Search PubMed⌕ Search

Biomedical subjects

S Shoji

Publications and source records attributed to S Shoji.

At least 145 records · Page 8Linked to original sources
PubMed1997

Synergistic effect of nitric oxide and vasoactive intestinal peptide on bronchoprotection against histamine in anesthetized guinea pigs.

Vasoactive intestinal peptide (VIP) and nitric oxide (NO) are considered to be nonadrenergic, noncholinergic (NANC) inhibitory neurostransmitters in the airways. It seems likely that these neurotransmitters may be coreleased and act as functional antagonists against bronchoconstrictor stimuli. In the present study, we examined the synergistic effect of NO and VIP on bronchoprotection against histamine in anesthetized guinea pigs. The NO donor, S-nitroso-N-acetylpenicillamine (SNAP) significantly inhibited histamine-induced bronchoconstriction in a dose-dependent manner. VIP also inhibited histamine-induced bronchoconstriction in a dose-dependent manner, but this bronchoprotective effect was short-lived. Additionally, VIP (10(-9) M) had no significant bronchoprotective effect, but a subthreshold dose of SNAP (10(-7) M) significantly potentiated VIP (10(-9) M)-induced bronchoprotection against histamine. Moreover, SNAP (10(-7) M) significantly enhanced VIP (10(-7) M)-induced bronchoprotection for a longer period of time. On the other hand, VIP (10(-9) M) also significantly potentiated SNAP-induced bronchoprotection against histamine. In conclusion, combination therapy with NO donor and VIP receptor agonist may have important advantages in the treatment of bronchial asthma, and both NO and VIP may contribute in complementary fashion to the NANC-induced relaxant response in guinea pig airways.

Anesthesia↗
PubMed1997

Serial magnetic resonance imaging (MRI) study of a patient with Balo's concentric sclerosis treated with immunoadsorption plasmapheresis.

A 28-year-old Japanese woman with Balo's concentric sclerosis developed a rapidly progressive form of encephalopathy. Magnetic resonance imaging (MRI) showed multiple concentric lesions in the central white matter and the cerebellum. The administration of corticosteroid regimen resulted in little benefit. Immunoadsorption plasmapheresis led to a remission within 1 month of onset. Serial MRI study was described here for the first time, which allowed us to observe the development of concentric structures. The observation indicated that, initially, a central core, a round demyelinated area, and surrounding edema appeared around a vessel. Subsequently, concentric demyelinated bands formed simultaneously, not centrifugally, with diminution of the edema. Analysis of cerebrospinal fluid showed elevated levels of interleukin-6 and tumor necrosis factor-alpha. The success of immunoadsorption plasmapheresis therapy in this patient suggests that both humoral demyelinating factors and cell-mediated immunity may be involved in the pathogenesis of this disorder.

Adult↗
PubMed1997

[Ataxic neuropathy in the elderly--clinicopathological study of six cases].

The combination of ataxia with peripheral neuropathy (ataxic neuropathy) is rare. Six elderly patients with peripheral neuropathy who developed ataxia were studied. Of the peripheral neuropathies, ataxic neuropathy was significantly more frequent in patients aged more than 65 years compared with younger patients. Ataxic neuropathy was associated with carcinoma (2 cases), Sjögren's syndrome (1 case), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP, 1 case) and chronic idiopathic ataxic neuropathy (2 cases). The two cases of carcinomatous neuropathy initially showed ataxia, which preceded detection of the carcinomatous lesions in the lung by approximately 1 year. The study cases had many clinical features in common. In the nerve conduction study, sural nerve action potential could not be measured in five of the cases; sural nerve biopsy revealed a decreased density of myelinated fibers in all cases. In particular, the large myelinated fibers were markedly decreased. These findings were common, regardless of the underlying disease, except in the case of CIDP in which there was only a slight decrease in the number of large myelinated fibers. Differential diagnosis based on the clinicopathological features was difficult. Therefore, in cases of ataxic neuropathy, systemic evaluation is necessary to rule out the possibility of carcinoma or various systemic diseases, especially in elderly patients.

Age Factors↗
PubMed1997

Chronic cocaine enhances gamma-aminobutyric acid and glutamate release by altering presynaptic and not postsynaptic gamma-aminobutyric acidB receptors within the rat dorsolateral septal nucleus.

Cocaine is a popular and sometimes deadly drug of abuse. Its mechanisms of action have previously not been linked with receptors localized to presynaptic sites for the major central nervous system amino acid transmitters gamma-aminobutyric acid (GABA) and glutamate. We demonstrate that, within the dorsolateral septal nucleus of in vitro brain slices from animals that had received cocaine chronically in vivo for 14 or 28, but not 7, days, control of both inhibitory (GABA) and excitatory (glutamate) amino acid transmission is impaired, due to the combined diminished effectiveness of presynaptic GABAB auto- and heteroreceptors. As a result, disinhibition of inhibitory and excitatory transmitters occurs, with enhanced transmitter release. Although the involvement of postsynaptic GABAB receptors has been suggested in the chronic actions of cocaine at other central nervous system nuclei, we do not see any change in the effectiveness of the postsynaptic GABAB receptors within the dorsolateral septal nucleus. Modulation of presynaptic GABAB receptors at central nervous system nerve terminals after chronic cocaine administration has not been reported previously. Our findings demonstrate that chronic intermittent cocaine administration for at least 14 days induces a persistent change in neuronal activity that involves both inhibitory and excitatory amino acid-mediated transmission within the dorsolateral septal nucleus. These results suggest that nerve terminal GABAB receptors have been overlooked as playing a role in either the etiology and treatment of chronic cocaine addiction or cocaine toxicity.

Animals↗
PubMed1997

[A case of frontal gait apraxia caused by hypoxic encephalopathy].

We reported a rare case who had hypoxic-encephalopathy causing frontal apraxia of gait. The patient, a 34-year-old female, was admitted in July, 1994, complaining of difficulty in walking after anoxic brain damage caused by ventricular arrhythmia. She had difficulty in raising her feet, which appeared to be rooted to the floor. There was no evidence of motor paralysis, spasticity, rigidity or sensory loss, but she did show frontal lobe signs such as foot grasp reflex and Gegenhalten. Cranial MRI showed slight atrophy of the frontal lobe. On T2 weighted image, high-intensity areas were detected at the posterior internal capsule and corona radiata. Single photon emission CT (123I-IMP) demonstrated a low perfusion area which included the inferomedical part of the frontal lobe. After 8 months of hospitalization, her postural instability and unsteady gait slowly improved without treatment as frontal signs such as foot grasp reflex disappeared. We speculate that her apraxia of gait may result from grasp reflex and Gegenhalten.

Adult↗
PubMed1997

[A case of potassium-sensitive periodic paralysis with cardiac dysrhythmia].

The authors reported a case of potassium-sensitive periodic paralysis with cardiac dysrhythmia. The patient was a 21-year-old male and had periodic paralysis and asymptomatic cardiac dysrhythmia since the age of 12. His attacks worsened in frequency and intensity which brought him to our hospital at the age of 21. Physical examination on admission revealed slight dysmorphic features such as hypoplastic mandible and high-arched palate. He had slight proximal muscle atrophy with no myotonia. Electrocardiogram showed multifocal ventricular arrhythmia. The serum potassium levels during his paralytic attacks were normal or slightly decreased (3.6-4.2 mEq/l). Both potassium and glucose tolerance tests provoked paralytic attacks. Glucose tolerance test also aggravated his cardiac dysrhythmia. Acetazoramide administration improved his paralytic attack. Potassium-sensitive periodic paralysis with cardiac dysrhythmia can not be defined by the classification of periodic paralysis based on the serum potassium concentration. Provocative tests should be done to make a definite diagnosis and treatment should be done taking into consideration both paralytic attack and cardiac dysrhythmia.

Abnormalities, Multiple↗
PubMed1997

[A case of mitochondrial encephalomyopathy showing ophthalmoplegia, diabetes mellitus and hearing loss associated with the A3243G mutation of mitochondrial DNA].

We report a 47-year-old female patient showing clinical features of chronic progressive external ophthalmoplegia (CPEO) without stroke-like episodes. Large scale deletion of mitochondrial DNA (mtDNA) was not found in her biopsied muscle, whereas the A-->G transition at position 3243 (A3243G) was detected. The patient's mother had diabetes mellitus, suggesting maternal inheritance. This mutation is usually associated with MELAS, but wide clinical variety of the mutation has been recognized. Although several patients of CPEO with A3243G mutation (CPEO3243) have been found in the Western countries, only one case has been reported in detail in Japan. The CPEO3243 patients, including ours, show retinopathy less frequently, but diabetes mellitus and hearing loss more frequently than CPEO patients with deletions of mtDNA (CPEO delta). CPEO3243 is usually inherited maternally, but almost all CPEO delta is sporadic. With regard to COX activity of biopsied muscles, CPEO3243 resembles CPEO delta more than MELAS3243. This suggests that how the mutant mtDNA is distributed among cells or tissues may have more significant effect on clinical phenotype than what type of mtDNA mutation exists. The presence of such a CPEO3243 patient like ours could be an important suggestion toward further understanding of mitochondrial diseases.

DNA, Mitochondrial↗
PubMed1997

[A case of post-poliomyelitis muscular atrophy with cranial nerve signs and widespread muscular atrophy of the extremities].

Here we report a case of a 56-year-old male with post-poliomyelitis muscular atrophy (PPMA), who presented with cranial nerve signs and widespread atrophy of the extremities. He had suffered from poliomyelitis at the age of 2 years. After recovery from the acute stage, the paralysis remained in his left arm. He noticed muscle weakness of the right upper and lower extremities at the age of 45 years and the muscle atrophy progressed to his arms, hip and thigh at the age of 55 years. Neurological examination revealed muscle atrophy of the neck and disturbance of left V, VIII, IX, X and bilateral XI cranial nerves. We diagnosed this case as PPMA from his history and electromyographic and muscle biopsy findings which suggested chronic denervation. Among the 21 PPMA cases in the past in which the acute poliomyelitis had resulted in paralysis of the only one limb, ours was the only case that had muscle atrophy of all the limbs. Cranial nerve involvement is known to occur in acute poliomyelitis; therefore, there is a possibility that the involvement of the cranial nerves in our case might be a delayed progressive symptoms.

Cranial Nerves↗
PubMed1996

Amyloid beta protein in plasma from patients with sporadic Alzheimer's disease.

Fibrillar amyloid beta protein (A beta) deposition is increased in the brains of patients with Alzheimer's disease (AD), and is manifested as senile plaques (SPs) and congophilic angiopathy (CA). A beta 40 and A beta 42(43), two chief species of A beta, are documented in SPs and CA, as well as in cerebrospinal fluid (CSF) and cell culture media. A beta 42(43) is the major component of diffuse plaques, the earliest form of SPs. Thus, we hypothesized that determination of the amount of A beta 42(43) in CSF or plasma might provide a diagnostic laboratory test for AD. We measured amounts of different A beta species in plasma from 28 patients with sporadic probable AD, 40 age-matched neurologic patients without dementia and 25 age-matched normal controls using enzyme-linked immunosorbent assays (ELISAs). Plasma concentrations of A beta 1-40 and A beta 1-42(43) did not significantly differ among these groups. These findings suggest the unlikelihood that plasma A beta assays would be useful as a diagnostic tool for AD.

Aged↗
PubMed1996

An additional form of rat Bcl-x, Bcl-xbeta, generated by an unspliced RNA, promotes apoptosis in promyeloid cells.

The bcl-2 oncogene product delays apoptotic cell death and prolongs the cell survival. We cloned two bcl-2-related cDNAs from a rat thymus cDNA library by low stringency hybridization with a rat bcl-2 fragment as a probe. One of these, designated bcl-xalpha, was a counterpart of the human bcl-xL reported previously as a bcl-2-related gene (Boise, L. H., Gonzalez-Garcia, M., Postema, C. E. , Ding, L., Lindsten, T., Turka, L. A., Mao, M., Nunez, G., and Thompson, C. B. (1993) Cell 74, 597-608). The other, designated bcl-xbeta, was novel and found to be generated by an unspliced mRNA, whereas bcl-xalpha was generated from a spliced transcript. The splice junction exactly corresponded to that found in the bcl-2 gene. bcl-xbeta was specifically expressed in cerebellum, heart, and thymus. When bcl-xbeta directed by a strong promoter was introduced into an interleukin-3-dependent promyeloid cell line, FDC-P1, DNA fragmentation was observed even in the growing state in the presence of interleukin-3 although not in the control transfectants. This finding suggests that the rat bcl-xbeta gene product promotes apoptosis in the promyeloid cells.

Animals↗
PubMed1996

A novel monoclonal antibody to N-myristoyl glycine moiety found a new N-myristoylated HIV-1 p28gag protein in HIV-1-infected cells.

A novel monoclonal antibody was raised against a synthetic N-myristoyl glycine that is characteristic of all N-myristoylated proteins. The immunoreaction suppressed in the presence of hemocyanin as well as albumin conjugated with N-myristoyl glycine and other N-myristoyl glycyl peptides, while underivatized and myristoyl amino acid proteins or various fatty acids other myristic acid exerted no effect. The antibody specifically reacted with N-myristoylated pp60c-src in human colon adenocarcinoma cells, N-myristoylated pp60v-src in Rous sarcoma virus-infected cells, and N-myristoylated Gag precursor protein Pr55gag in HIV-1 producing cells. Furthermore, the antibody immunoreacted with a new N-myristoylated p28gag derived from HIV-1 gag protein. The antibody is shown to be a very useful tool for identification of N-myristoylated proteins.

Adenocarcinoma↗
PubMed1996

Depletion of glucose causes presynaptic inhibition of neuronal transmission in the rat dorsolateral septal nucleus.

The role of glucose in synaptic transmission was examined in the rat dorsolateral septal nucleus (DLSN) with single-microelectrode voltage-clamp and slice-patch technique. Removal of glucose from the oxygenated Krebs solution caused an outward current associated with an increased membrane conductance. The current-voltage relationship (I-V curve) showed that the hypoglycemia-induced outward current was reversed in polarity at the equilibrium potential for K+. Exposure of DLSN neurons to the glucose-free solution for 5-20 min depressed the excitatory postsynaptic current (EPSC), the inhibitory postsynaptic current (IPSC), and the late hyperpolarizing current (LHC). Replacement of glucose with 2-deoxy-D-glucose (2DG), an antimetabolic substrate, mimicked the deprivation of glucose. Mannoheptulose (10 mM) and dinitrophenol, inhibitors of glucose metabolism, also depressed the PSCs, even in the presence of 10 mM glucose. Glucose-free perfusion did not significantly depress the glutamate-induced inward current, indicating that the inhibition of the EPSC by the glucose-free perfusion was presynaptic. gamma-Aminobutyric acid (GABA)-induced outward currents were depressed by the glucose-free solution. Intracellular dialysis of DLSN neurons with a patch-pipette solution containing 5 mM ATP attenuated the hypoglycemia-induced outward current. Glucose-free superfusion consistently inhibited the IPSC and the LHC without changing the GABA-induced outward current in ATP-treated DLSN neurons. It is suggested that glucose metabolism directly regulates the release of both excitatory amino acids and GABA from the presynaptic nerve terminals.

Animals↗
PubMed1996

Idiopathic portal hypertension associated with high serum titer of autoantibodies and liver dysfunction.

Idiopathic portal hypertension (IPH) is a condition marked by unexplained portal hypertension. Although a number of immunological abnormalities occur in patients with IPH, liver function is usually normal. We experienced an unusual case of IPH in a 49-year-old woman, who had pronounced splenomegaly. Laboratory data revealed pancytopenia, hypergammaglobulinemia, and liver dysfunction. Antinuclear antibodies were positive, with high titer at 1280 dilutions of sera. LE cell phenomena were also positive. Histological examination of biopsied liver showed only mild changes, but portal venous pressure was markedly elevated, at 38 cm H2O. This case was thus characterized by both a high serum titer of autoantibodies and liver dysfunction.

Autoantibodies↗
PubMed1996

Serum type III, IV collagens and TIMP in patients with type II diabetes mellitus.

We investigated serum levels of type III procollagen aminopeptide (CIII), 7S type IV collagen (CIV), and tissue inhibitor of metalloproteinase (TIMP) in 33 patients with type II diabetes mellitus (DM) without uremia (serum creatinine less than 1.5 mg/dl). The patients were divided into three groups based on measurement of the urinary albumin excretion (UAE) index obtained during two morning outpatient clinic visits: non-proteinuric patients (n = 11), UAE index less than 2.26 mg/mmol Cr; patients with microalbuminuria (n = 15), UAE index of 2.26 - 22.6 mg/mmol Cr; and patients with proteinuria (n = 7), UAE index more than 22.6 mg/mmol Cr. Serum levels of CIV and TIMP in patients with microalbuminuria and proteinuria were significantly higher than non-proteinuric patients (ANOVA, p <0.05). Serum levels of CIII in patients with proteinuria were significantly higher than those in non-proteinuric patients (p < 0.05). There was a significant positive correlation between CIV and TIMP (r = 0.502, p < 0.003), but no correlation was observed between CIII and TIMP. These results demonstrated that serum CIII and CIV increases as diabetic nephropathy progresses in terms of increasing proteinuria in type II DM patients, suggesting feasibility and usefulness of measuring serum CIV and CIII in assessing diabetic nephropathy. The increase in TIMP may be, at least in part, a possible cause for the increase in serum CIV in type II DM patients.

Adult↗
PubMed1996

Autosomal dominant pure cerebellar ataxia. A clinical and genetic analysis of eight Japanese families.

We carried out linkage analysis and clinical assessment on 41 patients with autosomal dominant pure cerebellar ataxia (ADCA) type III from eight Japanese families. The presenting symptom was gait ataxia in all patients, with the average age of onset at 46.0 +/- 9.0 (SD) years. The mean age of onset was 3.2 +/- 7.7 years earlier in offsprings than in their parents, suggesting mild, but not dramatic, anticipation. Other neurological features were restricted to cerebellar symptoms in spite of a long duration of illness of up to 41 years. The disease progression was uniformly slow, and earlier onset did not show different or severe clinical phenotype. Linkage analysis using four microsatellite markers (D11S905, D11S903, GATA2A01 and D11S913) excluded the first gene locus for ADCA type III [spinocerebellar ataxia (SCA) type 5]. The present study provides new genetic evidence, in addition to that suggested by clinical difference, that ADCA type III represents a group of heterogeneous conditions.

Adult↗
PubMed1996

Potentiation of the bronchoprotective effects of vasoactive intestinal peptide, isoprenaline, and theophylline against histamine challenge in anaesthetised guinea pigs by adrenomedullin.

BACKGROUND: Adrenomedullin is a hypotensive peptide recently discovered in human phaeochromocytoma which has been found to inhibit bronchoconstriction induced by histamine and acetylcholine. This study was designed to determine the manner in which adrenomedullin and other bronchodilators interact in modulating airway function. METHODS: A study was undertaken to determine whether adrenomedullin potentiated the bronchoprotective effects of isoprenaline, vasoactive intestinal peptide (VIP), and theophylline against histamine-induced bronchoconstriction in anaesthetised guinea pigs in vivo. RESULTS: Adrenomedullin in a concentration of 10(-9) M significantly inhibited histamine-induced bronchoconstriction but in a concentration of 10(-10) M it did not exhibit the bronchoprotective effect against histamine. VIP (10(-9) M) did not affect histamine-induced bronchoconstriction but it markedly inhibited the bronchoprotective effect against histamine in the presence of adrenomedullin (10(-10) M). VIP (10(-6) M) significantly inhibited histamine-induced bronchoconstriction but this effect was short lived. Adrenomedullin in a concentration of 10(-10) M potentiated bronchoprotection induced by VIP (10(-6) M) and prolonged it. Isoprenaline (10(-8) M) also significantly inhibited histamine-induced bronchoconstriction and this effect was enhanced in the presence of adrenomedullin (10(-10) M). Similarly, adrenomedullin (10(-10) M) significantly potentiated theophylline-induced bronchoprotection, and a sub-bronchoprotective dose of theophylline (20 mg/kg i.p.) was effective in preventing histamine-induced bronchoconstriction in the presence of adrenomedullin (10(-10) M). CONCLUSIONS: This study shows that adrenomedullin potentiates the bronchoprotective effects of different classes of bronchodilators against histamine challenge in anaesthetised guinea pigs.

Adrenomedullin↗