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Study finds THC rises in hemp due to genetics, not growing conditions – New Food

February 3rd, 2020 4:41 pm

Researchers from Cornell University studied hemp from two sites to determine whether the difference in growing conditions affected THC levels.

As the hemp industry grows, producers face the risk of cultivating a crop that can become unusable and illegal if it develops too much of the psychoactive chemical THC, according to researchers from Cornell University. The researchers have determined that a hemp plants propensity to go hot become too high in THC is determined by genetics, not as a stress response to growing conditions, which is said to be contrary to popular belief.

[People thought] there was something about how the farmer grew the plant something about the soil, the weather getting too hot, or drought, said Larry Smart, Horticulture Professor and senior author of the study, but our evidence from this paper is that fields go hot because of genetics, not because of environmental conditions.

Smart and his team conducted field trials at two sites, studying the genetics and chemistry of 217 hemp plants. They found that differences in growing conditions between the sites had no significant influence on which chemicals the plants produced. But when they compared the CBD (cannabidiol) and THC levels of each of the plants against their genomes, they found very high correlation between their genetics and the chemicals they produced.

Jacob Toth, first author of the paper and a doctoral student in Smarts lab, developed a molecular diagnostic to demonstrate that the hemp plants in the study fell into one of three genetic categories: plants with two THC-producing genes; plants with two CBD-producing genes; or plants with one gene each for CBD and THC.

To minimise the risk of plants going hot, hemp growers ideally want plants with two CBD-producing genes, the researchers explained.

While conducting the research, the team also discovered that as many as two-thirds of the seeds they obtained of one hemp variety which were all supposed to be low-THC hemp produced THC above legal limits.

The researchers explained that they hope their work will help address this problem by providing breeders with easy-to-use genetic markers that can be utilised much earlier on seedlings and both sexes of plants.

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Human Genetics Market 2020 Projections, SWOT Analysis, Size and Forecast by 2026 | QIAGEN, Agilent Technologies, Thermo Fisher Scientific – Jewish…

February 3rd, 2020 4:41 pm

Global Human Genetics market 2020 in depth research by industry competitive landscape, size, growth rate, strategy, trends and forecast 2026.

The report on the global Human Genetics market is just the resource that players need to strengthen their overall growth and establish a strong position in their business. It is a compilation of detailed, accurate research studies that provide in-depth analysis on critical subjects of the global Human Genetics market such as consumption, revenue, sales, production, trends, opportunities, geographic expansion, competition, segmentation, growth drivers, and challenges.

Get the Sample of this [emailprotected]https://www.qyresearch.com/sample-form/form/1494807/global-human-genetics-market

As part of geographic analysis of the global Human Genetics market, the report digs deep into the growth of key regions and countries, including but not limited to North America, the US, Europe, the UK, Germany, France, Asia Pacific, China, and the MEA. All of the geographies are comprehensively studied on the basis of share, consumption, production, future growth potential, CAGR, and many other parameters.

Market Segments Covered:

The key players covered in this studyQIAGENAgilent TechnologiesThermo Fisher ScientificIlluminaPromegaLabCorpGE

Market segment by Type, the product can be split intoCytogeneticsPrenatal GeneticsMolecular GeneticsSymptom Genetics

Market segment by Application, split intoResearch CenterHospitalForensic Laboratories

Regions Covered in the Global Human Genetics Market:

The Middle East and Africa (GCC Countries and Egypt) North America (the United States, Mexico, and Canada) South America (Brazil etc.) Europe (Turkey, Germany, Russia UK, Italy, France, etc.) Asia-Pacific (Vietnam, China, Malaysia, Japan, Philippines, Korea, Thailand, India, Indonesia, and Australia)

Highlights of the Report Accurate market size and CAGR forecasts for the period 2019-2025 Identification and in-depth assessment of growth opportunities in key segments and regions Detailed company profiling of top players of the global Human Genetics market Exhaustive research on innovation and other trends of the global Human Genetics market Reliable industry value chain and supply chain analysis Comprehensive analysis of important growth drivers, restraints, challenges, and growth prospects

The scope of the Report:

The report offers a complete company profiling of leading players competing in the global Human Genetics market with high focus on share, gross margin, net profit, sales, product portfolio, new applications, recent developments, and several other factors. It also throws light on the vendor landscape to help players become aware of future competitive changes in the global Human Genetics market.

Get Customized Report in your Inbox within 24 hours @https://www.qyresearch.com/customize-request/form/1494807/global-human-genetics-market

Strategic Points Covered in TOC:

Chapter 1: Introduction, market driving force product scope, market risk, market overview, and market opportunities of the global Human Genetics market

Chapter 2: Evaluating the leading manufacturers of the global Human Genetics market which consists of its revenue, sales, and price of the products

Chapter 3: Displaying the competitive nature among key manufacturers, with market share, revenue, and sales

Chapter 4: Presenting global Human Genetics market by regions, market share and with revenue and sales for the projected period

Chapter 5, 6, 7, 8 and 9 : To evaluate the market by segments, by countries and by manufacturers with revenue share and sales by key countries in these various regions

About Us:QYResearch always pursuits high product quality with the belief that quality is the soul of business. Through years of effort and supports from huge number of customer supports, QYResearch consulting group has accumulated creative design methods on many high-quality markets investigation and research team with rich experience. Today, QYResearch has become the brand of quality assurance in consulting industry.

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Don’t believe the conspiracy theories you hear about coronavirus and HIV – Massive Science

February 3rd, 2020 4:41 pm

The 2019 novel coronavirus (2019-nCoV) outbreak has sparked a speedy response, with scientists, physicians, and front-line healthcare professionals analyzing data in real-time in order to share findings and call out misinformation. Today, The Lancet published two new peer-reviewed studies: one which found that the new coronavirus is genetically distinct from human SARS and MERS, related viruses which caused their own outbreaks, and a second which reports clinical observations of 99 individuals with 2019-nCoV.

The first cases of the coronavirus outbreak were reported in late December 2019. In this new study, Nanshan Chen and colleagues analyzed available clinical, demographic, and laboratory data for 99 confirmed coronavirus cases at the Wuhan Jinyintan Hospital between Jan 1 to Jan 20, 2020, with clinical outcomes followed until 25th January.

Chen and colleagues reported that the average age of the 99 individuals with 2019-nCoV is around 55.5 years, where 51 have additional chronic conditions, including cardiovascular and cerebrovascular (blood flow to the brain) diseases. Clinical features of the 2019-nCoV include a fever, cough, shortness of breath, headaches, and a sore throat. 17 individuals went on to develop acute respiratory distress syndrome, resulting in death by multiple organ failure in 11 individuals. However, it is important to note here that most of the 2019-nCoV cases were treated with antivirals (75 individuals), antibiotics (70) and oxygen therapy (75), with promising prognoses, where 31 individuals were discharged as of 25th January.

Based on this sample, the study suggests that the 2019 coronavirus is more likely to affect older men already living with chronic conditions but as this study only includes 99 individuals with confirmed cases, it may not present a complete picture of the outbreak. As of right now, there are over 6,000 confirmed coronavirus cases reported, where a total of 126 individuals have recovered, and 133 have died.

In a second Lancet study, Roujian Lu and their fellow colleagues carried out DNA sequencing on samples, obtained from either a throat swab or bronchoalveolar lavage fluids, from eight individuals who had visited the Huanan seafood market in Wuhan, China, and one individual who stayed in a hotel near the market. Upon sequencing the coronaviruss genome, the researchers carried out phylogenetic analysis to narrow down the viruss likely evolutionary origin, and homology modelling to explore the virus receptor-binding properties.

Lu and their fellow colleagues found that the 2019-nCoV genome sequences obtained from the nine patients were very similar (>99.98% similarity). Upon comparing the genome to other coronaviruses (like SARS), the researchers found that the 2019-nCoV is more closely related (~87% similarity) to two bat-derived SARS-like coronaviruses, but does not have as high genetic similarity to known human-infecting coronaviruses, including the SARS-CoV (~79%) orMiddle Eastern Respiratory Syndrome (MERS) CoV (~50%).

The study also found that the 2019-nCoV has a similar receptor-binding structure like that of SARS-CoV, though there are small differences in certain areas. This suggests that like the SARS-CoV, the 2019-nCoV may use the same receptor (called ACE2) to enter cells, though confirmation is still needed.

Finally, phylogenetic analysis found that the 2019-nCoV belongs to the Betacoronavirus family the same category that bat-derived coronaviruses fall into suggesting that bats may indeed be the 2019-nCoV reservoir. However, the researchers note that most bat species are hibernating in late December, and that no bats were being sold at the Huanan seafood market, suggesting that while bats may be the initial host, there may have been a secondary animal species which transmitted the 2019-nCoV between bats and humans.

Its clear that we can expect new findings from the research community in the coming days as scientists attempt to narrow down the source of the 2019-nCoV.

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Bent into shape: The rules of tree form – Knowable Magazine

February 3rd, 2020 4:41 pm

Theres a place in West Virginia where trees grow upside-down. Branches sprout from their trunks in the ordinary fashion, but then they do an about-face, curving toward the soil. On a chilly December day, the confused trees bare branches bob and weave in the breeze like slender snakes straining to touch the ground.

Its really kind of mind-boggling, says plant molecular biologist Chris Dardick, waving toward the bizarro plum trees. Theyre completely messed up.

Im visiting an orchard at the Appalachian Fruit Research Station, an outpost of the US Department of Agriculture nestled in the sleepy Shenandoah Valley. Here, at Dardicks workplace, the disoriented plums are but one in an orchard of oddities, their outlines, seasonally stripped of leaves, standing out in stark relief.

There are trees with branches that shoot straight up, standing to attention in disciplined rows, with nary a sideways branch. There are trees with branches that elegantly arch, like woody umbrellas; others with appendages that lazily wander this way and that.

Dwarf trees crouch, sporting ball-like crowns akin to Truffula trees. Compact trees poke from the ground in clumps of scraggly, knee-high sticks. Apple trees with some hidden predicaments grow in a greenhouse nearby: Their roots reach sideways rather than down. The topsy-turvy growth of all of these trees comes from genetic variations that cause the dialing up, dialing down or elimination altogether of the activity of key genes controlling plant architecture.

Understanding these misfits has real-world applications: It could help grow the next generation of orchards that, densely packed with trees, produce more fruit while using less land and labor than today. But Dardick is also trying to answer a fundamental question: How do different trees get their distinctive shapes? From the towering spires of spruce and fir, the massive spreading limbs of an oak to the stately arching canopies of an elm, the skeletal shapes of trees offer signature silhouettes.

Dardicks work and that of other researchers also could help to explain how the shapes of individual trees are far from fixed. Trees, much more than we can, will morph in response to their literal neck of the woods. Limbs in the shade reach toward spots of sunlight. Trees on windswept hills bend trunk and branches into gnarled architectures.

The familiar shape of a regular plum tree (left) is transformed by dialing down the activity of certain plant architecture genes, leading to plums with erect branches that shoot straight up (middle) or plums with branches that cascade downward (right).

CREDIT: C. HOLLENDER (LEFT), C. DARDICK (CENTER AND RIGHT)

Work by breeders, biologists and botanists have revealed sizable pockets of knowledge about the hormones, genes and processes that yield the diverse shapes of trees and other plants, between species and within species. It has not been easy: Two of trees most appealing attributes their long lives and large sizes make them intractable research subjects.

But as scientists pursue these questions, commonalities are emerging between vastly different species. The puzzle of shape diversity and adaptability turns out to be tied to the fundamentals of being a plant: grappling with gravity, fighting for sunlight, all while anchored in one place for a lifetime.

Plants are stuck. The best they can do is grow toward something, says Courtney Hollender, a former postdoc of Dardicks who now runs her own lab in the Department of Horticulture at Michigan State University in East Lansing. Thats all theyve got; they cant run, they have to adapt to their environment. And theyve developed brilliant ways to do it.

Scientists have a word for the ability to adapt so readily: plasticity. In plants, this feature is both obvious and astounding. Most animals are born in specific shapes then just grow larger, but plants are modular they grow in various iterations of two building blocks: shoots and roots.

It is the first of these where and when a shoot grows or doesnt grow that governs the basic form a tree takes.

Some aspects are hardwired. Leaves emerge in a pattern that is usually fixed throughout the trees life, with structural arrangements that tend to be shared by members of a given plant family. And shoots emerge where leaves meet the stem. So, for example, plants in the maple family, which have leaves set opposite each other, have branches in the same format. Members of the beech family have leaves, and thus branches, that alternate up the stem.

But the interplay between physiology and external forces also plays a large part. Take your standard-issue plant with a main central stem that grows upward and has few side branches. Most plants, from basil to birch, start out this way, a growth habit that probably evolved because it enables them to quickly reach the light more rapidly than the competition. Called apical dominance (the tip of the plant is the apex), this is largely under the purview of the plant hormone indole acetic acid, also known as auxin. Made in the tip, auxin diffuses downward and blocks the growth of side branches.

This is why pinching the tips off of basil or geranium makes them bushy you are removing the source of that bossy auxin, freeing buds on the stems sides from the prohibition and allowing them to grow. (Though auxin is mighty, its not the only player here. Other plant hormones, along with light intensity and access to nutrients, also wield power.)

Another related and less-understood phenomenon occurs in some tree species. Called apical control, it also is imposed by the tip of a tree and probably also by auxin. But rather than operating at the scale of a branch, it commandeers the whole dang tree.

Think of a pine. At the top, theres a pointy tip, then upper branches that tend to reach skyward. Moving down, the branches become more horizontal, growing out more than up. But unlike a basil plant, a pine tree does not become bushy when you lop off the top. Instead, a new bud near the top grows upward, becoming the new leader. Or an existing branch reorients to grow up and become the new dominant tip.

These two principles are always in the back of arborists minds as they work. They have to consider, If we cut a branch here, that bud below is going to break and well just get a branch in basically the same spot, Dardick says. All of their rules of what to prune and where are based on these physiological factors that contribute to tree shape.

Physiology also underpins the plastic responses trees have to more extreme situations they may face. A tree on a high mountain peak or windswept coast must contend with exposure to mechanical forces that could topple and kill it. To survive, such trees become short and stocky, their bent, asymmetric crowns reducing drag and presumably protecting a tree from violent gusts. The driver is the winds very touch a response now called thigmomorphogenesis that has been observed for hundreds of years.

How it works is still unclear, but over the past decade researchers have made some headway. Theyre actively studying force-sensing proteins and processes that may be involved. And recent work suggests an important role for hormones such as jasmonate, which accumulates in all kinds of plants in response to damage and mechanical stress. In experiments with a weedy mustard called Arabidopsis, plants became stunted when researchers bent their leaves back and forth twice a day.Mutants that couldnt make jasmonate, though, grew normally.

Sometimes, wind does more than gust against a tree: It blows the whole tree over, and that tree, if still rooted, must reorient the growth of its branches and buds toward the sky. Avalanches, erosion and landslides deal similar fates. And trees in all sorts of circumstances must grow around obstacles, away from competitors and toward the light. To get these jobs done, trees make a special kind of wood called reaction wood.

Trees may become contorted in challenging physical environments, such as this ridge in the Rocky Mountains. The touch of wind and other forces prompt physiological responses by the plant that yield a shorter, stockier stature, gnarled asymmetric shape and the development of specialized wood. This characteristic tree form is called a krummholz (German for crooked wood).

CREDIT: BRYCE BRADFORD / FLICKR

Hardwoods such as maple, beech, oak and poplar form this tough stuff (in this case called tension wood) on the upper side of their stems. Incredibly, it creates a tensile force thatpullsthe stem upward. If you walk around the woods, you can see that most species, if not all species, have this kind of reaction wood response, says Andrew Groover, a research geneticist with the USDA Forest Services Pacific Southwest Research Station in Davis, California.

The hardwood tree first discerns that it is off-kilter using specialized gravity-sensing cells. Where these cells reside in trees the woody stem? the tip of new shoots? was unknown until Groover and colleagues detected them in woody and soft tissues of poplar, a few years back. The cells contain organelles called statoliths that sink down in the cell and indicate to the plant that its leaning one way or the other. This, in turn, causes that influential auxin to mobilize, triggering the growth of tension wood on the top. Cellulose with a peculiar gelatinous layer is thought to act as the muscle that generates the pulling-up force.

In this experiment, young, potted poplar trees were placed sideways to investigate the plantsgravity-sensing machinery. The poplar in this time-lapse movie, taken over two weeks, responded to being tipped on its side by reorienting its growth upward. The plant hormone auxin is key to this response. Mutants that cannot respond appropriately to auxins signaling instructions do not right themselves this way. (This particular poplar also received a dose of a chemical called gibberellic acid that interacts with auxin, so that scientists could learn more about its role.)

CREDIT: ANDREW GROOVER AND SUZANNE GERTTULA, US FOREST SERVICE, PACIFIC SOUTHWEST RESEARCH STATION DAVIS CA

Much of the knowledge about the architecture of plants is rooted in millennia of human efforts to alter crop shapes to make them more suitable for cultivation, and modern science is now revealing the genetic changes that lie behind these creations. The lessons, it turns out, apply broadly across the plant kingdom, to herbaceous and woody species alike.

It is hard to overstate the importance to human history of some of these plant-shape changes, says plant molecular geneticist Jiayang Li, who details some of their genetic underpinnings in the Annual Review of Plant Biology. A classic example is the transformation of the ancestor of corn (maize) into a key staple crop for much of the world. It arose from a species of the Central American grasses called teosintes bushy plants with many branches. Domestication, among other things, abolished that branching, yielding the single-stalked upright corn we plant today.

Similarly, explains Li, who works at the Chinese Academy of Sciences Institute of Genetics and Developmental Biology, the green revolution of the 20th century ushered in compact, dwarf varieties of wheat and rice. By modifying the height and thickness of the stems of these grasses, breeders developed varieties that could carry more grain without toppling over in wind and rain.

Much of Lis own research has focused on architectural variation in rice, although the work turns out to have implications for the architecture of plants in general, from lowly mosses to towering trees. Like other grasses, rice grows shoots called tillers specialized, grain-bearing branches that emerge from the base. In cultivated rice, the angle at which these tillers grow varies widely: Some varieties are squat and wide-spreading, others have shoots that are more upright. Breeders are interested in altering tiller angle because upright plants can be grown more densely, giving farmers more bang for their acreage.

In a key advance, in 2007, a team including Li reported theyd discovered the genetic cause of the spread-out architecture trait. The scientists named the responsible gene TAC1, short for tiller angle control. A functional TAC1 gene increases rices tiller angle, leading to open, widely branching plants. Mutations in TAC1 lead to the opposite: plants with erect shoots that reach up, instead of out.

That same year, Lis team and a group in Japan both reported another major achievement: finding a long-sought gene behind a curious trait in some rice varieties that gives plant branches a scruffy, lounging look. The trait, known as lazy, had intrigued plant breeders and geneticists since the 1930s, when researchers described its extreme manifestation in corn: The lazy plants grow along the ground, following the unevenness of the surface.

In ordinary rice (left), the hormone auxin helps to tell the plant which direction is up. Auxin transport within the plant goes awry when a gene called LAZY malfunctions, leading to confused plants with sprawling branches (right).

CREDIT: B. WANG ET AL / AR PLANT BIOLOGY 2018

The cause, it turns out, was errors in a gene that normally makes branches shoot straight up. Li and his colleagues surveyed some 30,000 mutant rice plants to pin down that gene, now called LAZY (names of genes, confusingly, often refer to what happens when a gene is mutated and doesnt work, rather than when it is functioning properly). And they provided convincing evidence for an idea batted around for decades that lazy plants have muddled perceptions of gravity and that auxin is centrally involved.

A common test for whether a plants gravity-perception machinery is working is to lay the plant on its side. If it knows up from down, it wont continue to grow sideways, but will start to grow up again, akin to the reaction-wood response of a toppled trees branches. An important step in this reorienting involves auxin pooling on the bottom side of the shoot. But in lazy mutants, proteins that help ferry auxin around the plant are malfunctioning, so instead of shoots growing in the correct direction, theyre prone to casually sprawl about.

Scientists now know that LAZY genes come in multiple versions. Some appear to operate in plant roots, telling them which way is down, probably using similar, auxin-related signals. If those genes are absent or inactive, confused roots grow upward. And though the genes were first found in monocots, a branch of the plant kingdom including rice and corn, researchers now know that LAZY genes exist in numerous plants, including the plums growing in the fruit research station in West Virginia.

A lazy mutant of corn (left) compared with normal corn (right). Such corn mutants were described nearly 100 years ago, but it took 21st century molecular biology to nail down the growth habitscause: genetic malfunctions that meddle with responses to gravity.

CREDIT: T.P. HOWARD III ET AL / PLOS ONE 2014

As our boots crunch along the uneven ground, Dardick points at an errant orchard cat watching our tree tour from a distance. One row of trees stands so upright that a fencepost at the end of it is enough to block the row from view. These regimented trees are pillar peaches, and they are favorites of landscapers (one reason: its easy to get around them with a lawnmower). They also were key to uncovering genes like LAZY and TAC1 at the Shenandoah Valley station.

By comparing ordinary peaches to pillar peaches, and drawing on decades of work by former lead scientist Ralph Scorza, a team of station scientists and others in the US and Germany discovered the cause of the pillar trait: mutations in the peach version of TAC1.

Many of the strange plant architectures under investigation existed as naturally occurring varieties that were developed by breeders for ornamental gardens or orchards; only recently have the genes underlying these forms been identified. Its now known that the upright growth habit of the pillar peach (center), available commercially under the nameCrimson Rocket,results from mutations in a gene that helps plants branch outward.

CREDIT: C. DARDICK

The team also found that LAZY was at work in many of their misfits. Just as with the corn plants described nearly 100 years ago, mutations in LAZY made plums grow topsy-turvy, their branches seeking the soil. Apple trees with LAZY mutations have similarly disoriented roots. And when multiple copies of LAZY genes malfunction in the weed Arabidopsis, its roots grow up, its shoots down.

In the last decade, researchers have found that TAC1 influences branch angle in plums, poplar trees, the grass Miscanthus and Arabidopsis, and it appears to affect leaf angle in corn. But LAZY genes have even deeper roots. Theyre found in all manner of plants, including the evolutionarily older Loblolly pine and even more ancient mosses.

This finding suggests a very old role for LAZY: It may have allowed plants to grow up, literally, when they first colonized land. Plants got their start in water. There, rootless and leafless, they were buoyed, unconcerned with gravity. The transition to land spurred the development of proper roots and stems, and plants then had to figure out up from down. LAZY seems to have allowed plants to orient their above-ground growth away from gravity and up toward the sun.

Scientists think that TAC1 evolved somewhat later, providing a counterpoint to LAZY ensuring that branches dont only grow straight up, but also reach out. Together, these genes laid critical groundwork for the diversity of plant forms we see today, all seeking sustenance in their own ways.

Once you start to grow up as a vascular plant, you need to maximize your resources, you need to capture as much sun as possible, says Hollender, who has been working on yet another gene, called WEEP, that when nonfunctional lends plants a weeping, waterfall-like structure seen here and there in trees of ornamental gardens. (But its probably not responsible for the shape of weeping willow trees.) Modifying your shoot angles is an important adaptive trait for plants that allows them to capture light. Its essential for them to survive.

This kind of research has broad economic implications. Fruit and nut trees bring $25 billion annually in the US alone and there are hefty costs associated with pruning, bending and tying branches; spraying hormones; and the manual labor of picking fruit from an unruly cacophony of limbs. Understanding the genetic controls behind tree architecture could help scientists breed trees that make the whole fruit-farming enterprise more efficient and environmentally friendly.

Orchard systems are not the most sustainable in the world, Dardick says. The idea is, if we can modify tree architecture, if we could reduce their size and limit the amount of area they take up, then we could plant them at higher density and potentially increase their sustainability.

And there may be odder outcomes than friendlier outdoor orchards: In collaboration with NASA, the USDA team is investigating genetic tweaks that might even help bring fruit to space. On that December day, Dardick takes me to a greenhouse tucked in a corner of the lab. In it are plum and apple trees whose shape is so transformed that they look more like the love children of shrubs and vines. This strange growth habit is a side-effect of efforts to breed plants that flower and make fruit sooner and then do so continuously, rather than flowering after growing for several years, and then only in the spring.

The genetic tweaks that sent the trees developmental program into overdrive have also transformed their architecture. In the greenhouse, these precocious trees sprawl, draping lazily along wire trellises, happily flowering and heavy with fruit. Theyre growing almost like tomatoes, Dardick says. So were broaching the concept of, can we bring an orchard indoors?

The strange, vine-like growth of this plum results when a gene controlling the timing of flower development malfunctions. Such unusually shapedtrees may facilitate indoororchards that produce fruit many months of the year.

CREDIT: C. SRINIVASAN

Those ambitions aside, Dardick has his hands full trying to answer numerous basic-science questions about how trees do what they do. Researchers still dont know how different tree species set the angles of their branches going wide like an oak, or arching like an elm. They dont know how trees alter those angles during the course of mature growth, as branches sprout from branches sprouted from branches, until some of them finally point down. Trees are both kindred and foreign to us, their various forms so familiar, but their architectural rules still in so many ways opaque.

I find myself looking at trees all the time now in a new way; they fill space so beautifully and efficiently, Dardick says. They are the biggest organism we have thats visible, thats in our face all the time. But theres so much we dont know.

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Viral epidemics, public health and universal vaccine against influenza, in international conference Viruses2020 – Mirage News

February 3rd, 2020 4:41 pm

This international conference will gather more than two hundred participants.

Professor Albert Bosch, from the Faculty of Biology of the UB, and the expert Eric O. Freed from the National Cancer Institute (United States).

The Long Road to a Universal Influenza Virus Vaccine is the title of the master conference to be given by the expert Peter Palese, from the School of Medicine at Mount Sinai (United States), in the opening ceremony for the conference Viruses2020 to take place on Wednesday, February 5, at 9 a.m. This international conference will gather more than two hundred participants and is promoted by a committee presided by Professor Albert Bosch, from the Department of Genetics, Microbiology and Statistics of the Faculty of Biology of the UB, and the expert Eric O. Freed from the National Cancer Institute (United States).

During his speech, Peter Palese will talk about the most recent studies on a protein from the surface of influenza hemagglutinin which could lead to the development of a vaccine against influenza, a viral infection that can create annual epidemics with about five million affected people and more than 600,000 deaths worldwide.

As part of this forum, which will take place from February 5 to 7 in the headquarters of Axa auditorium, the experts will show the latest advances in viral pathogenesis, innate immunity, viral replication and the evolution of viruses, among other content. In the 21st Century world, the challenge is to be always ready for the challenges that can come up regarding globalization and climate change, which contribute to the emergence of viral infections, notes Alfred Bosch, president of the Spanish Society of Virology (SEV).

Globalization, public health and viral epidemics

This work can only be based on solid knowledge on the molecular biology of the different viruses, continues Bosch. Regarding coronavirus, it is a fascinating group of viruses from the molecular perspective, which were not thought to be related to any important public health problem. When the SARS, MERS and 2019-nCoV (Wuhan) infectious episodes of coronavirus appeared, the basic knowledge of the scientific community have been determining to enable fast progress in the research on this coronavirus, as relevant as human pathogens.

Regarding the emerging viral infection episodes we should avoid panic and develop tools for diagnosis like in the coronavirus case- in order to establish control systems. Afterwards, we need knowledge on their transmission, reservoirs, etc. and this is the current phase we are in. The next step would be, therefore, to work on therapies, prophylactic therapies like vaccines, or antiviral ones.

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Is the medication you’re taking worth its price? – Salon

February 2nd, 2020 2:46 pm

Austin was three years old and Max was a newborn when their mother, Jenn McNary, learned they had a rare genetic condition called Duchenne muscular dystrophy. The doctor painted a grim picture: Her boys would stop walking by age 12 or 13 and, shortly thereafter, they would require nighttime ventilation. They would each need a tracheotomy, a feeding tube, or both by their late teens. Death would come a few years later.

It hasn't worked out that way, thanks to two new drugs that became available after the boys' 2002 diagnosis. Exondys 51, a medicine that targets their genetic mutation, slows the disease's progression, and Emflaza, a corticosteroid, mitigates some of its symptoms. Thanks to these treatments, Austin now attends college and interns at a biotech company. Max attends his local high school in Newton, Massachusetts. Both are able to get around in wheelchairs, and neither needs ventilation. McNary just rented an apartment for her boys because they can function on their own with the help of an aide.

By all accounts, the drugs have been transformative, McNary said. But, she added, her boys "aren't going to be cured," and extending and improving their life for an unknown period of time comes at a high price. Emflaza came onto the market in 2017 at an annual cost of $65,000. Exondys 51 appeared in 2016 at $748,500. Neither of the drugs will help the young men walk again and, in the eyes of some U.S. health economists, the drugs are not worth the price.

That's why McNary hates the quality-adjusted life year (QALY, pronounced "qua-lee"), an economic calculation that attempts to quantify the value of a medical intervention, based in part on the quality of life it bestows on recipients.

First developed by U.S. economists in the late 1960s and early 1970s, variations of the QALY have been used for years by governments around the world to help determine what treatments citizens can obtain under public health care. In America's free-market health care system, however, QALY calculations have largely been avoided. As McNary and others like her are finding out, that's starting to change.

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As policymakers and insurance companies scramble to get a handle on skyrocketing health care costs, they are promoting the idea of paying for value. In this view, drugs designated as higher-value should be prioritized over lower-value treatments. But this raises a thorny question: Who gets to define "value"? Health economists and insurance companies who seek to use limited health care dollars judiciously? Or patients, parents, and doctors who want to receive the best health care for their situation?

Because the quality-adjusted life year threatens her sons' ability to get the medicine they need, McNary is clear about her answer. "To me, the QALY is a measurement that says that keeping my sons alive by providing incremental benefit but not totally curing them is never going to be valuable," McNary said. "Just mull that around in your head if you are less than perfect, you are worth less money."

* * *

In QALY math, a year of perfect health is equal to 1; death equates to 0. The value of other health states is derived from surveys of patients, caregivers, or the general public. Paralysis might be valued at .35, for example, and mild Alzheimer's disease at .52, depending on the survey. Those numbers can then be plugged into a formula that allows the relative cost-effectiveness of treatments to be compared to identify the best buys.

Economists developed the QALY concept more than 40 years ago to address a fundamental question: "Where should we spend whose money to undertake what programs to save which lives with what probability?' Richard J. Zeckhauser and Donald Shepard asked in a 1976 article describing the basic QALY formula. The next year, as U.S. health care spending topped $120 billion, Harvard health policy professor Milton C. Weinstein and his colleague, cardiologist William B. Stason, sounded an alarm bell. "It is now almost universally believed that the resources available to meet the demands for health care are limited," they wrote in the New England Journal of Medicine. "We, as a nation, will have to think very carefully about how to allocate the resources we are willing to make available for health care."

Their article cited by other authors more than a thousand times in the past four decades pointed out that resources were already being allocated by millions of individual decisions: hospitals rationing beds where they didn't have room for all patients, for example, and insurers agreeing to pay for some tests and treatments but not for others. Such decisions, they argued, were often inconsistent with the "societal objective of deriving the maximum health benefits from the dollars spent," an objective that could be achieved by putting the QALY to work.

In the intervening decades, some countries the United Kingdom, the Netherlands, and Sweden, for example have embraced QALY-based evaluations. In the U.K., cost-effectiveness studies are used, in part, to determine which therapies the National Health Service will provide for residents. The publicly-funded health system does not cover Orkambi, the first cystic fibrosis treatment that targets the cause of the disease, for example, because its cost-per-QALY far exceeds the U.K. cost-effectiveness threshold.

In the United States, however, QALY-based assessments have not gained traction until recently. "Perhaps the general reason is that we as patients and our providers don't want to be limited in the treatment options available," said Louis P. Garrison Jr., an economist in the Pharmaceutical Outcomes Research and Policy Program at the University of Washington.

In fact, QALY-based cost-effectiveness reviews are so controversial that the federal government has repeatedly quashed their use. In 1992, the Department of Health and Human Services rejected Oregon's attempt to use QALY-based cost-effectiveness assessments to determine what services its Medicaid program would cover. In 2010, as part of the Patient Protection and Affordable Care Act, Congress prohibited the use of QALYs by the Medicare program. It also banned the federal Patient-Centered Outcomes Research Institute from using QALY thresholds in its assessments of comparative treatments.

* * *

A QALY Primer

A QALY reflects quality of life and length of life. A year in "perfect health" is worth 1 QALY, death is worth 0 QALYs, and other health states fall between 0 and 1. The amount that a drug lengthens or improves the quality of life is calculated as "QALYs gained." The cost of getting a certain level of health improvement is the "cost per QALY gained," shown here for several interventions targeting asthma.

But more than half of U.S. residents are covered by private insurance companies, which are not prohibited from using QALY-based assessments to decide which medicines they will cover for their members. Traditionally, however, private insurers have generally not used QALYs explicitly in their decisions about what tests and treatments they will pay for, according to a recent report by the National Council on Disability. Instead, when major U.S. insurers decide to limit access to a given medication, they usually cite insufficient data to justify its use in a given situation.

Indeed, until recently, U.S. insurers did not have a source for QALY-based cost-effectiveness reports. That began to change in 2014, when the Institute for Clinical and Economic Review, a nonprofit research organization based in Boston, turned its attention to high-cost drugs. Founded in 2006 as a research project based at Harvard Medical School, ICER initially issued reports on broad topics such as obesity management and palliative care. But when Sovaldi, a drug for deadly hepatitis C, came on the market at the then-shocking price of $84,000 for a 12-week course of treatment, ICER kicked into action. Despite the high price, its assessment found that Sovaldi is cost-effective for some patients. Insurers took notice.

Since then, the organization has been churning out several drug-assessment reports each year. Each report includes its opinion of how much the drug is worth; drugs priced higher than that are deemed not cost-effective. ICER has no authority over anyone, but its reports have become popular reading for U.S. insurers. "If there is a drug of note being approved by the FDA, there's also likely going to be an ICER assessment of that drug that can factor into their decision-making," said David Whitrap, the research organization's vice president of communications and outreach.

* * *

U.S. health care spending has risen dramatically since Weinstein and Stason expressed concern in the mid-1970s. In 2016, the U.S. spent nearly 18 percent of its gross domestic product on health care, far outstripping the average of 11 percent for 10 other high-income nations. High prices for prescription drugs is one reason. "We're seeing price tags now of $1 million, $2 million," said Seema Verma, administrator for the federal Centers for Medicare and Medicaid Services, at a conference recently. "That's completely unsustainable for the system."

That's why Peter Neumann, director of the Center for the Evaluation of Value and Risk in Health at Tufts Medical Center, said cost-effectiveness analyses are needed more than ever. But there are many reasons for the resistance, Neumann and his co-authors wrote in the Journal of the American Medical Association, including "an inclination on the part of many individuals in the United States to minimize the underlying problem of resource scarcity and the consequent need to explicitly ration care."

Further, Ari Ne'eman, a disability rights activist and consultant to Partnership to Improve Patient Care, a coalition of advocacy groups, said the idea that two health conditions can be numerically compared to one another is simply wrong. "Proponents of the QALY will say it is this mathematically perfect measure that gives us a superpower ability to compare depression drugs to cystic fibrosis drugs to cancer drugs even though all of those drugs do different things because it lets you translate them back to this common measure," he said. "Our concern is that when you engage in that process of translation, you lose some significant nuance in terms of the amount of benefit that's being delivered."

The Partnership argues the QALY calculation is flawed because it assumes quality of life can be captured by a certain number, despite the fact that different surveys arrive at different numbers. For example, a 2006 quality-of-life survey in the U.S. assigns blindness/low vision as .69 on the 0-to-1 scale, while a 2011 survey in the U.K. gives blindness/low vision a score of .78.

Beyond the methodological issues, Ne'eman said, "there are all kinds of ethical problems with it." People with disabilities and chronic medical conditions may value a treatment that offers an incremental improvement in the quality or length of their lives, even though the "QALYs gained" are less than those for a treatment that prevents the loss of perfect health.

Former U.S. Representative Tony Coelho, a Democrat from California and a primary author of the Americans with Disabilities Act, is the Partnership's chairman. "I worry that more focus is being given to what is most cost-effective for the 'average patient' than creating a system that works for each individual patient," he wrote in 2018. "The medication I take for epilepsy isn't 'high value' for every patient. But it's the only one that works for me."

That's why, Ne'eman said, cost-effectiveness analyses must consider the fact that not all patients respond the same way to a drug. Some patients need drugs that aren't deemed cost-effective for the general population. It's important to account for that, he said. "Otherwise we're giving insurers a tool to deny care to people who need it."

When an insurer decides to cover a specific drug, that decision affects everybody who pays into the insurance pool. Michael Sherman, chief medical officer for the insurer Harvard Pilgrim Health Care, uses the example of a gene therapy that costs $1 million to treat a child who will die without it. Under the ACA, families will hit their out-of-pocket maximum at about $16,000, and many health plans have out-of-pocket maximums far below that. "The rest of that million dollars is going to be paid by everyone else that's the way it works in insurance," he said. When insurers see that kind of unanticipated budget impact, they raise premiums or out-of-pocket cost-sharing for everyone.

Like other proponents of the QALY, Neumann sees it as an imperfect but useful tool. "Any single number is never going to capture everything," he said.

"The problem is, if you're not going to use QALYs, what are you going to use?"

* * *

That's an urgent question, particularly now when there is a huge pipeline for rare-disease therapies, often called orphan drugs. By 2024, orphan drug sales are expected to reach $242 billion.

In the U.S., a rare disease is defined as one that affects fewer than 200,000 people. While these conditions are individually rare, in the aggregate, an estimated 25 to 30 million Americans that's about one in 10 live with a rare disease. Most rare diseases affect children, and many are fatal or disabling.

Historically, drugmakers spent little effort developing treatments for rare diseases, but that changed with the passage of the Orphan Drug Act of 1983, which provides tax credits and a seven-year marketing exclusivity to companies that develop rare-disease treatments. Hundreds of such treatments have won FDA approval in recent years, with more than 560 medicines in the works.

Those treatments are generally expensive. On average, the per-patient cost for orphan drugs in the U.S. is almost 4.5 times more than for non-orphan drugs.

In the two decades ending in 2017, the average annual cost for orphan drugs was $123,543, based on the price at the time the drug launched, compared to $4,961 for traditional drugs. For Duchenne alone, more than 30 orphan therapies are in development. None of them are going to cure patients, McNary said. But she hopes new treatments, generally used in combination, will help her sons live longer, healthier lives and completely change the disease trajectory for younger patients whose disease has not yet progressed as far.

The barrier she worries about is cost-effectiveness analysis. In August, the Institute for Clinical and Economic Review published its assessment of treatments for Duchenne, which affects about 400 to 600 boys born in the U.S. each year. Emflaza, the corticosteroid, appears to be as good as or better than prednisone, another corticosteroid approved to treat the disease, but it would need a price cut of at least 73 percent to be considered cost-effective.

Exondys 51 approved by the FDA for about 13 percent of the Duchenne population got a worse review. In the clinical trials used to seek FDA approval, no clinical benefit, including motor function improvement, was demonstrated. (The FDA approved the drug because some of the patients treated with Exondys 51 had a slight increase in dystrophin levels in skeletal muscle.) In light of that, Exondys 51 was not deemed cost-effective at any price.

But Jenn McNary said the drug works for her sons. Austin, who was not eligible for the Exondys 51 clinical trial, stopped walking at age 10. Max got in the trial and started taking the drug at age 9."They have the same mutation, they have been raised by the same mother, so one would expect they would progress similarly," she said. "But Max walked until he was 17."

Austin was already in a wheelchair when, at age 15, he started taking Exondys 51. He regained some upper-body strength that changed his life, according to his mother. "He's able to use a urinal on his own, which makes is possible for him to have a job and to go to college without an aide," she said.

The Medicaid program in Massachusetts, where the McNarys live, won't pay for Max's Duchenne therapies. For the time-being, the drugmakers are giving him the drugs free through a patient-assistance program. Austin, because he's enrolled in college, is eligible for student coverage through Blue Cross Blue Shield of Massachusetts. The insurer, by policy, does not cover Exondys 51 for patients who can no longer walk. His mother appeals the insurance denial. Every six months, she sends a video of Austin in action, along with a letter from his doctor and so far, his medicines have been covered.

The payers made their coverage policies before the quality-adjusted life year analysis was published. Now, insurers who have been covering the Duchenne treatments have an independent analysis with which to rethink that decision.

For now, there is one thing that QALY supporters and critics agree on. "Very promising drugs are coming, and they're going to be very expensive," said Neumann, the health economist at Tufts. Increasingly, the QALY appears poised to influence how American health care money is spent.

* * *

Lola Butcher is a health care business and policy writer based in Missouri.

This article was originally published on Undark. Read the original article.

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Here are some tips, treatment options for acne – The Reporter

February 2nd, 2020 2:46 pm

According to the American Academy of Dermatology, acne affects up to a staggering 50 million Americans annually.

To make matters worse, blackheads, whiteheads, pimples, cysts and other acne-related blemishes seem to occur at the most inconvenient times: before a date, a meeting, class photos, you name it. Although acne is not a serious health threat, severe acne can lead to disfiguring and permanent scarring.

Why do I have acne? Acne is most commonly linked to the changes in hormone levels during puberty, but can start at any age. Certain hormones cause the grease-producing glands next to hair follicles in the skin to produce larger amounts of oil, or abnormal sebum. This abnormal oil changes the activity of harmless skin bacterium called P. acnes, or propionibacterium acnes, which becomes more aggressive and causes inflammation and pus. Certain medications, stress and a poor diet can also contribute to acne. There is also evidence of a genetic component to acne as well.

Types of treatments: Because acne is caused by a myriad of factors, treating it with one product or medicine usually is not enough. You may need to attack it from many angles with different types of treatments that all work differently.

While a pimple will eventually go away, if you have numerous outbreaks, you could end up with scars. This is when it is time to visit a dermatologist, who may suggest a cream, lotion, gel or some that contains ingredients that can help. Many can be bought without a prescription:

Benzoyl peroxide kills bacteria and removes extra oil.

Salicylic acid keeps pores from getting clogged.

Sulfur removes dead skin cells.

Stronger treatments: If some of these over-the-counter remedies do not get your acne under control, your doctor may prescribe a retinoid to be used on the skin. This comes in a cream or gel and helps unplug oil ducts. Antibiotics in cream, lotion, solution or gel form may be used for inflammatory acne.

Isotretinoin is a medicine used to treat severe acne. It is usually used for cystic acne that does not improve after treatment with other medicines. Brand names include Accutane, Amnesteem, Sotret and Claravis. Isotretinoin is the most effective long-term medication for acne but is associated with some risks that dermatologists are familiar with. Spironolactone blocks excess hormones.

When to seek medical help: Even mild cases of acne can cause distress and, in some cases, depression. If your acne is making you feel unhappy or you are having a hard time controlling your blemishes with over-the-counter medication, see your doctor. Try to resist the temptation to pick or squeeze the spots, because this can lead to scarring.

Treatments can take a few months to work, so do not expect immediate results. Once they do start to work, the results are usually good.

Dr. Daniel Shurman of Pennsylvania Dermatology Partners in Amity Township completed his dermatology training at Thomas Jefferson University. He is fellowship-trained in both Mohs micrographic surgery and procedural dermatology, and his research interests include medical genetics, antibiotics in dermatologic surgery and wound healing.

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The first case of coronavirus being spread by a person with no symptoms has been found – Science News

February 2nd, 2020 2:46 pm

As the 2019 novel coronavirus outbreak continues to spreadin China, researchers have found that people carrying the virus but not showingsymptoms may be able to infect others.

If infected people can spread 2019-nCoV while asymptomatic,it could be harder to trace contacts and contain the epidemic, which is alreadya globalhealth emergency (SN: 1/30/20).

An unnamed Shanghai woman passed the virus to businesscolleagues in Germanybefore she showed signs of the illness, doctors report January 30 in the New England Journal of Medicine. Thewoman had attended a business meeting at the headquarters of the auto supplierWebasto in Stockdorf on January 20 and flew back to China on January 22. Shebecame ill with mild symptoms on the flight back to China and tested positivefor the virus.

Meanwhile, one of her German colleagues fell ill on January24 with a fever, sore throat, chills and muscle aches. His illness was brief,and he returned to work on January 27, the same day that the woman informed thecompany she carried the virus. Nasal swabs and sputum, or phlegm, samples fromthe man contained high levels of the novel coronavirus even though his symptomshad passed.

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Three other employees of the company also tested positivefor the virus. Tracing their contacts, doctors conclude that the first man andanother person caught the virus from their Chinese colleague.

Whats also concerning is that the first man apparently passedthe virus to the other two coworkers, who both had contact with him before hedeveloped symptoms. All cases of the illness have been mild.

These cases suggest that people shed the virus before theyshow symptoms and after recovery from the illness, say Camilla Rothe, atropical medicine and infectious disease specialist at the University Hospital ofLudwig-Maximilians-Universitt in Munich, and her colleagues.

Asymptomatic spread, though common for influenza viruses forexample, would be a new trick for coronaviruses. The coronaviruses that causesevere acute respiratory syndrome, or SARS, and Middle East respiratorysyndrome, or MERS, are notcontagious before people show symptoms (SN:1/28/20).

Another coworker of the firm was confirmed to have the viruson January 30, and a child of one of the infected workers has also contractedthe virus, bringing the case count to six, health officials in the German stateof Bavaria said January 31. The company has closed its headquarters near Munichuntil February 2 and began testing contacts of the ill employees on January 29.

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Here is what you need to know about novel… – ScienceBlog.com

February 2nd, 2020 2:46 pm

Before a packed room at the Health Sciences Learning Center on the University of WisconsinMadison campus on Jan. 29, Associate Dean for Public Health and Community Engagement Jonathan Temte asked for a moment of silence for those affected by an outbreak of a virus that in a matter of weeks has sickened nearly 10,000 people around the world and killed more than 200 people in China as of Jan. 31.

The virus, a previously unknown member of a class of coronaviruses, was first described in late December 2019 after several cases of illness appeared in people in Wuhan, a city in Hubei province, China. Its name, for now, is 2019-nCoV.

As details of the virus and its effects continue to emerge, UWMadison gathered a panel of experts, including physicians, epidemiologists, public health officials, scientists and communication experts, to address questions and concerns from the public.

Watch a video of the livestreamed event.

The event came together on short notice after the director of the Centers for Disease Control and Prevention, Robert R. Redfield, had to cancel his previously scheduled talk in Madison in order to help manage the outbreak.

Here are some takeaways:

Coronaviruses are relatively common. What makes this coronavirus unique is that it has never been implicated in human disease before. There are several human coronaviruses that cause mild disease and we have known about them for decades now, said Kristen Bernard, a professor in the UW School of Veterinary Medicine. They are the cause for about 30 percent of common colds. They are also the viruses behind the 2003 SARS and 2012 MERS outbreaks, which both killed large numbers of people.

The original source of the virus is probably bats, which serve as a reservoir for large numbers of zoonotic diseases, or those that pass between animals and people. Most of these viruses rely on an intermediary species to render it infectious in people. With SARS, experts believe that species was civet cats, and with MERS, it was dromedary camels. Some early reports blamed snakes for the 2019-nCoV outbreak, but, said Chris Olsen, emeritus professor in the School of Veterinary Medicine: I think we need to take that with a very large grain of salt.

In people, 2019-nCoV is transmitted through coughing and contact with saliva, mucus or the tears of people sick with the virus. Symptoms of illness include cough, fever and shortness of breath. Public health officials are still working to determine whether infected people can transmit the virus to others if they are not symptomatic.

There have been six confirmed cases of 2019-nCoV in the United States since mid-January, and as of Jan. 30, officials in the U.S. reported the first case of person-to-person transmission. There have been no confirmed cases in Wisconsin, though experts continue to monitor patients for symptoms and have sent six potential cases to the CDC for testing. One came back negative for the virus and results are still pending on the remaining samples. Allen Bateman, assistant director in the communicable disease division of the Wisconsin State Lab of Hygiene, said the laboratory is working with local health departments and clinical labs across the state to help with testing and response.

There are no specific cures or treatments for people with 2019-nCoV, but as is the case with many viruses, said Medical Director of Infection Control at UW Hospital and Clinics Nasia Safdar, those who are sick are offered supportive care to relieve symptoms and mitigate complications. And because the symptoms of the novel coronavirus are similar to other kinds of viruses, she and colleagues are working with health care providers to train them on containment and help keep them safe.

There are no cases of 2019-nCoV in Wisconsin at this time, but we are prepared to react if things are changing, said Patrick Kelly, interim director of medical services at University Health Services. On campus, that has meant taking steps to keep more than 40,000 students safe and provide physical and mental health care as needed. It has also meant communicating often with students and their families. An all-campus message sent Jan. 24 shared information about the novel virus and was translated on short notice in five languages.

The state has also been working on the logistics of monitoring and preparing for the virus, said School of Medicine and Public Health (SMPH) Professor of Medicine Ryan Westergaard, also chief medical officer and state epidemiologist at the Wisconsin Department of Health Services. While some areas have couriers to transport samples from the clinic to the state lab for testing, police are serving that role in others. Its been a good learning experience, he said, with people from legislative offices and the governors office at the table to make sure we are coordinating well.

Its important to be prepared for a possible outbreak of coronavirus, but public health officials still remain more concerned about seasonal influenza. That virus has had a greater impact in Wisconsin, and in the U.S., so far this year. Right now, in Dane County and southern Wisconsin, were in the midst of a huge influenza outbreak, said Temte, also a family medicine physician. As of Friday (Jan. 24), 54 children across the country had died of influenza and influenza is one of these diseases for which we have effective vaccines and effective antivirals.

Scientists at UWMadison are monitoring research developments globally. Chinese scientists worked swiftly in the aftermath of the outbreak to decode the genetic sequence of 2019-nCoV and share it with other researchers worldwide. Thomas Friedrich, a professor in the School of Veterinary Medicine, said some researchers are working with that sequence to develop vaccines against the new coronavirus. Some journals where scientists publish, including the New England Journal of Medicine, require researchers to share their raw data for others to use, and many researchers are making data instantly available on widely-used pre-print servers. I think its very important for us to make our information available to the public as much as possible, he said.

Misinformation is easy to spread, so sticking with facts when discussing 2019-nCoV is imperative, said Emily Kumlien, media strategist at UW Health. We work with the experts to get the right information to share with the community at the right time. That includes using social media and other platforms to reach people in the places where they get their news, and where misinformation is most likely to live. I think its everybodys responsibility, said Ajay Sethi, SMPH professor of population health, to serve as educated, informed opinion leaders; to identify misinformation; and to find creative and strategic ways to dispel that.

Officials believe the novel coronavirus originated in a seafood and live animal market in Wuhan. But shutting down these kinds of markets broadly would be akin to telling Wisconsinites not to hunt deer, said Bernard. Thats part of their culture and we have to be sensitive to that. However, she added: There are things we can do and thats why basic research is so, so important.

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Snake venom can now be made in a lab and that could save many lives – CNN

February 2nd, 2020 2:46 pm

It involves milking snake venom by hand and injecting it into horses or other animals in small doses to evoke an immune response. The animal's blood is drawn and purified to obtain antibodies that act against the venom.

Producing antivenom in this way can get messy, not to mention dangerous. The process is error prone, laborious and the finished serum can result in serious side effects.

Experts have long called for better ways to treat snake bites, which kill some 200 people a day.

Now -- finally -- scientists are applying stem cell research and genome mapping to this long-ignored field of research. They hope it will bring antivenom production into the 21st Century and ultimately save thousands, if not hundreds of thousands, of lives each year.

Researchers in the Netherlands have created venom-producing glands from the Cape Coral Snake and eight other snake species in the lab, using stem cells. The toxins produced by the miniature 3-D replicas of snake glands are all but identical to the snake's venom, the team announced Thursday.

"They've really moved the game on," said Nick Cammack, head of the snakebite team at UK medical research charity Wellcome. "These are massive developments because it's bringing 2020 science into a field that's been neglected."

Hans Clevers, the principal investigator at the Hubrecht Institute for Developmental Biology and Stem Cell Research in Utrecht, never expected to be using his lab to make snake venom.

So why did he decide to culture a snake venom gland?

Clevers said it was essentially a whim of three PhD students working in his lab who'd grown bored of reproducing mouse and human kidneys, livers and guts. "I think they sat down and asked themselves what is the most iconic animal we can culture? Not human or mouse. They said it's got to be the snake. The snake venom gland."

"They assumed that snakes would have stem cells the same way mice and humans have stems cells but nobody had ever investigated this," said Clevers.

After sourcing some fertilized snake eggs from a dealer, the researchers found they were able to take a tiny chunk of snake tissue, containing stem cells, and nurture it in a dish with the same growth factor they used for human organoids -- albeit at a lower temperature -- to create the venom glands. And they found that these snake organoids -- tiny balls just one millimeter wide -- produced the same toxins as the snake venom.

The team compared their lab-made venom with the real thing at the genetic level and in terms of function, finding that muscle cells stopped firing when exposed to their synthetic venom.

The current antivenoms available to us, produced in horses not humans, trigger relatively high rates of adverse reactions, which can be mild, like rash and itch, or more serious, like anaphylaxis. It's also expensive stuff. Wellcome estimate that one vial of antivenom costs $160, and a full course usually requires multiple vials.

Even if the people who need it can afford it -- most snakebite victims live in rural Asia and Africa -- the world has less than half of the antivenom stock it needs, according to Wellcome. Plus antivenoms have been developed for only around 60% of the world's venomous snakes.

In this context, the new research could have far-reaching consequences, allowing scientists to create a biobank of snake gland organoids from the 600 or so venomous snake species that could be used to produce limitless amounts of snake venom in a lab, said Clevers.

"The next step is to take all that knowledge and start investigating new antivenoms that take a more molecular approach," said Clevers.

To create an antivenom, genetic information and organoid technology could be used to make the specific venom components that cause the most harm -- and from them produce monoclonal antibodies, which mimic the body's immune system, to fight the venom, a method already used in immunotherapy treatments for cancer and other diseases.

"It's a great new way to work with venom in terms of developing new treatments and developing antivenom. Snakes are very difficult to look after," Cammack said, who was not involved with the research.

Clevers said his lab now plans to make venom gland organoids from the world's 50 most venomous animals and they will share this biobank with researchers worldwide. At the moment, Clevers said they are able to produce the organoids at a rate of one a week.

But producing antivenom is not an area that pharmaceutical companies have traditionally been keen to invest in, Clevers said

Campaigners often describe snakebites as a hidden health crisis, with snakebites killing more people than prostrate cancer and cholera worldwide, Cammack said.

"There's no money in the countries that suffer. Don't underestimate how many people die. Sharks kill about 20 per year. Snakes kill 100,000 or 150,000," said Clevers.

"I'm a cancer researcher essentially and I am appalled by the difference in investment in cancer research and this research."

One challenge to making synthetic antivenom is the sheer complexity of how a snake disables its prey. Its venom contains several different components that have different effects.

Researchers in India have sequenced the genome of the Indian Cobra, in an attempt to decode the venom.

"It's the first time a very medically important snake has been mapped in such detail," said Somasekar Seshagiri, president of SciGenom Research Foundation, a nonprofit research center in India.

"It creates the blueprint of the snake and helps us get the information from the venom glands." Next, his team will map the genomes of the saw-scaled viper, the common krait and the Russell's viper -- the rest of India's "big four." This could help make antivenom from the glands as it will be easier to identify the right proteins.

In tandem, both breakthroughs will also make it easier to discover whether some of the potent molecules contained in snake venom are themselves worth prospecting as drugs -- allowing snakes to make their mark on human health in a different way to how nature intended -- by saving lives.

"As well as being scary, venom is amazingly useful," Seshagari said.

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How to live longer: How does fasting increase your life expectancy? What we know so far – Express

February 2nd, 2020 2:45 pm

It is well understood that eating a healthy, balanced diet is essential to living a long life, with certain foods offering protection against life-threatening health complications. With the spotlight placed firmly on what foods you should embrace and avoid, less attention has been devoted to the frequency of eating and its impact on longevity.

Pearson continues: It's after this period of time that processes such as autophagy and stem cell generation are triggered.

Autophagy is the body's way of cleaning out damaged cells, in order to regenerate newer, healthier cells, according to Priya Khorana, PhD, in nutrition education from Columbia University.

According to Pearson, profound regenerative changes have been shown with periodic water-only fasting but consuming nothing but water for days on end can be challenging for many.

To circumvent this challenge, professor Valter Longo, who has spearheaded much of the research in the field of fasting and longevity, developed the concept of Fasting Mimicking Diets (FMDs).

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Fast Mimicking Diets mimics fasting by tricking your body into a fasted state, while eating specially designed plant-based mini meals, explains Pearson.

FMDs have been shown to promote multi-system regeneration, enhanced cognitive performance, and health span.

Clinical studies on three, five day FMD cycles, spread over three months, show a spike in circulating stem cells that lead to delayed ageing by promoting regeneration in multiple systems.

Body weight, BMI, total body fat, trunk fat, waist circumference, systolic and diastolic blood pressure, cholesterol, insulinlike growth factor 1 (IGF1) and C-Reactive Protein (a marker of inflammation) were significantly reduced, particularly in participants at risk for diseases.

Curiously, scientists from the University of Wisconsin-Madison, and the Pennington Biomedical Research Center, Baton Rouge, Louisiana, reported that health and longevity improved with increased fasting time, regardless of what the mice ate or how many calories they consumed.

According to the study's lead author, Rafael de Cabo, Ph.D., chief of the Translational Gerontology Branch of the NIA Intramural Research Program, scientists have studied the beneficial effects of caloric restriction for more than a century, but the impact of increased fasting times has recently come under closer scrutiny.

"Increasing daily fasting times, without a reduction of calories and regardless of the type of diet consumed, resulted in overall improvements in health and survival in male mice," said de Cabo.

He added: Perhaps this extended daily fasting period enables repair and maintenance mechanisms that would be absent in a continuous exposure to food."

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Innovation in the treatment of COPD – Health Europa

February 2nd, 2020 2:43 pm

OmniSpirant Limited are a leading European biotech startup company with ambitions to change the paradigm of treatment for respiratory disease. Chronic Obstructive Pulmonary Disease (COPD) is an umbrella term used to describe progressive lung diseases including emphysema, chronic bronchitis, and refractory (non-reversible) asthma. This disease is characterised by increasing breathlessness, frequent chest infections and persistent wheezing. COPD currently cannot be cured or fully reversed.

This debilitating disease today has a solution, developed by OmniSpirant, as we explain below. Until now, the current COPD therapeutics market has lacked any effective disease modifying treatments and the clinical stage pipeline is weak, given the massive disease prevalence; COPD is arguably the disease with the most severely unmet medical and patient needs.

Smoking is indeed the primary cause of this devastating disease, but 15-20% of COPD cases are due to exposures to occupational dust, chemicals, vapours or other airborne pollutants in the workplace. Air pollution is also a likely and underappreciated driver of the growth of the disease and declining lung function in COPD is strongly associated with ageing.

COPD affects up to 500 million patients globally and is the worlds fourth leading cause of death. This dire situation is projected to worsen with COPD becoming the third leading cause of death globally in 2030 and the leading cause of hospitalisations in the industrialised world. COPD is classified as a priority disease by the EU and WHO as it is the only leading cause of death that is rising in prevalence globally. The burden of this chronic respiratory disease is growing rapidly, fuelled by an ageing demographic, persistent smoking habits, and air pollution.

A recent study has estimated that air pollution may be a factor in as many as 47,000 COPD deaths per annum across the 28 EU Member States. Epidemiologic studies have found a measured prevalence of COPD in Europe of between 4% and 10% of adults (European COPD Coalition). However, COPD is widely undiagnosed and untreated especially in its early stages, so the actual prevalence may be higher. New therapies that can slow disease progression desperately need to be developed.

The disease costs tens of billions of euros annually to healthcare payers in reimbursement for largely ineffective pharmacological and medical interventions. In the key United States market, COPD is responsible for USD $72bn (~65bn) per year in direct healthcare expenditures. In the EU, estimated spending on inpatient, outpatient and pharmaceuticals exceeds 10bn per year and productivity losses are estimated at 28.5bn year.

The disease also causes an estimated 300,000 premature deaths in the EU annually (European Respiratory Society). These startling figures are forecast to rise dramatically as the disease prevalence is set to rise sharply.

Current COPD treatments do not include an effective disease modifying therapy which can reduce the exacerbation of symptoms and/or slow down COPD from progressing and worsening. State of the art therapies for COPD consists of combinations of oral, injected or inhaled bronchodilators, anti-muscarinics, corticosteroids, anti-inflammatories, and antibiotics, all of which are used to treat symptoms and reduce exacerbations of COPD with only modest results.

Except for a small minority of Alpha one Antitrypsin (AAT) deficient COPD patients (five in 10,000 carry the mutation responsible for AAT deficiency on both chromosomes), there are no available therapies which modulate disease progression. AAT is a protein that protects the lungs from the destructive actions of common illnesses and exposures, particularly tobacco smoke.

Furthermore, the COPD pipeline is also devoid of disease modifying treatments. The COPD pipeline is full of incremental advances on existing mainstay therapies which merely treat disease symptoms and do not target the root causes of the disease. There are a few innovative therapies in development but a small molecule or biologic agent such as a monoclonal antibody (or even combinations of several of these agents) are highly unlikely to provide a curative or even therapeutically useful intervention in a complex disease like COPD.

OmniSpirant believe that the solution to the COPD epidemic can be found in the new era of advanced therapeutics by combining several technological advances in the fields of cell culturing, genetic engineering and their innovative exosome technology platform. OmniSpirant are developing inhaled bioengineered exosome therapeutics, delivered by a tailored aerosol delivery method based on vibrating mesh nebuliser technology.

In the first instance, the presenting problem is that patients have established lung damage and an increased risk of developing lung cancer (independent of smoking history). OmniSpirant believe that microRNA/mRNA engineered stem cell exosomes can provide powerful anti-inflammatory and regenerative effects and also reduce the risk of patients developing lung malignancies.

Exosomes are naturally produced by cells and recent research highlights the vast potential of stem cell exosomes as transformative regenerative medicines. Stem cell exosomes have shown great regenerative potential in animal models of COPD by stimulation of repair mechanisms and reversing damage to the lung. Stem cells have also shown some promising results in COPD clinical trials.

Donor (Allogeneic) MSCs delivered intravenously in repeat-dose clinical trials for COPD (Prochymal Osiris Therapeutics) were found to be safe and well tolerated and reduced systemic inflammation, but no significant improvements in lung function were observed. We believe that the use of exosomes, as the therapeutic essence of stem cells, delivered by the inhaled route of administration will be capable of far greater efficacy by delivering far higher doses of exosomes directly to the affected lung tissues than intravenous delivery while typically only requiring about 1% of the overall dose. Furthermore, our exosomes will have enhanced delivery (via proprietary surface engineering) and are also bioengineered to enhance efficacy.

OmniSpirants novel technology platform is capable of delivering high doses of these exosomes across the mucus barrier and through cell membranes to deliver the therapeutic payload directly into the diseased lung cells. Such delivery has proven problematic for competing gene transfer technologies because the mucus in the lungs is a barrier that traps the carriers used to deliver gene therapies such as nanoparticles and viral vectors. These trapped gene therapy carriers are mostly cleared from the mucus layer before they can penetrate into the underlying cells and introduce their genetic cargo.

The use of exosomes overcomes other issues associated with viral and non-viral vectors which include the generation of therapy-inactivating host immune responses and poor ability to cross cell membranes. Furthermore, traditional gene transfer vectors may be immunogenic and elicit adverse inflammatory responses.

OmniSpirants solution is a proprietary method of surface engineering exosomes so they can efficiently penetrate the protective mucus barrier and enter into the underlying cells. These stem cell exosomes are therapeutic (regenerative, anti-inflammatory, antimicrobial and antifibrotic), non-immunogenic, and can be tailored via genetic modification of the parent stem cells to create ideal inhaled gene therapy vectors for any lung disease.

The surface engineered exosomes have demonstrated 100% mucus penetration and target cell uptake in the gold standard in vitro model (well-differentiated bronchial epithelial cells in air liquid interface culture), which is game changing compared with the state of the art viral vectors which can achieve only 30% of cells at best. We believe that the enhanced delivery of stem cell exosomes can translate the promising regenerative effects witnessed in various animal models of inflammatory lung diseases into the clinic.

To treat COPD, our approach is to genetically modify the stem cells so that they produce exosomes carrying carefully selected nucleic acids which are tailored for treating the underlying causes of COPD, which has been linked to gene expression and cellular senescence. The genetic element to COPD runs much deeper than just AAT deficiency.

Abnormalities in scores of genes have been clearly shown to increase or decrease the risk of developing COPD and perturbed gene expression is apparent in hundreds of disease associated genes. MicroRNAs (miRNAs) are a recently discovered class of non-coding RNAs that play key roles in the regulation of gene expression and more than 2,000 miRNAs have been identified in the human genome to date. The fact that each miRNA has the ability to target multiple genes within a pathway makes miRNAs one of the most abundant classes of regulatory genes in humans, regulating up to 30% of human protein coding genes.

MiRNAs have been widely shown to be dysregulated in the affected lung tissues of COPD patients which makes an inhaled gene therapy a highly promising approach for treating COPD. Such a gene therapy could effectively modulate the disease altered microRNAs (and their target genes) to halt or even reverse the disease. Recent advances in cell culturing techniques, isolation of exosomes and proprietary cell engineering technologies hold the promise to bring this therapy to the afflicted masses. The BOLD project estimates that there are currently 36 million patients in the EU and US alone with GOLD Stage 2 disease or higher; we need to act quickly as this figure is set to rise dramatically in the coming decade.

OmniSpirant are currently seeking investors or partners to fund the preclinical development of OS002 and anticipate that clinical studies can be initiated within approximately four years an impactful investing opportunity as the rising prevalence of COPD means that by 2030 there may be over 4.5 million deaths annually worldwide and COPD is predicted to be the leading cause of hospitalisation. Lets work together to change those grim statistics.

OmniSpirant and their consortium partners were awarded a 9.3m Irish government grant award (Disruptive Technologies Innovation Fund) in December 2019 to advance the development of their novel COPD gene therapy.*

OmniSpirant have received funding from Horizon 2020, ReSpire, Grant agreement ID: 855463 and have been accelerated by EIT Health.

Gerry McCauleyCEOOmniSpirant Ltd+353 876306538gmccauley@omnispirant.comwww.omnispirant.com

Please note, this article will appear in issue 12 ofHealth Europa Quarterly, which will be available to read in February 2020.

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New Bedford firefighter dies of occupational cancer – SouthCoastToday.com

February 2nd, 2020 2:43 pm

NEW BEDFORD The New Bedford Fire Department is mourning the death of one of their own.

On Monday morning Russ Horn, who worked for the department for over 30 years, died of occupational cancer, according to the president of New Bedford Firefighters Union, Billy Sylvia.

Sylvia said Horn, who was in his 50s, was forced to retire from the department after being diagnosed with multiple myeloma.

According to a patient blog on the Dana Farber Cancer Institutes website, Horn was diagnosed with cancer of plasma cells in 2014 after a minor slip at work sent him to the emergency room. There they discovered he had two broken ribs and a punctured lung as a result of the cancer already attacking his bones.

After receiving stem cell transplants and participating in clinical trials, Horn retired from the department in 2017.

Firefighters face a 1.53 times greater risk of getting multiple myeloma, according to the Firefighter Cancer Support Network.

Sylvia said he has seen a lot of cancer diagnoses among his colleagues in his 14 years as a firefighter, its adding up really quickly... its more than a handful.

We have active guys dealing with this, we have guys that are contracting it after retirement... studies show how much more susceptible we are, Sylvia said.

Its more than just the smoke theyre breathing thats putting them at risk, according to Sylvia; firefighters also can end up absorbing things through their skin and some of its coming from the gear thats supposed to protect us.

The issue is affecting firefighters across the country, Sylvia said, Were learning more and more, trying to get it under control, but theres still a lot of work that can be done.

Sylvia said Horns family has been proactive about making firefighters aware of their cancer risk and teaching them what to look for and the importance of early cancer screenings.

He was a very strong individual, both mentally and physically, Sylvia said of Horn, Eventually it just took its toll.

In 2019, Horn told Dana-Farber, Id do it all again, referring to his 30 years as a firefighter. This has been really hard, but having the guys behind me 100 percent makes it all a little easier.

Both the New Bedford Fire Department and the union have updated their profile pictures on Facebook to include a black stripe over their logos, honoring Horn.

In a post to the unions Facebook page announcing Horns passing, Sylvia said, Russ was the perfect example of what a firefighter, husband, father, and friend, that anyone could ever be. He was surrounded by his family, friends, brother and sisters firefighters throughout his fight and now beyond.

Sylvia closed the post with, We Love You Russ, Well see you again At the Big One.

On their own Facebook page the New Bedford Fire Department posted, "Our hearts are broken as we learned this morning that our retired brother, FF Russell Horn has lost his brave and courageous battle. We will never forget you and we will keep your family in our thoughts and prayers."

This story will be updated as more information becomes available.

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Mucosal Barrier Injury-Laboratory Confirmed Bloodstream Infection in Patients Who Receive HSCT – Cancer Network

February 2nd, 2020 2:43 pm

Mucosal barrier injury-laboratory confirmed bloodstream infection (MBI-LCBI), in addition to any bloodstream infections (BSIs), were associated with significant morbidity and mortality after hematopoietic stem cell transplant (HSCT), according to this study published inJAMA Network Open.

The researchers indicated that further investigation into risk reduction should be a clinical and scientific priority for this patient population.

Reduction in MBI-LCBI will require a better understanding of its mechanisms and risk factors, and our data contribute to the knowledge needed to make important progress, the authors wrote.

According to the study, a BSI is defined as an MBI-LCBI if it resulted from 1 or more of a group of selected organisms known to be commensals of the oral cavity or gastrointestinal tract, and it occurred in a patient with specific signs or symptoms compatible with the presence of mucosal barrier injury, like gastrointestinal graft-vs-host disease (GVHD) and/or neutropenia.

Of this cohort of 16,875 patients, 13,686 underwent HSCT for a malignant neoplasm, and 3,189 (18.9%) underwent HSCT for a nonmalignant condition. The cumulative incidence of MBI-LCBI was 13% (99% CI, 12%-13%) by day 100, and the cumulative incidence of BSI-other was 21% (99% CI, 21%-22%) by day 100. The median time from transplant to first MBI-LCBI was 8 (<1 to 98) days, versus 29 (<1 to 100) days for BSI-other. Most cases of MBI-LCBI met the definition secondary to neutropenia alone (1,915 of 2,179 [87.9%]), with the other 12.1% (264 of 2,179) meeting criteria owing to the presence of gastrointestinal GVHD (166 of 2,179 [7.6%]) or gastrointestinal GVHD with neutropenia (98 of 2,179 [4.5%]).

Multivariable analysis exposed an increased risk of MBI-LCBI with poor Karnofsky/Lansky performance status (hazard ratio [HR], 1.21 [99% CI, 1.04-1.41]), cord blood grafts (HR, 2.89 [99% CI, 1.97-4.24]), myeloablative conditioning (HR, 1.46 [99% CI, 1.19-1.78]), and posttransplant cyclophosphamide GVHD prophylaxis (HR, 1.85 [99% CI, 1.19-1.78]). These findings support current efforts to use umbilical cord blood graft expansion to shorten the duration of neutropenia.

One-year mortality was significantly higher for patients with MBI-LCBI (HR, 1.81 [99% CI, 1.56-2.12]), BSI-other (HR, 1.81 [99% CI, 1.60-2.06]), and MBI-LCBI plus BSI-other (HR, 2.65 [99% Ci, 2.17-3.24]) compared with controls. Moreover, one-year TRM (non-relapse mortality) among patients with malignant disease increased for patients with any BMI. There was no association of any BSI with the development of chronic GVHD.

Infection was more often reported as a cause of death for patients with MBI-LCBI (139 of 740 [18.8%]), BSI (251 of 1,537 [16.3%]), and MBI-LCBI plus BSI (94 of 435 [21.6%]) than for controls (566 of 4,740 [11.9%]). Additionally, infection as an associated secondary cause of death was higher in patients with MBI-LCBI (158 of 740 [21.4%]), BSI only (343 of 1,537 [22.3%]), and MBI-LCBI plus BSI (116 of 435 [26.7%]) than in the control group (739 of 4,740 [15.6%]).

To our knowledge, this is the first large-scale study to evaluate MBI-LCBI, the authors wrote. The inclusion of multiple centers provides a diverse population of all ages, stem cell sources, and transplant types and minimizes overreporting or underreporting biases inherent in single-center studies.

Each year, more than 50,000 HSCTs are performed worldwide, according to the researchers. Though transplant strategies and supportive care has evolved, leading to improved overall survival, patients who have undergone HSCT are still at high risk for BSIs and associated morbidity and mortality.

Reference:

Dandoy CE, Kim S, Chen M, et al. Incidence, Risk Factors, and Outcomes of Patients Who Develop Mucosal Barrier Injury-Laboratory Confirmed Bloodstream Infections in the First 100 Days After Allogeneic Hematopoietic Stem Cell Transplant.JAMA Network Open. doi:10.1001/jamanetworkopen.2019.18668.

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Where Will Vertex Pharmaceuticals Be in 10 Years? – Nasdaq

February 2nd, 2020 2:43 pm

It's easy to grasp how Vertex Pharmaceuticals (NASDAQ: VRTX) got to where it is today. A decade ago, the biotech's market cap hovered around $8 billion. Vertex's lead pipeline candidate was hepatitis C virus (HCV) drugtelaprevir, which went on to win FDA approval in 2011. The drug was marketed under the brand name Incivek -- but only briefly. Vertex quit selling the HCV drug in 2014 because Gilead Sciences'HCV franchise was dominating the market.

However, Vertex had another program in development targeting cystic fibrosis (CF). Its first CF drug, Kalydeco, won FDA approval in 2012. The rest is history. Vertex went on to gain FDA approvals for three other CF drugs. It's now highly profitable with annual revenue approaching $4 billion. And its stock has skyrocketed more than 500% over the last 10 years.

Trying to predict where Vertex will be 10 years from now isn't as easy. But there are some clues from the present that point to the prospects for another highly successful decade for the biotech.

Image source: Getty Images.

The safest prediction of all for Vertex is that it will remain a juggernaut in CF in 2030. Vertex won FDA approval for its most powerful CF drug yet -- Trikafta -- in October 2019. European approval for the drug is likely on the way this year.

Vertex expects that Trikafta will expand the addressable patient population for its CF therapies by more than 50%. The company also has three other CF drugs in its pipeline, including two programs that, like Trikafta, are triple-drug combos.

Currently, there are no other approved drugs that treat the underlying cause of CF. AbbVie is evaluating a triple-drug CF combo that it picked up from Galapagosin a phase 1 clinical study, but it's way behind Vertex. Even if AbbVie's drug proves to be successful, it would at best be several years before the drug could win approval. By that time, Vertex will already have further entrenched itself in the CF market.

Although the patents for Kalydeco, Orkambi, and Symdeko will expire near the end of the decade, Vertex's patents for Trikafta won't expire until 2037. The company could face generic rivals for its older CF drugs, but there's no reason to expect that Vertex's CF franchise won't still be racking up huge sales.

Vertex doesn't plan on being a one-indication company 10 years from now, though. The biotech has been busy expanding its pipeline and advancing the most promising programs.

The most likely addition to Vertex's lineup in 2030 will be a pain medication. Vertex has already completed phase 2 clinical studies for experimental pain drug VX-150. Chief Medical Officer and soon-to-be CEO ReshmaKewalramanisaid in Vertex's Q3 conference call in October that the company is "advancing multiple selective NaV1.8 inhibitors through late-stage research and early clinical development."

I think that Vertex and its partner CRISPR Therapeutics also have a good chance of launching a few years from now a gene-editing therapy that effectively cures rare blood disorders beta-thalassemia and sickle cell disease. The two companies are currently evaluating gene-editing therapy CTX001 in phase 1/2 studies targeting both indications and have reported encouraging preliminary results.

Another indication that could be a big winner for Vertex by the end of this decade is alpha-1 antitrypsin deficiency (AATD). Like CF, AATD is a rare genetic disease caused by misfolding proteins. Vertex has two experimental AATD drugs in early stage testing. My hunch is that the company's CF expertise combined with the similarity between AATD and CF could boost the odds of success for this program.

Vertex also has an early stage program targeting APOL-1 mediated kidney diseases. The biotech hopes to advance a drug to phase 2 testing this year. If all goes well, this could be yet another new arena for Vertex to dominate by the end of the decade.

Then there's the huge potential game-changer. Vertex acquired privately held Semma Therapeutics for $950 million last year. Semma is developing a drug that could cure type 1 diabetes.

Semma's approach is to turnpluripotent stem cells into islets that produce insulin in the needed amounts to keep blood sugar levels in check. This program is in its very early innings right now. So far, Semma has conducted promising lab tests but hasn't initiated any clinical studies in humans.

Curing type 1 diabetes presents an enormous opportunity for Vertex. Over 1.5 million people have type 1 diabetes in the U.S. alone. Vertex has had its eye on several companies in recent years that have made progress in addressing issues related to islet transplantation to treat type 1 diabetes. The big biotech thinks that Semma has a solution and is confident enough about its prospects to write a really big check to acquire the small drugmaker.

Will Vertex really have successful drugs on the market that target five or more rare genetic diseases in addition to more common indications like pain and type 1 diabetes 10 years from now? There's no way to know for sure. Many promising early stage programs fail along the way.

However, there are some things we can be certain about with Vertex. It claims a commanding lead in CF. It has the expertise needed to develop therapies targeting other rare genetic diseases. It has plenty of money to continue investing in research and development and acquisitions. And it has multiple shots on goal. Not all of them have to pan out for Vertex to win.

My view is that Vertex is the best biotech stock on the market right now. I think that it's future looks really bright.

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Keith Speights owns shares of AbbVie, Gilead Sciences, and Vertex Pharmaceuticals. The Motley Fool owns shares of and recommends CRISPR Therapeutics and Gilead Sciences. The Motley Fool recommends Vertex Pharmaceuticals. The Motley Fool has a disclosure policy.

The views and opinions expressed herein are the views and opinions of the author and do not necessarily reflect those of Nasdaq, Inc.

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The special legacies left by people who died too soon – Wales Online

February 2nd, 2020 2:43 pm

We have all heard heartbreaking stories about those who have battled lifelong illnesses or died in sudden and unexpected circumstances.

But sometimes when tragedy strikes it can also act as a way of highlighting issues and helping others suffering similar heartache.

Here we look at some of the wonderful legacies that are working tirelessly to keep alive the memories of people across Wales who were taken too soon.

Mathew Mizen was just 25 years old when he suddenly died following a short mystery illness.

A popular postman from Cwmavon, in Neath Port Talbot, he had been playing rugby for his beloved Cwmavon RFC just three weeks before he died.

After suddenly becoming ill he began to deteriorate and was admitted to hospital.

While his death at the time remained a mystery to his loved ones, tests later showed he died from acute respiratory distress syndrome with an underlying diagnosis of T-cell lymphoma.

His parents, Rhidian and Myra Mizen, decided to set up The Mathew Mizen Foundation in his memory as a way to give back to the community of Cwmavon.

"Mathew passed away suddenly in 2008 when he was 25," his father said. "He was a postman and then he went off work sick.

"He went into hospital on Boxing Day and passed away on January 4. He was taken into Singleton Hospital before they sent him to Cardiff.

"We found out that he had acute respiratory distress syndrome (ARDS). We thought for a while that we should do something.

"Mathew was one of the village postmen and played for Cwmavon rugby and cricket clubs so we thought we will start something up because of his connections with the village and all the money raised we would use for people living in the village."

The foundation in his name has now been running for a decade and has built up a reputation for its annual January charity dip at Aberavon beach.

After first starting out with around 15 people heading into the freezing-cold sea, now around 50 people are brave enough to take the plunge.

Mr Mizen added: "It's been going for about 10 years now. At the time my wife and I had a caravan in Pendine and we went into the pub one day and they were advertising for a swim on Boxing Day and I thought 'I wouldn't mind trying that' so we set one up for the Sunday that's closest to when Mathew passed away.

"In the first year we had about 15 people doing it but this year we had about 48 so it seems to be growing bigger and bigger.

"We've also done a cycle ride between the Principality Stadium and Aberavon rugby club and we've put on shows. A husband and wife in the village have done a skydive.

"With the funds we have been able to buy interactive whiteboards for Cwmafan School, new kit for the rugby team in the school, a new walking frame for a girl with cerebral palsy, and the most we've given is 2,500 for a young boy to play cricket."

Mr Mizen said both he and his wife still get approached by people in the village with fond memories of their son.

"He was helpful. We often get people saying 'Mathew was my postman and he helped me'. One woman said that he helped her move her fridge," he added.

"He was outgoing and loved his rugby. He was full of fun and was known for his smile everybody remembers him for his smile.

"I think Mathew would be proud and if he was alive he would be doing the dip and the shows himself.

"I'm hoping that he's looking down on us and smiling."

In February 2012 Rhian Mannings' life was turned upside down when her one-year-old son George died suddenly after suffering a seizure at home.

It was later discovered that George was suffering with bronchial pneumonia and a severe strain of type A influenza.

Just five days later her grief-stricken husband Paul took his own life.

Amid her darkest hour the Pontyclun mum set up the charity 2 Wish Upon A Star which provides support to bereaved families.

"My one-year-old son died suddenly in an A&E department and we left with no idea where to go next," she said.

"Five days later my husband took his own life. We received no support and had nowhere to turn.

"Within a few months I knew I wanted to help our local community in Miskin as they were the only support we received.

"I set up a fund and within weeks it was clear that I had identified a gap across Wales.

"People contacted me saying 'this has happened to me' so I decided to give up my job as a teacher and tried to put things in place for people who have lost a child."

One of the aims that the charity has is to have memory boxes available at hospitals across Wales for families who have suffered a loss.

Families can also be offered a referral to the charity's counselling services if they wish to do so.

"When George died they had nothing to keep memories so we have put things in place at every hospital so families can leave with something," Rhian added.

"We make sure there are facilities for families and at the moment there are nine family rooms in hospitals to make sure there's somewhere for them to sit down.

"The ripple effect of such tragedy brought the community together and we have raised over 1m through fundraising alone.

"I can't thank the people of Miskin enough. So many families need our support."

Helping other families who are going through similar tragedy is Rhian's way of keeping her son's legacy going.

Earlier this year 2 Wish Upon A Star was given a boost when Coldplay recorded a special version of one of their biggest hits for the charity.

She added: "George was my youngest and he was the happiest, easiest little boy who completed our family.

"We were a lovely family of five and had everything we wanted life was brilliant.

"Life will never be the same but we share memories and photos around the house.

"It's my boy's legacy and it will always be bittersweet."

When Ben and Catherine Mullany married in July 2008 no-one could have predicted the tragedy that would take place just days later.

While on honeymoon in Antigua the health professionals, both aged 31 and from the Swansea Valley, were shot by intruders in their luxury chalet.

Mr Mullany was in his third year of training to become a physiotherapist while his new wife was a paediatrician training to become a GP.

Mrs Mullany died instantly after being shot in the head while her husband was taken to hospital before later being flown home on a life-support machine.

Doctors at Morriston Hospital proceeded with brain stem testing but the day after his arrival his life-support machine was switched off.

Following a two-month trial in Antigua Kaniel Martin and Avie Howell were found guilty of murdering the couple and sentenced to life imprisonment.

The Mullany Fund was set up in their memory with the aim of helping young people realise their potential.

The charity harnesses the couple's passion for life sciences and encourages and helps young people take a step closer to pursuing a career in the medical field.

Project manager at the charity, Sarah James, said: "The project was set up in 2008 as a remembrance charity for Ben and Catherine.

"As a whole we believe that all young people should have equal opportunities to succeed.

"We work with partners to promote and encourage the ability of young people particularly aged between 14 and 19.

"In 2015 the charity was successful in gaining funding for an online mentoring project for young people where we work with volunteers across the UK.

"We work with schools, community groups, and students in Swansea, Neath Port Talbot, Rhondda Cynon Taf, Bridgend, and Merthyr Tydfil."

The mentoring scheme introduces young people to professional mentors who offer them advice and guidance as well as an insight into life sciences.

The charity's objective is to give every young person, regardless of their background, the opportunity to access a career in life sciences by providing the support they need to follow their aspirations.

"About 600 people across the five areas have registered for Mullany e-mentoring," Sarah added.

"We have had very positive feedback from the people involved and the mentors are happy to be involved as they feel like they are giving back."

Paul Popham battled kidney failure for more than half of his life but in the words of his daughter "you wouldn't have known he was ill".

From the age of 30 he was undergoing kidney dialysis but in later life he was dealt another blow as he was diagnosed with kidney cancer.

In October 2008 Mr Popham, from Swansea, was given just nine months to live and told that his only hope of living longer was to take a drug called Sutent.

The National Institute for Health and Clinical Excellence initially refused to fund the 30,000-plus treatment but when Mr Popham's family began collecting signatures, lobbying politicians, and even taking their fight to Downing Street, the Assembly finally made the drug available in January 2009.

It wasn't until four years after his prognosis that Mr Popham died at the age of 67 in October 2012.

In the following months his family and friends decided to set up the Paul Popham Fund to help other renal patients across Wales.

His daughter Joanne said: "The Paul Popham Fund was set up in memory of my father.

"He had kidney failure for over half his life but he dealt with it in a positive manner. You wouldn't have known he was ill. It did not define him.

"He played football, worked shifts at Alcoa, and brought up a family of four.

"From the age of 30 he was on dialysis and in the later years he got kidney cancer."

Mr Popham was actively involved with St Joseph's AFC throughout his life and was even a founding member.

"He was very fun-loving and very positive," his daughter added.

"He played football all of his life and was a founding member of St Joseph's football club and they still support the charity.

"He absolutely loved that club and I think it was his second family.

"He was also a member of the Labour party. He loved his music and was a family man."

Mr Popham's family and friends hoped that the charity could help other patients "lead a better quality of life".

After initially setting out to raise funds for Morriston Hospital's renal unit, the charity has since gone on to offer a befriending and counselling service.

"He was a positive man and we wanted to do something positive in his memory so we got family and friends together to talk about what we wanted to do," Joanne added.

"We set it up in March 2013 with the aim was to raise funds in memory of my father and donate them to Morriston Hospital's renal unit.

"It's for his legacy and to do what my father did to help people lead a better quality of life.

"We now also run a befriending and counselling service and train kidney patients to befriend and provide support to new patients.

"He would be proud of the work that we are doing but he wouldn't want his name on it as he was a private man.

"In terms of the work, he owed his life to the NHS and would always champion it.

"To think we are supporting them and patients like him, he would be over the moon."

It was in the run-up to Christmas that the lives of one young family from Cardiff changed forever.

While the Bates family were returning home from a festive party the lives of the happy family of four were destroyed in a split second as a car ploughed into two of them as they crossed a road near Miskin.

Dad Stuart was tragically killed while seven-year-old son Fraser was left fighting for his life.

He was rushed to a specialist hospital in Bristol for emergency care but sadly died several hours later as his injuries were too severe.

Mum Anna Louise and daughter Elizabeth, who was just three at the time, were not injured during the incident but have had to live with the pain of losing both Stuart and Fraser.

Just over a week after the unimaginable loss Anna Louise made the decision to focus her energy and grief on helping others going through similar heartache.

She set up the charity Believe to offer support and education around organ donation as her husband and son saved several lives when their organs were donated.

"We set the charity up within a week of the loss of my husband and son," Anna Louise said.

"I had a situation that you would not wish on anybody. I had had this conversation with my husband just a few weeks before about organ donation and I knew what they would have wanted me to do.

"It just struck me that no-one knew about organ donation and I did not realise that I could override my husband's wishes, even though he had opted in.

"It became really clear that it was time to talk about this and we wanted to break down the taboo and talk about it.

"Death and grief; it's a very traumatic time and I wanted to assist and provide support to others."

In recent years the charity has managed to create an animation aimed at children to help them understand organ donation, which has reached eight million people around the world.

The animation even went on to win at the Charity Film Awards in 2019, while Anna Louise has also received numerous awards for her work including a Pride of Britain award and The Points of Light.

The charity has also been working with schools throughout Cardiff, as well as the WJEC, to incorporate organ donation into the national curriculum.

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‘I was scared’: Abilene parents and children remember their pediatric cancer struggles – Abilene Reporter-News

February 2nd, 2020 2:43 pm

Cancer is not just an adult problem.

Whether it's a health fightin the public's eye or in private, children across the world claw, scratch and rip away in theirbattle with "The Big C."

An American Cancer Society report last year estimated2019 would seemore than 11,000 children between the ages of 1 and 14 diagnosed with some form of cancer. Of them, 1,190 would not survive.

Abilene is no safe haven. Those youngsters who are diagnosed must deal with more than just their fragile and failing health.

For them, cancer isn't just a disease. There's also a social element becausethey're in school when not undergoing treatment or at checkups.

Third-grade student, Ciara Husing'sdiagnosis was a death sentence. Not for her body, but for her standing in the social circles.

"They (fellow classmates)would be rude," said Ciara, now 10. "One girl told me 'You know you're going to die.'"

First, it was relief. Then reality set in for McKenzie Husing.

On a typically hot August afternoon in 2018, alone in her vehicle, Husing heldan envelope in her hands.She began to cry.

Its contents weretest results after a mass was removed from the knee of her daughter, Ciara.

Breathing in, she tore it. Two years of struggle, fighting, pain and anguishnot justCiara's but also her own channeled into that motion. She reached in.

It's contents read, "Synovial sarcoma."

Not cancer, she thought.

Then reality hit hard. It most certainly is cancer, and Ciara, then 8, was in the fight for her life.

Sarcomas are cancers of soft tissue, according to Dr. Douglas Harrison, center director of the pediatrics department at University of Texas MD Anderson Cancer Center in Houston.

Synovial, Harrison said, refers to the long bones that the cancerous soft tissue is attached to.

While synovial sarcoma is one of the most common forms of sarcomas in terms of diagnosis, it's not typical in children, Harrison said.

"A pediatric (cancer) diagnosis is a pretty rare phenomenon," Harrison said. "And (specific types) getrarer and rarer. It's extremely rare to be diagnosed with synovial sarcoma (in a pediatric case). So, it's not great that it's synovial sarcoma."

The most common diagnosis for children is acute lymphoblastic leukemia, he said. That's a cancer of the blood-forming tissue. Children nextare most susceptible to brain cancer, then soft tissue cancers, including but not limited to sarcomas.

It was 2016. Ciara Husing, a kindergarten student, complained about a bump on her left knee. It hurt to the touch, McKenzie Husing recalledher daughter saying.

"I thought it was growing pains, at first," Husing said. To be safe, the family took Ciara to the hospital for an x-ray. It came back normal.

But Ciara's pain didn't go away. Neither did the bump. In fact, the bump got bigger. And bigger.

Eventually, after several doctor visits, the diagnosis came back. Ciara had developed a condition called Osgood-Schlatter Disease. Or so the family was told.

Ciara Husing, 10, plays basketball during a league practice at First Baptist Church Dec. 5. She was excited to be playing again after the fight for her life. Ciara was diagnosed with synovial sarcoma, a tissue cancer found in the body's extremities, in August 2018.(Photo: Ronald W. Erdrich/Reporter-News)

"This was her tag," Husing said. "As a mom, I thought, 'Finally we had a diagnosis.' I didn't second guess the doctors. And her pain was real."

According to the Mayo Clinic's website, Osgood-Schlatter manifests asa bony bump on the shin directly below the knee cap and associated most often with young athletes as they undergo growth spurts. It's typical among girls ages 10-13. Boys develop it at a slightly older age.

Ciara was 6.

MORE: Ward Elementary teacher in Abilene is a Life Changer, like it or not

In hindsight, itwasclue No. 1 that something was terribly wrong with the determination. There would be others.

Ciara's "diagnosis" came in September 2016. By December, Ciara was in the waiting room of an orthopedic doctor. Combined with Husing's input, the doctor fitted Ciara with a knee brace.

But that was just a stop-gap measure.

By the time Ciara started first grade the next summer, she was leaving the brace at home while at school. It never really helped her much anyway, Husing said.

And the bump kept getting bigger. So Husing sent her daughter to school with knee pads on under her clothes. It led to some confidence problems as some teasing came along with the bulging joints.

Under normal circumstances, Osgood-Schlatter has specific symptoms. The bump, medical reports say, is not painful to the touch. And the inflammation tends to subside with enough rest.

Clue Nos. 2 and 3, Husing said.

Yet the Osgood-Schlatter disease diagnose continued.

Emergency room trips, visits to Cook Children's Hospital in Fort Worth and local doctor visits piled up, each doctor confirming what the previous one said despite the abnormal presentation. And each bill dropping the family deeper down a rabbit hole.

Ciara kept complaining about pain. Nothing was being done about it.

"I tried everything over-the-counter, everyhome remedy," Husing said. "Nothing worked."

So Ciara's father suggested they go to the doctor every time she complained about anything.

Jack Marcelain, left, survived a benign brain tumor diagnosed in 2005, when Marcelain was 6 years old. He's now a social work student at Abilene Christian University, studying to one day help families who are enduring what he and his suffered through. His mother, Tammy Marcelain, right, supports him through his journey.(Photo: Ronald W. Erdrich/Reporter-News)

In 2005, 6-year-old Jack Marcelain was diagnosed with a type of benign brain cancer called pilocytic astrocytoma.

It was his last month of kindergarten, his mother said. Surgery at Children's Medical Center Dallas removed about 96 percent of the tumor. However,the 4 percent that remained, in Jack's brain stem, was acting as the heart of the tumor.

Tammy Marcelain, his mother, remembers it well. Jack? Not so much.

"I was so young at that point," he said, "I knew what cancer was, but I never really knew the whole gravity of the situation."

Though it's all burned into her synapses, what Tammy Marcelain remembers most is the immediate aftermath of the surgery. The danger of operating on the brain, especially the brain of a 6-year-old, became reality.

For four weeks, Jack was unable to use his eyes. He was unable to speak. He was unable to walk. His parents moved him into Our Children's House in Dallas while Jack was recovering.

You're mad, scared, petrified (in the moment). But you can't live like that. You have to know where he went and know where we're going. We have faith in our religion and our God.

At 9, after years of the tumor regenerating, Jack endured radiation treatment, aimed at addressing that tumor's heart in his brain stem. It resulted in two things: the right side of Jack's face is paralyzed and the tumor eventually was halted.

With that one caveat, mission accomplished.

"That was what eventually stopped the tumor from growing," Tammy Marcelain said. "Once he was cancer-free, he progressed like a pretty normal kid."

Jack Marcelain, now a social work student at Abilene Christian University, hopes to translate that experienceat least, what he remembers from being a young childhood cancer patient and survivorinto a career helping families in situations similar to were his family found itself all those 15 years ago.

He has singled out the pediatric hospital setting as his focus. He just wants to make sure future him can help in any way possible anyone avoid some of the struggles his family endured making sure he was receiving the proper care.

"Social work was never something I knew what it was," Marcelain said. "I knew you helped people. As I was coming into college, I had narrowed down my focus to between that and ministry. I knew I wanted to work with people and found this was a really good way to help people .... andmake that time a little less stressful."

In March 2018, Ciara was climbing on her bed with her siblings when she fell.

Thump! She landed on the bump. The noise she made was unlike anything Husing said she'd ever heard from her daughter.

It was questionable Ciara Husing, 10, would ever play sports again after she was diagnosed with synovial sarcoma. But she runs circles around people now, despite a large scar on her left leg.(Photo: Ronald W. Erdrich/Reporter-News)

Still, there was no change in the diagnosis. But the doctor prescribed crutches for Ciara.

"We know now that she had a tumor on her nerve and she hit the dang thing," Husing said.

In April, they finally were able to convince the hospital to order an MRI on Ciara's knee. It came back with an irregularity: a bursa, doctors said, had formed as a result of the Osgood-Schlatter disease.

The family argued with doctors, sick of hearing the same diagnosis. At this point, they were self-made experts and they knew their daughter had something, and it wasn'tOsgood-Schlatter.

"We argued, we yelled," Husing said. "Some bad words were said. But as we were scrolling through the images from the MRI, I saw a flash of something. When I pointed it out, it looked like a crescent moon, but when I pointed to it, the doctor said it could be the bursa."

A bursa is a fluid-filled sac that develops near joints due to friction.

Finally, there was a light at the end of a darktunnel, Husing said. While they had no idea what actually was happening, they knew there was a foreign body affecting her knee.

Again, Ciara's pain and struggle was justified.

'I knew something was wrong'

With the bursa identified, it was time to remove it. Surgery.

It happened in August. Husing said they were told it would take 20-30 minutes.

Hours ticked by.

Finally, the surgeon camethrough the doors. Husing said her stomach dropped.

"My heart stopped," she said. "I thought she'd died. I mean, that's what you see in movies when the doctor comes out."

When you hear those words, you don't know who to call. There is no speed dial for when you're told your kid has cancer. You pray about it but you don't know who to call.

Once she was able to move, they were ushered into Ciara's recovery room.

The surgeon sat between mom and dad and looked them in the eye. He told them they did a good thing getting her to surgery. He told them she needed him to cut into their daughter.

He told them he found a massof some kind.

"He said he'd never seen anything like it before," Husing said. "He said he got it out of her, cut it open and it was black inside."

That's where Husing's imagination took over. She kept thinking about the doctor's words. As she got home, she jumped on Google and searched out phrases like "pediatric knee mass."

The results weren't what she wanted.

"I thought it couldn't be cancer," she said. "But in my mind, I knew."

It's one of the worst feelings in the world, Husing said.

"When you hear those words, you don't know who to call," Husing said. "There is no speed dial for when you're told your kid has cancer. You pray about it but you don't know who to call."

Eventually, she called Ciara's pediatrician, one of the many doctors who, up to this point, classified it as Osgood-Schlatter disease. There was an apology, Husing said. And an offer to put her in touch with a child life specialist.

I was so young at that point, I knew what cancer was, but I never really knew the whole gravity of the situation.

Husing refused.

In her anger, she refused to allow anyone but herself deliver the information to her daughter and the rest of her family. Hours after opening the envelope, she sat with Ciara and began her explanation.

It didn't go well, Husing said.

"The cry she let out was awful," she said.

At that point, she hadn't slept much. Less sleep came in the next few days as she waited for test results on the mass to come back.

That's when she opened the envelope in her car. That's when reality confirmed both her worst-case scenario and her daughter's story.

Within 45 days of Ciara's diagnosis, the child had seen more of the United States than she ever thought possible.

Aside from the trips to Cook Children's in Fort Worth, they flew to Cincinnati in September 2018. There, she had a lymph node biopsy done to see if the cancer had spread. Nine days later, Ciara had traveled to the East Coast, inBoston for an official consultation.

She was going in for surgery.

There, she met with the man who helped change her young life around: Dr. Ernest "Chappie" Conrad III.

Specializing in both adult and pediatric sarcomas, Conrad was able to save Ciara's leg.

It's called limb salvage surgery, a procedure Conrad excels at and has pioneered.

Essentially, Conrad removed a section of herleg and replaced the missing piece witha donor bone.

Since that surgery, Husing and her daughter have been to Houston tomeet with Conrad, who serves as a professor of medicine in the University of Texas McGovern Medical School at MD Anderson Cancer Center.

Thomas Elementary School students released balloons in November 2012 to honor Rex Fleming, 10, who died earlier that week after a two-year bout with brain cancer. Students and football teams at Abilene Christian University, where his father was employed, and at Abilene High had rallied around Rex.

(Photo: Joy Lewis/Reporter-News)

When Jill Fleming sees pink pom-poms at football games, or National Football League players wearing pink cleats in October, she gets frustrated.

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Foundation donates $18M to expand psychosocial care for cancer patients – Daily Bruin

February 2nd, 2020 2:42 pm

A foundation has gifted $18 million to UCLA Health to expand an integrative patient-care program, according to a university press release Thursday.

The Simms/Mann Family Foundations donation will expand the Simms/Mann-UCLA Center for Integrative Oncology which focuses on psychosocial care intended for cancer patients and their families in California. This holistic approach includes psychiatric care, along with educational programs about nutrition and meditation.

The foundations donation is led by Victoria Mann Simms and Ronald Simms, who have previously donated to programs that work to advance integrative medicine and provide care to cancer patients. Their donation will provide funding for the center.

The endowment will also improve a training program offered by the center that trains providers in integrative care.

Since the centers founding, it has cared for over 50,000 patients, held more than 310 lectures and provided training for over 100 fellows for oncology-based psychosocial care around the country.

The Simms/Mann Foundation has now donated over $33 million to UCLA. The donors are also founding board members of the Geffen Playhouse and are credited with supporting other UCLA programs, such as the Jules Stein Eye Institute.

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Foundation donates $18M to expand psychosocial care for cancer patients - Daily Bruin

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5 Easy Ways to Start Meditating – Duke Today

February 2nd, 2020 2:42 pm

Rather than fight an energy dip with caffeine in the afternoon, Daniel Hatch closes his eyes and puts on headphones to block noise. He focuses on breathing deeply through his nose and out of his mouth for five minutes.

For me, Ive found that meditating in the afternoon is almost like taking a nap, said Hatch, a biostatistician for the Duke School of Nursing. I feel less anxious afterward. It calms me down and I feel refocused.

Meditation, the practice of observing your thoughts and feelings without judgment, can be a beneficial habit for reducing anxiety, depression and high blood pressure and improving sleep, according to the National Institution for Healths National Center for Complementary and Integrative Health.

Focusing on your breathing is one way to be in the moment. Take a look at four other pieces of advice from Duke University and Health System experts on starting your own meditation practice.

For two decades, Duke neurosurgeon Patrick Codd has practiced Zen, a sect of Buddhism that aims for enlightenment through meditation.

He suggests starting with two minutes of meditation each day and increasing to five, then 10 minutes, as youre able to complete each length of time. Codd started meditating in five minute increments and now does it two to three times a week. He sits on a comfortable cushion in a quiet room and turns his attention toward counting his breaths for about 30 minutes.

Youll get frustrated and give up if you over challenge yourself, Codd said. Know that its going to take some practice. Any little bit can count.

When Jocelyn Weiss needs to focus energy, she takes a short walk from her office to a Duke Integrative Medicine meditation room, where she sits on a cushion, closes her eyes and takes deep breaths.

Its good to have an area specifically for meditation, said Weiss, Duke Integrative Medicines education and training coordinator. Its like avoiding your bed for anything but sleep. You want your mind and body to know thespace is designated to meditate.

At home, Weiss uses a corner in her bedroom for meditation. She sits on a cushion and places incense and flowers on a low table.

Create a space that makes you comfortable and is free of distractions, offering the greatest opportunity to focus on your practice, Weiss said. If you need back support, you can lean against a wall. If you like certain aromas, then have them nearby.

By her sophomore year at Duke, Natasha Gupta had a hard time shaking anxiety about balancing coursework and social pursuits.

After years of ignoring her dads advice to meditate, she gave the practice a shot with Duke Universitys student-led Buddhist Meditation Community and fell in love with meditation.

I felt calmer and like I had more space in my head, said Gupta, now a senior majoring in economics and English. Meditation helped me come to terms with my emotions.

Gupta leads one of two weekly guided meditation classes at the Student Wellness Center. The classes continue through the academic year and are open to all Duke community members. Check the Student Wellness Centers website for updates on time and location.

Gupta said finding a community was essential to her practice. It gave her a designated time to meditate each week and friends to discuss her struggles and successes.

They helped me get started, she said. Now, they hold me accountable.

Sometimes Jocelyn Weiss needs a little assistance to get into the right headspace for meditation.

She gets help from InsightTimer, a free app for Apple and Android users that has about 30,000 guided meditation programs in a range of topics from helping the user prepare for sleep, to feeling more gratitude to dealing with stress.

Headspace is also available for a free trial on Apple and Android software. The app has guided meditation and mindfulness sessions to help with focus, anxiety, sport performance, sleep and more.

The app can be that little push I need to get me going, Weiss said.

WATCH our short video to learn about the benefits of practicing mindfulness.

Have a story idea or news to share?Shareit with Working@Duke.

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Need to tame your stress? Try mindfulness – The Detroit News

February 2nd, 2020 2:42 pm

Lu Quang Pham was just weeks into his first year of medical school at Oakland University last fall when he already felt completely overwhelmed.

There was endless studyingand classes. Before moving to Michigan, the California nativestruggled with panic attacks. Talking to his brother or parentsalways helped him feel better when one hit, but his family wasn't nearby anymore.

Then Pham, 28, heard about a special training program right on campus designed tohelp medical students better manage their stress,take care of themselves and prevent burnout. It was called Mindfulness-Based Stress Reduction.

Offered by Beaumont Hospital's Center for Mindfulness, Pham took the eight-week class late last year. Today, he feels so much better about the long, stressful road ahead to becoming a doctor.

Dr. Ruth Lerman, left, and Lucy Sternburgh extend their arms into a yoga position as part of one class.(Photo: Beaumont Hospital)

"I found it extremely valuable," Pham said. "It taught me to createa habit to dedicate time to my mind and toself-care."

Mindfulness -- a practice once considered on the fringesof treatment options-- is moving into the mainstream these days as an effective tool for reducing stress and even managing chronic pain.

There's a Mindful magazine. Time Magazine put the practice on its cover, calling it a "Mindful Revolution." And schools across the country are incorporating mindfulness into their curriculumsto ease student anxiety.

Mindfulness programs are popping up across Michigan. The Ann Arbor Center for Mindfulness offers a range of classes and has eight instructors. The University of Michigan Health System offers drop-in classes for staff and students. And the Grand Rapids Center for Mindfulness has classes for adults and children as young as 9.

"Students are drawn to our classes, retreats and events to learn more

about mindfulness, support their own practice and enhance their sense

of well-being," said Claire Weiner, an instructor at the Ann Arbor Center for Mindfulness.

Beaumont's Center for Mindfulness, which opened in 2014,teaches eight-week Mindfulness-Based Stress Reduction courses three times a year to both employees and the public.

Experts say mindfulness is a type of awareness that uses different methods, including yoga and meditation, to help people focus on their thoughts, physical feelings and surroundings in the present moment. But it isn't about relaxation.

Dr. Ruth Lerman, left, and Lucy Sternburgh, center, teach a class as part of Beaumont's Mindfulness-Based Stress Reduction course.(Photo: Elizabeth Debeliso)

"The primary intent behind mindfulness is not relaxation; it's awareness," said Dr. RuthLerman, a breast care specialist, mindfulness teacher and medical director of Beaumont Center for Mindfulness.

And research shows that it works. In a study published in 2012 in the Annals of Surgical Oncology by Lerman, Robert Jarski and several medical students, they found Mindfulness-based Stress Reduction helped improve the recovery of breast cancer survivors, significantly improving their quality of life and reducing symptoms of stress.

Lerman said she did the study because mindfulness wasn't on her colleagues' radar asa tool to help cancer survivors or to manage chronic pain.

"I had to put it in a context and a language that gave it validity," said Lerman.

Mindfulness-Based Stress Reduction was founded by Jon Kabat-Zinn, now aprofessor emeritus of medicine. In the latethe 1970s,he recruited chronically ill patients who weren't responding to traditional medicine to try a new stress reduction program. It has since become known as Mindfulness-Based Stress Reduction and Kabat-Zinn went on to found theStress Reduction Clinic and the Center for Mindfulness in Medicine, Health Care, and Society at the University of Massachusetts Medical School.

Lerman, a three-time breast cancer survivor, discovered Kabat-Zinn and mindfulness during her second bout with cancer. She said while she was emotionally able to process having cancer the first time, it hit her hard the second time. She reacted more like a regular person than a doctor, she said.

"I was scared," she said.

Looking for tools to cope,Lerman reached out to Rachel Remen, a renownedexpert on integrative medicine, who suggested she take up yoga. Yoga eventually led Lerman to Kabat-Zinn and mindfulness.

"It's about being present in what's happening in the moment," said Lerman, who eventually became an instructor and taught some of her first classes to doctors and cancer survivors.

Lucy Sternburgh,program manager of Beaumont's Center for Mindfulness, studied the mind-body connection during graduate school. She remembers working in Beaumont's cardiac rehab unitwhere they taught patientsphysical exercises but never touched on the stress component.

"For me, it was very apparent that there was a very unaddressed emotional and stress issue," said Sternburgh, who discovered Kabat-Zinn and Mindfulness-Based Stress Reduction while getting her doctorate.

Sternburgh, who at one point managed Beaumont's employee wellness programs,eventually started offering lunchtime mindfulness seminars to Beaumont employees. She said there's an "emotional overload" that health care workers face.

"And it manifests itself as a physical shutdown," said Sternburgh. "For health care workers, it's this sense of 'I have nothing left to give.' It's numbness."

But surveys taken before and after Beaumont's eight-week classes show mindfulness can help.

During a recent orientation session on a blustery day in late January, a group of roughly a dozen people of all ages and races, mostly women,gathered for an orientation session to learn more about Beaumont's eight-week course at Adat Shalom Synagogue in Farmington Hills. Classes also are offered at Royal Oak Beaumont.

Several people had been referred by the Karmanos Cancer Center. Some were battling breast cancer. One woman was a social worker. Another had heard about the training through a colleague and decided to check it out.

Sternburgh led the group through the history of Mindfulness-Based Stress Reduction and what would be required over the next eight weeks. At-home daily meditation is a requirement of the class. The course also culminates with a day-long silent retreat to really solidify each person's practice.

Alumni and current students of Beaumont's mindfulness program gather for an all-day silent retreat.(Photo: Elizabeth Debeliso)

During a brief 10-minute meditation session during the orientation, Sternburgh guided the group to pay attention to sounds, surroundings and how each person was feeling. When it was over, one woman began to cry. She'd recently lost her daughter, after both her husband and son had died.

"I had to let it out," she said.

Sternburgh believes one reason mindfulness has grown in popularity is because so many people feel isolatedin today's chaotic world.

"I really do think there's an epidemic of loneliness and isolation that is painful for people," she said. "And so much of digital and social media doesn't fill that void of meaningfulness and connection."

Surveys both before and after Beaumont's classes have found a decrease in burnout and increased feelings of peacefulness, said Sternburgh.

"Its like theyve been looking for the answers outwardly," said Sternburgh. "Theyve rarely seen their inner resources."

Lexi Gird, a graduate student who lives in Hazel Park, took Beaumont's course last year and calls it a "profound experience." She's still practicing what she learned, practicing daily meditation while attending a weekly meditation class and yoga.

"I just loved the whole process," she said. "Just being with the group and having just a dedicated space just to check in every week that was designated for stress reduction was just really important."

Gird even took her training a step further when she attended a five-day silent retreat -- which includes no cellphones and no talking at all -- at a center in Clarkston.

"It really solidified my practice," Gird said.

Dr. Ruth Lerman, center, leads an exercise during a mindfulness class.(Photo: Elizabeth Debeliso)

Lerman admits that mindfulness isn't for everyone. It takes practice. And Beaumont's classes aren't cheap -- they're $350 for an eight-week session, though scholarships are available.

But with home practice, "it's wonderfully transformational," said Lerman.

As for Pham, he's still practicing what he learned and thinks more medical students should take the training. He likes to do a walking meditation as he walks to class, focusing on how he's feeling at that moment.

He hasn't had a panic attack since he took the mindfulness course.

"I feel much less stressed," he said. "It's had such a positive impact on my well-being."

mfeighan@detroitnews.com

What is Mindfulness

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