Monthly Archives: January 2020

Human Behavior

Simple and effective- Best ways to dispose of plastic! – Times of India

India consumes an estimated 16.5 million tonnes, about 1.6 million truck full of plastic annually, of which 25-30% percent remains uncollected as per this June 2018 report. The plastic processing industry is estimated to grow to 22 million tonnes per year by 2020, as per another study. The sad part is that the current situation of disposing plastic is not easy to explain. One cannot dispose of plastic like other forms of garbage. Plastic is strong, flexible and durable, making it extremely useful and hard-to-break. As useful as it might be, it does create harm to the environment by entering the oceans every day and staying there forever, becoming toxic 'food' for marine life. Plastic Waste Crisis'; var randomNumber = Math.random(); var isIndia = (window.geoinfo && window.geoinfo.CountryCode === 'IN') && (window.location.href.indexOf('outsideindia') === -1 ); console.log(isIndia && randomNumber The consumption of plastic has been increasing by 10 percent year-on-year but the disposal methods of plastic have not evolved and that makes the situation murky for us. Multiple factors add to the problem - for instance, theres no segregation at the waste source, many amongst us still use one bin for all kinds of waste. Lack of awareness about segregation leads to a bigger problem. Plastic makes up about eight percent of total solid waste in India, according to the government and this plastic comes from the use of single-use plastic such as bags, cutlery and straws alone. It is estimated that 80% of marine litter comes from land and this hotchpotch ends up in landfills. However, it should be considered that plastic itself is not that bad, but the way people dispense it, that creates a negative environmental impact. We all need to work towards changing this.

Simple Habits Need To Change

The problem is irresponsible human behavior in disposing of plastic. If recycled, plastic can be made to form recycled polyester which in turn is made to produce a number of things like shoes, T-shirts, bags, etc. thereby causing less strain on natural resources, then plastic has value. Every individual can contribute by making small changes in their consumption and dumping patterns. To begin with, lets follow these simple, basic rules:

Be The Change You Want To See

We all know how we have polluted our surroundings by neglecting the way we use and dispose of plastic. To improve the quality of living, we will have to go back to the basics we had all learned in school:

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Simple and effective- Best ways to dispose of plastic! - Times of India

Human Behavior

Nature up close: Are humans really the smartest species? – Wink News

CBS NEWS

This story is by Sunday Morning contributing videographer Judy Lehmberg, who is a former college biology teacher who now shoots nature videos.

Ive been thinking and reading a lot about non-human animal intelligence recently. One thought that continues to run through my head is the meaning of the word anthropomorphic. The more I think and read, the more Ive come to feel it is a word that shouldnt exist.

Anthropomorphic, from anthropos (human) and morphe (form), means attributing human actions and thoughts to non-human animals. Fine. Except, who evolved from whom? Other animals didnt evolve from us. We, Homo sapiens, at a mere 200,000 or so years old, are one of the new kids on this Earth. We didnt directly evolve from wolves or moose or elephants, but they were here first. Therefore, it is logical that our thoughts and emotions evolved later than those of any other animal.

And since we share many similar structures and DNA with other organisms who were here first, it is logical to assume our brains evolved in a similar manner and have some of the same intelligence and emotions. We should be talking about gorillaopomorphic or chimpomorphic or even animalmorphic, not anthropomorphic. They arent emulating us; were emulating them, because they were doing it first.

The more time I spend watching animals, the more I see humans in them. Weve all heard stories about elephants mourning their dead, including seeming distraught due to the absence of a family member. Crows and ravens can pull up long strings tied to a horizontal bar with a piece of meat on the other end. They pull the string up as far as they can, trap it with a foot, and repeat until the morsel is within reach. A chimpanzee in a Swedish zoo was discovered to spend his early mornings hiding rocks behind logs and hay piles he created and later using them to throw at zoo visitors. Guess he didnt want company! Ive watched a female fox bury the remains of one of her babies after a badger killed and ate most of it. Ive seen bison and elk mourn the death of their babies for hours, sometimes all day long, after a wolf or bear got it. We once watched a bison mom who had given birth to a stillborn calf fend off wolves for hours, until she was exhausted. She then suddenly left only to return with some of her friends as reinforcements. There are many, many other examples.

One of the reasons I started thinking about animal intelligence was because of a story I heard years ago about an orangutan at a zoo that kept getting out of its locked enclosure and letting the rest of the orangutans out with him. I had believed that story because I knew orangutans were smart, but I didnt have any proof it was true, until the head zookeeper involved told it on NPRs Radiolab.

Jerry Stones was the head zookeeper in the 1960s at the zoo in Omaha, Nebraska. One day some of his keepers came to him and said all the orangutans were loose and up in the trees near the elephants. They all ran to the orangs, lured them back to their enclosure, and then tried to figure how they had gotten out. Jerry was sure one of the keepers had forgotten to lock the enclosure door. Over the next few weeks it happened several more times with the same results. The keepers swore they were making sure the door was carefully locked. Jerry threatened to fire someone. Several days after the last escape, one of the keepers came running to Jerry and said, You have to come see this. They snuck up to the orangutan enclosure and watched Fu Manchu, the dominant male, fiddling with the door lock. He had something in his hand, but they couldnt figure out what it was. As they watched they realized he had a piece of wire he slipped into the slit between the door and the door stop and skillfully get it around the door latch. Then he pulled on both ends of the wire and the latch pulled out of its hole. They were free!

Jerry and the other keepers were amazed but they still had the wherewithal to stop the orangutans, and confiscate the wire. They later realized Fu Manchu was hiding the wire in the area between his lower lip and teeth.

He was not only using a tool; he was using a tool in a way he had never been taught and he was storing it for future use. I guess his one mistake was that he was too nave to watch for people spying on him.

We know a growing number of animals, from Darwins finches to chimpanzees, are capable of using tools. But here was an animal hiding a tool he knew he would lose if discovered, and planning to use it in the future.

Many biologists who study animal behavior dismiss the idea of nonhuman higher intelligence or emotion. I had a very highly-respected animal behavior professor in college who was absolutely scornful of a young, uneducated woman who had the audacity to go to Africa and study chimpanzees and horror of all horrors! she also had the nerve to name them human names, such as David Greybeard and Frodo rather than Chimp 1, Chimp 2, Chimp 3, etc. Of course, that young woman was Jane Goodall, who has contributed so much to our knowledge of chimps and is now considered the worlds foremost chimp expert.

I wonder what we would discover if we were smart enough to understand their language? And if we really are the smartest species, why are we in the process of destroying the Earth with our overpopulation, global warming, destruction of habitat, etc.? Maybe we should be learning from them.

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Nature up close: Are humans really the smartest species? - Wink News

Cell Biology

Six is better than two: assay assesses multiple cellular pathways at once – Baylor College of Medicine News

Scientists strive to have a better understanding of the complex biological processes involved in health and disease, and what they can learn usually goes hand-in-hand with the number, quality and type of measurements techniques provide.

Cancer, for instance, usually originates through changes on many different genes and pathways, not just one, but currently most cell-based screening assays conduct single measurements, said Dr. Koen Venken, assistant professor of biochemistry and molecular biology, and pharmacology and chemical biology at Baylor. We thought that if we could see what happens to more than one cellular pathway at once, we could have a more complete picture of what goes on inside a cancer cell.

To get a more detailed picture of the cellular processes that differentiate normal versus cancer cells, researchers resort to conduct several independent screening assays at the expense of time and additional cost.

In his lab at Baylor College of Medicine, Venken and his colleagues apply state-of-the-art synthetic biology, cell biology, genetics, genome engineering and transgenic technologies to have a better understanding of the processes involved in cancer.

Our goal in this study was to measure multiple cellular pathways at once in a single biological sample, which would also minimize experimental errors resulting from conducting multiple separate assays using different samples, said Venken, a McNair Scholar and member of the Dan L Duncan Comprehensive Cancer Center at Baylor.

Dr. Alejandro Sarrion-Perdigones, first author of the paper, wanted to develop an experimental assay that would expand the number of molecular pathways that can be studied simultaneously in a cell sample.

He focused on developing a multiplexed method a method for simultaneously detecting many signals from complex systems, such as living cells. He developed a sensitive assay using luciferases, enzymes that produce bioluminescence. The assay includes six luciferases, each one emitting bioluminescence that can be distinguished from the others. Each luciferase was engineered to reveal the activity of a particular pathway by emitting bioluminescence.

To engineer and deliver the luciferase system to cells, we used a molecular Lego approach, said co-author Dr. Lyra Chang, post-doctoral researchers at the Center for Drug Discovery at Baylor. This consists of connecting the DNA fragments encoding all the biological and technological information necessary to express each luciferase gene together sequentially forming a single DNA chain called vector. This single vector enters the cells where each luciferase enzyme is produced separately.

Treating the cells with a single multi-luciferase gene vector instead of using six individual vectors, decreased variability between biological replicates and provided an additional level of experimental control, Chang explained. This approach allowed for simultaneous readout of the activity of five different pathways (a control makes number six), compared to just one using traditional approaches, providing a much deeper understanding of cellular pathways of interest.

The new assay is sensitive, saves time and expense when compared to traditional approaches, reduces experimental error and can be adapted to any research field where the dual luciferase assay is already implemented, and beyond.

In addition to applications in cancer research, as we have shown in this work, our multiplex luciferase assay can be used to study other cellular pathways or complex diseases across different research fields, Venken said. For instance, the assay can be adapted to study the effect of drugs on insulin sensitivity in different cell types, the immune response to viral infections or any other combinations of pathways.

Interested in this new technology? Find all the details in the journal Nature Communications.

Other contributors to this work include Yezabel Gonzalez, Tatiana Gallego-Flores and Damian W. Young, all at Baylor.

This work was supported by start-up funds provided by Baylor College of Medicine, the Albert and Margaret Alkek Foundation and the McNair Medical Institute at The Robert and Janice McNair Foundation. Additional support was provided by March of Dimes Foundation grant #1-FY14-315, the Foundation For Angelman Syndrome Therapeutics grant FT2016-002, the Cancer Prevention and Research Institute of Texas grants R1313 and R1314 and the National Institutes of Health grants 1R21GM110190, 1R21OD022981 and R01GM109938.

The authors dedicate this work to the memory of Dr. Alejandro Sarrion-Perdigones, who passed away before the paper was published.

By Ana Mara Rodrguez, Ph.D.

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Six is better than two: assay assesses multiple cellular pathways at once - Baylor College of Medicine News

Cell Biology

Scientists Have Grown Snake Venom Glands in The Lab. Here’s Why That’s Awesome – ScienceAlert

For the first time, scientists have produced snake venom toxins in the lab, opening up a much-needed path for developing drugs and venom antidotes that doesn't involve having to breed and milk real-life snakes.

The toxins have been produced through mini glands called organoids, following a process adapted from growing simplified human organs something that is already helping in a wide range of scientific and medical research projects.

In the case of the snakes, researchers were able to blow organoids matching the Cape coral snake (Aspidelaps lubricus cowlesi) and seven other snake species, and they say this new approach is a welcome upgrade on current methods of farming snakes to extract their venom.

"More than 100,000 people die from snake bites every year, mostly in developing countries," says molecular biologist Hans Clevers, from Utrecht University in the Netherlands. "Yet the methods for manufacturing antivenom haven't changed since the 19th century."

By tweaking the recently developed process for growing human organoids including reducing the temperature to match reptiles rather than mammals the researchers were able to find a recipe that supports the indefinite growth of tiny snake venom glands.

Tissue was removed from snake embryos and put into a gel mixed with growth factors, but access to stem cells which is how human and mouse organoids are usually developed wasn't required.

The cells quickly began dividing and forming structures, giving the team hundreds of growing samples in the space of a couple of months, and producing small white blobs from which venom toxins could be harvested.

Al least four distinct types of cell were identified by the researchers within the artificially grown venom glands, and they were also able to confirm that the venom peptides produced were biologically active, closely resembling those in live snake venom.

Snake venom gland organoids. (Ravian van Ineveld/Princess Mxima Center)

"We know from other secretory systems such as the pancreas and intestine that specialised cell types make subsets of hormones," says developmental biologist Joep Beumerfrom Utrecht University.

"Now we saw for the first time that this is also the case for the toxins produced by snake venom gland cells."

The use of snake venom toxins to develop medicines and treatments has been going on since the time of ancient Greece. In the modern age, drugs fighting everything from cancer to haemorrhages have been developed with the help of toxins we find in snake venom.

Having faster and more controlled access to these toxins could mean these treatments can be developed more easily and on a shorter time scale, say the researchers.

Besides drug development, these organoid venom glands should make it easier and faster to develop antivenoms and with so many people suffering deaths, injuries or disabilities because of snake bites, that will make a considerable difference.

"It's a breakthrough," snake venom toxicologist Jos Mara Gutirrez from the University of Costa Rica, told Science.

"This work opens the possibilities for studying the cellular biology of venom-secreting cells at a very fine level, which has not been possible in the past."

The research has been published in Cell.

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Scientists Have Grown Snake Venom Glands in The Lab. Here's Why That's Awesome - ScienceAlert

Cell Biology

Quench Bio emerges with $50M to treat severe inflammatory disease – FierceBiotech

Most treatments for inflammatory disease have single targets, such as an inflammation-promoting cytokine or a protein complex called an inflammasome. Quench Bio is taking aim at a family of proteins involved in inflammatory cell deathand its picked up $50 million to do so.

Incubated at Atlas Venture since its inception in 2018, Quench's first target is gasdermin D, the best understood member of the gasdermin family of proteins. With its $50 million in series A cash, the company expects to fund three years worth of research, as well as come up with its first clinical candidate, CEO Samantha Truex told FierceBiotech. It also hopes to screen for drug candidates that inhibit other members of the gasdermin family.

Gasdermin D plays a role in multiple inflammatory cell death pathways; when those pathways are activated, the protein forms pores in the cell membrane.

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By forming pores, it does two things: one is it allows for the release of inflammatory signals. Those can be inflammatory cytokines, alarmins, or what we call DAMPs: danger-associated molecular patterns, Quench CEO Samantha Truex told FierceBiotech.

In addition, once enough of those pores form, the cell membrane loses its integrity and the cell literally explodes in an inflammatory way, she added.

One of those types of cell death is called pyroptosis, derived from pyroliterally firewhile another is NETosis, a type of cell death linked to white blood cells called neutrophils. The hope is that inhibiting gasdermin D will delay cell death, or lead cells to die by apoptosis, a quieter, calmer, noninflammatory form of cell death, Truex said.

Gasdermin could be a more complete way to treat inflammatory disease as it is downstream of inflammasome targets like NLRP3 and upstream of pro-inflammatory cytokines, like IL-1 beta, Truex said. For example, targeting NLRP3 could stop cells on their way to pyroptosis if NLRP3 is indeed the inflammasome that is triggered, she said. But the drug would be ineffective if the cell has another inflammasome triggered, such as NLRC4 or pyrin, she said.

And Quench believes that going upstream of the release of cytokines and heading off explosive cell death could be a better approach than aiming to block a cytokine that is already being released. Truex said.

Its almost like an hourglass, with inflammatory targets at the top, and at the bottom there are things leaking out of the cell. If we hit at the middle, we can have an impact on all of it, she said.

Quench spent most of 2019 coming up with its clinical game plan. As it looks to 2020, the company still has much to learn about its targets.

We assessed over 25 diseases in the autoimmune, autoinflammatory and severe inflammatory category and we have come to the conclusion that pyroptosis and NETosis are known to be associated with numerous inflammatory diseases, Truex said. Those include rheumatoid arthritis, lupus, nonalcoholic steatohepatitis (NASH) and multiple sclerosis. The company isnt sharing yet which ones its going after first, but Truex noted that the company plans to work on treatments for diseases that have no treatments, or those that have many treatments, but still have unmet need.

We could start with rare diseases and subsets of patients with lupus and rheumatoid arthritis who appear specifically to have disease driven by gasdermin D. Our center of excellence in gasdermin biology will do more research in gasdermins role in those diseases in parallel with our efforts to discover inhibitors of gasdermin, she said.

Quench draws its series A funding from RA Capital Management and AbbVie Ventures, as well as Atlas Venture and Arix Bioscience.

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Quench Bio emerges with $50M to treat severe inflammatory disease - FierceBiotech

Cell Biology

A new study reveals a link between sleep and glowing skin – Times of India

If your skin has been looking dull and lifeless, then you need to look at your sleep pattern. A good night's sleep can actually be good for your skin, which is now backed by scientists. A new study by Nature Cell Biology shed light on how a good night rest can be good for your skin.The study was conducted on mice and their collagen. It was found out that the sleep phase can regulate the extracellular matrix, which provides structural support to cells in the form of connective tissue like bone, skin, cartilage, etc. Half of our body is made of matrix and half of it is collagen.The study discovered that collagen is made of two types of structure. One is a thicker form, which is fully formed by the age of 17. It remains the same for the rest of our lives and is permanent. The second type is the thinner structure, which breaks down under stress. The study found out that these structures can actually repair itself while we rest at night.The thinner fibres protect the permanent structures from the daily wear and tear on the skin cells."If you imagine the bricks in the walls of a room as the permanent part," says lead author Karl Kadler, B.Sc., Ph.D., "the paint on the walls could be seen as the sacrificial part which needs to be replenished every so often."Collagen is the most abundant protein in the body. It provides the glow and improves skin's elasticity and strength. Beauty sleep is pretty much real, as good rest can now actually help to boost collagen naturally.

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A new study reveals a link between sleep and glowing skin - Times of India

Cell Biology

Books in Brief: Lucky Caller by Emma Mills, From the Desk of Zoe Washington by Janae Marks; Wild Honey From the Moon by Kenneth Kraegel – Buffalo News

YOUNG ADULT

Lucky Caller by Emma Mills; Henry Holt, 323 pages ($17.99) Ages 14 and up.

...

Emma Mills has a gift for creating appealing characters, believable family situations and funny dialogue, and "Lucky Caller" is a well-crafted gem of a teen romance.

Hoping for an easy and fun elective her senior year, 17-year-old Nina signs up for a radio broadcasting class where she is teamed up with a volleyball player, a wooden-voiced guy named Joydeep and Jamie, a childhood friend she has been trying to avoid since an awkward incident in 8th grade. Her parents are divorced, and her absentee father is actually a popular deejay in California, but Nina struggles to master the technical side of broadcasting, accidentally broadcasting remarks that weren't meant to be public. Her team's grade will depend on how many listeners they can get for their "Sounds of the '90s" music show.

But classmates find ingenious ways to sabotage each other's radio shows, and Nina finds herself in a pickle when she invites her dad to guest-host a broadcast and a rumor spreads that the frontman of an obscure '90s band is going to appear on the show. The drama at school unfolds while Nina's home life is undergoing a major change: her mother is getting remarried, to a dentist who has a popular YouTube show offering paint-by-numbers tutorials. An unlikely hero emerges to save the day, offering a perfect ending to this sweet story.

Even the setting for much of the action an old apartment building called the Eastman in Indianapolis where Nina and Jamie both live is charming. There's also an incidental STEM aspect to the book. Nina's mother works in science; the author finished her PhD in cell biology while writing "Lucky Caller."

CHILDREN'S

From the Desk of Zoe Washington by Janae Marks; Katherine Tegen Books/HarperCollins, 286 pages ($16.99) Ages 8 to 12.

...

A 12-year-old girl works through conflicts with her mother and her best friend and turns her passion for baking into more than a hobby, all while fighting for justice for her imprisoned dad in this marvelous debut novel by Janae Marks for middle-grade readers.

Zoe lives with her mom and stepfather in the Boston area and knows very little about her biological dad, Marcus, who has been in prison since he was convicted of murder at the age of 19 before she was born. Then Zoe gets a birthday letter from Marcus, mailed from prison (he calls her "My Little Tomato"), and without telling her mother, she writes him back.

With each letter and song recommendation, she feels as though she's getting to know her real dad. He says he is innocent of the crime he was convicted of, but Zoe isn't sure whether to believe him. Why would an innocent person be in prison? Marks offers a compelling mystery as Zoe and her friend Trevor research the crime and then search for the alibi witness who was never called to testify at Marcus' trial.

Marks has managed to write a middle-grade novel that explores racial justice issues and addresses the routine bias Zoe faces (funny looks when she's out with her white stepfather, being tailed by clerks at stores while shopping with her mom) while also dealing with such coming-of-age issues as changing friendships with boys. She also offers a compelling portrait of a girl with a serious interest in pursuing her passion for baking, interning at a bakery where she experiments at inventing a new cupcake flavor that will wow the owner. The book also serves as a valuable introduction to The Innocence Project for its target audience.

PICTURE BOOK

Wild Honey From the Moon by Kenneth Kraegel; Candlewick Press ($17.99)

...

A mother shrew is willing to go to the moon and back to cure her sick young son in this whimsical, sweet story with delicate and distinctive illustrations by a self-taught artist. Young Hugo's "feet were hot, his head was cold, and he just slept and slept." According to "Dr. Ponteluma's Book of Medical Inquiry and Physiological Know-How," the only cure is "a teaspoon of wild honey from the moon." In lyrical and humorous style, Kraegel spins storyteller magic his appealing tale is divided into short chapters as mama shrew outwits a Great Horned Owl, falls into a raging stampede of "night mares," hitches a ride with a butterfly and braves swarms of angry bees to get what she came for.

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Books in Brief: Lucky Caller by Emma Mills, From the Desk of Zoe Washington by Janae Marks; Wild Honey From the Moon by Kenneth Kraegel - Buffalo News

Immunology

Quench Bio Closes $50M Series A Financing to Advance First-in-Class Medicines Targeting Gasdermin to Treat Severe Inflammatory Diseases – BioSpace

Experienced team focused on inhibiting inflammatory cell death underlying a range of severe inflammatory diseases

CAMBRIDGE, Mass., Jan. 27, 2020 /PRNewswire/ -- Quench Bio, a company leveraging new insights into gasdermin biology and innate immunology to develop medicines for severe inflammatory diseases, today announced the completion of a $50 million Series A financing led by RA Capital Management ("RA Capital"), with participation from new Investor Abbvie Ventures. Atlas Venture ("Atlas") and Arix Bioscience plc ("Arix", LSE: ARIX) who co-founded and seeded the company, also participated in the Series A. Quench Bio has incubated at Atlas since inception.

Led by a team of drug developers and scientists with deep experience in inflammation and small molecule drug discovery, Quench Bio's lead therapeutic approach centers on inhibiting Gasdermin D, which has been recently discovered as a key target at the core of multiple inflammatory cell death pathways, including pyroptosis and NETosis. When pyroptosis or NETosis pathways are activated, gasdermin is processed and forms lytic pores on the cell membrane, allowing release of inflammatory cytokines, alarmins, DNA and NETs. Pyroptosis and NETosis are associated with numerous inflammatory diseases, including rheumatoid arthritis, lupus, multiple sclerosis and nonalcoholic steatohepatitis (NASH), among others.

"Targeting gasdermin provides a unique therapeutic opportunity, as there are currently no marketed therapies inhibiting inflammatory cell death," said Samantha Truex, CEO of Quench Bio. "Unlike approaches that target individual inflammasomes or cytokines, by targeting gasdermin, we aim to simultaneously inhibit multiple inflammatory cell death pathways that drive severe inflammatory diseases."

"We are excited about Quench Bio's first-in-class approach to potentially enable effective treatments for important autoimmune diseases with significant unmet medical need and we look forward to supporting this exceptional team as they pioneer modulation of gasdermin biology, an important and promising novel target in inflammation," said Josh Resnick, M.D., Managing Director and co-head of Ventures at RA Capital, who will join the Quench Bio board as a new director alongside Adam Houghton, Head of AbbVie Ventures. Other board members include Samantha Truex as CEO, Bruce Booth of Atlas Venture, Jonathan Tobin of Arix Bioscience, Herbert Waldmann, Director at the Max Planck Institute and Jo Viney, President, CSO and Co-Founder of Pandion Therapeutics.

"Gasdermin inhibitors have the potential for impact across a broad range of indications, including severe inflammatory diseases with few current treatment options," said Bruce Booth, DPhil, Quench Bio board chairman and partner at Atlas Venture. "Having assembled a world-class team of leaders in drug discovery, inflammation and gasdermin biology, as well as a renowned board and advisory team, Quench Bio is well-positioned to harness this potential to discover new medicines for these patients."

Quench Bio was founded in 2018 by Atlas, Arix, Mark Tebbe, Ph.D., Chief Technology Officer, and Mike Nolan, Ph.D., Head of Biology, together with Arturo Zychlinsky and Herbert Waldmann, both Directors at The Max Planck Institute who collaborated with the Lead Discovery Center on inhibitors of NETosis and gasdermin.

About Quench Bio Quench Bio is a biotechnology company leveraging new insights into gasdermin biology and innate immunity to develop medicines for severe inflammatory diseases. Quench's lead compounds target and inhibit the pore-forming protein Gasdermin D, a central player in both pyroptosis and NETosis pathways that mediates the release of inflammatory cytokines, alarmins, DNA and NETs. Quench Bio launched in January 2020 with $50 million from leading life science investors including Atlas Venture, Arix Bioscience, RA Capital and AbbVie Ventures. To learn more, visit please visit http://www.quenchbio.com.

About Atlas VentureAtlas Venture is a leading biotech venture capital firm. With the goal of doing well by doing good, the company has been building breakthrough biotech startups for over 25 years. Atlas works side by side with exceptional scientists and entrepreneurs to translate high impact science into medicines for patients. Our seed-led venture creation strategy rigorously selects and focuses investment on the most compelling opportunities to build scalable businesses and realize value. For more information, please visit http://www.atlasventure.com.

About Arix Bioscience plcArix Bioscience plc is a global venture capital company focused on investing in and building breakthrough biotech companies around cutting edge advances in life sciences. Arix collaborates with exceptional entrepreneurs and provides the capital, expertise and global networks to help accelerate their ideas into important new treatments for patients. As a listed company, Arix is able to bring this exciting growth phase of our industry to a broader range of investors. For more information, please visit http://www.arixbioscience.com.

About RA CapitalRA Capital is a multi-stage investment manager dedicated to evidence-based investing in public and private healthcare and life science companies that are developing drugs, medical devices, and diagnostics. The flexibility of its strategy allows RA Capital to provide seed funding to startups and to lead private, IPO, and follow-on financings for its portfolio companies, both facilitating the crossover process and allowing management teams to drive value creation from inception through commercialization. For more information, please visit http://www.racap.com.

About AbbVie VenturesAbbVie Ventures is the corporate venture capital group of AbbVie. We are a strategic investor, investing exclusively in novel, potentially transformational science aligned with AbbVie's core R&D interests. We measure success primarily by the extent to which our investments foster innovation with potential to transform the lives of patients that AbbVie serves. AbbVie Ventures enables its portfolio companies with both funding as well as access to AbbVie's internal network of experts across all phases of drug development, from drug discovery through commercialization. For more information, please visit http://www.abbvie.com/ventures.

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Company Codes: LSE:ARIX

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Quench Bio Closes $50M Series A Financing to Advance First-in-Class Medicines Targeting Gasdermin to Treat Severe Inflammatory Diseases - BioSpace

Immunology

Should You Buy Allergan Before the AbbVie Acquisition Closes? – The Motley Fool

Allergan's (NYSE:AGN) days as a standalone company are numbered. We don't know exactly when AbbVie's (NYSE:ABBV) pending acquisition of Allergan will close, but it should happen sometime in the first quarter of 2020.

This deal certainly lit a fire beneath Allergan stock, with the drugmaker's shares soaring 45% since the transaction was first announced. But is Allergan still a stock to buy with the AbbVie acquisition likely to close so soon?

Image source: Getty Images.

It's first important to understand the terms of AbbVie's acquisition offer. Allergan shareholders stand to receive 0.866 AbbVie shares plus $120.30 in cash for each Allergan share that they own.

When the deal was announced in June 2019, this translated to a total transaction value of around $63 billion. Based on AbbVie's share price at the time, the acquisition valued Allergan at $188.24 per share.

Today, though, AbbVie's shares are trading more than 10% higher than they were seven months ago. And Allergan's share price is now around $192, a little higher than its valuation when AbbVie's plan to buy the drugmaker was disclosed.

These transaction terms should be at the forefront of investors' minds when considering whether or not to buy Allergan stock. The reality is that AbbVie and Allergan are already joined at the hip even before the deal is finalized.

If you're hoping to make a quick profit, Allergan's share price will depend largely on whether AbbVie's shares go up. Even if Allergan announces wonderful news over the next few weeks, shareholders will still only receive $120.30 in cash for each Allergan share they own. But any significant good news for Allergan should push AbbVie's share price higher, which in turn will benefit Allergan shareholders when the transaction closes.

Long-term investors thinking about buying Allergan stock should focus even more on AbbVie's prospects. This isn't a merger of equals. AbbVie is a much bigger company than Allergan is. AbbVie's shareholders will own 83% of the combined entity.

It's important to remember the main reason why AbbVie is buying Allergan. Sales are declining for AbbVie's top-selling drug, Humira, in the face of competition from biosimilars in Europe. Biosimilars will enter the U.S. market in 2023 -- and that's when the pain will really intensify for AbbVie. The Allergan acquisition is being made to reduce AbbVie's dependence on Humira, but the immunology drug will still contribute close to 40% of the company's total revenue even after the Allergan transaction closes.

Basically, there are only three reasons to buy Allergan right now:

If the first reason is your primary motivation for buying Allergan, my view is that you're making a mistake. There's no guarantee that either AbbVie or Allergan stocks will pop over the next few weeks before the acquisition closes.

However, I think that the second reason listed to buy Allergan right now makes sense. Although Humira's best days are behind it, AbbVie has other drugs that should drive growth, especially including cancer drugs Imbruvica and Venclexta and new immunology drugs Rinvoq and Skyrizi. Allergan's Botox and antipsychotic drug Vraylar should also boost AbbVie's sales.

If you're an income-seeking investor, buying Allergan before the AbbVie acquisition closes seems like a pretty astute move. You'll get a lot of your cash back relatively quickly thanks to the cash portion of AbbVie's acquisition offer. You'll also own shares of one of the more attractive dividend stocks on the market, with AbbVie's dividend currently yielding nearly 5.4%.

All this, of course, assumes that AbbVie's acquisition of Allergan will wrap up as expected. Could something derail the deal? It's possible but very unlikely at this point. If you're considering buying Allergan, your fortunes are almost certainly linked to AbbVie, too.

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Should You Buy Allergan Before the AbbVie Acquisition Closes? - The Motley Fool

Immunology

Research Roundup: Astronauts and osteoporosis, fungi diversity and new cancer drug – The Stanford Daily

Each week, The Dailys Science & Tech section produces a roundup of the most exciting and influential research happening on campus or otherwise related to Stanford. Heres our digest for the week of Jan. 19 Jan. 25.

Martian astronauts likely to develop osteoporosis

Future astronauts headed to Mars will likely develop osteoporosis, or brittle bones, by the time astronauts reach Mars or return to Earth, a study published on Jan. 22 in Public Library of Science One predicts.

If you have a fracture on the surface of Mars, it will take at least a year to get back to Earth, Eneko Axpe, a materials science and engineering postdoctoral fellow, told Stanford Medicine blog SCOPE. It puts the astronauts lives and the mission at risk.

Experimental models suggest that for a round trip of 400 to 600 days between Earth and Mars, astronauts may lose 15 to 22% of their bone mineral density. An estimated two-thirds of returning astronauts would develop osteopenia, a precursor to osteoporosis.

A lot of people focus on the technological challenges of getting to Mars, or the psychological challenges of being in a spacecraft for 1,000 days, but not necessarily the fact that your bones decay, materials science and engineering assistant professor Eric Appel told Stanford Medicine blog SCOPE. Can people even make it, or will they be jello by the time they get there?

Fungi diversity predicted to decrease in the next 50 years

North American pine forests could stand to lose over a quarter of ectomycorrhizal fungi species by 2070 due to the effects of climate change, a study published on Jan. 21 in Journal of Biogeography found.

Ectomycorrhizal fungi have a symbiotic relationship with trees and plants in forested areas. The fungi envelop a host root system to provide a larger surface area for resource absorption.

These are critical organisms for the functioning and the health of forests, associate biology professor Kabir Peay told Stanford News. We have evidence to suggest that these fungi are as susceptible to climate change as other kinds of organisms and their response may be even more important.

The researchers collected 1,500 soil samples from 68 pine forests in North America, then compared geographical fungi against historical climate data. The findings suggested climate strongly predicted the fungi patterns in North America. The team then used the data and applied it to future climate projections to understand how future climate would affect fungi diversity.

According to our models, climate change over the next 50 years could eliminate more than a quarter of ectomycorrhizal species inside 3.5 million square kilometers of North American pine forests, Brian Steidinger, a postdoctoral research fellow in biology, told Stanford News. Thats an area twice the size of Alaska.

One of the things thats kind of shocking and a little bit scary is that we predict there will be some pretty significant decreases in diversity in western North America, well known culturally for fungal diversity and for people who are interested in collecting edible mushrooms, Peay told Stanford News.

Newly developed cancer drug inspired by antiviral treatments

In developing treatments intended to fight viral diseases, collaborating researchers spanning different disciplines inadvertently developed a novel cancer drug class effective in mice, a study published on Jan. 22 in Science Translational Medicine reports.

Weve been working for many years on potent drugs that we had shown were important for viruses, Jeffrey Glenn, medicine, microbiology and immunology professor, told Stanford Medicine News. This is just an important target that hasnt really been appreciated in cancer, and we had the perfect drugs to get this started.

The cancer drug works by disrupting normal cellular functions that viruses and cancer cells utilize to grow and spread. The findings suggest the newly developed drug can shrink tumors and prevent spread in mice models.

I think thats the secret thing, having chemists physically in the lab with biologists, virologists and physician-scientists, Glenn told Stanford Medicine News. Weve leveraged the special enabling environment of Stanford to create a unique group that has never existed before here or in academia. Its allowed things to happen that just wouldnt have happened otherwise.

Contact Derek Chen at derekc8 at stanford.edu.

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Research Roundup: Astronauts and osteoporosis, fungi diversity and new cancer drug - The Stanford Daily