StemCell Therapy

Olly Mannand The Week delve behind the headlines and debate what really matters.

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In this weeks episode, we discuss:

The UK government has announced plans to allow gene-editing to be used in agricultural crops, diverging from an EU-wide ban on any genetic modification. Proponents of the technique say that it is more like accelerated selective breeding than genetic engineering - and that it could help farmers grow more produce while using fewer pesticides. But its opponents are worried that it will pave the way for riskier experiments.

A landmark legal case has begun between two stand-up comedians over who owns the rights to a comedy routine. One has hired Harbottle & Lewis, the lawyers best known for representing the Queen, to argue his case. So are we going to see lots of comedians taking one another to court? And how can you really establish who owns a joke anyway?

TikTok videos with the manifestation hashtag have been viewed a whopping ten billion times on TikTok, making it a buzzword of 2021. Its the latest incarnation of cosmic ordering - the practice of asking the universe to deliver what you expect from it, whether thats exam success or romantic fulfilment. Is it just harmless fun, or does it have a darker side to it?

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Gene editing, joke theft and manifesting - The Week UK

The University of Missouri at Kansas City (UMKC) has invited Vandana Shiva to speak on October 7th.According to a speaker booking website, her asking price for a lecture is a cool 100k.Lets give UMKC the benefit of the doubt, and assume they got a deal.It is hard to imagine a price for this world famous charlatan that gives good value.

It is a safe bet that most of us have never heard of Vandana Shiva, and this is, on balance, a good thing. Shiva has earned a measure of fame and a great deal of fortune railing against the use of modern technology in agriculture. She burst upon the scene by arguing that genetically modified cotton was causing hundreds of thousands of suicides amongst Indian farmers. Farmers have many reasons to be depressed, Dr. Shiva amongst them, but I can guarantee you that a technology that safely controls bugs that used to eat your crops isnt one of them. A 2011 study published in India found no correlation between genetically modified cotton seeds and farmer suicide, a conclusion which will surprise no one whose livelihood doesnt depend on believing the opposite, at one hundred thousand dollars per Zoom call.

In 1999, a cyclone caused ten thousand deaths in India. The U.S. sent grain and soybeans to help feed survivors. Shiva held a news conference to protest the donation, accusing the U.S. of using the victims of the cyclone as guinea pigs for genetically engineered products. When India accepted the food donations, she was highly critical. Better starvation than the unthinkable alternative of eating food that has been safely consumed billions of times.

Shiva has long been opposed to the introduction of Golden Rice, a genetically modified rice that helps prevent blindness by increasing vitamin A in the rice. Every year, about five hundred thousand children lose their sight because of vitamin A deficiency, and 70% of those children die within a year.Shiva has called the technology a hoax. Her appearance at UMKC is part of something called the Social Justice Book and Lecture series.Although social justice may be hard to define, Shivas position on this life-saving technology would surely be its opposite.

Agriculture owes a great debt to those who have worked so hard and so long to counter the arguments of Shiva and others against genetic engineering. For most of us the issue was long ago settled, the arguments stale, the battle won, and it was time to move on.

However much we might wish it to be so, the issue never really goes away. The fruits of Shivas long and lucrative fight against modernity pop up in the most unexpected places and in the most costly ways. The arguments against Covid vaccines mirror Shivas insane opposition to saving the lives of children, and even though the two sides have largely switched ideological labels, the horrendous costs in lives and fortunes are eerily similar.

It has to be heartening to GMO warriors that, despite the arguments of Shiva and the like, much of humanity consumes food improved by genetic engineering every day and Golden Rice is finally being approved in countries where it is so desperately needed. In the face of unending social media criticism of vaccines, some three-quarters of the U.S. population eligible for vaccines have availed themselves of the opportunity. Facts do prevail, usually, but it sometimes takes a very long time.

UMKC is a wonderful institution, doing valuable work. College students ought to have their ideas, beliefs, and biases challenged at every turn. The kids at UMKC who attend the virtual lecture will survive their exposure to Shiva, and may even be challenged to learn more about the relationship, largely beneficial, between agriculture and technology.Having said all that, this taxpayer would hope that social justice will be better served in the future by more discerning choices in speakers.

Blake Hurst is a farmer and greenhouse grower in Northwest Missouri.

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Opinion: Saving lives through real social justice - Agri-Pulse

CP Snow was a Cambridge scientist, a civil servant, and a novelist. He was, therefore, well placed to observe the gap between science, on one hand, and the arts and humanities on the other hand. He named it the two cultures divide, and his observations on it, in which he lamented the divides growing extent, formed the substance of his much-discussed Rede Lecture for 1959, subsequently published as a book.

His principal anxiety was that, whereas scientists can take a knowledgeable interest in the arts and humanities, the reverse is rarely true, and this is a problem because almost everyone in government in his day, whether politicians or civil servants, tended to be arts and humanities graduates, with little understanding of science but complete control of science policy and most of its funding.

The problem Snow identified had grown out of the extraordinarily rapid expansion of scientific knowledge in the period less than a century before he delivered his lecture, while the fundamentals of elite education, predicated on the classics and humanities, had not changed much. At the date of his lecture, science subjects were still looked down upon as bangs and smells, and were lumped together with engineering and technology as the domain of nerds with dirty fingernails and rows of pens in their top pockets, a far cry from the languid cravat-wearing aesthete with a volume of Shelley in one hand and a cigarette-holder in the other.

The real problem was that the depth and complexity of science had quickly resulted in a proliferation of specialisms, sometimes not fully accessible even to specialists in neighbouring areas of the same science. Competence in any area of, say, physics required a training and possession of mathematical abilities beyond the reach of most. This is even more true today. When Snow delivered his lecture, the Standard Model of the atom was still being formulated and the development of instruments of investigation was rudimentary in comparison to now, unsurprising given that when Snow wrote it was not much more than thirty years since quantum theory had been given, what might be called, its official imprimatur at the Solvay Conference of 1927.

In one very important respect, however, Snows two cultures division was incorrect. There was, in fact, not a division between two cultures but instead a three-way split, a triangle of cultures, though the third vertex of the triangle was so far beneath notice at the time Snow wrote that rather as one would expect from an Oxbridge don of the day it did not occur to him to include it. This third vertex is business. If the humanities student looked down his nose at the science student, neither of them even noticed the student of accountancy or commerce at the College of Further Education out in the suburbs.

This was the lingering attitude of snobbery about trade that had its origin in the far distant past in the classical Greek disdain for anything banausic, for buying and selling and taking an interest in money. Pythagoras said that people fell into three classes, mirroring those at the Games: competitors, spectators, and those who came to hawk their wares under the stands. He likened philosophers to spectators; in Greek to spectate is theorein, the source of our theory. Plato was disgusted by the sophists who offered to teach, for a fee, how to make a bad argument beat a good argument.

Statue of Plato, Athens (Alamy)

The unnoticed third vertex in Snows account has since risen into great importance in the triangle. Indeed, there has been a remarkable transformation in the respectability of business; successful businessmen and women are admired, the importance of business to the national economy is fully recognised, the wealth of top business people has risen hugely and given them significant influence in society and politics. Things had long been different in the US; there, money-making from business had been admired and encouraged at least since the years following the Civil War. In the unrestrained conditions of the expanding frontier and its abundant resources, together with a flow of both skilled and cheap labour through immigration, business millionaires became Americas aristocracy. That was still not the case in Snows Britain at the time he wrote. In the following decades it has become so; and it has radically changed the cultures divide he described.

It is still the case that few people can say what the Second Law of Thermodynamics is, which was Snows challenge to those who complained that scientists do not read poetry. But business entrepreneurs were not slow to recognise and profit from the scientific and technological advances which have transformed the world over the last half-century. It has made many of them rich, and they fuel the digital revolution by their energetic desire to see faster, smaller, more powerful, more capable technologies operative in many areas of activity. Meanwhile science genetics, biochemistry, neuroscience, particle physics, cosmology has continued to race ahead and astonish, with its applications via technology already outstripping our ability to manage its impacts (think of the potential downsides, along with the upsides, of artificial intelligence, genetic engineering, brain-chip interfaces, military robots, and the like).

The alliance between science and business and the prominence of both explains why the two areas of greatest pull in higher education are STEM subjects science, technology, engineering and mathematics and business studies. Between them they are the culturally dominant elements of the triangle, when in Snows day this role had been occupied by the humanities. In consequence, the humanities are withering. Parents and school advisers, together with the facts of life about what todays economies need in the way of skilled workforces, between them push and pull students into STEM or business studies in large and increasing numbers. In some universities the study of modern languages, literature, history and philosophy has vanished altogether; classics vanished from almost all universities long ago. The forces at work are Darwinian, and understandable.

You might cite the immortal words of Mandy Rice-Davies, He would say that, wouldnt he, in response to what I as a lifelong student of the humanities, and founder of a university college called New College of the Humanities (now part of Northeastern University) am about to say here. But note the concluding sentence of the preceding paragraph: I acknowledge the Darwinian imperatives, and do not propose to argue for a reassertion of the situation prevailing in Snows day. But allow me to recount an anecdote that explains why concentrating just on two vertices of the triangle at the expense of the third humanities is a mistake; as follows.

When Ronald Reagan was President he proposed that the US should develop an anti-ballistic missile system based on satellites in earth orbit the so-called Star Wars initiative so that an attack on the US by the Soviet Union could be interdicted in space. It eventually transpired that the suggestion was merely a propaganda device to turn the screws on the Soviet Union; there was, it seems, no real prospect of such a system being created. In the anxious debate that the suggestion prompted, however, one withering contribution was made by the physicist Steven Weinberg (pictured below, centre), who had won the Nobel prize for his contribution to showing how the weak nuclear force, responsible for radioactive decay in atomic nuclei, can be combined with the electromagnetic force that governs interactions between charged particles, thus yielding the electroweak force. He said (I paraphrase): It does not bother me that the President doesnt know any physics, but it does bother me that he doesnt know any history or philosophy, because if he did he would not dream of increasing tensions in the Cold War in this way.

Queen Beatrix with Christian de Duve and Steven Weinberg (centre)(Alamy)

This is a telling remark. History and philosophy and one might add literature, languages, the arts give us the insights, the overview, the understanding of human nature and the human condition, and with them the experiential and ethical dimensions of both individual and social existence, that provide context for how we use science, how we do business, how we direct public policy, and most importantly, why we do what we do in these respects. Weinbergs point concerned the larger human and social context, exactly the subject matter of historical and philosophical reflection.

The lessons learned in study of the humanities can be richly suggestive. Consider history: the Bronze Age Collapse around 1200 BCE was in significant part the result of disruption of supply chains, destroying economies and the political structures based on them. The French Revolution had, as a major cause, the social and economic injustices felt by those at the wrong end of a too great rich-poor gap. Personality politics rarely end well, from Caesar to Ceausescu. And so on. All three examples carry hints for very present discontents in our world.

Consider philosophy: ideas, beliefs, ideologies are the springs that vitalise society. Examining them and their implications, challenging them, exploring what is really at stake in this -ism or that, postulating fresh ways of thinking and seeing, are essential to a civilisations health. Think of what happens when an orthodoxy is imposed by force, and only one set of ideas is permitted and no discussion allowed, as in Kims North Korea. Think of the stagnation of any society under the heel of a monolithic ideology; history offers plenty of examples.

Consider literature: the stories we tell in novels, plays, poems, the cinema, are a million windows into human experience and feeling, extending our capacity if we are attentive to understand and sympathise with the variety in human motivation and to become acquainted with choices, perceptions, attitudes, ways of life, that we would not otherwise encounter. The same applies to learning languages, to appreciating the arts, to becoming receptive and perceptive as a result of being transported over the landscapes of human experience by all these expressive, communicative enterprises.

To become a research scientist, a chemical engineer, a financial advisor, one needs training. The complexities of science and business demand specialisation. A training is essential if one is to be successful in most of these fields. Therefore, training is important. But training is not education, and as the foregoing remarks show, what the humanities offer is education: the nourishing, equipping and expanding of mind and its capacities.

Oddly enough, a survey of what a complex modern economy requires shows that many of its arenas require precisely the sensibility that the arts and humanities offer to develop. They include journalism, politics, law, the civil service, creative industries, publishing, advertising, arts promotion and management, events, entertainment, human resources, education, performance, museology and curating, design, the tourism and hospitality industries, many aspects of retail, and more the list is long.

And this is to leave aside one enormously important point that most thinking about training and education ignores, with the result that the idea of education for its own sake has so significantly diminished. This is that people are not only their careers; they are not only infantry on the economic battlefield. They are also spouses, parents, voters, travellers, lovers, gardeners, readers, neighbours, dreamers, consumers, tennis players, cinema-goers, and much else again life is many things, and being awake to its variety and its possibilities requires much more equipment than just a training for a specific career.

My idea in founding the New College of the Humanities was to make a statement about two things: the importance of the humanities, and the fact that they can and should be combined with a full acknowledgment of the importance in our time of the other two vertices of the triangle, STEM and business. So I made it a requirement that throughout their undergraduate studies in the humanities my students take, for an additional diploma, courses in science literacy so that they would have an intelligent laypersons overview of the main developments in science and basic business studies, equipping them to understand entrepreneurship, the essentials of marketing, how to read a balance sheet, what is required in the world of work, and general financial literacy. In a world now so dependent on digital technologies, literacy and competence in these is a necessity too.

The thought was that the demand for appropriate preparation for life after formal education should not entirely displace the opportunity to explore ideas, the past and literature, but that what the humanities offer should be recognised as of great value in itself, and can readily be combined with practical considerations. Education and training do not have to be mutually exclusive. My design was to provide the opportunity for the humanities intellectual maturation and fertilisation, with an adjunct of practical knowledge, to overcome the false dichotomy of the two.

It is a principle of education viewed as the cultivation of a well-furnished and highly able mind that the beneficiary of it should develop a rich sense of context and connection. Someone interested in, say, medieval monasticism or Presocratic philosophy might relish the study of it for its own sake and find it absorbingly interesting, but might also see surprising relevances to his own life and times. This explains how, in the 18th and 19th centuries, Britain governed an empire by teaching Greek and Latin classics to those sent out to run it. For when you read and discuss the classics you read history, philosophy and literature, and through them you read about and discuss government, military affairs, ideas of justice and morality, statesmen and the way they handled problems, successes and disasters and what prompted either, subtleties of human nature, celebrations of virtue and condemnations of vice, poems of love and of mourning, the absurdity of certain beliefs, the nobility of certain ambitions and much besides of relevance to both the social and individual scales of life.

Of course, much of this might have gone over most of the heads of lazy and self-interested boys at their public schools we see an example of this vividly in our own day, alas but enough stuck so that the administration of empire was not always and everywhere a prejudiced and exploitative disaster. In any case, the point is that the aim of imparting the benefits of an education in the humanities might succeed often enough that the candles of civilisation will continue be carried, alight, over the floodwaters of time. Even if almost every educational institution should shed its commitment to the humanities, salvation would reside in that almost.

There might be another spin of the triangles orientation which changes which vertex is uppermost. Suppose most productive activity is taken over by artificial intelligence systems, with the result that more than enough wealth is generated to allow most of the population a comfortable national wage without having to work for a living. Then the arts and humanities will be at a premium, the practice and study of them the main avocation of many, the value of intellectual and educational attainment as great as the value of money-wealth is now. It is far from an impossibility that this might happen. It would be good if a flourishing tradition of the humanities were to survive into such a time.

CP Snow wished to see the two cultures divide closed, or at least narrowed. I say that that the three vertices of the triangle should be kept connected, because to lose the perspectives offered by the humanities would render our society technocratic and banausic merely, a fate it is already not far from. Snows anxiety was that science would be mishandled by uncomprehending humanists, whereas today the anxiety is very different; it is that technology and the imperatives of bottom lines will determine all our choices for us.

Perhaps one can sum up the matter by saying that whereas science and technology is about capability, and business is about profit and cost, the humanities are about value. That is a vertex of the triangle we cannot afford to lose.

We are the only publication thats committed to covering every angle. We have an important contribution to make, one thats needed now more than ever, and we need your help to continue publishing throughout the pandemic. So please, make a donation.

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Science, business and the humanities: CP Snow's 'Two Cultures' sixty years on - TheArticle

Researchers at the University of Toronto have found that immune cells from the upper respiratory tracts of children, taken years before the pandemic began, react with the virus that causes COVID-19.

The findings hint at a possible reason why children with COVID-19 are often asymptomatic or have mild symptoms, while many adults experience severe disease and even death.

We isolated B cells from tonsil tissues collected from children over five years ago, and found that some are reactive to the SARS-CoV-2 spike protein, saidGoetz Ehrhardt, principal investigator on the study and an associate professor ofimmunologyat U of TsTemerty Faculty of Medicine.

We found that antibodies generated from these B cells have neutralizing potential against the virus in lab experiments, reducing the ability of the spike protein to bind to its target protein on the cell surface.

The study,published in theJournal of Immunology, is one of just a few to examine the role of the mucosal immune system in COVID-19. Other studies have looked at immune components in the bloodoften after infection has taken hold or during recovery.

Mucosal surfaces comprise one of the largest components of the immune systemand include the gut, urogenital tract and respiratory system all of which teem with microbiota including bacteria, viruses and fungi.

The researchers at first assumed the B cells reacted to SARS-CoV-2 because they had encountered similar coronaviruses in the past, perhaps through common colds and other infections.

But the antibodies did not react to those coronaviruses in further testing, although they did share genetic sequence characteristics linked to other triggers.

Taken together, Ehrhardt said, the results suggest cross-reactivity in the B-cell antibodies. The immune system makes these antibodies toward certain agents or pathogensand as a by-product the antibodies react to SARS-CoV-2, he said. It will be interesting to find out what causes that reaction.

A better understanding of the antibody reaction could shed light on the mystery of COVID-19 susceptibility in children and adultsand inform clinical and public health decisions as well as therapeutic approaches.

Whatever the cause of the reaction, it is likely due to a common element in the childhood environment sinceall samples the researchers tested had the SARS-CoV-2-reactive B cells many of which were observed also in the immune systems naive or newly generated B cells that had not encountered any pathogen.

One explanation is that some of these B cells react to triggers in the microbiome, saidYanling Liu, lead author on the paper and a senior research associate in Ehrhardts lab.

Or it could still be that antibodies are reacting to endemic coronavirusesand we just didnt see that, Liu said. We dont really know, but one implication of our work is that it suggests children should respond to vaccines very well since they have those naive B cells ready to recognize vaccine in their lymphoid tissue.

Several other researchers were key to the study, Liu and Ehrhardt said, includingJames Rini, a professor ofbiochemistryandmolecular geneticsat U of T who provided purified spike proteins from viral samples.

Amin Ziaused computational biology to scan large databases and predict which antibodies would react to the virus. Zia was a post-doctoral researcherin the lab ofAlan Moses, a professor in U of Ts departments ofcell and systems biology,ecology and evolutionary biologyandcomputer science in the Faculty of Arts & Science.

About half the antibodies we generated were based on computer-generated predictions, said Ehrhardt. That was first for us, and it wont be a last.

Researchers atthe Hospital for Sick Children, with whom Ehrhardts lab has collaborated for years, supplied the tonsil tissue samples.

Mucosae are no doubt a very important interface for the immune systems response to a great variety of pathogens, but availability of samples has been a major impediment, said Ehrhardt. Research in this area is gathering steam, and it will be interesting to see where that takes us.

The research was funded by the Canadian Institutes of Health Research.

See the article here:
U of T research may help explain children's immune response to COVID-19 - News@UofT

"If it's not broken, don't fix it" is generally good advice for a lot of thingsyour favorite recipe, the gallery wall that took forever to put up, the workout routine your body has been lovingbut something it doesn't necessarily apply to? Your immune system.

While, no, you don't need to "fix" your immune system (nor could you), there are steps you can take to support it, even when you're feeling fantastic.

"Nothing is more critical for a healthy life than a well-functioning immune system," says clinical community pharmacist Kathy M. Campbell, PharmD. The goal, according to Dr. Campbell, is a Goldilocks approachyou want an immune system that's not too weak and not too strong.

"Nothing is more critical for a healthy life than a well-functioning immune system."

"A healthy, well-functioning immune system is an easy thing to take for granted," she says, but luckily, there are habits that can help support your immune systemsome of which you may already be doing. Eating nutrient-packed foods, prioritizing sleep, and getting some direct sunlight are all necessary for overall health, and they can also go a long way in supporting your immune system, Dr. Campbell says.

Assuming those habits are in check, turning to supplements for immune support can be a great next step. "Appropriately chosen, high-quality supplementation can be a very effective addition in supporting a healthy immune system," Dr. Campbell says.

Ready to start stocking up? First, talk to your healthcare provider. Next, turn to a trusted brand like Nature Made, which creates science-backed supplements for plenty of health needs, including immune support.

Okay, so yes, you want all of your supplements to be high-quality, but Dr. Campbell really emphasizes it for multivitamins. "It's important to provide a balance of all nutrients in an effort to minimize over-supplementation with a single nutrient," Dr. Campbell says. A high-quality multivitamin should do that balancing act for you.

Next up for supplements that support immune health? No surprise: good ole vitamin C. "Vitamin C is an essential nutrient, which cannot be synthesized by humans and therefore must be consumed by diet or supplementation," Dr. Campbell says. "Function is key in many biochemical processes within the immune system."

Vitamin D may already be high on your must-have list (hello, sunshine), but if you're supplementing with it, make sure to take it with vitamin K for the biggest impact, Dr. Campbell says. She also notes vitamin K can often be found in quality multis (pssstit's in Nature Made Women's Multivitamin Softgels). Vitamin D has multiple roles in the body, and can help support immune health, she says.

Optimal zinc levels help support a healthy immune system, Dr. Campbell says, but you'll also want to be careful not to overdue it. If you're supplementing with zinc, she recommends combining it with copper, which can often be found in multivitamins, likeyep, you guessed itNature Made Women's Multivitamin Softgels. Your immune system says thank you in advance.

Photo: Getty Images/shurkin_son

These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease.

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Im a Pharmacist, and These Are My Top 4 Go-To Immune-Support Supplements - Well+Good

Sam Antonios| Special to The Capital-Journal

While viruses aren't new to humans, COVID-19 is novel to the human species, so no one has immunity against it. Like many other viruses, this novel coronavirus survives, replicates and transmits itself in and among its primary hosts: human beings.

Our human immune system fights off viral infections by developing special cells that secrete anti-virus molecules. But first, our bodies must learn how to build that immunity.

This coronavirus is a virus with which our bodies have had no previous experience. Some people's bodies can quickly create an immune response before the virus has the opportunity to overwhelm them, usually through domination of their respiratory system. Others aren't as fortunate and their immune system's response is too little, too late, causing them to fall victim to the disease.

For years, weve used vaccination to help our bodies ward off viral infections such as hepatitis, rubella, measles, chickenpox, influenza and rotavirus. The concept is simple: Introduce a non-active chunk or image of the virus so that our body becomes familiar with it and begins its immunity generation.

Because no actual virus has been introduced, that allows us to begin immunity stockpiling without the threat of disease. This model has helped humans for years and continues to do so with COVID-19.

After being vaccinated, when the body is exposed to the COVID-19 virus, it is more ready to fight it off, not even giving it a chance to overwhelm the body. COVID-19 can cause terrible medical problems and death to people. The vaccines available in the United States have been well-tested.

More than 388 million doses of the vaccines have been given in the U.S. and more than 6 billion doses worldwide. The goal is to develop enough collective immunity to stop this strain of coronavirus from spreading and mutating further the way viruses are designed to do.

Real-life evidence shows that the vaccines are working. Although people who have been vaccinated can still get a "breakthrough" infection and potentially transmit the virus, that infection tends to be milder because of their body's preparation work, thanks to the vaccines.

These infections occur far less frequently than those happening among unvaccinated people. We know this to be true because we are seeing this at our own hospitals and clinics.

This is why we continue to urge people to get vaccinated for COVID-19. While it might be tempting to try to ride this out, time is of the essence. The impact of this highly transmissible virus on the health and well being of our community is widely felt, as the surge commands significant resources, causing disruptions and delays for patients needing all types of care.

The story of our immune system fighting off invaders is long, this is simply another chapter. Using what we know works, we can beat this thing.

Sam Antonios, MD, is the chief clinical officer at Ascension Via Christi.

The rest is here:
'The story of our immune system fighting off invaders is long': COVID vaccination gives immune system a chance - The Topeka Capital-Journal

A microscopic image of a normal mouse small intestine. Cells stained red express normal amounts of cell-surface tags (MHC-II) needed by immune cells to find threats like infections or cancer. High-fat diets reduce the levels of MHC-II tags in intestinal cells, and so the immune system has a harder time recognizing intestinal tumors. Credit: Beyaz lab/CSHL, 2021

The immune system relies on cell surface tags to recognize cancer cells. CSHL researchers discovered mice who ate high-fat diets produced less of these tags on their intestinal cells, suppressing the ability of immune cells to identify and eliminate intestinal tumors. The high-fat diet also reduced the presence of certain bacteria in the mices gut, which normally helps maintain the production of these tags.

A high-fat diet increases the incidence of colorectal cancer. Cold Spring Harbor Laboratory Fellow Semir Beyaz and collaborators from Harvard Medical School and Massachusetts Institute of Technology have discovered that in mice, fat disrupts the relationship between intestinal cells and the immune cells that patrol them looking for emerging tumors. Reconfiguring the gut microbiome may be a way to heal the relationship.

The immune system patrols tissues looking for and eliminating threats. Certain immune cells look for tags that distinguish between normal and abnormal cells. One tag, called MHC-II, helps target cells for destruction. Cell-surface MHC-II activates the immune system to destroy that cell, whether it is just worn out or about to become cancerous. Beyaz and his colleagues found that when mice ate diets high in fat, MHC-II levels were suppressed in intestinal cells. Cells with reduced levels of these tags were not recognized as abnormal and thus could grow into tumors. Charlie Chung, a Stony Brook University graduate student-in-residence in Beyazs lab, says, If we alter the level of these immune recognition molecules in a positive way, then the tumor will more likely be recognized by the immune cell. We hope this can be coupled with the existing strategies, such as immunotherapy, to eradicate tumors.

Intestinal cells of a mouse that were fed a high-fat diet. The intestinal cells express less of the MHC-II tag than found in a gut from mice fed a normal diet. Credit: Beyaz lab/CSHL, 2021

The researchers found that a high-fat diet changed the mouses intestinal microbiome (the mixture of microbes in the gut). Several bacteria, including ones called Helicobacter, increase MHC-II, which may help immune cells locate abnormal cells. The team did a dirty roommate experiment where mice without these bacteria were housed with ones that had it. The clean mice became infected with the Helicobacter bacteria and produced more of the MHC-II tag.

The scientists findings suggest a new way to boost current immunotherapy treatments against cancer. Increasing the production of this MHC-II tag, either by diet, drugs, or changing the microbes in the body, can help the immune system recognize and eliminate cancer cells. Beyaz says:

This interaction between diet, microbes, and immune recognition has the potential to help us explain how lifestyle factors can contribute to tumor initiation, progression, or response to therapy.

Cancer cells use many tricks to avoid being recognized as abnormal by the immune system, but Beyaz hopes hes found several ways to outwit them.

Reference: Dietary suppression of MHC class II expression in intestinal epithelial cells enhances intestinal tumorigenesis by Semir Beyaz, Charlie Chung, Haiwei Mou, Khristian E. Bauer-Rowe, Michael E. Xifaras, Ilgin Ergin, Lenka Dohnalova, Moshe Biton, Karthik Shekhar, Onur Eskiocak, Katherine Papciak, Kadir Ozler, Mohammad Almeqdadi, Brian Yueh, Miriam Fein, Damodaran Annamalai, Eider Valle-Encinas, Aysegul Erdemir, Karoline Dogum, Vyom Shah, Aybuke Alici-Garipcan, Hannah V. Meyer, Deniz M.zata, Eran Elinav, Alper Kucukural, Pawan Kumar, Jeremy P. Mc Aleer, James G. Fox, Christoph A. Thaiss, Aviv Regev, Jatin Roper, Stuart H. Orkin and mer H. Yilmaz, 15 September 2021, Cell Stem Cell.DOI: 10.1016/j.stem.2021.08.007

Funding: National Cancer Institute, Oliver S. and Jennie R. Donaldson Charitable Trust, Mathers Foundation, STARR Cancer Consortium, Mark Foundation For Cancer Research, National Institutes of Health, Massachusetts Institute of Technology Stem Cell Initiative, Pew Foundation, Howard Hughes Medical Institute, American Association of Immunologists Career Reentry Fellowship

Continued here:
How High-Fat Diets Allow Cancer Cells To Go Unnoticed by the Immune System - SciTechDaily

Treatment for breast cancer is highly effective. Five-year survival rates for breast cancer have increased dramatically in recent decades, and much of that success can be credited to cancer researchers and campaigns designed to inform women about the importance of screenings.

Breast cancer is highly treatable, but treatment typically leads to some unwanted side effects. According to Johns Hopkins Medicine, women undergoing treatment for breast cancer may experience a host of side effects, including fatigue, pain, headaches, and dental issues. Cancer treatments, most notably chemotherapy, also can take a toll on womens immune systems.

Why does chemotherapy affect the immune system?

Cancer is caused by an uncontrolled division of abnormal cells in the body. According to Breastcancer.org, chemotherapy targets these abnormal cells, but also can affect fast-growing cells that are healthy and normal. So chemotherapy can damage cells throughout the body, including those in bone marrow. When bone marrow is damaged, its less capable of producing sufficient red blood cells, white blood cells and platelets. Breastcancer.org notes that the body is more vulnerable to infection when it does not have enough white blood cells.

Does chemotherapy always weaken the immune system?

The effects of chemotherapy on the immune system depend on various factors. According to Breastcancer.org, a patients age and overall health may influence the effects of chemotherapy on their immune systems. Young, healthy patients may be less vulnerable to infections from weakened immune systems than aging, less healthy patients. However, Susan G. Komen notes that the median age for breast cancer diagnosis in the United States is 63, so many patients are likely to be affected by the impact that treatment can have on their immune systems. The length of treatment and amount of medicines patients receive also can affect the impact of chemotherapy on patients immune systems. Breastcancer.org notes that being administered two or more chemotherapy medicines at once is more likely to affect the immune system than just one medication.

Chemotherapy is not the only treatment that can affect breast cancer patients immune systems. The Cancer Treatment Centers of America notes that surgery, radiation, CAR T-cell therapy, stem cell transplants, and even immunotherapy can affect the immune system. Surgery can overtax the immune system and compromise its ability to prevent infections and heal wounds caused by the procedure. Like chemotherapy, radiation therapy can damage healthy cells and lead to an increased risk of infection. And while immunotherapy is designed to boost the immune system by helping it recognize and attack cells more effectively, it also can lead to an overactive immune system that attacks healthy cells.

Cancer treatment is often highly effective. However, patients may need to work with their physicians to combat treatment side effects that can adversely affect their immune systems.

Read more from the original source:
How breast cancer treatments can affect the immune system - Defiance Crescent News

Booster shots now available at FAMU. Photo Courtesy: wctv.com

Florida A&M University is now offering two booster shots of the COVID-19 vaccine for those with compromised immune systems.

The Pfizer and Moderna third dosage are available to, but not limited to, individuals with acquired immunodeficiency syndrome (AIDS), lupus, heart conditions and people who are prescribed drugs that suppress their immune system.

Jamal Stokes, a Tallahassee native and lupus patient, has already received his booster shot for the Pfizer vaccine.

As soon as I got word that the booster shot was available on FAMUs campus, I went right up there, Stokes said. I didnt have to bring a doctors note or anythingvery grateful that the university is offering this.

The university is not requiring individuals with compromised immune systems to bring a doctors note to prove their conditions, preregister, or make appointments. They are only required to fill out a form upon arrival.

Tanya Tatum, the FAMU Student Health Services director, discussed the purpose of this third dosage for those who are eligible.

The additional dose brings their immune systems up to par with those who have healthy immunes and are fully vaccinated, Tatum explained.

Some students at the university are hopeful that the booster shot will eventually be offered to all individuals, no matter their immune status. Students are trying their best to remain optimistic about not only the future of the university, but the United States.

I think its really important that the campus is offering the third dosage and all other vaccines because hopefully that will encourage students to get it, Tyla Ewards, a fourth year facilities management student with long qt syndrome said. Its free and super convenient being that you can go get your booster shot in between classes with no hassle.

For now, scientists are recommending the booster shots to those with convincing evidence that the initial doses of the vaccine do not offer enough immune protection.

The Food and Drug Administration Advisory Committee has posed the question of whether to wait for a booster designed to fight against multiple variants to be offered to those with normal immune systems.

The most common side effects by clinical trial participants who have received the booster dose of the vaccine were pain, redness and swelling at the injection site. Other side effects include headache, fatigue, joint or muscle pain and chills.

Both Pfizer and Moderna Vaccines are available at FAMU on 659 Ardelia Court, located off Robert and Trudie Perkins Way. The site is open from 9 a.m. to 5 p.m. on Monday through Saturday.

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Booster shots now offered at FAMU The Famuan - Famuan

Hospitals will begin contacting people over the age of 16, who have very weakened immune systems due to certain medical conditions, to offer them an additional Covid-19 vaccine.

Hospitals will identify the people who need an additional dose, the HSE said. You dont need to register or contact anyone.

People who need an additional dose will receive a text message with an appointment for their vaccine.

These additional doses will be given through a HSE vaccination centre near you, or your hospital if you are an inpatient. GPs may also vaccinate some people.

The HSE said this would happen from this week for those aged 16 and over.

As the vaccination programme for 12- to 15-year-olds started later, those aged 12 to 15 who have been identified for an additional dose will be offered an appointment at a later date.

This is to facilitate the two-month minimum interval from their last dose of Covid-19 vaccine.

Dr Colm Henry, Chief Clinical Officer of the HSE, said: It has been shown that people with weakened immune systems do not generate a full immune response to their first two doses of the Covid-19 vaccine.

This additional dose we are offering will mean they will get the maximum benefit from their primary vaccination course, giving them better protection against the serious effects of Covid-19.

It follows recommendations from the National Immunisation Advisory Committee (Niac) that people aged 12 years and older, who are immunocompromised at the time of vaccination due to disease or treatment, should receive one additional dose of a Covid-19 vaccine.

They will be offered a single dose of either Pfizer/BioNTech Covid-19 vaccine or Moderna vaccine. They need to continue to follow anti-Covid protection measures.

Read more from the original source:
Over-16s with weakened immune system to be offered third jab - Independent.ie

A new, sustainable immune health ingredient derived from carrot pomace is set to launch at the SupplySide West trade show in Las Vegas this October. Introduced by Dutch ingredients company NutriLeads (Wageningen, the Netherlands), BeniCaros is an ingredient suited for both dietary supplements and functional foods and beverages.

BeniCaros is a soluble fiber produced from upcycled carrot pomace, which is a byproduct of carrot juice production, making it a sustainable ingredient that is also label friendly.

NutriLeadss proprietary extraction process ensures the ingredient is rich in the immune-supporting polysaccharide rhamnogalacturonan-I (RG-I). The company says BeniCaros was shown in a clinical trial to help the immune system become more responsive to potential challenges as well as to stimulate beneficial gut microorganisms and their metabolites, at a daily dose of 0.3 grams. The firm says there is robust preclinical and clinical research showing the efficacy of BeniCaros.

In a press release, Ruud Albers, PhD, chief scientific officer for NutriLeads, said, I have been active in this field for more than 25 years and have never seen another ingredient with such distinctive data supporting its effectiveness. He added, There are many immune health ingredient options out there but very few that work like BeniCaros and even fewer that work with the same efficacy to support immune function.

Read more:
Immune health ingredient from carrots debuting at SupplySide West 2021 - Nutritional Outlook

Lots of people these days are asking what they feel is a completely legitimate question, "Is it safe to get the COVID vaccine and get my flu shot?" The quick answer is: Yes. ABSOLUTELY...According to the Centers For Disease Control and Prevention.

WWLP/News 22 Springfield is reporting that, according to the CDC,its safe for other vaccines to be administered at the same time as the COVID-19 vaccine.

This new guidance is a definite change from previous CDC recommendations which said that other vaccinations should not be administered within a 2-week window before or after the COVID-19 vaccine.

With colder weather on the horizon, many people are starting to think about the flu shot in addition to COVID vaccinations. But there are also many who are wondering, after last year's very mild flu season, if getting a flu shot is even essential.

Health officials caution that substantial flu activity happening at the same time as COVID-19 activity could seriously overwhelm our health care systems.

The Centers For Disease Control and Prevention estimates that every year, anywhere between 12,000 to 61,000 people die due to the flu. Last year, however, the combination of social distancing and wearing masks prevented the majority of cases.

In summation, you can get your flu shot at the same time you get your COVID vaccination or vice versa. The CDC recommends getting the flu vaccine by the end of October and to get the COVID-19 vaccine as soon as you can.

For more information, check out WWLP's website here.

KEEP READING: See 25 natural ways to boost your immune system

Here are some tips for self-care during the pandemic:

KEEP READING: 15 Natural Ways to Improve Your Sleep

Read the original here:
Health Officials Addressing Concerns Over Flu Shot, COVID Shot - Live 95.9

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A patient at The Ottawa Hospitals General campus has been diagnosed with legionellosis, forcing the hospital to turn off the water supply to a portion of the hospital in order to disinfect it.

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In a brief statement, the hospital said the water system at the General campus is undergoing hyperchlorination.

Ottawa Public Health said its infection prevention and control team was made aware of one case of legionellosis affecting a patient at the General campus and has worked closely with the hospital, locating the source and ensuring steps are taken to protect patients and staff.

There have been no further reports of legionellosis infection at The Ottawa Hospital, according to Ottawa Public Health. All cases must be reported to public health for follow up with the patient as well as investigation.

Ottawa Public Health performed environmental testing, with support from Public Health Ontario. The hospital continues to work with public health and has hired its own environmental consultants to lead the remediation.

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The illness is a form of pneumonia caused by exposure to Legionella, the common name for the bacterium L. pneumophila. It lives in water and may infect some people who inhale water droplets from a contaminated water supply, although most people will be unaffected.

For people with healthy immune systems the risk is low, but for those that have a suppressed immune system, there is a greater risk of infection, said the hospital.

The hospital said Tuesday it immediately turned off the water on the unit where the patient was, and the issue is being addressed.

During this time, water will be temporarily unavailable on certain units. We are working with care teams to ensure alternative water sources are available during this time, to minimize the impact on patient care.

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Rachel Muir, The Ottawa Hospital bargaining unit president with the Ontario Nurses Association, said the water has been shut off between the hospitals fourth and eight floors since the case of legionellosis was identified last Friday. She said the water isnt expected to be back on until later this week, possibly the weekend.

She said staff was notified last Friday that there was a case of legionellosis and the source was located in the water system in the unit.

Muir said drinking water and ice are being supplied to all the units affected and wipes and clean water are being provided for cleaning.

Patients will be freshened up but not showered until the system is back on.

Muir called it an inconvenience but said the hospital is working hard to minimize that and keep staff and patients informed.

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The hospital said it is working closely with public health and environmental experts to remediate the issue and to turn the water back on as soon as possible.

Legionnaires disease, named after a severe pneumonia outbreak at a convention centre in the U.S. in 1976, is the most common form of legionellosis. It can also cause less severe illness. According to the U.S. Centers for Disease Control and Prevention, healthy people usually get better after being sick with Legionnaires disease, but hospitalization is often required. About 15 out of 100 people who get it will die from the infection.

Many hospital patients have compromised immune systems because of illness, age or treatment. The General campus is home to The Ottawa Hospital Cancer Program where many patients are undergoing treatment that affects their immune systems ability to fight off infection.

Safety is our top priority, and we will continue to update patients and families to ensure they have all the information they need, said the hospital.

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Hospital disinfecting water system after patient at the General diagnosed with legionellosis - Ottawa Citizen

A recent study has found that despite effective antiretroviral therapy, low CD4/CD8 ratios and high CD8 counts are associated with a higher risk of Kaposis sarcoma and non-Hodgkin lymphoma, respectively. This increased risk is particularly present in people living with HIV who have CD4 cell counts above 500.

As expected, virological failure was a strong risk factor for both cancers. Findings are published in Clinical Infectious Diseases.

Kaposis sarcoma is a cancer that forms in the lining of blood and lymph vessels. The tumours can appear as painless purplish spots on the legs, feet or face, in the genital area, mouth or lymph nodes, and may also develop at a later stage in the digestive tract or lungs. The underlying cause of Kaposis sarcoma is infection with a virus called human herpes virus-8 (HHV-8). This virus causes no symptoms in healthy people. However, in people with a damaged immune system CD4 loss, but also an imbalance between CD4 and CD8 cell counts which allows it to multiply, HHV-8 has the potential to trigger Kaposis sarcoma.

Non-Hodgkin lymphoma is a type of cancer that begins in the lymphatic system, which is part of the bodys germ-fighting immune system. In non-Hodgkin lymphoma, lymphocytes grow abnormally and can form tumours throughout the body. Signs and symptoms may include swollen lymph nodes, abdominal pain, persistent fatigue, night sweats, fever, chest pain, coughing or trouble breathing. Non-Hodgkin lymphoma can be induced by the Epstein-Barr virus (EBV), herpes virus-8 (HHV-8) or human T-cell leukaemia/lymphoma virus-1 (HTLV-1) when the damaged immune system cannot regulate them adequately.

A molecule on the surface of some white blood cells. Some of these cells can kill other cells that are infected with foreign organisms.

Lesions on the skin and/or internal organs caused by abnormal growth of blood vessels. In people living with HIV, Kaposis sarcoma is an AIDS-defining cancer.

A type of cancer that starts in the tissues of the lymphatic system, including the lymph nodes, spleen, and bone marrow. In people who have HIV, certain lymphomas, such as Burkitt lymphoma, are AIDS-defining conditions.

A group of lymphomas (cancers of the lymphatic system). The many types of non-Hodgkin lymphoma (NHL) are classified according to how fast the cancer spreads. Although the symptoms of NHLs vary, they often include swollen lymph nodes, fever, and weight loss. Certain types of NHLs, such as Burkitt lymphoma and immunoblastic lymphoma, are AIDS-defining cancers in people with HIV.

A type of lymphoma. Lymphoma is a cancer of a part of the immune system called the lymph system. The first sign of Hodgkin disease is often an enlarged lymph node. The disease can spread to nearby lymph nodes, the lungs, liver, or bone marrow. The exact cause is unknown. See also non-Hodgkin lymphoma.

Despite the widespread use of effective antiretroviral therapy and the resulting long-term viral suppression and CD4 restoration, a higher incidence of Kaposis sarcoma and non-Hodgkin lymphoma persists in people living with HIV, compared to the general population. These events seem to be driven by immune activation and inflammation that even viral suppression may not control.

CD8 cells are part of the immune system: also known as T killer cells, they recognise and destroy cells infected with viruses or bacteria. CD8 cell counts increase in response to acute infections. However, they can remain high in chronic infections such as HIV and respond to treatment more slowly than CD4 cell counts.

The CD4/CD8 ratio is considered a reliable marker of immune activation during successful antiretroviral therapy. Its normal value ranges between 1 and 4. When it is lower than 1 in people with HIV receiving antiretroviral therapy, it correlates with the risk of AIDS-related mortality and non-AIDS defining events, especially cancers.

However, the impact of the CD4/CD8 ratio on the risk of AIDS-defining cancers, such as Kaposis sarcoma and non-Hodgkin lymphoma, had never been studied before.

Dr Fabienne Caby and colleagues from COHERE (Collaboration of Observational HIV Epidemiological Research Europe, composed of several major cohorts) used data from over 50,000 people living with HIV who were receiving effective antiretroviral therapy to assess the impact of the CD4/CD8 ratio on Kaposis sarcoma or non-Hodgkin lymphoma risks in this population. This analysis focused specifically on whether or not this biomarker provided additional information to the CD4 count, which is the usual immunological predictor for both cancers.

As starting antiretroviral therapy with a high CD4 count is more and more common, the investigators conducted a secondary analysis that focused only on people with CD4 cell counts above 500 after they achieved virological control.

To be included in the study, individuals had to be at least sixteen years old, to have started antiretroviral therapy in the 2000-2014 period and to have achieved virological control defined as viral load below 500 copies within nine months after starting their treatment. At least one CD4/CD8 measurement, done in the six months following virological control, was needed.

For both analyses, the baseline was considered as the time of the very first CD4/CD8 ratio measurement within six months after virological control. Individuals with a diagnosis of Kaposis sarcoma or non-Hodgkin lymphoma at baseline or before could not be included in the study.

To better understand the impact of immune factors on the risk of the two cancers, three statistical models were tested, respectively adjusted for the CD4/CD8 ratio; both the CD4 and the CD8 cell counts; and for both the CD4/CD8 ratio and the CD4 cell count. All models were also adjusted for virological failure, demographics and year.

Overall, 57,708 people living with HIV from twenty cohorts in twelve Western European countries were eligible for the study. Men who have sex with men accounted for 49% of these participants, and women for 25%. Most participants were of European origin (69%), whereas 15% were of sub-Saharan origin (5770 women and 2691 men).

At baseline, the median age was 38 years (interquartile range 32-45) and the median CD4 and CD8 counts were 414 (IQR = 296-552) and 936 (IQR = 670-1304), respectively. The median CD4/CD8 ratio was low at 0.43 (IQR = 0.28-0.65) and reached 1 in only 8% of participants. Also, a very low CD4/CD8 ratio (<0.5) was found in 59% of participants.

Finding these low CD4/CD8 ratios in people with a suppressed viral load is not uncommon. As explained above, CD8 cells take time to respond to HIV treatment, except when treatment is started during acute HIV infection.

Participants were followed up for a median of 59 (IQR = 30-96) months from baseline, accounting for 307,700 persons-years. Two years after baseline, the CD4/CD8 ratio was restored to 1 in only 28% of participants (46% of those with a baseline CD4 count over 500).

In the primary analysis, Caby and colleagues found that during follow-up, Kaposis sarcoma and non-Hodgkin lymphoma had been diagnosed in 221 and 187 cases, respectively. This corresponded to incidence rates of 72/100,000 persons-years for the former and to 61/100,000 persons-years (95% CI; 46-76) for the latter. Most cases of Kaposis sarcoma were diagnosed between 2 to 37 months after baseline, whereas non-Hodgkin lymphoma was diagnosed between 7 to 42 months.

Of note, 15% (33/221) of Kaposis sarcoma cases and 12% (23/187) of non-Hodgkin lymphoma cases occurred in a context of virological failure.

The secondary analysis showed that among the 19,133 participants with CD4 cell counts above 500 at baseline, 65 were diagnosed with Kaposis sarcoma and 50 with non-Hodgkin lymphoma. However, this time, occurrence of the two cancers in a context of virological failure amounted to 14/65 cases (21%) of Kaposis sarcoma and 11/50 cases (22%) of non-Hodgkin lymphoma, despite the patients high CD4 cell counts.

What were the risk factors associated with Kaposis sarcoma? In all three models described above, virological failure was the strongest, with a nearly 3-fold higher risk (hazard ratio 2.77 in the third model).

When the CD4/CD8 ratio was looked at as the only immune factor, the lower it was, the higher the risk. When CD4 and CD8 counts were looked at separately, their independent associations with the risk of Kaposis sarcoma were confirmed.

In the third model which was found to be the most accurate CD4 counts and CD4/CD8 ratios were found to be independently associated with Kaposis sarcoma. The better the CD4 restoration was, the lower the risk: hazard ratio from 1.57 with 350 CD4 cells, to 0.71 with 650 CD4 cells, when compared to 500 CD4 cells. Furthermore, the association between the CD4/CD8 ratio and the risk of Kaposis sarcoma was gradual: hazard ratio from 1.18 in participants with a CD4/CD8 ratio of 0.8, to 2.02 in those with a CD4/CD8 ratio of 0.3, when compared to a normal CD4/CD8 ratio of 1.

The investigators highlight that in participants with CD4 cell counts above 500, the association between the CD4/CD8 ratio and the Kaposis sarcoma risk was stronger than that seen in the entire study population. They also found that being a man who has sex with men and being older were associated with a higher Kaposis sarcoma risk.

As observed with Kaposis sarcoma, virological failure was a strong factor for non-Hodgkin lymphoma risk, increasing it two-fold. Contrary to what was seen with Kaposis sarcoma, the CD4/CD8 ratio was not as predictive as the CD4 count for non-Hodgkin lymphoma.

However, the model adjusted for the CD4 and the CD8 counts showed that the risk for non-Hodgkin lymphoma strongly increased when the CD8 count was very high: hazard ratio from 1.61 for 2000 CD8 cells, to 3.14 for 3000 CD8 cells, compared to 1000 CD8 cells. This association was even stronger among participants with CD4 cell counts above 500 at baseline.

The investigators identified being older and male sex as other independent factors associated with a higher non-Hodgkin lymphoma risk.

These results confirm that HIV-related diseases still occur in people living with HIV despite a suppressed viral load and a relative immune response restoration. HIV-related inflammation is reflected in persistently high CD8 cell counts and leads to unbalanced CD4/CD8 ratios, raising the risk of AIDS and non-AIDS-related diseases.

Caby and colleagues say that CD4/CD8 ratios and high CD8 counts may be biomarkers of particular interest to people living with HIV who have high CD4 counts. For those with persisting low CD4/CD8 ratios despite efficient antiretroviral therapy, closer monitoring could be beneficial.

However, they add, further studies are needed to clarify the impact of the CD4/CD8 ratio on the risk of other HIV-related diseases, to know which specific preventative measures could be implemented.

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Increased risk of Kaposi's sarcoma with low CD4/CD8 ratios and of non-Hodgkin lymphoma with high CD8 counts despite effective HIV treatment - aidsmap

RESEARCHERS have discovered a "cold environment" in a form of cancer which hides it from the immune system.

The findings mean immunotherapy- an emerging and advanced treatment which triggers the bodys own immune system to attack cancer cells - is unlikely to be effective in treating neuroendocrine tumours, a form of cancer which goes undetected by the immune system.

As a result, attention can now turn to understanding why this type of cancer is not recognised and finding ways to trigger an immune response to enable further treatments to be developed.

In this study, Dr Lulu Tanno, NETs research fellow at the University of Southampton, and her team studied samples of the tumours of 192 patients with pancreatic and small intestinal NETs at University Hospital Southampton.

The results, presented at the European Neuroendocrine Tumours Society, showed neither of these tumours contained any immune cells, known as tumour infiltrating lymphocytes (TILs), compared to hundreds found in the most common form of lung cancer.

Prior to this study very little was known about the quality and significance of the immune (anti-tumour) response in NETs but it is vital we know more with the emergence of immunotherapy as a potential treatment option, explained Dr Tanno.

What we have established is that there is no evidence of immune cells in pancreatic and small intestinal NETs, making it an immunologically cold environment and, therefore, unlikely to respond to current immunotherapy.

NETs are rare types of cancer which are usually found in the pancreas, bowel or lungs but can also develop in other parts of the body.

They arise from cells found throughout the body which form a link between the nervous system and the endocrine system, a collection of glands which produce hormones.

Around 4,000 new cases are diagnosed every year in the UK, though it is thought that a larger number of people are affected but remain undiagnosed as the cancers are slow growing.

If detected early they can often be cured with surgery but, at present, most are diagnosed at a later stage when they have already spread to other parts of the body.

Dr Tannos research programme was founded by the Robert White Legacy Fund and is part-funded by PLANETS Charity, which helps patients with pancreatic, liver, colorectal, abdominal and neuroendocrine cancer by funding patient support groups, innovative treatments and research.

She said NET patients curiosity and enthusiasm for knowing more about their condition was one of the major driving forces behind this research project.

See the article here:
Researchers discover 'cold environment cancer' which hides from the immune system - Daily Echo

As the subject of the 2018 Nobel Prize in Medicine, tumor immunotherapy has proven to be an exciting cancer treatment strategy. Most immunotherapies to date have focused on T cell function; however, more natural killer (NK) cell-based therapies that involve monoclonal antibodies (mAbs) that target tumor antigens are emerging. mAbs have shown clinical success for the treatment of both hematological cancers and previously difficult to treat solid tumors. One fundamental mechanism through which mAbs can kill tumor cells is antibody-dependent cellular cytotoxicity (ADCC). ADCC refers to when mAbs elicit an immune response through the activation of NK cells and is triggered by the bi-specific binding of an antibody to both a NK cell activation receptor (CD16) and a target cancer cell protein antigen. This binding results in the release of cyto-toxic molecules that lead to targeted cancer cell death. While promising, mAbs are potentially immunogenic, can degrade in vivo and experience difficulties trafficking to the site of solid tumors. Furthermore, large doses of the mAb need to be administered intravenously. This increases manufacturing costs, resulting in higher drug prices and limiting general patient accessibility. An approach to utilize tumor immunotherapeutic antibodies directly in vivo using small immune recruiting molecules coined as covalent immune recruiters (CIRs) was developed. CIRs selectively link to naturally abundant serum antibodies and redirect them to the sur-face of tumor cells. The resultant display of tumor coated antibodies activates stimulatory receptors on innate immune cells, such as CD16 on NK cells, and triggers an antitumor immune response. The efficacy of these CIRs as modulators of protein proximity can be characterized by the Octet Bio-Layer Interferometry (BLI) platform. Octet systems are capable of real-time, high-throughput analysis of small molecule and biomolecule binding kinetics under equilibrium conditions. Due to its flexibility and compatibility for alternative assay format arrangements, it is a powerful tool for characterizing the CIR dependent binding equilibrium (e.g., tumor antigen:CIR:Ab) in addition to its use in determining CIR-antibody covalent recruitment kinetics. The label-free and highly sensitive nature of the Octet BLI technology also enables analysis under dilute conditions, conserving expensive biologic reagents and attenuating aggregation phenomena intrinsic to isothermal titration calorimetry (ITC) and fluorescence polarization (FP) assays. Octet systems also present a unique method to simultaneously characterize multiple protein binding and covalent labeling processes and discern reversible binding from a covalent reaction. Octet system can be employed to efficiently characterize CIR binding affinities against both a prostate tumor antigen and human serum antibodies, as well as measure the selective covalent recruitment of these antibodies to the tumor antigen. These assays can accelerate the advancement of lead compounds to in vivo validation studies, and have additional utility in characterizing emerging classes of covalent inhibitor drugs.

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Synthetic Immune Recruitment - A New Way to Fight Tumors - Technology Networks

Every person, every mouse, every dog, has one unmistakable sign of aging: hair loss. But why does that happen?

Rui Yi, a professor of pathology at Northwestern University, set out to answer the question.

A generally accepted hypothesis about stem cells says they replenish tissues and organs, including hair, but they will eventually be exhausted and then die in place. This process is seen as an integral part of aging.

Instead Dr. Yi and his colleagues made a surprising discovery that, at least in the hair of aging animals, stem cells escape from the structures that house them.

Its a new way of thinking about aging, said Dr. Cheng-Ming Chuong, a skin cell researcher and professor of pathology at the University of Southern California, who was not involved in Dr. Yis study, which was published on Monday in the journal Nature Aging.

The study also identifies two genes involved in the aging of hair, opening up new possibilities for stopping the process by preventing stem cells from escaping.

Charles K.F. Chan, a stem cell researcher at Stanford University, called the paper very important, noting that in science, everything about aging seems so complicated we dont know where to start. By showing a pathway and a mechanism for explaining aging hair, Dr. Yi and colleagues may have provided a toehold.

Stem cells play a crucial role in the growth of hair in mice and in humans. Hair follicles, the tunnel-shaped miniature organs from which hairs grow, go through cyclical periods of growth in which a population of stem cells living in a specialized region called the bulge divide and become rapidly growing hair cells.

Sarah Millar, director of the Black Family Stem Cell Institute at the Icahn School of Medicine at Mount Sinai, who was not involved in Dr. Yis paper, explained that those cells give rise to the hair shaft and its sheath. Then, after a period of time, which is short for human body hair and much longer for hair on a persons head, the follicle becomes inactive and its lower part degenerates. The hair shaft stops growing and is shed, only to be replaced by a new strand of hair as the cycle repeats.

But while the rest of the follicle dies, a collection of stem cells remains in the bulge, ready to start turning into hair cells to grow a new strand of hair.

Dr. Yi, like most scientists, had assumed that with age the stem cells died in a process known as stem cell exhaustion. He expected that the death of a hair follicles stem cells meant that the hair would turn white and, when enough stem cells were lost, the strand of hair would die. But this hypothesis had not been fully tested.

Together with a graduate student, Chi Zhang, Dr. Yi decided that to understand the aging process in hair, he needed to watch individual strands of hair as they grew and aged.

Ordinarily, researchers who study aging take chunks of tissue from animals of different ages and examine the changes. There are two drawbacks to this approach, Dr. Yi said. First, the tissue is already dead. And it is not clear what led to the changes that are observed or what will come after them.

He decided his team would use a different method. They watched the growth of individual hair follicles in the ears of mice using a long wavelength laser that can penetrate deep into tissue. They labeled hair follicles with a green fluorescent protein, anesthetized the animals so they did not move, put their ear under the microscope and went back again and again to watch what was happening to the same hair follicle.

What they saw was a surprise: When the animals started to grow old and gray and lose their hair, their stem cells started to escape their little homes in the bulge. The cells changed their shapes from round to amoeba-like and squeezed out of tiny holes in the follicle. Then they recovered their normal shapes and darted away.

Sometimes, the escaping stem cells leapt long distances, in cellular terms, from the niche where they lived.

If I did not see it for myself I would not have believed it, Dr. Yi said. Its almost crazy in my mind.

The stem cells then vanished, perhaps consumed by the immune system.

Dr. Chan compared an animal's body to a car. If you run it long enough and dont replace parts, things wear out, he said. In the body, stem cells are like a mechanic, providing replacement parts, and in some organs like hair, blood and bone, the replacement is continual.

But with hair, it now looks as if the mechanic the stem cells simply walks off the job one day.

But why? Dr. Yi and his colleagues next step was to ask if genes are controlling the process. They discovered two FOXC1 and NFATC1 that were less active in older hair follicle cells. Their role was to imprison stem cells in the bulge. So the researchers bred mice that lacked those genes to see if they were the master controllers.

By the time the mice were 4 to 5 months old, they started losing hair. By age 16 months, when the animals were middle-aged, they looked ancient: They had lost a lot of hair and the sparse strands remaining were gray.

Now the researchers want to save the hair stem cells in aging mice.

This story of the discovery of a completely unexpected natural process makes Dr. Chuong wonder what remains to be learned about living creatures.

Nature has endless surprises waiting for us, he said. You can see fantastic things.

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Losing Your Hair? You Might Blame the Great Stem Cell Escape. - The New York Times

A lung transplant can mean the difference between life and death for people with diseases such as pulmonary fibrosis, chronic obstructive pulmonary disease (COPD) and even severe COVID-19. Yet, recipients of donor lungs must take daily medications to stave off damage caused by their own immune system, which attacks the organs it recognizes as foreigna process known as rejection.

A new University of Michigan Health study, published in the Journal of Clinical Investigation, has identified cells that appear to play a pivotal role in creating the scarring, or fibrosis, characteristic of chronic rejection following a lung transplant.

Almost 15 years ago, Vibha Lama, MBBS, M.S., a professor in the Division of Pulmonary Disease and Critical Care Medicine, and her lab described the presence of stem-cell-like cells, called mesenchymal stromal cells, in lung sample fluid from lung transplant recipients.

We found that even ten years post-transplant, these cells belonged to the donor, not the recipient, she explained. At that time, we had no clue where in the lung they were coming from or what role they played.

To figure this out, her lab generated a mouse model to recreate what happens within a lung transplant recipient. With the model, they followed a transcription factor known as FOXF1 as a sort of trail of breadcrumbs back to the cells original location.

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They discovered that these cells formed a reservoir of stem cells within the bronchovascular bundle deep inside the lung. These bundles contain a bronchus (airway), arteries, connective tissue and other structures and is the part of the lung which connects it to the outside environment.

In this study, explained Lama, who is senior author on the paper, they show that these specific stem cells are interacting with neighboring epithelial cells within that airway niche.

Epithelial cells line and protect the airways and produce a protein known as Sonic hedgehog. Via this protein, epithelial cells signal the stem-cell-like mesenchymal cells, which make up the scaffolding of the lungs, to make FOXF1, a repressor that keeps the stem cells in check.

We are just recently understanding that there are many different kinds of mesenchymal cells in the lung, said Lama. What we describe here is not only are there many kinds of mesenchymal cells, FOXF1 is retained only in these specific stem-cell-like cells.

In the case of lung transplant rejection, Lama hypothesized that immune cells from the recipient attack the epithelial cells which disrupts the balance between them and the mesenchymal cells.

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Because of the damage caused by rejection, the epithelial cells get damaged, Sonic hedgehog is reduced and that interrupts the signaling to the mesenchymal cells to keep quiet, she said. Because of that, these cells start dividing and they lay down more collagen, which leads to fibrotic scarring.

The work sets the stage for more research into the interaction of these cells with epithelial and other cells it their vicinity to further characterize what happens during chronic rejection and potentially how to prevent it. Furthermore, discovery of these cells is also important in understanding other airway diseases like asthma and COPD.

Paper cited: Transcription factor FOXF1 identifies compartmentally distinct mesenchymal cells with a role in lung allograft fibrogenesis, J Clin Invest. DOI: 10.1172/JCI147343

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Stem cells and their role in lung transplant rejection - Michigan Medicine

If you are human, you are going to die. This isn't the most comforting thought, but death is the inevitable price we must pay for being alive. Humans are, however, getting better at pushing back our expiration date, as our medicines and technologies advance.

If the human life span continues to stretch, could we one day become immortal? The answer depends on what you think it means to be an immortal human.

"I don't think when people are even asking about immortality they really mean true immortality, unless they believe in something like a soul," Susan Schneider, a philosopher and founding director of the Center for the Future Mind at Florida Atlantic University, told Live Science. "If someone was, say, to upgrade their brain and body to live a really long time, they would still not be able to live beyond the end of the universe."

Scientists expect the universe will end, which puts an immediate dampener on a mystery about the potential for human immortality. Some scientists have speculated about surviving the death of the universe, as science journalist John Horgan reported for Scientific American, but it's unlikely that any humans alive today will experience the universe's demise anyway.

Related: What happens when you die?

Many humans grow old and die. To live indefinitely, we would need to stop the body from aging. A group of animals may have already solved this problem, so it isn't as far-fetched as it sounds.

Hydra are small, jellyfish-like invertebrates with a remarkable approach to aging. They are largely made up of stem cells that constantly divide to make new cells, as their older cells are discarded. The constant influx of new cells allows hydra to rejuvenate themselves and stay forever young, Live Science previously reported.

"They don't seem to age, so, potentially they are immortal," Daniel Martnez, a biology professor at Pomona College in Claremont, California, who discovered the hydra's lack of aging, told Live Science. Hydra show that animals do not have to grow old, but that doesn't mean humans could replicate their rejuvenating habits. At 0.4 inches (10 millimeters) long, hydra are small and don't have organs. "It's impossible for us because our bodies are super complex," Martnez said.

Humans have stem cells that can repair and even regrow parts of the body, such as in the liver, but the human body is not made almost entirely of these cells, like hydra are. That's because humans need cells to do things other than just divide and make new cells. For example, our red blood cells transport oxygen around the body. "We make cells commit to a function, and in doing that, they have to lose the ability to divide," Martnez said. As the cells age, so do we.

We can't simply discard our old cells like hydra do, because we need them. For example, the neurons in the brain transmit information. "We don't want those to be replaced," Martnez said. "Because otherwise, we won't remember anything." Hydra could inspire research that allows humans to live healthier lives, for example, by finding ways for our cells to function better as they age, according to Martnez. However, his gut feeling is that humans will never achieve such biological immortality.

Though Martnez personally doesn't want to live forever, he thinks humans are already capable of a form of immortality. "I always say, 'I think we are immortal,'" he said. "Poets to me are immortal because they're still with us after so many years and they still influence us. And so I think that people survive through their legacy."

The oldest-living human on record is Jeanne Calment from France, who died at the age of 122 in 1997, according to Guinness World Records. In a 2021 study published in the journal Nature Communications, researchers reported that humans may be able to live up to a maximum of between 120 and 150 years, after which, the researchers anticipate a complete loss of resilience the body's ability to recover from things like illness or injury. To live beyond this limit, humans would need to stop cells from aging and prevent disease.

Related: What's the oldest living thing alive today?

Humans may be able to live beyond their biological limits with future technological advancements involving nanotechnology. This is the manipulation of materials on a nanoscale, less than 100 nanometers (one-billionth of a meter or 400-billionths of an inch). Machines this small could travel in the blood and possibly prevent aging by repairing the damage cells experience over time. Nanotech could also cure certain diseases, including some types of cancer, by removing cancerous cells from the body, according to the University of Melbourne in Australia.

Preventing the human body from aging still isn't enough to achieve immortality; just ask the hydra. Even though hydra don't show signs of aging, the creatures still die. They are eaten by predators, such as fish, and perish if their environment changes too much, such as if their ponds freeze in winter, Martnez said.

Humans don't have many predators to contend with, but we are prone to fatal accidents and vulnerable to extreme environmental events, such as those intensified by climate change. We'll need a sturdier vessel than our current bodies to ensure our survival long into the future. Technology may provide the solution for this, too.

As technology advances, futurists anticipate two defining milestones. The first is the singularity, in which we will design artificial intelligence (A.I.) smart enough to redesign itself, and it will get progressively smarter until it is vastly superior to our own intelligence, Live Science previously reported. The second milestone is virtual immortality, where we will be able to scan our brains and transfer ourselves to a non-biological medium, like a computer.

Researchers have already mapped the neural connections of a roundworm (Caenorhabditis elegans). As part of the so-called OpenWorm project, they then simulated the roundworm's brain in software replicating the neural connections, and programmed that software to direct a Lego robot, according to Smithsonian Magazine. The robot then appeared to start behaving like a roundworm. Scientists aren't close to mapping the connections between the 86 billion neurons of the human brain (roundworms have only 302 neurons), but advances in artificial intelligence may help us get there.

Once the human mind is in a computer and can be uploaded to the internet, we won't have to worry about the human body perishing. Moving the human mind out of the body would be a significant step on the road to immortality but, according to Schneider, there's a catch. "I don't think that will achieve immortality for you, and that's because I think you'd be creating a digital double," she said.

Schneider, who is also the author of "Artificial You: AI and the Future of Your Mind" (Princeton University Press, 2019), describes a thought experiment in which the brain either does or doesn't survive the upload process. If the brain does survive, then the digital copy can't be you as you're still alive; conversely, the digital copy also can't be you if your brain doesn't survive the upload process, because it wouldn't be if you did the copy can only be your digital double.

Related: What is consciousness?

According to Schneider, a better route to extreme longevity, while also preserving the person, would be through biological enhancements compatible with the survival of the human brain. Another, more controversial route would be through brain chips.

"There's been a lot of talk about gradually replacing parts of the brain with chips. So, eventually, one becomes like an artificial intelligence," Schneider said. In other words, slowly transitioning into a cyborg and thinking in chips rather than neurons. But if the human brain is intimately connected to you, then replacing it could mean suicide, she added.

The human body appears to have an expiration date, regardless of how it is upgraded or uploaded. Whether humans are still human without their bodies is an open question.

"To me, it's not even really an issue about whether you're technically a human being or not," Schneider said. "The real issue is whether you're the same self of a person. So, what really matters here is, what is it to be a conscious being? And when is it that changes in the brain change which conscious being you are?" In other words, at what point does changing what we can do with our brains change who we are?

Schneider is excited by the potential brain and body enhancements of the future and likes the idea of ridding ourselves of death by old age, despite some of her reservations. "I would love that, absolutely, she said. "And I would love to see science and technology cure ailments, make us smarter. I would love to see people have the option of upgrading their brains with chips. I just want them to understand what's at stake."

Originally published on Live Science.

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Will humans ever be immortal? - Livescience.com

RJ Pierce, Tech Times 05 October 2021, 09:10 am

Healthcare research has gone a long way from the dark days of old, when today's simplest illnesses can be a death sentence. And now, there's reason to look forward to a brighter future because of this news.

(Photo : Getty Images )

According to BigThink, a team from Iowa State University claimed that they've found a way to integrate human immune systems in pigs, as a way to study illnesses much closer.

In other words, they basically "humanized" the pigs to try and find out how to better treat human diseases in the future.

The implications of their research are quite profound, too. As per the researchers, this breakthrough could theoretically advance healthcare research in areas such as virus and vaccines, cancer, and even stem cell treatments.

Before this, scientists often used mice in their biotech and biomedical experiments. However, the problem is that mice-based results don't translate well to humans.

Aside from mice, primates have also been used in related fields of healthcare research due to their direct biological connections with humans. Nevertheless, a lot of ethical issues popped up, thus leading to the retirement of primates, including chimpanzees, from this type of research eight years ago.

This won't be the first time that healthcare research has produced what's basically human-animal hybrids to study illnesses.

Three years ago, a team of scientists from Rockefeller University in New York managed to create a human-chicken embryo, in an attempt to take a closer look at the intricacies of stem cell therapies.

Read also: Scientists Want To Create Part-Human Part-Animal Chimeras To Find Cure For Diseases

It started when the same scientists from Iowa State University discovered a genetic mutation in pigs that caused an illness called SCID (Severe Combined Immunodeficiency).

Some people may know this from the film "The Boy In The Plastic Bubble" from 1976, which tells the story of a child whose immune system never fully developed. As such, he was forced to literally live inside a sterile bubble because even the slightest cold would kill him.

Upon this discovery, the researchers then developed a pig that's far more immunocompromised compared to a person with SCID, then successfully "humanized" it by injecting human immune stem cells into the livers of piglets.

The researchers were able to do this by using ultrasound imaging as a guide.

Ultrasound imaging, also known as sonography, makes use of high-frequency waves to look inside the body.

(Photo : Getty Images )

The resulting pigs had excellent healthcare research potential, because they were found to have human immune cells in their blood, thymus gland, spleen, and liver.

However, the SCID-afflicted pigs are in constant danger of infections. As such, they have to be housed in so-called bubble biocontainment facilities. These facilities work by maintaining high positive pressure, which keeps dangerous pathogens out. All staff members have to wear sterile protective gear at all times.

They've basically turned into their own versions of the boy in the bubble.

Before this research, pigs have often been used to know more about the human body because of how strikingly similar their anatomy is to humans.

In fact, a few scientists even believe that with how biologically similar pigs are to humans, they might be classified into an animal family occupied by primates, reportedScience.org.au.

But of course, there have been ethical issues involving the use of these human-animal hybrids for healthcare research. Eventually, though, the National Institutes of Health (NIH) relaxed their regulations a bit back in 2016, which made it easier for scientists to transfer human stem cells into animal embryos.

Related: Scientists Grow Sheep Embryos With Human Cells To Revolutionize Organ Transplant

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Written by RJ Pierce

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Healthcare Researchers Are Putting HUMAN Immune Systems In Pigs To Study Illnesses-Here's The Tech Behind It - Tech Times