Abdominal obesity increases risk for esophageal cancer: a nationwide population-based cohort study of South Korea

Journal of Gastroenterology - The relationship between overall obesity, as measured by body mass index (BMI) and risk of esophageal squamous cell carcinoma (ESCC) has been reported to show a...     

Aquaporin 1 regulates GTP-induced rapid gating of water in secretory vesicles

The swelling of secretory vesicles has been implicated in exocytosis, but the underlying mechanism of vesicle swelling remains largely unknown. Zymogen granules (ZGs), the membrane-bound secretory vesicles in exocrine pancreas, swell in response to GTP mediated by a G(alpha)i3 protein. Evidence is presented here that the water channel aquaporin-1 (AQP1) is present in the ZG membrane and participates in rapid GTP-induced vesicular water gating and swelling. Isolated ZGs exhibit low basal water permeability. However, exposure of granules to GTP results in a marked potentiation of water entry. Treatment of ZGs with the known water channel inhibitor Hg2+ is accompanied by a reversible loss in both the basal and GTP-stimulatable water entry and vesicle swelling. Introduction of AQP1-specific antibody raised against the carboxyl-terminal domain of AQP1 blocks GTP-stimulable swelling of vesicles. Our results demonstrate that AQP1 associated at the ZG membrane is involved in basal as well as GTP-induced rapid gating of water in ZGs of the exocrine pancreas.     

Sleep duration and health-related quality of life in Korean adults: 2007-2015 Korea National Health and Nutrition Examination Survey

Sleep and Breathing - To evaluate the association of sleep duration with health-related quality of life (HRQOL) and examine the influence of age, sex, and common comorbidities on this association....     

A major histocompatibility complex class I-dependent subset of memory phenotype CD8+ cells

Most memory phenotype (MP) CD44(hi) CD8(+) cells are resting interleukin (IL)-15-dependent cells characterized by high expression of the IL-2/IL-15 receptor beta (CD122). However, some MP CD8(+) cells have a CD122(lo) phenotype and are IL-15 independent. Here, evidence is presented that the CD122(lo) subset of MP CD8(+) cells is controlled largely by major histocompatibility complex (MHC) class I molecules. Many of these cells display surface markers typical of recently activated T cells (CD62L(lo), CD69(hi), CD43(hi), and CD127(lo)) and show a high rate of background proliferation. Cells with this phenotype are highly enriched in common gamma chain-deficient mice and absent from MHC-I(-/-) mice. Unlike CD122(hi) CD8(+) cells, CD122(lo) MP CD8(+) cells survive poorly after transfer to MHC-I(-/-) hosts and cease to proliferate. Although distinctly different from typical antigen-specific memory cells, CD122(lo) MP CD8(+) cells closely resemble the antigen-dependent memory CD8(+) cells found in chronic viral infections.     

Plumbagin (5-hydroxy-2-methyl-1,4-naphthoquinone) induces apoptosis and cell cycle arrest in A549 cells through p53 accumulation via c-Jun NH2-terminal kinase-mediated phosphorylation at serine 15 in vitro and in vivo

This study first investigates the anticancer effect of plumbagin (5-hydroxy-2-methyl-1,4-naphthoquinone) in human nonsmall cell lung cancer cells, A549. Plumbagin has exhibited effective cell growth inhibition by inducing cancer cells to undergo G2/M phase arrest and apoptosis. Blockade of cell cycle was associated with increased levels of p21 and reduced amounts of cyclinB1, Cdc2, and Cdc25C. Plumbagin treatment also enhanced the levels of inactivated phosphorylated Cdc2 and Cdc25C. Blockade of p53 activity by dominant-negative p53 transfection partially decreased plumbagin-induced apoptosis and G2/M arrest, suggesting it might be operated by p53-dependent and independent pathway. Plumbagin treatment triggered the mitochondrial apoptotic pathway indicated by a change in Bax/Bcl-2 ratios, resulting in mitochondrial membrane potential loss, cytochrome c release, and caspase-9 activation. We also found that c-Jun NH2-terminal kinase (JNK) is a critical mediator in plumbagin-induced cell growth inhibition. Activation of JNK by plumbagin phosphorylated p53 at serine 15, resulting in increased stability of p53 by decreasing p53 and MDM2 interaction. SP600125 (anthra [1,9-cd]pyrazol-6(2H)-one-1,9-pyrazoloanthrone), a specific inhibitor of JNK, significantly decreased apoptosis by inhibiting the phosphorylation of p53 (serine 15) and subsequently increased the interaction of p53 and MDM2. SP6000125 also inhibited the phosphorylation of Bcl-2 (Ser70) induced by plumbagin. Further investigation revealed that plumbagin's inhibition of cell growth effect was also evident in a nude mice model. Taken together, these results suggest a critical role for JNK and p53 in plumbagin-induced G2/M arrest and apoptosis of human nonsmall cell lung cancer cells.     

Three Cases of Lichen Nitidus Associated with Various Cutaneous Diseases

Lichen nitidus (LN) is an uncommon, usually asymptomatic cutaneous eruption characterized by the presence of multiple, small, flesh-colored papules. The epidemiologic and pathophysiologic characteristics of LN have not yet been defined. Furthermore, LN has rarely been described in association with other cutaneous diseases. We herein report 3 cases of LN associated with various cutaneous diseases, including lichen striatus, oral lichen planus, and psoriasis vulgaris.     

Risk factors and effects on long-term outcomes of cardiac troponin I elevation after drug-eluting stent implantation in patients with stable coronary artery disease

This study evaluated the risk factors of postprocedure cardiac troponin I (cTnI) increase and its effects on repeat revascularization and on overall clinical outcomes in patients with angina and normal preprocedural cTnI levels who underwent successful drug-eluting stent implantation. Postprocedure cTnI increase (≥0.5 ng/ml) was observed in 207 of 802 patients (25.8%). Patients with cTnI increase had more extensive coronary disease than patients without cTnI increase, which necessitated for the cTnI group more multilesion interventions and a longer total stent length. In multivariate analysis, total stent length (odds ratio 1.02, 1.01 to 1.03, p = 0.001) and use of glycoprotein IIb/IIIa inhibitors (3.07, 1.54 to 6.11, p <0.001) were identified as independent predictors of cTnI increase. During a median follow-up of 42 months, however, there were no significant between-group differences in Kaplan-Meier estimates of any repeat revascularization (24.8% vs 18.4%, hazard ratio 1.085, 0.723 to 1.627, p = 0.694) and major adverse cardiovascular events (27.0% vs 22.4%, 1.022, 0.703 to 1.485, p = 0.911). In conclusion, patients with postprocedure cTnI increase had more severe baseline coronary disease and received more complex interventional procedures. However, cTnI increase after successful drug-eluting stent implantation was not associated with an increased risk of repeat revascularization or of other adverse events.