Detection of Mutant Peptides of SARS-CoV-2 Variants by LC/MS in the DDA Approach Using an In-House Database.

Equipped with a dramatically high mutation rate, which happens to be a signature of RNA viruses, SARS-CoV-2 trampled across the globe infecting individuals of all ages and ethnicities. As the variants of concern (VOC) loomed large, definitive detection of SARS-CoV-2 strains became a matter of utmost importance in epidemiological and clinical research. Besides, unveiling the disease pathogenesis at the molecular level and deciphering the therapeutic targets became key priorities since the emergence of the pandemic.

Isogenic hiPSC models of Turner syndrome development reveal shared roles of inactive X and Y in the human cranial neural crest network.

Modeling the developmental etiology of viable human aneuploidy can be challenging in rodents due to syntenic boundaries, or primate-specific biology. In humans, monosomy-X (45,X) causes Turner syndrome (TS), altering craniofacial, skeletal, endocrine, and cardiovascular development, which in contrast remain unaffected in 39,X-mice. To learn how human monosomy-X may impact early embryonic development, we turned to human 45,X and isogenic euploid induced pluripotent stem cells (hiPSCs) from male and female mosaic donors.

Monosomy X in isogenic human iPSC-derived trophoblast model impacts expression modules preserved in human placenta.

Mammalian sex chromosomes encode homologous X/Y gene pairs that were retained on the Y chromosome in males and escape X chromosome inactivation (XCI) in females. Inferred to reflect X/Y pair dosage sensitivity, monosomy X is a leading cause of miscarriage in humans with near full penetrance. This phenotype is shared with many other mammals but not the mouse, which offers sophisticated genetic tools to generate sex chromosomal aneuploidy but also tolerates its developmental impact.

Contiguous erosion of the inactive X in human pluripotency concludes with global DNA hypomethylation.

Female human pluripotent stem cells (hPSCs) routinely undergo inactive X (Xi) erosion. This progressive loss of key repressive features follows the loss of XIST expression, the long non-coding RNA driving X inactivation, and causes reactivation of silenced genes across the eroding X (Xe). To date, the sporadic and progressive nature of erosion has obscured its scale, dynamics, and key transition events.

Forged by , , and : How Tandem Repeats Shape the Active and Inactive X Chromosome.

Recent efforts in mapping spatial genome organization have revealed three evocative and conserved structural features of the inactive X in female mammals. First, the chromosomal conformation of the inactive X reveals a loss of topologically associated domains (TADs) present on the active X. Second, the macrosatellite emerges as a singular boundary that suppresses physical interactions between two large TAD-depleted "megadomains.

Metabolic syndrome in vitiligo patients among a semi-urban Maharashtrian population: A case control study.

Aim: To assess the prevalence of metabolic syndrome and its correlation with the severity and duration of vitiligo.

Methods: One hundred vitiligo patients and 100 age-and-sex matched controls were included, whose waist circumference and blood pressure were measured; fasting serum cholesterol, triglycerides and glucose levels quantified; disease severity assessed and metabolic syndrome defined by National Cholesterol Education Program (NCEP) criteria.

Results: Metabolic syndrome (24%:12%), hypertriglyceridemia (41%:24%), impaired glucose tolerance (25%:16%) [P<0.

Restoration of Pigmentation by Follicular Unit Extraction Transplant in Three Cases of Focal Vitiligo Recalcitrant to Therapy including with Previous Nonculture Melanocyte-keratinocyte Transplant.

Vitiligo is an acquired, idiopathic depigmentary disease resisting satisfactory repigmentation despite multimodal therapy. Based on the concept of activation of the existing undifferentiated stem cells in the outer root sheet of the hair follicles, follicular unit extraction (FUE) transplant is an interesting advancement in the field of minimally invasive surgery for vitiligo. We herein present three cases of vitiligo whose residual recalcitrant foci as well as poliosis - refractory to therapy including with previous nonculture melanocyte-keratinocyte transplant - repigmented satisfactorily after FUE transplant.

Stability of Norwalk Virus Capsid Protein Interfaces Evaluated by in Silico Nanoindentation.

Norwalk virus causes severe gastroenteritis for which there is currently no specific anti-viral therapy. A stage of the infection process is uncoating of the protein capsid to expose the viral genome and allow for viral replication. A mechanical characterization of the Norwalk virus may provide important information relating to the mechanism of uncoating.