Archive for April, 2022

Ancient skeletons, funerary practices, and DNA reveal layers of inequality in past societies.

November 26, 1922, marks what is arguably the most famous discovery in the history of archaeology. On that day, the British Egyptologist Howard Carter made a small hole through which he could insert a candle in the sealed doorway of Tutankhamuns burial chamber and thus lit the interior. As his eyes slowly adapted to the darkness, he was able to make out a chamber that had not been disturbed for over 3,000 years.

Tutankhamun was just an obscure pharaoh during his lifetime, and there is evidence that he was hastily buried; the second of the three nested coffins seems to have originally belonged to someone else. And yet the inner coffin, in which his mummy was discovered, is made of solid gold, weighing almost 250 pounds. One can barely imagine how impressive the burials of such powerful leaders as Khufu, Thutmose III, or Rameses II must have been; alas, they were all looted in antiquity.

But contrary to popular belief and cinematic glorification, most archaeologists would say that the search for spectacular treasures isnt their main research objective; they want to understand the daily life of past civilizations. Still, both extremes the fabulous wealth of kings and the hardscrabble existence of common people contribute to an understanding of what can be argued is one of the main goals of archaeology: to document and study the evolution of inequality in ancient societies. This also involves the question of how to recognize and quantify it.

One of the most obvious approaches would be through the assessment of differential goods deposited in graves. But richly furnished graves may not simply be evidence of social differentiation; rather, they may be an attempt to demonstrate the importance and distinction of a family in relationship to other kindreds a social importance that may not exist in reality. Moreover, social stratification can be based on wealth but can also be based on personal prestige and power. Therefore, it isnt always possible to assess social differences by comparing graves with goods to those without them.

Aztec society, even with its horrific human sacrifices, was at the time of the Spanish conquest more egalitarian than Mexico 200 years later.

Some archaeologists have attempted to apply economic principles to examine social differences at specific sites and, crucially, compare the data from different places. A study led by Samuel Bowles from the Santa Fe Institute and published in Nature in 2017 tried to address this question by applying the Gini coefficient a single number most commonly used to measure income inequality across a large number of sites from the archaeological record, both in the Old World and the Americas. The list of sites included paradigmatic cities such as atalhyk in Turkey, Pompeii in Italy, and Teotihuacan in Mexico; the authors measured the dimensions of houses as estimated indicators of wealth.

Among modern hunter-gatherers, the team found, the Gini coefficient is low around 17 (on a scale of 0 to 100). This is not surprising as few objects can be carried in nomadic societies, and consequently, personal qualities such as the ability to hunt count for more. This does not mean that some people didnt have a higher social status; material culture was probably so poor or so different from our perceptions of status that it is difficult to grasp social differences among past hunter-gatherers.

In the ancient farming societies under study the Gini coefficients are estimated to have been between 35 and 46; interestingly, the real measurements were lower than those obtained from records. For instance, among the ruins of Babylonia, researchers estimated a coefficient of 40, yet an estimate based on information from the Babylonian chronicles resulted in a higher coefficient of 46. The ancient accounts likely overemphasized the size of the largest houses in admiration. This is not unlike what happens when we return from a trip: We sometimes tend to exaggerate the things that weve seen.

Nevertheless, the most remarkable differences come from the comparison of the societies of the Old World and those of the Americas, with the latter being much more equal in the Gini coefficient, despite being highly hierarchical in some cases such as the mighty Aztec Empire. Researchers conclude that the root of these differences could be ecological since there were more and larger animals to be domesticated in Eurasia such as cows, horses, pigs, sheep, and goats than in the Americas, with only dogs and turkeys, and this trait alone created a differential system of accumulated wealth.

At the Aztec capital, Tenochtitln, for instance, houses had highly standardized dimensions and were all quite similar. Aztec society, even with its horrific human sacrifices, was at the time of the Spanish conquest more egalitarian than Mexico 200 years later, when the European elite had created the encomienda system, under which the indigenous population worked in semislavery. Within a few generations, the concentration of wealth had almost doubled in the colonial New World, with a consequent increase in inequality.

When did these differences between the Old and New Worlds emerge? Early farming societies had the possibility of generating and storing food surpluses, creating potential scenarios for differences in population size along with a certain degree of inter- and intrasettlement inequality. A recent application of the Gini coefficient to 90 sites from the Near East and Europe showed a remarkable increase of inequality thousands of years after the advent of agriculture a finding that would indicate it was not farming per se that created unequal societies. According to the authors, at some point some farmers were able to maintain specialized plow oxen that could cultivate 10 times more land than other farmers, thereby transforming the economy toward a higher value of land in detriment of human labor.

This emerging inequality at the end of the Neolithic could explain a remarkable example of wealth dating from that period: the Varna burial. This burial was found in a Copper Age cemetery in modern Bulgaria and is dated to 45604450 BCE; it contained more gold than the rest of the world possessed at that time. It contained an adult male likely a chieftain or king of some sort who was buried holding a gold war mace; curiously he also had a gold penis sheath of unknown meaning. Still, such findings are exceptional, and there is a general consensus that Neolithic societies were more egalitarian than later ones.

Inequality clearly increased with the arrival of metals, which partly allowed, from 3000 to 2000 BCE onward, the appearance and development of a social organization based on the emergence of elites. Once the initial power structure was established, it attempted to perpetuate itself dynastically by increasing social control and building up familial alliances with other chiefs. Control mechanisms often involved violence. The possibility of using horses and to lesser extent, camels as instruments of war determined the success of conquests that would alter the pattern of settlements across Eurasia at the end of the Neolithic. This would at least partially explain how 30 empires or large states that emerged between 3000 and 600 BCE were all found in the Old World, where these animals roamed.

Consequently, tombs with signs of wealth became more abundant in the archaeological record, such as the famous Amesbury Archer, found three miles southeast of Stonehenge in 2002 (near todays Salisbury) and dated to 2300 BCE. This grave includes more artifacts than any other Bronze Age British burial; besides numerous arrowheads, three copper knives, four boars tusks, two stone wrist guards that protected users from their bowstrings, and five pots that conformed to the Bell Beaker tradition, there were two gold hair ornaments the earliest pieces made of this metal ever found in the British Isles. The arrival of the Bell Beaker complex to the British Isles is associated with an almost complete replacement of the prior local population and subsequent emergence of social elites. The Amesbury Archer must be considered in the context of the spread of metalwork and supraregional exchange networks in a process that archaeologists sometimes call Bronzization.

The rise in inequality during this period, both in the Middle East and parts of western Europe, seems to be partly influenced by an increase in population density. This correlation is likely related to a growing complexity in modes of subsistence, trading networks, and political organization associated with population growth.

Although the highest Gini coefficients for past societies determined by the Santa Fe Institute were similar to those found in some present-day European countries (for instance, with values of around 60 in Pompeii and Kahun, an Egyptian settlement from the 12th dynasty), they remained below the values for the most unequal modern societies such as China and the United States (with Gini coefficients of 73 and 85, respectively), which obviously have larger populations.

From a historical perspective this would suggest that an increase in population size brings higher inequality an issue explored by the economist Thomas Piketty in recent times, but that likely has parallels in Bronze Age populations.

Still, the Gini coefficient cannot always be applied since some settlements have grown with time over the destruction of previous ones, piled one atop another like the layers of a cake. Many ancient sites could not possibly be studied in detail; for instance, at Hisarlik the old Troy at least 10 cities arose atop their predecessors in just 2,000 years, making them quite difficult to disentangle. In addition to this limitation, whether the Gini coefficient can be transferred between different cultural, geographic, and ecological environments to make direct comparisons has also been a subject of debate since such factors can influence their inhabitants differently. For example, a settlement established in a jagged terrain would favor smaller, more vertical houses than one extending over a vast plain.

The economic interpretation of past settlements has received some criticism from among the archaeological community; some argue that the quality and solidity of the building materials can be as important as the size of the houses. In our modern cities, were all aware that location for instance, close to the city center is usually more important than size. Finally, the ostentatious wealth opulent furniture, wall paintings, mosaics, and so on that can still be found in some excavated houses such as at Pompeii should be taken into consideration too, though such features arent usually well preserved.

One way around these limitations might be to compare the Gini coefficients with the so-called health inequality of each population, since buried human remains are sometimes better preserved than buildings. There are several skeletal indicators (dental cavities, arthrosis, traumas, vitamin deficiencies, etc.) that can reflect the health status of the population in each period. The frequencies of these pathological markers are in general higher during periods of higher inequality.

For example, the 20062013 excavation of nonelite cemeteries such as North Tombs Cemeteries at Amarna demonstrated deaths at an early age mainly of children, teenagers, and young adults widespread dietary deficiencies, and indications of hard labor, suggesting the poor state of health and substandard working conditions for most of this urban community. For instance, 16 percent of all children under 15 displayed spine injuries of the sort associated with carrying heavy loads; none of them had any grave goods, and sometimes were buried together with several others, with scant regard for the disposition of the bodies a grim image that contrasts with the glamorous depictions of the pharaohs family in the Amarna style.

The information retrieved from their DNA can be used, for the first time, to correlate ancestry with social power in each period.

An additional indicator would be evidence of a high infant mortality rate, although the preservation of childrens skeletal remains is invariably more difficult than that of adult bones due to differential conservation processes, and this could represent an insurmountable bias in the results. Changes in health status can be used to ascertain cultural and ancestral transitions too. In this sense, probably the most striking change observed is between hunter-gatherers and the first farmers in Europe. The latter not only show signs of poorer health such as cavities, almost unknown by the former but also higher infant mortality rates and even lower stature than previous hunter-gatherers.

Correlated with this information, recent developments in the stable isotope analysis of carbon and nitrogen ratios in bone collagen can provide information on nutritional status and mobility patterns associated with specific individuals. For instance, the analysis of a high-status burial in Helmsdorf, Germany, related to the ntice culture, showed that this person had a higher protein intake than other contemporaneous peers, suggesting as well that diet can be as much an indicator of social status as it is in todays societies.

Key to understanding the social panorama of the past is that ancient cemeteries can provide not only potential indicators of inequality in the form of grave goods and even differential health status but also genetic material preserved within human remains. The information retrieved from their DNA can be used, for the first time, to correlate ancestry with social power in each period. Furthermore, a crucial aspect of the accumulation of power is the possibility of bequeathing wealth to biological relatives something that can be tested as well via the interface between genetics and archaeology, which enables us to reveal family links.

Like funerary goods, a privileged resting place could serve as a status marker too. Around 6,500 years ago, the phenomenon of building large funerary stone structures known as megalithic tombs emerged, mainly across Europes Atlantic seaboard, and culminated in the great passage tomb complexes such as Newgrange in Boyne Valley (Ireland), which has a mound almost 300 feet in diameter and 50 feet high. The origins and meaning of these monuments, which required a heavy investment in labor, have been debated for more than a century, as has the social organization of the farming communities that built them. The genetic analysis of two-dozen individuals found in various megalithic tombs from Scandinavia to Orkney Island and Ireland yielded some interesting social clues.

In some places, notably the British Isles, more males than females were buried in these preeminent spots, pointing to a sex bias. In accordance with this observation, the descent of most individuals with kinship links could be traced through the paternal line. In one case it was possible to find two related males buried in two different megaliths just over a mile apart (Primrose Grange and Carrowmore in Ireland), indicating a geographic expansion of these dominant families. Genetic analyses of skeletal remains discovered within the most intricately constructed chamber of the Newgrange passage tomb revealed that they belonged to the incestuous son of a brother and sister (or a parent and child), and therefore a quarter of his genome had no genetic variation.

The fact that even children who died in infancy were buried with grave goods suggests as well that their status was inherited rather than acquired during their lifetime.

This kind of first-degree offspring is extraordinary, only having been cited in royal families of the past headed by god-kings such as the Egyptian pharaohs seeking to maintain a pure dynastic bloodline. (It is known, for instance, that Akhenaten married his eldest daughter, Meritaten, and much later, Ptolemy II married his sister, Arsinoe II hence his nickname, Philadelphus or sibling loving.) It has been suggested that this Neolithic elite may have claimed to possess divine powers to ensure the continuity of agricultural cycles by keeping the suns movements going.

The findings support the notion that these Neolithic communities were socially stratified and that the massive stone structures were used to bury transgenerational patrilineal members of these clans. Perhaps equally interesting is the fact that in one case relatives were separated by up to 12 generations, pointing to an unusual stability through time of both the funerary tradition and the stratified society where they lived.

One of the most illustrative examples of how the analysis of Bronze Age individuals that lived through continental-scale cultural changes can shed light on the process is a study led by researchers at the Max Planck Institute in Jena and published in 2019. Paleogenetic researchers analyzed more than 100 skeletons from 45 farmstead-related graveyards in the Lech River valley in southern Germany to explore the social mechanisms underlying the local spread of steppe ancestry across Europe. Additionally, isotope data were generated for these individuals to gather information on their lifetime mobility patterns, which could be correlated with differential composition in genetic ancestry.

Isotopic analyses revealed that females tended to be nonlocal (only 50 percent of them had values consistent with the local isotopic range) as compared to males and children from the same cemeteries (where 82 to 84 percent were deemed local). Isotopic data on early and late forming teeth in the same individuals the first and third permanent molars that emerge at six and 18 years, respectively suggested that females moved from their birthplaces during adolescence or later. One of them was found to come from a place at least 200 miles away. Most of the males carried the R1b Y chromosome lineage, while the mitochondrial DNA lineage composition was much more diverse. The results indicate that these Bronze Age settlements followed patrilocal residential rules that is, males stayed in the groups where they were born, while females moved away from them. The fact that most males descendants shared their ancestry with a single female also suggests that the social structure, besides being based on patrilineal links, was likely monogamous.

The researchers were able to reconstruct six pedigrees in different graveyards, three of which spanned at least four generations. They detected 10 parent-offspring relationships, six of them between mother and child. Interestingly, the latter were always male; there were no adult daughters present. Again, this suggests that females were interchanged between households as a way to establish alliances; it is likely that their status was secured once they had children in the new household. It was also possible to correlate grave goods (daggers, axes, chisels, and arrowheads for males, and body ornaments such as neck or leg rings for females) with kinship.

This indicates that wealth and social status were inherited and ran with families. The fact that even children who died in infancy were buried with grave goods suggests as well that their status was inherited rather than acquired during their lifetime. A further observation was that members of each clan were buried near each other in the cemeteries, thus clearly delimiting preeminent areas within them. It is likely that the inheritance system of these households was based on male primogeniture a custom by which the oldest son inherits all the familys properties at the fathers death. With time, forged alliances granted families access to larger, regional clans and eventually kingdoms.

An examination of the dynamics between kinship and social inequality can be applied to even more recent periods. The complex interactions underlying extended families and population levels can be better understood in geographically isolated places such as islands. Iceland remains the most studied island from a genetic point of view, mainly due to the efforts of a private company called deCODE Genetics that was founded in 1996 by neurologist Kri Stefnsson.

Iceland, a remote island in the north Atlantic, was first colonized around 874 CE, according to the Landnmabk, or settlement book, when the Norse chieftain Inlfr Arnarson arrived in the region of present-day Reykjavik. Over the next 150 years, groups of Viking migrants from Norway along with Celtic women and servants or slaves arrived on the island, establishing themselves on rather isolated farms. By 930 CE, all arable land was already occupied and all the forests were gone. The migratory influx slowed down afterward and almost ceased after the year 1000 CE. This resulted in a population that was small and isolated yet at the same time big enough to have all the common European diseases and genetic diversity and it suffered several demographic bottlenecks associated with volcanic eruptions, famines, and epidemics of the plague.

Until 1850, the Icelandic population never exceeded 50,000. The combination of two factors an isolated population and a well-known genealogical database makes Iceland an ideal laboratory for detecting genetic variants associated with common diseases that affect not only modern Icelanders but also the rest of Europe, where such information does not exist or the population is too big to make such an approach practical. Over the years, researchers from deCODE Genetics have generated a whole body of data on the genomics of modern Icelanders and also on how the original population was established. By working with uniparental markers from living Icelanders it could be observed that 62 percent of the mitochondrial DNA was Celtic in origin (meaning that the majority of these maternal markers derived from either the British Isles or Ireland), while 75 percent of the Y chromosomes were of Scandinavian origin. This suggested a settlement primarily established by Viking males and Celtic females.

In 2017, and thanks to paleogenomic techniques, it was possible to retrieve 27 ancient Icelandic genomes, most of them from the heathen period (prior to the year 1000 CE, when Icelanders decided to become Christians by the curious procedure of voting). At the nuclear genome level, these pioneers had a Norwegian-type ancestry (55.4 percent) that was greater than the Celtic one, and more prevalent among men (a recent genetic study of more than 400 Viking individuals has confirmed the spread of Norwegian ancestry mainly across the North Atlantic islands).

Modern Icelanders are not, however, a simple mixture of the two components; their ancestry demonstrates a differentiation from the two source populations at least partially due to genetic drift promoted by geographic isolation during the last thousand years. Interestingly, the Norwegian-type ancestry component in Iceland is nowadays 70.4 percent, suggesting an increase that was likely socially mediated. An example of this stems from seven individuals excavated in 1964 from a boat grave (a type of burial in which a ship is used as a container of the dead) at Vatnsdalur in the remote western fjords. The grave goods included a knife, 30 beads, a silver Thors hammer, a Cufic coin (dated circa 870930 CE), and various items of jewelry. Three of the four skeletons sequenced showed mostly Scandinavian ancestry. One of these individuals is among the few sequenced early settlers to be genetically similar to modern Icelanders, indicating that he contributed disproportionately to their ancestry.

One way or another, mortuary archaeology will always be an important subfield of this discipline, and one that will need to rely on the hard sciences such as genetics and forensics.

It seems that the Celtic servants brought to Iceland clearly had fewer opportunities to reproduce. Using isotopic analysis, it was also possible to detect that at least three people two Scandinavians and one Celt were first-generation migrants, having spent their childhood outside Iceland. One individual had mixed ancestry, indicating that his parents were from different places. The fact that the Celtic ancestry is still detectable decades after the first settlement also suggests that some kind of social discrimination between the two ancestral groups persisted for a while. After a few centuries, however, the admixing of the two communities was complete, to the point that Iceland has essentially become an extended family with a remarkably uniform population.

We have seen several case studies of past inequality correlating funerary archaeology with genetics that might no longer apply today, where legal regulations (and also the exponential increase of cremations) represent a certain degree of standardization in funeral practices. Nevertheless, an opposite trend could shape the future of the archaeology of death: the trend toward personalized coffins, unconventional funerary memorials, and special grave goods. One way or another, mortuary archaeology will always be an important subfield of this discipline, and one that will need to rely on the hard sciences such as genetics and forensics.

Perhaps one encouraging conclusion is that despite what we have seen on the archaeology of past inequality, societies have been able to evolve and change their social stratifications. One example is Iceland itself; the country has become one of the most egalitarian societies in the world. In 2018, Iceland passed a law that all companies employing more than 25 people will have four years to ensure gender-equal payment because, according to the head of the Equality Unit at Icelands Welfare Ministry, equality wont come about by itself, from the bottom up alone.

Carles Lalueza-Fox is Research Professor and Director of the Paleogenomics Lab at the Institute of Evolutionary Biology (CSIC-Universitat Pompeu Fabra) in Barcelona. He participated in the Neanderthal Genome Project and led the first retrieval of the genome of an 8,000-year-old European hunter-gatherer. He is the author of Inequality: A Genetic History, from which this article is adapted.

More here:
The Archaeology of Inequality - The MIT Press Reader

To the Editor:

Re Pills Are New Target in 50-Year Abortion Battle (front page, April 6):

The game plan of the anti-abortion movement is falling into place. First, impose strict restrictions on the surgical procedure (think Texas and Oklahoma). Next, let the Supreme Court jettison Roe v. Wade. And now, we read that abortion pills are the new battle line, as numerous states have adopted or are considering restrictions and penalties for pill takers and pill providers.

I am convinced that, after the surgery and the pills are gone, the next target will be birth control.

Abortion opponents, determined to impose their religious views upon the country at large, will not rest until all American women can experience the joys of living in the 13th century.

William DunhamBryn Mawr, Pa.

To the Editor:

Its time for a modern-day Underground Railroad to obtain self-medicated abortions. Its time to widely advertise the availability of these pills, and explain their safety, effectiveness and cost (much cheaper than a medical abortion). You report that in 2020, 54 percent of abortions were with these pills.

Tell women how to obtain these pills from Europe, Canada and Mexico. Attempts to ban pills via the mail will be futile. We need an underground movement to counter state efforts to stop abortions.

Steve GoldPhiladelphia

To the Editor:

Re Near-Total Ban on Abortion in Oklahoma (news article, April 6):

The near-total ban on abortion was approved by a male-dominated legislature. Oklahoma has among the lowest percentages of female legislators in the country.

These men dont seem to get that it takes two people to make a baby. While this law is meant to control the behavior of women, I know of no law that exerts any control over the behavior of the men who are fathering these children.

Martha MeyerChicago

To the Editor:

In the spring of 2005, while we were living in Tulsa, Okla., my wife became pregnant. However, our joy turned to concern and then sorrow as the fetal heartbeat slowed and eventually stopped. My wife had miscarried.

After consulting with our obstetrician, my wife decided to have a dilation and curettage procedure. We both hoped that by surgically extracting the fetal tissue rather than waiting for it to pass on its own, she would heal faster physically and psychologically.

A few weeks later, I received a letter from our insurance company, informing me that the procedure was not covered because it did not pay for abortions. My wife did not have an abortion, and she did not willingly terminate her pregnancy. After many letters and phone calls, I sorted out the situation with our insurance carrier.

However, under the bill passed by Oklahoma lawmakers, that simple insurance coding error or misunderstanding could have led to the arrest of my wifes physician. I suspect that many innocent people, providing appropriate health care to the women of Oklahoma, will face legal consequences as a result of this legislation.

James MonkCleveland

To the Editor:

Re Save Baseball by Nationalizing It, by Matthew Walther (Opinion guest essay, Sunday Review, April 10):

I grew up playing Little League Baseball and, later, N.C.A.A. softball. If my children dont play baseball, it wont be because the game is slow or uncool. Itll be because youth sports have become exorbitantly expensive, and as a result socioeconomically monolithic, shutting out a generation of enthusiasm and talent.

After equipment, uniforms, travel fees and hotels, youth baseball can cost families thousands of dollars per child, and thats if they live near a baseball field unlikely in a dense city or have jobs that allow them to drive their children to practice. Why go through the rigmarole when kids can play football in the park?

It makes sense, then, that Major League Baseballs fan base is overwhelmingly older and whiter even as America becomes younger and more diverse.

Baseball doesnt have a relevance problem. It has an equity problem. To survive as the American pastime, baseball needs youth leagues that are financially, geographically and socially accessible to American kids, and professional rosters that better represent the country.

And speaking as a girl who used to strike out the boys involving more women and girls wouldnt hurt.

Maddie UlanowCambridge, Mass.

To the Editor:

Baseballs future was sealed when, to maximize short-term revenues, it started broadcasting the World Series at night, too late for many young fans to watch. When you cant watch the World Series, it becomes hard to become a die-hard fan.

Rather than nationalize, why not return the World Series to daytime? It has a better chance of saving the game.

Chris BarnumWilmington, Del.

To the Editor:

Re Straight People Need Better Rules for Sex, by Christine Emba (Opinion guest essay, Sunday Review, April 10):

One concerning aspect of sexual encounters raised by Ms. Emba is the use of choking, say, or other porn-inspired violence.

As a psychotherapist and a couples counselor, I am seeing more and more young heterosexual couples where the use of choking and other acts that are violent or degrading to women has caused a significant rift in the relationship.

One suggestion I have for young men is to ask a question three times to get a true answer. Perhaps by asking three times we create that pause suggested by Epictetus. It might sound like: Is this OK? Is it really OK with you? Are you sure you want to do this?

As a society we need to teach men how actual sex with an actual woman might differ from the hard-core porn theyve been exposed to, and we need to educate men about what it means to bring respect, true consent and pleasure into the bedroom in a way that a woman might want.

Jennifer WoffordBrookline, Mass.

To the Editor:

The whole species needs better mores for social intercourse. Maybe we should mainstream manners. Courtesy dignifies our own and others value.

Deborah GriesbachWatertown, Conn.

To the Editor:

Re America Is Running Out of Money to Fight Covid, by Vivek H. Murthy and David A. Kessler (Opinion guest essay, nytimes.com, March 29):

The U.S. surgeon general and the chief science officer for the U.S. Covid-19 Response Team write that the federal government is running out of money to provide Americans with Covid-19 vaccines, booster shots and other supplies to address present and future risks from variants of the coronavirus. They write, It would be a grave mistake to assume Covid-19 no longer requires our action and investment.

As professors of health policy, we strongly agree that the risks are still substantial and likely to increase with a future variant. But our research, published in the Journal of the Royal Society of Medicine, shows that the U.S. is paying Pfizer, Moderna and other major companies more than 15 times the companies total net costs per dose, after subtracting the billions taxpayers already paid them for developing and manufacturing them. More than 95 percent of the $23 to $25 a dose the government now pays is pure profit for executives and shareholders.

If the government paid net costs plus a 20 percent profit, it would have plenty of money to fund its Covid-19 program and would be able to greatly increase global equity access.

Donald W. LightJoel R. LexchinDr. Light is a professor at the Rowan University School of Osteopathic Medicine. Dr. Lexchin is an emergency physician and professor emeritus at York University.

Link:
Opinion | Fighting the Latest Efforts to Outlaw Abortion - The New York Times

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Antiplatelet response to clopidogrel is associated with a haplotype in CYP2C19 gene in Pakistani patients | Scientific Reports - Nature.com

The Utah State Veterinarians office has identified several cases of trichomoniasis (Trich) positive bulls from a beef cattle herd.

This herd had grazed the summer of 2021 at a grazing association in southern Idaho with several other herds, including at least six herds from Utah. There are ten potentially exposed cattle herds that are awaiting test results; five herds belonging to the aforementioned grazing association and five herds that neighbor the affected properties.

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It is concerning to have this large of an outbreak of Trich in Utah cattle herds, said Dr. Dean Taylor, Utah State Veterinarian. Our office is working closely with local veterinarians to conduct testing and are taking measures to stop the spread of this disease.

Trich is a venereal disease of cattle caused by a protozoa (microscopic parasite). It is spread between cattle during breeding. Cows generally abort the fetus from this breeding and then clear the infection, but bulls remain infected for life.

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According to information from Texas A&M University, although losses are observed in the cow,T. foetus lives on the surface of the penis and prepuce of the bull and in the reproductive tract of the cow. Trich prefers a reduced oxygen environment, and it multiplies in the small folds of tissue (crypts) on the bulls penis. Because older bulls have more numerous and deeper crypts and are more easily infected, using young bulls is part of a disease management strategy. There are no obvious signs of Trich in the male, and pregnancy loss is the only sign of the disease in the female.

Cows exposed to Trich cannot be considered safe in calf until they are at least 120 days pregnant; open cows cannot be considered free of infection until they have had at least 90 days of sexual rest and are examined and cleared by a veterinarian. Only then should they be placed back into the breeding herd. All newly acquired cows that are less than 120 days pregnant should be isolated from the breeding herd. They may be placed in the breeding herd once they are four months pregnant.

Because approximately 2 percent of infected cows will have a swollen uterus that contains pus (pyometra) and remain infective, all open cows should be examined by a veterinarian. Cows with pyometra should be sent to slaughter. There is no treatment for infected bulls; send them to slaughter.

Trich should be suspected in herds with poor conception rates and extended calving seasons. Infected herds can produce conception rates that range from slightly subnormal to 50 percent or lower, depending on the length of time the disease is in the herd and the number of animals that are infected. Conception rates in herds with controlled breeding seasons of 90 days or less will be even poorer. Shorter breeding seasons expose the problem more dramatically and can actually reduce the long-term production and economic losses caused by herd infection.

Because Trich develops gradually and is not readily apparent, it is better to prevent exposing the herd to the disease rather than trying to control or eradicate it. Trich enters a herd or ranch only via infected bulls, cows or heifers. Again, transmission is from infected bulls to cows or from infected cows to bulls. To eliminate Trich from a herd, allow infected cows to clear the infection and eliminate infected bulls altogether.

There is no treatment for Trich and this disease can be economically devastating to cattle herds because of:

Culling of positive bulls and purchase of replacement bulls

Increased abortion rate leading to a reduced calf crop

Prolonged calving season and lower calf weights at sale

Culling of open cows

Loss of genetics

Utah requires yearly testing of all bulls for Trich, with the exception of dairy cattle who are kept in confinement and bison bulls. Animals from one positive herd moved into the grazing association in 2021 without proper paperwork. It is also suspected that bulls from this herd were leased to other ranches for breeding purposes.

Source: Utah State Veterinarian's Office and Texas A&M University.which is solely responsible for the information provided and is wholly owned by the source. Informa Business Media and all itssubsidiaries are not responsible for any of the content contained in this information asset.

Visit link:
Trich confirmed in Utah beef herd - Beef Magazine

By Dr. Amy Tan, M.D.

"Justice demands integrity. It's to have a moral universenot only know what is right or wrong but to put things in perspective, weigh things. Justice is different from violence and retribution; it requires complex accounting."

- bell hooks

Two toxic workplaces, almost a decade apart. Same person affecteda racialized woman physician but at different stages of her career. Two different provinces, two different institutions, two different chains of command, two different policies and procedures to navigate. Two different decisions about whether to submit a formal complaint for gendered racism (and ageism) for harmful behaviourby different white male physicians. Two different decisions and experiences once initial informal complaints made. Same outcome: no justice, no acknowledgement of the harm endured, no accountability. While I may have made the decisions to leave both of these workplaces, they were not actual choices I had due to the great harm that I endured. I still suffer from the trauma, and physical and psychological ramifications of ongoing injustice that I endured in both of these workplaces. My family has also endured the effects alongside me.

The most recent ordeal dragged on over the last 12 months until I excised myself from the horrendously toxic situation. As Im left picking up the pieces again, doing everything I can to bring down my blood pressure and stress hormone levels, and healing from what was a traumatizing formal complaint process, I cant help but ask, if I truly feel that both experiences have left me with the same outcome of feeling unheard, unseen, unacknowledged, and without justice with regards to my harmful experiences in the workplace with other physicians, then what real options do racialized (Black, Indigenous, Asian, and other Persons of Colour) women and nonbinary persons in medicine have when disrespect, gendered racism and other mistreatment occurs in the workplace? My two complaints were specific to certain male physicians and incidences that crossed the line for me. There have beencountlesscovert and overt racist aggressions Ive endured over the 23 years of training and my career in medicine. I could fill pages with stories of unwanted touching, or of being told to my face that I was a diversity hire, that Asians dont experience racism, so be quiet, that my English is so good, and that my people are responsible for the pandemic because of our disgusting eating habits by colleagues and patients. I have been mistaken innumerable times by patients and staff members to be a member of the housekeeping or food services staff in to collect dinner trays over my entire career. I know that Im not alone in suffering persistent racism throughout my years in medicine. A survey of physicians in Alberta (one of the provinces Ive trained and worked in for many years) that was published last month, showed thatover 75% of cisgender BIPOC women physicians surveyedhad experienced harassment and discrimination. 74% of the small number of physicians who reported such workplace harassment and discrimination were unsatisfied with the outcome due to retaliation or lack of satisfactory outcome. While I didnt complete this survey, these statistics completely resonate with my experiences. Theovertly violent and racist commentspublished in the report by white physicians, our colleagues, shows beyond any possible shadow of a doubt, the truly toxic and racist culture that people like me must endure in our careers.

With over50% of Canadian physiciansreporting burnout two years into the pandemic, I am stating clearly that without addressing the rampant racism experienced by Black, Indigenous, and racialized physicians (most especially women and nonbinary), along with all healthcare workers and patients, there will be no improved wellness for us.Wellness is more than the burnoutthat racialized women and nonbinary physicians are at increased risk for; it includesunderstanding and addressingthe fact that there arephysiological impacts on racialized physicians healthfrom being subjected to ongoing racial injustice in the healthcare system.

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The first time I tried to put in a formal complaint for two white male physicians, who I will call Jeff and Bob, I was told by the Department Chair that I should be warned of how hard a formal complaint process would be for me and my young family. Is this really what you want or need right now, Amy? You know it will simply become a he said, she said situation.

When I pushed back that I had a paper trail for Jeffs years-long mistreatment of me, and that the egregious way in which Bob treated me was witnessed by several other department members, the Chair responded, No, thats not how it works. Then he went on to say, Amy, you have to understand that they feel threatened by you. They see you as a young whippersnapper, 20-30 years younger than them and you make them look bad with how productive you are. What was alluded to in that conversation was that as anAsian woman leader, I was just expected to work so hard but not do it in a way that threatened anyone else. I wasnt to make any waves. I was to just do the work demanded of me and be quiet. I was supposed to know there was an unspoken societal agreement in that my age, identity and productivity would be seen by others as tacit justification of their bullying of me. The Chair would not support my request for a formal complaint; he would sit it out if it came to that.

I resigned and left that position six months after that conversation. I gave up my hard-earned tenure achieved at age 35 at that university after years of enduring this toxicity upheld by so many complicit colleagues, and for which there was no end in sight. It took me several years to process, unpack and undo the belief that I was the problem, as they had made me feel. Truthfully, it wasnt until Jeff had a very public run-in with the law that exposed his true lack of a moral compass, could I even start to believe that maybe I wasnt at fault for having to leave that institution.

Fast forward several years and another leadership position in another province within another institution. My past experiences had taught me a tremendous amount, and put me on the alert for any disrespect. In feminist scholarSara Ahmeds book,Complaint!,she writes, You cant go back to the person you were before the complaint, you cant unsee what you come to see through complaintbeing able to see what is going on, to see more, is also to see what you did not see before (Pg 29). In addition to not being able to unsee gendered racism and disrespect, I now had even more years of experience and expertise under my belt. I was not going to tolerate ongoing gendered racist undermining of my work and leadership 17 years into my career. As part of my ongoing anti-racist and anti-oppressive praxis, I actively call out power differentials and the elephants in the room when I perceive conflict and tensions between groups that must work together in an effort to actively address them and find workable solutions. At this new workplace, I was told at first that they appreciated my ability to call out power dynamics that were affecting working relationships and people's work (which was ultimately the care of patients and families). But they became more resistant to address these concerns as I kept bringing it up. It only took six months of subtle othering and subversion as the only racialized physician (and leader) in this group for a more overt gendered racist attack to occur that challenged my leadership in a public manner. Lets call this white male physician, Bill. It was immediately apparent as the only racialized physician in this group, that no one understood the gendered racist impact Bills comments had had on me, or that I was being punished by him for not conforming to the racist stereotypes of the subservient Asian woman who is not to take a stand. The people who could have intervened on my behalf were immobilized by their own white fragility. When I expressed my harm that had been witnessed and unconfronted by the other white physicians, I got the Oh, Im sure he didnt mean that, and No, were not racist, were (colour-blind) nice physicians types of reactions, including from the leaders who would receive the complaint. I had no choice but to proceed with the formal complaint process against Bill to be seen and heard; this process was horrendous and traumatized me even more.

There were so many points in this formal process where I endured even more harm and that exacerbated the threat I felt in my workplace: a) the notion that both the complainant (me) and the respondent were seen as onequalfooting as colleagues, completely disregarding the societal power differential of a white male physician with that of an Asian woman physician, in a virtual face-to-face alternative dispute resolution attempt where he could be allowed to exert his power and privilege over me without any restraint, b) the stance of neutrality by the institution in adjudicating this complaint of gendered racist harm, and c) the eight months of silencing during the investigation that fostered the ostracizing of me in my workplace with the whispers of my being difficult and unwell by my other (white) colleagues, while all the benefit of the doubt was given to Bill. The worst part was that my complaint was only handled by various white people, none of whom had eitheranyunderstanding or lived expertise to understand racism. The institution used a colonial legal framework and lawyers to determine whether I was treated differently than a white man, which is missing the point entirely. In making my complaint, I was not seeking to be treated the same as a white man (equality not yet achieved in society); I was seeking to be heard and seen as an individual with an incredibly different lived experience for which my psychological safety isnever assurednot only in spaces of vast whiteness, but also within the colonial healthcare system and society in Canada. Recognition that I would havedifferentneeds for how to be treated is, in fact, theequityI was seeking as a person who has less societal and systemic power and privilege than my white colleagues. We have not yet achieved equality in society and must stop deluding ourselves that treating everyone the same is appropriate. I was morally injured and mentally exhausted throughout the complaint process. I have come to recognize that the entire complaint process itself, and subsequent ostracization I endured for putting in a complaint were an extension of the harassment for which I complained. This in it of itself is the goal of harassment: to tire out and inflict weariness through the repetition of trying experiences (Ahmed 2021).

So to answer my own question that I had at the outset of this piece, I can honestly saythat neither option was helpful to me as a racialized woman physician leader.Neither option gave me any validation, acknowledgement, or any accountability for bad behaviour. Both options caused further trauma and harm that has affected my well-being and that of my family over the years. My well-being is affected not only by the psychological ramifications and burnout I suffered through this mistreatment, but the physical effects that coping with oppression at work have due toincreased stress and inflammatory responses(Marya and Patel 2021). There has been absolutelynojustice for what I endured.

The sad truth is that there arenogood choices to seek acknowledgement of harm, receive any accountability for harm, or have any systemic changes made that would make institutions less harmful for racialized women and nonbinary persons in healthcare to navigate. This is the despairing reality of the patriarchal, colonial, and racist medical culture in North America, and that of the Western world. I also live and work with disabilities due to ongoing neurological effects from surviving a near-death rollover motor vehicle collision that punctured my lung, broke several ribs, and crushed my backbone (vertebrae) in four places when I was a resident physician. I havent, however, even touched how the unwillingness of call groups to accommodate such disabilities in call schedules has resulted in even more oppression for me.

How is this acceptable?The ongoing pervasive nature of systemic racism means that the medical profession is not adequately supporting racialized women and nonbinary persons within the profession. This also elucidates that if colleagueswithinthe medical profession are subjected to ongoing racism, the racist harm that our profession causes the patients and families we serve to suffer is immense. The racialized physicians who are harmed within the profession are arguably those who would be most acutely aware of the need for cultural safety for patients and families. But, if we are not supported and holistically healthy as professionals, how can we work to ensure safety for our patients in a sustainable manner?

Another quote from the book,Complaint!, resonates with me, What I learned about institutions froma complaint led me to leave; at the time it did not feel like a choice but like what I had to do. If complaints are more likely to be received well when they are made by those with more power (Ahmed 2021 Pg 38), then how do we compel complaint systems (both informal and formal) to rectify this ongoing power imbalance that only serves to further harm racialized women/nonbinary people, and others from intersectional oppressed backgrounds who have the courage to make a complaint?

We must overhaul the colonial complaint system to better support and protect racialized women/nonbinary people in medicine. Physician wellness will be the most critical priority we have going forward as we continue through this pandemic to a post-pandemic recovery of the physician workforce for years to come. For racialized women and nonbinary physicians, addressing gendered racism in medicine will bethewellness issue that must be tackled if theres any hope to curb the burnout amongst us. We must have systems workforthose with less societal and institutional power by virtue of their social location and oppression. The system must workforthose who must fight daily to be seen, heard, and respected. We do not have the privilege of having existed as a white male in society who has always been afforded the benefit of the doubt. We continue in our careers to be denied the same privileges bestowed to white male physicians and to some degree, white women physicians, in our profession. We must acknowledge this hard truth. While white male physicians have been emboldened to take up space by being praised and rewarded for it, racialized women physicians are punished for daring to take up space, even when they have the expertise and job title with responsibilities that requires speaking up and making decisions. We must acknowledge that medicine is not immune to the systemic systems of oppression pervasive in society. To better support racialized women and nonbinary physicians, we must have a safe and effective accountability system to submit complaints that has the principles of equity as its foundation.

The systemmuststart out withbelieving victimsand those with intersectional identities that are oppressed who have the courage to submit a complaint about racism or oppression. The system currently treats the person who has been oppressively harmed and dares to file a complaint (to try to seek help), as the wrongdoer. Any complaint about racism (and/or any other oppressive harm) must be immediately directed to a specific pathway where only racialized people and actual experts in anti-racism and anti-oppression deal with the complaint. The people tasked with managing racism complaintsmust havelived expertise on having to navigate the world with racism on an ongoing basis.

Every complaint must have a power and privilege and power differential analysis at the outset. As Archbishop Desmond Tutu has said, the system cannot be neutral in the face of oppressive harm complaints.There is no neutral.The inordinate amount of effort in protecting the innocence until proven guilty and confidentiality of the (white)respondent of a racism complaint (who already is afforded the benefit of the doubt over the racialized complainant, societally) means continued harm to the complainant through the inequity in the colonial processes and policies. Clear boundaries and safety measures must be immediately put in place for the complainant, and monitored. While I had called the Canadian Medical Protective Association (CMPA) for legal advice on how to navigate this complaint process, I was informed, to my incredulity, that they were not positioned to advise or support me, as the complainant, despite being a physician member who pays my medical-legal protection dues as required to practice. The respondent, however, would have been supported by the CMPA in this complaint. Talk about the system upholding systemic racism, power and privilege within the profession.

Existing in this society with its dehumanizing messages about racialized and Indigenous people creates internalized racism within racialized people that take decades to unpack, understand and actively resist. The fact that a racialized person would have concluded that making a complaint was required would have only resulted after much internal torture, self-gaslighting, and introspection. We would have already tried to obtain informal help because we know that the system is not set up to protect and support us. In my two cases where I needed to proceed with complaints, I had sought help repeatedly from people who had the power and jurisdiction within the institution to help me. I had had several informal complaint meetings with my Chair, and his predecessor, regarding Jeff over six years to no avail. This was despite having a thick file full of documentation of the various incidents over the years and many belligerent emails from him. One very high level white male superior advised me that I just had to put more effort into making nice with them (in a patriarchal, condescending tone akin to being patted on the head), but that I was just to carry on as I was supported by leadership in my work. Another white male superior said that I just had to get some white hair, some wrinkles, and not look like I was twelve to command respect. No one in a position of power to help me deal with these bullies was willing to step in because they didnt want to upset the faculty members who had been at the institution for such a long time. In the situation regarding Bill, as detailed earlier, I was met with white fragility byeveryonedirectly involved who could have used their white privilege to help me. Be it the silence, staying out of it, remaining neutral, protecting oneself, outright dismissal of the impact on me, not seeing the racism, or defending Bill, these were all forms of furthercovert racisminflicted on me by these colleagues. While two people within the physician group acknowledged in private that they could see that I had been attacked by Bill, when it came to actually putting their privilege on the line to speak up for me, they choose not to. They actively chose, instead, to harm me further by upholding the status quo at a critical time. It is near impossible to recover from such disappointment and betrayal from your colleagues.

Oppressive harm requiresrestorative justiceto occur so that there is acknowledgement that violation of a person (and relationship) has occurred, not a violation of a law. Restorative justice focuses on healing of the individual harmed while requiring accountability from the respondent that also includes their own personal learning and growth. This process involves receiving an acknowledgement of harmful impact (regardless of intention), accountability for future incidents, and sending a clear message that lashing out at people in a gendered racist way is never acceptable, but especially in a workplace. The complaint process for racist and/or oppressive harm should be focused on the institution recognizing the complainants pain as ahuman being,not shielding those who cause harm and are already protected by the status quo of society and the institution. The person harmed should not be the person tasked with teaching everyone in the complaint process about racism and oppression, including racist gendered stereotypes, as I had to do ongoing over months to the several people who (mis)handled my complaint. This included, ironically, having to explain how covert racism exists to the third party white lawyers hired to investigate whether gendered racism had occurred. Leaders ateverylevel in medicine must be competent to not only support those on their teams who have been harmed, but more importantly, to not further perpetuate harm through their defensive responses.

Complaints about racism and other intersectional oppressive harm must be acted upon as urgent, and concluded quicklywithin 8 to 12 weeks. At the conclusion of the complaint process, there must be a wrap-up meeting that not only discusses actions or outcomes, but determines what ongoing needs, changes and system feedback is required to help complainants who have experienced oppressive harm going forward. Institutions must understand that regardless of a complaint investigation being concluded, the complainant will be forever changed for having gone through the original harmful event, and the complaint process that dehumanizes them.

I resigned from my position last fall before the conclusion of the investigation for my complaint. That was how untenable my situation became over the eight months of the complaint process. The last straw was receiving yet another harmful email. After several requests that I not be present in regular administrative meetings with the respondent of my complaint, I was told that it had been decided that I was to meet with the whole physician group, or none of the group. This email was from a white woman physician colleague who had heard through my tears and anguish in the preceding months, the immense toll and impact that this whole ordeal was having on me and my family. If I had broken my leg and the elevator to an upper floor was out of service, would they have denied my reasonable accomodation if I had requested a meeting in the lobby so that I wouldnt have to crawl up the stairs? If they did, this would be so disgustingly and overtly dehumanizing to make someone crawl up the stairs. My insistence that I not be in the presence of the person who was causing meongoingharm, and the respondent of an ongoing complaint (itself a harmful process) was treated as unreasonable. I was essentially barred from being able to do my job while trying to advocate for my own safety. As Sara Ahmed writes, You can be exhausted by not being accommodated; you can be exhausted by the work you have to do in order to [try to be] accomodated (Ahmed 2021).

I was demoralized, exhausted and dehumanized. I had to end that pain for myself, and my family by resigning.

As youre reading this, you might be thinking, what expertise do I have to demand such system changes? I have lived expertise as a racialized woman physician with disabilities working in Canadian healthcare institutions for 18 years, a medical educator who has supportedcountlessracialized and otherwise oppressed learners who have experienced hardship due to oppression in their training, and a physician who has gone through and been failed by both the informal and formal complaint process at different stages of my medical career. Do not perpetuateepistemic injusticeby thinking that my testimony, and my blood, sweat and tears in 18 years of experiences (23 years if you count my training years) do not carry any weight or expertise.

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In attempting to make sense of the injustices I have faced, I have read and researched this topic in the social psychology, sociology, psychology, medicine, social justice and anti-racism literature for years. As a qualitative medical researcher, I have attempted to make meaning from these injustices to enact institutional change to improve things for the next generation in medicine.

Epistemic injusticeprops up systemic racism within the policies and procedures in Canadian healthcare institutions. Epistemic racism plays out every day in Canadian society, in the silencing, exclusionary, and disbelieving responses to discussions of racism, be it in the national news, or within organizations and workplaces. The dominant narrative has been formed by white people in society over time and continues to this day. This means that the lived experiences of racialized people are not only undisclosed or unheard, they arenotbelieved and/or dismissed if heard because they dont fit the dominant narrative (ie: the dominant group doesnt suffer racism so does not see or understand racial harm). These exemplify the two ways in which epistemic racism exists:testimonial injustice(the person not being believed due to racism, subconscious or not) andhermeneutical injustice(not understanding or believing the interpretations of lived experiences by racialized persons because it doesnt fit the dominant narrative). Harm is perpetuated through the stories of only the dominant group who then make the rules and direct the narratives upon which racist and oppressive harm is adjudicated. This is why all the white physicians with whom I worked in the second complaint were so quick to confidently dismiss and punish me for daring to utter the word racism in relation to a colleague and their group, when they have zero understanding of racism. It is also why I was overtly denied any accommodation when asking for protection from the respondent in not being in his virtual or physical presence, despite my clear articulation of the threat he posed to me. As a result, I was forced to give up clinical shifts (and income) because I was so fearful that being in his (to me, threatening) presence on the wards would adversely distract me in caring for patients safely. It is also why when asking for help, that other leaders could dare to say, Well, none of the other physicians (all of whom are white) have stood up and supported you, so who are we to believe that racism occurred. I did not need an investigation to confirm what I knew to be gendered racism.

This is why white men (and women) are defended so quickly in media stories about oppressive harm. This is why many racialized people who aspire to the seductive power and privilege in society that centres whiteness will give white people the benefit of the doubt over racialized people, especially women and nonbinary people, even when they themselves are racialized. This occurred in my first complaint experience. Lateral violence from racialized colleagues in many ways, is more violent than racism from white people or institutions. How do we move past asking the question of does systemic and other forms of racism exist within our healthcare organization or institution to what can we do to minimize the harm to racialized people within our organization and the healthcare system? How can we support them better within the organization to strive towards achieving equity?

Ultimately, the question I have for all healthcare leaders across Canada is do our voices, perspectives, and our lived expertise in having a lifetime of navigating colonial society as racialized individuals not matter within healthcare? Why must we endure racist harm in the workplace in silence and isolation?

Every workplace policy must consider restorative justice principles to achieve what is earnestly being sought by complainants of oppressive harm; help to be seen and heard as a person with different needs, that impact matters more than intent, and that it is not punishment but accountability being sought. The complainant is simply trying to lessen their chances of such a harmful incident occurring again. We know it will occur again, especially if unchecked. This is our reality. We must not continue to exacerbate the harm of inequities in the workplace through complaint policies that only aggravate oppression by virtue of how they are written. More importantly, the process harms by being disconnected from the problem the policy is intended to address (Ahmed 2021). These policies themselves serve to only avoid the person harmed and the oppressive problems within the institution.

Since my most recent ordeal, some of my healing has been fostered through my work with the newly formedAnti-Racism Support Groupin UBCs Family Practice Residency Program. The decolonized approach to achieving restorative justice that our group strives for, led by an inspiring Indigenous Elder, gives me hope that colonial institutions can change and actively work towards safety and authentic support of racialized physicians in medicine. It is past due thatallinstitutions concretely address the problems that complaints bring forth to those who have less institutional and societal power within medicine. It is past time thatallinstitutions create explicit safety for racialized women and others who experience intersectional oppression, rather than continuing to burden those with less power and privilege, as the most affected, to fight to be seen and heard in these institutions. Only then, can physicians who are racialized women and other intersectional identities, and those who are coming after us, haveanyhope of surviving our careers in medicine.

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Why must Black, Indigenous, or otherwise racialized women and nonbinary physicians endure racist harm in the workplace in silence and isolation? - The...

The first thing to know is that not all sleep medications are the same. The myth is, It doesnt matter which one you choose, they all work the same way, they all do the same thing. They dont, said Dr. Andrew D. Krystal, a psychiatrist at the University of California, San Francisco, who specializes in sleep disorders. Some drugs, like zaleplon (Sonata), decrease the amount of time it takes to fall asleep, he said; while others, such as suvorexant (Belsomra), block signals in the brain that cause you to wake up. The hormone melatonin, as well as prescription drugs like ramelteon (Rozerem) that act on melatonin receptors, help regulate the bodys internal clock but dont necessarily help you stay asleep.

The best drug for you will largely depend on what causes your insomnia. It really is about choosing the right medication for the patient, said Dr. Aruna S. Rao, a neurologist at Johns Hopkins Medicine. If your problem is that you cant fall asleep at bedtime, then a drug that prevents you from waking in the middle of the night may not help. If you fall asleep easily but cant sleep toward the end of the night, then drugs that wear off within a few hours, like zaleplon (Sonata), arent going to do you much good, either.

Many people, too, have sleeping problems that wont be resolved with any sleeping pill. One such condition is sleep apnea, which afflicts 22 million people in the United States and causes frequent wake-ups, said Dr. Grace Pien, a pulmonary, critical care and sleep medicine physician at Johns Hopkins Medicine. Sleep apnea is best managed with a machine that provides continuous positive airway pressure (CPAP), not with medication.

Another issue is that many sleep aids dont have convincing data behind them. The over-the-counter antihistamines I used to take, which contain diphenhydramine, were never really systematically studied for their effects on sleep, Dr. Krystal said. Theyre recognized for their allergy benefits but are often used as a sleep aid because they cause drowsiness, he added. The few studies that have been done on diphenhydramine suggest that it doesnt help much at all: Clinical practice guidelines from the American Academy of Sleep Medicine say the antihistimines benefits, in terms of extra sleep, are below the level of clinically significant improvement.

Sleep aids can also have side effects, some of them serious. A 2017 study found that, when compared with older adults who did not take sleeping medications, those who took sleep aids of any kind recommended by their doctor were 34 percent more likely to suffer a fall, perhaps because the drugs affected their balance or incited clumsiness. Another study found that people who had recently, for the first time, been prescribed sleep medications such as temazepam, trazodone or zolpidem (Ambien) were 90 percent more likely to be involved in car crashes, and that their increased risk was on par with that of driving drunk. Some research even suggests that the long-term use of hypnotic drugs such as nordazepam, clonazepam (Klonopin), flurazepam (Dalmane) and zolpidem (Ambien) can more than double the risk of dementia.

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Using Melatonin or Benadryl to Sleep? Read this. - The New York Times

AstraZeneca SVP of Early Oncology Matthew Ellis/Courtesy AstraZeneca

With an eye on becoming a leading oncology company, AstraZeneca made a splash at the American Association for Cancer Research meeting in New Orleans with 60 different presentations highlighting the cancer programs that will bolster its three biggest assets: Enhertu, Lynparza and Tagrisso.

At the annual oncology conference, AstraZenecas team, led by Susan Galbraith, executive vice president of oncology research and development, highlighted several of its developmental programs. Prior to the start of AACR, Galbraith said the company is serious about pioneering new approaches to cancer treatment through the development of therapies that can target cancer at earlier stages and with greater precision. The first efforts of that goal were on display at the oncology conference where the company focused on MEDI5752, a novel bispecific antibody, and AZD5305, a next-generation PARP1-selective inhibitor.

AstraZeneca highlighted those two assets as well as AZD8205, a novel ADC that targets B7-H4, a protein that is overexpressed in multiple solid tumors. AZD8205 is the first ADC that uses the companys proprietary linker technology.

The U.K.-based pharma company has high hopes for these three assets. MEDI5752 is designed to simultaneously target the immune checkpoint proteins PD-1 and CTLA-4. AstraZeneca believes that the use of a bispecific antibody-like MEDI5752 is a promising immuno-oncology approach precisely because of the way it was engineered to block both proteins. MEDI5752 is designed to bind to CTLA-4 only in the presence of PD-1.

With that specific bit of engineering, it reduces the chances of off-target toxicities. The drug will bind only to those activated T-cells and broaden the therapeutic window for the medication. MEDI5752 is currently being assessed in a Phase I study, and the company presented data from the first 86 patients who were dosed with different levels in order to find the right level of efficacy and durability.

With its next-generation PARP1 inhibitor, AstraZeneca believes it has a new approach to killing cancer cells by targeting their DNA repair mechanisms. Not only that, but AstraZeneca also has early evidence that one of its experimental PARP1 inhibitors is capable of crossing the blood-brain barrier, which will potentially allow for new approaches to treating malignancies of the brain.

Galbraith is now supported by Matthew Ellis, senior vice president of early oncology. Ellis joined the big pharma in March after spending a year in academic research. He told BioSpace from AACR that after years of academic research focused on the tumor profiles of patients, he wants to close out his career by helping AstraZeneca develop new therapies for multiple cancer types.

I want to put together cures for AstraZeneca and patients, he said in an interview.

Ellis joined AstraZeneca from the Lester and Sue Smith Breast Center at Baylor College of Medicine, where he was the director who oversaw efforts to better understand the molecular profile of breast cancer in order to improve treatment. He was also the co-lead ofThe Cancer Genome Atlas Breast Cancer project, which revealed that the loss of the NF1 gene is an important driver of breast cancer resistance to hormone therapy.

As AstraZenecas assets were on display at AACR, he said he was excited about the potential of these therapies and how they can potentially improve patient care and, one day, help lead to an eradication of cancer. As a cancer survivor himself, Ellis said hes well aware of the needs of patients and keeps them at the forefront of what he intends to do at the pharma giant.

As a breast cancer physician, Ellis said hes prescribed PARP inhibitors on multiple occasions and expressed particular excitement about AZD5305, the next-generation PARP1 inhibitor. He noted that this particular asset has been designed to target PARP1, while engineering out PARP2. Current PARP inhibitors that include PARP2 have some off-target issues, he said.

This has improved the off-target profile, Ellis said, referring to AZD5305. The preclinical profile of it is remarkable the hematological toxicity is gone.

Ellis added that without the toxicity concerns from PARP2, there is a potential for using higher doses in patients. That could ultimately lead to its use as a medication that could prevent breast cancer patients from having to have a mastectomy and prevent prostate cancer patients from having invasive procedures.

Were still in early days with this molecule with early data, but its captured everyones imagination. This is something we intend to take advantage of, Ellis said.

He also expressed excitement about the ADC AZD8205, saying that early data suggests the therapy is a remarkable opportunity to replace chemotherapy. As an oncologist, Ellis said chemotherapy is a double-edged sword of treatment.

Replacing that with an ADC approach could be transformative. AZD8205 targets B7-H4, a protein overexpressed in a range of solid tumors. He said B7-H4 was carefully selected because of its overexpression and the current understanding of its role in the tumor. AstraZeneca plans to drive this into human testing next year, coming to a patient near you, soon, Ellis quipped.

As Ellis looked ahead at his future with AstraZeneca, he said he is excited about exploring new hypotheses in oncology drug research, and will also conduct a top-to-bottom review of the companys compounds in order to prioritize and accelerate development.

Ellis also said he intends to promote equity in clinical trials. He said ethnic minorities have been overlooked as participants in trials, and that is something that has to change. He expressed hope that some barriers to trials will be addressed in order to open them up to more people from all races.

The one thing Ive learned is the value of diversity. It creates an amazing environment, but we have to honor that diversity to make sure that everyone can get a drug and they wont be overlooked, Ellis said.

He added that he also hopes to become a champion for trial participation, pointing out that participation levels in the United States are at about 5% of patients. He would like to see that increase to 25%, which would help achieve those higher levels of minority participation.

Theres a societal responsibility to mitigate cancer in our different populations, he said.

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AstraZeneca Rolls into AACR with 60 Presentations, New SVP of Early Oncology - BioSpace

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Data Highlights In Vivo Research and the Potential Mechanism of Action in Pancreatic and Prostate Cancers

CARLSBAD, Calif., April 12, 2022 (GLOBE NEWSWIRE) -- Qualigen Therapeutics, Inc. (Nasdaq: QLGN), a diversified life sciences company focused on developing treatments for adult and pediatric cancers with potential for Orphan Drug Designation, while also commercializing diagnostics, today highlights three posters presented during the American Association of Cancer Research (AACR) held in New Orleans from April 8-13, 2022.

Qualigen Chairman and CEO Michael Poirier commented, Our lead therapeutic program QN-302 may have the potential to ultimately treat multiple tumor types that are characterized by genomic quadruplexes (G4) which are overrepresented in numerous cancer-related genes. The findings reported in these posters illustrate promising in vivo anti-proliferative activity against pancreatic cancer and metastatic prostate cancer. We are encouraged by the results of these studies as we progress toward our goal to benefit the lives of cancer patients, and are on-track to initiate IND-enabling studies.

Pancreatic cancer remains a high unmet medical need with limited treatment options. According to the American Cancer Society, about 62,210 will be diagnosed with pancreatic cancer in the United States. in 2022, and more than 49,830 patients will die from the disease -- the highest mortality rate of all major cancers. For advanced disease, chemotherapy (sometimes along with a targeted drug therapy) may lengthen survival.1

Poster 2926, Structure-based design of quadruplex-binding small molecule compounds: The essential role of water molecules (Dr. Stephen Neidle) Crystal structures and computer modelling were utilized to characterize the details of the interactions of substituted naphthalene diimides targeted against human DNA quadruplexes, and in particular the role of water molecules in the binding site. It is concluded that information on conserved water molecules is important for drug design and has been used in the design of a current lead compound QN-302.

1 https://pancreatic.org/pancreatic-cancer/pancreatic-cancer-facts/

VIEW AACR POSTER

Session Category: ChemistrySession Title: Structural and Chemical BiologySession Date and Time: Tuesday Apr 12, 2022 9:00 AM - 12:30 PMLocation: New Orleans Convention Center, Exhibit Halls D-H, Poster Section 40

Poster 4068, The potent quadruplex-binding compound QN-302 shows potent anti-proliferative activity in a prostate cancer cell panel and anti-tumor activity in anin vivomodel of metastatic prostate cancer (Dr. Stephen Neidle) demonstrated bioavailability and toleration at therapeutic doses in a prostate cancer cell line, PC3, which is derived from castration-resistant prostate cancer and is therefore relevant to the situation when hormone therapies are no longer effective. The in vivo study, which included the commonly used drug abiraterone, showed that QN-302 had statistically significant anti-tumor activity in this model (p=0.0008) relative to the controls, and was superior to abiraterone.VIEW AACR POSTER

Session Category: Experimental and Molecular TherapeuticsSession Title: New Chemotherapy AgentsSession Date and Time: Wednesday Apr 13, 2022 9:00 AM - 12:30 PMLocation: New Orleans Convention Center, Exhibit Halls D-H, Poster Section 27

Poster 4069, The potent quadruplex-binding compound QN-302 shows anti-tumor activity in patient-derived in vivo models of pancreatic cancer (Dr. Stephen Neidle) outlined a study in which QN-302 displayed substantial anti-tumor activity in three patient-derived xenograft (PDX) models for pancreatic ductal adenocarcinoma (PDAC). Immunocompromised mice were subcutaneously implanted with PDX tumor fragments. Mice intravenously received either QN-302, a vehicle, or in some models, gemcitabine. In three of these models, significant changes in tumor growth were observed in those that received QN-302, together with good tolerance and bioavailability at therapeutic doses.

VIEW AACR POSTER

Session Category: Experimental and Molecular TherapeuticsSession Title: New Chemotherapy AgentsSession Date and Time: Wednesday Apr 13, 2022 9:00 AM - 12:30 PMLocation: New Orleans Convention Center, Exhibit Halls D-H, Poster Section 27

QN-302 is the Companys genomic quadruplex (G4)-selective transcription inhibitor being developed as a potential treatment for PDAC, in addition to other tumors of high unmet clinical need. The abstracts accepted by AACR outline the potential binding to a quadruplex target for the compound, as well as significant anti-tumor activity in relevant animal models.

The AACR Conference, being held in New Orleans from April 8-13, 2022, is a focal point of the scientific cancer community where scientists, clinicians, other health care professionals, survivors, and patients review the latest advances in cancer science and medicine.

About Qualigen Therapeutics, Inc.

Qualigen Therapeutics, Inc. is a diversified life sciences company focused on developing treatments for adult and pediatric cancer, as well as maintaining and expanding its core FDA-cleared FastPack System, which has been used successfully in diagnostics for over 20 years. Our investigational QN-302 compound is a small molecule selective transcription inhibitor with strong binding affinity to G4s prevalent in cancer cells; such binding could, by stabilizing the G4s against unwinding, help inhibit cancer cell proliferation. Our investigational QN-247 compound inhibits nucleolin, a key multi-functional regulatory protein that is overexpressed in cancer cells; QN-247 may thereby be able to inhibit the cells proliferation. QN-247 has shown promise in preclinical studies for the treatment of acute myeloid leukemia (AML). The investigational compounds within Qualigens RAS-F family of RAS oncogene protein-protein interaction inhibitor small molecules are believed to inhibit or block the binding of mutated RAS genes proteins to their effector proteins, thereby leaving the proteins from the mutated RAS unable to cause further harm. In theory, such mechanism of action may be effective in the treatment of about one quarter of all cancers, including certain forms of pancreatic, colorectal, and lung cancers. In addition to its oncology drug pipeline, Qualigen has an established diagnostics business which manufactures and distributes proprietary and highly accurate rapid blood testing systems to physician offices and small hospitals for the management of prostate cancer and other diseases and health conditions.

For more information about Qualigen Therapeutics, Inc., please visit http://www.qualigeninc.com.

Forward-Looking Statements

This news release contains forward-looking statements by Qualigen that involve risks and uncertainties and reflect the Company's judgment as of the date of this release. These statements include those related to the Company's prospects and strategy for the development of therapeutic drug candidates. Actual events or results may differ from the Company's expectations. For example, there can be no assurance that the Company will successfully develop any drugs (including QN-302, QN-247 and RAS-F); that preclinical development of the Company's drugs (including QN-302, QN-247 and RAS-F, and the deprioritized infectious-disease drug candidate QN-165) will be completed on any projected timeline or will be successful; that any clinical trials will be approved to begin by or will proceed as contemplated by any projected timeline, or at all; that any future clinical trial data will be favorable or that such trials will confirm any improvements over other products or lack negative impacts; that any drugs will receive required regulatory approvals (or Fast Track designation or Orphan Drug status) or that they will be commercially successful; that patents will issue on the Company's owned and in-licensed patent applications; that such patents, if any, and the Company's currently owned and in-licensed patents would prevent competition; that the Company will be able to procure or earn sufficient working capital to complete the development, testing and launch of the Company's prospective therapeutic products (including QN-302, QN-247 and RAS-F, and QN-165); or that the Company will be able to maintain or expand market demand and/or market share for the Company's diagnostic products. The Company's stock price could be harmed if any of the events or trends contemplated by the forward-looking statements fails to occur or is delayed or if any actual future event otherwise differs from expectations. Additional information concerning these and other risk factors affecting the Company's business can be found in the Company's prior filings with the Securities and Exchange Commission, including its most recent Form 10-K, all of which are available at http://www.sec.gov.

The Company disclaims any intent or obligation to update these forward-looking statements beyond the date of this news release, except as required by law. This caution is made under the safe harbor provisions of the Private Securities Litigation Reform Act of 1995.

Contact:

Jules AbrahamJQA Partners, Inc.917-885-7378jabraham@jqapartners.com

Source: Qualigen Therapeutics, Inc.

AACR POSTER

Structural and Chemical Biology

AACR POSTER - CHART 1

New Chemotherapy Agents

AACR POSTER - CHART 2

Tumor Volumes for CTG-1128

AACR POSTER - CHART 3

Tumor Volumes for CTG-0952

AACR POSTER - CHART 4

Tumor Volumes for CTG-2184

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Qualigen Therapeutics Presents Three Posters of QN-302 at American Association of Cancer Research Conference - StreetInsider.com

On March 28, Gov. Ron DeSantis signed into law FloridasHouse Bill (HB) 1557, which disallows or limits schools from instructing children in certain sexual matters. The heart of the new law states, Classroom instruction by school personnel or third parties on sexual orientation or gender identity may not occur in kindergarten through grade 3 or in a manner that is not age-appropriate or developmentally appropriate for students in accordance with state standards.

The news was met in many quarters with histrionic outrage. The American Federation of Teachers presidentRandi Weingartengroused that the law will single out certain kids and families for derision and denigration. It is just wrong. Its intent is to divide our communities and make political hay, but it hurts children, hurts families and makes it hard for teachers to do their jobs.

Hardly. It simply doesnt allow teachers to discuss certain sexual identity issues with young children. Weingarten also inanely insisted that the law would shame LGBTQIA+people back into the closet by policing their identity.

Following the signing of the bill, a gay teacher in Parish, Florida, creepily bemoaned the fact that he canttalk about his love lifewith his kindergarteners anymore.

No one was more outraged than Joe Biden, however. On March 31 the day that some celebrate as the International Transgender Day of Visibility the president insisted that his administration is standing up for transgender Americansagainst hateful bills being passed at the state level and assured them, Youre so brave. You belong. And we have your back.

To show that Biden is really, really serious about his stance, his administrations Department of Health and Human Services raised the pink, white and blue striped Transgender flag at its D.C. headquarters.

Frighteningly, theDepartment of Justicegot into the act, issuing a press release on the Transgender Day of Visibility in which it proclaims that it sent a letter to all state attorneys general reminding them of federal constitutional and statutory provisions that protect transgender youth against discrimination, including when those youth seek gender-affirming care. The missive advises states that laws and policies that prevent individuals from receiving gender-affirming medical care may infringe on federal constitutional protections under the Equal Protection Clause and Due Process Clause of the Fourteenth Amendment. Not surprisingly, the word parent never once appeared in the document.

And California of course is doing what it can to maintain its reputation as the nations wackiest state. Democratic lawmakers areproposing to make California a havenfor transgender youth and their parents who are fleeing other states. State Senator Scott Wiener said apparently with a straight face They have a safe place to go if theyre threatened with prosecution. California will not be a party to this new wave ofdeadly L.G.B.T.Q. criminalization.

Its fascinating how a bill which doesnt allow for sexual identity issues to be discussed in grades k-3 can morph into deadly L.G.B.T.Q. criminalization. How could theBabylon Beepossibly satirize this?

In fact, California is actually the anti-Florida, and has done much do disempower parents. To wit:

AB 2119, which passed in September 2018, provides that the rights of minors and nonminors in foster careinclude the right to be involved in the development of case plan elements related to placement and gender affirming health care, with consideration of their gender identity. At the time, the American College of Pediatricians (ACPeds) filedtestimonyagainst the bill, urging legislators to reject it. Children with gender dysphoria believe they are not their biological sex, the groups March 2018 testimony read. A delusion is a fixed false belief. This bill proposes that foster children with gender dysphoria be socially affirmed into their delusion, and allowed to obtain experimental puberty blockers, and dangerous cross-sex hormones and surgery without parental consent.

In September 2021,AB 1184, a bill cosponsored by Planned Parenthood, became law. As the California Family Council explains, this diktat prohibits insurance companies from revealing to the policyholderthe sensitive services of anyone on their policy, including minor children (starting at age 12), even though the policy owner is financially responsible for the services. The term sensitive services refers to all health care services related to mental or behavioral health, sexual and reproductive health, sexually transmitted infections, substance use disorder, gender affirming care, etc. The bill doesnt detail the kindly sounding gender affirming care, but as defined by the University of California, San Francisco, itshormone therapy and a laundry list of surgeriesincluding vaginectomy, scrotoplasty, voice modification, etc., ad nauseam.

At a California Teachers Association conference in October 2021, teachers were advised on best practices for subverting parents, conservative communities and school principals on issues of gender identity and sexual orientation.

The Los Angeles Unified School Districts Office of Human Relations, Equity and Diversity hosted a 10-weekonline club for LGBT elementary schoolers, including children as young as four years oldin the fall of 2021.

And then theres Disney, which is in a state of rage over the passage of Floridas parental rights bill. As Christopher Rufo explains, Disney executives immediately organized a Reimagine Tomorrow Conversation Series meeting for its leaders and pledgedto mobilize the entire corporation in service of the LGBTQIA+ community. Those recruited included a black, queer, and trans person, a bi-romantic asexual, and the mother [of] one transgender child and one pansexual child, and announced ambitious new initiativesseeking to change everything from gender pronouns at the companys theme parks to the sexual orientation of background characters in the companys films.

Also, speaking in blunt terms, Disney executive producer Latoya Raveneau laid out the companys game plan. She said her team was implementing a not-at-all-secret gay agenda and regularly adding queerness to childrens programming. Production coordinator Allen Martsch, said his team has created a tracker to ensure that they are creating enough canonical trans characters, canonical asexual characters, [and] canonical bisexual characters. Corporate president Karey Burke said she supported having many, many, many LGBTQIA characters in our stories and reaffirmed the companys pledge to make at least 50 percent of its on-screen characters sexual and racial minorities.

The gender obsession has also extended to Disneys theme parks in Anaheim and Orlando. Diversity and inclusion manager Vivian Ware explains that Disney made the decision last year toeliminate all mentions of ladies, gentlemen, boys, and girlsin order to create that magical moment for children who do not identify with traditional gender roles.

It must be noted that Disney, whose name evokes warm and fuzzy images of Mickey, Donald, Goofy and Tinkerbell has been over the years the corporate equivalent of a heavy-breathing, sweaty guy in a trench coat lurking in a park. For example, a six-month investigation in 2014 revealed that at least35 Disney employees had been arrested for sex crimesagainst children, attempting to meet minors for sex, and possession of child pornography over the previous eight years. Additionally, other Disney employees were found to have exhibited an abiding interest in kiddie porn on the internet.

The transgender movement is cultish, and can have dire consequences. Brown University physician and researcher Lisa Littman released a study in 2018, which showed that rapid-onset gender dysphoria in young people may be driven in part by social and peer contagion. She stresses that nearly 70 percent of the teenagers were involved with a peer group in which at least one friend had identified as transgender. In some groups, the majority had done so. Nearly 65 percent of teens had spent an increased amount of time online and on social media, and parents reported that pro-transgender YouTube videos and blogs might have been influential. It is unclear how many of the kids who have joined the cult took it to the next level and actually engaged in hormone blockers and self-mutilation.

In reality, Sex is determined at conceptionby our DNA and is stamped into every cell of our bodies, asserts Dr. Michelle Cretella, President of the American College of Pediatricians. Human sexuality is binary. You either have a normal Y chromosome and develop into a male, or you dont, and you will develop into a female. There are at least6,500 genetic differences between men and women.Hormones and surgery cannot change this. Nor can Disney, Joe Biden, Randi Weingarten or any other gender zealot.

The good news is that a poll taken in late March reveals that when Americans are presented with the actual language of the new Florida law,61% are in favor, while just 26% oppose. Importantly, there is bipartisan support. Republicans are in favor by a 70%-23% margin, while Democrats support it by 55%-29%. And, indeed states are acting.Georgia lawmakers have alreadyintroduceda bill that would similarly restrict classroom discussion of sexual orientation or gender identity, and other bills targeting related content in schools arependingin Indiana, Tennessee, Oklahoma and Kansas. Hopefully, the other 44 states will get aboard soon.

First published at: For Kids and Country.

Photo by skyseeker, Attribution 2.0 Generic (CC BY 2.0).

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Global Genetic Testing Markets Forecasts, Applications and Technologies Research Report 2022 - ResearchAndMarkets.com - Galveston County Daily News

The UAB Cardiogenomics Clinic provides genetic testing and counseling for a gene variant associated with a risk of heart failure and death.

Researchers believe that the presence of the Val122Ile genetic variant in African Americans is believed to predispose them to the development of transthyretin amyloidosis, which can lead to higher risk of heart failure.A new study published in the Journal of the American Medical Association led by researchers from the University of Alabama at Birmingham Marnix E. Heersink School of Medicine found that being a carrier of a genetic variation known as Val122Ile in the transthyretin, or TTR gene, was significantly associated with an increased risk of heart failure and death. Research shows that this Val122Ile variation is more commonly seen among individuals of African ancestry.

Transthyretin protein is produced by the liver and helps circulate vitamin A and thyroxine through the body. This genetic variation causes misfolding of the transthyretin protein leading to hereditary transthyretin amyloidosis, a condition characterized by the buildup of abnormal deposits of a protein in the bodys organs and tissues. As buildup increases over time, the heart may become stiff, leading to cardiomyopathy, a disease of the heart muscle that makes it difficult to pump blood through the heart.

For this study, UAB researchers Vibhu Parcha, M.D., and Pankaj Arora, M.D., looked at this genetic variation in a cohort of 7,500 Black individuals living in the United States.

The TTR Val122Ile genetic variant is unfortunately more common among those of African ancestry with nearly three out of 100 individuals carrying the genetic variation, said Parcha, a clinical research fellow in the UAB Cardiogenomics Clinic and the UAB Division of Cardiovascular Disease.

Parcha says the presence of the Val122Ile genetic variant in African Americans is believed to predispose them to the development of transthyretin amyloidosis.

We wanted to examine whether carrying this genetic variant will lead to a higher risk of new-onset heart failure, death due to heart failure, cardiovascular causes or any other causes, Parcha said.

(Left) Vibhu Parcha, M.D., clinical research fellow in the UAB Cardiogenomics Clinic and the UAB Division of Cardiovascular Disease. (Right) Pankaj Arora, M.D., an associate professor in the Division of Cardiovascular Disease and director of the UAB Cardiogenomics Clinic.In this study, researchers analyzed participants from the REasons for Geographic and Racial Differences in Stroke study living in the United States without baseline heart failure. Among 7,514 Black participants, the population frequency of the TTR Val122Ile variant was 3.1 percent. Over a median follow-up of 10.9 years, Val122Ile variant carriers had a higher risk of incident heart failure compared with non-carriers. Over a median follow-up of 11.6 years, Val122Ile variant carriers had a higher risk of mortality compared with non-carriers. Overall researchers found that those with the TTR Val122Ile variant had a 2.5-fold higher risk of heart failure and a 40 percent higher risk of death from any reason.

Among those with the pathogenic TTR Val122Ile genetic variation, the heart may gradually become unable to function correctly, which will lead to heart failure and ultimately death, said Arora, an associate professor in the Division of Cardiovascular Disease and director of the UAB Cardiogenomics Clinic. However, the true probability of genetic variation being expressed in all those with the variant is not known, and further work is needed to understand this. The good news is that there are several new treatments approved or awaiting approval for this hereditary heart disease.

Medical facilities like the UAB Cardiogenomics Clinic provide genetic testing for this variant. At the clinic, those who carry this variant will have access to comprehensive genetic counseling and assessment of their heart structure and function.

Those with the variant may be eligible for getting access to evidence-based therapies that improve their heart health and improve their long-term outcomes, Arora said. It is also important to identify any family members who may have the genetic variation as they will benefit from early diagnosis and access to medical therapies that improve their health.

Learn more about the UAB Cardiogenomics Clinic here.

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Genetic variation common among Black individuals is associated with higher risk of heart failure and death - University of Alabama at Birmingham

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The major players covered in the direct-to-consumer (DTC) genetic testing market report are EasyDNA, Ancestry, 23andMe, Inc., Colour Genomics, Inc., Genesis HealthCare, Full Genomes Corporation, Inc., Helix OpCo LLC, IDENTIGENE, LLC, Living DNA Ltd, Mapmygenome, Pathway Genomics, Gene by Gene, Ltd., MyHeritage Ltd., 10X Genomics, Dante Labs, Inc., 24Genetics, LabCorp, Myriad Genetics, Inc., Quest Diagnostics Incorporated and Abacus Diagnostica Oy among other domestic and global players. Market share data is available for global, North America, Europe, Asia-Pacific (APAC), Middle East and Africa (MEA) and South America separately. DBMR analysts understand competitive strengths and provide competitive analysis for each competitor separately.

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Geographic Segment Covered in the Report:

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Direct-to-Consumer (DTC) Genetic Testing Market Trends Analysis, Top Manufacturers, Shares, Growth Opportunities, Statistics and Forecast by 2028 ...

11 April 2022

The world's first bedside genetic test that could prevent babies from losing their hearing has proven successful according to the NHS.

The 26 minutes genetic test, called the Genedrive MT-RNR1 test, can identify babies who carry a particular genetic variant that could make them permanently deaf when treated with a common emergency antibiotic. Babies admitted to intensive care with a suspected infection are routinely given an antibiotic called gentamicin within 60 minutes, which is used to safely treat approximately 100,000 babies a year. However, one in 500 babies carry the genetic variant that can make it cause permanent hearing loss. Researchers expect that the new genetic test could prevent permanent hearing loss in 180 babies in England every year.

'I am absolutely thrilled with the success of the study, and that this testing is now going to be used in three of our Trust's Neonatal Intensive Care Units it's actually going to make a real difference so babies are not going to lose their hearing for a preventable reason,' said one of the study's co-authors Professor William Newman, from the University of Manchester, and who led the initial Pharmacogenetics to Avoid Loss of Hearing (PALoH) study. 'The trial demonstrated that you can deploy rapid genetic testing in a clinical setting, and that the tests can be carried out within the 'golden hour' when severely unwell babies should be treated with antibiotics.'

In the current clinical trial, published in JAMA Pediatrics, researchers at two hospitals in Manchester used the Genedrive MT-RNR1 test to screen 424 newborn babies who required antibiotics for the MT-RNR1 genetic variant. Nurses conducted a cheek swab in the babies which was then inserted into a bedside machine for analysis.

The researchers also compared the mean times in giving the proper antibiotic to the babies screened with and without the new genetic test. They found that the mean times were almost the same, taking about 55 minutes. This means that including the new genetic test in clinical practice does not negatively impact the delivery of care.

To the researchers' knowledge, there are no genetic tests that could screen for the genetic variant in question within the critical first hour when antibiotics should be given to babies with severe infections. This is faster than previous genetic tests which normally would have taken several days.

The genetic test has already benefited some families as conveyed by first year nursing student Mary about her baby Khobi: 'Khobi was born with her bowel outside her tummy, which put her at risk of infection she needed antibiotics quickly but was given this new genetic test which showed she was susceptible to hearing loss from gentamicin... She was given an alternative antibiotic which didn't affect her hearing'.

Over 300 nurses are now being trained to use the machines across hospitals in Manchester, and it is expected the use of the test will become routine for babies who need antibiotic treatment in hospitalswithin weeks.

However, the new Genedrive MT-RNR1 genetic test should not be confused with gene drive a way of using genome editing to replace a natural gene with a new gene, that then gets passed on from generation to generation. Such gene drive technology only works on animals with short reproduction cycles, such as mosquitoes.

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Rapid genetic test to identify babies at risk of antibiotic-induced hearing loss - BioNews

PHILADELPHIA -- Robert H. Vonderheide, MD, DPhil, has been appointed to a second five-year term as director of the Abramson Cancer Center (ACC) at the University of Pennsylvania, following a highly successful tenure that saw 17 FDA approvals in oncology for therapies based on studies led or co-led by ACC investigators, high-impact basic and translational research discoveries, expansion of radiation oncology services to new sites across the Philadelphia region, and development of new methods for live tumor imaging during surgeries. Under his leadership, the ACC has also launched new cancer home care and telemedicine programs, and initiatives that drove improvements in germline genetic testing, cancer screenings and clinical trial participation by minority patients. He will continue in his roles as Vice President for Cancer Programs for the University of Pennsylvania Health System and Vice Dean for Cancer Programs in Penns Perelman School of Medicine.

In the next phase of his leadership, Dr. Vonderheide will build on the development of pathways to ensure that amid the increasingly complex landscape of cancer care and research patients across the entire health system are able to access leading-edge Penn Medicine care no matter where they live. Among key examples already underway: Proton therapy at Lancaster General Health and Virtua Health in New Jersey, both set to open this year; sub-specialty surgery consultation at outpatient sites and Penn Medicines regional hospitals; and telemedical options for genetic counseling and CAR T cell therapy and bone marrow transplant evaluation and education.

Patients can expect an exceptional experience at every location across our health system a place they are cared for by the most committed staff, specialized nurses, and top physician experts. Now, we are harmonizing that patient experience to ensure that every patient has the most seamless care and robust options across different sites of care, and the assistance to navigate easily between them, said University of Pennsylvania Health System CEO Kevin B. Mahoney. Under Dr. Vonderheides leadership, we are ensuring that every patient has every opportunity for the most personalized treatment and the very best chance at a cure through every door they enter across Penn Medicine.

Vonderheides renewal as ACC director includes a five-year, $130 million investment from the health system to provide resources and infrastructure to unify all missions of cancer care and research across Penn Medicine.

Growing access to cancer clinical trials is a key area of focus, through the development of a cancer clinical trials network, including more opportunities for patients at Penn Medicines regional hospitals to participate in clinical trials being led at the ACCs main campus sites in Philadelphia, and the expansion of other trial sites closer to patients homes. Additional efforts will harness the power of Penns unified electronic health record, from new approaches to involve patients in the Penn Medicine BioBank to expansion of programs providing patients with e-nudges to schedule mammograms and other tests and appointments through the MyPennMedicine portal.

This is a time of exciting, unprecedented momentum for cancer care and research. The cancer death rate has dropped faster in the past two years than ever before, due in part to the development of prevention strategies and of targeted and immunotherapies for an array of diseases, said J. Larry Jameson, MD, PhD, dean of the Perelman School of Medicine and Executive Vice President of the University of Pennsylvania for the Health System. Dr. Vonderheide embodies that momentum, as an exceptional collaborator who brings experts together across different disciplines to focus efforts on the most innovative ways to meet our shared goals of driving cancer discovery and improving patient care.

The ACC has continuously been designated as a Comprehensive Cancer Center by the National Cancer Institute (NCI) since 1973, one of 52 such Centers in the United States. It is among the nations most highly ranked cancer centers, providing care to adults during more than 300,000 outpatient visits annually across the six-hospital Penn Medicine Cancer System, as well as delivering more than 190,000 outpatient infusion therapies, over 130,000 radiation treatments and 330 stem cell transplants each year. The ACC was rated as exceptional during its competitive research funding review, the highest possible merit rating for an NCI Cancer Center.

Dr. Vonderheide is a leading authority in cancer immunology, leading a lab and clinical research focused on immunotherapies and vaccines for pancreatic, breast, and other cancers. He serves on the boards of directors for the American Association of Cancer Research, the American Association of Cancer Institutes, and the National Comprehensive Cancer Network. He is a member of the NCI Board of Scientific Advisers.

He received his bachelors degree in chemical engineering from the University of Notre Dame, and is a graduate of the Harvard Medical School, as well as Oxford University, where he earned a doctorate in immunology as a Rhodes Scholar. He completed residency training in internal medicine at Massachusetts General Hospital and a fellowship in medical oncology at the Dana Farber Cancer Institute.

Penn Medicineis one of the worlds leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of theRaymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nations first medical school) and theUniversity of Pennsylvania Health System, which together form a $9.9 billion enterprise.

The Perelman School of Medicine has been ranked among the top medical schools in the United States for more than 20 years, according toU.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $546 million awarded in the 2021 fiscal year.

The University of Pennsylvania Health Systems patient care facilities include: the Hospital of the University of Pennsylvania and Penn Presbyterian Medical Centerwhich are recognized as one of the nations top Honor Roll hospitals byU.S. News & World ReportChester County Hospital; Lancaster General Health; Penn Medicine Princeton Health; and Pennsylvania Hospital, the nations first hospital, founded in 1751. Additional facilities and enterprises include Good Shepherd Penn Partners, Penn Medicine at Home, Lancaster Behavioral Health Hospital, and Princeton House Behavioral Health, among others.

Penn Medicine is powered by a talented and dedicated workforce of more than 52,000 people. The organization also has alliances with top community health systems across both Southeastern Pennsylvania and Southern New Jersey, creating more options for patients no matter where they live.

Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2021, Penn Medicine provided more than $619 million to benefit our community.

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Penn Medicine Appoints Robert Vonderheide to Second Five-Year Term as Director of the Abramson Cancer Center - Penn Medicine

In 2014, Barbara Small was a pediatric nurse at Childrens Hospital of Philadelphia, enjoying her work, her family, and traveling with her husband, Dave. She was an active 55-year-old until she broke her hip in a bike accident.

A week after surgery to repair her hip, her vision became blurry. She went to the walk-in clinic at Penn Presbyterians Scheie Eye Institute and learned that her optic nerve was damaged, but that it didnt have anything to do with her accident or surgery.

Soon after, she awoke one morning and couldnt control her left side. The emergency room doctor told her shed had a stroke and sent her to a neurologist. An MRI revealed she had a brain lesion, apparently an area of tissue that had been damaged by the stroke.

Over the next few years, as her eyesight continued to deteriorate, repeated MRIs showed more brain lesions. Small visited a low-vision specialist, retinologist, endocrinologist, hematologist, rheumatologist and three cardiologists. She was tested for multiple sclerosis, diabetes, and a host of other diseases. She didnt have any of them.

I didnt think they would ever find anything, that the tests would all be negative, recalled Small, now 63. I wasnt optimistic about getting a diagnosis but I felt like I could overcome and manage whatever was wrong.

Doctors did diagnose a number of issues, including retinopathy, a disease of the retina that can impair vision, and neovascularization, the growth of blood vessels that are part of abnormal tissue, such as tumors, and of course, those lesions on her brain. She was also seeing a physical therapist for balance issues. But what connected these diagnoses remained elusive.

Small often thought about her mother, who died while in her 40s of an illness that was never diagnosed. When Small graduated from nursing school, she looked at her mothers medical records, which showed hardening of the arteries, arterial sclerosis, collagen disease, cardiac arrhythmias, and liver and kidney failure.

They summarized it as multisystem failures, Small said.

Her mother, who died in 1969, hadnt displayed any brain or eye symptoms, however. And her father, who lived into his late 80s, never spoke about his wifes illness.

In January 2018, almost four years after Smalls first symptoms, her neurologist sent her for genetic testing.

When I saw the geneticist, I said, This will be my last doctor, Small said. The geneticist tested me for four different genetic diseases that involve the brain and the eye and I tested positive for the TREX 1 gene mutation.

Small was diagnosed with RVCL retinal vasculopathy with cerebral leukoencephalopathy an extremely rare, inherited disease with no known cure.

Patients with RVCL are typically healthy until the fourth or fifth decades of life, and then they suddenly start to develop a variety of symptoms that can affect multiple organs, but especially the brain and the eye, said Jonathan Miner, associate professor of medicine and director of the RVCL Research Center at Penn Medicine.

Its a relentless disease that results in premature death in 100% of cases, in many cases within five or 10 years of onset.

As devastating as the news was, Small also had some measure of relief to be able to put a name to her constellation of issues.

I thought they would never find anything, that I would just have these odd symptoms, she recalled. Luckily, I had good doctors at Penn who did the research and were on this journey with me, trying to figure it out. They gave me a lot of resources so I felt very well-informed.

Uncovering Smalls diagnosis was difficult because RVCL is so rare just 43 families in the world are known to have it.

I suspect there are many more RVCL patients who just havent been diagnosed yet, Miner said. The disease can be confused with other diseases, like multiple sclerosis, lupus or brain tumors.

Disease of the retina is a hallmark of RVCL, but it can look very similar to diabetic eye disease.

The patients will end up losing vision, can develop glaucoma or blood vessel disease in the retina, dementia, cognitive impairment, memory problems, difficulty speaking or walking, and stroke symptoms, he said. A lot of patients have kidney, liver or thyroid disease. In all cases, without having a genetic test, these findings can end up being attributed to something else.

Within families with the disease, 50% will inherit the mutation that causes RVCL, and 100% of those with the mutation will develop the disease, Miner said. Since her diagnosis, Smalls family has undergone genetic testing that has uncovered more cases, including in one of her daughters and her brother. Small suspects that her mother had it, too, though her symptoms were different from her own.

Smalls brother, James Davis, 67, discovered that he had RVCL in July 2021. He had been getting injections in his right eye to treat vision problems for several years and later developed glaucoma. Otherwise, he felt fine until he didnt.

In June of 2021, I had extreme fatigue, loss of appetite, problems with my right eye, and funky walking, said Davis, who lives in Plymouth, Minn.

An MRI showed lesions concerning for possible malignancy, so he was expecting he might need treatment for brain cancer. When he shared the news with his sister, she put him in touch with Miner, who asked Davis to hold off on seeking additional evaluation until he had genetic testing. The test confirmed that Davis, too, had the TREX 1 gene mutation.

It was a big shock, said Davis. We talked to our financial planner to be sure theres sufficient money for my wife, Dale, and were trying to enjoy things as much as we can because my life expectancy is a lot shorter than we planned.

Davis son is 27 and plans to have genetic counseling and testing soon.

Shortly after Smalls diagnosis, her daughters Kimberly Antonelli, 35, and Lindsay Ward, 32, had genetic counseling, and were told that many people dont want to be tested because they fear the results and think that they cant do anything about them. They saw it differently.

Getting tested was a very easy decision for me, said Ward, who lives in West Deptford. Knowledge is power. But it was a very hard eight weeks waiting for the results.

She was especially anxious for her son, Declan, now 4. She does have the mutation, which means Declan might, as well.

I had prepared myself for the worst, she recalled. In a weird way I felt it was a positive for my mom because now were in this together. I always try to see the bright side of things but obviously I was devastated. To think my future might not be as long as I had anticipated was hard.

Hoping to become pregnant again, Ward went through preimplantation genetic diagnosis (PGD,) a laboratory procedure used in conjunction with in vitro fertilization (IVF) to reduce the risk of passing on inherited conditions.

We had seven embryos. Four had the mutation and three did not, she recalled. I did three rounds of IVF and all resulted in eventual miscarriage. It had taken such an emotional, physical and mental toll on me that I couldnt do it again. We had our son, Jason, who is now 8 months old, naturally.

Ward hopes that by the time her children grow up, there will be treatments or even a cure for RVCL, should they turn out to have the mutation. She has decided to wait on testing them so that they can make the choice together when they are older.

I take things more seriously and live more for the moment because at any point I could have the onset or my moms could get worse, she said. This morning we went to get a dozen specialty doughnuts, and, why not! Youve got to live life.

Her big sister, Kimberly, was relieved to find out that she doesnt have the gene, and so neither do her four children. Yet her joy for them is tempered by grief. Im happy that Im negative but Im sad that my other family members arent, said Antonelli, who lives near Pittsburgh. My sister and I are very close.

Another source of stress is the fact that few people can really understand what its like to have such a rare condition.

You can sympathize with people who have cancer because you understand it, Antonelli said. My mom has a death sentence but people cant appreciate how dangerous and unknown these rare diseases are. There are very few visible symptoms.

Miner, who came to Philadelphia from St. Louis in 2021 to lead Penn Medicines research center, is among numerous experts seeking answers to RVCL.

What motivates me is knowing that this is a solvable problem because its a disease caused by a single gene mutation, he said. This disease is going to be eventually treatable and hopefully cured, but we dont know how long its going to take, five years or 15 years.

Unlike many other diseases, RVCL is due to one protein encoded by one gene, said Miner. Now that we know the genetic cause, were hoping to be able to develop personalized medicines for these patients and their families. Understanding this particular gene and protein is about far, far more than this specific disease. The drugs that are being developed to target the TREX 1 protein are very likely to become useful for other diseases, as well.

Small has some weakness on her left side, which causes a slight limp; her vision is impaired; and she tires easily. She left her nursing job in October 2019.

Now that her husband, Dave, is retired, they are enjoying travel and spending time with their family. She maintains an optimistic outlook, hopeful that progress will be made in unlocking the mysteries of RVCL, if not for her then for her children, grandchildren and future generations.

My outlook is good, she said. My husband tells me Im going to live until Im 80. Im not going to live until Im 80 but thats OK. Im much more likely not to make it out of my 60s but that doesnt depress me. Its just the way its working out.

Read more from the original source:
Medical mystery: This woman's brain lesions led to a diagnosis that affected her entire family - The Philadelphia Inquirer

New York, United States The Predictive Genetic Testing And Consumer Genomics Market research report provides all the information related to the industry. It gives the outlook of the market by giving authentic data to its client which helps to make essential decisions. It gives an overview of the market which includes its definition, applications and developments and manufacturing technology. This Predictive Genetic Testing And Consumer Genomics market research report tracks all the recent developments and innovations in the market. It gives the data regarding the obstacles while establishing the business and guides to overcome the upcoming challenges and obstacles.

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Some of the Top companies Influencing in this Market include:23andMe, Inc., Myriad Genetics, Inc., F.Hoffmann-La Roche Ltd., Abbott Laboratories, Genesis Genetics, Agilent Technologies, Thermo Fisher Scientific, Inc., BGI, Bio-Rad Laboratories Inc., Illumina, Inc., Counsyl, Inc., ARUP Laboratories

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Firstly, this Predictive Genetic Testing And Consumer Genomics research report introduces the market by providing the overview which includes definition, applications, product launches, developments, challenges and regions. The market is forecasted to reveal strong development by driven consumption in various markets. An analysis of the current market designs and other basic characteristic is provided in thePredictive Genetic Testing And Consumer Genomics report.

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Market Segmentation: By Type

Genetic Susceptibility TestNutria GeneticsSkin & Metabolism GeneticsOthers

Market Segmentation: By Application

Breast & Ovarian CancerCardiovascular screeningDiabetic Screening & MonitoringOthers

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The region wise coverage of the market is mentioned in the report, mainly focusing on the regions:

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An assessment of the market attractiveness with regard to the competition that new players and products are likely to present to older ones has been provided in the publication. The research report also mentions the innovations, new developments, marketing strategies, branding techniques, and products of the key participants present in the global Predictive Genetic Testing And Consumer Genomics market. To present a clear vision of the market the competitive landscape has been thoroughly analyzed utilizing the value chain analysis. The opportunities and threats present in the future for the key market players have also been emphasized in the publication.

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Table of Contents

Global Predictive Genetic Testing And Consumer Genomics Market Research Report 2022 2029

Chapter 1 Predictive Genetic Testing And Consumer Genomics Market Overview

Chapter 2 Global Economic Impact on Industry

Chapter 3 Global Market Competition by Manufacturers

Chapter 4 Global Production, Revenue (Value) by Region

Chapter 5 Global Supply (Production), Consumption, Export, Import by Regions

Chapter 6 Global Production, Revenue (Value), Price Trend by Type

Chapter 7 Global Market Analysis by Application

Chapter 8 Manufacturing Cost Analysis

Chapter 9 Industrial Chain, Sourcing Strategy and Downstream Buyers

Chapter 10 Marketing Strategy Analysis, Distributors/Traders

Chapter 11 Market Effect Factors Analysis

Chapter 12 Global Predictive Genetic Testing And Consumer Genomics Market Forecast

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Predictive Genetic Testing And Consumer Genomics Market Report Covers Future Trends With Research 2022 to 2029 23andMe, Inc., Myriad Genetics ...

Breast pain can be worrisome, but its not usually a cause for concern.

Hormones play a big role in the development of breast tissue and the pain that can develop there. This is especially true in women, as hormone fluctuations cause ducts and glands in the breasts to grow and shrink in cycles.

This article will explore the causes of breast pain, as well as when to contact a doctor and how theyll diagnose your symptoms.

While anyone can experience breast pain, its more common in people with female sex hormones like estrogen and progesterone. These hormones play a big role in the fluctuation of breast tissue structure and size.

During significant hormonal shifts like pregnancy and while breastfeeding, breast pain or tenderness is actually expected.

Most types of breast pain fit into two categories: cyclic and noncyclic breast pain.

Cyclic breast pain is linked to your menstrual cycle and is believed to be caused in part by hormone changes. Pain can develop at different points in this cycle. But its most common at the start of the cycle or during ovulation.

Cyclic breast pain is barely noticeable for some people and excruciating for others. Its not uncommon for this pain to be felt in just one breast or the other. It is often a radiating pain that begins near the armpit.

Noncyclic breast pain can occur at any time and is not linked to your menstrual cycle. This type of pain is pretty uncommon. It can be caused by all kinds of things, like trauma, an injury to the breast tissue, or even arthritic pain. The type of pain can vary, but its usually a continuous pain that is felt in one specific area of the breast. It can be sharp, dull, or radiating.

Cyclic and noncyclic causes of breast pain include things like:

Most causes of breast pain will go away on their own with time, medications, or lifestyle changes. However, if youre experiencing any of the following symptoms, schedule an appointment with a doctor for an evaluation and diagnosis:

Your doctor will begin an examination for breast pain by asking you about your personal and family medical history. Theyll want to know which of your relatives if any have had breast cancer and at what age.

Genetic testing using your blood or saliva could provide clues about your cancer risk. But there are other considerations in your family history, too.

Your doctor may suggest a one-time or regular mammogram to examine your breast tissue more closely. The U.S. Preventive Services Task Force recommends that all women between the ages of 50 and 74 receive a mammogram at least once every 2 years. Get one more often if you have an increased risk of breast cancer.

Other tools that can help identify tissue changes, breast cancer, or other conditions may include:

Biopsies are the tool of choice when it comes to diagnosing breast lumps, which are often associated with a higher risk of cancer.

A mammogram is usually the go-to tool when it comes to diagnosing breast pain and other issues, but ultrasound imaging is sometimes more accurate in people under 30 years old. Mammograms are highly accurate at detecting cancer, though, especially in older adults.

Treatment of your breast pain depends on the cause. Breast cancer treatment is complex and depends on the cancer type and stage.

Most breast pain, however, can be addressed with medications or lifestyle changes. Some things that you can do to relieve breast pain:

Breast pain is common and usually not serious. Most women will experience breast pain at some point in their lives, but only a few will be diagnosed with a serious problem like cancer.

If you have concerns about your breast pain, talk with a doctor about your symptoms. Be sure to follow their recommendations for regular screenings.

Discussing your risk factors including family and genetic history can help you and your doctor make the best decisions regarding your breast health.

Excerpt from:
When to Worry About Breast Pain: Causes, Diagnosis, Treatment - Healthline

Did you know that your babys genetic makeup was determined at conception? From the moment the sperm met the egg, your little ones genetic code DNA began forming. Its made up of 23 pairs of chromosomes. Sometimes, though, extra chromosomes make their way into the mix and can result in something called a trisomy.

Edwards syndrome is also known as trisomy 18. It means a person has an extra copy of chromosome number 18, leading to issues with development. Heres more about the symptoms of this syndrome, what causes it, and what you might expect after a diagnosis.

Trisomy 18 is a rare genetic disorder that affects approximately 1 in every 3,315 births in the United States around 1,187 babies each year.

In typical development, a baby gets 23 pairs of chromosomes from its parents during conception 22 are called autosomes, and 1 set is made up of sex chromosomes (X and/or Y, depending on the babys sex).

The word trisomy means three bodies. When there are three copies of the chromosome versus the usual two, it creates an imbalance. As a result, a baby may be born with certain structural changes some of which may lead to miscarriage, stillbirth, or death after the baby is born.

Babies can be born with an extra copy of chromosome 18 in each cell in the body. This is called complete trisomy 18 and causes more serious health outcomes.

Mosaic trisomy 18 happens when only some cells in the body contain the extra chromosome. Around 5 percent of babies with trisomy 18 have the mosaic form. This generally leads to milder irregularities and longer life expectancy.

Partial trisomy 18 happens when an extra copy of chromosome 18 attaches to another chromosome. Again, the severity of the syndrome tends to be associated with the total number of cells affected by the trisomy. So, a partial trisomy tends to have less severe effects and longer life expectancy.

You may not notice anything different in your pregnancy if your baby has Edwards syndrome. In fact, you may not learn about your babys diagnosis until after your doctor orders certain prenatal screening tests, like:

Some families do not discover their childs diagnosis until birth, when the following physical features may include:

Other health issues may include:

Trisomy 18 is caused by any situation that leads to an extra copy of chromosome 18 in the body.

In most cases, it happens when the sperm meets the egg during conception. In one scenario, the reproductive material of either parent may spontaneously divide. In another, the trisomy may happen as cells divide after fertilization. Whatever the case, the extra chromosome happens at random.

Translocation is another possibility, which means that parts of chromosomes break off and attach to other chromosomes. This may happen randomly or through a balanced translocation, in which one parent has a set of chromosomes that arent typical but are balanced. When chromosomes are balanced, they dont cause medical issues. After reproduction, though, genetic information passed on may cause a trisomy.

Edwards syndrome may be diagnosed at some point during your pregnancy. You may have a cell-free DNA screening (cfDNA) at any time after 10 weeks of pregnancy and until delivery. cfDNA is a simple blood test that screens for genetic conditions. A positive result on this test means youll need further testing to confirm the results.

Other tests during pregnancy include:

Other times, trisomy 18 may not be diagnosed until after your baby is born. Your childs doctor may diagnose it based on:

There is no cure for trisomy 18. Since babies with this condition tend to have multiple health issues, youll work with a team of doctors to create a customized treatment plan. In more severe cases, some families favor palliative care or hospice care.

Treatments are more about making a child comfortable or correcting the issues that affect an individual child. For example, surgery may be an option to treat things like:

As a child grows, they may need support academically and physically. Early intervention and special education programs can help fill these gaps.

You may be surprised to learn that there are very few risk factors for Edwards syndrome.

There may be an increased chance of having a baby with a trisomy as you get older. While different reports show mothers in their late teens and 20s can have children with trisomy 18, the mean age is closer to 32.5 years old.

In rare cases, trisomy 18 may be inherited from a biological parent (through balanced translocation). If you already have had one child with a trisomy, your doctor may suggest getting genetic testing to assess your chances of having another child with a similar condition.

The vast majority of the time, though, Edwards syndrome happens by chance during conception when the sperm meets the egg.

Its important to be prepared for all possibilities with a condition like trisomy 18. Researchers share that nearly half of all babies born with Edwards syndrome who survive delivery may not live beyond the first week of life.

That said, the severity of the syndrome depends on the type (complete, mosaic, partial, etc.) and whatever effects it has on your individual child. All children are different, and all outlooks will be unique as a result.

Of children born with Edwards syndrome, nearly 50 percent will not survive beyond the first week of life. However, around 10 percent will reach their first birthday, and some may live to their teen years or even adulthood, but they will need medical support or therapies, including:

While you may be worried about your child and the outlook over the long term, try taking it day by day. And dont forget about yourself or your own mental health in the process.

There is support for families with children who have Edwards syndrome. Consider contacting the Trisomy 18 Foundation or the Support Organization for Trisomy 13, 18, and Related Disorders (SOFT). Your doctor may also be able to help connect you with a local group for support and other resources.

View original post here:
Trisomy 18: Diagnosis, Causes, Prognosis, and More - Healthline

After that, you sit back and you wait for your results to come in and you wait for information to come to you. So if there's a new survey that comes out, well let you know, and it's up to the individual, how much, or how little they want to participate. Again, we'd love everyone to continue to complete the surveys as they go along because the more information that we have about lifestyle, environment, family health history, social determinants of health, all of that helps researchers have a more dynamic and full understanding of what is going on. Not only with the individual, but they can see it on a larger scale in communities and different populations.

La Keisha Jones:One thing with a trial is that you are providing treatment. We do not provide treatment. We are just collecting information to create a data cohort of information for researchers to look at and that would be the difference there. The one thing that we do offer, though, is that if something is discovered individuals are notified. If there is something of health significance with the genetic results that is found, then a genetic counselor is offered to them to explain what this means to them and what it can mean to their family.

Our program is giving information back so that people can have more informed conversations. They can be more informed about their risk for a disease possibly, or the risks that they may or may not face. Again, if something comes back, it doesn't necessarily mean that disease could take place, but if they are aware of it, they can keep it to themselves or they could share it with their family, or they could take it to their doctor and just say, "Hey, you know, we would never have known this because genetic testing isn't on the list of things that normally take place and I might be at risk. What should we do about it?" Maybe it means earlier screenings. Maybe it means making healthier decisions.

There are also different levels of participation. Some people just decide they want to do the online portion. Some people want to provide genetic information but not to receive their results. You have the option to say yes, no, maybe, or I don't know yet.

Lakeisha Jones:Anyone over the age of 18 can enroll. It doesn't matter if you have any diseases or don't have any diseases, anything of that sort. We do ask individuals to have an address in the U.S. and contact information here in the U.S. for about six months out of the year, just so that when information is returned, they can make sure that they can be followed up with and be contacted. You don't need health insurance to participate and you do not need to be a U.S. citizen.

That's the beautiful thing about New York, too, we have a very diverse staff. Our staff is bilingual, English and Spanish.

To sign up online or find phone numbers of where to talk to someone about the program, you can visit the New York City Consortium websiteor call 212-205-9927.

Here is the original post:
The 'All of Us' Research Program Is Helping Make Medicine More Precise for Diverse Populations. Five Years In, How Is It Going? - Columbia | Neighbors

Familial cancer syndrome is a genetic condition that increases the risk of various cancers in related family members. Hereditary cancer disorders are caused by mutations in certain genes passed down from parents to offspring, and certain cancer patterns can be found in families with hereditary cancer syndrome.

This could be due to other causes like the fact that family members share certain activities or exposures that raise cancer risk, such as smoking. Rarely, factors that run in families, such as obesity, may also increase cancer risk.

The common cancers and associated syndromes:

Hereditary Breast and Ovarian Cancer (HBOC) syndrome: tumors are commonly found in women younger than the average age and are caused by a hereditary mutation in either the BRCA1 or BRCA2 gene.

Lynch syndrome: also known as hereditary non-polyposis colorectal cancer, is the most common genetic syndrome that raises a person's risk of colon cancer in those under the age of 50.

Li-Fraumeni syndrome: a rare genetic disease that causes a variety of malignancies in individuals in their twenties and thirties, including sarcoma, leukemia, brain tumors, adrenal cortex cancer, and breast cancer.

Genetic counseling and testing: People with a strong family history of cancer may be interested in learning more about their genetic composition. Since hereditary mutations impact all cells in a person's body, genetic testing on blood or saliva samples is frequently used to detect them.

Germline mutation

Any observable alteration within germ cells is referred to as a germline/germinal mutation. When a mutant sperm or oocyte combine to form a zygote, the only mutations that can be passed on to progeny are those in these cells.

Individuals with mutations in tumor suppressor genes or proto-oncogenes are more likely to develop tumors. About 5-10% of all cancers are inherited through defective inherited genetic alterations.

Because the protein produced inhibits tumors, those who inherit germline mutations in TP53 are prone to specific cancer types. Breast and ovarian cancer as well as hereditary non-polyposis colorectal cancer, are two further examples.

Indias stance on family cancer syndrome

According to the WHO and the American Cancer Society, cancer kills one out of every six people on the planet, more than HIV/AIDS, TB, and malaria combined.

Are these genetic tests available in India?

Yes, these genetic tests are now accessible in India and require only a simple blood test (Multi-gene panel testing).

Who must undergo these tests?

Strong family history of Cancers like Breast cancer, Ovarian cancer, Colon cancer etc. happening in multiple family members and or many generations needs to get tested.

When cancer happens at an early age say <30 years, needs to be tested again.

There are other situations where one needs to get tested for which they can consult their Oncologist or physician.

What preventive strategies are available?

Those who test positive for these syndromes have a few cancer prevention options like preventive surgeries, tablets, and also aggressive cancer screening programs to detect cancers at early stages and treat them effectively.

This data can help clinicians make better clinical management decisions. Furthermore, mutations in particular genes boost therapeutic response, contributing to precision/personalized medicine, in which patients are treated depending on their mutations.

Given the numerous benefits of detecting genetic differences in hereditary malignancies, the medical community has been working to make genetic testing more affordable and accessible to the general people, allowing for faster disease diagnosis, management, and treatment.

-The author Dr. Vivek Belathur is MD, DM, ECMO, Senior Consultant Medical Oncology at Fortis Hospitals, Bannerghatta Road. The views expressed are personal.

(Edited by : Priyanka Deshpande)

First Published:Apr 07, 2022, 08:42 PM IST

Read the original:
World Health Day | Family Cancer Syndrome: What genes tell us about the risk of developing cancer - CNBCTV18

DEDUCE study demonstrates AUC of 0.86 in overall cohort, including more than 700 prospective samples

AUSTIN, Texas, April 13, 2022 /PRNewswire/ --Natera, Inc. (NASDAQ: NTRA), a global leader in cell-free DNA testing, todayannounced that its clinical validation study1 on its donor-derived cell-free DNA (dd-cfDNA) test for the assessment of acute rejection in heart transplant patients, Prospera Heart, has been published in the Journal of Heart and Lung Transplantation - a leading journal with the highest impact factor in the transplantation sector2.

This multi-site clinical validation, named the DEDUCE study, was conducted in partnership with the University of Utah and the University of California, San Diego and evaluated 703 prospective and 108 retrospective samples, (811 samples total) from 223 patients. The patient cohort included a large number of biopsy-confirmed rejections - 32 samples correlating to antibody mediated rejection (AMR) and 17 samples correlating to acute cellular rejection (ACR). The Prospera Heart test exhibited excellent performance with an overall 0.86 AUC for identifying acute rejection. Notably, the performance was also exceptional in the prospective arm-alone (0.87 AUC3).

"There is a critical unmet need for an accurate and less invasive approach for rejection surveillance after heart transplant," said Josef Stehlik, senior author and medical director of the Heart Transplant Program and co-chief of the Advanced Heart Failure Program at the University of Utah School of Medicine. "Incorporation of a noninvasive assay to reduce or replace the use of endomyocardial biopsy requires a very high performance standard. The Prospera Heart test demonstrated performance that I believe the clinicians will be very excited about."

The study also included an analysis on the use of dd-cfDNA concentration alone to identify rejection. dd-cfDNA concentration demonstrated an AUC of 0.88 overall, and 0.89 in the prospective cohort, highlighting the potential (upon additional studies and evaluation) to further improve the performance of the Prospera Heart test by evaluating both dd-cfDNA concentration and donor fraction.

The Prospera Heart test was launched in late 2021 and will continue to be evaluated in a variety of additional studies, including the NIH-supported DTRT study, and the Natera-sponsored DETECT trial, expected to be the first randomized controlled trial comparing dd-cfDNA surveillance to endomyocardial biopsy surveillance in patients of all risk profiles from 30 days post transplant. Combined, these trials are expected to include more than 775 heart transplant patients across multiple centers, underscoring Natera's commitment to generating robust scientific evidence.

About the Prospera test

TheProsperatest leverages Natera's core single-nucleotide (SNP)-based massively multiplexed PCR (mmPCR) technology to identify allograft rejection non-invasively and with high precision and accuracy, without the need for prior donor or recipient genotyping. The test works by measuring the fraction of donor-derived cell-free DNA (dd-cfDNA) in the recipient's blood. It may be used by physicians considering the diagnosis of active rejection, helping to rule in or out this condition when evaluating the need for diagnostic testing or the results of an invasive biopsy. The Prospera test has been clinically and analytically validated for performance regardless of donor relatedness, rejection type, and clinical presentation. It has been developed and its performance characteristics determined by Natera, the CLIA-certified laboratory performing the test. The test has not been cleared or approved by the US Food and Drug Administration (FDA). CAP accredited, ISO 13485 certified, and CLIA certified.

About Natera

Natera is a global leader in cell-free DNA testing, dedicated to oncology, women's health, and organ health. Our aim is to make personalized genetic testing and diagnostics part of the standard of care to protect health and enable earlier and more targeted interventions that help lead to longer, healthier lives. Natera's tests are validated by more than 100 peer-reviewed publications that demonstrate high accuracy. Natera operates ISO 13485-certified and CAP-accredited laboratories certified under the Clinical Laboratory Improvement Amendments (CLIA) in Austin, Texas and San Carlos, California. For more information, visit http://www.natera.com.

Forward-Looking Statements

All statements other than statements of historical facts contained in this press release are forward-looking statements and are not a representation that Natera's plans, estimates, or expectations will be achieved. These forward-looking statements represent Natera's expectations as of the date of this press release, and Natera disclaims any obligation to update the forward-looking statements. These forward-looking statements are subject to known and unknown risks and uncertainties that may cause actual results to differ materially, including with respect to our efforts to develop and commercialize new product offerings, whether the results of clinical or other studies will support the use of our product offerings, our expectations of the reliability, accuracy and performance of our screening tests, or of the benefits of our screening tests and product offerings to patients, providers and payers. Additional risks and uncertainties are discussed in greater detail in "Risk Factors" in Natera's recent filings on Forms 10-K and 10-Q and in other filings Natera makes with the SEC from time to time. These documents are available atwww.natera.com/investorsandwww.sec.gov.

ContactsInvestor Relations:Mike Brophy, CFO, Natera, Inc., 510-826-2350Media:Kate Stabrawa, Communications, Natera, Inc., 720-318-4080[emailprotected]

References

SOURCE Natera, Inc.

Excerpt from:
Multi-Site Clinical Validation of Prospera Heart Test Demonstrates Outstanding Performance in Assessing Heart Transplant Rejection - PR Newswire

Image: Professor John Yarnold (left), Professor Pascal Meier (middle) and Professor Clare Isacke.Credit:soora.co.uk

As research efforts become bigger and more ambitious, there is a real need to bring together researchers with diverse scientific backgrounds and perspectives to solve complex scientific problems. This type of multidisciplinary approach taken by The Breast Cancer Team at the ICR and The Royal Marsden NHS Foundation Trusthas been critical to their success in making transformational discoveries in breast cancer.

Twelve researchers from the ICR and The Royal Marsden Breast Cancer Team have been awarded the 2022 Team Science Award from the American Association for Cancer Research (AACR). The award recognises the significant contributions to the breast cancer research community made by the multidisciplinary team spanning a spectrum of discovery biology, molecular pathology, trial statistics and clinical science.

Here, we celebrate the teams tremendous achievements, which are underpinned by more than two decades of research.

In 1995, Professor Alan Ashworth, then at the ICR but now President of the UCSF Helen Diller Family Comprehensive Cancer Center, was part of a team of researchers that discovered the second breast cancer susceptibility gene, BRCA2. Building on this work, Professor Ashworth and Professor Andrew Tutt(then Ashworths MRC Clinical Training Fellow and PhD student), along with a wider group in the Ashworth lab, uncovered the important role of the BRCA2 gene in DNA damage repair revealing how it might be targeted with drugs such as carboplatin.

Together with Professor Chris Lordwho had joined the lab, and Professor Steve Jacksonsteam at the UK biotech company KuDOS, in 2005, they went on to identify the first synthetic lethal interaction between the BRCA1/2 genes and the DNA damage repairing enzyme Poly-ADP-Ribose Polymerase 1, or PARP1.

The concept of synthetic lethality is based on the dependency between a pair of cancer genes, where loss of function of either individual gene will allow the cancer cell to survive, but loss of function of both genes simultaneously will cause the cancer cell to die.

The collaboration with the KuDOS team, who had discovered a PARP inhibitor drug called olaparib, showed that blocking PARP1 caused cancer cells carrying BRCA1 or BRCA2 mutations to die. The striking results from the Ashworth lab stimulated Professor Tutt and the Ashworth group to design a Phase I clinical trial in 2008, together with ICR clinician scientist Professor Johann de Bonoand Professor Stan Kayeat The Royal Marsden, that focussed on BRCA1/2 mutation carriers.

Commenting on the discoveries, Professor Lord said, I think we knew from a very early stage that this was quite a significant finding. But at the time, we didnt fully realise that it would go all the way to actually getting approved and used worldwide. For us lab scientists and clinician scientists, these are things that we came into research to do. From an emotional perspective, it is incredibly rewarding and an enormous privilege to be able to contribute to things that actually make a difference to people.

The teams collaborative efforts pioneered the use of synthetic lethality as a new therapeutic strategy in cancer. This has had a particular impact in breast cancer, as well as in ovarian, prostate and pancreatic cancer, where PARP inhibitors are also now used.

Phase III trials with olaparib, that followed the phase II proof of concept studies led by Professor Tutt in 2010, resulted in the drugs approval in treating advanced BRCA1/2 mutated breast cancers. Olaparib was approved for breast cancer by regulators in the US, the Food and Drug Administration (FDA), in 2018, and in Europe, the European Medicines Agency (EMA), in 2019. The FDA and EMA have also approved the use of olaparib in ovarian, prostate and pancreatic cancers.

The development and approval of olaparib has transformed how advanced BRCA1/2 mutated breast cancers are treated worldwide. Olaparib is the first cancer treatment targeted against an inherited genetic fault. This breakthrough has had a huge impact on thousands of people with breast cancer, enabling patients to live longer and have a better quality of life while receiving treatment.

More recently, the results from the OlympiA trial, that was led by Professor Tutt as the Breast International Groups Global OlympiA Steering Committee Chair,revealed that adding olaparib to standard treatment for early-stage breast cancer in patients with inherited BRCA1/2 mutations can improve survival and reduce the risk of recurrence. The trial also supports testing for germline BRCA1/2 mutations, which has now been established as an important part of treatment selection in early breast cancer. The teams findings have impacted international treatment guidelines for both breast cancer therapy and genetic testing.

Professor Tutt said, This work brought together fundamental biologists, geneticists, biotech companies, early phase trials leaders and international collaborators at the phase III study stage. The award recognises the teamwork and amalgamation of skillsets required to change the way breast cancer is treated.

While the use of PARP inhibitors has been largely successful, not all patients who have inherited a faulty BRCA1 or BRCA2 gene respond to PARP inhibitors. Professors Lord and Tutt and their team are trying to understand how cancer cells become resistant to these drugs. They are uncovering ways to overcome resistance by identifying molecules that can be targeted using different drug combinations.

Developing smarter, kinder treatments for patients is a continuous cycle from the lab to the clinic and back again. Professor Lord said, Our collaboration with The Royal Marsden allows us to be a truly translational research centre. We can do biological research that informs new drug discovery projects and design of clinical trials, but we can also take observations from the clinic and feed them back into the lab where they can be dissected at a molecular level. This provides useful insight that can help to make new discoveries to overcome drug resistance.

Our researchers regularly present their latest findings at the AACR Annual Meeting in the US.

Find our more about the AACR conference

Oestrogen receptor positive, or ER+, breast cancer is the most common form of the disease it makes up about 80 per cent of cases and this is where the joint team made another major contribution recognised by the award. These cancers rely on oestrogen for their growth and can be treated using aromatase inhibitors that block the effects of the hormone.

The ICR and The Royal Marsden played a key role in the clinical development of aromatase inhibitors assessing their effectiveness over the years. The teams work in this field has been critical to understanding the biology of ER+ breast cancers and improving our knowledge of how these cancers become resistant to conventional hormone treatment.

Early trials involving Professor Mitch Dowsettfound that aromatase inhibitors were better than tamoxifen another type of hormone therapy for breast cancer at preventing the recurrence of ER+ breast cancers.

A seminal trial co-led by Professor Judith Bliss, an expert trial statistician and methodologist, demonstrated improved relapse-free survival in patients that switched to the aromatase inhibitor exemestane after two to three years of tamoxifen treatment compared with tamoxifen alone for five years. This trial played an instrumental role in changing practice guidelines for use of aromatase inhibitors in the clinic.

Professor Stephen Johnston, a consultant oncologist at The Royal Marsden, led the large-scale international MonarchE trialwhich aimed to identify new treatments that overcome resistance in ER+ breast cancer. The results showed that adding the drug abemaciclib a CDK4/6 inhibitor that prevents cell growth to hormone treatment significantly reduced the risk of the disease coming back in high-risk patients with early breast cancers.

The MonarchE trial was based on many years of research done at the ICR and The Royal Marsden and was a collaboration between both organisations, Eli Lilly and numerous international investigators. Abemaciclib was approved for adjuvant therapy by the FDA in the US in 2021 and just this month by the EMA.

Professor Bliss said, The ICR and The Royal Marsden bring together discovery science, clinical expertise and dedicated cancer specific trials methodology, which is ideal for designing scientifically robust, efficient and practice-changing clinical trials.

Professor Dowsett and his team also discovered an important biomarker Ki67, which marks newly divided cancer cells to evaluate the effectiveness of aromatase inhibitors in patients. The biomarker was subsequently developed into a test that is used to identify patients who might particularly benefit from hormone therapy.

The POETIC trialinvolved Professor Dowsett, Professor Bliss and Professor Ian Smith, and enrolled postmenopausal women who were planned to receive an aromatase inhibitor for five years following surgery. By starting the aromatase inhibitor two weeks before surgery and looking at how the Ki67 biomarker changed in patients tumours following the short-term therapy, the researchers were able to distinguish groups of patients with different risks of their cancer coming back.

Some patients started with a low level of the biomarker which stayed low after two weeks of treatment. The patients in this group had a very low chance of their cancer coming back during the next five years, with many of these patients able to be treated with aromatase inhibitor therapy alone. A minority of these patients were likely to still require chemotherapy if they exhibited certain high-risk features in their cancer.

For patients who had higher levels of the biomarker before treatment, assessing the levels again after two weeks of therapy showed that biomarker changes during that period affected the patients long-term outcome. Many of these patients had tumours that exhibited low levels of the biomarker following treatment. Patients whose biomarker levels stayed high following the brief exposure to aromatase inhibitors had the highest risk of their cancer coming back.

These findings helped to identify high-risk patients whose cancer was likely to come back and so required additional treatment above the current standard of care. This national trial engaged patients and doctors throughout the UK and helped to promote the desire for Ki67 biomarker testing as part of routine practice in the clinic.

Professor Johnston said, The pioneering work done by The Royal Marsden and the ICR is unrivalled elsewhere. Our close collaborations with the Cancer Research UK-funded Clinical Trials and Statistics Unitat the ICR and the scientists involved in the development of biomarkers made it possible to do the POETIC trial and plan the follow up POETIC-A trial, which started in 2020. These trials help to increase our understanding of the disease and how we can overcome resistance.

A measure of cancer treatment is not only how effective it is, but also how well tolerated it is by patients. Its important that research is used to find smarter and kinder treatments, and the joint team has excelled in this area.

The award recognises approaches that have led to de-escalation of breast cancer treatment. Long-standing research conducted by Professor John Yarnoldand Professor Bliss, and their wider teams, has revolutionised the way radiotherapy is delivered to people with breast cancer. This work was done in partnership with many other clinical leads at hospitals across the UK.

The findings from their clinical trials demonstrated that patients could be treated safely and effectively with fewer and bigger radiotherapy doses. Their remarkable discovery changed the treatment, for some patients, from being delivered in 25 doses over five weeks to just five doses over one week, reducing overall treatment time, the burden of that time on patients and hospital costs. This was particularly impactful during the Covid-19 pandemic when patients needed to receive treatment but minimise the time spent in hospitals.

Professor Bliss spoke about the impact of the radiotherapy trials saying, These trials investigated the balance of being able to keep recurrence rates down without causing more side effects. Our findings have been practice-changing and have had a great impact on the treatment pathways for breast cancer patients worldwide. They have also reduced inequalities by expanding access to the best treatment for patients in an impartial manner.

The team have also developed a test, known as a liquid biopsy, that detects tumour DNA circulating in the blood. By analysing samples of blood plasma from breast cancer patients to see if that tumour DNA is present, researchers can predict which patients are at risk of recurrence. This work, led by Professor Nick Turner, provides a less invasive way to assess patients and their response to therapy, avoiding the need for repeat tumour biopsies.

A recent phase II trial (plasmaMATCH), involving Professor Turner, Professor Bliss and Dr Alistair Ring, assessed the feasibility and clinical use of liquid biopsies in breast cancer patients it has shown promising results. The team have launched additional trials to further assess the potential use of liquid biopsies in guiding cancer therapy.

While most people with primary breast cancer, which hasnt spread, have a high survival rate because of the availability of effective treatments and the accessibility of tumours for surgical intervention, metastatic disease is still considered incurable.

Progress in treating advanced disease is urgently needed and the award recognised the discovery of molecular changes in breast cancer that drive some of the more aggressive behaviours in advanced breast cancer.

Professor Clare Isacke and her teams research focuses on how breast cancer cells interact with their environment during the early stages of metastatic colonisation. They have developed new ways to study advanced breast cancer using metastasis models in mice, which has provided important insights into how breast cancer cells adapt to survive in secondary sites and evolve to resist treatment. Their discoveries about how certain cells, called cancer associated fibroblasts, nourish tumour seedlings, have revealed potential therapeutic targets for advanced breast cancer.

Professor Pascal Meierand his team, whose work centres on cell death, have discovered proteins that regulate cell survival and inflammation. They are trying to change the way cancer cells die so that it activates the immune system and helps to fight the tumour cells more effectively. Their work uncovering how breast cancer cells escape death may help to develop new strategies for cancer therapies.

Image: Picture of the winning team from the ICR and The Royal Marsden. Credit:soora.co.uk

The ICR and The Royal Marsden have a close partnership that goes back many decades, which has been particularly productive for breast cancer research. Professor Johnston said, We are a close-knit team and have worked together for over 20 years. The regular dialogue between the basic scientists who are studying the biology of the disease and clinician scientists who are translating that into better treatments for patients facilitates easy transfer of knowledge. Our collaboration advances our understanding of breast cancer and also enables clinical trials to be set up relatively seamlessly.

Professor Lord also emphasised the unique partnership between the two organisations saying, Our close collaboration means any potential opportunity to translate is not lost. This ultimately means we can get new cancer treatments out to patients quickly.

Breast Cancer Now and Cancer Research UKfunded much of the teams research at the ICR. Professor Isacke said: The partnership between the ICR and The Royal Marsden really provides the best environment to do cancer research. Its a huge credit to the Breast Cancer Now charity, which set up a dedicated research centreat the ICR and created the space for us to do our research. They have continued to fund our research and support us all these years.

Speaking about the Team Science Award, Professor Tutt said, Its an amazing honour to receive this award. The AACR is one of the worlds biggest and most prestigious cancer research organisations and for them to have recognised a UK based team for the work weve done in breast cancer is a massive achievement.

Its unusual for this to be awarded to a team outside of the US. For us to have been that team, in fact for the second time now for the ICR, is a testament to what the ICR and its clinical partners at the Royal Marsden can achieve. We want to make fundamental discoveries that improve the outlook for our patients with breast cancer, and to be recognised for that, I think is as good as it gets.

He stressed, Each named member is a figurehead for a wider team who have been involved in the work, so this victory is shared by many.

Professor Lord agreed, It really does take an entire army of people to deliver all of that work. The AACR Team Science Award neatly illustrates that if you want to achieve things that make a real difference to people who actually have cancer, it needs a multidisciplinary team and involves an enormous amount of teamwork.

The winners of the AACR Team Science Award are Professor Alan Ashworth, Professor Judith Bliss, Professor Mitch Dowsett, Professor Clare Isacke, Professor Stephen Johnston, Professor Chris Lord, Professor Pascal Meier, Dr Alistair Ring, Professor Ian Smith, Professor Nick Turner, Professor Andrew Tutt, and Professor John Yarnold.

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From bench to bedside and beyond: the team of scientists that transformed breast cancer treatment - The Institute of Cancer Research

Authorities said an arsonist likely burned down Knoxville's Planned Parenthood clinic on New Year's Eve in Dec. 2021.

KNOXVILLE, Tenn. It has been around 4 months since a Planned Parenthood medical clinic in East Knoxville was likely set on fire by an arsonist, according to the Knoxville Fire Department. It burned down on the morning of New Year's Eve in December 2021.

Leaders of the Planned Parenthood of Tennessee and North Mississippi branch said they planned to rebuild the clinic and welcome patients once again.

We will rebuild at our Cherry Street location," said Aimee Lewis, the vice president of external affairs. "We expect the design phase, which we are currently in, to take approximately 6 months and construction to take a year. While we work with our architects, builders and insurance to make this happen, we are exploring options to provide in-person services in some capacity in the meantime."

She said they are continuing to offer limited telehealth options and referrals for patients while trying to expand healthcare options by hiring more providers and staff.

In 2021, the clinic served almost 4,000 patients. More than 2,400 went to the medical facility for birth control and to test for sexually-transmitted diseases, while another 712 sought gender-affirming hormone therapy. Officials said 815 were there for abortion treatments.

The clinic had posted before burning down that it was closed for renovation "to enhance and expand our patient services."

Officials previously said they expected it would cost around $2.2 million to rebuild, in addition to the $2.2 million they had already spent on the renovation project the center burned down.

Recently, MacKenzie Scott donated a historic $275 million to support Planned Parenthood at the national level.

Regarding MacKenzie Scotts incredible generosity, Planned Parenthood of Tennessee and North Mississippi did not receive a donation," said Lewis. "However, this gift is a testament to the very strong health care network that the Planned Parenthood federation and its affiliates provide for its patients all over the country. Were excited to see what Ms. Scotts investment in our sister affiliates will do to bring care and education to the patients they serve.

Anyone with information about the arsonist or arsonists involved in the Knoxville branch's fire should reach out to KFD at 1-800-762-3017 or email them at KFDArson@Knoxvilletn.gov. They previously offered a reward of up to $10,000 for information.

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'We will rebuild' | Knoxville Planned Parenthood leader expects year-and-a-half of work to reopen clinic - WBIR.com

CULTURAL INDOCTRINATION WAR.Recently, leftist activists and their allies in the media had a big success labeling a bill passed by the Florida Legislature as the "Don't Say Gay" bill. They claimed, without evidence, that the Republican-sponsored bill would ban the mention of homosexuality in Florida schools. In fact, the bill, now signed into law by Gov. Ron DeSantis, prohibited "classroom instruction" on "sexual orientation or gender identity" by teachers or other adults in kindergarten through third grade. It also said such instruction after third grade must be "age-appropriate" or "developmentally appropriate." In other words, it specifically allowed classroom instruction on such matters after third grade. Nevertheless, LGBTQIA+ activists called the bill "Don't Say Gay." Many media outlets and commentators picked it up immediately.

Now, just a month later, the same alliance is at it again. The Alabama Legislature has passed a bill banning hormone treatment, puberty blockers, and surgery for minors who say they want to change their gender. "Minors, and often their parents, are unable to comprehend and fully appreciate the risk and life implications, including permanent sterility, that result from the use of puberty blockers, cross-sex hormones, and surgical procedures," the Republican-sponsored bill says. "For these reasons, the decision to pursue a course of hormonal and surgical interventions to address a discordance between the individual's sex and sense of identity should not be presented to or determined for minors who are incapable of comprehending the negative implications and life-course difficulties attending to these interventions." A "minor," for the purposes of this measure, is defined in Alabama law as "a person who is under 19 years of age."

So the law bans certain drastic treatments and procedures for children 18 and under. And this is the headline of the New York Times story reporting it: "Alabama Lawmakers Approve Ban on Medical Care for Transgender Youth."

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A ban on medical care? If a "transgender youth," that is, 18 or under, breaks his or her leg or catches pneumonia or is diagnosed with cancer is that person denied medical care under the new law? Would it be illegal for a doctor to treat them? Obviously not. And is there a consensus that puberty blockers, hormone treatments, amputations, and other surgeries, irreversible actions, are appropriate "medical care" for young people age 18 and under? Those are questions raised by the New York Times headline.

NPR took a slightly different route, headlining its story "Alabama Legislature votes to ban gender-affirming medical care for transgender youth." The phrase "gender-affirming" has entered wide use quite recently and is a euphemism for medical procedures not to affirm but to change one's gender. For example, this explainer from the Mayo Clinic mentions "gender affirming genital surgical procedures, such as penile inversion vaginoplasty." For its part, the New York Times article describes the Alabama law as the criminalization of "gender-affirming surgeries."

The Biden White House is fully on board. On Thursday, press secretary Jen Psaki said, "To be clear, every major medical association agrees that gender-affirming healthcare for transgender kids is a best practice and potentially lifesaving." The Alabama law, Psaki continued, "would target trans youth with tactics that threaten to put pediatricians in prison if they provide medically necessary, lifesaving healthcare."

On March 31, the Biden administration released a statement celebrating what is called the "Transgender Day of Visibility." The statement used the word "affirm" or "affirming" 29 times. Some examples: The administration pledged to strengthen federal measures to "protect transgender youth against discrimination, including when those youth seek gender-affirming care." It pledged to emphasize "the positive impact of gender-affirming care on youth mental health." It pledged to confirm that "providing gender-affirming care is neither child maltreatment nor malpractice." It pledged to create an information bank to show why "gender-affirming care ... is important to transgender, nonbinary, and other gender expansive young people's well-being." It pledged to use the Justice Department to knock down laws like Alabama's by "reaffirming that transgender children have the right to access gender-affirming health care."

And so on. You get the idea. Not surprisingly, the phrase "gender-affirming" and its variants are showing up more and more in the media discussion of puberty blockers, hormone treatments, and surgery. Such measures are also benignly described as "medical care." And who could be against medical care? Who could respond negatively to a positive word like "affirming?"

Just like the "Don't Say Gay" situation, supporters of the Florida bill and now the Alabama bill, and other bills like them around the country, face a battle of language as well as substance. And with the current administration, the activist world, and much of the media arrayed against them, it is an uphill battle.

For a deeper dive into many of the topics covered in the Daily Memo, please listen to my podcast, The Byron York Show available on the Ricochet Audio Network and everywhere else podcasts can be found. You can use this link to subscribe.

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Cultural indoctrination war - Washington Examiner

Amryt Pharma plc

Amryt Announces Positive Long-Term Safety and Efficacy Data for Mycapssa (oral octreotide) from the 2nd Year of OPTIMAL Open Label Extension Study in Acromegaly Patients

Acromegaly patients were exposed to Mycapssa during the OPTIMAL Phase 3 Trial, including its open label extension (OLE), for a maximum treatment duration of 3.2 years

Study demonstrated that 100% of evaluable patients who entered the 2nd year OLE phase of the study as responders - insulin-like growth factor 1 (IGF-1) within normal limits - maintained their long-term biochemical response at the end of the study

IGF-1 levels were stably maintained within normal limits at the end of the OLE period (mean IGF-1 levels at baseline and at the end of the OLE were 0.92 and 0.84 respectively)

Growth hormone (GH) levels also improved at the end of the OLE period (mean GH levels at baseline and at the end of the OLE were 0.79 and 0.45 respectively)

Long-term safety profile of Mycapssa during the OLE was consistent with that observed in prior studies

DUBLIN, Ireland, and Boston MA, April 13, 2022, Amryt (Nasdaq: AMYT), a global, commercial-stage biopharmaceutical company dedicated to acquiring, developing and commercializing novel treatments for rare diseases, today presents long-term safety and efficacy data from the 2nd year open-label extension (OLE) of its global Phase 3 OPTIMAL clinical trial that compared Mycapssa (octreotide capsules) to placebo for maintenance of biochemical response in patients with acromegaly. The OPTIMAL trial supported the approval of Mycapssa in the United States for long-term maintenance treatment in acromegaly patients who have responded to and tolerated treatment with injectable octreotide or lanreotide.

Susan L Samson, MD, PhD, at Mayo Clinic (Jacksonville, Florida), and lead investigator of the OPTIMAL study commented: These data together with the recently published positive results from the 3 years OLE period of the MPOWERED Phase 3 study further supports the long-term safety and efficacy of Mycapssa (oral octreotide) in acromegaly patients who were previously biochemically controlled on monthly injectable Somatostatin Receptor Ligands (iSRLs). The data showing that 100% of responders (IGF-1 within normal limits) maintained their response at the end of the 2nd year of the OLE, confirming the durability of response over time.

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Dr. Mark Sumeray, Chief Medical Officer of Amryt, commented: The OPTIMAL 2nd year OLE data show that acromegaly patients who were switched from iSRLs to Mycapssa may benefit from a daily oral treatment based on maintenance of long-term biochemical response.

OPTIMAL Phase 3 Trial Open-Label Long-Term Safety & Efficacy Data40 patients that completed the 9 months double-blind placebo controlled (DPC) core treatment phase elected to continue treatment with Mycapssa in the OPTIMAL open label extension study (20 patients that were originally randomized to Mycapssa and 20 that were randomized to placebo). Results from the first year were published previously and demonstrated that all patients who responded to Mycapssa (IGF-1 within normal limits) during the DPC period and enrolled in the OLE (n=14) completed the 48-week period and 93% (13/14) maintained their IGF-1 response within the normal limit at the end of this period. 32 patients continued treatment into the 2nd year of the OLE (18 of those originally randomized to Mycapssa during the DPC and 14 of those randomized to placebo).

Key 2nd year study outcomes included:

31 out of 32 patients (97%) of those enrolled to the 2nd year of the OLE completed 96 weeks in the OLE period

100% of evaluable patients, who entered the 2nd year OLE phase of the study as responders (IGF-1 within normal limits; N=17), maintained their long-term biochemical response at the end of the study. The average IGF-1 levels of enrolled patients were stably maintained within the normal limits at the end of the OLE period (mean IGF-1 levels at baseline OLE and at the end of the OLE were 0.92 and 0.84 respectively).

93% of all patients who entered the 2nd year OLE phase (N=32) were responders at the end of the 96 weeks OLE

The average GH levels of enrolled patients improved at the end of the OLE period (mean GH levels at baseline OLE and at the end of the OLE were 0.79 and 0.45 respectively)

Acromegaly patients were exposed to Mycapssa during the OPTIMAL study (including its OLE phase), for a median treatment duration of 2.1 years and a maximal exposure of 3.2 years

Patients in the OLE demonstrated a median compliance rate of 98% over this period of time

The long-term safety profile of Mycapssa during the OLE, was consistent with the safety profile observed during previous studies with Mycapssa with no new safety signals with long-term exposure

About the OPTIMAL Phase 3 TrialThe OPTIMAL trial (NCT03252353) was a randomized, double-blind, placebo-controlled, nine-month Phase 3 clinical trial of octreotide capsules in 56 adult acromegaly patients whose disease was biochemically controlled by injectable somatostatin analogs (octreotide or lanreotide). Patients were randomized on a 1:1 basis, to octreotide capsules or placebo. The primary endpoint of the trial was the proportion of patients who maintained their biochemical response (IGF-1 levels 1.0 ULN), at the end of the nine-month, double-blind, placebo-controlled period. Hierarchical secondary endpoints included: (i) proportion of patients who maintain GH response at 9 months; (ii) time to loss of response; and (iii) proportion of patients requiring reversion to prior treatment. The OPTIMAL study met the primary endpoint and all secondary endpoints which led to the US approval of Mycapssa, the first oral somatostatin analog, for the long-term maintenance treatment in acromegaly patients who have responded to and tolerated treatment with injectable octreotide or lanreotide.

FDA APPROVED INDICATION AND USAGEMycapssa delayed-release capsules, for oral use, is a somatostatin analog indicated for long-term maintenance treatment in acromegaly patients who have responded to and tolerated treatment with octreotide or lanreotide.

IMPORTANT SAFETY INFORMATIONWARNINGS AND PRECAUTIONSMycapssa can cause problems with the gallbladder. Monitor patients periodically. Discontinue if complications of cholelithiasis are suspected. Blood sugar, thyroid levels, and vitamin B12 levels should be monitored and treated accordingly. Bradycardia, arrhythmia, or conduction abnormalities may occur. Treatment with drugs that have bradycardia effects may need to be adjusted.

The full US Prescribing Information for Mycapssa is available at http://www.mycapssa.com.

About AcromegalyAcromegaly typically develops when a benign tumor of the pituitary gland produces too much growth hormone, ultimately leading to significant health problems. Common features of acromegaly are facial changes, intense headaches, joint pain, impaired vision and enlargement of the hands, feet, tongue and internal organs. Serious health conditions associated with the progression of acromegaly include type 2 diabetes, hypertension, respiratory disorders and cardiac and cerebrovascular disease. Amryt estimates that approximately 8,000 adult acromegaly patients are chronically treated with somatostatin analog injections in the United States.

About Amryt Amryt is a global commercial-stage biopharmaceutical company focused on acquiring, developing and commercializing innovative treatments to help improve the lives of patients with rare and orphan diseases. Amryt comprises a strong and growing portfolio of commercial and development assets.

Amryts commercial business comprises three orphan disease products metreleptin (Myalept/ Myalepta); oral octreotide (Mycapssa); and lomitapide (Juxtapid/ Lojuxta).

Myalept/Myalepta (metreleptin) is approved in the US (under the trade name Myalept) as an adjunct to diet as replacement therapy to treat the complications of leptin deficiency in patients with congenital or acquired generalized lipodystrophy (GL) and in the EU (under the trade name Myalepta) as an adjunct to diet for the treatment of leptin deficiency in patients with congenital or acquired GL in adults and children two years of age and above and familial or acquired partial lipodystrophy (PL) in adults and children 12 years of age and above for whom standard treatments have failed to achieve adequate metabolic control. For additional information, please follow this link.

Mycapssa (octreotide capsules) is approved in the US for long-term maintenance therapy in acromegaly patients who have responded to and tolerated treatment with octreotide or lanreotide. Mycapssa is the first and only oral somatostatin analog approved by the FDA. Mycapssa has also been submitted to the EMA and is not yet approved in Europe. For additional information, please follow this link.

Juxtapid/Lojuxta (lomitapide) is approved as an adjunct to a low-fat diet and other lipid-lowering medicinal products for adults with the rare cholesterol disorder, Homozygous Familial Hypercholesterolaemia ("HoFH") in the US, Canada, Colombia, Argentina and Japan (under the trade name Juxtapid) and in the EU, Israel, Saudi Arabia and Brazil (under the trade name Lojuxta). For additional information, please follow this link.

Amryt's lead development candidate, Oleogel-S10 is a potential treatment for the cutaneous manifestations of Junctional and Dystrophic Epidermolysis Bullosa (EB), a rare and distressing genetic skin disorder affecting young children and adults for which there is currently no approved treatment. Filsuvez has been selected as the brand name for Oleogel-S10. The product does not currently have regulatory approval to treat EB.

Amryts pre-clinical gene therapy candidate, AP103, offers a potential treatment for patients with Dystrophic EB, and the polymer-based delivery platform has the potential to be developed for the treatment of other genetic disorders.

Amryt also intends to develop oral medications that are currently only available as injectable therapies through its Transient Permeability Enhancer (TPE) technology platform. For more information on Amryt, including products, please visit http://www.amrytpharma.com.

Forward-Looking StatementsThis announcement may contain forward-looking statements and the words "expect", "anticipate", "intends", "plan", "estimate", "aim", "forecast", "project" and similar expressions (or their negative) identify certain of these forward-looking statements. The forward-looking statements in this announcement are based on numerous assumptions and Amryt's present and future business strategies and the environment in which Amryt expects to operate in the future. Forward-looking statements involve inherent known and unknown risks, uncertainties and contingencies because they relate to events and depend on circumstances that may or may not occur in the future and may cause the actual results, performance or achievements to be materially different from those expressed or implied by such forward-looking statements. These statements are not guarantees of future performance or the ability to identify and consummate investments. Many of these risks and uncertainties relate to factors that are beyond Amryt's ability to control or estimate precisely, such as future market conditions, the course of the COVID-19 pandemic, currency fluctuations, the behaviour of other market participants, the outcome of clinical trials, the actions of regulators and other factors such as Amryt's ability to obtain financing, changes in the political, social and regulatory framework in which Amryt operates or in economic, technological or consumer trends or conditions. Past performance should not be taken as an indication or guarantee of future results, and no representation or warranty, express or implied, is made regarding future performance. No person is under any obligation to update or keep current the information contained in this announcement or to provide the recipient of it with access to any additional relevant information that may arise in connection with it. Such forward-looking statements reflect the Companys current beliefs and assumptions and are based on information currently available to management.

ContactsJoe Wiley, CEO / Rory Nealon, CFO/COO, +353 (1) 518 0200, ir@amrytpharma.comTim McCarthy, LifeSci Advisors, LLC, +1 (212) 915 2564, tim@lifesciadvisors.com

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Amryt Announces Positive Long-Term Safety and Efficacy Data for Mycapssa (oral octreotide) from the 2nd Year of OPTIMAL Open Label Extension Study in...