Cell Ca2+ response to luminal vasopressin in cortical collecting tubule principal cells

Cell Ca2+ response to luminal vasopressin in cortical collecting tubule principal cells. Although vasopressin V1 receptors have been shown to exist in both luminal and basolateral membranes of rabbit cortical collecting duct (CCD), exact cell types having V1 receptors remain unestablished. To identify the distribution of V1 receptor by cytoplasmic Ca2+ response, we utilized the confocal imaging system in the microperfused rabbit CCD. Basolateral application of arginine vasopressin (AVP) increased [Ca2+]i mainly in one group of cells which were not stained by fluorescein-isothiocyanate-conjugated peanut agglutinin. Luminal application of AVP increased [Ca2+]i in the same cells which responded to basolateral AVP. These findings provide evidence that V1 receptors, as defined by the [Ca2+]i response, exist in both luminal and basolateral membranes of the rabbit principal cell

Development of a New Geomaterial for Base Isolation Foundations

Design method of rational composite foundation capable of reducing seismic response of structures was studied. Analysis of the effects of damping materials on the reduction of seismic response of a full-scale structure was performed. Shaking experiment and seismic observation for model foundations confirming the damping effects were conducted and development of new damping material are described

Comparison of conservative treatment versus transcatheter arterial embolisation for the treatment of spontaneously ruptured hepatocellular carcinoma

Purpose: To elucidate the prognostic factors in the spontaneous rupture of hepatocellular carcinoma (HCC) and to determine whether transcatheter arterial embolisation (TAE) is associated with better prognosis compared to conservative treatment. Material and methods: A retrospective multicentre study was conducted involving 71 patients with spontaneous rupture of HCC. A conservative treatment group (Cons T group) included 20 patients, while a transcatheter arterial embolisation group (TAE group) included 51 patients. Results: The median survival time (MST) in the Cons T group was only 16 days and the survival rate was 39% at one month, whereas the MST in the TAE group was 28 days and the one month survival rate was 63%. However, there is no statistically significant difference in the overall survival between Cons T and TAE groups (p = 0.213). Multivariable analysis identified only the presence of distant metastasis as an independent prognostic factor (p = 0.023). A subanalysis including patients without distant metastasis showed that the presence of portal vein tumour thrombosis was a significant prognostic factor (p = 0.015). Conclusions: Distant metastasis appears to be a prognostic factor in spontaneous rupture of HCC. In cases without distant metastasis, portal vein tumour thrombosis could influence the prognosis. Our data failed to prove any benefit of TAE as the primary management

Transforming Growth Factor-β1 as a Common Target Molecule for Development of Cardiovascular Diseases, Renal Insufficiency and Metabolic Syndrome

Transforming growth factor-β1 (TGF-β1) is a polypeptide member of the transforming growth factor β superfamily of cytokines. It is a secreted protein that performs many cellular functions including control of cell growth, cell proliferation, cell differentiation and apoptosis. In the cardiovascular system, TGF-β1 plays pivotal roles in the pathogenesis of hypertension, restenosis after percutaneous coronary intervention, atherosclerosis, cardiac hypertrophy and heart failure. In addition, TGF-β1 has been shown to be increased in adipose tissue of obese subjects with insulin resistance. Furthermore, TGF-β1 is a potent initiator of proliferation of renal mesangial cells leading to chronic kidney disease. Some currently available agents can manipulate TGF-β1 expression leading to amelioration of cardiovascular diseases. Thus, an understanding of interactions between chronic kidney disease and metabolic syndrome and the development of cardiovascular diseases is an important issue, and attention should be given to TGF-β1 as a crucial factor for regulation and modulation of those pathological conditions

Negative regulation of hepatitis B virus replication by forkhead box protein A in human hepatoma cells

AbstractHepatitis B virus (HBV) replication is controlled by liver-enriched transcriptional factors, including forkhead box protein A (FOXA) members. Here, we found that FOXA members are directly and indirectly involved in HBV replication in human hepatic cells. HBV replication was elevated in HuH-7 treated with individual FOXA members-specific siRNA. Reciprocally, the downregulation of HBV replication was observed in FOXA-induced HuH-7. However, the mechanism of downregulation is different among FOXA members at the level of HBV RNA transcription, such as precore/pg RNA and 2.1kb RNA. In addition, FOXA1 and FOXA2 suppressed nuclear hormone receptors, such as HNF4α, that are related to HBV replication

Induction of microRNA-214-5p in human and rodent liver fibrosis

BACKGROUND: miRNAs are non-coding RNAs that regulate gene expression in a wide range of biological contexts, including a variety of diseases. The present study clarified the role of miR-214-5p in hepatic fibrogenesis using human clinical tissue samples, livers from rodent models, and cultured hepatic stellate cells. METHODS: The expression of miR-214-5p and genes that are involved in liver fibrosis were analyzed in hepatitis C virus-infected human livers, rodent fibrotic livers, a human stellate cell line (LX-2), and the cells from intact mouse livers using real-time PCR. The effect of miR-214-5p overexpression in LX-2 cells on cell function was investigated. Twist-1 expression in the liver tissues of mouse models and primary-cultured stellate cells was also analyzed. RESULTS: miR-214-5p was upregulated in human and mouse livers in a fibrosis progression–dependent manner. miR-214-5p expression increased during the culture-dependent activation of mouse primary stellate cells and was significantly higher in stellate cells than in hepatocytes. The overexpression of miR-214-5p in LX-2 cells increased the expression of fibrosis-related genes, such as matrix metalloproteinase (MMP)-2, MMP-9, α-smooth muscle actin, and transforming growth factor (TGF)-β1. TGF-β stimulation induced miR-214-5p in LX-2 cells. Twist-1 was increased in fibrotic mouse livers and induced during mouse stellate cell activation. CONCLUSION: miR-214-5p may play crucial roles in the activation of stellate cells and the progression of liver fibrosis. Twist-1 may regulate miR-214-5p expression in the liver, particularly in stellate cells