In 1978, the first case of hepatitis E was identified as non-A, non-B hepatitis. Hepatitis E virus (HEV) infection is believed to be one of the common causes of enterically transmitted acute hepatitis in developing countries and is rare in developed countries, except in patients with a history of travel. However, an increasing number of chronic HEV infection cases have recently been reported in developed countries. In these countries, immunosuppressed patients with HEV infection, such as organ transplant recipients, human immunodeficiency virus (HIV)-infected patients or patients with haematological malignancies, could develop chronic hepatitis E (CHE) infection. Approximately 60% of HEV infections in immunocompromised patients after solid organ transplantation evolve to CHE without antiviral treatment. Clinical manifestations of CHE are often nonspecific symptoms. Many patients with CHE infection are asymptomatic, but some have jaundice, fatigue, abdominal pain, fever and asthenia. Several extrahepatic manifestations have also been reported. Although chronic HEV infection can result in progressive severe liver failure and cirrhosis, diagnosis is often controversial because of the lack of specific diagnostic criteria. Many CHE cases are diagnosed by HEV RNA-positive serum or stool for >6 months. Immunosuppressive drugs, interferon-alpha and ribavirin have been used for treatment. Diagnostic reverse-transcription polymerase chain reaction is useful for estimating treatment efficacy. Preventive measures for HEV infection have been discussed, while systematic guidelines have not yet been reported.

Tooth brushing, regular dental visits, and use of dentures are inversely associated with mortality in elderly individuals with tooth loss.

STAS is a prognostic factor of poor outcomes for sublobar resection in patients with lung cancer. The worse prognosis for sublobar resection would be associated with STAS.

Transcriptional dysregulation, which can be caused by genetic and epigenetic alterations, is a fundamental feature of many cancers. A key cytoprotective transcriptional activator, NRF2, is often aberrantly activated in non-small cell lung cancers (NSCLCs) and supports both aggressive tumorigenesis and therapeutic resistance. Herein, we find that persistently activated NRF2 in NSCLCs generates enhancers at gene loci that are not normally regulated by transiently activated NRF2 under physiological conditions. Elevated accumulation of CEBPB in NRF2-activated NSCLCs is found to be one of the prerequisites for establishment of the unique NRF2-dependent enhancers, among which the NOTCH3 enhancer is shown to be critical for promotion of tumor-initiating activity. Enhancer remodeling mediated by NRF2-CEBPB cooperativity promotes tumor-initiating activity and drives malignancy of NRF2-activated NSCLCs via establishment of the NRF2-NOTCH3 regulatory axis.

Background: The basal lipid peroxide concentration in the plasma of patients with hyperlipidemia may be related to atherosclerosis. Quantitative determination of lipid peroxides in the plasma is an important step in the overall evaluation of the biochemical processes leading to oxidative injury. Unfortunately, the currently available methods for lipid peroxidation lack specificity and sensitivity. Methods: Hyperlipidemic patients (44 males and 50 females), ages 12–82 years (mean ± SE, 53 ± 2.3 years for males, 58 ± 2.0 years for females, and 56 ± 14 years for total cases), and normolipidemic volunteers (controls, 32 males and 15 females), ages 13–90 years (49 ± 4 years for males, 65 ± 4 years for females, and 55 ± 24 years for total cases), were recruited in the present study. Plasma phosphatidylcholine hydroperoxide (PCOOH) was determined by chemiluminescence-HPLC (CL-HPLC). Results: Plasma PCOOH concentrations increased with age in both controls and hyperlipidemic patients. However, the mean plasma PCOOH concentration in patients with hyperlipidemia (331 ± 19 nmol/L; n = 94) was significantly (P <0.001) higher than in the controls (160 ± 65 nmol/L; n = 47). Plasma PCOOH concentrations were similar in three hyperlipidemic phenotypes: hypercholesterolemia (IIa), hypertriglyceridemia (IV), and combined hyperlipidemia (IIb). The mean plasma PCOOH in patients with treatment-induced normalized plasma lipids was 202 ± 17 nmol/L. There was no significant correlation between plasma PCOOH concentration and total cholesterol, triglycerides, or phospholipids in hyperlipidemic patients. For all subjects, there was a significantly positive correlation between plasma PCOOH and each lipid (total cholesterol, P = 0.0002; triglycerides, P = 0.0137; and phospholipids, P <0.0001). Analysis of fatty acids composition of plasma phosphatidylcholine showed significantly low concentrations of n-6 fatty acids moieties (linoleic acid and arachidonic acid) in patients compared with controls. Conclusions: Our results suggest that an increase in plasma PCOOH in patients with hyperlipidemia may be related to the development and progression of atherosclerosis, particularly in the elderly. Measurement of plasma PCOOH is useful for in vivo evaluation of oxidative stress.