Lifeboat Foundation

Scientists have identified a specific gene they believe could be a key player in the changes in brain structure seen in several psychiatric conditions, such as schizophrenia and autism.

The team from Cardiff University’s Neuroscience and Mental Health Research Institute has found that the deletion of the gene CYFIP1 leads to thinning of the insulation that covers nerve cells and is vital for the smooth and rapid communications between different parts of the brain.

The new findings, published in the journal Nature Communications and highlighted in the journal Nature Reviews Neuroscience, throws new light on the potential cause of psychiatric conditions and could ultimately point to new and more effective therapies.

After 10 years in remission, Derek Ruff’s cancer returned, this time as stage IV colon cancer. Despite aggressive rounds of chemotherapy, palliative radiotherapy and immunotherapy, his disease progressed. In February 2019, as part of a phase I clinical trial at Moores Cancer Center at UC San Diego Health, Ruff became the first patient in the world to be treated for cancer with a human-induced pluripotent stem cell (iPSC)-derived cell therapy called FT500.

Moores Cancer Center at UC San Diego Health treats the first patient treated for cancer with a human-induced pluripotent stem cell (iPSC)-derived cell therapy called FT500. Dan Kaufman collaborated with Fate Therapeutics to bring the iPSC-derived natural killer cell cancer immunotherapy to patients.

Neurotoxic anticancer drugs, such as platinum-based anticancer drugs, taxanes, vinca alkaloids, and proteasome/angiogenesis inhibitors are responsible for chemotherapy-induced peripheral neuropathy (CIPN). The health consequences of CIPN remain worrying as it is associated with several comorbidities and affects a specific population of patients already impacted by cancer, a strong driver for declines in older adults. The purpose of this review is to present a comprehensive overview of the long-term effects of CIPN in cancer patients and survivors. Pathophysiological mechanisms and risk factors are also presented. Neurotoxic mechanisms leading to CIPNs are not yet fully understood but involve neuronopathy and/or axonopathy, mainly associated with DNA damage, oxidative stress, mitochondria toxicity, and ion channel remodeling in the neurons of the peripheral nervous system. Classical symptoms of CIPNs are peripheral neuropathy with a “stocking and glove” distribution characterized by sensory loss, paresthesia, dysesthesia and numbness, sometimes associated with neuropathic pain in the most serious cases. Several risk factors can promote CIPN as a function of the anticancer drug considered, such as cumulative dose, treatment duration, history of neuropathy, combination of therapies and genetic polymorphisms. CIPNs are frequent in cancer patients with an overall incidence of approximately 38% (possibly up to 90% of patients treated with oxaliplatin). Finally, the long-term reversibility of these CIPNs remain questionable, notably in the case of platinum-based anticancer drugs and taxanes, for which CIPN may last several years after the end of anticancer chemotherapies. These long-term effects are associated with comorbidities such as depression, insomnia, falls and decreases of health-related quality of life in cancer patients and survivors. However, it is noteworthy that these long-term effects remain poorly studied, and only limited data are available such as in the case of bortezomib and thalidomide-induced peripheral neuropathy.

Platinum-based anticancer drugs (i.e., cisplatin, oxaliplatin), proteasome/angiogenesis inhibitors (bortezomib/thalidomide), vinca alkaloids (i.e., vincristine, vinorelbine) and taxanes (i.e., paclitaxel, docetaxel) are the most common anticancer drugs used as first-line chemotherapy for several cancers, including colorectal, gastric, breast and lung cancers, and multiple myeloma. Despite their different action mechanisms, all these anticancer drugs share a common adverse and disabling effect for patients, namely CIPN (Balayssac et al., 2011). CIPN has a considerable impact on cancer treatments and their related symptoms severely affect patients’ daily activities and quality of life. Thus CIPN is often the main adverse effect leading to the reduction or discontinuation of chemotherapy.

The evolving gene-editing technology CRISPR-Cas9 is useful for changing one gene, or maybe a few genes at a time. A team at ETH Zurich has tweaked the technology so they can change 25 different gene sites at once. Instead of using the Cas9 enzyme to do the DNA cutting, though, they used Cas12a. That allowed them to create a long “address list” of gene sites to target, they explained in the journal Nature Methods. They created a DNA molecule called a plasmid to store the list, inserted it in human cells and were able to modify several genes, they reported. (Release)

Chemotherapy and radiation suppress blood stem cells, often for several weeks or even months after cancer treatments are complete. This leaves patients vulnerable to infections and other health problems. Scientists at the University of California, Los Angeles have created a new drug that targets the protein tyrosine phosphatase-sigma (PTP-sigma), which is prevalent on blood stem cells. They showed that blocking the protein in rodent models with the drug, called DJ009, helped blood cells recover more quickly after they were damaged by radiation. They published their findings in the journal Nature Communications. (Release)

Ellen Swallow Richards was not going to be intimidated by a room full of health experts and officials. Children were dying and their parents, Boston’s taxpayers, and city officials were to blame. The tiny, square-chinned woman thought nothing of climbing over boulders in petticoats, collecting thousands of water samples by horseback, or exploring mines on her honeymoon. So when she took the podium at the 1896 meeting of the American Public Health Association, she wasted no time in laying out her evidence.

More than 5,000 cases of illness could be attributed to the illegal conditions in Boston’s public schools, she said. Buildings lacked ventilation. Sewer pipes were still open. Toilets were filthy. Some 41 percent of the floors had never been washed. Only 27 of the city’s 168 schools had fire escapes that worked. Fully half of Boston’s schoolhouses were “deleterious to health.” The public and parents should be charged with “the murder of some 200 children per year,” Richards declared, their deaths entirely preventable from environmental hazards.

The strident, accusatory tone of Richards’ speech was remarkable, given how tactful she had been in the first two decades of her career. That tact had been a coping strategy, characteristic of a pragmatic feminism. Richards had been the first woman admitted to the Massachusetts Institute of Technology and the university’s first woman instructor. To blend in, she made a conscious effort to appear as unthreatening and feminine as she possibly could to her male colleagues. She even mended their clothes when they asked.

The Defense Advanced Research Projects Agency (DARPA) launched the Pandemic Prevention Platform (P3) program in 2017, with the eventual goal of halting the spread of any infectious disease outbreak before it can escalate into a pandemic.

Current approaches for recent public health emergencies due to infectious diseases have not produced effective preventive or therapeutic solutions in a relevant timescale. Examples from recent outbreaks such as H3N2 (flu), Ebola, and Zika viruses highlight the significant lag in deployment and efficacy of life-saving solutions.

Before an A.I. system can learn, someone has to label the data supplied to it. Humans, for example, must pinpoint the polyps. The work is vital to the creation of artificial intelligence like self-driving cars, surveillance systems and automated health care.

Artificial intelligence is being taught by thousands of office workers around the world. It is not exactly futuristic work.

At iMerit offices in Kolkata, India, employees label images that are used to teach artificial intelligence systems. Credit Credit Rebecca Conway for The New York Times.

A team of scientists at UC San Francisco and the National Institutes of Health have achieved another CRISPR first, one which may fundamentally alter the way scientists study brain diseases.

In a paper published August 15 in the journal Neuron, the researchers describe a technique that uses a special version of CRISPR developed at UCSF to systematically alter the activity of genes in human neurons generated from stem cells, the first successful merger of stem cell-derived cell types and CRISPR screening technologies.

Though mutations and other genetic variants are known to be associated with an increased risk for many neurological diseases, technological bottlenecks have thwarted the efforts of scientists working to understand exactly how these genes cause disease.