Accurate Detection of Streptococcus pyogenes at the Point of Care Using the cobas Liat Strep A Nucleic Acid Test.

The performance of a polymerase chain reaction-based point-of-care assay, the cobas Strep A Nucleic Acid Test for use on the cobas Liat System (cobas Liat Strep A assay), for the detection of group A Streptococcus bacteria was evaluated in primary care settings. Throat swab specimens from 427 patients were tested with the cobas Liat Strep A assay and a rapid antigen detection test (RADT) by existing medical staff at 5 primary care clinics, and results were compared with bacterial culture. The cobas Liat Strep A assay demonstrated equivalent sensitivity (97.

DNA methylation regulates bromodomain-containing protein 2 expression during adipocyte differentiation.

Obesity is characterized by excessive accumulation of white adipose tissue. Bromodomain-containing protein 2 (Brd2), which belongs to the bromodomain and extraterminal domain family of proteins, suppresses adipocyte differentiation. DNA methylation is critical for several differentiation processes and possibly in adipocyte differentiation.

Brd2 inhibits adipogenesis via the ERK1/2 signaling pathway in 3T3-L1 adipocytes.

Bromodomain-containing protein 2 (Brd2) is a nuclear serine/threonine kinase involved in transcriptional regulation. In 3T3-L1 adipocytes, Brd2 normally co-represses PPARγ (peroxisome proliferator-activated receptor gamma) and inhibits adipogenesis. Here, we show that Brd2 over-expression in preadipocytes inhibits their differentiation into adipocytes, while Brd2 knockdown promotes adipogenic differentiation in vitro and forces cells to undergo adipogenesis independent of the MDI (methyisobutylxanthane, dexamethasone and insulin) induction.

Brd2 gene disruption causes "metabolically healthy" obesity: epigenetic and chromatin-based mechanisms that uncouple obesity from type 2 diabetes.

Disturbed body energy balance can lead to obesity and obesity-driven diseases such as Type 2 diabetes, which have reached an epidemic level. Evidence indicates that obesity-induced inflammation is a major cause of insulin resistance and Type 2 diabetes. Environmental factors, such as nutrients, affect body energy balance through epigenetic or chromatin-based mechanisms.

Brd2 disruption in mice causes severe obesity without Type 2 diabetes.

Certain human subpopulations are metabolically healthy but obese, or metabolically obese but normal weight; such mutations uncouple obesity from glucose intolerance, revealing pathways implicated in Type 2 diabetes. Current searches for relevant genes consume significant effort. We have reported previously a novel double bromodomain protein called Brd2, which is a transcriptional co-activator/co-repressor with SWI/SNF (switch mating type/sucrose non-fermenting)-like functions that regulates chromatin.

Establishment of new mouse embryonic stem cell lines is improved by physiological glucose and oxygen.

Embryonic stem cell lines are routinely selected and cultured in glucose and oxygen concentrations that are well above those of the intrauterine environment. Supraphysiological glucose and hyperoxia each increase oxidative stress, which could be detrimental to survival in vitro by inhibiting proliferation and/or inducing cell death. The aim of this study was to test whether isolation of new embryonic stem cell lines from murine blastocysts is improved by culture in physiological (5%) oxygen instead of approximately 20%, the concentration of oxygen in room air, or in media containing physiological (100 mg/dL) instead of 450 mg/dL glucose.

Glucose and Insulin Regulate Leptin Expression in 3T3-F442A Adipocytes.

Relative quantitation RT-PCR was used to investigate the regulation of leptin expression in 3T3-F442A adipocytes by glucose and insulin. The results showed that glucose and insulin stimulated the expression of leptin in 3T3-F442A adipocytes, but they did not act synergically. Over-high concentration of glucose suppressed the expression of leptin and the effect of insulin.