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Biomedical subjects

S Ohara

Publications and source records attributed to S Ohara.

At least 73 records · Page 4Linked to original sources
PubMed1999

Protein spot recognition on the non-denaturing and denaturing two-dimensional electrophoresis patterns using in situ immunosubtraction via Protein A agarose and antibodies.

Specific proteins in small amounts of human plasma were subtracted from patterns of non-denaturing two-dimensional electrophoresis (non-denaturing 2-DE) by layering a 7 microl aliquot of Protein A agarose-antibody complex on the top of an isoelectric focusing (IEF) gel before the loading of a plasma sample. The Protein A agarose suspension was recovered after non-denaturing IEF and was mixed with 8 M urea-5% 2-mercaptoethanol-1% NP-40 to extract the antibody and the specific plasma protein from Protein A agarose. The extract was then subjected to denaturing two-dimensional electrophoresis (denaturing 2-DE) and the location of the specific polypeptide was determined. The technique can be applied to the extraction and analysis of proteins in small amounts of samples.

Antibodies↗
PubMed1999

On the occurrence of neuronal sprouting in the frontal cortex of a patient with Down's syndrome.

We report on the autopsy of a 52-year-old Down's syndrome patient with a 9-year history of progressive dementia. Histologically, there was a marked neuronal loss in the cerebral cortices with numerous neurofibrillary tangles and senile plaques and congophilic angiopathy. The second cortical layer was spongy in appearance and the frontal and temporal white matter showed marked myelin pallor. Immunohistochemistry for MAP2 of the frontal and temporal cortices revealed great reduction in the number of large pyramidal neurons. On the other hand, a much stronger MAP2 immunoreactivity than that seen in the controls was observed in the second layer, which consisted of many small pyramidal neurons with features of aberrant sprouting. They were recognized in the frontal cortices but not in the temporal cortices, and were not immunolabeled with phosphorylated-tau nor MAP5. On double immunolabeling with MAP2 and beta-amyloid antibodies, these neurons were found to be not directly associated with the formation of senile plaques. Ultrastructurally, MAP2 was immunolocalized in an amorphous granular form in the neuronal somata and processes, and paired helical filaments were not immunolabeled. The observation may indicate the occurrence of a remarkable plastic response of small pyramidal cortical neurons in this patient with Down's syndrome.

Amyloid beta-Peptides↗
PubMed1999

Epalrestat prevents the decrease in gastric mucosal blood flow and protects the gastric mucosa in streptozotocin diabetic rats.

We have recently reported that steady-state gastric mucosal blood flow (GMBF) is decreased in streptozotocin (STZ) diabetic rats, and that their GMBF response to burn-stress is impaired, probably via a nitric oxide (NO)-mediated mechanism. Accordingly, this study was designed to investigate the relation of aldose reductase (AR) and NO synthase to the regulation of GMBF during chronic hyperglycemia. STZ rats were treated with or without chronic oral administration of an AR inhibitor, epalrestat (EPA) and/or an NO synthase inhibitor, N-nitro-L-arginine methyl ester (L-NAME). GMBF was measured by laser-Doppler velocimetry (LDV). In the STZ rats, GMBF after a 24-h fasting period was decreased significantly 4 weeks after the onset of diabetes and this was accompanied by an increase in the gastric ulcer index (UI) (a measure of the length of gastric erosions and ulcers). Chronic oral administration of EPA to the STZ rats dose-dependently inhibited the increased UI and the decreased GMBF after the fasting stress, whereas chronic oral administration of L-NAME further increased the UI and further decreased the GMBF. EPA administered in combination with L-NAME to the STZ rats reduced the effects of L-NAME, but the effects did not reach significance. These results suggest that EPA protects the gastric mucosa of diabetic rats, by preventing the decrease in GMBF that is, at least in part, caused by NO-related mechanisms.

Aldehyde Reductase↗
PubMed1999

Compensatory response of colon tissue to dextran sulfate sodium-induced colitis.

Depletion of goblet cells (the main mucin-producing cells in the colon) is one of the most reliable histological characteristics of ulcerative colitis, whereas a major symptom of this disease is bloody diarrhea containing a large amount of mucus. The discrepancy between these phenomena was investigated in a time-course study in rats with experimental colitis induced by treatment with oral dextran sulfate sodium (DSS) for 1, 3, or 5 days. Biochemical analysis showed a reduction in mucin content in the distal side of the colon that was proportional to the duration of DSS administration. In the proximal side of the colon, however, there was a significant increase in mucin content already on the first day of treatment with DSS. This increase in colonic mucin content continued for the 5 days of treatment. In the distal side, both sulfomucin and sialomucin decreased proportionally to the duration of DSS administration. In the proximal side, there was an increase in high iron diamine-Alcian blue-positive mucins, and confirming the proliferation of goblet cells. The proliferated glands were predominantly sialylated. Goblet cell depletion and an increase in mucin production occurred in different parts of the colon. This phenomenon may be a type of compensatory function of colon tissue in response to the localized decrease of mucin production in certain portions of the colon.

Animals↗
PubMed1999

Cell damage and proliferation in human gastric mucosa infected by Helicobacter pylori--a comparison before and after H pylori eradication in non-atrophic gastritis.

Helicobacter pylori (HP) is believed to be involved in the transition from normal gastric mucosa to atrophic gastritis and intestinal metaplasia. Infection with the organism is one of the risk factors for development of intestinal-type gastric adenocarcinoma, possibly through altered cell turnover. Medical eradication of HP is widely performed for the treatment of peptic ulcers and other upper gastrointestinal disorders. Eradication of HP may affect altered cell turnover of the gastric mucosa caused by the infection, but there are few reports comparing sterilized mucosa with HP-infected and non-infected mucosa. In this study, we examined cell damage using terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL), in situ nick translation (ISNT), and cell proliferation by Ki 67 immunohistochemistry staining in gastric mucosa before and after HP eradication and in non-infected gastric mucosa. We then compared these findings using endoscopic gastric biopsy specimens. Labeling indices of TUNEL (2.46 +/- 1.22), ISNT (1.13 +/- 0.42), and Ki67 (21.8 +/- 6.14) in tissue from which HP had been eradicated were significantly lower than those of HP-infected mucosa (6.36 +/- 2.26, 4.00 +/- 1.62, 45.8 +/- 5.35, for TUNEL, ISNT, and Ki67, respectively). There were no significant differences between formerly infected and non-infected mucosa (TUNEL: 2.26 +/- 0.69, ISNT: 1.29 +/- 0.63, Ki67: 23.5 +/- 8.20). These results indicate that medical HP eradication results in decreased cell proliferation and damage, restoring the condition seen in non-infected mucosa. Thus, HP eradication may be effective, not only in the treatment of gastric ulcers or gastric symptoms, but also in the prevention of gastric carcinoma.

Anti-Bacterial Agents↗
PubMed1999

Focal ictal direct current shifts in human epilepsy as studied by subdural and scalp recording.

In order to clarify further the characteristics of ictal direct current (DC) shifts in human epilepsy, we investigated them by subdural and scalp recording in six and three patients, respectively, both having mainly neocortical lobe epilepsy (five with frontal lobe epilepsy, two with parietal lobe epilepsy and two with temporal lobe epilepsy). By using subdural electrodes made of platinum, ictal DC shifts were observed in 85% of all the recorded seizures (89 seizures) among the six patients, and they were localized to just one or two electrodes at which the conventional initial ictal EEG change was also observed. They were closely accompanied by the electrodecremental pattern in all patients except for one in whom 1 Hz rhythmic activity was superimposed on clear negative slow shifts. Seizure control after resection of the cortex, including the area showing DC shifts, was favourable irrespective of histological diagnosis. Scalp-recorded ictal slow shifts were observed in 23% of all the recorded seizures (60 seizures) among the three patients. They were, like the subdurally recorded ones, mainly surface-negative in polarity, closely related to the electrodecremental pattern and consistent in their location. It seems that scalp-recorded DC shifts were detected particularly when seizures were clinically intense, while no slow shifts were observed in small seizures. It is concluded that at least subdurally recorded ictal slow shifts are clinically useful before epilepsy surgery to delineate more specifically an epileptogenic area as well as to further confirm the conventional initial ictal EEG change, and that scalp-recorded ictal slow shifts also have high specificity although their low sensitivity is to be taken into account.

Adolescent↗
PubMed1999

Cognitive motor control in human pre-supplementary motor area studied by subdural recording of discrimination/selection-related potentials.

To clarify the functional role of human pre-supplementary motor area (pre-SMA) in 'cognitive' motor control as compared with other non-primary motor cortices (SMA-proper and lateral premotor areas) and prefrontal area, we recorded epicortical field potentials by using subdural electrodes in five epileptic patients during presurgical evaluation, whose pre-SMA, SMA-proper, prefrontal and lateral premotor areas were defined by electric cortical stimulation and recent anatomical orientations according to the bicommissural plane and callosal grid system. An S1-Go/NoGo choice and delayed reaction task (S1-choice paradigm) and a warned choice Go/NoGo reaction task (S2-choice paradigm) with inter-stimulus intervals of 2 s were employed. The results showed (i) transient potentials with onset and peak latencies of about 200 and 600 ms, respectively, after S1 in the S1-choice paradigm mainly at pre-SMA and to a lesser degree at the prefrontal and lateral premotor areas, but not in the S2-choice paradigm. At SMA-proper, a similar but much smaller potential was seen after S1 in both S1- and S2-choice paradigms and (ii) slow sustained potentials between S1 and S2 in both S1- and S2-choice paradigms in all of the non-primary motor areas investigated (pre-SMA, SMA-proper and lateral premotor areas) and prefrontal area. It is concluded that pre-SMA plays a more important role in cognitive motor control which involves sensory discrimination and decision making or motor selection for the action after stimuli, whereas SMA-proper is one of the main generators of Bereitschaftspotential preceding self-paced, voluntary movements. In the more general anticipation of and attention to the forthcoming stimuli, non-primary motor cortices including pre-SMA, SMA-proper and lateral premotor area, and the prefrontal area are commonly involved.

Adult↗
PubMed1999

Helicobacter pylori infection inhibits reflux esophagitis by inducing atrophic gastritis.

OBJECTIVE: Although it is widely accepted that Helicobacter pylori (H. pylori) infection is an important cause of atrophic gastritis, few studies have examined the relationship between H. pylori-induced atrophic gastritis and the occurrence of reflux esophagitis. The present study was aimed to examine the relationship between H. pylori infection, atrophic gastritis, and reflux esophagitis in Japan. METHODS: A total of 175 patients with reflux esophagitis were compared with sex- and age-matched 175 control subjects. Diagnosis of H. pylori infection was made by gastric mucosal biopsy, rapid urease test, and serum IgG antibodies. Severity of atrophic gastritis was assessed by histology and serum pepsinogen I/II ratio. RESULTS: H. pylori infection was found in 59 (33.7%) patients with reflux esophagitis, whereas it was found in 126 (72.0%) control subjects. The grade of atrophic gastritis was significantly lower in the former than in the latter. Among the H. pylori-positive patients, atrophic gastritis was milder in the patients with reflux esophagitis than in the patients without it. CONCLUSIONS: These findings suggest that most cases of reflux esophagitis in Japan occur in the absence of H. pylori infection and atrophic gastritis, and it may also tend to occur in patients with milder gastritis even in the presence of H. pylori infection. Therefore, H. pylori infection may be an inhibitory factor of reflux esophagitis through inducing atrophic gastritis and concomitant hypoacidity.

Adult↗
PubMed1999

Coexpression of mineralocorticoid receptors and 11beta-hydroxysteroid dehydrogenase 2 in human gastric mucosa.

The role of mineralocorticoids in human gastrointestinal tract is well established. In the stomach, aldosterone is thought to regulate electrolyte transport associated with gastric acid secretion. In mineralocorticoid target organs, the action of the glucocorticoid inactivating enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) facilitates aldosterone binding to a nonselective mineralocorticoid receptor (MR) in the face of high levels of circulating glucocorticoids. In the present study, we examined 25 specimens of human stomach for the presence of MR and 11beta-HSD2 using a [3H]aldosterone binding assay, Northern blot analysis, RT-PCR, and immunohistochemistry. Specific [3H]aldosterone binding sites were detected in gastric fundic mucosa, but not in the antrum. In fundic mucosa the Kd was 0.72+/-0.05 nmol/L (mean +/- SE), and Bmax was 6.0+/-1.4 fmol per milligram of protein. Northern blot analysis demonstrated a faint band for MR mRNA at 6.0 kb, although message for 11beta-HSD2 was undetectable. However, RT-PCR demonstrated specific PCR products for both MR and 11beta-HSD2. Immunohistochemistry demonstrated the colocalization of MR and 11beta-HSD2 only in parietal cells. MR-positive cells were further characterized by electron microscopy, confirming the identity of parietal cells. This study shows that parietal cells contain both MR and 11beta-HSD2, suggesting that the human stomach is a novel target organ for mineralocorticoids. Aldosterone may, therefore, regulate biological functions of parietal cells including gastric acid secretion.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1999

[Recurrence rate of H. pylori after successful eradication and second eradication therapy after initial failure of treatment].

Three hundred thirty-three patient (116 gastric ulcer, 119 duodenal ulcer, 98 gastritis) who were successfully eradicated were enrolled in the study of H. pylori recurrence rate. H. pylori status was determined by histology, rapid urease test, 13C-urea breath test. The mean of the follow-up period was 13.3 months (2-56 months), and 15 patients showed negative to positive conversion of H. pylori. The recurrence rate was 4.4% for one year and 8.3% for two years using Kaplan-Meier analysis. Second eradication therapy after initial failure is another concern. Nineteen patients were assigned to receive an 1-week new triple therapy (clarithromycin, metronidazole and PPI), in whom a 2-week course of dual therapy (amoxicillin plus PPI) failed (group1). Another 15 patients in whom the 1-week new triple therapy failed were switched to the 2-week course of dual therapy plus ecabet sodium (group2). H. pylori was eradicated in 84.2% (16/19) of patients in group1 and 86.7% (13/15) in group2.

Amoxicillin↗
PubMed1999

[Increased acid secretion after Helicobacter pylori eradication is the important risk factor of acute duodenitis and reflux esophagitis].

The aims of this study were to investigate whether the changes in gastric acid secretion after H. pylori eradication might influence the development of acute duodenitis (AD) and reflux esophagitis (RE). Stimulated acid output was assessed by EGT (mEq/10 min), which is the new endoscopic method of gastric secretory testing described previously. Changes in the EGT values before and after eradication were divided into 4 groups; decreased group, no change group, increased group, markedly increased group. Results estimated by EGT demonstrated that AD and RE development after eradication significantly correlated with the increase of acid secretion. In conclusion, the increase of acid secretion was thought to be one of the most important risk factors of both AD and RE developed after H. pylori eradication.

Acute Disease↗
PubMed1999

[The expression of chemokines and the dynamics of inflammatory cell infiltration before and after H. pylori eradication].

We attempted to evaluate the relationship between the expression of IL-8 and RANTES and the dynamics of their target cells in human gastric mucosa of H. pylori associated gastritis, including their changes after H. pylori eradication. We performed the measurement of the mucosal level of IL-8 and RANTES protein by ELISA and immunohistochemistry. The neutrophil infiltration into the gastric mucosa was identified by the histological examination based on the Updated Sydney system and the measurement of MPO activity. The memory T lymphocyte and eosinophil were indicated by immunohistochemistry of CD45RO that is one of surface markers indicating memory T lymphocytes and MBP that is contained in the granules of eosinophils. H. pylori positive gastric mucosa demonstrated a remarkable increase in neutrophils. CD45RO positive cells and eosinophils, compared to H. pylori negative gastric mucosa. Gastric mucosal level of IL-8 and RANTES protein and MPO activity was significantly higher in H. pylori positive cases than that in H. pylori negative controls after H. pylori eradication, both of the level of IL-8 protein and MPO activity reduced at the same levels as negative controls. However, RANTES expression, CD45RO positive T lymphocytes and eosinophils remained in H. pylori eradicated gastric mucosa at the significantly high level, compared with H. pylori negative cases. Therefore, it seems possible that IL-8 might enhance the inflammation by facilitating the neutrophil infiltration into H. pylori infected gastric mucosa and that RANTES might play an important role in the specific immune response against H. pylori and the maintenance of the immune memory after H. pylori eradication.

Adult↗
PubMed1999

Clonic convulsion caused by epileptic discharges arising from the human supplementary motor area as studied by subdural recording.

In order to help clarify the mechanism of tonic convulsion, which is commonly seen in supplementary motor area (SMA) seizures, we investigated the temporal relationship between ictal discharges arising from the SMA and the associated EMG discharges in the foot, in a patient with SMA seizures, prior to surgical treatment. The patient's intractable seizures consisted of tonic followed by clonic convulsion of the left foot also involving at times, the left hand. Ictal EEGs were investigated by subdural electrodes placed on the SMA-proper and pre-SMA, which were defined by cortical stimulation and by recording cortical-evoked potentials. Interictally, repetitive spike discharges were seen at the pre-SMA. Each seizure initially had a tonic phase associated with an electrodecremental EEG pattern. It was followed by clonic convulsion as shown by clonic EMG discharges of the left tibialis anterior (TA) muscle. It had a duration of 300 to 500 msec, and on each occasion a positive cortical activity at the pre-SMA preceded the EMG onset by 110 msec, and a negative spike at the SMA-proper preceded the EMG onset by 50 to 60 msec. Epileptic discharges originating from the pre-SMA spread to the SMA-proper and possibly also to the primary motor cortex (MI) in this patient. Since both SMA-proper and MI could elicit EMG discharges through the independent corticospinal tracts having different conduction velocities, even a single spike arising from the SMA could give rise to a long EMG burst, which may play some role in the tonic convulsion which characterizes SMA seizures.

Adult↗
PubMed1999

Seizure with prominent tonic initial signs followed by psychomotor features: a case report clinically manifesting an unusual ictal evolution.

A clinically tonic seizure phase, immediately followed by psychomotor features (right hand dystonic posture, left hand and oral automatisms), was recorded by video and EEG, in a patient who had gliosis of the left temporal lobe and left hippocampal atrophy. Interictal epileptiform discharges were frequently seen in the left temporal area, and at the time of the tonic seizure phase, ictal spike discharges were continuously observed at the left posterior temporal area, which was recognized only by applying a high frequency filter (HFF) of 15 Hz to the digitally recorded EEG because EMG artifacts totally obscured the EEG with a HFF of 60 Hz. It is most likely that tonic seizure can occur in an adult patient with temporal lobe epilepsy, and it is speculated that an epileptogenic focus might activate a certain brain area which is regarded as a symptomatogenic zone for tonic seizures. If the tonic seizure phase is immediately followed by psychomotor features as seen in the present patient, the former could be due to focal epilepsy.

Adult↗
PubMed1998

Removal of specific protein spots on the patterns of non-denaturing two-dimensional electrophoresis using protein A agarose and antibodies.

Protein spots, such as immunoglobulin G (IgG), A (IgA) or alpha 2-macroglobulin, on the patterns of non-denaturing two-dimensional polyacrylamide gel electrophoresis (2-D PAGE) were selectively removed by the application of protein A or antibody-conjugated protein A agarose to the first-dimension gel top at the cathode side. A protein residing at pI 5.8 and with a molecular mass of about 200 kDa was clearly detected when the IgG and IgA spots were removed from the 2-D PAGE pattern.

Antibodies↗
PubMed1998

Hereditary motor and sensory neuropathy associated with cerebellar atrophy (HMSNCA): clinical and neuropathological features of a Japanese family.

We report clinicopathological features of a Japanese family with hereditary motor and sensory neuropathy associated with cerebellar atrophy (HMSNCA). Four affected members from a single generation were examined. They shared common clinical features, including insidious onset in teenage, slowly progressive cerebellar ataxia, amyotrophy, sensory disturbance, and dementia. In addition, all the patients showed hypoalbuminemia and hyperlipidemia and a marked atrophy of the cerebellum on magnetic resonance images. Autopsy of the proband revealed a severe loss of Purkinje cells, degeneration of posterior columns and spinocerebellar tracts of the spinal cord, and a marked loss of myelinated and unmyelinated fibers in the peripheral nerves. We consider that HMSNCA is a distinct form of hereditary multisystem neuronal degeneration.

Age of Onset↗