A simple injection of muscle tissue could control glucose in patients with type 2 diabetes (T2D). Genetic modification of skeletal muscle and subsequent intramuscular implantation could increase blood sugar absorption and become an effective and long-lasting treatment for this pathology. “We took mice satellite cells and we genetically altered to overexpress GLUT4,” Hagit Shoyhet, researcher at the Levenberg lab of stem-cell and tissue engineering, Technion (Israel), said at the European Association for the study of Diabetes (EASD) 58th Annual Meeting.
Synthetic cells (SCs) armed with recombinant growth factors could contribute to tissue regeneration and healing by promoting angiogenesis. This technology opens the door to its application in other therapies such as transplants that require the remodeling or formation of new blood vessels. In addition, they mark the way to produce intracorporeal biological drugs or the inhibition of the angiogenesis process itself when it comes to blocking the irrigation of a tumor.
Scientists from the University of Lisbon have described how telomeres can establish the maximum damage that a cancer cell can suffer. Above this threshold, the cell would stop dividing and die. The damage comes from the transcription of the telomeres themselves of an RNA molecule called TERRA. When TERRA’s levels increase, the cell can no longer multiply. This mechanism occurs in ALT (alternative lengthening of telomeres) cells, which do not elongate their telomeres through telomerase.
Sex differences at the cellular level could explain why men respond less well to glioblastoma (GBM) treatments, according to a study led by the Washington University School of Medicine in St. Louis (WUSTL). The researchers found that male and female GBM tumor cells had different metabolic needs. GBM cells from male surgical samples absorbed more glutamine and had different nutritional preferences for amino acids.
A new study has unveiled the signaling cascade involved in the progression of brain metastasis from breast cancer. A family of connexins participates in the process that regulate the expression of laminins that favor metastatic cells to colonize the brain.
The design of genetically modified exosomes that combine multiple targets killed cancer cells and conferred immunity against them. Scientists at the University of Southern California (USC) applied bioengineering techniques to introduce up to four antitumor functions in the same type of extracellular vesicles and destroy EGFR-positive triple-negative breast cancer (TNBC) tumor cells.
A new vaccine that uses the native-like HIV-1 envelope (Env) trimer CH505 and a Toll-like receptor (TLR) 7/8 agonist adjuvant, successfully evaluated in macaques, generated potent polyclonal neutralizing antibodies (nAbs) and a high protection against the infection of the homologous simian-human immunodeficiency virus (SHIV).
Surviving apoptosis after administration of a drug triggered a previously unknown evolutionary process that gave tumor cells greater resistance to subsequent therapies. A cancer cell that does not die gets stronger. Cancer reappears with those cells that escape death thanks to a mechanism that, at the same time, offers a potential therapeutic target. According to a study led by St. Jude Children's Research Hospital in collaboration with the University of Glasgow and University of Oxford, the alternative to the cell death program is a stress response pathway that generates a persister cell phenotype not described before.
A brief pulse of rapamycin before the onset of aging extended lifespan by triggering lasting increases in autophagy. The authors called this phenomenon "rapamycin memory." Elevated autophagy was accompanied by increased levels of LManV and lysozyme in fruit flies, in intestinal enterocytes in female fly models, and its Man2B1 homologue in mice. In mice, a 3-month treatment in early adulthood had the same effect as chronic treatment, even 6 months after rapamycin was withdrawn. In the study published in the Aug. 29, 2022, issue of Nature Aging and led by researchers at the Max Planck Institute, scientists showed that the lifespan-increasing response to rapamycin treatment decreased with the age at which treatment is started.
Communication between adipose tissue and the brain increases the risk of cognitive impairment in patients with insulin resistance through extracellular vesicles (EVs) containing microRNAs (miRNAs). Neurons could be damaged when these nucleotides reach the hippocampus guided by membrane proteins in prediabetic overweight people.
