Asexual reproduction has been one of the most fascinating biological features of some animals, who can reproduce on their own, hence the derivation of the term.

Unlike sexual reproduction, its counterpart does not rely on conventional mixture of sperm and egg for ovulation and fertilization to take place involving two opposite sexes.

In the process called parthenogenesis, dozens of vertebrate species are capable of asexually reproducing, wherein most animals include fish or lizards.

While it has a beneficial effect for survival, a new study found that asexual reproduction can lead to life-threatening genetic mutations.

The new research led by biologists from the University of Texas at Arlington found new details that support the theory that species have more harmful genes as a result of unnatural genetic changes compared to those utilizing sexual reproduction.

While the mutations are also present in offspring that are byproduct of sexual reproduction, the angle that such genetic alterations are present from asexual reproduction is relatively least explored.

With the new paper, the scientists expounded the premise that the genetic mutations are universal but varies depending on the type of reproduction.

(Photo : Photo by YURI CORTEZ/AFP via Getty Images)

In the study published on the journal Evolutionon May 17, the US-based biologists explored the aspect of sexual reproduction of being ubiquitous in the natural world, implying that sex could have extensive benefits to surpass the coast of males relative to asexual reproduction.

The research used a previous hypothesis that the advantage of reproduction based on sexual intercourse is that it removes faulty genetic mutations from the genome.

The theory predicted that a transition from sexual to asexual increases the risk of the accumulation of "slightly deleterious mutations."

In addition, the paper indicated that such transition suppresses recombination and segregation, which weakens natural selection.

Also Read:Male-less Reproduction: Strange Biological Switch Observed In Shark For The First Time

Authors of the study examined Aspidoscelis, a genus of whiptail lizards, as part of parthenogenesis and as summarized by phys.org.

The team also selected the reptiles due to their abundance and distribution throughout the southwestern part of the United States.

The scientists came up with their conclusion after using mitochondrial genome data from both asexual and sexual whiptail lizards.

The method aimed to test whether their prediction that parthenogenetic lineages result in faster genetic mutations than sexual lineages.

Both sexual and asexual reproduction have their own advantages and disadvantages, which some living things utilize to produce their own offspring, according to the University of Utah.

While some species are capable of both reproduction methods, the new research implies there is still limited data that needs addressing.

Although it was reportedly found that asexual production yielded unwanted genetic changes, it can still serve as a significant method when it comes to survivability and mating challenges.

In particular, previous wildlife documentaries and research showed that there are instances where physical sexual intercourse between two animal species is challenging, especially in hostile environments where competition is prevalent.

Related Article:How Certain Animal Species Survives Without Sexual Reproduction

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Asexual Reproduction: Species Reproducing on Their Own are Susceptible to Dangerous Genetic Mutations - Nature World News

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Society faces challenges to feed a growing population with a reliable supply of wholesome food, produced to high standards of safety and welfare. The development and adoption of new technologies such as precision breeding can help optimise the balance between productivity, health and welfare in modern livestock farming systems, says aquaculture breeder Alan Tinch.

It was disappointing that a minority of MPs used last weeks Second Reading debate on the Precision Breeding Bill to articulate their prejudice against modern livestock farming by suggesting that the legislation would be a step backwards for farm animal welfare.

Disappointing, but perhaps not entirely surprising given the high-profile campaigns by organisations such as Compassion in World Farming to draw an (unjustified) association between technological advance and worse outcomes for farm animal welfare.

This isnt a debate about whether or not we should farm livestock. We should be considering how new technology can be used to make farming even more sustainable, and deliberating ways to improve the health and welfare of livestock.

Genome editing itself is neutral in terms of animal health and welfare. It is a scientific tool which enables scientists and breeders to make targeted genetic changes more quickly and precisely, based on our improved understanding of genomics and genetic function.

Margaret Beckett, as Environment Secretary, once observed that opposing genetic technologies was like campaigning against the petri dish in other words, what matters is not the existence of specific scientific tools but the way they are used.

As this legislation progresses through Parliament, I hope that future debates will focus on the potential of the science, and avoid provocative references to cramming animals together in unsanitary conditions (Kerry McCarthy MP a vegan), or to intensive factory farming practices (Caroline Lucas MP a vegetarian).

It is also wrong to associate genome editing with any particular farming system or ideology, just as it is wrong to associate scientific innovation and technological advance with poorer animal health or welfare.

We understand from experience that any advance in our scientific knowledge can be deployed to deliver a range of outcomes. We should assess and deploy new technology to improve systems, not dismiss it because there are potential negative consequences. Overzealous precautionary approaches would have prevented use of new technologies such as the printing press, the steam engine, internal combustion engine, vaccines and others. We now consider the Locomotive Act disproportionate with its requirement to wave flags in front of motorised vehicles.

The development of Covid vaccines in record time is a clear example of how genetic technologies such as GM, genome editing and RNAi have unquestionably been used for the enormous benefit of humankind.

Current plans for the use of genome editing in the livestock sector relate either to human health applications or to improved health and welfare in farmed animals, primarily through improved genetic resistance to diseases such as Porcine Reproductive and Respiratory Syndrome (PRRS) and African Swine Fever in pigs, and avian influenza in poultry.

These devastating animal health conditions are not the result of factory farming, as Caroline Lucas suggests. They do not differentiate between animals kept in intensive or extensive systems.

Concern continues about the spread of avian influenza which is transmitted by wild birds and affects outdoor-reared and backyard poultry, and can potentially mutate to infect humans and begin the next global pandemic. Genome editing to control avian influenza infection in chickens has been proposed by scientists in the UK. How can it be ethical not to embrace and encourage scientific innovation which promises solutions to such devastating disease?

The Precision Breeding Bill itself does not set or change existing standards for farm animal welfare.

These standards are addressed through separate regulations applied at both research and farm level and which rightly focus on welfare outcomes, not on production or breeding methods. They are reinforced at farm level by independently accredited assurance schemes such as Red Tractor and RSPCA Assured.

Still often misjudged by the perceptions of 30 or 40 years ago, farm animal breeding today uses a balanced approach to select for a range of traits which optimise performance, health and welfare outcomes in new strains. Organisations such as the European Forum of Farm Animal Breeders (EFFAB) promote the use of a balanced range of traits in farm animal breeding, and UK breeders supported by world-leading livestock research and animal health institutes such as Roslin and Pirbright are recognised for developing novel methods of selecting animals with improved welfare characteristics including IPN resistance in Atlantic salmon, and real-time X-ray assessment of leg strength in broilers.

By using genome editing constructively, animal breeders and farmers can deliver further improvements the health, welfare and sustainability of farmed animals. Personally, I consider it immoral not to deploy technology that can be used to improve the health and welfare of the animals in our care. We wouldnt argue against the development of a new vaccine because farmers might increase stocking density and exactly the same argument applies to precision breeding technologies such as genome editing.

In addition, the Bill makes provision for a separate welfare assessment to be applied specifically to genome edited animals as a further assurance that the welfare of the animal (or its progeny) would not be adversely affected by any trait resulting from precision breeding.

Modern animal breeders welcome objective methods to assess animal welfare and include assessment of welfare-associated traits into their breeding programmes. By open and transparent consideration of precision breeding technology, animal breeders can demonstrate that modern farming continues to improve the health, welfare and sustainability of livestock production.

Alan Tinch receiveda Ph.D. in genetics from the University of Edinburgh, and has been the VP of the Center for Aquaculture Technologies. During his career he has worked with aquatic and terrestrial species such as Atlantic salmon, chickens and pigs in the UK and worldwide. Follow Alan on Twitter @aetinch

A version of this article was posted at Science for Sustainable Agriculture and is used here with permission. Check out Science for Sustainable Agriculture on Twitter @SciSustAg

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Viewpoint: Why genetic engineering of livestock is compatible with the sustainable and human treatment of animals - Genetic Literacy Project

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Everybody gets older, although not everyone ages in the same way. For many people, late life includes a deterioration of health brought on by age-related disease. Yet there are also people who retain a more youthful vigor, and around the world, women typically live longer than men. Why is that? In this episode, Steven Strogatz speaks with Judith Campisi and Dena Dubal, two biomedical researchers who study the causes and outcomes of aging to understand how it works and what scientists know about postponing or even reversing the aging process.

Listen on Apple Podcasts, Spotify, Google Podcasts, Stitcher, TuneIn or your favorite podcasting app, or you can stream it from Quanta.

Steven Strogatz (00:03): Im Steve Strogatz, and this is The Joy of Why podcast from Quanta Magazine that takes you into some of the biggest unanswered questions in science and math today. In this episode, were going to be talking about aging. Why exactly do we age? Whats happening at the cellular level as our bodies get older?

(00:22) Scientists are still chasing many of the answers, but there have been some important advances in understanding the distinctive changes we call aging. Someday, that progress might not only help us live longer, but live better too. After all, living many years may not be much of a bargain if it means suffering from diseases like Alzheimers or Parkinsons. Well ask what role do our genes play in aging? And why do women tend to live longer than men on average? And also, what is research finding out about the ways we might slow down the process of aging?

(01:00) Later in this episode, well be hearing from Dr. Dena Dubal, associate professor in the department of neurology at the Weill Institute for Neurosciences at the University of California, San Francisco. But first, joining me now is Dr. Judith Campisi, a biochemist and cell biologist and professor at the Buck Institute for Research on Aging. Her lab there focuses on cellular senescence, a concept that well be unpacking very shortly. She is co-editor in chief of the Aging journal. Judy, thanks so much for joining us today.

Judith Campisi (01:34): My pleasure.

Strogatz (01:35): Im very excited to be talking to you about this. Well, of course, all of us are getting older, and we all feel it. It raises so many questions, though, like why is it happening? Is it something that nature is doing on purpose? Is it that our bodies are kind of wearing out like an old machine? Or how should we think about it?

Campisi (01:54): I think the way we have to think about it is in the context of evolution. If you think about humans, our lifespan, over the course of our evolution, aging never happened. There was no Parkinsons disease, no Alzheimers disease, there was no cancer. Everybody was dead by the age of 40 or 45. So evolution put into place ways of keeping young, reproductively fit organisms healthy for only a few decades, certainly not for the larger number of decades that were living through.

(02:35) Now, many of the processes that happen during aging really happen as a consequence of the declining force of natural selection. That is, there was no natural selection for these diseases. The process we study, cellular senescence, its now clear and certainly in mouse models that this process, the cellular process, drives a large number of age-related diseases, everything from macular degeneration, to Parkinsons disease, cardiovascular disease, and even late-life cancer, but it evolved to protect young organisms from cancer.

(03:19) So we certainly dont want to stop it when were young. It also helps fine-tune certain structures during embryogenesis. And it initiates labor in women in the placenta. So these are the things that evolution is selecting for. And this is why we have to be careful in how we intervene. And thats true for almost everything that happens with age. Evolution didnt try to make us old. Evolution tried to make us young and healthy. And sometimes that came at a cost.

Strogatz (03:56): Its a fascinating perspective, actually, that the things that are healthy for us when were young and that would be selected by evolution can have this inadvertent consequence. That as weve been able to extend lifespan I suppose through better diet or medicine, all kinds of things that now what used to help us can hurt us.

Campisi (04:15): Yes, this idea that whats good for you when youre young, can be bad for you when youre old. It was proposed in the 1950s by a guy named George Williams, an evolutionary biologist named George Williams. There was no molecular data at that time, you know. No genomes had been sequenced. He pointed out evolution never had to fine-tune the prostate. If you dont have a good prostate, you dont have good babies. You dont make good babies. On the other hand, almost inevitably with age, over the age of, say, 50 or so, the prostate begins to enlarge and of course it becomes a possibility of developing into cancer. Yet that didnt happen for most of our evolutionary history.

Strogatz (05:02): Wow. So lets go into cells because this its so rich and wonderful what you and your students and colleagues have been discovering at the cellular level. So could you please define what it means for a cell to be senescent?

Campisi (05:17): It is a state that the cell enters, in which it adopts three new traits. One of them is it gives up almost forever, almost forever, the ability to divide. It will tend to resist dying. And most important, it tends to secrete a lot of molecules that can have effects on neighboring cells, and also in the circulation. Not that many cells have been studied when they become senescent. And almost everything else we know about senescence is slowly changing as we learn more and more about different cell types and different ways that cells enter senescence.

(06:00) Okay, so they stopped dividing. And that makes sense that that would prevent cancer. The other thing is they become relatively resistant to cell death. That is they stick around. And this could explain why they increase with age, and they do. Many people now have looked in many, many vertebrate tissues. And it just seems that the older the tissue, the more senescent cells are present.

(06:29) The caveat to that statement is, there are still very few of them even in very old and very diseased tissue. A few percent at the most. So why do people think this has anything to do with aging? That has to do with the third thing that happens when cells become senescent is they begin to secrete a large number of molecules that have biological activity outside the cell. And that means that those senescent cells can call immune cells to the site where they are, it can cause neighboring cells to fail to function. And it basically causes a situation that is classically termed chronic inflammation. You know, and of course, chronic inflammation is also a great risk for developing age-related cancer. Not so much childhood cancers, but age-related cancers.

Strogatz (07:26): So a certain small subset of cells that stopped dividing hang around for a long time, dont dont die, and yet secrete molecules that call immune cells or other parts of the immune system to come. And what I mean, are they signaling come and kill me? Or whats going on? Why are they, what are they secreting for?

Campisi (07:50): Yeah, so theyre secreting a large number of molecules. So some of them are growth factors. And we reported some time ago, that at least on a mouse, if you make a wound, like a skin wound just a little punch biopsy on the back of the mouse at the site of that wound, senescent cells form within a few days, and they secrete growth factors that help the wound heal.

(08:17) This is why evolution selected for this phenotype. Its not all bad. On the other hand, if you have a pre-cancerous cell nearby, and those growth factors are now being secreted, and this cancer cell sees them, its possible that that cancer cell will wake up and start to form a tumor. So again, good for you when youre young, bad for you when youre old.

Strogatz (08:44): Well, let me ask some basics while were talking about senescent cells, because I think there are some things Im curious about. For instance, should I think of them as having started out like any other kind of cell and something set them on a pathway to become senescent? Or are we born with them? Or whats, whats the right way to think about this?

Campisi (09:04): I think where the field is right now is were beginning to realize that all senescent cells are not equal. And then the question is, why would what starts out as a normal cell so youre right, you start out with a normal cell. What would make it enter this strange state where it doesnt divide? And its got all these molecules it has to make and secrete. And the answer is, the kinds of stresses that we tend to associate with both cancer and aging. So for example, anything that damages the genome or even damages what we now call the epigenome. The way genes are organized within the nucleus, anything that damages that has the potential to drive a cell into this senescent state.

(09:51) On the other hand, there are also stresses that we dont think about as normally associate certainly, not associated with cancer. But things, for example, like advanced glycation end products, the chemical reactions that take place when glucose levels are too high. And so this is a big problem with people who have diabetes or pre-diabetic conditions. So those, those chemicals can also cause the cell to become senescent. So its more appropriate to call it a stress response, except not all stresses result in senescence.

Strogatz (10:30): Let us, if we could, talk about the mouse experiments that you and your, your group have done really pioneering experiments where youve used the technique in molecular biology of transgenic mice. Maybe first, you should tell us what they are, and then how you use them as a kind of testbed for how to get rid of bad senescent cells.

Campisi (10:49): So right now in biology, its pretty straightforward and easy to insert DNA into the genome of a mouse, and then have that mouse develop into a full-blown adult mouse and have that adult mouse make babies. And so the mouse that we made, this trans. So thats called a transgene, the transgenic mouse we made, carried a piece of DNA that had a foreign protein made when cells become senescent. And that foreign protein had three parts. A molecule that was what we call luminescent, meaning we could image the cells in a living animal. It had a fluorescent protein, which meant that we could sort senescent cells from the tissues of that mouse. But most importantly, it had a killer gene, a gene that would normally be totally benign. But if you feed a drug, which is also very benign, that drug and the presence of that foreign gene will cause senescent cells to die.

(12:01) So we made this mouse quite a while ago. And weve shared it with dozens and dozens of academic labs that are studying different diseases of aging: Alzheimers disease, Parkinsons disease, cardiovascular disease, age-related cancers, osteoporosis, osteoarthritis, et cetera. And the results are just astounding.

(12:27) If you eliminate senescent cells, it is possible to do one of three things to an age-related pathology: You either make it less severe, or you postpone its onset, or and this is, of course, the one we all love in a few cases, you can even reverse that pathology.

Strogatz (12:49): Oh wow.

Campisi: I know. Thats true for osteoarthritis so far. And so this has now sort of given meat to the idea that developing drugs that can do what our transgenes can do. Its too late for any adult to get their transgenes. But if you have an unborn baby, it may be possible.

Strogatz (13:09): Oh, I see where youre going with that. I mean, thats, of course, thats a big can of worms for us, isnt it to think that, you know

Campisi (13:15): I know, its too political. Its already been done.

Strogatz (13:17): Oh, really?

Campisi (13:19): Well, its been done. Its been done in China. Right?

Strogatz (13:22): Youre saying that fetuses or before fetuses

Campisi (13:25): Thats correct. Was engineered. Yeah. I dont know the guy who did it, the Chinese guy who did it was condemned by the community because there were not enough controls there. No oversight, et cetera, et cetera. But its possible. Theres no intellectual reason why we cant make transgenic people. And my guess is, its not just China.

Strogatz (13:45): Okay, in terms of what was actually we know that youve done in you and the other people doing transgenic mice, if I just make sure I got that. You said there were three parts to the transgene, two of which it sounds like were for detecting. So theres the luminescent and the fluorescent part. But the, the killer part is the part that is playing the role of in the future drugs, I suppose, that could kill off the bad senescent cells. You had this genetic mechanism

Campisi (13:46): Thats exactly right. So the drug that we use to kill senescent cells in the mouse would not work in humans because humans are not transgenic. But the idea would be now to develop new drugs. And they are being developed. There, there are already some that are being used in mice, and even a few in early-stage clinical trials in people with the idea that they would mimic what our transgene can do in the presence of this otherwise benign drug.

Strogatz (14:13): And so the punchline here is that if this really comes to pass, this gives us hope for, as you said, postponing, ameliorating or in some cases maybe again, were dreaming, but its like theres science behind this or possibly reversing some of these many age-related diseases. Just that you told us about. Yes. Wow.

Campisi (15:01): Youll die on the tennis court at 110. But youll be winning.

Strogatz (15:06): Thank you very much, Judy. This has been just a delightful conversation, my pleasure.

Announcer (15:14): Explore more science mysteries in the Quanta Magazine book Alice and Bob Meet the Ball of Fire, published by The MIT Press. Available now at Amazon.com, Barnesandnoble.com or your local bookstore. Also, make sure to tell your friends about The Joy of Why podcast and give us a positive review or follow where you listen. It helps people find this podcast.

Strogatz (15:39): Why we age and what happens to our bodies as we age are two of the biggest mysteries about aging. Another mystery has to do with sex differences. Women tend to live longer than men. Its often said that they live three to five years longer. But really, if you look at the global statistics, you see that in some places, women live more than 10 years longer. So what is it about being female that makes women more resilient? The body of a 70-year-old woman may be younger than her 70 years biologically when compared to that of a 70-year-old man. Researchers on aging say that an epigenetic clock runs differently for each.

(16:19) If we can understand why a womans brain might also age differently than a mans, we might be able to develop therapies to help everyone. Research into this question gets us into proteins and sex chromosomes and hormones. The goal is to understand all of this better. Can we slow down the aging process somehow?

(16:39) Joining me now to discuss all this is Dr. Dena Dubal. Shes an associate professor of neurology at the University of California, San Franciscos Weill Institute for Neurosciences. Her lab studies female longevity and the aging brain. What makes it resilient against cognitive decline? Dr. Dubal is also an investigator with the Simons Collaboration on Plasticity and the Aging Brain. Dena, thank you so much for joining us today.

Dena Dubal (17:06): My pleasure. Thank you for inviting me.

Strogatz (17:08): Well, Im really pumped up by this. You know, I think in my own family about how sharp some of the women were in their 90s, even. I recently had an aunt who just passed away just shy of her 100th birthday. She had smoked her whole life. But she was sharp. And I dont know how she could have managed to live so long. The men were all gone, the husbands had all died.

Dubal (17:32): Yeah, I noticed something similar in my family of origin, when I was very young, and that is that women live longer than men. And every summer growing up, my parents would take me back to India, their country of origin. Theyre immigrants from India. And we would spend time in a very small village in western Gujarat. And it was really remarkable that the elderly were, were really mostly women. And I had a great-grandmother, whose name was Rumba, who was just a remarkable woman, not educated, but really smart. And she lived almost to her 90s. And her husband, my great grandfather, despite being robust, tall, handsome and also very smart, he died in his early 40s. And so her lifespan was nearly double that of his. And this was seen really throughout my extended family, that the women live longer than the men and I always wondered why that was.

Strogatz (18:41): I mean, Im sure that many of our listeners are thinking the same thing. Its a pretty commonplace experience that the, the women outlive the men. Of course, its not universal. There are exceptions for all kinds of reasons, but, but its just an amazing general trend.

Dubal (18:55): So in every society that records mortality across the world, women live longer than men. From Sierra Leone, where lifespan is lower, to Japan and Sweden, where lifespan is much longer. But heres a really interesting piece of information: When we look historically across multiple countries and societies, at times of extreme mortality, like famine and like epidemics, the girls will live longer than the boys and the women will live longer than the men.

(19:34) And this, this really suggests to us that there is a biologic underpinning for female longevity, because even when there is very high and equal stress in the environment with very high mortality, the girls are outliving the boys and the women are outliving the men. Theres some very, very sad and really remarkable times that, that demonstrate this including the Irish famine and many, many other examples in our world history.

Strogatz (20:04): Its, its really fascinating to think that its somehow so intrinsic, that theres something you know, youve mentioned the cultural aspects, but it does feel like theres something purely biological also going on. And I wonder if we could get into that. I mean, is there something happening in the body itself that could account for these differences?

Dubal (20:26): There can be, really I would say, four main reasons. If we think about this, biologically, why there could be sex differences and human longevity. One has to do with sex chromosomes, our genetics, our genetic code, and every single one of our cells in our bodies. And that is that female mammals and certainly female human mammals have two X chromosomes in every cell. One of them is inactivated during development, but there are two X chromosomes, and that is the sex chromosome complement of women and girls. In contrast, boys and men have one X and one Y.

(21:12) And so here already at the outset, there is a very clear and striking difference in our genetics. And so with this difference, and XX in females compared to XY in males, there, there arises for biologic reasons, for sex differences in longevity. One is that in males, theres a presence of a Y. And it is thought, although not experimentally shown, that maybe there are toxic effects or deleterious effects of the presence of a Y chromosome.

Strogatz (21:48): Wow, what an idea. Well, why do living things get old at all? Why dont we live forever? What causes aging in the first place?

Dubal (21:56): Thats a very simple yet philosophical question. I would say that aging is what happens with the passage of time to the biology of cells. There is a change in biologic functions that leads to dysfunction and vulnerability to diseases. One major cause is genetic instability. So over time, our genetic code becomes more unstable. Some mutations will occur. Parts of our genes kind of jump around those are called transposons and disrupt other parts of our genetic code. There are changes that occur epigenetic, that means on top of our genes that ultimately change the way that our cells express themselves. And that becomes dysregulated and more dysfunctional over time with aging.

Strogatz (22:54): All right, well, so theres, the story of why we age then is a very multi-faceted one, apparently.

Dubal (23:01): Yeah, yeah, and the loss of what we call homeostasis. But really, what that is, is housekeeping of proteins. How theyre turned over, how theyre modified, how theyre folded, what is done with the proteins in our cells. And the housekeeping of these proteins declines with aging. And so then theres this buildup of essentially gunk, of like clutter, that really jams up cellular processes and contributes to aging as well. Mitochondria are the powerhouses of our cells, and they have more dysfunction with aging.

(23:40) This brings us back to another possible biologic reason for female longevity, it brings me to something called the mothers curse. So all the mitochondria in all of your cells, Steve, and all of mine, are inherited from our mothers. So in the process of, of cellular division and the creation of a zygote, mothers pass on their mitochondria, not fathers. And so this, this becomes really important because mitochondria can only undergo evolution in a female body. Males will never pass their mitochondria on.

(24:24) And so at the end of the day, what that predicts is that mitochondrial function is more evolved to female physiology, when compared to male physiology. And this may make a difference with aging when things begin to go awry. The female cells may be more fit because their mitochondria are more evolved to the female cells compared to male cells. For males, that would be a mothers curse.

Strogatz (24:50): And then a mothers blessing for females, maybe. Interesting. This is this is an interesting thing. Wow. So that gives me a very good big picture about whats happening. So living longer, though, is just one aspect of what well be discussing here. Theres also the issue of living better, right? In terms of not in the case of people, not experiencing the cognitive decline that we or reducing that, that we all associate with getting older.

Dubal (25:18): Yeah. So, lifespan is one thing, right? How, how long does one live? And right now the oldest recorded person in history has lived to approximately 122 years old. But then health span is really a measure of how many healthy years of life is one living. Thats what we really aspire to, is really good healthy health span, where we are not suffering from cancers, cardiovascular disease, neurodegenerative diseases, like Alzheimers, cognitive decline and more that happens with aging.

(25:58) So with a very good health span, one lives a healthy life without these chronic debilitating conditions until, lets say, 100 and then one dies peacefully in ones sleep from pneumonia, lets say. But that is health span. Its really life lived without diseases. And, you know, the reason that we are so interested in lifespan is that the things that help us to live longer tend to help us to live better.

(26:32) So if we can understand the molecules that work together to conspire toward longevity, we can harvest those molecules to help fight disease. And thats why were so interested in, Wow, why is it that women live longer than men? Is there some biology of aging that can be discovered, learned and then harvested toward better health span in males and females?

Strogatz (27:02): Well, let us start getting into that, then. I mean, I suppose our common sense would say that its got to be about sex hormones. That we associate testosterone with men, estrogen with women. Is it estrogen thats the secret here that, that thats somehow protective? Or lets, lets start with that. Is it, is this a story of estrogen?

Dubal (27:24): Yeah, its a golden question. So this brings me to the fourth biologic reason for sex differences in longevity. One was, could it be the presence of a Y that increases mortality? Is it an extra X in females that extends lifespan? Is it a mothers curse of mitochondrial inheritance from mothers only that works against males? And fourth, what about sex hormones? Could it be that testosterone is decreasing lifespan in males and estrogen is increasing it in females?

(27:58) I think this is a really important possibility and considering sex differences in biology and in longevity. And we have some very interesting clues from natural human experiments and experiments in animals.

(28:16) There is some support that removing testosterone prolongs life. The Korean Chosun dynasty had a population of Korean eunuchs, that were castrated. They were useful and respected members of the dynasty and of the imperial court. And they lived a very long life, a significantly longer life than men of the same socio-economic status that lived at the same time on average, 15 years longer.

Strogatz (28:49): This is amazing.

Dubal (28:51): Right?

Strogatz (28:52): Wow!

Dubal (28:52): It suggests that decreasing testosterone prolongs life. And we do see this, actually. There have been animal studies in which sheep are castrated and will live longer compared to those that are not. And some very robust studies in dogs. Of course, we spay our dogs and castrated male dogs will live longer than non-castrated male dogs.

(29:16): But, Steve, I have to tell you that this question that you asked was burning me for many, many years. Could it be the hormones that contribute to female longevity? Is it estrogen, or could it be sex chromosomes that contribute to longevity? And to that point, we did a really neat experiment to be able to dissect out those two causes, and Id love to explain it if this is a good time.

Strogatz (29:42): Its perfect and, and I like that you, you describe it as neat because I read in reading about it to prepare for our conversation. I thought this was such an elegant and you know, this is like primo science. This is the scientific method, to ask this tricky question and find a way to get a good approximation to an answer to it.

Dubal (30:04): It was a really exciting experiment to do. And it mattered not what the results were, we were to follow the science and the science would tell us something about the cause of sex differences in longevity.

(30:18) And so to be able to dissect out whether female longevity was driven by hormones, or by sex chromosomes, we used a really elegant, as you said, animal model, called the FCG model, the four core genotypes model. And in these mice, theres, theres a genetic manipulation, theres a genetic engineering thats taken place. And that is on the Y chromosome, there is this SRY, or a testis-determining factor, theres a gene that causes male differentiation and the production of testes and testosterone.

(30:58) So in this model, SRY is taken off of the Y chromosome and added to any other autosomes, the non-sex chromosomes. And what this allows is the inheritance of this testicular determining factor, the SRY, the inheritance of it by males that are XY or by females that are XX. So at the end of the day, this genetic engineering enables the creation of mice that have four sexes: XX mice with ovaries, that is the typical female biologic genotype and phenotype. XX mice that have developed as male with testes. And thats again, because they inherited the testicular determining factor SRY and they have differentiated as males and they, they cannot be distinguished from other male mice, except that theyre XX. So they have testes, they have male reproductive behaviors, they ejaculate. They fight in their cages. They are male mice, except theyre XX.

Strogatz (32:10): Hmm. So Ive got it. I want to make sure everyone listening has got it because its so incredible this way of doing things that the, you can make. I mean, let me put it crudely I think its approximately right phenotypically, on the outside, they look like males but inside, in terms of their chromosomes, they look like females.

Dubal (32:29): Thats right. Thats right. And then we do the same in males, in that we produce XY males that lack the testis determining factor and have developed by default as females that is, that they are indistinguishable from other female mice. They have ovaries, they have a uterus, they cycle, they have female reproductive behaviors, they are female mice, except their genetics are XY. And then we have the typical male, that is XY male that has developed a male phenotype.

(33:08) So this model produces four sex genotypes with males and females, XX and XY that developed with either ovaries or testes. And this allows us to really track which mice will live longer. Is it the mice that have ovaries regardless of being XX or XY? Or is it the mice that are XX, that have female genetics, regardless of growing up with ovaries or testes?

Strogatz (33:37): Before you reveal the answer? Let me ask the question a different way because I want everyone to mull this question over in their head, and guess what the answer is. So the question is, youve created this thing thats a little hard to wrap our minds around, but I think weve got it. These four sexes, a traditional male, a traditional female, a male genetically, but I dont know which one you call the male. Do you call you call, you refer to male as anything thats XY, is that right?

Dubal (34:07): I do. But its, its a matter of taste and, and style.

Strogatz (34:11): Okay, but so its an, its an organism thats XY but has ovaries, yes. Or you can have an organism thats X. Its not an organ. Its a mouse that has XX, but has testes.

Dubal (34:24): Its, its sudoku. Its like this is scientific sudoku.

Strogatz (34:30): Thats great.

Dubal (34:30): Yeah, we actually didnt have a specific hypothesis, we were going to follow the science. And what we found very clearly, is that the mice with two X chromosomes lived longer than those that were XY. So the XX mice, regardless of growing up with ovaries and having lots of estrogen, or regardless of having testes and lots of testosterone, it was the XX mice that lived longer compared to the XY. So this was a decisive genetic experiment that showed us really for the first time that sex chromosomes contribute to female longevity.

(35:14) Now, there was more that the experiment taught us too. The mice that lived the longest of all the groups, or the mice that had ovaries combined with the XX chromosomes, those lived to maximal longest lifespan, suggesting that the hormones produced by the ovaries, that ovaries and the hormones also contribute to female longevity. And that maybe testosterone is deleterious. So the answer was, the main statistical effect was that sex chromosomes contribute to female longevity. However, the hormones did have an effect in there as well.

Strogatz (35:56): So of the four sexes that we could choose from in this sudoku that you created, the traditional female, if I can keep referring to it as that, seems to be the winner?

Dubal (35:56): In living the longest. Yes.

Strogatz (36:12): What about the worst? What about the one living the shortest is what I would guess?

Dubal (36:16): The XY with testes? The XX mice, whether they grew up with ovaries or testes, lived longer than the XY mice that grew up with ovaries or testes. XX mice lived about 15 to 20% longer than XY mice.

Strogatz (36:33): Thats an enormous difference. It really, I mean, I assume by any statistical measure was considered significant. Your statisticians must have said, is that right?

Dubal (36:41): Absolutely. Very, very clearly significant, a very clear sex chromosome effect.

Strogatz (36:47): Well, thank you on that very inspiring and thoughtful note, Dena. You know, this was a really just an outstanding discussion. Thanks so much for joining us today.

Dubal (36:55): My pleasure.

Announcer (36:58): Wants to know whats happening at the frontiers of math, physics, computer science and biology? Get entangled with Quanta Magazine, an editorially independent publication supported by the Simons Foundation. Our mission is to illuminate basic science and math research through public service journalism. Visit us at quantamagazine.org.

Steve Strogatz (37:22): The Joy of Why is a podcast from Quanta Magazine, an editorially independent publication supported by the Simons Foundation. Funding decisions by the Simons Foundation have no influence on the selection of topics, guests, or other editorial decisions in this podcast or in Quanta Magazine. The Joy of Why is produced by Susan Valot and Polly Stryker. Our editors are John Rennie and Thomas Lin, with support by Matt Carlstrom, Annie Melchor and Leila Sloman. Our theme music was composed by Richie Johnson. Our logo is by Jackie King, and artwork for the episodes is by Michael Driver and Samuel Velasco. Im your host, Steve Strogatz. If you have any questions or comments for us, please email us at quanta@simonsfoundation.org. Thanks for listening.

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Ten years ago, Hanna Rosins book, The End of Men, argued that feminism had largely achieved its aims, and that it was time to start worrying about the coming obsolescence of men. American women were getting more undergraduate and graduate degrees than American men, and were better placed to flourish in a feminized job market that prized communication and flexibility. For the first time in American history, they were outnumbering men in the workplace. The modern economy is becoming a place where women hold the cards, Rosin wrote.

The events of the past decadethe rise of Trump, the emergence of the #MeToo movement, the overturning of Roe v. Wadehave had a sobering effect on this sort of triumphalism. The general tone of feminist rhetoric has grown distinctly tougher and more cynical. Cheerful slogans about the femaleness of the future have receded; the word patriarchy, formerly the preserve of womens-studies professors, has entered the common culture. Last year, in an article about womens exodus from their jobs during the pandemic, Rosin recanted her previous thesis and apologized for its tragic navet. Its now painfully obvious that the mass entry of women into the workforce was rigged from the beginning, she wrote. American work culture has always conspired to keep professional women out and working-class women shackled.

Men, especially conservative men, continue to wring their hands over the male condition, of course. (Tucker Carlson appropriated the title of Rosins book for a documentary, advertised this past spring, about plummeting sperm counts.) But feminist patience for twilight of the penis stories has run out. All that time they spend snivelling about how hard it is to be a poor persecuted man nowadays is just a way of adroitly shirking their responsibility to make themselves a little less the pure products of patriarchy, Pauline Harmange wrote in her 2020 screed, I Hate Men. More recently, the British journalist Laurie Penny, in her Sexual Revolution (Bloomsbury), notes the systemic underpinnings of such snivels: The assumption that oozes from every open pore of straight patriarchal culture is that women are expected to tolerate pain, fear and frustrationbut male pain, by contrast, is intolerable. Penny is careful to distinguish hatred of masculinity from hatred of men, but she nonetheless defines the fundamental political struggle of our time as a contest between feminism and white heterosexual male supremacy. In Daddy Issues (Verso), Katherine Angel calls for #MeToo-era feminists to turn their attention to long-overlooked paternal delinquencies. If the patriarchy is to be defeated, she argues, womens reluctance to criticize their male parents must be interrogated and overcome. Even the modern, civilized father must be kept on the hook, she recommends, and daughters must reckon with their desire for retribution, revenge and punishment.

The combative tone taken by these writers is hardly a surprise. One might argue that a movement currently scrambling to defend some vestige of womens reproductive rights can be forgiven for not being especially solicitous of mens sperm counts. One might argue that it isnt feminisms job to worry about how men are doingany more than its the job of hens to fret about the condition of foxes. But two recent books claim otherwise. A History of Masculinity: From Patriarchy to Gender Justice (Allen Lane), by the French historian Ivan Jablonka, and What Do Men Want?: Masculinity and Its Discontents (Allen Lane), by Nina Power, a British columnist with a background in philosophy, both contend that the drift toward zero-sum war-of-the-sexes language is a bad thing for feminism. Although their diagnoses of the problem are almost diametrically opposed, both authors make the case for a more generous and humane feminist discourse, capable of recognizing the suffering of men as well as of women. Hens, they acknowledge, have legitimate cause for resentment, but foxes have feelings, too.

Jablonkas dense, copiously researched book, which became a surprise best-seller in France when it was published there, in 2019, takes an ambitious, key-to-all-mythologies approach to its subject. Jablonka, who is a professor at the Universit Sorbonne Paris Nord, begins in the Upper Paleolithic, examining its mysterious, corpulent Venus figurines, and moves suavely across the millennia all the way to the successive waves ofmodern feminism. He has an eye for striking, often grim, detailsunder the Babylonian Code of Hammurabi, a daughter might be killed as punishment for a murder committed by her fatherand relishes drawing parallels across eras. From ancient times to the present day, it seems, the central totems of masculinityweapons, locomotive vehicles, and meat (particularly rare meat)have remained remarkably consistent. Likewise, from the fall of Rome to the Weimar Republic, men have consistently attributed political disaster and cultural decline to the corrupting influence of feminine values.

Jablonkas thesis about how patriarchy arose is a fairly standard one. Paleolithic societies already had a sexual division of laborSpanish cave paintings from as early as 10,000 B.C. show male archers hunting and women gathering honeybut it was relatively benign. In the Neolithic era, with the advent of agriculture and the move away from nomadic existence, birth rates increased and women became confined to the domestic sphere, while men started to own land. From then on, each new development, be it metal weapons, the rise of the state, or even the birth of writing, further entrenched the power of men and the subjugation of women.

Until now, that is. Patriarchy has declined, according to Jablonka, but men remain caught in pathologies of the masculine, trying to live up to a symbolic role that doesnt reflect their reduced dominance. The result is an almost tragic level of alienation, he writes, and feminists, instead of mocking or dismissing male anguishthereby leaving men vulnerable to the revanchist fantasies of Tucker Carlson and his ilkshould recognize this moment as a crucial recruitment opportunity. Now is the time to convince men that their obligatory model of virility has immiserated them far more than it has empowered them. The masculinity of domination pays, but it comes at a high cost: an insecure ego, puerile vanity, disinterest in reading and the life of the mind, atrophied inner life, the narrowing of social opportunities... and to top it all, a diminished life expectancy.

Feminism has been slow to empathize and collaborate with men, Jablonka claims, because too many in the movement remain wedded to a Manichean world view of male oppressors and female victims. Some feminists are unreconstructed leftist types, who reject any evidence of womens progress as mystification designed to hide the persistence of male domination. Others are duped by a pro-women romanticism into believing that women are innately nicer and more progressive than men. Jablonka rejects this sort of essentialist thinking, which he says provides a spurious biological rationale for traditional gender roles. If women are naturally kinder and more nurturing than men, and if men are intrinsically imbued with a culture of rape, why bother trying to change the status quo? Testosterone and other androgens may have something to do with a male propensity for aggression, he concedes, but human beings are hostage neither to their biology nor their gender. Mens history of brutish behavior is the product of patriarchal culture, and only by insisting on the fundamental identity between men and women can feminism realize its proper aima redistribution of gender, in which new masculinities abound and the selection of any given way of being a man becomes a lifestyle choice.

Whats saved to the cloud gets printed in Hell.

Cartoon by Michael Shaw

To claim that masculinity is a patriarchal construct, however, is not so much an explanation as the postponement of an explanation. Who or what created the patriarchy? Evolutionary biologists maintain that our earliest male ancestors had an evolutionary incentive to maximize the spread of their genes by violently competing for, and monopolizing access to, women. Jablonka is eager to avoid such biological imperatives, but in doing so he reaches for a kind of just-so story that renders much of the history he has laid out beside the point. Patriarchy, he speculates, was motivated by simple resentment of womens wombs. Deprived of the power that women have, men reserved all the others for themselves, he writes. This was the revenge of the males: their biological inferiority led to their social hegemony.

Thus it is that successive patriarchal lites have spent the past several millennia shoring up their illegitimate rule, by defining manliness as a set of superior qualities denied to women. Not that Jablonka thinks there is only one, eternal masculine style; rather, all models of masculinity since antiquity have been mechanisms for asserting and imposing patriarchal power. The extroversion and swagger of the toreador look very different from the gallantry of the Victorian gentleman, which is, in turn, quite distinct from the laconic glamour of the cowboy, but they are all equally culpable expressions of the masculine-superiority complex.

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New Feminist Considerations of Masculinity, Reviewed - The New Yorker

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Hari Jones, six, from Gwynedd, has X Linked Myotubular Myopathy (XLMTM), which affects about one in every 50,000 male births - he cannot walk or sit up and is connected to a life support machine that needs constant monitoring

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Wales: Boy with rare genetic disorder desperately needs care

A family says they are at a "breaking point" as they wait for a full care package for their son who has a rare genetic disorder.

Hari Jones, six, from Gwynedd, has X Linked Myotubular Myopathy (XLMTM), which affects about one in every 50,000 male births.

He cannot walk or sit up and is connected to a life support machine that needs constant monitoring.

The parents say they've been told he would get a full care package, but because of "ongoing issues" they have stepped up as Hari's carers while they wait.

Hari is unable to attend school and requires constant supervision in case the tube in his throat blocks or his breathing stops.

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Dad Michael Jones had told the BBC that "poor management" has "let them down as a family" and it is harming their physical and mental health as they have to step up as carers.

He says that he also has health conditions and was in a coma in 2018, which means a lot of care has fallen onto Hari's mum Ellen.

Mr Jones said: "She's with him day and night, mainly because I'm still really unwell so Ellen's life is basically next to Hari, she can't go out of the house, she's constantly with him and making sure he's safe.

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"She's a nurse for him, a doctor, a physiotherapist, she manages all his stock, she does absolutely everything for him day and night - to the point where she doesn't sleep for days and days so it's a lot of stress for her.

"At the worst, Ellen's done 12 days and 12 nights non-stop and her basic hours are 36 hours without sleep, so it's a lot of work."

Mr Jones added: "They should just find answers - it's not something that happened overnight for them.

"They've known that this was going to happen, and happening, since March last year so they should have had something in place to help us by now."

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The health board has said it would need time to recruit and train staff said due to Hari's complex needs it would take time to recruit and train staff.

A spokeswoman said the board was recruiting more staff and "continuing to work closely" with the family.

Hari spent four years on and off at Alder Hey Children's Hospital in Liverpool.

He was then assigned a care package that included carers being with the family almost 24 hours a day.

The health board took over from a private company in early 2021 - and the family say it reduced contact hours and used agency staff who were unable to fulfil the hours.

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The family say they were offered respite care at a hospice in Chorley, Lancashire, which is three hours from their home.

Neeru Naik, of Muscular Dystrophy UK - a charity which supports more than 60 conditions including XLMTM - said there were "inconsistencies" in regards to care packages.

Dr Catrin Edwards from the Carers Trust said there was "huge pressure" on families and unpaid carers.

"There's no doubt that our health and social care system is totally dependent on unpaid carers and we have to acknowledge the strain on them.

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"We have to remember that carers have legal rights and an individual has to be willing and able to provide care. However, when there are so many gaps existing in the workforce, many carers feel they have no choice but to continue, despite the personal strain."

Betsi Cadwaladr health board said Hari's care needs were set at 168 hours per week, a plan which had been agreed upon by a multidisciplinary team and the family.

It said it "compares favourably with other packages of care across the country".

Liz Fletcher, Assistant Area Director for Childrens Services in the West of Betsi Cadwaladr University Health Board, told The Mirror: We are continuing to work closely with Haris parents, Mr and Mrs Jones, to discuss the plans we have made to ensure that Hari has safe and ongoing care.

We are fully committed to providing the package of care for Hari and his family as an in-house arrangement, rather than via an external provider.

"We have taken this decision due to the complexity of the package required and the lack of suitable agencies and care providers nationally that can fulfil the familys needs.

"However, due to Haris complex needs, it will take time for us to recruit and train the number of appropriately skilled staff required to deliver this care package in full.

Two Health Care Support Workers and three registered nurses are now providing regular consistent care and we are actively recruiting more staff who will work as a team to support Hari.

"The team will be gradually introduced over a phased period according to a plan that has been discussed and shared with Mr and Mrs Jones.

We recognise there are challenges at times with staffing and when this occurs it is communicated to the family, who are updated regularly throughout the week.

"We do continue to offer meetings with Mr and Mrs Jones to discuss the package of care and any ongoing concerns they have.

We continue to look at all possible ways to support Hari at home recognising the challenges for everyone involved.

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Rocio Cifuentes, the children's commissioner for Wales, told The Mirror: "For children and young people throughout Wales who have complex needs, there are often difficulties in accessing the help and support they need.

"We want care to be much easier to access for children, and we want it to fit around them and their needs.

"Access to robust support at home, and regular short breaks is a hugely important part of any care package - so improving access to this for children and families across Wales must be a focus for services going forward."

A Welsh Government spokesperson told The Mirror: "We are investing heavily to support the recruitment and retention of social care staff in Wales, including paying social care workers the real living wage.

"Local authorities are also working closely with health boards to increase the number of domiciliary care workers. We've delivered record numbers of NHS staff - a 54% increase over the last 20 years - and more qualified nurses, hospital consultants and ambulance staff than ever before."

The Mirror contacted the Carers Trust for comment.

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Family at 'breaking point' amid difficulties caring for son with rare genetic disorder - The Mirror

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JOB VIGIL North Platte Telegraph

NORTH PLATTE Across Nebraska, corn tassels wave in the breeze as the crop moves toward pollination and on into harvest.

Managing that pollination specifically for seed or field corn determines the quality for the following season. Randy Lloyd, research facility coordinator at West Central Research, Extension and Education Center in North Platte, said getting the most out of the harvest depends on a lot of factors, one of which is hybridization.

Hybrids are a cross of two parents to create a new, stronger seed. Corn that self-pollinates inbred Lloyd said, is not high producing or high quality.

When you cross dog breeds or whatever it is, you get what they call hybrid vigor, which means the offspring is stronger than the parents, Lloyd said. Thats why sometimes you get these purebred dogs that have all these problems like hip (dysplasia) and such.

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A similar situation occurs with corn, Lloyd said, in that hybrid corn is much stronger because the best DNA from each plant is combined to produce stronger seed.

Back in the late 1800s, farmers just grew their corn, Lloyd said. The pollen (interacted) with whatever was around it and the seed developed on the ear and thats what they collected.

What geneticists found is there is an inherent improvement when you cross two parents creating hybrid seeds.

Corn is really a neat plant, because you can hybridize it so easily, Lloyd said.

To make hybrid strands, farmers and researchers have to separate male and female plants. The tassel is the male part of the plant and the ear is the female. Detasseling a plant ensures a female plant, Lloyd said.

What farmers will do is they will plant typically two or four rows of male and then upwards of eight rows of the female, Lloyd said. Theyll put them side by side through the field and youll see them alternate like that.

In hybridization, the farmer wants to ensure the proper pollen is being used and that is the reason for detasseling, so the plants cant self-pollinate.

Historically, detasseling was all done by hand, Lloyd said. Certainly in Nebraska where a lot of seed is produced in that Doniphan, York area, Ive heard stories of multi-generational detasselers.

The industry has developed some mechanical ways to detassel as well.

Corn production in the United States from the 1870s to the mid-1930s was mostly static. The average yield was about 25 bushels per acre.

A lot of the reason was, one, we didnt need that much corn back then, Lloyd said. If you think of what was available from a farming perspective we had no equipment, we had no fertilizers, we had no herbicides, we had nothing.

The way farmers collected seed for the next year in the early days of field corn production was to walk their fields and pick out what appeared to be the healthiest-looking ears.

That was their selection for seed and it was all open pollinated, Lloyd said. They planted it, the pollen came from this field, and it just pollinated whatever plant was ready to receive pollen.

When researchers began to develop hybrids, farmers saw their yields start to grow significantly.

(Hybridization) really didnt catch on that much with farmers until the Dust Bowl, Lloyd said.

Farmers saw yields going up due to drought-tolerant hybrids that were being developed at the time.

For a little while there, we started gaining about .9 bushels per acre until about the mid-1950s, Lloyd said. Then in the mid-1950s there was kind of an explosion of both technology and genetics, so we really started focusing on hybridization.

Along with continuing to improve hybrid seeds after World War II, Lloyd said equipment got better, fertilizers got better and herbicides came into the picture. Since that time, the way science manages genetics is improving each year.

Almost 95%-plus of the corn today is hybrid corn, Lloyd said, and the reason detasseling hybrid corn is important is for control that improves the quality of the corn.

Tassels have begun to show at the tops of corn around the area. Lloyd said the tassel, if its a good tassel, will have anywhere from 2 million to 5 million pollen grains. As the ear develops, it will have small kernels on it and it starts sending out silks.

It always starts at the bottom, Lloyd said. These (silks) are going to start to elongate up through the husk and then theyre going to come out the top of the ear.

Once the kernels are pollinated, the silks drop off.

If you have 30,000 plants per acre, which is a typical population, Lloyd said, youre getting 2 to 5 million pollen grains per tassel. Thats why when you come out of the fields youre covered in pollen, because theres so much of it.

With farmers paying almost $300 a bag for seed corn, Lloyd said, the farmer wants to be sure what he is purchasing is pure and gives him the best opportunity to produce a quality crop. Field corn is big business and companies work with farmers directly.

Typically a company will go to the farmer and say, we want you to grow this seed in your field and when you harvest it we want the seed, Lloyd said. Theyll take it back to their plant, clean it, do whatever they have to do to it, treat it and put it in a bag. This is almost all contract work.

The companies are particular about the types of herbicides, fungicides and fertilizer used to produce the crop.

Typically the company will send out a consultant to go look at the field several times during the year to make sure things are going well, Lloyd said.

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There are valid reasons so many Nebraska kids have spent their summers detasseling corn - Scottsbluff Star Herald

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image:One of the samples of ancient herpes DNA used in the study came from a male of 26-35 years old, excavated near the banks of the Rhine. The man was a fervent smoker of clay pipes. Traces of the habit are visible in multiple places on the teeth, where the hard clay pipe, usually put in the same place in the mouth, has worn the teeth. view more

Credit: Dr Barbara Veselka

Ancient genomes from the herpes virus that commonly causes lip sores and currently infects some 3.7 billion people globally have been uncovered and sequenced for the first time by an international team of scientists led by the University of Cambridge.

Latest research suggests that the HSV-1 virus strain behind facial herpes as we know it today arose around five thousand years ago, in the wake of vast Bronze Age migrations into Europe from the Steppe grasslands of Eurasia, and associated population booms that drove rates of transmission.

Herpes has a history stretching back millions of years, and forms of the virus infect species from bats to coral. Despite its contemporary prevalence among humans, however, scientists say that ancient examples of HSV-1 were surprisingly hard to find.

The authors of the study, published in the journal Science Advances, say the Neolithic flourishing of facial herpes detected in the ancient DNA may have coincided with the advent of a new cultural practice imported from the east: romantic and sexual kissing.

The world has watched COVID-19 mutate at a rapid rate over weeks and months. A virus like herpes evolves on a far grander timescale, said co-senior author Dr Charlotte Houldcroft, from Cambridges Department of Genetics.

Facial herpes hides in its host for life and only transmits through oral contact, so mutations occur slowly over centuries and millennia. We need to do deep time investigations to understand how DNA viruses like this evolve, she said. Previously, genetic data for herpes only went back to 1925.

The team managed to hunt down herpes in the remains of four individuals stretching over a thousand-year period, and extract viral DNA from the roots of teeth. Herpes often flares up with mouth infections: at least two of the ancient cadavers had gum disease and a third smoked tobacco.

The oldest sample came from an adult male excavated in Russias Ural Mountain region, dating from the late Iron Age around 1,500 years ago.

Two further samples were local to Cambridge, UK. One a female from an early Anglo-Saxon cemetery a few miles south of the city, dating from 6-7th centuries CE. The other a young adult male from the late 14th century, buried in the grounds of medieval Cambridges charitable hospital (later to become St. Johns College), who had suffered appalling dental abscesses.

The final sample came from a young adult male excavated in Holland: a fervent clay pipe smoker, most likely massacred by a French attack on his village by the banks of the Rhine in 1672.

We screened ancient DNA samples from around 3,000 archaeological finds and got just four herpes hits, said co-lead author Dr Meriam Guellil, from Tartu Universitys Institute of Genomics.

By comparing ancient DNA with herpes samples from the 20th century, we were able to analyse the differences and estimate a mutation rate, and consequently a timeline for virus evolution, said co-lead author Dr Lucy van Dorp, from the UCL Genetics Institute.

Co-senior author Dr Christiana Scheib, Research Fellow at St. Johns College, University of Cambridge, and Head of the Ancient DNA lab at Tartu University, said: Every primate species has a form of herpes, so we assume it has been with us since our own species left Africa.

However, something happened around five thousand years ago that allowed one strain of herpes to overtake all others, possibly an increase in transmissions, which could have been linked to kissing.

The researchers point out that the earliest known record of kissing is a Bronze Age manuscript from South Asia, and suggest the custom far from universal in human cultures may have travelled westward with migrations into Europe from Eurasia.

In fact, centuries later, the Roman Emperor Tiberius tried to ban kissing at official functions to prevent disease spread, a decree that may have been herpes-related. However, for most of human prehistory, HSV-1 transmission would have been vertical: the same strain passing from infected mother to newborn child.

Two-thirds of the global population under the age of 50 now carry HSV-1, according to the World Health Organisation. For most of us, the occasional lip sores that result are embarrassing and uncomfortable, but in combination with other ailments sepsis or even COVID-19, for example the virus can be fatal. In 2018, two women died of HSV-1 infection in the UK following Caesarean births.

Only genetic samples that are hundreds or even thousands of years old will allow us to understand how DNA viruses such as herpes and monkeypox, as well as our own immune systems, are adapting in response to each other, said Houldcroft.

The team would like to trace this hardy primordial disease even deeper through time, to investigate its infection of early hominins. Neanderthal herpes is my next mountain to climb, added Scheib.

Ancient herpes simplex 1 genomes reveal recent viral structure in Eurasia

27-Jul-2022

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In an age of universal communications via satellites circling the globe when any human on the planet who has a capable device may offer up opinions and speculations about any subject known to humankind it is not unreasonable, given the testimony of history, to assume some of these ideas will be of such content so as to stretch the mind to its furthest capacity of acceptance.

In short, there is a lot of crazy stuff on the internet. Let me pass along a couple of these offerings as they may, or may not, have passed through the ether:

Do you ever wonder how some people become famous but have zero talent? It is a known fact in the late 1930s three scientists in a country that cannot be named for fear of reprisal discovered a small entity within our solar system, which they first thought was nothing more than collected gases, but upon further investigation they discovered it was of a gelatinous nature, more blob than solid matter, but seemed to be inhabited by creatures with the same jelly-type body.

After months of observation the scientists documented that the populace of what was now deemed, by them, a planet was amorphous and could, chameleon-like, replicate whatever object they observed; much like the shape shifters of some Native American cultures. According to the scientists global rotation calculations, the planet would pass closest to Earth on Feb. 4, 1944, its closest point directly above a hospital in Los Angeles, Calif., USA. It is believed that on this occasion a creature from the planet occupied the body of a newborn male infant at that facility.

In the early morning hours of New Years Day 1944, after a night of celebration, an unexplained fire took the lives of the three scientists and destroyed all compiled data. A short note naming the planet written to a friend by one of the scientists was the only remaining evidence of their undisclosed discovery, and as result the world would never learn what became of the planet the scientists dubbed Kardashia.

There is no known phenomenon between a verified body in space and the birth of Robert George Kardashian (1944-2003).

There is an explanation of what creature these unsuspecting hikers came across, but governments around the world have hidden the true story. It is a known fact that just after the turn of the 20th century at a convention of genetic scientists in Paris, France, there was a paper submitted that outlined a process by which human genes could be spliced with primate genes thus producing a human being with the capabilities of a primate; a combination thought by the geneticist author to produce a manageable race to be used as working class for menial labor and soldiering.

The author of the paper, a scientist from China, had his paper and his ideas rejected by the scientific community, but volumes of his research and initial findings of experiments were copied by some of those attending the conference and were taken with them back to their home countries. What the research revealed was that the Chinese scientist had separated the DNA from a creature found frozen in a cave about 26 miles (41 kilometers) east of Mount Everest in Nepal.

Based on findings from other parts of China, speculation is the creature may have been a preserved Bunopithicus sericus. It is then believed he attempted to cross this DNA with tribesmen of the area for a number of years before submitting his findings at the 1912 convention. The scientist died in 1916 and a subsequent search of his abandoned facility, the Yuang Experimental and Testing Institute, led authorities to believe there were numerous studies done on human subjects, and subsequently the facility and all documents were destroyed by government authorities.

But oral history recounts testimony of local residents who reported hearing loud primal screams and odors described as musky and like a dirty wet dog coming from the compound where barracks sat alongside the laboratory. A handful of Sherpas had for years reported smells and sounds in the upper reaches of the Himalayas, and of seeing large human-like footprints in the snow. It is not known how many foreign scientists who availed themselves of the Yuang research papers conducted their own experiments nor what if any results may have occurred.

There is no known evidence of any research by any genetic scientists in the early part of the 20th century in any country involving gene splicing humans with other species (see Myths: Abominable Snowman, Sasquatch, Bigfoot, Yeti).

It is a known fact in the witch haven of Bad Durkheim Palatinate in Rhineland-Germany that a sorceress by the name of Juliana Maria Rodenroth (born circa 1667-70) pronounced a curse upon the family of her grandson when he married below his station in life and moved from the ancient land of his ancestors, many of whom were considered practitioners of occultism and witchery, to Kallstadt Palatinate of the Kingdom of Bavaria.

Oral tradition of the area relates the curse was that within her grandsons lineage there would be one born who would by inherited bounty and nefarious means rise to great power only to use that power to bring about great shame upon her grandsons name and the name of his heirs for generations to come.

As yet all data has yet to be compiled upon the generations of Juliana Maria Rodenroth, the mother of Johann Sebastian Trump (1699-1756) (see Select Committee Hearing to Investigate the January 6 Attack on the United States Capitol).

***

I dont usually get political, but cmon folks, sometimes there is just an abundance of honest people giving honest account about a dishonest human being.

Take care. Peace.

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Funny Papers Again Column | Idiotologies vs The Review and Research Posse - King City Rustler

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The US has an abundance of national parks of varying shapes and sizes. From the grandeur of Colorados best national parks to the beauty of Californias stunning parks, they are home to hundreds (if not thousands) of plants and animals. Thus, nature-loving and adventure-seeking tourists have ample opportunity to witness these creatures thrive in their natural habitats when visiting national parks in the US. Whether one goes backcountry camping, hiking, or even kayaking, these US parks offer opportunities for viewing wildlife in its natural habitat!

Yosemite National Park is familiar with crowds of tourists wanting to visit its majesty and whimsy. This California park receives hundreds of thousands of visitors annually, providing an array of activities for many to enjoy its natural wonders. Take a guided tour of the park while riding a horse, bike through the trails, or get some bait to try some fishing at Yosemite. This famous national park is also home to over 165 species of birds, making it an ideal destination for avid birdwatchers.

Michigans Isle Royal National Park is nothing to scoff at; being an archipelago, it encompasses over 400 islands! With 36 campgrounds and approximately 165 miles (or 266 km) of trails, experienced backpackers can take a backcountry trip to Michigans massive park, exploring its many nooks and crannies. Otherwise, this natural area is also great for families, offering activities like scuba diving, fishing, paddling, and canoeing. Plus, its possible to spot local wildlife here, including red foxes, squirrels, bats, and certain reptiles.

Located 290 miles (or 470 km) away from Las Vegas, the Great Basin National Park provides a quieter hangout compared to the bright lights of The Strip. The park is known for the strenuous Wheeler Summit Trail and the Lehman Caves. However, nature-loving tourists can also find a plethora of wildlife at the Great Basin National Park. Hikers may spot species like the bighorn sheep, pygmy rabbit, water shrews, porcupines, and beavers.

The most beautiful wildflowers are found in Alaskas Katmai National Park. Thus, plant lovers who visit this Northern national park can find vascular plants like fireweeds, Kamchatka lilies, and Alaskas Nootka lupine. However, despite its faunal diversity, tourists flock to Katmai for one reason: brown bears! With their population in the thousands (particularly about 2,200), backcountry campers and curious tourists love watching these cuteyet mightymammals at Katmai every year. Bear-watching usually occurs between June to September, so travelers wishing to see these beautiful beasts can book a bear-watching trip through a reputable local tour operator.

RELATED: A Guide On Where To Find All The Summer Action In Virginia Beach

Sitting near the US-Mexican border, the Big Bend National Park lies far away from bustling cities. However, this desert park, located in Far West Texas, offers breathtaking views of the Chisos Mountains and its dramatic canyons. While backcountry camping or kayaking along the Rio Grande, visitors may spot local critters like jackrabbits, deer, bobcats, or the collared peccary.

Colorados Rocky Mountain National Park is a popular attraction for wildlife viewing year-round. Whether visitors take a relaxing road trip through the Rocky Mountains or embark on its 350+ mile worth of hiking trails, the Rocky Mountain National Park has an abundance of flora and fauna. Regardless of how travelers explore this Colorado park, from a distance, they may spot some unique wildlife like the yellow-bellied marmot, bighorn sheep, black bears, coyotes, or the white-tailed ptarmigan.

Covering over 1.5 million acres of wetland, this south Floridian national park is a must-visit for nature-loving travelers. Thus, the Everglades National Park offers visitors many opportunities to appreciate its wildlife. Go birdwatching in Homestead to see mangrove cuckoos, purple gallinules, or warblers in their natural habitat, or venture to the Everglades City entrance to witness bald eagles and wood storks. Alternatively, canoeing (or kayaking) is a fun way to explore the mangrove forests and marshes in the park while spotting local alligators, crocodiles, or manatees!

RELATED: Not Everyone Enjoys The Summer, And These U.S. Destinations Always Feel Like Fall

The Grand Canyon National Park is undoubtedly beautiful and a popular tourist attraction in Arizona. However, theres something beautiful about the Saguaro National Park. Home of the giant saguaro cacti, visitors can take a scenic road trip around the park or hike along its trails with picnic areas. Plus, depending on the month of ones visit, those exploring the parkespecially during the warmer monthsmay spot some local amphibians and reptiles, including canyon treefrogs, leopard frogs, Gila monsters, tortoises, and rattlesnakes.

Just a stone's throw away from the Yellowstone National Park, Grand Teton features breathtaking views of the Teton Range, alongside countless lakes and rivers. Its expansive size and lush surroundings make it an ideal destination for passionate, experienced backcountry campers. Simultaneously, Grand Teton National Park is home to hundreds of animals and flora that can be easily spotted while driving (or camping), such as mule deer, bears, moose, elk, bison, and grizzly bears.

Known as the worlds first national park (and in the US), Yellowstone National Park welcomes millions of nature-seeking tourists every year. Visit this national park by entering one of its five entrances to appreciate some of natures best sites (and wildlife)! This UNESCO World Heritage Site always dazzles visitors with its incredible views of the Grand Canyon and the world-famous Grand Prismatic Spring. Additionally, Yellowstone is rich in biodiversity, where visitors (at a respectable distance) can watch animals like buffalo, moose, grizzly bears, wolves, and bald eagles thrive in their natural habitat.

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10 US Parks Where You Can Watch Wildlife In Its Natural Habitat - TheTravel

Recommendation and review posted by Bethany Smith

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Autologous Cell Therapy Market 2021-2025: Scope

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We provide a detailed analysis of around 25 vendors operating in the autologous cell therapy market, including Bayer AG, Brainstorm Cell Therapeutics Inc., Daiichi Sankyo Co. Ltd., FUJIFILM Holdings Corp., Holostem Terapie Avanzate Srl, Osiris Therapeutics Inc., Takeda Pharmaceutical Co. Ltd., Teva Pharmaceutical Industries Ltd., Sumitomo Chemical Co. Ltd., and Vericel Corp. among others. The key offerings of some of these vendors are listed below:

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Autologous Cell Therapy Market Scope

Report Coverage

Details

Page number

120

Base year

2020

Forecast period

2021-2025

Growth momentum & CAGR

Accelerate at a CAGR of 14.16%

Market growth 2021-2025

USD 4.11 billion

Market structure

Fragmented

YoY growth (%)

13.5

Regional analysis

North America, Europe, APAC, and South America

Performing market contribution

North America at 43%

Key consumer countries

US, UK, Germany, Canada, and Japan

Competitive landscape

Leading companies, competitive strategies, consumer engagement scope

Companies profiled

Bayer AG, Brainstorm Cell Therapeutics Inc., Daiichi Sankyo Co. Ltd., FUJIFILM Holdings Corp., Holostem Terapie Avanzate Srl, Osiris Therapeutics Inc., Takeda Pharmaceutical Co. Ltd., Teva Pharmaceutical Industries Ltd., Sumitomo Chemical Co. Ltd., and Vericel Corp.

Market Dynamics

Parent market analysis, market growth inducers and obstacles, fast-growing and slow-growing segment analysis, COVID-19 impact and future consumer dynamics, market condition analysis for the forecast period

Customization purview

If our report has not included the data that you are looking for, you can reach out to our analysts and get segments customized.

Table Of Contents :

Executive Summary

Market Landscape

Market Sizing

Five Forces Analysis

Market Segmentation by Product

Customer landscape

Geographic Landscape

Vendor Landscape

Vendor Analysis

Appendix

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Technavio is a leading global technology research and advisory company. Their research and analysis focus on emerging market trends and provide actionable insights to help businesses identify market opportunities and develop effective strategies to optimize their market positions. With over 500 specialized analysts, Technavio's report library consists of more than 17,000 reports and counting, covering 800 technologies, spanning across 50 countries. Their client base consists of enterprises of all sizes, including more than 100 Fortune 500 companies. This growing client base relies on Technavio's comprehensive coverage, extensive research, and actionable market insights to identify opportunities in existing and potential markets and assess their competitive positions within changing market scenarios.

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Technavio ResearchJesse MaidaMedia & Marketing ExecutiveUS: +1 844 364 1100UK: +44 203 893 3200Email: [emailprotected]Website: http://www.technavio.com/

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Autologous Cell Therapy Market Size to Grow by USD 4.11 billion, Bayer AG and Brainstorm Cell Therapeutics Inc. Among Key Vendors - Technavio - PR...

Recommendation and review posted by Bethany Smith

The British Heart Foundation announced the winner of its $36 million Big Beat Challenge, one of the largest non-commercial awards ever given for heart research.

The winning team, CureHeart, brings together researchers from the U.K., U.S. and Asia, including Eric Olson, professor and chair of the Department of Molecular Biology at UT Southwestern Medical Center.

Olson is the founding chair of the department and directs the Hamon Center for Regenerative Science and Medicine and the Wellstone Center for Muscular Dystrophy Research. He holds the Robert A. Welch Distinguished Chair in Science and the Annie and Willie Nelson Professorship in Stem Cell Research.

He has spent his career investigating heart and muscle development and disease, leading to his participation on the CureHeart team. The Olson Lab at UTSW has been incredibly successful in muscular research, most recently providing a new way to correct the mutation that causes Duchenne muscular dystrophy through gene editing.

CureHeart made the top of the list with its gene editing therapy aimed at curing inherited heart muscle diseases, known as cardiomyopathies.

A BHF release said the technology will seek to develop the first cures for inherited heart muscle diseases by pioneering revolutionary and ultra-precise gene therapy technologies that could edit or silence the faulty genes that cause these deadly conditions.

The project will use gene-editing technology CRISPR to complete base and prime editing in the heart for the first time.

It works by correcting or silencing a faulty gene in the pumping machinery of the heart, either by re-writing the DNA at a single location or by switching off the entire copy of the faulty gene.

The technique was described as molecules that act like tiny pencils to rewrite the single mutations that are buried within the DNA of heart cells in people with heart conditions.

It can also help the heart produce enough proteins to function normally, again by fixing or stimulating the faulty gene.

With ultra-precise base editing technology, we hope to be able to correct a single letter and larger errors in the genetic code. This would mark a breakthrough for not only genetic cardiomyopathies, but for many heart conditions, said Olson in the release.

The project is the next step toward a real-world application, having already proved successful in animals with cardiomyopathies and in human cells. Members of the team believe therapies could be delivered through an arm injection, slowing or stopping the progression of cardiomyopathies, or even curing the disease entirely.

If successful, the research could have enormous impacts.

Every year in the US, around 2,000 people under the age of 25 die of a sudden cardiac arrest, often caused by one of these inherited muscle diseases, said the release. Current treatments do not prevent the condition from progressing, and around half of all heart transplants are needed because of cardiomyopathy.

The researchers believe it could also be successful in preventing the disease from being expressed if inherited. Children who receive the faulty gene from their parents could receive the injection and never develop cardiomyopathy in the first place.

Over the last 30 years, we have made extraordinary advancements in our understanding of the genetic mistakes that cause cardiomyopathy. CureHeart is a once-in-a-generation opportunity to transform this knowledge into a cure, said Olson in the release.

The technology is still in the research and development phase, but Olson said the funds will be used to optimize the method and expand it to a larger number of genetic diseases of the heart, and could move to clinical trials in the next few years.

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UTSW researcher part of team awarded $36 million heart research grant - The Dallas Morning News

Recommendation and review posted by Bethany Smith

SEATTLE--(BUSINESS WIRE)--Curi Bio, a leading developer of human stem cell-based platforms for drug discovery, today announced the commercial launch of the Mantarray platform for human-relevant 3D heart and skeletal engineered muscle tissue (EMT) contractility analysis. Curis Mantarray platform enables the discovery of new therapeutics by providing parallel analysis of 3D EMTs with adult human-like functional profiles of healthy and disease models. Over the past three years, Curi Bio has developed the Mantarray platform in close beta testing and development partnerships with several leading global pharma companies, biotech companies, and regulatory agencies for use in their drug discovery and development projects. With this commercial launch, the Mantarray instrument and consumables will be available worldwide, on a first-come, first-served basis.

Lack of clinical translatability in current preclinical models, which often rely upon surrogate biomarkers or poorly translational animal models, may be to blame for the unacceptably high clinical trial failure rates plaguing the industry. For cardiac and skeletal muscle diseases, direct assessment of contractile output constitutes the most reliable metric to assess overall tissue function, as other proxy measurements are poor predictors of muscle strength. 3D EMTs derived from human induced pluripotent stem cells (iPSCs) offer a promising route to model the contractile deficiencies seen in the heart and muscles of patients. However, the bioengineering strategies required to generate these predictive models at sufficient scale are oftentimes out of reach for most researchers.

Curis solution to this problem is the Mantarray platform: an easy-to-use, scalable, and flexible biosystem for assaying EMTs. The Mantarray platform leverages a proprietary, label-free, electromagnetic measurement system for parallel contractility assessment of up to 24 3D EMTs simultaneously and can utilize a variety of contractile cell types. The system has built-in electrical stimulation capabilities, enabling users to easily create individual stimulation protocols for each well, for both short and long-term pacing of cardiac and skeletal muscle models. Curi has developed consumable Mantarray plates that are specifically designed for cardiac and skeletal muscle applications. 3D Mantarray tissue models will also be compatible with Curis new Nautilus system (optical mapping system for voltage and calcium analysis).

Additionally, Curi offers services and partnerships leveraging the Mantarray technology for applications in drug discovery, disease modeling, and safety and efficacy screening. Companies interested in fully accessing or licensing Curis proprietary disease models, next-generation iPSC platforms, gene therapy technologies and technical expertise can do so with Curis new Technology Access Partnership program. Further details of this Technology Access Partnership program will be announced at a later date.

High-fidelity models of human diseases can be created and tested on the Mantarray platform using human iPSC-derived cells or patient-derived myoblasts from healthy or affected individuals. For example, Mantarray 3D EMTs can be formed from cells harboring disease-causing mutations (patient-derived or gene-edited; iPSC-derived or primary) to model human diseases such as Duchenne muscular dystrophy, myotonic dystrophy type 1, hypertrophic and dilated cardiomyopathies, and more. Multi-modal data captured with the 3D platform shows enhanced disease stratification for a number of monogenic disorders. Curi Bio is accelerating the path to investigational new drugs, making personalized medicine a reality through clinically-translatable human disease models.

Safety and efficacy testing can also be performed with the Mantarrays novel magnetic detection of drug-induced contractile changes. Acute drug responses can be measured on the order of seconds to minutes with enough sensitivity to detect dose-response-like behavior. Alternatively, chronic experiments can be performed over the course of days to weeks for longer-term studies. Mantarray brings clinically-relevant functional data into the earliest stages of preclinical testing of new therapeutics.

At Curi Bio, our goal is to provide researchers with innovative solutions to accelerate the discovery of new medicines, said Curi CEO Michael Cho. The Mantarray platform provides drug developers with clinically-relevant preclinical models that more closely recapitulate human cardiac and skeletal muscle tissues. With this key milestone, Curi is closing the gap between preclinical results and clinical impact. Our clients are using this data in direct support of IND applications.

To learn more about how the Mantarray system can improve the predictive power of your experiments, or about Curis other human-relevant preclinical platform technologies and services, please reach out at http://www.curibio.com/contact.

About Curi Bio

Curi Bios preclinical discovery platform combines human stem cells, systems, and data to accelerate the discovery of new medicines. The Curi Engine is a comprehensive, bioengineered platform that integrates human iPSC-derived cell models, tissue-specific biosystems, and AI/ML-enabled phenotypic screening data. Curis suite of human stem cell-based products and services enable scientists to build more mature and predictive human iPSC-derived tissueswith a focus on cardiac, musculoskeletal, and neuromuscular modelsfor the discovery, safety testing, and efficacy testing of new drugs in development. By offering drug developers an integrated preclinical platform comprising highly predictive human stem cell models to generate clinically-relevant data, Curi is closing the gap between preclinical data and human results, accelerating the discovery and development of safer, more effective medicines.

For more information, please visit http://www.curibio.com.

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Curi Bio Launches Mantarray Platform 3D Engineered Muscle Tissues for Discovery of New Therapeutics - Business Wire

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New research clarifies how stem cells repair the intestines.

To act as a robust barrier against pathogens while also absorbing needed nutrients, the lining of the intestines must regenerate on a daily basis to remain equal to the task.

The intestines resident stem cells are responsible for meeting this need for constant repair and replenishment, but each stem cell faces decisions that depend on the overall conditions of the intestine and the needs of the moment.

Bad decisions and poor coordination could result in intestinal diseases or cancer.

A new study suggests that stem cells are able to integrate cues from their surroundings and coordinate their behavior across the tissue through networks of vasculature in their close vicinity.

The researchers found that lymphatic capillariesfine vessels that transport immune cells and drain fluids from tissuesrepresent a signaling hub that communicates with stem cells to regulate their activity. With molecular guidance from the lymphatics, the stem cells produce daughter cells to repopulate the intestinal lining or self-renew to restock the stem cell reserve.

The findings in the journal Cell Stem Cell provide new insights about primary intestinal components whose disrupted communication may contribute to intestinal disorders, such as inflammatory bowel disease.

The key to treating these diseases will be to figure out who talks to whom in this ecosystem and how we can reset the communication networks, says Rachel Niec, a clinical scholar in the laboratory of Elaine Fuchs at Rockefeller University.

The intestinal stem cells reside in so-called crypts, found at the base of densely packed indentations in the intestinal lining. The stem cells may renew and stay in the crypt, or differentiate into specialized cells, which then migrate out of the crypt to replenish the gut lining.

To understand how stem cells balance self-renewal with differentiation, we needed a more complete picture of crypt niches, says Marina Schernthanner, a graduate student in the Fuchs lab.

To zoom in on the crypt, the team used a suite of techniques, including single-cell and spatial transcriptomics, which allowed them to identify cell types at specific locations and study their signaling molecules.

The results showed that lymphatic capillaries, which form an intimate connection with the stem cells in the crypt, produce a number of proteins known to be important for stem cell functioning.

One previously underappreciated protein, REELIN, emerged as a top candidate for mediating communications between lymphatics and stem cells. By manipulating the amount of REELIN in lab-grown intestinal organoid cultures in some experiments and genetically suppressing it in mice in others, the researchers found that REELIN directly governs the regenerative behavior of intestinal stem cells.

The involvement of the lymphatic system in stem cell functioning is a relatively new concept. A previous study by the Fuchs team revealed that lymphatics are also closely involved with stem cells of the skin and play a key role in hair regeneration. There, however, it is the hair follicle stem cells that signal to lymphatic capillaries. By controlling their interactions with lymphatics, the stem cells synchronize hair regeneration across the tissue.

This suggests that lymphatics may be a conserved feature of stem cell niches, but their relationship to stem cells are likely tailored around the needs of each tissue, Niec says.

Source: Rockefeller University

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How your intestines repair and renew themselves - Futurity: Research News

Recommendation and review posted by Bethany Smith

Cells with the highest Hlf-tdTomato expression levels have bone marrow reconstitution capacity

We previously reported that HSCs have higher levels of tdTomato than other hematopoietic progenitors in the fetal livers of Hlf-tdTomato KI mice25. Transplantation experiments were performed to confirm the stem cell potential of bone marrow cells with higher levels of Hlf-tdTomato in the bone marrow of the tibia. Flow cytometry analysis showed that 47.04.4% of whole bone marrow cells from adult long bones of Hlf-tdTomato KI mice were positive for CD45, which is a panhematopoietic marker (Fig.1a, left panel, n=4). Cells with the top 0.011% tdTomato intensity within the CD45-positive cells (0.0049% of the whole bone marrow cells) were defined as Hlf-tdTomatohi cells (Fig.1b). All the Hlf-tdTomatohi cells were located within the Sca-1+c-Kit+ fraction, including phenotypic HSCs (CD150+CD48) and short-term HSCs (CD150CD48) (Fig.1a, right panel and Supplementary Fig.1). To determine whether Hlf-tdTomatohi cells show a high frequency of functional HSCs within the bone marrow of the tibia, we compared engraftment capacity between the Hlf-tdTomatohi and Hlf-tdTomato cells (44.3% of the whole bone marrow cells) by the transplantation assay (Fig.1b). A total of 100 Hlf-tdTomatohi cells were capable of engraftment after primary and secondary transplantation, whereas 5000 Hlf-tdTomato cells were not capable (Fig.1c, d). These results indicate that functional HSCs were enriched within the Hlf-tdTomatohi fraction in the bone marrow of the long bones.

a Hlf-tdTomato expression in the bone marrow blood cells obtained from long bones. The black box indicates the Hlf-tdTomatohi population. b Flow cytometry sorting of Hlf-tdTomato cells. The Hlf-tdTomatohi box population was used for transplantation experiments. The tdTomato box population was used as a negative control. c Bone marrow transplantation (BMT) experiments. Irradiated mice were transplanted with 100 tdTomatohi/CD45+ cells or 5000 tdTomato/CD45+ cells. d Second BMT experiments.

Next, we developed a method to observe the dynamics of Hlf-tdTomatohi HSCs in the tibial bone marrow in vivo (Fig.2). Previous studies have used drilled tibia for intravital imaging of HSCs in the long bones14,15,16,17. However, drilling of the long bones precluded the comparison of the HSC dynamics between adults and neonates for two reasons. First, drilling could disturb the microenvironment of the bone marrow, and second, the long bone of neonates is too fragile to be drilled, and it is not possible to avoid bleeding from the blood vessels penetrating the neonatal tibia (Supplementary Fig.2a and Supplementary Movie1). A multiphoton imaging system equipped with a bone-penetrating fiber laser (average power, >2W; pulse width, 55> fs; wavelength, 1070nm) was established to overcome the limitations of the conventional methods (Fig.2a). In our system, tdTomato-positive cells were observed under the intact tibial bone tissue, which was visualized with second harmonic generation (SHG) signals in adult mice (3 months old) in vivo (Fig.2b; Supplementary Movie2). Blood capillaries in the bone marrow were visualized by intravenous injection of an infrared fluorescent dye Qtracker 655 to confirm the location of the tdTomato-positive cells within the tibial bone marrow. Intravital imaging showed that tdTomato-positive cells were located around the blood capillary network (Fig.2c, d), which are typical blood vessel patterns in the bone marrow of long bones28. These results suggest that Hlf-tdTomato-positive cells in the intact tibial bone marrow can be observed by the method developed in the present study.

a Experimental schema of intravital imaging of the tibial bone. The tibial bone was exposed, and the bone marrow was imaged without bone drilling using a high-powered infrared laser. b Z-stack images obtained via in vivo imaging of the bone marrow in the undrilled tibia of Hlf-tdTomato KI mice. Hlf-tdTomato-positive cells were observed in the bone marrow cavity. Bone surface, bone, and bone marrow cavities. The depth is indicated in the upper right corner of each panel. SHG, second harmonic generation. c Orthogonal view of 3D images confirmed that Hlf-tdTomato-positive cells were in the bone marrow under the tibial bone. Blood capillaries in the tibial bone marrow were visualized by intravenous injection of Qtracker 655. Cells indicated with arrows 1 and 2 are shown in higher magnification in (d). See also Supplementary Movie2. d Higher magnification images of Hlf-tdTomato-positive cells located around the bone marrow capillary. e Intravital imaging of a Runx1-GFP mouse before drilling. Depth is 155m from the bone surface. f Intravital imaging of the Runx1-GFP mouse after drilling. The same region in (d) was reimaged after drilling. Background signals were imaged in the red channel, suggesting that most signals in the green channel were artificial backgrounds. Arrows indicate Runx1-GFP cells that had no background signals in the red channel.

The technical advances of our method were evaluated by comparing it with the conventional method. For the conventional method, intravital imaging of Runx1-GFP transgenic mice, in which HSCs and progenitor cells strongly express GFP29, was conducted using a short wavelength (920nm) laser which does not easily penetrate bone. Intravital imaging showed that Runx1-GFP labeled cells in the bone marrow were blurred without drilling (Fig.2e), and GFP signals were only clearly observed after drilling (Fig.2f), indicating that drilling is essential for the conventional method. As previously reported11, artificial background signals were observed in the green channel (Fig.2f), whereas these were rarely seen using our imaging method (Fig.2b). These results highlight the advances of the intravital imaging developed in the present study.

There were 18.21.0 tdTomato-positive cells in the volume of the intravital images (around 600m600m100m=3.6107m3; n=5 volumes from five mice). Immunohistochemical staining of the tibial bone sections obtained from Hlf-tdTomato KI mice was conducted (Fig.3a) to determine which tdTomato-positive cells in the intravital images corresponded to the Hlf-tdTomatohi HSCs that were identified in the flow cytometry analysis (Fig.1). In the histological sections of the tibial bone, there were 18,201933 CD45-positive cells and 1,630269 tdTomato-positive cells within the same volume as the in vivo-imaged volume (n=3 sections from three mice; Fig.3b, c). Since the cells with the top 0.011% tdTomato intensity in CD45-positive cells were defined as Hlf-tdTomatohi cells (Fig.1), those with the top two tdTomato fluorescent intensities in the in vivo images corresponded to Hlf-tdTomatohi cells (18,201 cells0.011%=2 cells; Fig.3c). We defined the remaining Hlf-tdTomato-positive cells with lower intensity in the intravital images that include differentiated progenitor cells25 as Hlf-tdTomatolow cells (16 cells in Fig.3c), which had lower stem cell potential (Supplementary Fig.3). Most of the tdTomato-positive cells in the histological sections were not visible using intravital imaging due to the very low intensity (1612 cells in Fig.3c). These results suggested that the cells with top two tdTomato fluorescent intensities in the in vivo image were HSCs.

a Immunohistochemical staining of tibial bone sections was obtained from an adult Hlf-tdTomato KI mouse. Ter-119, red blood cell marker; CD45, blood cell marker except for mature red blood cells and platelets; DAPI, nuclear marker. b Fluorescence distribution of tdTomato signals in CD45-positive cells in the histological sections of the tibial bone. The number of CD45-positive cells within the same volume as the in vivo-imaged volume was 18,201933 cells. Error bars indicate standard error. c The number of CD45 and tdTomato-double-positive cells within the same volume as the in vivo-imaged volume was 1630269 cells. The number of tdTomato-positive cells was 18.21.0 cells, suggesting that the remaining 1612 cells were not visible in the intravital images due to the very low fluorescent intensity. The cells with the top 0.011% tdTomato intensity in CD45-positive cells were defined as Hlf-tdTomatohi cells (Fig.1); therefore, the cells with the top two tdTomato fluorescent intensities in the in vivo images correspond to the Hlf-tdTomatohi cells (18,201 cells0.011%=2 cells). We defined the remaining Hlf-tdTomato-positive cells with lower fluorescent intensity (16 cells in average) as Hlf-tdTomatolow cells for quantitative analysis of Hlf-tdTomato-positive cell dynamics in Figs.4 and 5.

Three-dimensional time-lapse imaging of undrilled tibial bone marrow was performed to observe the in vivo dynamics of Hlf-tdTomatohi HSCs (Fig.4a and Supplementary Movie3). Artifactual movement of the image area, mainly caused by the heartbeat, was corrected using image registration. Hlf-tdTomatohi HSCs were stationary (Fig.4b), although they showed oscillatory movements in the restricted area. In contrast, Hlf-tdTomatolow cells migrated (Fig.4c). Quantitative analysis of the HSC migration using TrackMate30 revealed that the velocity of the Hlf-tdTomatohi HSCs (0.0960.019m/min, 10 cells from five mice) was significantly lower than that of Hlf-tdTomatolow cells (0.1690.017m/min, 81 cells from five mice; p=0.008; t=2.886; g=0.505; Fig.4d). We also showed long-term engraftment of Hlf-tdTomatohi cells (Fig.1c, d and Supplementary Fig.1), indicating that HSCs were stationary but oscillatory. However, differentiated cells were motile in the bone marrow of adult long bones. Therefore, our findings demonstrate that Hlf-tdTomato KI mice, the inside-bone intravital imaging system and quantitative bioimaging analysis facilitate the evaluation of the migration dynamics of endogenous HSCs in the native microenvironment of long bones.

a Hlf-tdTomato-positive cells in the tibial bone marrow were imaged for 2h in vivo. Arrows indicate Hlf-tdTomatohi HSCs and arrowheads indicate Hlf-tdTomatolow cells. See also Supplementary Movie3. b Higher magnification time-lapse images of Hlf-tdTomatohi HSCs. c Higher magnification time-lapse images of Hlf-tdTomatolow cells. d Quantitative comparison of the migration dynamics between Hlf-tdTomatohi cells (ten cells from five mice) and Hlf-tdTomatolow cells (81 cells from five mice).

Neonatal HSCs are characterized by fast cell cycling and higher mitochondrial membrane potential4, indicating changes in the cellular properties between adult and neonatal HSCs. Gene expression patterns were compared between developing HSCs and matured HSCs using RNA-seq to evaluate changes in the properties of neonatal HSCs.

Gene set enrichment analysis (GSEA) showed significant enrichment in cell migration-related genes in neonatal HSCs (Supplementary Fig.4a, b). Consistently, changes in the expression of genes related to the cytoskeleton and cell adhesion were observed in neonatal HSCs (Supplementary Fig.4cf). Differences in the cell migration-related genes indicated differences in the migration dynamics of neonatal and adult HSCs in the tibial bone marrow. From these results, we focused on the migration dynamics in subsequent experiments for intravital imaging of neonatal mice.

Migration of HSCs into the bone marrow from other hematopoietic organs has been hypothesized since adult-type definitive HSCs are generated from the aortagonadmesonephros region8,25. However, the migration dynamics of HSCs during development is unclear. Therefore, three-dimensional time-lapse imaging of the bone marrow was performed in the undrilled tibia in neonates (postnatal day 2; Fig.5a, left). The orthogonal view confirmed that the intravital imaging of the intact tibial bone marrow enabled the observation of endogenous tdTomato-positive cells in neonatal Hlf-tdTomato KI mice (Fig.5a, right; Supplementary Movie4). Quantitative analyses showed that the velocity of Hlf-tdTomatohi cells (1.5161.010m/min, six cells from three mice; top two fluorescent intensities) was much higher than that of Hlf-tdTomatolow cells (0.0780.010m/min, 24 cells from three mice; p=0.002; Z=3.059; r=0.558) in neonates (Fig.5b). Furthermore, the velocity of Hlf-tdTomatohi cells in neonates was much higher than that in adults (p=0.017; Z=2.386; r=0.597, Supplementary Fig.2b). These results suggest that HSCs are motile in the tibial bone marrow of neonates.

a Tibial bone was exposed on postnatal day 2 (left). Orthogonal view image of the tibial bone marrow (right). See also Supplementary Movie4. b Quantitative comparison of the migration dynamics between Hlf-tdTomatohi cells (six cells from three mice) and Hlf-tdTomatolow cells (24 cells from three mice) in neonates. c Time-lapse images of developing (P2) bone marrow showing migration of an Hlf-tdTomatohi cell in the blood vessels. White arrows indicate migrating cells in the blood vessel and yellow arrows indicate stable cells outside the blood vessels. See also Supplementary Movie5. d Another example of an Hlf-tdTomatohi cell migrating in the bone marrow blood vessels in a neonatal mouse (P1).

Intravital imaging was conducted after visualizing blood vessels by injecting Qtracker 655 via the superficial temporal vein31 to check whether the motile Hlf-tdTomatohi cells were extravascular or intravascular. Some of the Hlf-tdTomatohi cells rapidly migrated in the blood vessels (Fig.5c, d, white arrows). Moreover, Hlf-tdTomatohi cell attached to the vessels during the imaging session, indicating extravasation and homing to the bone marrow (Fig.5c, 63 and 100min; Supplementary Movie5). In contrast, Hlf-tdTomatohi cells located outside the capillaries, which appeared to be extravasated prior to the imaging session, were stationary (Fig.5c, yellow arrows). These results suggest that motile Hlf-tdTomatohi cells migrate in the blood vessels of the neonatal tibia.

Finally, migration of HSCs from outside the bone marrow was observed using time-lapse imaging of the tibial bone cavity, where the blood vessels that penetrate the bone are located (Fig.6a). An Hlf-tdTomatohi cell was observed to rapidly migrate within the bone cavities (Fig.6b and Supplementary Movie6). Interestingly, the distance between the observed cell and the inner bone surface appeared to be increased (Supplementary Fig.5a, b), suggesting migration of the cell to the deeper part of the bone. Taken together, these results indicate that HSCs migrate in the bone cavities and bone marrow during tibial bone marrow formation.

a Two-photon images showing the blood vessels penetrating the bone cavity in the tibial bone in a neonatal mouse (P3). Yellow arrows indicate bone cavities. b Time-lapse images of Hlf-tdTomatohi cells migrating from the bone surface to the bone marrow cavity. White arrows indicate a migrating cell in the bone cavity. See also Supplementary Movie6. c Transient vessel penetration model for HSC homing during bone marrow formation. HSCs migrate from outside the tibia to inside via transient blood vessels penetrating the bone during bone marrow formation.

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Bone marrow imaging reveals the migration dynamics of neonatal hematopoietic stem cells | Communications Biology - Nature.com

Recommendation and review posted by Bethany Smith

LAS VEGAS, NV, Aug. 01, 2022 (GLOBE NEWSWIRE) -- via NewMediaWire Meso Numismatics, Inc. (Meso Numismatics or the Company) (MSSV), a technology company specializing in Biotech and Numismatics, is pleased to announce additional global expansion by opening stem cell therapy and regenerative medicine facilities in Indonesia. The new facilities emphasize Global Stem Cells Group's objective of introducing its therapies and technology to meet market demands in populous parts of the world.

In partnership with the Dr. Yanti Aesthetic Clinics, which currently has 6 branches across Indonesia, this latest GSCG expansion will promote high standards of service in regenerative medicine across the country. As part of this effort, through GSCG the International Society for Stem Cells Applications (ISSCA) has granted Dr. Yanti Aesthetic Clinics membership and use of its brand, products, therapies, and training on how to apply stem cell therapies.

This new partnership seeks to expand the Global Stem Cells Group (GSCG) brand and create centers of excellence in cell therapy to meet the high demand within the vast Asian markets, said David Christensen, CEO of MSSV. GSCG is rapidly expanding its global operations as it seeks to become a significant player in the lucrative regenerative medicine industry. To achieve our expansion plans, our organization is partnering with healthcare providers specializing in regenerative medicine with at least five years of experience in the healthcare sector.

Video: https://youtu.be/T2CFjsps9qk

The vision behind the effort.

The Indonesia addition is the latest part of an expanding medical network of partners, and it will formalize and strengthen ties, establishing a global center of excellence to guarantee that we effectively use the underlying basic stem cell technology for medical conditions, where traditional therapeutic approaches seem to have failed. This is consistent with GSCG's overall strategy for developing regenerative medicine through data-driven studies, disease modeling, and cell-based therapeutics.

The Dr. Yanti Aesthetic Clinic is a key partnership because it provides the organizational and physical infrastructure needed to disseminate need-based stem cell locally. And Global Stem Cells Group's outstanding cell and stem cell biology and disease pathophysiology give an edge to patients for which they are prescribed.

The opening in Indonesia also presents the perfect opportunity to translate breakthrough therapies from basic discoveries to useful products by drawing upon the skills and local knowledge promoted within Dr. Yanti Aesthetic Clinics.

GSCG group managing director, Benito Novas, provided a clear description of the new strategic direction and objectives. "Our goal is to make regenerative medicine benefits a reality for both doctors and patients all around the world. We recently launched a very similar effort in Pakistan. Additional announcements are planned in the near future as we attempt to expand our presence." Meso Numismatics and Global Stem Cells Group Expand its Global Footprint

The current market outlook.

Stem cell therapy is striving to become an increasingly effective clinical solution to treat conditions that traditional or mainstream medicine offers only within palliative care and pain management. Patients all over the world are searching for a natural regenerative alternative without the potential risks and side effects sometimes associated with mainstream pharmaceuticals. With the opening of each new treatment center in populous regions such as Indonesia, GSCG is working to help stem cell therapy and regenerative medicine to eventually move from alternative and elective procedures to mainstream protocols.

This new clinic effort will play a significant role in the development of regenerative medicine in Indonesia and indeed the rest of the world by adding yet another opportunity for continuous improvement through research and development, Christensen continued. By adding busy clinics in population centers, we plan to consistently generate high volumes of reliable clinical data to assist us with the development and refinement of even more medicines and treatments.

About Dr. Yanti Aesthetic Clinics

Dr. Yanti Aesthetic Clinics is a premier cosmetic and aesthetics clinic based in Kelapa Gading, Jakarta Utara. Since its inception in 2004 in Surabaya by Dr. Khoe Yanti Khusmiran, the clinic has expanded to over 6 branches throughout Indonesia. Dr. Yanti clinics provide a range of skin and body enhancement treatments through minimally invasive and non-invasive procedures the expertise of which are a natural fit for the addition of a variety of stem cell therapies.

"Indonesians have a growing need for the latest medical technology that is reliable, potent, has reduced side effects, and leverages the bodys own healing biochemistry to resolve injury and aging, said Dr. Yanti. We are honored to be a part of GSCG, which has a proven 10-year track record in the market with a strong and growing international reputation. This new partnership is expected to create a wide variety of custom treatment options we can offer our patients and treat injury and illness in ways we could not before.

The newly formed partnership will deliver revolutionary medicines through Dr. Yanti clinics to assist patients in avoiding permanent harm and live a healthier life, while changing the paradigm from asymptomatic treatments to cures that may improve and restore quality of life.

More about Global Stem Cells Group

GSCG delivers leadership in regenerative medicine research, patient applications, and training through our strategic global networks. We endeavor to enable physicians to treat otherwise incurable diseases using stem cell therapy and to improve the quality of life and care across the world.

For this reason, GSCG works with innovative, next-generation therapy providers like Dr. Yanti Aesthetic Clinics to give access to one-of-a-kind holistic and safe treatment options.

More information regarding this transaction and the Global Stem Cells Group may be found at GSCG.

This press release should be read in conjunction with all other filings on http://www.sec.gov

For more information on Global Stem Cells Group please visit: http://www.stemcellsgroup.com

About Meso Numismatics: Meso Numismatics, Corp is an emerging Biotechnology and numismatic technology company. The Company has quickly become the central hub for rare, exquisite, and valuable inventory for not only the Meso region, but for exceptional items from around the world.

Meso has now added Biotechnology to its portfolio and will continue to grow the company in this new direction. With the Company's breadth of business experience and technology team, the Company will continue to help companies grow.

Forward-Looking Statements

Some information in this document constitutes forward-looking statements or statements which may be deemed or construed to be forward-looking statements, such as the closing of the share exchange agreement. The words plan, "forecast", "anticipates", "estimate", "project", "intend", "expect", "should", "believe", and similar expressions are intended to identify forward-looking statements. These forward-looking statements involve, and are subject to known and unknown risks, uncertainties and other factors which could cause the Company's actual results, performance (financial or operating) or achievements to differ from the future results, performance (financial or operating) or achievements expressed or implied by such forward-looking statements. The risks, uncertainties and other factors are more fully discussed in the Company's filings with the U.S. Securities and Exchange Commission. All forward-looking statements attributable to Meso Numismatics, Inc., herein are expressly qualified in their entirety by the above-mentioned cautionary statement. Meso Numismatics, Inc. disclaims any obligation to update forward-looking statements contained in this estimate, except as may be required by law.

For further information, please contact:investor.relations@mssvinc.com Telephone: (800) 956-3935

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Global Stem Cells Group Expands Its Stem Cell Therapy and Regenerative Medicine Centers to Indonesia - GlobeNewswire

Recommendation and review posted by Bethany Smith

Breast cancer survivors often experience symptoms of declining estrogen levels, including hot flashes, night sweats, vaginal dryness, and urinary tract infections. While hormone replacement therapy (HRT) can be an effective treatment for these adverse effects, some types of HRT have been associated with a higher risk of breast cancer recurrence, according to BreastCancer.org.

The American Cancer Society warns that higher estrogen levels may heighten the risk of breast cancer growth, and doctors may caution women with a history of breast cancer to not take types of systemic HRT that affect the entire body. HRT has also been linked to cardiovascular risks, such as heart disease, stroke, and blood clots.

A study published this month in the Journal of the National Cancer Institute, however, found that menopausal hormone therapy for breast cancer survivors is not associated with breast cancer reoccurrence.

Scientists in Denmark analyzed data from the countrys national prescription registry regarding postmenopausal women diagnosed between 1997 and 2004 with early-stage breast cancer who received no treatment or five years of hormone therapy. Among 8,461 women who had not received vaginal estrogen therapy or menopausal hormone therapy before a breast cancer diagnosis, 1,957 and 133 used vaginal estrogen therapy or menopausal hormone therapy, respectively, after diagnosis.

In accordance with national treatment guidelines during the study period, all patients were allocated either to five years of tamoxifen (one of the most widely used breast cancer treatments) or an aromatase inhibitor (which lowers estrogen levels by stopping an enzyme in fat tissue), or both treatments in sequence.

The researchers observed no higher odds for cancer returning or death in those who had the therapy compared with those who didnt.

These results suggest that breast cancer survivors on tamoxifen with severe symptoms [of genitals and urinary tract] can take vaginal estrogen therapy without experiencing an increase in their risk for breast cancer recurrence, said Elizabeth Cathcart-Rake, MD, who wrote in an accompanying editorial to the investigation.

Study authors noted, however, that a subgroup analysis revealed an increased risk of recurrence, but not death, in patients receiving vaginal estrogen therapy with aromatase inhibitors.

Patients who are taking aromatase inhibitors should try alternative strategies for management of genitourinary symptoms because vaginal estrogen therapy will likely increase their risk for breast cancer recurrence, said Dr. Cathcart-Rake, who is a physician at the Mayo Clinic in Rochester, Minnesota.

Overall, Cathcart-Rake sees the investigation helping to clarify the potential safety and hazards of taking such treatments. This large cohort study helps to inform the nuanced discussions between clinicians and breast cancer survivors about the safety of vaginal estrogen therapy, she said.

BreastCancer.org recommends that because the risks and benefits are different for every woman, breast cancer patients should educate themselves and talk to their doctor to decide if HRT is right for them.

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Hormone Replacement Therapy Not Linked to Breast Cancer Recurrence, Study Finds - Everyday Health

Recommendation and review posted by Bethany Smith

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Association of hormone replacement therapy with risk of gastric cancer: a systematic review and meta-analysis | Scientific Reports - Nature.com

Recommendation and review posted by Bethany Smith

FLINT, Mich., Aug. 2, 2022 /PRNewswire/ -- Forum Health Akron, integrative and functional medicine practice part of the nationwide Forum Health network, has welcomed Tammy Guseman MHA, MSN, APRN, CNP to its practice.

Forum Health Akron, formerly Revitalize Med, is led by board-certified physicians including Dr. Tara Scott. Using a functional and integrative approach, this clinic specializes in women's health, hormonal imbalance, thyroid disorders, infertility, nutrition, and more to optimize its patient's health and well-being.

"Tammy is a welcome addition to our growing team," said Dr. Scott. "Her years of experience in family medicine, and dedication to a functional and integrative approach make her a great fit."

Tammy Guseman is a board-certified family nurse practitioner who has experience in both inpatient and outpatient settings. She made the decision to focus her career on using an integrative approach to hormone balancing after her own positive experience with functional medicine.

"I am excited to continue my career with Forum Health Akron," said Tammy. "Functional care has benefitted me personally and I have seen first-hand the profound healing it offers my patients."

Tammy received her bachelor's and master's degrees from Walsh University, and a master's degree in healthcare administration from Ohio University. She is continuing to expand her education in bio-identical hormone replacement therapy through coursework from the American Academy of Anti-Aging Medicine (A4M).

"Adding Tammy to the team will allow us to continue to provide top-quality service to our patients," said Adam Puttkammer, president of Forum Health. "We are always striving to support our teams with experienced and knowledgeable providers."

"Tammy's commitment to continued education and personal interest in functional and integrative medicine aligns perfectly with our values at Forum Health," said Phil Hagerman, chief executive officer at Forum Health.

For more information on Forum Health, including how to join one of our practices, visit http://www.forumhealth.com.

About Forum Health, LLC

Forum Health, LLC is a nationwide provider of personalized healthcare. Steeped in the powerful principles of functional and integrative medicine, Forum Health providers take a root-cause approach to care. They listen and dig deep exploring lifestyle, environment, and genetics to help each patient achieve their ultimate health goals. Members have access to advanced medical treatments and technology, with care plans informed by data analytics and collaborative relationships. To learn more, visit forumhealth.com.

SOURCE Forum Health, LLC

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Forum Health Akron Welcomes Experienced Nurse Practitioner to Growing Team - PR Newswire

Recommendation and review posted by Bethany Smith

South Carolina became the seventh state last month to permit health care providers to decline to serve people if they feel doing so would violate their religious beliefs.

As a result, more than 1 in 8 LGBTQ people now live in states where doctors, nurses and other health care professionals can legally refuse to treat them, according to the Movement Advancement Project, an LGBTQ think tank. In addition to South Carolina, Mississippi, Alabama, Arkansas, Tennessee, Ohio and Illinois have similar measures in effect.

The conflict between patient needs and religious directives has been a serious problem in the past, and I dont see any sign of that issue being resolved quickly and easily.

Jenny Pizer, lambda legal

Advocates and legal experts say the laws will further raise the barriers to health care for lesbian, gay, bisexual, transgender and queer patients.

We often are worried that the expansion of religious rights in these contexts will be taken as a license to discriminate, said Jenny Pizer, the law and policy director for the LGBTQ legal advocacy group Lambda Legal.

Proponents of such legislation, however, say the measures dont allow providers to discriminate against or target LGBTQ people.

South Carolina state Sen. Larry Grooms, who supported his states law, the Medical Ethics and Diversity Act, told NPR in June that its based on procedure, not on patients.

This is America, where you should have the freedom to say no to something you dont believe in, he told NPR.

Although religious freedom or conscience measures, as theyre often called, dont explicitly list LGBTQ people among those who may be refused treatment, advocates say that in practice they are affected disproportionately.

Ivy Hill, the community health program director for the Campaign for Southern Equality, which promotes LGBTQ equality across the South, said transgender people are among those who will be the most negatively affected.

When we have laws in place that make it easier for providers to discriminate, of course its not going to do anything but make it worse, said Hill, who uses gender-neutral pronouns. The people who are already on the margins of the margins are going to be the ones who are most deeply impacted by stuff like this.

Even before the new law went into effect, they said, many trans people they work with in South Carolina struggled to find gender-affirming health care providers in the state willing to help them gain access to hormone therapy, leading some of them to travel to North Carolina to get care.

Hill said doctors usually dont tell trans people that they wont treat them for religious reasons, which makes it hard to know how often it happens. Research has found that LGBTQ people, particularly transgender people, are more likely to face medical discrimination.

A study published in 2019 found that 16 percent of LGBTQ adults, or about 1 in 6, reported experiencing discrimination in health care settings. A 2020 survey from the Center for American Progress, a liberal think tank, found that 16 percent of LGBTQ people, including 40 percent of transgender respondents, reported postponing or avoiding preventive screenings because of discrimination.

Maggie Trisler, who works in tech, said she had a great relationship with her primary care provider in Memphis, Tennessee, for about a year and a half in 2016 and 2017. He asked her in-depth questions about her health and the band she plays in, and he said he was going to take his wife to see her play.

Then, in March 2017, Trisler came out to him as transgender, and she said he suddenly became very cold and told her he doesnt know anything about the standards of care for transgender people. He began to blame pain she was having on her weight, she said.

It suddenly went from the best doctor-patient relationship Ive ever had to just the absolute least helpful, most frustrating that Ive had, she said.

Three months later, Trisler said, the doctor effectively although not explicitly told her he couldnt see her anymore.

He did say that he was deeply uncomfortable treating me with [hormone replacement therapy], he wasnt comfortable providing HRT, and if I was seeking that elsewhere, then maybe I should seek medical care elsewhere, she said.

Trisler added that she was lucky to have good insurance and that it was easy for her to change doctors, although she acknowledged that she is coming from a rather privileged position and that what was just a nuisance for her could have been a critical roadblock for others.

While LGBTQ people have long faced barriers to health care because of religious refusals, Pizer said, such religious objections can violate both state and federal law in some cases.

Pizer pointed to a 2005 case in which the North Coast Womens Medical Care Group in Southern California denied infertility treatments to her client Guadalupe Lupita Benitez because she is a lesbian. The providers argued that it was within their religious rights to refuse to offer treatment to Benitez, but the California Supreme Court decided that religious rights protected under California law dont excuse violations of the states nondiscrimination law.

The court found that when doctors are practicing in a particular field and offering services generally, according to patient needs in their field, they cant pick and choose among patients in ways that violate the nondiscrimination law, Pizer said.

Pizer said the problem with laws like South Carolinas Medical Ethics and Diversity Act is that they use broad language that doesnt give examples of situations in which a religious objection in medicine would violate medical standards or federal law. Many hospitals, including some that are religiously affiliated, receive federal funding. As a result, if they were to provide fertility treatments to heterosexual people and not to LGBTQ people, they would violate Section 1557 of the Affordable Care Act, which the Biden administration hopes to strengthen to better protect access to abortion and gender-affirming services.

Pizer said the issue is becoming more prominent and contentious as Catholic-affiliated institutions control an increasing proportion of the U.S. hospital system. As NBC News reported recently, more than 1 in 7 U.S. hospital patients are cared for in Catholic facilities.

The conflict between patient needs and religious directives has been a serious problem in the past, and I dont see any sign of that issue being resolved quickly and easily, Pizer said. A hospital thats operating in a community to serve the community more broadly should not be imposing their religious beliefs on people that are not part of that faith or that are at the hospital for medical services, not religious services.

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More than 1 in 8 LGBTQ people live in states where doctors can refuse to treat them - NBC News

Recommendation and review posted by Bethany Smith

For this episode ofThe Vitals,Oncology Nursing News met with Sarah Donahue, MPH, NP, a nurse practitioner at the University of California San Francisco Health, to discuss findings from the findings of DESTINY-Breast04 trial (NCT03734029).

DESTINY-Breast04, a phase 3, open-label pivotal trial, randomly assigned patients with unresectable or metastatic HER2-low breast cancer to receive the fam-trastuzumab deruxtecan-nxki (Enhertu) at 5.4 mg/kg every 3 weeks (n = 373) or physicians choice chemotherapy at locally approved dosing (n = 184). All enrolled patients had already received at last 1 prior line of therapy in the metastatic setting.1,2

The primary end point was progression-free survival (PFS) in patients with hormone receptorpositive breast cancer. The median PFS in the primary end point population was 10.1 months (95% CI, 9.5-11.5) with the antibody-drug conjugate vs 5.4 months (95% CI, 4.4-7.1) with standard of care (HR, 0.51; 95% CI, 0.40-0.64;P< .0001). The median overall survival was 23.9 months (95% CI, 20.8-24.8) vs 17.5 months (95% CI, 15.2-22.4), respectively (HR, 0.64; 95% CI, 0.48-0.86;P= .003).1,2

These findings, according to Donahue, will result in the addition of another therapy that patients with unresectable or metastatic HER2-low breast cancer can benefit greatly from.

One significant part [of] this trial is that included such a large population of patients, Donahue says. It really captured most patients with metastatic breast cancer[there were] patients with liver metastases, lung metastases, and brain metastases that were stable. It really covered a very large representative group of patients.

Further, Donohue adds, The data that were presented at the [2022 ASCO Annual Meeting] showed that the patients that received the trials trastuzumab deruxtecan had a much [improved] PFS compared with those patients that were on the physicians choice of chemotherapy. [Investigators] found that they could increase the median PFS from 5 months to about 10 months, so they could double it, Donahue explains. It was similar with the patients with hormone [receptor]positive diseases, as with the entire population. It did not matter what the hormone receptor status was for these patients, [they all] received that benefit.

If you liked todays episode ofThe Vitals, please consider subscribing to our podcast on Apple Podcasts, Spotify, Google Podcasts, Amazon Music, and many of your other favorite podcast platforms, to get a notification every time a new episode is posted. While you are there, please take a moment to rate us!

Thanks again for listening toThe Vitals. Be sure to never miss a beat withOncology Nursing News.

References

Read more:
Sarah Donahue Highlights Destiny-Breast04 Trial Takeaways for Patients With HR+, HER2-Low Metastatic Breast Cancer - http://www.oncnursingnews.com/

Recommendation and review posted by Bethany Smith

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At-home PCOS tests may provide an insight into hormone levels that a person can then share with their doctor or healthcare professional. However, alone, they are unable to diagnose PCOS.

Sex and gender exist on spectrums. For the purposes of this article, we use female to refer to a persons sex assigned at birth.

Polycystic Ovary Syndrome (PCOS) is a common condition that affects a females ovaries. People with PCOS are often unable to ovulate which can lead to irregular menstrual cycles. PCOS is also linked with the development of other conditions in later life, such as type 2 diabetes and high cholesterol levels, and other cardiovascular issues. PCOS is also one of the most common causes of infertility.

The exact cause of PCOS is unknown, although researchers and healthcare professionals usually cite a combination of genetic and environmental factors. According to a 2019 study, although PCOS is proven to be extremely heterogenetic, it has not yet been possible to find a single gene variant that underlies to condition.

Some common symptoms of PCOS are:

Symptoms usually appear in a females teenage years or early twenties, with most caused by higher than average androgen levels, also known as the male sex hormone.

A 2021 study found that hyperandrogenism facilitates the growth and advancement of PCOS. Higher levels of androgen can also cause the follicles to enlarge, forming cysts on the ovaries.

When diagnosing PCOS, doctors and healthcare professionals typically use the Rotterdam Criteria. The criteria include:

A person must display two of the three criteria for a doctor to diagnose PCOS.

When diagnosing PCOS, doctors and healthcare professionals look for three or more typically indicative symptoms. If a person experiences this number of symptoms, or if they have any general concerns about PCOS, they should speak with their doctor as soon as possible.

At-home PCOS tests look for female hormonal imbalances, with high androgens levels possibly indicating PCOS.

The types of samples needed for an at-home test include:

The majority of tests provide a lancet so a person can take a blood sample using the finger-prick method.

Results are typically available within a few days of the lab receiving the test samples from the female.

Only a doctor or qualified healthcare professional can make a formal PCOS diagnosis.

However, anyone can use an at-home PCOS test if they feel they may have a hormonal imbalance. The results from such tests can help a doctor in their diagnosis.

Below, we look at some at-home PCOS tests that a person may consider.

This at-home test measures key hormone levels. The hormones tested include those related to stress, sex, and those responsible for the development of ovarian follicles. However, the test is not suitable for those on hormonal contraception, hormone replacement therapy, steroid or testosterone-containing medications including gels, creams, patches, and oral medication.

A person orders their test online and the company will deliver the test for free, in a discrete package.

Individuals should collect their samples in the morning, before eating or drinking. They should collect the saliva sample first, as taking blood can sometimes raise cortisol levels.

A person should then return their packaged sample on the same day, using the prepaid shipping label provided. The sample is sent to one of the companys CLIA-certified and ISO-accredited laboratories for analysis.

Results will display via an individuals online LetsGetChecked account, within 25 days. If necessary and at no extra cost, a person can discuss their results with a member of the companys nursing team for advice on the next steps.

It is important to note that, due to state restrictions, this test is not permitted for use in New York.

Some pros and cons of the LetsGetChecked PCOS Test include:

Pros

Cons

Modern Fertility is a reproductive health company that gives personalized fertility tests and follow-up information from a licensed nurse. Part of its fertility test includes looking at the hormones associated with PCOS, due to its link to fertility difficulties.

The Modern Fertility Hormone Tests measures up to eight hormones, two of which link to PCOS testosterone and androgens. It also looks at AMH levels, that, when raised, AMH may indicate large numbers of undeveloped follicles in ovaries.

Initially, a person orders their test online that a doctor will review and personalize based on any birth control they may take. They can then choose to take the test at home or opt to visit a local Quest Diagnostics lab.

If taking the test at home, a person should follow the sample collection and packaging instructions and return the test the same day. The company will provide results via an individuals online profile within a few days.

The company offers aftercare that includes:

There are some pros and cons that a person may consider, such as:

Pros

Cons

Everlywell Womens Health test is suitable for people at all stages of life. It tests for hormonal imbalances which could indicate PCOS.

A person orders an online test that comes with prepaid return packaging. Upon receipt of the testing kit, the individual must register the test on the companys website, using the unique ID number provided.

The test has easy-to-follow instructions so a person can take a finger-prick blood sample and a saliva sample that they should return the same day. The results are available to view via the companys online platform within a few days.

The results include a personalized report explaining the results and some online resources for continued learning with healthcare professionals.

Below are some pros and cons for a person to consider:

Pros

Cons

A person orders their test online and the company will ship a testing kit. Shipping is free for those in the U.S., Canada, Puerto Rico, and the U.S. Virgin Islands.

The test is urine-based, and according to the companys website, it tests urine because it provides more accurate results than simply testing cortisol or sex hormones alone. DUTCH requires a person to collect four or five dried urine samples over 24 hours, using the test strips the company provides. The dried samples are suitable for international shipping as they are stable for several weeks.

A full timeline of how and when to collect the samples is available via the company website. Once an individual returns their samples and the lab receives them, they will process the samples and provide results within 510 days.

The company advises people not to take oral DHEA 48 hours prior to testing, or oral estrogen or pregnenolone 72 hours prior to testing.

Restrictions apply for ordering tests in New York, Rhode Island, and Maryland.

Some pros and cons that a person may consider, include:

Pros

Cons

Individuals should speak with a doctor if they are experiencing symptoms that interfere with their everyday life.

If a female has taken an at-home PCOS test, they should share their results with their doctor to help them provide a formal diagnosis. Although at-home PCOS tests can provide information on hormonal imbalances, only a doctor can provide an official PCOS diagnosis.

Here are some common questions about at-home PCOS tests.

A person may notice if they experience symptoms of PCOS, but only a doctor can officially diagnose it. At-home PCOS tests can provide a doctor with the results to help with diagnosis.

There is no test that definitively diagnoses PCOS. However, many people with PCOS have a hormonal imbalance. Hormone testing can help to identify whether key hormones are outside of expected limits and help a healthcare professional make a more accurate diagnosis.

A doctor can diagnose PCOS by initially discussing a females medical history and symptoms. They may then complete physical exams or arrange for an imaging test, such as an ultrasound.

PCOS is a hormonal disorder that affects a persons ovaries. Symptoms can range from mild to severe and include pelvic pain, oily skin, and weight gain. Symptoms typically present in a persons teenage years through to their early 20s.

At-home PCOS tests look at an individuals hormones, as for many people, hormonal imbalances are a typical sign of PCOS. Testing samples are typically blood, saliva, or urine.

Although at-home test results can show irregularities with hormones, they are not indicative of a formal PCOS diagnosis. For this, a person must consult with a doctor or qualified healthcare professional.

Read more:
4 at-home PCOS tests in 2022: What to know, how to choose, and more - Medical News Today

Recommendation and review posted by Bethany Smith

Having a normal blood pressure level is necessary for overall well-being.Blood pressure is essential because it helps the flow of blood from the heart to other areas of the body like organs, tissues and arteries and having high blood pressure can cause serious long-term health issues. But the good news is there's several ways to get blood pressure under control. Eat This, Not That! Health spoke with Dr. Bayo Curry-Winchell, Urgent Care Medical Director and Physician, Carbon Health and Saint Mary's Hospital who shares causes of high blood pressure and how to help prevent it. Read onand to ensure your health and the health of others, don't miss these Sure Signs You've Already Had COVID.

Dr. Curry-Winchell says, "Your blood pressure is the (normal) pressure created by blood flowing in your arteries. This pressure might change throughout the day based on multiple things such as exposure or response to mental or physical stressors. It's important to remember having high blood pressure is considered a silent disease. Therefore, there is no guarantee you will experience any symptoms or warning signs that you have high blood pressure (defined as a number greater than 120/80). The only way to know is to get your blood pressure checked."

Dr. Curry-Winchell tells us, "A blood pressure greater than 120/80 can increase your risks of having a stroke, heart attack or developing heart disease. A higher-than-normal blood pressure can cause damage to the arteries affecting the amount of blood flow to organs such as your eyes, brain, heart, and kidneys."

"You can't always tell! Not everyone gets a warning sign they have elevated blood pressure," says Dr. Curry-Winchell. "Because high blood pressure is a silent disease some of my patients discover they have high blood pressure after a heart attack or stroke. The only way to know is to get it checked. I recommend purchasing a blood pressure cuff that you can use at home that records your readings."

According to Dr. Curry-Winchell, "You are at increased risk if you have a family history of hypertension, getting older (aging), diagnoses with chronic health conditions such as diabetes, eat a high salt diet, are considered overweight, drink large amounts of alcohol, and use tobacco."6254a4d1642c605c54bf1cab17d50f1e

Dr. Curry-Winchell explains, "There are several causes that increase your risk for developing high blood pressure including family history, age, lifestyle choices, etc. It is often socialized that elevated blood pressure is more common amongst African Americans. The reason is multi-faceted and not due to race/ethnicity; it is due to access to quality care, medical racially based algorithms, distrust of healthcare, and social, economic, and environmental determinants of health to name a few."

Dr. Curry-Winchell shares the following ways to have a normal blood pressure level.

"Stay Active

Participating in low or high impact exercising for approximately 5 days a week for approximately 30 minutes a day can lower your risks.

Lower Stress

I encourage my patients to find ways to lower their stress each day. Take the time to invest in yourself and find ways to bring a sense of joy or relaxation to your day. It can be as simple as closing your eyes and thinking about absolutely nothing, listening to music, singing in the shower, or reading one page in the book you have been wanting to read.

Eating Heart Healthy Foods

A balanced diet of fruits, vegetables, carbohydrates, and protein that includes low sodium (salt) options can help decrease your risks.

Quit Smoking

Smoking (nicotine) cigarettes causes your heart rate and blood pressure to increase. When this happens over an extended period and multiples times a day you increase your risks of developing hypertension.

Drink Less or Refrain from Alcohol

Alcohol increases several hormones such as renin, vasopressin (antidiuretic) and cortisol (stress hormone) which helps regulate blood pressure. Why does this matter? An increase in these hormones such as renin causes blood vessels to narrow, decreasing the amount of blood flowing to organs. Vasopressin, an antidiuretic hormone, allows your body to hold on to more fluid. Alcohol quells this function which in turn increases urination and risks for dehydration."

Heather Newgen

More:
The #1 Cause of High Blood Pressure According to Science Eat This Not That - Eat This, Not That

Recommendation and review posted by Bethany Smith

To the Editor:

Re Why Is the Right Forcing Women Who Miscarry to Suffer?, by Michelle Goldberg (column, July 19):

They dont tell you this in medical school, but to be an OB-GYN physician is to know heartache up close and personal, over and over again. I have been a practicing physician in Portland, Ore., for the last 37 years. My colleagues span the political spectrum, but almost everyone I have known has put the interest of the mothers life before that of the embryo or fetus. And if for reasons of conscience they could not, they would find another provider who could.

With the Dobbs decision, my specialty has been thrown into disarray. Miscarriage is one of the most common conditions we treat, as it occurs in about 10 to 20 percent of known pregnancies.

These new laws in anti-choice states just ban termination of pregnancy, some immediately after fertilization. They have no subtlety, they have no algorithms to guide practice.

Now providers are in an extremely precarious situation, risking prosecution. When the only exception for pregnancy termination is the mothers risk of death, how close must she be for them to act? Most pregnant people are young and healthy, and they cope well with blood loss and infection, until suddenly they do not, and by then it may be too late to save them.

America will now see what happens when politicians exploit the care of women for their political gain. It is brutal. Anyone who thought it would take a long time to see the consequence of banning a common medical procedure will soon see the tears, blood and death that we told them was coming. It is inevitable, and it will continue.

Marguerite P. CohenPortland, Ore.The writer is a fellow of the American College of Obstetricians and Gynecologists.

To the Editor:

Re Risks to Patients as Doctors Deal With Abortion Exceptions (news article, July 21):

As a Missouri resident living under a new abortion ban, I am enraged and disgusted. Advocates warned of the dangers of bans for years, unheeded. Even now, as doctors describe how pregnant women will die from substandard care as a result of this ban, our leaders shrug.

Days after Missouri enacted an abortion ban except in medical emergencies, I called the attorney generals office for clarification. I shared that I had experienced two life-threatening conditions in my last pregnancy, and I was concerned that my obstetrician might be constrained if a similar complication arose today.

The staff attorney told me that he was unable to offer guidance, as giving legal advice could jeopardize his law license. I replied that this ban could jeopardize my life. His response? That I could leave the state.

Unfortunately, I worry that many Missouri families like mine will take him up on his suggestion. I worry that our womens health providers will choose to practice elsewhere. I worry that Missouris elected officials will be shortsighted enough to celebrate these losses. The state deserves better.

Katy NimmonsSt. Louis

To the Editor:

Re Im Terrified for My Patients, by David N. Hackney (Opinion guest essay, July 10):

Dr. Hackney describes the pain experienced by a pregnant woman who learns that her child has a lethal condition yet has no option but to carry to term. While accurate, the potential pain of learning your fetus has a serious abnormality goes well beyond this.

A variety of severe, life-altering birth defects and genetic syndromes can be diagnosed prenatally, and many of these conditions are not lethal or not lethal immediately but serious enough that the affected child faces a lifetime of severe disability and, in many cases, pain.

Being told in the middle of a much wanted pregnancy that your child will have severe neurological or physical disabilities, that she will never walk, or talk or even be able to roll over by herself, and yet will survive, is as devastating as being told your child will die at birth, but with far different consequences.

Despite Justice Amy Coney Barretts assertion, these children are unlikely to be adopted. It is unethical to diagnose a medical condition and not provide the patient with reasonable and safe therapeutic options, but the laws of many states now make it impossible to do the ethical thing. More pain for everyone.

Katharine WenstromProvidence, R.I.The writer is a professor at the Alpert Medical School of Brown University and past president of the Society for Maternal Fetal Medicine.

To the Editor:

Dr. David Hackney joins so many doctors highlighting the serious life and health risks pregnant women now face. President Biden and Congress cannot restore comprehensive abortion rights in any manner that will survive future elections.

So congressional Democrats should immediately legislate a strong national right to abortion if continued pregnancy would risk the life, physical health or mental health of the mother, or if the fetus will not survive.

Further, there should be reasonable protection for medical providers who perform these medically necessary procedures. Otherwise, physician hesitation may cost womens lives.

I would hope there might be bipartisan support for this.

Without these protections, hikes to doctors liability insurance could render obstetrics care grossly overpriced and take already scarce funding away from all medical care.

Mary Jo NapoliColumbus, Ohio

To the Editor:

Re Abortion Bans Will Affect Both Rich and Poor Americans (Opinion guest essay, July 7):

Elizabeth Spiers describes the impact of abortion restrictions as a crisis for all American women, with delays in therapeutic abortions resulting in fatal consequences. As an emergency physician who routinely cares for women with pregnancy-related complications, I echo Ms. Spierss concerns.

I frequently treat obstetric emergencies. In recent weeks I cared for pregnant women with the following complications: ectopic pregnancy, undetectable fetal heartbeat with decreasing pregnancy hormone levels, and copious vaginal bleeding with an open cervix.

My patients were not asked their political affiliation or religious persuasion. I didnt need to know whether their pregnancies were planned or desired. My focus was on the timely care of three vulnerable patients, with pain and bleeding, who looked to our medical team for compassionate treatment and emotional support. All three patients had therapeutic abortions.

As abortion bans proliferate throughout our country, I feel fortunate to practice in New York Citys public hospital system, where the law supports sound medical decision making combined with a womans choice. No time for complacency, however. The lives and well-being of millions of women will depend on it.

Bonny J. BaronBrooklyn

Read this article:
Opinion | New Risks Facing Doctors and Their Pregnant Patients - The New York Times

Recommendation and review posted by Bethany Smith

Study participants

We evaluated data from 70 consecutive patients with PAI on conventional steroid treatment in a real-life study. Patients were consecutively referred to the Division of Endocrinology of Palermo University from January 2012 to December 2020. Patients were on conventional steroid treatment (cortisone acetate and HC), administered twice or three times a day. Thirty-five patients, 15 males and 20 females, maintained conventional steroid therapy (17 cortisone acetate and 18 HC) (group A) while the other 35, (16 who were on cortisone acetate and 19 who were on HC), 11 males and 24 females, were switched from conventional steroid treatment to DR-HC (group B) administered orally in the morning in a fasting state. Patients had a 60-month follow-up. In group A there were 5 women in menopause, while in group B there were 6 women in menopause. Exclusion criteria were the following: age18years, secondary AI (SAI), treatment with other steroids (prednisone), pregnancy, breastfeeding, premature ovarian failure, hypoparathyroidism, hyperparathyroidism, treatment with estrogens and underweight (BMI<18.5kg/m2). The switch to DR-HC was judged to be appropriate on clinical grounds in those patients who complained of fatigue and weakness, presented hyponatraemia (<134mmol/L) or hypoglycaemia (2.78mmol/L) or showed more than two comorbidities such as diabetes, osteoporosis/osteopenia, arterial hypertension and central obesity. The switch from HC to DR-HC was made with an equivalent dose, while the dose was reduced from cortisone acetate to DR-HC taking into consideration the minor steroid activity of cortisone acetate compared to HC and patients clinical characteristics.

PAI was diagnosed as recommended by international guidelines9.

In detail, among the total of 70 patients, 42 had autoimmune polyglandular syndrome (APS), while 28 had isolated autoimmune AI. Among patients with APS, 26 had combined Addisons disease and autoimmune thyroid disease, 6 had combined Addisons disease, type 1 diabetes mellitus and autoimmune hypothyroidism and 10 had combined Addisons disease, autoimmune hypothyroidism and celiac disease. Patients with celiac disease were on a stable gluten-free diet. All patients with PAI were also on stable treatment with fludrocortisone (0.050.1mg/day, once). Patients with hypothyroidism were treated with levo-thyroxine at the average dose of 1.21.5 mcg/kg. Patients with type 1 diabetes were on basal-bolus treatment on flash blood glucose monitoring. Five postmenopausal women had been treated with DHEA for a ranging period of 618months, before being included in the study.

During the 60-month treatment period, the conventional steroid and the DR-HC doses were changed based on the physicians judgement of a patients need in both groups of patients (Table 1). Each patient received instructions for treatment in special or emergency situations. Patients treated with DR-HC were instructed to add a rescue dose of HC during an intercurrent illness or stress (5 or 10mg according to severity of stress and symptoms). Overall, 8 patients had to take a rescue dose of HC, 5 of them less than 10 times and 3 of them from 20 to 30 times during the 60-month period.

The current study was carried out in accordance with the recommendations of the Paolo Giaccone Policlinico ethics committee, with written informed consent from all subjects. All subjects gave written informed consent in accordance with the Declaration of Helsinki. The protocol was approved by the Paolo Giaccone Policlinico ethics committee (protocol 06/2021).

At baseline and after 18, 36 and 60months of conventional steroid and DR-HC treatment, clinical and bone metabolic parameters were evaluated.

Anthropometric parameters such as BMI and waist circumference (WC), measured at the midpoint between the lower rib and the iliac crest, were evaluated. In addition, sodium, potassium, serum 25hydroxyvitamin-D (vitaminD), parathyroid hormone, calcium, phosphorus, creatinine, osteocalcin and bone alkaline phosphatase were assayed.

The blood sample was taken about 2h after steroid administration (patients took the dose in the morning on waking) to avoid patients experiencing fatigue or other symptoms due to delayed intake of the drug.

In both groups, hypovitaminosis D was observed at baseline and a pharmacological supplementation was started in 26 patients of group A and 25 of group B, at the mean dose of 800 UI/day and maintained during the follow-up. Hypovitaminosis D was defined as a serum 25-hydroxy vitamin D level below the normal range (<30ng/ml). All patients supplemented with vitamin D reached the threshold of 30ng/ml.

BMD was measured by DXA at lumbar spine and femoral neck (Hologic Horizon Inc., QDR-4500W Waltham, MA) at baseline and after 18, 36 and 60months of follow-up.

In patients aged 50 or more, BMD was expressed as the T-score, comparing the results with those obtained in a sex-matched Caucasian population at the peak of bone mass. A T-score less than or equal to 2.5 SD at the neck or spine was defined as osteoporosis, whereas osteopenia was defined as a T-score between 1 and 2.5 SD. In patients younger than 50years, the results were expressed as a/the Z-score, comparing the results with those obtained in an age and sex-matched Caucasian population. A Z-score of 2.0 SD or lower was used to define a BMD below the expected range for age10. The coefficients of variation in the DXA measurements for BMD, bone mineral content (BMC) and area were 0.61%, 2.98% and 2.89%, respectively.

We also evaluated rib, femoral neck and hip fractures rate during the follow-up in both groups.

Sodium, potassium, serum 25hydroxyvitamin-D (vitamin-D), parathyroid hormone, calcium, phosphorus, creatinine, osteocalcin and bone alkaline phosphatase were measured with standard methods (Modular P800, Roche, Milan) at our hospital centralized laboratory. The intra- and interassay coefficients of variation were the following: Sodium 0.5% to 1.2% and 1.28% to 1.44%, respectively; potassium 1% to 2.1% and 2.2% to 3.08%, respectively; vitaminD 0.9% to 1.6% and 1.7% to 2.56%, respectively, parathyroid hormone 1.2% to 2.6% and 2.8% to 3.9%, respectively; calcium 1.8% to 3.5% and 3.75% to 4.23%, respectively; phosphorus 1.6% to 3.3% and 3.5% to 4.2%, respectively; creatinine 1.7% to 2.9% and 3.3% to 4.6%, respectively; osteocalcin 1.9% to 3.3% and 3.6% to 4.9%, respectively; bone alkaline phosphatase 2.7% to 3.6% and 3.8% to 5.2%, respectively.

The Statistical Packages for Social Science SPSS version 19 (SPSS, Inc., IBM, New York, USA) were used for data analysis. The normality of quantitative variables was tested with the Shapiro-Wilk test. The baseline characteristics of the groups were presented as meanSD for continuous variables, while the rates and proportions were calculated for categorical data. The differences between groups were performed using ANOVA for quantitative variables and the 2-test for categorical variables. A comparison between numerical variables at baseline, 18-, 36- and 60-month follow-up was performed with the Friedman analysis. In addition, multiple linear regression analysis was performed to identify independent predictors of the dependent variables lumbar spine and femoral neck T and Z scores and of dependent variable fracture. A p value<0.05 was considered statistically significant.

Read more:
Long-term outcomes of conventional and novel steroid replacement therapy on bone health in primary adrenal insufficiency | Scientific Reports -...

Recommendation and review posted by Bethany Smith

For anyone who doesnt have a thyroid condition, it might be easy to forget about the gland in the front of their neck that controls hormone production. But behind the scenes, the thyroid does a lot of work to help metabolize and maintain blood pressure, body temperature and heart rate.

Thyroid disease affects approximately 20 million people in the US and about one in eight women. The two most common types of thyroid disorders are hyperthyroidism and hypothyroidism.

Hyperthyroidism produces too much thyroxine hormone (an overactive thyroid) and hypothyroidism does not produce enough (an underactive thyroid). Although the two conditions have different signs and symptoms, there can be some overlap.

There is no replacement for getting the proper diagnosis and starting medication when necessary, said Vatche Zohrabian, DO, primary care physician with the Hartford HealthCare Medical Group, but there are some lifestyle modifications that can help augment conventional treatment and help keep your thyroid on track.

Here are the five things Dr. Zohrabian recommends you do to upkeep a healthy thyroid:

Dr. Zohrabian encourages anyone who experiences the following symptoms to have their thyroid function checked by their primary care provider:

Continue reading here:
Five Easy Steps to Keep Your Thyroid Healthy - Health News Hub

Recommendation and review posted by Bethany Smith