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Biomedical subjects

S Shoji

Publications and source records attributed to S Shoji.

At least 163 records · Page 9Linked to original sources
PubMed1996

Role of endogenous nitric oxide in airflow obstruction in smokers.

OBJECTIVE: The aim of this study was to examine the relationship between endogenous nitric oxide (NO) level and airflow obstruction in smokers using single-breath measurement of exhaled NO with the sequential breath-holding method. SETTING: A university hospital. PATIENTS: Nine nonsmoking and ten smoking healthy volunteers. MEASUREMENTS: NO in exhaled air was measured using a chemiluminescence analyzer. Pulmonary function tests were performed using an autospirometer. RESULTS: The level of exhaled NO was higher in nonsmokers than in smokers, and the difference became larger as the breath-holding time increased. To evaluate the correlation between endogenous NO level and the degree of airflow obstruction in smokers, we used a new parameter, the NO concentration difference (delta NO). Our findings indicate that reduced level of NO in exhaled air is an indicator of decreased NO synthesis within the respiratory system and is associated with the development of airflow obstruction in smokers (r = 0.678; p < 0.01). CONCLUSIONS: delta NO is a good indicator of the synthesis of endogenous NO within the respiratory system, and it appears likely that the reduced synthesis of NO may be a contributing factor to airflow obstruction in smokers.

Adult↗
PubMed1996

A novel phospholipase C inhibitor, S-PLI produced by Streptomyces sp. strain no. A-6288.

S-PLI, an inhibitor of phospholipase C (PLC) produced by Streptomyces sp. strain No. 6288, was purified from the culture filtrate by salting-out with solid ammonium sulfate, column chromatography on CM-cellulose and gel filtration on Sephadex G-75. The molecular weight of S-PLI was estimated to be 65,000 by SDS-polyacrylamide gel electrophoresis. The inhibitor was found to be a glycoprotein with a composition of 609 amino acids and 19 glucose residues having an isoelectric point at 7.8. S-PLI was stable from pH 3 to 10 at 37 degrees C and up to 40 degrees at pH 6.0. The inhibitory activity showed pH- and temperature-dependence with a maximum around pH 7.0 at 50 degrees C. S-PLI inhibited phospholipase C in a competitive manner (Ki value; 9.5 x 10(-6) mM), but did not inhibit S-Hemolysin, phospholipase A2; phospholipase B, phospholipase D and phosphatases. S-PLI is the first reported example of a glycoproteinaceous inhibitor of microbial origin which is able to specifically inhibit phospholipase C.

Amino Acids↗
PubMed1996

[Small-cell lung cancer and subacute sensory neuropathy in a patient positive for the anti-Hu antigen].

We encountered a case of small-cell lung cancer in a patient with subacute sensory neuropathy that began 5 months before the cancer was diagnosed. A 60-year-old man complained of abnormalities in the functioning of his peripheral sensory systems (senses of pain, touch, position, and vibration). A chest X-ray film obtained on admission showed an anterior mediastinal tumor. The anti-Hu antibody was found in his serum. The diagnosis was small-cell lung cancer. Combination chemotherapy (cisplatin and irinotecan, CPT-11) was begun and the response was a complete remission. The symptoms of neuropathy continued. The anti-Hu antibody was useful in the diagnosis in the case of small-cell lung cancer combined with subacute sensory neuropathy.

Acute Disease↗
PubMed1996

[Two siblings of galactosialidosis with marked progression of cardiac involvement during 10 years].

Two brothers, aged 34 and 30 showed signs of gargoylism, macular cherry-red spots, angiokeratoma, vertebral deformities, epilepsy, action myoclonus and ataxia. In 1985, they were diagnosed as juvenile galactosialidosis due to the decrease in activity of beta-galactosidase and neuraminidase when they had slight valvular involvement with mild heart murmur. On admission in 1994, their echocardiograms revealed marked progression of the cardiac involvement, i.e. thickening of the valvular and left ventricular wall with valvular regurgitation. These findings suggested that accumulation of abnormal materials was increased during the past 10 years. The change in the echocardiographic findings was more severe in the younger brother who had milder physical and neurological manifestations, although severity of neurological symptoms correlated with those of other symptoms in some reports. This study indicates that an evaluation in cardiac involvement may be very important in patients with galactosialidosis, even those with very mild neurological manifestations. Thus echocardiogram is very useful for this purpose.

Adult↗
PubMed1996

[Keratitis and corneal edema associated with levodopa use--a case report].

We report a patient who developed keratitis and corneal edema during treatment with carbidopa-levodopa. The patient was a 34-year-old woman who complained of apraxic gait after anoxic brain damage caused by ventricular arrhythmia. She had difficulty in walking. While doses of droxidopa, flecainide acetate and amantadine HCl were kept at the same levels as before several weeks, administration of carbidopa-levodopa was gradually increased from an initial dose of 100 mg per day to 300 mg per day over a period of 10 days in an attempt to relieve her apraxic gait. Ten days after initiation of treatment with carbidopa-levodopa, her postural instability and unsteady gait slightly improved. However, after 8 days of treatment with carbidopa-levodopa, she complained of blurred vision. Ophthalmologic examination showed keratitis (corneal endothelitis) and corneal edema. After stopping carbidopa-levodopa, the keratitis dramatically improved. Cessation of the drug therapy resulted in a return of vision to normal levels by the 7th day. Although there had been no previous reports of corneal lesion caused by levodopa, we suspected that keratitis and corneal edema were associated with carbidopa-levodopa use, especially in combination treatment with flecainide acetate, and amantadine HCl. The process was reversible and presumably could have been prevented by a shorter term of medication.

Adult↗
PubMed1996

[Pseudoradicular sensory impairment caused by parietal lesions: report of two cases].

Here we report two cases of pseudoradicular sensory impairment (PRSI) caused by cerebral infarctions. Case on was a 49-year-old male who presented with dysesthesia in the left ulnar nerve distribution, and case 2 was a 57-year-old male who developed dysesthesia and weakness in the left radial nerve distribution. In both cases, the symptoms began with dysesthesia, followed by disturbance of cortical sensation, and distal motor weakness of the left upper extremity. Although the temperature, superficial pain, tactile, and vibratory sensations were well preserved, position sense, and cortical sensations such as two-point discrimination, material discrimination and stereognostic sensations were severely disturbed. No abnormalities were found in nerve conduction studies or cervical magnetic resonance imaging (MRI). Findings of somatosensory evoked potential (SEP) indicated that cortical components (N20, P24, N35 and P55) were missing in the left ulnar nerve in case 1, and in the median nerve in case 2. MRI of the brain revealed cerebral infarctions in the right parietal lobe including the postcentral gyrus. From the above results sensory disturbances of these two cases are caused by infarctions of the right parietal lobe. The characteristics of sensory disturbances caused by parietal lesions in our cases are similar to the previous reports. In addition, we found that the impaired cortical and subcortical areas were larger than the predicted areas indicated by Penfield's somatosensory homunculus. From the thermography, we found that the dermal regions with sensory impairment were more or less hypothermal. This suggests that cortical and subcortical infarctions may lead to localized sympathetic dysfunctions of the skin.

Cerebral Cortex↗
PubMed1996

Sural nerve biopsy in vasculitic neuropathies: morphometric analysis of the caliber of involved vessels.

We performed histologic and morphometric analyses of the sural nerve in 13 patients with vasculitic neuropathies. The ratio of vessels with vasculitis, the caliber of involved vessels, and pathologic changes of myelinated fibers were evaluated. In patients with polyarteritis nodosa (PN), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE), marked vasculitis with inflammatory cell infiltration and occlusion were observed in epineurial arteries greater than 100 microns in diameter, and mild vasculitic changes were noted in arterioles 40 to 100 microns in diameter. In vessels less than 40 microns, mild vasculitis with perivascular cuffing was noted in patients with RA and SLE, but not in PN. In a patient with microscopic PN, mild inflammatory cell infiltration was encountered around small vessels at diameters less than 40 microns as well as those greater than 100 microns. In a patient with nonsystemic vasculitic neuropathy, vasculitic changes were identified only in vessels less than 40 microns. In patients with Churg-Strauss syndrome (CSS), there were no distinct findings of vasculitis in any biopsy material. In conclusion, morphometric analyses of the caliber of involved vessels may be useful in the differential diagnosis and classification of underlying vasculitic neuropathies.

Aged↗
PubMed1995

Determination of N-myristoyl peptide sequence both by MALDI TOF MASS and with an N-myristoyl cleaving enzyme (polymyxin acylase).

Polymyxin acylase isolated from Pseudomonas sp. M-6-3 was used as an N-myristoyl cleaving enzyme in order to determine a part of the N-terminal amino acid sequence of N-myristoyl proteins. The enzyme hydrolyzed a number of N-myristoyl oligopeptides at various hydrolysis rates but not N-myristoyl proteins. The oncogenic protein (N-myristoyl-pp60c-src) was isolated from human colon adenocarcinoma cell line COLO 320DM by two-dimensional polyacrylamide gel electrophoresis. The protein was digested with trypsin and the resultant tryptic N-myristoyl tetrapeptide (N-myristoyl-Gly-Ser-Asn-Lys) was purified by HPLC and the structure was determined both by matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI TOF MASS) and by a gas-phase protein sequencer before or after treatment with the polymyxin acylase. The results suggest that the N-myristoyl peptide sequence derived from N-myristoyl proteins was clearly determined by the combined use of MALDI TOF MASS and the N-myristoyl cleaving enzyme.

Amidohydrolases↗
PubMed1995

Carboxyl end-specific monoclonal antibodies to amyloid beta protein (A beta) subtypes (A beta 40 and A beta 42(43)) differentiate A beta in senile plaques and amyloid angiopathy in brains of aged cynomolgus monkeys.

Senile plaques (SPs) and cerebral amyloid angiopathy (CAA) in the brains of five aged (20-26 years old) cynomolgus monkeys were investigated immunohistochemically using two monoclonal antibodies (anti-A beta 40 (BA27) and anti-A beta 42(43) (BC05)) that can differentiate the carboxyl termini of amyloid beta protein (A beta) subtypes. In four of five animals, all types of SPs (i.e. diffuse, primitive, and classical plaques; DPs, PPs, and CPs, respectively) were identified by BC05. However, BA27 did not label DPs and stained only about one third of PPs and CPs, mainly labeling granular structures and cored portions, respectively. In CAA, lesions of cortical capillaries reacted to BC05 in four of five cases, but rarely and weakly to BA27 in two of five cases. On the other hand, lesions of parenchymal and meningeal arterioles were stained by both BA27 and BC05. These staining profiles of SPs in cynomolgus monkeys correspond well to those in humans, although there are two remarkable features in cynomolgus monkeys. First, BA27 stained PPs associated with granular structures. Secondly, capillary A beta reacted intensely to BC05 but only slightly to BA27. Despite these unique features, the results suggest that aged cynomolgus monkeys can be used to investigate the pathogenesis of A beta deposition in SPs and CAA.

Amyloid beta-Peptides↗
PubMed1995

Erythromycin suppresses interleukin 6 expression by human bronchial epithelial cells: a potential mechanism of its anti-inflammatory action.

We evaluated the effects of several antibiotics on IL-6 expression by human bronchial epithelial cells, potent sources of this proinflammatory cytokine important in airway inflammation. Among those tested, erythromycin (EM) and clarithromycin (CAM) uniquely suppressed mRNA levels as well as the release of IL-6 at the therapeutic and non-cytotoxic concentration (10(-6)M). Our findings suggested that these macrolide antibiotics had suppressive effect on cytokine expression in human cells, and this new mode of action may have relevance to their clinical effectiveness in airway inflammatory diseases.

Anti-Bacterial Agents↗
PubMed1995

Amyloid beta protein 1-42/43 (A beta 1-42/43) in cerebellar diffuse plaques: enzyme-linked immunosorbent assay and immunocytochemical study.

Diffuse plaques are immature and amorphous senile plaques and believed to be in the initial phase of plaque formation. In contrast to amyloid angiopathy and the plaque core amyloid, diffuse plaques failed to be purified in preserved forms from the brain. Here, we studied the diffuse plaques in the cerebellar region of the Alzheimer's disease brain based on immunocytochemistry and ELISA using two different monoclonal antibodies specifically recognizing the carboxyl termini of A beta molecules (BA27 for A beta 1-40 and BC05 for A beta 1-42/43). We found that the amount of A beta 1-40 was in proportion to the staining degree on amyloid angiopathy by immunohistochemistry. We found that A beta 1-42/43 comprised diffuse plaques as the major component in the cerebella of AD brains. Taking these findings into consideration, diffuse plaques, the earliest pathological change in the brain with AD, are concluded to be composed mainly of A beta 1-42/43, implicating the critical importance of this kind of A beta species deposition in the pathogenesis of AD.

Adult↗
PubMed1995

Superoxide dismutases of muscle in mitochondrial encephalomyopathies.

Immunohistochemical analyses were made of the superoxide dismutases (Mn-SOD and Cu/Zn-SOD) in biopsied muscles from 7 patients with mitochondrial encephalomyopathies that included mitochondrial encephalomyopathy, lactic acidosis and strokelike episodes (MELAS), and chronic progressive external ophthalmoplegia (CPEO). Mn-SOD mainly was present in the subsarcolemmal region, but it also was found in a coarsely granular, reticular, or diffuse pattern of staining within the muscle fibers. These Mn-SOD-positive fibers corresponded almost completely to the ragged-red fibers. The immunoreaction for Cu/Zn-SOD was weakly positive in some of the muscle fibers positive for Mn-SOD. In CPEO, Mn-SOD-positive fibers predominantly showed decreased cytochrome c oxidase (COX) activity. In MELAS, Mn-SOD-positive fibers tended to be stained deeply for COX although a few were COX-negative. These findings suggest that Mn-SOD-positive fibers can be used to make a differential diagnosis between CPEO and MELAS and that in mitochondrial encephalomyopathies Mn-SOD in the ragged-red fibers may protect against oxidative stress.

Adult↗
PubMed1995

Ubiquitinated alpha B-crystallin in glial cytoplasmic inclusions from the brain of a patient with multiple system atrophy.

Glial cytoplasmic inclusions (GCIs) have been observed in oligodendroglia-like cells, specifically in the brains of patients with multiple system atrophy (striatonigral degeneration, olivopontocerebellar atrophy and Shy-Drager syndrome). We have investigated GCIs from brains of patients with multiple system atrophy biochemically and immunochemically. While most GCIs have been reported positive for both ubiquitin and alpha B-crystallin in immunocytochemical studies, the components of GCIs have not been identified biochemically. GCI-bearing cells were partially purified from the OPCA brain by sieving with nylon meshes and discontinuous sucrose density gradient centrifugation. The fraction containing GCI-bearing cells was also found to contain a 32 kDa and a 40 kDa protein, both of which were specifically recognized by anti-ubiquitin and anti-alpha B-crystallin antibodies, neither of which was found in the same fraction derived from control brain. These immunochemical results suggest that ubiquitinated alpha B-crystallin is present in GCIs from the brains of patients with multiple system atrophy.

Amino Acid Sequence↗
PubMed1995

Calbindin-D 28k immunoreactivity in the cerebellum of spinocerebellar degeneration.

We studied immunoreactivity for calbindin-D 28k (CaBP), an intracellular calcium-binding protein, in the cerebellum of control subjects and of patients with spinocerebellar degeneration (SCD) including sporadic olivopontocerebellar atrophy and familial cortical cerebellar atrophy. In the cerebellum, CaBP immunoreactivity was seen exclusively in the Purkinje cell in both SCD and control groups. However, the number of CaBP-immunoreactive Purkinje cells was significantly reduced in SCD. CaBP immunohistochemistry also disclosed abnormal morphological changes of Purkinje cells, which was not visualized on conventional strains or not clearly demonstrated on immunohistochemistry for neurofilaments. Moreover, reduced CaBP immunoreactivity was observed even in some remaining Purkinje cells of SCD suggesting that loss of CaBP precedes neuronal loss of Purkinje cell. We conclude that CaBP is a useful marker for Purkinje cell degeneration, and that reduced CaBP expression might have some association with the mechanism of the Purkinje cell degeneration in SCD.

Aged↗