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H Ueda

Publications and source records attributed to H Ueda.

At least 289 records · Page 16Linked to original sources
PubMed1998

Meta-analysis of association of insertion/deletion polymorphism of angiotensin I-converting enzyme gene with diabetic nephropathy and retinopathy.

An insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene has repeatedly been shown to be associated with ischaemic heart disease, but the association of this genetic marker with diabetic microangiopathy is controversial. To assess the association of the genotypes with the development of diabetic nephropathy or retinopathy, we performed a meta-analysis of data from the literature, using Mantel-Haenszel method followed by the Breslow-Day test for assessing homogeneity among data. In a total of 4773 diabetic patients from 18 studies with (n = 2495) and without (n = 2278) renal complications, the D allele was significantly associated with diabetic nephropathy (p < 0.0001) in a dominant model (summary odds ratio 1.32, 95% confidence interval: 1.15 to 1.51). There was no significant evidence against homogeneity of the odds ratios (chi(2) = 18.9, 20 df; p = 0.53). The association was significant both in non-insulin-dependent (p < 0.005) and in insulin-dependent diabetes mellitus (p < 0.05). Likewise, in a total of 2010 diabetic patients with (n = 1008) and without (n = 1002) retinopathy, there was no association of the I/D polymorphism with diabetic retinopathy. These data suggest that the ACE I/D polymorphism affects the risk for diabetic nephropathy, but not for diabetic retinopathy.

Alleles↗
PubMed1998

Association of distal chromosome 2q with IDDM in Japanese subjects.

An insulin-dependent diabetes mellitus (IDDM)-susceptibility gene (IDDM13) has recently been mapped to a region of distal chromosome 2q, which is syntenic to the region of mouse chromosome 1 containing a murine susceptibility gene for IDDM, Idd5. To determine the contribution of this region to IDDM disease susceptibility further and to narrow the region for positional cloning of susceptibility genes, we have studied the association of distal chromosome 2q with IDDM in the genetically distinct Japanese population. A 137 mobility unit (mu) allele at D2S137 locus was significantly associated with IDDM (odds ratio 1.92, p = 0.0016). Other markers, D2S301 and D2S143, located in the same region were not associated with IDDM, indicating that IDDM13 is in linkage disequilibrium with D2S137, but not with D2S301 or D2S143. The association of D2S137 with IDDM was observed in patients lacking one of two high risk HLA alleles, DQBI*0303 and DQBI*0401, but not in patients with either of these alleles. The frequency of high risk HLA alleles was significantly lower in patients with the susceptible allele at D2S137, suggesting that IDDMI3 contributes to IDDM susceptibility in subjects without high risk genotypes at IDDM1. Demonstration of allelic association of D2S137 with IDDM localizes IDDM13 in the close vicinity (<2 centiMorgans) of D2S137, greatly facilitating fine structure mapping and positional cloning of IDDM13.

Adolescent↗
PubMed1998

Immunocytochemical study of lysosomal proteins with a new monoclonal antibody directed against epithelioid macrophages.

A monoclonal antibody, EPI-1, was produced against macrophages in epithelioid granulomas induced in rat foot pads by muramyl dipeptide. This EPI-1 antibody reacted to lysosome-like structures in epithelioid macrophages, peritoneal and pulmonary macrophages, and also in other tissues such as liver, testes, and kidneys. Western blot analysis of epithelioid granulomas, liver, testes, and kidneys revealed the same positive band of 62 kDa. Immunoelectron microscopic study of foot pad granulomas and hepatocytes demonstrated the EPI-1 antigen located in lysosomes and autophagic vesicles, preferentially along their membranes. These findings suggest that the EPI-1 antibody may recognize a novel antigen related to lysosomal membrane proteins in macrophages and other cells, which is useful for identifying lysosomes and their related structures.

Animals↗
PubMed1998

Hepatocyte nuclear factor-1alpha gene and non-insulin-dependent diabetes mellitus in the Japanese population.

Recently, hepatocyte nuclear factor-1alpha(HNF-1alpha, which is encoded by the TCF1 gene) mutations were reported in a subset of patients with maturity onset diabetes of the young (MODY3). We studied the contribution of TCF1 to genetic susceptibility to common non-insulin-dependent diabetes mellitus (type 2) in Japanese subjects by investigating allelic association with type 2 diabetes use of three markers. We also studied the frequency of the G191D mutation, the only mutation of TCF1 reported so far in late-onset type 2 diabetes. A total of 356 subjects were studied. There were no significant differences in allele frequency of the three markers between patients with type 2 diabetes and control subjects. A G191D mutation was not found in the subjects studied, giving a frequency of less than 0.4% in common type 2 diabetes. The lack of association of type 2 diabetes with three markers in and near TCF1 suggests that mutations in TCF1 derived from a limited number of founders are not a major cause of common type 2 diabetes even in the genetically homogeneous Japanese population. The data also indicate that the G191D mutation in TCF1 plays little, if any, role in susceptibility to common type 2 diabetes in the Japanese.

Adult↗
PubMed1998

Detection of human serum antibody to encapsulated strains of Staphylococcus aureus by enzyme-linked immunosorbent assay inhibition test.

A specific and rapid enzyme-linked immunosorbent assay (ELISA) inhibition test was employed for detection of immunoglobulins to Staphylococcus aureus (S. aureus) capsular polysaccharide in human serum. Cap-sular polysaccharide antigens obtained from Smith diffuse (capsular type 2), Reynolds (capsular type 5), or Becker (capsular type 8) strains of S. aureus were added to microplates coated with these strains. Seventy-four patients with open fractures (31 serum samples from those with staphylococcal infections, 10 serum samples from those with non-staphylococcal infections, and 33 serum samples from the non-infected group) and 28 serum samples from healthy controls were then added. The plates were incubated at 37 degreesC for 2 h and the ELISA was performed. The ELISA inhibition assay showed remarkable inhibition with the capsular type 2, 5, and 8 polysaccharides in the 33 serum samples from the non-infected group and in the 28 serum samples from the healthy controls, but low inhibition was observed with the 31 sera with staphylococcal infections. Positive immunoglobulin (Ig)G and IgM titers showed marked inhibition with this assay, but IgA titer were not seen in any samples. These results indicate that the quantitation of human serum antibody against S. aureus capsular polysaccharide by the ELISA inhibition assay is useful for the demonstration of protective activities against S. aureus.

Antibodies, Bacterial↗
PubMed1998

Lack of tolerance in peripheral opioid analgesia in mice.

We recently developed a sensitive peripheral analgesic test in mice. Bradykinin, a representative pain-producing substance, when given subcutaneously through a polyethylene tube into the plantar of the limb connected to a transducer, induced a flexor reflex response, in a dose dependent manner. When morphine, a mu-opioid receptor agonist, was added to the plantar through another polyethylene tube, bradykinin-induced responses were completely abolished in a naloxone-reversible manner. These peripheral analgesic effects were also observed with DAMGO, another mu-opioid receptor agonist, and U-69,593, a kappa-opioid receptor agonist, but not DSLET, a delta-opioid receptor agonist. When morphine was given subcutaneously to the back, a potent analgesia in the tail pinch test was observed. Repeated administrations of morphine once per day for 5 days showed a marked tolerance or reduction in morphine analgesia on the 6th day, while there was no significant reduction in the peripheral analgesia of morphine. These findings suggest that tolerance to morphine analgesia is mediated through synaptic plasticity in the central nervous system, but not through a receptor desensitization at the level of the single cell.

Analgesia↗
PubMed1998

Parallel stimulations of in vitro and in situ [35S]GTPgammaS binding by endomorphin 1 and DAMGO in mouse brains.

Metabotropic activities of endomorphin 1, a candidate for endogenous mu-opioid receptor ligands, were examined in comparison with the actions of [D-Ala2, N-Me-Phe4, Gly5ol]-enkephalin/DAMGO, a well-known synthetic mu-opioid agonist. Endomorphin 1 stimulated [35S]GTPgammaS binding to synaptic membranes from the mouse amygdala in a naloxone-reversible manner. DAMGO had the same effect in such preparations. In in situ [35S]GTP-gammaS binding experiments using brain sections, both endomorphin 1 and DAMGO similarly stimulated this binding in specific cellular locations throughout the brain regions. These findings strongly support the view that endomorphin 1 selectively acts on a mu-opioid receptor.

Amygdala↗
PubMed1998

Melittin, a metabostatic peptide inhibiting Gs activity.

Some basic amphiphilic peptides are known to directly stimulate heterotrimeric GTP-binding proteins (G proteins). Mastoparan and melittin are known to stimulate Gi activities. Here, we found melittin inhibited guanine nucleotide-dependent adenylyl cyclase activity in synaptic membranes of the rat cerebral cortex. However, in insect cell membranes overexpressing specific heterotrimeric G proteins using baculovirus expression system, melittin showed unique effects different from those by mastoparan on G protein activities. This peptide markedly stimulated Gi1 and G11 activities, whereas it did inhibit Gs activities. Kinetic studies revealed that the inhibition of Gs activity by melittin is attributed to the inhibition of GDP release in exchange for added guanine nucleotides (or the association of guanine nucleotides). Thus, melittin may be the first metabostatic peptide inhibiting G protein (Gs) activity, and both mechanisms through the stimulation of Gi and inhibition of Gs might be involved in the melittin-induced inhibition of adenylyl cyclase.

Adenylyl Cyclases↗
PubMed1998

Attempts to classify dependence-liable drugs by using a simple drug-discrimination test in mice.

1. In a simple discrimination test using a two-compartment shuttle box with mice, we examined the action properties of dependence-liable drugs. In mice trained to discriminate morphine from saline, neither methamphetamine (MAP) nor cocaine (COCA) was generalized to the discriminative stimulus effects of morphine. 2. Similarly, in mice trained to discriminate MAP from saline, COCA, which is known to have neuronal mechanisms in common with MAP, was generalized to the stimulus effects of MAP, but morphine was not. 3. Dihydroetorphine (DHE), which has receptor mechanisms in common with morphine, was generalized to the discriminative stimulus effects of morphine, whereas it was not generalized to the effects of MAP. Thus, the present discrimination test might be useful for the first screening of compounds with unknown neuronal mechanisms, particularly for classification into groups having separate neuropharmacological mechanisms in common.

Analgesics, Opioid↗
PubMed1998

Developmental regulation of myotonic dystrophy protein kinase in human muscle cells in vitro.

From our previous studies, myotonic dystrophy protein kinase: gene product of myotonic dystrophy is localized at the terminal cisternae of sarcoplasmic reticulum of human adult muscle. Now we have studied the developmental expression of myotonic dystrophy protein kinase in aneurally cultured human muscles and contracting cross-striated muscles innervated with fetal rat spinal cord using a semi-quantitative reverse transcription-polymerase chain reaction method for myotonic dystrophy protein kinase messenger RNA expression, Western blot analysis, immunohistochemical examinations by laser scanning confocal microscopy and immunoelectron microscopy. About 65,000 mol. wt myotonic dystrophy protein kinase was detected in aneurally cultured muscles. Myotonic dystrophy protein kinase messenger RNA was expressed in both aneurally and innervated cultured muscles, but in early innervated cultured muscles the message was transiently lower than in aneurally cultured muscles and innervated cultured muscles in long-term co-culture. In aneurally cultured muscles, immature aneurally cultured muscles show a diffuse and irregular distribution of myotonic dystrophy protein kinase in the deeper cytoplasm near the nuclei. Ultrastructurally the immuno-products against myotonic dystrophy protein kinase were observed as dense deposits in parts of the membranes near the mitochondria. In innervated cultured muscles, immunofluorescent microscopy showed myotonic dystrophy protein kinase to be localized regularly in the I bands and A-I junctions. Ultrastructurally myotonic dystrophy protein kinase was localized in branched duct-like membranes in the early stage of innervated cultured muscles and then in small sacs at the I bands and A-I junctions of the sarcolemma in the mature stage. Our present studies strongly suggest that innervation plays an important role in the localization of myotonic dystrophy protein kinase in human skeletal muscle during development. We conclude that the expression of myotonic dystrophy protein kinase during development is under neuronal influence.

Animals↗
PubMed1998

Effects of effusion in the middle ear and perforation of the tympanic membrane on otoacoustic emissions in guinea pigs.

The influence of fluid in the middle ear and of perforation and closure of the tympanic membrane (TM) on otoacoustic emissions (OAEs) was evaluated in guinea pigs. Click-evoked otoacoustic emissions (CEOAEs) and distortion product otoacoustic emissions (DPOAEs) were measured after the auditory bulla was opened. Neither OAE level changed significantly when fluid filled only half the space in the bulla, but both OAE levels disappeared when fluid completely filled the bulla. These changes were reversible. Thus, the presence of fluid in the bulla influenced CEOAE and DPOAE levels only when its volume filled more than half the space of the bulla. Changes in both CEOAE and DPOAE levels were affected by the size of the perforation of the tympanic membrane. For the smallest perforation, the reduction in both CEOAE and DPOAE levels was restricted to the lower frequencies. However, as the size of the perforation increased, a decrease in high-frequency function occurred. Thus, the results indicate that the magnitude of both OAEs was proportional to the size of the perforation. Both OAE levels improved after the perforation was closed. Because CEOAEs were more sensitive than DPOAEs to perforation and closure of the TM, DPOAEs may be better suited for OAE measurement in ears with perforated TMs.

Acoustic Stimulation↗
PubMed1998

An electrophysiologic study of the guinea pig inner ear following low pressure barotrauma.

We examined electrophysiologic and morphologic changes following low pressure barotrauma in 25 guinea pigs. Compound action potentials (CAPs), cochlear microphonics (CMs), and transiently evoked otoacoustic emissions (TEOAEs) were elicited by tone bursts (1, 2, 4 and 8 kHz) or non-linear clicks immediately following barotrauma. CAP threshold elevations were observed in 19 out of 25 cochleas, mainly at lower stimulus frequencies. Furthermore, CM and TEOAE thresholds were significantly increased, while CAP and CM amplitudes demonstrated reductions at all stimulus frequencies and intensities. CAP N1 latencies exhibited slight elongations at all stimulus frequencies and intensities. The regression coefficient between the mean CAP thresholds of four stimulus frequencies and TEOAE thresholds was statistically significant. Scanning electron microscopy (SEM) study of six electrophysiologically abnormal cochleas revealed stereocilia morphology in four, but no changes in two. We hypothesize that low pressure barotrauma can injure inner ear hair cells through an early threshold shift secondary to dislocation of the basement membrane.

Acoustic Stimulation↗
PubMed1998

Immunolocalization of myotonic dystrophy protein kinase in corbular and junctional sarcoplasmic reticulum of human cardiac muscle.

The subcellular localization of myotonic dystrophy protein kinase has been examined in human cardiac muscles with confocal laser-scanning microscopy and electron microscopy. A polyclonal antibody was produced against the synthesized peptide from a human kinase cDNA clone. We checked the antibody specificity for cardiac myotonic dystrophy protein kinase using an immunoblotting technique. Immunoblotting of extract from human cardiac muscles showed mainly 70 kDa and 55 kDa molecular weight bands. Confocal images of the protein kinase immunostaining showed striated banding patterns similar to those of skeletal muscles. In addition, the kinase was strongly detected around the intercalated disc. Immunoelectron microscopy showed that the kinase was mainly expressed in both corbular and junctional sarcoplasmic reticulum, but not in network sarcoplasmic reticulum. These results suggest that myotonic dystrophy protein kinase may be involved in the modulation of Ca2+ homeostasis in cardiac myofibres.

Blotting, Western↗
PubMed1998

The ultrastructure of anionic sites in rat articular cartilage as revealed by different preparation methods and polyethyleneimine staining.

The ultrastructure of anionic sites in the middle layer of rat articular cartilages was studied by two methods, the quick-freezing and deep-etching method, and the quick-freezing and freeze-substitution method. The anionic sites were visualized with a cationic tracer, polyethyleneimine. They were also compared with those revealed in tissues subjected to conventional fixation, such as pre-embedding or post-embedding. With the deep-etching method, three-dimensional meshwork structures were observed more clearly in the extracellular matrix compared with those seen in conventional ultrathin sections. In combination with polyethyleneimine staining, in which no chemical contrast was needed for visualization of anionic sites, numerous stained particles were detected around filaments in the extracellular matrix, indicating that they were anionic sites consisting mainly of proteoglycans. With the pre-embedding method and polyethyleneimine staining, the shapes of aggregated stained particles varied with different preparation procedures, including chemical fixation and contrasting. The fine meshworks were also observed with the post-embedding method and polyethyleneimine staining. It is suggested that such images of anionic sites, as revealed by the deep-etching method and the post-embedding polyethyleneimine-staining method with low-temperature dehydration, are probably closer to native states than those revealed by the conventional pre-embedding polyethyleneimine-staining method.

Animals↗
PubMed1998

Antiamnesic action of cromakalim, a potassium channel opener, in mice treated with hypoxia- and cerebral ischemia-type stress stimuli.

1. The amnesia induced by various stress stimuli through hypoxia and cerebral ischemia was evaluated by the shortening of the response latency in a step-through task in mice. 2. The hypoxia-induced amnesia was reduced by cromakalim, a K+ channel opener (KCO), given 10 min before or immediately after the hypoxic treatment. 3. Similarly, the ischemia-induced amnesia was also reduced by cromakalim given 30 min before the occlusion. 4. In ischemic-induced amnesic mice, pyknotic cells, indicating the condensation of chromatin, were observed histochemically at the dentate gyrus granule cells in hippocampal regions 96 hr after ischemic treatment. In addition, cromakalim inhibited the induction of pyknotic cells. 5. These results suggest that KCOs might produce prophylactically neuroprotective effects against hypoxia- and cerebral ischemia-induced amnesia.

Amnesia↗
PubMed1998

In vivo signal transduction of tetrodotoxin-sensitive nociceptive responses by substance P given into the planta of the mouse hind limb.

1. We developed a simple and sensitive peripheral analgesic test in mice. 2. Substance P (SP) given into the planta (i.pl.) of the mouse hind limb produced a flexor response. The flexor response was dependent on SP doses (0.1-100 pmol, i.pl.). When SP (10 pmol) was given every 5 min, there were stable flexor responses. These nociceptive responses were completely abolished by CP-96,345, a neurokinin 1 receptor antagonist. 3. SP-induced responses were also blocked by several signal transduction-related compounds, such as tetrodotoxin, EGTA, and U73122, a selective phospholipase C inhibitor. 4. These findings suggest that SP depolarizes peripheral nerve endings, possibly through inositol trisphosphate (Ins P3)-gated Ca2+ influx, followed by induction of action potentials in the peripheral axons of primary afferent neurons.

Action Potentials↗
PubMed1998

Low-density induced apoptosis of cortical neurons is inhibited by serum factors.

1. We investigated the survival of neurons under serum-free conditions without any exogenous signal molecules, using primary cultures of rat cerebral cortex. 2. Survival activity, measured with Alamar Blue, showed a cell density dependency under serum-free conditions. 3. The addition of fetal bovine serum suppressed the apoptotic cell death accompanied by DNA-laddering and fragmentation specific in low-density cultures, resulting in the disappearance of the cell density dependency of survival. 4. These findings suggest that serum factors may substitute for endogenous survival factors from cortical neurons in high-density cultures.

Animals↗