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T-cell transfer therapy is a type of immunotherapy that makes your own immune cells better able to attack cancer. There are two main types of T-cell transfer therapy: tumor-infiltrating lymphocytes (or TIL) therapy and CAR T-cell therapy. Both involve collecting your own immune cells, growing large numbers of these cells in the lab, and then giving the cells back to you through a needle in your vein. T-cell transfer therapy is also called adoptive cell therapy, adoptive immunotherapy, and immune cell therapy.

The process of growing your T cells in the lab can take 2 to 8 weeks. During this time, you may have treatment with chemotherapy and, maybe, radiation therapy to get rid of other immune cells. Reducing your immune cells helps the transferred T cells to be more effective. After these treatments, the T cells that were grown in the lab will be given back to you via a needle in your vein.

Toronto, Ontario —A new ultra-high-performance brain PET system allows for the direct measurement of brain nuclei as never before seen or quantified. With its ultra-high sensitivity and resolution, the NeuroEXPLORER provides exceptional brain PET images and has the potential to spur advances in the treatment of many brain diseases. This research was presented at the 2024 Society of Nuclear Medicine and Molecular Imaging (SNMMI) Annual Meeting, and the grouping of images highlighting targeted tracer uptake in specific brain nuclei has been selected as the 2024 SNMMI Henry N. Wagner, Jr., Image of the Year.

Each year, SNMMI chooses an image that best exemplifies the most promising advances in the field of nuclear medicine and molecular imaging. The state-of-the-art technologies captured in these images demonstrate the capacity to improve patient care by detecting disease, aiding diagnosis, improving clinical confidence, and providing a means of selecting appropriate treatments. This year, the SNMMI Image of the Year was chosen from more than 1,500 abstracts submitted for the meeting.

The image quality of PET systems has improved in recent years, mostly by increases in sensitivity, including enhanced time-of-flight capabilities. However, these systems have shown only minimal improvement in intrinsic resolution. To address these issues, researchers designed the NeuroEXPLORER PET scanner with a focus on ultra-high sensitivity and resolution, as well as continuous head motion correction.

Restraining or slowing ageing hallmarks at the cellular level have been proposed as a route to increased organismal lifespan and healthspan. Consequently, there is great interest in anti-ageing drug discovery. However, this currently requires laborious and lengthy longevity analysis. Here, we present a novel screening readout for the expedited discovery of compounds that restrain ageing of cell populations in vitro and enable extension of in vivo lifespan.

Using Illumina methylation arrays, we monitored DNA methylation changes accompanying long-term passaging of adult primary human cells in culture. This enabled us to develop, test, and validate the CellPopAge Clock, an epigenetic clock with underlying algorithm, unique among existing epigenetic clocks for its design to detect anti-ageing compounds in vitro. Additionally, we measured markers of senescence and performed longevity experiments in vivo in Drosophila, to further validate our approach to discover novel anti-ageing compounds. Finally, we bench mark our epigenetic clock with other available epigenetic clocks to consolidate its usefulness and specialisation for primary cells in culture.

We developed a novel epigenetic clock, the CellPopAge Clock, to accurately monitor the age of a population of adult human primary cells. We find that the CellPopAge Clock can detect decelerated passage-based ageing of human primary cells treated with rapamycin or trametinib, well-established longevity drugs. We then utilise the CellPopAge Clock as a screening tool for the identification of compounds which decelerate ageing of cell populations, uncovering novel anti-ageing drugs, torin2 and dactolisib (BEZ-235). We demonstrate that delayed epigenetic ageing in human primary cells treated with anti-ageing compounds is accompanied by a reduction in senescence and ageing biomarkers. Finally, we extend our screening platform in vivo by taking advantage of a specially formulated holidic medium for increased drug bioavailability in Drosophila. We show that the novel anti-ageing drugs, torin2 and dactolisib (BEZ-235), increase longevity in vivo.

Researchers at the Okinawa Institute of Science and Technology (OIST) have developed a potentially transformative approach to treating Alzheimer’s disease, A team from the former Cellular and Molecular Synaptic Function Unit have reported significant progress in reversing cognitive decline and restoring memory in transgenic mice using a synthetic protein. The findings, published in Brain Research, offer hope for a viable treatment to alleviate the debilitating symptoms associated with this neurodegenerative condition.

“We successfully reversed the symptoms of Alzheimer’s disease in mice,” explained Dr Chia-Jung Chang, first author of the study and presently a member of the Neural Computation Unit at OIST. “We achieved this with a small, synthetic peptide, PHDP5, that can easily cross the blood-brain barrier to directly target the memory center in the brain [1].”

Longevity. Technology: There is a pressing need to find effective treatments for Alzheimer’s; along with other forms of dementia, this debilitating disease currently affects approximately 55 million people worldwide, and this number is predicted to nearly double every 20 years, reaching 78 million in 2030 and 139 million in 2050. As well as a health burden, Alzheimer’s is an economic burden – the annual global cost of dementia has now rocketed to more than US$1.3 trillion, with a projected rise to US$2.8 trillion by 2030 on the horizon [2].

Magnetic stimulation therapy could aid patients who don’t respond to antidepressants. Scientists from the University of Helsinki and Stanford University are refining techniques that may lead to personalized treatments in the future.

Not every patient with depression benefits from medication. Recent research highlights potential improvements in an alternative approach, transcranial magnetic stimulation (TMS), for treating depression. TMS is distinct from electroconvulsive therapy (ECT), another treatment option for depression.

Researchers from the University of Helsinki and Stanford University investigated which factors in targeting TMS influence the brain’s electrical responses. They examined the behavior of a specific electrophysiological marker. This marker could potentially be used as a biomarker in the future to measure the efficacy of TMS treatment and thus help target and tailor the therapy.

Lovely essay by Sara Walker on how tech is biology. She closely mirrors my own thinking on this. “The technologies we are and that we produce are part of the same ancient strand of information propagating through and structuring matter on our planet.”


Our best estimates place the origin of life on this planet at approximately 3.8 billion years ago. Biological beings alive today are part of a lineage of information that can be traced backward in time through genomes to the earliest life. But evolution produced information that is not just genomic. Evolution produced everything around us, including things not traditionally considered “life.” Human technology would not exist without humans, so it is therefore part of the same ancient lineage of information that emerged with the origin of life.

Technology, like biology, does not exist in the absence of evolution. Technology is not artificially replacing life — it is life.

It is important to separate what is meant by “life” here as distinct from “alive.” By “life,” I mean all objects that can only be produced in our universe through a process of evolution and selection. Being “alive,” by contrast, is the active implementation of the dynamics of evolution and selection. Some objects — like a dead cat — are representative of “life” (because they only emerge in the universe through evolution) but not themselves “alive.”

A new gene editing technique derived from bacterial “jumping genes” can add, remove, recombine and invert DNA sequences, potentially overcoming some of the limitations of CRISPR.

The approach is made possible by a molecule called bridge RNA, the discovery of which came about through a joint effort led by scientists at the Arc Institute in Palo Alto, California, in collaboration with the University of Tokyo. They described their work in a pair of papers published June 26 in Nature.

As part of the 2024 Prostate Cancer Patient Conference, Dr. Eric Small discusses systemic therapy treatment in advanced prostate cancer, including AR-targeted therapy. The presentation includes definitions of disease states, categories of treatment types, and standards in treatment selection.
Recorded on 03/09/2024. [Show ID: 39768]

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So, they get very healthy but only live 24% longer no matter how many more times they use the treatment. I wonder what the telomere effect is. And what they are doing is not the same as what Aubrey’s mouse experiment is doing.


Altos Labs Co-founder and Chief Scientist Rick Klausner participated in a panel discussing efforts to increase human healthspan by combatting age-related diseases at this year’s Aspen Ideas Health conference.

In a panel that included Laura Deming and Kristen Fortney, Klausner discussed an Altos experiment in Spain (likely to be research conducted by Universidad Católica de Murcia and Altos Labs in collaboration with the Hospital Clínic de Barcelona), Klausner reported that if old kidneys are transplanted into young people they do not function nearly as well as transplanting young kidneys – but organ donations donors are getting older and older, and therein lies the rub.

We’ve been doing these experiments with the transplant team at Barcelona where we remove a kidney from different animals, and now we’re preparing to do this in the clinic. You take an old kidney and you transplant it into a young rat versus [transplanting] a young kidney and you see a tremendous difference in overall survival and kidney function. But when we take the old rat organ and we introduce these components that rejuvenate, this reprogramming cocktail, just for 45 minutes they’re exposed to it and then they survive as well if not better than the young organs that are transplanted.