Impact of Fish Intake Frequency on Cardiovascular Disease-Specific Survival in Hemodialysis Patients.

Introduction: Cardiovascular disease (CVD) is the leading cause of death in hemodialysis patients (HPs). As a food source, fish contains both CVD-preventive and CVD-promoting fatty acids; however, there is no consensus on fish consumption as a preventive measure for CVD in HPs. This single-center longitudinal cohort study aims to assess the impact of fish intake frequency (FIF) per week on CVD in Japanese HPs.

A case of adrenal myelolipoma complicated with Prader-Willi syndrome.

Introduction: Prader-Willi syndrome is a congenital disorder that occurs in one in 10 000-30 000 children and is characterized by obesity, short stature, and intellectual disability.

Case Presentation: A 24-year-old male patient with Prader-Willi syndrome presented with an enlarged adrenal tumor. Computed tomography detected a well-defined mass.

Human skin gas profile of individuals with the people allergic to me phenomenon.

Recent studies have shown that some people claim that their skin gases provoke allergy-like reactions in people in their near vicinity. Such a phenomenon or symptom is called 'people allergic to me (PATM)'. Although numerous people suffer from PATM, the actual conditions are unknown.

Intake of New Zealand Blackcurrant Powder Affects Skin-Borne Volatile Organic Compounds in Middle-Aged and Older Adults.

Skin volatile organic compounds (VOCs) can cause body odor or reveal human disease and may result from lipid peroxidation or activity by skin bacteria. We examined the effect of intake of New Zealand blackcurrant (NZBC) powder for 77 skin VOCs in middle-aged and older adults in a crossover design. Fourteen adults (nine males, age: 55 ± 5 yrs) consumed NZBC powder for 7 days (6 g·day with 138.

Novel pi-expanded radialene macrocycles with inner cavity.

[structure: see text] Polyenyne macrocycles with pi-extended [9]- and [12]radialene frameworks have been synthesized. These radialenes exhibit restricted rotation of the aromatic rings, and the D3- and D4-symmetric structures in solutions have been determined by dynamic NMR. The macrocyclic radialenes bear small to medium inner cavities, and the small cavity of the pi-extended [9]radialene can incorporate a silver cation.

Possible involvement of atypical protein kinase C (PKC) in glucose-sensitive expression of the human insulin gene: DNA-binding activity and transcriptional activity of pancreatic and duodenal homeobox gene-1 (PDX-1) are enhanced via calphostin C-sensitive but phorbol 12-myristate 13-acetate (PMA) and Gö 6976-insensitive pathway.

Pancreatic and duodenal homeobox gene-1 (PDX-1) is a transcription factor which regulates the insulin gene expression. In this study, we tried to elucidate the role of PDX-1 in the glucose-induced transcriptional activation of the human insulin gene promoter in MIN6 cells. Electrophoretic mobility shift assay (EMSA) and chloramphenicol acetyltransferase (CAT) assay demonstrated that both DNA-binding activity and transcriptional activity of PDX-1 were increased with 20 mmol/l glucose more than with 2 mmol/l glucose.

Impact of natural IRS-1 mutations on insulin signals: mutations of IRS-1 in the PTB domain and near SH2 protein binding sites result in impaired function at different steps of IRS-1 signaling.

Insulin receptor substrate-1 (IRS-1) is one of the major substrates of insulin receptor tyrosine kinase and mediates various insulin signals downstream. In this study, we have examined the impact of three natural IRS-1 mutations identified in NIDDM patients (G971R, P170R, and M209T) on insulin signaling. G971R is located near src homology 2 protein binding sites, and P170R and M209T are located in the phosphotyrosine binding domain of IRS-1.

Molecular scanning of the insulin receptor substrate-1 (IRS-1) gene in Japanese patients with NIDDM: identification of five novel polymorphisms.

Since the insulin receptor substrate-1 (IRS-1) is the major substrate of the insulin receptor tyrosine kinase and has been shown to activate phosphatidylinositol (PI) 3-kinase and promote GLUT4 translocation, the IRS-1 gene is a potential candidate for development of non-insulin-dependent diabetes mellitus (NIDDM). In this study, we have identified IRS-1 gene polymorphisms, evaluated their frequencies in Japanese subjects, and analysed the contribution of these polymorphisms to the development of NIDDM. The entire coding region of the IRS-1 gene of 94 subjects (47 NIDDM and 47 control subjects) was screened by polymerase chain reaction-single stranded conformation polymorphism (PCR-SSCP) analysis.

Roles of insulin, guanosine 5'-[gamma-thio]triphosphate and phorbol 12-myristate 13-acetate in signalling pathways of GLUT4 translocation.

Insulin, guanosine 5'-[gamma-thio]triphosphate (GTP[S] and phorbol 12-myristate 13-acetate (PMA) trigger the translocation of Gl UT4 (type 4 glucose transporter; insulin-sensitive glucose transporter) from an intracellular pool to the cell surface. We have developed a highly sensitive and quantitative method to detect GLUT4 immunologically on the surface of intact 3T3-L1 adipocytes and Chinese hamster ovary (CHO) cells, using c-myc epitope-tagged GLUT4 (GLUT4myc). We examined the roles of insulin, GTP[S] and PMA in the signalling pathways of GLUT4 translocation in the CHO cell system.

Bradykinin enhances GLUT4 translocation through the increase of insulin receptor tyrosine kinase in primary adipocytes: evidence that bradykinin stimulates the insulin signalling pathway.

It has been suggested that bradykinin stimulates glucose uptake in experiments in vivo and in cultured cells. However, its mechanism has not yet been fully elucidated. In this study, the effects of bradykinin on the insulin signalling pathway were evaluated in isolated dog adipocytes.

Frequency of mutations of insulin receptor gene in Japanese patients with NIDDM.

To examine the prevalence of abnormalities in the insulin receptor structure gene in Japanese with non-insulin-dependent diabetes mellitus (NIDDM), a population of 51 patients with NIDDM was screened for mutations in this gene. Patient genomic DNAs of both alleles corresponding to 22 exons of the gene were amplified by polymerase chain reaction (PCR). The PCR products on pUC19 were sequenced.

Possible domains responsible for intracellular targeting and insulin-dependent translocation of glucose transporter type 4.

Translocation of the type 4 glucose transporter (GLUT4) to the cell surface from an intracellular pool is the major mechanism of insulin-stimulated glucose uptake in insulin-target cells. We developed a highly sensitive and quantitative method to detect GLUT4 immunologically on the surface of intact cells, using c-myc epitope-tagged GLUT4 (GLUT4myc). We constructed c-myc epitope-tagged glucose transporter type 1 (GLUT1myc) and found that the GLUT1myc was also translocated to the cell surface of Chinese hamster ovary cells, 3T3-L1 fibroblasts and NIH 3T3 cells, in response to insulin, but the degree of translocation was less than that of GLUT4myc.

Platelet-derived growth factor triggers translocation of the insulin-regulatable glucose transporter (type 4) predominantly through phosphatidylinositol 3-kinase binding sites on the receptor.

Insulin is the only known hormone which rapidly stimulates glucose uptake in target tissues, mainly by translocation to the cell surface of the intracellular insulin-regulatable glucose transporter (glucose transporter type 4, GLUT4). We have developed a cell line for direct, sensitive detection of GLUT4 on the cell surface. We have suggested that insulin-activated phosphatidylinositol (PI) 3-kinase may be involved in the signaling pathway of insulin-stimulated GLUT4 translocation.

Epidermal growth factor triggers the translocation of insulin-responsive glucose transporter (GLUT4).

In a novel cell line we developed for direct, sensitive detection of insulin-responsive glucose transporter (GLUT4) on the cell surface, we considered that insulin-activated phosphatidylinositol 3-kinase (PI 3-kinase) may be involved in the signaling pathway of insulin-stimulated GLUT4 translocation. We report here evidence that epidermal growth factor (EGF), which stimulates PI 3-kinase activity, also triggers GLUT4 translocation in Chinese hamster ovary (CHO) cells stably overexpressing the EGF receptor. The EGF-dependent GLUT4 translocation is possibly mediated by two independent pathways: one by PI 3-kinase and the other by protein kinase C (PKC); the PI 3-kinase-mediated pathway predominates.

The role of insulin in activation of two enhancers in the mouse GLUT1 gene.

We identified two enhancer elements of the mouse GLUT1 gene responsive to serum, growth factor, and oncogenes; the first enhancer element (enhancer-1) is located 2.7 kilobases upstream of the cap site of the gene, and the second one (enhancer-2) is located in the second intron of the gene (Murakami, T., Nishiyama, T.

Expression of the gene encoding the tyrosine kinase-deficient human insulin receptor in transgenic mice.

Defects in the insulin receptor (IR) in diabetic patients have been given much attention. To address the role of such defects, we generated a transgenic (TG) mouse carrying the cDNA encoding a tyrosine-kinase (TK)-deficient human IR (hIR), under the control of the native promoter. The TG mouse expressed the transgene (TG) mRNA in the liver, as identified in Northern blots.

Insulin-stimulated GLUT4 translocation is relevant to the phosphorylation of IRS-1 and the activity of PI3-kinase.

We examined the role of 185-kDa insulin receptor substrate-1 (IRS-1) and phosphatidylinositol 3-kinase (PI3-kinase) in the signaling pathway of insulin-stimulated GLUT4 translocation. We had already developed a novel cell line to detect GLUT4 on the cell surface, directly and sensitively (Kanai, F., Nishioka, Y.

Direct demonstration of insulin-induced GLUT4 translocation to the surface of intact cells by insertion of a c-myc epitope into an exofacial GLUT4 domain.

Stimulation of glucose transport is the main physiological effect of insulin in target tissues. This effect is linked to translocation of the GLUT4 glucose transporter from an intracellular pool to the cell surface. To elucidate the molecular mechanisms involved in this effect, we developed a simple direct sensitive method to detect GLUT4 immunologically on the cell surface.

Familial primary hyperparathyroidism: study of the pedigree in three generations.

The familial occurrence of primary hyperparathyroidism in which the proband is a 55-year-old man is reported. His 58-year-old sister and 40-year-old brother had undergone partial parathyroidectomy, and histological examination revealed hyperplasia in both cases. Their father and a daughter of the proband had a history of nephrolithiasis.

[An epidemiological study on relationship between life style and colorectal cancer].

In Kumamoto prefecture, 2,359 cases were diagnosed as colorectal cancer and operated in 5 years from 1983 to 1987. Their records were analysed to determine the annual incidences in the cecum, ascending, transverse, descending, sigmoid colon and rectum. The female age-adjusted mortality from cancer of the cecum and ascending colon was slightly surpassed that of the male's.