Optical photometry of GM Cep: evidence for UXor type of variability

Results from optical photometric observations of the pre-main sequence star GM Cep are reported in the paper. The star is located in the field of the young open cluster Trumpler 37 - a region of active star formation. GM Cep shows a large amplitude rapid variability interpreted as a possible outburst from EXor type in previous studies. Our data from BVRI CCD photometric observations of the star are collected from June 2008 to February 2011 in Rozhen observatory (Bulgaria) and Skinakas observatory (Crete, Greece). A sequence of sixteen comparison stars in the field of GM Cep was calibrated in the BVRI bands. Our photometric data for a 2.5 years period show a high amplitude variations (Delta V ~ 2.3m) and two deep minimums in brightness are observed. The analysis of collected multicolor photometric data shows the typical of UX Ori variables a color reversal during the minimums in brightness. On the other hand, high amplitude rapid variations in brightness typical for the Classical T Tauri stars also present on the light curve of GM Cep. Comparing our results with results published in the literature, we conclude that changes in brightness are caused by superposition of both: (1) magnetically channeled accretion from the circumstellar disk, and (2) occultation from circumstellar clouds of dust or from features of a circumstellar disk.Comment: 7 pages, 3 figures, accepted for publication in Ap&S

Epidemiology of Escherichia coli bacteraemia in England: results of an enhanced sentinel surveillance programme

Background: Escherichia coli causes over one third of the bacteraemia cases in England each year, and the incidence of these infections is increasing. Aim: To determine the underlying risk factors associated with E. coli bacteraemia. Methods: A three month enhanced sentinel surveillance study involving 35 National Health Service hospitals was undertaken in the winter of 2012/13 to collect risk factor information and further details on the underlying source of infection to augment data already collected by the English national surveillance programme. Antimicrobial susceptibility results for E. coli isolated from blood and urine were also collected. Findings: A total of 1,731 cases of E. coli bacteraemia were included. The urogenital tract was the most commonly reported source of infection (51.2% of cases) with prior treatment for a urinary tract infection being the largest independent effect associated with this infection source. Half of all patients had prior healthcare exposure in the month prior to the bacteraemia with antimicrobial therapy and urinary catheterisation being reported in one third and one fifth of these patients. Prior healthcare exposure was associated with a higher proportion of antibiotic non-susceptibility in the blood culture isolates (P=0.001). Conclusion: Analysis of risk factors suggests potential community and hospital-related interventions particularly better use of urinary catheters and improved antibiotic management of urinary tract infections. As part of the latter strategy, antibiotic resistance profiles need to be closely monitored to ensure treatment guidelines are up to date to limit inappropriate empiric therapy

Inhibition of MAP4K4 signaling initiates metabolic reprogramming to protect hepatocytes from lipotoxic damage.

The primary hepatic consequence of obesity is non-alcoholic fatty liver disease (NAFLD), affecting about 25% of the global adult population. Non-alcoholic steatohepatitis (NASH) is a severe form of NAFLD characterized by liver lipid accumulation, inflammation, and hepatocyte ballooning, with a different degree of hepatic fibrosis. In the light of rapidly increasing prevalence of NAFLD and NASH, there is an urgent need for improved understanding of the molecular pathogenesis of these diseases. The aim of this study was to decipher the possible role of STE20-type kinase MAP4K4 in the regulation of hepatocellular lipotoxicity and susceptibility to NAFLD. We found that MAP4K4 mRNA expression in human liver biopsies was positively correlated with key hallmarks of NAFLD (i.e., liver steatosis, lobular inflammation, hepatocellular ballooning, and fibrosis). We also found that the silencing of MAP4K4 suppressed lipid deposition in human hepatocytes by stimulating β-oxidation and triacylglycerol secretion, while attenuating fatty acid influx and lipid synthesis. Furthermore, downregulation of MAP4K4 markedly reduced the glycolysis rate and lowered incidences of oxidative/endoplasmic reticulum stress. In parallel, we observed suppressed JNK and ERK activation and increased AKT phosphorylation in MAP4K4-deficient hepatocytes. Together, these results provide the first experimental evidence supporting the potential involvement of STE20-type kinase MAP4K4 as a component of the hepatocellular lipotoxic milieu promoting NAFLD susceptibility