Heat Convection of Compressible Viscous Fluids. I.

The stationary problem for the heat convection of compressible fluid is considered around the equilibrium solution with the external forces in the horizontal strip domain z_0 < z < z_0 + 1 and it is proved that the solution exists uniformly with respect to z_0 larger than Z_0 . The limit system as z_0 goes to infinity is the Oberbeck-Boussinesq equation

Deficiency in Galectin-3 Promotes Hepatic Injury in CDAA Diet-Induced Nonalcoholic Fatty Liver Disease

Nonalcoholic fatty liver disease (NAFLD) is increasingly recognized as a condition in which excess fat accumulates in hepatocytes. Nonalcoholic steatohepatitis (NASH), a severe form of NAFLD in which inflammation and fibrosis in the liver are noted, may eventually progress to end-stage liver disease. Galectin-3, a β-galactoside-binding animal lectin, is a multifunctional protein. This protein is involved in inflammatory responses and carcinogenesis. We investigated whether galectin-3 is involved in the development of NASH by comparing galectin-3 knockout (gal3−/−) mice and wild-type (gal3+/+) mice with choline-deficient L-amino-acid-defined (CDAA) diet-induced NAFLD/NASH. Hepatic injury was significantly more severe in the gal3−/− male mice, as compared to the gal3+/+ mice. Data generated by microarray analysis of gene expression suggested that galectin-3 deficiency causes alterations in the expression of various genes associated with carcinogenesis and lipid metabolism. Through canonical pathway analysis, involvement of PDGF and IL-6 signaling pathways was suggested in galectin-3 deficiency. Significant increase of CD14, Fos, and Jun, those that were related to lipopolysaccharide-mediated signaling, was candidate to promote hepatocellular damages in galectin-3 deficiency. In conclusion, galectin-3 deficiency in CDAA diet promotes NAFLD features. It may be caused by alterations in the expression profiles of various hepatic genes including lipopolysaccharide-mediated inflammation

Factors influencing caregiver burden in chronic pain patients: A retrospective study

Chronic pain coexists with disability, anxiety, depression, and sleep disturbances, which are factors of pain chronicity in the fear-avoidance model. Self-efficacy for managing pain plays a protective role against pain chronicity. For chronic pain sufferers, social support from caregivers is important. However, such caregivers face enormous physical and mental burdens. This study aimed to assess how self-efficacy and factors related to the fear-avoidance model affect caregiver burden. Participants were 135 chronic pain patients and their caregivers who visited our outpatient pain special clinic. In clinical assessments, numeric rating scale (NRS), pain catastrophizing scale (PCS), hospital anxiety and depression scale (HADS), Athens insomnia scale (AIS), pain disability assessment scale (PDAS), pain self-efficacy questionnaire (PSEQ) for the patients and Zarit Burden Interview (ZBI) for their caregivers were evaluated. Participants were divided into 2 groups (L group ZBI = 24 points) and compared. Regression analyses were conducted to identify factors correlated with the ZBI scores. Compared to L group, H group showed significantly higher NRS and HADs depression scores, and lower PSEQ scores. In univariate regression analysis, ZBI scores were significantly correlated with NRS, PCS, HADS anxiety, HADS depression, PDAS and PSEQ. Multiple linear regression analysis revealed that ZBI scores were significantly correlated with PSEQ. The caregivers who perceived high caregiver burden had significantly higher patients' pain intensity, depression, and lower self-efficacy than those who perceived low caregiver burden. Caregiver burden correlated with the pain intensity, pain catastrophizing, anxiety, depression, disability, and self-efficacy of chronic pain patients. Among these factors, self-efficacy was the most negatively correlated with caregiver burden. Treatments focused on increasing self-efficacy for managing pain have the potential to reduce caregiver burden

Clinical Course before and after Cataract and Glaucoma Surgery under Systemic Infliximab Therapy in Patients with Behçet's Disease

www.karger.com/cop This is an Open Access article licensed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs 3.0 License (www.karger.com/OA-license), applicable to the online version of the article only. Distribution for non-commercial purposes only

A Tool Path Modification Approach to Cutting Engagement Regulation for the Improvement of Machining Accuracy in 2D Milling With a Straight End Mill

In two-dimensional (2D) free-form contour machining by using a straight (flat

Mechanical stretch increases CCN2/CTGF expression in anterior cruciate ligament-derived cells

Anterior cruciate ligament (ACL)-to-bone interface serves to minimize the stress concentrations that would arise between two different tissues. Mechanical stretch plays an important role in maintaining cell-specific features by inducing CCN family 2/connective tissue growth factor (CCN2/CTGF). We previously reported that cyclic tensile strain (CTS) stimulates alpha 1(I) collagen (COL1A1) expression in human ACL-derived cells. However, the biological function and stress-related response of CCN2/CTGF were still unclear in ACL fibroblasts. In the present study, CCN2/CTGF was observed in ACL-to-bone interface, but was not in the midsubstance region by immunohistochemical analyses. CTS treatments induced higher increase of CCN2/CTGF expression and secretion in interface cells compared with midsubstance cells. COL1A1 expression was not influenced by CCN2/CTGF treatment in interface cells despite CCN2/CTGF stimulated COL1A1 expression in midsubstance cells. However, CCN2/CTGF stimulated the proliferation of interface cells. Our results suggest that distinct biological function of stretch-induced CCN2/CTGF might regulate region-specific phenotypes of ACL-derived cells

Lamivudine treatment in patients with HBV-related hepatocellular carcinoma--using an untreated, matched control cohort.

Lamivudine is widely used to treat patients with hepatitis B. However, the outcomes in patients with hepatocellular carcinoma (HCC) treated with lamivudine have not been established. This study was conducted to evaluate the outcomes of lamivudine treatment for patients with HCC using an untreated, matched control group. Thirty patients with controlled HCC orally received lamivudine. As controls, 40 patients with HCC who were not treated with lamivudine and matched for clinical features were selected. The lamivudine-treated and untreated groups were compared with respect to changes in liver function, HCC recurrence, survival, and cause of death. In the lamivudine-treated group, there was significant improvement in the Child-Pugh score at 24 months after starting treatment, while no improvement was observed in the untreated group. There was no significant difference in the cumulative incidence of HCC recurrence and survival between the groups. However, there was a significant difference in the cumulative incidence of death due to liver failure (P= 0.043). A significant improvement in liver function was achieved by lamivudine treatment, even in patients with HCC. These results suggest that lamivudine treatment for patients with HCC may prevent death due to liver failure. Further prospective randomized studies using a larger number of patients are required.</p