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Biomedical subjects

F Umeda

Publications and source records attributed to F Umeda.

At least 73 records · Page 4Linked to original sources
PubMed1995

Ectodermal dysplasia syndrome in siblings with true keloids, stenosis of the esophagus after operations for congenital achalasia and renovascular hypertension due to stenosis of renal artery.

Ectodermal dysplasia syndrome (EDS) is a rare hereditary disease, with symptoms brought about by dysplasia of ectodermal tissue (such as skin, teeth, nails, and hair). This report details the cases of two siblings (41 and 43 year old sisters) with autosomal recessive and hydrotic EDS complicated by esophageal achalasia, postoperative stenosis of esophagus, true keloids, renovascular hypertension, incomplete malrotation of the bowel, and demyelination of the brain.

Adult↗
PubMed1995

[Enteroglucagon].

Explore the source record for details and available documents.

Glucagon-Like Peptides↗
PubMed1995

Immunohistochemical localization of a novel peptide, prostacyclin-stimulating factor (PSF), in human tissues.

In a recent study, we purified and cloned a newly identified bioactive factor that stimulates prostacyclin (PGI2) production by vascular endothelial cells (ECs) using conditioned medium (CM) from cultured human diploid fibroblast cells. The present study was undertaken to clarify whether PSF is expressed in ECs and vascular smooth muscle cells (SMCS) of human tissues at a protein level. In an immunohistochemical study of seven human autopsy cases, all arteries in all lungs (n = 4) and kidneys (n = 6) examined stained positive to variable extents for PGI2-stimulating factor (PSF). PSF was predominantly expressed by SMCs in the media of small arteries. Staining for PSF was weaker in SMCs of aortic media (n = 3) and strong in SMCs of vaso vasorum (n = 3). PSF staining was also found in the SMCs of human bronchi (n = 4). Immunoblot analysis confirmed that PSF is present in CM from cultured bovine aortic SMCS.

Adult↗
PubMed1994

Human fibroblast cells produce a factor that stimulates prostacyclin synthesis by vascular endothelial cells.

The prostacyclin (PGI2) produced by vascular endothelium plays a key role in maintaining vascular homeostasis. The present study demonstrated that the conditioned medium (CM) of human diploid fibroblast cells contained PGI2-stimulatory activity (PSA) for bovine aortic endothelial cells (BAEC) and human umbilical vein endothelial cells (HUVEC). CM significantly stimulated the production of 6-keto-PGF1 alpha, a stable PGI2 metabolite, by both cultured BAEC and HUVEC in a concentration-dependent manner. Since the factor responsible for the PSA seemed to be negatively charged, PSA was partially purified using a DEAE-5PW high performance liquid chromatography column. The partially purified PSA was completely inhibited by preincubation with 15 microM indomethacin, a cyclooxygenase inhibitor. However, partially purified PSA was partially inhibited by preincubation with 50 microM mepacrine, a phospholipase A2 inhibitor. These findings suggest that PSA stimulates preferentially cyclooxygenase relative to phospholipase A2 in vascular endothelial cells. The partially purified PSA showed no effect on thromboxane A2 production by human washed platelets, and had no growth-promoting activity on BAEC. We conclude that cultured human fibroblast cells produce factor that stimulate the synthesis of prostaglandin by vascular endothelial cells but not by platelets.

Animals↗
PubMed1994

Purification and molecular cloning of prostacyclin-stimulating factor from serum-free conditioned medium of human diploid fibroblast cells.

We attempted to identify the factor that stimulated prostacyclin (PGI2) production using conditioned medium from cultured human diploid fibroblast cells subjected to a series of purification steps using h.p.l.c. on DEAE-5PW, Heparin-5PW, Protein-Pak 300, and an insulin-like growth factor-1 ligand affinity column. The purified prostacyclin-stimulating factor (PSF) ran as a single band with a molecular mass of 31 kDa by SDS/PAGE. Analysis of the purified PSF by C4 reversed-phase h.p.l.c. showed a single sharp peak in 31% (v/v) acetonitrile. The material was purified 8000-fold with an overall yield of about 18%. The purified PSF stimulated PGI2 production by cultured bovine aortic endothelial cells at a concentration of about 10 ng/ml; maximal stimulation was achieved at a concentration of 25 ng/ml. A cDNA coding for PSF was cloned and sequenced, revealing an apparently novel protein with no obvious sequence similarity to known proteins.

Amino Acid Sequence↗
PubMed1994

Expression of prostacyclin-stimulating factor, a novel protein, in tissues of Wistar rats and in cultured cells.

We recently purified and cloned a newly identified PGI2-stimulating factor (PSF). In the present study, we examined the PSF expression in the tissues of Wistar rats and in cultured cells, such as fibroblast cells (FCs), endothelial cells (ECs), and smooth muscle cells (SMCs). The expression of PSF was observed in many tissues of Wistar rats, such as brain, lung, liver, kidney, skeletal muscle, and fat tissue. Especially, lung and kidney showed a greater expression than the other tissues. PSF was also expressed in cultured FCs, ECs, and SMCs. These results indicate that PSF is conserved over species, suggesting that PSF plays a significant role in regulating PGI2 production.

Animals↗
PubMed1994

Insulin treatment improves relative hypersecretion of amylin to insulin in rats with non-insulin-dependent diabetes mellitus induced by neonatal streptozocin injection.

The dissociated release of insulin and amylin in the hyperglycemic state has been reported. This relative hypersecretion of amylin is thought to provide an important insight into how amylin aggregates to form islet amyloid deposits in non-insulin-dependent diabetes mellitus (NIDDM). The aim of the present study was to characterize the alterations of amylin hypersecretion in NIDDM with exacerbation or amelioration of diabetic control. For this purpose, neonatally streptozocin (nSTZ) diabetic rats were treated with dexamethasone (0.25 mg/kg) or Lente insulin (3 to 5 U/kg) daily for 14 days, and responses of amylin and insulin to 16.7 mmol/L glucose or 10 mmol/L arginine were evaluated in vitro using an isolated perfused pancreas system. nSTZ rats exhibited moderate elevations of plasma glucose compared with normal rats. In the isolated perfused pancreas, the molar ratio of secreted amylin to insulin in response to 16.7 mmol/L glucose by nSTZ pancreas (1.8% +/- 0.2%) was significantly greater than that of normal rat pancreas (1.2% +/- 0.1%). Plasma glucose levels in nSTZ rats (7.3 +/- 0.4 mmol/L) increased with dexamethasone treatment (17.8 +/- 1.1 mmol/L, P < .005) and decreased with insulin treatment (5.8 +/- 0.4 mmol/L, P < .05). The secreted amylin to insulin ratio in dexamethasone-treated nSTZ rats was significantly greater than that of the controls (P < .05). Moreover, insulin-treated nSTZ rats exhibited decreased amylin to insulin molar ratios compared with saline-treated nSTZ rats (P < .05), which had the same levels as normal rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Amyloid↗
PubMed1994

Correlation of peripheral nerve fatigue following vibratory stimulation with hyperglycemia in diabetic patients.

To determine whether the vibratory perception threshold (VPT) was altered in patients with diabetes, we measured this parameter after 5 min of conditioning vibration in 59 patients with non-insulin-dependent diabetes mellitus (NIDDM), with (n = 36) and without clinical neuropathy (n = 23). Thirty-seven healthy volunteers served as controls. VPT in the diabetic patients was significantly correlated with fasting plasma glucose (FPG) level, but not with age. Although VPT increased in all three groups, the increase disappeared completely within 5 min in controls, but was sustained for over 5 min in the diabetic groups. delta-VPT, the difference between VPT 10 s after activation and the baseline VPT, was significantly larger in the diabetic groups than in the control group, and in diabetic patients, was closely correlated with FPG, but not baseline VPT or age. These findings indicate that VPT is markedly increased in diabetic patients following repetitive vibratory cutaneous stimulation and does not recover easily, perhaps as a result of defects in peripheral nerve excitability linked to glycemic control.

Adult↗
PubMed1994

[Conjugal transfer of chemolithoautotrophically growing ability from hydrogen-oxidizing bacterium Alcaligenes hydrogenophilus to useful material-producing bacteria].

The plasmid genes encoding the ability to grow chemolithoautotrophically with H2 and CO2 from a H2-oxidizing bacterium Alcaligenes hydrogenophilus were in vivo cloned using the broad host range Inc P1 R-plasmid R68.45. The genes of H2-oxidation enzymes were expressed by a novel alternative sigma 54-like factor encoded on the chromosome. The sigma 54-like factor was also in vivo cloned using R68.45. Both R68.45-primes, one carrying plasmid genes and the other carrying chromosome genes, were in vivo recombined and a recombinant plasmid carrying both genes from plasmid and chromosome was obtained. The conjugal transfer of chemolithoautotrophically growing ability was carried out using the resulting recombinant plasmid. Seventeen bacterial strains, including useful material-producing bacteria, grew up to be able to grow with H2 and CO2 as the H2-oxidizing bacteria. Some patent strains registered for the production of antibiotics were ascertained to produce some products which inhibited the growth of the testing-bacteria, under not only heterotrophic conditions but also chemolithoautotrophilic conditions. The results obtained in our studies will be available in the future research for the production of useful material from CO2.

Alcaligenes↗
PubMed1994

Catechol estrogens are more potent antioxidants than estrogens for the Cu(2+)-catalyzed oxidation of low or high density lipoprotein: antioxidative effects of steroids on lipoproteins.

In order to clarify the mechanism of antiatherogenic action of several steroids such as estrogens, dehydroepiandrosterone (DHEA) and dexamethasone, we investigated the effects of various steroids on the copper (Cu2+)-catalyzed oxidation of low density lipoprotein (LDL) or high density lipoprotein (HDL) in 0.15 M NaCl by measuring thiobarbituric acid-reactive substances (TBARS). At a concentration of 10(-5) M, estrogens strongly protected against LDL oxidation by 0.5 microM Cu2+ in the following order of inhibition: estradiol (E2) (75%), estrone (E1) (35%) and estriol (E3) (30%). However, the corresponding metabolites of these estrogens, the catechol estrogens, had an even more protective effect on LDL oxidation by 0.5 microM Cu2+ in the following order of inhibition: 2-hydroxyestradiol (2-OHE2) (98%), 2-OHE1 (97%) and 2-OHE3 (96%). E2 and 2-OHE2 from 10(-7) M to 10(-5) M inhibited LDL oxidation in a dose-dependent manner, with a more marked effect for oxidation by 0.1 microM Cu2+ than by 0.5 microM Cu2+. 10(-5) M dexamethasone produced a slight (10%) but significant inhibition of LDL oxidation by 0.5 microM Cu2+. In addition, the estrogens and catechol estrogens were also effective in protecting against HDL oxidation by 0.5 microM Cu2+. Other steroids including DHEA and DHEA-sulfate had no antioxidative effects on either LDL or HDL in this system. These results indicate that estrogens and their metabolites, the catechol estrogens, exert antioxidative effects on both LDL and HDL. The catechol estrogens may be more important antioxidants than estrogens for both LDL and HDL.(ABSTRACT TRUNCATED AT 250 WORDS)

Antioxidants↗
PubMed1994

Normalization of diacylglycerol-protein kinase C activation by vitamin E in aorta of diabetic rats and cultured rat smooth muscle cells exposed to elevated glucose levels.

Hyperglycemia and diabetes have been shown to increase diacylglycerol (DAG) level and activate protein kinase C (PKC) activity in the vascular tissues, possibly altering vascular function. We have characterized the effects of D-alpha-tocopherol (vitamin E) on PKC activities and DAG levels in rat aortic smooth muscle cells (ASMCs) cultured with elevated glucose levels as well as in the vascular tissues obtained from control and diabetic rats. In ASMCs, the specific PKC activity from the membraneous fraction and total DAG level were increased by 31 +/- 4% (P < 0.05) and 50 +/- 7% (P < 0.05), respectively, when the glucose levels were changed from 5.5 to 22 mmol/l. The addition of D-alpha-tocopherol and another lipophilic antioxidant, probucol, prevented the glucose-stimulated increases in DAG level and PKC activity. By immunoblotting studies, D-alpha-tocopherol treatment was able to reduce the enhancement of PKC beta II isoform in the membraneous fraction isolated from ASMCs. Comparing streptozotocin-induced diabetic rats with their nondiabetic controls, both membraneous-specific PKC activities and total cellular DAG levels were increased in aorta by 162% (P < 0.05) and 60% (P < 0.05), respectively. Intraperitoneal injection of D-alpha-tocopherol (40 mg/kg) every other day prevented the increases in membraneous-specific PKC activities and total DAG levels in parallel with a significant increase of D-alpha-tocopherol contents in the aorta and plasma. These findings have demonstrated that D-alpha-tocopherol can prevent the activation of PKC activities in the vascular cells and tissues induced by hyperglycemia by lowering DAG levels, possibly via its antioxidant effect.

Animals↗
PubMed1994

Utility of Albusure test in screening for early stage of diabetic nephropathy.

All diabetic patients should be screened for the early stage of diabetic nephropathy, because microalbuminuria has a great prognostic significance. The albusure test (AT), alatex agglutination nephelometric immunoassay, is a rapid and low cost test for the detection of microalbuminuria of 30 mg/L or more. We compared the results of AT and of radioimmunoassay (RIA) for urinary albumin to evaluate the clinical utility of AT using fresh urine samples from 74 diabetic patients without persistent proteinuria and from 11 healthy subjects. Urinary albumin levels measured by RIA were 6.0 +/- 2.3 mg/L in the healthy subjects, 11.0 +/- 8.7 mg/L in the AT-negative group (n = 61), and 38.1 +/- 10.2 mg/L in the AT-positive group (n = 13). Using a cut-off value of 30 mg/L by RIA, the rate of coincidence between AT and RIA was 89.2%, although five subjects were false-positive by AT, and three were false-negative. These results show that AT may provide a useful monitor microalbuminuria, a reliable early mark of diabetic nephropathy.

Adult↗
PubMed1994

[A case of syndrome X whose hyperglycemia, hyperlipidemia and hypertension were improved as accompanying with decreased insulin resistance].

A 60-year-old man was admitted to the Kyushu University Hospital because of poor glycemic control of diabetes mellitus. Although he had been treated with glicrazide and nifedipine for his diabetes and hypertension, the controls of the diseases were unsatisfactory. Plasma triglyceride level was 186 mg/dl. Furthermore, extreme insulin resistance was found by measuring glucose infusion rate with an euglycemic hyperinsulinemic clamp method. These findings were compatible to those seen in syndrome X. After admission, diet therapy of 1,800 Cal was started and his metabolic disorders such as hyperglycemia, hyperlipidemia, and hypertension were all improved. Moreover, euglycemic hyperinsulinemic clamp study also revealed a decreased insulin resistance after diet therapy. Our experience from the case suggested that insulin resistance may closely related with the metabolic disorders of the disease "syndrome X".

Diet, Reducing↗
PubMed1994

[Etiology and molecular biology of hyperproinsulinemia].

Clinical hyperproinsulinemia occurs not only in familial hyperproinsulinemia, but also in insulinoma, renal failure, and even in non-insulin-dependent diabetes mellitus (NIDDM). The etiology of hyperproinsulinemia is divided into (1) abnormality of pro-insulin molecules, (2) abnormality of pancreatic beta-cells other than proinsulin molecules, (3) retardation of proinsulin clearance. Hyperproinsulinemia is now thought to be both a result of the above-mentioned diseases and a cause of atherosclerosis in patients with NIDDM. Recent developments in molecular biology have deepened our knowledge of the biosynthesis and role of proinsulin, especially the prohormone sorting mechanism into secretory granules in pancreatic beta-cells.

Animals↗
PubMed1994

A point mutation in the bile acid biosynthetic enzyme sterol 27-hydroxylase in a family with cerebrotendinous xanthomatosis.

Cerebrotendinous xanthomatosis (CTX) is a rare familial disorder characterized by progressive neurological dysfunction, atherosclerosis, and xanthomas with sterol storage in the nervous system, vessels, and tendons. Increased serum cholestanol, derived from intermediates of cholesterol catabolism, may possibly be a major cause of the disease. An examination was made of the cDNA encoding cytochrome P450 sterol 27-hydroxylase (CYP27) in hepatic mitochondria, considered a defective enzyme inducing CTX, in a Japanese housewife afflicted with CTX and her family. The proposita and one of her brothers, who also had CTX symptoms and hypercholestanolemia, were found to be homozygotic, carrying a point mutation in the CYP27 gene at Arg104 (CGG) to Trp104 (TGG). The mutant position has a 100% conserved positive charge in all known vertebrate cytochrome P450s and even in bacterial cytochrome P450cam. The mother of the proposita and another brother were both free of CTX symptoms and were heterozygotic for the mutation, although their plasma cholesterol increased moderately. An increase in plasma cholestanol alone would, thus, not appear to be a direct cause of sterol storage in CTX, while CTX is strongly suggested to be caused by defects in both alleles of the CYP27 gene.

Aged↗
PubMed1993

Hypersecretion of amylin from the perfused pancreas of genetically obese (fa/fa) rats and its alteration with aging.

To evaluate the relationship between the development of obesity and the hypersecretion of amylin by the pancreas, we examined the effects of 16.7 mmol/L glucose and 10 mmol/L arginine on the secretion of amylin and insulin by isolated perfused pancreata from genetically obese (fa/fa) and lean (Fa/?) Zucker rats at 9, 18, and 54 weeks of age. Concentrations of amylin and insulin in the effluent were measured by radioimmunoassay (RIA). Pancreata of obese rats secreted greater amounts of amylin in response to 16.7 mmol/L glucose and 10 mmol/L arginine than did those of lean rats at all ages. The hypersecretion of amylin by obese rats was particularly marked at 18 weeks of age, when they showed the most rapid increase in body fat mass. This hypersecretion became obscure at 54 weeks of age, when obese rats showed the maximum body weight. The pattern of amylin release resembled that of insulin in all groups. However, the relative amount of amylin to insulin secreted following stimulation with 16.7 mmol/L glucose and 10 mmol/L arginine in obese rats exceeded that in lean rats at all ages. Differences in the secreted amylin to insulin molar ratios between obese and lean rats were significant when pancreata were stimulated with glucose at 18 weeks (obese, 1.23% +/- 0.05%; lean, 0.99% +/- 0.04%; P < .01), glucose at 54 weeks (P < .01), and arginine at 54 weeks (P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗