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Archive for the ‘Female Genetics’ Category

What’s behind the abundance of twins born in the Sea to Sky? – Pique Newsmagazine

When my husband and I found out we were pregnant with twins, we were shocked. They didnt run in my family and we werent doing any fertility treatments that might have increased our chances of twins, but there they were, two little blobs on the ultrasound printout. A few scans later and we found out they shared a placenta, which about 70 per cent of identical twins do, known as monochorionic twins. We also learned they were identical twins, which dont typically run in families the same way fraternal twins do.

As my belly grew, and grew, and grew, the more I talked to friends, neighbours and complete strangers about my pregnancy and how Id got two-for-one baking in the oven. And thats when I heard it, the bit of local hearsay that inspired this article. What I heard went something like this: Youre having twins? Did you know that the Sea to Sky corridor has one of the highest rates of twins in North America along with a small potato-farming town in the States? If only one person had mentioned it to me, I would have likely forgotten about it, but I heard it over and over from different people. Then, last summer, I got into my friends truck with three other women to go for a bike ride and one of them commented how crazy it was that not only were all four of us mothers of twins, but we all live in the same neighbourhoodthree of us even on the same street! What were the odds?

When I started researching this article, I reached out to the Sea to Sky Multiples group on Facebook (yes, its a thing) and a lot of them had heard almost exactly the same hearsay I had. I was not alone (or crazy).

I have 20-month-old identical twins and I have been told this many times by random people at Strong Start (Sea to Sky Community Services program) and at the park. Sarah Ewing, identical twin girls, Squamish.

I have heard that. I actually blamed the carrots after hearing this because I was eating a lot of Pemby carrots when I got pregnantsame soil! Jasmine Robinson, fraternal twin boys, Whistler.

When I was pregnant with my twins, nearly 10 years ago, my OBGYN in North Van said something about a study, but I never asked for specifics. Anon, Squamish.

I actually have heard that, but I dont know where. Someone also once said there were studies done in the area or they were going to do studies on the high number of twins in the area. Im not sure how true it is though! Jen Bang, fraternal twin girls, Whistler.

So, does this hearsay have any truth to it? Do we have a high number of twins in the Sea to Sky? If so, why? Can potatoes actually play any role in it? As it turns out, these questions dont have simple answers.

Youre going to need to ask some detailed questions to really understand this, explained Dr. Marina Tourlakis, life sciences tutor in molecular genetics at Squamishs Quest University, in an email. Fraternal, or non-identical twins, can result from fertility treatment, which often induces the release of more than one egg during a womans menstrual cycle (super-ovulation). Fertility issues are prevalent in our society and hence increased twinning rates, if non-identical, might be explained by increased awareness of, and accessibility to, fertility treatments. Hence, Id wonder if the proposed high rates of twinning in Whistler are of identical or fraternal twins as these are two very different questions to ask.

If the average age of the mothers in Whistler is high, and we are talking about fraternal twins, then Id wonder if this is indeed linked to an increase in fertility treatment (since fertility drops precipitously with age). Given that fertility treatments are expensive and Whistler is typically associated with an affluent demographic, this too would make me wonder if this is the main factor at play.

Statistics Canada helped me compare the number of twins born in the Sea to Sky to the rest of Canada between 2000 and 2020. For 12 out of those 20 years, Squamish, Whistler and Pembertons combined twin percentage rate was higher than the Canadian average. For six straight years spanning 2012 to 2017, the corridor remained above the national average. Its worth noting, however, that the mean average of those years puts the twinning rate at 3.1 per cent, in line with the rest of Canada, while a median average puts us at 3.3 per cent, just over.

Statistics Canada does not collect information on whether twins are identical or fraternal, or if they were conceived using fertility treatments, but for 60 per cent of that 20-year period, weve had more twins than the national average, so the hearsay about the Sea to Sky having an above-average amount of twins could be somewhat true, although the reasons why are an educated guess without more robust data.

What Tourlakis was saying about fertility treatment being the major driver in increased fraternal twin rates is echoed in a comprehensive, global study led by Christiaan Monden, a professor of sociology and demography at Oxford University. The research shows that over 40 years, the twinning rate worldwide has increased by a third, which means that one in every 42 babies is now born a twin.

Our results show that twinning rates were recently peaking at a historical high, with rates of over 15 twin deliveries per 1,000 deliveries in many countries, including the USA, Canada, the European Union, Israel, South Korea, Taiwan, and almost all African countries, the study says.

The report goes on to say the reasons for the increase are driven by fertility treatments (responsible for two-thirds of the increase) in combination with households delaying childbearing, in other words, older mothers (responsible for one-third of the increase).

An international collaboration (2020) involving researchers at The University of Western Australia (UWA), DePauw University in Indiana and the London School of Hygiene and Tropical Medicine found that women are more likely to conceive fraternal twins once they reach their 30s as a result of an evolutionary response to combat declining embryo viability.

This research offers important insights into how our evolutionary past still influences our modern lives, with fraternal twinning rates increasing as women increasingly delay childbearing, said Associate Professor Joseph Tomkins, UWA School of Biological Sciences.

Note that this research refers to fraternal twins specifically, as the reason an egg randomly splits to create identical twins is still a mystery. However, new research into epigenetics might be the start of unravelling this biological enigma.

Epigenetics refers to the turning on and turning off of genes, explains Dr. Nancy L. Segal, a professor of psychology, director of the Twin Studies Center at California State University, Fullerton and author of seven books on twins, speaking on the podcast, Speaking of Psychology: What Studying Twins Can Teach Us About Ourselves. What environmental triggers are there before birth and sometime after birth, that will activate a gene or perhaps silence it. And this is where identical twins, who differ in fundamental ways, may be of greatest use to us in the medical sciences because we know that the similarity rate of identical twins with diabetes or multiple sclerosis is only 50 per cent, schizophrenia maybe 40 per cent, so, if they come out into the world with the same genes, why is it that one twin expresses it and the other one does not? This is information we can all use to assist individuals in the non-twin population.

A 2019 CBC article stated that B.C. has the highest number of older mothers in Canada, with the average age of first-time mothers being 31.6 compared to the national average of 29.2. It went on to say that in B.C., between 2000 and 2017, the number of mothers aged 35 to 39 increased by 60 per cent, and the number of mothers aged 40 to 44 doubled.

Statistics Canada helped me dig into the Sea to Sky numbers and in 2020, the average age of a mother in the corridor was 33.5, so above both the national average (31.3) and the B.C. average (32.1). Of the children born to mothers in the corridor, 78 per cent were born to mothers aged 30 to 39. In 2000, that figure was just 54 per cent. UBC professor Paul Kershaw, founder of research and advocacy group Generation Squeeze, is quoted in the CBC article saying the numbers didnt come as a surprise. This is the province where hard work pays off the least for younger people in their prime childbearing years, Kershaw said.

Kershaws research compared todays young adults to those of a generation ago and found that the full-time incomes of British Columbians have dropped the most in Canada during that time while housing prices have increased the most.

The nature of work, housing, and the propensity towards play in the Sea to Sky could be a factor in people deciding to wait longer to start a family. The result? More issues conceiving, possibly fewer kids, but also a slightly higher chance, biologically speaking, of these women producing twins. Interestingly, while older mothers might have issues getting pregnant, they are statistically more likely to have a successful multiple pregnancy if one does occur, said researchers at Columbia University Irving Medical Center in a 2017 study.

A U.S. study by the National Center for Health Statistics spanning from 1980 to 2009 showed that the national twin birth rate rose an incredible 76 per cent over that period, from 18.9 to 33.3 per 1,000 births. Increases were seen across all 50 states and by more than 100 per cent in five statesConnecticut, Hawaii, Massachusetts, New Jersey, and Rhode Island.

The report notes that Connecticut had the highest number of twin births at five per cent in 2009. More recent figures published by Statista in May 2021 also show Connecticut as the state with the highest twin birth rate from 2017-19.

While it is known for its stunning fall foliage, Yale University and being the home of ESPN, Connecticut is not exactly known for potatoes. So, the Sea to Skys connection to a small, potato farming town in the U.S.? Still possible, but again, without more data, its difficult to say for sure. (The U.S. CDC was unable to narrow down where this mythical potato town with the high twinning rate is located.) Seed potatoes have been farmed in Pemberton for more than a century, so wouldnt the numbers of twins stay consistently high or spike when we had bumper crops? What a woman eats and drinks have not been scientifically linked to the subsequent production of twins, although some people think it could be.

Anna Capria, a human genetics and genomic data analytics masters student, led me to an article on a small Nigerian town called Igbo-Ora. Nigeria has one of the largest populations of twins in the world and the highest dizygotic/fraternal twinning rate (45 per 1,000). A recent 2020 study delved into the local peoples beliefs as to why this might be, and mentioned a soup produced with okra leaves and a local delicacy made from cassava, a root vegetable.

Since the same foods are consumed in neighbouring communities that have lower rates of twinning, we conjecture that nutritional and other environmental factors may produce epigenetic modifications that influence high DZ twinning rates in Igbo-Ora community. We conclude that more directed scientific studies based on these findings are required to further elucidate the etiology of the high rate of DZ twinning in Igbo-Ora, the study says.

My post on the Sea to Sky Multiples group helped to unearth other twin-heavy places in Brazil and India. In an article about Kodinh, a small village in India that counts more than 400 sets of twins, it was interesting to read that some of the pervasive reasoning for multiple births, like more mature mothers and access to fertility treatments, are not a factor there. The doctor interviewed mentioned that he thinks its something in the food or water in the area, but again, theres no concrete evidence.

One long-held twin myth that has recently been busted is the notion that identical twins dont run in families. We thought that for a very long time, says Segal. And yet, some recent research from Sweden and Singapore looking at inbred populations has found that there are these pockets of people around the world in India and Iran, where there are multi-generations of identical twins. And so, we think that within some families that theres a tendency towards zygotic splitting.

In the podcast, Segal goes on to explain that the offspring of two pairs of identical twins would be first-cousins and full siblings, because each parent is genetically interchangeable, which is rarebut a trend thats not so rare is identical twins marrying unrelated people, and that their children would be genetic half-siblings. Mind-blowing.

Whats become clear over the course of digging into this hearsay is that there is a serious lack of comprehensive research on twins, part of a longer trend in academia that tends to skew towards a male perspective.

Female reproduction has a long tradition of being studied primarily from a male lens (because researchers and medical doctors were primarily male) and poorly at that (perhaps because the funding bodies deciding what research to fund were also primarily male), says Tourlakis. Recently there has been a surge in attention (perhaps due to an aging mother population, and perhaps also due to increased numbers of women in research positions) to reproductive studies, which is leading to all kinds of interesting new findings about fertility, so I imagine we will continue to have exciting new findings hitting our science news feeds in the coming years.

So, one day we might be able to debunk or uphold this strange bit of Sea to Sky hearsay, but for now, its still a bit of a mystery.

Being the mother of twins in the Sea to Sky area these days may seem commonplace, but it doesnt take away from how incredibly special it is to have them. Sarah Lindsay, identical twin boys, Squamish.

Writers Note: Thank you to Dr. Marina Tourlakis and Anna Capria for explaining genetics basics and to David Raffo for patiently helping me draw some answers from the data.

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What's behind the abundance of twins born in the Sea to Sky? - Pique Newsmagazine

Calendar of events, awards and opportunities – ASBMB Today

Every week, we update this list with new meetings, awards, scholarships and events to help you advance your career.If youd like us to feature something that youre offering to the bioscience community, email us with the subject line For calendar. ASBMB members offerings take priority, and we do not promote products/services. Learn how to advertise in ASBMB Today.

The International Union of Biochemistry and Molecular Biology is offering $500 to graduate students and postdocs displaced from their labs as a result of natural disaster, war or "other events beyond their control that interrupt their training." The money is for travel and settling in. Learn more and spread the word to those who could use assistance.

This conference, to be held in person in Athens, Ga., will address the multitude of roles that the O-GlcNAc protein modification has in regulating nuclear and cytosolic proteins. It will bring together researchers from diverse fields to share their research, tools and experience in O-GlcNAc biology. The abstract deadline is April 26, and the early registration deadline is May 9. Submit an abstract.Learn more in this Q&A with organizers Gerald Hart and Lance Wells.

The ASBMB Lipid Research Division features the work of young investigators at noon Eastern on Wednesdays. If you are interested in presenting, please contactJohn Burke. Registeronce to access the whole series.

The next seminar on April 27 will be aboutregulation of plasma membrane dynamics by PIP kinases. It will feature Nirmalya Bag of the Indian Institute of Technology and Federico Gulluni of the University of Turin in Italy.

The Sphingolipid Biology webinar seriescontinuesApril 27 with two talks on lysosomal storage diseases. Elsa Rodrigues ofUniversidade de Lisboa will give atalk titled "CYP46A1 as a therapeutic target in Niemann-Pick type C disorder," and Janet Deane of the Cambridge Institute for Medical Research will give a talktitled "Identifying new players in Krabbe disease: How galactosphingolipids alter membrane protein abundance." Register.

The National Institutes of Health will host speaker Joanna Fares of Emergence Therapeutics and Jenn Symonds of Spherix Consulting Group on April 27 for an 11 a.m. Eastern webinar on careers in scientific project management. Register.

Endpoints News is hosting a webinar titled "The R&D challenge: What are the best practices in drug development today?" Speakers/panelists include: Alise Reicin, president and chief executive officer of Tectonic Therapeutic; Arie Belldegrun, is executive chairman and co-founder of Allogene; Norbert Bischofberger, president and CEO of Kronos Bio; David Schenkein, a general partner at GV; and Abhay Kini, director of life sciences at Egnyte. Learn more.

DDN is hosing a seminar about interventions that target the bloodbrain barrier to facilitate drug delivery. It will feature Zhenpeng Qin of the Center for Advanced Pain Studies at the University of Texas at Dallas, Olaf van Tellingen of the Netherlands Cancer Institute, Costas Arvanitis, of the Georgia Institute of Technology and Emory University, and Graeme F. Woodworth of the Greenebaum Comprehensive Cancer Center at the University of Maryland. Learn more.

The ASBMB Annual Awards are given to outstanding professionals who have been recognized by their peers for contributions to their fields, education and diversity. In addition to a monetary award, recipients will give talks about their work at the 2023 annual meeting in Seattle.Know someone who deserves to be recognized for their work? Check out the available awards and submit your nomination today.

The American Neurological Association and the National Research Mentoring Network have teamed up for this lunchtime webinar about distance mentorship. Here's how they characterize it: "Distance mentorship allows mentormentee partners to continue to work together despite geography and continue to flourish virtually. Whether the mentorship is a long-distance one from the start or evolves to one over time, several best practices exist to succeed. This webinar is a roundtable discussion with mentors and mentees who will discuss the successes, challengesand tips that allowed their relationships to thrive." Register.

We were contacted by Caroline Mueller, assistant professor at Ohio University, about a survey for early-career medical educators. She wrote: "We hope that through this survey, we will identify the needs of early-career medical educators and develop appropriate resources for new faculty." Learn more and complete the survey by April 30.

The Genetics Society of America's DeLill Nasser Award for for Professional Development in Genetics "supports geneticists in their graduate or postdoctoral career stages by subsidizing participation in conferences and laboratory courses." The prize (up to $1,000) can be used for attending virtual or in-person events. Applicants must be members of GSA. Learn more.

The U.S. Department of Energy's Office of Science Graduate Student Research program is accepting applications until May 4. The program supports U.S. graduate students seeking to conduct part of their thesis research at a DOE national lab or host site with a DOE scientist. The program is open to Ph.D. students who are conducting their thesis research in targeted areas of importance to the DOE Office of Science. Learn more.

The 2020 documentary Coded Bias explores biases embedded into technology. These biases affect the behaviors, outputs and consequences of countless devices, tools and digital spaces and often lead to or perpetuate inequity. Self-driving cars, facial recognition software, motion-activated appliances, job applicant screens and algorithms used for medical decision making theyre only as good as the code that defines their functions. The film describes in chilling fashion numerous prejudicial and even dangerous outcomes caused by biases hard-wired into data-centric technologies, and it makes the case for systemic changes needed to safeguard users and hold the tech industry accountable. Interested? The ASBMB Women in Biochemistry and Molecular Biology Committee is hosting a screening and virtual panel discussion at 4 p.m. EDT on May 4. Committee member Meghna Gupta will moderate, and Jeff Kapler and Marina Holz will be panelists. The link to access the film will be sent to all registered attendees two weeks prior to the event. (The film also can be streamed on Netflix.) Register.

This in-person meetingin Kansas City, Mo., will showcasethe most recent insights into the cis-regulatory code, how cis-regulatory information is read out by transcription factors, signaling pathways and other proteins, how cellular diversity is created during development and how we can study this problem using cutting-edge genomics technology and computational methods.The meeting will simultaneously examine the problem from an evolutionary perspective: how cis-regulatory elements evolve, how regulatory variation affects gene expression and phenotypes, how these changes have shaped development and parallel evolution, and how noise affects regulatory circuits and their evolution. The abstract deadline for those who'd like to be considered for talks is May 6. The abstract deadline for poster presenters and the registration deadline is May 25.Submit an abstract.Learn more in this Q&A with two of the organizers.

The National Institutes of Health Office of Research on Womens Healthhas issued a request for information "on research gaps, clinical practice needs, and research opportunities to inform research priority setting at the intersection of the COVID-19 pandemic and/or long COVID and the health of women." Read the RFI.

The National Institutes of Health Office of Research on Womens Health is hosting its annual Vivian W. Pinn Symposium on May 12 to markNational Women's Health Week. The event will focus on the impacts of the COVID-19 pandemic on the careers of women in science. Learn more.

This five-day conference will be held Aug. 1418 in person in Cambridge, Massachusetts, and online. It will be an international forum for discussion of the remarkable advances in cell and human protein biology revealed by ever-more-innovative and powerful mass spectrometric technologies. The conference will juxtapose sessions about methodological advances with sessions about the roles those advances play in solving problems and seizing opportunities to understand the composition, dynamics and function of cellular machinery in numerous biological contexts. In addition to celebrating these successes, we also intend to articulate urgent, unmet needs and unsolved problems that will drive the field in the future. Registration and abstract submission begins Nov. 1. Abstracts are due May 16. Learn more.

The Protein Society is hosting a virtual workshop on emerging approaches in membrane protein design. It'll include presentations by Joanna Slusky of the University of Kansas, Anastassia Andreevna Vorobieva of the VIB-VUB Center for Structural Biology, Sarel Fleishman of the Weizmann Institute of Science, and Patrick Barth of EPFL, who is also the event organizer. Register.

For the Versatile PhD's webinar series, career coach Tina Li will provide advice on launching and building your brand online and offline. Learn about the series.

The Marion B. Sewer Distinguished Scholarship for Undergraduates offers financial support to students who demonstrate an interest in the fields of biochemistry and molecular biology and enhance the diversity of science. Students whose social, educational or economic background adds to the diversity of the biomedical workforce or who show commitment to enhancing academic success of underrepresented students are eligible. The scholarship provides up to $2,000 toward undergraduate tuition costs for one academic year and can be applied to fall or spring tuition of the year following scholarship award notification. Up to ten scholarships will be awarded each academic year. Applications by individuals from underrepresented groups are encouraged, although all qualified applicants will be considered without regard to race, gender, color, ethnicity or national origin. Apply.

The Oklahoma Cobre in Structural Biology at the University of Oklahoma is hosting its 10th annual structural biology symposium on June 16. Confirmed speakers include Hao Wu of Harvard University, Breann Brown of Vanderbilt University School of Medicine, Lorena Saelices of University of Texas Southwestern Medical Center, Satish Nair of the University of Illinois Urbana-Champaign and Erica Ollman Saphire of the La Jolla Institute for Immunology. Check here for details and to register.

The Journal of Science Policy & Governance, the United Nations Educational, Scientific and Cultural Organization and the Major Group for Children and Youth announced in February a call for papers for a special issue on "open science policies as an accelerator for achieving the sustainable development goals." The deadline for submissions is July 10. To help authors prepare their submissions, the group will be hosting a series of webinars (April 8 & 29, May 20, and June 10) and a science policy paper-writing workshop (March 2627). Read the call for submissions and learn more about the events.

Head to beautiful Denver, Colorado, for a summer experience as a PRIDE (Programs to Increase Diversity Among Individuals Engaged in Health-Related Research) scholar. PRIDE is an initiative of the National Heart, Lung and Blood Institute that trains junior faculty from underrepresented backgrounds and/or with disabilities to advance their scientific careers and make them more competitive for external research funding. The University of Colorado PRIDE (led by Sonia C. Flores, who also leads the ASBMB Minority Affairs Committee) is one of nine national PRIDE sites. Its focus is on the "impact of ancestry and gender on omics of lung and cardiovascular diseases" (which is why it's called PRIDEAGOLD). The program consists of two consecutive summer institutes (two and one week, respectively) that offer comprehensive formal instruction on multi-omics, data sciences and bioinformatics, with an emphasis on interpretations based on ancestry and/or gender; career development and grant-writing tools; pairing with expert mentors; and pilot funds to develop a small research project. Learn more.

This in-person meeting will be held Sept. 29 through Oct. 2 in Snowbird, Utah. Sessionswill cover recent advances and new technologies in RNA polymerase II regulation, including the contributions of non-coding RNAs, enhancers and promoters, chromatin structure and post-translational modifications, molecular condensates, and other factors that regulate gene expression. Patrick Cramer of the Max Planck Institute will present the keynote address on the structure and function of transcription regulatory complexes. The deadline for oral presentation abstracts is July 14. The deadline for poster presentation abstracts is Aug. 18.Learn more.

Most meetings on epigenetics and chromatin focus on transcription, while most meetings on genome integrity include little attention to epigenetics and chromatin. This conference in Seattle will bridge this gap to link researchers who are interested in epigenetic regulations and chromatin with those who are interested in genome integrity. The oral and poster abstract deadline and early registration deadline is Aug. 2. The regular registration deadline is Aug. 29.Learn more..

The ASBMB provides members with a virtual platform to share scientific research and accomplishments and to discuss emerging topics and technologies with the BMB community.

The ASBMB will manage the technical aspects, market the event to tens of thousands of contacts and present the digital event live to a remote audience. Additional tools such as polling, Q&A, breakout rooms and post event Twitter chats may be used to facilitate maximum engagement.

Seminars are typically one to two hours long. A workshop or conference might be longer and even span several days.

Prospective organizers may submit proposals at any time. Decisions are usually made within four to sixweeks.

Propose an event.

If you are a graduate student, postdoc or early-career investigator interested in hosting a #LipidTakeover, fill out this application. You can spend a day tweeting from the Journal of Lipid Research's account (@JLipidRes) about your favorite lipids and your work.

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Calendar of events, awards and opportunities - ASBMB Today

4 Tips to Include Bovine In Vitro Fertilization into Breeding Season – Drovers Magazine

Well-worn variations of the saying, busier than a, realistically capture how cow/calf producers feel during day-to-day management of their female herd. Consideration of how and whether or not bovine in vitro fertilization (IVF) will fit and bring success to their cattle breeding plans is often dismissed as impossible for numerous reasons.

Operations strive for accelerated genetic progress, but advancement is often hampered by rigid timelines of conventional embryo flushing or limitations of follicle stimulating hormone (FSH) deliveries.

Bruno Sanches, Vytelles VP of Operations, believes plans no longer need to follow this outdated pattern.

At Vytelle, our process is very attractive and accessible for all operations, he says. With our hormone free bovine in vitro fertilization program, any customer can access our cutting-edge technology simply by bringing their selected female donor to one of our satellite locations. She doesnt need any preparation or labor associated pre-oocyte collection. Its the most accessible, reliable and predictable way of using IVF.

Producers can research the best fit for their donor needs and access hormone-free IVF services at several locations scattered throughout the country. Without a hormone treatment protocol, oocyte collections can be performed from the same donor on a weekly basis allowing those with limited numbers time to build a well-stocked frozen embryo bank before breeding season.

The speed of genetic progress by quickly multiplying offspring from elite performing animals and shortening generation intervals through reproductive efficiency can be improved exponentially using four basic IVF tips.

Ensure Nutrition Management of Donors and Recipients

First, for producers to ensure the highest success rates to accelerate their herd, Sanches explains nutrition and management are key as they directly impact the oocyte quality and collection capabilities of donors and effectively support embryo transfers (ET) in recipients.

If we dont have a good egg, we cant make the quality embryos a customer expects, he said. Using accurate nutrition practices meeting energy, crude protein, mineral and vitamin requirements is critical for consistent follicular growth and oocyte quality.

He urges producers to begin stabilizing their donors nutrition levels early, at least 60 to 90 days prior to breeding season as correcting deficiencies and building oocyte quality and embryo development takes time.

Likewise, recipients must also be suitably maintained to create a successful embryo transfer.

He suggests working with a nutritionist to assess condition and develop proper rations supportive of lactation requirements and post-calving needs, preferably at least 30 days prior to ET for strong synchronization responses and pregnancy success.

They need to be in good shape to receive an embryo and carry through a productive pregnancy. At times, people mistakenly assume recipients arent as important and cut corners with nutrition. Then, we transfer an expensive embryo into them, and they lose money.

Optimize Collection Time Based off Breeding

Many producers believe IVF is limiting and difficult to keep on the right track, but Sanches explains hormone-free IVF expands rather than limits options.

Donor choice is extensive, ranging from prepubertal, as young as 6 months of age, to 15 days post-calving, plus pregnant females within the first 100 days of gestation. Additionally, without the need for FSH injections, producers can select donors and allow them to remain in their natural environment until the day of collection.

Sanches adds with such a wide range of availability, producers can focus on collecting from their elite donors, while ensuring their reproduction goals, by storing frozen embryos pre-breeding-season to meet their expanded needs. During breeding season, the producer can continue to collect from their donors and transfer fresh embryos into recipients and supplement with frozen embryos from their tank.

If we wait to collect embryos, transfers will be spread across an entire cattle breeding season. Many breeders prefer to start with all embryos transferred in the first few weeks. Then, recipients are released for natural service. I strongly suggest developing an embryo bank before breeding season so theres plenty to come out of the gate in good shape.

For those wanting to breed their donors, he recommends harvesting oocytes during the last collection, but leaving the most dominant follicles in the ovaries.

We know this egg will be ovulated, and she will breed successfully after a last collection. Its a natural process.

As producers realize they dont need to utilize IVF only on their problem or nonresponding cows; today, its become the first choice for their best animals. They can replicate the right genetics faster with hormone-free IVF rather than conventional flushing.

Capitalize on Post Breeding Opportunities

Sanches outlines oocyte collection doesnt need to end once a donor becomes pregnant.

Its an exciting aspect that we may begin using IVF again approximately 15 days after calving, 40 days post breeding and after a pregnancy confirmation, he said. Herd genetics are accelerated while keeping donors on track naturally, right up to 100 days of pregnancy. After confirmation, we can collect up to four more times before the fetus and the uterus drop out of reach.

He believes keeping donors on a regular schedule is important but admits everything is flexible and heavily dependent on a customers needs and numbers. He recommends collection every other week but the logistics of both donors and recipients need to be evaluated.

Planning ahead before cattle breeding season and having the donors on a schedule matching all the involved logistics is critical, he stressed. Know which satellite location will be used, where the embryos will be made and where the recipients are located. Donors and recipients might be in different states. We work with clients to understand their needs, explain our platform and help them be successful.

Pregnancy Checking and Live Calf Data

Once plans are in motion and oocytes have been collected, the fertilization process will take place in a laboratory. After eight days, viable embryos will be available for producers, fresh or frozen, depending on the producers request.

Producers can synchronize their receiving females to maximize the transfers possible in one day. Transfer services are commonly utilized; typically, IVF companies can provide or recommend a trusted partner.

Most US beef operations complete embryo placements early in the breeding season and follow up with natural service bulls. Sanches stresses its vital they work with their veterinarian to complete a pregnancy check.

If we dont confirm a pregnancy from an embryo or a bull, we cant track the due date, he said. The timing difference and due date will be around 15 to 25 days. If its not tracked, we may have calves overdue which can become a problem during the calving season. Ideally, we like to check at 45 and again at 90 days, but I encourage at least one check for reliable data to be gathered.

To optimize results with IVF embryos and help ensure the success of resulting calves, accurate record keeping should include pregnancy confirmation, gestation length, calf sex, birth weight and subsequent health status information.

Its a powerful technology but many people still have the misconception bovine in vitro fertilization is very expensive making it out of reach to progress their entire herds genetics, Sanches said. Some believe its time consuming, labor intensive and requires extensive preparation protocols. Its really a natural process with zero donor preparation. Plus, lastly, our customers love that they only pay for viable embryos. It changes the game for how breeders can use the technology.

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4 Tips to Include Bovine In Vitro Fertilization into Breeding Season - Drovers Magazine

Veterinary Artificial Insemination Market to Reach USD 8.42 Billion by 2030; Increasing Government Initiatives, Technological Advancements, and…

Brainy Insights Pvt. Ltd.

Asia-Pacific is the greatest contributor in terms of veterinary artificial insemination market revenue due to rising demand for dairy and animal-based protein and government performance.

Pune, April 11, 2022 (GLOBE NEWSWIRE) -- As per the report published by The Brainy Insights, the global veterinary artificial insemination market is expected to grow from USD 4.74 billion in 2021 to USD 8.42 billion by 2030, at a CAGR of 6.6% during the forecast period 2022-2030.

The main advantage of artificial insemination is that it reduces the danger of disease transmission involved with animal reproduction. The need for high cow efficiency and milk composition is expected to rise due to artificial insemination. To address the ever-increasing demand, industry participants are employing synthetic insemination processes to generate high-quality cattle breeds and boost productivity. This factor is expected to grow the global veterinary artificial insemination market during the forecast period. Global population growth, urbanization, and an increase in the average population's purchasing power are all expected to enhance the production of high-quality dairy and allied goods. In the following years, the global veterinary artificial insemination market is likely to be driven by an increase in demand for high-quality dairy products.

Get a sample of the report from: https://www.thebrainyinsights.com/enquiry/sample-request/12681

The growing worldwide population and expanding need for animal-based protein drive the demand for artificial insemination in household farmed animals. Improving veterinarian services and increased animal healthcare costs are also urging market expansion. Moreover, the main businesses are forming strategic alliances to increase their range of animal genetics and boost their position in other sectors. The procedure of achieving conception withoutsperm or sperm in the female uterus is known as artificial insemination. Cattle are bred with freshly, uncooked, or cold straw of semen. Insemination is a method of obtaining pregnancy in animals using in vitro fertilization. It is also utilized in assisted reproduction and contraceptive innovations to allow animals to reproduce in heat. Veterinary artificial insemination is an excellent technological tool for enhancing animal heredity and production.

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Key players operating in the global veterinary artificial insemination market are:

Genus CRV URUS Group LP Viking Genetics SEMEX Swine Genetics International STgenetic Select Sires Inc. Stallion AI Services Ltd Shipley Swine Genetics

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To enhance their market position in the global veterinary artificial insemination market, the key players are now focusing on adopting the strategies such as product innovations, mergers & acquisitions, recent developments, joint ventures, collaborations, and partnerships.

For example, Genus plc, a leading animal genetics firm, collaborated with Beijing Capital Agribusiness Co. Ltd, a prominent Chinese animal protein breeding firm, to investigate and produce virus-resistant procedures in pigs. For example, Elanco Animal Health established cooperation with Ducks Unlimited in April 2021 to promote sustainable development and agriculture - especially beef cattle development across North America. To fulfill the increased demand, LIC, an agritech co-operative established in New Zealand, will open a sexed sperm lab in the nation in September 2021.

In 2021, the swine type dominated the market with a market share of 22.12%.

The animal type segment is divided into cattle, equine, sheep, swine, canine, and others. In 2021, the swine type dominated the market with a market share of 22.12% and market revenue of 1.04 billion. The expanding output of organic pig meat due to increased animal welfare awareness will offer momentum to the industry. The rising demand for high-quality hog meat has compelled producers to expand their production facilities, which will benefit the market. Customers' increasing use of pig meat in various forms like ham, ham, steaks will allow the industry to expand quickly. The increasing popularity of pork in Western European countries will increase swine commerce and production in the near future.

In 2021, normal semen accounted for the largest share of the market, with 56.7%.

The product segment is divided into sexed semen and normal semen. In 2021, normal semen accounted for the largest share of the market, with 56.7% and market revenue of 2.68 billion. This growth is due to the low cost of normal sperm and the firm conception and low death rates.

The veterinary clinics accounted for the largest share of the market, with 37.3% for veterinary artificial insemination in 2021.

The end-user segment is divided into veterinary clinics, veterinary hospitals, others. The veterinary clinics accounted for the largest share of the market, with 37.3% and market revenue of 1.76 billion for veterinary artificial insemination in 2021. Clinics often provide wellness checks concentrating on preventative treatment and routine checkups for pets.While they can undertake spaying and neutering operations, they will need to send out more complicated cases to a better-equipped institution. They will have treatments and medicines, but they may not be as well-stocked as a vet clinic.

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Regional Segment Analysis of the Veterinary Artificial Insemination Market

North America (U.S., Canada, Mexico) Europe (Germany, France, U.K., Italy, Spain, Rest of Europe) Asia-Pacific (China, Japan, India, Rest of APAC) South America (Brazil and Rest of South America) The Middle East and Africa (UAE, South Africa, Rest of MEA)

Among all regions, the Asia Pacific region emerged as the largest market for the global veterinary artificial insemination market, with a market share of around 38.14% and 1.08 billion of the market revenue in 2021. Due to several significant players in this region, Asia-Pacific is the greatest contributor in terms of market revenue. This is due to rising demand for dairy and animal-based protein and government performance, which is driving market expansion in this area.

About the report:

The global veterinary artificial insemination market is analyzed based on value (USD Billion). All the segments have been analyzed on a worldwide, regional, and country basis. The study includes the analysis of more than 30 countries for each piece. The report offers an in-depth analysis of driving factors, opportunities, restraints, and challenges for gaining critical insight into the market. The study includes porter's five forces model, attractiveness analysis, raw material analysis, supply, demand analysis, competitor position grid analysis, distribution, and marketing channels analysis.

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Veterinary Artificial Insemination Market to Reach USD 8.42 Billion by 2030; Increasing Government Initiatives, Technological Advancements, and...

Minnesota family confirmed as tallest in the world – Guinness World Records

A family in Esko, Minnesota, USA, has achieved a record that not many can measure up to - quite literally!

Meet the Trapp family of five; Scott, Krissy, Savanna, Molly, and Adam.

On 6 December 2020, the Trapps were confirmed as the tallest family in the world with an average height of 203.29 cm (6 ft 8.03 in).

The family's combined height is equal to the length of half a tennis court!

The youngest (but certainly not the smallest) member of the family is 22-year-old Adam Trapp, who towers over his siblings and parents at an astounding 221.71 cm (7 ft 3 in) tall.

Savanna Trapp-Blanchfield, 27, is next, measuring in at203.6 cm (6 ft 8 in). Last is their sister Molly Steede, 24, standing at 197.26 cm (6 ft 6 in) tall.

Unsurprisingly, all three Trapp kids played sports throughout their lives and were recruited by colleges for either basketball or volleyball.

"Coaches always said to us 'you can't teach height. Youre either tall or youre not,'" said Molly.

Although they have many tall extended family members, its clear that the Trapp kids followed in their parents' (very large) footsteps.

Krissy, their mom, comes in as the shortest among the Trapp family at 191.2 cm (6 ft 3 in), while the father, Scott, is a towering 202.7 cm (6 ft 8 in).

"I love saying that Im the shortest person in the worlds tallest family." Krissy Trapp

Measuring up to such a record-breaking achievement was a tall task. Savanna credits her "super tall, little brother," Adam, for inspiring her to reach out to Guinness World Records.

In December 2020, the family went to Dr. Anna Sudoh, an orthopaedics doctor at Essentia Health, to be measured.

Each family member had to be measured three times throughout the day, both standing up and lying down. This average of these measurements is used to calculate their height.

After meeting all the criteria to qualify for a place in the record books, the Trapps were thrilled to learn they had become the new title holders.

"My sister called the family up to tell us that we officially got the record. Everyone was excited about it, and it was almost hard to believe, said Adam.

The family feels that the worldwide recognition theyve received makes up for the downside of being so tall.

"Our friends and family are so proud of us and like to use us for bragging rights, saying they know a world record holder," said Savanna.

Qualifying to be recognized as the tallest family certainly came along with some growing pains, both literally and figuratively.

"I have always been tall but had a growth spurt where I grew an inch and a half in one month." Savanna Trapp-Blanchfield

"The growing pains were unreal. I have stretch marks on the back of my legs, Savanna continued.

The Trapps each realized they were unusually tall early on, constantly standing out among their peers.

When I was in the first grade, I was taller than my teacher, said Scott.

But whats it like to look down at everyone you meet?

It's a dilemma this super-tall family understands all too well. The Trapps have grown used to the frequent comments and stares they get in public.

Being taller than nearly everyone they meet, except for the occasional basketball player, means the family attracts attention everywhere they go.

They have learned to embrace their genetics and use their height as a way of engaging in conversations and educating others.

"Being able to meet new people when they come up and ask me questions about my height is something I like the most," said Adam.

The Trapps also encounter trying situations that most average-sized individuals dont even have to think about.

"If I stand up too fast, Ill faint and its a long way to fall," Savanna joked.

Besides having to duck to get through doorways, frustrating shopping experiences and difficulties driving a car because of their long legs, the Trapps agree that their spectacular size brings far more ups than downs.

"My height is useful for household projects. I dont ever need a ladder." Scott Trapp

Aside from their incredible accomplishment, the Trapps are just the same as any other family.

"I still put on my pants one leg at a time like most people. They're just really long pants," said Adam.

The family loves being able to share their most unique characteristic, which they feel has made them a strong family unit.

Since they can each relate to the trials and tribulations that come along with their stature, the Trapps often lean on each other for support.

"Its nice to have a shoulder thats tall enough for you to lean on. Who better to understand what youre going through than the people who are even taller than you are?" Molly Steede

The Trapp family hopes to continue using their height to their advantage.

While Savanna dreams of eventually pursuing acting, modelling, or breaking the record for the largest hands on a living person (female), Molly is looking forward to one day starting her very own tall family.

The Trapps hope that their record-breaking tallness will empower others who are unique or feel different.

They want the world to know that any one attribute shouldnt define you and encourage people to judge others by who they are deep down inside rather than what they look like.

"There is joy and freedom in embracing who you are," said Savanna.

"Rock what you got. There is nobody else like you and that is fantastic."

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Minnesota family confirmed as tallest in the world - Guinness World Records

The upregulation of circFNDC3B aggravates the recurrence after endoscopic submucosal dissection (ESD) in early gastric cancer (EGC) patients |…

Patient recruitment

In this study, a total of 96 EGC patients (TNM classification: T1A) who were subjected to ESD treatment were recruited and their expression of circFNDC3B was measured for grouping. Subsequently, the median circFNDC3B expression was calculated and utilized as the indicator to divide the patients into a Low expression group (N=48, including all EGC patients whose expression level of circFNDC3B was at or above the median expression of circFNDC3B) and a High expression group (N=48, including all EGC patients whose expression level of circFNDC3B was below the median expression of circFNDC3B). Therefore, for further analysis, since the patients were grouped according to their median, there are same number of patients in each group. The demographic and clinic parameters of both patient groups, including their sex, age, BMI, status of H. pylori infection, history of alcohol abuse and smoking, tumor site, as well as clinical grade of ESD was collected by reviewing their medical records, carrying out breath test for H. pylori infection, serological examinations, as well as bacterial culture, and the demographic and clinic parameters of the two patient groups were compared using Students test. In this study, ESD was defined as a type of adenocarcinoma constrained to the mucosa tissues or submucosa tissues in the stomach. All subjects with a past ESD history or those who received treatment for multiple ESD were not enrolled. An endoscopic forceps biopsy operation was carried out in each patient to collect ESD tissue samples for subsequent Western blot, qPCR and IHC assays. ESD follow-ups were carried out 2, 3, 6, 9, 12, 24, as well as 36months after the initial ESD operation. The level of gastric atrophy was assessed using histological evaluation results based on the endoscopic atrophy border scale developed previously (Kimura et al. 1969; Ito et al. 1996; Satoh et al. 1996). Institutional ethical committee of Chinese PLA NO.254 Hospital has approved the protocol of this study. All methods were performed in accordance with the last vision of the Declaration of Helsinki. Written informed consent was obtained from all patients before the study.

In this study, MKN28 cells, a extensively-studied gastric tubular adenocarcinoma cell line which were established from a 70-year-old female patient, were used to carry out cellular experiments. In brief, MKN28 cells were acquired from American Type Culture Collection (ATCC, Manassas, VA) and cultured according to the recommended conditions provided by the manufacturer, i.e., the cells were cultured in a Roswell Park Memorial Institute 1640 (RPMI 1640) medium (Gibco, Thermo Fisher Scientific, Waltham, MA) supplemented along with 10% of fetal bovine serum as well as 1% of penicillin and 100 U/ml of streptomycin. The culture conditions were 37C, 5% CO2 and saturated humidity. Furthermore, all cells were regularly examined to affirm the absence of Mycoplasma. When the cells reached 70% confluence, they were sub-cultured and divided into different groups. In cell model I, the MKN28 cells were divided into 2 groups, i.e., 1. pGL group (MKN28 cells transfected with an empty plasmid); and 2.pGL-FNDC3B group (MKN28 cells transfected with a pGL3 plasmid inserted with the circFNDC3B fragment). In cell model II, the MKN28 cells were also divided into 2 groups, i.e., 1. NC siRNA group (MKN28 cells transfected with a scramble negative control NC siRNA); and 2.pGL-FNDC3B group (MKN28 cells transfected with circFNDC3B siRNA to silence the expression of circFNDC3B). In cell model III, we utilized the MKN28 cells to establish a H. pylori-infected gastric cancer cell model in comparison with un-infected cell model. The MKN28 cell were established as 2 groups, i.e., 1. Control group (MKN28 cells in unprocessed medium); and 2. rTip- group (MKN28 cells cultured in medium containing 12.5g/mL rTip-).

According to protocols provided by a previous publication22, to obtain rTip-, we transfected Tip- into Escherichia coli for subsequent amplification. And the amplified rTip- was purified for subsequent cell model establishment. All transfections were carried out using Lipofectamine 2000 (Invitrogen, Carlsbad, CA) according to the recommended transfection conditions provided by the manufacturer, and the transfected cells were harvested 48h after the start of transfection to analyze the expression of target genes.

The harvested cell as well as tissue samples were treated by utilizing a miRCURY RNA Isolation Kit (Exiqon, Qiagen, Germantown, MD) according to the recommended assay methods provided by the assay kit manufacturer to isolated cellular RNA. Then, the isolated RNA was assayed on an Agilent 2100 Bioanalyzer (Agilent Technologies, Mountain View, CA) in conjunction with an RNA 6000 Pico assay kit (Agilent Technologies, Mountain View, CA) according to the recommended assay methods provided by the assay kit manufacturer to quantify the RNA concentration. In the next step, 1g of isolated total RNA was converted into cDNA by making use of a QuantiTect Reverse Transcription assay kit (Qiagen, Germantown, MD) according to the recommended assay methods provided by the assay kit manufacturer. Finally, real time quantitative polymerase chain reaction (RT-qPCR) was performed on a BX-384 real time PCR apparatus (Bio-Rad laboratories, Hercules, CA) by making use of a QuantiTect SYBR Green PCR assay kit (Qiagen, Germantown, MD) according to the recommended assay methods provided by the assay kit manufacturer to evaluate the relative expression of circFNDC2B, miR-942, miR-510, CD44 mRNA as well as CDH1 mRNA in each sample using the 2Ct approach. The expression of GAPDH in each sample was used as the internal control.

We utilized online bioinformatic tools including TargetScan (http://www.targetscan.org/vert_80/) and miRDB (http://mirdb.org/) to compare the sequences of circFNDC2B, miR-942, miR-510, CD44 mRNA and CDH1 mRNA. Accordingly, we detected a putative binding site of miR-942 on circFNDC3B, while a putative binding site of miR-942 was detected on the 3UTR of CD44 mRNA. Similarly, we detected a putative binding site of miR-510 on circFNDC3B, while a putative binding site of miR-510 was detected on the 3UTR of CDH1 mRNA. In the next step, we performed luciferase assays in MKN28 cells to confirm the regulatory relationship of circFNDC2B/miR-942, circFNDC2B/miR-510, miR-942/CD44 mRNA, and miR-510/CDH1 mRNA. In brief, the wild type sequences of circFNDC2B, CD44 mRNA, and CDH1 mRNA containing the corresponding miRNA binding sites were cloned into pGL plasmid vectors to generate wild type plasmids of circFNDC2B, CD44 mRNA, and CDH1 mRNA. At the same time, the sequences of circFNDC2B, CD44 mRNA, and CDH1 mRNA containing the corresponding miRNA binding sites were subject to site-directed mutagenesis to generate mutant type sequences of circFNDC2B, CD44 mRNA, and CDH1 mRNA containing the corresponding miRNA binding sites, which were also cloned into pGL plasmid vectors to generate mutant type plasmids of circFNDC2B, CD44 mRNA, and CDH1 mRNA. In the next step, MKN28 cells were co-transfected with the plasmids carrying wild type or mutant type circFNDC2B, CD44 mRNA, and CDH1 mRNA along with miR-510 and miR-942. At 48h post transfection, the luciferase activity of transfected cells was assayed by utilizing a GloMax Multi Detection assay kit (Promega, Madison, WI) according to the recommended assay methods provided by the assay kit manufacturer.

The recurrence-free rate of the patients was analyzed by using R statistical software (version 3.0). The recurrence-free rate in each group was calculated at various follow-up time points, and the recurrence-free rates of the two groups were compared at the level of statistical significance of 0.05. The KaplanMeier survival curves were generated for high and low groups of circFNDC3B expression.

Cells as well as tissue samples were first lysed in a phosphatase- and protease-inhibitor containing 1X RIPA buffer (Thermo Fisher Scientific, Waltham, MA) according to the recommended assay methods provided by the assay kit manufacturer. The collected lysates were then centrifuged to collect proteins in the supernatant, whose concentration of total proteins was examined by using a BCA protein assay kit (Pierce, Thermo Fisher Scientific, Waltham, MA) according to the recommended assay methods provided by the assay kit manufacturer. In the next step, the protein in each sample was resolved by 10% SDS-PAGE and blotted onto nitrocellulose membranes (Hybond, GE Medical Care, Pittsburgh, PA), which was blocked with TBSS containing 5% of skim milk and subsequently incubated with primary anti-CD44 and anti-CDH1 antibodies as well as HRP-conjugated secondary antibodies in sequence according to the recommended antibody incubation conditions provided by the assay kit manufacturer (Abcam, Cambridge, CA). Finally, after the protein blots (all original protein blots are shown in Supplementary file) were developed by using an enhanced chemiluminescence Western blot substrate (Pierce, Rockford, IL) according to the recommended assay methods provided by the assay kit manufacturer, the relative protein expression of CD44 and CDH1 in each sample was calculated.

Collected tissue samples were paraffin embedded, sliced into 4 um sections, deparaffinized, gradient alcohol hydrated, and incubated with primary anti-CD44 antibodies and biotin-labeled secondary antibodies in sequence according to the recommended antibody incubation conditions provided by the assay kit manufacturer (Abcam, Cambridge, CA) to determine the positive protein expression of CD44 in each sample under a Zeiss Axioskop microscope.

Unless otherwise specified, all results are presented as meanS.E.M of 4 independent tests. Statistical evaluations were done by making use of the Student's t test in SPSS 21.0 software (IBM, Chicago, IL) and Prism 8.0 program (GraphPad, San Diego, CA), and P<0.05 was deemed as statistically significant.

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The upregulation of circFNDC3B aggravates the recurrence after endoscopic submucosal dissection (ESD) in early gastric cancer (EGC) patients |...

Is ‘Boba Fett’ a Clone? – We Got This Covered

One of the most popular characters in the Star Wars universe, Boba Fett was introduced theatrically in Star Wars: Episode V Empire Strikes Back. Not much was known about the masked character after the film was released, with fans becoming attached to the mysterious nature of the bounty hunter, and his glorious Mandarloian armor. The character has been a fan favorite throughout the years, but some fans waver on the characters popularity. Recently the character starred in his own Disney + series, The Book of Boba Fett which was met with mixed reviews.

It wouldnt be until Star Wars: Episode II Attack of the Clones that Star Wars fans would learn the truth about Boba Fetts origin with the controversial decision to make him a clone. Star Wars fans were outraged upon learning that Boba Fett had really been a clone the entire time, someone with the same origin as the stormtroopers who couldnt shoot straight, claiming that the origin ruined the character. But was Boba Fett really a clone like those who fought in the clone wars?

In Star Wars: Episode II Attack of the Clones, Obi-Wan Kenobi uncovered a secret, that a Jedi named Sifo-Dyas had employed a cloning facility on Planet Kamino, to create a clone army for the Republic. Kenobi was under the impression that Sifo-Dyas had been dead for years prior, and it was discovered later that he was killed by Count Dooku, so seemingly Darth Sidious had ordered the clone army. It was later revealed that all of these clones were made from a single specimen, a Mandalorian bounty hunter named Jango Fett.

The cloning facility had compensated Jango Fett quite well, paying him twenty million credits but he also requested one clone for himself, Boba Fett, in addition to his payment. The ordinary clones would be aged up to adulthood and also had their behavior modified which made them better soldiers by making them easier to control. Boba Fett, however, was not aged up and was only a child when Obi-Wan Kenobi met Jango Fett.

Boba Fett was a child when Jango was killed in the Battle of Geonosis by Mace Windu, so Jango had some time to teach the character his bounty hunting ways before he died. Because Jango requested that Boba be untampered with, Jango had made him entirely unique compared to any other clone made. Lets take a look at the few different types of clones we have seen throughout Star Wars and how Boba Fett differs from them.

As mentioned previously, all the Clone Troopers were conditioned to be soldiers and were easier to control. In addition to that, Boba Fett was not changed when Order 66 was launched. A large majority of the clones had a chip implanted in their head which, when activated by launching Order 66, the clones would suddenly turn on the Jedi, which they did in Star Wars: Episode III The Revenge of the Sith when Darth Sidious launched the order, which resulted in the Jedi Purge. Boba Fett did not have the chip implanted in him because of Jangos wish to raise him by himself, unaltered by the Kaminoans. Because he was unaltered, Boba Fett also aged naturally and would be older than the original Clone Troopers.

This first batch of clones were trained to be soldiers, whereas Boba Fett had to learn to be as good as Jango, even though he still had the same genetics. Boba was also more determined than the Clone Troopers throughout The Clone Wars as shown in Star Wars: The Clone Wars, as Boba Fett started his journey fueled by revenge. Boba attempted to assassinate Mace Windu for killing Jango Fett. He also ended up in prison and encountered many criminals which he would have learned from, such as Cad Bane and Asajj Ventress. The Clone Troopers rarely learned from one another, taking orders from the Jedi at first, then taking their orders from the Empire after Order 66. The Clone Troopers were also seen by some Jedi and the Empire as disposable, whereas there was only one Boba Fett.

Debuting in the final season of Star Wars: The Clone Wars, The Bad Batch was a group of clones who were deemed to be genetically altered. These clones all had some mutations which caused them to be proficient in different areas, therefore furthering their genetic differences from Boba Fett. These troopers were spun off into their own animated series on Disney + named Star Wars: The Bad Batch. Although Boba Fett is different from these clones, they are not regular clones either so this doesnt necessarily mean that Boba Fett is different from all clones, just that he is unique.

Introduced in Star Wars: The Bad Batch was the character called Omega, who surprisingly is quite similar to Boba Fett. Seemingly without Jango Fetts permission, the Kaminoans created a perfect genetic clone of Jango Fett who was female. Another thing that sets her apart from the other members of The Bad Batch and other clones is that she was not aged like the other clones, aging naturally like Boba Fett. She might be the one clone that is most like Boba Fett, genetically at least.

The main difference between Boba Fett and the clones who served in the Empire as stormtroopers is that they are different from the Clone Troopers who fought in The Clone Wars, especially those who appeared sooner in the original Star Wars trilogy. There was a percentage of stormtroopers who were not clones but the comparison between Boba Fett and the stormtroopers is only for those who were clones. The clones would either be quite old, having already been grown adults in The Clone Wars, or they would not be of the same genetic material as the Clone Troopers.

Either the stormtroopers were a copy of the Clone Troopers, therefore a clone of a clone and would be a worse soldier than the Clone Troopers and Boba Fett. Or they were mixed with other genetic material, lessening the impact of Jango Fetts. And as Jango Fett was considered one of the galaxys best bounty hunters this would be a disservice to the stormtroopers and would prove that Boba Fett was the superior specimen.

So there you have it, Boba Fett is technically a clone, but because of Jango Fett and his insistence that he have an unaltered, true copy of himself, he stands apart from the rest of the clone army. Many clones were created on Kamino but not all of them were the same, with Boba Fett and Omega being the outliers. Hopefully, the origins of the character do not sour your love for the character, as Boba Fett is still one of the coolest designed characters in the Star Wars universe.

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Is 'Boba Fett' a Clone? - We Got This Covered

Polygenic prediction of educational attainment within and between families from genome-wide association analyses in 3 million individuals – Nature.com

Department of Economics, School of Business and Economics, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands

Aysu Okbay,Hyeokmoon Kweon&Philipp D. Koellinger

Institute for Molecular Bioscience, University of Queensland, Brisbane, QLD, Australia

Yeda Wu,Julia Sidorenko,Jian Yang,Loic Yengo&Peter M. Visscher

National Bureau of Economic Research, Cambridge, MA, USA

Nancy Wang,Hariharan Jayashankar,Michael Bennett,Grant Goldman,Tamara Gjorgjieva,Steven F. Lehrer,David Cesarini&Daniel J. Benjamin

UCLA Anderson School of Management, Los Angeles, CA, USA

Seyed Moeen Nehzati,Chelsea Watson,Jonathan Jala,Daniel J. Benjamin&Alexander I. Young

23andMe, Inc., Sunnyvale, CA, USA

Yunxuan Jiang,Barry Hicks,Chao Tian,David A. Hinds,Michelle Agee,Babak Alipanahi,Adam Auton,Robert K. Bell,Katarzyna Bryc,Sarah L. Elson,Pierre Fontanillas,Nicholas A. Furlotte,Karen E. Huber,Aaron Kleinman,Nadia K. Litterman,Jennifer C. McCreight,Matthew H. McIntyre,Joanna L. Mountain,Carrie A. M. Northover,Steven J. Pitts,J. Fah Sathirapongsasuti,Olga V. Sazonova,Janie F. Shelton,Suyash Shringarpure,Joyce Y. Tung,Vladimir Vacic&Catherine H. Wilson

Department of Government, Uppsala University, Uppsala, Sweden

Rafael Ahlskog,Sven Oskarsson&Karl-Oskar Lindgren

Swedish Twin Registry, Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden

Patrik K. E. Magnusson,Robert Karlsson,Paul Lichtenstein&Nancy L. Pedersen

MRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Western General Hospital, Edinburgh, UK

Caroline Hayward,Jennifer E. Huffman,Jonathan Marten,Veronique Vitart,James F. Wilson&Alan F. Wright

Centre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, University of Edinburgh, Western General Hospital, Edinburgh, UK

Archie Campbell&David J. Porteous

Usher Institute, University of Edinburgh, Edinburgh, UK

Archie Campbell&David J. Porteous

Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, UK

David J. Porteous

Department of Sociology, Stanford University, Stanford, CA, USA

Jeremy Freese

McCourt School of Public Policy, Georgetown University, Washington, DC, USA

Pamela Herd

Department of Sociology, Princeton University, Princeton, NJ, USA

Dalton C. Conley&Dalton Conley

Robert M. La Follette School of Public Affairs, University of Wisconsin-Madison, Madison, WI, USA

Philipp D. Koellinger

Department of Economics, Stockholm School of Economics, Stockholm, Sweden

Magnus Johannesson

Department of Economics, Harvard University, Cambridge, MA, USA

Olga Rostapshova,David I. Laibson&David Laibson

Center for Translational Bioethics and Health Care Policy, Geisinger Health System, Danville, PA, USA

Michelle N. Meyer

Department of Psychology, University of Minnesota Twin Cities, Minneapolis, MN, USA

Michael B. Miller,William G. Iacono,Matt McGue,Robert F. Krueger&James J. Lee

Big Data Institute, Li Ka Shing Centre for Health Information and Discovery, University of Oxford, Oxford, UK

Augustine Kong

Department of Economics, New York University, New York, NY, USA

Kevin Thom&David Cesarini

Center for Experimental Social Science, New York University, New York, NY, USA

David A. Hinds&David Cesarini

Department of Economics, University of Southern California, Los Angeles, CA, USA

Patrick Turley

Center for Economic and Social Research, University of Southern California, Los Angeles, CA, USA

Mark Alan Fontana&Patrick Turley

Interdisciplinary Center for Economic Science and Department of Economics, George Mason University, Fairfax, VA, USA

Jonathan P. Beauchamp

Human Genetics Department, UCLA David Geffen School of Medicine, Los Angeles, CA, USA

Daniel J. Benjamin&Alexander I. Young

Center for the Advancement of Value in Musculoskeletal Care, Hospital for Special Surgery, New York, NY, USA

Mark Alan Fontana

The Novo Nordisk Foundation Center for Basic Metabolic Research, Section of Metabolic Genetics, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

Tune H. Pers,Pascal Timshel,Tarunveer S. Ahluwalia&Thorkild I. A. Srensen

Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark

Tune H. Pers&Pascal Timshel

Institute for Behavior and Biology, Erasmus University Rotterdam, Rotterdam, the Netherlands

Cornelius A. Rietveld,S. Fleur W. Meddens,Ronald de Vlaming&A. Roy Thurik

Department of Applied Economics, Erasmus School of Economics, Erasmus University Rotterdam, Rotterdam, the Netherlands

Cornelius A. Rietveld,Ronald de Vlaming&A. Roy Thurik

Department of Epidemiology, Erasmus Medical Center, Rotterdam, the Netherlands

Cornelius A. Rietveld,Ronald de Vlaming,Najaf Amin,Frank J. A. van Rooij,Cornelia M. van Duijn,Henning Tiemeier,Andr G. Uitterlinden&Albert Hofman

Queensland Brain Institute, University of Queensland, Brisbane, QLD, Australia

Guo-Bo Chen,Zhihong Zhu,Andrew Bakshi,Anna A. E. Vinkhuyzen,Jacob Gratten&Jian Yang

Icelandic Heart Association, Kopavogur, Iceland

Valur Emilsson,Albert V. Smith&Vilmundur Gudnason

Faculty of Pharmaceutical Sciences, University of Iceland, Reykjavk, Iceland

Valur Emilsson

Department of Complex Trait Genetics, Center for Neurogenomics and Cognitive Research, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands

S. Fleur W. Meddens,Christiaan de Leeuw&Danielle Posthuma

Amsterdam Business School, University of Amsterdam, Amsterdam, the Netherlands

S. Fleur W. Meddens&Mal P. Lebreton

New York Genome Center, New York, NY, USA

Joseph K. Pickrell

Department of Biological Psychology, VU University Amsterdam, Amsterdam, the Netherlands

Abdel Abdellaoui,Jouke-Jan Hottenga,Gonneke Willemsen&Dorret I. Boomsma

Copenhagen Prospective Studies on Asthma in Childhood, Herlev and Gentofte Hospital, University of Copenhagen, Copenhagen, Denmark

Tarunveer S. Ahluwalia,Klaus Bnnelykke,Johannes Waage&Hans Bisgaard

Steno Diabetes Center, Gentofte, Denmark

Tarunveer S. Ahluwalia&Johannes Waage

Department of Obstetrics and Gynecology, Institute of Clinical Sciences, Sahlgrenska Academy, Gothenburg, Sweden

Jonas Bacelis&Bo Jacobsson

Research Unit of Molecular Epidemiology, Helmholtz Zentrum Mnchen, German Research Center for Environmental Health, Neuherberg, Germany

Clemens Baumbach&Christian Gieger

Institute of Epidemiology II, Helmholtz Zentrum Mnchen, German Research Center for Environmental Health, Neuherberg, Germany

Clemens Baumbach&Christa Meisinger

deCODE Genetics/Amgen, Inc., Reykjavik, Iceland

Gyda Bjornsdottir,Gudmar Thorleifsson,Bjarni Gunnarsson,Bjarni V. Halldrsson,Kari Stefansson&Unnur Thorsteinsdottir

Department of Cell Biology, Erasmus Medical Center Rotterdam, Rotterdam, the Netherlands

Johannes H. Brandsma&Raymond A. Poot

Istituto di Ricerca Genetica e Biomedica U.O.S. di Sassari, National Research Council of Italy, Sassari, Italy

Maria Pina Concas,Simona Vaccargiu&Mario Pirastu

Psychology, University of Illinois, Champaign, IL, USA

Jaime Derringer

Institute for Computing and Information Sciences, Radboud University Nijmegen, Nijmegen, the Netherlands

Tessel E. Galesloot&Lambertus A. L. M. Kiemeney

Department of Medical, Surgical and Health Sciences, University of Trieste, Trieste, Italy

Giorgia Girotto,Dragana Vuckovic,Ilaria Gandin,Paolo Gasparini&Nicola Pirastu

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Polygenic prediction of educational attainment within and between families from genome-wide association analyses in 3 million individuals - Nature.com

Mercer professor’s podcast among the best about women in STEM – Mercer University

A Mercer University professors podcast highlighting women in science, technology, engineering and math has been recognized among the best in its niche.

Dr. Sabrina Walthall, associate professor of science in the College of Professional Advancement, hosts the STEM Lab Podcast, which was ranked No. 13 among the Best 45 Women in STEM Podcasts. The ranking by Feedspot, a web content reader, was based on traffic, social media followers, domain authority and freshness.

Dr. Walthall said she created the STEM Lab Podcast two years ago to highlight women, especially those from marginalized groups, in STEM.

I realized that the news media only seemed to highlight women who, of course, had done something just spectacular and over the top, she said. But I knew a lot of women, who I either went to graduate school with or met at conferences, who were doing great things. These are a lot of women already in the community, doing work in their own community, but no one really knows.

And so, I just felt the podcast was a great way to put the story out there.

Each episode, released monthly, features an interview with a woman who uses science, technology, engineering or math in her work. Episodes have featured two women who hold both M.D. and Ph.D. degrees, a registered nurse, an environmental neuroepidemiologist and a viral immunologist. A recent episode featured an unconventional woman in STEM a celebrity cake artist.

The baker was very unconventional, which I love because I dont think people think of STEM in that way, and then just talking to her I realized, All you do is STEM all day long, Dr. Walthall said.

Her podcast also dives into the challenges women, in particular marginalized women, face in STEM. One of her favorite episodes was an interview with Dr. Ansley Booker, director of diversity and inclusion initiatives at Mercer.

In order for STEM to move forward, we really have to look at diversity, equity and inclusion, Dr. Walthall said.

Representation of women in STEM varies widely, according to a recent Pew Research Center analysis of the STEM workforce.

While women make up half of those employed in STEM careers, they are overrepresented in health-related jobs but underrepresented in other fields, such as the physical sciences, computing and engineering. Meanwhile, Black and Hispanic workers (male and female) are underrepresented in the STEM workforce across the board, the analysis shows.

A lot of times the reason all this is happening, and why I also try to work with girls in STEM, is because of gender stereotypes, Dr. Walthall said. Its just been ingrained in us since we were young that certain careers belong to men and are masculine, and certain careers belong to women.

And you dont always hear of young girls being told that they should grow up to be a scientist or that they can be the engineer or that maybe they can be the mathematician.

She said she hopes a young girl might hear the STEM Lab Podcast and discover she can be like the women being interviewed.

Dr. Walthalls own love for STEM began when she was young. She became fascinated with science after being assigned a report on the heart.

I learned the heart was not the shape of the candy box, but it was the size of our fist, and that fascinated me, she said. And I just remember learning all the information and just going around the house, spouting it to anybody who would listen to it.

She went on to earn a bachelors degree in biology from Emory University and a doctorate in biochemistry and molecular genetics from the University of Alabama at Birmingham. She completed her postdoctoral training with the UAB Community for Outreach Development where she worked on rebuilding science education at the K-12 level in Alabama and discovered her passion for the science of teaching and learning.

Through a National Science Foundation fellowship, she was able to go into an Alabama high school and teach genetics. She realized she really enjoyed it.

I would always make a story out of the science because thats the way Ive always seen science. Its really, literally, a cartoon in my head, she said. I realized I could start a concept in a fun way and then build up to where we understand it truly scientifically, but I had to start them somewhere.

In addition to her work at Mercer, prior to the COVID-19 pandemic, Dr. Walthall volunteered with the Real Impact Center, a Macon-based nonprofit dedicated to exposing girls to STEM careers.

She enjoyed the work so much that she incorporated it into her courses as a service-learning project, which included college students working with youth during events like STEM-tastic Saturdays and a Macon STEM Pop-Up.

The STEM Lab Podcast is available on Apple and Google Podcasts, Anchor, Spotify and YouTube.

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Mercer professor's podcast among the best about women in STEM - Mercer University

‘Break that glass ceiling’: Omahan Marian Andersen has relished a life filled with firsts – Kearney Hub

There arent enough hours in the day, Marian Andersen says.

Marian Andersen with her dog, Ashley. She reads four newspapers daily and enjoys watching all kinds of sports. Gonzaga is her pick to win the NCAA basketball tournament.

At 93, shes still reading four newspapers daily. Magazines and books also keep her busy.

Im not giving up on newspapers, she said.

She couldnt wait for the NCAA basketball tournament to start she picked Gonzaga to win it all. Baseball is another love, and with a fall trip to Texas, shes seen every major league stadium.

Shes also a huge Nebraska football fan. People are astounded to learn shes been attending games for 90 years. Her father took her to her first one when she was 3 years old.

Marian Andersen at age 5. She went to her first Nebraska football game at the age of 3.

Her social calendar is packed she enjoys playing bridge and attending the movies. Thank goodness for younger friends, she said, since many of her older ones have sadly passed away.

One of the amazing things about Marian is her positive attitude and zest for life and her genuine interest in other people, longtime assistant Jackie Wrieth said. Not only does she want to know everything about you, but also about your kids and grandkids and she remembers it all.

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A mutual friend always said if youre attending a banquet you want to sit at Marian Andersens table. Shes one of a kind.

Marian Andersen and her husband, former Omaha World-Herald publisher Harold W. Andersen, at the Ak-Sar-Ben pre-coronation in October 1994.

Life has always been full for Andersen, who still lives in her home with a cocker spaniel, Ashley. Ashley doesnt cook, Andersen jokes, but shes great company.

Shes got family here, too. Son David, his wife, Leslie, and three grandkids live in the Omaha area as well as San Francisco. Daughter Nancy Andersen and her three sons live in Denver.

Her husband, the late Harold W. Andersen, was publisher of The Omaha World-Herald from 1966 to 1989. Although she didnt have a full-time career, Marian didnt sit home on the sideline. As a longtime community volunteer, she has been a pioneer.

She was the first woman chairman of the University of Nebraska Foundation and the first woman board chair for the Red Cross in Omaha.

Marian Andersen, center, leaves the stage with her daughter Nancy Andersen, left, and son David Andersen after she was honored during the United Way of the Midlands Excellence in Impact event in 2017.

She was on the board and co-chair of the committee that hired the first woman president of the national Public Broadcasting System. The Andersens made significant contributions locally and nationally to PBS.

She was also pleased recently to make the acquaintance of Ava Thomas, The World-Heralds second woman publisher.

Im all for women to break that glass ceiling, she said.

Together, she and Harold supported a long list of organizations.

She was named the United Way of the Midlands Citizen of the Year in 1994. With her husband, she was a co-founder of the Alexis de Tocqueville Society, a group of contributors who donate a minimum of $10,000 to the annual United Way campaign.

She also received the Distinguished Nebraskalander Award from the Nebraskaland Foundation and was named outstanding sustainer by the Junior League of Omaha. She was a past president of Planned Parenthood and co-chairman of the Nebraska Shakespeare Festival.

Marian Andersen in 1974. She was an active volunteer.

Brian Hastings, the president and CEO of the Nebraska Foundation, said Marian Andersen has a long history of supporting the foundation. She is its longest-serving trustee, since 1962, served as the chair of the board of directors in 1984 and 1985 and was the first woman to do so.

She liked to say she broke the glass ceiling for her husband, Harold, who became chair of our board later, in 1991 through 1993, Hastings said. She and Harold were the volunteer chairs of a comprehensive campaign that ran from 1993 through 2000. The goal was to raise $250 million for the University of Nebraska. It raised $727 million due to Marian and Harolds leadership. She is one of the foundations and universitys most ardent and faithful supporters.

Andersen said shes just always been a leader, from when she was student council president at Lincoln High and president of Kappa Kappa Gamma sorority at the University of Nebraska-Lincoln, where she also was a Phi Beta Kappa.

Marian Andersen in 1951. She said she's always been a leader.

I never was intimidated, she said.

After she married at 23, which at that time she said was almost an old maid, she and her husband saw the world. They visited 60 countries and every state.

Another great love of Andersens is tennis, and shes been to the grand slam of tournaments: the Australian Open, the U.S. Open, Wimbledon and the French Open.

During womens history month, Andersen said shes most proud of two things.

I think my family, she said, and the fact that I have maybe made a difference in some of the organizations.

Marian Andersen and her dog, Ashley, at her home in Omaha. She jokes that Ashley cant cook, but shes good company.

2. Standing Bear

c. 1829-1908

Native leader

A renowned Ponca chief, Standing Bear, in 1879, became the first Native to be legally recognized as a person.

In 1877, the federal government forced the Ponca from their northeast Nebraska land to Indian Territory in what is now Oklahoma. A year later, honoring the wish of his 16-year-old son to be buried along the Niobrara River, Standing Bear led a band of tribe members back to Nebraska.

Arrested for leaving the reservation, Standing Bear stood trial at Fort Omaha, his lawyers filing a writ of habeas corpus contesting the detention. The judge ruled in favor of Standing Bear and the U.S. Supreme Court upheld the ruling.

4. George W. Norris

1861-1944

Politician

Called the very perfect, gentle knight of American progressive ideals by President Franklin D. Roosevelt, Norris served five terms in the U.S. House of Representatives (1903-13) and five terms in the U.S. Senate (1913-43), all save the final term as a Republican.

An Ohio native, Norris moved to Beaver City in 1885 to practice law. He established an office in McCook in 1899, practicing law before beginning his political career.

Norris promoted the unicameral Legislature in Nebraska, approved by voters in 1934, and led the creation of the Tennessee Valley Authority, and the Rural Electrification Act, both championing public power.

5. Wm. Jennings Bryan

1860-1925

Politician

A famed orator and leader of the populist wing of the Democratic Party, Bryan was the Democratic presidential nominee three times in 1896, 1900 and 1908. He served two terms in Congress from Nebraska and was Secretary of State under Woodrow Wilson.

Born in Salem, Illinois, The Great Commoner settled in Lincoln in 1887 to practice law. Known for his oratory, Bryan was a champion of free silver and delivered his famous Cross of Gold speech in 1896.

Touring the country as a public speaker, Bryan worked for peace, Prohibition and womens suffrage and opposed the teaching of evolution, joining the prosecution in the famed Scopes Monkey Trial in 1925.

6. John Neihardt

1881-1973

Poet

The writer, poet and historian is best known for "Black Elk Speaks," the biography of the Oglala Lakota holy man Neihardt published in 1932.

Born in Illinois, Neihardt moved to Wayne in 1892 as an 11-year-old. Bancroft became his home in 1901. He became a published author at age 19, started his major work, "The Cycle of the West," at 31 and became Nebraska's Poet Laureate at 40.

At 45, he was literary editor for the St. Louis Post-Dispatch, and at 68 became poet-in-residence and lecturer in English at the University of Missouri. He returned to Nebraska in his 80s, continuing to write until his death at 92.

9. Charles Dawes

1865-1951

Vice president

Dawes (above with pipe) pursued two careers in his lifetime, one in business/finance, the other in public service, with the two coming together in 1925 when he won the Nobel Peace Prize while serving as Calvin Coolidge's vice president.

Dawes moved to Lincoln in 1887, where he practiced law until 1894. Purchases of gas companies in LaCrosse, Wisconsin, and near Chicago started investments that made him rich. The Republican activist took his first government position in 1898.

A self-taught musician, he composed what eventually became the pop standard "It's All in the Game."

10. Ted Sorensen

1928-2010

Presidential adviser

In 1953, the Lincoln native and University of Nebraska College of Law graduate became chief legislative aide for Sen. John F. Kennedy and, after the 1960 election, became President Kennedys chief aide and speechwriter.

Responsible for crafting Kennedys famous inaugural address, Sorensen served as a key adviser during the 1962 Cuban missile crisis and penned the letter to Soviet Premier Nikita Khrushchev that defused the crisis.

After his White House years, Sorensen joined a prominent New York City law firm and built an international law practice.

11. J. Sterling Morton

1832-1902

Politician

Founder of Arbor Day, Morton moved to Nebraska City in 1854 and became editor of the local paper. He served as acting governor in 1858 and again in 1861 and was U.S. Secretary of Agriculture from 1893-1897.

12. Tom Osborne

1937-

Football

The Hastings native played professional football before becoming a Nebraska assistant coach in 1964. Named head coach in 1972, Osborne led the Huskers for 25 years, winning three national championships. He served in Congress from 2001-2007 and as UNL athletic director from 2007-2013.

13. John J. Pershing

1860-1948

Military

In 1891, Army officer Pershing became professor of military science at the University of Nebraska where he earned his law degree in 1893. Black JackPershing served in the Spanish-American War and became the leading American commander in World War I.

14. Harold Edgerton

1903-1990

Engineer

Fremont-born Edgerton grew up in Aurora and received his engineering degree from the University of Nebraska in 1925. In 1927, he began working with stroboscopes and in 1937 began collaborating with a photographer to make his motion capture images.

15. Loren Eiseley

1907-1977

Nature Writer

The Lincoln native began writing while attending the University of Nebraska. In 1947, he began teaching at the University of Pennsylvania. In the 1940s, he began writing his acclaimed nature essays and books combining natural science with literature.

16. Dick Cavett

1936-

Television

Born in Gibbon, Cavett grew up in Lincoln before attending Yale University. Hired as a writer for The Tonight Show in 1960, Cavett also worked in stand-up comedy before landing The Dick Cavett Show, which ran from 1968 to 2007.

17. Bob Kerrey

1943-

Politician

Winning the Congressional Medal of Honor for his service in Vietnam, Lincolns Kerrey was elected governor in 1982, became a U.S senator in 1989 and was a Democratic presidential candidate in 1992. He also served on the 9/11 Commission.

18. Henry Fonda

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'Break that glass ceiling': Omahan Marian Andersen has relished a life filled with firsts - Kearney Hub

What Does It Mean When When You Have Bad Cramps? – The List

If your bad cramps aren't caused by a workout or period pain, there can be another reason: pelvic inflammatory disease (PID). According to the Centers for Disease Control and Prevention (CDC), PID is the infection of the female reproductive organs, and can result from untreated sexually transmitted diseases (STDs) or the use of an improperly placed intrauterine device (IUD).

The only way to avoid PID is to avoid all sexual activity. If you are sexually active, use protection or be smart about your choice of partners, making sure they also test negative for STDs. If you notice abnormal bleeding or severe cramping in the abdomen, it is best to get a diagnosis, as it is always better to treat a disease in its earlier stages because the cause could be PID.

WebMD shared that "PID is an infection of the organs of a women's reproductive system. They include the uterus, ovaries, fallopian tubes, and cervix." This affects about 770,000 women in the U.S. every year, and can ultimately also affect fertility. Consult a doctor if you are sexually active and experience severe pain in your tummy that seems more unusual than period cramps. It can be treated with antibiotics, but serious cases may require hospitalization.

Ultimately, no matter what is causing them, we've got you covered with the best ways to relieve stomach cramps.

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What Does It Mean When When You Have Bad Cramps? - The List

The Top 10 Insect-Powered Biotech Companies – Labiotech.eu

Insects are often seen as pests, but many species can provide new sources of food, materials, and even ways to clean up plastic waste. Here are 10 companies in this space that we think are worth watching.

Many people think of insects simply as pests that eat crops and carry diseases such as malaria. While this is true in some cases, insects have also been an inspiration to scientists for many years. Biotechs and researchers are now applying this knowledge to create new and sustainable food sources for both humans and animals, as well as fertilizers to grow other foods.

The unique biology and chemistry found in insects has inspired the creation of packaging materials, bioplastics, glue, and other biomaterials. Some scientists have even found moth larvae that eat plastic and other, more early-stage research, is looking at ways to repurpose spider venom to treat pain or create insecticides for use on plants.

The number of biotech companies working in the insect or yellow biotechnology space is constantly increasing. Here are 10 firms we think are worth paying attention to.

Founded: 2005

Headquarters: Madrid, Spain

Madrid-based Algenex uses insects and insect cells to produce proteins needed to develop drugs, vaccines, and diagnostics. Jos Escribano founded the company in 2005 and is now CSO.

The company has two main products: CrisBio and TopBac. The former, validated by the EMA last year, uses chrysalises of the cabbage looper moth Trichoplusia ni as living bioreactors to produce medicinal proteins. Living insects can regulate their own temperature and oxygen levels, making them easier than cells to manufacture at scale. The insects are infected with a modified virus, harmless to humans, known as a baculovirus. Prior to infection, the virus is genetically engineered to ensure production of the desired protein. The chrysalises can then produce enough protein to extract in less than a week.

The other product, TopBac, is a DNA sequence that contains instructions necessary to express certain genes in cells. It can be used to improve both the productivity and quality of the proteins produced by the insect cells.

The company has already produced more than 200 types of medicinal proteins used for human and animal diagnostics and therapeutics. Funded by Columbus Venture Partners, Chamber Ventures, and Vita Advisory, the company raised a 8.75M Series B round in 2020 and a 4M Series A financing in 2019.

Founded: 2011

Headquarters: Paris, France

nsect was founded in 2011 in Paris by a group of scientists and environmental activists. The company uses insects to produce high-protein products for animal and fish food, as well as the fertilizer industry, in a sustainable and environmentally friendly way.

The company has created technology that allows vertical production of the yellow mealworm beetle Tenebrio molitor. In 2019, nsect raised 110M in Series C funding the largest-ever amount for agriculture technology outside of the USA to fund the construction of the worlds largest automated insect farm. This was extended to 343M in 2020, bringing its total funding to approximately 391M. Last year, the company acquired Dutch mealworm breeding company Protifarm to expand its reach across Europe.

In January 2021, the European Food Safety Authority concluded that mealworms are safe for human consumption, a positive development for nsects mission to enter the human food market.

Last month, nsect announced the launch of nfabre, an industrial program dedicated to the genetics of these insects. The initiative is designed to bring expertise from different fields together to develop improved phenotyping and genotyping tools, as well as more efficient industrial processes.

Founded: 2002

Headquarters: Abingdon, UK

A spin-off from the University of Oxford founded in 2002, Oxitec genetically engineers mosquitoes with a self-limiting gene to help control diseases such as malaria and dengue. By introducing a gene that kills the female offspring of mosquitoes, the company has claimed massive success in reducing local populations of disease-carrying mosquitoes in locations including Brazil, India, and Panama.

Since its founding, Oxitec has diversified and is applying similar technology to pest insects that attack crops such as the diamondback moth, a massive problem for vegetable farmers, and others such as the soybean looper and the fall armyworm. According to the company, the advantage of this technology is that, unlike chemical insecticides, it does not kill harmless insects like bees and other pollinators.

Oxitec was acquired by US-based Intrexon Corporation in 2015, acting as a separate subsidiary. In 2020, Intrexon sold off Oxitec and other non-healthcare assets to another US company, Third Security.

Founded: 2009

Headquarters: Dongen, The Netherlands

Protix was founded by Kees Aarts and Tarique Arsiwalla in 2009. The company uses a combination of high-tech control systems, artificial intelligence, breeding programs, and robotics to produce lipids, proteins, and pure from larvae of the black soldier fly (Hermetia illucens). It also plans to expand to crickets, locusts, and mealworms in the future.

The company opened its first industrial-scale factory in 2019 in Bergen op Zoom and has a number of different animal food products on the market used to make nutritious food for pets, chickens, and fish. The firm also produces a fertilizer from the byproducts of its industrial process.

Protix started a collaboration with the animal breeding specialist Hendrix Genetics in 2018 and recently announced that they have successfully bred black soldier flies with bigger larvae that will increase yield in their insect farms.

Last month, Protix attracted a 50M investment from BNP Paribas, Monaco Asset Management, and the Luxembourg-based European Circular Bioeconomy Fund. The company has now accrued over 120M in total funding and plans to expand internationally.

Founded: 2014

Headquarters: Salamanca, Spain

Tebrio, previously known as MealFood Europe, was founded by Adriana Casillas and Sabas de Diego in 2014. Similar to nsect, Tebrio focuses on transforming the T. molitor mealworm beetle into different ingredients for a wide variety of uses.

Tebrio has three main product streams: sustainable fish, pet, and animal feed; biofertilizer for plants that also acts as an insect repellant; and chitosan extracted from the insects to make biodegradable plastic that can dissolve in water. Chitosan has many other uses; for example, it can be used for water treatment, as a base for coagulants, or for medical uses as an antibacterial component of dressings and bandages.

In 2020, the company closed a Series A funding round co-led by Caixa Capital Risc and the Spanish Centre for Industrial Technological Development (CDTI). While the total amount of the round was undisclosed, Tebrio announced the cash would allow the firm to develop a 50M insect breeding project.

Founded: 2017

Headquarters: Karmei Yosef, Israel

Smart Resilin is an Israeli biotech, set up in 2017, that is harnessing the power of resilin in its products. Resilin is a rubber-like protein found in the outer skin of most insects that helps them jump large distances and fly by allowing their wings to beat.

The company was spun out of the Hebrew University of Jerusalem by a team including materials scientist and serial entrepreneur Professor Oded Shoseyov, now CSO of the company. The researchers behind the company succeeded in identifying the genetics of resilin production and engineered bacteria to produce the protein.

Experiments have shown that resilin can be very useful in industry. For example, as an addition to glue, resilin improves elasticity and fatigue resistance. The company also plans to use it for other applications such as manufacturing training shoes. Resilin is also biodegradable, sustainable, and compostable, making it attractive for consumers.

Founded: 2016

Headquarters: Meath, Ireland

Hexafly is another company on the list that focuses on the black soldier fly (H. illucens). The company feeds its insects waste materials from breweries so the farm is totally waste-free. Founded by Alvan Hunt and John Lynam, Hexafly is based in Meath, Ireland and runs the countrys only vertical insect farm.

The company makes animal and fish food with their products from proteins and oils extracted from the flies, as well as dried grubs. The team also makes frass, a natural fertilizer for plants that can double up as a pesticide, for example, by reducing the impact of aphids.

The company received 2.2M seed funding in 2018 and has since then set up a pilot plant and received 3M in Series A funding.

Founded: 2020

Headquarters: Jarfalla, Sweden

Norbite, was founded in 2020 by Nathalie Berezina, previously nsect CTO/CSO. The firm was founded based on observations of the greater wax moth (Galleria mellonella) that showed caterpillars of this species are capable of eating plastic.

While the initial observations of the plastic-munching caterpillars occurred accidentally, they have now been confirmed. Greater wax moth larvae can consume around 80% of plastics including polyethylene and polystyrene, which have a similar chemical formulation to the wax they normally consume.

While it is still early days for Norbite, the company hopes to build a plant capable of processing 30,000 tons of plastic within five years. Many industrial biotechs find scaling up a challenge and Norbite will need to overcome major technical and economic obstacles to breed these insects on a wide scale and make its plastic degradation proposal an affordable reality.

Founded: 2016

Headquarters: Kongens Lyngby, Denmark

BioPhero was founded in 2016 by Irina Borodina as a biotechnology spin-out from the Technical University of Denmark. The company uses yeast fermentation technology to produce sustainable and safe insecticide replacements with the same makeup as insect pheromones. Applying pheromones to crops can mask the pheromones that female insects use to attract males, stopping them from mating.

The company currently targets four main pests with its pheromones, the cotton bollworm (Helicoverpa armigera), the diamondback moth (Plutella xylostella), rice stem borers (Chilo suppressalis and Scirpophaga incertulas), and the fall armyworm (Spodoptera frugiperda).

In March last year, BioPhero announced a 15.6M Series A funding round led by DCVC Bio with participation from FMC Ventures, as well as existing investors Syngenta Group Ventures and Novo Holdings.

Founded: 2021

Headquarters: Limburg, The Netherlands

Sib was named after a Costa Rican deity who taught people to work together with nature. It is still at the seed funding stage and was founded last year in the Netherlands by Costa Ricans Daniela Arias and Alejandro Ortega.

Sib is focused on the development and supply of insect-based food ingredients and water-soluble proteins from crickets and yellow mealworms.

The company will carry out technological processing of the insects in the Netherlands at the Brightlands Chemelot Campus in Limburg. The insect farming itself will take place in Costa Rica to ensure a fair deal for farmers in the developing country.

Sibs technology, named Entowise, allows fine separation of nutritional components such as protein, fats, and cytosine from powdered insects. The technology is precise enough that it could be used to extract vitamins such as B12 from insects.

Cover image via Elena Resko

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The Top 10 Insect-Powered Biotech Companies - Labiotech.eu

The Times view on the trans debate: Back to Basics – The Times

Accusations of unfairness surround trans athletes such as the swimming champion Lia Thomas, far right, in womens sport

RICH VON BIBERSTEIN/GETTY IMAGES

The governments dithering over whether to ban conversion therapy has left policy on this sensitive issue in utter confusion. A double U-turn saw the prime minister at first cast aside a pledge that he would outlaw attempts to change peoples sexual orientation, before reinstating the commitment with measures to ensure it would not affect counselling offered to those suffering from body dysmorphia who want to transition to the opposite sex.

Lobby groups on all sides shrilly condemn discrimination. Mr Johnson had previously described all conversion therapy as abhorrent. However, feminists fear that womens rights are now in jeopardy. And the general public is bemused by arguments that seem as obscure as they are virulent. It is time common sense was brought to the trans debate.

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The Times view on the trans debate: Back to Basics - The Times

Hunting alters animal genetics. Some elephants are even losing tusks. – Vox.com

Sometime in the distant past, well before humans walked the Earth, the ancestors of modern-day elephants evolved their iconic tusks. Elephants use their bleach-white incisors theyre technically giant teeth, like ours but longer to dig, collect food, and protect themselves.

Then Homo sapiens arrived, and elephant tusks became a liability. Poachers kill the massive animals for their tusks, which are worth about $330 a pound wholesale as of 2017. Hunters slaughter roughly 20,000 elephants a year to supply the global ivory trade, according to the World Wildlife Fund.

But just as tusks evolved because they provide a number of benefits, a striking new study shows that some populations of African elephants have rapidly evolved to become tuskless. Published in the journal Science, the papers authors found that many elephants in a park in Mozambique, which were heavily hunted for their ivory during a civil war a few decades ago, have lost their tusks presumably because tuskless elephants are more likely to survive and pass the trait on to their offspring.

While scientists have known about this trend for a while its not uncommon to see tuskless elephants in places with lots of poaching the study provides strong evidence that the trait is rooted in genetics, something previous research failed to do, said Andrew Hendry, an evolutionary biologist at McGill University who was not involved in the research. In other words, the study shows evolution in action.

The results also offer a vivid example of how animals can quickly adapt under human pressures such as poaching and climate change. Past research has shown that creatures can evolve new colors, shapes, and even behaviors to better tolerate the increasingly inhospitable world weve created for them. The problem is that even rapid evolution has its limits and many species are already on the brink.

Social conflict and the decline of wildlife are often closely linked, the authors of the Science study write. Few locations reveal a clearer picture of this than Gorongosa National Park, a protected area in central Mozambique where Shane Campbell-Staton, an evolutionary biologist at Princeton University, led the research.

During a 16-year civil war that began in 1977, poachers on both sides of the conflict slaughtered a huge number of elephants in the park for their ivory, which they sold to finance their efforts, according to the study. Over that period, the number of large herbivores (like elephants) at Gorongosa fell by more than 90 percent.

Thats not all that changed in the park. Between 1970 and 2000 a period that encompassed much of the impact of the long-running war the portion of female elephants without tusks nearly tripled. The researchers best guess was that it had something to do with genetics: A trait visible only in females suggests it might be associated with changes to genes on the X chromosome. (Female elephants have two X chromosomes, whereas males have an X and a Y chromosome.)

This study all but proved it. The first bit of evidence was that female calves born from tuskless mothers were often themselves tuskless, indicating that the trait is passed on from one generation to the next. A heritable trait is pretty strong evidence of a genetic basis, said Robert Pringle, a biology professor at Princeton and a co-author of the study.

The authors also identified a couple of regions in the animals DNA that appear to be associated with a lack of tusks. Sure enough, There is strong evidence for mutations on a particular region of the X chromosome, Pringle said. Mutations, or variations in an organisms DNA, are an important engine of evolution. If they result in traits that are beneficial such as tusklessness, for certain populations of female elephants theyre more likely to get passed to the next generation and drive evolution.

Remarkably, one of the genes associated with tusklessness is also present in humans, where its linked to a condition that limits the growth of our lateral incisors. These are essentially the same teeth that, in elephants, evolved into tusks millions of years ago.

What makes this study so fascinating is that it offers evidence of rapid evolution in an animal that has a pretty long lifespan 50 or 60 years in the wild, said Hendry and Fred Allendorf, a professor emeritus at the University of Montana who was not involved in the research.

Studies of elephants rarely can say anything about the genetic basis of tusklessness, Hendry said. For years, researchers assumed that rapid evolution was common only in small species with short life cycles. Given these results, Nobody can argue that evolution isnt occurring, even in the biggest and longest-lived species, he added.

In theory, its advantageous to be born without tusks in areas where poachers are active, Hendry said. But tusklessness also has its downsides. Elephants need their tusks to dig, lift objects, and defend themselves. The hulking incisors are not useless appendages.

The genes that seem to make female elephants tuskless also appear to prevent mothers from giving birth to male calves thats why all the tuskless elephants in the park are female, Pringle said. (Some mothers did give birth to males with tusks, who likely didnt inherit the gene.) Over time, a shift in the sex of elephants could have consequences for population growth.

There are also potential costs to African grasslands, which are among the rarest and most biodiverse ecosystems on Earth, the study authors write. By turning over soil in search of food and minerals and gouging trees with their tusks, African savanna elephants prevent forests from growing too dense and help maintain grasslands. Thats why theyre considered engineers of the ecosystem. If they lose their tusks, a whole web of plants and animals may feel the impact.

This evolutionary change could have massive cascading ecological influences, Hendry said.

Humans have shaped the environment around them for centuries, down to the very genetics of wild plants and animals. The tuskless elephants in this study are just one example in a long list of species that have adapted in response to the pressures weve placed on them.

Human-induced changes are creating conditions for fast biological evolution so rapid that its effects can be seen in only a few years or even more quickly, a team of scientists wrote in a landmark intergovernmental biodiversity report in 2019.

One of the earliest and most famous examples is the peppered moth in the UK. Before the Industrial Revolution, most of the moths flitting about England were white with speckles of black, which helped them blend in with lichen and tree bark. Then, in the mid- to late-1800s, coal-fired power plants and mills started belching dark soot that blackened trees in parts of the country. White moths stood out against the newly dark background and were more likely to be eaten by birds, whereas the once-rare black ones were camouflaged and survived. In a matter of years, some populations of peppered moths inverted from white to mostly black. The phenomenon was deemed industrial melanism.

Scientists have measured similar changes in recent decades. One study from 2003, for example, found that bighorn sheep in Alberta, Canada, evolved smaller horns in roughly 30 years. The reason? Trophy hunters tend to target rams with larger horns. Another study, published in November 2020, suggests that a type of lily found in the mountains of China is evolving less-colorful leaves so it doesn't stand out in regions where its harvested as a traditional herb.

Rising temperatures from climate change also appear to be making some animals, including birds and mammals, smaller, as I previously reported. Smaller bodies cool off more easily than larger ones, so shrinking could be an adaptive response in warming environments (though its not yet clear whether these particular changes are genetic).

Then there are species changing in less conspicuous ways. In Japan, populations of mamushi snakes that are heavily hunted for their perceived medicinal and nutritional benefits seem to be better at evading predators, compared to snake populations that hunters have ignored. Many species, including plants and insects, have evolved resistance to pesticides, which is why farmers often use several at once and chemical companies must constantly develop new solutions.

Theres something like hope behind the idea of rapid evolution. Humans are deforesting, polluting, and exploiting the Earth at an alarming pace, yet in some cases, animals are adapting to live another day. Theres even a term for this resilience, Hendry said: evolutionary rescue.

Still, this evolution, as fast-tracked as it may be, still often isnt quick enough to overcome the many threats species face. And because adaptations can also come with drawbacks, there are untold and unpredictable consequences for the ecosystem at large.

Plus, not all species can adapt their way out of crisis. Consider rhinoceroses, which poachers kill for their horns. Three of the five rhino species have been hunted almost to extinction, yet none appear to have evolved hornlessness.

In Gorongosa National Park, the ecosystem has largely recovered from the war, Pringle said. Poaching has subsided, but tusks havent bounced back. After the war, the park successfully rebuilt its infrastructure, ramped up law enforcement, and put social development programs into place. The presence of tuskless elephants is now akin to a scar from an injury thats healed, Pringle said. So while evolution may have helped these creatures survive, the real remedy is putting an end to the underlying forces that triggered it in the first place.

Original post:
Hunting alters animal genetics. Some elephants are even losing tusks. - Vox.com

Old heifer-raising ideals may not be the way of the future – Progressive Dairy

As I travel around the country and go from farm to farm, I see a good trend beginning to take hold as dairy producers are understanding the value of carrying extra heifer inventory.

Since the inclusion of sexed semen into dairy breeding programs, dairies can easily be heavy on heifer numbers. This is an amazing technology that allows us to produce more heifers than may be needed, but when we look at the drain these animals can put on the dairy economy, several things come into view. Replacement cost, calf value, production standards, genetic progress and labor concerns are just a few of the items that need to be processed to make an informed decision on your heifer inventory choices.

To begin this discussion, we do have to get a little philosophical. For the known history of dairy production in North America, management has dictated that heifers be cherished and treasured as the lifeblood of sustainability for your dairy. I have heard over and over, Yeah, growing up I knew I was going to be in trouble if we lost any calves. Make no mistake, I am in no way suggesting we should not have good husbandry for our youngstock. In fact, I would suggest we care for and manage them even better than before but only the ones we choose to retain.

Keep in mind, there is a ratio of first-lactation animals in your herd that is the most productive. Heifers by physiology are about 80% to 85% of the size and the production value of a periparturient cow. So just adding first-lactation animals into the herd because we have them may in fact cost us production in the herd. So what are some ideas to think about that will allow us to capitalize on this untapped potential in our herds?

In the last 10 years, beef on dairy or dairy beef phrases have taken off like wildfire as a way to make some extra income from drop calves or to capitalize on higher prices and better growth rates for feeders or finish cattle. I think we need to bring in another technique from our friends in the beef world and start looking at only retaining the heifers we need. Beef producers do not cull mother cows unless they absolutely must, as they are the breadwinners of the herd. Heifers will be inserted into the management chain only as needed to fulfill a need, whether for space or replacement. If we investigate doing this similarly in dairy management, we need to reverse our thinking and start from the end of a heifers life cycle.

To begin, we need to decide on the number of heifers we would ideally like to insert into the herd every month to maintain current population but not overwhelm the lactation ratio we choose. Dr. Jud Heinrichs from Penn State University has published equations to help us figure it out.

First, we calculate the heifers we need: (herd size[total]) x (cull rate) x (age at first calving 24) x (1 + non-completion rate for heifers). The non-completion rate being heifers that are born alive but never make it to the milk barn. Second, we calculate the number we produce: (herd size[total]) x (12 calving interval) x (percent female calves) x (1 calf mortality rate) x (24 age at 1st calving). Calf mortality counts deaths in first 48 hours after birth.

These two equations allow us to get an idea of our heifer surplus. These are the animals we carry in inventory that are costing us money, space or potential. Opinions vary, but I have seen operations as low as 33% and as high as 45% with first-lactation animals in the herd. If we are going to limit ourselves to raising fewer heifers than we are producing, where can we find advantages? Do we raise dairy beef or do we look at exclusively sexed semen, or embryo transfer for high genetic potential, or should we have cows that only milk and dont get pregnant? What can we do with the extra cow womb space now that we dont need every cow to deliver a calf into the herd?

There are a few items we need to investigate to realize the financials for this management change:

Economically, every dairy is different in lots of ways. Whether you sell extra feed, raise beef for sale, buy less feed, this analysis and change in philosophy may be of benefit. There will be considerable effort required to make change happen and for it to work.

First steps to get started are to use the two equations above, add 5% to 10% for safety and look at exactly how many heifers you need every month to maintain your herd. We cannot automatically say this will work for you, as this discussion is much more in-depth than an article can address. As with almost everything on a dairy operation, quality management and a team approach can make these scenarios achievable.

PHOTO:To maximize production, farms should evaluate their replacement heifer numbers and only raise the ones they need. Dairy beef may be a great option to fill extra cow womb space.Photo by Mike Dixon.

Original post:
Old heifer-raising ideals may not be the way of the future - Progressive Dairy

Germline Testing in Prostate Cancer: When and Who to Test – Cancer Network

Abstract

The results of multiple studies have shown that a substantial proportion of men with advanced prostate cancer carry germline DNA repair mutations. Germline testing in prostate cancer may inform treatment decisions and consideration for clinical trials. There are 2 FDA approved PARP inhibitors (PARPi), olaparib (Lynparza) and rucaparib (Rubraca), for the treatment of advanced prostate cancer with DNA repair deficiency. Increasing demand for germline testing in prostate cancer and a shortage of genetic counselors have created a need for alternative care models and encouraged oncologists to take a more active role in performing germline testing. This article summarizes recommendations for germline testing in prostate cancer and describes care models for providing counseling and testing.

Genetic testing in men with prostate cancer has become more widespread since the discovery that men with metastatic prostate cancer are more likely to carry germline DNA repair gene mutations and the approval of PARP, or poly adenosine diphosphate-ribose polymerase, inhibitors (PARPi) for prostate tumors with DNA repair deficiency. The resulting substantial increase in men with prostate cancer who are eligible for germline testing, with time-sensitive treatment implications, challenges the traditional in-person, time- and resource-intensive cancer genetics care delivery model, and calls for alternative approaches. Urologists, oncologists, and other medical providers are encouraged to take a more active role in delivering germline testing, and they should be aware of current guidelines and optimal pretest and posttest counseling components. This article focuses on the implementation of germline testing in the care of patients with prostate cancer.

Germline genetic testing evaluates for inherited mutations (otherwise known as pathogenic or likely pathogenic variants) that are found in virtually all cells of the body and are derived from the fundamental DNA of an individual. DNA from no cancerous, healthy cells (eg, leucocyte or saliva/buccal swab cells) are used for germline genetic testing. The goals of germline genetic testing are to evaluate for an inherited cancer syndrome; to inform individual and family cancer risks; and to guide cancer prognosis and treatment decisions. Germline testing should be distinguished from recreational and somatic (tumor-specific) testing. Direct-to-consumer recreational genetic testing consists of an at-home test that is advertised to help understand the customers ancestry. Recreational genetic panels look for inherited variants in saliva/buccal swab cells to inform genealogy, and they are not primarily intended to guide medical decisions as they lack gene coverage and clinical-grade precision. None of the recreational genetic tests include a comprehensive assessment of the BRCA1/2 or other DNA damage repair genes and are inadequate for medical purposes. Somatic testing panels are designed to identify alterations in a tumors DNA. A somatic test may occasionally identify mutations expected to be germline, in which case follow-up dedicated germline tests are needed. Examples of somatic panels that report germline mutations include Tempus and UW-Oncoplex. However, many somatic panels use bioinformatics algorithms that may filter out, miss, and/or choose not to report germline mutations. Thus, in general, somatic panels should not be considered adequate for germline conclusions; at most, they should prompt confirmatory germline testing. This articlefocuses on dedicated clinical-grade germline testing.

Germline testing in men with prostate cancer is being performed more often since an important number of prostate cancer cases have a heritable component.1,2 Germline mutations in DNA repair genes, such as BRCA1/2, contribute to hereditary prostate cancer risk and are present in up to 11.8% of men with metastatic prostate cancer,3 compared with 4.6% among men with localized prostate cancer and 2.7% in persons without a known cancer diagnosis.3,4

Germline BRCA1/2 mutations are associated with increased risk of prostate cancer: up to a 3.8-fold increase with BRCA1 and an 8.6-fold increase with BRCA2 mutations.5 Men who carry germline BRCA1/2 mutations are not only at increased risk of developing prostate cancer but are also at risk of a more aggressive prostate cancer phenotype. In their study, Castro et al found that patients with prostate cancer with germline BRCA1/2 mutations at the time of diagnosis were more likely to have higher Gleason score (8) and more advanced stage (T3/4, nodal involvement, and metastases) compared with noncarriers. Men with germline BRCA1/2 mutations also had shorter cancer-specific survival (CSS) than noncarriers (15.7 vs 8.6 years; P=.015).6 Men with localized prostate cancer and germline BRCA1/2 mutations have worse outcomes after definitive treatment with surgery or radiation compared with noncarriers: 5-year metastasis-free survival, 72% vs 94%; P <.001; 5-year CSS, 76% vs 97%; P <.001.7 The prospective PROREPAIR-B study found that germline BRCA2 status is an independent prognostic factor for CSS in patients with metastatic castration-resistant prostate cancer (mCRPC; 17.4 vs 33.2 months; P = .027).8

Based on the study results above and others, the current National Comprehensive Cancer Network (NCCN) guidelines for prostate cancer (version 1.2022)9 recommend germline testing for the subsets of patients with prostate cancer who are more likely to have germline DNA repair mutations (Figure 1).

The NCCN guidelines recommend offeringgermline testing to the following groups of patients with prostate cancer9:

I. Men with node positive, high-risk or very highrisk localized prostate cancer

II. Men with metastatic prostate cancer

III. Men meeting family history criteria (Table 1)

NCCN recommends considering germline testing for men with personal history of prostate cancer and:

I. intermediate risk prostate cancer and intraductal/cribriform histology

II. personal history of exocrine pancreatic, colorectal, gastric, melanoma, pancreatic, upper tract urothelial, glioblastoma, biliary tract or small intestinal cancers

Several commercial vendors provide germline testing panels, including Invitae, Color, and Ambry. Further details and information on available panels can be found on the vendors websites. Panel sizes vary from dedicated BRCA1/2 testing to 91-gene panels. The NCCN guidelines for prostate cancer9 recommend that germline testing panels include genes associated with Lynch syndrome (MLH1, MSH2, MSH6, PMS2) and homologous recombination genes (BRCA1/2, ATM, PALB2, CHEK2).9,10 Broader panels might be appropriate for men with mCRPC, especially if clinical trial participation is being considered. Average turnaround time for germline testing is between 10 and 30 days, which varies depending on the particular panel. The cost of germline testing varies depending on insurance coverage. Some companies offer provide testing for a flat out-of-pocket fee (eg, $250), and a benefit of participating in certain research studies may be no-cost testing.

NCCN guidelines recommend germline testing for a large subset of patients with prostate cancer, but the best care model to offer education and testing is unclear. The traditional clinical care delivery model for cancer genetics includes 2 in-person visits with a genetic counselor, the first for pretest risk assessment and education and the second to discuss the results. This is the most established pathway and, historically, has been utilized the most. However, broadening recommendations for germline testing create great demand that cannot be currently met in a timely fashion by the approximately 4000 genetic counselors in the United States.11,12 Therefore, oncologists and other providers are increasingly performing pretest counseling, ordering genetic testing, and providing posttest counseling for their patients, or following hybrid models (Table 2).13

The provider-led germline testing model has been tested in breast and ovarian cancer but is new in prostate cancer.14-18 Scheinberg et al reported results of a multicenter prospective study evaluating provider-led germline testing for men with prostate cancer. Twelve oncologists received training about the role of germline testing and in counseling patients, and then offered germline testing to patients with mCRPC in their practice. Those patients who accepted germline testing received pretest counseling and educational materials, and later discussed test results in the oncologists office. If a germline mutation was identified, the patient was referred to a genetic counselor to discuss the further implications of the results and to initiate cascade testing. Most patients (63 of 66; 95%) accepted the germline testing and high satisfaction rates were achieved among both oncologists and patients.19 A provider-led germline testing model in the Veterans Affairs health care system was also evaluated. Patients with metastatic prostate cancer were offered germline testing by their oncologists during regular clinic visits. Pretest counseling was provided by oncologists and study coordinators and saliva for the test was collected in the clinic. Posttest counseling sessions with genetic counselors were provided over the phone by the testing panel company. Again, most patients (190 of 227 approached veterans; 84%) accepted testing, and the test completion rate was 80% (182/227).20 Results of early studies suggest that provider-led germline testing in prostate cancer could be effective and satisfactory for both patients and providers.

The need to streamline germline testing also calls for the utilization of new technologies, such as video- or phone-based counseling. The EMPOWER study (NCT04598698) assessed mens preference of in-person genetic counseling vs video-based genetic education21; results indicated that in-person genetic counseling was preferred by men with less education and higher anxiety levels, and it resulted in greater improvement of cancer genetics knowledge. The rates of genetic testing uptake were similar for video-based and in-personcounseling groups.21 Video-based counseling was also evaluated by Tong et al, who compared 2 models of streamlined germline testing in prostate cancer: (a) a take-home genetic kit provided by an oncologist, followed by referral to a genetic counselor if subsequent results are concerning; and (b) a genetic testing station, at which the patient participated in a video call from a genetic counseling assistant for genetics education and collection of family history, which was followed by saliva sample collection and, later, referral to a genetic counselor if any mutation was identified. The latter approach resulted in a lower rate of incomplete tests and a higher rate of follow-up with genetic counselors for positive results. Authors suggested that utilization of video education and involvement of genetic counselor assistants may improve access to germline testing among patients with prostate cancer.22 Several studies are ongoing to evaluate other care models to provide genetic testing in prostate cancer (eg, NCT02917798, NCT03076242, NCT03328091, NCT03503097).23

Oncologists who choose to perform germline testing need to be comfortable with several aspects of genetic counseling and to remain current on the ethics of informed consent and posttest counseling for germline testing (Figure 2). The 2019 Philadelphia Prostate Cancer Consensus Conference suggests that optimal pretest consent should include discussion of the purpose of testing, types of possible results (ie, pathogenic/likely pathogenic; benign/likely benign; variant of unknown significance; no variants identified), the possibility of identifying hereditary cancer syndrome and/or other cancer risks, testings potential cost, the importance of cascade family testing, and the Genetic Information Nondiscrimination Act (GINA) law.12 The GINA law protects against discrimination based on genetics in employment and health insurance; however, it is not applicable to life insurance, long-term care disability insurance, Indian Health services, and patients enrolled into federal employee, Veterans Administration, and US military health benefit plans.23,24 These gaps in protection by GINA law are important to discuss with patients, who may need to consider them before proceeding with the germline testing. Providers should also consider discussing the different panels available for testing, the privacy of genetic tests, and genetic laboratories policies related to sharing and selling of data.12

Providers ordering germline tests also must accept responsibility to follow up with patients if reclassification occurs of a variant of (currently) unknown significance (VUS). VUS are reported in about 30% of men with prostate cancer who undergo germline testing.4 VUS results do not change clinical recommendations, and the majority of them end up being reclassified as benign.25,26 In the Find My Variant Study, 38 of 63 VUS (61%) were reclassified: 32 of 38 (84%) as benign/likely benign and 6 of 38 (16%) as pathogenic/likely pathogenic.27,28 In the rare case when a VUS is reclassified as pathogenic or likely pathogenic, the provider who ordered the test is notified and they are responsible for disclosing the reclassification to the patient. Regardless of the model used, genetic counselor referral is recommended if a patient has a germline mutation identified and/or if clinical suspicion is high for an inherited cancer predisposition. Collaborative efforts are needed to educate oncology providers on aspects of germline testing counseling and to create shared printed and video resources for patients to facilitate informed consent.

Germline testing in men with prostate cancer can potentially benefit not only the patient but also family members. If a germline mutation is identified in a patient, testing for the same mutation in family members (cascade testing) should be performed. For instance, identifying family members with BRCA1/2 mutations could inform potentially lifesaving risk-reducing interventions, eg, prophylactic salpingo-oophorectomy for female BRCA1 mutation carriers. The IMPACT study (Identification of Men with a Genetic Predisposition to Prostate Cancer: Targeted screening ingBRCA1/2mutation carriers and controls) evaluated the utility of prostate-specific antigen (PSA) screening in men aged 40 to 69 years with germline BRCA1/2 mutations compared with its utility in noncarriers.29,30 The study enrolled 3027 men with no personal history of prostate cancer: 919 BRCA1 carriers, 902 BRCA2 carriers, 709 BRCA1 noncarriers, and 497 BRCA2 noncarriers. Preliminary results, reported after 3 years of follow-up, showed that BRCA2 mutation carriers, compared with noncarriers, have a higher incidence of prostate cancer and a younger age of diagnosis. The results for BRCA1 carriers were not definitive, and further investigation is needed. The results from IMPACT suggest annual PSA screening for BRCA2 mutation carriers aged between 40 and 69 years, using PSA cutoff of 3.0 ng/ml.30 Studies evaluating the predictive value of lower PSA cutoff and prostate MRI are ongoing (eg, NCT03805919, NCT01990521).

Advanced disease

PARPi. Patients with DNA repair mutations have higher responserates toPARPiand platinum chemotherapy.31,32 In 2020, two PARPi received FDA approval for treatment of mCRPC with germline or somatic DNA damage repair gene mutations. Rucaparib was approved based on the phase 2 TRITON2 (NCT02952534) study; it reported a 51% (50/98) radiographic response rate among men with mCRPC and BRCA1/2 alterations.33 The benefit for men with non-BRCA DNA repair mutations was less clear, and rucaparib is currently approved only for carriers of BRCA1/2 mutations. 33-35 The olaparib label includes a larger number of mutated genes eligible for treatment (BRCA1, BRCA2, ATM, BRIP1, BARD1, CDK12, CHEK1, CHEK2, FANCL, PALB2, RAD51B, RAD51C, RAD51D, RAD54L), based on results of the phase 3 ProFOUND study (NCT02987543). ProFOUND compared olaparib with enzalutamide or abiraterone and showed improved radiographic progression-free survival (5.8 months vs 3.5 months) with olaparib. 36 Several other ongoing studies are evaluating the efficiency of PARPi monotherapy and combined therapies in mCRPC. Table 3 summarizes study results reporting response rates to PARPi in prostate cancer. 37

Platinum chemotherapy. Historically, platinum chemotherapy has been used to treat tumors, such as ovarian or pancreatic cancer, that have a high frequency of DNA repair mutations.38,39 Early data suggest that platinum chemotherapy is also effective in prostate tumors with DNA repair deficiency.40-43 A retrospective case series by Cheng et al showed that 3 of 3 patients with prostate cancer who had biallelic inactivation of BRCA2 had an exceptional response to platinum chemotherapy after progressing on several therapies.40 The results of a larger retrospective study supported this observation, reporting that 75% (6/8) of patients with mCRPC and withgermline BRCA2 mutations had a PSA50 response (ie, decline of prostate-specific antigen by 50% from baseline) to platinum chemotherapy compared with 17% (23/133) of mCRPC patients without gBRCA2 mutations.41 Mota et al reported a 53% (8/15) PSA50 response to platinum chemotherapy among men with mCRPC and DNA damage repair mutations (ie, BRCA2, BRCA1, ATM, PALB2, FANCA, and CDK12).43

NCCN guidelines recommend considering DNA repair mutation status when discussing the possibility of active surveillance. Germline mutations in BRCA1/2 or ATM are associated with a higher likelihood of grade reclassification among men undergoing active surveillance.44 Mutation carriers should be closely monitored; they could potentially benefit from an earlier definitive treatment approach.

BRCA1/2 carriers have worse outcomes with conventional definitive therapies. Castro et al evaluated the response of BRCA1/2 carriers with localized prostate cancer to 2 radical treatmentsdefinitive radiation and radical prostatectomyand reported that BRCA status is an independent prognostic factor for metastasis-free survival (HR, 2.36; P = .002) and CSS (HR, 2.17; P = .016).7 New treatment approaches in earlier disease stages are being evaluated in clinical trials for patients with prostate cancer and DNA repair deficiency. Targeted therapies, such as PARPi, are being actively investigated in the biochemically recurrent stage of prostate cancer (eg, NCT03047135, NCT03810105, NCT04336943, NCT0353394) and as neoadjuvant therapy in localized disease (eg, NCT04030559).

Germline testing is becoming more commonplace with advances in precision oncology and expanding treatment implications of the results of this testing. The NCCN prostate cancer guidelines recommend germline testing for men with high-risk or very highrisk localized prostate cancer; men with metastatic prostate cancer; patients with intraductal histology of the prostate; and patients meeting family history criteria. These recommendations have created a need for germline testing of many prostate cancer patients, which calls for a change in the traditional cancer genetics delivery model to meet the new demand.45 Oncologists are encouraged to take a more active role in performing germline testing, but the optimal approach is unclear. Until the results of larger trials focusing on various testing delivery models are available, joint efforts are needed to build collaborative relationships between oncologists and genetic specialists. Further efforts are required to create dedicated resources to support providers in this new era of genetic testing and precision oncology in prostate cancer, which is marked by near-constant change.

ACKNOWLEDGMENTS: We gratefully acknowledge support from the Institute for Prostate Cancer Research, NIH/NCI CCSG P30CA015704, NIH SPORE CA097186, NCI T32CA009515 award, Congressional Designated Medical Research Program (CDMRP) award W81XWH-17-2-0043, and the Prostate Cancer Foundation.

Conflict of interest/disclosures: AOS has no conflicts to disclose; HHC receives research funding to her institution fromClovis Oncology, Color Genomics, Janssen Pharmaceuticals, Medivation, Inc. (Astellas Pharma Inc), Phosplatin Therapuetics, and Sanofi S.A., and has a consulting or advisory role withAstraZeneca.

Sokolova is from the Division of Medical Oncology at Oregon Health Science University (OHSU) and the OHSU Knight Cancer Institute.

Cheng is from the Division of Medical Oncology at the University of Washington and the Division of Clinical Research at Fred Hutch Cancer Research Center.

1. Mucci LA, Hjelmborg JB, Harris JR, et al; Nordic Twin Study of Cancer (NorTwinCan) Collaboration. Familial risk and heritability of cancer among twins in Nordic countries. JAMA. 2016;315(1):68-76. doi:10.1001/jama.2015.17703

2. Hjelmborg JB, Scheike T, Holst K, et al. The heritability of prostate cancer in the Nordic Twin Study of Cancer. Cancer Epidemiol Biomark Prev. 2014;23(11):2303-2310. doi:10.1158/1055-9965.EPI-13-0568

3. Pritchard CC, Mateo J, Walsh MF, et al. Inherited DNA-repair gene mutations in men with metastatic prostate cancer. N Engl J Med. 2016;375(5):443-453. doi:10.1056/NEJMoa1603144

4. Nicolosi P, Ledet E, Yang S, et al. Prevalence of germline variants in prostate cancer and implications for current genetic testing guidelines. JAMA Oncol. 2019;5(4):523-528. doi:10.1001/jamaoncol.2018.6760

5. Giri VN, Beebe-Dimmer JL. Familial prostate cancer. Semin Oncol. 2016;43(5):560-565. doi:10.1053/j.seminoncol.2016.08.001

6. Castro E, Goh C, Olmos D, et al. Germline BRCA mutations are associated with higher risk of nodal involvement, distant metastasis, and poor survival outcomes in prostate cancer. J Clin Oncol. 2013;31(14):1748-1757. doi:10.1200/JCO.2012.43.1882

7. Castro E, Goh C, Leongamornlert D, et al. Effect of BRCA mutations on metastatic relapse and cause-specific survival after radical treatment for localised prostate cancer. Eur Urol. 2015;68(2):186-193. doi:10.1016/j.eururo.2014.10.022

8. Castro E, Romero-Laorden N, Del Pozo A, et al. PROREPAIR-B: a prospective cohort study of the impact of germline DNA repair mutations on the outcomes of patients with metastatic castration-resistant prostate cancer. J Clin Oncol. 2019;37(6):490-503. doi:10.1200/JCO.18.00358

9. NCCN Clinical Practice Guidelines in Oncology. Prostate cancer, version 1.2022. https://www.nccn.org/professionals/physician_gls/pdf/prostate.pdf. Accessed 9/10/2021

10. Cheng HH, Sokolova AO, Schaeffer EM, Small EJ, Higano CS. Germline and somatic mutations in prostate cancer for the clinician. J Natl Compr Cancer Netw. 2019;17(5):515-521. doi:10.6004/jnccn.2019.7307

11. Abacan MA, Alsubaie L, Barlow-Stewart K, et al. The global state of the genetic counseling profession. Eur J Hum Genet. 2019;27(2):183-197. doi:10.1038/s41431-018-0252-x

12. Giri VN, Knudsen KE, Kelly WK, et al. Implementation of germline testing for prostate cancer: Philadelphia Prostate Cancer Consensus Conference 2019. J Clin Oncol. 2020;38(24):2798-2811. doi:10.1200/JCO.20.00046

13. Giri VN, Hyatt C, Gomella LG. Germline testing for men with prostate cancer: navigating an expanding new world of genetic evaluation for precision therapy and precision management. J Clin Oncol. 2019;37(17):1455-1459. doi:10.1200/JCO.18.02181

14. George A, Riddell D, Seal S, et al. Implementing rapid, robust, cost-effective, patient-centred, routine genetic testing in ovarian cancer patients. Sci Rep. 2016;6:29506. doi:10.1038/srep29506

15. Yoon SY, Bashah NSAhmad, Wong SW, et al. LBA4_PR. Mainstreaming genetic counselling for genetic testing of BRCA1 and BRCA2 in ovarian cancer patients in Malaysia (MaGiC study). Ann Oncol. 2017;28(suppl 10):x187. doi:10.1093/annonc/mdx729.004

16. Enomoto T, Aoki D, Hattori K, et al. The first Japanese nationwide multicenter study of BRCA mutation testing in ovarian cancer: CHARacterizing the cross-sectionaL approach to Ovarian cancer geneTic TEsting of BRCA (CHARLOTTE). Int J Gynecol Cancer. 2019;29(6):1043-1049. doi:10.1136/ijgc-2019-000384

17. Kemp Z, Turnbull A, Yost S, et al. Evaluation of cancer-based criteria for use in mainstream BRCA1 and BRCA2 genetic testing in patients with breast cancer. JAMA Netw Open. 2019;2(5):e194428. doi:10.1001/jamanetworkopen.2019.4428

18. Colombo N, Huang G, Scambia G, et al. Evaluation of a streamlined oncologist-led BRCA mutation testing and counseling model for patients with ovarian cancer. J Clin Oncol. 2018;36(13):1300-1307. doi:10.1200/JCO.2017.76.2781

19. Scheinberg T, Goodwin A, Ip E, et al. Evaluation of a mainstream model of genetic testing for men with prostate cancer. JCO Oncol Pract. 2021;17(2):e204-e216. doi:10.1200/OP.20.00399

20. Sokolova A, Cheng HH, Montgomery B. Implementation of systematic germline genetic testing (GT) for metastatic prostate cancer (mPC) patients at the Puget Sound VA Prostate Oncology Clinic. J Clin Oncol. 2020;38(15 suppl):abstr 1578. doi:10.1200/JCO.2020.38.15_suppl.1578

21. Giri VN, Bowler N, Hegarty S, et al. Video vs. in-person genetic counseling for men considering germline prostate cancer testing: a patient-choice study. J Clin Oncol. 2020;38(15 suppl):abstr 1577. doi:10.1200/JCO.2020.38.15_suppl.1577

22. Tong B, Borno H, Alagala F, et al. Streamlining the genetics pipeline to increase testing for patients at risk for hereditary prostate cancer. J Clin Oncol. 2021;39(6 suppl):abstr 66. doi:10.1200/JCO.2021.39.6_suppl.66

23. Paller CJ, Antonarakis ES, Beer TM, et al; PCCTC Germline Genetics Working Group. Germline genetic testing in advanced prostate cancer; practices and barriers: survey results from the Germline Genetics Working Group of the Prostate Cancer Clinical Trials Consortium. Clin Genitourin Cancer. 2019;17(4):275-282.e1. doi:10.1016/j.clgc.2019.04.013

24. Genetic discrimination. National Human Genome Research Institute. Updated September 16, 2020. Accessed April 27, 2021. https://www.genome.gov/about-genomics/policy-issues/Genetic-Discrimination

25. Mersch J, Brown N, Pirzadeh-Miller S, et al. Prevalence of variant reclassification following hereditary cancer genetic testing. JAMA. 2018;320(12):1266-1274. doi:10.1001/jama.2018.13152

26. Slavin TP, Manjarrez S, Pritchard CC, Gray S, Weitzel JN. The effects of genomic germline variant reclassification on clinical cancer care. Oncotarget. 2019;10(4):417-423. doi:10.18632/oncotarget.26501

27. Tsai GJ, Raola JMO, Smith C, et al. Outcomes of 92 patient-driven family studies for reclassification of variants of uncertain significance. Genet Med. 2019;21(6):1435-1442. doi:10.1038/s41436-018-0335-7

28. Sokolova AO, Shirts BH, Konnick EQ, et al. Complexities of next-generation sequencing in solid tumors: case studies. J Natl Compr Canc Netw. 2020;18(9):1150-1155. doi:10.6004/jnccn.2020.7569

29. Page EC, Bancroft EK, Brook MN, et al; IMPACT Study Collaborators. Interim results from the IMPACT study: evidence for prostate-specific antigen screening in BRCA2 mutation carriers. Eur Urol. 2019;76(6):831-842. doi:10.1016/j.eururo.2019.08.019

30. Eeles RA, Bancroft E, Page E, Castro E, Taylor N. Identification of men with a genetic predisposition to prostate cancer: targeted screening in men at higher genetic risk and controlsthe IMPACT study. J Clin Oncol. 2013;31(6 suppl):abstr 12. doi:10.1200/jco.2013.31.6_suppl.12

31. Athie A, Arce-Gallego S, Gonzalez M, et al. Targeting DNA repair defects for precision medicine in prostate cancer. Curr Oncol Rep. 2019;21(5):42. doi:10.1007/s11912-019-0790-6

32. Carlson AS, Acevedo RI, Lim DM, et al. Impact of mutations in homologous recombination repair genes on treatment outcomes for metastatic castration resistant prostate cancer. PLoS ONE. 2020;15(9)e0239686. doi:10.1371/journal.pone.0239686

33. Abida W, Bryce AH, Balar AV, et al. TRITON2: an international, multicenter, open-label, phase II study of the PARP inhibitor rucaparib in patients with metastatic castration-resistant prostate cancer (mCRPC) associated with homologous recombination deficiency (HRD). J Clin Oncol. 2018;36(6 suppl):abstr TPS388. doi:10.1200/JCO.2018.36.6_suppl.TPS388

34. Abida W, Campbell D, Patnaik A, et al. Non-BRCA DNA damage repair gene alterations and response to the PARP inhibitor rucaparib in metastatic castration-resistant prostate cancer: analysis from the phase II TRITON2 study. Clin Cancer Res. 2020;26(11):2487-2496. doi:10.1158/1078-0432.CCR-20-0394

35. Sokolova AO, Yu EY, Cheng HH. Honing in on PARPi response in prostate cancer: from HR pathway to gene-by-gene granularity. Clin Cancer Res. 2020;26(11):2439-2440. doi:10.1158/1078-0432.CCR-20-0707

36. de Bono J, Mateo J, Fizazi K, et al. Olaparib for metastatic castration-resistant prostate cancer. N Engl J Med. 2020;382(22):2091-2102. doi:10.1056/NEJMoa1911440

37. Sokolova AO, Cheng HH. Genetic testing in prostate cancer. Curr Oncol Rep. 2020;22(1):5. doi:10.1007/s11912-020-0863-6

38. Alsop K, Fereday S, Meldrum C, et al. BRCA mutation frequency and patterns of treatment response in BRCA mutation-positive women with ovarian cancer: a report from the Australian Ovarian Cancer Study Group. J Clin Oncol. 2012;30(21):2654-2663. doi:10.1200/JCO.2011.39.8545

39. Chetrit A, Hirsh-Yechezkel G, Ben-David Y, Lubin F, Friedman E, Sadetzki S. Effect of BRCA1/2 mutations on long-term survival of patients with invasive ovarian cancer: the national Israeli study of ovarian cancer. J Clin Oncol. 2008;26(1):20-25. doi:10.1200/JCO.2007.11.6905

40. Cheng HH, Pritchard CC, Boyd T, Nelson PS, Montgomery B. Biallelic inactivation of BRCA2 in platinum-sensitive, metastatic castration-resistant prostate cancer. Eur Urol. 2016;69(6):992-995. doi:10.1016/j.eururo.2015.11.022

41. Pomerantz MM, Spisk S, Jia L, et al. The association between germline BRCA2 variants and sensitivity to platinum-based chemotherapy among men with metastatic prostate cancer. Cancer. 2017;123(18):3532-3539. doi:10.1002/cncr.30808

42. Mota JM, Barnett E, Nauseef J, et al. Platinum-based chemotherapy in metastatic prostate cancer with alterations in DNA damage repair genes. J Clin Oncol. 2019;37(15 suppl):abstr 5038. doi:10.1200/JCO.2019.37.15_suppl.5038

43. Mota JM, Barnett E, Nauseef JT, et al. Platinum-based chemotherapy in metastatic prostate cancer with DNA repair gene alterations. JCO Precis Oncol. 2020;4:355-366. doi:10.1200/PO.19.00346

44. Carter HB, Helfand B, Mamawala M, et al. Germline mutations in ATM and BRCA1/2 are associated with grade reclassification in men on active surveillance for prostate cancer. Eur Urol. 2019;75(5):743-749. doi:10.1016/j.eururo.2018.09.021

45. Carlo MI, Giri VN, Paller CJ, et al. Evolving intersection between inherited cancer genetics and therapeutic clinical trials in prostate cancer: a white paper from the Germline Genetics Working Group of the Prostate Cancer Clinical Trials Consortium. JCO Precis Oncol. 2018;2018: PO.18.00060. doi:10.1200/PO.18.00060

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Germline Testing in Prostate Cancer: When and Who to Test - Cancer Network

The Different Ways That ADHD Symptoms Present in Women And How It Affects Everyday Life – YourTango

A generation ago, clinical wisdom strongly suggested that ADHD rarely existed in girls, much less adult women. Researchon ADHD almost exclusively focused on boys and men.

However, research now shows that ADHD in women and girls simply presentsdifferently. This is why the myth that only males have ADHD has persisted for decades.

ADHD in boys is often fairly noticeable because they're disruptive at home and at school. ADHD symptoms in boys often affectothers.

They "act out"aggressively, are hyperactive, restless, and interruptive. Their problems are very noticeable to teachers and parents, so they're more likely to be assessed, diagnosed, and treated.

RELATED:6 Common But Often Overlooked Symptoms Of ADHD In Adults

In some cases, this is also mixed with hyperactivity.

Generally, these girls tend to turn their emotions and behaviors inward that inward vs. outward focus is apparent in many of the behaviors, reactions, and disorders that affect both men and women.

A leading ADHD expert in womens and girls ADHD, Stephen Hinshaw Ph.D.,says that girls', and later womens, symptoms include that they "tend to take their problems out on themselves rather than others. Compared with boys who have the disorder, as well as with girls without it, girls with ADHD suffer more mood disorders such as anxiety and depression as well."

Due to these differences in presentation, teachers and parents often believe girls are just daydreamers, absent-minded, "dumb,"or socially awkward.

Since they often turn inward, they "act out" less and are not as disruptive as boys. Thus parents and teachers often miss these more subtle clues and their significance.

Or they focus solely on concerns about the girls' home lifeor depressive and anxious behaviors, missing the ADHD part of the picture altogether.

Recent research posits that potential adult-onset cases of ADHD are more likely to exist in females.

Research has not been conclusive so far however as to whether this is due to the factors explained above that it's just not seen or assessed due to presenting differently or if it's truly absent before adolescence or young adulthood in more females than males.

There's evidence that genetics plays a large role. Statistics indicate levels of genetic impact align with disorders such as schizophrenia or bipolar disorder.

Genetic factors are thought to contribute up to 40 percent of causes when it comes to these disorders.

Whether it's geneticsor another factor such as nurture orsituational aspects or all of these factors together in some measure, young, older onset, and ongoing adult female ADHD has been found to have a profound impact in womens lives.

The bad news is thatgirlsand young women with undiagnosed ADHDcan become women with higher risk for multiple social and emotional problems,intimate partner violence, self-harm (NSSI, "nonsuicidal self-injury,"harming themselves through cutting, etc.) as well as have a greater incidence of actual suicide attempts.

Females with ADHD have been shown to have impulsive behaviors that lead to factors likestrikingly high rates of unplanned pregnancies, substance abuse, and other "impulse control"problems.

Research has shown that40 percent of women with ADHD encounter these life events versus just 10 percent of young women without ADHD.

Obviously, these effects can come from many factors besides ADHD including situational factors likeexposure to trauma, poverty, or societal/community harms.

RELATED:Im A Lost Girl Of ADHD

Women with ADHD often site their ability to focus for long periods of timeusually called "hyperfocus" as a benefit of ADHD.

Some feel the eclectic point of view ADHD can bring allows them to be more creative. Many have an artistic bent and believe they are able to think outside of the box more easily due to ADHD.

While self-report tests can try to answer the question, "Do I have ADHD?", most professionals believe such tests are only indicators that consultation with an expert is needed.

Assessment and diagnosis are very important. Most women report a sense of relief and clarity upon being diagnosed. They experience a boost in self-esteem and improved functioning when they understand their diagnosis and prognosis.

Another benefit towomen with ADHD and symptoms of ADHD is understanding that no matter the cause of their ADHD,it is treatable.

Some believe medication is the answer.

Medications likeAdderall (mixed amphetamine salts) greatly improve focus for some and lessen anxiety. The majority of therapists and doctors agree that the most beneficial treatment includes a blend of medication and talk therapy.

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A combination of Cognitive Behavioral Therapy (CBT) and Relational Multicultural Theory (RMT)-based therapycan be the most helpful to women experiencing ADHD.

Research backs up this view.

While Cognitive Behavioral Therapy provides a structured way to challenge ones automatic thoughts and choose new ones that better fit our current life circumstances and beliefs, RMT can provide an important addition, especially for women.

Relational Multicultural Theory (RMT) addresses the social anxiety and sense of self or self-esteem aspects of ADHD in women.

RMT was developed by the Stone Center at WellesleyCollege which bases its longitudinal research on girls and women and how they develop and grow.

Their research shows that most teen, young adult, and adult women with ADHD benefit from discussion, education, and therapy experiences that focus on their unique needs as females.

Therapy should include assistance with interactions in relationships, realistic and aspirational relational and personal expectations, and a connection with a therapist that is positive and supportive.

RMT addresses these concerns to help women with ADHD see themselves, their own needsand others' needs, and their path forward in a clearer and more positive light.

This blend of CBT, RMT, and improved research and treatment can help women with this disorder improve their lives and regain their sense of agency in the world.

Though ADHD in women and girls receives less attention than ADHD in men and boys, there are viable options for individuals to lead successful, healthy lives.

RELATED:How Adult ADD & ADHD Can Impact Healthy Relationships

Tracy Deagan is a psychotherapist with a strong background in working with those that experience PTSD, Dissociative disorders, and Healthy Multiplicity from traumatic experiences.

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The Different Ways That ADHD Symptoms Present in Women And How It Affects Everyday Life - YourTango

Breast cancer and genetics: Can it skip a generation? – Medical News Today

There are a number of genes that can cause a person to develop breast cancer. Some of these genes are inheritable, meaning they pass from parent to child. However, having the gene for breast cancer does not always mean a person develops it.

This article will go into detail about the role of genetics in breast cancer, whether breast cancer can skip a generation, and the next steps for a person who has a breast cancer gene.

The American Cancer Society (ACS) notes that inherited genetic factors do not cause the majority of breast cancers. However, there are certain inherited genes that increase a persons chances of developing breast cancer.

A gene is a sequence of DNA that determines certain traits, such as eye or hair color. Genes are transmitted in pairs from biological parents to their child. A child inherits one copy from each parent. Sometimes, a child can inherit a gene with mutations, which means that the gene does not function correctly.

Approximately 510% of breast cancer cases in people are hereditary.

Learn more about breast cancer genes here.

Other forms of breast cancer can occur due to gradual changes in a persons DNA.

These forms of breast cancer, known as somatic mutations, are not due to inherited factors. Somatic mutations occur for a variety of reasons, such as aging or exposure to certain chemicals.

Inherited breast cancer genes cannot skip a generation.

If a person has inherited a gene that causes breast cancer, they have a 50% chance of passing it on to their children. If a persons child does not inherit the mutated gene, the child cannot then pass it on to their future children.

However, while genes cannot skip a generation, the cancer can. Having a mutated gene is not a guarantee that a person will have breast cancer.

A mutated gene is still inheritable, even if the person does not develop breast cancer. This means that a persons child may inherit the mutated gene from them and could develop breast cancer.

There are various inherited gene mutations that can cause a person to develop breast cancer. The most common causes of inherited breast cancer are mutations in the genes BRCA1 and BRCA2.

The BRCA genes are responsible for repairing damage to cells in a persons body. These genes also help certain cells, such as breast or ovarian cells, to grow as expected.

When mutations occur in these genes, it can lead to atypical cell growth. Atypical cell growth can lead to the development of cancer.

If a female inherits a harmful BRCA gene, their risk of developing breast cancer by age 7080 is between 4569%.

Additionally, the ACS notes that males with the BRCA2 gene have a lifetime risk of 6 in 100 for developing breast cancer. Those with the BRCA1 gene have a lifetime risk of 1 in 100.

However, while there has been extensive research on the risk of breast cancer in females with the BRCA1 and BRCA2 genes, there has been less research on the cancer risk in males. As a result, these statistics might not be a true reflection.

Learn more about the BRCA gene here.

The ACS notes that most females who have breast cancer have no family history of the condition. However, having a family history of breast cancer can increase a persons chances of developing it.

A females chances of developing breast cancer double if they have a first degree relative with the condition. A first degree relative is an immediate family member, such as a sister, mother, or daughter.

Breastcancer.org states that a female has a higher risk of inheriting a genetic mutation linked to breast cancer if they have:

The risk of a person developing breast cancer increases with each additional family member who has it. Additionally, having a male relative who has breast cancer also increases a females chances of having it.

More research is necessary to determine the effects of family history on a males chances of developing breast cancer.

If a person is concerned that they may have inherited a breast cancer gene, they should speak with a doctor. A doctor may suggest for a person to undergo genetic counseling.

Genetic counseling involves a person speaking with a genetic counselor about their chances of developing breast cancer. Genetic counselors can also provide a person with resources and support.

This type of counseling can also help a person decide if they would like to take part in genetic testing or not. Genetic testing involves checking a persons genetic profile for breast cancer-causing genes.

Genetic testing for cancer usually involves a person submitting a blood sample. However, other forms of genetic testing can use cell samples from a persons:

If a person knows they have a BRCA gene, there are various medical options available to them.

These options include the following:

Breastcancer.org suggests that a person with a high risk of developing breast cancer may benefit from having more frequent screenings.

A person can speak with a doctor about how often they should get screened for breast cancer.

This can involve:

There are certain medications that can help reduce a persons chances of developing hormone receptor-positive breast cancer.

Hormone receptor-positive breast cancers contain hormone receptors that are activated by certain hormones. When these hormones bind to the hormone receptors, they can stimulate growth in the cancer.

Hormonal therapy medications reduce the amount of these hormones in a persons body.

These medications include:

A person may choose to have risk-reduction surgery if they have a high risk of developing breast cancer.

According to the National Cancer Institute, risk-reduction surgery for breast cancer can involve removing one or both breasts, ovaries, or both pairs. There are two types of risk-reducing surgeries: bilateral prophylactic mastectomy and salpingo-oophorectomy.

Bilateral prophylactic mastectomies involve removing both breasts, including a persons nipples, which is known as a total mastectomy. The other option is a subcutaneous mastectomy, which involves removing as much breast tissue as possible while leaving a persons nipples intact.

A total mastectomy reduces a persons risk of developing breast cancer better than a subcutaneous mastectomy.

A salpingo-oophorectomy involves the removal of a persons ovaries and fallopian tubes. Removing the ovaries reduces the amount of estrogen in someones body, which can slow the growth of some breast cancers. Estrogen can promote the growth of some types of breast cancer.

For people with a mutation in the BRCA1 and BRCA2 genes, a bilateral prophylactic mastectomy can reduce the risk of breast cancer by at least 95%.

It can also reduce the risk of breast cancer in people with a strong family history of this condition by up to 90%.

A salpingo-oophorectomy can reduce the chances of breast cancer in people with a high risk by 50%.

For people with mutated BRCA genes, premenopausal removal of their ovaries and fallopian tubes can reduce breast cancer risk by 50% and ovarian cancer risk by 8595%.

Ovary removal may also increase a persons chances of survival if they do develop breast cancer due to mutated BRCA genes.

Inherited genetic factors may cause a person to develop breast cancer. However, a person who inherits a breast cancer gene may not always develop cancer.

This means that a breast cancer gene can appear to skip a generation, even though it does not.

If a person has a family history of breast cancer, they are at a higher risk of developing it. A person can speak with a doctor about their risk of breast cancer to see if they may qualify for or benefit from genetic counseling.

A person can then decide if they would like to have genetic testing.

If a person has a mutated BRCA gene, there are various medical options available to them. A person should speak with a doctor about which option is right for them.

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Breast cancer and genetics: Can it skip a generation? - Medical News Today

Gordon Stenhouse, Grizzly whisperer, on humans sharing the world with bears – Maclean’s

Biologist Gordon Stenhouse has observed grizzlies respect for humans. He wishes wed return the favour.

I wanted to be a veterinarian, but I didnt get into vet school. So I went into wildlife biology. In the early 80s, I got a job studying polar bears and, over many years in the Arctic, I was fortunate to also work on many other speciesDall sheep, peregrine falcons, Arctic-nesting geese, barren-ground caribou. Of all the species I worked on, I enjoyed polar bears the most.

I worked for the Northwest Territories government out in Manitobas Cape Churchill, where congregations of polar bears gather every fall waiting for the sea ice to form. My job was to figure out how to keep polar bears and people apartwhat we call bear deterrence. I lived with an assistant in a fire tower, basically an eight-by-eight-foot box on a tower, just watching the bears and taking notes. I couldnt really go down on the ground much, because there were bears all around us. I thought I had the best job in the world.

Later, I moved to Alberta and worked for a forestry company, which was a very good jobI had a pension and benefits, all that. But I left it for a one-year position to work with grizzly bears, getting paid by the hour. Just imagine, coming home and telling your wife that when you have two small kids.

MORE:Arctic narwhals have a new enemy: the noise of passing ships

Scientists had just figured out how to do DNA population inventories. You get hair samples from bears and run DNA profiles on themjust like the CSI stuff you see on TV, but it takes more time. We learned there were fewer bears than expected. After a few years of inventory work, the Alberta government put a stop to the spring bear hunt [in 2006]. We began to think, how do we recover bear populations? We learned about how road densities affect the survival of bears and that we needed to manage roadswhich is really managing people.

(Courtesy of Gordon Stenhouse)

We used radio collars to understand bear movements. In the early days, we would have to fly around in a helicopter and find the bear, then send a signal to the collar to get the data. One day were flying and I see people walking on this trail up the hillside. And going down toward these people is our collared bear, a big male. I thought, oh no, this is going to be a wreck. We were going to stop our work and go chase the bear away, but before we could descend, the bear walked off the trail and sat down about 20 m away, the way a dog would sit, on his haunches. He watched these people walk by, and then he went back to the trail and kept walking. Generally bears want to stay away from people, but theyll share their world with us. And its our responsibility to show them the same respect.

Every time I capture and handle a bear, I think this better be worth it. This bear is minding his own business, and you come in with a helicopter and dart him, put a collar on him and when he wakes up, hes missing a tooth. When someone shoots a collared bear that youve followed for many years, you think, how can humans be like this? Here are bears, sharing their world with us, tolerating us, walking by us on the trail. And this is how we treat them?

I think its possible to balance the needs of humans and bears, but its not easy. We have to make decisions that certain areas are more important for wildlife than for humans. It doesnt mean we cant use those areas, but it has to be controlled usemaybe hiking only, maybe no trucks or quads. Or we cant disturb the landscape for natural resource extraction, we just leave it as it is.

READ:Tseketi, the 100-year-old B.C.sturgeon thats here to save her species

We just finished two inventory projects over the last few years, and the populations in two areas have doubled. Weve also learned that some of the changes made for forestry, like taking big patches of old forest and making them into younger patches, can be good for bears. We have produced, in my view, the most comprehensive database of grizzly bears in North America, and this amazing genetic database. Its a gold mine of data. In my office, I had boxes and boxes stacked to the ceiling. While watching the 2014 Sochi Olympics, I realized that they werent using blood samples to test athletes prior to the Gamesthey were taking hair samples, because hair contains long-term signatures of chemicals. So I thought, we must be able to do something more with this hair. We started looking at hair cortisol, to look at stress and reproductive hormones. Id never imagined that we would be able to do that with hair samples when we collected them.

Sometimes in science, you just happen upon a finding. In grad school, we were taught that grizzlies are a solitary species that only come together when they mate, and then the mom is on her own with the cubs. But one year, in 2012, we had three adult female bears collared. And, from the genetics, we knew they were relateda female, her sister and her daughter. All three of these females had cubs, and they met up on a mountain, and over the course of the next few weeks, those bears were together all the time, with their six little cubs running around. They travelled together, bedded down together. It made me think of a family reunion, when people meet at the summer cottage. And I always say to myself, I wonder if they took the right cubs with them when they left?

Despite all the research, we will likely never know everything about the lives of bears. I find it pleasing that we still have much to learn. Canadians are fortunate to have many wildlife species that other parts of the world dont have. We have an environment that represents wilderness, and bears to me are a symbol of wilderness. I like to think that if we can manage their habitat and give them what they need, they will be around for future generations. I hope that we can conserve them for many, many years to come.

As told to Michelle Cyca

This article appears in print in the November 2021 issue of Macleans magazine with the headline, Here be bears. Subscribe to the monthly print magazine here.

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Gordon Stenhouse, Grizzly whisperer, on humans sharing the world with bears - Maclean's

Care of men with cancer-predisposing BRCA variants – The BMJ

Men and women are equally likely to inherit or pass on a cancer-predisposing BRCA variantfamily history of cancers needs to encompass both sides of the family

Men with cancer-predisposing BRCA variants have an increased risk of developing breast cancer and are advised to be breast aware

Men with cancer-predisposing BRCA2 variants have an increased risk of developing aggressive prostate cancer (men with cancer-predisposing BRCA1 variants may also have an increased risk); it is not yet known whether prostate specific antigen screening reduces mortality in men with cancer-predisposing BRCA variants

The European Association of Urology recommends that PSA screening is offered to men with cancer-predisposing BRCA2 variants from 40 years of age after discussion of the risks and benefits

Around one in 260 men (~0.4%) inherits a cancer-predisposing BRCA variant that increases their risk of developing prostate, pancreatic, and breast cancer and may affect the health of their family.12 Most of these men are currently unaware that they have a cancer-predisposing BRCA variant, but as genetic testing becomes more common, more men will need medical advice about what having such a variant means for them and their families.

Men are just as likely as women to have a cancer-predisposing BRCA variant, but many people perceive these variants as only being relevant to women. Paradoxically, this could lead to women at very high risk of breast and ovarian cancer missing out on screening and risk-lowering treatment despite a concerning paternal family history. Clinicians might also be less attuned to paternal family history of cancer in assessing womens breast cancer risk.3 This practice pointer covers what cancer-predisposing BRCA variants are, who might be tested; and what health issues men and their clinicians need to know about. We refer to men, but the article also applies to transwomen and some non-binary

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Care of men with cancer-predisposing BRCA variants - The BMJ

Cheetah Cubs Are Born at the Smithsonian Conservation Biology Institute – Smithsonian’s National Zoo and Conservation Biology Institute

Carnivore keepers at the Smithsonian Conservation Biology Institutein Front Royal, Virginia, welcomed a litter of fivecheetah cubs today. Five-year-old female Rosalie birthed the cubs at 5:20 a.m., 8:24 a.m., 9:42 a.m., 10:33 a.m and 11:17 a.m. ET. The family can be viewed via the Cheetah Cub Cam. Ten-year-old Nick, who was the first cheetah born at SCBI, sired this litter. Animal care staff will leave Rosalie to bond with and care for her cubs without interference, so it may be some time before they can determine the cubs'sexes. The cubs appear to be strong, active, vocal and eating well. Keepers will perform a health check on the cubs when Rosalie is comfortable leaving them for an extended period of time.

Staff are closely monitoring Rosalie and her cubs behaviors via webcam.Virtual visitors can observe Rosalie and her cubs on this temporary platform until the cubs leave the den. Keepers provided Rosalie with access to multiple dens, so it is possible she may move the cubs to an off-camera location.

"Seeing Rosalie successfully care for this litterher firstwith confidence is very rewarding,"said Adrienne Crosier, cheetah reproductive biologist at SCBI and head of the Association of Zoos and Aquariums'Cheetah Species Survival Plan. "Being able to witness the first moments of a cheetahs life is incredibly special. As webcam viewers watch our cheetah family grow, play and explore their surroundings, we hope the experience brings them joy and helps them feel a deeper connection to this vulnerable species."

SCBI is part of the Cheetah Breeding Center Coalitiona group of 10 cheetah breeding centers across the United States that aim to create and maintain a sustainable North American cheetah population under human care. These cubs are a significant addition to the Cheetah SSP, as each individual contributes to this program.

The SSP scientists determine which animals to breed by considering their genetic makeup, health and temperament, among other factors. Rosalie and Nick were paired and bred July 9 and 10. Keepers trained Rosalie to voluntarily participate in ultrasounds, and SCBI veterinarians confirmed her pregnancy Aug. 16. Since 2007, 16 litters of cheetah cubs have been born at SCBI.

Cheetahs live in small, isolated populations mostly in sub-Saharan Africa. Many of their strongholds are in eastern and southern African parks. Due to human conflict, poaching and habitat and prey-base loss, there are only an estimated 7,000 to 7,500 cheetahs left in the wild. The International Union for Conservation of Nature considers cheetahs vulnerable to extinction.

The Zoos legacy of conservation work extends beyond the public Zoo in Washington, D.C., to SCBI in Front Royal, Virginia. Scientists at SCBI study and breed more than 20 species, including some that were once extinct in the wild, such as black-footed ferrets and scimitar-horned oryx. Animals thrive in specialized barns and building complexes spread over more than 3,200 acres. The sprawling environment allows for unique studies that contribute to the survival of threatened, difficult-to-breed species with distinct needs, especially those requiring large areas, natural group sizes and minimal public disturbance.

SCBI spearheads research programs at its headquarters in Virginia, the Zoo in Washington, D.C., and at field research stations and training sites worldwide. SCBI scientists tackle some of todays most complex conservation challenges by applying and sharing what they learn about animal behavior and reproduction, ecology, genetics, migration and conservation sustainability.

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Cheetah Cubs Are Born at the Smithsonian Conservation Biology Institute - Smithsonian's National Zoo and Conservation Biology Institute

Maryland scientists mapped the DNA of a blue crab for the first time. It could unlock new clues to understanding the species. – Frederick News Post

In the basement of a lab at Baltimores Inner Harbor, The Chosen One was born.

At least, thats what the researchers at the University of Marylands Center for Environmental Science called her. She was the blue crab who would be the foundation of a breakthrough scientific discovery the first map of the species DNA.

Through a process known as genome sequencing, the scientists created a virtual blue crab encyclopedia, which appears on a computer screen as a color-coded network of thousands of nucleotides the genetic building blocks that make a blue crab a blue crab.

The genomes contents, researchers say, hold a range of potential clues to help them better understand and protect the states beloved crustacean. It could help pinpoint what mutations drive disease, for example, or track how climate change affects the species in the wild. It could even provide a blueprint on how to breed the meatiest crabs in a lab for Maryland picnic tables in summers to come.

Scientists had published genome assemblies for 67 different crustaceans, from the Chinese mitten crab to the shrimp. But until this year, the genetic road map of the blue crab remained largely a mystery.

The project took four researchers about four years a timeline that included raising The Chosen One in the lab. Its an arduous process, but one thats become more achievable thanks to technological advancements. By comparison, a first draft of the human genome was unveiled in 2000, but completing it took until this summer.

The work began on the waters of the Chesapeake Bay one day in October 2018. UMCES professor J. Sook Chung boarded a crabbers boat off Pasadena and harvested dozens of young female crabs to bring back to her lab at the Institute of Marine and Environmental Technology in downtown Baltimore.

After years of raising crabs in her lab, one question plagued her: Why is it that one mother crab can produce millions of eggs, but only a lucky few survive to adulthood?

Genomic sequencing could provide the answer.

To get there, the scientists had to raise the chosen crab, which then gave birth in the lab to dozens of healthy babies, proving her genetic viability. Then, they extracted as much blood and soft tissue from that crab and sent those samples to a lab in Rockville for DNA extraction.

Then, Baltimore scientists received a trove of information from the Rockville lab that they had to piece together, bit by bit. It was terabytes upon terabytes of data, which had to be processed by a computer for five to six months at a time. Thats because the results were full of extra, repetitive genetic information, which they had to comb through to craft each individual chromosome.Its a little bit like ads when youre watching Hulu and you get the same ads again and again, said Tsvetan Bachvaroff, another professor at the University of Maryland center.

When the intricate jigsaw puzzle was complete, the group determined that blue crabs have 40 to 50 chromosomes. Thats nearly double the number in humans, but each one is considerably shorter than ours. There are still some small gaps in the blue crab genome, but future research could fill in the holes.

The scientists article was published last month in the peer-reviewed journal G3: Genes, Genomes, Genetics. The entire sequence will soon be available for public viewing.

The Maryland scientists are now able to compare the DNA of other blue crabs to the model theyve created to understand what drives any differences between them. For instance, what genes decide the crabs size and color? What genetic differences separate a Maryland crab from one native to the waters of, say, Venezuela?

In Baltimore, theyve already determined which part of the sequence encodes the hormone that controls molting, when crabs shed their shells so they can grow. Manipulating this gene could pave the way for improvements in large-scale blue crab farming, Chung said. Thats important because when blue crabs grow in a tank, they molt at different times. Crabs with soft bodies are vulnerable to their bloodthirsty brethren.Blue crabs are sort of notorious for cannibalistic behaviors. They dont care if theyre siblings. If you culture them in a communal tank thousands of them eventually, theres just one big crab. They will eat each other, Chung said. If you synchronize all of the animals sharing the water shedding the shell at the same time, you can remove those cannibalistic behaviors.

Molting is also a vulnerable time for crabs in the wild, and the environment theyre in during that time has a profound impact on their future health and size, said Genine McClair, blue crab program manager for the Maryland Department of Natural Resources. Understanding more about what drives the process could help fisheries managers adjust harvest practices in pursuit of the best crabs, she said.

Now, we have this starting point to ask all these questions, and researchers from all over the country can ask these questions, but they have to reference back to Maryland as where it all began, she said.

All told, the sequencing project cost less than $250,000, much of which came from Maryland-based donors like Mike and Trish Davis of Severna Park. The couple, who ran a software company for decades before their retirement 12 years ago, was looking to support projects that might have trouble getting off the ground without an initial burst of donor funds.Its just a tough project because we dont know exactly what the benefits will be, and people dont like to fund that sort of thing, Mike Davis said.

Slowly, Davis and his wife assembled a group of donors, who collectively gave about $140,000 to the genome project, Davis said.

There was a competitive spirit that helped the scientists in Baltimore make their case, Davis said. The scientists joked about a general rivalry with counterparts in Virginia who also study blue crabs.

They told us: Well, its going to get mapped, its just a matter of who, Davis said. We dont want Virginia to do this, of course, as proud Marylanders.

On a recent afternoon, Chung fed the labs latest crop of blue crabs from the bay, each stored in an orange Home Depot bucket, with oxygen tubes piping bubbles into their watery homes. Its a seven-day-a-week job, she said, to keep the crabs healthy and note their progress.

Sporting a red T-shirt with an image of blue crab sewn on the back, Chung weaved between vast blue tanks to a dark corner of the lab, where minuscule baby crabs grow. Each with their own underwater cubicle, illuminated only by gentle red light, the dime-sized crabs are delicate creatures.

In a way, its fitting Chung was part of the genome sequencing work. Her first name, Sook, is another word for a mature female blue crab, as shes quick to point out. And her earlier work had unveiled some of the creatures more carefully guarded secrets. In 2014, for example, she was part of a team that discovered a new sex hormone in the eyestalks of female blue crabs.

But this recent project feels the most significant, she said the equivalent of passing a baton to the relay runners of tomorrow.

This is a digitized legacy to those who are coming for the next generation of scientists, she said. Thats the way I see it. I left something behind.

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Maryland scientists mapped the DNA of a blue crab for the first time. It could unlock new clues to understanding the species. - Frederick News Post

Weight Loss and Hair Loss: Connection, Prevention, and More – Greatist

Have your luscious locks lost their luster lately? While hair loss can be a normal part of getting older, rapid hair loss could be a sign that somethings up. If youve also been losing weight, its important to understand whether your weight loss and hair loss could be related.

Sudden or rapid weight loss is associated with a condition called telogen effluvium (TE). Its the most common cause of widespread hair loss.

Why does it happen? Stress or trauma may temporarily mess with your hairs growth cycle and cause too much hair to shed at once.

Nutrient deficiencies also seem to be connected to this condition, but that doesnt mean its always a good idea to hit the supplement aisle. In some cases, getting too much of certain vitamins can actually make hair loss worse or put you at risk of toxicity.

A healthcare professional can help you decide whether supplements are right for you.

Keep in mind that TE usually lasts only about 6 months and tends to clear up on its own.

If youre following a very restrictive diet to lose weight, you may be cutting out entire food groups. This can lead to deficiencies in nutrients like zinc, protein, iron, and fatty acids. And those deficiencies can be bad news for your hair health.

A 2015 study of 180 women with hair loss found that iron deficiency and psychological stress were common causes of hair loss.

Research suggests that very low calorie crash diets are another culprit for these nutrient deficiencies. Dieting can also cause psychological stress, which is a major hair loss trigger.

Its important to talk with a healthcare professional before starting a new diet. In general, aim for a balanced diet that includes a variety of fresh fruits, vegetables, grains, and proteins.

Amino acids help your body produce the main structural protein of hair, called keratin. Deficiencies in specific amino acids (like leucine, histidine, valine, and cysteine) are common in folks with hair loss.

A 2017 study in 100 people with hair loss found that a large portion of the participants had leucine and histidine deficiencies. Cysteine and valine deficiencies were also common.

To up your amino acid intake, you can add more protein to your diet. Meat is a solid source of protein, but there are vegetarian and vegan protein options too. Some popular choices are:

Weight loss surgery (such as sleeve gastrectomy) has been linked to low levels of protein, vitamins, and minerals and those deficiencies can lead to hair loss.

A 2018 study of 50 folks who underwent a sleeve gastrectomy found that 56 percent of participants experienced hair loss. Researchers also noted that the peeps who had hair loss also had low levels of vitamin B12 and zinc before and after surgery.

Its tough to say exactly how long hair loss will last after weight loss surgery. In a 2021 study of 112 women who had sleeve gastrectomy surgery, 72 percent of participants experienced hair loss after surgery. In 79 percent of those people, the hair loss started 3 to 4 months after surgery and resolved in about 5.5 months.

Hair loss during weight loss tends to be triggered by rapid weight loss or a diet-related nutrient deficiencies. Try to stick to a sustainable weight loss program instead of an overly restrictive diet. And aim to maintain a balanced diet that includes all the vital vitamins and nutrients your body needs.

Always talk with a healthcare pro before making any major changes to your lifestyle. They can customize a diet or supplement regimen to help get your hair growth back on track.

Hair loss itself isnt a risk to your health, but it can be a sign of an underlying medical condition. Its important to contact a doc ASAP if you experience:

Hair loss is a common side effect of rapid weight loss or nutrient deficiencies. While the hair loss itself isnt dangerous, the underlying cause might be more serious.

Talk with a healthcare pro if you start to notice that your hair is shedding or thinning rapidly, if you notice bald patches, or if clumps of your hair start to fall out. They can help you figure out the cause and the best treatment plan for you.

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Weight Loss and Hair Loss: Connection, Prevention, and More - Greatist

The five biggest threats to our natural world and how we can stop them – The Guardian

The worlds wildlife populations have plummeted by more than two-thirds since 1970 and there are no signs that this downward trend is slowing. The first phase of Cop15 talks in Kunming this week will lay the groundwork for governments to draw up a global agreement next year to halt the loss of nature. If they are to succeed, they will need to tackle what the IPBES (Intergovernmental Science-Policy Platform on Biodiversity and Ecosystem Services) has identified as the five key drivers of biodiversity loss: changes in land and sea use; direct exploitation of natural resources; climate change; pollution; and invasion of alien species.

1

Changes in land and sea use

Its hidden destruction. Were still losing grasslands in the US at a rate of half a million acres a year or more.

Tyler Lark, from the University of Wisconsin-Madison, knows what he is talking about. Lark and a team of researchers used satellite data to map the expansion and abandonment of land across the US and discovered that 4m hectares (10m acres) had been destroyed between 2008 and 2016.

Large swathes of the United States great prairies continue to be converted into cropland, according to the research, to make way for soya bean, corn and wheat farming.

Changes in land and sea use has been identified as the main driver of unprecedented biodiversity and ecosystem change over the past 50 years. Three-quarters of the land-based environment and about 66% of the marine environment have been significantly altered by human actions.

North Americas grasslands often referred to as prairies are a case in point. In the US, about half have been converted since European settlement, and the most fertile land is already being used for agriculture. Areas converted more recently are sub-prime agricultural land with yields 70% lower than the national average, which means a lot of biodiversity is being lost for diminishing returns.

Our findings demonstrate a pervasive pattern of encroachment into areas that are increasingly marginal for production but highly significant for wildlife, Lark and his team wrote in the paper, published in Nature Communications.

Boggier areas of land, or those with uneven terrain, were traditionally left as grassland, but in the past few decades, this marginal land has also been converted. In the US, 88% of cropland expansion takes place on grassland, and much of this is happening in the Great Plains known as Americas breadbasket which used to be the most extensive grassland in the world.

According to the UNs Convention on Biological Diversity there arefive main threatsto biodiversity. In descending order these are: changes in land and sea use; direct exploitation of natural resources; climate change; pollution and invasive species.

1.For terrestrial and freshwater ecosystems, land-use change has had the largest relative negative impact on nature since 1970.More than a third of the worlds land surface and nearly 75% of freshwater resources are now devoted to crop or livestock production.Alongside a doubling of urban area since 1992, things such as wetlands, scrubland and woodlands which wildlife relies on are ironed out from the landscape.

2. The direct exploitation of organisms and non-living materials,including logging, huntingand fishing and the extraction of soils and water are allnegatively affecting ecosystems.In marine environments, overfishing is considered to be the most serious driver of biodiversity loss.One quarter of the worlds commercial fisheries are overexploited, according to a 2005Millennium Ecosystem Assessment.

3. The climate crisis is dismantling ecosystems at every level. Extreme weather events such as tropical storms and flooding are destroyinghabitats.Warmer temperatures are also changing the timing of natural events such as theavailability of insects and when birds hatch their eggs in spring. The distribution of species and their range is also changing.

4. Many types of pollution are increasing. In marine environments, pollution from agricultural runoff (mainlynitrogen and phosphorus)do huge damage to ecosystems. Agricultural runoff causes toxic algal blooms and even"dead zones"in the worst affectedareas.Marine plastic pollution has increased tenfold since 1980,affecting at least 267 species.

5. Since the 17th century, invasive species havecontributed to 40%of all known animal extinctions. Nearly one fifth of the Earths surface is at risk of plant and animal invasions. Invasive species change the composition of ecosystems by outcompeting native species.

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Hotspots for this expansion have included wildlife-rich grasslands in the prairie pothole region which stretches between Iowa, Dakota, Montana and southern Canada and is home to more than 50% of North American migratory waterfowl, as well as 96 species of songbird. This cropland expansion has wiped out about 138,000 nesting habitats for waterfowl, researchers estimate.

These grasslands are also a rich habitat for the monarch butterfly a flagship species for pollinator conservation and a key indicator of overall insect biodiversity. More than 200m milkweed plants, the caterpillars only food source, were probably destroyed by cropland expansion, making it one of the leading causes for the monarchs national decline.

The extent of conversion of grassland in the US makes it a larger emission source than the destruction of the Brazilian Cerrado, according to research from 2019. About 90% of emissions from grassland conversion comes from carbon lost in the soil, which is released when the grassland is ploughed up.

The rate of clearing that were seeing on these grasslands is on par with things like tropical deforestation, but it often receives far less attention, says Lark.

Food crop production globally has increased by about 300% since 1970, despite the negative environmental impacts.

Reducing food waste and eating less meat would help cut the amount of land needed for farming, while researchers say improved management of existing croplands and utilising what is already farmed as best as possible would reduce further expansion.

Lark concludes: I think theres a huge opportunity to re-envision our landscapes so that theyre not only providing incredible food production but also mitigating climate change and helping reduce the impacts of the biodiversity crisis by increasing habitats on agricultural land.PW

2

Direct exploitation of natural resources

From hunting, fishing and logging to the extraction of oil, gas, coal and water, humanitys insatiable appetite for the planets resources has devastated large parts of the natural world.

While the impacts of many of these actions can often be seen, unsustainable groundwater extraction could be driving a hidden crisis below our feet, experts have warned, wiping out freshwater biodiversity, threatening global food security and causing rivers to run dry.

Farmers and mining companies are pumping vast underground water stores at an unsustainable rate, according to ecologists and hydrologists. About half the worlds population relies on groundwater for drinking water and it helps sustain 40% of irrigation systems for crops.

The consequences for freshwater ecosystems among the most degraded on the planet are under-researched as studies have focused on the depletion of groundwater for agriculture.

But a growing body of research indicates that pumping the worlds most extracted resource water is causing significant damage to the planets ecosystems. A 2017 study of the Ogallala aquifer an enormous water source underneath eight states in the US Great Plains found that more than half a century of pumping has caused streams to run dry and a collapse in large fish populations. In 2019, another study estimated that by 2050 between 42% and 79% of watersheds that pump groundwater globally could pass ecological tipping points, without better management.

The difficulty with groundwater is that people dont see it and they dont understand the fragility of it, says James Dalton, director of the global water programme at the International Union for Conservation of Nature (IUCN). Groundwater can be the largest and sometimes the sole source in certain types of terrestrial habitats.

Uganda is luxuriantly green, even during the dry season, but thats because a lot of it is irrigated with shallow groundwater for agriculture and the ecosystems are reliant on tapping into it.

According to UPGro (Unlocking the Potential of Groundwater for the Poor), a research programme looking into the management of groundwater in sub-Saharan Africa, 73 of the 98 operational water supply systems in Uganda are dependent on water from below ground. The country shares two transboundary aquifers: the Nile and Lake Victoria basins. At least 592 aquifers are shared across borders around the world.

Some of the groundwater reserves are huge, so there is time to fix this, says Dalton. Its just theres no attention to it.

Inge de Graaf, a hydrologist at Wageningen University, who led the 2019 study into watershed levels, found between 15% to 21% had already passed ecological tipping points, adding that once the effects had become clear for rivers, it was often too late.

Groundwater is slow because it has to flow through rocks. If you extract water today, it will impact the stream flow maybe in the next five years, in the next 10 years, or in the next decades, she says. I think the results of this research and related studies are pretty scary.

In April, the largest ever assessment of global groundwater wells by researchers from University of California, Santa Barbara, found that up to one in five were at risk of running dry. Scott Jasechko, a hydrologist and lead author on the paper, says that the study focuses on the consequences for humans and more research is needed on biodiversity.

Millions of wells around the world could run dry with even modest declines in groundwater levels. And that, of course, has cascading implications for livelihoods and access to reliable and convenient water for individuals and ecosystems, he says.PG

In 2019, the European heatwave brought 43C heat to Montpellier in France. Great tit chicks in 30 nest boxes starved to death, probably because it was too hot for their parents to catch the food they needed, according to one researcher. Two years later, and 2021s heatwave appears to have set a European record, pushing temperatures to 48.8C in Sicily in August. Meanwhile, wildfires and heatwaves are stripping the planet of life.

Until now, the destruction of habitats and extraction of resources has had a more significant impact on biodiversity than the climate crisis. This is likely to change over the coming decades as the climate crisis dismantles ecosystems in unpredictable and dramatic ways, according to a review paper published by the Royal Society.

There are many aspects of ecosystem science where we will not know enough in sufficient time, the paper says. Ecosystems are changing so rapidly in response to global change drivers that our research and modelling frameworks are overtaken by empirical, system-altering changes.

The calls for biodiversity and the climate crisis to be tackled in tandem are growing. It is clear that we cannot solve [the global biodiversity and climate crises] in isolation we either solve both or we solve neither, says Sveinung Rotevatn, Norways climate and environment minister, with the launch in June of a report produced by the worlds leading biodiversity and climate experts. Zoological Society of London senior research fellow Dr Nathalie Pettorelli, who led a study on the subject published in the Journal of Applied Ecology in September, says: The level of interconnectedness between the climate change and biodiversity crises is high and should not be underestimated. This is not just about climate change impacting biodiversity; it is also about the loss of biodiversity deepening the climate crisis.

Writer Zadie Smith describes every countrys changes as a local sadness. Insects no longer fly into the house when the lights are on in the evening, the snowdrops are coming out earlier and some migratory species, such as swallows, are starting to try to stay in the UK for winter. All these individual elements are entwined in a much bigger story of decline.

Our biosphere the thin film of life on the surface of our planet is being destabilised by temperature change. On land, rains are altering, extreme weather events are more common, and ecosystems more flammable. Associated changes, including flooding, sea level rise, droughts and storms, are having hugely damaging impacts on biodiversity and its ability to support us.

In the ocean, heatwaves and acidification are stressing organisms and ecosystems already under pressure due to other human activities, such as overfishing and habitat fragmentation.

The latest Intergovernmental Panel on Climate Change (IPCC) landmark report showed that extreme heatwaves that would usually happen every 50 years are already happening every decade. If warming is kept to 1.5C these will happen approximately every five years.

The distributions of almost half (47%) of land-based flightless mammals and almost a quarter of threatened birds, may already have been negatively affected by the climate crisis, the IPBES warns. Five per cent of species are at risk of extinction from 2C warming, climbing to 16% with a 4.3C rise.

Connected, diverse and extensive ecosystems can help stabilise the climate and will have a better chance of thriving in a world permanently altered by rising emissions, say experts. And, as the Royal Society paper says: Rather than being framed as a victim of climate change, biodiversity can be seen as a key ally in dealing with climate change. PW

On the west coast of Scotland, fragments of an ancient rainforest that once stretched along the Atlantic coast of Britain cling on. Its rare mosses, lichens and fungi are perfectly suited to the mild temperatures and steady supply of rainfall, covering the crags, gorges and bark of native woodland. But nitrogen pollution, an invisible menace, threatens the survival of the remaining 30,000 hectares (74,000 acres) of Scottish rainforest, along with invasive rhododendron, conifer plantations and deer.

While marine plastic pollution in particular has increased tenfold since 1980 affecting 44% of seabirds air, water and soil pollution are all on the rise in some areas. This has led to pollution being singled out as the fourth biggest driver of biodiversity loss.

In Scotland, nitrogen compounds from intensive farming and fossil fuel combustion are dumped on the Scottish rainforest from the sky, killing off the lichen and bryophytes that absorb water from the air and are highly sensitive to atmospheric conditions.

The temperate rainforest is far from the sources of pollution, yet because its so rainy, were getting a kind of acid rain effect, says Jenny Hawley, policy manager at Plantlife, which has called nitrogen pollution in the air the elephant in the room of nature conservation. The nitrogen-rich rain thats coming down and depositing nitrogen into those habitats is making it impossible for the lichen, fungi, mosses and wildflowers to survive.

Environmental destruction caused by nitrogen pollution is not limited to the Scottish rainforest. Algal blooms around the world are often caused by runoff from farming, resulting in vast dead zones in oceans and lakes that kill scores of fish and devastate ecosystems. Nitrogen-rich rainwater degrades the ability of peatlands to sequester carbon, the protection of which is a stated climate goal of several governments. Wildflowers adapted to low-nitrogen soils are squeezed out by aggressive nettles and cow parsley, making them less diverse.

About 80% of nitrogen used by humans through food production, transport, energy and industrial and wastewater processes is wasted and enters the environment as pollution.

Nitrogen pollution might not result in huge floods and apocalyptic droughts but we are slowly eating away at biodiversity as we put more and more nitrogen in ecosystems, says Carly Stevens, a plant ecologist at Lancaster University. Across the UK, we have shown that habitats that have lots of nitrogen have fewer species in them. We have shown it across Europe. We have shown it across the US. Now were showing it in China. Were creating more and more damage all the time.

To decrease the amount of nitrogen pollution causing biodiversity loss, governments will commit to halving nutrient runoff by 2030 as part of an agreement for nature currently being negotiated in Kunming. Halting the waste of vast amounts of nitrogen fertiliser in agriculture is a key part of meeting the target, says Kevin Hicks, a senior research fellow at the Stockholm Environment Institute centre at York.

One of the biggest problems is the flow of nitrogen from farming into watercourses, Hicks says. In terms of a nitrogen footprint, the most intensive thing that you can eat is meat. The more meat you eat, the more nitrogen youre putting into the environment.

Mark Sutton, a professor at the UK Centre for Ecology & Hydrology, says reducing nitrogen pollution also makes economic sense.

Nitrogen in the atmosphere is 78% of every breath we take. It does nothing, its very stable and makes the sky blue. Then there are all these other nitrogen compounds: ammonia, nitrates, nitrous oxide. They create air and water pollution, he says. He argues that if you price every kilo of nitrogen at $1 (an estimated fertiliser price), and multiply it by the amount of nitrogen pollution lost in the world 200bn tonnes it amounts to $200bn (147bn) every year.

The goal to cut nitrogen waste in half would save you $100bn, he says. I think $100bn a year is a worthwhile saving.PG

On Gough Island in the southern Atlantic Ocean, scores of seabird chicks are eaten by mice every year. The rodents were accidentally introduced by sailors in the 19th century and their population has surged, putting the Tristan albatross one of the largest of its species at risk of extinction along with dozens of rare seabirds. Although Tristan albatross chicks are 300 times the size of mice, two-thirds did not fledge in 2020 largely because of the injuries they sustained from the rodents, according to the RSPB.

The situation on the remote island, 2,600km from South Africa, is a grisly warning of the consequences of the human-driven impacts of invasive species on biodiversity. An RSPB-led operation to eradicate mice from the British overseas territory has been completed, using poison to help save the critically endangered albatross and other bird species from injuries they sustain from the rodents. It will be two years before researchers can confirm whether or not the plan has worked. But some conservationists want to explore another controversial option whose application is most advanced in the eradication of malaria: gene drives.

Instead of large-scale trapping or poisoning operations, which have limited effectiveness and can harm other species, gene drives involve introducing genetic code into an invasive population that would make them infertile or all one gender over successive generations. The method has so far been used only in a laboratory setting but at Septembers IUCN congress in Marseille, members backed a motion to develop a policy on researching its application and other uses of synthetic biology for conservation.

If a gene drive were proven to be effective and there were safety mechanisms to limit its deployment, you would introduce multiple individuals on an island whose genes would be inherited by other individuals in the population, says David Will, an innovation programme manager with Island Conservation, a non-profit dedicated to preventing extinctions by removing invasive species from islands. Eventually, you would have either an entirely all male or entirely all female population and they would no longer be able to reproduce.

Nearly one-fifth of the Earths surface is at risk of plant and animal invasions and although the problem is worldwide, such as feral pigs wreaking havoc in the southern United States and lionfish in the Mediterranean, islands are often worst affected. The global scale of the issue will be revealed in a UN scientific assessment in 2023.

We have to be very careful, says Austin Burt, a professor of evolutionary genetics at Imperial College London, who researches how gene drives can be used to eradicate malaria in mosquito populations. If youre going after mice, for example, and youre targeting mice on an island, youd need to make sure that none of those modified mice got off the island to cause harm to the mainland population.

In July, scientists announced they had successfully wiped out a population of malaria-transmitting mosquitoes using a gene drive in a laboratory setting, raising the prospect of self-destructing mosquitoes being released into the wild in the next decade.

Kent Redford, chair of the IUCN Task Force on Synthetic Biology who led an assessment of the use of synthetic biology in conservation, said there are clear risks and opportunities in the field but further research is necessary.

None of these genetic tools are ever going to be a panacea. Ever. Nor do I think they will ever replace the existing tools, Redford says, adding: There is a hope and I stress hope that engineered gene drives have the potential to effectively decrease the population sizes of alien invasive species with very limited knock-on effects on other species.PG

Find more age of extinction coverage here, and follow biodiversity reporters Phoebe Weston and Patrick Greenfield on Twitter for all the latest news and features

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The five biggest threats to our natural world and how we can stop them - The Guardian

Hunting: How can you tell the age of a deer? Here are some tips – pressherald.com

When most folks talk about aging deer theyre referring to venison, and the process of hanging a deer for an extended period to improve flavor and tenderness. However, with the rise in popularity of trail cameras, increasingly more hunters are sharing photos on social media and asking, How old is this deer?

When it comes to the answers you have to consider the source. A lot of well-meaning keyboard biologists offer their opinions, often of questionable accuracy. Fortunately, there are some fairly reliable though not foolproof methods for properly aging deer on the hoof, or from a photo. Lets start with does as they can only be reliably divided into two or three age classes. Early in the season its easy to distinguish does from fawns but as the youngsters grow it becomes more difficult, especially if you dont have multiple deer present for comparison.

First, look at the head and face. A fawns forehead and nose will appear much shorter (think: 8-ounce soda bottle) in comparison to the adult does longer nose (16-ounce soda bottle) and larger head. Next, look at the body. Fawns also have short, square bodies, short necks and less muscle development. An adult does body will be larger and more rectangular-shaped. Necks appear longer and older does may have swayed backs or sagging bellies.

Yearling does look somewhere in between and are best judged in the presence of older and/or younger deer. Its not uncommon for female deer to travel in family groups consisting of several generations, often a mature doe, her fawns and her yearling female offspring from the previous year. The same guidelines apply to buck fawns, though they may show a more square head than a doe, and sometimes you can distinguish tiny nubs or buttons that will eventually become antlers.

Now for the antlered bucks. Yearling bucks appear dainty, with thin necks, somewhat resembling a doe with antlers. Their legs appear long and slender compared to their body. Antler development can be highly variable depending mostly on nutrition and genetics. Many will sport spikes or forked antlers but some may carry a rack of six or even eight points. Regardless, main beams and points are usually thin and short.

Two-year-old bucks generally look somewhat gangly and awkward, though a healthy Maine buck could fool a lot of folks into thinking its older. Legs also appear long for their body, and theyll have a thin waist and shoulders and limited neck swelling. During the rut, tarsal glands may be dark, but very small and round. Rack size also varies but six-, eight- or even 10-point racks that score in the 120s and even 130s are not unusual, and a 2-year-old might dress out somewhere between 140 and 180 pounds, possibly more further north. Antler beams will still be relatively narrow at the base but thicker than a yearling and possibly have more rounded points.

Three-year-old bucks will have a fuller, thickly-muscled neck. The chest appears deeper than the hindquarters, giving a race horse appearance. Horizontal lines of the back and stomach are still straight and taut. Another good characteristic is that you can usually distinguish where the neck meets the shoulders. Tarsal glands during the rut will be dark but small, and staining does not extend down the leg to the hoof. Antler beams become thicker and could be 3 1/2 inches in diameter at the base.

At age 4, bucks reach maturity. Skeletal structure stops growing so they can direct more nutrition to body weight and antler mass. Their fully muscled neck now blends seamlessly into a deep chest. Their rump appears full and rounded and legs may appear slightly short for the body. The stomach and back do not sag, yet. Jaw skin is tight and tarsal glands will be noticeably large and dark. Rack size still varies but most of these deer will fall into what most hunters would consider the trophy category. The base of the beams will be thick, about the same diameter as a deers eye, and may show more dark staining.

Not many deer make it that long in heavily hunted areas but a few do, more so in the big woods where hunting pressure is less. Their neck and brisket will appear to be one continuous muscle and their neck will show heavy swelling. Now the legs really appear too short for the big, blocky body. Their waistline will be even (parallel) with the chest and they may start to show a pot belly and sagging back. Tarsals appear noticeably large and very dark with staining down the inside of the leg to the hoof during the rut. Again, rack size varies but even if they dont carry a crown of thorns, beams will be thick and heavy, especially at the bases.

There are objective criteria for what distinguishes a trophy buck, but for most hunters its a personal and very subjective judgement. A yearling might be a trophy for an inexperienced or unlucky hunter. Many 2- and 3-year-old bucks eventually make their way to the taxidermist. And a gnarly old north woods buck that wont score well in the record book but will pull the scales down well past the 200-pound mark might make the grade for big woods hunters. Still, if you plan to be selective, its nice to know what to look for.

Bob Humphrey is a freelance writer and Registered Maine Guide who lives in Pownal. He can be reached at:[emailprotected]

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