Lifeboat Foundation

Two months ago, Musk said he was too busy to look into his company’s role in mass censorship in India. It’s only gotten worse.

Why do cancer immunotherapies work so extraordinarily well in a minority of patients, but fail in so many others? By analyzing the role of neutrophils, immune cells whose presence usually signals treatment failure, scientists from the University of Geneva (UNIGE), from Harvard Medical School, and from Ludwig Cancer Center have discovered that there is not just one type of neutrophil, but several. Depending on certain markers on their surface, these cells can either promote the growth of tumors, or fight them and ensure the success of a treatment. By boosting the appropriate factors, neutrophils could become great agents of anti-tumor immunity and reinforce the effects of current immunotherapies. These results have been published in the journal Cell.

Immunotherapy involves activating immune cells —mainly T cells—to recognize and destroy cancer cells. While this treatment is very efficient for some patients, and sometimes even exceeds expectations, it is unfortunately not the case in most cases. “The reasons for these failures remain largely unknown,” says Mikaël Pittet, full professor at the UNIGE Faculty of Medicine, holder of the ISREC chair in immuno-oncology, director of the Centre for Translational Research in Onco-Hematology and member of the Ludwig Cancer Center, who directed this work. “This is why deciphering the immune components involved is key to develop more advanced treatments and make immunotherapies a real therapeutic revolution.”

Neutrophils are the most abundant immune cells in the blood and are very useful in infections or injuries by being quickly mobilized to the affected area and releasing antimicrobial factors. In the context of cancer, however, their presence is generally bad news as they promote vascularization and tumor progression.

In a recent study on the medRxiv preprint server, researchers identified an interleukin 6 (IL-6) dependent alternative pathway as a therapeutic strategy against coronavirus disease 2019 (COVID-19).

Study: A Complement Atlas identifies interleukin 6 dependent alternative pathway dysregulation as a key druggable feature of COVID-19. Image Credit: MarynaOlyak/Shutterstock.com

“You won’t live forever” is a catchphrase which has often been touted and has so far remained the proven truth of life — of humans and almost every other living being on planet earth. But soon, this catchphrase may well become the truth of the past, as humanity steps forward to attain immortality.

A former Google scientist has made a prediction, which if proven right, may redefine human civilisation as we know it. Ray Kurzweil, whose over 85 per cent of 147 predictions have been proven right, has predicted that humans will become immortal by 2029.

The revelation came when the 75-year-old computer scientist dwelled upon genetics, nanotechnology, robotics and more in a YouTube video posted by channel Adagio.

The expanded availability of opioid use disorder-related telehealth services and medications during the COVID-19 pandemic was associated with a lowered likelihood of fatal drug overdose among Medicare beneficiaries, according to a new study.

“The results of this study add to the growing research documenting the benefits of expanding the use of telehealth services for people with opioid use disorder, as well as the need to improve retention and access to medication treatment for opioid use disorder,” said lead author Christopher M. Jones, PharmD, DrPH, director of the National Center for Injury Prevention and Control, Centers for Disease Control and Prevention. “The findings from this collaborative study also highlight the importance of working across agencies to identify successful strategies to address and get ahead of the constantly evolving overdose crisis.”

Published today in JAMA Psychiatry, this study is a collaborative research effort led by researchers at the National Center for Injury Prevention and Control, a part of CDC; the Office of the Administrator and the Center for Clinical Standards and Quality, both part of the Centers for Medicare & Medicaid Services (CMS); and the National Institute on Drug Abuse, a part of the National Institutes of Health.

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Advances in antiaging drug/lead discovery in animal models constitute a large body of literature on novel senotherapeutics and geroprotectives. However, with little direct evidence or mechanism of action in humans—these drugs are utilized as nutraceuticals or repurposed supplements without proper testing directions, appropriate biomarkers, or consistent in-vivo models. In this study, we take previously identified drug candidates that have significant evidence of prolonging lifespan and promoting healthy aging in model organisms, and simulate them in human metabolic interactome networks. Screening for drug-likeness, toxicity, and KEGG network correlation scores, we generated a library of 285 safe and bioavailable compounds. We interrogated this library to present computational modeling-derived estimations of a tripartite interaction map of animal geroprotective compounds in the human molecular interactome extracted from longevity, senescence, and dietary restriction-associated genes. Our findings reflect previous studies in aging-associated metabolic disorders, and predict 25 best-connected drug interactors including Resveratrol, EGCG, Metformin, Trichostatin A, Caffeic Acid and Quercetin as direct modulators of lifespan and healthspan-associated pathways. We further clustered these compounds and the functionally enriched subnetworks therewith to identify longevity-exclusive, senescence-exclusive, pseudo-omniregulators and omniregulators within the set of interactome hub genes. Additionally, serum markers for drug-interactions, and interactions with potentially geroprotective gut microbial species distinguish the current study and present a holistic depiction of optimum gut microbial alteration by candidate drugs. These findings provide a systems level model of animal life-extending therapeutics in human systems, and act as precursors for expediting the ongoing global effort to find effective antiaging pharmacological interventions.

Communicated by Ramaswamy H. Sarma.

Advanced age is a shared risk factor for many chronic and debilitating skeletal diseases including osteoporosis and periodontitis. Mesenchymal stem cells develop various aging phenotypes including the onset of senescence, intrinsic loss of regenerative potential and exacerbation of inflammatory microenvironment via secretory factors. This review elaborates on the emerging concepts on the molecular and epigenetic mechanisms of MSC senescence, such as the accumulation of oxidative stress, DNA damage and mitochondrial dysfunction. Senescent MSCs aggravate local inflammation, disrupt bone remodeling and bone-fat balance, thereby contributing to the progression of age-related bone diseases. Various rejuvenation strategies to target senescent MSCs could present a promising paradigm to restore skeletal aging.

Periodic prolonged fasting (PF) extends lifespan in model organisms and ameliorates multiple disease states both clinically and experimentally owing, in part, to its ability to modulate the immune system. However, the relationship between metabolic factors, immunity, and longevity during PF remains poorly characterized especially in humans.

This study aimed to observe the effects of PF in human subjects on the clinical and experimental markers of metabolic and immune health and uncover underlying plasma-borne factors that may be responsible for these effects.

In this rigorously controlled pilot study ( ClinicalTrial.gov identifier, NCT03487679), 20 young males and females participated in a 3D study protocol including assessments of 4 distinct metabolic states: 1) overnight fasted baseline state, 2) 2-h postprandial fed state, 3) 36-h fasted state, and 4 ) final 2-h postprandial re-fed state 12 h after the 36-h fasting period. Clinical and experimental markers of immune and metabolic health were assessed for each state along with comprehensive metabolomic profiling of participant plasma. Bioactive metabolites identified to be upregulated in circulation after 36 h of fasting were then assessed for their ability to mimic the effects of fasting in isolated human macrophage as well as the ability to extend lifespan in Caenorhabditis elegans.