Category Archives: Longevity Medicine

LONDON, Sept. 21, 2022 /PRNewswire/ -- Smith+Nephew (LSE:SN, NYSE:SNN), the global medical technology company, today announces it is expanding the reach of its medical education curriculum through a suite of advanced simulation technologies. Healthcare professionals can now conveniently access core orthopaedic, robotics and sports medicine procedural skills-training using virtual and augmented reality, haptics, and 3D interactive gaming at every Smith+Nephew Academy centre of excellence around the world.

Healthcare professionals are universally acknowledging the benefits that simulation technology can deliver as part of their continuous education journey. Reinforcing procedural, psychomotor and cognitive skills by simulating a surgeons decision making process delivers an immersive learning experience that traditional training methods cannot match.

Mr. Stephen Mitchell, Consultant Trauma & Orthopaedic Surgeon at University Hospitals Bristol NHS Foundation Trust recently led a hip fracture management course for Smith+Nephew using virtual reality. He commented, "There is a huge opportunity with virtual reality for future training applications to drive both an accelerated learning process and distance training. It lends itself perfectly to the 2D/3D nature of trauma, arthroscopy and arthroplasty procedures."

Recent randomized controlled trials have generated data which indicates that virtual reality training programs can be a more effective modality of learning orthopaedic surgical techniques compared to passive learning tools such as a standard guide training.1 The training groups completed their assessments faster, with a higher Global Rating Score, and demonstrated greater retention with higher scores upon re-testing at two weeks.1

A recent Smith+Nephew survey for participants in a virtual reality training course concluded that they felt the workshop increased their surgical procedure knowledge and better prepared them for the cadaveric lab because of the instrumentation walk through.2 When asked if they would like to see more virtual reality sessions as part of future medical educational programmes, 90% of the participants responded "yes".2

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"Central to Smith+Nephew's commitment to being a global leader in medical education and improving patient outcomes isproviding a state-of-the-art, interactive learning environment tailored to the needs of the healthcare professional," said Cindy Walker, Senior Vice President of Global Medical Education for Smith+Nephew. "With Smith+Nephew Academy, we are actively transforming the way we educate our customers around the world by surrounding them with leading edge technology, clinical content and scientific data."

A number of educational VR modules are currently available including the world's first for arthroscopic meniscal repair launched earlier this year. Additionally, a module for the JOURNEY II BCS Total Knee Arthroplasty using a robotic-assisted CORI Surgical System will launch globally in October.

If you are a healthcare professional and you wish to learn more about Smith+Nephew's world-class medical education offerings, please visit our booth at OSET (#110) and our global platform Education Unlimited https://educationunlimited.smith-nephew.com/

References1. Blumstein G, Zukotynski B, Cevallos N, et al. Randomized Trial of a Virtual Reality Tool to Teach Surgical Technique for Tibial Shaft Fracture Intramedullary Nailing. J Surg Educ. 2020;77(4): 9699772. Smith+Nephew survey results on file

About Smith+NephewSmith+Nephew is a portfolio medical technology business focused on the repair, regeneration and replacement of soft and hard tissue. We exist to restore people's bodies and their self-belief by using technology to take the limits off living. We call this purpose 'Life Unlimited'. Our 18,000 employees deliver this mission every day, making a difference to patients'lives through the excellence of our product portfolio, and the invention and application of new technologies acrossour three global franchises of Orthopaedics, Sports Medicine & ENT and Advanced Wound Management.

Founded in Hull, UK, in 1856, we now operate in more than 100 countries, and generated annual sales of $5.2 billion in 2021. Smith+Nephew is a constituent of the FTSE100 (LSE:SN, NYSE:SNN). The terms 'Group' and 'Smith+Nephew' are used to refer to Smith & Nephew plcand its consolidated subsidiaries, unless the context requires otherwise.

For more information about Smith+Nephew, please visitwww.smith-nephew.comand follow us onTwitter,LinkedIn,InstagramorFacebook.

Forward-looking StatementsThis document may contain forward-looking statements that may or may not prove accurate. For example, statements regarding expected revenue growth and trading margins, market trends and our product pipeline are forward-looking statements. Phrases such as "aim", "plan", "intend", "anticipate", "well-placed", "believe", "estimate", "expect", "target", "consider" and similar expressions are generally intended to identify forward-looking statements. Forward-looking statements involve known and unknown risks, uncertainties and other important factors that could cause actual results to differ materially from what is expressed or implied by the statements. For Smith+Nephew, these factors include: risks related to the impact of COVID-19, such as the depth and longevity of its impact, government actions and other restrictive measures taken in response, material delays and cancellations of elective procedures, reduced procedure capacity at medical facilities, restricted access for sales representatives to medical facilities, or our ability to execute business continuity plans as a result of COVID-19; economic and financial conditions in the markets we serve, especially those affecting health care providers, payers and customers (including, without limitation, as a result of COVID-19); price levels for established and innovative medical devices; developments in medical technology; regulatory approvals, reimbursement decisions or other government actions; product defects or recalls or other problems with quality management systems or failure to comply with related regulations; litigation relating to patent or other claims; legal compliance risks and related investigative, remedial or enforcement actions; disruption to our supply chain or operations or those of our suppliers (including, without limitation, as a result of COVID-19); competition for qualified personnel; strategic actions, including acquisitions and dispositions, our success in performing due diligence, valuing and integrating acquired businesses; disruption that may result from transactions or other changes we make in our business plans or organisation to adapt to market developments; and numerous other matters that affect us or our markets, including those of a political, economic, business, competitive or reputational nature. Please refer to the documents that Smith+Nephew has filed with the U.S. Securities and Exchange Commission under the U.S. Securities Exchange Act of 1934, as amended, including Smith+Nephew's most recent annual report on Form 20-F, for a discussion of certain of these factors. Any forward-looking statement is based on information available to Smith+Nephew as of the date of the statement. All written or oral forward-looking statements attributable to Smith+Nephew are qualified by this caution. Smith+Nephew does not undertake any obligation to update or revise any forward-looking statement to reflect any change in circumstances or in Smith+Nephew's expectations.

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Now humans

Renewal Bios precise technical plan remains under wraps, and the companys website is just a calling card. Its very low on details for a reason. We dont want to overpromise, and we dont want to freak people out, says Omri Amirav-Drory, a partner at NFX who is acting as CEO of the new company. The imagery is sensitive here.

Some scientists say it will be difficult to grow human embryo models to an advanced stage and that it would be better to avoid the controversy raised by imitating real embryos too closely.

Its absolutely not necessary, so why would you do it? says Nicolas Rivron, a stem-cell scientist at the Institute of Molecular Biotechnology in Vienna. He argues that scientists should only create the minimal embryonic structure necessary to yield cells of interest.

For his part, Amirav-Drory says he hasnt seen a technology with so much potential since CRISPR gene-editing technology first emerged. The ability to create a synthetic embryo from cellsno egg, no sperm, no uterusits really amazing, he says. We think it can be a massive, transformative platform technology that can be applied to both fertility and longevity.

To create the succession of breakthroughs, Hannas lab has been combining advanced stem-cell science with new types of bioreactors.

A year ago, the stem-cell specialist first showed off a mechanical womb in which he managed to grow natural mouse embryos outside of a female mouse for several days. The system involves spinning jars that keep the embryos bathed in nutritious blood serum and oxygen.

A. AGUILERA-CASTREJON ET AL., NATURE 2021

In the new research published this week, Hanna used the same mechanical womb, but this time to grow look-alike embryos created from stem cells.

Remarkably, when stem cells are grown together in specially shaped containers, they will spontaneously join and try to assemble an embryo, producing structures that are called embryoids, blastoids, or synthetic embryo models. Many researchers insist that despite appearances, these structures have limited relation to real embryos and zero potential to develop completely.

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This startup wants to copy you into an embryo for organ harvesting - MIT Technology Review

JERUSALEM, Israel A fountain-of-youth drug could soon make the problems of aging a thing of the past. Researchers in Israel say they have identified a group of molecules that repair the damaged parts of cells which break down over time. That discovery may also lead to a new pill that prevents age-related diseases such as Alzheimers.

Scientists from the Hebrew University of Jerusalem note that modern medicine has helped to increase the average life expectancy worldwide. However, as people live longer, they face more and more problems associated with old age. With that in mind, the team set out to balance the benefits of longevity with a better quality of life in our later years.

During their study, the researchers developed a drug which protects human cells from damage, making it possible for a persons tissues to retain their proper function for a longer period of time.

Study authors say a major factor in the aging process is the drop in effectiveness in a cells quality-control mechanism. When this system starts to break down, it leads to a buildup of defective mitochondria the power plants of the cells.

Mitochondria, the cells power plants, are responsible for energy production. They can be compared to tiny electric batteries that help cells function properly. Although these batteries wear out constantly, our cells have a sophisticated mechanism that removes defective mitochondria and replaces them with new ones, Professor Einav Gross explains in a media release.

However, this mechanism breaks down as people grow older. The result is cell dysfunction and the deterioration in tissue activity which can cause diseases like Alzheimers, Parkinsons, and heart failure to develop.

The team is hopeful that their study has found an innovative compound that may help treat these diseases. Turned into an easy-to-take pill, the molecules may also act as a preventative measure, repairing cellular aging before it has a chance to trigger disease.

In the future, we hope we will be able to significantly delay the development of many age-related diseases and improve people quality of life, says co-author Shmuel Ben-Sasson.

The researchers, together with Yissum, Hebrew Universitys tech transfer company, have created the startup company Vitalunga to further develop this compound into an anti-aging drug.

Ben-Sassons and Grosss findings have significant value for the global aging population, notes Itzik Goldwaser, CEO of Yissum. As Vitalunga advances towards pre-clinical studies, theyre closer than ever to minimizing the unbearable burden that aging-related diseases, such as Alzheimers and Parkinsons, has on individuals, their families and our health care systems.

The findings are published in the journal Autophagy.

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Miracle longevity drug? Scientists identify molecules that reverse the aging process - Study Finds

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MyMD Pharmaceuticals, Inc. (Nasdaq: MYMD) (MyMD or the Company), a clinical stage pharmaceutical company committed to developing novel therapies for age-related diseases, autoimmune and inflammatory conditions, announced today the publication of data in the Journal of Gerontology: Biological Sciences (JGBS) from a pre-clinical study of MYMD-1 demonstrating four-fold greater improvements than rapamycin in delaying aging and extending the life of mice who began treatment at the human equivalent of 60 years of age. The study was led by principal study investigator Patrizio P. Caturegli, MD, MPH, a professor of pathology at the Johns Hopkins University School of Medicine.

We are very excited that this important early data with our lead product MYMD-1 has been published in a prestigious medical journal, said Chris Chapman, MD, President, Director, and CMO of MyMD Pharmaceuticals. These results further validate the potential of MYMD-1 in delaying aging. Our ongoing Phase 2 study of MYMD-1 in sarcopenia/frailty, a result of a pathological aging process, is going well. Since TNF-alpha is a key player in the aging process, we also believe MYMD-1 has real potential to address autoimmune and inflammatory conditions by modulating inflammation, even when begun at an advanced age.

MYMD-1, an oral selective inhibitor of tumor necrosis factor-alpha (TNF-), that drives chronic inflammation, is being studied to slow the aging process, prevent sarcopenia and frailty, and extend healthy lifespan. A Phase 2 multi-center double-blind, placebo controlled, randomized study (NCT05283486) to investigate the efficacy, tolerability and pharmacokinetics of MYMD-1 in the treatment of chronic inflammation associated with sarcopenia/frailty is currently ongoing. The companys scientific advisory board met recently and agreed to move to the next higher dose in the study.

Aging is closely linked to multi-morbidities, frailty, and death due to conditions such as neoplastic, cardiovascular, neurodegenerative, metabolic, or autoimmune diseases.i Similarly, frailty, or a decline in physical function leading to greater risk of hospitalization, disability, and death, increases with age independent of underlying conditions or demographical characteristics.ii

Results from the JGBS Study

The study compared MYMD-1, an oral inhibitor of TNF-, to rapamycin, the best characterized drug endowed with anti-aging properties. In vivo, a longitudinal cohort of C57BL/6 mice, was randomized to receive either MYMD-1, high-dose rapamycin, or low-dose rapamycin plus metformin. Each of these three treatment arms of 18 mice (10 females and 8 males) was followed for 13 months or until death. Lifespan was significantly longer in the MYMD-1 group compared to rapamycin (P=0.019 versus high-dose and P=0.01 versus low-dose) in a Cox survival model that accounted for sex and serum levels of IL-6, TNF-, and IL-17A (see figure above). MyMD-1 also improved several health span characteristics in the study, resulting in milder body weight loss, maintenance of greater muscle strength, and amelioration of progression to frailty.

Additionally, using a panel of 12 human primary cell systems (BioMAP Diversity PLUSTM) where a total of 148 biomarkers were measured, MYMD-1 possessed anti-proliferative, anti-inflammatory, and anti-fibrotic properties. Many were shared with rapamycin, but MYMD-1 was more active in the inhibition of pro-inflammatory cytokines and pro-fibrotic biomarkers.

About MYMD-1

MYMD-1, an oral selective inhibitor of tumor necrosis factor-alpha (TNF-), a driver of chronic inflammation, is being studied to slow the aging process, prevent sarcopenia and frailty, and extend healthy lifespan. MYMD-1 has shown effectiveness in pre-clinical and clinical studies in regulating the immune system. Unlike other therapies, MYMD-1 has been shown in these studies to selectively block TNF- when it becomes overactivated in autoimmune diseases and cytokine storms, but not block it from doing its normal job of being a first responder to any routine type of moderate infection.

MYMD-1s ease of oral dosing is another differentiator compared to currently available TNF- blockers, all of which require delivery by injection or infusion. No approved TNF inhibitor has ever been dosed orally. In addition, the drug is not immunosuppressive and has not been shown to cause the serious side effects common with traditional therapies that treat inflammation. Because it can cross the blood-brain barrier and gain access to the central nervous system (CNS), MYMD-1 is also positioned to be a possible treatment for brain-related disorders. Its mechanism of action and efficacy in diseases including multiple sclerosis (MS) and thyroiditis have been studied through collaborations with several academic institutions.

About MyMD Pharmaceuticals, Inc.

MyMD Pharmaceuticals, Inc. (Nasdaq: MYMD), a clinical stage pharmaceutical company committed to developing novel therapies for autoimmune and inflammatory conditions, is focused on developing two novel therapeutic platforms that treat the causes of disease rather than only addressing the symptoms. MYMD-1 is a drug platform based on a clinical stage small molecule that regulates the immune system to control TNF-, which drives chronic inflammation, and other pro-inflammatory cell signaling cytokines. MYMD-1 is being developed to delay aging, increase longevity, and treat autoimmune diseases. The Companys second drug platform, Supera-CBD, is being developed to treat chronic pain, addiction and epilepsy. Supera-CBD is a novel synthetic derivative of cannabidiol (CBD) and is being developed to address and improve upon the rapidly growing CBD market, which includes both FDA approved drugs and CBD products not currently regulated as drugs. For more information, visit http://www.mymd.com.

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MyMD Pharmaceuticals (MYMD) Announces Data Showing MYMD-1 May Extend Life and Improve Health Published in the Journal of Gerontology: Biological...

Healthy aging is a shared goal of most humans, but the body has a nasty habit of breaking down over time. Tantalizing research suggests it is possible to develop nutrition and lifestyle interventions that can delay aging and extend healthspan. In model organisms, including rodents and nonhuman primates, caloric restriction (CR) has proven to be an effective method for mitigating aging-related deterioration of biological functions and for extending healthspan and life-span. But more than 80 years since its discovery, the underlying mechanisms by which caloric restriction extends either are still largely undefined.

Researchers have linked a number of biochemical pathways to longevity, including those involved with nutrient signaling, metabolism, growth, genome stability, and oxidative stress. Translating this knowledge, derived mostly from mouse studies, to humans is an additional barrier that must be overcome. For example, it is almost impossible for the majority of people to maintain severe dietary restriction over their lifetime. Thus, more viable solutions for promoting health- and lifespan in humans must be found.

We have been studying the behavioral effects of CR in mice and have found that it leads to dramatic changes in feeding behavior. In contrast to mice given continual access to unlimited food, which spread their daily food consumption over the course of the day and night, mice on caloric restriction adopt a stark feeding and fasting pattern in which they consume all of the food provided within a few hours each day. Thus, under CR, mice not only consume fewer calories, they voluntarily adopt a time-restricted feeding pattern with a long fasting interval. All these factors have been shown to have numerous health benefits, again primarily in animal models.

More than 80 years since its discovery, the underlying mechanisms by which caloric restriction extends lifespan are still largely undefined.

To disentangle the contributions to longevity of calorie restriction, periods of fasting, and alignment of eating with an animals circadian clock, we recently completed a comprehensive study that contrasts these three factors. We found that CR is sufficient to extend lifespan but that the pattern and circadian alignment of eating act synergistically to extend life-span further. While CR alone increases lifespan by approximately 10 percent, eating that CR diet only at night, when mice are normally awake, extends life-span by more than 35 percent compared to mice eating regular diets. We also found that circadian alignment of feeding enhances CR-mediated benefits for survival independently of fasting duration (2 vs. 22 hours) and body weight. Aging promotes increases in inflammation and decreases in metabolism in the livers of mice with constant access to food, whereas a CR diet fed at night ameliorates most of these aging-related changes. Thus, eating only at certain times of day appears to promote longevity in animals and could provide a new mechanism for the treatment and management of aging in humans.

A significant aspect of our study was that there were no significant effects of the pattern or time of eating on body weight in mice. In addition, body weight was not associated with lifespan. This finding is consistent with a recent report in the New England Journal of Medicine (NEJM) comparing weight loss in two groups of human subjects that were assigned to CR alone or CR with an 8-hour time-restricted eating window. The authors of this paper report no differences between these groups and conclude that there was no benefit of time-restricted eating for body weight. As we showed in our study, however, body weight does not serve as a good biomarker for longevity under CR conditions. So it would have been more useful in the NEJM study to have measured other endpoints besides body weight, such as inflammatory biomarkers associated with aging. In addition, previous studies that demonstrated health benefits of time-restricted eating were performed under conditions of overeating, not CR. Obviously, CR and overeating engage fundamentally different metabolic processes, and thus time-restricted eating of a CR diet should not be expected to yield the same results as time-restricted eating of a calorie-rich diet.

Our discovery that CR functions in concert with time-restricted eating and circadian alignment to optimally extend healthspan and lifespan is potentially transformative because it may yield a novel method for promoting healthy aging and lifespan increases in humans. Because lifespan in humans is primarily determined by lifestyle (less than 25 percent is genetically determined), these findings may be translated in future work to humans and are amenable to widespread adoption because they can be achieved by behavioral intervention: a CR diet eaten at the correct circadian time of dayi.e., when one is normally awake. This might involve, for example, a 12-hour eating window that begins at breakfast time.

A significant aspect of our study was that there were no significant effects of the pattern or time of eating on body weight in mice.

In addition, ongoing research in our labs seeks to test whether enhancing circadian clock function by behavioral (lifestyle), genetic, or pharmacological means can delay the aging process. Pharmaceutical agents were identifying in our labs that enhance circadian clock function may one day be used in humans as comprehensive therapies for aging. For now, were planning experiments for testing their anti-aging and pro-longevity effects in mice. Our lab and others have already provided evidence that the circadian clock system is an upstream regulator of all of the known anti-aging and pro-longevity pathways. So enhancing circadian clock function may rescue multiple aging pathways at the same time. We are testing this hypothesis by boosting Clock gene expression in genetically engineered mice. These animal studies can then lay the groundwork for the isolation of small molecules that target the Clock protein and the development of drugs that might safely modulate clock function and enhance health and longevity in people.

Joseph S. Takahashiis an investigator in the Howard Hughes Medical Institute and professor and chair of the Department of Neuroscience at the University of Texas Southwestern Medical Centers Peter O Donnell Jr. Brain Institute. He is also a member ofThe ScientistEditorial Advisory Board. Carla B. Green is a professor and Distinguished Scholar in the Department of Neuroscience at the same institution.

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Opinion: Changing When and How Much We Eat May Extend Health Span - The Scientist

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the progressive loss of motor neurons in the brain and spinal cord responsible for voluntary movements and muscle control.

In a new study, published July 11, 2022 in the journal Theranostics, researchers at University of California San Diego School of Medicine report that a gene therapy approach, developed at UC San Diego, measurably delayed disease onset in humanized mouse and rat models of familial ALS, an inherited form of the disease that runs in families. (Most ALS cases are sporadic, of unknown cause, though environmental and genetic factors may play a part.)

In previous research, senior author Brian P. Head, PhD, adjunct professor in the Department of Anesthesiology at UC San Diego School of Medicine and research health scientist at the VA San Diego Healthcare System and colleagues had crossed a mouse model genetically engineered to express a neuroprotective protein called caveolin-1 with a transgenic mouse model of ALS. The double transgenic model exhibited better motor function and longer survival.

The latest work involved injecting a harmless adeno-associated viral vector carrying synapsin-Caveolin-1 cDNA (AAV9-SynCav1) into the spinal cords of familial ALS mice to see if it would delay disease progression and preserve physical strength and mobility.

Researchers found that SynCav1 protected and preserved spinal cord motor neurons and extended longevity in the mice. Subsequent experiments with a rat model of ALS produced similar results.

These data suggest that SynCav1 might serve as a novel gene therapy for neurodegenerative conditions in ALS and other forms of central nervous system disease of unknown etiology, the authors wrote, advocating for further studies.

The Theranostics paper follows a study published in 2021 in which Head and colleagues used a SynCav1 gene therapy approach to prevent learning and memory loss in a mouse model of Alzheimers disease (AD), a key step toward eventually testing the approach in humans with the neurodegenerative disease.

Because the neuroprotective efficacy afforded by SynCav1 occurred independent of targeting the known toxic monogenic protein (i.e., mutant hSOD1), these findings suggest that SynCav1 may serve as a novel gene therapy for other neurodegenerative conditions in addition to ALS and AD, said Head. However, it is essential for further studies to determine the effect of SynCav1 on disease progression at later stages of the disease.

Incidence of ALS is approximately 3 to 5 per 100,000 persons globally. The disease affects approximately 18,000 persons in the United States. Current approved pharmaceutical treatments, such as Rilutek and Radicava, may slow disease progression and improve quality of life, but there is no cure. Mean survival time after diagnosis is two to five years.

The SynCav1 gene therapy is patented through UC San Diego and the Department of Veterans Affairs, and licensed to Eikonoklastes Therapeutics, based in Cincinnati, Ohio.

Co-authors include: Shanshan Wang, Taiga Ichinomaya, Paul Savchenko, Donsheng Wang, Xiaojing Li, Tiffany Duong, Wenxi Li, Jacqueline A. Bonds, Atushi Miyanohara, David M. Roth, Hemal H. Patel, Piyush M. Patel and Martin Marsala, all at UC San Diego; Atsushi Sawada, University of the Ryukyus, Japan; Eun Jung Kim, UC San Diego and Yonsei University College of Medicine, South Korea.

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11-Jul-2022

Study co-authors Dave M. Roth, Hemal H. Patel, Piyush M. Patel and Brian Head hold equity and are non-paid consultants to Eikonoklastes Therapeutics.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

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Gene therapy approach shows promise in treating ALS - EurekAlert