CRISPR Is The Future.
Welcome to the future!
It is the year 2050, and the world is facing a crisis. Climate change has caused widespread devastation, and the planet’s resources are dwindling. Famine and disease are rampant, and humanity is on the brink of collapse. But amidst the chaos, a new hope emerges.
O.o!!!
A fungal superbug called Candida auris is spreading rapidly through hospitals and nursing homes in the US. The first case was identified in 2016. Since then, it has spread to half the country’s 50 states. And, according to a new report, infections tripled between 2019 and 2021.
This is hugely concerning because Candida auris is resistant to many drugs, making this fungal infection one of the hardest to treat.
Continue reading “New Deadly Superfungus Can Now Be Found in Half of US States” »
A team of scientists at the Sloan Kettering Institute have identified the STING cellular signaling pathway as a key player in keeping dormant cancer cells from progressing into aggressive tumors months, or even years, after they’ve escaped from a primary tumor.
The findings, which were published in Nature on March 29, suggest that drugs to activate STING could help prevent the spread of cancer to new sites throughout the body—a process known as metastasis.
In mouse models of lung cancer, treatment that stimulated the STING pathway helped eliminate lingering cancer cells and prevent them from progressing to aggressive metastases. Known as micrometastases, these cells, which can be found individually and in small clusters, are too small to be detected with standard imaging tests.
The hNSCs used in the study have been produced and characterised in the Cell Factory and Biobank of Santa Maria Hospital (Terni, Italy), authorised by the Italian Medicine Agency (AIFA) for the production of hNSCs to be used for clinical trials (aM 54/2018). The methodology applied to isolate, expand, characterise and cryopreserve the lines is based on the Neurosphere Assay26,41,54, and has been used for the production of the cells utilised in phase I trials for Amyotrophic Lateral Sclerosis patients (NCT0164006723) and for Secondary Progressive Multiple Sclerosis patients (NCT03282760, ongoing).
The entire production process, starting from tissue procurement to cryopreservation is compliant to cGMP guidelines and approved by AIFA. The hNSCs are obtained from foetal brain tissue derived from fetuses that underwent miscarriage or natural in utero death upon receiving the signed informed consent from the mother. Forty-eight hours prior to implantation, hNSCs were plated in the growth medium at a concentration of 10,000 cells/cm2. On the day of surgery, hNSCs were collected by centrifugation, viable cells were counted by Trypan blue exclusion criteria, and the correct number of cells were re-suspended in HBSS for the transplant.
SOD1 transgenic male rats were randomly divided into three experimental groups: (i) transplanted with hNSCs (hNSC rats, n = 15); (ii) treated with HBSS (HBSS rats, n = 15) and (iii) untreated (CTRL rats, n = 22). An additional group of non-transgenic littermates (wild-type, WT, n = 9) were used as controls for symptomatic evaluation of the colony. Tacrolimus (FK506) and cyclosporine (cyclosporin A) are the principal immunosuppressive drugs that have been applied for solid organ transplantation55,56 and have been translated to stem cell treatments for PD57 and ALS22. In animal models, despite differences in potency, both drugs showed excellent survival rates for grafts across many comparative studies58,59. Our previous results44,45 showed that hNSCs can survive—without signs of rejection—in the rat brain up to 6 months under transient immunosuppression treatment, with cyclosporin A. On the bases of these results, we applied the same immunosuppressive treatment with administration of cyclosporine A (15 mg/kg/day subcutaneous; Sandimmne, Novartis) that was initiated on the day of transplantation and continued for 15 days after surgery (for all animal groups).
Alzheimer’s disease is a very common illness that affects older people worldwide, and it is one of the main causes of dementia. Researchers have been working for more than twenty years to find out what causes Alzheimer’s, but they have not yet discovered the exact reason, and there is no cure for the disease.
Huntington’s disease (HD) is a neurodegenerative disease caused by a CAG repeat expansion in the Huntingtin (HTT) gene. The resulting polyglutamine (polyQ) tract alters the function of the HTT protein. Although HTT is expressed in different tissues, the medium spiny projection neurons (MSNs) in the striatum are particularly vulnerable in HD. Thus, we sought to define the proteome of human HD patient–derived MSNs. We differentiated HD72 induced pluripotent stem cells and isogenic controls into MSNs and carried out quantitative proteomic analysis. Using data-dependent acquisitions with FAIMS for label-free quantification on the Orbitrap Lumos mass spectrometer, we identified 6,323 proteins with at least two unique peptides. Of these, 901 proteins were altered significantly more in the HD72-MSNs than in isogenic controls. Functional enrichment analysis of upregulated proteins demonstrated extracellular matrix and DNA signaling (DNA replication pathway, double-strand break repair, G1/S transition) with the highest significance. Conversely, processes associated with the downregulated proteins included neurogenesis-axogenesis, the brain-derived neurotrophic factor-signaling pathway, Ephrin-A: EphA pathway, regulation of synaptic plasticity, triglyceride homeostasis cholesterol, plasmid lipoprotein particle immune response, interferon-γ signaling, immune system major histocompatibility complex, lipid metabolism and cellular response to stimulus. Moreover, proteins involved in the formation and maintenance of axons, dendrites, and synapses (e.g., Septin protein members) were dysregulated in HD72-MSNs. Importantly, lipid metabolism pathways were altered, and using quantitative image, we found analysis that lipid droplets accumulated in the HD72-MSN, suggesting a deficit in the turnover of lipids possibly through lipophagy. Our proteomics analysis of HD72-MSNs identified relevant pathways that are altered in MSNs and confirm current and new therapeutic targets for HD.
Improving the seasonal influenza vaccine and public health specialists’ ability to predict pandemic potential in new flu strains may be possible, due to new findings from scientists at St. Jude Children’s Research Hospital. The key is the stability of a viral protein that gains entry into human cells. The findings were published today in Science Advances.
“We found that the protein flu viruses use to enter cells, hemagglutinin, needs to be relatively stable and resistant to acid in an effective H3N2 flu vaccine,” said senior and co-corresponding author Charles Russell, Ph.D., St. Jude Department of Infectious Diseases. “We found a mutation in hemagglutinin that makes the virus grow better in eggs also causes a mismatch in the vaccine. The mutation makes the virus unstable and makes it look less human-like.”
The H3N2 virus is a subtype of Influenza A and is one of the culprits behind the seasonal flu. Many flu vaccines are made by growing the virus in chicken eggs, but the virus can gain mutations during that process. Some of those changes, like the one uncovered by the St. Jude group, make the vaccine less effective in generating the ideal immune response. At the same time, other mutations have more beneficial impacts.
A large case-control study by international researchers at the RIKEN Center for Integrative Medical Sciences (IMS) in Japan has found that people who carry certain genetic risk factors for gastric (stomach) cancer have a much greater risk if they have also been infected by the bacterium Helicobacter pylori. The study, published in The New England Journal of Medicine, could contribute to the development of tailored genomic medicine for treating stomach cancer.
Stomach cancer is the fourth leading cause of cancer death worldwide and has both environmental and genetic risk factors. Environmentally, infection by H. pylori increases the risk of stomach cancer. Because the virulence of H. pylori in East Asia is high, the incidence of stomach cancer is higher in countries like Japan. Genetically, while hereditary gene variation is why we have different colored eyes and are unique as individuals, sometimes gene variants are associated with the risk of disease. For example, individuals who carry a certain hereditary pathogenic variant of the CDH1 gene have an increased risk of gastric cancer.
Testing for the presence of pathogenic variants is now one of several measures being taken for cancer prevention, surveillance, and treatment selection. However, because large-scale, case-control studies are lacking, and because those that exist have not assessed how the risk for stomach cancer changes when pathogenic variants interact with environmental factors like H. pylori, it remains unclear what actual clinical measures can be taken. To address this issue, researchers therefore evaluated the risk of gastric cancer in a large case-control study of Japanese people, considering whether they were carriers of pathogenic variants and whether they had been infected by H. pylori.
Jennifer Garrison is an assistant professor at the Buck Institute for Research on Aging and also holds appointments in the Department of Cellular and Molecular Pharmacology at University of California, San Francisco (UCSF) and the Davis School of Gerontology at the University of Southern California.
Over 321 books from 170 plus interviews over 5 years.
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Altered dystrophin expression was found in some tumors and recent studies identified a developmental onset of Duchenne muscular dystrophy (DMD). Given that embryogenesis and carcinogenesis share many mechanisms, we analyzed a broad spectrum of tumors to establish whether dystrophin alteration evokes related outcomes. Transcriptomic, proteomic, and mutation datasets from fifty tumor tissues and matching controls (10,894 samples) and 140 corresponding tumor cell lines were analyzed. Interestingly, dystrophin transcripts and protein expression were found widespread across healthy tissues and at housekeeping gene levels. In 80% of tumors, DMD expression was reduced due to transcriptional downregulation and not somatic mutations. The full-length transcript encoding Dp427 was decreased in 68% of tumors, while Dp71 variants showed variability of expression.
