Archive for the ‘Male Genetics’ Category

People of all sexes can have risk genes that are often assumed to affect only women. A new name could aid cancer prevention and treatment, argues Colin C. Pritchard. I recently had a conversation with my parents about genetic testing for cancer risk. You mean men also have the BRCA genes? asked my dad. I thought those were the breast-cancer genes, chimed in my mom.

My parents are far from alone in not realizing that people of all sexes (including transgender people) can have mutations in BRCA1 and BRCA2 genes. These genes do encode the proteins associated with susceptibility to breast cancer. But they are also associated with an increased risk of prostate and pancreatic cancer, among others.

Because this is not widely understood, testing is not being done for the right people at the right time. Those who identify as men are especially less likely to be tested.1 And people who are tested can have difficulty understanding the full meaning of their results regarding both their own cancer risk, and the risks to their family members.

In the past year, I was involved in the care of a man with late-stage prostate cancer. He knew that his sister carried a BRCA2 mutation, but he had not been tested for it because none of his medical practitioners had recommended the test. Hed been unable to walk because of cancer-related pain, and was considering hospice care when a new oncologist suggested a genetic test. Finding out that he carried the BRCA2 mutation allowed him to start a more effective cancer treatment, and in weeks he was able to play golf. Whats more, the man had two daughters who thought they werent at risk for the BRCA2 mutation because it was on their fathers side. Both were tested and used the results to take preventive measures that substantially reduce their chances of developing breast and ovarian cancer.

In my view, part of the confusion stems from the fact that people with mutations in BRCA1 or BRCA2 are said to have hereditary breast and ovarian cancer syndrome, or HBOC. This term is not only misleading, it is also cumbersome and hard to remember. Fortunately, there is a simple solution: rename the syndrome.

Whats in a name?Depending on the population, between 1 in 40 and 1 in 400 people carry a mutation in BRCA1 or BRCA2. As such, I estimate that this confusion could be affecting thousands of people with cancer, and their families.

All sexes have the same rate of BRCA1 or BRCA2 mutation; all are equally likely to pass these mutations to their children. Yet a study last year found that, in the United States, over ten times more women were tested for these mutations than were men1 (see Missed tests); rates of testing for genes associated with colon-cancer risk were equal. Other studies have shown that men who have been tested for BRCA1 or BRCA2 mutations and diagnosed with HBOC are often uncertain about their risks of developing cancer, and sometimes keep the information from their families for fear of stigmatization.2,3

As is the case for many terms in medicine, the precise origin of HBOC is difficult to pin down. It first appeared in the scientific literature in the early 1990s, around the time when the BRCA1 gene was identified. In previous decades, people had described hereditary breast cancer and hereditary ovarian cancer as distinct entities, on the basis that such cancers cluster in families. The discovery of BRCA1, and then of BRCA2, allowed clinicians to link HBOC with a specific genetic cause. But at that time, the full spectrum of cancers associated with these two genes was not known.

I propose that HBOC be renamed King syndrome. This is easy to remember. It doesnt imply that the condition affects only one sex, or that people with BRCA1 or BRCA2 mutations will develop only certain types of cancer. And it would recognize the seminal contributions of pioneering cancer geneticist Mary-Claire King, the discoverer of BRCA1 (see Cancer-genetics pioneer).

In the mid-1970s, Mary-Claire King (pictured) was the first to recognize that hereditary breast and ovarian cancer could be accounted for by a single gene; in 1990, she and her group at the University of California, Berkeley, identified the location of the BRCA1 gene.13,14Now at the University of Washington, Seattle, King is recognized15 as a founder of cancer genetics and a long-term advocate for BRCA1 and BRCA2 testing.

Hundreds of thousands of people have been tested for mutations in these genes, and many lives have been saved through cancer prevention. Yet, with an estimated 19 million mutation carriers worldwide at least, we have only scratched the surface.

Instant impactChanging HBOC to King syndrome could have immediate benefits for health-care providers and for all patients.

Flexibility. Removing the sex and cancer specificity from the name would allow more flexibility as scientific knowledge evolves.

People with mutations in genes other than BRCA1 and BRCA2 can have a syndrome that is similar to HBOC. In fact, some investigators have suggested renaming the gene PALB2 as BRCA3. (PALB2 encodes a protein that is involved in the same DNA-repair pathway as the BRCA2 protein, and mutations in both have similar effects.4) In short, the term King syndrome would enable researchers to link other genes to the syndrome more easily as scientific understanding advances.

Communication. Changing the name would also make it easier for people to appreciate that the syndrome occurs in all sexes, can be passed through the male lineage, and can be linked to genes that are not specifically named for breast or ovarian cancer.

Take prostate cancer. The latest US clinical guidelines recommend that people with the most advanced form of prostate cancer are tested for BRCA1 and BRCA2 mutations. This stems from the discovery that a high proportion of people with prostate cancer that has spread to other areas (metastatic) carry mutations in these genes, as well as in other related DNA-repair genes conventionally associated with breast and ovarian cancer. The recommendation also arises from the finding that the presence of such mutations has an impact on the effectiveness of treatments.58

Yet it is only recently that guidelines on prostate cancer were updated to recommend BRCA1 and BRCA2 testing. Before 2017, health-care providers in the United States would have found recommendations seemingly focused on breast and ovarian cancer. Specifically, the information could be found only in guidelines titled Genetic/Familial High-Risk Assessment: Breast and Ovarian.9

In good companyThere is precedent for renaming a cancer-risk syndrome after a leading scientist for clarity.

For several years, health-care providers and others referred to people with mutations in any of four genes involved in a certain type of DNA-repair mechanism as having hereditary non-polyposis colorectal cancer syndrome, or HNPCC. But over the past ten years, specialists have returned to the original terminology: Lynch syndrome. (US physician Henry Lynch, who died last month, did much of the pioneering work in the 1960s and 1970s to identify the familial syndrome.10)

As with HBOC, clinicians and others found the name HNPCC misleading, because it did not accurately reflect the types of cancer to which it has been linked. People with Lynch syndrome are more likely to get colorectal cancer, but can also develop cancer of the endometrium (which begins in the uterus), stomach and ovaries, as well as some forms of bladder cancer, among many others. These individuals are also at risk of developing pre-cancerous lesions in the colon (colorectal polyps), making the non-polyposis part of the old name especially misleading.

Some might disagree that King syndrome is the best choice for a new name, because it doesnt describe the syndrome. They might instead favour something like homologous recombination DNA repair deficiency syndrome. But such a name would again be hard to remember for providers and patients.

Others might worry that testing rates among cisgender women (whose gender is the same as their birth sex) could decrease under the new name (especially given the male connotations of the word king), and that related health care could suffer. I acknowledge the potential downsides, but think that these would be outweighed by improvements in care that could follow. The name could help people to understand that their cancer risk is not limited to breast and ovarian cancer. It might also help them to better communicate the risks to their family members, or to a new health-care provider, and so increase the chance that testing is done.

Renaming HBOC could even spark a wider discussion around confusing names for cancer genetic syndromes. Hereditary diffuse gastric cancer syndrome, for instance, is caused chiefly by inherited mutations in CDH1, which encodes a protein that helps to establish and maintain the shape of epithelial cells, such as those found in the gut lining. People with these mutations are much more likely than the general population to develop a certain type of breast cancer,11 and the children of families with this syndrome are at risk of having some types of congenital malformation, such as a cleft lip.12

Ultimately, using names that are simple and flexible, instead of obtuse and out of step with emerging understanding, could save lives by improving communication and awareness.

Written by: Colin C. Pritchard, Associate Professor, Department of Laboratory Medicine, University of Washington and Head of Precision Diagnostics, Brotman Baty Institute for Precision Medicine, Seattle, Washington

References:1. Childers, K. K., Maggard-Gibbons, M., Macinko, J. & Childers, C. P. JAMA Oncol. 4, 876879 (2018).2. Rauscher, E. A., Dean, M. & Campbell-Salome, G. M. J. Genet. Couns. 27, 14171427 (2018).3. Strmsvik, N., Rheim, M., yen, N., Engebretsen, L. F. & Gjengedal, E. J. Genet. Couns. 19, 360370 (2010).4. Antoniou, A. C. et al. N. Engl. J. Med. 371, 497506 (2014).5. Castro, E. et al. J. Clin. Oncol. 31, 17481757 (2013).6. Mateo, J. et al. N. Engl. J. Med. 373, 16971708 (2015).7. Na, R. et al. Eur. Urol. 71, 740747 (2017).8. Pritchard, C. C. et al. N. Engl. J. Med. 375, 443453 (2016).9. National Comprehensive Cancer Network. Genetic/Familial High-Risk Assessment: Breast and Ovarian Version 2.2019 (2019).10. Lynch, H. T., Snyder, C. L., Shaw, T. G., Heinen, C. D. & Hitchins, M. P. Nature Rev. Cancer 15, 181194 (2015).11. Hansford, S. et al. JAMA Oncol. 1, 2332 (2015).12. Figueiredo, J. et al. J. Med. Genet. 56, 199208 (2019).13. Hall, J. M. et al. Science 250, 16841689 (1990).14. King, M. C. Science 343, 14621465 (2014).15. King, M. C., Levy-Lahad, E. & Lahad, A. J. Am. Med. Assoc. 312, 10911092 (2014).

Nature. 2019 July 4; vol 571, 27-29 doi: 10.1038/d41586-019-02015-7.

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Rename Breast-Cancer Syndrome to Help Save Lives - UroToday

The legal team advocating the repeal of Section 377A of the Penal Code which criminalises acts of gross indecency between men argued before the High Court on Mon (18 Nov) that sexual orientation is a product of genetic and environmental factors, and cannot be changed at will.

Lawyers Eugene Thuraisingam, Suang Wijaya and Johannes Hadi of Eugene Thuraisingam LLP, on behalf of applicant DJ Johnson Ong Ming, said that the preponderance of scientific evidence shows that human sexual orientation ranges along a continuum, from completely heterosexual to completely homosexual.

In between are bisexuals who have varying degrees of preference for either sex, the lawyers added.

Homosexuals, like heterosexuals, cannot wilfully change their sexual orientation and/or attraction. There is no credible scientific evidence which supports the proposition that therapy aimed at changing sexual orientation (such as reparative or conversion therapy) is safe or effective, they argued.

Consequently, the crux of the legal teams argument is that Section 377A in the Penal Code violates two provisions in the Singapore Constitution, namely Article 9 of the Constitution which guarantees the right to life and personal liberty, and Article 12 which guarantees equal protection before the law.

Sexual activity between consenting adult males in private, according to Mr Ongs lawyers, neither harms nor impinges upon the rights or interests of any other persons.

Section 377A therefore violates Article 9 and 12 of the Constitution. It is absurd, irrational and discriminatory to criminalise a person on the basis of his natural, unchangeable identity and for non-harmful private acts, they added.

The relevant section in the Penal Code also reinforces the majoritys good old-fashioned discrimination against male homosexuals, who are a minority in Singapore, according to Ongs legal team.

The role of our Constitution and the Court is to protect minorities against the absurd, irrational prejudices of the majority, his lawyers argued.

Three medical experts were called by Mr Ongs legal team in the immediate case, namely:

The Attorney-Generals Chambers (AGC), the respondent in all three cases, called the following experts:

Little to no scientific evidence in support of proposition pinpointing socio-environmental factors as cause for homosexuality and bisexuality, according to medical experts on both sides

Experts from both sides concurred that genetic and non-social environmental factors (like the womb environment) contribute to the causality of sexual orientation and/or attraction.

There is little if any scientific evidence which supports the proposition that social environmental factors (like culture, parenting) play any role in the causality of sexual orientation and/or attraction, said Mr Ongs lawyers.

One of the sources cited by Dr Cai is a study by Bailey, J.M., Vesey, P.L., Diamond, L.M., Breedlove, S.M., Villian, E,M & Epprecht, M. (in press), titled Sexual orientation controversy, and science, Psychological Science in the Public Interest, 2016, Vol 17(2) 45-101 summarises the position, which details the following:

No causal theory of sexual orientation has yet gained widespread support. The most scientifically plausible causal hypotheses are difficult to test. However, there is considerably more evidence supporting non-social causes of sexual orientation than social causes.

This evidence includes the cross-culturally robust finding that adult homosexuality is strongly related to childhood gender non-conformity; moderate genetic influences demonstrated in well sampled twin studies; the cross-culturally robust fraternal birth order effect on male sexual orientation; and the finding that when infant boys are surgically and socially changed into girls, their eventual sexual orientation is unchanged (i.e., they remain sexually attracted to females).

In contrast, evidence for the most commonly hypothesized social causes of homosexuality sexual recruitment by homosexual adults, patterns of disordered parenting, or the influence of homosexual parents is generally weak in magnitude and distorted by numerous confounding factors.

Citing Dr Cais report, the lawyers argued that it can be inferred that Dr Cais findings align with those of Dr Rajesh, who posited that biological and non-social environmental factors influence sexual orientation, and that [e]vidence for the most commonly hypothesised social causes of homosexuality have generally been debunked.

First, Dr Cai states that [s]exual orientation is no unchanging in everyone, and cites studies showing that some individuals have been found to experience spontaneous and naturally-occurring changes in sexual orientation, as opposed to willful changes.

Second, Dr Cai does not cite any literature or study supporting the proposition that sexual orientation can be willfully changed, such as through sexual orientation change efforts, conversion therapy or reparative therapy.

Mr Ongs lawyers also argued that Dr Cai has offered no credible evidence that sexual orientation can be willfully changed.

Studies showing that some individuals experience spontaneous and naturally occurring change in sexual orientation is nothing to the point, they argued, citing two reasons, namely:

i) spontaneous and naturally-occurring change is not willful change as demonstrated by the literature cited by Dr Cai himself; and

(ii) the studies show that close to 100% of homosexual males do not experience even any spontaneous or natural change.

Secondly, said Ongs lawyers, the literature cited by Dr Cai himself supports the point that persons do not experience choice over their sexual orientation and/or sexual attraction.

Ongs legal team added that the literature cited by Dr Cai demonstrates that there is no credible evidence for the purported effectiveness of conversion therapy, reparative therapy, and other forms of intervention to change sexual orientation are effective, which have been known present a significant risk of harm to individuals undergoing such interventions.

Genetics and other biological factors, including non-social environmental factors, contribute strongly to the development of sexual orientation

Another source cited by Dr Cai is a study by Roselli, C.E. titled Neurobiology of Gender Identity and Sexual Orientation, published in Journal of Neuroendocrinology, 2018, which states the following:

Most people experience little or no sense of choice about their sexual orientation. There Is no scientifically convincing research to show that therapy aimed at changing sexual orientation (ie, reparative or conversion therapy) is safe or effective. The origin of sexual orientation is far from being understood, although there is no proof that it is affected by social factors after birth. On the other hand, a large amount of empirical data suggests that genes and hormones are important regulators of sexual orientation

The data summarised in the present review suggest that both gender identity and sexual orientation are significantly influenced by events occurring during the early developmental period when the brain is differentiating under the influence of gonadal steroid hormones, genes and maternal factors. However, our current understanding of these factors is far from complete and the results are not always consistent

Our current understanding suffers from many limitations in the data Despite these limitations, the existing empirical evidence makes it clear that there is a significant biological contribution to the development of an individuals identity and sexual orientation.

Ongs lawyers pointed out thatDr Cai accepted the proposition that it is not disputed by experts in the field that genetics has some contribution to the causation of homosexuality.

Secondly, the lawyers highlighted that Dr Cai cited, in approval, papers which conclude that there can be little doubt that [sexual orientation] is influenced by environmental factors.

The environmental factors referred to by the papers cited by Dr Cai are non-social environmental factors such as the womb environment, not social environmental factors, Mr Ongs legal team highlighted, adding that Dr Cai has already cited various studies and literature pointing to genetic and non-social environmental factors of sexual orientation.

Dr Cai, according to the lawyers, also cited studies indicating that hormones play a part in the causation of sexual orientation, and the fraternal birth order effect play a role in shaping a persons sexual orientation.

Mr Ongs lawyers also rejected Dr Tays assertion that cultural and social environmental factors are also likely to play a role in determining sexual orientation, as the expert has cited no material that supports such an assertion.

This assertion is also demonstrably false, Mr Ongs lawyers argued.

The closed High Court hearing on Mon was the second out of three cases to be presented against Section 377A this month.

The current cases, according to a statement by Mr Ongs legal team, set a precedent in examining legal questions on the nature of sexual orientation, as expert evidence is now presented before the courts.

Previously, the court was only asked to take judicial notice of scientific facts which required a different legal test, Mr Ongs legal team added.

The AGC began its submissions on Mon, and will conclude its submissions at the next hearing on Wed.

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Section 377A constitutional challenge: Expert evidence reveal sexual orientation cannot be changed at will, lawyers argue - The Online Citizen

Henry Cavill is Superman, yesbut the legend of the British actor's physique isn't limited to his role as the Man of Steel.

He's become one of Hollywood's most dependable hardbodies, even without the good fortune of being named Chris. Cavill's powerful arms even became a rare non-superhero physique meme when the Mission Impossible: Fallout trailer dropped, showcasing a mind-melting moment when he appears to reload his biceps mid-fight, sprouting 5 o'clock shadow and creating a breast pocket on a shirt that previously had none. This was more likely an editing mistake than a power up, but it looks absolutely awesome.

Cavill has had to train hard for those muscles. The actor opened up to Men's Health for a wide-ranging cover story, and he shared that he was teased growing up for being "a chubby kid." Now, he's built up a meme-worthy frame with Dave Rienzi, who is also Dwayne Johnson's strength and conditioning coach (yes, even The Rock has a coach). Rienzi has worked with Cavill through Superman shoots to now, as the actor takes on the lead role of Geralt in Netflix's fantasy epic The Witcher.

The MH team caught up with Cavill and Rienzi in the weight room to get a behind the scenes look at the actor's Witcher routine. Every morning, Cavill started his day with fasted cardio. Cavill also hit the weights hard, whenever he was able to fit in a workout with his busy shoot schedule.

Importantly, Cavill notes that the exercises he and Rienzi highlighted for MH aren't meant to be performed all together as one complete routine. "Those are moves that we put into workouts, depending on which muscle group or muscle groups we're working that particular day," he told the MH crew. The list covers his whole body, from the posterior chain to core to biceps.

Cavill is also quick to point out that not everyone is Supermanand that's perfectly okay. "The most important thing to remember is that you are you," he says. "Everyone has a different genetic makeup, everyone is at a different stage of fitness or training or even has a different amount of calories going in. So you do you, and just make sure that every workout is as hard as you can do it."

If you want to train like Cavill, mix these exercises into your workouts on the appropriate training days, with posterior chain movements in lower body sessions and arm movements for upper days.

4 second negative, 2 second pause

2 second hold at the top

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Henry Cavill Breaks Down His 'The Witcher' Workout Routine - menshealth.com

An Australian woman risked her own life when she saw an injured koala trying to escape the flames of a major brushfire. The woman, who was not identified, jumped out of her car and rushed over to save the injured animal. She took off her shirt and used it to wrap up the marsupial as she carried it away from the flames.

Once she brought the koala to safety, she poured water over it to wash away some of the soot from the fire. A male passenger in her car grabbed a blanket and wrapped it around the wet koala so they could transport it to a nearby animal hospital.

Hundreds of wildfires are burning across Australia, threatening the local wildlife populations. The intense flames have made it nearly impossible for rescue workers to go in and move the animals to safety. One of the fires spread to the Lake Innes Nature Reserve, which is a well-known habitat for koalas, which number between 50,000 and 100,000. Officials fear that over 350 koalas perished in the fire.

In NSW, the firestorms ripped through, and they burnt everything. So koalas caught up in trees had no chance of survival, unfortunately," Claire Smith, founder of Wildlife Rescue Sunshine Coast, told Yahoo News Australia. The loss of that volume of animals is going to dramatically affect the genetic diversity of the species over the next 20 years.

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Video Captures Australian Woman Braving Brushfire To Save Injured Koala - KFI AM 640

A rare genetic disorder caused three siblings' blood to flood with fat and turn "milky" white, according to a new report of the unusual case.

The three siblings consisted of one set of fraternal twins (a daughter and son) and an older son, all born to a first-cousin couple in a Pennsylvania Dutch family. In their teens and early 20s, all three siblings experienced mysterious symptoms, including bouts of abdominal pain. They had all been diagnosed with hypertriglyceridemia, a fairly common disorder that causes fatty molecules called triglycerides to build up in the blood.

Now in their 50s, the siblings recently underwent genetic testing and learned that they have a condition that's much more rare, affecting only 1 in every million people, according to the case report, published today (Nov. 18) in the journal Annals of Internal Medicine.

Those with the ultrarare disorder, known as familial chylomicronemia syndrome (FCS), may accumulate more than 1,000 milligrams of triglycerides per deciliter (mg/dL) of blood. For comparison, normal blood levels of the fat should fall below 150 mg/dL, and 500 mg/dL would be considered "very high" in a healthy person, according to the National Institutes of Health.

Indeed, in people with FCS, blood fat levels are so high that the normally crimson fluid turns the color of milk. (FCS is not the only condition that can cause milk-colored blood; the symptom may also appear in people with severe hypertriglyceridemia.)

Related: The Color of Blood: Here Are Nature's Reddest Reds (Photos)

The three siblings had long struggled to keep their triglyceride levels under control and suffered frequent inflammation of the pancreas, also known as pancreatitis a serious condition that can cause abdominal pain, fever and vomiting. At the hospital, the male twin's triglyceride levels reached as high as 5,000 mg/dL, while the other brother's levels peaked at around 6,000 mg/dL. The female twin's triglyceride levels soared highest of all, reaching 7,200 mg/dL at maximum.

The siblings hoped their doctors could help subdue those aggressive symptoms.

To confirm the sibling's rare diagnosis, the doctors looked to their patients' genes. Triglycerides typically build up in the blood due to multiple malfunctioning genes and other related health conditions, such as diabetes or high-blood pressure, according to the Journal of the American Board of Family Medicine. But when doctors probed the siblings' genetic code, the researchers spotted only one mutated gene that was key for breaking down triglycerides in the body.

In healthy people, the gene contains instructions to build a protein called lipoprotein lipase (LPL), which typically coats the blood vessels that run through muscles and fatty tissues in the body, according to the Genetics Home Reference. LPL breaks down fats carried in the blood; without an adequate supply, the siblings' blood plasma ran thick with excess triglycerides.

Related: How to Speak Genetics: A Glossary

Each sibling carried two copies of the mutated LPL gene, meaning both their parents passed down the mutated genetic code to the children, the case report noted. What's more, the particular genetic mutation in the siblings had never been seen before, the authors said. The doctors placed the siblings on a fat-restricted diet, which successfully stabilized their triglyceride levels and quelled their bouts of pancreatitis. Sometimes, when triglyceride levels spike, doctors must manually replace the fat-filled blood of their patients with healthy blood from donors, Live Science previously reported. Thankfully, the siblings' condition could be curtained with diet alone.

Originally published on Live Science.

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A Rare Genetic Disorder Turned These Siblings' Blood 'Milky' White - Livescience.com

She said: It is also fair to say that there are another minority of trans people who agree with me that the terms biological male and biological female are accurate terms but are afraid to speak out because not only is there an extremely toxic debate on Twitter where they are being attacked from both sides. But also, within our community, the idea around gender identity is very intolerant of any dissent.

Ms Harrison, who haslivedas a transgender woman for two decades, said she shares Ms Forstaters gender critical beliefs and has been labelled a "Nazi facilitator" and "scum" for expressing them.

The process of having surgery or hormone treatment cannot ultimately transform your sex, Ms Harrison told the tribinal. Every cell in my body has male chromosomes. I have a prostate. These things cannot be completely deconstructed. It is not possible to be biologically female. But that does not mean I cant live a fulfilling life being treated as a woman.

Writing in her witness statement, Ms Harrison said that attempts to legally coerce society into treating males as females in all circumstances is inevitably doomed to fail.

As Churchill once said, The truth is incontrovertible. Malice may attack it, ignorance may deride it, but in the end, there it is, she added.

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Transgender people who agree with using terms 'men' and 'women' too afraid to speak out, tribunal hears - The Telegraph

The latest edition of Pig Progress is available for reading digitally. The latest copy zooms in on health issues as well as breeding and genetics.

To start with the last theme breeding and genetics Pig Progress was fortunate enough to take a little look into DanBreds new boar manual. The Danish breeding company publishes a step-wise manual with many chapters how to deal with its male animals.

Pig Progress had a sneak preview and chose the chapter as to how to train the boars. Dummies, stroking, boards, feeding many tips and tricks are discussed by DanBreds Trine Lund Pedersen on pages 6-7.

On the verge of health and breeding issues is Hendrix Genetics pig division, i.e. Hypor. This company has been very prominent in South Korea and sees this country confronted with African Swine Fever (ASF) in recent months. Boerderij reporter Judith Waninge and Pig Progress editor Vincent ter Beek learned about the BioHypor system a well thought-through biosecurity approach which should keep farms free from ASF. Pages 16-17

Hugues (Hugo) Six, general manager East and South-East Asia for Hendrix Genetics. Photo: Vincent ter Beek

And whilst we were in Asia, we also took a look into the situation in the Philippines. Dr Steven McOrist has an insight view as to what has been going on there in recent months and shares his experiences on pages 12-14.

Photo: Dr Steven McOrist

Also in this months farm visit, health issues were never far off. With the help of German syringe manufacturer Henke-Sass, Wolf, Pig Progress was allowed to visit Albesa Ramadera, an innovative model farm near Lleida, Spain. The farm aims to combine animal welfare, precision farming and a good health status. Throw all these philosophies in the blender and the result is a fascinating visit on pages20-23.

Laia Calder Puig (left) and Cristina Sanmartn Ruz vaccinating a piglet against PCV2. Note the yellow light in the vaccination device. Photo: Vincent ter Beek

More on-site visits in this edition as we also took a look at a feed production site of the Brazilian cooperative Lar. This is one of the larger agro-industrial cooperatives in Brazil. As African Swine Fever in Asia is likely to offer great export opportunities, the cooperative is keen to keep its business clean and free from any potential pathogenic hazards. Pages 8-10

The Lar feed mill in Santa Helena, PR, Brazil. Photos: Vincent ter Beek

Pig Progress has been truly on the move over the last few months as colleagues Rosie Burgin and Vincent ter Beek also paid a visit to Qingdao, China, mid-September, to take a look at the 2 large international trade shows that were held simultaneously there. VIV Qingdao took place in western Qingdao, whereas EuroTier China was organised 50km down the road in this huge city. The shows were held in a time when ASF has rampaged the Chinese swine industry. How did the virus affect the shows? Let us take you back to VIV Qingdao (pages 28-29) and EuroTier China (pages 30-31).

The Cosmopolitan Exposition centre in Qingdao welcomed over 20,000 visitors during the 3-day event. Photo: Vincent ter Beek

A trade show is always a good time to launch new products. Challenge Animal Health introduced various new types of antibiotics at EuroTier China.

Pig Progress also took a look at the Animal AgTech Summit, held 1-2 October in Amsterdam, the Netherlands. This relatively new concept aims to get companies in the international animal agribusiness together to discuss applications and innovations with regard to precision farming. Various interesting new companies were present and explained their case we highlight 5 of them on pages 26-27.

One of the ways precision farming can benefit pig producers is through the possibility of benchmarking. After all, being able to monitor and measure all kinds of developments inside pig farms, also allows farmers to compare performance with others. In Canada, financial benchmarking has become popular, as correspondent Treena Hein explains on pages 24-25.

Benchmarking starts with knowing exactly what is going on inside the pig houses. Photo: Bert Jansen

Columnist John Gadd continues where he left off in October with his series on immunity, and discusses now which type of stressors exist for pigs and what can be done about them (page 15). Then, Dr Monique Pairis-Garcia discusses the different types of animal welfare definitions and delves into the value of knowing what an animal experiences (page 34).

To view these articles online or other issues of the magazine just click on our digital magazine section and then on issue nr 9. Registration is free.

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Biosecurity, boars and benchmarking in Pig Progress 9 - Pig Progress

BUFFALO, N.Y. The role of zoos has taken on critical importance in both preservation and conservation of increasingly threatened species such as the rhinoceros.

The Buffalo Zoo has been very active in working with rhinos. Its two adult rhinos, Tashi and George, are helping to increase the global population of greater-one horned rhinos. Tashi, a 23 year old female, recently gave birth to a male calf named Mohan. The zoo tried to breed George and Tashi, but it didn't take, so they had to resort to artificial insemination.

RELATED: It's a boy! Baby rhino born at the Buffalo Zoo

It's a complex process guided by the American Species Survival Plan, which was developed in 1981 by the American Association of Zoos and Aquariums. The SSP program was created to help ensure the survival of selected species in zoos and aquariums, most of which are threatened or endangered in the wild.

"We look at the genetics of each individual animal, and then match them best who matches best with who to know where to send them with, who to breed them with, how many offspring can they have, are they over represented, are they under represented," said Buffalo Zoo Assistant Curator Joe Hauser. "So there's a lot of factors to the genetic portion, and where the animals go."

Hauser says that Tashi has given birth four times, two naturally and two artificially. Young Mohan's birth went off smoothly, as anxious zoo keepers watched from a distance.

"We stayed out of the barn when she is giving birth, we wanted to make sure she's paying attention to giving birth, and not trying to disturb that," he said. "So we watched her on the camera and your heart's pounding the whole time, and fortunately with Mohan, he hit the ground and was kicking right away."

In a few years, Mohan will hopefully father more rhinos. And though unsuccessful in breeding with Tashi this time, George is just entering his prime breeding years. His genes will also contribute to the overall success of his species.

"George is actually the third most genetically valuable male in North America, so he's very valuable," Hauser said.

The Buffalo Zoo has also helped Rhinos in Indonesia, raising $14,000 over the summer for the organization.

International Rhino Foundation

The zoo's efforts to help these ancient mammals doesn't stop with breeding. Over the summer Hauser and the zoo raised $14,000 to donate to the Sumatran Rhino Rescue, an Indonesian organization dedicated to saving the Sumatran rhino, the most critically endangered large mammal on earth. There are less than eighty left in existence.

"The government of Indonesia along with International Rhino Foundation and other NGO's they recently developed the Sumatran Rhino Rescue, which is a plan to be able to capture the remaining Sumatran Rhinos that are out in the wild, bring them into human care, put them in managed breeding situations, increase their numbers, and then re-release them back out into the wild," Hauser said.

There are less than 80 Sumatran Rhinos left in the wild. The Sumatran Rhino Rescue is working to preserve them.

International Rhino Foundation

It will take the entire global community to ensure the future of the rhino, and the zoo is rightfully proud of its contribution to the cause.

"And I hope that we can pass that along to our zoo guests, and the zoo community, and the Western New York community, and all across the United States, we can do this, and you can take a lot of pride in knowing you played a part in saving a species," Hauser said.

To help support the Buffalo Zoo's efforts, click here.

To learn more about Sumatran Rhino Rescue, click here.

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2 the Outdoors: Saving a species - WGRZ.com

Fertility tech startup Mojo is coming out of stealth to announce a 1.7 million (~$1.8M) seed round of funding led by Nordic seed fund Inventure. Also participating are Doberman and Privilege Ventures (an investor in Ava), plus a number of angel investors including Josefin Landgard (founder and ex-CEO of Kry) and Hampus Jakobsson (venture partner at BlueYard, BA in Clue & Kind.app).

Mojos mission, says co-founder and CEO Mohamed Taha, is to make access to fertility treatment more affordable and accessible by using AI and robotics technology to assist in sperm and egg quality analysis, selection and fertilization to reduce costs for clinics. Only by reducing clinics costs will the price fall for couples, he suggests.

What the AI does in our technology stack from now until our roadmap is completed, product wise, is to look at sperm, look at eggs, look at data and ensure that the woman or the couple get precise treatment or the precise embryo that yields healthy baby, he tells TechCrunch. The role of robotics is to ensure that the manipulations/procedures are done precisely and at reduced time compared to nowadays, and also accurately.

The idea for the business came to Taha after he was misdiagnosed with a kidney condition while still a student. His doctor suggested freezing his sperm as a precaution against deterioration in case he wanted to father a child in the future, so he started having regular sperm tests. I was super annoyed with one particular fact, he says of this. Every time I do a sperm test I get a different result.

After speaking to doctors the consensus view of male fertility he heard was I shouldnt care about my fertility worst case scenario all that they need from me is one sperm. He was told it would be his future partner who would be put on IVF to take the treatment for me. Doctors also told him there was little research into male fertility, and therefore into sperm quality such as which sperm might yield a healthy baby or could result in a miscarriage. And after learning about what IVF entailed, Taha says it struck him as a tough deal for the woman.

Its completely blackbox, he says of male fertility. I also learned that in terms of IVF or ART [assisted reproductive technologies] everything, pretty much, is done manually. And everything, pretty much, also is done at random you select a random sperm, they fertilize it with a random egg. Hopefully the technician whos doing it manually knows his or her job. And in the end theres going to be an embryo that will be implanted.

He says he was also struck by the fact the trial and error process only works 25% of the time in high end laboratories, yet can prospective parents between 40,000-100,000 for each round of treatment. This is where the idea of the company came from, he adds. Mojos expectation for their technology is that it will be able to increase IVF success rates to 75% by 2030.

The team started work in 2016 as a weekend project during their PhDs. Taha initially trained as an electrical engineer before going on to do a PhD in nanotechnology, investigating new and affordable materials for use as biosensors. It was the microscopes and robotic arms that he and his co-founder Daniel Thomas, were using in the labs to examine nanoparticles and select specific particles for insertion into other media that led them to think why not adapt this type of technology for use in fertility clinics as an alternative to purely manual selection and fertilization.

The other two co-founders are Fanny Chesa and Tobias Boecker.

We just completely automate everything to ensure that the procedure is done faster, better and at the same time more reliably, Taha says of the concept for Mojo. No randomness. Understand the good from the bad.

That at least is the theory. To be clear, they dont yet have their proposition robustly proved out nor productized at this stage. Their intended first product, called Mojo Pro, is still pending certification as a medical device in the EU, for example. But the plan, should everything go to plan, is to get it to market next fall, starting in the UK.

This product, a combination of microscopy hardware and AI software, will be sold to fertility clinics (under a subscription model) to offer an analysis service consisting of a sperm count and quality check as a first service for couples to determine whether or not the man has a fertility problem.

Initially, Mojos computer vision analysis system is focused on sperm counts, automating what Taha says is currently a manual process, as well as assessing some basic quality signals such as the speed and morphology of the sperm. For example, a sperm with two heads or two tails would be an easy initial judgement call to weed out as bad, he suggests.

The first product is to look at the sperm and say if this man experiences infertility or not. So we have a smart microscopy built custom in-house. And this is where the element of the robotics comes in, he explains. At the same time we put on it an AI that looks at a moving sperm sample. Then, through looking at this, the system on Mojo Pro will tell us what is the sperm count, what is the sperm mobility (how fast they move) and what is the predominant shape of the sperm.

The second part is the selection of the sperm [i.e. if the sample is needed for IVF]. Now we ensure that good sperm is being selected. This microscopy will look at the same and visually will guide the embryologist to pick the good sperm thats highlighted around, for example, by a green box. Good sperm have green boxes around them, bad sperm have red boxes around them so they can pick up through their current techniques the sperm that are highlighted green.

Based on internal testing of Mojo Pro the system has achieved 97% of the accuracy of a manual sperm count so far, per Taha, who says further optimization is planned.

Though he admits theres no standardization of sperm counts in the fertility industry which means such comparative metrics offer limited utility, given the lack of robust benchmarks.

The way we are going with this is were really choosing the best of the best practitioners and we are just comparing our work against them for now, is the claim. (Mojos lab partner for developing the product is TDL.)

We will try to introduce new standards for ourselves, he adds.

The current research focus is: What are the visuals to make sure the sperm is good or bad; how to actually measure the sperm sample, the sperm count; in terms of morphology how we can incorporate a protocol that can be the gold standard of computer vision or AI looking at sperm?

The wider goal for the business is to understand much more about the role that individual sperm and eggs play in yielding a healthy (or otherwise) embryo and baby.

Taha says the teams ultimate goal is automating the fertilization process, again with the help of applied AI and robotics (and likely also incorporating genetic testing to screen for diseases).

He points out that in many markets couples are choosing to conceive later in life. The big vision, therefore, is to develop new assisted reproductive technologies that can support older couples to conceive healthy babies.

Generally speaking we leave our fertility to chance which is sex So theres a little bit of randomness in the process. This doesnt necessarily mean its bad its how the body functions. But when you hit later ages, 30 or 40, we face biological deficiencies which means the quality of the eggs are not good any more, the quality of the sperm might not be good any more, if fertilization happens with old gametes you are not sure there is a healthy baby. So we need technology to play a role here.

Imagine a couple at the age of 40 who want to conceive a baby ten, twelve years from now. What happens if this couple have the possibility of the sperm of the man to be shipped somewhere, the egg of the woman to be shipped somewhere and they get fertilized using high end technology, and they get informed once the embryo is ready to be implanted. This is where we believe the consumer game will be in the future, he says.

We envisage ourselves going from just working with clinics in the coming ten years making our AI and our robotics really flawless at manipulation, and then we are envisaging of having as consumer-facing way where we ensure people have healthy babies. Not necessarily this will be a clinic but it will be somehow where fertilization will happen in our facilities.

Im not speaking about super humans or designer babies, he adds. Im speaking about ensuring at a later stage of the conception journey to have a healthy baby. And this is where we see ART can actually be the way to procreate at later stages in order to ensure that the baby is healthy then there should be new technologies that just give you a healthy baby and not mess up with your body.

Of course this is pure concept right now. And Taha concedes that Mojo doesnt even have data to determine good sperm from bad beyond some basic signifiers.

But once samples start flowing via customers of the first product they expect to be able to start gathering data (with permission) to support further research into the role played by individual sperm and eggs in reproduction looking at the whole journey from sperm and egg selection through to embryo and baby.

Though getting permission for all elements of the research they hope to do may be one potential barrier.

Once the first module is in the market we will be collecting data, he says. And this data that well be collecting will go and be associated with the live births or the treatment outcome. And with that well understand more and more what is a good sperm, what is a bad sperm.

But we need to start from somewhere. And this somewhere right now what were relying on is the knowledge that good practitioners have in the field.

Taha says he and his co-founders actively started building the company in January 2018, taking in some angel investment, along with government grants from France and the EUs Horizon 2020 research pot.

Theyve been building the startup out of Lyon, France but the commercial team will shortly be moving to the UK ahead of launching Mojo Pro.

In the short term the hope is to attract clinics to adopt the Mojo Pro subscription service as a way for them to serve more customers, while potentially helping couples reduce the number of IVF cycles they have to go. Longer term the bet is that changing lifestyles will only see demand for data-fuelled technology-assisted reproduction grow.

Now we help streamline laboratory processes in order to help the 180M people who have fertility problems have access to fertility at an affordable price and reliable manner but also we have an eye on the future what happens when genetic testing [plays] an important role in the procreation and people will opt for this, he adds.

Go here to read the rest:
Fertility startup Mojo wants to take the trial and error out of IVF - TechCrunch

Editors' Note: This is the transcript of the podcast we published last week on Invitae (NYSE:NVTA). We hope you enjoy.

Daniel Shvartsman: Welcome to the Razor's Edge. I'm Daniel Shvartsman. I'm joined by Seeking Alpha author Akram's Razor on this show. Each episode we take an investing idea or theme that Akram has been looking at for his personal investing as well as the Seeking Alpha marketplace service he runs, also called The Razor's Edge. We look at the ideas themselves, stress test them, try to figure out where they might go right or wrong, talk about what's been going on, and talk about the research and analysis that led to this take.

The idea to share some current investing ideas here into consideration, but also get the ins and outs of deep fundamental market research today. This week's topic has a lot behind it. The ticker symbol is NVTA. The stock is Invitae. Akram released a short case on the company on Seeking Alpha on October 11th, that went long in terms of breaking down why the genetic testing company was more like a WeWork than an Amazon. In other words, the company has had prodigious revenue growth, but it's come at a cost of increasingly negative cash flows and limited competitive advantage, in Akram's view. Was a thoroughly researched short case and as is often the case it's attracted a lot of attention, both positive and negative.

On today's Razor's Edge, we're going to talk about what brought Akram to this case, what investors are missing, and some of the reactions since he went public on Invitae. We're also joined by a colleague of Akram's, James who can add some insight on this topic based on research he's done on the stock as well.

Before we begin a quick disclaimer and disclosure; The Razor's Edge is a podcast on Seeking Alpha's The Investing Edge channel. The views discussed belong to either Akram, James in this case, or me respectively, and nothing on this podcast should be taken as investment advice. We'll disclose any positions in any stocks discussed at the end of the podcast, though upfront I can say I have no positions in any of the stocks we plan to discuss, Akram is short Invitae and long Myriad Genetics, and James is short, Invitae. We're recording this on the morning of November 4th.

Listen to or subscribe to The Investing Edge on these podcast platforms:

All right, guys. Good morning. Welcome.

Akram Razor: Good morning.

James: Good morning. Thanks.

DS: So let's just go really basic, why Invitae? What brought -- why does your radar get on this stock? Where did they come up?

AR: That's definitely an interesting part of the story. I guess the starting point was, there was people shorting Myriad. So I follow the Southern Investigative Reporter. And they've done a couple short pieces on that. And I kind of have taken a look at it briefly, which caused me to take a brief look at Invitae, and that was probably like, May or June. And then Ilumina missed big time on earnings, and I've traded Ilumina several times of the year. I've never traded any of these other stocks in terms of that. But it kind of got me interested in the space. And I guess what kind of, I mean, like, I think I had pinged James on it a couple times being like this is like this is worth looking into, but like neither of us had really gotten that excited about it.

And then there was a report that came out by a short seller, recommending the stock is an amazing long idea, which I read, because I know the short seller and his work. Once I read that, I was like, I need to look at this company a little closer. And then just the typical process, like pulling up their filings, seeing exactly what's going on financially, and I was just like, wow, this is just an incinerator. What are they doing? Why is -- like, what's the business model?

And that brought me to, there's an author on Seeking Alpha who had published a lot on this over the years, capital markets, laboratories and read their work, and they made these Amazon compares where, obviously, that's where you get a little bit of a heightened radar, when a laboratory diagnostic company is being compared to Amazon, which I mean, I don't know also if you know -- and I had like a brief experience with Theranos in 2000 it was say like, early 2014, like back when it was like -- I was picking on the Decacorns then, my favorite, like when I used to write my market commentary and I'd have a little bit of fun with it.

At the time, the two I was having fun with were Zenefits and Theranos. But I mean in Theranos' case, like I was just curious as far as what like -- I mean, it was a private company, $10 billion, obviously a lot of hype. I was like, wow, do I short Quest and LabCorp, right? I mean, I can't make -- I can't invest in Theranos. But if this company is so revolutionary like it, there's this pretty simple thesis out there in the public markets where I mean, if they're going to stick a lab in a box, I should go short Quest Diagnostics and LabCorp.

And I have, on the medical side, an extensive network of friends and family. So I ended up doing just one call with someone who'd been at Quest and in the laboratory diagnostic space, pretty senior for about 20 years. And like, I mean, it was like a 30 minute conversation. I felt stupid by the time it was over. It was just like, he's like, are you an idiot, you can't stick a Lab-in-a-Box. It was like -- it was literally like that, after like being very polite for a little while. So that type of stuff kind of intrigued me. And Theranos ended up being Theranos. I never really did much more with it after that. And then Wall Street Journal came after it, and it became this cautionary tale. I don't know if James -- did you follow Theranos very closely, I don't even know if we really discussed that?

J: No, I had heard from some VC friends who were very skeptical of it all the way through. But I wasn't that close to the name myself.

AR: Yeah, I mean, neither of us I would say, I would characterize myself as close to it. But I mean, I did take the time to literally be like, hey, do I short these stocks because of Theranos, right? It was like an investment idea at the time.

So yeah, I mean, I guess that's what started it, right. I mean, like Theranos had this -- and then the message was just kind of just like affordable blood testing for all, a social cause being compared more to, like technology differentiating companies and I mean, Elizabeth Holmes like to associate herself when she talked about things, when she compared herself to the Google Founders and Facebook and like, I mean, if you saw the documentaries like here we were at, in Brazil, and this is where we -- who was sitting there, and the Google guys, and the Amazon and Facebook, and we are the stars of the show, right?

And if you look at Invitae, I mean, like on the surface, it's like there's a social enterprise element to it, right? Where it's just like, we have a mission, and this mission is to make genetic testing affordable for all. I mean, like, they don't care, they don't describe themselves as like a laboratory diagnostics company, right?

DS: Well, they --

AR: That was a genetic information company. Go ahead.

DS: Yeah. I mean, if you look, I have got their 10-K open, their last one and it's -- our goal is to aggregate a majority of the world's genetic information into a comprehensive network that enables sharing of data among network participants to improve healthcare and clinical outcomes. So it's this.

AR: Yeah, so what does that mean?

DS: Right. You know, it is this very -- it is very big mission, right. It is very big.

AR: Yeah, I mean, James, obviously has some views on this. Like, I mean, what do you think of that part?

J: Well, I think that really comes down to the crux of the investment case here, which is, just because something sounds good as a sound bite doesn't mean that it actually makes sense in business. And so the idea of accumulating the world's genetic information, you would argue, seems like if you could do that would allow you to capture rents on that database. But there are very real issues with that. Namely the company has said that they won't do that. And then when they're pressed about how -- whether or not they will do that, they kind of seem to give non answers what I can tell.

So that's one of the questions right that that I think would be very helpful for the company to lay out there, very specifically, which is, if we gather all this data up, and specifically what data is being gathered? Are they -- is that data, they've also released to a common database, like they say they have been doing, is there additional data that they're not releasing?

AR: Well, I mean, the data that they're sharing with the common database is the variant of unknown significance data, right? So I mean, that's what they're contributing to Clinvar. We don't really know. But like, I mean, I'll be honest, like if I was to go in and have hereditary cancer test, I would have never thought once about, like, who the lab doing the test is or ask the oncologist anything, but like literally now knowing this business, I mean like, make sure you're not using Invitae, because I have no clue what they're going to do with that data.

Like my DNA is a product for them to figure out somewhere down the road just to do something with it, I mean, it's so -- like James just said, it's very bizarrely unclear, which is decidedly convenient when you're running a business model like this.

DS: So step back for a second. So the thesis -- the company's thesis is that they're providing genetic tests. And then they're aggregating that, they provide it at -- arguments are they providing it for below the cost that they actually have to pay to their providers to actually deliver the test but low cost testing that they can then -- if we're going to use the Silicon Valley jargon, that they get the flywheel of more genetic data and improve, they get a lot of volume, and eventually, that's both going to give them scale to lower the costs, but then also they're aggregating this huge genetic database, which as you kind of point out, Akram, they're going to have to do something with to make it reasonable, which raises concerns in of itself. But the idea is that eventually they'll get scale from offering at cost that will allow them to become a profitable business, I think. That's how I understood the company's take and the company's argument.

AR: I mean, like James just said the company hasn't explained that. So if you look at this company's history, this isn't like a startup, number one, right. So this company was founded in 2009. They've been at this for a decade, okay. Initially, they were kind of rare disease focused, right?

Like where they're deriving the revenue, if they were to actually describe themselves accurately, they would be like, we do hereditary cancer testing far cheaper than Myriad, right? And I mean, like, I think that's an important thing to look at this. I mean, there are sources of revenue, which is generally speaking what has attracted people to the stock, it's not science, right. It's not like you've developed a test or you're like Foundation Medicine and you've got this companion diagnostic clinical trials and you are about to do something where you're going to earn a high margin, because you've developed something nobody else has. That's typically, what people get excited about in science and biotechnology, right?

You get rewarded for R&D, okay. These guys have approached the market that Myriad discovered the BRCA mutation in 1994, okay. That's like what the indication of hereditary cancer right? I understand cancer, 90% of it is not hereditary. So you're looking -- when you talk hereditary, there's a less than 10% chance that it's something hereditary. That's helpful from a clinical standpoint, as far as your treatment for cancer diagnosis, whether it's early or late stage or whatnot.

So this company came into this space in the sense that Myriad had a monopoly on this gene, right? They started doing their first BRCA testing lab kit was like 1996. They had the patent on that gene till 2013 when the Supreme Court struck it down, right. So these guys entered this space, essentially, from that standpoint as a competitor against Myriad. And once that space kind of opened up in hereditary cancer testing, I mean like, well, you can't patent these genes, right? Which is great for competition, but what's the flip side of it?

If I make a major discovery on gene X correlates to disease Y, right? And I can't patent it and I'm running like a test that kind of identifies that historically, kind of tough to build a very profitable business around it. So when we go back to like what you were saying about like this whole genetic information and whatnot, the most interesting thing about this business is look at the rest of the landscape. Nobody's selling the story, like Myriad's still the revenue leader in hereditary cancer testing.

The other space the company is in deriving revenue from is reproductive health, carrier screening, non-invasive prenatal screens. And that's the most crowded market ever. It's got Ilumina and Sequenom, which is owned by LabCorp, like pretty much, they control the IP there. And then there's like a half a dozen other competitors owned by large companies.

So like, in hereditary cancer, you've got Myriad. And then you kind of have this like at a huge, huge, huge discount to Myriad prices, Invitae, right? I mean, like now they're running what, $99 tests, okay? So you look at it and you can sit here we can just, like figuring out what they want to do data wise and the fact that it's Vegas kind of important. It's also important in the context of -- well, there's a whole industry here, right? I mean, this is at least what -- we got some heat when we cautioned this like, some of this has attracted obviously a lot of retail investors by using the Amazon compare. And, in the initial thesis it was like a cautionary mention at the end, like that the laboratory diagnostic space doesn't need another Theranos.

And at least in Theranos' case, what they were selling to investors was we're building a better mousetrap essentially, right? Like we've got -- we've engineered something that's going to change the way we are able to do testing. And that's not the story here. The story here, I mean, if you go back to the founder in 2016, there's a couple of interviews with him. And he literally says like, we're providing the same test that everyone else is providing, we're just making them more affordable. That was that's their initial story, right.

So I mean, you do kind of run into something like that, which is where, like some people may think it like, you know, oh, it's very, self-serving or opportunistic to compare this to WeWork. It is, exactly like WeWork from a business standpoint. Like you can't get around that fact. And I think the Amazon like -- and this is not like some guy writing a really bullish Seeking Alpha article and using hyperbole, the management sticks to compares. I mean, they -- literally they have a slide in their investor deck, what we can learn from Amazon, and they make statements like our competitors -- what did they say, James, is like the competitors margin is our opportunity or

J: Yeah, something that effect. Yeah, you've heard a lot of ground there, Akram. I think the important aspect of what you've said and the commonality among all those points is that the management team has made some very high level statements about the promise of this industry and the promise of their company. And they could really answer a lot of these questions if they wanted to, right? They could say, okay, here is our revenue breakdown from cancer or nips [ph], kind of other panels, which don't have necessarily the clinical efficacy.

Or they could say, here's our -- here's what we're getting from the various cost cutting or network effects or economies of scale that we promised. And here's how this is going to develop, but they don't they just say, trust us, it's all going to work out. And the way that it's not [ph] going to work out is that it worked out for Amazon. So it's there's not much transparency, there's a lot of just kind of big picture verbiage I would say.

AR: Yeah. I mean, 100% and like, I mean, you get the Amazon story, Daniel, right. I mean, if you look at it, people like, if you look, well, come on, Amazon was losing money. No, Amazon was improving operating cash flow from literally from day one. I mean, people forget, like, you make money selling DVDs and books online, particularly if you don't pay your suppliers for 100 days, right? I mean, like, where was Amazon after a decade? It was already a behemoth, right?

So when you look at it, Amazon had someone else, i.e., their suppliers funding their growth. It's free, cheap capital. This company went and IPOed in 2015, at $16 a share, had like 25 million shares outstanding. They're at 100 now, four years later, right? I mean, it's like, they keep going back to the well. So if you're an investor and you're looking at it from a return on investment on money, you're giving them. I mean, you have a serious problem. And if you look at it, and you say, hey, I'm going to compare myself to Amazon. Well, Amazon had a cost structure that attacked this cost structure of brick and mortar, okay?

They benefited from so many things. We didn't have sales taxes, if you were paying on Amazon as a consumer. They benefited from the fact that they went into markets with huge existing volume already, books and DVDs. They didn't have to convince people to buy X, Y and Z. They were already huge volume markets. I mean, I'm sorry, but like hereditary cancer testing. It's not something people get excited about to go online or buy as a gift for a friend.

I mean, like, we get the DTC space, and even that has already slowed down drastically, and that's Ancestry. And if Ancestry slowed down at like 30 million tests, right, like, you really think people are going to be super excited as individual consumers to be like, I really need to figure out whether I have a history of cancer right now. I mean

J: Well, and more importantly, more importantly, I think there's a healthy amount of skepticism in the medical community whether or not these tests are useful, right? Like the issue with any test is, if you find something, an indicator of a disease. Does that help you catch the disease? Does it help you catch it earlier than existing testing or physical exams, or other ways of seeing the diseases there? And then can you do anything about it?

So, I think one of the issues here is even if you were to send your saliva [ph] sample out, and you came back with saying indication that you might have liver cancer potentially. A, you wouldn't know, if that were real, because it's really just a correlation at this point. There's not enough data. B, even if you knew, it was real, there's really not much to do except worry about it. And so you have a lot of additional burdens on the patient and the healthcare system in terms of emotional and financial burdens, without any clear benefit.

And so I think within -- as I'm saying, within breast cancer, that there is a clear benefit in terms of efficacy and outcomes. But for the rest of the space, it's really not clear. And that's why, if you look at the treatment protocols for most of the commercial payers, they don't pay for all these tests, because the research doesn't demonstrate that they should.

DS: So one of the things I'm -- as we're throwing around these comparisons. I'm thinking about the -- there's a notion in Silicon Valley and sort of abroad, the market, the idea of tech, tech as a category is becoming less and less meaningful, because companies are adopting online models or tech models to different verticals. And what I think about with Theranos and Invitae, specifically, healthcare is a very complicated sector, both in terms of the way payers work and we can get into Medicare in a little bit, but the way the payment system works.

And I'm not talking even about what might or might not happen in the future with changes to insurance. But just -- that's, I think, always been fairly -- you have to really work through it. And the articles for example, there's looking at the different reimbursement codes and that sort of thing. Like, it's more than you have to do to figure out, well, are they going to buy this software tool or not?

And then also, Theranos is a problem, because they were actually -- there were issues of fraud around people, things that were supposed to help people's health. And so I guess I'm just kind of, I guess, I wanted to hear a little bit more about like, because -- a lot of the response.

AR: Well, I mean, look -- let's, I mean, if you think about Theranos, where really was the fraud. The fraud like, I mean, if you read the indictment, what she's really on the hook for the biggest time is misleading investors, okay. I mean, that's the biggest part.

Yes, correct, like at the end, there was issues with the lab testing and they were getting inaccurate results because by the time she did that deal with Walgreens, and clearly they were at a point where they were desperate for showing meaningful revenue, because they need to raise more cash, right? Because they still haven't made the Edison work, right? They're trying to engineer a problem. They're working on it.

She didn't set out to commit fraud, right? She set out to build -- to stick a Lab-in-a-Box, right? But she had bigger aspirations. She wanted to take -- that she wanted to aggregate your data. She wanted to stick it in this cloud called Yoda, right? I mean, if you look today, you still have people who defend -- I mean, what's his name?

DS: Yeah.

AR: Tim Draper has really defended her. And what does he defend her on the point, and his point is that look, she had this vision to give you a movie of your health, i.e. like look, I get my blood work once a month, and that goes into a cloud, right? And my physician can track it. And I'm building a historical picture of a trend, by having more real time information on my blood work, cholesterol, everything right? So that creates preventative medicine in their view, right? Like your ability to have an earlier and more accurate versus a snapshot, right?

So he's like, look, she had that and was great and I genuinely have discussed this with James. I believe if she had IPOed this company and the company had started out as like, hey, she's got this Edison and this finger stick. It would have been just like binary tech play, right? She either makes it or she doesn't. And people would have debated that and thought that out there would been the believers. And then there would have been the skeptics, but she would have had plenty of time, as she gauged how that was working, okay?

To find something that generates revenue, which investors are willing to pay for, like with her inflated market cap on the Edison optimism, where she could just do regular lab testing like Quest and like LabCorp, but she would obviously do it at a lower price, right? But she would sell you the story that I'm going to stick this in the cloud, and you're going to pay a subscription fee, right? And that subscription fee to that cloud, Yoda, where all your information is and your general practitioner can access it and whatnot, that's the business. That's where I make money.

Of course, what's the problem with that business? And that business is -- well, I mean, that you're going to be like, well, you're losing a lot of money per test, doing your tests at a lower price than Quest and LabCorp or whatever to provide this back end service, why can't they do that, right? I mean, like, that becomes the same thing because you're going to need the same infrastructure. That's where she ran into issues. She's collecting data and she doesn't have the lab infrastructure to do it at the scale that these guys are doing.

If she'd been like these DTC companies, 23AndMe ancestry, she could have actually struck a deal, which is like, I'll be the cloud and I'll outsource the testing to them. And I will take a loss on the tests, because my investors are going to subsidize it, right? I mean, there was -- there would have been many Ways, but of course, she was also trying to kill their businesses. So it didn't work, right, with her engineering. but like, I mean, the bottom-line is, is if you look at it, like, it's something where you had a potential business model in that sense, where we would be asking the same questions that you'd ask about in detail, right? Like what are you doing that's different?

If you look at them today, Quest and LabCorp, they've entered into direct-to-consumer testing. I can go online and order my own tests and schedule the appointment and go pick them up, right? I'd like it's really, like, it's something where I don't even need to go through my medical practitioner if I want to get tested. And I don't know, to the degree I mean, I've discussed this with other people in the medical community on the testing side and I'm just, why isn't there a VIP service like, if I'm an extremely wealthy individual, where they come to my house, do the work, store in a cloud. And there's access to my blood work, on let's say -- but we don't have to do a monthly but let's say every three months, right?

These -- I mean like these are obviously options. So when you look at something like that and you see what went wrong with this company, her biggest mistake was being private. It's like -- because with her turtlenecks and Steve Jobs and Stanford dropout, I mean, the benefit of doubt, she would have gotten, if you look at the benefit of doubt, for example, that this company, Invitae has gotten. I mean, their CEO says one thing, and then he does the other three months later and nobody has cared like, at all. No one's asking questions. I mean, I don't know if you -- have you watched the CNBC, the Invitae interview with him on CNBC, Daniel?

DS: No. No, I haven't pulled that up.

AR: If you watch that, you would not understand what the company does. It's like we are the company the key opinion leaders turn to and this -- like, he does not say I'm a laboratory diagnostics genetic testing company, who derives primarily its revenue from doing these types of tests. And we're doing them at a significant discount to a competitor, who has had a monopoly in the space for ages. And we're using that to generate volume and we're hoping to parlay that into other sectors. And this is like -- this is our business model. Because to be -- to tell you the truth, if you look at this closely, I don't think they figured it out. They are trying to figure it out as they go along and that's part of the problem here.

DS: Isn't -- you said, if Theranos that they could have arguably sold tests below costs, but then put the -- like, isn't that essentially what the Invitae has? They haven't maybe laid out that vision but they're essentially selling below cost to get into -- like they could build that into the cloud sort of approach like?

AR: Okay. No, let's not make that mistake, okay? I'm saying that Theranos, if they wanted to, okay, and wanted to pivot for a story to sell, that sells well, when you're dressed like Steve Jobs, and you dropped out of Stanford, and you're a unique character and you're -- you've got a Board that has these people on it. And you've convinced Tim Draper and Larry Ellison to invest in you and whatnot, right? When you've dressed something like that, and you've ticked all those boxes, okay, you could just be like, hey, I'm going to do the same blood work everyone else is doing, I'm going to do it cheaper. So come to me. And how I'm going to make money off of it down the road, is I'm going to store that data, and it's going to give you a real time picture.

Now if you were to compare this on genetic information, my DNA isn't constantly changing, right? So if I'm doing -- if my focus is hereditary screening, i.e., what's been passed on to me, and what does that indicate?

What is the usefulness of that sitting there, right? Number one. And number two, in her case, it would be like, well, you still need to build the lab infrastructure to do the tests. You're going to have to do huge volume. So any business that -- like I mean, if you listen to the CEO, he literally sits on conference calls. And he's like, we hope to do half a million tests this year and reach a million people next year, and on our way to billions across the world. Well, what kind of infrastructure, you need Amazon infrastructure for that, right? I mean, how many geneticists do you need, genetic counselors? The industry doesn't even have the employees. I mean, we were discussing this, like, how big is that industry James.

J: It's well smaller than then I thought it was. I think it's in the thousands of genetic counselors. I forget it, 10,000 or 15,000.

AR: So you're going to need lab technicians, genetic counselors, you're going to need the physical footprint. You're going to need logistics. I mean have you looked -- like part of the thing that like -- we found kind of interesting is just look at Quest Diagnostics. I mean, there was a $100 price target slapped on this thing. That's the market cap of Quest, okay? They have 3,500 trucks like 26 planes, 6,000 patient access points, right? They have infrastructure to test everybody.

The internet bull on this stock, he's been close to management. He's done a lot of write ups on it. One of his write ups was just recently, and I read it and he's like, I visited the company and the CEO told me that they're actually paying for the trucks to go to FedEx, to pick up the samples and bring them back instead of waiting for FedEx to bring them to the lab. And he's like, I've never seen a company who cares about the customer so much. And I am like -- I mean, sorry, logistics are part of his business. Collecting the samples and the turnaround time and what the infrastructure you need to do it, right?

Like that's not something of like, hey, I really care about my customer. It's something you have to do and unfortunately, Quest and LabCorp are sitting there with huge economies of scale and scope and infrastructure and the same machines available to them, and the lab technicians and the geneticists and everything to flip this switch on, and they're not flipping it on. Why?

DS: Right.

AR: It doesn't make money, because the volume isn't significant enough and the cost isn't at that point. So when this company talks about driving down costs, no, they're not driving down costs. Everyone else has a lower cost per test already established, because they have higher volumes in the space, right? If you look at it Myriad's cost per sample is in the $140, $150 range. If you look across all these other labs, who are doing the stuff and the testing on the reproductive health they're all far lower, right?

So this is a last person in the space coming and trying to get to the volume, trying to get to the economies of scale and trying to drive it down, right? But they still are subject to the same cost infrastructure limits. It's not amazon.com. They haven't eliminated the blockbuster employees sitting, that when they're competing against in DVDs like a Netflix or an Amazon or whatnot, they haven't eliminated the huge physical retail footprint that a Barnes & Noble needed, right? Like, they still have the same limitations, from a cost standpoint. They're relying on Ilumina machines, consumables, Agilent, Read [ph] everybody -- like it's the vials from, what's the company that sells the vials?

J: OraSure

AR: OraSure, right, like you're buying the same stuff from the same people. So it's when you look at it from that standpoint, like if they were to sell you a story about data or whatever, it's like, well, everybody else can sell us a story about data. Why are they selling it to us?

J: It's an interesting dynamic here, because when there was the rebuttal by this bullish commentator/endorsed analyst of the company, there was a comment that, hey, it's not just the raw data, it's not just the genetic information that is useful, because genetic information in and of itself doesn't tell you enough about the disease. And I think that's a partial indictment of the whole process. But more importantly, what the analyst said is, what the company does is they take that information and they combine it with a patient's medical record. That includes all of their scans, their CTs, their MRIs, all their historical blood tests, all their physical exams, and then it takes that data. And if you get enough of that data, then you can start running effectively very large statistical relationships and figure out, okay, which genetic mutations might be associated with which diseases.

The problem with that is, as far as we know, that's not what's happening. And yet the company, again, they've kind of endorsed this, this guy is an analyst of record, the company hasn't come out and said that. But that's not what's happening. Because if it is what is happening, I think they're serious privacy concerns. So I think it's very different, if you as patients and [indiscernible] into 23AndMe, you might sign a paper, some paperwork somewhere, but if they're actually signing away the rights to all their medical records. Again, I don't believe they are, but again, this is what would need to happen in order for this data to be proprietary and useful. Then I would imagine the consumers are not aware of that.

And so you kind of have this catch 22, if you're getting the data, whatever, this guy refers to it as the golden data, whatever it is, if you're getting that data, such that it's useful, you're probably in violation of some privacy laws, whether or not you are in terms of you're covered legally, I think just patients don't understand that's what's happening. And if you're not getting that data, then there's a very real question as to what exactly is the use of just this genetic information without putting it into -- in context without kind of correlating it to these other disease markers?

And again, this is a question that could -- that's very answerable by the company as far as we know, has decided not to answer.

J: I mean, look, there's also two elements of that, right. If you remember also, in his rebuttal, he pointed out to a subscription model, right ,where he was even saying that this should be looked at from a dollar-based retention standpoint like a SaaS company. So I mean, again, if he's saying this, it's something that well was spoon fed to him, okay? And that's part of the element here, when you're dealing with something like this, and you look at that, it's like, all right, so like, I go in, I do a test for cancer, but you know, a BRCA screen. And you're saying -- are you essentially saying that, in year one, you generated revenue off of the actual testing, but then in year two, and year three, supposedly, my DNA is something that just sits there, and they can find ways to make money off of, by farming it for some sort of data that they can sell to pharma.

And it's tenuous at best to even understand how that model would work, because if you look at the rest of the industry, you just have to assume, they're all idiots. I mean, how many tests has Myriad done? I mean, look, when you go back to this thesis, Daniel, one of the most important things here is, when I put this on, this company was bigger than Myriad, literally in enterprise value, it was bigger than a company with $850 million in revenue, 20 years of testing. They've done 6 million tests through some -- to that effect I think it is at this point.

They have a database that they've made a trade secret since 2004, as far as variant data. They have four times the employees of Invitae. I mean, if you were to look at this company from there -- one notable institutional bull in the space, like this bull doesn't own any Myriad, okay. And they have a genetic spawn, and they did like kind of throw like a little bit of a shade at this thesis when it came out. And I mean, I can imagine they got a lot of questions because they own a lot of the stock and they were like, these are the companies leading in AI.

And then they like -- they listed Invitae like two other names. And then they put in their tweet, which was almost essentially directed, not my gen [ph], which I mean, for someone like me, I just -- I didn't even really spend much time getting into the AI nonsense. But if you look at Myriad how many people with machine learning backgrounds and data scientists do they employ, plenty.

You could just go on LinkedIn, look at it, and draw your conclusion. But they're not out running around saying, hey, we got AI, we're doing stuff. We're literally running machine learning models on your DNA. We're figuring out better ways, a secret sauce. Like who would advertise that? If you actually have made the data a trade secret, and you refuse to share it and they've gotten a lot of heat for it, literally the whole industry had to band together to contribute data freely to Clinvar, because Myriad won't share, because they're like, hey, fine, you took away our patent, but who cares about that. Our ability to interpret this is better than everybody else at this juncture.

So again, you look at it, at something like that, and you're just like, well, there's companies who've been doing this for decades. And you're just supposed to assume that like data science is completely irrelevant to them. But the company that acquired an AI startup in July, by September is a leader in this space. I mean what, you know.

DS: Solet me -- so there are a few directions to go here. But let's quickly touch on Myriad. It's -- you're using it as a payer here, as I think you mentioned, it's -- short sellers have kind of had their eyes on it. Somebody like Southern Investigative Reporting Foundation has reported about it. Why are you comfortable with that as the other side of this trade given the fact that they've also come under fire?

AR: I mean, I don't know James, you want to tackle this? I'm obviously a lot more bullish on Myriad then most people. I would say, like, I can't really get my head around the short thesis, and I can't get my head around the short thesis in a relative context. I mean, if you've looked at the space there are some companies with some pretty crazy valuations. Myriad is not a hard business to understand. They have a cash cow in hereditary cancer. They've used that to diversify into companion diagnostics, into carrier screening, now into these pharmaco-genetic tests, psychotropic like for depression, which is a very controversial area.

A lot of a lot of volatility around Myriad lately, let's say the last six months, has been tied to this gene site division, and the way the FDA wants to treat these tests, where I get a DNA test that like tells me, I'm more tolerant for Zoloft over Prozac. And no science has shown any clinical efficacy yet, and it's a controversial area, because there's obviously some doctors, and they've been doing -- they've been running clinical studies to try to get this approved. And they missed the primary endpoints on it. But there's also an argument that in depression, which is like opioids, a national crisis, essentially speaking, and it's not going to get better, that there's nothing, and something is better than nothing. I mean, two-thirds of antidepressants are prescribed by general practitioners. Not -- you're not talking about the psychiatry side here. These are not experts on these drugs or on mental health.

And the argument is that maybe you give them something that starts this out with a little bit more direction, however little incremental it is. Now when the stock got hammered in the summer, on its last earnings, was because they said the FDA is pushing back on them on the labeling. And then recently, there was another genetic psychotropic-related test company where the FDA allowed them to resume sending the test information, but to the doctors. So the patient just gets this, like here's what your genetics say, but nothing about the drugs. But the doctor actually gets the drug indications. And then that doctor can see that and that doctor can use that as part -- like as a helpful part of his treatment.

But again, you go back to -- they haven't been able to show scientifically and it's hotly debated. I mean, there was just recently something in -- two Harvard doctors had published something in one of the big journals on mental health, same thing with oncology, like outside of BRCA, like there was a recent paper basically like these other genes are like no better than a placebo.

So this is part of the problem in the space but I mean, I haven't -- I don't have the numbers in front of me. I mean, James do you remember off the top of your head, but I mean, I think it's like $850 million in revenue and like $150 million in EBITDA, something like that against a company with -- that did what, like $144 million in revenue last year and lost what $100 million.

J: Yeah, but larger now.

DS: Yeah, $850 million, trailing 12 months revenue, looks like EBITDA of over $100 million at least.

AR: Yeah. So like, you can look at that, I mean, and this is something when you look at stocks, I mean I was long, some Pinterest against the Snapchat short. And I thought about closing it before earnings. And the reason I thought about closing it is that you know, Snap is $16 billion and Pinterest is 15 billion and Twitter after its 35% decline is 18.2 billion AV. Yeah, Twitter's growing slower than the other two. But it's like three to four times the revenue base. And you got to kind of adjust for that, when you get to that point.

And you're like, this is a company that is in the advertising space, and it's doing -- it's going to do whatever issues its got, it's going to do 3.5 times what this is going to do and their enterprise values are a hair apart. So when you -- like this wasn't -- this is a case where if you would look at an Invitae, you'd be like, this has got to be like a quarter a fifth of the size of like, even if you are a believer and you're willing to buy into the speculation of a Myriad.

And then the other problem you have with it is that they're interrelated. All the revenue growth that is coming for Invitae is coming because Myriad hasn't come down in pricing. They've been fighting this price decline, because they've had the luxury to fight it as the leader in the space and they're extracting a premium for their testing, because they -- like there's a compelling argument, at least from their end, that based on the data we have in the history, our tests can more accurately predict what you have, as far as a likelihood of a hereditary cancer and indication reliably.

And it's ironic, and we were discussing this when we were working on this, like this company throw shade at who -- I mean, they throw shade at the DTC companies. Like they literally just gave a scientific presentation at this Houston Cancer Conference with Genetics or whatever, just like two weeks ago, where they were like, here's 23andMe's tests, okay, and this is what's wrong with it. Like 23AndMe gives you a BRCA test, that only is designed to detect three variants. Basically, if you're not an Ashkenazi Jew, it's useless.

But it's literally a report that is bundled in with the ancestry, with the health with the 50, 60, 70 reports, you get for $100 okay. It's not like you're going into buy this or you're going to your doctor and you're like, okay, I had breast cancer, I'm worried about a potential recurrence. Let's see family history. Do I need to get a mastectomy early because I have this mutation and that's a good preventative measure, et cetera, et cetera. They're not looking at 23AndMe. Like, it's -- you're competing in the clinical grade medical diagnostics market. But here's this company attacking the DTC companies who are not really their competitors.

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Breaking Down The Invitae Short (Podcast Transcript) - Seeking Alpha

The health of black men worries Dr. Charles Modlin. The numbers are clear. Theyre many times more likely to contract various serious illnesses than other Americans. So the Cleveland Clinic urologist is doing something about it.

In 2003, he launched the Minority Mens Health Fair in Cleveland. Now he is bringing the Clinics 20-plus institutes together under an umbrella organization to address the glaring health disparities in a comprehensive way.

Dr. Charles Modlin launched the Minority Mens Health Fair in Cleveland in 2003 to help eliminate health disparities among black men.Theres a lot of helplessness and hopelessness that minority men feel, Modlin says. They may think that whatever happens to them, society doesnt really care. Through this health fair and other activities, I think weve shown that we do care, they do matter to their families, their community and society.

The annual health fair was a good start, he says. The first disease we wanted to target was prostate cancer, which was twice as common in African-American men as white men and where the death rate was twice as high, Modlin says. A lot of it is delayed presentation. We know that if we can diagnose prostate cancer in the early stages, then we can cure black men at the same rate as white men.

Now Modlin, an African-American kidney transplant surgeon who has completed more than 500 transplants at the Clinic in the past 20 years, is stitching together the Clinics new Multicultural Health Center of Excellence. It will help the Clinics diverse institutes develop their own programs and approaches to address the health disparities, building on the success of the health fair, as well as the Minority Mens Health Center, which Modlin also helped launch in 2003.

What were doing basically is getting ready to take this to the next level, amplify it and spread it across the entire Cleveland Clinic, he says.

Dr. Charles Modlin talks with a patient at the Minority Mens Health Center at the Cleveland Clinic.Many doctors are unaware of health disparities and how to address them, says Modlin, who is the only black transplant surgeon in the Clinics history. A lot of times, poor communication may lead to poor patient compliance and follow-up, he says. A patient may think a caregiver doesnt care about them or is not listening to them. At the same time, patients also need to be more health literate.

Several new programs already have been launched under the Multicultural Health Center of Excellence. One is the Clinics Minority Stroke Program, which is housed under the Cerebrovascular Center in the Neurological Institute. Its goal is to increase stroke awareness among minority groups in order to lower stroke rates and improve stroke outcomes, according to its website.

Another example is the Clinics Center for Multicultural Cardiovascular Care, which is housed under the Arnold Miller Family Heart and Vascular Institute. It aims to research and understand the nature of heart and vascular diseases that are unique to special groups, identify appropriate testing for high risk populations, provide access to treatment, and understand how treatments differ among races and cultures.

The list of other new Clinic programs under the umbrella is long. They include the Neurological Institute's Minority Stroke Center; the Glickman Urological & Kidney Institute Minority Kidney & Hypertension Center; the Orthopedic & Rheumatologic Institute Minority Center; and the Respiratory Institute Minority Lung Health Center.

The Clinics marketing department is working internally on creating standardized individual webpages for each of these "center" programs before going live externally.

The Minority Men's Health Fair in 2018.The launch of this new initiative shows that the Clinic is committed to reducing health disparities, Modlin says. The directive is for us to try to take care of patients even when theyre not in front of us in an exam room. One example is that its now built into physicians schedule every week that they have time to stop and manage patients. There may be patients that we know are not coming back, patients who missed lab draws or didnt get that X-ray we ordered, and we proactively call them and remind them that they missed their appointment and ask, Whats going on, what can we do to help you?

Another mission of the Center for Multicultural Health Excellence will be to champion diversity in the field. Having more minority doctors is important because it can improve minority patient outcomes, says Modlin, who is one of only an exceedingly small number of African-American transplant doctors in the U.S.

The new center will also conduct more research into the causes behind minority health disparities, with the aim of identifying genetic variants that cause varying responses in disease and health. For example, the newly launched African-American Male Biobank houses a growing collection of blood and urine samples, accompanied by a database of donor demographics, including age, medical history and family history. The biobank, which is one of the only African-American biobanks in the nation, is approved by the Cleveland Clinic Institutional Review Board.

Efforts to reduce health disparities across the U.S. are beginning to see results, but much more work is needed, Modlin says. Since physicians have been taking a proactive approach to screening for prostate cancer, we have actually seen a lessening of some of the gaps, he says, citing one example.

Yet he has seen firsthand how efforts to reduce health disparities can make a difference. I cant tell you how many times people say, I never would have come in without this doctor, or how many times weve saved peoples lives at the health fair, he says.

The Clinics Minority Mens Health Fair, which takes place annually in April, has expanded to four Northeast Ohio locations and has reached more than 35,000 people with free early prevention screenings.

Three Calls to Action:

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Cleveland Clinic doctor leads effort to reduce health disparities among black men - freshwatercleveland

On Marlon Taylors health Hes going to be out a while; its going to be another few weeks. We are going to go back and look at something in the foot. He still has some issues in his foot that we need to get addressed so I think the earliest he will be back is in two to three weeks. I think our goal would be to have him back by the East Tennessee State game. I think that would be a realistic goal for him to come back in the middle of December but if not then right after Christmas. We are going to be without him for an extended period. We will shut him down and recalibrate on a few things.

On Trendon Watfords performance Trendon (Watford) is off to a really good start. Every time you get a five-star kid, everyone says this and this. You look at how he stacks up against the other guys in the country and he is way out performing the other guys that are supposed to be in his class. I think he is playing extremely well, obviously we need to clean up some of the stuff at the free throw line and some of the turnovers. I think a lot of it is him playing in tighter spaces. He is playing like I said, with the adjustment of the speed, so it takes some time. (VCU) is as tough as environment as we have played in.

"You put a freshman out there at VCU, it is not easy, it is not high school. I think he has adjusted well and there are certainly some other ways we can help him get the ball closer to the basket a little easier without him having to dribble it eight times to get down there which increases the margin for error. It is part of the reason we started him at the three the other night.

"It puts our biggest lineup out there and Charles (Manning) is so smart he sees thing really well coming off the bench. It helps him get in the flow of the game, I thought he played better in that role. Theres some mismatches we can take advantage of at the three that we sometimes cant take advantage of when he is playing at the post spot. I think he is off to a very good start. He is going to continue to get better and continue to move forward.

On the players in the recruiting class Jalen (Cook) has such a good personality. He committed to us first. Hes got a great pride about LSU, hes got a great pride about Louisiana and representing the state and representing the boot. Hes been to the Under Armour camp, he was at NBA Top 100 camp. It is the same 150 players that go to all the same stuff together.

"Whether its USA Basketball, the camps, the top 100, its the same 100-125 guys that go to everything together so they develop relationships and get to know each other. (Jalen) Cook has a good personality, so people like to be around him. Certainly, having Bradley (Ezewiro) there at Oak Hill didnt hurt anything. Bradley is someone who is aggressive. Hes aggressive on the court, hes aggressive how he goes and gets rebounds. That is really his nature.

We have to sign a big class. We have three signed and we have to sign another three or four before its all done. We have some work ahead of us and we need to add some big guys. We need to add a wing that can help us replace what Marlon (Taylor) brings us. We need to add another ball handler, but we have some good irons in the fire. All those guys certainly know each other and are very close. Any time you get a high-level player like Cameron (Thomas), (Jalen) Cook and Bradley (Ezewiro), other guys want to play with those guys.

On other teams focusing on playing LSU We probably snuck around on some folks last year. I dont think people just circle LSU on their schedule for basketball. I think certainly there are other programs in our league that get that. I think if you ask the average SEC fan who won the regular season SEC title last year, they probably wouldnt know.

"That stuff moves on as time does. I think you develop a target more as you go through the season and you pile up wins. I think at the end of the year we had a target on our back when we were winning and we were a threat to win the SEC. It is our job to regain the target. You have to embrace it, if you have it, you have to embrace it. You can run from it or you can run to it and you better run to it. We have to get to the point where we have that.

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Everything Will Wade said ahead of LSU-UMBC - 247Sports

A warty-skinned octopus living about 9,000 feet below the surface of the ocean. Credit: (c) ROV Jason

Deep beneath the oceans surface, surprisingly cute warty pink octopuses creep along the seafloor. But not all these octopuses look alike. While we humans love a good Is your skin oily, dry, or combination? quiz, members of one octopus species take variations in skin texture to a whole new level. Some have outrageous warts, while others appear nearly smooth-skinned. Scientists werent sure if these octopuses were even members of the same species, and they didnt know how to explain the differences in the animals looks. But in a new study, scientists cracked the case: the deeper in the ocean the octopuses live, the bumpier their skin and the smaller their bodies. DNA revealed even though the octopuses looked different, they were the same species.

If I had only two of these animals that looked very different, I would say, Well, theyre different species, for sure. But variation inside animal species can sometimes fool you, says Janet Voight, associate curator of zoology at the Field Museum and the lead author of the paper in the Bulletin of Marine Science. Thats why we need to look at multiple specimens of species to see, does that first reaction based on two specimens make sense?

An octopus with comparatively smooth skin, living 5,000 feet below the oceans surface. Credit: Ocean Networks Canada/ CSSF-ROPOS

To figure out if the smooth and warty octopuses were the same species, the scientists examined 50 specimens that were classified as Graneledone pacificathe Pacific warty octopus. Plunging deep into the ocean in ALVIN, a human-occupied submersible vehicle, Voight collected some of the octopuses from the Northeast Pacific Ocean. The team also studied specimens loaned from the University of Miami Marine Laboratory and the California Academy of Sciences. They looked at specimens from up and down the Pacific, from as far north as Washington State to as far south as Monterey, California, and from depths ranging from 3,660 feet to more than 9,000 feet below the oceans surface.

The researchers counted the number of warts in a line across each octopuss back and its head and the number of suckers on their arms. They found that the octopuses from deeper in the ocean looked different from their shallower counterparts. The deep-sea specimens were smaller, with fewer arm suckers, and, most noticeably, bumpier skin than those from shallower depths. The thing is, there werent two distinct groups; the animals appearances changed according to how deep they live. Comparing the octopuses DNA sequences revealed only minor differences, supporting the idea that they were all the same species, despite looking so different.

A deep-sea octopus with very warty skin. Credit: (c) Field Museum, John Weinstein

Sometimes when animals look different from each other, scientists can be tempted to jump the gun and declare them separate speciesespecially in the deep sea, where very little is known about animal life and scientists often dont have many specimens to compare. But looking different doesnt necessarily mean that animals are members of different species; take Chihuahuas and Great Danes, which are both the same species of Canis lupus familiaris. Dogs different appearances are due to selective breeding by humans, but in the case of the warty octopuses in this study, their different appearances seem to result from environmental influences, because their appearance changes depending on where the octopuses are from.

Scientists arent sure why the variations in skin texture occur with depth. But they do have a hunch about the size difference.

Voight thinks that these octopuses usually eat creatures from the sediment on the ocean floor, passing food from sucker to sucker and then crushing their prey like popcorn. Theres less food as you get deeper in the ocean. So these animals have to work harder to find food to eat. And that means at the end of their lives, theyll be smaller than animals who have more food. If youre a female whos going to lay eggs at the end of your life, maybe your eggs will be smaller, says Voight. Smaller eggs mean smaller hatchlings.

Support for this hypothesis comes from the number of suckers on the males arm that transfers sperm packets to females.Earlier research by Voight found that male hatchlings have a fully formed arm with all its suckers in place. The researchers documented that the number of suckers on this arm was way smaller in males from greater depth, and Voight hypothesizes it relates to egg size.

The octopus hatchlings in shallower water, only 3,660 feet, are bigger. Their eggs had more yolk. As the embryos grew, they developed farther inside the egg than the ones from 9,000 feet, who were developing in smaller eggs. They had less energy to fuel their growth before they left the egg, so they made fewer suckers, says Voight. Seeing these physical manifestations of octopuses food limitation provides a hint of how they might fare as climate change progresses and the octopuses food supply fluctuates.

Voight notes that this study, which shows that different-looking octopuses can still be the same genetic species, could help researchers down the line trying to identify life forms in the deep sea. Remotely operated vehicles (ROVs) collect video footage of the ocean floor, and it can be used to estimate the number of species presentif we know what they look like. Thats why, Voight says, its so important to examine specimens in person and use characteristics you cant see on video to identify species boundaries.

Theres still just so much we dont know about the deep sea. We need to be able to understand the information thats becoming available from ROV footage. And we can only do it by knowing what the animals look like.

Reference: A depth cline in deep-sea octopods (Cephalopoda: Graneledone) in the northeast Pacific Ocean by Janet R Voight, Jessica A Kurth, Richard E Strauss, Jan M Strugnell and A Louise Allcock, 7 October 2019, Bulletin of Marine Science.DOI: 10.5343/bms.2019.0039

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Scientists Cracked the Case of Why Octopuses of the Same Species Can Look Totally Different - SciTechDaily

The international group of scientists knew they were setting out to investigate an explosive subject: the hereditary basis of human same-sex behavior. Even so, the members of the prestigious Broad Institute in Cambridge, Massachusetts, may not have anticipated the magnitude of the public furor that erupted when they published their study, which identified several markers in certain genetic loci in the human genome related to same-sex sexual experience. The storm of reactions ranged from those who welcomed something seen as heralding significant progress in the field, to others who maintained that it would have been better if the scientists hadnt published anything.

The research results were published in full in the journal Science, at the end of August. This was the most extensive study of its kind ever conducted (there were about a half a million subjects), in which use was made of the GWAS (genome-wide association studies) method to analyze genetic big data. The researchers discovered five genetic markers (frequent, minor changes in the DNA segments of certain chromosomes) that appeared repeatedly among individuals who reported having had same-sex sexual experiences. Slight and frequent genetic variations were identified in both women and men, two others in men only and one more only in women.

No less important in the study, entitled Large-scale GWAS reveals insights into the genetic architecture of same-sex sexual behavior, is the scientists claim that a large number of genetic markers, perhaps even thousands, might operate simultaneously together although each in and of itself is of minuscule weight and influence ones same-sex orientation. Moreover, their study led the researchers to the conclusion that human genetics can explain up to 32 percent of same-sex sexual behavior.

What is at issue here, however, is not what the study contains but what it does not contain. As Melinda Mills, a sociology professor at Oxford, writes in the same issue of Science, there is no way that the researchers findings can be used as a tool to accurately predict same-sex behavior. Specifically, the fact that genetics can explain up to 32 percent of the fact that someone is gay or lesbian, does not mean that sexual identity is determined primarily by environmental factors not to mention social ones. This story is far more complex and has not yet been fully deciphered. Mills views are shared by Andrea Ganna, one of the chief authors of the new study.

What we basically do is statistical associations between having and not having these genetic markers and having or not having same-sex behavior, Ganna told Haaretz in a phone interview. Because we had this uniquely large study, he continued, which allowed us to have robust conclusions, and because we had the technology to measure the genetic markers of so many individuals, the time was right to confirm something that we expected: There is no one specific gay gene. Instead there are a lot of relatively common genetic markers, genetic mutations, that have a small effect on same-sex behavior.

At the same time, adds Ganna, a geneticist at Harvard Medical School and at Finlands Institute of Molecular Medicine, Not everyone is interpreting the fact that theres no single gay gene in the right way.

Gannas concern is shared by scientists around the world. Theyre worried that the researchers findings will fuel prejudice and discrimination against the LGBTQ community, and even spark calls for genetic engineering and genetic diagnosis among its members. So serious are these apprehensions that some have wondered whether the study would not do more harm than good.

As a queer person and a geneticist, I struggle to understand the motivations behind a genome-wide association study for non-heterosexual behavior, Joseph Vitti, a postdoctoral researcher at the Broad Institute, wrote on its blog, adding, I have yet to see a compelling argument that the potential benefits of this study outweigh its potential harms [T]he results presented not only oversimplify the question of biological causality, but also threaten direct damage by perpetuating the stereotype of LGBTQIA+ people as imprudent, while also likening same-sex attraction to a medical or psychological disorder.

Moreover, a website called The American Conservative posted an article entitled Not Born This Way After All? which wondered, skeptically: If the study proves that homosexuality is related to the environment, above all, and not to heredity why isnt it right and proper, in scientific terms, to allow those who so desire to undergo treatment in order to reduce their same-sex desires, which have now been shown not to be genetic?

That, however, is a simplistic reading of the studys findings. According to Michael Bailey, a professor of psychology at Northwestern University in Illinois, who was not involved in the study but has been conducting research on sexual orientation for 30 years, Its very important to understand that environment does not simply refer to social surroundings, like what your parents teach you and what kids you know, trauma and so on theres also a biological environment that begins right after conception.

Three years ago, Bailey and several colleagues published a survey of all the studies and professional literature in the field. The best studies have shown that genes are probably important but not overwhelmingly important, he tells Haaretz. We estimated in our 2016 review that 30 percent of the variation in sexual orientation is due to genetic variations. It may be this finding that led him to conclude that it is the biological environment that is mostly important. Bailey is convinced that men are born with their sexual orientation and that it is not subsequently acquired at any stage. He notes that there are several cases, I think there are seven throughout the professional literature, in which a baby boy was changed into a girl for medical reasons and was raised as a girl. When you follow these individuals through adulthood, you find that they are attracted to women and not to men.

In Baileys view, the best example of how biological-environmental factors can influence sexual orientation is the fraternal birth order effect. The phenomenon, whose existence is well established, he says, shows that the more older brothers a man has, the more likely he is to be homosexual. In practice, every older biological brother increases the probability that the youngest brother will be gay by about 33 percent. Thus, if the probability that a man with no older brothers will be gay is 2 percent, one older brother will increase the probability to 2.6 percent, and a second, third and fourth brother to 3.5 percent, 4.6 percent and 6 percent, respectively. Whats not yet clear is the reason for this.

In my mind, Bailey suggests, the best hypothesis as to why this happens is that a mothers immune system becomes increasingly active and produces antibodies against male proteins over successive births.

Fingers and hands

Behind this hypothesis is one of the most influential figures in the field, American-Canadian clinical psychologist and sexologist Ray Milton Blanchard. He was also among those who linked the fraternal birth order effect to another phenomenon of interest to scientists: the connection between being left-handed and having a same-sex orientation. The most extensive study in this regard was conducted in 2000, incorporating 20 different studies involving 7,000 gay male and female subjects and 16,000 heterosexual ones. It was found that gay men were 34 percent more likely to be left-handed. The situation was more extreme among lesbians: They were seen to have a 91 percent greater chance than straight women of writing with their left hand.

As a result, six years later, a research team led by Blanchard argued that the fraternal birth-order effect is relevant only among right-handed men. The reason is that, in any case, left-handed men who dont have older brothers already have a greater likelihood of being gay than right-handed men with such siblings.

A persons dominant hand turns out to be significant in another sense as well. An article published two years ago (about a study in which all the subjects had taken part in a gay pride parade in Toronto) found a connection between that hand and the gay persons role in bed: that is, the proportion of left-handed gays who defined their sexual behavior as passive or versatile (i.e., sometimes passive, sometimes not) was significantly higher than among those who described themselves as actives who clearly tended to be right-handed.

In research conducted over the years on the subject of the connection between sexual orientation and other attributes of the body, the hand holds a place of honor. But while Blanchard developed his theory on the basis of the whole hand, sometimes a few fingers are also enough: two, to be exact. In his 1998 study, British biologist John Manning confirmed a relatively old hypothesis, first put forward in Germany almost 150 years ago. Its gist is that the proportion between the length of index and ring fingers is, typically, different in men and women. Manning found that this phenomenon was detectable as early as age 2, which led to the observation that its source lies in the differences in testosterone and estrogen levels that already exist in the womb hereinafter: a biological-environmental factor.

Manning did not emphasize the element of sexual orientation in the two books and over 60 articles he wrote on this subject, but in the two decades that have elapsed since his study, more than 1,400 papers have been written on the ratio between the length of the second and fourth fingers (known as 2D:4D) and the connection between it and the level of risk of contracting certain diseases, as well as personality traits, cognitive and athletic abilities and sexual orientation.

One such study, published in 2010, maintained that straight and lesbian women are differentiated by the ratio between the length of the index and ring fingers, with lesbians tending to show a more masculine ratio i.e., closer to the average difference between the length of the fingers, among men. However, no such differences were found between gay and straight men.

Last year a team of scientists led by a British psychologist measured the fingers of 18 pairs of identical female twins, one lesbian, the other straight. Overall, differences in proportion were documented only in the lesbians and only in their left hand, and were comparable to the situation among men. This fact, the team concluded, could indicate a heightened exposure to testosterone in the womb but their study was based on a very small sample and drew much criticism. The critics charged that the conclusion was based on an overly simple means of measurement: of the way only two variables impacted each other. And, they added to bolster their argument, findings of studies involving those fingers have not been replicated in scientific experiments.

The field of gay science has been on a roll in recent years, but has a far longer history. Its modern phase dates to the early 1990s, when scientists began to publish increasing numbers of studies arguing that sexual orientation has a biological component. A leading scientist in this field is British-American neurobiologist Simon LeVay, who in 1990 performed autopsies on the bodies of 41 people: 19 gay men, 16 straight men and nine women. He discovered that the brain cells known as INAH-3 among the deceased gay men were relatively small, and closer in size to those of women than to heterosexual males.

In 1991, LeVay told Haaretz in a phone conversation, I published a study that got a lot of media attention, related to my observation that there was a region inside the hypothalamus that was different in size between men and women, and also between gay and straight men My additional finding was the difference in size between gay and straight men in this region inside the hypothalamus that is involved in the regulation of sexual behavior.

Adds LeVay, My general feeling is that there are certainly strong biological influences on peoples sexual orientation, but we cant say everything is genetic.

In the spirit of the period, and in light of the AIDS epidemic at the time, LeVay tried to be as cautious as possible about his conclusions. Its important to stress what I didnt find, he said in an interview to Discover magazine, in 1994. I did not prove that homosexuality is genetic, or find a genetic cause for being gay. I didnt show that gay men are born that way, [which is] the most common mistake people make in interpreting my work.

Three decades after publishing his study, he still thinks media coverage is doing an injustice to research even if its not his. Ive seen some headlines saying, basically, that this study [i.e., that of Ganna and his associates] shows its not genetic, or that are no gay genes, or something like that; and, of course, its not what the study shows at all.

Truly gay

In recent decades, scientific research (on men and women alike) in this realm has relied on an additional field: molecular genetics. The pioneer is geneticist Dean Hamer, who in 1993 conducted the first study of its kind.

We noticed that being gay, for males, tended to pass down through the mothers side of the family, he told Haaretz. And that is characteristic in genetics of something on the X chromosome because males get their X chromosomes from their moms That led us to look in families where there were gay brothers, to see if they shared anything on the X chromosome.

And thus, recalls Hamer, he and his team discovered Xq28: a genetic marker that plays a part in determining whether a person will be heterosexual or gay. He emphasizes that this is a factor, its not the factor and actually, overall, its not even the most important factor. He adds, Whats good about genetic studies, is that you know that whatever you find is a causal factor, because of course people are born with their genes, and its not something that changes over time.

LeVay, he explains, is looking directly at the brain, and were looking at what we think is building the brain and genes. Yet, its very difficult to know whether one was born with a brain like that, or whether that brain developed that way because of your behavior the causality is rather unknown.

At the same time, Hamer adds, That doesnt mean there arent specific pathways, because there has to be some sort of a pathway in the brain that controls sexual orientation. We know, for example, that the reason you become a male or a female is very simple: If you have a certain gene on the Y chromosome, you will produce male hormones, and if you have those you make a penis and scrotum and you become male. Accordingly, Theres probably some pathway in the brain that does same thing for sexual orientation, but were not going to discover it from genetics The answer will probably emerge from some sort of very sophisticated brain and developmental studies.

For 35 years, Hamer accumulated experience as a scientist at the National Institutes of Health in Bethesda, Maryland. That period is behind him. He doffed the white coat and now lives in Hawaii, where he makes films. But even if hes no longer occupied with research, it still occupies him.

Hamer: Back in the 1990s, I, along with all the scientists involved, believed that if we did good genetic studies wed find the important genes. For example, well find a gene that is responsible for the production of testosterone, and if its functioning was low, it would be possible to say that this is the cause of homosexuality in a particular person. But it turns out that it doesnt work that way. For every mental trait that has been studied everything you can imagine in the brain, for every single trait, theres a [vast number of] genes not to mention a host of complex societal and environmental factors.

For his part, Hamer has much praise for the Broad Institute study: The new GWAS study is really important, because for the very first time they used a huge sample and they mapped every inch of the genome. And this has never been done before. All the other studies were much smaller, or used many fewer genetic markers. But he also demurs: Whats very important is to look at what they actually analyzed. They didnt analyze people who were gay or lesbian, but anyone who had one single same-sex experience, which is quite different... They were measuring something more like openness to sexual experimentation.

As Hamer sees it, If you look for those five markers, or even just the three strongest markers, they are not necessarily found in people who actually identify as gay or lesbian. If you take people who are gay, like me, and look for those markers theyre not significantly there.

Hamer thinks that the whole field is lagging behind because of insufficient research, owing to the stigmas that plague the subject. I dont think sexuality is any more complicated than many other areas of human personality and individual differences, he observes, noting, We formally established that male sexuality is something that is deeply ingrained in people, its not any sort of choice really. It starts really early in life, and it has a major biological component to it. But, how it works? What the biological component is? Were completely unaware and dont know anything, and we barely know more than we did 25 years ago, or in the 1940s, when Kinsey did his work, to be honest.

Hamer was referring to biologist Alfred Kinsey, who in 1948 stunned the American public with his book, Sexual Behavior in the Human Male, which addressed previously taboo subjects, and challenged the traditional beliefs and existing knowledge about human sexuality. Kinsey had conducted a survey of men, which found that 37 percent of his subjects said they had undergone a homosexual experience of some kind, and 10 percent said they had been exclusively gay for three years of their adult life a statistic which to this day is generally said to represent the proportion of people engaging in same-sex behavior.

At the same time, subsequent studies reveal that the percentage of people who define themselves as exclusively homosexual is far lower, though it fluctuates from one article to the next. For example, a 2011 survey of nine different studies on the subject revealed that approximately 3.5 percent of Americans identify themselves as gays, lesbians or bisexuals. A poll involving 1,000 Jewish Israelis in 2012 found that 11.3 percent of the male respondents and 15.2 percent of the female ones said they felt an attraction to members of the same sex. However, only 8.2 percent of the men categorized themselves as gay or bisexual, while 4.8 percent of the women said they were lesbian or bisexual.

For his part, Ganna, of the Broad Institute, understands some of the criticism of his research. What we studied is not related directly to the biology, but to extended environmental factors related to it. Its not about our sample size once you have a lot of individuals, you can capture very small effects. But are these directly influencing same-sex behavior, or other things related to this topic? As a medical example, think about a study that looks for associations between genetic markers and lung cancer. In that example, what we found are genetic variants regarding how much you smoke, which is related to lung cancer.

One of the lessons, and one of the most interesting points arising from the study has to do, says Ganna, with the mode of measurement that had been in use since 1948, when Kinseys scale ranked individuals as being between 0 (totally heterosexual) and 6 (totally homosexual).

Ganna: Basically, the tendency is to locate individuals on a continuum. You can supposedly be anywhere between 100 percent heterosexual to 100 percent homosexual, which implies that the more youre homosexual, the less youre heterosexual, and vice versa. We show that this assumption actually doesnt hold water: When we look at the genetic data, its not that straightforward, theres no simple continuum of sexuality.

So, actually, you are refuting the Kinsey scale?

Ganna: Thats exactly one of our conclusions. What were now doing is, rather than asking people to put themselves on a scale somewhere between being exclusively heterosexual or exclusively homosexual, we ask them how much theyre attracted to men and women. You could be attracted to either of them, very attracted to both of them or to one more than the other. And that information will be crossmatched with genetic markers.

In the final analysis, he adds, We showed that this is just another natural human variation. Sexual orientation, similar to many other behavioral traits, is complicated and is composed of different factors. The interesting thing is how genetics and environment work together. If you think about how much more prevalent same-sex behavior has become lately, people engage in it more than in the past. And thats clearly not because our genetics are changing. Its because of the environment, because society is becoming more open and laws are changing.

Further research should focus on the relationship between environmental factors and genetics, Ganna says, and on how they interact. Its somewhat misleading to think of nature and nurture as separate aspects; they both contribute. So, it would be wrong to say that you can use only DNA to predict if someone will engage in same-sex behavior, but you also cant say its simply a [matter of] choice.

In summary, he says, I think that the more people who will understand that there are genetic and environmental components to sexual behavior, the better and this is a message that goes beyond just sexuality.

Choice and lifestyle

However, the relationship between science and the environment, and particularly the people living in it, is a complicated one. The subject definitely should be studied, but the social aspect of it is problematic, says LeVay, the neurobiologist. I am gay myself, and I feel strongly that gay people should be valued and accepted into society, regardless of what caused their sexual orientation. I dont think its vital for gay liberation to prove that gay people cant help but be gay there are plenty of other reasons [for accepting them], including basic human rights.

At the same time, he adds, this issue is socially relevant, because of traditional notions that see same-sex relations as a choice, a lifestyle or sinful behavior.

In recent years, there have been many studies showing that peoples attitudes toward homosexuality are closely tied to their beliefs about what makes people gay, says LeVay, citing a survey that showed there was a high probability that people who think homosexuality is a choice will object to a gay person being their childrens teacher which in a way might make sense, he adds: If you think being gay is something infectious, socially contagious, and you didnt want your kid to be gay, then you wouldnt want their teacher to be gay ... It follows that demonstrating that biological factors are involved, helps counter those ideas. Still, Im a bit ambivalent about the use of this type of research as some sort of a political weapon in the struggle for gay rights.

The Broad Institute study contains a reminder of the problems and stigmas that still exist with regard to the LGBTQ community. One of the parameters it considers are genetic correlations between genes that are ascribed to homosexuality, and certain psychological problems.

Bailey, the psychologist: One thing that was perceived as controversial, was to look for and find a genetic overlap between homosexual sex genes and genes associated with depression. Its not the same as saying all people who engage in homosexual sex are depressed for genetic reasons, but its also not something that can be easily ignored. There are assumptions that the higher rates of depression among gay men and lesbians is due to the way they are mistreated by society, but the evidence for that is not so overwhelming. There is also the fact, for example, that you have as high a rate of depression among homosexual men in the Netherlands, which is very tolerant, as you have in some less tolerant places, like the United States.

Ganna, for his part, tries to soften that criticism: Even if we see genetic overlap, or correlation, it is not set in stone that weve found a biological mechanism that causes depression and same-sex behavior, he says. There are many explanations for why this one genetic marker is associated with both things. But finding these correlations help us study human traits in general.

In the meantime, there is a price to be paid for conducting research in this realm, which all those involved must be aware of. Reminders of this abound, and are almost routine. In some cases whats at stake is not even a groundbreaking study or one of tremendous scientific importance. In 2017, for example, two researchers from Stanford published an article stating that gay men are predicted to have smaller jaws and chins, slimmer eyebrows, longer noses, and larger foreheads; the opposite should be true for lesbians. In the next stage, they created a facial-recognition program with the aid of more than 14,000 images taken from a singles site of straights and LGBTQs. The program was able to distinguish between gays and lesbians and heterosexuals with an accuracy of 81 percent for men and 71 percent for women, in contrast to an average rate of successful human guesses of 61 percent and 54 percent, respectively. Even though the program achieved relatively impressive results, the study as such drew widespread criticism not unusual for researchers engaged in such studies.

The Stanford gays identification program may be an extreme example, in this respect, but its also a byproduct of the considerable surge in studies in this field, a trend that began in the early 1990s. Together with the scientific community, media interest in the subject of same-sex orientation and its causes has contributed substantially to transmitting messages and shaping public opinion.

In the United States, this can be seen in a series of polls conducted by Gallup, Inc. The first one, conducted in 1977, found that only 13 percent of the respondents believed that homosexuality is an innate tendency, while 56 percent attributed it to environmental factors. This approach remained largely constant until the period between 1989 and 1996, when the rate of those supporting the innate thesis leaped from 19 percent to 31 percent; by 2001, it stood at 40 percent. Almost a decade and a half later, the annual poll produced, for the first time, a larger proportion who agreed with the innate argument. The latest survey, from the end of last year, showed this trend continuing: More than half of the American public believes that gay people are born with their sexual orientation, whereas only 30 percent attribute it to environmental factors (10 percent said both factors play a part, 4 percent cited other factors and 6 percent said they werent sure).

Changes in the perceptions of the origins of sexual orientation are having a pronounced effect on the struggle LGBTQ individuals are waging for equal rights. The latest Gallup poll shows that an absolutely majority (88 percent) of those who believe that homosexuality is an innate trait also support legitimizing same-sex marriages. In contrast, most of those who see this orientation as being environmentally driven (61 percent) are against.

When it comes to public opinion, which is very important, the born this way idea has been really resonant and has had a very positive impact on society, Hamer maintains. Public opinion polls asked people whether they think [gays] were born this way or not, and we know that believing that homosexuality is innate correlates with having positive feelings toward gay rights. Overall, its been important in educating the public about who we are, as gay people.

Such messages are reaching Israel as well. A poll conducted by the Dialog Institute for Haaretz at the end of 2013 found that 70 percent of those questioned favored full rights for same-sex couples, while 64 percent specifically backed their right to surrogacy. However, two polls conducted in the wake of the surrogacy law protest in July 2018 presented slightly lower numbers: About 57 percent of respondents expressed support for the right of same-sex male couples to surrogacy.

These polls did not ask Israelis whether they believe the origin of same-sex orientation is innate or environmental. If you ask Bailey, though, that doesnt really matter.

Ive gone to great lengths to try to persuade people not to base equal rights for gay people on the causal hypothesis, he says. Its a terrible idea to say gay people should have equal rights because they were born that way. Its terrible in part because some criminals might be born that way, and you dont want to them to have the same rights. Being gay doesnt harm anybody, other than people who are close-minded and easily offended. Preventing people from expressing their homosexuality is quite destructive for them. Thats true whether gay people are born that way or not.

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Is sexual orientation genetic? Yes and no, an extensive study finds - Haaretz

The women of the 19th-century urban poor were at it. Sneaking around, getting some. That, anyway, is the conclusion drawn from some recently reported DNA research, published in the journal Current Biology.

The authors of the paper compared the Y chromosomes of 513 pairs of men who supposedly share a common ancestor to determine the prevalence of what they called extra-pair paternity over the past 500 years in other words, the number of times in the mens family trees that the father named on the birth certificate wasnt the same as the man who supplied the sperm.

For most of the period, the rate was stable at one in 100. But the researchers analysis identified a spike in the 19th century, when the level went up to six in 100. What caused this? The Industrial Revolution.

While procreation stayed closely tied to marriage bonds in the countryside, the rapidly increasing urban population lived in an intimacy with each other that made sex outside marriage more possible that ever before. This was reported as an uptick in adultery, although the researchers acknowledged that sexual violence played a part too: not every extra-pair paternity event was consensual.

Theres an inevitable glint of salaciousness in the way this has been reported. And the idea of the Victorian woman loosening her stays for a passing fancy fellow, then presenting the resulting baby to her clueless husband as his own, has a certain piquancy to the kind of man who hangs around on internet forums inveighing against the general untrustworthiness of females.

As presented, extra-pair paternity sounds like a kind of con that modern science can at last unravel, the cuckoos in the nest finally revealed and the unhappy chaps who raised another mans child made subject to retrospective sympathy.

But such a view forgets that life for women in the urban working classes was precarious at best (something that the historian Hallie Rubenhold has written about movingly in her book The Five, a group biography of the victims of Jack the Ripper). The available jobs were poorly paid and unreliable. To be a woman alone was to skirt along the bleakest fringes of existence; to be a woman alone with a baby was to have almost no prospects at all. The imperative was to find a man who could provide some legal standing, some financial security and some social shelter in an inhospitable world.

Did all the men raising children who werent genetically their own know? Of course not. But many would have done and though the researchers may be correct that extra-pair paternity is little studied from a genetic standpoint, the private mythologies of families abound with these stories, few of which sit safely within the prudish label of infidelity.

The parlour maid whose master ruined her, but set her up with a dowry with which she could be safely married off to a male servant. The deserted woman who supported herself and her children with a makeshift procession of temporary husbands of no lawful status.

And, yes, the one who was having a good time and got away with it. Marriage is a patriarchal invention and nothing the patriarchy made was ever done in womens interests: marriage exists precisely because men sought to control the female body and not all female bodies have submitted easily to that control.

The untidy true story of paternity is really the story of how insufficient our institutions can be when they try to contain the messy truth of human feelings. Desire will defy lawful bonds, brute survival will best romance, and love those fathers who cared for their sons, regardless of extra-paternity events will refuse the mean calculus of genetics.

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Whos the daddy? Difficult to say in Victorian times - The Guardian

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Researcher Tom Cappola tells us about the latest clinical trials and medical breakthroughs to be announced during Scientific Sessions.

Chief of the cardiovascular medicine division in the Perelman School of Medicine at the University of Pennsylvania, Tom Cappola.

For the first time in its near 100-year history, the American Heart Association (AHA)will host its annual meeting in Philadelphia. AHAs Scientific Sessions is the largest cardiovascular meeting in the United States. On November 16-18, the meeting will attract nearly 18,000 attendees from more than 100 countries to the Pennsylvania Convention Center, and an additional two million medical professionals who will participate virtually in lectures and discussions about basic, translational, clinical and population science innovations aimed at reducing disability and deaths caused by cardiovascular disease and stroke.

The American Heart Association is excited to be in Philadelphia, said Michelle Kirkwood, director of National Science Media Relations for AHA. It has been on our wish list for some time, especially since the renovations at the Pennsylvania Convention Center and the citys landmark, robust nonsmoking laws that align directly with the American Heart Associations health and wellness goals. We are excited for our thousands of attendees to visit Philadelphia.

More than 610,000 people die of heart disease in the United States every year, according to the CDC. While heart disease is a leading cause of death for both men and women, it claims the lives of over 400,000 American women each year, or one death every 80 seconds. During the three-day meeting, more than 12,000 leading physicians, scientists, cardiologists and healthcare professionals in the global cardiovascular health community will host 850 educational sessions and more than 4,100 original research presentations to unveil the late-breaking science, clinical trials, and novel therapeutics and pathways that are shaping the future of cardiovascular care.

Its very fitting for Scientific Sessions to be here, chief of the cardiovascular medicine division in the Perelman School of Medicine at the University of Pennsylvania Tom Cappola said. We have the first medical school in the country and the first teaching hospital in the country. It makes sense that these new innovations would be presented in a place where theres already been so much innovation.

Cappola will be one of several Penn researchers leading the Cardiovascular Expert Theater, Innovations in Cardiovascular Therapies session during the meeting. Here are just a few big trends in heart care that Cappola says we can expect to learn more about during this weekends meeting:

Using artificial intelligence to monitor heart health

Artificial intelligence (AI) is having a big impact on cardiovascular care. Results from two preliminary studies to be presented this weekend will show AI can be used to accurately examine electrocardiogram (ECG) test results to possibly predict irregular heartbeat and risk of death. There will also be a presentation on the Apple Heart Study, which found that the Apple Watch and other wearable remote monitoring devices may be capable of detecting atrial fibrillation (aFib), an irregular and often rapid heartbeat that can lead to blood clots, stroke, heart failure and other complications.

Identifying new risk factors for aFib and stroke

George Mason University researchers will present results from two studies that found young people who smoke marijuana regularly have an increased risk of stroke. According to the study findings, young adults between the ages 18 and 44 who reported frequent use of marijuana, cigarettes and e-cigarettes were three times more likely to suffer stroke than young adults who did not smoke marijuana at all. The study also found that African-American males between the ages of 15 and 24 faced the highest risk of being hospitalized for arrhythmia.

In one Penn study to be presented this weekend, researchers found women who are diagnosed with peripartum cardiomyopathy (PPCM) during late pregnancy or within a month following delivery are more likely to experience restored cardiac function and improved outcomes compared to those who are diagnosed later in the postpartum period. The findings underscore the need for increased awareness and monitoring of heart failure symptoms, particularly among black women, who, on average, are diagnosed significantly later than white patients, according to study results.

Making advances in genetics and genomics

Another big trend at this years meeting will be the continued advancement in genetics and genomics, and how thats impacting cardiovascular care.

I think that genomic medicine has arrived and its arriving in waves, but it will ultimately affect all aspects of cardiovascular care, Cappola said. We have lots of people getting their 23andMe for sort of recreational purposes and they dont know what to do with it. But were starting to figure out what to do with that genetic information to improve care.

Another Penn Medicine study to be presented during the meeting will show why taller people may have an increased risk of developing atrial aFib. The research found a strong link between the genetic variants associated with height and ones risk for AFib, for the first time demonstrating that height may be a causal not correlated risk factor for the condition. Researchers hope insight from human genetics in large studies like this one will help them better understand causal risk factors for common disease.

It takes expertise to find links like this. Thats why researchers go to the American Heart Association meetings. You get all the experts together, they share their knowledge and this helps us to actually figure out what to do with this genetic information, Cappola said. Thats true across the board, but its particularly important for genomic medicine as it continues to advance.

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The American Heart Association's Annual Conference Comes to Philly This Weekend - Philadelphia magazine

Heres a batch of fresh news and announcements from across Imperial.

From a study showing a genetic link for obesity, to a new centre for wildfire research, here is some quick-read news from across the College.

An international team has discovered a new genetic link for a type of obesity which affects pathways in the brain as well as in the pancreas.

Caused by mutations in a single gene called MRAP2, the condition is associated with excessive hunger and linked to early onset diabetes and high blood pressure.

Professor Philippe Froguel, who worked with French researchers in Lille on the discovery, hopes the findings could lead to new treatments targeting the MRAP2 protein. He said: Discoveries such as these could help to tackle genetic forms of obesity. Finding the genetic basis is the key to targeting excessive hunger.

Froguels team previously identified the MC4R gene and a treatment to activate the protein and affect appetite. The treatment is expected to become available from next year.

Read more in Nature Medicine: Loss-of-function mutations in MRAP2 are pathogenic in hyperphagic obesity with hyperglycemia and hypertension

When it comes to asthma, neutrophilsmay not be the bad guys people thought they were.

Severe asthma is caused, in part, by inflammation of the branching airways inside the lungs which makes it hard to breathe. White blood cells called neutrophils are a major component of this inflammation, and researchers previously thought these cells were driving much of the lung damage and ensuing symptoms.

But new research fromDr Robert SnelgroveandDr Dhiren Patel, from Imperials National Heart and Lung Institute,hasfound that neutrophils are not all bad in the context of asthma. They show targeting neutrophils can also have a negative effect, as they have a regulatory role over other inflammatory cells in the lung.

Read the full paper in Science Immunology: Neutrophils restrain allergic airway inflammation by limiting ILC2 function and monocytedendritic cell antigen presentation

Professor Ricardo Martinez-Botas, from the Department of Mechanical Engineering, has received an Honorary Doctorate in Engineering from Universiti Teknologi Malaysia (UTM).

Professor Martinez-Botas is the co-Director of UTMs Centre for Low Carbon Transport (LoCARtic) and has supervised more than ten PhD students from UTM and other institutions in Malaysia.

In 2018, the Prime Minister of Malaysia Tun Dr Mahathir bin Mohamad visited Imperial and toured Professor Martinez-Botass Turbo Group lab, learning about the latest developments in low-carbon transport and electric motors, as well as major collaborations with UTM.

Matoha Instrumentation, founded by Imperial scientists and entrepreneurs, has won an Institute of Physics Business Start-Up Award.

The company make technologies that quickly and cheaply analyse the chemical composition of materials that visually look the same, allowing them to be more easily sorted for recycling. They have made two platforms: one that identifies and analyses plastics, and one that works with fabrics.

The technology uses a combination of near-infrared spectroscopy and machine-learning algorithms to continuously improve performance. The small and low-cost nature of the technology means it can also be used where larger, automatic detectors are not feasible, instead providing a better pair of eyes to manual sorters. The team behind Matoha Instrumentation previously won the Faculty of Natural Sciences Make-A-Difference competition.

Read more on the Institute of Physics website

The Equality, Diversity and Inclusion Centre marked the end of Black History Month and six years of the IMPACT talent development programme for Black, Asian and Minority Ethnic (BAME) staff with a special reunion event. Delegates and mentors, old and new, gathered at the event to reflect on and celebrate their time on the programme.

Gabriella Gordon-Kerr, Equality, Diversity and Inclusion Coordinator, has been at the helm of the IMPACT programme since it started in 2014. She said: It was great to gather our delegates and mentors in one room, and to reflect on the success of the IMPACT programme. At our reunion event, we looked at the history of the programme and heard stories of progression from delegates.

We asked delegates to sign a guest book on the day, and one of the quotes that resonated with us said: IMPACT has left an ever-lasting impact on my life in more ways than one. Heres hoping to another great six years.

BBC Security Correspondent Gordon Corera presented the 10th Vincent Briscoe Lecture of Imperials Institute for Security Science and Technology this week.

He spoke of the intertwining history of technology and espionage over the last century, from the most classified heart of the national security state. From Bletchley Park through the Cold War to Google and Huawei he explored how data, encryption and computers transformed what we think of as secret and what this means for us.

This marks the tenth anniversary of the lecture, which was named in honour of Professor Vincent Briscoe, a distinguished inorganic chemist at Imperials Department of Chemistry.

Dr Jackie Bell has won the Rising Star Award from WISE a campaign that promotes the work of women in STEM.

The annual awards recognise inspiring individuals who actively promote these subjects to girls and women. Dedicated to raising aspirations and changing peoples beliefs that science isnt for them, Dr Bell has given talks to schools and community groups across the UK, and helps Imperial and other institutions develop inclusive community outreach approaches.

Jackie is currently developing the Department of Computings outreach strategy, committing to at least 50 per cent female participation for all activities. Jackie said: Im a strong supporter of the WISE Campaign and all that is being done to achieve gender balance. To have my work recognised like this is an honour and winning the Rising Star award has given me a greater platform to bring about positive change.

Imperial held the launch of a new research centre studying the science and impact of wildfires. Speakers from the Leverhulme Centre for Wildfires, Environment and Society were joined by Marc Castellnou, a Strategic Fire Analyst working with Bombers de Catalunya (Firefighters of Catalonia), who warned that warm and wet winters, followed by extremely hot summers are a perfect storm for the most dangerous wildfires.

Historically common in Mediterranean countries, evidence shows these conditions have arrived in the United Kingdom, Ireland and Scandinavia as a result of climate change. The Centres new Director, Imperials Professor Colin Prentice, said, We need a better understanding of how and why wildfires occur, knowledge to make seasonal forecasts, and an urgent need to understand how to live with wildfires.

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Gene targets for obesity and wildfire research: News from the College | Imperial News - Imperial College London

On September 7, 1936, the last Tasmanian tiger died in captivity in Hobart's Beaumaris Zoo.

Or so we thought.

Last month, Tasmania's Department of Primary Industries, Parks, Water and Environment released a document that revealed Australian citizens have been reporting Tasmanian tiger sightings. In the last two years, there have been eight reported sightings; the most recent was in July.

The tiger was a member of the Thylacine family of carnivorous marsupials. It was recognizable by its yellow-brown fur and a pallet of black stripes across the lower back and tail (hence the tiger moniker).

Tasmanian tigers preyed on kangaroos, wombats, and occasionally sheep and livestock, which brought them into conflict with British colonists who settled in Tasmania in 1803.

Some 130 years later,the last wild Tasmanian tiger was thought to have been hunted to extinction.

Here's everything we know about the elusive animal and why some experts and hunters think it may not be extinct after all.

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The Tasmanian tiger is thought to have gone extinct in 1936, but mysterious sightings suggest the creature might still be out there - INSIDER

14 November, 12:50pm

On a crisp Port Elizabeth morning, 14-year-old Mike Willemse stood gawping pitchside, utterly transfixed by a schoolboy monster, claret gushing from his face and fury burning in his eyes.

As a junior pupil at the storied Grey High, Willemse was expected to brandish the school flag and roar on the older students in their ferociously contested matches.

South African schools rugby is a ruthless proving ground. Enormous teenage specimens, not all of them purely the product of extreme toil and fortunate genetics, lock horns on paddocks as hard as granite against the backdrop of unyielding pride and tradition that dates back decades.

There was one boy who stood above them all for Willemse. It was on that morning that the young hooker first laid eyes on Siya Kolisi, the snarling township urchin who would become a World Cup-winning captain.

Kolisi was not yet 17, but already there was an avalanche of hype building around this back row phenomenon. The kid was a colossus, a schoolboy encased in the body of a giant.

(Continue reading below)

Siya was captain of the under-16 As and he got hit in the mouth and he was bleeding, Willemse told RugbyPass. I just remember him grabbing the ball and not even caring, bouncing guys and carrying on.

He completely dominated, brushing through players like they werent even there. Hed come on for the last 15 minutes to win games for us. Honestly, wed have people from other schools coming to watch our games instead of their own teams just because of Siya. He was incredible.

Since the Springboks glorious triumph in Japan, the astonishing story of Kolisi has been told and retold. The flanker had been reared in obscene poverty, left school aged 10 to look after his ailing grandmother, suffered the most heinous bereavements and spoke not a word of English before winning a bursary to study and play at Grey.

His impact, even in those days, went well beyond what he did on the pitch. Because he had played and done so well for so long, the whole school respected him, explained Willemse. He was a prefect, house captain and whatnot.

And also just being a player of colour of that stature at that time was very inspiring for a lot of people. The way he did things was inspiring for everyone. Through that, he gained so much respect and he handled it well. Thats why he was a leader.

Everyone was in awe of him. He was a seriously good player and a natural-born leader from the get-go. He made his first-team debut at grade ten, so he was playing three years above his age. You dont often hear of that in South African schools rugby.

The way he dominated the schoolboy rugby scene is what people talk about sometimes more than how he is playing now. He was probably the best schoolboy rugby player anyone had ever seen.

I only really got to know him very well after school because at school you stay in your age groups. He was my dorm prefect and often you dont really build a tight connection with your prefect. They instil discipline and that is what he did very well.

After their school days, Willemse and Kolisi played together with the Stormers and became close friends. The Edinburgh hooker has heaps of mates in Kolisis group of immortals. In his days at Newlands and with the Southern Kings, he played alongside Steven Kitshoff, Makazole Mapimpi, Duane Vermeulen, Bongi Mbonambi, Cheslin Kolbe, Lukhanyo Am and a pile more besides.

On the morning of the World Cup final, Edinburgh were in Treviso preparing for a PRO14 match against Benetton. That didnt stop the hulking South African contingent threatening to reduce the team hotel to rubble as the hammering unfolded not least because their coach, Richard Cockerill, is typecast as the very depiction of the pugnacious Englishman.

They thought after the All Blacks game they had already won it. But the whole of South Africa just had a quiet confidence about us, said Willemse.

It was life-changing for them and for SA as a whole. What Rassie Erasmus has done and the way the players have bought into what he was trying to do was seriously special. You can see the determination to stick to that plan and do damage with it.

Compared to the horrors of Kolisis upbringing, Willemse has not seen true hardship. But in a pure rugby sense, he has known extreme deprivation. For four seasons, some as captain, he grafted for the Kings, a team hopelessly handicapped by its meagre budget, ramshackle infrastructure and the bruising annual poaching of its top assets.

After being booted out of Super Rugby in 2017, they and the Cheetahs found a home in the PRO14. The Kings have won only four games out of 48 since.

In Willemses time, they had few of the modern tools that professional teams regard as a given no GPS units, and only a handful of backroom staff. During pre-season, their search for a new head coach became so compromised by leaks, controversy and unseemly public malcontent that it had to be aborted.

The scary thing about it is that because you know you dont have the gear and the support staff all of the teams over here do, the minute something goes wrong, its so easy to look for excuses, explained Willemse.

It was so easy to look elsewhere and not at ourselves. We were almost mentally oppressed. As much as we were saying we could do it, I dont think we really believed we could. That was the biggest struggle.

Youre losing games week in, week out. Its tough to try and get guys up for it. Youve got to take it down a whole lot of levels and look at the smaller things and be positive about things you did well on the field.

There were no chartered planes for the Kings squad on their tours of the north. In fact, the travel itineraries often read like extracts from Christopher Columbus diary, leaving players stiff and exhausted on the eve of matches.

Youre leaving on the Tuesday to play on the Saturday, flying from Port Elizabeth to Johannesburg, Johannesburg to Istanbul, Istanbul to Heathrow, and from there youre either flying to Scotland or Ireland or bussing it to Wales.

You couldnt train the next day. You almost lost three or four days of training. Wed have a captains run to try and freshen up and then you have got to play. I dont care what you say, you cant be as physically up for it in those circumstances all the time.

We tried as best as we could, we tried to get decent enough hotels with pools and saunas to make an effort with recovery, but you can only do so much before fatigue sets in. A lot of our games we were up for it in the first half and come the last 40 we were completely off our feet.

Willemse is better for the chaos he endured but grateful that it is now behind him. In Edinburgh, the hooker has joined a cleverly assembled squad with a mountain of depth and designs on the PRO14 play-offs.

After winning four of their first six league matches, they begin their European Challenge Cup voyage in Agen this Friday, before Bordeaux-Begles come to Murrayfield a week later. The fact that Edinburgh are competing in the second tier having scalped Montpellier and Toulon and reached the giddying heights of the Champions Cup quarter-finals last season is a trifle embarrassing.

But the group Cockerill has built this time around is far better equipped to compete on two fronts. With Matt Scott and Mark Bennett fit and flourishing in midfield, Edinburgh are finding extra gears in attack, the pack is rumbling around with its typical venom, and the World Cup contingent are being steadily filtered back into contention.

Edinburgh werent as attack-minded last year as they are now. Theres real excitement about our attack, our counterattack, Willemse said. Our backs are really making an impact on the game and we know from previous seasons how good the pack is. Thats what Richard expects and demands from us.

The pack really grinds a lot harder than anyone else in training and rightly so, because youre doing a lot more than anyone else on the field.

Weve got ourselves in a good position and weve yet to reach our full potential. Now that the internationals are making their way back into the team, weve created so much depth that its really exciting we can hopefully make a claim to play-offs and go further from there.

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'Siya got hit in the mouth at school and was bleeding... I just remember him bouncing guys and carrying on' - RugbyPass

Every superhero's life can get complicated, and the same could be said for their families. That holds especially true in the world of the X-Men, which features more time-traveling, alternate dimensions and clones than any other major superhero franchise.

From the earliest days of the franchise to Johnathan Hickman and Leinil Francis Yu's ongoing run on X-Men, Cyclops has been one of the franchise's most consistent core characters. Naturally, Scott Summers has amassed quite a family during his adventures with the rest of Marvel's mutants. Now, we're going to break down the rest of his very extended family from across the Marvel Multiverse to see who knows who in this family of mutant royalty.

RELATED: The New Mutants Are Betrayed By a Classic Marvel Team

Major Christopher Summers was am Air Force pilot, who, on one fateful day, had his aircraft shot out of the sky by the Shi'ar. This plane crash would forever alter the lives of his children, Alex and Scott Summers. After the crash, Chris and his wife, Katherine Anne were taken to the Shi'ar Imperial Throneworld of Chandilar, where Katherine was murdered by Emperor D'Ken.

While imprisoned, Chris met Cho'd, Cr'reee, Hepzibah, and Raza. Together, they escaped and formed the Starjammers, a group of space pirates who sought vengeance on the Shi'ar starting in Chris Claremont and Dave Cockrum's Uncanny X-Men. Chris became Corsair, the swashbuckling leader of the group and years later, he was reunited with his sons, Scott and Alex. During Ed Brubaker, Billy Tan and Clayton Henry's "The Rise and Fall of the Shi'ar Empire" arc i, Corsair was seemingly killed by his long lost son, Vulcan. However, he appeared alive and well in the short-lived ongoing series Cyclops, where he spent time roaming the galaxy with a time-displaced version of Scott.

When Corsair's plane went down, Alex held onto Scott as the brothers jumped out of the plane. When the two were found, Scott became comatose as a result of his head injury, and Alex was placed in an orphanage. Alex was soon adopted by the Blandings, a family who tried to mold Alex into the memory of their dead son, Todd. During this period in his life, he discovered his own mutant powers.

After Arnold Drake and Don Heck introduced him to the X-Men, he reunited with Scott and went on to become an X-Man of his own. As Havok, he played a part on the main X-Men team and adjacent teams like X-Factor. During the aftermath of Brubaker's "The Rise and Fall of the Shi'ar Empire," he became the leader of the Starjammers, taking his late father's role. While Havok has been manipulated into becoming a villain more than once, he's also led the Avengers and currently lives with the Summers family on the Moon.

RELATED: Marvel's X-Men are Making Black Panther a Future Enemy

For years there were inklings of a third Summers brother, but it wasn't until Ed Brubaker and Trevor Hairsine'sX-Men: Deadly Genesis that readers learned the truth about him. Gabriel Summers, also known as Vulcan, was the Summers brother no one knew existed --and Charles Xavier wanted it to stay that way. When Corsair and Katherine Summers were captured, Katherine was pregnant with Gabriel. The fetus was removed from Katherine's body and placed in an incubation accelerator, allowing Gabriel to reach adolescence at an accelerated rate. He was sent to Earth to become a slave for Erik the Red but was found by Moira MacTaggert instead. Moira took him in and soon, Charles noticed his existence as well.

Alongside Petra, Darwin, and Sway, Vulcan became an X-Man and was tasked with a mission to rescue the original X-Men from Krakoa. The mission went awry, and Gabriel developed a deep hatred for the Summers clan after he was left adrift in space. Charles Xavier even wiped all memories of Gabriel from Scott's mind. For a while, Vulcan served as a major cosmic villain, ruthlessly ruling the Shi'ar Empire and wreaking havoc on his family members in various ways, even killing Corsair. Now, he lives at the Summers' lunar base, seemingly on good terms with his once-estranged family.

Jean Grey and Scott Summers' romance started all the way back in the early years of X-Men comics, becoming something of a staple for the series. After 1980's "Dark Phoenix Saga" ended, Jean Grey was thought to have died. However, then the hear-broken Scott met Madelyne Pryor, the genetic clone of Jean who was created by Mister Sinister. Sinister wanted to carry on the Summers/Grey bloodline, so he used Madelyne to make that happen, although neither Scott nor Maddie herself was initially aware of this.

Out of grief, Scott retired from the X-Men and moved to Alaska to settle down, engaging in a whirlwind romance with Madelyne Pryor. Noting her striking resemblance to Jean, he found himself questioning who she was. His suspicions certainly weren't helped by the fact that she had gaps in her memory. Nonetheless, the two wed and eventually, they had a son, Nathan Christopher Summers.

RELATED: X-Men: Marvel's Strangest Mutants are the Keys to Dawn of X

For all Scott's talk about moving on and starting a new life, he couldn't quite get his lost first love out of his mind. Scott and Maddie's relationship suffered and by 1986, Jean Grey had returned. Scott rushed to see her, leaving his wife and child behind to join the new mutant team, X-Factor. As it turned out, Jean hadn't died in the "Dark Phoenix Saga" at all --she was merely suspended in a cocoon at the bottom of Jamaica Bay.

While her physical form was healing, the Phoenix had assumed Jean's identity. After theInfernostoryline, a crazed Madelyne (then going by the Goblin Queen) confronts Jean. Jean ends up absorbing the remnant of the Phoenix Force housed inside Madelyne, giving her the memories of both Madelyne and the Phoenix. In 1994, Jean and Scott finally wed but were transported to the future to raise their son, Nathan. Although they were separated by death for most of the 2000s, Scott and Jean seem to have gotten back together.

When Cable first appeared, he was baby Nathan Christopher Summers, the son of Scott Summers and Madelyne Pryor. However, shortly after theInfernostoryline, Nathan contracted a techno-organic virus that was rapidly killing him. In order to save his son, Scott was forced to give him to the Mother Askani, who promised to heal himin a future timeline. Nathan returned to the X-Men from the future around that same time, appearing as the time-traveling, gun-toting Cable. Eventually, it was revealed that Cable was really Nathan, Scott's long lost son. During theExterminationevent, Cable was murdered --by a younger version of himself. This Kid Cable is the one currently found in X-Men comics and he lives at the Summer Home with his family.

Nate Grey --who's also known as X-Man-- is an alternate version of Cable, who hails from the "Age of Apocalypse" reality. Nate is the biological child of Scott Summers and Jean Grey, born from Mr. Sinister's genetic tampering. Unlike Cable, Nate was not infected by the techno-organic virus, allowing him increased telepathic and telekinetic powers. Nate Grey was the antagonist in the recentAge Of X-Manstoryline, where he stayed behind to tend to the universe of his own creation.

Rachel is the biological daughter of Scott Summers and Jean Grey, hailing from the apocalyptic "Days of Future Past" timeline. She was drugged and brainwashed, forced to hunt down other mutants until she broke her own conditioning. Eventually, she found her way into the 616 timeline and after a while, Scott learned of her true identity and came to view her as his own daughter.

RELATED: Marvel's New X-Force Isn't a Team -It's a Mutant CIA

She joined several teams including Excalibur and the X-Men, and formed close bonds with heroes like Nightcrawler and Kitty Pryde. It was later revealed that a future version of Rachel was the Mother Askani who brought Nathan into the future to heal him. In the future, she also has a romantic relationship with Franklin Richards, another incredibly powerful mutant. She takes after her mother, inheriting her powerset and is one of the few mutants capable of controlling the Phoenix force. She currently lives on the Moon with her parents and brother.

Hope was the first mutant born after the Scarlet Witch decimated the mutant population inHouse of M.To some, she was seen as the mutant's messiah, someone who could save their dying race with her mutant power to borrow and activate other mutants' powers.

Eventually, Cyclops put Hope in the care of Cable, wanting to save her from being raised into this world. As such, Cable raised Hope as an adoptive daughter in the future and since then, she has appeared in severalX-Mencomics. Unlike the other characters on this list, she does not have any biological connection to Cyclops or the other Summers, but she is an accepted adoptive member of the family. She currently resides on Krakoa as one of the Five, a group of young mutants who can effectively bring back the dead.

Ruby is the daughter of Scott Summers and Emma Frost, hailing from the dystopian future of Earth-1191. Alongside her father and Layla Miller, she is a founding member of the Summers Rebellion in the same future that Bishop hails from.

Like her father, she can fire force beams from her eyes, though hers are colored black. Similarly to Emma's diamond form, Rubycan turn her body into organic ruby. An alternate version of Ruby was briefly seen in one of the realities inSecret Wars. Unlike the other characters on this list, Ruby still hasn't appeared in the main Marvel Universe, even though she's present in multiple alternate timelines.

KEEP READING: Make More Mutants: A Major X-Men Couple Wants a Baby

Wonder Woman Is Humbled Before a More Powerful Wonder-Woman... From China

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Cyclops and the Summers: The X-Men Family Tree, Explained | CBR - CBR - Comic Book Resources

Apolipoprotein E (APOE) 4 is associated with younger age at ischemic stroke onset but not with stroke outcomes, according to study results published in Neurology.

Previous studies have shown that APOE genotype is a predictor of outcome after hemorrhagic stroke, but there are conflicting data regarding the effect of this genotype on ischemic stroke. In the current study, researchers investigated the interplay among the 3 common APOE alleles (2, 3, and 4), age at ischemic stroke onset, severity, sex, and outcome.

The study cohort included 6165 cases from the genome-wide association study within the Genetics of Ischemic Stroke Functional Outcome network. Effects of APOE allele 4 and 2 were compared with those of the most common allele, 3.

The study revealed an association between increasing allele count of 4 and younger age at stroke onset (P <.001), which was evident in both sexes and in cases with first-stroke only. However, there was no evidence for direct effect of 4 on outcome after stroke as, following adjustment for age and stroke severity, there was no association between 4 allele count and favorable outcome. In men only, there was a statistically significant association between 2 allele count and poor outcomes following adjustment for ancestry, age, and stroke severity.

The researchers acknowledged several study limitations, including those of Genetics of Ischemic Stroke Functional Outcome study that were previously reported, as well as the relatively small sample size for the sex-stratified analyses and use of imputed values from single nucleotide polymorphism arrays to establish common APOE alleles.

This study shows that APOE 4 carriers have a younger age at ischemic stroke onset. We also detected worse functional outcome in male 2 carriers, a result needing replication, concluded the researchers.

Reference

Lagging C, Lorentzen E, Stanne TM, et al. APOE 4 is associated with younger age at ischemic stroke onset but not with stroke outcome. Neurology. 2019;93:849-853

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The Role of Apolipoprotein E on the Age of Ischemic Stroke Onset and Stroke Outcome - Neurology Advisor

By Michael Le Page

Celebrating the Birth by Jan Steen, 1664. The Wallace Collection, London

In the 19th century, poorer families living in cities in Europe had a higher rate of children who werent biologically related to their legal fathers. This is according to a genetic study that looked at how this rate differs for different socio-economic groups.

It is widely assumed many men arent the biological fathers of their children. The rate of extra-pair paternity, as this is called, has been claimed to be as high as 30 per cent today. They look just like the milkman, goes the popular joke that no parent finds funny.

However, over the past two decades DNA studies in several countries have shown the average rate is low around 1 per cent. Maarten Larmuseau at KU Leuven in Belgium, who authored one of these studies, wondered whether there was a difference between groups.

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He suspected, for example, that the rate was higher among aristocrats in the 17th century, as there was often a large age gap between husband and wife. Extra-pair paternity is depicted in the 1664 painting Celebrating the Birth by Jan Steen, which shows a wealthy Dutch father holding his newborn child. But behind him a man is making the sign of the cuckolds horns, meaning the child was fathered by another.

Larmuseaus team identified 500 pairs of men in Belgium and the Netherlands where, according to genealogical records, each pair descended from the same male ancestor through a male lineage. Half of these ancestors were born before 1840 and the oldest was from 1315.

The men in each pair should have inherited their shared ancestors Y chromosome, as it comes from the father. When DNA testing revealed a mismatch, the team tested other male descendants to narrow down when a son had been fathered by someone other than the husband. All the men were volunteers and the team didnt test close relatives to avoid uncovering recent cases.

What we found was completely the opposite to what we expected, says Larmuseau.

The rate of extra-pair paternity among farmers and more well-to-do craftsmen and merchants was about 1 per cent, rising to 4 per cent among labourers and weavers and nearing 6 per cent among working class people who lived in densely populated cities in the 19th century. This was in comparison to a rate of around 0.5 per cent among the more well-off.

What the study cannot reveal is why people were more likely to be in this situation. We cannot give an explanation, Larmuseau says. We cannot interview them.

One possibility is that poorer women in cities were more vulnerable to male sexual violence and exploitation.

The overall rate was still low, at 1.6 per cent per generation. But that still means a very large number of people alive today may not be aware of their biological parentage. Larmuseau says 30 million people worldwide have done ancestry tests, which suggests up to 500,000 could have made a shocking discovery about their father. Companies offering these tests dont provide any counselling, he says.

Journal reference: Current Biology, DOI: 10.1016/j.cub.2019.09.075

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Genetic study reveals the family secrets of people in the 1800s - New Scientist News

Psoriasis in ankylosing spondylitis (AS) is not related to axial psoriatic arthritis (PsA), a type of psoriasis that causes lower back inflammation and pain similar to AS, according to a study published in Rheumatology.

The study included approximately 1303 patients with PsA and 766 patients with AS from 2 Canadian clinics. Of the patients with PsA, 477 had axial PsA and 826 had peripheral PsA. In the AS group, 91 participants had psoriasis and 675 did not.

Patients at both clinics were followed and assessed using a variety of diagnostic tools, with visits every 6 to 12 months for an average of 12.6 years for patients with axial PsA and 6.7 years for the patients with peripheral PsA. The average follow-up for AS with psoriasis was 5.4 years and 3.5 years for those without psoriasis.

The analysis showed that overall, patients with AS were younger at diagnosis, with an average age of 21.3 years in patients with psoriasis and 22.9 years in those without psoriasis compared with axial patients with PsA who had an average age at diagnosis of 34.4 years. There were also more males in both AS groups compared with the axial PsA group.

Spondyloarthritis is a family of inflammatory diseases causing arthritis and involves areas where ligaments and tendons attach to bones. AS is the most common form of spondyloarthritis and mainly affects the joints at the base of the spine where it meets the pelvis.

More patients in both AS groups tested positive for HLA-B27, a genetic marker for inflammatory arthritis of the spine and joints. Of the AS patients with psoriasis, 82% tested positive, while 75% of those without psoriasis tested positive. In the axial PsA group, only 19% tested positive.

Approximately 90% of patients with AS with psoriasis and 92% without psoriasis reported back pain compared with only 21% of patients with axial PsA. Furthermore, compared with patients with axial PsA, patients with AS and with and without psoriasis had a higher grade of sacroiliitis, or inflammation of the joints connecting the lower spine to the pelvis.

When the data were analyzed over time, there was also an increase in joint swelling in both patients with axial PsA and patients with peripheral PsA, whereas patients with AS with or without psoriasis were more likely to have back pain and a higher BASMI, or Bath Ankylosing Spondylitis Metrology Index, a measure of AS disease severity.

The study reveals that axial PsA and AS with psoriasis are 2 different diseases with different genetics, demographics, and disease expression, according to the study authors.

Reference

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Nancy Battick, Special to The County November 14, 2019

Finding the maiden name of a female ancestor can be a challenge. Mens names were recorded in town vital records but the wife was usually listed by her given name only.

Finding the maiden name of a female ancestor can be a challenge. Mens names were recorded in town vital records but the wife was usually listed by her given name only.

Heres the definition of terms Im using: Given name is the first name; maiden name was usually the womans fathers last or surname; the womans married surname was that of the husband. When searching for an ancestors maiden name your success often depends on the time period involved. The census may help but unless a woman was a widow or head of a household, her name didnt appear in our censuses until 1850. Widows were usually listed as Widow Carter. So, how do you go about locating these ladies hidden by history? In this and the following column Ill try to give you some pointers.

In the U.S. Census youll find a wifes name enumerated beneath her husbands, showing her first name and usually an initial, such as Mary C. While C. could be a middle initial it is more often a clue to her maiden name. Assuming the couple didnt move into the town already married, start your search by combing the neighborhood for surnames beginning with C. Check earlier censuses to see if there is a daughter Mary of the correct age.

Also, note all living in the couples household is there a mother, brother, or sister-in-law listed. Note their surname because its most likely the wifes family.

Youre fortunate if the lady youre seeking has a less common first name such as Sophronia. Lets suppose youve found a possible Sophronia and her family. Now check to see if you can find a will or a deed settling her fathers estate. You may find an entry that states the name of the daughter and her husband among the heirs.

Another familiar situation in remote areas was that brothers often married women who came from the same family. If youve exhausted conventional sources, try searching the family tree. Check the marriages of your male ancestors brothers and trace their marriages. Chances are you might find connections. Im researching a line where two brothers married two sisters and another brother married a first cousin of the sisters. This happened more often than realized and unless there was a genetic disposition to certain diseases caused no problems. We all know the jokes about shopping for a wife at family reunions, but it happened, and rare is the tree without a cousin marriage of one degree or the other.

Should your ancestor have moved to your town complete with a family, dont despair. Here in Maine until the late 19th century, most immigrants came from our sister New England states. These states kept detailed records from their earliest settlements so dont be daunted if you learn your ancestor came from Duxbury, Massachusetts. The Massachusetts records are really good. Odds are youll find information on your ancestors marriage.

In my next column Ill have a few more tips in seeking the unknown maiden names of female ancestors.

Columnist Nancy Battick of Dover-Foxcroft has researched genealogy for over 30 years. She is past president of the Maine Genealogical Society, author of several genealogical articles and co-transcribed the Vital Records of Dover-Foxcroft. Nancy holds an MA in History from UM and lives in DF with her husband, Jack, another avid genealogist. Reader emails are welcome at nbattick@roadrunner.com.

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Tips on finding female ancestors - The County

John Plechl survived World War II, moving to Salem and becoming a referee in 1964. At 86, he stays active to keep up with the kids running up and down the field.

John Plechl makes a call during a recent soccer match in Salem.(Ron Cooper/Special to Salem Reporter)

John Plechl watched as the girls junior varsity soccer team from North Salem High School warmed up for their match.

The 5-foot-tall referee with glasses and white hair, standing in a yellow shirt and black shorts, finally gave a sharp whistle and called for the team captains.

After the coin toss, Plechl tells the girls with his German accent, Okay, have a good game.

And Oregons oldest referee goes to work, jogging back and forth on the field, keeping up with the teenage athletes.

For more than 55 years, Plechl has been a fixture on the soccer field, blowing his whistle and doling out advice.

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Plechl was born in former Yugoslavia, before his parents and siblings moved to Germany in 1944 to escape being killed or put in a concentration camp under the reign of Josep Broz, commonly known as Tito.

Plechl started playing goalkeeper in an Austrian league as a teen after his family had moved to Austria a year before World War II ended. Back then, soccer balls were made of leather and heavy.

When it was raining when the ball was coming towards you, the coach said, Dont head the ball when it comes like that, but dont chest it because itll kill you. Plechl said.

They practiced barefoot and when the shoemaker made them leather soccer shoes, Plechl got blisters breaking them in.

In 1955, Plechls family immigrated to the U.S., following Plechls sister, who had married an American soldier.

Plechl remembers his first job, picking up rocks at the future site of the Lebanon High School football field.

He went on to become a tailor, working at Meier and Frank for most of his life, retiring at 67 as the demand for tailoring dwindled.

But he continued with soccer, becoming one of the pioneers of the sport in Salem.

John Plechl has been refereeing in Salem since 1964. (Ron Cooper/Special to Salem Reporter)

At 86, he is one of the oldest soccer referees in the nation, maybe even the world. Plechl is the same age as the Guinness World Record holder, who was the worlds oldest soccer referee at age 83 in 2016.

During peak soccer season, Plechl will referee a game, which typically last an hour and 20 minutes, each day.

He also works out regularly, going to the Courthouse Club Fitness in west Salem several times a week.

Plechl doesnt have a distinct answer as to why he stays involved with the sport, but its clear his passion for the game is the culprit.

What has changed is my immense, immense respect for this man, said Jose Maciel, the commissioner of the Salem Soccer Referee Association Knowing I can give him a call hey I have this game up in Molalla.

And Plechl will typically respond, Oh yeah Jose, no worries.

Over the 15 years Maciel has known Plechl, hes grown to appreciate the referees dependability and willingness to help.

Everybody whos been in the presence of Johnnie in the officiating world has positively been effected by it and it motivates whats going on, Maciel said.

Harry Garabedia got involved in the Salem soccer scene in the mid-1970s when there was only one amateur team the Salem Kickers.

Plechl helped found the Salem Kickers in the 1960s and started refereeing in 1964 at the recommendation of a friend.

In those days, Garabedia said, Plechl was the only referee in town.

He did anything and everything, he said. Anytime you would call John, he was there.

John Plechl referees a recent soccer game in Salem. (Ron Cooper/Special to Salem Reporter)

Dick Horner met Plechl when he played on Salems second mens soccer team, the Hot Spurs.

Horner put down the soccer ball and donned a whistle more than 40 years ago.

Horner said a successful referee must be fit, decisive, knowledgeable about the rules and have the ability to manage people in a stressful situation.

Referees have just over a second to make a call before players and coaches start saying hey, Horner said.

For Plechl, The most important thing for a referee is to be honest. You see something, you have to call the same on them as on everybody else. Most of the people who watch, they recognize that.

He knows almost everyone in Salems soccer community, and if someone doesnt know Plechl then their grandparents probably do, Horner said.

John Plechl makes a call during a recent soccer match in Salem. (Ron Cooper/Special to Salem Reporter)

Most all Plechls family members have played soccer at some point.

Plechls son Kevin coaches the Sprague High School girls soccer team for which his granddaughter plays.

It might be just part genetic, Kevin said.

Kevin Plechl would go out with his dad when he was 11 and be whats now called the assistant referee, raising a flag when a player was offsides or out of bounds.

Kevin said he was young, but he understood the laws of the game well.

There were a few times that he was cussed out as a young guy, he said, but I always felt dad was there to protect me.

The Plechls had season tickets for Portland Timbers games in the 1970s and Kevin remembers piling into a Volkswagen bus with his dads soccer buddies to go to games.

Sometimes its hard to get a word in, his friends will say, but they always see him with a positive attitude.

Honestly if you were to see my dad and hang out with him, you really never see him with any sort of negative attitude or in a bad mood. You dont see him grumpy, Kevin said. He just enjoys being around the game and being around people.

Hes an institution to say the least, Garabedia, the soccer referee, said.

Have a tip? Contact reporter Saphara Harrell at 503-549-6250,saphara@salemreporter.comor @daisysaphara.

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