Working in connectomics means creating comprehensive maps of brain and nervous system networks. Your research includes the identification and measurement of all parts of each neuron: the soma, dendrites, axonal path and branching patterns and combining that data with the synapses and gap junctions of the entire circuit.
Your microscopy challenges are extensive; submicron resolution is required over long distances inside large volumes of dense and complicated tissues.
Can aging be reversed? Dr. Michael West explains telomerase, cellular immortality, stem cells, tissue regeneration, and the future of longevity.
LifeCraft Sciences:
https://lifecraftsciences.com/
In this episode, I sit down with pioneering molecular gerontologist and biotechnology entrepreneur Dr. Michael D. West to explore telomeres, telomerase, cellular senescence, stem cells, tissue regeneration, and the possibility of reversing biological aging.
One of our central topics is the groundbreaking telomerase program West founded and led at Geron. That research helped establish how restoring telomerase activity can protect the ends of chromosomes and allow normal human cells to move beyond their usual replicative limit while retaining youthful characteristics in laboratory culture. We unpack what scientists mean when they say a cell has been “immortalized,” why cellular immortality is very different from making a person immortal, and how telomerase connects the biology of aging with the biology of cancer.
We also explore West’s work in regenerative medicine and his early vision of pluripotent stem cells as a “parts supply store” for the human body. Could youthful cells eventually be used to repair damaged tissues, replace worn-out biological components, and restore regenerative capabilities lost with age? West discusses the early isolation of human embryonic stem cells, therapeutic cloning, developmental reprogramming, and what cloned animals taught researchers about resetting cellular age.
Finally, we discuss LifeCraft Sciences and RESTORE, the company’s experimental approach combining telomerase with developmental regulators to return aged cells to a more youthful, regenerative state. It is a fascinating conversation about the history of longevity science, the future of tissue repair, and one of biology’s biggest questions: can aging eventually be reversed rather than merely slowed?
Preface (pdf); Contents with subsections
I Artificial Intelligence
1 Introduction … 1
2 Intelligent Agents … 36
II Problem-solving
3 solving problems by searching … 63.
In humans and other mammals, spinal cord injuries can be devastating, leading to permanent loss of movement, sensation and bladder control. When severed axons (the long fibers that carry messages between nerve cells) cannot regrow, a dense scar forms, preventing nerve signals from passing the injury site.
But the situation is different for some primitive invertebrates, which can rapidly reconnect severed nerves by fusing them. Inspired by this natural phenomenon, scientists led by Michael Lebenstein-Gumovski at the Sklifosovsky Institute for Emergency Medicine in Russia report that they have successfully reconnected severed spinal cords in pigs, enabling them to walk again.
When a spinal cord is completely cut, the two severed ends naturally pull away from each other. In microscopic roundworms, for example, the nerve ends automatically find each other and fuse together. The researchers realized that to recreate a natural fusion process like this, they needed a material to fill the empty space and hold the two ends together.
Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, impulsivity and/or hyperactivity. In recent years, metabolic alterations, primarily obesity, insulin resistance, and diabetes, have emerged as frequent comorbidities in individuals with ADHD, suggesting a bidirectional relationship between neurodevelopmental and metabolic dysfunctions. Emerging evidence indicates that dysregulation of dopaminergic signaling, disturbances in the hypothalamic-pituitary-adrenal (HPA) axis, and chronic low-grade inflammation are central to both ADHD symptomatology and metabolic impairments. For instance, alterations in dopamine-related genes (e.g., DRD4, DAT1) not only affect cognitive and behavioral functions but also play a role in appetite regulation and glucose homeostasis. Epidemiological studies further demonstrate that individuals with ADHD exhibit poorer glycemic control and a higher prevalence of both type 1 and type 2 diabetes, while early-life metabolic challenges such as maternal diabetes may predispose offspring to ADHD. This review aims to comprehensively synthesize the epidemiological, genetic, and pathogenetic evidence linking ADHD to metabolic alterations. We discuss key pathophysiological pathways—including dopaminergic dysregulation, HPA axis disturbances, inflammation, and oxidative stress—and evaluate their contributions to the co-occurrence of ADHD and metabolic disorders. In addition, we explore the clinical implications and integrated treatment approaches that encompass lifestyle modifications, pharmacological therapies, and multidisciplinary care. Finally, we outline future research directions to develop personalized and holistic interventions.
Known by acronyms that need no explanation, viruses like COVID, SARS and Ebola conjure images of medics in protective suits and spark fear in populations worldwide.
Vaccines for individual viruses have provided some relief, but new strains pose a constant challenge.
Now, new AI-aided vaccine technology developed by scientists at Cambridge University offers potential immunity against whole families of viruses and could even prevent the next pandemic, according to researchers.
Ma et al. present a pan-cancer analysis of 61 cancers that defines a TP53-based tripartite classification: TP53_top, TP53_plus, and Non_TP53. Analysis of 80,524 mutations and network integration reveals mutational heterogeneity, dysregulated transcription factor regulatory networks, and signaling pathway networks, providing a framework for precision oncology.
A Monash University-led study has found that an unusual pairing of two commonly used antibiotics can kill and stop the spread of resistance in a highly drug-resistant bacterium, Pseudomonas aeruginosa, which can cause life-threatening bloodstream infections, pneumonia and meningitis.
Published in The Lancet Microbe, Monash Institute of Pharmaceutical Sciences (MIPS) researchers used a validated laboratory infection system in which they were able to expose bacterial samples from infected patients to simulated antibiotic dosing regimens, as would actually occur in hospitalized patients.
The discovery of the combination regimen of two so-called β-lactam antibiotics—the most commonly used antibiotic class against serious infections—comes in the context of the World Health Organization’s designation of Pseudomonas aeruginosa as a high-priority pathogen requiring rapid and sustained action.
Every echocardiogram is a moving story. For a baby born with a complex heart condition, the gray and black images on the ultrasound screen can influence some of the earliest and most important decisions a medical team makes: What exactly is wrong with the heart? How urgent is surgery? What should doctors watch for after repair?
In our recent work, we focused on tetralogy of Fallot, often shortened to TOF. It is one of the most common cyanotic congenital heart defects. The condition involves several structural abnormalities of the heart, and many children with TOF need careful evaluation, surgery and long-term follow-up. The research is published in the journal eBioMedicine.
Echocardiography is central to that process. It is widely used, noninvasive and rich in clinical information. But it is also demanding. Clinicians must identify the correct views, interpret moving images, measure small cardiac structures, and combine these pieces of information with the patient’s clinical course. Even experienced clinicians can face heavy workloads, and interpretation can vary between observers.