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Biomedical subjects

S Terao

Publications and source records attributed to S Terao.

At least 37 records · Page 2Linked to original sources
PubMed1996

Expression of mRNAs for neurotrophic factors (NGF, BDNF, NT-3, and GDNF) and their receptors (p75NGFR, trkA, trkB, and trkC) in the adult human peripheral nervous system and nonneural tissues.

The steady-state mRNA levels of the four neurotrophic factors of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) and glial cell line-derived neurotrophic factor (GDNF) and their receptors (p75NGFR, trkA, trkB and trkC) in the adult human peripheral nervous system (PNS) as well as nonneural tissues were examined using quantitative reverse transcription-polymerase chain reaction (RT-PCR). NGF and BDNF mRNA levels were high in the heart and spleen as well as in the dorsal root ganglia (DRG) and spinal cord, showing similar spatial expression patterns, while NT-3 mRNA levels were more pronounced in the liver and spleen. In contrast to these neurotrophins, GDNF mRNA expression occurred at the highest levels in the muscle, and it was also comparatively high in the spinal cord. p75NGFR mRNA was expressed extensively throughout the PNS tissues and in the spleen. The spatial expression patterns differed among trkA, and trkB and trkC mRNAs. trkA mRNA was greatly expressed in the DRG, sympathetic ganglia and spleen, while the trkB and trkC mRNA levels were high in the DRG, spinal cord and brain. The levels of trkB and trkC mRNAs with tyrosine kinase domain, compared to those with extracellular domain, were relatively high in the DRG, whereas they were low in the spinal cord and brain. The spatial patterns of the distributions of neurotrophic factors and their receptors mRNA levels in the adult human PNS and nonneural tissues are largely similar to those reported in other mammals, but these findings provide further, more specific, understanding relevant to the therapeutic approach to human diseases.

Adult↗
PubMed1996

Age-related changes in human spinal ventral horn cells with special reference to the loss of small neurons in the intermediate zone: a quantitative analysis.

A cytoarchitectonic study of spinal ventral horn cells was performed to identify age-related changes. The diameter distribution of ventral horn neurons of the fourth lumbar segment of the spinal cord and their size and topographical distributions were investigated in 14 autopsy cases. These cases represented patients of 18-100 years of age who had died of non-neurological diseases. The results indicate that small neurons widely distributed in the intermediate zone of the ventral horn significantly diminished with aging (P < 0.0005, r = -0.898), whereas medium-sized and large neurons located in the medial and lateral nuclei showed only a slight decrease with advancing age. The total number of neurons in the whole ventral horn was also noted to decrease significantly with aging (P < 0.0005, r = -0.899). While small neurons in the intermediate zone of the ventral horn are thought to be mostly interneurons, their physiological function still remains obscure in many respects. The findings of this study provide insight into age-related cell loss in terms of size and location.

Adolescent↗
PubMed1996

Infarction of superior cerebellar artery presenting as cerebellar symptoms.

BACKGROUND: MRI of the brain has facilitated the diagnosis of cerebellar infarction in the territory of the superior cerebellar artery (SCA). We analyzed the data on patients with SCA infarction who presented with only cerebellar symptoms in an attempt to define its underlying pathophysiology. SUMMARY OF REPORT: Ten patients with SCA infarction who presented with cerebellar symptoms were studied by brain MRI, angiography, and underlying pathology. Brain MRI demonstrated an infarct in the SCA territory in the anterior rostral cerebellum of all patients. None had abnormalities in the brain stem. In four patients, a hemorrhagic infarct was present in the same region. Cerebral angiography revealed no obvious SCA occlusion or atherosclerotic vascular disease in any patient. Eight of the 10 patients had heart disease, such as atrial fibrillation or old myocardial infarction. The presumed diagnosis was occlusion of the SCA in its periphery due to cardiogenic embolism. CONCLUSIONS: When a patient presents with only cerebellar symptoms and has cerebellar infarction demonstrated by brain MRI, the SCA branch is probably occluded by cardiogenic embolism.

Aged↗
PubMed1996

Selective loss of small myelinated fibers in the lateral corticospinal tract due to midbrain infarction.

Small myelinated fibers in the lateral corticospinal tract (LCST) were selectively diminished as compared with large myelinated fibers in a patient with an old paramedian midbrain infarct involving the red nuclei, oculomotor nuclei, and inferior olivary pseudohypertrophy. Although the physiologic function of small myelinated fibers in the LCST is unknown in humans, we hypothesize that some of these fibers may include the rubrospinal tract.

Cerebral Infarction↗
PubMed1996

Stereoselective synthesis and thromboxane A2 (TXA2) receptor antagonistic activity of optically active phenol derivatives.

Enantiomers of four potent nonprostanoid thromboxane A2 (TXA2) receptor antagonists, (+/-)-7-(4-fluorophenyl)-7-(2-hydroxyphenyl)heptanoic acids (1-4), were synthesized stereoselectively by direct ortho-alkylation of phenols under modified Mitsunobu conditions. The reaction of 5 eq of phenols (6a-c) with 1 eq of (S)- or (R)-methyl 7-(4-fluorophenyl)-7-hydroxyheptanoate ((S)- or (R)-7) afforded ortho-alkylated phenol derivatives (6a-c) enantioselectively in 33 to 42% chemical yield and 90 to 93% ee. In these compounds, the (R)-enantiomers (1-4) exhibited potent TXA2 receptor antagonistic activity and the (S)-isomer (3) was much less active. In particular, compound (R)-3 strongly inhibited U-46619-induced human platelet aggregation (IC50 = 48 nM), and also showed a very potent inhibitory effect with a minimum effective dose (MED) of 0.3 mg/kg (p.o.) on U-46619-induced bronchoconstriction in guinea pigs.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1996

[A case of erythroleukemia found after multiple cerebral hemorrhage].

A 61-year-old man without hypertension was admitted for unconsciousness. Brain CT showed multiple cerebral hemorrhage of the left frontal lobe and right occipital lobe. The hemoglobin was 7.0 g/dl, the platelet count 7,000, the white-cell count 7,600 with erythroblasts, and the fibrinogen 327 mg/dl. No disseminated intravascular coagulation was found. Bone marrow examination demonstrated 69.2% erythroblasts including abnormal types of nucleus, 12.8% myeloblasts, 12.8% neutrophils, 0.8% monocytes, 4% lymphocytes, and 0.4% reticulocytes. Chromosomal examination showed 7 of 20 bone marrow cells were variously abnormal. A diagnosis of erythroleukemia with major karyotype aberrations (MAKA) was made. The patient died 5 days after admission. Histologically, cerebral hemorrhagic lesions showed complete necrosis, but neither invasion of leukemic cells nor amyloid angiopathy. We suspected that the cause of cerebral hemorrhage was severe loss of platelets. This is a rare case of erythroleukemia found after multiple cerebral hemorrhage. As a cause of cerebral hemorrhage in an old man without hypertension, one should consider not only cerebral amyloid angiopathy but also leukemia.

Cerebral Hemorrhage↗
PubMed1996

[Favorable prognosis in a case of recurrent cerebral infarctions caused by chronic disseminated intravascular coagulation due to ovarian carcinoma].

We report a 53-year-old woman who developed a cerebral infarction in the left middle cerebral artery area. Although she did not have a hemorrhagic tendency, the results of her examination showed a chronic disseminated intravascular coagulation (DIC) and a left ovarian carcinoma. Gabexate mesilate (FOY) and nafamostat mesilate (FUT) were not effective for her DIC. One month after admission, she had another cerebral infarction in the right posterior cerebral artery area. She was treated by heparin sodium and her chronic DIC improved. Then, she was operated on for ovarian carcinoma; the histologic finding was clear cell adenocarcinoma. No recurrence of DIC nor cerebral infarction was observed postoperatively. Patients with cerebral infarctions caused by chronic DIC due to ovarian carcinoma have been reported in the literature, but few patients had a favorable prognosis such as the present case. Heparin therapy appears to be the treatment of choice for chronic DIC rather than FOY or FUT, if there is no hemorrhagic tendency. When a patient with DIC develops cerebral infarction, one should always investigate for possible malignant tumors.

Adenocarcinoma, Clear Cell↗
PubMed1996

[Somatoparaphrenia caused by the lesion in the dominant cerebral hemisphere--a case report].

We reported a rare case of cerebral infarction with somatoparaphrenia (SP) caused by involvement of the dominant cerebral hemisphere. The patient was 77-year-old right-handed woman who was noted to have atrial fibrillation, right hemiplegia, hemisensory disturbance and ipsilateral homonymous hemianopsia. Neuropsychologically, there were anosognosia (AG) for hemiplegia and SP arguing her hand as doctor's hand. In addition, there also were noted disorientation, right unilateral spatial neglect and mild amnestic aphasia. Brain CT and MRI demonstrated infarctions in the left lateral thalamus, internal capsule, lateral geniculate body, hippocampus, caudate nucleus and medial occipitotemporal gyrus. IMP-SPECT showed extensive hypoperfusion areas in the left cerebral hemisphere. These lesions were thought to have resulted from occlusion of the left anterior choroidal artery and partial occlusion of the left middle and posterior cerebral arteries caused by cardiogenic embolism. AG persisted and SP disappeared 80 days after the onset. While AG and SP are generally believed to be associated with non-dominant hemispherical lesion, the present case suggests the possibility that those symptoms were seen in the case of dominant hemispherical lesion without severe aphasia.

Aged↗
PubMed1996

[Clinical features of anterior inferior cerebellar artery territory infarcts--a study of ten patients].

Clinical features of the anterior inferior cerebellar artery (AICA) territory infarcts were investigated in ten patients, ranging in age from 38 to 76 years. In all patients, there were MR images of infarction located in the area supplied by the AICA. The lesion was on the left side in 6 patients and right side in 4. The lesion of brain stem including the middle cerebellar peduncle was found in 7 patients and that extended to the cerebellum was in 3 patients. The main ipsilateral neurological signs were the VII and VIII cranial nerves palsy and cerebellar ataxia. The V and VI cranial nerves palsy. Horner's syndrome, and dysphagia were also present. The main contralateral sign was superficial sensory disturbance, but no hemiplegia. The underlying pathology included chiefly hyperlipidemia, hypertension, and diabetes mellitus. Cerebral angiography was performed in 8 patients, most of which was observed severe arteriosclerosis suggesting poor hemodynamics in the vertebral and basilar arteries. The prognosis was relatively good, but the VII, VIII, and V cranial nerves palsy and contralateral superficial sensory disturbance remained as the sequelae. As mentioned above, there were various neurological findings and MR images in AICA territory infarcts. Especially there were some patients whose lesion extended to the upper medulla and neurological findings were similar to the Wallenberg syndrome. It is important that one investigates not only axial slices but also coronal slices of MR image to estimate the extension of AICA territory infarct.

Adult↗
PubMed1996

[Central facial weakness due to medullary pyramidal infarction; a case report].

We reported a hypertensive 40-year-old man who developed sudden right hemiparesis, deep sensory disturbance, left hypoglossal nerve palsy, and mild right central facial weakness. MRI of the brain showed an infarct located in the left upper medullary pyramid. Course and connection of the corticobulbar pathway are not well known in human. Recently Cavazos (1996) described a hypothesis that some facial corticobulbar fibers descend caudally ipsilaterally as low as the upper medulla, making a loop before decussating and ascending to the contralateral facial nucleus Contralateral central facial weakness may result from interruption of these descending fibers.

Adult↗
PubMed1995

Magnetic resonance imaging of the corticospinal tracts in amyotrophic lateral sclerosis.

In 13 patients with amyotrophic lateral sclerosis (ALS), corticospinal tract lesions on spinal cord, brain and brain stem were examined by MR imaging. In 9 patients, areas of high signal intensity located in the dorsolateral columns coinciding with the lateral corticospinal tracts, were detected on axial T2*-weighted MR imaging of the cervical spinal cord using a gradient echo technique. In two patients, these spinal cord MR abnormalities corresponded well to the postmortem pathological findings of lateral corticospinal tract degeneration. T2-weighted abnormal MR signals along the corticospinal tract at the brain and brain stem were detected in 4 patients, all of whom also showed abnormal signals on cervical cord MR imaging. Four of 13 patients did not show any abnormal signals on brain and brain stem or spinal cord MR imaging. Spinal cord MR imaging provides a useful information regarding upper motor neuron lesions in ALS.

Adult↗
PubMed1995

Effects of 6-(10-hydroxydecyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone (idebenone) and related benzoquinones on porcine pancreas phospholipase A2 activity.

6-(10-Hydroxydecyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone (idebenone) has been found to have a membrane-stabilizing activity in studies using lysosomes. Using dimyristoyl L-alpha-phosphatidylcholine (DMPC) as a substrate, the effects of idebenone and related benzoquinones on phospholipid digestion by phospholipase A2 (PLA2) was investigated. Free myristic acid, released from DMPC upon PLA2 treatment, was anthrylmethylated with 9-anthryldiazomethane (ADAM) and determined by reversed-phase HPLC. Idebenone and a related benzoquinone, 2,3-dimethoxy-5-methyl-6-(10-morpholinodecyl)-1, 4-benzquinone hydrochloride (QS-10.Mor), inhibited the hydrolysis of the substrate with PLA2 in a dose-dependent manner. It is suggested that the effect of idebenone on PLA2, in addition to its antioxidant activity lipid peroxidation, can be attributed to membrane-stabilizing activity.

Animals↗
PubMed1995

[Cerebellar infarction in the territory of the superior cerebellar artery, presenting a predominant cerebellar symptom--with special reference to its pathophysiology].

Clinical features of cerebellar infarction in the territory of the superior cerebellar artery (SCA) were investigated in six male patients, ranging in age from 50 to 69 years. In all patients, there were MR images of infarction located in the area supplied by the SCA. The lesion was on the left-side in 2, right-side in 3 and bilateral (recurrent) in 1 patient. The onset of disease occurred with nausea, vomiting and floating sensation, with no overt brain stem signs other than symptoms of unilateral cerebellar ataxia and dysarthria. Five of the 6 patients had heart disease and cerebral angiography without definite evidence of SCA occlusion, strongly suggesting occlusion of the artery at its periphery due to cardiogenic embolism. A comparison of these 6 patients with those reported previously in Japan suggests that patients with SCA occlusion may be divided into two distinct subgroups: one manifesting diffuse brain stem signs in addition to cerebellar signs, and the other showing cerebellar signs as the only neurologic manifestation. In the former group, comprising the vast majority of patients, SCA occlusion occurred at the origin of the vessel due to a thrombus under a state of hypertension, diabetes mellitus or malignancy, producing signs of brain stem involvement, such as dissociating sensory disturbance and Horner's sign. While in the latter group, which included these 6 patients, paucity of brain stem signs, absence of definite cerebral angiographic evidence of SCA occlusion, and the presence of heart disease were distinguishing clinical features. Cardiogenic cerebral embolism was probably the underlying pathology in many of the cases and the functional prognosis was favorable.

Aged↗
PubMed1995

[Disturbance of hypothalamic-pituitary hormone secretion in familial chorea-acanthocytosis].

An endocrinological study was performed dopaminergic regulation of the hypothalamic-pituitary axis of 3 patients with familial chorea-acanthocytosis (females, 38 to 47 years of age). All 3 patients exhibited low basal levels of triiodo-thyronine (T3), and 2 patients had a slightly elevated baseline plasma prolactin (PRL) level. The patients had a delayed plasma thyroid stimulating hormone (TSH) response and plasma PRL excessive response to thyrotropin releasing hormone (TRH), and a low plasma growth hormone releasing hormone (GRF) response to L-dopa. These TSH, PRL and GRF responses represent a secretion pattern due to a hypothalamic disorder, suggesting impaired regulation of hormone secretion by the dopaminergic system, primarily in the hypothalamus. In addition, an increased growth hormone (GH) response secretion following TRH (paradoxical response) was observed in 2 patients, suggesting that the pituitary was also involved. An oral glucose tolerance test (75g-OGTT) revealed a diabetic pattern in all 3 patients, indicating frequent association with impaired glucose tolerance.

Acanthocytes↗
PubMed1994

Age-related changes of the myelinated fibers in the human corticospinal tract: a quantitative analysis.

A quantitative analysis was made of the myelinated fibers in the lateral corticospinal tract (LCST) at the levels of the 6th cervical, 7th thoracic and 4th lumbar spinal segments in 20 patients between 19 and 90 years old, and who died of non-neurological diseases. The diameter frequency histograms of myelinated fibers of LCST showed a bimodal pattern with a sharp peak of the small myelinated fibers and broad slope of the large myelinated fibers. The ratio of small fiber to large fiber densities was significantly higher in the 6th cervical (P < 0.05) and 4th lumbar segments (P < 0.01) than in the 7th thoracic segments. The density of small myelinated fibers was significantly lowered with advancing age (P < 0.05-0.001), while that of large myelinated fibers was not significantly decreased in the aged patients, although it showed a slight age-dependent declining tendency. Age-dependent decline of small fiber density was more prominent in the cervical and lumbar segments. Retraction of the axon-collaterals from large-diameter myelinated fibers, which are abundant in the cervical and lumbar segments, may contribute to the age-related diminution of the small myelinated fibers in the LCST.

Adult↗
PubMed1994

Disease-specific patterns of neuronal loss in the spinal ventral horn in amyotrophic lateral sclerosis, multiple system atrophy and X-linked recessive bulbospinal neuronopathy, with special reference to the loss of small neurons in the intermediate zone.

The ventral horn cells of the fourth lumbar segment were morphometrically analysed in six cases of amyotrophic lateral sclerosis (ALS; there common forms and three pseudopolyneuritic forms), six of multiple system atrophy (MSA) with autonomic failure, four of X-linked recessive bulbospinal neuronopathy (X-BSNP), and seven age-matched autopsy cases of non-neurological disorders. In the common form of ALS, large and medium-sized neurons of the medial and lateral nuclei were markedly lost; small neurons in the intermediate zone were slightly diminished but fairly well preserved. In the pseudopolyneuritic form of ALS, marked loss was present in the large and medium-sized neurons, and in the small neurons located in the intermediate zone as well. In the MSA, in contrast to ALS, there was a marked reduction in small neurons in the intermediate zone, and large and medium-sized neurons of the medial and lateral nuclei tended to be preserved. In X-BSNP, large and medium-sized neurons were almost completely lost and small neurons were also markedly depopulated. These findings indicated that the pattern of neuron loss in the ventral horn is distinct among these diseases depending on size, location and function of the ventral horn cell population. These disease-specific patterns of neuron loss suggest a difference in the process of neuronal degeneration of ventral horn cells among the disease examined.

Adult↗