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Biomedical subjects

A Taniguchi

Publications and source records attributed to A Taniguchi.

At least 109 records · Page 6Linked to original sources
PubMed1997

Gazelle herpesvirus 1: a new neurotropic herpesvirus immunologically related to equine herpesvirus 1.

A herpesvirus was isolated from Thomson's gazelle (Gazella thomsoni) kept at a zoological garden in Japan during an outbreak of epizootic acute encephalitis. The virus, gazelle herpesvirus 1 (GHV-1), was serologically related to equine herpesvirus 1 (EHV-1). However, DNA fingerprints of GHV-1 were different from those of EHV-1 and other equine herpesviruses. Southern hybridization with probes of cloned BamHI fragments derived from UL and US segments of EHV-1 revealed differences in the DNA restriction profiles throughout the entire genome. Nucleotide sequences were determined for a conserved region of an essential envelope glycoprotein B (gB) gene and a type-specific glycoprotein G (gG) homologue gene. The predicted amino acid sequence of GHV-1 gB showed 97, 92, 61, and 57% identity to EHV-1, EHV-4, feline herpesvirus, and pseudorabies virus, respectively, indicating that GHV-1 was closer to EHV-1 than any other herpesvirus. The GHV-1 gG gene showed 93.2, 92.3, and 53% identity to EHV-1, EHV-8, and EHV-4 gGs, respectively. GHV-1 was virulent to suckling mice of the ICR strain by intracerebral inoculation and was virulent to 4-week-old BALB/c mice by intranasal inoculation, causing neurological symptoms and death. We conclude that GHV-1 is a new type of equine herpesvirus with strong neurotropism.

Amino Acid Sequence↗
PubMed1997

Decreased glucose effectiveness but not insulin resistance in glucose-tolerant offspring of Japanese non-insulin-dependent diabetic patients: a minimal-model analysis.

The aim of the study was to estimate insulin sensitivity (SI), insulin secretion, and glucose effectiveness (SG) in 10 subjects with normal glucose tolerance (eight men and two women) with a family history of non-insulin-dependent diabetes mellitus (NIDDM offspring). Ten glucose-tolerant subjects (eight men and two women) without a family history of NIDDM served as control subjects. All subjects were Japanese. They underwent a modified frequently sampled intravenous glucose tolerance test (FSIGT): glucose (300 mg/kg body weight) was administered, and insulin (20 mU/kg over 5 minutes) was infused from 20 to 25 minutes after glucose. SI and SG were estimated by Bergman's minimal-model method. No significant difference was observed in body mass index (22.6 +/- 1.5 v 21.5 +/- 0.6 kg/m2) and fasting glucose (5.1 +/- 0.1 v 5.2 +/- 0.1 mol/L) and insulin (40.7 +/- 6.3 v 42.6 +/- 6.7 pmol/L). SI was not different between the two groups (0.83 +/- 0.11 v 0.94 +/- 0.15 x 10(-1).min-1.pmol/ L-1, P > .05). The acute insulin response to glucose (AIRglucose) estimated by intravenous glucose tolerance testing was significantly lower in the offspring than in the normal controls (2,139 +/- 265 v 3,438 +/- 318 pmol/L.min, P < .05). The glucose disappearance rate (KG) and SG were significantly diminished in the offspring versus normal controls (KG, 1.50 +/- 0.22 v 2.10 +/- 0.15 min-1, P < .05; SG, 0.016 +/- 0.003 v 0.023 +/- 0.002 min-1, P < .05). Thus, glucose-tolerant Japanese NIDDM offspring with normal insulin sensitivity are characterized by a reduced AIRglucose and diminished SG. This is the first report that glucose resistance but not insulin resistance already exists in glucose-tolerant Japanese NIDDM offspring.

Blood Glucose↗
PubMed1997

Intravenous glucose tolerance test-derived glucose effectiveness in bulimia nervosa.

The aim of the present study was to estimate insulin secretion, insulin sensitivity (SI), and glucose effectiveness at basal insulin (SG) in subjects with bulimia nervosa. Eight bulimic patients and eight age-, body mass index-, and sex-matched healthy control subjects without a family history of diabetes were studied. The subjects all had normal glucose tolerance. They underwent a modified frequently sampled intravenous glucose tolerance test; glucose (300 mg/kg body weight) was administered, and insulin (4 mU/kg body weight/min) was infused from 20 to 25 minutes after administration of glucose. SI and SG were estimated by Bergman's minimal model method. Basal insulin (27 +/- 3 v 45 +/- 3 pmol/L) was significantly lower in bulimic patients than in normal controls (P < .05), but basal glucose was similar between the two groups (4.5 +/- 0.1 v 4.9 +/- 0.1 mmol/L, P > .05). The glucose disappearance rate (KG) and acute insulin response to glucose estimated by the intravenous glucose tolerance test (AIR(glucose)) were similar between the two groups (KG, 1.35 +/- 0.29 v 2.20 +/- 0.21 min(-1), P > .05; AIR(glucose), 2,920 +/- 547 v 2,368 +/- 367 pmol/L x min, P > .05). No significant difference was observed in SI between the two groups (1.34 +/- 0.18 v 1.25 +/- 0.20 x 10(-4) x min(-1) x pmol/L(-1), P > .05). On the other hand, glucose effectiveness at basal (SG) and zero (GEZI) insulin was significantly diminished in comparison to normal controls (SG, 0.011 +/- 0.002 v 0.024 +/- 0.002 min(-1), P < .01; GEZI, 0.008 +/- 0.002 v 0.017 +/- 0.003 min(-1), P < .01). Thus, bulimic patients with normal glucose tolerance without a family history of diabetes were characterized by normal insulin secretion, normal SI, and reduced SG and GEZI.

Adult↗
PubMed1997

Generation and molecular characterisation of monoclonal IgG4 rheumatoid factor from a patient with rheumatoid arthritis.

OBJECTIVE: To characterise IgG4 rheumatoid factor (RF) at the molecular level from a patient with rheumatoid arthritis. METHODS: B cells were cloned from the peripheral blood of a patient with rheumatoid arthritis, using EB virus transformation. The supernatants of the clones were screened for IgG RF activity by ELISA. Nucleotide sequences of the expressed immunoglobulin heavy and light chain genes of one IgG RF producing clone were determined by direct sequencing of the products of a polymerase chain reaction. RESULTS: One clone producing monospecific IgG4 RF was obtained. Sequence analysis of the heavy and light chain genes suggested the accumulation of somatic mutations resulting in amino acid replacement in complementarity determining regions. CONCLUSIONS: The results may suggest an antigen driven response in the generation of IgG4 RF in rheumatoid arthritis disease processes.

Amino Acid Sequence↗
PubMed1997

Autosomal dominant hyaline body myopathy presenting as scapuloperoneal syndrome: clinical features and muscle pathology.

Hyaline bodies are rare subsarcolemmal aggregates in type 1 fibers of the skeletal muscle, stain pale pink with hematoxylin-eosin and pale green with the modified Gomori trichrome, and lack reactivity for glycogen and oxidative enzymes. We report clinical findings of autosomal-dominant hyaline body myopathy in seven members in four generations and muscle biopsy findings in two of them. Slowly progressive muscle weakness and atrophy developed with scapuloperoneal distribution; age at onset was from the first to the fifth decade. Muscle biopsy showed subsarcolemmal hyaline bodies in approximately 20% of type 1 fibers. Hyaline bodies showed myofibrillar ATPase activity after acid pre-incubation. Immunohistochemically, they stained intensely with myosin heavy chain (slow), but not with myosin heavy chain (fast). Ultrastructurally, they consisted of granules sometimes in linear array, filaments, and amorphous materials. These findings suggest that hyaline bodies may be products of degeneration of myosin heavy chain (slow).

Adult↗
PubMed1997

Sclerosing cholangitis associated with hypereosinophilic syndrome.

A 15-year-old male with hypereosinophilic syndrome was admitted to our hospital because of general malaise and abnormal liver function tests. Endoscopic retrograde cholangiopancreatography demonstrated bile duct changes consistent with primary sclerosing cholangitis. The patient's liver profile tests returned to normal after treatment with prednisolone and ursodeoxycholic acid. In this case, eosinophils might have played an important role in the pathogenesis of the bile duct lesion.

Adolescent↗
PubMed1997

[Cyclophosphamide pulse therapy for refractory rheumatic diseases].

We studied the efficacy of cyclophosphamide pulse therapy (CYP) for refractory rheumatic diseases except for lupus nephritis. Thirty-five patients were included in all, that is 9 patients with systemic lupus erythematosus (SLE), 10 with rheumatoid arthritis (RA), 7 with polymyositis/dermatomyositis (PM/DM), 2 with progressive systemic sclerosis (PSS), 2 with anti-phospholipid antibody syndrome (APS), 1 with mixed connective tissue disease (MCTD), 1 with juvenile rheumatoid arthritis (JRA), 1 with Behcet's disease (BD), 1 with Wegener's granulomatosis (WG) and 1 with allergic granulomatous angiitis (AGA). Moderate to marked improvement was noted in 4 patients with SLE (2 with CNS-lupus and 2 with vasculitis), 7 with RA (2 with interstitial pneumonia:IP, 2 with vasculitis and 2 with refractory arthritis), 4 with PM/DM (2 with IP and 2 with refractory myositis), 1 PSS with IP, 2 APS with thrombocytopenia, 1 JRA with vasculitis and BD with CNS disturbance. On the other hand, adverse reactions were observed in 9 out of 35 patients (25.8%). CYP should apply in the treatment for such refractory rheumatic diseases as CNS disturbance, vasculitis, IP and autoimmune thrombocytopenia.

Arthritis, Rheumatoid↗
PubMed1996

Similarity of in vivo somatic mutations at an autosomal adenine phosphoribosyltransferase locus between T- and B-cells in human peripheral blood.

In vivo somatic mutations have been detected at several human loci by using clonal cultures of peripheral blood T-cells. It has not been fully understood whether or not the somatic mutations in T-cells are similar to those of other cell types. To address this issue, we cloned, from human peripheral blood, T- and B-cells with mutations at an autosomal adenine phosphoribosyltransferase (APRT) locus. For the efficient detection of somatic mutations at the APRT locus, a blood sample from a human individual heterozygous for germline APRT deficiency was used. T- and B-cells deficient in APRT enzyme activity were cloned from peripheral blood mononuclear cells using a selecting agent, 2,6-diaminopurine. The APRT-deficient mutant frequencies were on the order of 10(-4) in both T- and B-cells. The single-strand conformation polymorphism analysis of the APRT DNA of mutant B-cell clones suggested that the molecular mechanisms leading to the APRT deficiency in B-cells were similar to those in T-cells. Our observations suggest that both the frequency and the mode of in vivo somatic mutations occurring spontaneously at general autosomal loci in B-cells are similar to those in T-cells.

Adenine Phosphoribosyltransferase↗
PubMed1996

Induction of the HPV16 enhancer activity by Jun-B and c-Fos through cooperation of the promoter-proximal AP-1 site and the epithelial cell type--specific regulatory element in fibroblasts.

The epithelial cell type-specific enhancer of the human papillomavirus (HPV) type 16 termed the long control region (LCR) carries three AP-1 binding sites. We investigated the roles of the AP-1 sites for transactivation of the LCR by Jun-B that may be a cell type specific-transactivator for the HPVs in human fibroblasts in which expression of the endogenous Jun-B gene is low. Transient expression of Jun-B alone poorly activated transcriptional activity of the LCR. However, when combined with c-Fos, Jun-B activated the LCR. The promoter-proximal AP-1 site was required for transactivation of the LCR by Jun-B:c-Fos, but the site itself was not sufficient for the maximal response. The proposed cell type specific--regulatory element that harbors binding sites for NF1 as well as TEF-1 and PEA3 motifs, but neither other AP-1 sites nor the proximal enhancer region, could augment the transcriptional response of the promoter-proximal AP-1 site to Jun-B:c-Fos.

Cell Line↗
PubMed1996

Role of SOD-1 and nitric oxide/cyclic GMP cascade on neurofilament aggregation in ALS/MND.

A number of free radicals such as superoxide and nitric oxide may cause damage to motor neurons but the exact mechanism remains to be elucidated. A potent free radical, peroxynitrite, is readily formed from superoxide and nitric oxide, which captures superoxide three times faster than SOD-1. Peroxynitrite may nitrate tyrosine residues of light neurofilaments (NF-I), thereby altering NF assembly and causing NF accumulation in motor neurons. To test this hypothesis we have probed the massive NF aggregates which are histopathological hallmarks of ALS/MND with immunohistochemistry. We investigated localization of reaction products related to SOD-1, nitric oxide synthase (NOS) and cyclic GMP activities. Our studies show colocalization of NF aggregates with SOD-1/b-NOS/calmodulin /citrulline/cGMP and nitrotyrosine in upper motor neuron conglomerates (Cgl) and lower motor neutron axonal spheroids (Axs). This strongly supports the notion that peroxynitrite deranges NF phosphorylation and assembly, by nitrating tyrosine residues in NF-L. Impaired phosphorylation of NF subunits, either at NF-I or at NF-H, may affect the slow axonal transport culminating in proximo-distal accumulation of NF and slowly progressive motoneuron death.

Aged↗
PubMed1996

Effects of a single bout of exercise on glucose effectiveness.

The effects of a single bout of exercise on glucose effectiveness (SG) and insulin sensitivity (SI) in 22 sedentary subjects were estimated with a minimal model approach. The intravenous glucose tolerance test (IVGTT) was performed 1) 11 h after an exercise bout on a cycle ergometer at the lactate threshold level (mild exercise) for 60 min, 2) 11 h after an exercise bout at the 4 mM lactate level (hard exercise) for 36 +/- 1 min, 3) 11 h after an exhaustive-exercise bout (exhaustive exercise) for 96 +/- 7 min, or 4) without any prior exercise (control). Only the exhaustive exercise increased the glucose disappearance constant (2.69 +/- 0.28 vs. 2.05 +/- 0.13%/min; P < 0.05) and SI (15.0 +/- 2.0 vs. 10.3 +/- 0.9 x 10(-5) min/pM: P < 0.05) in comparison with the control condition. The SG and SG at zero insulin (GEZI) were not affected by any exercise condition. However, a marked individual difference in GEZI emerged after the exhaustive exercise and could be divided into two subgroups: one decreased in GEZI (0.014 +/- 0.001 vs. 0.007 +/- 0.001 min-1) and the other increased in GEZI (0.014 +/- 0.001 vs. 0.021 +/- 0.003 min-1). The former subgroup was accompanied by elevated levels of plasma creatine kinase (100 +/- 16 vs. 598 +/- 315 IU/l; P < 0.05) and myoglobin (Mb; 46 +/- 4 vs. 126 +/- 47 ng/ml; P < 0.05), whereas the latter subgroup showed no significant change in creatinine kinase (99 +/- 10 vs. 128 +/- 9 IU/l; P > 0.05) and Mb (50 +/- 7 vs. 51 +/- 4 ng/ml; P > 0.05). In both subgroups, SI was similarly increased after the exhaustive exercise. These results thus suggest that a single bout of exercise that results in muscle damage or changes in muscle permeability, as reflected in the increased creatine kinase and Mb levels, decreases GEZI, whereas exhaustive exercise without such alterations increases GEZI.

Adult↗
PubMed1996

[Sevoflurane inhalation reduced bronchospasm after extubation].

A 73-year-old female was scheduled for left upper lobectomy. She had no history of asthma or chronic obstructive pulmonary disease. During the operation, respiratory sound was clear. As spontaneous breathing was regular and stable after the reversal of neuromuscular blockade, an endotracheal tube was extubated. But soon after the extubation, wheezing and gasping respiration occurred and she complained of dyspnea. Therefore, we administered aminophylline and steroid intravenously, and the patient's lungs were ventilated manually with 100% oxygen. But after 10 minutes, there was no improvement in symptoms, and sevoflurane inhalation was started immediately. Inspiratory sevoflurane concentration was 4% at first, and was decreased to 2%. About 20 minutes after starting sevoflurane inhalation, wheezing was reduced. Sevoflurane may be useful in the treatment of bronchospasm after extubation.

Administration, Inhalation↗
PubMed1996

[A case report of mild from of phenylketonuria].

We report a 19-year-old man with mild form of phenylketonuria. The diagnosis was first made when he was examined for the tremor at 19 years of age. He had not received the Guthrie's screening test for phenylketonuria in infancy. His development of speech and walking was almost normal. Action and positional tremor developed at two years of age, and psychomotor deterioration at five years. His intelligence was of borderline, and he entered the special class for the mentally retarded at elementary school and junior high school. His skin and iris were less pigmented than those of Japanese young adults, and his hair was rather reddish. He had mild action tremor. He showed mild mental retardation, and the WAIS was 46 in PIQ, 70 in VIQ and 53 in total IQ. T2-weighted MRI of the brain showed high signal of the deep white matter around the posterior conus of the lateral ventricles. EEG showed paroxysmal abnormalities. Serum aminogram disclosed a marked elevation of phenylalanine. Analyses of pteridine in the serum and urine disclosed a low ratio of neopterine/biopterine. An assay of the dehydropteridine reductase in erythrocytes was normal. These laboratory data indicated that his condition was caused by a deficiency of phenylalanine hydroxylase deficiency.

Adult↗
PubMed1996

[Anesthetic management of a patient complicated with restrictive cardiomyopathy for gastrectomy].

Restrictive cardiomyopathy is a rare condition characterized with endomyocardial fibrosis, which interferes diastolic ventricular filling. A 52-year-old man with a 38 year history of dyspnea on effort presented with advanced gastric cancer. Subtotal gastrectomy under general anesthesia was scheduled. Preoperative examination showed biventricular dysfunction, impaired liver function and chronic renal failure. General anesthesia was induced using fentanyl, pancuronium and isoflurane, and maintained with nitrous oxide/oxygen, isoflurane and fentanyl. Extensive invasive monitoring included arterial blood pressure, central venous pressure, pulmonary artery pressure and oxygen saturation of mixed venous blood as indices of left-sided pump function. Dopamine and nitroglycerin infusion was also started after the tracheal intubation. Although a transient improvement of cardiac function was noted after the removal of ascites 5 liter, restricted fluid administration induced desaturation of mixed venous blood and tachycardia. The start of low dose prostaglandin E1 markedly improved cardiac output without hypotension, while an increase of intravenous nitroglycerin did not prove to be beneficial. PGE1 was more selective in decreasing left ventricular afterload, while nitroglycerin produces greater decrease of preload.

Alprostadil↗
PubMed1995

Insulin sensitivity, insulin secretion, and glucose effectiveness in obese subjects: a minimal model analysis.

The aim of the present study was to estimate insulin sensitivity (SI), insulin secretion, and glucose effectiveness in 14 obese subjects who were further divided into two groups: one with normal glucose tolerance and the other with impaired glucose tolerance (IGT). Glucose tolerance was determined by criteria of the World Health Organization. All subjects were Japanese. They underwent a modified frequently sampled intravenous glucose tolerance test: glucose (300 mg/kg body weight) was administered, and insulin (20 mU/kg body weight given over 5 minutes) was infused from 20 to 25 minutes after administration of glucose. SI and glucose effectiveness at basal insulin (SG) were estimated by Bergman's minimal model method. Body mass index (33.0 +/- 1.8 v 30.9 +/- 1.5 kg/m2, P > .05) and fasting insulin level (127.9 +/- 30.0 v 107.4 +/- 14.4 pmol/L, P > .05) were higher in obese IGT subjects than in normal obese subjects, but were not statistically significant. With regard to fasting glucose level, obese subjects with IGT (5.9 +/- 0.3 mmol/L) had significantly higher levels than those with normal glucose tolerance (5.1 +/- 0.2 mmol/L, P < .01). There was no significant difference in SI between the two groups (0.53 +/- 0.10 v 0.56 +/- 0.13 x 10(-4).min-1.pmol/L-1, P > .05). Pancreatic insulin secretion expressed as the integrated area of plasma insulin above the basal level during the first 19 minutes was significantly lower in obese subjects with IGT (3,366 +/- 1,495 pmol/L.min) than in those with normal glucose tolerance (16,400 +/- 4,509 pmol/L.min, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

[Polymyositis with rimmed vacuoles in a case of chronic thyroiditis].

We report a 37-year-old woman who developed chronic thyroiditis, and polymyositis with rimmed vacuoles (RVs). She developed paresthesia of glove and stocking type, muscle weakness of the lower extremities, and slowness in motion. On examination, her lower legs were atrophic and weak, more prominent on the right, while proximal muscles in the upper and lower extremities were slightly affected. Deep tendon reflexes of the upper and lower extremities were normal except for the absent Achilles tendon reflexes. Serum CK was high (1,809 IU/l), and laboratory data indicated chronic thyroiditis and hypothyroidism. Muscle CT showed severe fatty changes in the gastrocnemius and soleus muscles, more marked on the right, and slight atrophy of the thigh muscles. Electromyography and nerve conduction velocity study revealed peripheral neuropathy. Muscle biopsy revealed numerous myofibers with RVs, together with myofiber necrosis, phagocytosis and lymphocyte infiltration, consistent with myositis. Nerve biopsy was indicative of slight axonal degeneration. A diagnosis of polymyositis with RVs in combination with chronic thyroiditis was made. Prednisolone combined with levothyroxine markedly improved muscle weakness though atrophy and weakness of the lower legs were barely improved. Distal-dominant asymmetric affection of the leg muscles and many myofibers with RV on the biopsied muscle are atypical and rare findings of polymyositis. Associated chronic thyroiditis and neuropathy may be related to the formation of marked rimmed-vacuolar degeneration of myofibers in the present case.

Adult↗
PubMed1995

[A case of optic neuropathy, recurrent transverse myelopathy and hypertrophic pachymeningitis associated with perinuclear anti-neutrophil cytoplasmic antibodies (p-ANCA)].

A 77-year-old woman developed recurrent transverse myelopathy of the thoracic cord about a year after acute retrobulbar optic neuropathy on the left. Neurological examination revealed paraplegia, total sensory loss down from the level of the sixth thoracic cord and sphincteric disturbances. Her clinical features resembled multiple sclerosis, but magnetic resonance imaging (MRI) of the brain and spinal cord revealed no evidence of demyelination or inflammation. MRI of the brain showed the tentorium cerebelli on the right of low signal in T1- and T2-weighted images with marked enhancement by gadolinium, indicating pachymeningitis. Characteristically, perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA) together with antinuclear antibody was positive, whereas lupus anticoagulant and anti-cardiolipin antibody were negative. A high dose of corticosteroid including pulse therapy did not improve her symptoms. In the present case, the optic neuropathy, recurrent transverse myelopathy and hypertrophic pachymeningitis may have been caused by some common inflammatory processes related with p-ANCA.

Aged↗