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Biomedical subjects

H Yamanouchi

Publications and source records attributed to H Yamanouchi.

At least 19 recordsLinked to original sources

Influence of the estrous cycle at gamma-ray exposure on radiation-induced mammary tumorigenesis in virgin rats.

Wistar rats received whole body irradiation with 260 cGy gamma-rays at 10 a.m. of individual phases of their estrous cycle and then had diethylstilbestrol pellets implanted for 1 year. When the radiation was given during di-estrus II, the highest incidence (73.3%) of mammary tumorigenesis was observed, and mean latency until the first tumor appearance was 8.5 +/- 0.7 months. Also, rats irradiated on estrus had significantly lower incidence (35.3%) of mammary tumors than those irradiated on pro-estrus and di-estrus II, but there was no significant difference in latency period. Iball's indices of total mammary tumors, fibroadenoma plus adenocarcinoma, were 14.3 +/- 0.9, 28.8 +/- 2.1, 23.3 +/- 0.8 and 12.2 +/- 0.2 in rats irradiated during di-estrus I, di-estrus II, pro-estrus and estrus respectively. The percentage of adenocarcinomas was comparatively uniform (25.0 to 34.8%) throughout the various phases of the estrous cycles. Also, Iball's indices calculated from adenocarcinoma indicated no significant differences between all groups. From our results, the highest incidence of mammary tumors arose in rats after irradiation at di-estrus II with minimum level of prolactin in serum. We discuss different mechanisms of radiation-induced and chemical-carcinogen-induced tumorigenesis of mammary glands.

Adenocarcinoma

Dementia in cerebral amyloid angiopathy: a clinicopathological study.

Dementia is in addition to cerebral haemorrhage major symptom of cerebral amyloid angiopathy (CAa). In order to explore the pathological basis for dementia in CAa-related conditions, we made a clinicopathological analysis of CAa, with special attention to dementia. Among 150 patients (mean age 78.6 years) with autopsy-proven intracranial haemorrhage in Tokyo Metropolitan Geriatric Medical Center, CAa with cerebral haemorrhage accounted for 8.0% (12 cases), associated with hypertension and metastatic brain tumour. Among 38 patients with lobar haemorrhage, CAa represented the second most common cause (21.1%) of intracranial haemorrhage after hypertension. A total of 20 patients with CAa (mean age 82.5 years) were studies clinically and pathologically. Hypertension was present in 50%. Thirteen had a history of stroke and others had either ill-defined or no strokes. The average number of strokes 2.9. Fifteen patients (75%) had dementia. Based on the clinicopathological grounds for dementia, CAa-related conditions could be divided into three subtypes: "haemorrhagic", "dementia-haemorrhagic" and "dementia" type. Haemorrhagic type (30%, 6 cases) showed multiple recurrent lobar haemorrhages caused by CAa. Hypertension was present in only 1 patient. The incidence of senile plaques and neurofibrillary tangles was generally correlated with age. Only 1 patient had dementia. The dementia-haemorrhagic type (40%, 8 patients) had recurrent strokes with cerebral haemorrhage after preceding dementia. There were two different neuropathological subsets: CAa with atypical senile dementia of Alzheimer type (SDAT) and CAa with diffuse leucoencephalopathy. Patients with CAa with atypical SDAT had multiple cerebral haemorrhages caused by CAa combined with atypical Alzheimer-type pathology. Patients with CAa with diffuse leucoencephalopathy had cerebral haemorrhages in combination with diffuse white matter damage like Binswanger's subcortical vascular encephalopathy (BSVE). The incidence of senile changes correlated with age. Patients with the dementia type (30%, 6 patients) showed progressive dementia with or without haemorrhage. All had hypertension. They had a combined condition of Alzheimer-type pathology with conspicuous CAa with BSVE. Dementia in CAa-related conditions may be responsible for multiple factors including not Alzheimer-type degeneration, but also diffuse leucoencephalopathy like Binswanger's disease. We also found an asymptomatic type, an ischaemic type, a vasculitis type and an hereditary type in this condition.

Aged

Congenital focal muscle dysplasia in the lower extremities from probable abnormal innervation: a case report.

A two-year-seven-month-old girl with pes equinovarus congenita, muscle hypotonia and weakness limited to the lower extremities is presented. Upon admission to our hospital, she could stand with support but could not walk alone. Serum creatine kinase level was normal and the electromyogram was nondiagnostic. The muscle CT disclosed an almost total absence of bilateral vastus lateralis and medialis, rectus femoris and gastrocnemius muscles. The biopsied vastus lateralis muscle was almost completely replaced by fat tissue, and a small amount of muscle tissue showed uniform type 1 fiber and an aggregate of atrophic fibers in one fascicle. Because of an absence of progressive muscle weakness and neurogenic EMG findings, the authors conclude that the muscle pathology was due to the congenital anomalous condition of probable abnormal innervation to developing muscles.

Child, Preschool

Elevated fibrinopeptide A (FPA) in patients with Lesch-Nyhan syndrome.

The detection of elevated fibrinopeptide A (FPA) level in a patient with the Lesch-Nyhan syndrome complicated with cerebral infarction prompted us to examine FPA level in 3 other patients with the syndrome. FPA level significantly increased in all patients. Fibrinopeptide B beta 15-42 (FPB beta 15-42) level was increased in two, and both beta-thromboglobulin (beta TG) and platelet factor 4 (PF4) levels were elevated in one patient. These results suggest coagulation abnormalities in patients with Lesch-Nyhan syndrome.

Adolescent

Unilateral brain damage after prolonged hemiconvulsions in the elderly associated with theophylline administration.

The brains of 14 elderly patients who died after status epilepticus were examined pathologically. Three of the 14 patients showed unilateral brain damage which corresponded to the side of the seizures, and the lesions were thought to be caused by seizures. In these three and two other patients, no causative lesion related to the seizures was found. In these five patients, status epilepticus occurred during theophylline therapy and thus the seizures in these five patients were assumed to be induced by theophylline. In the three patients with unilateral brain damage, the damage was seen in the hippocampus, amygdala and thalamus in two patients, while in the third, the whole hemisphere was damaged, including the hippocampus, amygdala, thalamus, basal ganglia and cerebral cortex. The distribution of pathological changes within the thalamus was described. It is suggested that the thalamus was primarily affected by seizures, rather than by secondary degeneration from the cortex.

Aged

Effects of brain natriuretic peptide and C-type natriuretic peptide infusion on urine flow and jejunal absorption in anesthetized dogs.

Effects of brain natriuretic peptide (BNP) or C-type natriuretic peptide (CNP) on urinary excretion and jejunal absorption of fluid and electrolytes were examined in anesthetized dogs. Intravenous infusion of BNP increased urinary fluid and electrolyte excretion and decreased jejunal fluid and electrolyte absorption. CNP had a similar effect on jejunal absorption as BNP. However, CNP had no significant effect on renal fluid or electrolyte excretion. These results indicate that: 1) BNP is a powerful natriuretic peptide comparable to ANP and; 2) CNP may also contribute to the regulation of body fluid homeostasis by way of inhibiting net jejunal fluid and electrolyte absorption.

Animals

[Clinical characteristics of Wernicke's encephalopathy in the elderly].

Clinical characteristics were examined in 5 elderly patients whose brain showed typical features of Wernicke's encephalopathy at the autopsy. All 5 were females with a mean age of 67 +/- 4 years old. The pathological diagnosis of Wernicke's encephalopathy was based on the presence of bleeding or atrophy of bilateral mammilary bodies, proliferation of capillaries and increase of macrophages in mammilary bodies, midbrain periaqueductal gray matter and periventricular area, with relatively intact neurons. Wernicke's encephalopathy was diagnosed clinically only in one case. The remaining four had no clinical diagnosis of Wernicke's encephalopathy. Underlying diseases were varied including neurological, metabolic, gastrointestinal disorders and malignancy. The predominant symptom, consciousness disturbance, was seen in 4 cases. Two of them showed a comatose state. Ocular symptoms and ataxia were observed in 2 cases. Laboratory findings revealed leukocytosis and anemia in 3 cases, hypoproteinemia in 4 cases. One case was alcoholic, but the other four were non-alcoholics and developed the disease after prolonged malnutrition. At the onset of the disease, 4 cases were receiving glucose and electrolyte infusion without vitamins, at the onset of the disease. We propose that in elderly patients with consciousness disturbance of unknown cause, Wernicke's encephalopathy should be taken into consideration even in non-alcoholics, and thiamine infusion should be commenced at once when the disease is suspected even when typical symptoms are lacking.

Aged

[Cerebral infarctions in elderly patients with anemia].

The authors investigated the cause of cerebral infarctions in elderly patients with anemia. Among 411 patients with acute cerebral infarctions, eight patients showed anemia (Hb < 10 g/dl) at the time of stroke. Only 2 patients had strokes during hospitalization were aware of their anemias before stroke. They were classified into two groups. One was the sudden onset group (4 patients) of whom 3 had malignant tumors, and 2 showed disseminated intravascular coagulations (DIC). There were no patients with atrial fibrillation or cardiac disease. All patients showed cortical infarction, and two died soon after stroke. Autopsy revealed verruca formation of the mitral valve in one patient and thrombus in the right ventricle in another. We thought that non-bacterial thrombotic endocarditis (NBTE) was the major cause of cerebral infarctions in this group. The other group consisted of 4 cases of thrombotic stroke. Their neurological symptoms appeared to be progressive. They also showed cortical infarctions except for one case of pontine infarction. Severe stenosis of the cerebral arteries was revealed by angiography in two patients and by autopsy in one. We concluded that cerebral infarctions in elderly patients with anemia can be important signs of underlying malignant tumors in sudden onset strokes or cases of severe cerebral artery stenosis with thrombotic strokes.

Aged

[Slowly progressive dysarthria and impaired language function--a case report].

A 68-year-old right-handed woman was admitted to Tokyo Metropolitan Geriatric Hospital because of slowly progressive dysarthria and writing disability over 2-year period. On admission, severe dysarthria was observed, but no dysphagia. The dysarthria mostly resembled a type of pseudobulbar palsy, although it was associated with effortful speech production. An oro-facial apraxia was also found. She could name objects, and could understand spoken words correctly. Examination using the Western Aphasia Battery showed diminution of word fluency, impaired repetition and perseveration and writing errors. On the Wechsler Adult Intelligence Scale-R verbal IQ was 100 and performance IQ was 87. These scores did not suggest any significant degree of general intellectual deterioration. Wisconsin card sorting test disclosed mild frontal dysfunction. Magnetic resonance imaging showed cortical atrophy in the bilateral frontal and temporal lobes. Measurements of regional cerebral metabolic rate by 18F-FDG-PET demonstrated decreased uptake in the latero-dorso-inferior area of the bilateral frontal lobes, especially on the left side. The present case showed slowly progressive dysarthria and progressive aphasia without generalized dementia, and without typical aphasia. These symptoms are speculated to be related to the atrophy in the bilateral frontal and temporal lobes shown by MRI and the decreased metabolic rate in the left dominant bilateral frontal lobes on PET study. The pathologic process responsible for these lesions remains obscure.

Aged

[A case of transient parkinsonism due to mesencephalic hemorrhage].

A 68-year-old man was admitted because of sudden onset gait disturbance and bradykinesia. He experienced left putaminal bleeding following mild right hemiparesis and emotional incontinence without any difficulties in his daily life since three years before admission. On neurological examination the patient was alert and oriented. He showed forced crying. Myerson's sign was positive. There were no abnormal findings in ocular movements, pupillary reflexes and other cranial nerves. Muscle tone was increased with cog-wheel phenomenon in bilateral upper extremities. Coordination was preserved. He showed severe akinesia and small steppage gait with stooped posture. Freezing phenomenon was observed in initiation of gait and turning. The deep tendon reflexes were increased in the right side with bilateral pathological reflexes. There was no definite weakness and sensory disturbance in all extremities. Brain CT revealed a small high density lesion in the medial side of right cerebral peduncle and a lens-shaped low density lesion in the left putamen. On T1 and T2 weighted images of MRI, right peduncular lesion showed low signal. It extended to the substantia nigra which was partially destructed. His parkinsonism was rapidly improved and completely disappeared within following two weeks. High density lesion of right peduncle on CT also disappeared. We discussed the mechanisms of parkinsonism following unilateral mesencephalic hemorrhage in this patient.

Aged

[Absence attacks with secondary bilateral synchrony].

Three cases with petit mal absence attacks with secondary bilateral synchrony were presented. The interictal EEG showed unilateral focal epileptic discharges in the frontal area with normal background activity. The ictal EEG disclosed 3-Hz generalized symmetrical spike-wave patterns preceded by unilateral focal discharges, which were elicited by hyperventilation. None of the three cases had abnormal neurological findings or abnormal CT findings. All three cases had normal psychomotor development. One case had a history of febrile convulsions. The ictal manifestations were as follows; impairement of consciousness without any other signs in one case, with decreased posture tone in the second, and automatism in the third. The authors suggest that there can be petit mal absence with 3-Hz generalized spike-wave discharges induced by secondary bilateral synchrony.

Child

[A case report of cerebral achromatopsia with bilateral occipital lesion].

An 80-year-old right-handed man suddenly became impossible to recognize any color 7 years prior to admission. He complained that everything looked like of the same color, monochromatic. On admission, he could not discriminate any color and any familial face. Left homonymous hemianopsia associated with right lower partial visual filed defect was observed, but visual acuity of both eyes was well preserved. Visual-visual color tasks (Ishihara, matching, Hue test, Panel-D15) disclosed the disturbances in color perception. However, he could roughly distinguished red or brown from the other colors. The color test was also impaired regarding the visual-verbal color tasks (naming, pointing). However, verbal description of the color concept, which was shown by the verbal-verbal color tasks, was well preserved. In addition, we observed left hemispatial neglect, disturbance of face recognition and topographical disorientation. MRI revealed old hemorrhagic infarcts in the bilateral occipital and temporal lobes, including the bilateral lateral and medial occipito-temporal gyri. Disturbance of color recognition in this case was diagnosed as cerebral achromatopsia on the basis of clinical characteristics and MRI findings. This is the first case of cerebral achromatopsia of which lesions were detected by MRI in detail.

Aged

Palatal myoclonus in Krabbe disease.

A seven-year-old girl with Krabbe disease presenting palatal myoclonus only when awake is reported. The patient was diagnosed as having Krabbe disease enzymatically at the age of eleven months. She developed rhythmical contractions of the soft palate, pharynx, larynx, lips and tongue at two years. The surface electromyography showed rhythmical 2 Hz electrical activities. The MRI disclosed markedly attenuated intensity in the midbrain, pons and medulla oblongata on T2-weighted images. Palatal myoclonus was not controlled by carbamazepine in therapeutic doses, but disappeared when the patient was asleep. This is the first reported case of Krabbe disease with palatal myoclonus.

Brain

Does the variability of casual blood pressure contribute to progressive subcortical vascular encephalopathy of Binswanger's type?

Our hypothesis was that progressive subcortical vascular encephalopathy of Binswanger's type (PSVE) in the elderly can be induced by repeated hypotension or greater variability of blood pressure in hypertensives, regardless of antihypertensive therapy. We retrospectively studied PSVE blood pressure, and compared them with those in atherothrombotic cerebral infarction (ACI) or in hypertensive cerebral hemorrhage (HCH). During the last seven years prior to death, neither the annual variability nor the annual mean value of systolic or mean arterial blood pressures in PSVE was different from that in ACI or in HCH. The present study did not support our hypothesis.

Aged

Loss of white matter oligodendrocytes and astrocytes in progressive subcortical vascular encephalopathy of Binswanger type.

To study whether oligodendrocytes and astrocytes can be affected in progressive subcortical vascular encephalopathy of Binswanger type (PSVE), the number of oligodendrocytes and astrocytes was counted in the white matter of frontal lobe. A sum of the number of oligodendrocytes and astrocytes in the deep white matter in PSVE accounted for approximately half of that in the age-matched controls. The number of oligodendrocytes, which were defined as the cells with small, round and solid nuclei in the present study, also decreased in PSVE showing half of that in the deep white matter of the controls. The present data suggest that the loss of oligodendrocytes and astrocytes can play a role to the process of nerve fibres loss in PSVE, which has been reported in my previous study (1), although the possibility that nerve fibres loss results in the secondary loss of oligodendrocytes can not be ruled out.

Aged

[Guillain-Barré syndrome preceded by diarrhea with the infection of Campylobacter jejuni].

We report a 77-year-old woman with Guillain-Barré syndrome following Campylobacter jejuni infection. She was admitted complaining of mild weakness in the left leg. Seven days before, she had severe diarrhea, which continued several days. After admission, the weakness soon worsened resulting in tetraparesis, and the respiration became so impaired that she was supported by the artificial ventilator. Deep tendon reflexes were absent in four limbs, and no sensory disturbance was noted. CSF contained the protein as low as 20.4 mg/dl in concentration; no pleocytosis was seen. Muscle action potentials evoked by the stimulation of nerves were markedly reduced in amplitude, but conduction velocity along the nerve was decreased mildly. Campylobacter jejuni was detected by bacterial culture of the stool; the antibody was positively raised against this bacteria in serum. By 90 hospitals days, she was restored to spontaneous respiration.

Aged

[Persistent amnestic syndrome due to infarction of the genu of the left internal capsule].

An 85-year-old housewife was admitted owing to the sudden onset of amnestic syndrome on June 27, 1986. There was no history of abulia or somnolence. Though she showed severe amnesia, her understanding was not impaired. There was no aphasia, no dysarthria or other focal sings. The CT showed a low density area in the genu of the left internal capsule. The patient's amnestic syndrome did not improve during the following four years and thus she was readmitted for further examination in July, 1990. Although her WAIS scores were fairly good and intelligence was considered normal, she showed very poor performance on the Wechsler memory scale-R and Benton visual retention test. MRI of the brain showed infarction which extended from the genu to the anterior limb of the left internal capsule. The longstanding amnesia in the present case was induced probably by the infarction of the genu of the left internal capsule, where some fibers of memory pathways, such as the anterior thalamic peduncle, ansa peduncularis, and stria terminalis, may pass.

Aged