MIAMI (CBSMiami) Scientists are working to create a robot that can detect all kinds of emotions. They say the benefits could help patients with a range of mental health disorders.

The robot is called Abel, and it is learning to smile, snarl, and frown. Twenty motors under his artificial skin give the robot emotions just like us. Engineers hope someday Abel will be a friend for people with behavioral, social, or cognitive disorders like autism or Alzheimers.

We want Abel to know how people are feeling to keep them healthy, not just physically, but mentally and emotionally, researcher Lorenzo Cominelli said.

To make Abel look eerily real, engineers teamed up with special effects artist Gustav Hoegen. His company has created animatronics for Hollywood hits Star Wars and Jurassic Park.

Right now, someone has to wear sensors for the robot to recognize their emotions. The next step may seem like something out of science fiction. Researchers say they want to give Abel a human brain with the help of tissue taken from stem cells.

Organoids are basically an aggregate of stem cells which self-assemble and self-organize to resemble the structure and function of a mini-human organ, researcher Arti Ahluwalia said.

Scientists say that would allow Abel to read our expressions all on his own. And if theyre successful, expect the team and Abel to look a bit smug.

Researchers acknowledge they are years away from their goal, but they believe Abel will one day not only be able to recognize emotions on his own but be able feel them too.

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Scientists Working On Robot That Can Detect All Kinds Of Emotions In Hopes Of Helping Patients With Mental Health Disorders - CBS Miami

Skin Stem Cells Comments Off on Scientists Working On Robot That Can Detect All Kinds Of Emotions In Hopes Of Helping Patients With Mental Health Disorders – CBS Miami | June 8th, 2021

In March, Australian scientists announced a worldwide important model of an early human Embryo, blastoids, using skin cells. The finding was crucial because it enables researchers to explore the reasons for infertility, developmental abnormalities, and miscarriage in a period of human development that is not yet accessible without human embryos. The International Stem Cell Science Organization published.

In the past week of May, new criteria for early human life research are to be conducted. The International Stem Cell Research Society guidelines include current progress such as the iBlastoid models and offer several recommendations that assist scientists in understanding more about the early phases of human life. The procedures also include: There are also apparent indications, such as genetic tampering, of what should not be permitted.

The most significant proposal is to modify the 14-day limit, a regulatory line-in-the-sand that scientists cannot experiment with human embryos in Australia and nearly a dozen nations. The 14-day limit stems from the 1980s when human seeds could not be grown longer than roughly six days after fertilization. Although modern technology currently allows scientists to cultivate embryos beyond 14 days in the laboratory, the rule is that research to take them further has not taken place.

Why fourteen days? On day 14, a human embryo is no longer a cell ball. It develops the primitive stripe, the beginning of the neural cord, eventually leading to the central nervous system. At a period when embryo research was a reasonably novel notion with the twin advantage of creating confidence while at the same time allowing space for early human development study, the deadline offered total certainty. Since scientists can cultivate human embryos for longer, revisions to these standards have been called for a long time.

What restrictions can instead be established to manage research on human embryos? The recommendations suggest that researchers who wish to develop human briefings above the two-week mark should assess their project by case to determine when they have to terminate investigations, subject to many rounds of assessment. The recommendation of the ISSCR for embryos or models from human stem cells, like the blastoids produced by Professor Jose Polo with his colleagues at Monash University, is of particular relevance to Australian science.

The new rules declare because most laws worldwide do not regard such embryo models to be identical to human embryos that they are not subject to the 14-day rule limitations. This statement directly contradicts the guidelines with the Australian law of 2002, which defines an embryo not only as an egg and sperm product. But as an embryo created by any other process that initiates organized development of a biological entity with a human nuclear genome or an altering human nuclear genome that may develop.

iBlastoids can simulate several elements of embryo development, making it a fantastic study tool. However, they have sufficient molecular and cellular composition modifications that scientists see as differing from human embryos. However, under Australian laws, iBlastoids are subject to existing human embryo research regulations, including a research license and the fourteen-day limit, as the National Health and Medical Research Council decided. Australian iBlastoid research will require discussion on the concept of a human embryo and maybe regulatory reform under the latest international principles.

To identify reasons for ingratitude, developmental anomalies, and malfunction, we have operated with human embryos and human embryo models ethically and responsibly. A timely reminder is made of the complete and bold ISSCR standards, which frequently need a change in the legislation to comply with science and allow advances such as IVF to occur.

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Embryo research law requires updating to match up with science - Cleveland American

Skin Stem Cells Comments Off on Embryo research law requires updating to match up with science – Cleveland American | June 8th, 2021

Every skin care fanatic has a favorite step of their routinethe layer of the ritual that brings them the most joy. And while I love the tender act of massaging in a dense face cream or slipping on an oil at night, there is nothing I appreciate more than washing my face. Yes, it's a semi-controversial skin care take (as controversial as those can be), but it's true: I love the ritual of cleaning my skin.

But face washes are a deceptively tricky category. For some time, the reigning options were of the strip-your-face variety. (You know the ones: Those sudsy numbers that left you feeling squeaky and dry.) But now, there are so many that experiment with textures, infuse deliciously hydrating actives, and elevate sensorial experiencesand finally, they're getting due attention.

There's no better example of this than the cleansing balm. (Even saying "cleansing balm" feels like slipping into a cashmere sweater.) The subcategory of face washes is marked by their thick, gel-cream texture and hydrating benefits; of course, there are subtle differences between them that make them unique, but that's the throughline.

Now, if all of the above has you thinking you need to get your hands on one, here are our favorites for you to try. Enjoy, won't you?

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The Creamiest, Dreamiest Way To Wash Your Face: 13 Must-Try Cleansing Balms - mindbodygreen.com

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Abel has 20 motors under his human-like skin that allow him to show feelings just like us.

LONDON, UK Scientists in Italy are working to create a robot that can detect all kinds of emotions.

The robot is called Abel, and it is learning to smile, snarl, and frown. Twenty motors under his artificial skin give the robot "emotions" just like us. Engineers hope someday Abel will be a friend for people with behavioral, social, or cognitive disorders like autism or Alzheimer's.

Researcher Lorenzo Cominelli says, "We want Abel to know how people are feeling - to keep them healthy, not just physically, but mentally and emotionally."

To make Abel look eerily real, engineers teamed up with special effects artist Gustav Hoegen. His company has created animatronics for Hollywood hits "Star Wars" and "Jurassic Park."

Right now, someone has to wear sensors for the robot to recognize their emotions. The next step may seem like something out of science fiction. Researchers say they want to give Abel a human brain with the help of tissue taken from stem cells.

Researcher Arti Ahluwalia says, "Organoids are basically an aggregate of stem cells which self-assemble and self-organize to resemble the structure and function of a mini-human organ." Scientists say that would allow Abel to read our expressions all on his own. And if they're successful, expect the team and Abel to look a bit smug.

Researchers acknowledge they are years away from their goal, but they believe Abel will one day not only be able to recognize emotions on his own but be able feel them too.

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Humanoid robot has super realistic facial expressions and it's kind of eerie - KHOU.com

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Aging is the ultimate risk factor for most diseases, such as cancer, neurodegenerative, cardiovascular, diabetes, degenerative fibrosis and many others. When we are young, we are typically healthy, despite a predisposition that will lead inevitably to a specific degenerative condition. However, the degenerative processes do not kick in until a certain age, when we are older. It looks like when we are younger, the body can compensate cumulative stress and damage caused to our cells in the tissues, allowing to maintain that equilibrium, called homeostasis, that keeps our organs functional and healthy. However, over time this buffering capacity becomes thinner and thinner, until things wear off: our tissues stop working as they used to. These changes are typically caused by an initial small number of rare but bad cells, that progressively increase over time, causing additional damage to the good cells that eventually stop working efficiently, causing a vicious cycle. Eventually the bad cells take over leading to the onset of a disease.

Our body is equipped with a number or regenerative and healing functions. Some are intrinsic in every cell, such as DNA repair mechanisms that are triggered when something compromises the integrity of our genomic structures. These are important functions that enable a cell, for example when it replicates, to repair errors and other damages that might have happened to our DNA. For example, two large proteins called ATM and ATR, involved in the cellular response to DNA damage, are responsible to maintain genomic instability caused by intrinsic and external DNA-damaging agents, such as UV light or various chemicals and toxins. A lack of functions of these proteins results in progressive neurodegeneration, immunodeficiency, predisposition to malignancy or radiation sensitivity. Mutations on the genes encoding these proteins can cause premature aging and premature development of these diseases, but this occurs also naturally, over time.

Cells also have an intrinsic immune system, producing factors called interferons employed by the cells as antiviral agents and to modulate other immune functions. It can be triggers by a viral infection so when a cell is infected will release interferons, protecting the neighbor cells against potential infection. Interferons can also suppress growth of blood vessels preventing tumors to get nutrients and growing. They can also activate immune cells so they can better fight viruses, tumors and others agents. Unfortunately, an age-related decline or impaired innate interferon functions in the cells results in a number of negative consequences in the body, such as increased susceptibility of the elderly to infections, tumors and damage.

In the body there are several cell types responsible to keep the tissues in check. The immune system is specialized to recognize remove and remember damaging agents. Those could be external, such as virus, bacteria or parasites, or internal, such as tumorigenic cells or senescent cells (see below). The immune system is a very sophisticated network of cell types, intercommunicating with each other to maintain the body clean from damaging factors. As we age the immune system also ages and loses capacity to recognize or responding to these damaging agents. It also become exhausted by an increasing chronic inflammation that progressively accumulate as we age, phenomenon also called inflammaging.

Another important repairing mechanism is the regenerative tissue functions, driven by the stem cells. Those cells are progenitor cells, often dormant in a quiescent state in the tissue and waiting to be activated by some damage. Stem cells are critical because once activated they can generate a progeny of daughter cells capable of re-growing the damaged tissue back to its original structure and function. Stem cells have another important function: they can regenerate themselves, in a process called self-renewal. This is important so that the new repaired tissue can repeat the process if a new damage occurs. The regenerative capacity of our body is remarkable, allowing our tissues to keep their integrity, health and functions. However, over time also stem cells age or respond to the aged microenvironment where they live (called the niche), and they become less efficient to repair tissues or to self-renewing. As a result, our tissues change, become atrophic, fibrotic or dysfunctional leading eventually to diseases.

In regenerative medicine, the application of stem cells resulted of the generation of multiple new therapeutic opportunities. A promising area uses stem cells to generate bioengineering strategies to grow new tissues in a petri dish to be then transplanted in the body to repair damaged tissues. Some applications are already in clinical use, such as for skin grafts. Many others are on their way, either in preclinical development or in clinical trials for many different tissue types and for different clinical indications.

Another promising stem cells application is the direct transplantation into damaged tissues, where they can grow and engraft repairing. However, as we age stem cells become less efficient. What if we If we could rejuvenate them? We could restore their capacity to repair our tissues and maintain homeostasis. Promising and exciting strategies are advancing in that direction. For example, we and others showed that it is possible to reprogram epigenetically a cell so it can become the younger and healthier version of itself (Sarkar et al., 2020). This is a mechanism that every cell has encoded in its DNA, but normally works only in the germline (the sperm and the egg) during the embryogenesis to make sure that the cellular clock is turned back to zero, before initiating the cellular programs to generate the embryo. This important for example to prevent making old newborn babies. This intrinsic rejuvenative mechanism is locked in the other somatic cells of the body. We found it is possible to re-activate it transiently and safely, without changing the identity of the cell, enabling to push back the cellular clock of aged human cells to make them healthier and restore their functions. These technologies are under development to be translated into therapeutics with the promise that one day could rejuvenate the aged cells in the body so they can become the younger version of themselves, repeating the process over time when needed.

Among many of the drivers of the aging process, there is one that seems to stands out as the lower hanging fruit among the emerging space of the longevity therapeutics. This is cellular senescence. Every damage that occurs to the cells in our body can push the cells to stop what they are doing and activate a safety mechanism that locks them into an arrested state called cellular senescence. Senescent cells cannot replicate anymore preventing them to cause additional damage, such as becoming cancer cells. All sort of damage can trigger this response leading to cellular senescence such as, oxidative stress, mitochondrial dysfunctions, DNA damage, viral infection, cigarette smoking, pollutions, chemicals, etc. They all can induce that safety lock and push damage cells to become senescent.

Senescent cells dont die easily but they stick around in the tissue, accumulating slowly over time. Importantly, cellular senescence is a pleiotropic mechanism, meaning it can be both good or bad. When we are young, we can efficiently get rid of senescent cells. The body uses them positively such as for tissue repair, wound healing or tissue remodeling. However, as we age, and our immune system ages (partially trough cellular senescence, a phenomenon called immune-senescence), our body become less efficient in removing senescent cells, which then start to accumulate.

Being able to make a new generation of drugs that are very selective for senescent cells, will enable the promise to achieve rejuvenative clinical results in humans similarly to what we found in preclinical results. On that end, we recently published a targeted strategy with the goal to advance the field in that direction (Doan et al., 2020). Using a prodrug, we engineered a small molecule to generate a selective senolytic compound to develop a targeted therapy. This prodrug is inactive in non-senescent cells but activated by senescent cells, taking advantage of an enzymatic function of those cells. In geriatric mice this prodrug showed to be well tolerated but also efficacious to clear senescent cells, resulting in restored cognitive functions, muscle functions, stem cells functions, vitality and overall health. As we advance senolytic drugs to the clinic to treat age-related diseases, it is very important to be mindful that elderly individuals, who are frail, with co-morbidities and exposed to multiple medications, will not well tolerate drugs that are not safe and effective. Importantly, not all senescent cells are the same. They are rare, interspersed in the tissues but are also very heterogeneous. Being able to hit the right senescent cells, in the right diseased tissue will be key to enable effective therapies. Developing drugs that are very potent, selective and potent and safe will be pivotal.

The longevity therapeutics space is emerging, but is already disrupting the medical industry. The goal of longevity therapeutics is not just to add years to life, extending lifespan. The true goal is to add life to years and extend health span. A target that gets closer every day.

Marco Quarta is CEO, Rubedo Life Sciences.

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The Rise of Longevity Therapeutics - Pharmaceutical Executive

Skin Stem Cells Comments Off on The Rise of Longevity Therapeutics – Pharmaceutical Executive | May 28th, 2021

NEW ORLEANS (WGNO) Several contract workers were burned during a gas well explosion on Belle Isle along the Gulf of Mexico on Tuesday.

Of those wounded, three were reported taken to University Medical Center the regions only Level I verified trauma and verified burn center.

According to Dr. Jeffrey Carter, Medical Director of the UMC Burn Center and professor of surgery at LSU Health-New Orleans, speed is of the essence when it comes to successful treatment of burn victims.

At 2:56 pm, Acadian received a report of a well fire. We sent 4 helicopters and 5 ground units to Morgan City (LA). We transported two patients by air (1 to NOLA and 1 to Lafayette area) and 2 patients by ground (both to NOLA)

Delays in medical treatment can result in increased amounts of resuscitation, increased length of hospital stays, increased infection risks and increased kidney problems.

Its important to realize here in Louisiana, we have a fair number of risks. About 85 percent of all hazardous waste travels through our port or rail here in New Orleans, said Dr. Carter.

There are over 3,000 rigs, gas and pipeline areas here that are at risk along the gulf. When we have injuries that occur from industrial accidents, what we find is that the mortality is increased by about 20 percent if there is a delay of about two hours in transporting the patient to a center where they can get definitive care.

Dr. Carter says being an academic medical research center, UMC is able to offer the latest technology in the treatment of severe burns.

On the forefront of burn care is the use of RECELLs spray-on skin by Avita Medical, in which the doctors take a small portion of the patients own skin, dissolve it and pull the stem cells, and then -apply it at the time of surgery.

Dr. Carter explained and demonstrated the use of RECELL during a Zoom interview with WGNOs Aaron S. Lee on Wednesday.

He also discussed how the use of artificial intelligence will soon revolutionize how burn victims are treated and how quickly they recover.

That video clip can be seen below:

According to Dr. Carter, half of his patients suffer burns to their hands and face as these are areas not covered, especially in the deep south. This can be worrisome to the victim after recovery as those are places people notice first when interacting with another person.

Not to mention, the face is extremely complex with the amount of movement and how it changes over time.

The use of RECELL on a burn victims face is making skin grafts a thing of the past.

A skin graft is like putting a piece of plywood on your roof when it has a hole in it, explained Dr. Carter. It doesnt look the same. It doesnt act the same. It doesnt behave the same.

While its OK for some types of injuries, said Dr, Carter, its not necessarily the best thing.

Dr. Carter goes on to explain the benefits of using of the RECELL system and ultimately allowing burn patients to heal themselves using their own cells during recovery.

The FDA is considering RECELL for pediatric burns, with Dr. Carter serving as one of the clinical trial investigators.

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Burn victims like the wounded Belle Isle contractors in good hands at UMC, spray-on skin at forefront of care - ArkLaTexHomepage

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CRANFORD, N.J., May 25, 2021 /PRNewswire/ --Citius Pharmaceuticals, Inc. ("Citius" or the "Company") (Nasdaq: CTXR), a biopharmaceutical company dedicated to the development and commercialization of first-in-class critical care products with a focus on anti-infective products in adjunct cancer care, unique prescription products and stem cell therapy, today announced that it has received the Best Poster Award at the prestigious International Society for Cell and Gene Therapy (ISCT) 2021 Annual Meeting.

The poster, titled "Novel Induced-Mesenchymal Stem Cells (i-MSCs) Attenuate Severity of ARDS in Septic Sheep," will be presented today, May 25, 2021 by Dr. Perenlei Enkhbaatar, Professor and Director of the Translational Intensive Care Unit at The University of Texas Medical Branch.

"The ISCT annual meeting brings together the brightest minds in cell and gene therapy and highlights cutting edge research in the field," stated Dr. Myron Czuczman, Chief Medical Officer and Executive Vice President of Citius. "We are honored to be selected for the Best Poster Award from among this distinguished peer group. The interim results demonstrate a marked improvement in i-MSC treated animals over control animals in key clinical parameters including: improved oxygenation, less systemic shock, and reduced bacterial burden and vascular injury to the lungs. We are encouraged by the data and welcome the support and engagement of the scientific research community," concluded Dr. Czuczman.

Myron Holubiak, President and Chief Executive Officer of Citius added, "We are grateful to be recognized by our peers for this award as we advance our novel stem cell program for the treatment of ARDS. In parallel to the expansion of our proof-of-concept ARDS sheep study, we are following guidance from the U.S. Food and Drug Administration (FDA) in the development of a cGMP Master Cell Bank of i-MSCs. I am pleased to report that we have completed the development of an i-MSC Accession Cell Bank (ACB) which is to serve as the basis for a scalable cGMP compliant manufacturing capability to support all of our planned pre-clinical and clinical trials. Compared with donor-derived cells that require a continuous supply of new donors, we believe our i-MSCs,derived from a single clonal induced pluripotent stem cell (iPSC), offer multiple advantages including consistent and scalable manufacturing and a potentially limitless supply of i-MSCs to meet our future needs. Moreover, we believe that our i-MSC stem cell program has the potential to meaningfully impact the treatment of ARDS and we appreciate the recognition received from the cell and gene therapy community as we advance our program."

Citius' i-MSCs are derived from iPSCs originating from a qualified single-donor dermal fibroblast, resulting in one homogeneous, validated source for all future cells. A patented synthetic, non-immunogenic mRNA high efficiency cell reprogramming technique is applied to create a clonal iPSC Master Cell Bank from which our i-MSCs are differentiated and expanded to create an i-MSC Accession Cell Bank. Citius has completed the development of its i-MSC ACB and is currently testing (as per FDA guidance) and expanding the cells to create an allogeneic cGMP i-MSC Master Cell Bank to support all future i-MSC needs.

The poster will be available to conference attendees via the conference website. The poster will be available on Citius' website once the event commences.

Conference Details:

Abstract Title:

"Novel Induced-Mesenchymal Stem Cells (i-MSCs) Attenuate Severity of ARDS in Septic Sheep"

Authors:

K. Hashimoto, N. Bazhanov, P. Enkhbaatar, M. Angel, A. Lader, M. Czuczman, and M. Matthay

Abstract Number:

100

Date and Time:

May 25, 2021

Session I

12:30 2:00 PM EDT

Session II

8:00 9:30 PM EDT

About Acute Respiratory Distress Syndrome (ARDS)

ARDS is an inflammatory process leading to build-up of fluid in the lungs and respiratory failure. It can occur due to infection, trauma and inhalation of noxious substances. ARDS accounts for approximately 10% of all ICU admissions and almost 25% of patients requiring mechanical ventilation. Survivors of ARDS are often left with severe long-term illness and disability. ARDS is a frequent complication of patients with COVID-19. ARDS is sometimes initially diagnosed as pneumonia or pulmonary edema (fluid in the lungs from heart disease). Symptoms of ARDS include shortness of breath, rapid breathing and heart rate, chest pain (particularly while inhaling), and bluish skin coloration. Among those who survive ARDS, a decreased quality of life is relatively common.

About Citius Pharmaceuticals, Inc.

Citius is a late-stage biopharmaceutical company dedicated to the development and commercialization of first-in-class critical care products, with a focus on anti-infectives in adjunct cancer care, unique prescription products, and stem cell therapy. The Company's lead product candidate, Mino-Lok, an antibiotic lock solution for the treatment of patients with catheter-related bloodstream infections (CRBSIs), is currently enrolling patients in a Phase 3 pivotal superiority trial. Mino-Lok was granted Fast Track designation by the U.S. Food and Drug Administration (FDA). Through its subsidiary, NoveCite, Inc., Citius is developing a novel proprietary mesenchymal stem cell treatment derived from induced pluripotent stem cells (iPSCs) for acute respiratory conditions, with a near-term focus on Acute Respiratory Distress Syndrome (ARDS) associated with COVID-19. For more information, please visit http://www.citiuspharma.com.

Safe Harbor

This press release may contain "forward-looking statements" within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934. Such statements are made based on our expectations and beliefs concerning future events impacting Citius. You can identify these statements by the fact that they use words such as "will," "anticipate," "estimate," "expect," "plan," "should," and "may" and other words and terms of similar meaning or use of future dates. Forward-looking statements are based on management's current expectations and are subject to risks and uncertainties that could negatively affect our business, operating results, financial condition and stock price. Factors that could cause actual results to differ materially from those currently anticipated are: risks relating to the results of research and development activities, including those for our NoveCite stem cell therapy; uncertainties relating to preclinical and clinical testing; the early stage of products under development; our dependence on third-party suppliers; our ability to successfully undertake and complete clinical trials and the results from those trials for our product candidates; the estimated markets for our product candidates and the acceptance thereof by any market; the ability of our product candidates to impact the quality of life of our target patient populations; our need for substantial additional funds; market and other conditions; risks related to our growth strategy; patent and intellectual property matters; our ability to attract, integrate, and retain key personnel; our ability to obtain, perform under and maintain financing and strategic agreements and relationships; our ability to identify, acquire, close and integrate product candidates and companies successfully and on a timely basis; our ability to procure cGMP commercial-scale supply; government regulation; competition; as well as other risks described in our SEC filings. These risks have been and may be further impacted by Covid-19. Accordingly, these forward-looking statements do not constitute guarantees of future performance, and you are cautioned not to place undue reliance on these forward-looking statements. Risks regarding our business are described in detail in our Securities and Exchange Commission ("SEC") filings which are available on the SEC's website at http://www.sec.gov, including in our Annual Report on Form 10-K for the year ended September 30, 2020, filed with the SEC on December 16, 2020 and updated by our subsequent filings with the SEC. These forward-looking statements speak only as of the date hereof, and we expressly disclaim any obligation or undertaking to release publicly any updates or revisions to any forward-looking statements contained herein to reflect any change in our expectations or any changes in events, conditions or circumstances on which any such statement is based, except as required by law.

Investor Relations for Citius Pharmaceuticals:

Andrew ScottVice President, Special ProjectsT: 908-967-6677 x105E: [emailprotected]

Ilanit AllenVice President, Corporate Communications and Investor RelationsT: 908-967-6677 x113E: [emailprotected]

SOURCE Citius Pharmaceuticals, Inc.

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Citius Pharmaceuticals Selected to Receive Best Poster Award at the International Society for Cell and Gene Therapy 2021 Annual Meeting - PRNewswire

Skin Stem Cells Comments Off on Citius Pharmaceuticals Selected to Receive Best Poster Award at the International Society for Cell and Gene Therapy 2021 Annual Meeting – PRNewswire | May 28th, 2021

If you have certain types of cancer, your doctor might suggest Keytruda (pembrolizumab) as a treatment option for you.

Keytruda is a prescription medication thats used to treat certain advanced forms of the following kinds of cancer in adults and some children:

Keytruda can also be used to treat these kinds of cancer in some children as well as adults:

Keytruda comes as a solution a healthcare professional injects into your vein over a period of time. This is called an intravenous infusion.

Keytruda is a biologic, which is a treatment made from parts of living organisms. It isnt available in a biosimilar form. Biosimilars are like generic drugs. But unlike generics, which are made for non-biologic drugs, biosimilars are made for biologic drugs.

For more information about Keytruda, including details about its uses, see this in-depth article on the drug.

Like other drugs, Keytruda can cause mild and serious side effects. Keep reading to learn more.

Some people may experience mild or serious side effects during their Keytruda treatment. These side effects can vary depending on whether Keytruda is used alone or with other cancer drugs.

Examples of Keytrudas commonly reported side effects include:

* To learn more about this side effect, see Side effects explained below.

Read on to learn about other possible side effects of Keytruda.

Keytruda may cause mild side effects. These side effects can vary depending on whether Keytruda is used alone or with other cancer drugs.

Examples of mild side effects that have been reported with Keytruda include:

* To learn more about this side effect, see Side effects explained below.

In most cases, these side effects should be temporary. And some may be easily managed, too. But if you have any symptoms that are ongoing or that bother you, talk with your doctor or pharmacist. And dont stop using Keytruda unless your doctor tells you to.

Keytruda may cause mild side effects other than the ones listed above. See the Keytruda medication guide for more information.

Note: After the Food and Drug Administration (FDA) approves a drug, it tracks side effects of the medication. If youd like to notify the FDA about a side effect youve had with Keytruda, visit MedWatch.

Serious side effects may occur with Keytruda. These side effects can vary depending on whether Keytruda is used alone or with other cancer drugs.

Many of Keytrudas serious side effects happen because of an overactive immune system. These are called immune-mediated side effects, and they often cause inflammation (damage and swelling) to tissues. Examples include:

Other serious side effects that have been reported with Keytruda include:

* To learn more about this side effect, see Side effects explained below.

If you develop serious side effects while using Keytruda, call your doctor right away. If the side effects seem life threatening or if you think youre having a medical emergency, immediately call 911 or your local emergency number.

Get answers to some frequently asked questions about Keytrudas side effects.

In most cases, Keytrudas side effects should be temporary. Most should go away soon after you start or stop the drug.

But Keytruda can cause serious side effects that may lead to long-term problems. In some cases, these problems can take many weeks or months to resolve. Here are some examples, all of which cause inflammation (damage and swelling) in different parts of the body:

If you have questions about what to expect long term while using Keytruda, talk with your doctor or pharmacist. But dont stop using Keytruda unless your doctor recommends it.

Yes, in rare cases, Keytruda may cause serious eye side effects (sometimes called ocular side effects).

Examples of eye problems that may happen while using Keytruda include:

Symptoms of eye side effects from Keytruda will depend on the exact eye problem you have. But possible symptoms that may happen with one or both eyes include:

Tell your doctor right away if you have any symptoms of eye problems while using Keytruda.

Keytruda is prescribed to treat many types of cancer, including non-small cell lung cancer and small cell lung cancer. The side effects of Keytruda are expected to be the same regardless of the type of cancer its treating. For a full list of the cancers Keytruda is used to treat, see this in-depth article on the drug.

To learn more about possible side effects of Keytruda, see the What are the mild side effects of Keytruda? and What are the serious side effects of Keytruda? sections above.

If you have questions about what to expect when using Keytruda to treat lung cancer, talk with your doctor.

Yes, confusion is a possible side effect of Keytruda. In fact, confusion was a common side effect of Keytruda in studies of the drug.

Confusion can make you feel as though you cant think clearly. You may also have problems making decisions or focusing on a task. This side effect can also lead to abnormal or slurred speech.

Its important to remember that encephalitis (inflammation of your brain) may cause confusion. Encephalitis is a rare but serious side effect of Keytruda. For this reason, you should tell your doctor right away if you experience confusion while using Keytruda. Theyll likely check you for signs of encephalitis.

Learn more about some of the side effects Keytruda may cause.

Muscle pain or bone pain are common side effects of Keytruda.

You can relieve muscle or bone pain by:

Before using OTC drugs with Keytruda, talk with your doctor or pharmacist. And ask your doctor about other ways to relieve bothersome muscle or bone pain that Keytruda may cause.

In rare cases, some people may have hair loss while using Keytruda. In studies, hair loss was more common when Keytruda was used with chemotherapy drugs than when used alone.

Hair loss as a side effect of Keytruda is usually temporary. If you have hair loss from using Keytruda, your hair should start growing back several weeks after your last dose.

Cooling caps, which are caps designed to keep your scalp cold, might help prevent hair loss. Cooling caps lessen the blood flow to your scalp, which may decrease the effect of Keytruda or chemotherapy on your hair. Ask your doctor if a cooling cap is right for you.

When your hair does start to return, dont overuse hair styling tools that are harsh on hair. These include blow dryers and hair straighteners. You should also avoid bleaching or coloring your hair so it stays healthy enough to grow.

If you experience bothersome hair loss while using Keytruda, talk with your doctor about ways to help with this side effect.

You may have itchy skin or rash from using Keytruda. Itchy skin and mild rashes are common side effects of the drug.

In rare cases, Keytruda may also cause severe rashes and other skin reactions. These include Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). With SJS and TEN, you have a rash along with painful sores on your eyes, genitals, mouth, or throat.

Here are a few tips for helping relieve itching and rash:

If you have a severe skin reaction to Keytruda, youll likely need treatment in a hospital. If you have severe skin peeling or blisters after using the drug, call 911 or your local emergency number right away. These may be signs of a serious skin reaction, which can be life threatening.

If youre concerned about your risk for a severe skin reaction from using Keytruda, talk with your doctor.

Like most drugs, Keytruda can cause an allergic reaction in some people.

Symptoms can be mild or serious and can include:

If you have mild symptoms of an allergic reaction, such as a mild rash, call your doctor right away. They may suggest an over-the-counter antihistamine you can take by mouth, such as diphenhydramine (Benadryl), or a product you can apply to your skin, such as hydrocortisone cream, to manage your symptoms.

If your doctor confirms you had a mild allergic reaction to Keytruda, theyll decide if you should continue using it.

If you have symptoms of a severe allergic reaction, such as swelling or trouble breathing, call 911 or your local emergency number right away. These symptoms could be life threatening and require immediate medical care.

If your doctor confirms you had a serious allergic reaction to Keytruda, they may have you switch to a different treatment.

During your Keytruda treatment, consider keeping notes on any side effects youre having. Then, you can share this information with your doctor. This is especially helpful to do when you first start taking new drugs or using a combination of treatments.

Your side effect notes can include things like:

Keeping notes and sharing them with your doctor will help your doctor learn more about how Keytruda affects you. And your doctor can use this information to adjust your treatment plan if needed.

Keytruda is used to treat certain types of cancer in some children. (For information about the cancers Keytruda can treat in children, see this detailed article on the drug.)

Most side effects that occur in children receiving Keytruda are similar to those that adults experience. However, some side effects of Keytruda are more common in children. These include:

Talk with your childs doctor about their risk for side effects from Keytruda.

Keytruda may not be right for you if you have certain medical conditions or other factors that affect your health. Talk with your doctor about your health history before you take Keytruda. Factors to consider include those in the list below.

Allergic reaction. If youve had an allergic reaction to Keytruda or any of its ingredients, you shouldnt take Keytruda. Ask your doctor what other medications are better options for you.

Receiving certain other treatments for multiple myeloma. Using Keytruda with certain other treatments for multiple myeloma can be fatal. (Multiple myeloma is a cancer that affects a type of white blood cell called a plasma cell.) Before using Keytruda, tell your doctor if youre taking any treatments for multiple myeloma.

Received an organ transplant. Before using Keytruda, tell your doctor if youve had an organ transplant. Keytruda can raise the risk for your immune system attacking the transplanted organ. If youve had a transplant, your doctor will tell you what symptoms of organ rejection you should watch for while using Keytruda.

Received or plan to receive a stem cell transplant. Before using Keytruda, tell your doctor if youve received stem cells from a donor in the past or plan to do so. You may be at a higher risk for graft-versus-host disease. This condition causes your immune system to attack the transplant stem cells. Talk with your doctor about whether Keytruda is safe for you to use.

It should be safe to drink alcohol while using Keytruda.

But be aware that alcohol can cause side effects that are similar to some of Keytrudas. These include diarrhea, fatigue (lack of energy), and nausea. If you drink alcohol during Keytruda treatment, it may make these side effects worse.

Talk with your doctor about the amount of alcohol thats safe for you to drink while using Keytruda.

You shouldnt use Keytruda while pregnant or breastfeeding.

Keytruda hasnt been studied during pregnancy. But based on how the drug works, Keytruda may cause harm to infants born to pregnant females* who used the drug during pregnancy.

For this reason, you should use birth control while taking Keytruda if you or your partner can become pregnant. And you should continue to use birth control for at least 4 months after your last dose.

It isnt known if Keytruda can pass into breast milk. To be safe, you shouldnt breastfeed while using Keytruda and for at least 4 months after your last dose.

Before starting Keytruda treatment, tell your doctor if youre pregnant or planning to become pregnant. Also tell them if youre breastfeeding or planning to breastfeed. They can discuss your options with you.

* In this article, we use the term female to refer to someones sex assigned at birth. For information about the difference between sex and gender, see this article.

Keytruda is a drug used to treat certain types of cancer in adults and some children.

Some people who use Keytruda may have mild side effects. Although rare, serious side effects can occur with Keytruda. Many of these happen because of an overactive immune system. Keep in mind that the side effects of Keytruda can vary depending on whether Keytruda is used alone or with other cancer drugs.

Talk with your doctor or pharmacist if you have questions about Keytrudas side effects. Here are a few questions you may want to ask:

Disclaimer: Healthline has made every effort to make certain that all information is factually correct, comprehensive, and up to date. However, this article should not be used as a substitute for the knowledge and expertise of a licensed healthcare professional. You should always consult your doctor or other healthcare professional before taking any medication. The drug information contained herein is subject to change and is not intended to cover all possible uses, directions, precautions, warnings, drug interactions, allergic reactions, or adverse effects. The absence of warnings or other information for a given drug does not indicate that the drug or drug combination is safe, effective, or appropriate for all patients or all specific uses.

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Keytruda Side Effects: What They Are and How to Manage Them - Healthline

Skin Stem Cells Comments Off on Keytruda Side Effects: What They Are and How to Manage Them – Healthline | May 28th, 2021

Founded to meet the future protein demands of an expanding global population, Australias Magic Valley is developing cell-cultured lamb products including mince, strips, steaks and chops. With lambs currently slaughtered at an incredibly young age using traditional farming methods, its founder tells us this particular meat became the obvious choice for the companys first product range.

There is absolutely no need for the mass slaughter of animals for food and hopefully intensive animal agriculture will soon be a thing of the past

Vegconomist spoke with Founder Paul Bevan, who says that he had become frustrated by the pace of change and effectiveness of his own activism so he turned his attention to technology, specifically the development of slaughter-free cultured meat, beginning with lamb.

Utilising induced pluripotent stem-cells and FBS-free media, Magic Valley is able to grow real animal meat from animal cells, using animals such as Lucy, who Paul refers to as cell volunteers.

Eventually we would like to expand into developing cultured meat products for all other animal species

Lucy the lamb is our very special cell donor. From just a tiny skin biopsy less than 4mm in diameter we are able to generate an infinite number of muscle and fat cells without ever having to interfere with an animal again. That is one of the distinct advantages of our technology and using induced pluripotent stem cells.

Meanwhile, Lucy gets to live out the entirety of her natural life (up to 20 years of age) happy and unharmed, blissfully unaware that her cell donation has potentially saved the lives of billions of lambs that would otherwise have been slaughtered at just 6 months of age.

Magic Valleys team consisting of Australias leading scientists have extensive experience in both stem cell biology and livestock production. As part of its ambitions to become a leader in the field, the company also announced this week the onboarding of industry pioneer Dr. Sandhya Sriram, PhD, Co-Founder & CEO of the cell-based crustacean producers Shiok Meats, to its advisory board.

Eventually we would like to expand into developing cultured meat products for all other animal species that have traditionally been farmed for human consumption. With the advancement of this technology, there is absolutely no need for the mass slaughter of animals for food and hopefully intensive animal agriculture will soon be a thing of the past, Bevan commented to vegconomist.

Our immediate goal is to develop the safest, healthiest and tastiest cultured lamb products possible. We know that to be successful, cultured meat products have to become the obvious choice for consumers and that means taste, price & convenience are paramount. We know that ethical or environmental concerns alone are not enough to change consumer behaviour it has to be a better product.

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Australia's Magic Valley On How to Turn Cells From "Cell Volunteer" Lucy the Lamb Into Lamb Steaks and Chops - vegconomist - the vegan...

Skin Stem Cells Comments Off on Australia’s Magic Valley On How to Turn Cells From "Cell Volunteer" Lucy the Lamb Into Lamb Steaks and Chops – vegconomist – the vegan… | May 28th, 2021

Skin is the largest and heaviest organ of the body. It consists of three main layers; the epidermis, dermis, and hypodermis. Skin can either be thin or thick. The main difference is the thickness of the epidermis and dermis, which are the top two layers of skin.

Thin skin covers most of the body and can vary in thinness, with the thinnest skin covering the eyelids. Thick skin is present on the soles of the feet and palms of the hands.

In addition to differing thicknesses, the skin also differs in what is present in the layers. For example, thick skin has no hair follicles or sebaceous glands, whereas thin skin does.

In this article, we look at the differences in appearance, structure, and function of thin and thick skin.

Thin skin covers most of the body, except on the soles of the feet and palms of the hands, and contains fewer cellular layers than thick skin.

The epidermis of thin skin ranges from 0.070.15 millimeters (mm). Thin skin can vary in thickness in different parts of the body and is particularly thin across the eyelids. Thin skin is thickest on the upper back.

Thin skin also contains hair follicles, sweat glands, and sebaceous glands.

Thick skin is present on the soles of the feet and palms of the hands. This is because these areas receive more friction than other areas of the body, and thicker skin helps to protect from potential damage.

The epidermis of thick skin can be up to 1.5 mm. Thick skin does not contain any hair follicles or sebaceous glands. Thick skin also contains no arrector pili muscles, which cause goosebumps.

Thick skin is thicker due to it containing an extra layer in the epidermis, called the stratum lucidum. Thick skin actually has a thinner dermis layer than thin skin, but is still thicker due to the stratum lucidum layer present in the epidermis.

Thick and thin skin appear differently under a microscope. Thin skin contains four layers in the epidermis, while thick skin contains a fifth layer. These layers include:

The stratum basale, also known as the stratum germinativum, is the deepest layer of the epidermis. It is the layer just above the dermis.

This layer continuously produces new skin cells. It also contains melanocytes, which are cells that produce skin pigment and help protect the skin from sun damage.

The stratum spinosum consists of eight to ten layers of cells. People may refer to the stratum spinosum as the prickle cell layer because of the irregular structure of cells, which look like spines or prickles.

The stratum granulosum consists of three to five layers of cells. The stratum granulosum contains granules, which are rich in lipids.

Only thick skin contains the stratum lucidum layer. The stratum lucidum is a thin, transparent layer consisting of two to three layers of cells. It contains a protein called eleidin.

The stratum corneum is the upper layer of the epidermis. It consists of 2030 layers of cells. It contains keratin and horny scales, which make it tougher and able to thicken into calluses.

The stratum corneum contains dead keratinocytes, which produce defensins. Defensins are strings of amino acids that protect the body from infection.

Connecting the dermis and epidermis are structures called dermal papillae. Dermal papillae are more prominent in thick skin than thin skin.

Dermal papillae increase the surface area between the epidermis and dermis, allowing for more oxygen, food, and waste to pass between the layers.

The following table summarizes the key structural differences between thin and thick skin:

Skin in general has many different functions, such as protection, sensation, and thermoregulation. Both thin and thick skin have properties that allow the skin to function correctly.

For example, thin skin contains hair follicles, which are important in producing hair to help regulate temperature and protect from ultraviolet radiation. Hair follicles also provide epithelial stem cells, which help repair wounds.

In addition, thin skin contains sebaceous glands, which produce sebum. Sebum helps to lubricate the skin and protect against infections.

Thin skin also contains eccrine and apocrine sweat glands. Sweat glands help to regulate body temperature by releasing sweat to cool the body, and also help to repair skin damage.

Thick skin provides protection from damage in areas that experience more friction and abrasion, such as the palms of the hands and the soles of the feet. Thick skin also contains eccrine sweat glands to help regulate body temperature.

Skin is a large, complex organ with a wide range of vital roles. Thin skin and thick skin have different structures and functions in the body. The layers they contain provide their thickness and allow them to carry out their roles.

Thin skin is present on most of the body, and helps to protect against infections, regulate temperature, and allows hair to grow. Thick skin covers the palms of the hands and the soles of the feet and protects these areas from extra abrasion and friction.

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Thin skin vs. thick skin: What is the difference? - Medical News Today

Skin Stem Cells Comments Off on Thin skin vs. thick skin: What is the difference? – Medical News Today | May 15th, 2021

The Medical Skin Care Products Market report by Persistence Market Research throws light on the fact that the healthcare industry is more towards value-based care and continuous improvements based on the feedback. The mainstreaming of this practice is increasing all through. As such, the healthcare providers could make way for customized, lasting, and effective solutions to render utmost care to patients.

Medical skin care products are used for beautifying or to address some other skin care problems. The cosmetic industry is booming and skin care forms a very huge part of this industry. The aesthetic appearance is so important that people spend a lot on skin care products and treatment. People being more technologically aware of the various new skin care products trending in the market. In addition to the aesthetic application, the medical skin care products are also used to address issues such as acne, pimples or scars.

The medical skin care products is primarily driven by the need of natural based active ingredients products which are now trending in the market. Consumers demand medical skin care products which favor health and environment. Moreover, the consumers are updated with the trends so that various companies end up providing such products to satisfy the customers. For instance, a single product face mask has thousands of different variants. This offers consumers different options to select the product depending on the skin type. Moreover, the market players catering to the medical skin care products are offering products with advanced technologies. For instance, Santinov launched the CICABEL mask using stem cell material based on advanced technologies. The stem cells used in the skin care product helps to to protect and activate the cells and promote the proliferation of skin epidermal cells and the anagenesis of skin fibrosis.

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Medical Skin Care Products Market: Segmentation

On the basis of product type the medical skin care products market can be segmented as:

On the basis of application, the medical skin care products market can be segment as:

On the basis of distribution channel, the medical skin care products market can be segment as:

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Medical skin care products are used to address basic skin problems ranging from acne to scars. There are various advancements in the ingredients used to offer skin care products to the consumers. For instance, the use of hyaluronic acid and retinoids is the latest development in the industry. The anti-aging creams are at the forefront as the help treating issues such as wrinkles, scars, acne, and sun damage. Another, product in demand is the probiotic skincare which include lactobacillus and bifidobacterium.

In terms of geography, medical skin care products market has been divided into five regions including North- America, Asia- Pacific, Middle-East & Africa, Latin America and Europe. North America dominated the global medical skin care products market as international players are acquiring domestic companies to make their hold strong in the U.S. LOral is accelerating its U.S. market by signing a definitive agreement with Valeant Pharmaceuticals International Inc. to acquire CeraVe, AcneFree and Ambi skin-care brands for US$ 1.3 billion. The acquisition is expected LOreal to get hold of the brands in the price-accessible segment. Asia Pacific is expected to be the fastest growing region owing to the increasing disposable income and rising awareness towards the skin care products.

Some of the medical skin care products market participants are Avon Products Inc., Beiersdorf AG, Colgate-Palmolive Company, Kao Corporation, LOral S.A., Procter & Gamble, Shiseido Company, The Estee Lauder Companies Inc., Unilever PLC, Revlon, Clinique Laboratories, llc., Murad, LLC., SkinCeuticals, RMS Beauty, J.R. Watkins and 100% PURE.

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Global To Drive The Substantial Growth Of The Medical Skin Care Products Market KSU | The Sentinel Newspaper - KSU | The Sentinel Newspaper

Skin Stem Cells Comments Off on Global To Drive The Substantial Growth Of The Medical Skin Care Products Market KSU | The Sentinel Newspaper – KSU | The Sentinel Newspaper | May 15th, 2021

City University of Hong Kong (CityU) scientists have created a new microneedle patch to deliver cell therapies but rather than using traditional materials for their needles, they used ice.

The challenge: Cell therapies use living cells to treat medical conditions. Stem cell transplants are a form of cell therapy, as are some types of cancer immunotherapy.

These cells are typically transplanted into the patient via an implant, injection, or surgical graft. Not only can those delivery methods be painful and invasive, they also carry a risk of infection and must be administered by an experienced professional.

That limits the use of cell therapy to people who are willing to subject themselves to the transplantation process and who also have access to professionals capable of administering them.

Ice, ice baby: Microneedle patches are a growing trend in drug delivery. They're usually about the size of a postage stamp and are covered in tiny needles made of biodegradable substances packed with drugs.

Press the patch down on the skin like a band aid, and the needles break off from the back of the patch. They then dissolve into the skin, painlessly delivering the drug.

CityU created the microneedles for its patch out of ice, packed with living cells, coated in a protective medium.

Ice is easier to make and work with than the materials traditionally used for dissolving micropatches, but it melts just as readily. Even better, the icy microneedles can preserve the viability of living cells something other types of patches can't do.

The freezing cold water: Because the microneedles are made of ice, they would have to be transported and stored frozen, which could be a limiting factor in some places.

Additionally, the icy microneedle patch performed well when used to deliver a cell therapy to mice as a proof of concept, but it still needs to be proven safe and effective in humans.

What's next: If CityU's microneedle patch is cleared for use in people, it could have applications even beyond cell therapy.

"This device can also package, store, and deliver DNA, vaccines, and more."

"This device can also package, store, and deliver other types of bioactive therapeutic agents, such as proteins, peptides, mRNA, DNA, and vaccines," lead researcher Xu Chenjie said in a press release.

"I hope this device offers an easy-to-use and effective alternative method for the delivery of therapeutics in clinics."

We'd love to hear from you! If you have a comment about this article or if you have a tip for a future Freethink story, please email us at [emailprotected].

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Icy Microneedle Patch Delivers Cell Therapy, Then Melts - Freethink

Skin Stem Cells Comments Off on Icy Microneedle Patch Delivers Cell Therapy, Then Melts – Freethink | May 15th, 2021

South Korea and Japan have given the beauty world many gifts cleansing balms, glass-skin serums, inventive masks for making skin gleam. And at this time of unprecedented violence against Asians in this country, the Allure family is more passionate than ever about championing Asian innovation and Asian voices. We will speak out against racism and intolerance and do more than ever to support Asian-owned beauty brands, starting with this special edition of the Allure Beauty Box. Inside are some of the most influential K-beauty and J-beauty products of all time ones that have revolutionized our editors routines and the entire beauty industry. Sulwhasoo First Care Activating Serum is an innovative prep step for glowing skin (one bottle is sold every 10 seconds worldwide) and AHC Essential Real Eye Cream for Face, a unique eye and face cream hybrid, is cherished in South Korea (where one is sold every three seconds.) We hope they become as beloved by you as they are by us! And if you would like to get involved in the movement to Stop Asian Hate, you can also join Allure editors in donating to the Asian American Legal Defense and Education Fund and to GoFundMe's AAPI Community Fund to Stop Asian Hate at gofundme.com/aapi.

- The editors of Allure

You can find all these products and more in this limited-edition box. For just $60 (or $40 exclusively for Allure Beauty Box members), you'll get ten of our favorite J-Beauty and K-Beauty products, worth over $200 in value. Quantities are limited, so order now to take advantage of this exclusive offer before they're sold out.

Check out what's in this limited-edition box.

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The Limited-Edition J-Beauty + K-Beauty Allure Beauty Box - Allure

Skin Stem Cells Comments Off on The Limited-Edition J-Beauty + K-Beauty Allure Beauty Box – Allure | May 15th, 2021

During a virtual Targeted Oncology Case-Based event, Pashna N. Munshi, MD, associate clinical director, Stem Cell Transplant and Cellular Immunotherapy Program, assistant professor of Medicine, Georgetown University School of Medicine at MedStar Georgetown University Hospital, discussed the case of a 48-year-old male patient with acute graft-versus-host-disease (GVHD).

Targeted OncologyTM: What factors contribute to the risk of acute GVHD in a patient like this one?

MUNSHI: A lot of donor-recipient factors and other conditions increase the risk of acute GVHD. [These include] gender matching, human leukocyte antigen disparity, degree of mismatch, and having an older donor. Theres also [blood group] incompatibility and definitely CMV mismatched status. Though now that the FDA has approved letermovir [Prevymis] for patients who are undergoing allogeneic transplant if they have a CMV-positive donor,1 were seeing very little CMV reactivation. That has been a bit of a game changer for the good.

Patients have an increased risk of GVHD if they receive a transplant from a peripheral blood stem cell source versus a bone marrow graft, because the peripheral blood has more T cells in its composition. The myeloablative regimens [are associated with greater risk of GVHD than] reduced-intensity regimens.2

Do you agree with these poll results? Would you start with systemic therapy for this patient?

It can get a little tricky whether you want to give patients systemic steroids or wait and see if something gentler might work. I tend to agree that, at this point, the patient needs to immediately start with systemic steroids, because there are 2 organ systems involved. Once the lower gastrointestinal [GI] tract gets involved, it surely portends a poor prognosis if the grade becomes worse. And they become refractory to steroids very quickly: 50% of these patients will eventually not respond to steroids.

How would you stage this patients GVHD?

There are many criteria for staging GVHD. The criteria that most clinical trials use are the Mount Sinai Acute GVHD International Consortium [MAGIC] criteria.3 They are adapted from the Glucksberg criteria, which are very similar.4

Three organ systems [are involved in] acute GVHD: the skin, the liver, and the GI tract. Skin involvement is graded on the basis of the body surface area involved. Liver involvement is graded on the basis of the total bilirubin level. Upper GI involvement is graded on the basis of anorexia, nausea, and vomiting, and it just comes in stage 0 or stage I, depending on if its persistent or not. To determine lower GI tract involvement, we measure stool volume, especially when patients are admitted to the hospital. But once they go home, we cant do that, so we ask them how many times a day they have diarrhea. Is it watery? Is it muddy? Whats the volume? Is it large or small?

The patient can characterize the stool and tell their doctor how many times per day: 4 times, 5 times, 6 times. This patient is having 4 episodes per day; that puts them in stage I lower GI GVHD. But with a 60% body rash, that puts them in stage III skin GVHD. So really getting up there with skin, but not so much yet for GI. Once each organ [involvement is] staged, theres an aggregate score based on the combination of these organs. Then we come up with the grade.

In this patient, with a stage III rash, stage I upper GI, and stage I lower GI GVHD, they have a total score of a grade 2 acute GVHD. This is still in the mild to moderate zone. Anything above grade 2 is considered very severe GVHD.

Would you recommend that this patient receive systemic steroids?

In the scheme of things, somebody who didnt have symptoms and now is having active symptoms, especially with lower GI tract involvement, definitely needs high-dose steroids to get in there and [stop] the inflammation.

On what would you base a prognosis for this patient?

We can risk stratify these patients on the basis of the stage of organ involvement.5 Broadly, they can be at a standard risk or at a high risk [of poor response to treatment, mortality, and transplant-related mortality]. The patient is at high risk once they have very active GI involvement [or] if they have 2 organs involved. This is one more reason to think about starting these patients early on steroids. Why is this important? Because once a patient has high-risk GVHD, the chance of response to steroids is even lower, and once they dont respond to steroids, there is a higher [risk of] transplant-related mortality. The probability of transplant-related mortality is 44% for patients with high-risk acute GVHD flares, [versus] 22% for patients with low-risk GVHD [P < .001]. These are a few things to think about. Act very swiftly if a patient has 2-organ involvement, especially the lower GI tract.

Can biomarkers guide treatment decisions in this case?

In the field of GVHD, biomarkers are a very exciting advancement. We want a prognostic model of which patients will get GVHD. Can biomarkers in the blood [help] prevent GVHD and improve transplant outcomes?

A large prospective trial was done through the Bone and Marrow Transplant Clinical Trials Network where a set of 6 biomarkers were tested at several time points after the transplant.6 They saw that they could predict when GVHD happened by using these biomarkers. They could see that as the levels of these biomarkers increased, the patients had higher scores of GVHD. Once treatment was started, if specific biomarkers went down it was predictive of response at day 28 [56% vs 17%; odds ratio, 6.32; P = .001] and also predictive of [decreased] transplant-related mortality by day [180 (49% vs 87%; P < .0001)]. If all these biomarkers went up aggressively, overall survival was lower [P < .0001].

The MAGIC Consortium also tried to test biomarkers.7 They looked at 2 biomarkers, REG3Athe regenerating islet-derived 3-alpha, which is specific for the GI tract and ST2. Looking at these 2 biomarkers, they came up with an algorithm of prediction. On the basis of how these biomarkers responded at the time of GVHD and to treatment, they could predict mortality by 6 months. In clinical practice, it is difficult to use this day in and day out. We still use our clinical skills to assess the degree of GVHD. But all patients eventually get treated the same waywith high-dose steroidsdespite biomarkers being elevated or not.

At this point, [biomarker data] may tell us an association rather than a causality. Were not openly using biomarkers to guide our practice, but I think were learning to use them a bit more and knowing that theres something out there that could be used as a predictive tool. It is an exciting development.

Are there alternatives to systemic steroids?

Steroids remain the mainstay. We need to see if we can move to other therapies that are coming down the pipeline.

Data from the REACH1 [NCT02953678] and REACH2 [NCT02913261] trials led to ruxolitinib [Jakafi] approval.8,9 If we can use ruxolitinib in an up-front setting, [maybe we] can use the newly approved rho-kinase or ROCK2 inhibitors as well.10 We want to think about steroid-sparing agents. Maybe biomarkers can guide us in the future for that. But right now, in terms of, Do I start my patient on treatment? or Will they respond to this treatment, I find that [biomarkers are] still not a very useful tool because at the end of the day, the patients all still need to be started on steroids.

The minute you see that your patient is not responding to steroids, very quickly start them on a JAK2 inhibitor.

How do you dose steroids?

This patient received 2 mg/kg of prednisone per day for 14 days. Two mg/kg is a very high dose. The standard is 1 to 2 mg/kg.11 There are data to show that 2 mg isnt any different from 1 mg.12 But a lot of times, if its a very active, severe flare, we will use 2 mg/kg. Im not sure if I would have done 2 mg/kg in this case, but its certainly not out of the realm of treating these patients.

The goals of primary therapy for acute GVHD are to stabilize the organ manifestations, or improve them, and limit long-term treatment toxicity. We want to improve functional capacity and prevent any reduction in quality of life. First-line therapy is always with corticosteroids. Now ruxolitinib is approved for second-line therapy.8 There have been data to show that it can improve overall survival.

How do you taper glucocorticosteroids after achieving initial response?

If the patient is taking 2 mg/kg of steroids, an average 70-kg person, thats over 100 mg of steroids. After 2 weeks, they probably are not getting up from a seated position anymore with all the muscle wasting that can happen.

[As soon as they start to show improvement, it would be safe to start to taper the dose.] Traditionally, [the patient receives the full dose for] at least a week or 10 days. Then it is traditional to decrease the dose 10% every 5 to 7 days, gently coming down, making sure that the patient is not having any flares.

Describe the multidisciplinary teambased approach that you use for acute GVHD.

The incidence of acute GVHD in the patient population is anywhere from 30% to 50%, despite the best [efforts at] prophylaxis. Most patients will get some form of acute GVHDit can go up to even 80%. This [necessitates] a multidisciplinary team approach. If the patient is having diarrhea, theyre having malnourishment. Theres nausea or anorexia, so theyre not eating on top of that. Then theres skin rash, so the risk of infections and cellulitis. Theyre in pain. A dermatologist probably should be involved at some point. A nutrition team is also needed. If theyre on high-dose steroids, physical therapy should be involved up front. So early involvement of a whole team is very important. Thats usually how I treat my patients and usually how centers of excellence continue to treat active patients with GVHD after transplantation.

How do you determine if a patients GVHD is steroid refractory?

The strict definition of steroid refractoriness or resistance is if theres progression of acute GVHD within 3 to 5 days of starting high-dose steroids, or theres failure to improve within 1 week of starting these steroids, or theres incomplete response after more than 28 days of any immunosuppressive treatment.13 So, by and large, in 3 days or a maximum of 7 days, [it will be clear] if the patients GVHD is going to be steroid refractory or not.

Steroid dependence is [defined as when] the patients GVHD initially responded to steroids, but the disease flares when the dose is tapered, so they cannot be taken off the steroids.

Steroid intolerance is when the patient develops [unacceptable toxicity from steroids such as] uncontrolled diabetes or myopathies. Then it becomes hard to keep them on steroids.

What are the treatment options for patients with steroid-refractory GVHD?

Ruxolitinib now has been FDA approved for steroid-refractory acute GVHD, and its a category 1 definition.8,11 Ibrutinib [Imbruvica] has also been approvedits only FDA-approved indication is for chronic GVHD.14 There are many other treatment options [in the National Comprehensive Cancer Network guidelines].11 Oncologists always end up using some combination or other depending on which of these different immune suppression medications they are comfortable using.

What new treatments are in the pipeline?

In terms of BTK inhibitors, I dont think theres anything other than ibrutinib at this time point. There are many JAK inhibitors being studied.15 Baricitinib is another JAK inhibitor thats actively being studied for chronic GVHD, as well as for pulmonary GVHD.16 Then there are other rho-kinase inhibitors, called ROCK2 inhibitors. This is really making waves. Were very excited about this drug because the response rates are very high, about 70%.10 Its a smaller study, but clearly it has antifibrotic pathways. So I think thats going to be used much more in the up-front setting.

Then theres also alpha-1 antitrypsin, which targets the liver and macrophages and has very promising results from trials done at Dana-Farber Cancer Institute and Michigan.17 So I think were going to see very different characteristics of how to approach GVHD.

What data support the use of ruxolitinib in this setting?

The REACH1 study led to the approval of ruxolitinib for steroid-refractory acute GVHD.9,18 In this phase 2 trial, patients with steroid-refractory acute GVHD got ruxolitinib (5 mg twice a day) with or without a calcineurin inhibitor. They were allowed to remain on steroids. The primary end point of this trial was overall response rate [ORR] at day 28. They also looked at response rates at day 56 and day 100, biomarkers, failure-free survival, and durability of these responses. The ORR at day 28 was very high: 54.9%.18 The best ORR, which was at any given time during the treatment, which was as high as 73.2%. The median time to response was 7 days. So this was very quick. The median duration of response was 345 days, with more than 6 months follow-up. Nonrelapse mortality at 6 months was 44.4%. There were deaths from infections, etc, but not related directly to ruxolitinib.

Subsequently there was a phase 3 trial, REACH2.19 They looked at higher doses of ruxolitinib in steroid-refractory acute GVHD. They started off with 10 mg [of ruxolitinib] twice a day. This study had a similar primary end point of ORR at day 28. This was compared with best available therapy. This was done in Europe, so [the comparison was to the] best available therapy used in Europe, like anti-thymocyte globulin, sirolimus [Rapamune], etanercept [Enbrel], photopheresis, or other therapies; all things that we would use in the United States as well. They looked at similar key secondary end points, [including] duration of response at day 56.

The ORR for ruxolitinib was 62% at day 28, compared with the best available therapy arm, which was 39% [odds ratio, 2.64; 95% CI, 1.65 to 4.22; P < .001].19 Durable overall response at day 56 [was higher in the ruxolitinib group than it was in the control group (40% vs 22%, odds ratio, 2.38; 95% CI, 1.43-3.94; P < .001)].19

The lower grade acute GVHD, which was grade 2, had the highest complete response rate with ruxolitinib: 50.9% compared with just 26.4% with best available therapy.19 This is quite remarkable to have a complete response in GVHD so quickly. When you get to higher grades of GVHD, the complete response rate for ruxolitinib is not as impressive; its less than 30%. But its still much higher than the [response rates of] other therapies we would have otherwise treated these patients with in steroid-refractory disease. The key point is to diagnose steroid refractoriness early. Then get ruxolitinib in there to break the cycle and break the progression of organ grade to something higher.

The loss of response wasnt statistically significant. The estimated cumulative incidents for the loss of response at 6 months was 10% in ruxolitinib compared with 39% in the control arm.19 So patients continued to maintain responses, which, again, is what we want to see. We dont want to see flares if they come off steroids.

[Of the 4 organ systems involved in GVHD], the skin responses were the best with ruxolitinib. Lower GI and liver GVHD did have good responses, but the responses were not as remarkable. Ruxolitinib is an ideal drug in this setting, on the basis of the organ responses.

A secondary end point was failure-free survival, basically indicating a time point from randomization to either nonrelapse-related death or any new GVHD. This was not statistically significant because it was not designed to compare ruxolitinib survival outcomes with control therapy. But there were 5.0 months median failure-free survival with ruxolitinib compared with 1.0 month with control [hazard ratio for relapse or progression of hematologic disease, nonrelapse-related death, or addition of new systemic therapy for acute GVHD, 0.46; 95% CI, 0.35-0.60]. That tells you that the responses were maintained, and the treatment was still working.

[Most of the adverse events associated with ruxolitinib] were expected; the bone marrow is recovering so its a bit fragile. [The most common was] thrombocytopenia. You can reduce the dose of ruxolitinib down to 5 mg adjusted accordingly or support patients with transfusions. CMV reactivation was also common. But again, with letermovir, that happens less and less.

References:1. Merck receives FDA approval of Prevymis (letermovir) for prevention of cytomegalovirus (CMV) infection and disease in adult allogeneic stem cell transplant patients. News release. Merck. November 9, 2017. Accessed April 7, 2021. https://bit.ly/3fS6S0Q

2. Scott BL. Long-term follow up of BMT CTN 0901, a randomized phase 3 trial comparing myeloablative (MAC) to reduced intensity conditioning (RIC) prior to hematopoietic cell transplantation (HCT) for acute myeloid leukemia (AML) or myelodysplasia (MDS) (MAvRIC Trial). Biol Blood Marrow Transplant. 2020;26(3):S11. doi:10.1016/j.bbmt.2019.12.07

3. Harris AC, Young R, Devine S, et al. International, multicenter standardization of acute graft-versus-host disease clinical data collection: a report from the Mount Sinai Acute GVHD International Consortium. Biol Blood Marrow Transplant. 2016;22(1):4-10. doi:10.1016/j.bbmt.2015.09.001

4. Martino R, Romero P, Subira M, et al. Comparison of the classic Glucksberg criteria and the IBMTR Severity Index for grading acute graft-versus-host disease following HLA-identical sibling stem cell transplantation. International Bone Marrow

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A groundbreaking new study led by the University of Minnesota, Twin Cities has shown for the first time that lab-created heart valves implanted in young lambs for a year were capable of growth within the recipient.

The valves also showed reduced calcification and improved blood flow function compared to animal-derived valves currently used when tested in the same growing lamb model.

Currently, researchers have not been able to develop a heart valve that can grow and maintain function for paediatric patients. The only accepted options for these children with heart defects are valves made from chemically treated animal tissues that often become dysfunctional due to calcification and require replacement because they dont grow with the child. These children will often need to endure up to five (or more) open heart surgeries until a mechanical valve is implanted in adulthood. This requires them to take blood thinners the rest of their lives.

Minnesota Professor Robert Tranquillo and his colleagues used a hybrid of tissue engineering and regenerative medicine to create the growing heart valves. Over an eight-week period, they used a specialised tissue engineering technique they previously developed to generate vessel-like tubes in the lab from a post-natal donors skin cells. To develop the tubes, the researchers combined the donor sheep skin cells in a gelatine-like material, called fibrin, in the form of a tube and then provided nutrients necessary for cell growth using a bioreactor.

The researchers then used special detergents to wash away all the sheep cells from the tissue-like tubes, leaving behind a cell-free collagenous matrix that does not cause immune reaction when implanted. This means the tubes can be stored and implanted without requiring customised growth using the recipients cells.

The next step was to precisely sew three of these tubes (about 16 mm in diameter) together into a closed ring. The researchers then trimmed them slightly to create leaflets to replicate a structure similar to a heart valve about 19 mm in diameter.

After these initial steps, it looked like a heart valve, but the question then became if it could work like a heart valve and if it could grow, Prof Tranquillo said. Our findings confirmed both.

This second generation of tri-tube valves was implanted into the pulmonary artery of three lambs. After 52 weeks, the valve regenerated as its matrix became populated by cells from the recipient lamb, and the diameter increased from 19 mm to a physiologically normal valve about 25 mm. The researchers also saw a 17 to 34% increase in the length of the valve leaflets as measured from ultrasound images. In addition, researchers showed that the tri-tube valves worked better than current animal-derived valves, with almost none of the calcification or blood clotting that the other valves showed after being implanted in lambs of the same age.

We knew from previous studies that the engineered tubes have the capacity to regenerate and grow in a growing lamb model, but the biggest challenge was how to maintain leaflet function in a growing valved conduit that goes through 40 million cycles in a year, said Zeeshan Syedain, a senior research associate in Prof Tranquillos lab. When we saw how well the valves functioned for an entire year from young lamb to adult sheep, it was very exciting.

This is a huge step forward in paediatric heart research, Tranquillo said. This is the first demonstration that a valve implanted into a large animal model, in our case a lamb, can grow with the animal into adulthood.

If confirmed in humans, the new heart valves could prevent the need for repeated valve replacement surgeries in thousands of children born each year with congenital heart defects. The valves can also be stored for at least six months, which means they could provide surgeons with an off the shelf option for treatment.

The study has now been published in the journal Science Translational Medicine, while the valve-making procedure has been patented and licensed to University of Minnesota start-up company Vascudyne. Prof Tranquillo said the next steps are to implant the tri-tube valve directly into the right ventricle of the heart to emulate the most common surgical repair and then start the process of requesting approval from the US Food and Drug Administration (FDA) for human clinical trials over the next few years.

If we can get these valves approved someday for children, it would have such a big impact on the children who suffer from heart defects and their families who have to deal with the immense stress of multiple surgeries, Prof Tranquillo said. We could potentially reduce the number of surgeries these children would have to endure from five to one. Thats the dream.

Image credit: Syedain, et al, Tranquillo Lab, University of Minnesota.

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Skin Stem Cells Comments Off on Lab-created heart valves grow with the recipient – Lab + Life Scientist | May 3rd, 2021

CRISPR is revolutionary. Its also a total brute.

The classic version of the gene editing wunderkind literally slices a gene to bits just to turn it off. Its effective, yes. But its like putting an electrical wire through a paper shredder to turn off a misbehaving light bulb. Once the wires are cut, theres no going back.

Why not add a light switch instead?

This month, a team from the University of California, San Francisco (UCSF) reimagined CRISPR to do just that. Rather than directly acting on genesirrevocably dicing away or swapping genetic lettersthe new CRISPR variant targets the biological machinery that naturally turns genes on or off.

Translation? CRISPR can now flip a light switch to control geneswithout ever touching them directly. It gets better. The new tool, CRISPRoff, can cause a gene to stay silent for hundreds of generations, even when its host cells morph from stem cells into more mature cells, such as neurons. Once the sleeping beauty genes are ready to wake up, a complementary tool, CRISPRon, flips the light switch back on.

This new technology changes the game so now youre basically writing a change [into genes] that is passed down, said author Dr. Luke Gilbert. In some ways we can learn to create a version 2.0 of CRISPR-Cas9 that is safer and just as effective.

The crux is something called epigenetics. Its a whole system of chemicals and proteins that controls whether a gene is turned on or off.

If that sounds confusing, lets start with what genes actually look like inside a cell and how they turn on. By turning on, I mean that genes are made into proteinsthe stuff that builds our physical form, controls our metabolism, and makes us tick along as living, breathing humans.

Genes are embedded inside DNA chains that wrap very tightly around a core proteinkind of like bacon-wrapped asparagus. For genes to turn on, the first step is that they need a bunch of proteins to gently yank the DNA chain off the asparagus, so that the genes are now free-floating inside their cellular space capsule, called the nucleus.

Once that chunk of bacon-y DNA is free, more proteins rush over to grab onto the gene. Theyll then roll down the genes nucleotides (A, T, C, and G) like a lawn mower. Instead of mulch, however, this biological machine spews out a messenger that tells the cell to start making proteinsmRNAs. (Yup, the same stuff that makes some of our Covid-19 vaccines.) mRNA directs our cells protein factory to start production, and voil, that gene is now turned on!

Anything that disrupts this process nukes the genes ability to turn into proteins, essentially shutting it off. Its enormously powerfulbecause one single epigenetic machine can control hundreds or thousands of genes. Its a master light switch for the genome.

The team started with a CRISPR system that has a neutered Cas9. This means that the protein normally involved in cutting a gene, Cas9, can no longer snip DNA, even when tethered to the correct spot by the other component, the guide RNA bloodhound. They then tacked on a protein thats involved in switching off genes to this version of CRISPR.

Heres the clever part: the protein is designed to hijack a natural epigenetic process for switching genes off. Genes are often shut down through a natural process called methylation. Normally, the process is transient and reversible on a gene. CRISPRoff commandeers this process, in turn shutting down any targeted gene but for a far longer period of timewithout physically ripping the gene apart.

Thanks to epigenetics enhancing power, CRISPRoff lets researchers go big. In one experiment targeting over 20,000 genes inside immortalized human kidney cells with CRISPRoff, the team was able to reliably shut those genes off.

Not satisfied with a one-way street, the team next engineered a similar CRISPR variant, with a different epigenetics-related protein, dubbed CRISPRon. In cells inside petri dishes, CRISPRon was able to override CRISPRoff, and in turn, flip the genes back on.

We now have a simple tool that can silence the vast majority of genes, said study author Dr. Jonathan Weissman. We can do this for multiple genes at the same time without any DNA damage and in a way that can be reversed.

Even crazier, the off switch lasted through generations. When the team turned off a gene related to the immune system, it persisted for 15 monthsafter about 450 cellular generations.

The edits also lasted through a fundamental transformation, that is, a cells journey from an induced pluripotent stem cell (iPSC) to a neuron. iPSCs often start as skin cells, and are rejuvenated into stem cells through a chemical bath, when they then take a second voyage to become neurons. This process often wipes away epigenetic changes. But to the authors surprise, CRISPRoffs influence remained through the transformations. In one experiment, the team found that shutting off a gene related to Alzheimers in iPSCs also reduced the amount of subsequently encoded toxic proteins in the resulting neurons.

What we showed is that this is a viable strategy for silencing Tau and preventing that protein from being expressed, said Weissman, highlighting just one way CRISPRoffand controlling the epigenome in generalcan alter medicine.

This isnt the first time someones tried to target the epigenome with CRISPR. The same team previously experimented with another set of CRISPR variants that tried the same thing. The difference between the two is time and stability. With the previous setup, scientists struggled to keep the light switch off for a single generation. The new one has no trouble maintaining any changes through multiple divisionsand transformationsin the genome.

A reliable CRISPR tool for epigenetics is insanely powerful. Although we have drugs that work in similar ways, theyre far less accurate and come with a dose of side effects. For now, however, CRISPRoff and CRISPRon only work in cells in petri dishes, and the next step towards genomic supremacy would be to ensure they work in living beings.

If thats the case, it could change genetic editing forever. From reprogramming biological circuits in synthetic biology to hijacking or reversing ones to prevent disease, epigenetic reprogramming offers a way to do it all without ever touching a gene, nixing the threat of mutationswhile leading to lasting effects through generations.

I think our tool really allows us to begin to study the mechanism of heritability, especially epigenetic heritability, which is a huge question in the biomedical sciences, said study author Dr. James Nuez.

Image Credit: nobeastsofierce/Shutterstock.com

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From NIH Research Matters

Long-term, or chronic, stress puts people at risk for a variety of health problems. These can include depression and anxiety, as well as problems with digestion and sleep. Chronic stress has also long been linked to hair loss, but the reasons werent well understood.

Hair growth involves three stages. In growth (anagen), strands of hair push through the skin. In degeneration (catagen), hair ceases to grow, and the follicle at the base of the strand shrinks. In rest (telogen), hair falls out and the process can begin again. Hair is among the few tissues that mammals can regenerate throughout their lifetime.

The hair growth cycle is driven by stem cells that reside in the hair follicle. During growth, stem cells divide to become new cells that regenerate hair. In the resting period, the stem cells are inactive. Until now, researchers hadnt determined exactly how chronic stress impaired hair follicle stem cells.

A team led by Dr. Ya-Chieh Hsu of Harvard University studied the underlying mechanisms that link stress and hair loss. The study was supported in part by NIHs National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). Results appeared in Nature, on March 4, 2021.

The researchers began by testing the role of the adrenal glands, which produce key stress hormonescorticosterone in rodents and cortisol in humans. Removing the adrenal glands from mice led to rapid cycles of hair regrowth. Hair follicle regeneration didnt slow as these mice grew older, like it did in control mice. Rather, hair follicle stem cells continued to enter the growth phase and regenerate hair follicles throughout the animals lifespans. The team was able to restore the normal hair cycle by feeding the mice corticosterone.

Subjecting mice to mild stress over many weeks increased corticosterone levels and reduced hair growth. Hair follicles remained in an extended resting phase. Together, these findings supported the role of corticosterone in inhibiting hair regrowth.

The scientists next examined how corticosterone affects hair follicle stem cells. They found that the stress hormone was not regulating stem cells directly. By deleting the receptor for corticosterone from different cells, they determined that the hormone acts on a cluster of cells underneath the hair follicle called the dermal papilla.

Further studies revealed that corticosterone prevented the dermal papilla from secreting GAS6, a molecule they showed can activate hair follicle stem cells. Delivering GAS6 into the skin restored hair growth in mice fed corticosterone or undergoing chronic stress.

Last year, findings from Hsus team advanced the understanding of how stress causes gray hair. These results reveal a key pathway involved in hair loss from chronic stress. These findings may also lead to further insights into how stress affects tissue regeneration in other parts of the body.

In the future, the Gas6 pathway could be exploited for its potential in activating stem cells to promote hair growth, says first author Dr. Sekyu Choi of Harvard University. However, further study is needed to understand whether the same mechanism is at work in people.

by Erin Bryant

This research was supported in part by NIA grant R01AG048908.

Reference: Corticosterone inhibits GAS6 to govern hair follicle stem-cell quiescence. Choi S, Zhang B, Ma S, Gonzalez-Celeiro M, Stein D, Jin X, Kim ST, Kang YL, Besnard A, Rezza A, Grisanti L, Buenrostro JD, Rendl M, Nahrendorf M, Sahay A, Hsu YC. Nature. 2021 Mar 31. doi: 10.1038/s41586-021-03417-2. Online ahead of print. PMID: 33790465.

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In response to emailed questions, Cellino Biotech CEO and Co-founder Dr. Nabiha Saklayen, talked about the formation of the company and its goal to make stem cell therapies more accessible for patients.

Why did you start this company?

I see a huge need to develop a technology platform to enable the manufacture of cell therapies at scale. We recently closed a $16 million seed financing round led by Khosla Ventures and The Engine at MIT, with participation from Humboldt Fund. Cellino is on a mission to make personalized, autologous cell therapies accessible for patients. Stem cell-derived regenerative medicines are poised to cure some of the most challenging diseases within this decade, including Parkinsons, diabetes, and heart disease. Patient-specific cells provide the safest, most effective cures for these indications. However, current autologous processes are not scalable due to extensive manual handling, high variability, and expensive facility overhead. Cellinos vision is to make personalized regenerative medicines viable at large scale for the first time.

How did you meet your co-founders?

Nabiha Saklayen.

I met my co-founder Marinna Madrid in my Ph.D. research group. We had worked together for many years and had a fantastic working relationship. I then met our third co-founder Matthias Wagner through a friend. Matthias had built and run three optical technology companies in the Boston area and was looking to work with a new team. I was thrilled when we decided to launch the startup together at our second meeting. Matthias built the first Cellino hardware systems in what I like to call Matthias garage. In parallel, I was doing hundreds of expert interviews with biologists in academia and industry, and it started to narrow down our potential applications very quickly. Marinna was doing our first experiments with iPSCs. We iterated rapidly on building new versions of the hardware based on the features that were important to industry experts, such as single-cell precision and automation. Its incredible to witness our swift progress as a team.

What specific need or pain point are you seeking to address in healthcare/life sciences?

In general, autologous therapies are safer for patients because they do not require immunosuppression. The next iteration of cell therapies would use patient-specific stem cells banked ahead of time. Anytime a patient needs new cells, such as blood cells, neurons, or skin cells, we would generate them from a stem cell bank.

Today, patient-specific stem cell generation is a manual and artisanal process. A highly skilled scientist sits at a bench, looks at cells by eye, and removes unwanted cells with a pipette tip. Many upcoming clinical trials are using manual processes to produce stem cells for about ten to twenty patients.

At Cellino, we are converging different disciplines to automate this complex process. We use an AI-based laser system comes to remove any unwanted cells. By making stem cells for every human in an automated, scalable way, we are working towards our mission at Cellino to democratize personalized regenerative medicine.

What does your technology do? How does it work?

Cellinos platform combines label-free imaging and high-speed laser editing with machine learning to automate cell reprogramming, expansion, and differentiation in a closed cassette format, enabling thousands of patient samples to be processed in parallel in a single facility.

In general, autologous, patient-specific stem cell-derived therapies do not require immunosuppression and are safer for patients. Today, patient-specific stem cells are made manually, by hand. To scale the stem cell generation process, Cellino converges different disciplines to automate this complex process. We train machine learning algorithms to characterize cells before our AI-based laser system removes any unwanted cells. By making stem cells for every human in an automated, scalable way, our mission at Cellino is to democratize personalized regenerative medicine. Thats why our vision statement is Every human. Every cell.

Whats your background in healthcare? How did you get to where you are today?

When I arrived at Harvard University for my Ph.D. in physics, I wanted to be closer to real-world applications. Biology is inherently complex and beautiful, and I was interested in developing new physics-based tools to engineer cells with precision. During my Ph.D., I invented new ways to edit cells with laser-based nanomaterials. I collaborated with many brilliant biology groups at Harvard, including the Rossi, Scadden, and Church labs. Working closely with them convinced me that lasers offer a superior solution to editing cells with high precision. That realization compelled me to launch Cellino.

Do you have clinical validation for your product?

Our immediate goal for the next year is to show that our platform can produce personalized, high-quality, R&D-grade stem cells for different patients, which has not been established in an automated manner in the regenerative medicine industry so far. There is significant patient-to-patient variability in manual cell processing, which we eliminate with our platform.

Photo: Urupong, Getty Images

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When it comes to Alzheimers versus science, science is on the losing side.

Alzheimers is cruel in the most insidious way. The disorder creeps up in some aging brains, gradually eating away at their ability to think and reason, whittling down their grasp on memories and reality. As the worlds population ages, Alzheimers is rearing its ugly head at a shocking rate. And despite decades of research, we have no treatmentnot to mention a cure.

Too much of a downer? The National Institutes of Health (NIH) agrees. In one of the most ambitious projects in biology, the NIH is corralling Alzheimers and stem cell researchers to come together in the largest genome editing project ever conceived.

The idea is simple: decades of research have found certain genes that seem to increase the chance of Alzheimers and other dementias. The numbers range over hundreds. Figuring out how each connects or influences anotherif at alltakes years of research in individual labs. What if scientists unite, tap into a shared resource, and collectively solve the case of why Alzheimers occurs in the first place?

The initiatives secret weapon is induced pluripotent stem cells, or iPSCs. Similar to most stem cells, they have the ability to transform into anythinga cellular Genie, if you will. iPSCs are reborn from regular adult cells, such as skin cells. When transformed into a brain cell, however, they carry the original genes of their donor, meaning that they harbor the original persons genetic legacyfor example, his or her chance of developing Alzheimers in the first place. What if we introduce Alzheimers-related genes into these reborn stem cells, and watch how they behave?

By studying these iPSCs, we might be able to follow clues that lead to the genetic causes of Alzheimers and other dementiaspaving the road for gene therapies to nip them in the bud.

The iPSC Neurodegenerative Disease Initiative (iNDI) is set to do just that. The project aims to stimulate, accelerate, and support research that will lead to the development of improved treatments and preventions for these diseases, the NIH said. All resulting datasets will be openly shared online, for anyone to mine and interpret.

In plain language? Lets throw all of our new biotech superstarswith CRISPR at the forefrontinto a concerted effort against Alzheimers, to finally gain the upper hand. Its an Avengers, assemble moment towards one of our toughest foesone that seeks to destroy our own minds from within.

Alzheimers disease was first recognized in the early 1900s. Ever since, scientists have strived to find the cause that makes a brain waste away.

The most prominent idea today is the amyloid hypothesis. Imagine a horror movie inside a haunted house with ghosts that gradually intensify in their haunting. Thats the amyloid horrora protein that gradually but silently builds up inside a neuron, the house, eventually stripping it of its normal function and leading to the death of anything inside. Subsequent studies also found other toxic proteins that hang around outside the neuron house that gradually poison the molecular tenants within.

For decades scientists have thought that the best approach to beat these ghosts was an exorcismthat is, to get rid of these toxic proteins. Yet in trial after trial, they failed. The failure rate for Alzheimers treatmentso far, 100 percenthas led some to call treatment efforts a graveyard of dreams.

Its pretty obvious we need new ideas.

A few years ago, two hotshots strolled into town. One is CRISPR, the wunderkind genetic sharpshooter that can snip way, insert, or swap out a gene or two (or more). The other is iPSCs, induced pluripotent stem cells, which are reborn from adult cells through a chemical bath.

The two together can emulate Dementia 2.0 in a dish.

For example, using CRISPR, scientists can easily insert genes related to Alzheimers, or its protection, into an iPSCeither that from a healthy donor, or someone with a high risk of dementia, and observe what happens. A brain cell is like a humming metropolitan area, with proteins and other molecules whizzing around. Adding in a dose of pro-Alzheimers genes, for example, could block up traffic with gunk, leading scientists to figure out how those genes fit into the larger Alzheimers picture. For the movie buffs out there, its like adding into a cell a gene for Godzilla and another for King Kong. You know both could mess things up, but only by watching what happens in a cell can you know for sure.

Individual labs have tried the approach since iPSCs were invented, but theres a problem. Because iPSCs inherit the genetic baseline of a person, it makes it really difficult for scientists in different labs to evaluate whether a gene is causing Alzheimers, or if it was just a fluke because of the donors particular genetic makeup.

The new iNDI plan looks to standardize everything. Using CRISPR, theyll add in more than 100 genes linked to Alzheimers and related dementias into iPSCs from a wide variety of ethnically diverse healthy donors. The result is a huge genome engineering project, leading to an entire library of cloned cells that carry mutations that could lead to Alzheimers.

In other words, rather than studying cells from people with Alzheimers, lets try to give normal, healthy brain cells Alzheimers by injecting them with genes that could contribute to the disorder. If you view genes as software code, then its possible to insert code that potentially drives Alzheimers into those cells through gene editing. Execute the program, and youll be able to observe how the neurons behave.

The project comes in two phases. The first focuses on mass-engineering cells edited with CRISPR. The second is thoroughly analyzing these resulting cells: for example, their genetics, how their genes activate, what sorts of proteins they carry, how those proteins interact, and so on.

By engineering disease-causing mutations in a set of well-characterized, genetically diverse iPSCs, the project is designed to ensure reproducibility of data across laboratories and to explore the effect of natural variation in dementia, said Dr. Bill Skarnes, director of cellular engineering at the Jackson Laboratory, and a leader of the project.

iNDI is the kind of initiative thats only possible with our recent biotech boost. Engineering hundreds of cells related to Alzheimersand to share with scientists globallywas a pipe dream just two decades ago.

To be clear, the project doesnt just generate individual cells. It uses CRISPR to make cell lines, or entire lineages of cells with the Alzheimers gene that can pass on to the next generation. And thats their power: they can be shared with labs around the world, to further hone in on genes that could make the largest impact on the disorder. Phase two of iNDI is even more powerful, in that it digs into the inner workings of these cells to generate a cheat codea sheet of how their genes and proteins behave.

Together, the project does the hard work of building a universe of Alzheimers-related cells, each outfitted with a gene that could make an impact on dementia. These types of integrative analyses are likely to lead to interesting and actionable discoveries that no one approach would be able to learn in isolation, the authors wrote. It provides the best chance at truly understanding Alzheimers and related diseases, and promising treatment possibilities.

Image Credit: Gerd Altmann from Pixabay

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Are you stressed out? Your skin can show it. Studies show that both acute and chronic stress can exert negative effects on overall skin wellness, as well as exacerbate a number of skin conditions, including psoriasis, eczema, acne, and hair loss.

But its not just a one-way street. Research has also shown that skin and hair follicles contain complex mechanisms to produce their own stress-inducing signals, which can travel to the brain and perpetuate the stress response.

You may already have experienced the connection between the brain and skin. Have you ever gotten so nervous that you started to flush or sweat? If so, you experienced an acute, temporary stress response. But science suggests that repeated exposure to psychological or environmental stressors can have lasting effects on your skin that go far beyond flushing and could even negatively affect your overall well-being.

The brain-skin axis is an interconnected, bidirectional pathway that can translate psychological stress from the brain to the skin and vice versa. Stress triggers the hypothalamus-pituitary-adrenal (HPA) axis, a trio of glands that play key roles in the bodys response to stress. This can cause production of local pro-inflammatory factors, such as cortisol and key hormones in the fight-or-flight stress response called catecholamines, which can direct immune cells from the bloodstream into the skin or stimulate pro-inflammatory skin cells. Mast cells are a key type of pro-inflammatory skin cell in the brain-skin axis; they respond to the hormone cortisol through receptor signaling, and directly contribute to a number of skin conditions, including itch.

Because the skin is constantly exposed to the outside world, it is more susceptible to environmental stressors than any other organ, and can produce stress hormones in response to them. For example, the skin produces stress hormones in response to ultraviolet light and temperature, and sends those signals back to the brain. Thus, psychological stressors can contribute to stressed-out skin, and environmental stressors, via the skin, can contribute to psychological stress, perpetuating the stress cycle.

Psychological stress can also disrupt the epidermal barrier the top of layer of the skin that locks in moisture and protects us from harmful microbes and prolong its repair, according to clinical studies in healthy people. An intact epidermal barrier is essential for healthy skin; when disrupted, it can lead to irritated skin, as well as chronic skin conditions including eczema, psoriasis, or wounds. Psychosocial stress has been directly linked to exacerbation of these conditions in small observational studies. Acne flares have also been linked to stress, although the understanding of this relationship is still evolving.

The negative effects of stress have also been demonstrated in hair. One type of diffuse hair loss, known as telogen effluvium, can be triggered by psychosocial stress, which can inhibit the hair growth phase. Stress has also been linked to hair graying in studies of mice. The research showed that artificial stress stimulated the release of norepinephrine (a type of catecholamine), which depleted pigment-producing stem cells within the hair follicle, resulting in graying.

While reducing stress levels should theoretically help to alleviate damaging effects on the skin, theres only limited data regarding the effectiveness of stress-reducing interventions. There is some evidence that meditation may lower overall catecholamine levels in people who do it regularly. Similarly, meditation and relaxation techniques have been shown to help psoriasis. More studies are needed to show the benefit of these techniques in other skin conditions. Healthy lifestyle habits, including a well-balanced diet and exercise, may also help to regulate stress hormones in the body, which should in turn have positive effects for skin and hair.

If you are experiencing a skin condition related to stress, see a dermatologist for your condition, and try some stress-reducing techniques at home.

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