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Biomedical subjects

Y Kobayashi

Publications and source records attributed to Y Kobayashi.

At least 343 records · Page 19Linked to original sources
PubMed2000

Reduced expression of DMAHP/SIX5 gene in myotonic dystrophy muscle.

In myotonic dystrophy (DM), the expansion of CTG triplet repeats in the 3'-untranslated region of DM-protein kinase (DMPK) is a causal gene mutation. However, the pathogenic molecular mechanism of CTG repeat expansion for DM phenotypic expression is unclear. To investigate this issue, we examined the influence of CTG repeat expansion on the expression levels of DMPK gene and 3'-flanking DM locus-associated homeodomain protein (DMAHP)/SIX5 gene in the muscles of DM patients. We isolated RNA from muscle tissues of six DM patients and six controls, and performed a competitive reverse transcriptional polymerase chain reaction (RT-PCR) assay. The total mRNA level of DMAHP/SIX5 was significantly lower in DM than in controls, but the DMPK mRNA level was unchanged. Our results suggest that CTG repeat expansion influences the expression of genes other than DMPK to cause the DM phenotype.

Adult↗
PubMed2000

The skirt technique: A stenting technique to treat a lesion immediately proximal to the bifurcation (pseudobifurcation).

We report a new stenting technique employed in 10 patients to treat lesions immediately proximal to a bifurcation (pseudobifurcation). A stent is mounted on two balloon catheters and advanced into the lesion immediately proximal to the bifurcation until the distal portion of the balloon catheters enters each branch at the bifurcation. This is followed by kissing balloon inflation for stent deployment. In all 10 cases, the final angiogram showed a good result at the lesion site and no ostial compromise of any of the branches. Cathet. Cardiovasc. Intervent. 51:347-351, 2000.

Aged↗
PubMed2000

Regulation of intestinal glucose transport by tea catechins.

Intestinal glucose uptake is mainly performed by its specific transporters, such as SGLT 1, GLUT 2 and 5 expressed in the intestinal epithelial cells. By using human intestinal epithelial Caco-2 cells we observed that intestinal glucose uptake was markedly inhibited by tea extracts. While several substances in green tea seem to be involved in this inhibition, catechins play the major role and epicatechin gallate (ECg) showed the highest inhibitory activity. Since our Caco-2 cells did not express enough amount of SGLT 1, the most abundant intestinal glucose transporter, the effect of ECg on SGLT 1 was evaluated by using brush border membrane vesicles obtained from the rabbit small intestine. ECg inhibited SGLT 1 in a competitive manner, although ECg itself was not transported via the glucose transporters. These results suggest that tea catechins could play a role in controlling the dietary glucose uptake at the intestinal tract and possibly contribute to blood glucose homeostasis.

Animals↗
PubMed2000

Transient infiltration of neutrophils into the thymus in association with apoptosis induced by whole-body X-irradiation.

Generally, the process of apoptosis does not cause leakage of noxious cytosolic contents and is therefore non-inflammatory. However, as previously shown, macrophages ingesting apoptotic CTLL-2 cells produced pro-inflammatory cytokines, particularly interleukin-8 (IL-8) and macrophage inflammatory protein-2 (MIP-2), a murine IL-8 homolog. This predicted that rapid and massive apoptosis may induce neutrophil accumulation in vivo. In this study, we tested this prediction by inducing apoptosis by whole-body X-irradiation in mice. After exposure to 4 Gy X-ray irradiation, mice exhibited considerable apoptosis of thymic cells, which was associated with transient infiltration of neutrophils as well as MIP-2 mRNA expression. In contrast, in p53-deficient mice in which irradiation-induced apoptosis was suppressed, as has been reported, infiltration of neutrophils into the thymus was less than that found in p53+/+ mice. Taken together, these results suggest that massive and rapid apoptosis can result in infiltration of neutrophils.

Animals↗
PubMed2000

Liver-infiltrating T lymphocytes are attracted selectively by IFN-inducible protein-10.

We have demonstrated that interferon-inducible protein-10 (IP-10) is produced in hepatocytes surrounded by infiltrative mononuclear cells in chronic hepatitis. To clarify the role of IP-10 in hepatitis, we examined the chemoattractive activity of IP-10 on liver-infiltrating lymphocytes in experimental animal models of hepatitis. IP-10 was specifically induced in the livers of mice treated intravenously (i.v.) with Con A, while monocyte chemotactic protein-1 (MCP-1) showed a much lower level of induction and neither RANTES nor macrophage inflammatory protein-1alpha (MIP-1alpha) was detected. The liver-infiltrating lymphocytes in Con A-induced hepatitis were attracted only by IP-10, and not by other chemokines such as RANTES, MCP-1 and MIP-1alpha. The chemoattractive effect of IP-10 was dose-dependent and was neutralized by monoclonal antibodies to IP-10. The specific effect of IP-10 on liver-infiltrating lymphocytes was also seen on those obtained from rat livers with fulminant hepatitis induced by sequential treatment with killed Propionibacterium acnes (P. acnes) and LPS. Peripheral blood lymphocytes were slightly attracted by IP-10 as well as RANTES and MIP-1alpha, while hepatic resident lymphocytes were not. On the other hand, thioglycolate-elicited peritoneal macrophages did not respond to IP-10, although they did show a response to RANTES, MCP-1 and MIP-1alpha. These results indicated that IP-10 is a specific chemoattractant for T lymphocytes in the inflammatory liver tissues and may play a specific role in the development of hepatitis.

Animals↗
PubMed2000

Serum levels of ifn-inducible PROTEIN-10 relating to the activity of systemic lupus erythematosus.

IFN-inducible protein-10 (IP-10) is supposed to act as a specific chemoattractant for Th(1)cells. Since Th(1)cells and IFN-gamma are shown to be important for developing systemic lupus erythematosus (SLE), we examined the relationship between serum IP-10 levels and the disease activity. Serum IP-10 levels were markedly increased in the SLE patients depending on the level of disease activity, whereas not in the patients with rheumatoid arthritis (RA). On the other hand, serum MCP-1 levels were increased to a similar extent both in RA and inactive SLE patients, and a little more elevated in active SLE patients. Serum IP-10 levels in SLE patients correlated positively and negatively with levels of anti-DNA antibody and complements, respectively, whereas MCP-1 levels correlated less or not at all. These results suggest that serum IP-10 levels could be a good indicator for the activity of SLE and that IP-10 could play an important immunological role in SLE.

Adolescent↗
PubMed2000

c-myc overexpression is not mandatory in aggressive-phase multiple myeloma with Burkitt's type translocation.

This report concerns a case of aggressive-phase multiple myeloma (AGMM) with Burkitt's type translocation t(8;14)(q24;q32), detected by Giemsa-banding. Double-color fluorescence in situ hybridization identified the breakpoint on 8q24 at a comparatively centromeric site, which was at least 300 kb and possibly 600 kb distant from the c-myc coding region. The breakpoint on 8q24 of the present case was far removed from that seen in other B-cell neoplasms with t(8;14)(q24;q32). Despite the presence of t(8;14)(q24;q32), neither rearrangement nor overexpression of the c-myc gene was observed in this case. Although our case may be a special case of multiple myeloma, it nevertheless suggests that overexpression of c-myc is not mandatory in an AGMM patient with Burkitt's type translocation. t(8;14)(q24;q32) which was seen in our case represents one of the first to be mapped at more than 300 kb 5' of c-myc. It should also be noted that this result could mean that a centromeric boundary 5' of c-myc exists where the influence of the immunoglobulin (Ig) H enhancer on c-myc transcription is not effective.

Aged↗
PubMed2000

Moyamoya disease associated with a brain stem glioma.

An 8-year-old boy was found to have primary moyamoya disease associated with a brain stem glioma. For over 3 years the child had experienced transient ischemic attacks induced by hyperventilation. One month before referral to our hospital he had presented with progressive left facial nerve palsy. Magnetic resonance imaging showed a cystic mass in the lower pons. Angiography revealed severe bilateral stenosis of the internal carotid arteries and prominent moyamoya vessels in the basal ganglia. Partial resection of the tumor yielded a histological diagnosis of pilocytic astrocytoma. Local radiation therapy reduced the size of the tumor. Anastomosis of the superficial temporal arteries and middle cerebral arteries on both sides was then performed. After direct bypass surgery, the patient remained in a good condition for a 5-year follow-up period. Clinical investigation of the coincidence of primary moyamoya disease and brain stem glioma led the authors to conclude that these two diseases coexisted independently.

Astrocytoma↗
PubMed2000

Intracytoplasmic hyaline inclusions in the hippocampal neurons of two cattle.

This report deals with the large intracytoplasmic hyaline inclusions observed in hippocampal large pyramidal cells of two Holstein-Friesian cattle. These inclusions were round to elongated polyhedral in shape with consistently homogeneous glassy appearance; they varied in size and were positive for the periodic acid-Schiff reaction and silver impregnation. Electron microscopic examination revealed that the inclusions consisted of granular materials showing moderate electron density and were bounded by a unit membrane. On the external surface of the unit membrane, there were direct connections to cellular organelles, including ribosome, rough endoplasmic reticulum, and mitochondria. These findings suggest that the inclusions might be derived from neuronal endoplasmic reticulum.

Animals↗
PubMed2000

Lithium activates mammalian Na+/H+ exchangers: isoform specificity and inhibition by genistein.

Replacement of external NaCl with LiCl induced cytoplasmic alkalinization in CCL-39 cells and rat L6 myoblasts expressing the endogenous Na+/H+ exchanger isoform NHE1. This Li+-induced alkalinization is due to activation of the Na+/H+ exchanger because it was completely inhibited by 100 microM ethylisopropylamiloride (apparent Kd=1 microM) and because it did not occur in exchanger-deficient PS120 cells. The effect of Li+ was not mimicked by Na+, K+, Cs+ and choline+. Li+ caused cytoplasmic alkalinization in PS120 cells expressing NHE1 or NHE2, but not NHE3, when Li+ was added to cells at a concentration high enough to saturate their external transport sites as predicted from Li+ affinities. Li+ did not induce phosphatidylinositol (PI) turnover or intracellular Ca2+ mobilization. Li+-induced alkalinization was not affected by protein kinase C down-regulation, loss of glycogen synthase kinase 3beta caused by antisense oligonucleotide treatment, or pretreatment with calphostin C, pertussis toxin, MEK inhibitor PD98059 and PI3-kinase inhibitor LY294002. However, it was markedly suppressed by the tyrosine kinase inhibitor genistein (10 microM). Thus, externally added Li+ activates NHE1 and NHE2 via a mechanism possibly involving a tyrosine kinase, causing an increase in cytoplasmic pH that could potentially affect various cell functions.

Alkalies↗
PubMed2000

Alterations of basement membrane in di-isopropanolnitrosamine-induced carcinogenesis of the rat thyroid gland: an immunohistochemical study.

Alterations of basement membrane (BM) in di-isopropanolnitrosamine (DIPN)-induced carcinogenesis of the rat thyroid gland were examined by means of immunohistochemical localization of collagen type IV (CN-IV), laminin (LN), and fibronectin (FN) in prenodular and nodular thyroid lesions, correlating with the morphogenesis and proliferative activity of these lesions. Adult male rats of the Wistar strain were injected s.c. in the back with DIPN, and the thyroid glands were removed at the 15th and 30th week of treatment. Each of 133 thyroid lesions was histochemically analyzed. The follicular epithelial BM as revealed by CN-IV and LN was discontinued or completely lost during the progression of thyroid lesions from pre-nodular to nodular lesions and finally overt carcinomas. At the same time, the BM of vascular endothelial cells demonstrated a loss of dense capillary networks of follicles, a sinusoidal dilatation and, predominantly in carcinomas, development of interstitial-type blood vessels. However, FN, which was hardly stained in the normal thyroid tissue, was remarkably deposited in the interstitium of invasive carcinomas. These observations strongly suggested that alterations of BM structure play a key role in the morphogenesis of rat thyroid tumors, and that the expression of FN is an important step in the invasive growth of thyroid tumors.

Animals↗
PubMed2000

Interferon treatment on glomerulonephritis associated with hepatitis C virus.

We report on a 10-year-old girl with glomerulonephritis associated with hepatitis C virus infection, who was treated with interferon-alpha. On the first renal biopsy at 8 years of age, mild mesangial hypercellularity in a segmental to semiglobal pattern was present in all glomeruli. After 6 months interferon-alpha therapy, proteinuria diminished completely. However, mesangial proliferation was advanced on the second biopsy at 10 years of age. We concluded that the interferon-alpha was effective in the treatment of proteinuria despite the lack of pathological improvement.

Antiviral Agents↗
PubMed2000

Association of systemic lupus erythematosus and hemolytic uremic syndrome in a child.

We describe a 10-year-old girl with systemic lupus erythematosus (SLE) who first presented with hemolytic uremic syndrome (HUS). Diagnoses were based on the classic HUS triad, including the observation of fragmented red blood cells, and on the American College of Rheumatology criteria for SLE. Plasma exchange may have been effective against both HUS and SLE in this patient, as it was associated with improvement of platelet counts, renal function, and serological findings.

Child↗
PubMed2000

A new variant of apolipoprotein E (apo E Maebashi) in lipoprotein glomerulopathy.

We have previously reported an 8-year-old girl with lipoprotein glomerulopathy. Assessment of serum apolipoprotein E (apo E) in this patient showed a discrepancy between phenotype and genotype, suggesting that she may have a variant of apo E. The present report concerns our analysis of DNA sequences of the apo E gene in the patient: nine base pairs were found to be deleted from exon 4. This mutation would appear to encode a new apo E variant lacking three amino acids. This variant may be associated with the pathogenesis of lipoprotein glomerulopathy.

Apolipoproteins E↗
PubMed2000

Recent advances in bilirubin metabolism research: the molecular mechanism of hepatocyte bilirubin transport and its clinical relevance.

Bilirubin is taken up from blood into hepatocytes by sinosuidal membrane transporters and then excreted into bile through the bile canalicular membrane mainly as bilirubin glucuronides. (1) Mechanism of bilirubin uptake into hepatocytes: many organic anions are incorporated into hepatocytes by organic anion transporting polypeptides (rat, oatp1, oatp2, oatp3; human, OATP), liver-specific transporter (rlst/HLST), and/or by organic anion transporters (OAT2, OAT3). Oatp1 and HLST transport bilirubin monoglucuronide. However, a transporter of unconjugated bilirubin in the sinusoidal membrane has not as yet been identified. Unconjugated bilirubin may also go across the hepatocyte sinusoidal membrane by a diffusion process. (2) Intrahepatic transport and conjugation of bilirubin: ligandin carries bilirubin to the endoplasmic reticulum (ER) of hepatocytes. In the ER, bilirubin is conjugated by bilirubin uridine diphosphate (UDP)-glycosyltransferase (bilirubin UGT; UGT1A1) to form mono- and diglucuronides of bilirubin. (3) Transport mechanism of bilirubin glucuronides across the hepatocyte canalicular membrane: at the canalicular membrane, bilirubin glucuronides are excreted into bile by multidrug resistance-associated protein 2 (MRP2), a member of the ATP-binding cassette transporter family. (4) Regurgitation of bilirubin glucuronides into blood: MRP3, which is located in the lateral membrane, transports bilirubin glucuronides into blood under conditions of impaired biliary bilirubin excretion.

Anion Transport Proteins↗
PubMed2000

Different subtypes of human lung adenocarcinoma caused by different etiological factors. Evidence from p53 mutational spectra.

Human lung adenocarcinomas are only relatively weakly associated with tobacco smoke, and other etiological factors need to be clarified. These may also vary with the histopathology. Because the p53 mutation status (frequency and spectrum) of a carcinoma can provide clues to causative agents, we subclassified 113 adenocarcinomas into five cell types: hobnail, columnar/cuboidal, mixed, polygonal, and goblet (54, 23, 18, 13, and 5, respectively) and investigated relationships with p53 mutations and smoking history. In the hobnail cell type, a low mutational frequency (37%) and a high proportion of transitions (65%), especially G:C to A:T transitions at CpG dinucleotides (45%) associated with spontaneous mutations, were found with a weak relation to tobacco smoke. In contrast, a high mutation frequency (70%) with a higher proportion of transversions (50%), especially G:C to T:A (44%) on the nontranscribed DNA strand, caused by exogenous carcinogenic agents like tobacco smoke, were observed for the columnar cell type, as with squamous cell carcinomas. These results indicate that two major subtypes of lung adenocarcinoma exist, one probably caused by tobacco smoke, and the other possibly due to spontaneous mutations. For the prevention of lung adenocarcinomas, in addition to stopping tobacco smoking, the elucidation of endogenous mechanisms is important.

Adenocarcinoma↗
PubMed2000

Heterologous enzyme immunoassay for serum androstenediol.

A heterologous enzyme immunoassay for serum androstenediol (Adiol: 3beta, 17beta-dihydroxy-androst-5-ene) was established. The combination of anti-Adiol antiserum raised in rabbit against Adiol 7-O-(carboxymethyl)oxime (Adiol 7-CMO) conjugated bovine serum albumin (Adiol 7-CMO-BSA) and Adiol 7-iminomethylcarboxylic acid conjugated alkaline phosphatase was used for the assay. The sensitivity of the heterologous assay system was superior to that of a homologous assay system in which an antibody raised in rabbit against Adiol 7-CMO-BSA and enzyme labeled antigen, Adiol 7-CMO conjugated alkaline phosphatase, were used. The minimal amount of Adiol detected was 0.4 ngml(-1) and the measurable range was from 0. 4 to 150 ngml(-1). Intra-assay coefficients of variation (C.V.) were 8.6% (1.52+/-0.13 ngml(-1), mean+/-S.D., n=10) and 6.7% (13.4+/-0.9 ngml(-1), n=10). Inter-assay C.V. were 12.9% (1.63+/-0.21 ngml(-1), n=8) and 11.5% (12.2+/-1.4 ngml(-1), n=8). A linear relation was observed between the serum sample dilution and the Adiol concentration. For recovery study, authentic Adiol was added to serum sample (original concentration: 1.43 ngml(-1)). The calculated final Adiol concentration was 2.99 ngml(-1). The recovery was 98.6% (n=5). The Adiol concentrations in healthy subjects measured by the proposed assay (male: 1.1+/-0.3 ngml(-1) (mean+/-S.D.), range: 0.7-1. 7 ngml(-1), age: 22-50, n=10; female: 0.6+/-0.4 ngml(-1), range: 0. 2-1.6 ngml(-1), age: 23-48, n=20) were consistent with reported values.

Adult↗