A light-activated enzyme morphed round starfish egg cells into different shapes. This technology could one day be useful for wound healing therapies.
Category: genetics – Page 2
Driven by genetic and environmental factors, aging is a physiological process responsible for age-related degenerative changes in the body, cognitive decline, and impaired overall wellbeing. Notably, premature aging as well as the emergence of progeroid syndromes have posed concerns regarding chronic health conditions and comorbidities in the aging population. Accelerated telomere attrition is also implicated in metabolic dysfunction and the development of metabolic disorders. Impaired metabolic homeostasis arises secondary to age-related increases in the synthesis of free radicals, decreased oxidative capacity, impaired antioxidant defense, and disrupted energy metabolism. In particular, several cellular and molecular mechanisms of aging have been identified to decipher the influence of premature aging on metabolic diseases. These include defective DNA repair, telomere attrition, epigenetic alterations, and dysregulation of nutrient-sensing pathways. The role of telomere attrition premature aging in the pathogenesis of metabolic diseases has been largely attributed to pro-inflammatory states that promote telomere shortening, genetic mutations in the telomerase reverse transcriptase, epigenetic alteration, oxidative stress, and mitochondrial dysfunctions. Nonetheless, the therapeutic interventions focus on restoring the length of telomeres and may include treatment approaches to restore telomerase enzyme activity, promote alternative lengthening of telomeres, counter oxidative stress, and decrease the concentration of pro-inflammatory cytokines. Given the significance and robust potential of delaying telomere attrition in age-related metabolic diseases, this review aimed to explore the molecular and cellular mechanisms of aging underlying premature telomere attrition and metabolic diseases, assimilating evidence from both human and animal studies.
Aging is defined as a physiological phenomenon driven by genetic and biological processes, which are related to the lifespan of an individual and are associated with all age-related pathologies (Li et al., 2021). The aging process increases the susceptibility of individuals to factors leading to death as they grow older. Aging is a complex multifactorial phenomenon that involves the simultaneous interaction between various factors at different levels of functional organization. The role of genetic and environmental factors is represented by the heterogenous aging phenotype across different individuals, hence, these factors influence the lifespan of an individual via the process of aging (Jayanthi et al., 2010). With the deterioration of physiological functions critical to the survival and fertility of humans, the process of aging is known to relate to the notion of natural selection (Gilbert, 2000).
Recent advancements in in-vitro gametogenesis (IVG) suggest that lab-grown eggs and sperm could become viable within the next decade. This technology holds the promise of revolutionizing fertility treatments, particularly for individuals facing infertility and same-sex couples desiring biological children. However, it also raises significant ethical and medical considerations that must be carefully addressed.
The Human Fertilisation and Embryology Authority (HFEA), the UK’s fertility regulator, has reported that the development of lab-grown gametes, known as in-vitro gametogenesis (IVG), may become a practical option within the next decade. This technology involves creating eggs and sperm from reprogrammed skin or stem cells, potentially transforming fertility treatments by removing age-related barriers and enabling same-sex couples to have biological children.
IVG represents a significant advancement in reproductive science. By generating gametes in the laboratory, scientists can overcome challenges associated with traditional fertility treatments. This approach could provide new avenues for individuals with infertility issues and offer same-sex couples the opportunity to have children genetically related to both partners.
Researchers at the University of Cologne and University Hospital Cologne have determined that the novel mRNA-based COVID-19 vaccines not only induce acquired immune responses such as antibody production, but also cause persistent epigenetic changes in innate immune cells.
The study, “Persistent epigenetic memory of SARS-CoV-2 mRNA vaccination in monocyte-derived macrophages,” led by Professor Dr. Jan Rybniker, who heads the Division of Infectious Diseases at University Hospital Cologne and is a principal investigator at the Center for Molecular Medicine Cologne (CMMC), and Dr. Robert Hänsel-Hertsch, principal investigator at the CMMC, was published in Molecular Systems Biology.
The immune system comprises two immunity strategies: the innate and the acquired (adaptive) immune system. The innate immune system provides general protection from pathogens and must react quickly. The adaptive immune system adapts to new pathogens and is highly specific in its response. Both systems work closely together.
Researchers at Children’s Hospital of Philadelphia (CHOP) developed a longitudinal atlas of neuroblastoma, a common and potentially deadly childhood cancer, to gain a deeper understanding into precise molecular mechanisms underlying why and how certain treatments eventually become ineffective.
The findings, which offer insights that could potentially lead to new personalized medicine approaches in neuroblastoma treatment, were published today in the journal Nature Genetics.
Despite significant advances in the standard of care, the 5-year survival rate of high-risk neuroblastoma after diagnosis remains less than 50%. Neuroblastoma cells within the same tumor can vary greatly, which creates challenges in treatment efficacy. Until now, the scientific community lacked understanding of how the tumor microenvironment changes during treatment.
A new multicenter study by researchers at the Icahn School of Medicine at Mount Sinai, in collaboration with the Clinical Proteomic Tumor Analysis Consortium (CPTAC) and colleagues around the world, has discovered that the genes we are born with—known as germline genetic variants—play a powerful, underappreciated role in how cancer develops and behaves.
Published in the April 14 online issue of Cell, the study, “Precision Proteogenomics Reveals Pan-Cancer Impact of Germline Variants,” is the first to detail how millions of inherited genetic differences influence the activity of thousands of proteins within tumors.
Drawing on data from more than 1,000 patients across 10 different cancer types, the research illustrates how a person’s unique genetic makeup can shape the biology of their cancer.
Researchers have identified mutations in the non-coding gene RNU2-2 as a cause of a newly defined neurodevelopmental disorder, often accompanied by severe epilepsy.
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