Pre-endoscopy coronavirus disease 2019 screening and severe acute respiratory syndrome coronavirus-2 nucleic acid amplification testing in the Veterans Affairs healthcare system: clinical practice patterns, outcomes, and relationship to procedure volume.

Background And Aims: The coronavirus disease 2019 (COVID-19) pandemic has had profound impacts worldwide, including on the performance of GI endoscopy. We aimed to describe the performance and outcomes of pre-endoscopy COVID-19 symptom and exposure screening and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) nucleic acid amplification testing (NAAT) across the national Veterans Affairs healthcare system and describe the relationship of SARS-CoV-2 NAAT use and resumption of endoscopy services.

Methods: COVID-19 screening and NAAT results from March 2020 to April 2021 were analyzed to determine use, performance characteristics of screening, and association between testing and endoscopic volume trends.

Physician support of HPV vaccination school-entry requirements.

School-entry requirements in the US have led to high coverage for several vaccines, but few states and jurisdictions have adopted these policies for human papillomavirus (HPV) vaccination. Because physicians play a key role in advocating for vaccination policies, we assessed physician support of requiring HPV vaccine for school entry and correlates of this support. Participants were a national sample of 775 physicians who provide primary care, including vaccines, to adolescents.

Left ventricular assist device-associated infections.

The left ventricular assist device (LVAD) is a mechanical pump that supplements or replaces the function of a damaged left ventricle. Although LVAD support is associated with improved survival and quality of life, infectious complications remain a major limitation. The authors examine the epidemiology of LVAD-associated infections and review current diagnostic, treatment, and management strategies.

Synergistic premalignant effects of chronic ethanol exposure and insulin receptor substrate-1 overexpression in liver.

Aim: Insulin receptor substrate, type 1 (IRS-1) transmits growth and survival signals, and is overexpressed in more than 90% of hepatocellular carcinomas (HCCs). However, experimental overexpression of IRS-1 in the liver was found not to be sufficient to cause HCC. Since chronic alcohol abuse is a risk factor for HCC, we evaluated potential interactions between IRS-1 overexpression and chronic ethanol exposure by assessing premalignant alterations in gene expression.

Aspartyl-(asparaginyl)-beta-hydroxylase regulates hepatocellular carcinoma invasiveness.

Background/aims: We measured aspartyl (asparaginyl)-beta-hydroxylase (AAH) gene expression in human hepatocelluar carcinoma and surrounding uninvolved liver at both the mRNA and protein level and examined the regulation and function of this enzyme.

Methods: Since growth of HCC is mediated by signaling through the insulin-receptor substrate, type 1 (IRS-1), we examined-if AAH is a downstream gene regulated by insulin and IGF-1 in HCC cells. In addition, IRS-1 regulation of AAH was examined in a transgenic (Tg) mouse model in which the human (h) IRS-1 gene was over-expressed in the liver, and an in vitro model in which a C-terminus truncated dominant-negative hIRS-1 cDNA (hIRS-DeltaC) was over-expressed in FOCUS HCC cells.

Oncogenic role of the frizzled-7/beta-catenin pathway in hepatocellular carcinoma.

Background/aims: The molecular mechanisms of hepatocarcinogenesis remain largely unknown. Previous studies suggest that activation of the Wnt/beta-catenin pathway is important during hepatocyte transformation but the role of Frizzled receptor (FZD) in this process has not been defined. Here we investigate activation of this pathway by FZD using transgenic hepatocellular carcinoma (HCC) murine models.

Potential role of PTEN phosphatase in ethanol-impaired survival signaling in the liver.

Chronic ethanol consumption can cause sustained hepatocellular injury and inhibit the subsequent regenerative response. These effects of ethanol may be mediated by impaired hepatocyte survival mechanisms. The present study examines the effects of ethanol on survival signaling in the intact liver.