Ballarddickens7464

BACKGROUND Coxsackievirus B3 (CVB3) is the primary cause of infectious myocarditis. Aggressive immunological activation and apoptosis of myocytes contributes to progressive dysfunction of cardiac contraction and poor prognosis. MG-132, a proteasome inhibitor, regulates mitochondrial-mediated intrinsic myocardial apoptosis and downregulates NF-κB-mediated inflammation. Here, we determined whether AMPK pathway participates in MG-132-mediated myocardial protection in viral-induced myocarditis. METHODS AND RESULTS Acute viral myocarditis models were established by intraperitoneal inoculation of CVB3 in male BALB/c mice. Myocarditis and age-matched control mice were administered MG-132 and/or BML-275 dihydrochloride (BML) (AMPK antagonist) intraperitoneally daily from the day following CVB3 inoculation. MG-132 improved hemodynamics and inhibited the structural remodeling of the ventricle in mice with myocarditis, while BML largely blunted these effects. TUNEL staining and immunochemistry suggested that MG-132 exerts anti-apoptotic and anti-inflammatory effects against CVB3-induced myocardial injuries. BML attenuated the effects of MG-132 on anti-apoptosis and anti-inflammation. CONCLUSION MG-132 modulated apoptosis and inflammation, improved hemodynamics, and inhibited the structural remodeling of ventricles in a myocarditis mouse model via regulation of the AMPK signal pathway. Hepatocellular carcinoma (HCC) is one of the most common cancers in the world and one of the most lethal. MGN-3/Biobran is a natural product derived from rice bran hemicelluloses and has been reported to possess a potent anticancer effect in a clinical study of patients with HCC. The current study examines the mechanisms by which Biobran protects against chemically induced hepatocarcinogenesis in rats. The chemical carcinogen used in this study is N-nitrosodiethylamine (NDEA) plus carbon tetrachloride (CCl4). Rats were treated with this carcinogen, and the animals were pretreated or posttreated with Biobran via intraperitoneal injections until the end of the experiment. Treatment with Biobran resulted in 1) significant alleviation of liver preneoplastic lesions towards normal hepatocellular architecture in association with inhibition of collagen fiber deposition; 2) arrest of cancer cells in the sub-G1 phase of the cell cycle; 3) increased DNA fragmentation in cancer cells; 4) down-regulated expression of Bcl-2 and up-regulated expression of p53, Bax, and caspase-3; and 5) protection against carcinogen-induced suppression of IkappaB-alpha (IκB-α) mRNA expression and inhibition of nuclear factor kappa-B (NF-κB/p65) expression. Additionally, the effect of Biobran treatment was found to be more significant when supplemented prior to carcinogen-induced hepatocarcinogenesis as compared to posttreatment. We conclude that Biobran inhibits hepatocarcinogenesis in rats by mechanisms that include induction of apoptosis, inhibition of inflammation, and suppression of cancer cell proliferation. Biobran may be a promising chemopreventive and chemotherapeutic agent for liver carcinogenesis. An animal laboratory in a teaching hospital is a possible cause of cross infection. We aimed to assess the infection control in our animal laboratory and evaluate the disinfectant effects of a portable pulsed xenon ultraviolet (PX-UV) machine. Samples were taken from the surface of research tables, other high touch places, such as doorknobs, weighing scales, and handles of trolleys, and from air in the barrier system pre- and post-manual cleaning and post-PX-UV disinfection. The bacteria types were identified. We found that routine manual cleaning significantly reduced bacterial colony form unit (CFU)/cm2 (P = .02), and the median of CFU/cm2 reduced from 0.5 pre-cleaning to zero post-cleaning. PX-UV disinfection also significantly reduced residual bacterial counts (P = .002), with the highest counts 10 pre-PX-UV disinfection and 1 afterwards. Without manual cleaning, PX-UV disinfected surfaces significantly (P  less then  .001), median count 6 pre-PX-UV disinfection and zero afterwards. PX-UV significantly reduced bacterial colony counts in the air with the median count falling from 6 to zero (P  less then  .001). Some of the 21 species of pathogens we identified in the current study are pathogenic, resistant to antibiotics, and able to cause nosocomial infections and zoonosis. check details PX-UV reduced counts of most of the pathogens. PX-UV is an effective agent against these pathogens. OBJECTIVES To understand the prognostic value of laboratory markers at presentation on post-treatment survival of patients 50 and older following cervical spine fracture. PATIENTS AND METHODS We obtained clinical data on patients 50 and older treated for cervical spine fracture in a single healthcare system (2006-2016). Our primary outcome consisted of 1-year mortality, with mortality within 3-months of presentation considered secondarily. Our primary predictors included serum glucose, serum creatinine, platelet-lymphocyte ratio (PLR) and neutrophil-lymphocyte ratio (NLR) at presentation. We used multivariable logistic regression to adjust for confounding from sociodemographic and clinical characteristics. Point estimates and 95 % confidence intervals (CI) from the final model were refined using Bayesian regression techniques. RESULTS We included 1781 patients in this analysis, with an average age of 75.3 (SD 12.0). The mortality rate at 3-months was 12 % and 17 % at 1-year. In multivariable testing, neither elevated PLR or NLR were significant predictors of 1-year mortality. Elevated serum creatinine was associated with increased mortality at 1-year (OR 1.89; 95 % CI 1.30, 2.74), as was hyperglycemia (OR 1.50; 95 % CI 1.06, 2.13). Elevated serum creatinine remained influential (OR 1.64; 95 % CI 1.06, 2.54) on mortality at 3-months. CONCLUSIONS This is the first study to evaluate laboratory values at presentation in conjunction with survival following cervical fractures. The results can be used to help forecast natural history and in expectation management. They may also help formulate treatment plans, especially when the need for surgical intervention is not clearly defined.