Biomedical subjects

M Endoh

Publications and source records attributed to M Endoh.

501 records · Page 28Linked to original sources

PubMedDate not supplied

Chronic experimental allergic encephalomyelitis in guinea pigs induced by proteolipid protein.

A chronic experimental allergic encephalomyelitis (EAE) was produced in Hartley guinea pigs with bovine white matter proteolipid protein (PLP), in which the levels of myelin basic protein (MBP) and galactocerebroside (GC) were less than 0.014% and 0.13%, respectively, by our method of purification. Cells of an MBP-specific T-cell line did not proliferate in the presence of 100 micrograms of PLP and antigen-presenting cells. Eleven animals were sensitized with 250 micrograms of PLP in Freund's complete adjuvant. Three guinea pigs developed paraplegia about 45 days after sensitization. Histological examination of the three animals revealed marked demyelinating lesions in the spinal cord, particularly in the dorsal columns and subpial regions of the lateral and anterior columns. Another guinea pig without apparent clinical symptoms had demyelinating plaques in the dorsal columns of the spinal cord and periventricular white matter of the brain. Antibodies to PLP were highly elevated in the animals with demyelinating plaques but antibodies to MBP and GC were not elevated in the serum samples. Skin response to PLP was positive in sensitized animals, but was not related to the clinical state. Since none of four strain 13 guinea pigs developed chronic EAE, it seems to be strain specific. These results suggest that PLP is encephalitogenic and produces demyelination in the central nervous system without contamination by MBP or GC in Hartley guinea pigs.

Animals↗

PubMedDate not supplied

Studies of experimental allergic encephalomyelitis in old mice.

In old BALB/c mice susceptibility to experimental allergic encephalomyelitis (EAE) with bovine proteolipid apoprotein (PLP) is reduced significantly. Eleven of 21 8-week BALB/c mice developed clinical signs of EAE following injection of PLP but only two of 18 12-month BALB/c mice and one of 19 24-month BALB/c mice showed clinical signs of EAE. Susceptibility to EAE induced by either PLP or bovine myelin basic protein (MBP) also was reduced in old SJL mice. However, the aging process had no effect on the clinical signs of EAE in both strains, if EAE appeared. Some old BALB/c mice developed histologic EAE with significant demyelination without clinical signs. Lymphocyte proliferative response to mitogens and antigens, and interleukin-2 (IL-2) production, also were depressed in the aged mice (24-month BALB/c and 18-month SJL) probably due to the functional defect of T cells, since the function of macrophages as antigen-presenting cells was not affected in the old mice. PLP-sensitized spleen cells (SPC) from 8-week mice were able to adoptively transfer EAE to young and aged recipients. PLP-sensitized T cells from 8-week mice, reconstituted with young or old monocytes, also were able to transfer EAE into young mice. In contrast, spleen cells from aged mice did not induce EAE, so the reduction of EAE susceptibility was mainly explained by the failure of T cell activity. This T cell defect was not restored by exogenous IL-2.

Aging↗

PubMedDate not supplied

Immunofluorescence staining of renal biopsy samples in patients with diabetic nephropathy in non-insulin-dependent diabetes mellitus using monoclonal antibody to reduced glycated lysine.

This is the first report on immunofluorescence staining of renal biopsy samples in human diabetic nephropathy (DN) using monoclonal antibodies to reduced glycated lysine. In order to detect the localization of glycated lysine in the mesangial matrix and/or the glomerular basement membrane (GBM), we examined immunofluorescence staining using antibodies against reduced glycated lysine in the glomeruli of 16 patients with DN and ten age-matched patients with diffuse mesangial proliferative glomerulonephritis without IgA deposition (DPGN) as controls. In the early stage of DN, immunofluorescence microscopy revealed the presence of intense staining for reduced glycated lysine in the GBM as well as in part of the tubular basement membrane, but not in the mesangial area. In contrast, immunofluorescence microscopy revealed less staining for glycated lysine in the GBM in the advanced stage of DN, and no reaction with any part of the renal tissue in patients with DPGN. It was concluded that detection of reduced glycated lysine in GBM in the early stage of DN might be associated with the initial pathogenesis of this disease.

Adult↗

PubMedDate not supplied

Immunohistochemical analysis of platelet-derived growth factor-B expression in myocardial tissues in hypertrophic cardiomyopathy.

Intimal and/or medial hyperplasia of intramyocardial small vessels is thought to be one of the causes of myocardial ischemia in hypertrophic cardiomyopathy (HCM). However, the pathogenesis of such vascular lesions in HCM is not yet known. To evaluate the pathogenic role of platelet-derived growth factor (PDGF-B) and basic fibroblast growth factor (b-FGF), which have a potential to induce cellular and molecular changes observed in the vessels in HCM, we examined the expression of these molecules and PDGF receptors in cardiac tissues from six patients with HCM and seven controls using immunohistochemistry. The percentage of PDGF-B positive cells in the myocyte population in HCM was significantly higher than that in controls (52.6 +/- 16.2 (mean +/- SD) vs. 21.6 +/- 9.6, p < 0.01). PDGF-B was also observed in vascular regions in HCM (61.1 +/- 25.5% of arterioles) but not in controls. There were no significant differences in the expression of b-FGF and PDGF receptors in the myocyte and non-myocyte populations and the vascular regions between the HCM and control groups. Our study revealed that the expression of PDGF-B protein was up-regulated in HCM, suggesting the contribution of this molecule to the development of intramyocardial vasculopathy.

Adolescent↗

PubMedDate not supplied

Expression of apoptosis in placentae from mice lacking the prostaglandin F receptor.

This study aimed to investigate the changes in apoptosis in the placenta and decidua of pregnant mice lacking the prostaglandin F receptor. Mouse placentae were removed from fetuses on days 10-23 of pregnancy. Apoptotic cells were examined by a DNA fragmentation assay and the terminal deoxynucleotidyl transferase-mediated dUDP nick end-labelling (TUNEL) technique. The placenta and decidual weight increased before day 18 and 14 of pregnancy, and then decreased with gestational day. After day 19, the fetuses gradually died in the uterus. All fetuses died in the uterus on day 23 of pregnancy. The number of apoptosis was not significantly different between wild type and FP-deficient mice before day 18 of pregnancy by DNA fragmentation and TUNEL staining. The DNA fragmentation was always more pronounced in decidual tissue on each day of pregnancy. DNA laddering on placentae was more extensive on day 22 than day 18. In placenta, most TUNEL-positive cells were detected in trophoblast and stromal cells. A higher intensity of apoptotic cells was in the decidual basalis. The main area was the centre of the decidual basalis, and was in decrease toward to margin of placenta. The index of TUNEL positive cells increased as gestation progressed toward termination. Especially, it was prominent in the placentae on day 22 compared with that day 18 of pregnancy. The increased TUNEL-positive staining in syncytiotrophoblast surface was found in placenta at post-term, compared with those at term. Apoptosis may provide insights into both normal placental development and placental dysfunction during an abnormal pregnancy from post-term pregnancy.

Animals↗

PubMedDate not supplied

Increase of IgA in pharyngeal washings from patients with IgA nephropathy.

The levels of IgA and total proteins in pharyngeal washings were examined in patients with IgA nephropathy and other glomerular diseases in order to determine whether secretory IgA, IgA1 and IgA2 were increased in these patients. Thirty patients with IgA nephropathy, 21 patients with other glomerular diseases and 15 healthy adults were examined. The levels of IgA were quantitated by radial immunodiffusion and laser nephelometry. The levels of total proteins in pharyngeal washings were quantitated by Tonein-TP. It was demonstrated that the levels of IgA in pharyngeal washings were significantly increased in patients with IgA nephropathy compared to those with other glomerular diseases and healthy adults. The levels of total proteins in pharyngeal washings were increased in patients with IgA nephropathy, and the ratio of IgA and total proteins in the washings from patients with IgA nephropathy was not significantly different from those healthy adults. There was a significant correlation between the levels of IgA in pharyngeal washings and those of IgA in sera from patients with IgA nephropathy. The IgA observed in pharyngeal washings contained secretory components, IgA1 and IgA2, in patients with IgA nephropathy. It is suggested that the increase of IgA in the pharyngeal washings in parallel with the increase of total proteins might be associated with local inflammation.

Humans↗

PubMedDate not supplied

Modification by islet-activating protein of direct and indirect inhibitory actions of adenosine on rat atrial contraction in relation to cyclic nucleotide metabolism.

Adenosine decreased the force of contraction of isolated rat left atria (direct action) and inhibited the positive inotropic action of isoproterenol (indirect action). The direct action of adenosine was not accompanied by changes in cyclic nucleotide levels, while the isoproterenol-induced increase in cyclic AMP level was reduced by the nucleoside. Reserpine pretreatment and pindolol did not affect the direct action of adenosine. Both the direct and indirect actions of adenosine were enhanced by dipyridamole and dilazep and inhibited by 1-methyl-3-isobutylxanthine and theophylline. Among adenosine derivatives, N6-phenylisopropyladenosine was most potent, and 2'-deoxyadenosine was least effective in inducing the negative inotropic action in the absence and presence of isoproterenol. In atria pretreated with islet-activating protein (IAP) both the direct and indirect actions of adenosine, and the actions of N6-phenylisopropyladenosine were markedly attenuated compared with those in nontreated atria. The isoproterenol-induced increase in cyclic AMP level was not reduced by adenosine in IAP-treated atria. These results indicate that adenosine produces a dual action on rat atria: it decreases the force of contraction directly by a mechanism independent of cyclic AMP metabolism, and inhibits the positive inotropic action of isoproterenol by reducing the drug-induced accumulation of cyclic AMP. IAP attenuates both of these inhibitory actions of adenosine on rat atria.

Adenosine↗

PubMedDate not supplied

Effects of nicorandil and its interaction with isoproterenol on force of contraction and cyclic nucleotide levels of canine atrial muscle: comparison with carbachol.

Experiments were carried out on isolated canine right atria to investigate the effects of N-(2-hydroxyethyl)nicotinamide nitrate (nicorandil, SG-75) and its interaction with beta-adrenoceptor stimulation on the cyclic nucleotide levels accompanying inotropic changes. The results were compared with those during muscarinic receptor stimulation. The effects of nicorandil were similar to those of carbachol insofar as its negative inotropic effect was accompanied by a significant elevation of cyclic GMP levels in the absence of beta-adrenoceptor stimulation. However, the effects of nicorandil differed strikingly from those of carbachol in that the negative inotropic action of nicorandil was readily counteracted by isoproterenol, while that of carbachol was not. This difference may be ascribed to differences in cyclic AMP metabolism caused by these agents: carbachol but not nicorandil decreased the isoproterenol-induced elevation of cyclic AMP levels. The negative inotropic effects of muscarinic receptor stimulation on canine atria are associated with two different sorts of changes in cyclic nucleotide metabolism, i.e., cyclic GMP elevation and cyclic AMP reduction; nicorandil mimics the former but not the latter process.

Animals↗

PubMedDate not supplied

Alpha-1-antichymotrypsin is not associated with the increased frequency of apolipoprotein-E-epsilon-4 allele in elderly non-demented leprosy patients.

In our previous study, elderly leprosy patients showed a low prevalence of senile dementia of the Alzheimer type, but the frequency of apolipoprotein E (APO-E) epsilon 4 was elevated in non-demented elderly leprosy patients. Recent study has shown that Alzheimer's disease risk associated with APO-E epsilon 4 is significantly increased by the alpha 1-antichymotrypsin (ACT) genotype AA. Therefore we examined an association between ACT polymorphism and the APO-E epsilon 4 allele in 350 leprosy patients. None of our data showed an association of ACT genotype and APO-E epsilon 4 allele in leprosy patients. The allelic frequencies of the ACT gene did not differ even between demented patients with leprosy and age-matched controls. Our present data suggest that ACT polymorphism is not associated with the increased frequency of APO-E epsilon 4 in leprosy patients.

Adult↗

PubMedDate not supplied

Cross-reactivity of eluted antibodies from renal tissues of patients with henoch-Schönlein purpura nephritis and IgA nephropathy.

A study on the specificity of antibodies eluted from renal biopsy specimens from patients with Henoch-Schönlein purpura (HSP) nephritis, IgA nephropathy and other glomerular diseases is described. The specimens were treated with citrate buffer, pH 3.2, and the 'eluate' was neutralized by sodium hydroxide. The 'eluate' was then applied to the acid-treated sections obtained from the same patients and from other patients with HSP nephritis as well as to the sections from patients with IgA nephropathy and other glomerular diseases. The sections were stained with FITC-labeled heavy-chain specific anti-human IgA antisera and then examined with a fluorescent microscope. It was demonstrated that the antibodies obtained from patients with HSP nephritis specifically recombined with the glomerular mesangial areas in patients with IgA nephropathy and vice versa, whereas they did not combine with renal tissues obtained from patients without IgA nephropathy. These antibodies did not show antimesangial activity since they did not react with normal glomeruli or nephritic glomeruli other than those from cases with HSP nephritis and/or IgA nephropathy. The specificity of IgA antibodies was confirmed by various tests using anti-human IgA antisera, human IgA myeloma protein, whole serum samples, human gamma-globulin absorbed with anti-human IgG and/or IgM antisera or clostral IgA. It is suggested that some common antigens may be involved in the development of HSP nephritis and IgA nephropathy.

Antibodies↗

PubMedDate not supplied

Detection of viral antigens in patients with IgA nephropathy.

Immunofluorescent analysis of viral antigens in the cultured fibroblasts and renal tissues in patients with IgA nephropathy was described. Freeze and thawed extracts of pharyngeal cells obtained from patients with IgA nephropathy, chronic proliferative glomerulonephritis without IgA deposition (PGN) and healthy adults were cultured with human fibroblasts, i.e. Hel cells, with or without addition of 5-iodine 2'-deoxy-uridine (IUDR) at 37 degrees C for 2 weeks. These fibroblasts and renal sections were stained with several kinds of FITC-labeled antiviral antibodies. Deposition of adeno, herpes simplex, varicella zoster or parainfluenza 3 was observed not only in the renal sections but also in the nuclear regions and/or cytoplasm of Hel cells after incubation of extracts of pharyngeal cells with or without IUDR from patients with IgA nephropathy. It is indicated that antigenic stimulation in the upper respiratory tracts may be due to several different types of DNA and/or RNA viruses in patients with IgA nephropathy. It appears that these antigenic substances show some heterogeneity among these patients.

Adenoviruses, Human↗

PubMedDate not supplied

Idiopathic acute interstitial nephritis associated with uveitis.

A case of acute interstitial nephritis associated with uveitis is presented, An 18-year-old man developed uveitis followed by renal dysfunction. Moderate renal dysfunction (sCr 3.0 mg/dl), and increased levels of urinary beta 2 microglobulin (over 8,000 micrograms/I) were observed. Renal tissue obtained by open renal biopsy revealed severe infiltration of mononuclear cells in the tubulo-interstitial area. The majority of infiltrating cells were CD4-positive T cells demonstrated by immunoperoxidase staining, suggesting the involvement of T cell-mediated delayed hypersensitivity. Corticosteroid was effective against both uveitis and renal dysfunction. The possible pathogenesis of this syndrome is reviewed from the literature.

Adolescent↗

PubMedDate not supplied

Abnormal glucose tolerance in patients with chronic glomerulonephritis without renal failure.

An oral glucose tolerance test and an assay of insulin receptor activity were performed in patients with chronic glomerulonephritis (CGN) to elucidate the aberration of glucose metabolism in such patients. Ninety of 123 patients with CGN without renal failure showed abnormal glucose tolerance, including 72.6% with IgA nephropathy, 81% with benign recurrent hematuria, 87% with chronic proliferative glomerulonephritis, 100% with membranoproliferative glomerulonephritis, and 80.0% with membranous nephropathy. Insulin responses in CGN patients during oral glucose tolerance tests showed lower levels of basal insulin and significantly higher levels after 90, 120, and 180 min compared with those of normal controls. The binding of radiolabeled insulin to blood mononuclear cells in 22 CGN patients with abnormal glucose tolerance was significantly (P = 0.0023) decreased in comparison with 5 normal controls. However, plasma obtained from such patients showed no significant (P = 0.4761) inhibition of the binding of insulin to normal mononuclear cells. It was concluded that glucose tolerance capacity was impaired in 80.4% of patients with CGN without renal failure. Such impairment of glucose metabolism might be due to decreased activity of insulin receptors on cells in CGN patients.

Adolescent↗

PubMedDate not supplied

Usefulness of redox tolerance test in evaluating fatty liver.

BACKGROUND/AIMS: In living-related liver transplantation, fatty liver should be exactly detected in the healthy donor with noninvasive measurement before the surgery. The study aimed to investigate the usefulness of redox tolerance test in diagnosing fatty liver. METHODOLOGY: The subjects were 32 patients who underwent an abdominal surgery. They did not show any abnormal values in biochemical evaluations, nor had they diabetes. Under informed consent, liver specimens were obtained intraoperatively, and the subjects were divided into three groups according to the degree of hepatic fatty deposit: group A has fatty deposits at less than 10% of hepatocytes (n = 12), group B showed the deposits at 10-30% (n = 10), group C has the deposits of more than 30% (n = 10). Before the surgery, redox tolerance test was performed as follows; arterial blood samples were obtained successively at 75 g oral glucose load over a 120-min period, and the arterial ketone body ratio and blood glucose level were determined. The ratio of increased arterial ketone body ratio (AKBR) to increased blood glucose (BG) level (100 x delta AKBR/delta BG) was calculated as redox tolerance index. RESULTS: After fasting state, arterial ketone body ratio and blood glucose level did not differ among the three groups. However, the values of redox tolerance index in groups B (0.73 +/- 0.08) and C (0.46 +/- 0.04) were significantly lower than those in group A (1.85 +/- 0.31). CONCLUSIONS: The redox tolerance test was exceedingly sensitive indicator for objectively diagnosing the fatty liver.

3-Hydroxybutyric Acid↗

PubMedDate not supplied

The effect of dialysate glucose on phagocyte superoxide generation in CAPD patients.

OBJECTIVE: In the present study, we investigated the influence of dialysate glucose on superoxide (O2-) generation by peripheral and peritoneal phagocytes in continuous ambulatory peritoneal dialysis (CAPD) patients. DESIGN: Peripheral polymorphonuclear leukocytes (PMNL) and mononuclear leukocytes (MNL), and peritoneal cells were isolated from peripheral blood and peritoneal effluents, respectively, and their oxidative metabolism was assessed by measuring O2- generation after stimulation with a soluble stimulant [phorbol myristate acetate (PMA), 1 mg/mL, Sigma Chemical, St. Louis, MO, U.S.A.] using the chemiluminescence method. Dialysate glucose effect on O2- generation was also studied in vitro by exposing peripheral PMNL and MNL from healthy controls to peritoneal dialysis fluid (PDF) containing glucose or amino acids at a neutral pH for different time periods. RESULTS: The amount of O2- generation by both peripheral and peritoneal phagocytes in CAPD patients was significantly higher than that in the control, and the response was greater in patients who were dialyzed with high glucose dialysate than those using low glucose dialysate. In an in vitro study, all incubated cells, except the control, showed suppression of O2- generation in the early dwell time (2 hr), and subsequently showed increased responses (peaking at 6 hr), although lower in degree than those observed in vivo. In contrast, amino acid-based PDF exhibited no such effect on O2- generation at identical pH with similar or lower osmolality. Furthermore, the respective increased or decreased oxidative responses with the increased or decreased PDF glucose concentrations in the same patient confirmed the positive effect of PDF glucose on phagocyte O2- generation. CONCLUSION: It is suggested that increased O2- generation by peritoneal and circulating phagocytes in CAPD patients is at least partly due to the enhancement of hexose monophosphate shunt activity by increasing glucose metabolism in phagocytes, and the increased O2- generation might be involved in long-term complications of CAPD. Therefore, a suitable alternative osmotic agent is needed to provide a more physiological environment to minimize the adverse effects of glucose on cell functions.

Adult↗