Archive for the ‘Male Genetics’ Category

Have you ever wondered just exactly how your corn develops in the cob? Understanding how corn makes a cob, successful kernels, and packs in starch can be a key component of an agronomic plan.

This top part is the tassel, and that is the male part of the plant, says Sara Meidlinger, market development agronomist for Pride Seeds. Then we have the ear here, its going to develop silks, and its the female part of the plant.

In this episode of Corn School, Meidlinger gives us an overview of how pollination happens and what to expect during a corn crops reproductive stages.

The tassel will emerge and start to shed pollen, and kernels in the ears will shoot up a silk. Every kernel in a cob starts from a developing a silk, which is then fertilized by pollen from the tassel. A pollen tube develops, where the male genetics will travel down the silk towards the kernel. The whole process will take about seven to 10 days. Peak pollen shed from the tassel happens about three to four days after the process has started.

Meidlinger suggests pulling off some ears and getting familiar with your crop over the next couple of weeks. There are six stages that get that cob of corn to maturity:

If you happen to come across European corn borer or cutworm perhaps youve had corn heavy in the rotation it might be a good opportunity to switch to a different hybrid. While youre checking on your corns maturity, its a good time to scout for any insect issues, too.

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Corn School: The birds and the bees of corn that, is - RealAgriculture

Corporate scientists have received final approval from the Environmental Protection Agency (EPA) to release hundreds of millions of genetically altered mosquitoes into the Florida Keys. The goal? To begin reining in the mosquito population, which is only expected to increase as climate change continues to warm and flood the low-lying, tropical Keys. But some environmental groups object strongly to the move.

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Heres how the plan is designed to work: Local officials want to use these neobugs as an alternative to insecticides. The genetic modification, which is a common one being explored by scientists around the world, involves making female larvaeresponsible for laying eggsdie off very young before they can reproduce.

Male mosquitoes spread the gene, and in practice, this means any males spend their, uh, best years passing around a population-reducing time bomb. By generations, the population continues to dwindle.

But does this plan actually work?

While it's hard to find coverage of these events that arent from groups that lobby against genetically modified organisms, that doesnt necessarily mean these groups are wrong. In 2019, a controlled release in Brazil made news around the world when the genetically modified mosquitoes not only lived into fruitful adulthood, but began interbreeding and maybe even strengthening the local mosquito populations. That was a few years after a promising release killed 95 percent of problematic mosquitoes in a Brazilian trial.

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This has led to accusations that biotech firms that plan these events have taken the wrong lesson, to say the very least, from genetic engineering cautionary tales like Jurassic Park. Scientists continue to research ways to self-limit insects using genes, like invasive moths that destroy crops and are resistant to existing chemical technology. With mosquitoes, the stakes are even higher because of the diseases they carry.

Discussing evolution and genetics can end up assigning agency in a strange wayas though an animal chooses something to become, or that the environment chooses which organisms will survive. Whats interesting about breeding self-limiting pests is that a naturally occurring organisms with a gene like this would rapidly die out. Theres no way to breed a natural population the way you might breed flowers of a certain color or a new designer cat breed.

Sponsoring organization Oxitec has focused on the positives of a project like this, and indeed, mosquitoes are gigantic pests that cause almost unfathomable disease spread around the world. Theyre such a bane that people freely suggest wiping them all the way out, which isnt the panacea it sounds like due to, again, those pesky unforeseen environmental consequences.

The Oxitec experiment has gone through layers of approval, from local all the way up to the EPA. Oxitec must notify state officials 72 hours before releasing the mosquitoes and conduct ongoing tests for at least 10 weeks to ensure none of the female mosquitoes reach adulthood, CNN reports.

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Release 750 Million Genetically Modified Mosquitoes Into the Wild, They Said - Popular Mechanics

750 million genetically-modified mosquitos will be released in Florida, as a project to use the mutant bugs to try to control dengue fever, Zika, and other diseases gets the green light. The controversial Oxitec project was granted EPA approval earlier this year, but it was only this week that local regulators gave the go-ahead to the trial.

At the heart of it is a specially customized mosquito. All male, and non-biting, its designed to breed with wild female mosquitoes of the invasive Aedes aegypti species. Its this type which has been found to transmit diseases like dengue, yellow fever, Zika, and chikungunya.

Problem is, theyre also increasingly resistant to pesticides, and that growing tolerance has made chemical attempts to kill the mosquitos off less effective over time. As a result, the Florida Keys Mosquito Control District (FKMCD) has been working with Oxitec on the genetically modified bugs instead.

The idea is straightforward. The male, modified mosquitoes mate with the wild female ones, but also carry a protein thats designed to kill female offspring before they reach the stage where they too would begin biting. Male offspring, however, will survive, but carry on the tweaked genetics to further expand the trial.

The FKMCD board voted four to one in favor of the trial, following Federal and State approvals of an Experimental Use Permit issued by the EPA in May 2020. Part of the requirements set out by the EPA limit where the modified mosquitoes can be released, including not permitting them near to circus orchards, and reporting any adult female mosquitoes found to have reached that age with the OX5034 generic construct.

Its not been a smooth path to this point, however. Environmentalists have pushed back against Oxitecs plans, accusing the company of testing unproven science in public, and raising concerns that the midst of a pandemic is not the right time for it. There are also worries among some that unforeseen mutations could lead to even more resistant versions of the bugs.

Contesting those fears, Oxitec points to similar demonstration projects that took place in Brazil. There, the modified mosquitoes reportedly suppressed disease-carrying Aedes aegypti mosquitoes by up to 95-percent in a high 2-week rolling average after 13 weeks, compared to untreated control sites in the same city.

Exactly when the Florida release will go ahead has not been settled upon. The exact time and location of the trial has yet to be determined, the FKMCD says, but the current Experimental Use Permit granted to Oxitec dictates trials must be completed by 2022. Both the FKMCD and Oxitec have previously said that they plan sometime in 2021 for the launch.

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Mutant mosquitoes approved to help Florida fight dengue and Zika - SlashGear

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With many parents still working from home in the midst of a global pandemic as students return to the virtual classroom, some may wonder if the shows theirkids are streaming when they're not in class are doing anything to stimulate their minds.

Or are they just distracting the kids enough for you to get your work done when they could be doing both?

The good news is, there are plenty of options now available on streaming services to sneak some education into any student's viewing diet while for all they know they're merely being entertained.Choices include shows such as "Avatar: The Last Airbender," "Connected: The Hidden Science of Everything,"or"The World According to Jeff Goldblum."

Keep in mind not everything on this list will be appropriate for every child.

This educational comedy series features comedian Adam Conover debunking common misconceptions by using his magical TV host powers but also by referencing peer-reviewed articles and reaching out to experts in the field.

Each episode ends with a positive takeaway explaining how the knowledge you've just gained is better for you than the comfort of the misconceptions he's just ruined.

The Wall Street Journal said of Conover, "In short, he's irritating. But he owns it. Which makes his quasi-educational comedy series so goofily endearing."

Fast Company called him "the lovechild of Debbie Downer and the coolest, most contrarian college professor you ever had."

All three seasons of "Avatar: The Last Airbender" premiered on Netflix on May 15. Since the world is still in quarantine, now is a great time to watch it yourself for the first time or binge the series for the 50th time.(Photo: Courtesy of Forbes)

This animated series portrays the adventures of 12-year-old Aang, the last surviving Airbender, who awakens from a century in suspended animation to find the world at war.

As the spirit of light and peace in human form, Aang controls the elements and is tasked with keeping the Four Nations at peace.

Critics praised the series for addressing concepts rarely touched on in entertainment aimed at young kids, from war to genocide, imperialism, colonialism, totalitarianism and free choice.

It has a critics score of 100 on Rotten Tomatoes. Vanity Fair named it one of the best animated series since "The Simpsons," noting that it "teaches without tryingand is a shining example of what it means to show unconditional devotion to a greater cause."

This Pixar animated feature wasinspired by Da de los Muertos.

It tells the story of 12-year-old Miguel, who's magically transported to the Land of the Dead, where he enlists his deceased great-great-grandfather to help him return to the land of the living and reverse his family's ban on music.

Rolling Stone's Peter Travers praised this "loving tribute to Mexican culture," saying "Of course, a lesson is being preached to children about the need to respect elders. But Pixars 19th feature brings a soulful core to that message."

The Wrap said, "If an animated movie is going to offer children a way to process death, it's hard to envision a more spirited, touching and breezily entertaining example than Coco."

It was named best animated film of 2017 by the National Board of Review, the Golden Globes and the Critic's Choice Movie Awards.

Latif Nasser in Netflix's "Connected."(Photo: Netflix)

Here's a fun way to sneak in some science.

Latif Nasser, director of research at an award-winning New York Public Radio show called "Radiolab," investigates the surprising and intricate ways in which we're all connected to each other, the world and the universe in this six-part 2020 docuseries.

There are episodes on how surveillance pervades our lives, the power of dust, important lessons of nuclear bombs and a law of numerical probability that applies to classical music, contemporary social media, tax fraud and perhaps the universe at large.

It helps to have a host with the nerdy charisma Nasser brings to the proceedings. As Decider wrote, "This is a man who can turn weave a jaw-dropping story out of probability."

What were the odds?

CrashCourse is an educational YouTube channel started by John and Hank Green and funded by YouTube's $100 million original channel initiative.

Since launching a preview in late 2011, the channel has earned more than 10 million subscribers and 1 billion views.

At first, the channel focused on humanities and science courses, having launched with episodes on world history and biology. But after partnering in later 2014 with PBS Digital Studios, the brothers were able to expand the curriculum, recruiting additional hosts.

A second channel, Crash Course Kids, is hosted by Sabrina Cruz and has completed its first series, Science.

A collaboration with Arizona State University titled Study Hall began in 2020, offering less structured learning.

This Netflix docu-series has been around longer than "History 101" but follows a similar format.

Each episode is devoted to a single mini-lesson lasting less than 20 minutes.

Among the more serious topics the series has explored are the racial wealth gap, designer DNA, monogamy, political correctness, why women are paid less and the world's water critics. But other episodes have ranged from K-pop to cricket.

The show has had some interesting guest narrators, from Christian Slater talking cryptocurrency to John Waters on beauty, Kristin Bell on whether we can live forever (spoiler alert: we can't) and Carly Rae Jepsen on music.

"Explained" has spawned three spin-off miniseries: "The Mind, Explained," "Sex, Explained" and "Coronavirus, Explained."

Cynthia Erivo plays Harriet Tubman in "Harriet."(Photo: Glen Wilson)

Born into slavery, famed abolitionist Harriet Tubman escaped to Philadelphia in 1849, returning to the South rescue family members and eventually a total of approximately 70 enslaved people via the Underground Railroad, a network of safe houses.

Cynthia Erivo, who stars as Tubman, brought home acting nominations from the Academy Awards, Golden Globes and the Screen Actors Guild.

How accurate is it? Fairly.

A story in Slate says the filmmakers "take some considerable liberties with both the timeline of events and the creation of several characters."

And director Kasi Lemmons told USA Today the film's creators took creative liberties in fleshing out the character of her slave owners vengeful grandson, Gideon.

Now streaming on several HBO platforms.

This Netflix documentary series definitely makes good on the Intro to History implications of its title. Each episode is ahistory mini-lessonconsisting of archival footage, facts and graphs about various topics.

Since the series premiered in May, those mini-lessons have included episodes on fast food, the space race, the rise of China, plastics, oil and the Middle East, robots, feminism, nuclear power and genetics.

A review of the series at Ready Steady Cut! concluded "History 101" season 1 is worth a binge it wont take long and you may learn something new."

Jamie Hyneman (left) and Adam Savage, hosts of the Discovery Channel show 'MythBusters.'(Photo: Handout courtesy of Discovery Channel)

This show is a blast quite often literally.

In its first nine seasons, 12 tons of explosives were used as special effects experts Adam Savage and Jamie Hyneman employed the scientific method to test the validity of urban legends, rumors, myths, adages, movie scenes, videos and news.

The duo used a two-step method of replicating the circumstances tosee if they could duplicate the alleged results. By the end of each episode, the myths were rated busted,plausibleor confirmed.

The series premiered in 2003 on the Discovery Channel and ran through 2016 before being revived in 2017 with new hosts on the Science Channel. The original series is streaming now on Hulu.

The human body is the focus of this British children's television series, hosted by twin brothers Dr. Chris and Dr. Xand van Tulleken, who were joined in 2019 by a third host, Dr. Ronx.

In the interest of demystifying what happens in hospitals for younger viewers while explaining how our bodies work, the doctors undergo experiments on their own bodies.

Those experiments have ranged from scrambling their own brain signals to show how they control body movements to charting what happens to food in the digestive tract with a special camera pill.

So yes, it has been known to get a little gross. You'll find out the medical uses of maggots, for instance.

Each episode also follows children admitted to hospitalwards from diagnosis to recovery.

Marie Curie (Rosamund Pike) at work in the lab in a scene from 'Radioactive.'(Photo: Laurie Sparham)

"Radioactive" tells the inspiring tale of Marie Curie and the pioneering work she did that resulted in Curie becoming the first woman to be honored with a Nobel Prize.

Filmed in Hungary with great costuming and a brilliant performance from Rosamund Pike in the title role, it touches on the discrimination she faced as a Polish woman in Paris as well as her struggles to be heard in the male-dominated scientific community.

Scientific American said it portrayed Curie as "a woman of the future."

However, somehave criticized the film for taking far too much creative license with the truth, inspiring STEM on Stage to compile a list of historic inaccuracies.

Parents should also know that it contains brief nudity.

Streaming now on Prime Video.

This PBS series is hosted by a physicist named Dr. Derek Muller, who spends each episode unlocking the mysteries as well as explaining the history and uses of uranium, one of Earth's most controversial elements.

In Part 1: The Rock That Became a Bomb, Muller explores how uranium becomes lead in the process of radioactive decay, the harmful effects of radiation and the use of uranium as a nuclear weapon.

The episode ends with the bombing of Hiroshima at the end of World War II.

In Part 2: The Rock That Changed the World, he looks at the use of uranium in cancer treatment and visits Chernobyl and Fukushima, where nuclear disasters have occurred.

Did you know that dinosaurs didn't roar? Or that astronauts shrink in space? I can almost guarantee you didn't know that in 16th Century England, it was considered good luck to throw shoes at the bride and groom at weddings? THAT'S who throws a shoe.

Whether hunting for dinosaur fossils or flying planes, the science-loving Engelman siblings that host this National Geographic Kids series explore the weird but true science that makes this world or in the case of shrinking astronauts, this universe a fascinating place.

This show is clearly aimed at younger kids, who should respond well to the goofy children's-entertainer energy the Engelmans invest in making learning fun and often funny (if admittedly seven miles over-the-top for viewers past a certain age).

Jeff Goldblum: Oct. 22, 1952.(Photo: Monica Schipper/Getty Images)

The premise of this series is as quirky as the host himself.

He prepares for an episode by doing as little research as humanly possible on the topic at hand, from ice cream to RVs, relying instead on his ownunderstanding of the topicjust from living in this world.

But there's a method to this seeming madness, as the actor explained at a panel reported by IGN,

"I kind of encounter interesting people around these subjects and you see me, you go along with me, if you're so inclined, and we have this experience together," he said. "That's the idea. Its all a surprise to me. I don't even meet the people, see the places, before they turn on the camera. Its all me kind of like a chick popping out of its shell."

Reach the reporter at ed.masley@arizonarepublic.com or 602-444-4495. Follow him on Twitter @EdMasley.

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Try these streaming options to add some educational viewing to your kids screen time - AZCentral

Once known as a paradigm changing class of precision oncology, or targeted, drugs,1 Bruton tyrosine kinase (BTK) inhibitors are now well established as treatment for several hematological malignancies. They are named for Lt Col Ogden C. Bruton, MD, chief of pediatrics at Walter Reed Army Medical Center in the 1950s, who in 1951 discovered the first host immunodeficiency in humans, X-linked agammaglobulinemia.2,3

The BTK protein is essential to helping B cells develop and mature into functional and specialized white blood cells; these are part of the adaptive immune response in producing antibodies, or immunoglobulins.4 But mutations in the BTK gene, more than 600 of which have been identified, can lead to a sizeable reduction in the number of circulating B cells, along with reduced ability to fight infection, absence of the BTK protein, production of abnormal BTK protein, or cancer cell growth.5,6

Mutated immunoglobulins essentially malfunction in their roles as antigen receptors on the surfaces of B cells, especially in the cancer space, by not recognizing antigens as damaging or by not sending the correct signals to destroy the malignant cells.

This is where BTK inhibitors come in: They help to trigger cell death by blocking the B-cell receptor signaling that leukemias and lymphomas use to grow and survive.7 The first-generation BTK inhibitor ibrutinib (Imbruvica) came to market in 2013, when it was approved by the FDA to treat adult patients with mantle cell lymphoma. A targeted treatment, it stops cancer cells from surviving and multiplying by blocking abnormal protein signaling.8 Other indications, as monotherapy or in combination, have been approved for chronic lymphocytic leukemia, Waldenstrm macroglobulinemia, small lymphocytic lymphoma, relapsed/refractory marginal zone lymphoma, and chronic graft-versus-host disease.9 Ibrutinib is a once-daily oral agent and can be used in the frontline and relapsed settings.10

Despite its many benefits and indications, however, ibrutinib as BTK inhibition is also associated with numerous adverse effects (AEs) on nonmalignant cells, which range from common to uncommon and from mild to severe, making ibrutinibs toxicity profile notorious.7

Among the most severe AEs are hemorrhage; high blood pressure; heart rhythm irregularities, including ventricular arrhythmias, atrial fibrillation, and atrial flutter; second primary cancers (eg, skin, other organs); and tumor lysis syndrome.11 Some of the most common AEs, occurring in more than 30% of patients, are hematological (eg, decreased platelets, neutrophils, and hemoglobin), musculoskeletal, and respiratory in nature.

Additional possible AEs include diarrhea, constipation, vomiting, skin infections, dizziness, dehydration, petechiae, arthralgia, stomatitis, rash, and fatigue.12 Ibrutinib carries warnings for use among those with bleeding problems, liver problems, and for those who are planning surgery or recently had surgery; women who are pregnant or thinking of becoming pregnant; women who breastfeed or plan to do so; and men with female partners capable of pregnancy.

Second-generation BTK inhibitors seek to improve upon first-generation agents like ibrutinib by having less cardiotoxicity, fewer AEs that result in stopping treatment, and fewer off-target effects. For example, ibrutinib inhibits the activity of 3 major off-targets: epidermal growth factor, which can result in severe skin toxicities13; interleukin-2 inducible kinase, which impairs natural killer cells cytotoxic abilities14; and the Tec family of kinases, decreasing their ability to aid in phosphorylation.15

In updated results of the ASPEN trial presented at this years virtual American Society of Clinical Oncology (ASCO) 2020 Annual Meeting, zanubrutinib (Brukinsa), the most recent second-generation BTK inhibitor to hit the US market, was shown to have a survival advantage over ibrutinib in patients with Waldenstrm macroglobulinemia who lacked the MYD88 mutation typically associated with successful treatment.16

ASPEN first compared zanubrutinib with ibrutinib in patients with Waldenstrm macroglobulinemia who have the MYD88 mutation, and zanubrutinib was shown in December 2019 to increase the incidence of complete response (CR) or very good partial response (VGPR) by close to 46% compared with ibrutinib28.9% vs 19.8%, respectivelyin patients with relapsed or refractory disease.17

The updated results, from 5 additional months of data, widened this gap, showing a 30.4% CR plus VGPR rate for zanubrutinib compared with 18.2% for ibrutinib, as well as less occurrence of atrial fibrillation/flutter of any grade, bleeding of any grade, major hemorrhage, diarrhea, and hypertension. In addition, patients without the MYD88 mutation had an overall response rate of 80.8%, which included a 50.0% major response ratewhich itself included a VGPR rate of 26.9%and 12-month progression-free survival of 72.4%.18

Lead investigator, Constantine Tam, MBBS, MD, a clinical hematologist and professor at the Peter MacCallum Cancer Centre in Victoria, Australia, noted of zanubrutinib, Those patients who potentially have a history of hypertension or have a history of atrial fibrillationor have an abnormal ECG or abnormal echocardiogrammaybe theyre the ones who would be better off on [zanubrutinib] compared with ibrutinib. We think its how clean the targeting is.19

Zanubrutinib is associated with less incidence of muscle spasm, peripheral edema, pneumonitis, and pneumonia. In essence, fewer overall AEs with second-generation BTK inhibitors means less of a need to reduce dosing and a greater likelihood of being able to stay on treatment longer. Tam noted that most AEs happen with zanubrutinib during the first year on treatment, before their incidence plateaus, whereas prolonged treatment with ibrutinib has a greater chance of inflicting cumulative damage to the vascular system.20 Compared with first-generation BTK inhibitors, the second-generation drugs are associated with fewer concerns about primary and acquired drug resistance. For example, ibrutinib use among patients with relapsed/refractory mantle cell lymphoma has been shown to both have no effect on the disease and have a negative impact on additional therapies.21

These resistance mechanisms of action are 2-fold. They are molecular, in that they involve sustained distal B-cell receptor signaling through PIK3-AKT (protein kinase B) pathway activation, NFkB pathway activation, and cell cycle progression. They also are therapeutic, in that lines of therapy administered after BTK inhibitors do not produce prolonged responses or exceptional overall survival.21

Less Cardiotoxicity in Second Generation

Some of the strongest gains in this newer generation of BTK inhibitors, however, can be seen in the cardiovascular space, when compared with the toxicities of the first-generation inhibitors

that often lead to treatment discontinuation, especially among older, sicker patients who have a history of cardiac disease. In fact, most BTK inhibitors are prescribed for older patients, because the class of drugs is used primarily to treat chronic lymphocytic leukemia, for which the average age of onset is older than 60 years.22

I think its that a lot of the toxicities are related to off-target effects, meaning the binding of the BTK inhibitor drug to receptors or molecules that are not the ones that that theyre supposed to be treating the cancer for, said Michael Kolodziej, MD, FACP, vice president and chief innovation officer, ADVI Health, in an interview with Evidence-Based Oncology.

The big ones that were identified with the first-generation inhibitors were cardiovascular, or hypertension and atrial arrhythmias, atrial fibrillation. And they were not rare side effects.

Kolodziej explained that the second-generation drugs have fewer off-target effectsless cardiovascular toxicity, atrial arrhythmias, and hypertensionbecause of their improved toxicity profile, largely because the drugs are just better at being BTK inhibitors. Its not any more complicated than that.

The chief challenge of the first-generation BTK inhibitors is that the AEs cause clinicians and patients to stop treatment with them, Kolodziej noted. The cancer does not become resistant, but the toxicities become unbearable and the patients become intolerant, he emphasized.

The thinking is that the reduced cardiovascular side effects, the reduced bleeding, are going to allow a better persistence on the second-generation drugs, he explained.

Tolerability and Payers

Indeed, in a pooled analysis of clinical trials of the second-generation BTK inhibitor acalabrutinib (Calquence), also presented in May at ASCO, lead author Richard R. Furman, MD, of Weill Cornell Medicine in New York, found that at a median follow-up of 26.4 months, 65% of patients were still on treatment. Of the 34% of patients who stopped acalabrutinib, half (17%) did so because their disease progressed; only 9% stopped due to treatment-related AEs.23

Tolerability, especially as patients define it, is increasingly important to payers, starting with Medicare. The Center for Medicare and Medicaid Innovation has announced that it will incorporate patient-reported outcomes (PROs) into the Oncology Care First model, the proposed successor to the Oncology Care Model.24 Advocates for including PROs in payment models are encouraging drug developers to broaden definitions of tolerability, to include quality-of-life data in trial designs.25

Its a straightforward idea: When patients can tolerate treatment, it improves their chances of survival. This is important, Tam said during ASCO. The longer you take the drug, the better your responses become.19

Author Information

Maggie L. Shaw is associate editor, The American Journal of Managed Care.

References

1. Erba HP. BTK inhibition in B-cell lymphomas: an overview of Bruton tyrosine kinase inhibition. Targeted Oncology. June 21, 2019. Accessed July 18, 2020. https://www.targetedonc.com/view/btk-lymphoma

2. Wyckoff AS. Dr. Brutons discovery set the stage for modern clinical immunology. American Academy of Pediatrics News. May 31, 2018. Accessed July 18, 2020. https://www.aappublications.org/news/2018/05/31/dyk053118

3. Buckley RH. [Commentary:] agammaglobulinemia, by Col. Ogden C. Bruton, MC, USA, Pediatrics, 1952;9:722-728. Pediatrics. 1998;102(suppl 1):213-215. https://pediatrics.aappublications.org/content/102/Supplement_1/213

4. Deane P. B cells: the antibody factories of the immune system. Life Extension Advocacy Foundation. August 22, 2017. Accessed July 18, 2020. https://www.lifespan.io/news/b-cells/

5. BTK gene: Bruton tyrosine kinase. US National Library of Medicine/Genetics Home Reference. Updated July 7, 2020. Accessed July 18, 2020. https://ghr.nlm.nih.gov/gene/BTK#

6. Bruton tyrosine kinase inhibitor. Science Direct. Accessed July 18, 2020. https://www.sciencedirect.com/topics/medicine-and-dentistry/bruton-tyrosine-kinase-inhibitor

7. BTK inhibitors. Drugs.com. Updated January 7, 2020. Accessed July 18, 2020. https://www.drugs.com/drug-class/btk-inhibitors.html

8. Ibrutinib. MedlinePlus. Updated May 15, 2019. Accessed July 19, 2020. https://medlineplus.gov/druginfo/meds/a614007.html

9. Imbruvica approval history. Drugs.com. Updated 2020. Accessed July 19, 2020. https://www.drugs.com/history/imbruvica.html

10. Berger JA. The evolving role of BTK inhibitors in treating chronic lymphocytic leukemia BTK inhibition: disease state effectiveness. Targeted Oncology. April 16, 2020. Accessed July 19, 2020. https://www.targetedonc.com/view/evolving-btk-cll?seriesVid=2

11. How does Imbruvica work? Imbruvica (ibrutinib). April 20, 2020. Accessed July 19, 2020. https://imbruvica.com/cll/how-does-imbruvica-work

12. Imbruvica. Chemocare. Accessed July 19, 2020. chemocare.com/chemotherapy/drug-info/imbruvica.aspx

13. Ghasoub R, Albattah A, Elazzazy S, et al. Ibrutinib-associated sever[e] skin toxicity: a case of multiple inflamed skin lesions and cellulitis in a 68-year-old male patient with relapsed chronic lymphocytic leukemia case report and literature review. J Oncol Pharm Pract. 2020;26(2):487-491. doi:10.1177/1078155219856422

14. Bennett C. Ibrutinib may impair natural killer cell cytotoxic activity, study suggests. Cancer Therapy Advisor. June 19, 2019. Accessed July 19, 2020. https://www.cancertherapyadvisor.com/home/cancer-topics/lymphoma/ibrutinib-for-mantle-lymphoma-mcl-may-impair-naturalcyto-toxic-activity/

15. Patel V, Balakrishnan K, Bibikova E, et al. Comparison of acalabrutinib, a selective Bruton tyrosine kinase inhibitor, with ibrutinib in chronic lymphocytic leukemia cells. Clin Cancer Res. 2017;23(14):3734-3743. doi:10.1158/1078-0432.CCR-16-1446

16. Garcia-Sanz R, Dimopoulos MA, Lee H-P, et al. Updated results of the ASPEN trial from a cohort of patients with MYD88 wild-type (MYD88WT) Waldenstrm macroglobulinemia (WM). J Clin Oncol. 2020;38(15 suppl; abstr e20056). doi:10.1200/JCO.2020.38.15_suppl.e20056

17. Tam CSL, Opat S, DSa S, et al. ASPEN: results of a phase III randomized trial of zanubrutinib versus ibrutinib for patients with Waldenstrm macroglobulinemia (WM). J Clin Oncol. 2020;38(15 suppl; abstr 8007). doi:10.1200/JCO.2020.38.15_suppl.8007

18. BeiGene presents updated head to head results from phase 3 trial of zanubrutinib vs. ibrutinib in patients with Waldenstrms macroglobulinemia at the 2020 American Society of Clinical Oncology (ASCO) Virtual Scientific Program. News release. BeiGene; May 29, 2020. Accessed August 3, 2020. https://www.globenewswire.com/news-release/2020/05/29/2040883/0/en/BeiGene-Presents-Updated-Head-to-Head-Results-from-Phase-3-Trial-of-Zanubrutinibvs-Ibrutinib-in-Patients-with-Waldenstrm-s-acroglobulinemiaat-the-2020-American-Society-of-Clini.html

19. Caffrey M. Zanubrutinib pulls away from ibrutinib in update, shows durable responses in Waldenstrom patients lacking key mutation. The American Journal of Managed Care. May 30, 2020. Accessed July 21, 2020. https://www.ajmc.com/conferences/asco-2020/zanubrutinib-pulls-away-from-ibrutinib-in-update-shows-durable-responses-in-waldenstrom-patients-lacking-key-mutation

20. Dr Constantine Tam discusses the benefits of zanubrutinib on cardiac effects. The American Journal of Managed Care. May 31, 2020. Accessed July 22, 2020. https://www.ajmc.com/conferences/asco-2020/dr-constantine-tam-discusses-the-benefits-of-zanubrutinib-on-cardiac-effects

21. Hershkovitz-Rokah O, Pulver D, Lenz G, Shpilberg O. Ibrutinib resistance in mantle cell lymphoma: clinical, molecular and treatment aspects. Br J Haematol. 2018;181(3):306-319. doi:10.1111/bjh.15108

22. Chronic lymphocytic leukemia. CancerWall. Accessed July 24, 2020. https://cancerwall.com/chronic-lymphocytic-leukemia-lifeexpectancy-symptoms/

23. Furman RR, Byrd JC, Own RG, et al. Safety of acalabrutinib (acala) monotherapy in hematologic malignancies: pooled analysis from clinical trials. J Clin Oncol. 2020;38(suppl 15; abstr 8064). doi:10.1200/JCO.2020.38.15_suppl.8064

24. Bekele B, Macher D, Ferguson S, et al. Emerging trends in oncology management. Avalere Health. June 2, 2020. Accessed July 31, 2020. https://avalere.com/insights/emerging-trends-in-oncology-management

25. Basch E, Campbell A, Hudgens S, et al. A Friends of Cancer research white paper: broadening the definition of tolerability in cancer clinical trials to better measure the patient experience. Friends of Cancer Research. October 24, 2018. Accessed July 31, 2020. https://www.focr.org/sites/default/files/Comparative%20Tolerability%20Whitepaper_FINAL.pdf

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Human genetics, study of the inheritance of characteristics by children from parents. Inheritance in humans does not differ in any fundamental way from that in other organisms.

Britannica Quiz

Genetics Quiz

Which of these congenital disorders is characterized by an extra chromosome?

The study of human heredity occupies a central position in genetics. Much of this interest stems from a basic desire to know who humans are and why they are as they are. At a more practical level, an understanding of human heredity is of critical importance in the prediction, diagnosis, and treatment of diseases that have a genetic component. The quest to determine the genetic basis of human health has given rise to the field of medical genetics. In general, medicine has given focus and purpose to human genetics, so the terms medical genetics and human genetics are often considered synonymous.

A new era in cytogenetics, the field of investigation concerned with studies of the chromosomes, began in 1956 with the discovery by Jo Hin Tjio and Albert Levan that human somatic cells contain 23 pairs of chromosomes. Since that time the field has advanced with amazing rapidity and has demonstrated that human chromosome aberrations rank as major causes of fetal death and of tragic human diseases, many of which are accompanied by intellectual disability. Since the chromosomes can be delineated only during mitosis, it is necessary to examine material in which there are many dividing cells. This can usually be accomplished by culturing cells from the blood or skin, since only the bone marrow cells (not readily sampled except during serious bone marrow disease such as leukemia) have sufficient mitoses in the absence of artificial culture. After growth, the cells are fixed on slides and then stained with a variety of DNA-specific stains that permit the delineation and identification of the chromosomes. The Denver system of chromosome classification, established in 1959, identified the chromosomes by their length and the position of the centromeres. Since then the method has been improved by the use of special staining techniques that impart unique light and dark bands to each chromosome. These bands permit the identification of chromosomal regions that are duplicated, missing, or transposed to other chromosomes.

Micrographs showing the karyotypes (i.e., the physical appearance of the chromosome) of a male and a female have been produced. In a typical micrograph the 46 human chromosomes (the diploid number) are arranged in homologous pairs, each consisting of one maternally derived and one paternally derived member. The chromosomes are all numbered except for the X and the Y chromosomes, which are the sex chromosomes. In humans, as in all mammals, the normal female has two X chromosomes and the normal male has one X chromosome and one Y chromosome. The female is thus the homogametic sex, as all her gametes normally have one X chromosome. The male is heterogametic, as he produces two types of gametesone type containing an X chromosome and the other containing a Y chromosome. There is good evidence that the Y chromosome in humans, unlike that in Drosophila, is necessary (but not sufficient) for maleness.

A human individual arises through the union of two cells, an egg from the mother and a sperm from the father. Human egg cells are barely visible to the naked eye. They are shed, usually one at a time, from the ovary into the oviducts (fallopian tubes), through which they pass into the uterus. Fertilization, the penetration of an egg by a sperm, occurs in the oviducts. This is the main event of sexual reproduction and determines the genetic constitution of the new individual.

Human sex determination is a genetic process that depends basically on the presence of the Y chromosome in the fertilized egg. This chromosome stimulates a change in the undifferentiated gonad into that of the male (a testicle). The gonadal action of the Y chromosome is mediated by a gene located near the centromere; this gene codes for the production of a cell surface molecule called the H-Y antigen. Further development of the anatomic structures, both internal and external, that are associated with maleness is controlled by hormones produced by the testicle. The sex of an individual can be thought of in three different contexts: chromosomal sex, gonadal sex, and anatomic sex. Discrepancies between these, especially the latter two, result in the development of individuals with ambiguous sex, often called hermaphrodites. Homosexuality is unrelated to the above sex-determining factors. It is of interest that in the absence of a male gonad (testicle) the internal and external sex anatomy is always female, even in the absence of a female ovary. A female without ovaries will, of course, be infertile and will not experience any of the female developmental changes normally associated with puberty. Such a female will often have Turner syndrome.

If X-containing and Y-containing sperm are produced in equal numbers, then according to simple chance one would expect the sex ratio at conception (fertilization) to be half boys and half girls, or 1 : 1. Direct observation of sex ratios among newly fertilized human eggs is not yet feasible, and sex-ratio data are usually collected at the time of birth. In almost all human populations of newborns, there is a slight excess of males; about 106 boys are born for every100 girls. Throughout life, however, there is a slightly greater mortality of males; this slowly alters the sex ratio until, beyond the age of about 50 years, there is an excess of females. Studies indicate that male embryos suffer a relatively greater degree of prenatal mortality, so the sex ratio at conception might be expected to favour males even more than the 106 : 100 ratio observed at birth would suggest. Firm explanations for the apparent excess of male conceptions have not been established; it is possible that Y-containing sperm survive better within the female reproductive tract, or they may be a little more successful in reaching the egg in order to fertilize it. In any case, the sex differences are small, the statistical expectation for a boy (or girl) at any single birth still being close to one out of two.

During gestationthe period of nine months between fertilization and the birth of the infanta remarkable series of developmental changes occur. Through the process of mitosis, the total number of cells changes from 1 (the fertilized egg) to about 2 1011. In addition, these cells differentiate into hundreds of different types with specific functions (liver cells, nerve cells, muscle cells, etc.). A multitude of regulatory processes, both genetically and environmentally controlled, accomplish this differentiation. Elucidation of the exquisite timing of these processes remains one of the great challenges of human biology.

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As a great deal of recent public discourse makes clear, black Americans have been disproportionately impacted by the fallout from the coronavirus pandemic. Though hampered by limited and fragmented data, recent public health reports suggest that in eight states, blacks are at least three times more likely to be infected by coronavirus than their white counterparts, and nationally, blacks are twice as likely to die from such infections. County-level and city-level data have typically suggested similarly troubling trends. These realities largely mirror patterns of racial disparity that exist on a wide range of adverse social indicators.

As someone who studies gun violence, the recent discourse on coronavirus disparities has called to my mind long-standing narratives around gun violence and black men. While typically well intended, these disparity discourses share a number of problems that have often done more to obscure than to advance our understanding of these issues, as well as how we might effectively confront them. Such problems include: (1) the tendency to treat race as a biological category and to presume that racial identity is a discrete risk factor for coronavirus or gun violence, (2) the promotion of public health interpretations that focus on behavioral norms and lend themselves to austerity-minded interventions, and (3) the treatment of racial disparities as distinct from broader patterns of structural inequality. At the intersection of these discourses, moreover, epidemiological metaphors of racism and gun violence as diseases akin to coronavirus are often invoked in lieu of more nuanced and historically grounded analyses of these issues.

In the end, these accounts are largely devoid of class analysis and have little to offer in terms of meaningfully tackling these issues. We need an alternative lens for understanding and addressing the common roots of these issues.

In the early weeks of the emerging coronavirus pandemic in the United States, a rumor that black people were somehow immune to the virus was going viral on social media and beyond. Atlanta rapper Waka Flocka, for example, asserted in a radio interview in early March that minorities cant catch coronavirus. Name one. It doesnt touch them soul food folks. While the very public March 11 diagnosis of NBA player Rudy Gobert, a Frenchman whose father is of Afro-Caribbean descent, and the subsequent diagnoses of other high-profile black celebrities, put a swift end to this ridiculous rumor, its racialist premise of biological determinism regarding the coronavirus has unfortunately persisted including in some perhaps surprising corners.

Citing early data on racial disparities in pandemic-related hospital admissions, for example, the Centers for Disease Control and Prevention (CDC) identified race as a potentially discrete risk factor for infection, although they cautioned that its potential impact as such need[s] to be confirmed with additional data. In mid-April, the head of the British Medical Association called for an urgent investigation into the possible greater vulnerability of black, Asian and minority ethnic people to COVID-19 following the pandemic-related deaths of ten doctors from these demographic groups, the first such deaths in the United Kingdom. An April letter to pharmaceutical companies working on coronavirus treatments from a group of US senators, including Bernie Sanders and Elizabeth Warren, similarly emphasized the critical need for comprehensive demographic and racial data to ensure that new treatments work for all Americans with the obvious premise being that a persons racial identity may play some role in their physiological response to medical treatment.

Similar narratives around racial genetics and biological determinism emerged forcefully during the 1980s and 1990s, when dramatic increases in gun violence, much of it involving young people associated with the burgeoning urban crack cocaine trade, gave rise to a moral panic that found its ultimate expression in the term superpredator. John DiIulio, a political scientist at Princeton University, coined the phrase in 1995 to describe a young juvenile criminal who is so impulsive, so remorseless, that he can kill, rape, maim, without giving it a second thought. The term became part of the popular lexicon, with law enforcement and elected officials on both sides of the aisle deploying it in service of promoting tough-on-crime policies. While peddlers of the superpredator theory never explicitly tied the phenomenon to genetics, the convergent discourse around crack babies children born to crack cocaine users certainly did. These children were unabashedly categorized as a bio-underclass, a generation of physically damaged cocaine babies whose biological inferiority is stamped at birth. In the case of both superpredators and crack babies, these youngsters were cast, both explicitly and implicitly, as urban African Americans.

Such talk of race science and biological determinism, whether clearly reactionary, as in the case of gun violence, or seemingly well-intentioned, as in the case of coronavirus, is troubling and wrongheaded. It is rooted in a long and sordid history in which black Americans have been labeled as inherently disease and violence-prone, among various other vicious and dehumanizing stereotypes. But as a purely historical social construction without genetic or scientific basis, race can be neither an explanation for violent behavior nor a risk factor for coronavirus infection or mortality. As sociologist Karen Fields and historian Barbara Fields note, however, belief in the biological reality of race outranks even astrology, the superstition closest to it in the competition for dupes among the ostensibly educated, a dynamic that permit[s] the consequence under investigation in this case, disparities in coronavirus and gun violence victimization among those defined as African American to masquerade among the causes. As historian and public health scholar Merlin Chowkwanyun warns, moreover, the belief in biological race can not only lead to claims of racial superiority or inferiority, but, less conspicuously, can also obfuscate a complex litany of explanations for . . . observable population differences.

Such is the case with the coronavirus, as it was with gun violence. Though dangerous biological theories of violence persist in some corners, the superpredator and crack-baby theories have long been exposed as the junk they always were. We should be mindful of these lessons as we think about the current coronavirus pandemic.

In comparison to the pernicious race science described above, other public health explanations offer a step in the right direction in accounting for high rates of coronavirus infection and death among African Americans. For example, the Centers for Disease Control and Prevention (CDC) has published a web page on COVID-19 entitled Health Equity Considerations and Racial and Ethnic Minority Groups that identifies economic and social conditions that are more common among some racial and ethnic minorities than whites that may be contributing to observed disparities. These include living conditions such as neighborhood population density and multigenerational households that make social distancing and quarantining more difficult, work factors such as employment in essential industries and lack of sick leave that heighten chances of exposure, lack of health insurance and access to affordable care that decreases the likelihood of early detection and treatment, and chronic health conditions such as heart and lung disease that increase the likelihood of severe symptomatology and death.

Similarly, public health has recently emerged as a nearly ubiquitous framework for understanding gun violence, promoted by everyone from the World Health Organization and the American Medical Association to Barack Obama and Donald Trump. While the 1996 passage of the National Rifle Associationbacked Dickey Amendment effectively banned the CDC from studying gun violence, the agencys information on youth violence though a much more widely construed phenomenon offers a generally useful proxy for gun violence, especially given the dearth of comprehensive data elsewhere.

Specifically, the risk factors for youth violence identified by the CDC include individual factors such as violence exposure and victimization, emotional distress, substance abuse, various types of problematic parenting and familial dynamics, association with delinquent peers, and residence in high-poverty neighborhoods. Though the CDC does not comment specifically on racial disparities in violence, the conclusion one is inevitably left with is that racial disparities in violence involvement are simply the result of a higher prevalence of these risk factors among African Americans.

One issue typical of the public health approach, however, is that there is little to no exploration of how these risk factors themselves come to be. Accordingly, there are few insights into the genesis of the racial disparities they purport to explain. Cure Violence, for example, the widely celebrated gun violence prevention model that likens violence directly to a pandemic disease, reduces violence to a learned behavior rooted in acute and chronic exposure to violence and broader community norms that promote such behavior.

While equating a pattern of social behavior the use of firearms to settle disputes and grievances to the workings of a submicroscopic infectious agent operating at the cellular level may benefit from a patina of medical credibility, such an account fails to provide any meaningful insight into the etiology of the behavior in question: Why does the disease of violence infect some communities but not others? Or, stated differently, why do some communities in a given city experience no homicides in a typical year, while nearby communities in the same city experience dozens of homicides?

Lacking any historically grounded explanation for such divergences, the public health model is susceptible to reframing these issues in cultural terms communities with healthy cultures, and therefore healthy norms, have low levels of coronavirus infection and gun violence, while those with pathological cultures and norms have high levels. At worst, these explanations simply reflect a reframing of biological race in polite language.

In any case, as historian Thomas Adams and political scientist Cedric Johnson argue, such accounts obscure issues that are firmly political and structural in nature by reinventing them as cultural phenomena, an approach that betrays a deep unwillingness to grapple with political and social causation. And if these phenomena are observed across groups with different cultural proclivities certainly, blacks are not the only victims of coronavirus or gun violence, nor do all blacks share a monolithic culture, for that matter then what we are witnessing is not race or culture, as such.

Yet this type of narrow and misplaced emphasis is evident in public healths proposed strategies for addressing these issues. The CDC promotes the view that the primary way to combat the coronavirus disparity among African Americans and other communities of color is by harnessing the strengths of these groups via shared faith, family, and cultural institutions that can empower and encourage individuals and communities to take actions to prevent the spread of COVID-19, care for those who become sick, and help community members cope with stress.

The role of the federal government, meanwhile, is limited to collecting data to monitor and track disparities, and the various recommendations for public health professionals, community organizations, and health care providers amount to little more than disseminating information on healthy practices and trying to connect people with resources. A similarly limited approach has been a selling point for Cure Violence, which proudly touts that the public health model is able to reduce violence in places with awful economies, without healing the economy, just as it has done with malaria, HIV, and other diseases throughout the world. (That the organization has often failed to actually reduce violence according to its model is an important aside.)

In short, in much of the public health discourse, structural inequality is reified, recast in terms of behavioral deficits to be rectified by information campaigns. While specific material circumstances that contribute to racial disparities may be acknowledged to varying degrees, the ultimate causes of these circumstances remain unaccounted for and are as likely as not to be explained as products of the alleged cultural pathologies of these populations themselves. This is not a helpful perspective for understanding these issues, nor for addressing them.

While the public health framework tends to present disparities in health outcomes as natural social facts devoid and undeserving of meaningful explanation, others espouse a ready and seemingly obvious explanation: racism (typically modified as structural, institutional, or systemic). For example, David Williams of Harvard Universitys TH Chan School of Public Health stated, We are looking at societal policies, driven by institutional racism, that are producing the results that they were intended to produce. Its been hard for Americans to understand that there are racial structural disparities in this country, that racism exists, offered Camara Phyllis Jones, an epidemiologist, family physician, and senior fellow at the Morehouse School of Medicine, adding, But COVID-19 and the statistics about black excess deaths are pulling away that deniability. Officials in Franklin County, Ohio, meanwhile, declared racism a public health crisis due to racial disparities in coronavirus deaths and other health outcomes. Other cities and counties have followed suit.

Racial disparities in gun violence have long been discussed in similar terms. In the 1980s and 1990s, this discourse coalesced around narratives that political scientists Willie Legette and Nikol Alexander-Floyd, respectively, refer to as the crisis of the black male and the Endangered Black Male. Though this specific language has largely disappeared from popular discourse on gun violence, its underlying premises have been widely internalized as cultural common sense, distilled in tropes about black-on-black violence and black urban neighborhoods as war zones. In recent years, however, the discourse of black male peril has reemerged forcefully in relation to a different kind of (typically) gun violence: police violence. Indeed, although acknowledgment of black female and LGBT victimization has been an explicit dimension of Black Lives Matter from its inception, the predominant understanding of police violence in the United States is one of black male crisis.

What has been almost entirely absent from the dominant public discourse on police violence is any meaningful class analysis. Yet even a cursory examination of the long and tragic list of high-profile police killings of black men reveals an unmistakable pattern: nearly all of these victims were poor or, at best, members of the working class. Indeed, their class status often directly precipitated their contact with police and/or shaped its trajectory: the use of an allegedly counterfeit $20 bill, the unlicensed selling of cigarettes or bootleg CDs, fleeing a police stop because of a suspected warrant for unpaid child support, vehicle violations caused and compounded by an inability to pay tickets or make needed repairs.

These dynamics, in turn, should be understood within a broader context of an approach to policing that emerges from an imperative to contain and suppress the pockets of economically marginal and sub-employed working class populations produced by revanchist capitalism. The now seemingly ubiquitous notion that racism or white supremacy is the lone factor driving police killings of black men obscures the complexity of these dynamics while also failing to explain police killings of whites, who comprise roughly half of all such victims.

To be clear, there is no doubt that black people and other people of color face racist discrimination in a wide variety of settings and situations that deleteriously affect their lives. There is also no doubt that such discrimination contributes to persistent racial disparities on nearly every adverse social indicator. But racism does not explain the existence of those adverse social indicators or the fundamental realities of inequality, which are produced by a political economy that concentrates incredible amounts of power and wealth in the hands of a small minority on one hand and fails to ensure a stable and dignified material existence for the majority of people, whatever their racial identities, on the other.

Patterns of inequality, then, are reproduced not only via racist discrimination, but via the logic of capitalist social reproduction the former of which, as historian Tour Reed points out, operates within the confines of the latter, not outside of it. A narrow focus on racial disparities and an understanding of them as solely by-products of an ostensibly all-encompassing, transhistorical racism, then, risks reifying broader patterns of inequality and the mechanisms by which they are (re)produced. After all, issues like coronavirus, gun violence, and police violence do not exclusively nor, in sheer numerical terms, even primarily affect African Americans. As political scientist Adolph Reed Jr and Merlin Chowkwanyun argue, disparity discourse thus fails to provide a holistic causal account of these phenomena and obscures the fact that inequalities that appear statistically as racial disparities are in fact embedded in multiple social relations.

As with gun violence, the routine appropriation of medical metaphors likening racism to a disease, an epidemic, or a public health problem further clouds the historical nature of racism and leaves unquestioned the political-economic processes that produce inequality, of which racial disparities constitute one abhorrent manifestation. Yet such a perspective dovetails well with the view that a transcendental racism is alone responsible for racial disparities if not the totality of suffering experienced by black people and, on the flip side, that racial disparities themselves are proof of that fact. This type of circular reasoning means that the discourse on racial disparities has the tendency to borrow from Barbara Fieldss appraisal of historical studies of whiteness to produce no conclusions that it does not begin with as assumptions.

In the end, racial disparities in coronavirus infections and deaths, as in rates of victimization by gun violence or police violence, for that matter cannot be explained by racialist biological determinism, simplistic references to behavioral or cultural norms, or an understanding of racism as operating outside of political economy and of disparities as distinct from broader patterns of inequality.

In the case of coronavirus, racial disparities cannot be divorced from an analysis of our fragmented, profit-oriented health insurance industry; the hollowing out of the public health care sector; a woefully inadequate residual-model welfare state; and eroding unionism, diminishing protections, and increasing precarity for working people. Similarly, racial disparities in gun violence must be understood as a by-product of the deplorable conditions in urban working-class black communities, including low levels of human and economic development, high levels of inequality, a weak and illegitimate state, and large populations of desperate young men involved in collective violence in other words, the same exact conditions associated with elevated levels of violence throughout the world. For their part, working-class white communities that have been similarly devastated by deindustrialization, job loss, and increasing despair in recent decades are facing a gun violence crisis of their own.

Rhetorical maneuvers likening gun violence and racism to pandemic diseases ultimately fail to illuminate the roots of these issues or their effects on variously raced populations. Indeed, even a meaningful appraisal of the societal and demographic impact of coronavirus an actual pandemic disease must be placed within the broader context of the political-economic factors described above. In the end, then, efforts to address racial disparities in pressing issues such as coronavirus, gun violence, and police violence should be understood as an indispensable dimension of a broader assault on the intensifying inequality and precarity facing working people, and as a part of political struggles to create a dignified material existence for all.

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To Talk About Racial Disparity and COVID-19, We Need to Talk About Class - Jacobin magazine

Scientists estimate that about 80 percent of an individuals height is determined by the DNA sequence variants they have inherited, but which genes these variants are in and what they do to affect height are only partially understood. Some rare gene mutations have dramatic effects on height (for example, variants in the FGFR3 gene cause achondroplasia, a rare condition characterized by short stature). For most individuals, though, height is controlled largely by a combination of genetic variants that each have more modest effects on height, plus a smaller contribution from environmental factors (such as nutrition). More than 700 such gene variants have been discovered and many more are expected to be identified. Some of these variants are in genes that directly or indirectly affect cartilage in growth plates, which are areas in the long bones of the legs and arms where new bone is produced, lengthening the bones as children grow. The function of many other height-associated genes remains unknown.

In addition to the FGFR3 gene, researchers have identified hundreds of other genes involved in rare disorders that have an extreme effect on height. These genes (and the conditions they are associated with) include FBN1 (acromicric dysplasia, geleophysic dysplasia, Marfan syndrome), GH1 (isolated growth hormone deficiency), EVC (Ellis-van Creveld syndrome, Weyers acrofacial dysostosis), and GPC3 (Simpson-Golabi-Behmel syndrome). By studying the dramatic effect that altered versions of these genes have on height, scientists hope to better understand the complex interactions among genes that contribute to normal height. Some genes, such as ACAN, contain rare variants that cause severe growth disorders, and also other variants with milder effects on height in individuals without a related health condition. Identifying other height genes, and variants with large or small effects, is an active area of genetic research.

Because height is determined by multiple gene variants (an inheritance pattern called polygenic inheritance), it is difficult to accurately predict how tall a child will be. The inheritance of these variants from ones parents helps explain why children usually grow to be approximately as tall as their parents, but different combinations of variants can cause siblings to be of different heights. Height is influenced by other biological mechanisms (such as hormones) that may also be determined by genetics, although the roles of these mechanisms are not fully understood.

In addition to genetic and biological determinants, height is also influenced by environmental factors, including the nutritional status of the mother during pregnancy, whether she smoked, and her exposure to hazardous substances. A well-nourished, healthy, and active child is likely to be taller as an adult than will be a child with a poor diet, infectious diseases, or inadequate health care. Socioeconomic factors such as income, education, and occupation can also influence height. In some cases, ethnicity plays a role in adult height, but studies on immigrant families have shown that moving to a country with better access to nutritious food, healthcare, and employment opportunities can have a substantial influence on the height of the next generation; this suggests that some differences in height between ethnicities are explained by non-genetic factors.

Lango Allen H, Estrada K, Lettre G, et al. Hundreds of variants clustered in genomic loci and biological pathways affect human height. Nature. 2010 Oct 14;467(7317):832-8. doi: 10.1038/nature09410. Epub 2010 Sep 29. PubMed: 20881960. Free full-text available from PubMed Central: PMC2955183.

Marouli E, Graff M, Medina-Gomez C, Lo KS, et al. Rare and low-frequency coding variants alter human adult height. Nature. 2017 Feb 9;542(7640):186-190. doi: 10.1038/nature21039. Epub 2017 Feb 1. PubMed: 28146470. Free full-text available from PubMed Central: PMC5302847.

McEvoy BP, Visscher PM. Genetics of human height. Econ Hum Biol. 2009 Dec;7(3):294-306. doi: 10.1016/j.ehb.2009.09.005. Epub 2009 Sep 17. PubMed: 19818695.

Perola M. Genome-wide association approaches for identifying loci for human height genes. Best Pract Res Clin Endocrinol Metab. 2011 Feb;25(1):19-23. doi: 10.1016/j.beem.2010.10.013. PubMed: 21396572.

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Is height determined by genetics? - Genetics Home ...

Bison are currently gathering in the Hayden and Lamar Valleys, moving into massive aggregations of hundreds, if not thousands, of the iconic animals of Yellowstone National Park.

Massive bulls, some as large as 2,500 pounds, are fighting for the chance to breed. Challenges begin with bellows, as other bulls enter their territory. If the challenger replies, the bulls will begin to plow the ground, throw their huge frames on the ground and wallow, attempting to dust up.

From a distance, the clouds of dust look like the smoke from dozens of small fires, catching the sunlight in hues of yellow. What comes next is one of the most amazing displays of raw power in the park. The bulls move close head to head and unless one is willing to back down, the fight is on.

It will culminate then in essentially a fight to the death as they butt each others heads. Many bison are killed there, said Chris Geremia, Yellowstones top bison biologist. Theres really nowhere else in the world to see a breeding season like this with thousands of bison breeding.

Less than two centuries ago, there were as many as 30 to 60 million bison moving across the plains. Though there are far fewer now, the middle of a bison rut is still one of the most dangerous places to be in the park. The fighting can happen anywhere, including on the road through Yellowstones famous valleys. Still, visitors will clog pullouts and roadways during late July and the first three weeks in August some of the busiest weeks in the park hoping for a chance to see the spectacle.

Every year bison injure visitors, goring them or tossing them aside like rag dolls.

Give them some space, let them do their thing, Geremia said. Even if youre doing the right thing, theres a really good chance that those bison will move in your direction. We encourage people to get in their vehicles and move away Try and get to the next safest spot to observe.

Yellowstone doesnt keep track of property damage and injuries caused by bison. Most injuries happen when visitors, underestimating the speed and aggressive nature of the massive creatures, get too close. Bison can run at 35 mph and jump 5 feet in the air. Humans are no match for their athleticism. Every year the species cause property damage and injuries, Geremia said, so use your best judgement.

On Wednesday, the Park Service posted a video of one bison sending a rival partially airborne during a fight on a park road.

Geremia is currently working on research projects, including the effects of thousands of bison on the parks flora. The herd, estimated at approximately 5,000 individuals, is constantly on the move and constantly feeding. Bison migrate over 70 miles each year, Geremia said, and they walk more than 1,000 miles while searching for food during the year. Wolves and grizzly bears keep them moving, just like in pre-colonial times.

Weve realized that, as the bison population has gotten larger over the last decade, its changed the entire way that plants grow in the park, Geremia said So much so that it affects how spring green-up occurs across the park and how the plants ground down when it dries out in summertime.

The effects of the herds on plants is so dramatic, you can see a distinct difference in the way the park greens up in spring from space, he said. It was really stunning to me just because weve got wild bison roaming across the spaces.

Geremia is also testing genetics of the population and how it varies between these breeding areas. The PhD started as a field technician in 2002, collecting fecal samples and studying brucellosis in the population. He later became the program biologist and then was promoted to the bison team leader in 2018.

Bison make this ecosystem intact again, Geremia said. And the recovery of large predators and large herbivores is essential to making Yellowstone a full ecosystem, where youve got top predators and giant herbivores influencing what the land looks like.

Park visitors get the benefit and get to see this interaction happening, he added. Theres nowhere else in North America where you can see what you can see here.

As Yellowstones bison population has grown, park managers have taken actions to reduce the size of herd, culling hundreds of animals on an annual basis. Some have been transferred to Native American tribes.

This month, the InterTribal Buffalo Council will transfer 40 former Yellowstone bison to 16 tribes in nine states. These transfers will help develop and sustain tribally-managed herds while preserving the unique genetics and lineage of the largest and continuously free-roaming herd. The transfers are a victory of Native American tribes and represents the culmination of nearly 30 years of advocacy by the council on behalf of its member tribes, said council president Ervin Carlson.

Many Native American Tribes have been working to restore buffalo across the U.S., where they now number in the tens of thousands. Bison managed by Yellowstone National Park have never been interbred with cattle and will be used to help increase the long-term health of many populations across tribal lands.

The fight to protect Yellowstone bison is significant to many Native Americans, who disagree with management strategies which have led to the slaughter an estimated more than 10,000 since the early 1990s, according to the council.

The Choctaw Nation and Fort Belknap Tribes provided land and resources to support the development of bison quarantine facilities in 2018. The facility was built by the Fort Peck Tribes, funded in part by the council, and was approved for use in post-quarantine assurance testing by the State of Montana. Since then, the council says, quarantine operations have saved over 200 bison from slaughter.

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A fight to the death Bison rut is on in Yellowstone - Powell Tribune

PULASKI How does life face the onslaught of a force as powerful as death, totally unnecessary death? Coronavirus is schooling us in that question now, and we are a powerful force in ourselves. But, how does a little bird face it? A five-inch, four-ounce, little thing against all of nature and the power of man. A little life that 90 years ago numbered 1,000 pairs, but today only numbers 64. How does a little bird stand up to that?

Claire Nellis is 26, a Pulaski native, a 2015 graduate of Paul Smiths College majoring in wildlife sciences and fisheries and presently the Piping Plover Project Coordinator for the New York State Office of Parks, Recreation, and Historical Preservation on a grant from the U.S. Fish and Wildlife Service to save that little bird, the piping plover, a tiny shorebird, somewhat similar to the sandpiper, that has been decimated to the point of near-extinction, earning it an inglorious spot on the federal endangered species list, here on Sandy Island Beach, the only place in the state it has returned to make its stand against annihilation. And Claire Nellis, and an impressive array of others, are here to help it make that stand.

Just as the plovers have returned to Sandy Island Beach, Claire Nellis has returned to her hometown. For the last five years, shes been far from home, working always with wildlife, in Missouri for three years working with prairie chickens and turkeys and before that, in Idaho with owls. Now, since May 21 of this year, shes back.

I grew up in Pulaski, she said, and I kind of took the uniqueness of the beaches that we have for granted. I didnt realize how rare they were. And its really an amazing ecosystem. Its fragile and resilient in lots of ways. Its changed a lot over time. Im thrilled to be part of their story of recovery here, and its great to be working on conservation in my hometown.

The plovers, she said, returned to Lake Ontario in 2015 at Lakeview Wildlife Management Area. A local birder spotted one and couldnt believe their eyes, because theyve been missing for 30 years. They notified DEC and let them know. And then in 2016, there was a pair that nested at Sandy Island Beach State Park, which is where I work, and another pair nested at Lakeview Wildlife Management Area, which is just north of the park, in the same habitat. So, since they were there, U.S. Fish and Wildlife Service got involved as a federally endangered bird. The federal agency stepped in. Then 2017, there were prospecting adults (plovers) that checked out the area, but it was such high water, they unfortunately werent able to nest. And then, the Piping Plover Project Coordinator position, which is the position Im in now, started in 2018. Alivia Sheffield filled that position the first two years, and she did a lot of really phenomenal work, a lot of the beginning groundwork of monitoring them and building relationships with people out at the beach and doing a lot of outreach and education. Ive benefited a lot from all of her hard work.

The advent of that one nesting pair was, of course, a major development and defining moment in the nationwide work to bring the piping plover back to numbers representative of a healthy population. But just as one swallow does not a summer make, one pair of piping plovers does not signal the end of their plight. They are a fragile little bird, and it takes a lot of the right conditions to see to it there will be more of them.

Theres still only one pair nesting here unfortunately, Nellis said. The first year, in 2016, they lost their nest due to fox predation, and then in 2018, to help compensate for that, they were able to put up a nest exclosure, metal fencing, kind of like chicken wire, but large enough that the plover can get back and forth through but a fox or a raccoon wouldnt be able to. Its probably about five or six feet across, she explained, and it goes all the way around the nest, and it has a top layer to it as well, so that they (predators) cant just climb over.

That helped, and the plovers have been fruitful and multiplied. In their own rather humorous way, the pair comes together, seemingly for life, in a courtship ritual Nellis described.

The male actually helps with nest brooding and care, she said, and he will lay his belly on the ground and use his back legs to kick out a scrape. Its really just a little indentation in the sand. And then the female will watch him do that and come along and sit in it and either approve or more often, disapprove. Once they pick a scrape that they like, theyll line it with shells, and then just lay their eggs right in that. They usually lay four eggs.

Im not sure what her criteria are, Nellis said of the female plover, but he will often make many scrapes before she decides which ones the best. Its just part of their courtship. I dont know if its the placement on the beach or how deep he scrapes it or what, but sometimes its right, and usually its not.

After that, the pair stays together, at least in a sense, more like a married couple that takes separate vacations. Weve had the same pair, and they have individual bands that mark them, so we know whos who. So, the last three years, weve had the same adults nesting at Sandy Island.

Then comes the turn in the weather, and the plovers, who fly very little while nesting and living at Sandy Island Beach, fly long distances, separately, to the warm south.

They migrate south anywhere from North Carolina to the Bahamas, but primarily in Georgia and Florida, Nellis said. Theyll go to very similar habitat of the open beach where they can run down to the shoreline and eat invertebrates and then run back up into dunes for protection.

They migrate very long distances, so, they are good flyers, but theyre also good at walking. Their anatomy allows them to mostly be running on the ground rather than exerting the effort to fly everywhere.

While migrating, she said, they do stop over at beaches along the way. So sometimes well get reports that our female, shell leave our beach up here in Pulaski and then stop at a beach in Pennsylvania and feed for a day or two to refuel. And then shell continue her way south.

They all migrate separately. The female typically leaves first, and then, the male will leave after, and then the chicks will migrate.

So, the adults will leave, and the chicks will stay and continue feeding and growing and practicing flying for a little while before they take off south. Amazingly, they know where to go. And often theyll wind up in similar areas, Nellis said. Theres been research thats shown they can end up even within kilometers of each other. And they dont necessarily winter together either. They might not meet up down there even if they happen to be on the same beach, its not like theyre spending quality time together. Then they migrate north again and meet up sometimes hours or days apart at the same beach.

Sometimes theyre in different states (during the winter), Nellis continued. I think our pair, we havent seen the male, and the female was spotted in Georgia, and one of the chicks was spotted in Florida.

And then they individually head back north about the same time and meet up back at the same beach.

Our pair has done that three times, Nellis said.

Of course, you cant monitor and care for these little creatures and leave them as just anonymous blobs of feathers. So, they name them.

Theyve all got names, Nellis said. The first year that the male and female came they got named Aragorn and Arwen, and then their chicks all had Lord of the Rings-themed names too. 2019, they went with Star Wars-themed names, so they named the chicks Chewie, Yoda, and Leia. It was pretty exciting because Chewie was spotted down in Florida, and they reported that to us, and then she attempted to nest in Canada near downtown Toronto at a beach, and she stopped back over at Sandy Island Beach on her way south, July 4th, of all days, busy day. Thats the first time weve had a chick return to the habitat at Sandy Island. Even though she didnt attempt to nest, just stopping over was good to see her.

The chicks hatched June 14 this year, and thats about average. Ninety percent of chicks hatch between June 3 and July 14. Im glad that they successfully fledged and have officially migrated. The days are already starting to get short, and Im not sure why shore birds tend to migrate sooner than song birds, but evenings are starting to get colder, and they just head out as soon as theyre able. The adults arrived in early May. The female left July 10, and then the male left July 13. We had two chicks successfully fledge. This year they were named Fleetwood, Buckingham, and Stevie Nicks. Unfortunately, we lost Fleetwood before the female even left, I think the first week of July, so the chick was about two weeks old. We dont know what happened, probably a natural predator like an owl or possibly a fox or a raccoon got it. It couldnt fly, so we know something happened to it on the beach. Mostly its predation that gets them. Predation is a pretty heavy threat for them, and also, loss of habitat and the pressure of habitat use. In the 1930s, when their populations started to decline, it was from beachfront home construction and beach use. So, especially, off-road vehicles later becoming popular would just go right over them or their nests. And as that was mitigated in the 1980s, as they were listed as a federally endangered bird under the Endangered Species Act, theyve gotten more protections for their habitat, and so, theres no longer off-road vehicles allowed, beachfront construction has slowed down. But just the presence of people and dogs on the beach has increased significantly, and so, having less area available to them to be able to forage, because they eat most of the day, theyre really small birds, and theyre just eating invertebrates, so getting to their food source is really important, and the stress of feeling like theyre constantly being chased by people or dogs around can decrease their survivorship. And so, at Sandy Island Beach, we have part of their habitat, its about 100 meters of shoreline thats roped off for them. So, people can still walk by, but they cant set up and hang out there. And so, that keeps some area available to them.

In the 1930s, Nellis went on, at our beach there were 14 nesting pairs. In all of the Great Lakes, I think there were right around 1,000. So, having only 17 pairs in 1984, they declined pretty quickly. But theyre slowly making a comeback. The goal for de-listing them, or getting them off the endangered species list, is to have 150 breeding pairs, and 100 of them need to be in Michigan and then 50 more spread throughout the Great Lakes. Were still about 90 pairs away from that. I would be thrilled to be unemployed from this position in two or three years, if we could get that many pairs, but its likely that theyll still be endangered.

They need that open beach, she said, so that their little legs can navigate through it. A lot of dune stabilization efforts are important to hold the dunes in place. Without some vegetation there, they just blow away and erode. But over-vegetation can be hard for the plovers to navigate. Storms at certain times of the year are good, because it washes out some of that vegetation and makes more habitat available, but if theres a storm when the chicks are very young, they cant stay dry and warm, and they can die from that. If their nest on the ground gets washed out and flooded, thats problematic as well.

Once they settle, they typically stay on that beach, and they can travel up to a mile. But when they are trying to find good habitat for the first time, many times, theyll go back to their original birth place where they were hatched, but obviously, thats not what ours did, so a certain percentage of them fly around and try to find other suitable habitat. Theres a 17-mile stretch of the dune wetland ecosystem along eastern Lake Ontario. It starts with Deer Creek Wildlife Management Area, which is just south of Sandy Island, and goes north up to Eldorado and Black Pond Wildlife Management Area. So, they would prospect along that. But they also could fly all the way across Lake Ontario and check out beaches in Canada. The main population of Great Lakes piping plovers are in Michigan. 2018 was the first year that there were piping plovers on all the Great Lakes again.

If I got to pick and control things, Nellis said, which I dont, I would love for one of our chicks to come back and find a mate from an area such as Michigan or Canada to increase the genetics a little bit. So, its possible that two chicks from a different year or Aragorns brother, who we dont have a name for, he has visited the beach as well, and not stayed around, but he attempted to nest with one of our chicks in Canada. So, kind of funny in human terms that our chick tried to nest with her uncle. I know genetically theres a possibility that it could be detrimental, but at this point, with such a small population, it would overall still be a good thing if they were able to nest together.

They nest on areas that people frequent, and often large volumes of people, and they can still successfully nest, which is pretty impressive. And sometimes, well see people walking by them, and the person doesnt notice the bird, and the bird just continues foraging. But more often than not, the person doesnt notice the bird because theyre just enjoying the beach day, and the bird is running away from them as a perceived threat, or if the chicks are there, theyll do that broken wing act, where they kind of put their belly on the ground and flop their wings around, making it look like they cant fly away, but theyre trying to. And so, that would attract the predators attention, and it would go towards them rather than the chicks, and then it would make a short flight and do it again that would keep leading the predator away, and then fly back once the predators far enough away.

Both the male and female do that behavior.

We observe it more often in the males than the female, Nellis said. The female tends to not be quite as good of a parent as the male. But the male is really protective, and he will do the broken wing act, he will brood the chicks in his feathers to keep them warm, and hell also mob gulls. If a gull is getting too close to one of the chicks, hell fly over it and kind of peck at it. Gulls dont actively seek the chicks out, but gulls are such generalists and opportunists that if one is nearby and they could pick it up and eat it, they definitely would. Weve been fortunate that that hasnt happened with our pair in New York, but in other populations, its been demonstrated.

Plovers are primarily ground-dwelling shore birds. Thats one of the main distinctions between shore birds and sea birds. Sea birds, like terns and seagulls, will fly out and get fish, and then kind of land on the beach to rest or to eat. But shore birds, like plovers or sandpipers, will have that behavior where they run down the beach and eat at the shoreline, and then they run back up the beach to rest.

That running style is one of their distinctive traits.

Once you know what youre looking for, you can pick them out on the landscape, Nellis said, but oftentimes when Im talking to the public, if they havent seen them before, we have to get a spotting scope out to really zoom in on them. They have the same color feathers as the sand, so they blend in real well, and theyre also very small, and I think people are so used to looking at seagulls or the larger terns that fly around out there, a small bird just running along the shore is hard to pick out. Especially, they have a run, stop, movement where theyll run a short way and then kind of stop and look around or squat down in the sand even and then run again. So, they can be real hard to pick out. Even when I first started out working with them this spring, I had a horrible time. I was like, I cant believe this is my job and I cant even find the bird. But once you know what youre looking for, you kind of have that search image. And the chicks, especially, are even more difficult to find. When they first hatch, they are about the size of a cotton ball, and they weigh the same as two pennies. Theyre just so tiny, and incredibly well camouflaged. Their behavior also, when they get scared, is to flatten against the sand. They just really disappear right into it, which works great for aerial predators, like merlin or other hawks, but for ground predators, or even ground-going mammals like ourselves and dogs, even if theyre not maliciously seeking out the bird, it perceives us as a threat, it squats down, we dont see it, and they can easily be stepped on.

And the adults arent too big either.

Theyre very small, Nellis said. What we tell people on the beach, to give them an idea, is an adult weighs the same as a stick of butter.

But at least an adult plover has a chance of getting out of your way.

The adults will fly away once you get close, Nellis added. But the chicks cant fly. They can walk around within the first few hours of birth, so, theyre mobile but also vulnerable since theyre not in that nest. But they cant fly until about 20 to 25 days after they hatch.

All the plovers are uniquely banded with different-colored bands and a metal band on the other leg with a longer individual identification number on it.

They dont have a radio tracker on them, Nellis said. They just have the individual bands. So, if theyre traveling around to other beaches and not staying long, and they dont get sighted by a birder or a researcher thats up there, we dont really know where they go.

But in one way somewhat similar to salmon, plovers tend to return to where they were born. They have pretty high site fidelity, as its referred to, Nellis said.

That also means, she said, returning to where theyve successfully nested year after year, as well. Where youve been successful, you tend to head back. And maybe thats true for Claire Nellis too. All she knows for sure is, shes proud of her community.

Because this land was originally private, and so many of those families still live on the pond and enjoy that area, they all have a sense of ownership and pride in taking care of it, and thats something that I am proud of Pulaski and my community recognizing, she said. And having the piping plovers return to this area, theyre the only nesting pair in New York state, I think is really special and really a marker of how hard the community has worked to improve the ecosystem.

Nellis credits many others with helping her in this project.

We work with SUNY ESF and Jonathan Cohens lab, Nellis said. He has a permit that allows us to capture them and band them. Were only allowed to handle them for half-an-hour before they have to be released back to the parents. Theyre a well-oiled machine. We were fortunate enough to observe and help out a little bit, but he had graduate students come out whove worked with them before, capture them and place bands and then release them again.

Nellis also credited the U.S. Fish and Wildlife Service; the Onondaga Audobon Society; New York State Department of Environmental Conservation; Jonathan Cohens graduate Ph.D. student, Allison Kocek; Robyn Niver and Tim Sullivan, both at U.S. Fish and Wildlife Service; Irene Mazzocchi at the Department of Environmental Conservation; my supervisor, Tom Hughes, the regional biologist; Kelly Morrissette, the manager of the state park; and all the members at the Eastern Lake Ontario Dune Coalition have been really helpful, she said, especially noting Tom Hart, Sandy Bononno, and Patricia Schulenberg. Were lucky to have an organization like that that cares so much and helps with getting everybody on the same page.

Right now, its very likely there are more people trying to save the piping plover than there are piping plovers. But in the face of what oftentimes seem like overwhelming odds, the persistence of dedicated people and the resiliency of nature combine to perform what almost seems a miracle. That miracle may very well be in the making right now at Sandy Island Beach.

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The piping plover making a comeback at Sandy Island Beach, Pulaski native who's come home to help - NNY360

Local researchers are asking Southeast Alaska residents to keep an eye out for a white killer whale, seen recently near Petersburg, and believed to be part of a pod known to travel as far north as Haines.

Id like people to know how rare a white killer whale is and how wonderful it is being so close, said Stephanie Hayes, a Petersburg-based doctoral student with the University of Alaska Fairbanks. We can actually record and learn more about these rare killer whales.

Tluk, as whale T046B1B is known, is about 2 years old and is believed to be a male. However, since the animal is still a juvenile, Hayes said researchers cant be entirely sure of the sex yet. Hayes said Tluk is a regular around Vancouver Island, but he was seen recently near Kake. She was able to snap a photo of the whale with its pod near Petersburg on Aug. 6, and on Monday Tluk was seen again near Petersburgs Sandy Beach, she said.

The name is Coast Salish for moon, Hayes said, and when hes seen in the water, Tluks whiteness makes him look almost like hes glowing, something which might be a problem later in life. Killer whales are hunters, Hayes said, and being easily spotted isnt exactly advantageous to a predator.

Youre kind of a beacon, she said of being a brightly pigmented hunter. Its going to be more difficult to hunt a sea lion if it can see you coming.

Since Tluk is still only a juvenile, he hasnt strayed too far from his pod, Hayes said, but once he does its unknown if hell be accepted into other pods. Some males leave their home pods and join others in their lifetime, but not all whales are accepted by other pods. These males can become what Hayes called loners, who live mostly independently. But those animals dont glow brightly in the water, and can easily hunt on their own. Whether or not other pods will accept a white whale, or if Tluk will be able to hunt on his own an open question, she said.

[Shoes stand in for protesters at Capitol]

The scarcity white killer whales in the world meant Tluks presence is Southeast presented an unlikely opportunity to collect data not just on white killer whales, but orcas in general, Hayes said. There are still a lot of unknowns about killer whales in general which makes knowing what might happen to Tluk hard to predict.

Tluk is not fully white, and doesnt have pink eyes, which leads Hayes to believe he probably doesnt have albinism, a condition defined by a complete lack of pigmentation. Hayes believes Tluk has whats called leucism.

With leucism theres a lack of vibrancy in the pigmentation, Hayes said. The colors are more muted and not fully expressed. You can still see the spots but it looks like a ghostly color.

Leucism is certainly a possibility, according to Brad Hanson, a wildlife biologist with the National Oceanic and Atmospheric Administration Fisheries Department, but because theres so little data on white killer whales its too soon to tell.

There was a white killer whale named Chimo at Sealand of the Pacific, a former aquarium near Victoria, British Columbia, in the 1970s, but it is still hard to say what was causing the whitewashing of the orcas skin.

More white killer whales have been reported in the past few decades, according to Hayes, and there is some research to suggest leucism was ultimately the result of increased inbreeding due to declining whale populations. Theres not yet enough data to be conclusive, but genetic research on whales has improved, she said, and researchers in Switzerland have theorized increased instances of leucism could be the result of a lack of genetic diversity.

Its difficult to know what is considered typical for killer whale populations as good data is sparse and only goes back a few decades, she said. The lack of general knowledge about killer whales was something Hanson noted when asked about the potential link between inbreeding and leucism. It is an interesting theory he said, but wasnt sure he agreed.

My perspective is that because theres been increased effort in looking at killers whales, it wouldnt surprise me were detecting more, (instances of abnormalities), Hanson, whos based in Seattle, said in a phone interview Monday.

All the genetics on transient populations is unclear, we dont have a definitive idea of what the stock structure is, he said, referring to transient orcas, who hunt mammals and are biologically different from other kinds of killer whales.

We did detect some inbreeding in one of the pods. I dont think we have enough information to evaluate it at this point, he said.

But collecting information is exactly what Hayes says people can help do.

[Four whales struck by vessels this year in Southeast]

Its super important and super easy, she said.

Theres a number of websites tracking whale movements and a lot of the data is collected by everyday people uploading pictures of when and where they saw a particular whale.

Hayes mentioned HappyWhale.com as a site where members of the public can upload pictures of whales with time, date and location and that data will become public information for researchers around the globe. Pictures of dorsal fins on animals backs are best, Hayes said, as scientists use those markings to identify individual whales.

White whales or not, tracking whales is useful information and helps NOAA better understand habitat use, Hanson said, giving a better picture of the overall health of the ecosystems.

Tluk and his pod are here to eat, Hayes said, and where they go is entirely up to them. Historically Tluks pod has come to Southeast, but this is the first time the white whale has been seen in Alaskan waters, she said.

We know the pod has been coming up and we can keep an eye out for them, she said. We have a chance to actually see the white killer whale. It could be headed your way.

Contact reporter Peter Segall at psegall@juneauempire.com. Follow him on Twitter at @SegallJnoEmpire.

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Rare white killer whale spotted in Southeast - Juneau Empire

Rs 599, 282pp; HarperCollins

Prairie voles (Microtus ochrogaster) are said to be the paragons of monogamy. These brown mouse-like creatures, smaller than a palm squirrel, are among only 3 to 5 per cent of about 5,000 mammals to stick to one partner all their lives. When one of a couple dies, its mate most often lives a solitary life. But some studs give the lie to their species monogamous lifestyles. They trespass upon other voles home ranges, sneaking sex and scrapping with strangers. Female partners in stable relationships arent above having a casual fling. Their regular mates dont father even as much as a quarter of the litters. Still, a majority stick with their first sex partner, and thats a rarity in the animal world.

Philandering males of these small North American rodents hit the reproductive jackpot, producing more babies than their monogamous counterparts. But being unfaithful is not all fun and frolic. While these males are gallivanting, their lonely mates may also seek sex with others. These cuckolded males that are busy cuckolding others are more likely to raise a rivals offspring. Neither monogamy nor polygamy has an edge, and prairie voles practice both.

What makes some stick to one mate and the others wander?

Vasopressin, a hormone produced by the brains hypothalamus, influences social behaviour such as aggression, bonding with mates and care of offspring. It suffuses the brains of monogamous voles that have more vasopressin receptors (V1aR) in the ventral pallidum, the reward-seeking part of the brain. It is the same with faithful men. When receptor rich voles have sex for the first time, they imprint on their partners and thereafter stay true to them.

Meadow voles (Microtus pennsylvanicus), closely related to prairie voles, are promiscuous. By injecting vasopressin receptors into the males brains, researchers turned them monogamous.

The receptors were not the only things keeping male prairie voles in line. A lot has to do with their sense of geography, say Steven Phelps of the University of Texas at Austin, US, and his colleagues. They discovered rodents with more vasopressin receptors in the brains retrosplenial cortex, known for its role in memory and navigation, stayed within the confines of their homes. These rodents recalled sites where they had fights with rivals and avoided them.

The ones with fewer vasopressin receptors had a poorer understanding of their territories. They wandered over large areas, intruding on others territories and perhaps only dimly recollecting where their nests were located. The result: promiscuity.

A meadow vole. (Shutterstock)

Why didnt the prairie voles stick to either monogamy or polygamy? Mariam Okhovat and other students in Phelps lab used genetics in the lab combined with radio telemetry data gathered in a previous study to find out. They examined the gene avpr1a, known for predicting sexual fidelity in males and encoding the vasopressin receptors V1aR.

The specific arrangement of the four nucleotides in a DNA sequence is called encoding. It is the recipe for producing a particular protein that plays a unique role. In this case, the gene avpr1a produces a protein that acts as a receptor for vasopressin.

Not only did the number of V1aR in the ventral palladium and retrosplenial cortex anticipate male behaviour, but variations in the sequence of the gene also mattered.

The researchers discovered avpr1a comes with two alleles that they call HI and LO. The structure of the V1aR produced by the HI and LO alleles is the same, but they produce different amounts, says Okhovat. Males with the HI allele producing more vasopressin in the retrosplenial cortex were faithful and stayed within the bounds of their home range. The ones with the LO allele produced low levels of the hormone in the retrosplenial cortex and bumbled far out of their territories. Although the researchers noticed this correlation, this relationship between geography and vasopressin in the retrosplenial cortex hasnt been confirmed.

The two alleles didnt affect the amount of V1aR receptors in the ventral palladium, which regulates motivations, emotions and behaviour. The gene variations only affected receptors in parts of the brain involved in remembering places and sexual fidelity.

Phelps says his team was shocked by what they found. This brain variation isnt just there by chance. It isnt random. Natural selection had maintained the alleles in prairie voles for a long time so they had to benefit the species.

Janaki Lenin(Courtesy HarperCollins)

Since these effects are stronger in captive voles than in wild ones, the researchers say the traits cannot be explained by heredity alone. Environment and population may also influence the degree of males faithfulness.

Like many rodents, their populations boom or crash depending on food supply. Numbers explode at feast times, and home ranges shrink in size, with more than 600 rodents jammed in a hectare. Such situations are a perfect playground for promiscuous voles with little sense of territory, and a headache for possessive male voles, keen on keeping their mates away from strangers charms.

During famines, vole populations crash, leaving only one or two in a hectare. Those with better navigation and memory skills are at an advantage. They dote on their partners, defend their territories and mates from philandering males, and make successful parents.

Extending these conclusions to human behaviour is tempting, but research hasnt advanced that far. A 2014 study of 7,400 twins in Finland is the latest to suggest genes could influence faithfulness. It is possible vasopressin receptors control fidelity in women and, to a lesser degree, in men. Surprisingly, oxytocin, commonly thought to be at work when women bond with their partners, seems to have little effect. Philandering in humans may have some biological basis, but it is complicated by personality and environment.

Of his findings in voles, Phelps says, When it comes to social behaviour, maybe there isnt a normal brain. Many genes may have subtle variations so that individuals of a species can respond with flexibility to circumstances.

Wandering voles go astray in more ways than one.

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Excerpt: Every Creature Has A Story by Janaki Lenin - Hindustan Times

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Asia Pacific (China, Japan, India, and Rest of Asia Pacific)Europe (Germany, the UK, France, and Rest of Europe)North America (the US, Mexico, and Canada)Latin America (Brazil and Rest of Latin America)Middle East & Africa (GCC Countries and Rest of Middle East & Africa)

Global Male Breast Cancer Market is highly fragmented and the major players have used various strategies such as new product launches, expansions, agreements, joint ventures, partnerships, acquisitions, and others to increase their footprints in this market. The report includes market shares of Male Breast Cancer Market for Global, Europe, North America, Asia-Pacific, South America and Middle East & Africa.

Reasons To Buy: Make strategic business decisions using in-depth historic and forecast market data associated with the Male Breast Cancer market, and every category within it.Extensive price charts draw particular pricing trends within recent yearsPosition yourself to realize the most advantage of the Male Breast Cancer markets growth potentialTo understand the latest trends of the Male Breast Cancer marketTo understand the impactful developments of key players within the market, their strategic initiatives and comprehensively study their core competencies

For Customised Template PDF Report:https://www.reporthive.com/request_customization/2414230

Table of Contents

Report Overview:It includes major players of the global Male Breast Cancer Market covered in the research study, research scope, and Market segments by type, market segments by application, years considered for the research study, and objectives of the report.

Global Growth Trends:This section focuses on industry trends where market drivers and top market trends are shed light upon. It also provides growth rates of key producers operating in the global Male Breast Cancer Market. Furthermore, it offers production and capacity analysis where marketing pricing trends, capacity, production, and production value of the global Male Breast Cancer Market are discussed.

Market Share by Manufacturers:Here, the report provides details about revenue by manufacturers, production and capacity by manufacturers, price by manufacturers, expansion plans, mergers and acquisitions, and products, market entry dates, distribution, and market areas of key manufacturers.

Market Size by Type:This section concentrates on product type segments where production value market share, price, and production market share by product type are discussed.

Market Size by Application:Besides an overview of the global Male Breast Cancer Market by application, it gives a study on the consumption in the global Male Breast Cancer Market by application.

Production by Region:Here, the production value growth rate, production growth rate, import and export, and key players of each regional market are provided.

Consumption by Region:This section provides information on the consumption in each regional market studied in the report. The consumption is discussed on the basis of country, application, and product type.

Company Profiles:Almost all leading players of the global Male Breast Cancer Market are profiled in this section. The analysts have provided information about their recent developments in the global Male Breast Cancer Market, products, revenue, production, business, and company.

Market Forecast by Production:The production and production value forecasts included in this section are for the global Male Breast Cancer Market as well as for key regional markets.

Market Forecast by Consumption:The consumption and consumption value forecasts included in this section are for the global Male Breast Cancer Market as well as for key regional markets.

Value Chain and Sales Analysis:It deeply analyzes customers, distributors, sales channels, and value chain of the global Male Breast Cancer Market.

Key Findings: This section gives a quick look at important findings of the research study.

About Us:Report Hive Research delivers strategic market research reports, statistical surveys, industry analysis and forecast data on products and services, markets and companies. Our clientele ranges mix of global business leaders, government organizations, SMEs, individuals and Start-ups, top management consulting firms, universities, etc. Our library of 700,000 + reports targets high growth emerging markets in the USA, Europe Middle East, Africa, Asia Pacific covering industries like IT, Telecom, Semiconductor, Chemical, Healthcare, Pharmaceutical, Energy and Power, Manufacturing, Automotive and Transportation, Food and Beverages, etc. This large collection of insightful reports assists clients to stay ahead of time and competition. We help in business decision-making on aspects such as market entry strategies, market sizing, market share analysis, sales and revenue, technology trends, competitive analysis, product portfolio, and application analysis, etc.

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Trending Today Corona impact on Global Male Breast Cancer Market 2025: Outlook by Key Companies and Growth Forecast 2020| Pfizer, Roche,...

Global Male Breast Cancer Treatment Market Report 2020 by Key Players, Types, Applications, Countries, Market Size, Forecast to 2026 (Based on 2020 COVID-19 Worldwide Spread)

Global Male Breast Cancer Treatment Market Report offers an entire study of the Impact of COVID-19 on Male Breast Cancer Treatment Market, Industry Outlook, Opportunities in Market, and Expansion By 2025 and also taking into consideration key factors like drivers, challenges, recent trends, opportunities, advancements, and competitive landscape. This report offers a clear understanding of this also as a future scenario of the worldwide Male Breast Cancer Treatment industry. Research techniques like PESTLE and SWOT analysis are deployed by the researchers. They need also provided accurate data on Male Breast Cancer Treatment production, capacity, price, cost, margin, and revenue to help the players gain a clear understanding of the general existing and future market situation.

>>> Get Free Sample PDF (including COVID19 Impact Analysis, full TOC, Tables and Figures) of Male Breast Cancer Treatment Market:

Male Breast Cancer Treatment Market competition by top manufacturers/Key player Profiled:Pfizer, Roche, GlaxoSmithKline, Sanofi, Novartis, Bayer, Bristol-Myers Squibb, Eli Lilly, AstraZeneca, Teva Pharmaceutical, Sun Pharmaceutical, BioNumerik Pharmaceuticals, Seattle Genetics, Accord Healthcare

The study objectives of Male Breast Cancer Treatment Market report are: 1.To identify opportunities and challenges for Global Male Breast Cancer Treatment.2.To provide insights about factors affecting market growth. To analyze the Male Breast Cancer Treatment market based on various factors- price analysis, supply chain analysis, SWOT analysis, etc.3.To identify and analyze the profile of leading players involved within the manufacturing of worldwide Male Breast Cancer Treatment.4.To provide country-level analysis of the market regarding the present Male Breast Cancer Treatment market size and future prospective.5.To examine competitive developments like expansions, new product launches, mergers & acquisitions, etc., in Global Male Breast Cancer Treatment.6.To provide a detailed analysis of the market structure alongside forecast of the varied segments and sub-segments of the worldwide Male Breast Cancer Treatment market.

By Types, the Male Breast Cancer Treatment Market can be Splits into:

MedicationChemotherapyOthers

By Applications, the Male Breast Cancer Treatment Market can be Splits into:

HospitalsClinicsOthers

The global Male Breast Cancer Treatment market is expected to reach xxx Million USD by 2025, with a CAGR of xx% from 2020 to 2025.

Click Here For Best Discount: https://www.reporthive.com/request_customization/2414231

Regions Covered in these Report:

Asia Pacific (China, Japan, India, and Rest of Asia Pacific)Europe (Germany, the UK, France, and Rest of Europe)North America (the US, Mexico, and Canada)Latin America (Brazil and Rest of Latin America)Middle East & Africa (GCC Countries and Rest of Middle East & Africa)

Global Male Breast Cancer Treatment Market is highly fragmented and the major players have used various strategies such as new product launches, expansions, agreements, joint ventures, partnerships, acquisitions, and others to increase their footprints in this market. The report includes market shares of Male Breast Cancer Treatment Market for Global, Europe, North America, Asia-Pacific, South America and Middle East & Africa.

Reasons To Buy: Make strategic business decisions using in-depth historic and forecast market data associated with the Male Breast Cancer Treatment market, and every category within it.Extensive price charts draw particular pricing trends within recent yearsPosition yourself to realize the most advantage of the Male Breast Cancer Treatment markets growth potentialTo understand the latest trends of the Male Breast Cancer Treatment marketTo understand the impactful developments of key players within the market, their strategic initiatives and comprehensively study their core competencies

For Customised Template PDF Report:https://www.reporthive.com/request_customization/2414231

Table of Contents

Report Overview:It includes major players of the global Male Breast Cancer Treatment Market covered in the research study, research scope, and Market segments by type, market segments by application, years considered for the research study, and objectives of the report.

Global Growth Trends:This section focuses on industry trends where market drivers and top market trends are shed light upon. It also provides growth rates of key producers operating in the global Male Breast Cancer Treatment Market. Furthermore, it offers production and capacity analysis where marketing pricing trends, capacity, production, and production value of the global Male Breast Cancer Treatment Market are discussed.

Market Share by Manufacturers:Here, the report provides details about revenue by manufacturers, production and capacity by manufacturers, price by manufacturers, expansion plans, mergers and acquisitions, and products, market entry dates, distribution, and market areas of key manufacturers.

Market Size by Type:This section concentrates on product type segments where production value market share, price, and production market share by product type are discussed.

Market Size by Application:Besides an overview of the global Male Breast Cancer Treatment Market by application, it gives a study on the consumption in the global Male Breast Cancer Treatment Market by application.

Production by Region:Here, the production value growth rate, production growth rate, import and export, and key players of each regional market are provided.

Consumption by Region:This section provides information on the consumption in each regional market studied in the report. The consumption is discussed on the basis of country, application, and product type.

Company Profiles:Almost all leading players of the global Male Breast Cancer Treatment Market are profiled in this section. The analysts have provided information about their recent developments in the global Male Breast Cancer Treatment Market, products, revenue, production, business, and company.

Market Forecast by Production:The production and production value forecasts included in this section are for the global Male Breast Cancer Treatment Market as well as for key regional markets.

Market Forecast by Consumption:The consumption and consumption value forecasts included in this section are for the global Male Breast Cancer Treatment Market as well as for key regional markets.

Value Chain and Sales Analysis:It deeply analyzes customers, distributors, sales channels, and value chain of the global Male Breast Cancer Treatment Market.

Key Findings: This section gives a quick look at important findings of the research study.

About Us:Report Hive Research delivers strategic market research reports, statistical surveys, industry analysis and forecast data on products and services, markets and companies. Our clientele ranges mix of global business leaders, government organizations, SMEs, individuals and Start-ups, top management consulting firms, universities, etc. Our library of 700,000 + reports targets high growth emerging markets in the USA, Europe Middle East, Africa, Asia Pacific covering industries like IT, Telecom, Semiconductor, Chemical, Healthcare, Pharmaceutical, Energy and Power, Manufacturing, Automotive and Transportation, Food and Beverages, etc. This large collection of insightful reports assists clients to stay ahead of time and competition. We help in business decision-making on aspects such as market entry strategies, market sizing, market share analysis, sales and revenue, technology trends, competitive analysis, product portfolio, and application analysis, etc.

Contact Us:

Report Hive Research

500, North Michigan Avenue,

Suite 6014,

Chicago, IL 60611,

United States

Website: https://www.reporthive.com

Email: [emailprotected]

Phone: +1 312-604-7084

Read the original here:
Global Covid-19 impact on Male Breast Cancer Treatment Market Report 2025 by Global Market Insights, Outlook and Driving Trends 2020| Pfizer, Roche,...

INDIANAPOLIS, Ind. --Raena Eldridge of the Texas A&M womens swimming and diving team earned a conference-level nomination for NCAA Woman of the Year, as announced by the NCAA Tuesday afternoon. While 161 female student-athletes in total were nominated, Eldridgeis one of 59 student-athletes nominated from the Division I level. She is joined by Kentuckys Asia Seidt as the Southeastern Conferences nominees.

The NCAA Woman of the Year program is rooted in Title IX and has recognized graduating female college athletes for excellence in academics, athletics, community service and leadership since its inception in 1991.

Eldridge graduated from A&M in May with degrees in animal science and genetics, while also earning a business minor. She boasted a 3.979 cumulative GPA through her five years in Aggielandand has begun Vet School at NC State. Eldridge wasnamed the Arthur Ashe, Jr., Female Sports Scholar of the Year, awarded to one male and one femalestudent-athlete each year that exhibit academic excellence as well as community activism in addition to their athletic contributions.The Rockwall, Texas, native was A&M's female nominee for the H. Boyd McWhorter Scholar-Athlete Post-Graduate Scholarship, and for the second year in a row, was named the Bill Erwin Female Scholar-Athlete of the Year at A&M's annual Building Champions Awards. She earned College Swimming and Diving Coaches Association of America (CSCAA) Academic All-America honorable mention accolades as a sophomore and garnered first team honors as a junior and senior.

A team captain for her final two seasons, Eldridge was a part of four consecutive SEC Team Championships throughout her career. She was a two-time CSCAA All-American and earned All-SEC Second Team honors as a sophomore. Eldridge helped earn big points for the Aggies at SEC Championships as a sophomore, helping the 200 medley relay team reach the podium with a second-place finish, while adding a fifth-place finish with the 200 free relay squad. Individually at SEC Championships, she contributed a pair of top 16 finishes in the 100 back and 50 free that season. Eldridge also swam on winning teams in the 400 free relay and 400 medley relay to help the Aggies win the team title at the 2017 U.S. Open.

Away from the pool and the classroom, Eldridge served as a Student Technician at the Genetics Research Lab and as a member of the Pre-Vet Society. She was a project leader for the Aggie Research Scholars Program and started SPLASH, a non-profit organization that teaches swimming and swim safety. Eldridge also contributed her time at Save Our Streets Ministries in Bryan since 2016, mentoring elementary school girls.

The Woman of the Year Selection Committee, made up of representatives from the NCAA membership, will now choose the Top 30 honorees 10 from each division from the conference-level nominees. The Top 30 honorees will be announced in September. From there, the selection committee will narrow the pool to three finalists from each division. The NCAA Committee on Womens Athletics will select the 2020 Woman of the Year from the nine finalists.

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Eldridge Earns Conference-Level NCAA Woman of the Year Nomination - KBTX

DENVER, Aug. 11, 2020 In a pioneering study, CCRM Fertility has identified epigenetic alterations in sperm from men age 50 and older that predispose children to neurodevelopmental disorders, such as autism, bipolar disorder and schizophrenia. CCRM Fertility's groundbreaking research was published in the July issue of Aging Cell.

Led byCCRM Fertility's Scientific and Genetics DirectorMandy Katz-Jaffe,Ph.D.,the study examined sperm samples of men age 50 and older compared to their younger counterparts, as well as embryos that were created using donor eggs from young, fertile women.

By analyzing the sperm's DNA through a process known as whole-genome bisulfite sequencing, CCRM Fertility found significant methylation (the "on and off switch" for the expression of genes) alterations in both sperm and embryos from fathers age 50 and older. The abundance of methylation alterations was most associated with genes associated with neurodevelopmental disorders including autism, schizophrenia and bipolar disorder.

"While we have known that there is a correlation between advanced paternal age and risks of offspring neurodevelopmental disorders, this is the first time we've been able to identify an associated mechanism and inheritance," explains Dr. Katz-Jaffe. "It's an exciting breakthrough as we continue our researchinvestigating the male sperm genome, advanced paternal age risks and future healthy offspring."

William Schoolcraft, M.D., CCRM Fertility founder and medical director, adds,"Oftentimes, men fail to realize there is an ideal timeframe for their own roles in fertility. We hope our research raises further awareness around the male biological clock and encourages men in their 30s and 40s who plan to have children in the future to consider freezing their spermto maximize the chance of having a healthy baby."

About CCRMFertilityFounded by Dr. William Schoolcraft in 1987, CCRM(Colorado Center for Reproductive Medicine)Fertilityis the nation's leader in fertility care and research.CCRMFertilityspecializes in the most advanced fertility treatments, with deep expertise in in vitro fertilization (IVF), fertilityassessment, fertility preservation, genetic testing, third party reproduction and egg donation.Unlike many other fertility clinics that outsource their specialists and testing needs, CCRMFertilityleverages its own data, as well as a dedicated team of in-house reproductive endocrinologists, embryologists and geneticists in order to deliver industry-leading outcomes. CCRMFertilityoperates 11 fertility centers (including 26 offices) throughout North America, serving prospective parents in major metropolitan areas, including Atlanta, Boston, Dallas-Fort Worth, Denver, Houston, New York, Northern Virginia, Minneapolis, Orange County, San Francisco Bay Area and Toronto. For more information, visitwww.ccrmivf.com,become a fan onFacebook,or follow us onInstagramandTwitter.

SOURCE CCRM Fertility

See the article here:
CCRM Fertility Identifies Epigenetic Alterations in Sperm and Embryos of Older Men that Predispose Children to Autism and Other Neurodevelopmental...

Alcohol abuse is a serious problem worldwide. In England alone, over 350,000 alcohol-related hospital admissions and over 5,000 alcohol-related deaths were reported in 2018. Long-term alcohol abuse can have many harmful effects on our body. But one of the organs most affected by alcohol is the brain. Even moderate consumption changes brain structure and leads to cognitive issues, such as declines in memory and problem-solving.

Alcohol use is habit forming and can eventually lead to alcoholism. And though there are many treatments available for alcoholism, research shows these interventions often fail with less than 20% of patients remaining alcohol free after intervention. Like every addiction, alcoholism is a disease and not a choice, so finding the root cause of it will make treatment easier.

Although genetics and the environment you live in are known to play a role in developing alcoholism, these factors dont tell us how dependence occurs.

However, past research has found hints that the brains immune system cells (known as microglia) may be involved in addiction, including to cocaine and tobacco). One study even found that alcohol exposure and withdrawal in rats increased microglia numbers in the brain, before any other signs of alcohol-induced decline.

Another two recent studies have investigated brain changes seen in people and animals with alcohol dependence. Each of these studies found a common culprit: inflamed microglia.

Microglia are the brains resident immune system cells. Their main role is to guard and maintain balance in the brain. When microglia detect a threat, they respond by becoming inflamed and attacking. Normally, they return to normal after the threat is gone, but sometimes when inflammation becomes uncontrollable such as with Alzeimers disease it can lead to brain degeneration.

One recent study used mice to study the effect of alcohol dependence on the brain.

In the brains of male mice that had alcohol dependency, research found there were more microglia cells in the medial prefrontal cortex, a region associated with pain, decision making, and memory processes. Similar results have also previously been found in humans.

They then examined what effects microglia depletion had on alcohol dependent mice by looking at their alcohol seeking behaviour, and anxious behaviour during alcohol withdrawal. The researchers found both factors were lowered when the microglia cells were reduced in the brain.

They also saw gene changes with microglia depletion. Genes involved in inflammation and immune responses were expressed less after depletion. The expression of genes involved in alcohol consumption, and alcohol dependence also changed when microglia had decreased. They also found that microglia depletion weakens brain circuits involved in the development of dependence and relapse behaviour in rodents.

A second study looking at both rodent and human brains also showed microglia is involved in alcohol dependence.

The researchers of this study used brain imaging, microglia depletion, and studies of post mortem brains, to examine changes that occur in alcohol dependence. For the brain imaging part, they used a variation of MRI scans, called DTI-MRI in humans and rats, focusing on a measure called mean diffusivity.

As DTI-MRI is based on the diffusion of water in tissues, mean diffusivity essentially shows the amount of diffusion of water molecules in tissues, with more dense and structurally-intact tissues having lower mean diffusivity. Mean diffusivity has previously been shown to change in the brain in inflammatory and degenerative conditions (including Alzheimers Disease and even psychosis). The researchers therefore chose to look at mean diffusivity as neuroinflammation is also involved in alcoholism. The researchers wanted to examine whether changes in mean diffusivity would be found between alcoholics and non-alcoholics, which hasnt been done before.

Indeed their findings showed that mean diffusivity is overall higher in the brain of alcohol dependent rats and humans. They also found additional changes in how certain neurotransmitters including dopamine, which is involved in alcohol dependence move and are distributed in the brain.

The researchers went on to examine the microglia in the brains of rats with alcohol dependence, and rats with previous dependence who had abstained from alcohol for a week. They found a decreased amount of microglia in specific brain regions of dependent rats (including the hippocampus, which is involved in memory, and the nucleus accumbens, which is involved in the reward system). The microglia in the brains of alcohol dependent rats were also in their inflamed form.

Although this study showed a decrease in microglia numbers whereas the previous study saw an increase this might be because the researchers looked at different brain regions and used different research methods and animal models. However, both studies give hints towards how microglia functions during alcohol consumption and dependence, may differ in different brain regions.

The researchers also found that depleting microglia from the brain, or inducing microglias inflammatory response, led to similar results to each other, as both increased the mean diffusivity. Changes in microglias form when inflamed were also similar to the ones they observed in dependent rats. They concluded that the changes in the brain areas they studied could be explained by an inflammatory reaction of microglia caused by alcohol.

One limitation of both studies findings is that they used both only male rodents and male humans. However, both studies exhibit how alcoholism is a complex disease that produces clear changes in the brain.

Examining how exactly microglia is involved, and being able to interfere with their responses, could lead to better understanding and detection of addiction to alcohol, and give a good stepping stone for future targeted interventions.

Read more:
Alcohol addiction: could the brain's immune system be the key to understanding and treating alcoholism? - The Conversation UK

MedicalResearch.com Interview with:

Caspar van der Made, MDResident in Internal Medicine, PhD-studentAlexander Hoischen, PhDGeneticist, Assistant professor,Departments of Human Genetics and Internal Medicine

Radboud University Medical enterNijmegen, The Netherlands

First author Caspar van der Made is a resident in Internal Medicine and PhD-student on the topic of immunogenomics.Alexander Hoischen is geneticist with a special focus on the application of genomic technologies in primary immunodeficiencies and last author of this study.

MedicalResearch.com: What is the background for this study?

Response: This study was initiated to investigate the presence of monogenic factors that predispose young individuals to develop a severe form of COVID-19. It has become clear that several general risk factors such as obesity, hypertension and diabetes mellitus increase the risk of developing severe coronavirus disease. However, even though differences in interindividual genetic make-up are thought to influence the immune response to SARS-CoV-2, such specific genetic risk factors had not yet been identified.

We therefore chose to study young brother pairs (sharing half of their genomes) without any general risk factors that nevertheless contracted severe COVID-19.

We hypothesized these highly selected case series may offer the most optimal chance of identifying a (possible X-linked) primary immunodeficiency specific to COVID-19.

MedicalResearch.com: What are the main findings?

Response: In this case series, two young brother pairs of which all four individuals with a mean age of 26 years required mechanical ventilation at the ICU were enrolled and studied. We performed rapid clinical whole-exome sequencing of the patients and segregation in available family members to identify loss-of-function variants of the X-chromosomal TLR7. This gene encodes the toll-like receptor 7 protein that plays a critical role in the innate immune response against coronaviruses, predominantly by mediating the production of type I interferons. Especially in SARS-CoV-2 infections this response is crucial, as the virus has evasive mechanisms to disrupt a proper type I interferon response. In primary peripheral blood mononuclear cells extracted from the patients, we have shown that the transcription of type I-interferon genes was lower in patients upon stimulation with the TLR7 agonist imiquimod, as compared to controls. Furthermore, the production of the type II interferon IFNg was also decreased in patients.

MedicalResearch.com: What should readers take away from your report?

Response: To our knowledge this is the first report that proposes a specific monogenic factor to develop severe COVID-19. We aim to highlight the important contribution of genetics in the susceptibility to develop COVID-19 and hope to create awareness among physicians to consider genetic evaluation of young patients with unexplained severe COVID-19.

The finding of TLR7 deficiency in these patients furthermore underlines the importance of an intact type I and II interferon response to fight off SARS-CoV-2 and provides insight in the timing of possible treatment options.

MedicalResearch.com: What recommendations do you have for future research as a result of this work?

Response: While the TLR7 deficiency is most likely a rare phenomenon, with an estimate of 1:10,000 TLR7 mutation carriers in the general population; our findings shall be replicated and expanded by others. Similar to other rare disease genetic studies, this shall allow additional insides into disease pathogenesis in general. Further research should focus on the elucidation of the exact role of TLR7-signaling in the pathogenesis of SARS-CoV-2 and ultimately the exploration of rational treatment options.

Also, these findings may provide part of the explanation for the male sex bias observed in COVID-19, which should be addressed more in-depth. More generally, we encourage further studies towards the identification of other genetic risk factors and applaud the efforts already undertaken by other large consortia.

MedicalResearch.com: Is there anything else you would like to add?

Response: We are very grateful to the families that participated in this study, and would like to acknowledge our interdisciplinary team of collaborators.

Any disclosures?

No relevant conflict of interest for any of the authors.

Citation:

van der Made CI, Simons A, Schuurs-Hoeijmakers J, et al. Presence of Genetic Variants Among Young Men With Severe COVID-19.JAMA.Published online July 24, 2020. doi:10.1001/jama.2020.13719

https://jamanetwork.com/journals/jama/fullarticle/2768926

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The information on MedicalResearch.com is provided for educational purposes only, and is in no way intended to diagnose, cure, or treat any medical or other condition. Always seek the advice of your physician or other qualified health and ask your doctor any questions you may have regarding a medical condition. In addition to all other limitations and disclaimers in this agreement, service provider and its third party providers disclaim any liability or loss in connection with the content provided on this website.

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Genetic Change Detected in Brothers Helps Explain Why COVID-19 More Severe in Men - MedicalResearch.com

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In the past, the medicine people took for their ailment was primarily their food, the vegetables and other natures proceeds that were used as medicinal herbs. These served as nutritious food and medication, they boosted the bodys immune system and helped it fight various health conditions.

With the coming of scientific research, many of these modes of treatment phased out and were replaced by scientific inventions, the conventional drugs as they are known as today. However, interest and research on the benefits of some of these plants and herbs have been rekindled.

This is even more so now that it is known that they have various health benefits. One of such plants is the hemp plant.

Known botanically as cannabis sativa, this is a plant that has gained much relevance and popularity today because of both its fiber and edible seeds content. Many times, many people confuse it with the cannabis from which marijuana is made.

This is mostly because they are both from the cannabis family. The main difference however is in the amount of THC that they both contain. THC is the compound responsible for the psychoactive effect you can get from using marijuana. Marijuanas THC content is high while that of the hemp plant is low and wouldnt get you high. You can read more about it here.

One of the unique qualities of this plant is that it is a dioecious plant which means that it produces plant with both male and female characteristics. The opposite of this would be to be monoecious, which means that it would contain both male and female characteristics in it.

However, what is mostly used and is more popular is the female cannabis sativa. Thus, when it comes to the cultivation of cannabis, the females are usually more regarded because they are responsible for creating the flowers and the seed.

The fact that the female hemp plant is more used doesnt make the males less useful. They are actually very important. In fact, their uses are quite many. Some of its uses include the following:

You can visit https://cheefbotanicals.com/do-male-hemp-plants-produce-cbd/ to find out more its other uses.

At about six weeks, farmers should be able to differentiate between the sex of their produce, however, for newbies and even for old hands, a careful reminder is always a good thing.

This difference can be deduced when the crux of their branches, more popularly known as the plant nodes, are carefully observed. While the male plants grow small pollen sacks, the females grow bracts and as they mature, its bracts will grow hair like wisps that will catch the pollens from the males. It is also important to know that there are hermaphrodite species that have both male and female characteristics. While they might be useful to the farmer early on, the genetics of their offspring will only get weaker and weaker and there wouldnt be any variety amongst them.

The point is this, though it may seem that the male hemp plant does not have much market value compared to the female, they still remain quite useful.

If you previously had no idea that this plant family was divided into two genders, this article has brought that to your attention. If you on the other hand already knew this but did not know that the male variation offered any kind of value, now you also know differently thanks to this article.

With the information you have received in this article, you are now better informed and will now look at this previously despised plant differently.

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Uses of the Male Hemp Plant - Trill

LONDON--(BUSINESS WIRE)--Aug 5, 2020--

GlaxoSmithKline plc (LSE/NYSE: GSK) announced the US Food and Drug Administration (FDA) has approved BLENREP (belantamab mafodotin-blmf) as a monotherapy treatment for adult patients with relapsed or refractory multiple myeloma who have received at least four prior therapies including an anti-CD38 monoclonal antibody, a proteasome inhibitor and an immunomodulatory agent. This indication is approved under accelerated approval based on response rate. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials. BLENREP is the first anti-BCMA (B-cell maturation antigen) therapy approved anywhere in the world. i

Dr. Hal Barron, Chief Scientific Officer and President R&D, GSK, said: As the second most common form of blood cancer in the US, multiple myeloma is an incurable and devastating disease. BLENREP is the first approved anti-BCMA therapy and has the potential to transform the treatment of patients with relapsed or refractory myeloma who have limited treatment options today.

BLENREP is GSKs fifth major medicine approval in 2020 across areas of significant unmet medical need such as cancer, HIV and chronic kidney disease. This approval marks the second FDA approval for GSKs oncology portfolio in four months.

BLENREP employs a multi-faceted mechanism of action and is directed toward BCMA, a cell-surface protein that plays an important role in the survival of plasma cells and is expressed on multiple myeloma cells. ii The approval of BLENREP was based on six-month primary results from the pivotal DREAMM-2 study, which enrolled patients with relapsed or refractory multiple myeloma who had actively progressing disease that had worsened despite current standard of care.

Dr. Sagar Lonial, MD, Chief Medical Officer, Winship Cancer Institute of Emory University in Atlanta, Georgia, Chair of Emory Department of Hematology and Medical Oncology and Principal Investigator for DREAMM-2, said: While treatable, refractory multiple myeloma is a significant clinical challenge with poor outcomes for patients whose disease has become resistant to the current standard of care. Due to the limited options currently available, these patients are often retreated with drugs from the same classes after they relapse, which is why the approval of BLENREP, the first anti-BCMA therapy, is significant for both patients and physicians alike.

In the DREAMM-2 study, treatment with single-agent BLENREP 2.5 mg/kg every three weeks demonstrated a clinically meaningful overall response rate (ORR) of 31% (97.5% CI; 21-43) in patients who had received a median of seven prior lines of treatment (n=97). The median duration of response (DoR) had not been reached at the six-month analysis, but 73% of responders had a DoR equal to or greater than six months. The most commonly reported adverse events (20%) were keratopathy, decreased visual acuity, nausea, blurred vision, pyrexia, infusion-related reactions, and fatigue. Keratopathy is characterized as changes in the corneal epithelium as seen on eye examination, which can manifest with or without symptoms.

Ocular adverse reactions occurred in 77% of the 218 patients in the pooled safety population and included keratopathy (76%), changes in visual acuity (55%), blurred vision (27%), and dry eye (19%). Corneal adverse events were monitored with eye exams prior to each dose, allowing for dose reductions or interruptions as appropriate. Patients also used preservative-free eye drops. Keratopathy leading to treatment discontinuation affected 2.1% of patients in the 2.5 mg/kg cohort. iii

BLENREP is available through participation in the BLENREP Risk Evaluation and Mitigation Strategy (REMS), which was developed to ensure appropriate use of the medicine. The program requires education for all physicians prescribing BLENREP and their patients regarding the ocular risks associated with treatment as well as monitoring. Additional information about the BLENREP REMS can be found at http://www.blenreprems.com or 1-855-209-9188.

Paul Giusti, President and CEO of the Multiple Myeloma Research Foundation (MMRF), said: The approval of BLENREP is an important advancement for patients with relapsed or refractory multiple myeloma, as it brings a much-needed new treatment to patients who face limited options due to their progressing disease. We are grateful for GSKs continued commitment to myeloma patients and their families.

In 2017, BLENREP was granted Breakthrough Therapy designation by the FDA, which is intended to facilitate the development of investigational medicines that have shown clinical promise for conditions where there is significant unmet need.

Making Our Products Affordable and Accessible

GSK is actively involved in creating solutions that allow patients to have access to new scientific breakthroughs. We remain committed to helping patients access GSK medications and have a long history of providing patient assistance programs. Patients and healthcare professionals can access more information about our oncology specific resources on insurance coverage and financial support at: http://www.TogetherwithGSKOncology.com or call: 1-844-4GSK-ONC (1-844-447-5662).

About Multiple Myeloma

Multiple myeloma is the second most common blood cancer in the US and is generally considered treatable, but not curable. iv In the US, more than 32,000 people are estimated to be diagnosed with multiple myeloma this year and nearly 13,000 people will die from the disease. v Research into new therapies is needed as multiple myeloma commonly becomes refractory to available treatments. vi

AboutBLENREP(belantamab mafodotin-blmf)

BLENREP is an antibody drug conjugate comprising a humanized anti-B cell maturation antigen (BCMA) monoclonal antibody conjugated to the cytotoxic agent auristatin F via non-cleavable linker. The drug linker technology is licensed from Seattle Genetics; monoclonal antibody is produced using POTELLIGENT Technology licensed from BioWa.

IMPORTANT SAFETY INFORMATION FOR BLENREP

WARNING: OCULAR TOXICITY

BLENREP caused changes in the corneal epithelium resulting in changes in vision, including severe vision loss and corneal ulcer, and symptoms such as blurred vision and dry eyes.

Conduct ophthalmic exams at baseline, prior to each dose, and promptly for worsening symptoms. Withhold BLENREP until improvement and resume, or permanently discontinue, based on severity.

Because of the risk of ocular toxicity, BLENREP is available only through a restricted program under a Risk Evaluation and Mitigation Strategy (REMS) called the BLENREP REMS.

WARNINGS AND PRECAUTIONS

Ocular Toxicity: Ocular adverse reactions occurred in 77% of the 218 patients in the pooled safety population. Ocular adverse reactions included keratopathy (76%), changes in visual acuity (55%), blurred vision (27%), and dry eye (19%). Among patients with keratopathy (n = 165), 49% had ocular symptoms, 65% had clinically relevant visual acuity changes (decline of 2 or more lines on Snellen Visual Acuity in any eye), and 34% had both ocular symptoms and visual acuity changes.

Keratopathy: Keratopathy was reported as Grade 1 in 7% of patients, Grade 2 in 22%, Grade 3 in 45%, and Grade 4 in 0.5% per the KVA scale. Cases of corneal ulcer (ulcerative and infective keratitis) have been reported. Most keratopathy events developed within the first 2 treatment cycles (cumulative incidence of 65% by Cycle 2). Of the patients with Grade 2 to 4 keratopathy (n = 149), 39% recovered to Grade 1 or lower after median follow-up of 6.2 months. Of the 61% who had ongoing keratopathy, 28% were still on treatment, 9% were in follow-up, and in 24% the follow-up ended due to death, study withdrawal, or lost to follow-up. For patients in whom events resolved, the median time to resolution was 2 months (range: 11 days to 8.3 months).

Visual Acuity Changes: A clinically significant decrease in visual acuity of worse than 20/40 in the better-seeing eye was observed in 19% of the 218 patients and of 20/200 or worse in the better-seeing eye in 1.4%. Of the patients with decreased visual acuity of worse than 20/40, 88% resolved and the median time to resolution was 22 days (range: 7 days to 4.2 months). Of the patients with decreased visual acuity of 20/200 or worse, all resolved and the median duration was 22 days (range: 15 to 22 days).

Monitoring and Patient Instruction: Conduct ophthalmic examinations (visual acuity and slit lamp) at baseline, prior to each dose, and promptly for worsening symptoms. Perform baseline examinations within 3 weeks prior to the first dose. Perform each follow-up examination at least 1 week after the previous dose and within 2 weeks prior to the next dose. Withhold BLENREP until improvement and resume at same or reduced dose, or consider permanently discontinuing based on severity. Advise patients to use preservative-free lubricant eye drops at least 4 times a day starting with the first infusion and continuing until end of treatment. Avoid use of contact lenses unless directed by an ophthalmologist. Changes in visual acuity may be associated with difficulty for driving and reading. Advise patients to use caution when driving or operating machinery. BLENREP is only available through a restricted program under a REMS.

BLENREP REMS:BLENREP is available only through a restricted program under a REMS called the BLENREP REMS because of the risks of ocular toxicity. Notable requirements of the BLENREP REMS include the following:

Further information is available at http://www.BLENREPREMS.com and 1-855-209-9188.

Thrombocytopenia: Thrombocytopenia occurred in 69% of 218 patients in the pooled safety population, including Grade 2 in 13%, Grade 3 in 10%, and Grade 4 in 17%. The median time to onset of the first thrombocytopenic event was 26.5 days. Thrombocytopenia resulted in dose reduction, dose interruption, or discontinuation in 9%, 2.8%, and 0.5% of patients, respectively. Grade 3 to 4 bleeding events occurred in 6% of patients, including Grade 4 in 1 patient. Fatal adverse reactions included cerebral hemorrhage in 2 patients. Perform complete blood cell counts at baseline and during treatment as clinically indicated. Consider withholding and/or reducing the dose based on severity.

Infusion-Related Reactions: Infusion-related reactions occurred in 18% of 218 patients in the pooled safety population, including Grade 3 in 1.8% . Monitor patients for infusion-related reactions. For Grade 2 or 3 reactions, interrupt the infusion and provide supportive treatment. Once symptoms resolve, resume at a lower infusion rate. Administer premedication for all subsequent infusions. Discontinue BLENREP for life-threatening infusion-related reactions and provide appropriate emergency care.

Embryo-Fetal Toxicity: Based on its mechanism of action, BLENREP can cause fetal harm when administered to a pregnant woman because it contains a genotoxic compound (the microtubule inhibitor, monomethyl auristatin F [MMAF]) and it targets actively dividing cells. Advise pregnant women of the potential risk to a fetus. Advise females of reproductive potential to use effective contraception during treatment with BLENREP and for 4 months after the last dose. Advise males with female partners of reproductive potential to use effective contraception during treatment with BLENREP and for 6 months after the last dose.

ADVERSE REACTIONS

The pooled safety population described in Warnings and Precautions reflects exposure to BLENREP at a dosage of 2.5 mg/kg or 3.4 mg/kg (1.4 times the recommended dose) administered intravenously once every 3 weeks in 218 patients in DREAMM-2. Of these patients, 194 received a liquid formulation (not the approved dosage form) rather than the lyophilized powder. Among the 218 patients, 24% were exposed for 6 months or longer.

The safety of BLENREP as a single agent was evaluated in DREAMM-2. Patients received BLENREP at the recommended dosage of 2.5 mg/kg administered intravenously once every 3 weeks (n = 95). Among these patients, 22% were exposed for 6 months or longer.

Serious adverse reactions occurred in 40% of patients who received BLENREP. Serious adverse reactions in >3% of patients included pneumonia (7%), pyrexia (6%), renal impairment (4.2%), sepsis (4.2%), hypercalcemia (4.2%), and infusion-related reactions (3.2%). Fatal adverse reactions occurred in 3.2% of patients, including sepsis (1%), cardiac arrest (1%), and lung infection (1%).

Permanent discontinuation due to an adverse reaction occurred in 8% of patients who received BLENREP; keratopathy (2.1%) was the most frequent adverse reaction resulting in permanent discontinuation.

Dosage interruptions due to an adverse reaction occurred in 54% of patients who received BLENREP. Adverse reactions which required a dosage interruption in >3% of patients included keratopathy (47%), blurred vision (5%), dry eye (3.2%), and pneumonia (3.2%).

Dose reductions due to an adverse reaction occurred in 29% of patients. Adverse reactions which required a dose reduction in >3% of patients included keratopathy (23%) and thrombocytopenia (5%). The most common adverse reactions (20%) were keratopathy (71%), decreased visual acuity (53%), nausea (24%), blurred vision (22%), pyrexia (22%), infusion-related reactions (21%), and fatigue (20%). The most common Grade 3 or 4 (5%) laboratory abnormalities were lymphocytes decreased (22%), platelets decreased (21%), hemoglobin decreased (18%), neutrophils decreased (9%), creatinine increased (5%), and gamma-glutamyl transferase increased (5%).

USE IN SPECIFIC POPULATIONS

Lactation: There is no data on the presence of belantamab mafodotin-blmf in human milk or the effects on the breastfed child or milk production. Because of the potential for serious adverse reactions in the breastfed child, advise women not to breastfeed during treatment with BLENREP and for 3 months after the last dose.

Females and Males of Reproductive Potential: BLENREP can cause fetal harm when administered to pregnant women. There are no available data on the use of BLENREP in pregnant women to evaluate for drug-associated risk. No animal reproduction studies were conducted with BLENREP.

Pregnancy Testing: Pregnancy testing is recommended for females of reproductive potential prior to initiating BLENREP.

Infertility: Based on findings in animal studies, BLENREP may impair fertility in females and males. The effects were not reversible in male rats but were reversible in female rats.

Geriatric Use: Of the 218 patients who received BLENREP in DREAMM-2, 43% were aged 65 to less than 75 years and 17% were aged 75 years and older. Keratopathy occurred in 80% of patients aged less than 65 years and 73% of patients aged 65 years and older. Among the patients who received BLENREP at the 2.5-mg/kg dose in DREAMM-2 (n = 95), keratopathy occurred in 67% of patients aged less than 65 years and 73% of patients aged 65 years and older.

Renal Impairment: No dose adjustment is recommended for patients with mild or moderate renal impairment (estimated glomerular filtration rate [eGFR] 30 to 89 mL/min/1.73m 2 as estimated by the Modification of Diet in Renal Disease [MDRD] equation). The recommended dosage has not been established in patients with severe renal impairment (eGFR 15 to 29 mL/min/1.73 m 2 ) or end-stage renal disease (ESRD) with eGFR <15 mL/min/1.73 m 2 not on dialysis or requiring dialysis.

Hepatic Impairment: No dose adjustment is recommended for patients with mild hepatic impairment (total bilirubin upper limit of normal [ULN] and aspartate aminotransferase (AST) >ULN or total bilirubin 1 to 1.5 ULN and any AST). The recommended dosage of BLENREP has not been established in patients with moderate or severe hepatic impairment (total bilirubin >1.5 ULN and any AST) .

INDICATION

BLENREP is indicated for the treatment of adults with relapsed or refractory multiple myeloma who have received at least 4 prior therapies, including an anti-CD38 monoclonal antibody, a proteasome inhibitor, and an immunomodulatory agent.

This indication is approved under accelerated approval based on response rate. Continued approval for this indication may be contingent upon verification and description of clinical benefit in a confirmatory trial(s).

The full Prescribing Information, including BOXED WARNING and Medication Guide, will be available here.

GSK in Oncology

GSK is focused on maximizing patient survival through transformational medicines. GSKs pipeline is focused on immuno-oncology, cell therapy, cancer epigenetics, and synthetic lethality. Our goal is to achieve a sustainable flow of new treatments based on a diversified portfolio of investigational medicines utilizing modalities such as small molecules, antibodies, antibody drug conjugates and cells, either alone or in combination.

About GSK

GSK is a science-led global healthcare company with a special purpose: to help people do more, feel better, live longer. For further information please visit http://www.gsk.com/about-us.

Editors Note: In addition to the FDAs approval of BLENREP, GSK has received four major medicine approvals to date in 2020 for CABENUVA (cabotegravir and rilpivirine) in Canada, DUVROQ (daprodustat) in Japan and ZEJULA (niraparib) and RUKOBIA (fostemsavir) in the US.

Cautionary statement regarding forward-looking statements

GSK cautions investors that any forward-looking statements or projections made by GSK, including those made in this announcement, are subject to risks and uncertainties that may cause actual results to differ materially from those projected. Such factors include, but are not limited to, those described under Item 3.D "Risk Factors" in the company's Annual Report on Form 20-F for 2019 and as set out in GSKs Principal risks and uncertainties section of the Q2 Results and any impacts of the COVID-19 pandemic.

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References

i NCI Drug Dictionary - Anti-BCMA Antibody-Drug Conjugate GSK2857916. National Cancer Institute. https://www.cancer.gov/publications/dictionaries/cancer-drug/def/anti-bcma-antibody-drug-conjugate-gsk2857916.

Accessed May 2020.

ii Trudel S, Lendvai N, Popat R, et al. Antibodydrug conjugate, GSK2857916, in relapsed/refractory multiple myeloma: an update on safety and efficacy from dose expansion phase I study. Blood Cancer Journal. 2019;9(4).

doi:10.1038/s41408-019-0196-6.

iii Lonial, S, et al. Belantamab mafodotin for relapsed or refractory multiple myeloma (DREAMM-2): a two-arm, randomised, open-label, phase 2 study. Lancet Oncol. 2020; 21(2):20721.

iv Estimated number of incident cases worldwide, both sexes, all ages. World Health Organization. https://gco.iarc.fr/ Published 2020. Accessed May 2020.

v SEER Cancer Facts & Figures 2019. Available at: https://seer.cancer.gov/statfacts/html/mulmy.html. Accessed December 19, 2019.

vi Nooka AK, Kastritis E, Dimopoulos MA. Treatment options for relapsed and refractory multiple myeloma. Blood. 2015;125(20)

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Original post:
FDA Approves GSK's BLENREP (belantamab mafodotin-blmf) for the Treatment of Patients with Relapsed or Refractory Multiple Myeloma - The Baytown Sun

Since 1909, J.W. Jung Seed Co., has supplied Wisconsin gardeners with seeds, plants, shrubs and trees. Two seasons ago, Richard Dick Zondag, president and grandson of founder John William Jung, had been introduced to hemp and worked with specialist in the industry to develop a technique of rooting female plants. This season, they offered abacus strain hemp in rooted cuttings, as well as seedlings and seeds.

Jung is headquartered in Randolph, Wis. They also have garden centers throughout Madison and in Stevens Point. (Jung Seed Genetics, suppliers of farm seed, spun off from J.W. Jung Seed in the early 2000s and is now owned by Monsanto; the two companies are not affiliated.)

Zondag says he chose the abacus strain because its one of the most commonly used varieties, and he found it to be an early flowering variety; ideal for our upper Midwest climate. You need an early flowering variety for Wisconsin because our growing season is shorter than most. Theres a lot of hemp grown on the West Coast for CBD oil because they have a much longer growing season, he says.

J.W. Jung Seeds hemp experimentation started with seedlings. They planted all of their seedling populations and then removed the male plants when they started to flower. Then we went through the field and picked out 10 different plants that seemed to have the structure that we wanted, and the early flowering. That was a determining factor for our clonesand of course, they had to be female plants.

They chose to focus on rooted cuttings because, Zondag explains, hemp is a dioecious plant, meaning that it has male and female flowers on separate plants. Other examples of dioecious plants include honey locust. With hemp, you want females because the CBD oil is produced on the flowers of the hemp plant. Female flowers produce a lot more CBD oil when the flowers are not fertilized, he says. Thats why we use cuttings use rather than seedlings. Unless you really know what youre doing, if you have a cutting, the plant produced from a cutting will be the same as the plant it came from.

With seeds, youre taking a chance of ending up with male or female plants, he affirms. All rooted cuttings sold by J.W. Jung Seed for the 2020 growing season were cloned from female plants.

Zondag says they did have some cuttings and seedlings left over after farmers completed their spring planting. The market was becoming saturated, he says. The number of licenses (issued by the Wisconsin Department of Agriculture, Trade and Consumer Protection) were down instead of up. I think a lot of farmers that went into hemp farming didnt have a lab to extract the CBD oil. They got stuck with the crop and didnt make any money. Next spring, were going to produce hemp cuttings by contract only.

He hopes the market will stabilize because its a good secondary crop for farmers to diversify. He also sees a good opportunity to grow hemp for fiber, and for seed used in health products. When youre growing it for fiber, you dont have to pay attention to whether plants are male or female. The hemp plant is very woody when it matures, so theres a lot of fiber. It offers a lot of different purposes.

For more information, visit jungseed.com.

To read more Cannabis Connection articles,click here.

To read more articles by Sheila Julson,click here.

Sheila Julson is a freelance writer who enjoys capturing the stories behind Milwaukees happening food, beverage and urban farming scenes. She also pens articles about holistic health, green living, sustainability and human-interest features.

Aug. 04, 2020

10:14 a.m.

See the article here:
J.W. Jung Seed Specializes in Hemp Cuttings - Shepherd Express

Disclaimer: Early release articles are not considered as final versions. Any changes will be reflected in the online version in the month the article is officially released.

Author affiliations: Ghent University, Merelbeke, Belgium (E. Vandoorn, A. Parys, K. Van Reeth); Ghent University and Ghent University Hospital, Ghent, Belgium (I. Leroux-Roels, G. Leroux-Roels); National Animal Disease Center, Ames, Iowa, USA (A. Vincent)

Humans and swine are susceptible to influenza A viruses (IAVs) of hemagglutinin (HA) subtypes H1 and H3, which are widespread in both species. Human IAVs frequently are transmitted to swine, after which the HA surface protein generally undergoes slower antigenic evolution (drift) in swine than in humans (13). Therefore, swine can be considered a reservoir for past human IAVs. Because antigenic drift variants of human IAVs replace each other over time, younger persons only have been exposed to more recent strains and human population immunity against older human IAVs gradually decreases (4). Consequently, human-origin swine IAVs (swIAVs) can be reintroduced into the human population after a certain period and cause a pandemic, as illustrated by the influenza A(H1N1)pdm09 virus (pH1N1) (5). The H1 of this swine-origin virus is related to the H1 of human seasonal H1N1 IAVs that circulated in 19181950. In 2009, only persons born before the 1950s had cross-reactive antibodies against H1N1 viruses, so a pandemic was possible (6,7).

The evolution of swIAVs is different from and more complex than that of human IAVs because of multiple introductions of human IAVs into swine and geographic separation of swine populations (8). H1 swIAV colloquial names indicate their origin and region of circulation. An improved classification system subdivides H1 swIAVs into 3 lineages and 28 clades on the basis of H1 nucleotide sequence homology (9). The lineages are 1A, 1B, and 1C, with the number representing the subtype (H1) and the letter representing the lineage. Clades and subclades are indicated with 13 digits. Classical swine lineage 1A contains IAVs with the human 1918 pandemic H1N1 virus as a common ancestor. Most clades are restricted to America and Asia, but pH1N1 viruses (1A.3.3.2) circulate in swine and humans worldwide. Human seasonal lineage 1B contains swIAVs with an H1 derived from human seasonal IAVs. These human-like H1 swIAVs emerged in Europe in the late 1980s and in North America in the early 2000s. Eurasian avian lineage 1C contains swIAVs that originated from avian IAVs. These avian-like swIAVs emerged in Europe in 1979 and spread to Asia in 1993 (1013). Apart from antigenic evolution in the HA, IAVs also can evolve via exchange of gene segments with other IAVs of different subtypes or clades infecting the same cell, called reassortment (14), which frequently occurs in pigs. A reassortant IAV with an antigenically novel HA and the capacity to infect and spread in humans could cause a pandemic.

Since 2010, 35 zoonotic infections with H1 swIAVs were reported in North America and 10 in Europe (1517; Parys et al., unpub. data). Human population immunity is a major factor determining the pandemic risk for swIAVs. Hemagglutination inhibiting (HI) and virus neutralizing (VN) antibodies in serum are accepted correlates of protection (18). Evaluating humans of different age groups for HI and VN antibody titers against a range of antigenically different swIAVs might help clarify the public health risk.

In a previous seroprevalence study for H3 swIAVs in humans from Luxembourg, we demonstrated a correlation with the nature of the swIAV and its relation to human IAVs on the one hand and the persons birth year on the other (19). A large comparative seroprevalence study for H1 swIAVs is lacking. Previous studies examined limited numbers of H1 swIAVs or samples or did not evaluate the relation between birth year and antibody responses (12,13,2025). In addition, most studies were conducted before or during the 2009 pandemic, but the circulation of pH1N1 viruses in humans likely changed the serologic profile against H1 swIAVs. We assessed prevalence and titers of protective antibodies against all major H1 swIAV clades in various age groups in Belgium in 2017. We also examined the relation between antibodies against human-like swIAVs and their presumed human seasonal ancestor IAV. The results will help assess the public health risk for different H1 swIAVs.

During August 2017January 2018, a total of 549 anonymized serum samples were collected from immunocompetent persons with unknown influenza vaccination or infection history born during 19202017 at Ghent University Hospital (Ghent, Belgium). Samples included 6 per birth year with 1:1 ratio between male and female patients. Exclusion criteria included active oncologic disease or hematologic malignancies, immunosuppressive treatment, organ transplantation, admission to intensive care, and end-stage renal disease on dialysis treatment. This study was approved by the Commission for Medical Ethics of the Ghent University Hospital (approval no. 2017/0834).

Samples were evaluated for antibodies against 11 viruses representing 7 major H1 swIAV clades circulating in Europe, North America, and Asia; 2 human seasonal progenitor IAVs for European and North American human-like swIAVs; and 1 human seasonal IAV that circulated right before the pH1N1 virus (Table 1). We used epidemiologic data (1012) and the H1 classification system (9) to select major H1 swIAV clades. We selected test viruses on the basis of amino acid homology and antigenic relatedness to currently circulating swIAVs of each clade. We selected the human progenitor IAVs based on the literature (26,27).

We downloaded nucleotide sequences of the viruses HA1, the main target of neutralizing antibodies, from Genbank and translated these to amino acids. We used the MUSCLE algorithm for sequence alignment and the Jones-Taylor-Thornton model and nearest-neighbor-interchange heuristic method to construct maximum-likelihood trees in MEGA7 (28). We determined the percent of amino acid homology between test viruses and numbers of identical amino acids in presumed antigenic sites (29) with MEGA7 and R version 3.2.2 (30).

We obtained North American swIAVs and corresponding swine serum from the U.S. Department of Agriculture-Agricultural Research Service. We obtained human seasonal IAVs and corresponding ferret serum from Francis Crick Institute (London, UK), and Asian swIAV from Hong Kong University (Hong Kong). We antigenically characterized test viruses in cross-HI and cross-VN assays with postvaccination swine serum for swIAVs or postinfection ferret serum for human seasonal IAVs. Because serum against A/Brisbane/59/2007 was not available, we used ferret serum against A/Egypt/10/2007 instead; the HA sequence is identical in both. We propagated viruses in MDCK cells; all passages were <6. We calculated antigenic distances from HI and VN titers as described previously (31) and converted these into antigenic dendrograms by using the neighbor-joining method in MEGA7. One antigenic unit represents a 2-fold difference in HI or VN titer.

We tested individual samples in HI assays and pooled samples per birth year in VN assays for antibodies against each test virus. Both assays were performed according to standard procedures (32,33). We expressed antibody titers for HI as the reciprocal of the highest serum dilution showing complete hemagglutination inhibition of 4 hemagglutinating units of virus or, for VN, 50% neutralization of 100 TCID50 (50% tissue culture infective doses) of virus. The starting dilution was 1:20, and we considered a titer of 40 positive.

We calculated geometric mean titers (GMTs) and 95% CIs for HI and VN antibody titers of samples from each birth decade against each test virus by using log2-transformed data. Samples with a titer <20 were assigned a titer of 10. For non-stratified data, we calculated Spearman correlation coefficients (CCs) between HI titers or between VN titers against different viruses. We used Kruskal-Wallis and Mann-Whitney U tests to compare antibody titers between age groups for a certain virus or between viruses for a certain age group. We used Fisher exact test to compare proportions of positive samples. For all statistical tests, we applied Bonferroni adjustment of the p values and we considered corrected p values of <0.05 statistically significant. We performed all analyses by using R version 3.2.2.

Figure 1

Figure 1. Epidemiologic, phylogenetic, and antigenic relationship between influenza A test viruses from classical swine lineage 1A, human seasonal lineage 1B, and Eurasian avian lineage 1C. A) Schematic representation of the H1 IAV...

We tested samples for antibodies against 11 IAVs from the classical swine 1A, human seasonal 1B, or Eurasian avian 1C lineage. HA1 aa sequence homology between viruses of different lineages was <75% with 1935/50 identical amino acids in presumed antigenic sites. Classical swine and avian-like IAVs were phylogenetically most closely related (Figure 1, panel A; Table 2). Within-lineage HA1 aa homology was 82%97%, with 3649 identical amino acids in antigenic sites. Human-like swIAVs and their presumed human seasonal progenitor IAV shared 90%94% aa in the HA1 and 3642 aa in antigenic sites.

Antigenic dendrograms based on cross-HI and cross-VN assays showed similar trends to the phylogenetic tree, except for swOK13 (Tables 35; Figure 1). This North American human-like 1b swIAV (1B.2.2.2) clustered separately from other IAVs of its lineage, including its presumed human ancestor, NC99.

Figure 2

Figure 2. Number of positive human serum samples in the hemagglutination inhibition assay (titer >40) for each test virus compared with the total number of samples tested per birth cohort. Birth cohorts...

Figure 3

Figure 3. Number of positive human serum samples in the virus neutralization assay (titer >40) for each test virus compared with the total number of samples per birth cohort. Birth cohorts are...

We tested human serum samples against human seasonal IAVs related to 1B swIAVs from 1986 (TW86), 1999 (NC99), and 2007 (BR07) to evaluate a persons potential exposure to or vaccination with these IAVs. Overall, 39% were seropositive for TW86, 31% for NC99, and 22% for BR07 in HI and 48% were seropositive for TW86, 51% for NC99, and 29% for BR07 in VN (Figures 2, 3). Seroprevalences and GMTs against TW86 were highest for persons born during 19771986 and lowest for the 2 youngest groups, those born during 19972017 (Tables 6, 7). For NC99 and BR07, HI responses were highest for those born during 19871996, and VN responses were highest for those born during 19371946 (NC99 only) and 19972006. Persons born during 20072017 had minimal responses. Antibody responses against human seasonal IAVs were related to birth year and the year of virus isolation, with peak responses in persons born right before the virus circulated and lowest responses in persons born afterwards.

The major avian-origin swIAV clades are European avian-like 1C.2.1, represented by swG10, and Asian avian-like 1C.2.3, represented by swHK11. For swG10, 10% of all samples tested positive in HI and 7% in VN (Figures 2, 3). Seroprevalence was <20% and GMTs were <20 for all age groups except the oldest, those born during 19201926, with 40% seropositive in HI and GMTs for HI and VN of 24 (Tables 6, 7).

For swHK11, overall seroprevalence was 25% in HI and 34% in VN. Like swG10, responses against swHK11 were highest for those born during 19201926; 52% in HI, 72% in VN, and GMTs 38. Responses were minimal in both HI and VN for persons born during 19471956; 11% in HI, 10% in VN, and GMTs <20.

European human-like swIAV swG12 (1B.1.2.1) represents the human-like H1 swIAV clade circulating in Belgium, and TW86 was selected as its presumed human ancestor virus. At least half of all samples tested positive for swG12, 50% in HI and 59% in VN (Figures 2, 3). We noted statistically significant differences in seroprevalences and GMTs, which were higher (62% in HI and 74% in VN; GMTs 44) in persons born before 1996 than in persons born during 19972017 (5% in HI and in VN; GMTs <20; p<0.001) (Tables 6, 7). GMTs peaked (87) in HI in those born during 19771986 and in VN for those born during 19671976. Results for swG12 were similar to those for its presumed human ancestor virus, TW86.

North American human-like H1 swIAVs (1B.2) result from the introduction of a human IAV in the early 2000s, and we selected NC99 as their presumed human ancestor. For the most prevalent 1 clade (1B.2.2), swAL16 represents subclade 1a (1B.2.2.1), whereas swIL10 and swOK13 represent subclade 1b (1B.2.2.2).

Among samples, 24% tested positive for swAL16 in HI and 39% in VN (Figures 2, 3). Seroprevalences and GMTs were highest in those born during 19871996 in HI (55%; GMT 35) and in those born during 19471956 in VN (70%; GMT 59), but no antibodies against swAL16 were detected in the youngest group, those born during 20072017 (Tables 6, 7). Like for European human-like virus swG12 (1B.1.2.1), antibody responses against North American 1a virus swAL16 (1B.2.2.1) resembled those against its presumed human ancestor virus, NC99.

For the 1b swIAVs (1B.2.2.2), <10% were seropositive (swIL10, 10% in HI and VN; swOK13, 5% in HI and 4% in VN) (Figures 2, 3). We did not see statistically significant differences in seroprevalences between the 2 1b swIAVs or between age groups, with following exceptions. HI-seroprevalence of those born during 19271936 was statistically significantly higher for swIL10 (13%) than for swOK13 (2%; p<0.04). HI seroprevalence for swOK13 of those born during 19771986 was statistically significantly higher (21%) compared with groups born during 19271936 (2%), 19571966 (0), and 20072017 (0; p<0.04). GMTs were <20 in all age groups except those born during 19371956, who had VN GMTs of 2230 against swIL10 (Tables 6, 7). Unlike the other 2 human-like swIAVs tested, responses against 1b swIAVs (1B.2.2.2) did not concur with those against the presumed human ancestor virus NC99. Responses against swIL10 and swOK13 were generally statistically significantly lower than against NC99 (p<0.05).

We used swOH07 as reference virus to evaluate antibody responses against classical swine virus clade (1A.3.3.3) and CA09 as reference virus to evaluate classical swine virus clade pH1N1 (1A.3.3.2), which derived its HA from swIAVs. Overall, 50% of the samples tested positive for swOH07 (50% in HI; 78% in VN) and CA09 (54% in HI; 81% in VN), with high seroprevalences in all age groups (36%100% in HI; 50%100% in VN), except in those born during 19471956 in HI (swOH07, 17%; CA09, 24%) (Figures 2, 3). HI titers peaked in the 2 oldest groups, those born during 19201936; VN titers peaked in the 2 oldest groups and in those born during 19972006 (Tables 6, 7). No statistically significant difference was noted in responses against classical swine (1A.3.3.3) and pH1N1 (1A.3.3.2) IAVs.

Antibody titers against epidemiologically related human and swine IAVs were highly correlated for classical swine viruses swOH07 (1A.3.3.3) and CA09 (1A.3.3.2), European human-like swIAV swG12 (1B.1.2.1) and human ancestor IAV TW86, North American human-like 1a swIAV swAL16 (1B.2.2.1) and human ancestor IAV NC99, and European and Asian avian-like swIAVs swG10 (1C.2.1) and swHK11 (1C.2.3) (CC=0.680.86 in HI; CC=0.630.77 in VN; Table 8). Of note, titers against avian-like and classical swine IAVs also were strongly correlated (CC=0.550.68 in HI; CC=0.490.67 in VN). In contrast, CCs were low between titers against North American human-like 1b viruses swIL10 and swOK13 (1B.2.2.2) and human ancestor virus NC99 (0.420.43 in HI; 0.300.39 in VN [the first value of which is not statistically significant]).

Our results show that serum antibody responses of immunocompetent persons in Belgium against major H1 swIAV clades depend on the swIAV tested and its relation to human seasonal IAVs and the persons birth year. Overall seroprevalences were high (50%) for classical swine (1A.3.3.2, 1A.3.3.3) and for European human-like (1B.1.2.1) swIAVs, intermediate (24%) for North American human-like 1a (1B.2.2.1) and Asian avian-like (1C.2.3) swIAVs, and low (<10%) for North American human-like 1b (1B.2.2.2) and European avian-like (1C.2.1) swIAVs. Our results are consistent with previous studies that aimed to compare antibody responses in nonswine workers with those in persons with frequent swine contact (7,2025), although those studies examined only a limited number of swIAV clades or samples. Overall, most previous studies showed lower seroprevalences for Asian avian-like (2%10%) and European avian-like (05%) swIAVs in the general population or in nonswine workers (13,20,2224). A 2010 study in the United Kingdom also found a lower seroprevalence of 11% for a European human-like (1B.1.2.1) swIAV (24). The major difference between our study and studies conducted before or during the 2009 pandemic is the lower seroprevalence of 3%15% for classical swine IAVs in previous studies (13,20,2224). The circulation of pH1N1 viruses (1A.3.3.2) likely contributes to increased seroprevalence rates against these related classical swine IAVs. In our study, the oldest group, those born during 19201926 who are 9197 years of age, had the highest antibody responses against H1 swIAVs of classical swine (1A.3.3) and avian-like (1C.2) lineages, for which antibody titers were correlated (13,20,21). Responses against human seasonal IAVs and related European and North American 1a human-like H1 swIAVs (1B) generally were highest in those born during 19771996, who are 2140 years of age, and lowest in those born during 19962017, who are 020 years of age. Responses against North American 1b human-like H1 swIAVs (1B.2.2.2) generally were low across all age cohorts.

Antibody responses against past human seasonal IAVs TW86, NC99, and BR07 generally peaked in persons born near the time during which the respective IAV or similar viruses circulated, whereas responses were low in most persons born after. Within an age group, responses generally were highest against an antigenic representative of the virus encountered first. These findings concur with the theory of antigenic seniority: humans are expected to have antibodies against human seasonal IAVs that circulated after their birth, with highest responses against the virus encountered first. Antigenic seniority likely occurs because of periodic boosting of these antibodies by subsequent exposures to related human seasonal IAVs (4,34,35). Antibody titers against European human-like swIAV swG12 (1B.1.2.1) and North American human-like 1a swIAV swAL16 (1B.2.2.1) concur with those against their respective human ancestor viruses TW86 and NC99 because of close antigenic relationship to their ancestor IAV. Overall high seroprevalences against pH1N1 virus CA09 (1A.3.3.2) and antigenically closely related classical swine virus swOH07 (1A.3.3.3) can be explained by recent exposure to currently circulating pH1N1 viruses. Because the oldest persons were born during 19201936, when human IAVs closely related to the 1918 pandemic virus, the ancestor of classical swine IAVs, circulated, they could have had cross-reactive antibodies against classical swine IAVs before 2009. These antibodies might have been boosted by later exposure to pH1N1 viruses, which might account for the high responses in this group (6,7). Consistent with results for serum samples collected after pH1N1 virus infection in a previous study (21), cross-reactivity was higher against the Asian than against the European avian-like H1 swIAV, which differ by only 1 aa in antigenic sites (Table 2). Whether this single amino acid mutation is the reason for the difference in seroprevalence is still unknown (36,37).

European human-like (1B.1.2.1) and North American human-like 1a (1B.2.2.1) H1 swIAVs are antigenically more closely related to their human ancestor than North American human-like 1b (1B.2.2.2) H1 swIAVs (Figure 1; Tables 3, 4). North American human-like H1 swIAVs (1B.2) have been shown to drift 4 times faster than European human-like H1 swIAVs (1B.1). Increased antigenic diversity of the former since 2008 has led to the emergence of swIAVs that are antigenically distinct from the human precursors, mainly within the 1b subclade (3,27). This evolution can explain the recognition of selected European human-like and North American human-like 1a but not North American human-like 1b H1 swIAVs by human serum samples. Because the human ancestor IAVs no longer circulate in humans, swine can be considered a reservoir for old human IAVs. Seroprevalences for European human-like and North American human-like 1a H1 swIAVs are expected to decrease over time because the youngest age groups were never exposed to these human IAVs. On the basis of our results, we estimate that it could take <80 years for the population to become fully susceptible.

Seroprevalences of immunocompetent persons in Belgium for swIAVs representing major H1 swIAV clades suggest that North American human-like 1b (1B.2.2.2) and European avian-like (1C.2.1) H1 swIAVs currently pose the highest risk to public health. North American human-like 1b (1B.2.2.2) swIAVs rapidly drifted away from its human ancestor, whereas European avian-like (1C.2.1) swIAVs never circulated in humans. Seroprevalences of <10% for these viruses are comparable to 2%19% against the pH1N1 virus right before the pandemic (7). Our results suggest that the risk of reintroduction of these H1 swIAVs in the human population might be higher than for H3 swIAVs, given that 20% of persons 0100 years of age from Luxembourg tested seropositive for representative European and North American cluster IV H3 swIAVs in 2010 (19). Seroprevalences against the other currently circulating human-like H1 swIAV clades were higher than against 1B.2.2.2 and 1C.2.1, but these viruses, along with H3 swIAVs, also keep evolving in swine. As they continue to drift away from their human ancestor and population immunity wanes with lack of exposure, these viruses might also pose a risk to public health soon.

We evaluated human population immunity against H1 swIAVs on the basis of serum HI and VN antibodies, which are directed against the highly variable head region of the HA. We did not measure antibodies or T-cell responses against the HA stalk, the neuraminidase, or internal viral proteins, such as the nucleoprotein. Although these immune mechanisms are much less potent than neutralizing anti-HA antibodies, their targets are more conserved between IAVs of humans and swine (3842). Therefore, persons with minimal antibody titers in our study still might have some degree of immunity and protection against zoonotic infection with swIAVs. Furthermore, population immunity is only one aspect determining the pandemic potential of swIAVs (18). Another factor is their ability to spread in humans, which is difficult to investigate (43). Our results stress the need for continuous surveillance and characterization of circulating swIAVs and frequent monitoring of humans for antibodies against these swIAVs.

Ms. Vandoorn was a PhD student at the Laboratory of Virology, Faculty of Veterinary Medicine, Ghent University, during the study period. Her primary research interests are swine influenza A virus surveillance in Belgium and the Netherlands and broadly protective vaccination strategies for influenza A viruses.

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Suggested citation for this article: Vandoorn E, Leroux-Roels I, Leroux-Roels G, Parys A, Vincent A, Van Reeth K. Detection of H1 swine influenza A virus antibodies in human serum samples by age group. Emerg Infect Dis. 2020 Sep [date cited]. https://doi.org/10.3201/eid2609.191796

The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors' affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above.

More:
Detection of H1 Swine Influenza A Virus Antibodies in Human Serum Samples by Age Group - CDC

dingo, bigger, growth, poison baiting, Michael Letnic, Mathew Crowther

DINGOES have gotten around 6-9 per cent bigger over the past 80 years, according to new research - but the growth is happening only in areas where poison baiting is used. The findings, published in the Biological Journal of the Linnean Society over the weekend, compared the sizes of dingoes that lived in three baited regions (Kalgoorlie, Pilbara and pastoral South Australia), with those from an unbaited region that stretched from Northern Territory to South Australia. The scientists measured the skull size - which is a marker of animal size - of nearly 600 dingo specimens originating from the sites. "Skulls from the baited regions grew by about four millimetres since poison baiting was introduced," Michael Letnic, lead author of the paper and professor in conservation biology and ecosystem restoration at UNSW Science, said. "This equates to roughly a kilogram in body mass." While both male and female dingoes grew, female dingoes had the biggest growth spurt: Their skulls increased by 4.5 millimetres, which is almost nine per cent body mass. Male skulls grew by 3.6 millimetres, or six per cent body mass. The question is: Why are dingoes in poison-baited areas growing? "The most likely theory is that dingoes who survive baiting campaigns have less competition for food," co-author Associate Professor Mathew Crowther from the University of Sydney said. He said dingoes' primary prey, kangaroos, have been shown to increase in numbers when dingo populations are suppressed. "With more food in abundance, dingoes' physical growth is less restricted," Prof Crwother said. The pesticide sodium fluoroacetate - known as 1080 - is commonly used across Australia to control dingo and other pest populations. A flavourless white powder, 1080 is usually stuck into meat baits and left in dingo hotspots, often via helicopter drops. Baiting was rolled out in Kalgoorlie, Pilbara and pastoral South Australia over the 1960s and '70s. Dingoes from the unbaited region - which included Indigenous-owned lands and conservation reserves - saw no change in body size. This is not the first time a pesticide has been linked to changes in animal bodies. "Our interventions have consequences - and they're actually quite predictable consequences," Prof Letnic said. "Whatever pressures we put on animal populations - be it pesticides or not - there will be side effects." Scientists usually observe these impacts in invertebrate pests: for example, some insects - like cockroaches - are becoming more resistant to the insecticides used on them. However, this study is one of the first to show that vertebrates, like dingoes, also change from pesticide use. "Poison baiting campaigns could be favouring the survival of larger dingoes," Prof Crowther said. "Smaller dingoes need less poison for a lethal dose, so are more likely to be killed by baiting. This leaves the larger dingoes to survive and breed." As a result of their growing size, the 1080 dose required to kill a dingo in the baited regions has increased since the toxin was introduced. "The reaction to this finding may be to add more poison to the baits, or to find a new poison," Prof Letnic said. "But, eventually, the cycle will start again." The exact mechanisms at play are still unclear - but a greater abundance of food post-baiting and dingoes adapting to the poison are likely the most influential factors, the researchers believe. Other factors that could have potentially led to the dingoes' growth, like climate change or interbreeding with dogs, seem unlikely. "We only tested dingoes in areas that have very low dog hybridisation rates, making it highly unlikely that dog genetics are contributing to the size growth," Prof Letnic said. Most dingo-dog hybridisation, he said, occurs on the east coast of Australia. The researchers also suggest that - if anything - a warming climate would decrease dingoes' body size, as cooler conditions favour larger animals. Further studies that use a broader sample of dingoes from across Australia could help better understand the cause of the dingo body change. In the meantime, the researchers hope to explore other ecological impacts of 1080 baiting. "Baiting is changing dingoes, so it could be changing other animal populations," Prof Letnic said. "Animals respond to human interventions, whether directly or indirectly. The changes could well be adaptive, and we must think about that."

https://nnimgt-a.akamaihd.net/transform/v1/crop/frm/36cb5pgMzenMnrRDPitnuXV/44edfa0d-f29b-4735-906b-c5f05b4ba610.jpg/r0_224_2396_1578_w1200_h678_fmax.jpg

DIGEST

August 5 2020 - 6:00AM

DINGOES have gotten around 6-9 per cent bigger over the past 80 years, according to new research - but the growth is happening only in areas where poison baiting is used.

The findings, published in the Biological Journal of the Linnean Society over the weekend, compared the sizes of dingoes that lived in three baited regions (Kalgoorlie, Pilbara and pastoral South Australia), with those from an unbaited region that stretched from Northern Territory to South Australia.

The scientists measured the skull size - which is a marker of animal size - of nearly 600 dingo specimens originating from the sites.

"Skulls from the baited regions grew by about four millimetres since poison baiting was introduced," Michael Letnic, lead author of the paper and professor in conservation biology and ecosystem restoration at UNSW Science, said.

"This equates to roughly a kilogram in body mass."

While both male and female dingoes grew, female dingoes had the biggest growth spurt: Their skulls increased by 4.5 millimetres, which is almost nine per cent body mass. Male skulls grew by 3.6 millimetres, or six per cent body mass.

The question is: Why are dingoes in poison-baited areas growing?

"The most likely theory is that dingoes who survive baiting campaigns have less competition for food," co-author Associate Professor Mathew Crowther from the University of Sydney said.

He said dingoes' primary prey, kangaroos, have been shown to increase in numbers when dingo populations are suppressed.

"With more food in abundance, dingoes' physical growth is less restricted," Prof Crwother said.

The pesticide sodium fluoroacetate - known as 1080 - is commonly used across Australia to control dingo and other pest populations.

A flavourless white powder, 1080 is usually stuck into meat baits and left in dingo hotspots, often via helicopter drops. Baiting was rolled out in Kalgoorlie, Pilbara and pastoral South Australia over the 1960s and '70s.

Dingoes from the unbaited region - which included Indigenous-owned lands and conservation reserves - saw no change in body size.

This is not the first time a pesticide has been linked to changes in animal bodies.

"Our interventions have consequences - and they're actually quite predictable consequences," Prof Letnic said.

"Whatever pressures we put on animal populations - be it pesticides or not - there will be side effects."

Scientists usually observe these impacts in invertebrate pests: for example, some insects - like cockroaches - are becoming more resistant to the insecticides used on them.

However, this study is one of the first to show that vertebrates, like dingoes, also change from pesticide use.

"Poison baiting campaigns could be favouring the survival of larger dingoes," Prof Crowther said.

"Smaller dingoes need less poison for a lethal dose, so are more likely to be killed by baiting. This leaves the larger dingoes to survive and breed."

As a result of their growing size, the 1080 dose required to kill a dingo in the baited regions has increased since the toxin was introduced.

"The reaction to this finding may be to add more poison to the baits, or to find a new poison," Prof Letnic said.

"But, eventually, the cycle will start again."

Looking for an explanation

The exact mechanisms at play are still unclear - but a greater abundance of food post-baiting and dingoes adapting to the poison are likely the most influential factors, the researchers believe.

Other factors that could have potentially led to the dingoes' growth, like climate change or interbreeding with dogs, seem unlikely.

"We only tested dingoes in areas that have very low dog hybridisation rates, making it highly unlikely that dog genetics are contributing to the size growth," Prof Letnic said. Most dingo-dog hybridisation, he said, occurs on the east coast of Australia.

The researchers also suggest that - if anything - a warming climate would decrease dingoes' body size, as cooler conditions favour larger animals.

Further studies that use a broader sample of dingoes from across Australia could help better understand the cause of the dingo body change.

In the meantime, the researchers hope to explore other ecological impacts of 1080 baiting.

"Baiting is changing dingoes, so it could be changing other animal populations," Prof Letnic said.

"Animals respond to human interventions, whether directly or indirectly. The changes could well be adaptive, and we must think about that."

See the original post:
Dingoes getting bigger where baiting is used: research - The Macleay Argus

Womens health research continues to be marginalized. To address and reverse this trend requires committed, accountable leadership, inclusion of diversity of thought and critical social science issues, in addition to the more well-funded basic traditional and clinical research.

There are several areas that contribute to this marginalization, first, with respect to pregnant women. Optimizing pregnancy outcome would significantly improve world health, as babies, if born early and often thus small have higher risks of heart disease, diabetes, and asthma.

Therefore, a baby born without complications, at the right time and weight, has the potential for a healthier life. Similarly, optimizing a womans health both for a healthier pregnancy and outcome and for her long-erm health also has the potential to improve world health. A womans health is known to impact her family, including both younger and older generations, thus strategies to address womens health are essential.

Funding for womens health research is limited. The National Institutes of Health (NIH) categorizes research funding to provide consistent and transparent information on the categories of disease, conditions, and research areas.

The categorization uses sophisticated text data mining based on scientific experts to define a research category. Incredibly, 2019 was the first year that federal funding for womens health research was classified based on scientific relevance, rather than based on the percentage of female subjects included in the studies.1

The rationale for using the percentage of females enrolled in a study to count as womens health research is unclear, and unfounded, as women certainly are enrolled in studies that are not focused on womens health.In 2019, the NIH funded $4,749M in womens health research, with the largest percent (26%) by the National Cancer Institute (Figure 1).

As examples, the genetics, neurosciences, biotechnology, brain disorders, pediatrics, and aging research categories all had more NIH funding in 2019 than womens health.

To prevent transmission of the virus, all non-essential visits and encounters have been appropriately stopped, thus all ongoing clinical research has effectively ceased aside from that impacting clinical care. As I mentioned in my editorial in April, when there were only 51 studies2 - and now substantiated in 588 studies3 - pregnant and breastfeeding women are yet again excluded from research, notably from participating in COVID-19 clinical trials during this pandemic.

This is a major missed opportunity as results with therapies studied in men and nonpregnant women may not be generalizable. Furthermore, therapies are potentially not being offered to women, or if they are offered, are not being systematically studied in this population to provide needed data with which to guide therapy.

The impact of COVID-19 on womens health research highlights the long-standing inequities in including this population in research. Only in the last few decades were women required to be included in clinical research.

Yet even with this mandate, subsets of women remain excluded.

Despite mandated inclusion of women in research, womens health research remains marginalized, as are women researchers and physician-scientists. Although data suggest that women submitting NIH research project grant (RO1) applications for the first time have the same grant success rate as men4, they are half as likely to apply for those grants5, despite the fact that just as many women as men are receiving advanced degrees.

A natural history experiment using the investigator-initiated Canadian Institutes of Health Research Grant Programmes demonstrated that gender gaps in funding were due to female principal investigators being evaluated less favorably than male principal investigators - and not related to the quality of their research proposals.6

This marginalization of women researchers is rampant. As reported in numerous studies, women are less likely to be promoted, achieve tenure, or be selected for leadership roles (Supplemental figure).

Similarly, women with equal stature are less likely to be selected to participate in think tanks than men. As an example, a recent article outlining a research strategy for womens health with 17 authors included only 4 (24%) women.7

Furthermore, of the nine physician authors, only one is an ob/gyn and four are pediatricians. The themes from the think tank neglect critical areas of research, focusing on traditional sciences and emphasize genetics, overlooking the role of racial disparities and health inequities.

As noted by the 2018 NIH Gender Inequality Task Force Report, Sustainable change in representation of women, and of all individuals from underrepresented groups, requires committed, accountable leadership along with effective tools to accomplish this important goal.8 It is troubling that gender diversity in leadership positions is lacking nationally.

Using 2019 data, only 19% of department chairs (both interim and permanent) are held by women. Extrapolating the trend lines suggests another 50 years are needed to attain parity of department chairs and medical school deans by gender (Figure 2).

This diversity is not due to a lack of qualified women, as since 2002, women have earned the majority of all doctorates9 and in 2019, women comprise the majority of enrolled US medical students.10

Underrepresentation creates a culture that perpetuates inequalities. For our patients, for ourselves, for our families, we must correct this course. This is not easy, and will require a change of culture led by a committed, accountable, proactive leadership.

Equally important will be the inclusion of diversity and broadening of the research agenda to include critical social science issues, health disparities, and social determinants of health.

One ray of hope to address these pressing issues is the formation of the Womxns Health Collaborative, a group determined to identify and initiate actionable steps.

If you are interested in participating, I encourage you to contact Dr. Michal Elovitz at womxnshealth@gmail.com.

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See more here:
Addressing inequalities in women's health research - Contemporary Obgyn

Chris McGregor, right, who farmed with his father, David, near Antrim, has opended a new veterinary practice in Scotland, and is pictured with his business partner, Ross Wilson.

David McGregor, who farms 130 cows on robots near Antrim was one of the first farmers to take on the new system of genetic improvement.

He explained: We had two reasons for starting the RMS Optimise Program. Firstly, we knew from experience, that Genus ABS had the expertise to provide the service and the bull stud to back up the genetics. Secondly, my son, who had been heavily involved with the fertility program in the herd, was starting up Tinto Farm Vets, a new veterinary practice in Scotland, so his focus was moving to that business venture. We started to investigate the options. Gareth Bell, breeding advisor with Genus ABS suggested RMS Optimise. We studied the system in depth and decided that it fitted in with our plans for the dairy enterprise.

David outlined his experience with the RMS Optimise program: The Technician, Michael Scott, calls at the same time everyday to detect cows on heat and ensures they are mated with the appropriate genetics for our overall aims for the herd and the cows individual genetic requirements. In addition he looks after all the paperwork, providing detailed fertility reports which enable us to ensure that our feeding program, compiled by David from FarmGate Nutrition, complements our overall aims for the herd.

David emphasised; A successful dairy enterprise needs a team effort, with input from breeding adviser, nutritionist, vet etc. and Genus ABS takes account of all aspects when advising on our breeding program.

The net result has been a decrease of nearly 50 days off our calving interval which now has a projected calving interval of 383 days. Milk yield has increased from 34 litres per day up to 39 litres at present. Our pregnancy rate has improved greatly - we are now hitting 25%.

Simon Logan, explains: Pregnancy rate is the measure of how fast your herd is becoming pregnant and is your conception rate multiplied by your submission rate. Basically, the UK average is around 13%. David and Chris have almost doubled this in their first year of RMS Optimise which is a fantastic achievement.

David added: We have more milk in the tank and less cows culled due to infertility and so we have been able to sell surplus heifers and generated more income. We have also generated quite a few British blue calves not to mention a lot of valuable Sexcel pregnancies.

Simon Logan emphasised that the new RMS Optimise program has many more additional benefits. He explained: Farmers who utilise this program can create 67% of pregnancies with easy calving British Blue sires which should produce a cash crop of high value calves. All of the benefits will, in turn, mean increased milk production and pregnancy rates, a decreased calving interval, minimise the number of low value Holstein male calves and provide detailed management reports.

He added: In our first year of launching the Optimise service we had 19 customers all coming on for various reasons. It has been exciting to be a part of something that has really helped a lot of our customers. We have had 13 years of providing the RMS service in Northern Ireland and it now includes almost 40,000 cows improving the fertility and management of these herds. RMS Optimise further enhances this service and, in turn, the financial performance of the farm. We have had a lot of interest in the service and are aiming to accommodate more customers, although space will be limited so please contact your local Genus ABS representative for a free on farm consultation.

Read the original here:
One year on from the launch of RMS Optimise from Genus ABS - Farming Life