Cell and gene therapies are overlapping fields of research and treatments. While both aim to treat and potentially cure diseases, they have slightly differing approaches and have different historical backgrounds. Due to growing interest surrounding this field, the general public still has much to learn and understand about each of these potentially life-saving therapies.

Below, we provide a general overview and brief historical context for each type of therapy.

Cell therapyis the process of replacing damaged or dysfunctional cells with new, healthy ones by transferring live cells into a patient. These can be autologous (also known as self-to-self, using cells from the patient receiving the treatment) or allogeneic (using cells from a donor for the treatment). While this field of treatment has recently begun to expand, some forms of cell therapy like the cancer-treating hematopoietic stem cell transplantation(HSCT) have been in practice for decades.

While many people have heard of bone marrow transplants, few realize that this procedure is a stem cell therapy. While stem cells can be derived from many sources, such as umbilical cord blood and mobilized peripheral blood, bone marrow derived stem cell therapy is the most commonly used today and has been for more than 50 years.

The first transfusion of human bone marrow was given to a patient with aplastic anemia in 1939. After World War II researchers diligently worked to restore bone marrow function in aplasia patients caused by exposure to radiation produced by the atomic bomb. After a decade of work they were able to show, in a mouse model, that aplasia could be overcome by bone marrow treatment.

The first allogeneic HSCT, which led the way to current protocols, was pioneered by E. Donnall Thomas and his team at the Fred Hutchinson Cancer Research Center and reported in the New England Journal of Medicine in 1957. In this study six patients were treated with radiation and chemotherapy and then received intravenous infusion of bone marrow rich stem cells from a normal donor to reestablish the damaged or defective cells. Since then the field has evolved and expanded worldwide. While almost half of HSCT are allogeneic, the majority of HSCT are autologous, the patient's own stem cells are used for treatment, which carries less risk to the patient.

In 1988, scientists discovered that they could derive stem cells from human embryos and grow the cells in a laboratory. These newly derived stem cells, referred to as embryonic stem cells (hESCs), were found to be pluripotent, meaning they can give rise to virtually any other type of cell in the body. This versatility allows hESCs cells to potentially regenerate or repair diseased tissue and organs. Two decades after they were discovered, treatments based on hESCs have been slow in coming because of controversy over their source and concerns that they could turn into tumours once implanted. Only recently, testing has begun as a treatment for two major diseases: heart failure and type 1 diabetes.

In 2006, researchers made a groundbreaking discovery by identifying conditions that would allow some cells to be 'reprogrammed' genetically. This new type of stem cell became known as induced pluripotent stem cells (iPSCs). Since this discovery, the field has expanded tremendously in the past two decades. Stem cell therapies have expanded in use and have been used to treat diseases such as type 1 diabetes, Parkinson's and even spinal cord injuries.

There has also been a growing focus on using other immune cells to treat cancer. Therapies such as CAR T-cellare dependent upon a patient's T-cells, which play a critical role in managing the immune response and killing cells affected by harmful pathogens. These cells are then reengineered to target and kill certain cancerous cells. Several CAR T-cell therapies have been FDA approved, with the first approval being given in 2017 for Yescarta and Kymriah, to be used for the treatment of B-cell leukemia in children and young adults.

Gene therapyis a process that modifies the expression of a gene or alters the biological process of living cells for therapeutic use. This process can take the form of replacing a disease-causing gene with a new, healthy one, inactivating the mutated gene, or introducing a new gene to help the patient's body fight a disease.

While the use of gene therapy to treat humans is fairly new, the science behind it has been used in science for decades. Farmers and geneticists have collaborated for years on crop improvement using cross pollination, genetic engineering and microinjection techniques to create stronger, more resilient crops.

The first human patient to be treated with gene therapy was a four-year old girlsuffering from severe combined immunodeficiencyin 1990. She received treatment for a congenital disease called adenosine deaminase (ADA). Since then, gene therapies have been used to treat diseases such as cancer, cystic fibrosis and hemophilia.In 2017, the FDA gave its first approval of a gene therapy called Luxturna, which is used to treat patients with established genetic vision loss that may result in blindness. Gene therapies are still being studied and developed, with over 1,000 clinical trialscurrently underway.

ThermoGenesis Holdings Inc., is a pioneer and market leader in the development and commercialization of automated cell processing technologies for the cell and gene therapy fields. We market a full suite of solutions for automated clinical biobanking, point-of-care applications and large-scale cell processing and manufacturing with a special emphasis on the emerging CAR-T immunotherapy market. We are committed to making the world a healthier place by creating innovative solutions for those in need.

For more information on the CAR-TXpress multi-system platform, please contact our Sales team.

Disclaimer

Thermogenesis Holdings Inc. published this content on 13 April 2021 and is solely responsible for the information contained therein. Distributed by Public, unedited and unaltered, on 13 April 2021 07:10:03 UTC.

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ThermoGenesis : The History of Cell and Gene Therapy - marketscreener.com

LCol Laura Laycock on deployment.

LCol Laura Laycock

It was Oct. 7, 2019, and life was not just good, it was amazing.

My career in the Royal Canadian Air Force was going great. I loved my job and was getting promoted. Throughout my Canadian Armed Forces career of over 20years, I had represented Canada around the world with NORAD, NATO and the UN. I had married the most incredible man. We relocated to Ottawa, started to travel the world together, and were ready to start a family.

Then, on Oct. 8, 2019, everything changed.

I was diagnosed with Chronic Myeloid Leukemia(CML) after blood work for vertigo showed extremely elevated white blood cell counts. CML is a blood cancer where the bone marrow overproduces white blood cells, which eventually impairs the development of white and red blood cells and platelets. Its usually caused by a spontaneous mutation in DNA, which contains our genetic code.

LCol Laycock

Twenty years ago, researchers developed a new line of drugs that combat this overproduction of white blood cells. These targeted oral chemotherapy pills have been revolutionary in the fight against CML. Most people who take them do so for the rest of their lives and have good survival rates; however, a stem cell transplant remains the only actual cure. But its risky and not needed for most people.

Its now been about 17months since my diagnosis and my body has not tolerated this targeted chemotherapy. I fall into that small fraction of people who get debilitating or life-threatening side effects from this medication. My doctors are discussing other treatment options, one of which is a stem cell transplant, but my mixed ethnicity (European/Middle Eastern) has made it difficult to find a donor match.

My journey since my diagnosis has been to slow down and educate myself so that I can heal and advocate for my care; to appreciate every little moment of joy; and to do my best to overcome each challenge that arises. I have found strength in the extraordinary support Ive received from my family, my friends and my community, both old and new.

With the help of family and friends, I recently began a social media campaign to increase stem cell donor education and registration in Canada and around the world. Many people are unaware of the potentially lifesaving role they can play by registering to become stem cell donors. Stem cell transplants are vital treatment options for people with a range of medical conditions including spinal cord injuries, heart disease, diabetes, and some cancers.

The process to donate is simple. First, you register online with Canadian Blood Services or Hma-Qubec and do a mail-in cheek swab., and then you wait. It could be months or years before you are identified as a match. During this waiting period, you should update your contact information with the registry if it changes.

When you are matched, you will be contacted to continue with the donation process. This process is similar to giving blood, but it has its differences. The cells are usually collected intravenously from peripheral blood in a non-surgical procedure but, in rare cases, they are collected directly from the bone marrow in a surgical procedure. In either case, the risks associated with donating are minor.

In Canada, individuals aged17 to 35 can register to become stem cell donors (ages18 to 35 in Quebec). Both CBS and Hma-Qubec are part of an international network of donor registries from over 50countries. This network has a pool of over 38million donors but, unfortunately, matches are rare.

Your stem cells could potentially help others around the world, and throughout this process donor privacy is assured at all times.

LCol Laycock on her wedding day.

Stem cell matching relies on Human Leukocyte Antigen typing, which is highly influenced by ethnicity. This means that a patients best chance of finding a matching donor is from those who share similar ethnic backgrounds. Research conducted by Gragert et al.(2014) has shown that the likelihood of finding a match for certain ethnic groups can be as low as 16 percent and as high as 75 percent for others. This disparity highlights the need for more ethnically diverse stem cell donors in our registries.

Today, I am calling on my DND and CAF families to register as stem cell donors to help people, like me, who are fighting for our lives. If you arent able to register, please share this call with those who can. You, or someone you know, could be the match that saves a life a simple swab is all it takes to be a hero.

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Stem cell treatment needed to fight the good fight - Victoria Lookout

From an insight perspective, this research report has focused on various levels of analysis industry trends analysis, top players analysis, company profiles, which discuss the basic views on the competitive landscape, emerging and high-growth segments of Autologous Stem Cell Based Therapies market, and high-growth regions. Besides, drivers, restraints, challenges, and opportunities pertaining to Autologous Stem Cell Based Therapies market are also predicted in this report.

Get Sample Copy of Autologous Stem Cell Based Therapies Market Report at:https://www.globalmarketmonitor.com/request.php?type=1&rid=643098

Major Participators LandscapeThese market players enjoyed broad industry coverage, outstanding operational ability, and strong financial resources. Manufacturers are focusing on product innovation, brand extension, and the introduction of new brands to cater to the preferences of consumers. Some of them will be endowed with vital future while others will show a weak growth during the prospective timeframe.Major market participators covered in our report are:US STEM CELL, INC. Med cell Europe Pluristem Therapeutics Inc Mesoblast Tigenix Brainstorm Cell Therapeutics Regeneus

To Get More Information on The Regional Analysis Of Autologous Stem Cell Based Therapies Market, Click Here:https://www.globalmarketmonitor.com/reports/643098-autologous-stem-cell-based-therapies-market-report.html

Autologous Stem Cell Based Therapies Application AbstractThe Autologous Stem Cell Based Therapies is commonly used into:Neurodegenerative Disorders Autoimmune Diseases Cardiovascular Diseases

Autologous Stem Cell Based Therapies Type AbstractBased on the basis of the type, the Autologous Stem Cell Based Therapies can be segmented into:Embryonic Stem Cell Resident Cardiac Stem Cells Umbilical Cord Blood Stem Cells

Table of Content1 Report Overview1.1 Product Definition and Scope1.2 PEST (Political, Economic, Social and Technological) Analysis of Autologous Stem Cell Based Therapies Market2 Market Trends and Competitive Landscape3 Segmentation of Autologous Stem Cell Based Therapies Market by Types4 Segmentation of Autologous Stem Cell Based Therapies Market by End-Users5 Market Analysis by Major Regions6 Product Commodity of Autologous Stem Cell Based Therapies Market in Major Countries7 North America Autologous Stem Cell Based Therapies Landscape Analysis8 Europe Autologous Stem Cell Based Therapies Landscape Analysis9 Asia Pacific Autologous Stem Cell Based Therapies Landscape Analysis10 Latin America, Middle East & Africa Autologous Stem Cell Based Therapies Landscape Analysis 11 Major Players Profile

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Major countries of North America, Europe, Asia Pacific, and the rest of the world are all exhaustive analyzed in the report. Apart from this, policy mobilization, social dynamics, development trends, and economic development in these countries are also taken into consideration.

Target Audience for this Report Autologous Stem Cell Based Therapies manufacturers Autologous Stem Cell Based Therapies traders, distributors, and suppliers Autologous Stem Cell Based Therapies industry associations Product managers, Autologous Stem Cell Based Therapies industry administrator, C-level executives of the industries Market Research and consulting firms Research & Clinical Laboratories

Report SpotlightsDetailed overview of marketChanging market dynamics in the industryIn-depth market segmentationHistorical, current and projected market size in terms of volume and valueRecent industry trends and developmentsCompetitive landscapeStrategies of key players and products offeredPotential and niche segments, geographical regions exhibiting promising growthA neutral perspective on market performanceMust-have information for market players to sustain and enhance their market footprints

About Global Market MonitorGlobal Market Monitor is a professional modern consulting company, engaged in three major business categories such as market research services, business advisory, technology consulting.We always maintain the win-win spirit, reliable quality and the vision of keeping pace with The Times, to help enterprises achieve revenue growth, cost reduction, and efficiency improvement, and significantly avoid operational risks, to achieve lean growth. Global Market Monitor has provided professional market research, investment consulting, and competitive intelligence services to thousands of organizations, including start-ups, government agencies, banks, research institutes, industry associations, consulting firms, and investment firms.ContactGlobal Market MonitorOne Pierrepont Plaza, 300 Cadman Plaza W, Brooklyn,NY 11201, USAName: Rebecca HallPhone: + 1 (347) 467 7721Email: info@globalmarketmonitor.comWeb Site: https://www.globalmarketmonitor.com

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Global Autologous Stem Cell Based Therapies Market Survey Report, 2020-2027 KSU | The Sentinel Newspaper - KSU | The Sentinel Newspaper

Kaytlyn Gerbin, left, runs the Wonderland Trail around Mount Rainier. She completed the 93-mile loop in just under 19 hours. Her friend Tara Fraga helped with pacing between miles 30-55. (Ryan Thrower Photo)

When Kaytlyn Gerbin moved to Seattle 10 years ago to attend graduate school at the University of Washington, a friend took her to Kerry Park in the Queen Anne neighborhood on her first visit. The celebrated viewpoint offered Gerbin a glimpse of Mount Rainier that ignited an ongoing passion.

At the time, I had absolutely no idea there was a trail all the way around it, and didnt know the first thing that went into climbing to the summit or running even a few miles on the trails, Gerbin said. Since then, Ive climbed Rainier 10 times, and spent countless hours on the mountain and trails in that park.

Along with her drive to get to know Washington states most famous landmark more intimately, Gerbin achieved her PhD in bioengineering at UW, where her research was focused on the therapeutic and regenerative potential of cardiac cells. For the past four years shes been a scientist at Allen Institute for Cell Science, where she studies stem cells and cardiomyocytes, or cardiac muscle cells.

Our latest Geek of the Week, Gerbin is an accomplished ultrarunner, and she now knows a lot more about that trail that encircles Mount Rainier.

With COVID-19 lockdowns impacting her international race season last summer, Gerbin, a sponsored athlete for The North Face, went after the fastest known time, or FKT, for a run around the Wonderland Trail. Together with teammate Dylan Bowman of Portland and a small crew of local filmmakers, they made Summer of Wonder, a short film about the experience, which you can watch in full here:

The average thru-hiker takes 10-14 days to complete the 93-mile Wonderland Trail, with its 24,000 feet of elevation gain. Gerbin did it in 18 hours, 41 minutes, 53 seconds, and the film is a breathtaking look at her endurance feat.

Gerbins passion for running started with 3-mile commutes back and forth between her apartment, her research lab, and campus during grad school. Eventually she started trail running,essentially as a life hack to see if she could squeeze a five-day backpacking route into a weekend between experiments.

It turned out I was actually pretty good at that, and that opened up opportunities to start racing at some of the most competitive trail races in the U.S. and Europe, Gerbin said.

Shes since raced with Team USA at the Trail World Championships, reached the podium at the iconic Western States 100, and won races such as the Canary Islands Transgrancanaria and Cascade Crest 100 in Washington. She also still holds the womens self-supported FKT for the Rainier Infinity Loop (set in 2019), which combines the Wonderland Trail with two summits and descents of Mount Rainier.

Her preferred racing distance is anything between 50-100 miles long, the more elevation gain and technical the trail, the better. During peak training, Gerbin is usually hitting between 70-90 miles with over 20,000 feet of elevation gain each week. She calls the Pacific Northwest the best outdoor playground there is.

Although I love running fast, Im also really excited about pushing myself on more challenging terrain. So many of my other FKT goals and route ideas are along these lines, with more technical traveling than actual running, she said.

COVID permitting, her highest race priority this year is Ultra Trail du Mont Blanc, which is the most competitive world-stage for ultrarunning, at the end of August. The race circumnavigates Mont Blanc, passing through France, Italy, and Switzerland and covering around 105 miles and 33,000 feet of elevation gain.

While Gerbins experience as a scientist does inform her appreciation for what shes putting her body through during ultrarunning, shes equally passionate in the lab. At the Allen Institute shes seeking answers to broad questions about how cells work, including how single cells and all of their components are integrated into a functional system, while using imaging to build predictive models of cell behavior.

I get the opportunity to work with a multidisciplinary team of badass scientists, biologists, and engineers on really cool problems in cell biology, she said.

Learn more about our latest Geek of the Week, Kaytlyn Gerbin:

What do you do, and why do you do it? Science and ultrarunning for me have always come down to problem solving.

As a scientist, problem solving is inherent to experimental design, data analysis, and interpreting results. By asking hard questions, Im interested in pushing the field of cell biology forward, and challenging the current way of thinking.

As an ultrarunner, its a different kind of problem solving, but I lean on the same mindset to figure out how to push my athletic limits further and faster.

One thing that always amazes me is how adaptable the human body is. My training in cell science gives me context for how all of these stressors and inputs were putting on our bodies are fundamentally happening at the single cell level, and it keeps me thinking about the cells response to external cues in my research.

Whats the single most important thing people should know about your field? Yes, I do think about science and when Im running, and no, I do not geek out on heart rate monitors and training zones and all those numbers when Im running.

Where do you find your inspiration? Im inspired by brilliant women that are pushing whats possible in both science and in sports. I think we often set boundaries for ourselves about what we think is possible, without ever letting ourselves really hit that limit. Im inspired by women who set bold goals and bring others up and along for the ride, redefining whats possible.

Whats the one piece of technology you couldnt live without, and why? My Garmin 935. I use this watch daily to track miles run, elevation gain, etc. The battery life has lasted me for 100 miles of running and ~24 hrs, but its small enough to wear every day.

Whats your workspace like, and why does it work for you? Prior to 2020, I was splitting my time between the tissue culture hood (passaging cells, differentiating cardiomyocytes, setting up experiments), conference rooms (team science and collaboration means a lot of group discussions!), and my computer for writing and analysis. Since then, Ive shifted my work to be more remote while I work on a few different manuscripts. I have an office set up at home with a window, some good tunes, plenty of coffee, and a chair for my dog to wait impatiently on.

Your best tip or trick for managing everyday work and life. (Help us out, we need it.) I have always been a to-do list person. Most mornings start with me listing out tasks (and breaking those down into many sub-tasks). I feel productive as I cross things off, and it also helps me prioritize and plan ahead to make sure I can also fit my training runs in.

Mac, Windows or Linux? Mac as a personal preference, Windows for my work computer (I do work at the Paul Allen Institute

Transporter, Time Machine or Cloak of Invisibility? Transporter. I just promise not to use it in races.

Greatest game in history: Lode Runner. I havent played it since I was a kid, but the memories of yelling at the computer with my sister frantically hitting up-down-up-down arrows make me feel like it was just yesterday.

Best gadget ever: Garmin inReach mini satellite messaging and SOS call, all in a device small enough to throw in the bottom of a pack (or shorts pocket) and forget its there. I bring this with me anytime Im headed out into the wilderness/mountains, but I hope I never need to use it.

First computer: iMac G3.

Current phone: iPhone 11.

Favorite app: I have a love/hate relationship with Strava. Ive also been using DuoLingo during the pandemic and have a strong daily streak going!

Most important technology of 2021: COVID vaccines!!

Most important technology of 2023: Advancements in remote/low-resource medical care.

Final words of advice for your fellow geeks: Most problems can be solved with more snacks and some time (works for science and running).

Twitter: @kaytlyn_gerbin

LinkedIn: Kaytlyn Gerbin

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Kaytlyn Gerbin is blazing trails in cell science and as an ultrarunner who has conquered Mount Rainier - GeekWire

Children and young adults who underwent an allogeneic hematopoietic stem cell transplant (alloHSCT) after achieving complete response with CD19 CAR T-cell therapy experienced durable B-cell acute lymphoblastic leukemia (B-ALL) control, according to the results of a phase 1 trial (ClinicalTrials.gov Identifier: NCT01593696) published in the Journal of Clinical Oncology.

Although a proportion of patients who undergo CAR T-cell therapy go on to receive alloHSCT, the study authors stated that The role for [alloHSCT] following CD19-CAR T-cell therapy to improve long-term outcomes in [children and young adults] has not been examined.

The phase 1 trial evaluated 50 children and young adults with B-ALL who received CD19.28 CAR T-cell therapy. The primary objective was to determine the maximum tolerated dose of CAR T cells, toxicity, and feasibility of generating CAR T cells in the study population. In addition, this analysis retrospectively evaluated the effect of alloHSCT on survival after CAR T-cell therapy.

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At baseline, the median age was 13.5 years (range, 4.3-30.4), and 40 (80%) of the patients were male. The median number of prior regimens was 4 (range, 4.3-30.4); 22 (44%) patients had at least 1 prior HSCT, 2 (4%) had prior CD19-targeted therapy, and 5 (10%) of the patients had prior treatment with blinatumomab.

Complete response was achieved in 31 (62%) of the patients. Among these patients, 28 (90.3%) were negative for minimal residual disease. Higher rates of complete response were associated with primary refractory disease, fewer prior lines of therapy, M1 marrow, or fludarabine/cytarabine-based lymphodepletion. The median overall survival was 10.5 months (95% CI, 6.3-29.2) during a median follow-up of 4.8 years.

Of the 28 patients who achieved complete response, 21 (75%) proceeded to undergo consolidative alloHSCT. The median overall survival for these patients was 70.2 months (95% CI, 10.4-not estimable), with an event-free survival not yet reached. The rate of relapse after alloHSCT was 4.8% (95% CI, 0.3-20.3) at 12 months and 9.5% (95% CI, 1.5-26.8) at 24 months.

Any grade cytokine release syndrome (CRS) developed among 35 (70%) patients, with 9 (18%) experiencing grade 3 to 4 CRS. Of the 10 patients (20%) who developed neurotoxicity, 4 cases were severe. One cardiac arrest occurred during CRS. All patients with CRS, neurotoxicity, and cardiac arrest recovered.

The authors concluded that CD19.28 CAR T cells followed by a consolidative alloHSCT can provide long-term durable disease control in [children and young adults] with relapsed or refractory B-ALL.

Disclosure: Please see the original reference for a full disclosure of authors affiliations.

Reference

Shah NN, Lee DW, Yates B, et al. Long-term follow-up of CD19-CAR T-cell therapy in children and young adults with B-ALL. J Clin Oncol. Published online March 25, 2021. doi:org/10.1200/JCO.20.02262c

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Durable B-ALL Control With Allogeneic Transplant After CAR T-Cell Therapy - Cancer Therapy Advisor

By Guest Blogger Rich Whittle, Bioastronautics & Human Performance Lab at Texas A&M UniversityThe recent landing of the probe Perseverance on Mars, and the excitement generated by the high-resolution images currently being broadcast back to Earth, has inevitably started people thinking about human exploration of the Red Planet. However, the challenges faced by a manned journey to Mars are much more than just technical, but reflect some fundamental aspects of human physiology. In this guest article, Rich Whittle of the Bioastronautics and Human Performance Lab at Texas A&M University, reflects on some of the key issues.

NASA has ambitious plans to begin manned exploration of Mars, although its current focus is on sending the next man and first woman to the Moon as part of the Artemis programme, which will establish a permanent human presence there in the coming decade. A key part of this latter objective is to place a spaceship called Gateway in orbit around the Moon, from which landers will take astronauts to the surface and support their activities. Gateway will also conduct a wide variety of human and scientific missions, and in particular study the physiological effects of long journeys into space, in preparation for that first manned voyage to Mars.

The human body has evolved over hundreds of thousands of years to flourish on the surface of the Earth, and it is perhaps not surprising that the stresses of spaceflight pose unique physiological and medical problems. In fact, many of the basic issues associated with spaceflight, such as hypoxia, dysbarism, acceleration, and thermal support, have been well studied through aviation and diving medicine in the years prior to spaceflight. But while the last 50 years of manned space exploration have shown that humans can adapt to space, remaining productive for up to 1 year and possibly longer, there are still many problems associated with the prolonged exposure to a unique combination of stressful stimuli including acceleration, radiation, and weightlessness. The latter condition is a critical feature of spaceflight and has significant effects on human physiology, many of which were quite unexpected at the beginning of space exploration.

Scientists have known for a long time that the human body responds in specific ways to the microgravity environment of spaceflight. For example, a person who is inactive for an extended period loses overall strength, as well as muscle and bone mass. Unsurprisingly spaceflight has a similar effect, resulting in loss of bone mineral density (BMD), and increasing the risk of bone fractures in astronauts. It is predicted that a third of astronauts will be at risk for osteoporosis during a predicted 7-month long human mission to Mars. It is however possible to compensate for this loss of muscle and bone mass using resistive exercise devices that NASA has developed to allow for more intense workouts in zero gravity.

Overall, the pathophysiological adaptive changes that occur during spaceflight, even in well-trained, highly selected, and healthy individuals, have been likened to an accelerated aging process, and are being studied in research groups around the world. My own research at Texas A&M focuses on changes to the cardiovascular system caused by the microgravity environment of spaceflight. In an upright position under the Earths standard 1G gravity, arterial blood pressure is lower above the heart and higher below the heart. But in a weightless environment the body experiences a uniform arterial pressure, which decreases the cardiac workload, and reduces the need for blood pressure regulatory mechanisms. As a result, the muscles of the heart and blood vessels begin to atrophy, and consequently some astronauts experience orthostatic intolerance, the difficulty or inability to stand because of light headedness after return to Earth. During spaceflight, cardiovascular changes are noticeable immediately after the onset of weightlessness, with astronauts exhibiting characteristically puffy faces, stuffed noses, and chicken legs, as approximately 2L of fluid is shifted from the legs towards the head.

These fluid shifts affect not only the cardiovascular system but also the brain, eyes, and other neurological functions. The apparent increase in fluid within the skull is potentially linked to a collection of pathologies of the eye known as Spaceflight Associated Neuro-ocular Syndrome (SANS). This is principally manifested through a hyperopic shift in visual acuity, which in some cases does not resolve on return to Earth.

We believe that many of these problems can be overcome through effective countermeasures during spaceflight, and are often reversible after landing. Physical exercise programs are the main countermeasure used during spaceflight to protect the cardiovascular system. The technology involved has advanced from a rowing ergometer used in the early Skylab missions, through a motorized treadmill used in the ISS. This has been recently joined by a device for performing resistive exercise, and now rowing ergometers are once again being looked at for longer duration missions to Mars due to their small footprint.

However, some astronauts have returned from the ISS with unexpectedly stiff arteries, of a magnitude expected from 10 20 years of normal aging. Arterial stiffening is often linked to an increased blood pressure and elevated risk for cardiovascular disease. Additionally, other studies have suggested that insulin resistance occurs during spaceflight, possibly due to reduced physical activity, which could lead to increased blood sugar and increased risk of developing type 2 diabetes. These results suggest that the astronauts exercise routine did not always counteract the effect of the microgravity environment and indicated that further countermeasures might be needed to help maintain astronaut health. Here at Texas A&M we are looking at both lower body negative pressure (LBNP) and artificial gravity generated through short radius centrifugation as exciting new countermeasures that could be used in long duration spaceflight.

As we begin to further understand the effects of spaceflight on human physiology, scientists are now starting to study some of the underlying cellular mechanisms using model organisms, cell cultures, organs on a chip and stem cells. And because many of the observed changes seen in space, such as cardiovascular dysfunction due to inflammation, lack of exercise, intracranial hypertension, and hormonal and metabolic changes, resemble those caused by aging or illnesses, the research we conduct may have important applications on Earth. Hopefully, our push for manned exploration of the planets of the solar system will lead to tangible benefits to the health and well-being of humans on our home planet.

More:
The Physiological Challenges of Spaceflight - Cambridge Wireless

The 1997 film Gattaca promised a future where humans would be free of disease and babies born on demand with the latest upgrades, including enhanced speed, intelligence, and beauty. Much like a new Tesla Roadster. However, despite the technological predictions offered by Hollywood moviemakers, were still living in a time when synthetic biology is working hard to make a dent in the world. No designer babies in sight. And stem cell technology promised so many radical breakthroughs back in the late 1990s, including growing organs for transplants and regenerating whole body parts, but the challenge of growing whole organs has been shown to be more complex than previously believed, including technologies like 3D bioprinting and xenotransplantation.

Despite the challenges and setbacks, investors believe were living in a different time, with more money pouring into the space over the last few years:

Indeed, the science and technology behind manipulating biological matter are still promising when it comes to health and medicine, especially with the rise of CRISPR gene editing. The idea that we could potentially switch on or off genes that cause disease using a cocktail of enzymes is just fantastical. While inserting CRISPR enzymes into a live human being is a bit challenging, there are regions of the body that are easily accessible, such as the eye. In a landmark clinical trial approved by the FDA and led by Editas Medicine (EDIT) and Allergan, now owned by AbbVie (ABBV), a CRISPR-Cas9 gene therapy was administered directly to patients to remove rare mutations that can cause childhood blindness.

McKinsey is calling this emerging technological renaissance the next Bio Revolution, with advances in biological sciences being accelerated by automation and artificial intelligence. The speed at which scientists and researchers were able to sequence the genome of the Rona virus is a testament to the power of these converging technologies. McKinsey predicts that synthetic biology could have a direct economic impact of $4 trillion per year, nearly half of which will be in the domain of human health.

Lets take a look through five companies that are harnessingthe revolutionary power of synthetic biology to design new therapies and treathuman diseases.

Founded in 2017 and headquartered in Alameda, California, Scribe Therapeutics is a biotechnology startup that is producing therapeutics using custom-engineered CRISPR enzyme technology. The company has raised a whopping $120 million from the likes of Andreessen Horowitz to build out a suite of CRISPR technologies designed to treat genetic diseases. Scribe Therapeutics was co-founded by Dr. Jennifer Doudna, the UC Berkeley biochemist who discovered and developed CRISPR gene-editing technology and won the Nobel Prize in Chemistry in 2020 for her pioneering work.

The team at Scribe Therapeutics has designed its XEditing (XE) technology by evolving the native CRISPR gene-editing enzymes available to us to redesign and engineer them to suit different needs. More specifically, they want to be able to modify or silence the genes of live humans to treat genetic diseases such as Huntingtons, Parkinsons, Sickle Cell Anemia, and Amyotrophic Lateral Sclerosis (ALS). Anything your parents unwittingly handed down to you, Scribe Therapeutics is looking to treat it. The research team tests thousands of redesigned enzymes and selects those with greater editing ability, specificity, and stability compared to current enzymes. Scribe Therapeutics is starting with a pipeline of therapeutics to treat neurodegenerative diseases and has its sights set on other, less common genetic conditions down the road.

Canadian biotechnology startup Notch Therapeutics was founded in 2018 and has raised $86 million to develop immune cell therapies against pre-cancer cells. The companys cell therapies are based on induced pluripotent stem cells (iPSC), which are pre-differentiated cells with the limited capacity to transform into different mature cell lines. Based on its Engineered Thymic Niche (ETN) platform, the company is developing universally compatible stem cell-derived immune cell therapies.

Normally, human immune cells only recognize othercells found in the same individual and will target cells from other individuals,which appear foreign to the immune system. Thats why donor organs can sometimesbe rejected by the recipients body the immune system sees the organ as a foreignobject. Notch Therapeutics is designing a system where the immune cellsproduced from the stem cells will be universally recognizable by allindividuals, bypassing the need to create immune cells from pluripotent stemcells derived from each recipient. These manufactured immune cells, whichinclude T cells or natural killer cells, can be programmed to target cancercells and eliminate them from the patient.

Founded in 2016, Massachusetts-based bit.bio is a synthetic biology startup thats working on merging the world of coding with biology. The company has secured $42 million after a Series A round that was completed in June 2020. A spinout of Cambridge University, bit.bio is looking to commercialize its proprietary platform, opti-ox, which can reprogram human stem cells to do its bidding cure diseases. Touted as the Cell Coding Company, bit.bio was founded by Dr. Mark Kotter, a neurosurgeon at the University of Cambridge who studied regenerative medicine and stem cell technology.

While the ability to program mammalian stem cells has been around since 1981, the company claims it can consistently reprogram human adult cells into pluripotent stem cells, and then transform them into other mature human cells within days. Currently, stem cell technology produces a statistical mixed bag of mature, differentiated cells, some of which can have potential side effects. opti-ox uses a precise combination of transcription factors to ensure stem cells mature into cardiac, muscle, liver, kidney, or lung cells with high efficiency. The holy grail for the company is to be able to produce every cell in the human body for any cell therapy safely, on-demand, and with purities approaching 100%. And well be here, waiting for that stem cell therapy for erectile dysfunction promised by the medical community.

Founded in 2020, Delonix Bioworks is a Shanghai-based synthetic biology company designing therapeutic solutions against infectious diseases. The startup received $14 million from a Seed round just back in March. The Delonix Bioworks team is focusing its initial efforts on anti-microbial resistant (AMR) infections. The emergence of resistance in some bacteria species against common antimicrobial compounds, so has led to an increasing number of infections that are difficult to treat with conventional strategies. These superbug strains are mostly spread in hospital or clinical settings due to the overuse of antibiotics.

The company is engineering attenuated, live bacteria thatcan act as vaccines against these types of infections. By introducing reprogrammed,but weakened, bacteria to express specific antigens on the surface of theirmembrane that match those of the strains that cause AMR infections into anindividual, the individuals immune system can recognize those antigens andrespond to future infections with greater speed. Its no different from how antiviralvaccines are designed, except most vaccines introduce an attenuated or inactivatedvirus to activate the immune system instead. And for those of you who skipped highschool biology, no, this is not a mind-control scheme orchestrated by biotech companies.

Founded in 2018, Octarine Bio is a Danish synthetic biology company thats building out a pipeline for high-potency cannabinoids and psilocybin derivatives for the pharmaceutical industry. Octarine Bio has brought in $3 million after a Seed round that was also completed in March. Medical studies on psychotropic compounds have been shown to help reduce anxiety, depression, and pain, and may have the potential to serve as novel psychiatric medications. A few companies have recently emerged to commercialize existing psychedelics. Octarine Bio believes it can do better by harnessing the power of synthetic biology to engineer microorganisms to produce these psychotropic compounds with better pharmacokinetic and therapeutic effects.

Normally, natural products are produced by plant and fungal species as an ill-defined mixture. The psychoactive properties of these compounds primarily stem from only a handful of compounds because their natural concentration is much higher than other derivatives in the organic material. For example, tetrahydrocannabinol (THC) is the main psychoactive agent in marijuana while psilocybin is the one found in mushrooms from the Psilocybe and other psilocybin-producing genera. However, these are just a few out of hundreds of potential psychoactive derivatives produced by these species.

Molecular derivatives may be produced at too low of concentration to test and analyze, or the plant or mushroom may have a deactivated metabolic pathway that could lead to a superior compound. By tweaking the molecular structure of the product compounds using both synthetic biology and traditional organic chemistry, the team at Octarine Bio is creating a platform to discover new potential therapeutics that may not have been available before. Magic mushrooms are about to get an upgrade for an extra potent trip.

Much like what was said about software by Marc Andreessen back in 2011, synthetic biology is starting to eat the world. While were a long way away from a dystopian future where babies are engineered with supernatural talents, were already seeing the potential side-effects of using CRISPR on the Chinese twin girls originally to immunize them from HIV, including enhanced cognition and memory. The cure for stupid is possibly lurking in the vaults of this pioneering technology. For now, well wait and see how synthetic biology and CRISPR gene editing shape up as potential therapeutics for real diseases.

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5 Novel Therapies Using Synthetic Biology - Nanalyze

Cut off a piece of a zebrafish heart, and the little creature wont be at the top of its game for a few days.

But after a month, the heart will grow back to normal and life goes on as normal.

Given that a heart attack in humans known as a myocardial infarction is akin to losing a piece of your heart (because tissue dies), scientists for years have been trying to understand how zebrafish heal themselves, with a view to replicating the process in people.

Now, scientists at the Victor Chang Cardiac Research Institute have identified the genetic switch in zebrafish that prompts heart cells to divide and multiply after a heart attack, resulting in the complete regeneration and healing of damaged heart muscle in these fish.

Dr Kazu Kikuchi, who led the research, published in Science on Friday, said he was astonished by the findings.

Our research has identified a secret switch that allows heart muscle cells to divide and multiply after the heart is injured, Dr Kikuchi said in a statement.

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It kicks in when needed and turns off when the heart is fully healed. In humans where damaged and scarred heart muscle cannot replace itself, this could be a game changer.

The researchers investigated a critical gene known as Klf1, which previously had only been identified in red blood cells.

They discovered Klf1 plays a vital role in healing damaged hearts.

The gene works by making uninjured heart muscle cells called cardiomyocytes more immature and changing their metabolic wiring, a process called dedifferentiation.

This allows them to divide and make new cells

Cardiomyocytes are the heart cells primarily involved in the contractile function of the heart that enables the pumping of blood around the body.

Ordinarily, adult mammalian hearts have a limited ability to generate new cardiomyocytes whereas zebrafish will keep making new cells until their hearts are completely healed.

Its been known for more than a decade that cardiomyocytes become more youthful in order to regenerate and Dr Kikuchi was one of the researchers to demonstrate this.

What wasnt known was how this was made to happen.

Our new paper suggests it is Klf1 which triggers this, Dr Kikuchi said.

This isnt the same as stem cell technology. In fact, dedifferentiating cardiomyocytes has proved to be a more effective healing process than stem cells.

It all comes down to that genetic switch.

Dr Kikuchi said that when the gene was removed, the zebrafish heart lost its ability to repair itself after an injury such as a heart attack, which pinpointed it as a crucial self-healing tool.

Professor Bob Graham, head of the Institutes Molecular Cardiology and Biophysics Division, says this world-first discovery made in collaboration with the Garvan Institute of Medical Research may well transform the treatment of heart attack patients and other heart diseases.

The team has been able to find this vitally important protein that swings into action after an event like a heart attack and supercharges the cells to heal damaged heart muscle. Its an incredible discovery, Professor Graham said.

The gene may also act as a switch in human hearts. We are now hoping further research into its function may provide us with a clue to turn on regeneration in human hearts, to improve their ability to pump blood around the body.

Importantly, the team also found the Klf1 gene played no role in the early development of the heart and that its regenerative properties were only switched on after a heart injury.

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Australian scientists discover secret switch for the heart to heal itself - The New Daily

Synthego, the genome engineering company, today announced the launch of Eclipse, a new high-throughput cell engineering platform designed to accelerate drug discovery and validation by providing highly predictable CRISPR-engineered cells at scale through the integration of engineering, bioinformatics, and proprietary science. The launch of this unique CRISPR-based platform is driving the companys growing impact in biopharma R&D, reinforcing Synthegos position as the genome engineering leader.

CRISPR-engineered cells have a wide range of applications in research and development across disease areas, including in neuroscience and oncology. Synthego created the Eclipse Platform to enhance disease modeling, drug target identification and validation, and accelerate cell therapy manufacturing.

"By industrializing cell engineering, Synthegos Eclipse Platform will enable economies of scale, turning a historically complex process into one that is flexible, reliable, and affordable, said Bill Skarnes, Ph.D., professor and director of Cellular Engineering at The Jackson Laboratory and Synthego advisory board member. Offering CRISPR edits at scale, similar to what Synthego did with sgRNA reagents, puts researchers on the cusp of being able to study thousands of genes, and examine hundreds of variants of those genes. This will allow scientists to more faithfully model the complexity of a human disease, which could lead to the development of therapeutic drugs or next-generation gene therapies for many serious diseases.

To ensure the success of any type of edit, Eclipse uses machine learning to apply experience from several hundred thousand genome edits across hundreds of cell types. With this machine learning, combined with automation, the new platform can reduce costs and increase the scalability of engineered cell production. The Eclipse Platform is modular in design, allowing for fast deployment of upgrades or add-ons. It is engineered to use a cell-type agnostic process and immediately benefit researchers working with induced pluripotent stem (iPS) cells and immortalized cell lines.

We are living in a new era of life sciences innovation one that has added to DNA sequencing and being able to read out of biology, now being able to write into and engineer biology. We created our Eclipse Platform at the convergence of science and technology to make genome editing more precise, scalable, and accessible, said Paul Dabrowski, CEO and co-founder of Synthego. We are excited to expand our impact on advancing the life sciences innovation with the launch of this unique CRISPR-based platform.

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Synthego Launches Eclipse Platform to Accelerate Research and Development of Next-generation Medicines - The Scientist

Google is discontinuing the Google Play Movies and TV app for Samsung, LG and Vizio smart TVs, as well as Roku devices. Come June 15th, 2021, you wont be able to access the software on those platforms anymore. Instead, youll need to go through YouTube to watch any content youve bought in the past. Any Google Play credits associated with your account will still be there, allowing you to buy new movies and TV shows. However, your Watchlist wont transfer over, and support for family sharing is more limited.

Google shared the news last month, but it went mostly unnoticed until after websites like Liliputing and 9to5Google published stories on the shutdown earlier today following an email the company sent to users. To be clear, Play Movies and TV itself isnt joining the Google graveyard on June 15th. Google plans to eventually merge the app with its new Google TV software, but that's an ongoing process with the former still available to download on Android and iOS.

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The Google Play video app will leave Roku, Vizio, LG and Samsung's TV platforms - Yahoo Canada Finance

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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How stress causes hair loss | National Institute on Aging - National Institute on Aging

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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Cellino Biotech developing tech to help scale stem cell therapies - MedCity News

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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A Massive New Gene Editing Project Is Out to Crush Alzheimer's - Singularity Hub

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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Stress may be getting to your skin, but it's not a one-way street - Harvard Health Blog - Harvard Health

Leukemia cutis can happen when leukemia cells enter your skin. This rare condition causes patches of discolored skin to appear on the body.

In some cases, the appearance of leukemia cutis lesions on the skin is the first sign of leukemia a cancer of the blood and bone marrow.

Along with standard leukemia therapies, this complication can usually be addressed with topical treatments to help heal the damaged skin. If you have leukemia cutis, your outlook will usually depend on your age and the type of leukemia you have.

Leukemia cutis is an uncommon complication, affecting only about 3 percent of people with leukemia. However, it is often a sign that the cancer is at an advanced stage.

With leukemia, malignant leukocytes (white blood cells) are usually only present in the bloodstream. In the case of leukemia cutis, the leukocytes have entered the skin tissue, causing lesions to appear on the outer layer of your skin. The word cutis refers to the skin, or dermis.

Generally, leukemia cutis results in one or more lesions or patches forming on the outer layer of skin. This condition can mean that the leukemia is more advanced and may have spread to your bone marrow and other organs.

Because there are fewer healthy white cells to combat infections caused by other diseases, rashes and sores may be more common among people with leukemia. Low blood platelets from leukemia can cause damage to blood vessels that appear as red spots or lesions on the skin.

These may include:

However, these skin changes are different than those brought on by leukemia cutis.

While the legs are the most common area for leukemia cutis lesions to appear, they can also form on the arms, face, trunk, and scalp. These skin changes can include:

The lesions usually dont hurt. However, with certain types of leukemia particularly acute myeloid leukemia (AML) the lesions may bleed.

A dermatologist may initially diagnose leukemia cutis based on a physical examination of the skin and a review of your medical history. A skin biopsy is needed to confirm the diagnosis.

Leukemia cutis is a sign of leukemia. It wont develop if the body isnt already dealing with this type of blood cancer.

But leukemia isnt just one disease. There are multiple types of leukemia, each one classified by the kind of cell affected by the disease.

You can also have an acute or a chronic form of leukemia. Acute means it comes on suddenly and usually with more severe symptoms. Chronic leukemia develops more slowly and often with milder symptoms.

The types of leukemia that most commonly trigger leukemia cutis are AML and chronic lymphocytic leukemia (CLL).

Scientists arent sure why cancerous leukocytes migrate to skin tissue in some people with leukemia. It may be that the skin is an optimal environment for healthy leukocytes to transform into cancerous cells.

One possible risk factor that has emerged is an abnormality in chromosome 8, which has been found more often in individuals with leukemia cutis than in those without it.

Treating leukemia cutis usually includes treatment for leukemia as the underlying condition.

The standard leukemia treatment is chemotherapy, but other options may be considered depending on your overall health, your age, and the type of leukemia you have.

Other leukemia treatment options include:

For blood cancers, external beam radiation is a typical form of treatment. With this therapy, a focused beam of radiation is delivered outside the body from various angles. The goal is to injure the DNA in cancer cells to stop them from reproducing.

Immunotherapy, a type of biological therapy, uses the bodys own immune system to fight cancer. It is typically given by an injection that either stimulates immune system cells activity or blocks the signals cancer cells send to suppress the immune response.

Immunotherapy may also be given orally, topically, or intravesically (into the bladder).

Stem cell transplantation is more commonly known as a bone marrow transplant. Bone marrow is where blood stem cells develop. Stem cells can become any type of cell.

Through stem cell transplantation, healthy blood stem cells replace stem cells damaged by the cancer or by chemotherapy or radiation therapy. However, not everyone is a good candidate for this treatment.

Only treating the leukemia cutis lesions will not address the underlying disease of leukemia. That means treatments designed to remove or reduce lesions should be done in combination with systemic treatment for leukemia itself.

Treatments for leukemia cutis symptoms can include:

Again, these treatments will only treat the leukemia cutis lesions, but systemic treatment of the leukemia itself will be needed as well.

The length of time leukemia cutis lesions may last depends on many factors, including how well the leukemia itself is responding to treatment. If the leukemia goes into remission, its unlikely more lesions will appear.

With effective treatment, existing lesions could fade. However, other factors, including your age and overall health, can affect how widespread the lesions are and how long they may last.

There are encouraging trends in the treatment of leukemia, but it remains a challenging disease to treat and live with.

For people with AML who dont have leukemia cutis, research suggests that the survival rate at 2 years is about 30 percent. However, the survival rate drops to 6 percent among people with the skin lesions.

A separate study of 1,683 people with AML found that leukemia cutis was associated with a poor prognosis, and that those with AML and leukemia cutis may benefit from more aggressive treatment.

The outlook for people with CLL is better, with about an 83 percent survival rate at 5 years. The presence of leukemia cutis doesnt seem to change that outlook very much, according to a 2019 study.

Leukemia cutis is a rare complication of leukemia. It happens when malignant leukocytes invade the skin and cause lesions on the skins outer surface.

AML and CLL are more often associated with leukemia cutis than other types of leukemia.

While leukemia cutis usually means the leukemia is in an advanced stage, there are treatments for both the cancer and this uncommon side effect that may help extend life and improve its quality.

The rest is here:
Leukemia Cutis: Symptoms and Treatment - Healthline

(The Conversation is an independent and nonprofit source of news, analysis and commentary from academic experts.)

Christopher Tuggle, Iowa State University and Adeline Boettcher, Iowa State University

(THE CONVERSATION) The U.S. Food and Drug Administration requires all new medicines to be tested in animals before use in people. Pigs make better medical research subjects than mice, because they are closer to humans in size, physiology and genetic makeup.

In recent years, our team at Iowa State University has found a way to make pigs an even closer stand-in for humans. We have successfully transferred components of the human immune system into pigs that lack a functional immune system. This breakthrough has the potential to accelerate medical research in many areas, including virus and vaccine research, as well as cancer and stem cell therapeutics.

Existing biomedical models

Severe Combined Immunodeficiency, or SCID, is a genetic condition that causes impaired development of the immune system. People can develop SCID, as dramatized in the 1976 movie The Boy in the Plastic Bubble. Other animals can develop SCID, too, including mice.

Researchers in the 1980s recognized that SCID micecould be implanted with human immune cells for further study. Such mice are called humanized mice and have been optimized over the past 30 years to study many questions relevant to human health.

Mice are the most commonly used animal in biomedical research, but results from mice often do not translate well to human responses, thanks to differences in metabolism, size and divergent cell functions compared with people.

Nonhuman primates are also used for medical research and are certainly closer stand-ins for humans. But using them for this purpose raises numerous ethical considerations. With these concerns in mind, the National Institutes of Health retired most of its chimpanzees from biomedical research in 2013.

Alternative animal models are in demand.

Swine are a viable option for medical research because of their similarities to humans. And with their widespread commercial use, pigs are met with fewer ethical dilemmas than primates. Upwards of 100 million hogs are slaughtered each year for food in the U.S.

Humanizing pigs

In 2012, groups at Iowa State University and Kansas State University, including Jack Dekkers, an expert in animal breeding and genetics, and Raymond Rowland, a specialist in animal diseases, serendipitously discovered a naturally occurring genetic mutation in pigs that caused SCID. We wondered if we could develop these pigs to create a new biomedical model.

Our group has worked for nearly a decade developing and optimizing SCID pigs for applications in biomedical research. In 2018, we achieved a twofold milestone when working with animal physiologist Jason Ross and his lab. Together we developed a more immunocompromised pig than the original SCID pig and successfully humanized it, by transferring cultured human immune stem cells into the livers of developing piglets.

During early fetal development, immune cells develop within the liver, providing an opportunity to introduce human cells. We inject human immune stem cells into fetal pig livers using ultrasound imaging as a guide. As the pig fetus develops, the injected human immune stem cells begin to differentiate or change into other kinds of cells and spread through the pigs body. Once SCID piglets are born, we can detect human immune cells in their blood, liver, spleen and thymus gland. This humanization is what makes them so valuable for testing new medical treatments.

We have found that human ovarian tumors survive and grow in SCID pigs, giving us an opportunity to study ovarian cancer in a new way. Similarly, because human skin survives on SCID pigs, scientists may be able to develop new treatments for skin burns. Other research possibilities are numerous.

Pigs in a bubble

Since our pigs lack essential components of their immune system, they are extremely susceptible to infection and require special housing to help reduce exposure to pathogens.

SCID pigs are raised in bubble biocontainment facilities. Positive pressure rooms, which maintain a higher air pressure than the surrounding environment to keep pathogens out, are coupled with highly filtered air and water. All personnel are required to wear full personal protective equipment. We typically have anywhere from two to 15 SCID pigs and breeding animals at a given time. (Our breeding animals do not have SCID, but they are genetic carriers of the mutation, so their offspring may have SCID.)

[Deep knowledge, daily. Sign up for The Conversations newsletter.]

As with any animal research, ethical considerations are always front and center. All our protocols are approved by Iowa State Universitys Institutional Animal Care and Use Committee and are in accordance with The National Institutes of Healths Guide for the Care and Use of Laboratory Animals.

Every day, twice a day, our pigs are checked by expert caretakers who monitor their health status and provide engagement. We have veterinarians on call. If any pigs fall ill, and drug or antibiotic intervention does not improve their condition, the animals are humanely euthanized.

Our goal is to continue optimizing our humanized SCID pigs so they can be more readily available for stem cell therapy testing, as well as research in other areas, including cancer. We hope the development of the SCID pig model will pave the way for advancements in therapeutic testing, with the long-term goal of improving human patient outcomes.

Adeline Boettcher earned her research-based Ph.D. working on the SCID project in 2019.

This article is republished from The Conversation under a Creative Commons license. Read the original article here: https://theconversation.com/were-creating-humanized-pigs-in-our-ultraclean-lab-to-study-human-illnesses-and-treatments-156343.

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We're creating 'humanized pigs' in our ultraclean lab to study human illnesses and treatments - Alton Telegraph

Last year, something new was grafted to the tree of life.

Somewhere between a living organism and a robot, these tiny, living machines were created from clumps of stem cells from the African clawed frog. Stem cells from the heart gave them muscle, while skin stem cells provided structure.

Dubbed "Xenobots" (after the frog's scientific name not, alas, xenomorphs), their creators found that the living machines that could complete simple tasks in Petri dishes, as Freethink's Amanda Winkler explained last year.

Those same researchers, from Tufts and the University of Vermont, have now developed a second iteration, Xenobots 2.0, if you will, which can "self-assemble a body from single cells, do not require muscle cells to move, and even demonstrate the capability of recordable memory," as Tufts Now explains.

These Xenobots are also faster, can make their way through more complex environments, live longer than their predecessors, work in concert, and heal themselves.

Yeah, that sounds a lot like the T-1000 to me, too.

First generation Xenobots were constructed with a "top-down" approach, as Tufts put it. The researchers manually placed and surgically sculpted the heart and skin cells to form tiny biological robots in a variety of shapes.

Their shapes chosen with the help of a digital Xenobots simulator then impacted their various movements.

The original Xenobots were capable of "crawling, traveling in circles, moving small objects or even joining with other organic bots to collectively perform tasks," Winkler reported.

But to create Xenobots 2.0, the researchers utilized a "bottom up" approach, published in the journal Science Robotics.

Rather than crafting the frog heart and stem cells, the researchers simply scraped off some skin stem cells from frog embryos. Left to their own devices, the cells glommed together into spheroids on their own.

They could survive for 10 days without food and even grow if some sugar's in the mix.

"We've grown them for over four months in the lab," Tufts' Doug Blackiston, study coauthor, told Science News. "They do really interesting things if you grow them," including forming new, balloon-like shapes.

Some of the cells adapted to grow cilia a few days in. Usually used by cells to push away pathogens and ensure a nice coating of protective mucus, the Xenobots used their cilia to move around, eliminating the need for heart stem cells.

It's an example of life's remarkable plasticity, the researchers say.

"In a frog embryo, cells cooperate to create a tadpole. Here, removed from that context, we see that cells can re-purpose their genetically encoded hardware, like cilia, for new functions such as locomotion," Michael Levin, professor of biology and director of Tufts' Allen Discovery Center and study corresponding author told Tufts Now.

"It is amazing that cells can spontaneously take on new roles and create new body plans and behaviors without long periods of evolutionary selection for those features."

Along with those new body plans came new abilities. Xenobots 2.0 can move around just like the first iteration did, but they are faster than what the researchers constructed. They're also better at sweeping up junk a swarm of them can round up iron oxide particles in a Petri dish and they can coat flat surfaces and shimmy through narrow capillaries.

Because they are biological, the Xenobots could also heal themselves, forming back together after injury even recovering from full-length lacerations halfway through their "bodies" in just 5 minutes.

"In a frog embryo, cells cooperate to create a tadpole. Here, removed from that context, we see that cells can re-purpose their genetically encoded hardware, like cilia, for new functions such as locomotion."

Just like before, the Tufts team turned to computer simulations to tease out the best Xenobot layouts. Researchers at the University of Vermont did the data crunching, using the Vermont Advanced Computing Core's supercomputer cluster, called Deep Green.

Deep Green comes in because "it's not at all obvious for people what a successful design should look like," UVM computer scientist and robotics expert Josh Bongard told Tufts Now. "That's where the supercomputer comes in and searches over the space of all possible Xenobot swarms to find the swarm that does the job best."

The hope is that eventually Xenobots will be able to perform tasks like clearing microplastics from the ocean, or decontaminating soil.

Performing those jobs would be a hell of a lot easier with the ability to retain and access memory for guiding their actions something the original Xenobots lacked. This time around, the researchers gave them the ability to hold on to one piece of information.

The researchers injected the frog stem cells with mRNA carrying the instructions for a protein called EosFP. This protein normally glows green, but when exposed to a specific wavelength of light, it turns red instead.

Armed with their little running light, the Xenobots could now keep a record of being exposed to certain wavelengths of blue light in their environment. Further work could potentially allow them to keep track of multiple variables, or even alter their behaviors accordingly.

"When we bring in more capabilities to the bots, we can use the computer simulations to design them with more complex behaviors and the ability to carry out more elaborate tasks," Bongard said. "We could potentially design them not only to report conditions in their environment but also to modify and repair conditions in their environment."

The researchers' original work already opened questions of what, exactly, Xenobots are. Are they lifeforms? Robots, but made of biological material, in lieu of nuts and bolts?

As you can imagine, these improved iterations which organize on their own are provoking more of the same.

Tel Aviv University evolutionary biologist Eva Jablonka, who is unaffiliated with the work, told Quanta Magazine that she considers them a new form of life "defined by what it does rather than to what it belongs developmentally and evolutionarily."

Armed with a special protein that changes color from green to red, the next generation Xenobots could keep a simple record of their exposure to blue light. Credit: Doug Blackiston & Emma Lederer, Tufts University

University of Melbourne digital ethics researcher Kobi Leins believes new ethical issues arise with the creation of new forms of life. "Scientists like to make things, and don't necessarily think about what the repercussions are," she told Science News.

(For what it's worth, Levin agrees, telling Science News the questions raised by the Xenobots are like "finding a whole galaxy of weird new things.")

Levin hopes that within that galaxy, the Xenobots will do more than perform tasks: they may help us understand how biological life itself develops.

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]

Excerpt from:
The Next Generation of Living Machines: Xenobots 2.0 - Freethink

Using blobs of skin cells from frog embryos, scientists have grown creatures unlike anything else on Earth, a new study reports. These microscopic living machines can swim, sweep up debris and heal themselves after a gash.

Scientists often strive to understand the world as it exists, says Jacob Foster, a collective intelligence researcher at UCLA not involved with this research. But the new study, published March 31 in Science Robotics, is part of a liberating moment in the history of science, Foster says. A reorientation towards what is possible.

In a way, the bots were self-made. Scientists removed small clumps of skin stem cells from frog embryos, to see what these cells would do on their own. Separated from their usual spots in a growing frog embryo, the cells organized themselves into balls and grew. About three days later, the clusters, called xenobots, began to swim.

Normally, hairlike structures called cilia on frog skin repel pathogens and spread mucus around. But on the xenobots, cilia allowed them to motor around. That surprising development is a great example of life reusing whats at hand, says study coauthor Michael Levin, a biologist at Tufts University in Medford, Mass.

And that process happens fast. This isnt some sort of effect where evolution has found a new use over hundreds of thousands of years, Levin says. This happens in front of your eyes within two or three days.

Xenobots have no nerve cells and no brains. Yet xenobots each about half a millimeter wide can swim through very thin tubes and traverse curvy mazes. When put into an arena littered with small particles of iron oxide, the xenobots can sweep the debris into piles. Xenobots can even heal themselves; after being cut, the bots zipper themselves back into their spherical shapes.

Scientists are still working out the basics of xenobot life. The creatures can live for about 10 days without food. When fed sugar, xenobots can live longer (though they dont keep growing). Weve grown them for over four months in the lab, says study coauthor Doug Blackiston, also at Tufts. They do really interesting things if you grow them, including forming strange balloon-like shapes.

Its not yet clear what sorts of jobs these xenobots might do, if any. Cleaning up waterways, arteries or other small spaces comes to mind, the researchers say. More broadly, these organisms may hold lessons about how bodies are built, Levin says.

With the advent of new organisms comes ethical issues, cautions Kobi Leins, a digital ethics researcher at the University of Melbourne in Australia. Scientists like to make things, and dont necessarily think about what the repercussions are, she says. More conversations about unintended consequences are needed, she says.

Levin agrees. The small xenobots are fascinating in their own rights, he says, but they raise bigger questions, and bigger possibilities. Its finding a whole galaxy of weird new things.

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Frog skin cells turned themselves into living machines - Science News Magazine

Newswise March 30, 2021 As cancer survival rates improve, more people are living with the aftereffects of cancer treatment. For some patients, these issues include chronic radiation-induced skin injury which can lead to potentially severe cosmetic and functional problems.

Recent studies suggest a promising new approach in these cases, using fat grafting procedures to unleash the healing and regenerative power of the body's natural adipose stem cells (ASCs). "Preliminary evidence suggests that fat grafting can make skin feel and look healthier, restore lost soft tissue volume, and help alleviate pain and fibrosis in patients with radiation-induced skin injury after cancer treatment," says J. Peter Rubin, MD, MBA, FACS, American Society of Plastic Surgeons (ASPS) President-Elect and Chair of the Department of Plastic Surgery at University of Pittsburgh Medical Center. He is one of the authors of a new review of the clinical evidence on fat grafting for radiation-induced skin and soft tissue injury.

"But while promising, available research has some key weaknesses that make it difficult for us to determine the true benefits of fat grafting right now," Dr. Rubin adds. The review appears in the April issue of Plastic and Reconstructive Surgery, the official medical journal of the ASPS.

More than half of patients diagnosed with cancer receive radiation therapy. Because skin cells turn over rapidly, they are exquisitely sensitive to the damaging effects of radiation. In the first few months after treatment, many patients develop acute radiation injury with skin inflammation, peeling, swelling, pain and itching. In most cases, symptoms resolve over time. However, if inflammation continues, radiation-induced skin injury can become a chronic problem leading to tight, stiff skin (fibrosis) with a risk of poor wound healing, ulcers, and tissue loss.

Fat grafting procedures transferring the patient's own fat cells from one part of the body to another have become widely used in many cosmetic and reconstructive plastic surgery procedures. In their review, Dr. Rubin and colleagues round up promising research on fat grafting for patients with radiation-induced skin injury.

In studies of breast cancer patients, fat grafting procedures have reduced pain and other symptoms of radiation-induced skin injury backed up by more-normal cellular appearance of skin cells under the microscope. In other studies, fat grafting has led to reduced risks and better outcomes of breast reconstruction after mastectomy.

For patients with radiation-induced skin injury after treatment for head and neck cancer, fat grafting has led to improvements in voice, breathing, swallowing, and movement. Good outcomes have also been reported in patients with radiation-induced skin injury in the area around the eye or in the limbs.

"The good news is fat grafting has the potential to really help patients with discomfort and disability caused by radiation-induced skin damage," according to Dr. Rubin. While research is ongoing, the benefits of fat grafting seem to result from the wide-ranging effects of ASCs including anti-scarring, antioxidant, immune-modulating, regenerative, and other actions.

"However," he adds, "the available evidence has a lot of shortcomings, including small sample sizes, lower-quality research designs, and a lack of comparison groups." Variations in fat cell collection and processing, as well as the timing and "dose" of fat grafting, make it difficult to compare results between studies. There are also unanswered questions regarding potential risks related to ASC injection and concerns that fat grafting might affect cancer follow-up.

The reviewers outline some steps for further research to clarify the benefits of fat grafting for radiation-induced skin and soft issue injury, including approaches to clinical assessment and imaging studies, testing of skin biomechanics and circulation, and cellular-level analyses. For all of these outcomes, standardized measures are needed to achieve more comparable results between studies.

"We hope our review will inform efforts to establish the benefits of specific types of fat grafting procedures in specific groups of patients," says Dr. Rubin. "To do that, we'll need studies including larger numbers of patients, adequate control groups, and consistent use of objective outcome measures."

Click here to read Fat Grafting in Radiation-Induced Soft-Tissue Injury: A Narrative Review of the Clinical Evidence and Implications for Future Studies.

DOI: 10.1097/PRS.0000000000007705

###

Plastic and Reconstructive Surgery is published in the Lippincott portfolio by Wolters Kluwer.

About Plastic and Reconstructive Surgery

For more than 70 years, Plastic and Reconstructive Surgery (http://www.prsjournal.com/) has been the one consistently excellent reference for every specialist who uses plastic surgery techniques or works in conjunction with a plastic surgeon. The official journal of the American Society of Plastic Surgeons, Plastic and Reconstructive Surgery brings subscribers up-to-the-minute reports on the latest techniques and follow-up for all areas of plastic and reconstructive surgery, including breast reconstruction, experimental studies, maxillofacial reconstruction, hand and microsurgery, burn repair and cosmetic surgery, as well as news on medico-legal issues.

About ASPS

The American Society of Plastic Surgeons is the largest organization of board-certified plastic surgeons in the world. Representing more than 7,000 physician members, the society is recognized as a leading authority and information source on cosmetic and reconstructive plastic surgery. ASPS comprises more than 94 percent of all board-certified plastic surgeons in the United States. Founded in 1931, the society represents physicians certified by The American Board of Plastic Surgery or The Royal College of Physicians and Surgeons of Canada.

About Wolters Kluwer

Wolters Kluwer (WKL) is a global leader in professional information, software solutions, and services for the clinicians, nurses, accountants, lawyers, and tax, finance, audit, risk, compliance, and regulatory sectors. We help our customers make critical decisions every day by providing expert solutions that combine deep domain knowledge with advanced technology and services.

Wolters Kluwer reported 2019 annual revenues of 4.6 billion. The group serves customers in over 180 countries, maintains operations in over 40 countries, and employs approximately 19,000 people worldwide. The company is headquartered in Alphen aan den Rijn, the Netherlands.

Wolters Kluwer provides trusted clinical technology and evidence-based solutions that engage clinicians, patients, researchers and students with advanced clinical decision support, learning and research and clinical intelligence. For more information about our solutions, visit https://www.wolterskluwer.com/en/healthand follow us onLinkedInand Twitter@WKHealth.

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Fat grafting shows promise for cancer patients with radiation-induced skin injury - Newswise

The Augustinus Bader story hasbecome a beauty legend. Professor Bader, one of the worlds leading stem-cell experts, makes a groundbreaking wound gel that rehabilitates the skin of burns victims,without the need for grafts or scarring. At a dinner hosted by Robert Friedland, the self-made billionaire and long-time mentor to Steve Jobs, Bader meets Charles Rosier, a young French financier. They are kicking around ideas forfunding the necessary clinical trials forthe product, which would likely run intothetens of millions. Pharmaceutical companies arent interested because most burns victims are in emerging countries, where the market for sophisticated healing products is negligible.

Rosier has a flash of inspiration: couldBader use what he knows about wound healing to make an anti-ageing cream? Yes, answers Bader unhesitatingly. Two years and much cajoling later, the professor makes a prototype skincare cream, and pretty soon anyone who has ever had more than a passing interest in face cream is talking about it.

According to Deloitte, as many as 90per cent of beauty launches fail within ayear. By contrast, the Augustinus Bader skincare brand has grown from a turnover of $7m in 2018 to $70m in 2020. It has also shattered traditional conventions of luxury skincare along the way. For a start, the company launched with just two face products, The Cream (fornormal/oily skin) and The Rich Cream (dry skin) and insisted that apart from cleanser andSPF theyre all you need to use. No eye cream, no neck cream, no serum underneath, no primer ontop just one cream, and a very specific two pumps at that. This was intriguing. Most luxury-skincare brands (the creams retail at205 each) dont just sell you a dream they sell you a regime.

Charles Rosier believes that their inexperience in the beauty industry helpedat first. If Id known how complex and competitive the industry is, maybe Iwouldnt have had so much passion for it. But because I had seen what Augustinuss science could do, I was truly convinced thathe could create a product that was new, disruptive and of higher quality than whatever else was in the market.

As it turned out, it was. Celebrities normally paid handsomely to endorse beauty brands were not only recommending the Augustinus Bader cream unprompted butinvesting in the company too (Courteney Cox, Melanie Griffith and Carla Bruni to note). Usually cynical beauty editors discussed it with the fervour of addicts (myself included). And in February, a panel of more than 300 industry experts voted The Cream and The Rich Cream as Womens Wear Dailys Greatest Skincare Product ofAll Time (Crme de la Mer, launched in 1965, took second place and Este Lauder Advanced Night Repair, from 1982, took third), neatly capping off a pleasing statistic of 36 awards in 36 months.

Bader a softly spoken, bow tie-wearing 61-year-old German is both asthrilled and bemused by the brands success as youd hope. Before making the face cream, he says, he had never used a skincare product in his life. But he likes the fact that now, when he uses the cream before shaving, he no longer cuts himself. It would never have occurred to him to have created a cleanse/tone/moisturise-type regime. Beauty is always from inside, he says. You dont need a routine, as many people have been used to. The idea is that just after washing your face, you use The Cream or The Rich Cream. Everything is in that one product.

Before making the face cream, Bader had never used a skincare product inhis life

It would be tempting to paint Bader asthe sneery scientist, dabbling with the beauty world as a means to an end(close to10per cent of the brands profits in 201920 went to wound-healing research and other charities). The opposite is true: what finally convinced him to embark onthe project was his patients reaction tohisearly prototype: When I gave theproduct to patients with diabetic wounds, their skin became healthier-looking and stronger, and I could see how happy it made them...so for me, even though it was just a skincare product, it developed a kind of medical meaning.

Also subversive is the brandsconspicuous lack ofmiracle ingredients. Baderswork is guided by theprinciple that your skin contains all it needs already its the communication between thecells thats important, notapplying endlessnew ingredients that your skin doesnt recognise. Conventional medicine very often tries to helpby treating symptoms, but what the patientreally wants is a healing process, he says. The creams themselves contain a complex called TCF8, which hesays is mainly made out of vitamins, amino acids and lipid structures.

$70mThe brands turnoverin2020

10%The profits in 20192020 thatwent towards wound-healing research and other charities

11The number of products in the Augustinus Bader line

50%The acceleration in healing time experienced by patientsusing Baders wound-healing gel

According to Charles Rosier, Bader isprobably the person in the team who is strictest about only using gentle ingredients which means the brand is able to satisfy the current appetite for clean skincare too. Thats why theres no SPF; because Bader is vehemently opposed to chemical sun filters and has so far found it hard to make sufficiently premium-feeling sun protection without them. And, says Bader, a little bit of sun is good for your skin as is a little bit of stress (and carrot juice: he says that people who eat a lot of carrots generally have good skin).

Last month the brand also launched avegan version of The Rich Cream, with original ingredients such as beeswax and lanolin removed and a slightly upgraded formulation. It has the same rich texture and the same uncanny ability which fans can eulogise about for hours to hug your skin within seconds of applying.

But is it getting harder to avoid the pull of the beauty mainstream? Some devotees have taken a recent spate of new launches to mean that the brand is moving away from its original one cream is all you need philosophy, and that as a result has lost some of its outsider charm. In the second half of 2020, launches came thick and fast: theres now anEssence, Face Oil, Cleansing Balm, Cleansing Gel and Lip Balm, plus body oils and lotions.

Rosier points outthat most of their competitors have around 200 products and that last years bottleneck of launches was largely due to hold-ups in the lab, as well as Covid-19. Perhaps our philosophy has switched a little from Well give you one cream to Wellgive you the essential basics of a skincare routine, he concedes. Well never do 20 serums, but well do products where we feel they can be better than otherthings that exist in the market, and allow you to have an Augustinus Bader routine and not have to mix our products with other brands.

Given how feverish the current Baderobsession is, it seems unlikely thatcustomers would need much convincingnot to mix other brands products into their routines. What isdebatable is how long this brand can remain a disrupter. Ever the renegade, Bader is less interested in being a beauty outsider than encouraging the rest of the field toraise its game.

This new beauty side of mywork is interesting because, ultimately, healthy skin contributes to beauty and for me, thats notsomething superficial, its something absolutely relevant to all the work that I do, including the medical research. In a way, Ihope that perhaps what we can do is be a little bit game-changing about what a skincare product may want to achieve. And that, to me, sounds like real hope in a jar.

Original post:
Augustinus Bader and the making of a $70m phenomenon - Financial Times