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Biomedical subjects

S Ohara

Publications and source records attributed to S Ohara.

At least 199 records · Page 11Linked to original sources
PubMed1988

Changes of rat gastric mucus glycoproteins in cytoprotection: influences of prostaglandin derivatives.

The effects of two synthetic prostaglandin E derivatives on mucus glycoproteins in the stomachs of rats were evaluated. Neither derivative caused change in mucus glycoprotein content in the gastric corpus or antrum, but both increased the biosynthetic activity of mucus glycoproteins in these regions (about 15-30%). Furthermore, the effects of the pretreatment of these derivatives on conserving mucus glycoproteins in ethanol-induced gastric lesions were examined. Treatment with these derivatives 60 min prior to 70% ethanol administration markedly inhibits the decrease in gastric mucus glycoprotein content caused by 70% ethanol. But the glycoprotein content under these pretreatment conditions was significantly less (12-19%) than that in the control group without any drug treatment.

Alprostadil↗
PubMed1988

MR imaging of CSF pulsatory flow and its relation to intracranial pressure.

In a retrospective study of magnetic resonance (MR) images obtained in 289 neurosurgical patients, loss of signal intensity (signal-void phenomenon, SVP) of the cerebrospinal fluid (CSF) in the mesencephalic aqueduct was observed in 77 patients. This SVP was noted in the MR studies of 12 of 14 patients with communicating hydrocephalus who showed a normal mean intracranial pressure (ICP) and normal pulse pressure, but in only seven of 50 patients with high mean ICP and high pulse pressure (such as those with a supratentorial tumor). The difference in the incidence of SVP between these two disease groups was statistically significant by Fisher's direct probability test. Based on MR images triggered by electrocardiography (EKG) waves, graphs were plotted to show the signal intensity of ventricular CSF versus time after the EKG R-wave. These graphs showed six distinct patterns which changed after the ICP was lowered by the withdrawal of CSF via a lumbar puncture. It is known that CSF in the cranial cavity flows toward the spinal space in a to-and-fro manner in response to the pulsations of the brain. The SVP reflects the capacity of the craniospinal cavity to buffer pressure changes within it. It may be possible to differentiate normal from increased ICP by the MR signal intensity of the CSF in the ventricular system.

Central Nervous System↗
PubMed1988

[Mitochondrial angiopathy in the cerebral blood vessels of MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and strokelike episodes)].

MELAS is a distinctive syndrome manifested by mitochondrial myopathy, encephalopathy, lactic acidosis, and recurrent stroke-like episodes such as seizures, alternating hemiparesis, hemianopsia, or cortical blindness. Pathologically the disorder is characterized by multiple, solitary or continuous foci of necrosis (infarct or softening), varying in size and stage, predominantly involving the bilateral cerebral cortices and to a lesser degree cerebral white matter, basal ganglia, brainstem and cereblum. The distribution of the lesions does not correspond to vascular territories, suggesting that they are not due to usual thrombotic or embolic process. The exact nature and pathogenesis of these lesions with characteristic distribution pattern remain to be elucidated. We studied systematically cerebral blood vessels from two autopsied patients with MELAS by electron microscopy. All the main cerebral arteries including anterior, middle and posterior cerebral, basilar and vertebral arteries were examined at their proximal portions at the cerebral base and at their peripheral portions at the cortical surface as well as within brain parenchyma. We found marked accumulation of mitochondria in the cell bodies of smooth muscle cells and endothelial cells and numerous smooth muscle cells showing degeneration or necrosis, sporadically or in clusters in the tunica media. These abnormalities were most prominent in the walls of pial arterioles and small arteries up to 250 mu in diameter, and less frequent and severe in the larger pial arteries and intracerebral arterioles and small arteries. These vascular changes are different from any of those described in various disorders known to involve the cerebral blood vessels and are thus characteristic to the cerebral blood vessels of MELAS. We think that these peculiar vascular changes called mitochondrial angiopathy are caused by primary mitochondrial dysfunction in the vascular smooth muscle cells and endothelial cells themselves, as is the same in the skeletal and cardiac muscles in this disease, and that they constitute the pathogenic base of the brain lesions with unusual distribution pattern and nature in MELAS.

Acidosis, Lactic↗
PubMed1988

[Huge jugular foramen neurinoma extending to the pharyngeal region: a case report].

The authors report a rare case of a huge jugular foramen neurinoma extending to pharyngeal region in a 64 year-old woman who visited an otolaryngologist with complaints of dysphagia, hoarseness and headache in 1984. At that time a submucosal lump was noted in her left pharyngeal region. Biopsy of the tumor proved it to be neurinoma. A CT scan disclosed a dumbell shaped jugular foramen neurinoma and noncommunicating hydrocephalus. Because her symptoms slowly progressed and cerebellar signs as well as signs of increased intracranial pressure was noted, she was referred to our hospital in 1986. She had shown typical sings of left Vernet syndrome, VIIth, VIIIth cranial nerve impairment as well as cerebellar, long tract and increased ICP signs. A subtotal removal was performed from the extracranial and posterior fossa in one stage. The tumor seemed to originate from the Xth cranial nerve. The histological diagnosis of neurinoma was confirmed. Postoperatively, although her dysphagia increased for several weeks, a tracheostomy was not necessary. She was discharged 2 months later and returned to her usual occupation as a house wife. Slight dysphagia and hoarseness were her only chronic symptoms. So far, 88 cases of jugular foramen neurinoma have been reported, 15 of them including our case from Japan. Our case is probably the largest of these reported tumors. Tumors in jugular foramen often masquerade as an acoustic neurinoma or other tumor. However, recently this can usually be diagnosed preoperatively with a careful neurological examination and by means of neuroradiological investigations such as jugular venography, CT scan and MRI.

Cerebral Angiography↗
PubMed1987

Prophylactic treatment for superficial bladder cancer following transurethral resection.

A total of 130 primary cases with superficial bladder cancer were entered in the prospective randomized group study. The prophylactic treatments compared consisted in intravesical instillation of adriamycin (20 mg/-40 ml or 30 mg/30 ml), mitomycin C (20 mg/40 ml) or thio-TEPA (30 mg/30 ml), and noninstillation treatments with etretinate or tegafur; control patients were also studied. All agents were administered for 2 years. Recurrences were significantly suppressed in the instillation groups compared with control and non-instillation groups. Significant suppression of recurrence was observed in stage 1 or grade 2 disease treated with prophylactic instillation administered over the first 24 months of a 48-month observation period. These results may indicate the clinical usefulness of prophylactic instillation, but the long-term effect of intravesical instillation is still uncertain. A long-term follow-up study is therefore necessary.

Administration, Intravesical↗
PubMed1987

Esthesioneuroepithelioma: a tumor of true olfactory epithelium origin. An ultrastructural and immunohistochemical study.

A case of esthesioneuroepithelioma was investigated ultrastructurally and immunohistochemically, using antibodies against neurofilament protein (NFP), glial fibrillary acidic protein (GFAP), keratin, neuron-specific enolase (NSE), S-100 protein (S-100), and tyrosine hydroxylase (TH). The tumor initially manifested as an epidural mass in the anterior cranial fossa in a 64-year-old man, and about 3 1/2 years later, autopsy further revealed extensive metastases to the lymph nodes of the neck and thoracic cavity. In the cranial and nasal cavities, the tumor was composed of fairly uniform, ill-defined cells arranged in nests which were surrounded by a fibrovascular stroma. These histological features were reproduced in the metastatic tumor nodules with frequent occurrence of tubular arrangements of the tumor cells. Ultrastructurally, two different cell types were well recognized by their characteristic morphological features, which were reminiscent of sensory neurons and sustentacular cells of the olfactory epithelium. No dense-cored secretory granules were observed in the tumor cells. Immunohistochemically, the tumor showed a variable number of cells positive for NFP, keratin, NSE and S-100. NFP was present in a relatively small number of cells, which were found diffusely in the nests. Keratin was observed in the cells mainly located at the periphery. NSE-positive cells tended to form irregular clusters in the center. A few S-100-positive cells were found, without any particular arrangement.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1987

Mitochondrial angiopathy in cerebral blood vessels of mitochondrial encephalomyopathy.

We studied cerebral blood vessels of two autopsied patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). All the main cerebral arteries in the proximal portion at the brain base and more distal portion at the cortical surface, as well as within the brain parenchyma were examined by electron microscopy. There was a striking increase in number of mitochondria in the smooth muscle and endothelial cells, which were most prominent in the pial arterioles and small arteries up to 250 micron in diameter and less frequent and severe in the larger pial arteries and intracerebral arterioles and small arteries. These vascular changes have not hitherto been described in MELAS, or in other disorders affecting blood vessels of the brain and other organs. It is suggested that the vascular changes are caused by primary mitochondrial dysfunction in the vascular smooth muscle and endothelial cells of the brain and that they constitute the pathogenic base of the brain lesions and their unusual distribution pattern in MELAS.

Adolescent↗
PubMed1987

MPTP-induced parkinsonian model in mice: biochemistry, pharmacology and behavior.

The effects of MPTP administered to mice were examined biochemically and pharmacologically. The dopamine level in the striatum of the mice injected with MPTP decreased markedly, but recovered to 50% of the control level 6 weeks later. Amine fluorescence showed a decrease in the amount of amine especially in the lateral part of the striatum. Of the four neuropeptides, only the concentration of somatostatin changed with time. These findings indicate that the time elapsed after MPTP treatment should be taken into consideration when MPTP-treated mice are used as a parkinsonism model. Six weeks after MPTP treatment, the concentration of the striatal muscarinic cholinergic receptor decreased significantly but recovered to the normal level after the administration of L-dopa. Such a change was not detected with the dopamine D2-receptor. The therapeutic efficacy of medication in MPTP-treated mice as examined by the pole test showed that L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS), which is considered to be the precursor of norepinephrine, enhances the effect of L-dopa.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1987

Endoscopic findings of bleeding esophageal varices and experimental study.

It has been considered that the rupture of esophageal varices occurs with high incidences, and once bleeding occurs it sometimes cause fetal massive bleeding. However, from our experiences with the active application of emergency endoscopy, the incidence of bleeding from varix was unexpectedly low. From these results, we studied the rupture signs of esophageal varices in experiments on dogs and clinical cases. The actual rupture signs of varices were summarized as active bleeding, adhesion of fresh clot, mucosal protrusion in a conical shape and white discoloration of its top area and mucosal slight elevation and attachment of fibrin thrombi. Further studies, however, are required to determine whether there are any varicose bleedings which do not show the above rupture signs.

Adult↗
PubMed1987

Endocrine cells of gastric aberrant pancreas by PAP staining method.

Histopathological classification of gastric aberrant pancreas has been done by Heinrich's criteria. However in some case it was difficult to detect incomplete Langerhans' island consisting of several endocrine cells or a single endocrine cell by usual H-E staining. To identify the distribution of incomplete Langerhans' islands and endocrine cells, we applied an enzyme antibody method utilizing PAP method for 7 cases of gastric aberrant pancreas. It became easy to identify the endocrine cells such as single cell and islet cells by using the PAP method. In all 3 cases of aberrant pancreas classified as Heinrich type II and one of 2 case of type III, Langerhans' islands or endocrine small cell groups and single cells were found. The PAP staining method was useful to determine the Heinrich's classification of the aberrant pancreas.

Adult↗
PubMed1987

[Observation of CSF pulsatile flow in MRI--the signal void phenomenon].

In a comparative study of MR images of 289 neurosurgical patients, loss of the signal intensity (signal void phenomenon) of CSF in the aqueduct was observed in 77 patients. This signal void phenomenon was seen most frequently in infants with chronic subdural hematoma (12 of 18) and patients of all age groups suffering from communicating hydrocephalus (10 of 14). It is known that CSF in the cranial cavity flows toward the spinal CSF space in to and fro manner responding to brain parenchyma pulsations. The velocity of this flow is to be faster in the narrower parts through the ventricular systems such as the aqueduct, Monro's foramen and the 4th ventricles. We think that in T2 weighted images signal void phenomenon reflects "high velocity signal loss" due to CSF flow. When the subarachnoid adhesions secondary to subarachnoid hemorrhage stagnate CSF flow in the subarachnoid space, the intraventricular CSF flow forms the main buffer for changes of the brain volume. This causes an increase in the amplitude of the pulsatile flow in the ventricular systems. Therefore the signal void phenomenon in the aqueductal CSF becomes more pronounced. It may be possible to differentiate normal circulation of CSF from abnormal with the bigger amplitude of CSF pulsatile flow, to understand the mechanisms of the normal pressure hydrocephalus or to diagnose a shunt malfunction. Therefore more insight in the CSF flow as imaged by MRI is needed, quantification of CSF flow will be the subjects of our further research.

Aged↗