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Biomedical subjects

K Kosaka

Publications and source records attributed to K Kosaka.

At least 361 records · Page 20Linked to original sources
PubMed1981

Striatonigral degeneration combined with Alzheimer's disease.

An autopsy case with clinical features of progressive parkinsonism and dementia of presenile occurrence was characterized by the following neuropathological findings: (1) severe degeneration in the striatonigral system and (2) widespread occurrence of numerous senile plaques and Alzheimer's neurofibrillary tangles in the cerebral cortex. We believe this is to be a very rare case of striatonigral degeneration combined with Alzheimer's disease, because, as far as we know, only two similar cases have been reported and they had not such typical characteristics of Alzheimer's disease as ours did. In addition, in our case the biochemical examination revealed that the activity of one of the dopamine-synthesizing enzymes, tyrosine hydroxylase, was greatly decreased in the nigro-striato-pallidal system.

Alzheimer Disease↗
PubMed1981

Nasu-Hakola's disease (membranous lipodystrophy). A case report.

An autopsy case of Nasu-Hakola's disease (membranous lipodystrophy) was reported. A 29-year-old Japanese woman whose younger sister had been affected with typical Nasu-Hakola's disease with skeletal and neuropsychiatric syndromes and membrano-cystic lesions in the bones developed forgetfulness and lack of initiative. The clinical features were characterized by diminished drive, apathy, euphoria, disturbance of attention, amnestic syndrome, and gait disturbance. The clinical course of her illness was 8 years. The neuropathologic examination revealed marked symmetrical gliosis of the cerebral white matter (sclerosing leukodystrophy) predominantly in the frontal and temporal lobes with slight or moderate demyelination (dissociation glio-myelinique) and widespread axonal changes such as fragmentation and spheroid in the white matter of the cerebral hemisphere, cerebellum, basal ganglia, and brain stem. The ultrastructure of spheroids showed neurofilamentous accumulation. We discussed the importance of axonal changes with regard to the pathogenesis and etiogenesis of the disease.

Adult↗
PubMed1981

Pallido-nigro-luysial atrophy with massive appearance of corpora amylacea in the CNS.

A case of pallido-nigro-luysial atrophy, characterized by symptoms typical of progressive supranuclear palsy, presented (1) severe symmetrical abiotrophic degeneration of the globus pallidus, substantia nigra, and subthalamic nucleus and (2) widespread accumulations of corpora amylacea in the CNS. The former is thought to be consistent with pallido-nigro-luysial atrophy and we regard it as a combined system degeneration of both the pallido-nigral and the pallido-luysial systems. The significance of the latter is quite obscure. As far as we know, only three cases of pallido-nigro-luysial atrophy have been reported. However, there is no reported case of this disorder with such widespread and massive accumulations of corpora amylacea as in our case.

Aged↗
PubMed1981

Reciprocal changes, caused by insulin and glucagon, of adipose tissue lipoprotein lipase in rats in vitro.

Effects of insulin and glucagon on lipoprotein lipase activity in rat adipose tissue were studied in vitro. Adipose tissue from normal or streptozotocin-diabetic rats was incubated in Krebs-Ringer bicarbonate buffer for 60 min at 38 degrees C in the presence of heparin and lipoprotein lipase released from the tissue into the incubation medium was measured. Diabetic rats showed markedly low activities of adipose tissue lipoprotein lipase. Insulin (500 microU/ml) increased lipoprotein lipase activity in adipose tissue from diabetic rats. Glucagon (500 pg/ml), on the other hand, decreased the enzyme activity in normal rat adipose tissue. The results indicate that insulin and glucagon cause reciprocal changes of lipoprotein lipase activity in rat adipose tissue.

Adipose Tissue↗
PubMed1981

Myotonic dystrophy and thymoma: a necropsy case report.

This report describes a 46 year old woman having both thymoma and myotonic dystrophy. Laboratory studies revealed an anterior mediastinal mass, lymphocytopenia, anergic reaction to dinitrochlorobenzene and electrophysiological evidence of myotonia. Postmortem examination disclosed a thymoma with predominant proliferation of epithelial cells. This paper is the second necropsy report of myotonic dystrophy associated with thymoma.

Dinitrochlorobenzene↗
PubMed1981

Neurophysin biosynthesis in vitro in oat cell carcinoma of the lung with ectopic vasopressin production.

The incorporation of labeled compounds into neurophysins of a transplantable human oat cell carcinoma of the lung with ectopic vasopressin production was studied in vitro. Neurophysins in cell extracts and in incubation media were isolated by immunoprecipitation and analyzed by sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis. When cells were incubated with L-[35S]cysteine for 12 h, SDS-polyacrylamide gel electrophoresis of the immunoprecipitates from cell extract and medium resolved two forms of neurophysins with apparent molecular mass of 10,000 (10K) and 20,000 (20K). Both forms of [35S]-neurophysins were completely displaced from the immunoprecipitates by excess human neurophysin. Incubation of cells with L-[35S]cysteine and D-[3H]-glucosamine hydrochloride revealed that glucosamine was incorporated into the 20K neurophysin region, but not into 10K species. To observe the kinetics of labeling of the two forms of neurophysins, cells were incubated with L[35S]cysteine for varying periods of time. After short labeling periods, most of the radioactivity resided in 20K species, which plateaued after 1 h, whereas 10K neurophysin progressively increased in its height. When cells were chased with unlabeled cysteine after the exposure to a short pulse of labeling, 20K neurophysin peak gradually decreased with an apparent initial half-life of 1 h. In contrast, the label in 10K neurophysin steadily increased, which exceeded the former by 3 h of chase. Analysis of 20K neurophysin in cell extract by isoelectric focusing on polyacrylamide gel demonstrated that it was principally composed of a protein with an apparent isoelectric point (pI) of 5.7. These results suggest that neurophysin is synthesized in ectopic vasopressin-producing tumors by post-translational processing from a glycosylated proneurophysin with an apparent molecular mass of 20,000 daltons and a pI of 5.7.

Animals↗
PubMed1981

Basic peptide with insulin-like activity in human serum.

A peptide with insulin-like activity was isolated from human plasma. In the purification, insulin-like activity (ILA) was monitored by radioreceptor assay for insulin, using human placental membrane and [125I]-insulin. ILA was extracted from Cohn fraction III with acid-ethanol and chromatographed on Sephadex G-75 in 1% formic acid. When the active fractions were subjected to ion-exchange chromatography with CM-cellulose, the ILA was adsorbed to the column at pH 5.0 and was eluted with a gradient of ammonium acetate. The chromatographic behavior of the ILA was not identical to that of somatomedin A as determined by radioreceptor assay (RRA) for the latter. On isoelectric focusing of the ILA from the CM-cellulose column, insulin-like activity was distributed over a wide pH range. The ILA that was focused at pH 7.5-9.0 was further purified by gel filtration on Sephadex G-50 in 1 M acetic acid. The specific activity of the basic ILA was approximately 200 mU insulin equivalent /mg protein. The apparent molecular weight of the material was estimated to be 7,000. It stimulated [14C]-glucose oxidation in rat epididymal fat cells and had sulfation activity in chick chondrocytes. Furthermore, the basic ILA had a potent mitogenic activity in Balb/c-3T3 cells. Thus, the basic ILA is qualified as an 'insulin-like growth factor' (IGF). It is obviously different from somatomedin A, and may be closely related to IGF-I or somatomedin C. Subsequently, RRA for the basic ILA was developed in serum concentration of the basic ILA were determined. The serum concentrations of the basic ILA were high in acromegalics and low in patients with hypopituitarism. Thus, the basic ILA is entitled to be one of the IGFs.

Chromatography, Gel↗
PubMed1981

Insulin secretory responses in patients with glucose intolerance due to extra-pancreatic causes. Comparison with idiopathic diabetes mellitus.

Insulin responses during 100 g glucose tolerance tests (GTT) were compared between three groups of patients with varying degrees of glucose intolerance. Patients who had no disease known to be associated with secondary diabetes were classified as patients with idiopathic diabetes mellitus. Those whose present and past fasting blood glucose (FBG) exceeded 140 mg/100 ml were assigned to Group A, and the rest of the patients to Group B. Group C included patients with liver disease, thyrotoxicosis, or myocardial infarction, or those treated with corticosteroids or who had undergone gastrectomy. Patients in Group A were found to have consistently subnormal insulin responses whether glucose tolerance was normal (i.e. previous abnormality of glucose tolerance), borderline, or diabetic. In contrast, patients in Group C without fasting hyperglycemia had enhanced rather than decreased insulin responses when glucose tolerance was the more impaired. Patients in Group B had insulin responses similar to those either of Group A or of Group C. The relationship between the sum of six insulin and six blood glucose values during GTT (sigma IRI and sigma BG) was examined. The sigma BG-sigma IRI plot revealed distinctly different distribution zones for Group A and Group C (Zones A and C). In Group A, sigma IRI values were below 300 microU/ml irrespective of sigma BG values. In Group C, sigma IRI tended to increase, paralleling the increase in sigma BG values in the range of sigma BG values lower than 1400 mg/100 ml. In patients whose sigma BG rose above 1400/100 ml during corticosteroid treatment, the sigma IRI values decreased and entered into Zone A. After the cessation of corticosteroids in a few of these patients, the sigma IRI values recovered and reentered Zone C, concomitant with an improvement in glucose tolerance. Similar recovery of insulin response from Zone A to Zone C was also observed after the treatment of two obese diabetic patients. Thus, patients with glucose intolerance due to extra-pancreatic causes may secrete insulin at a higher rate than normal so long as the FBG level remains below 120 mg/100 ml, but a further deterioration in glucose metabolism may lead to a failure of insulin secretory mechanisms.

Adolescent↗
PubMed1981

Insulin binding of erythrocytes in hypoinsulinemic diabetics and its relationship to metabolic states.

We studied the insulin binding of erythrocytes from 26 "well-controlled" (FBG less than 120 mg/dl), and 28 "poorly-controlled" (FBG less than 120 mg/dl) non-obese diabetic patients, and 51 age-matched normal subjects. The capacity of insulin receptors was significantly decreased in well controlled (33.7 +/- 2.2) and poorly controlled (32.4 +/- 2.3) groups compared with normal subjects (43.1 +/- 2.3 sites/cell), while fasting insulin levels of diabetics were comparable to normal subjects but their insulin response to a glucose challenge was considerably decreased. However, the "empty sites" affinity (Ke) was significantly increased in both the well controlled group (5.2 +/- 0.3) and the poorly controlled group (4.8 +/- 0.3) compared with normal subjects (4.0 +/- 0.2 X 10(8) M-1). Thus, the capacity of insulin receptors to bind erythrocytes was decreased but binding affinity was increased in hypoinsulinemic diabetics. The amount of insulin bound in well-controlled diabetics was comparable to that in control subjects at physiological insulin concentrations.

Diabetes Mellitus↗
PubMed1981

Pituitary apoplexy in acromegaly during bromocriptine therapy.

Two cases of pituitary apoplexy occurring in the course of long-term bromocriptine therapy for active acromegaly are described. Although bromocriptine was effective in lowering serum growth hormone levels and concomitant clinical improvement was achieved, both patients developed an acute episode suggesting pituitary apoplexy when the therapy was continued for 6 and 24 months, respectively. Surgery verified marked haemorrhage and necrosis of an eosinophilic pituitary adenoma in each case. Bromocriptine may have suppressed the growth of these pituitary adenomas resulting in necrosis of the tumour, followed by haemorrhage into the adenoma. Pituitary apoplexy has not been documented as a complication of bromocriptine therapy. This report points out a possible role of bromocriptine in the development of this catastrophe and that careful follow-up is required when long-term treatment with bromocriptine is attempted.

Acromegaly↗
PubMed1981

Disturbances of rhythm formation in patients with hemispheric lesion.

A total of 191 patients with hemispheric lesion mainly due to CVD were examined by the finger-tapping test, and their disturbances of rhythm formation, 'hastening phenomenon' (HP), were compared with those of Parkinson's disease. HP was observed in 56% of the right and 49% of the left hemiplegic patients. HP in the intact hand of the patient was highly correlated with that of the affected hand. CT scans were examined in 86 of 191 patients, and HP was specifically correlated with unilateral striatal lesions. Thus, the disturbances of rhythm formation in hemiplegia, together with those in Parkinson's disease, Huntington's chorea, SND and OPCA, were attributed either to organic or functional deficits in the striatum.

Cerebrovascular Disorders↗
PubMed1981

Dual effects of veratridine on glucagon and insulin secretion: dependence upon extracellular and intracellular calcium.

The stimulatory effect of the sodium ionophore, veratridine (10, 25 and 50 microM), on glucagon and insulin secretion was investigated using monolayer cultures of newborn rat pancreas. The results suggest that intracellular accumulation of sodium modulates hormone secretion from both alpha- and beta-cells. The action of veratridine is dependent, at least in part, on the extracellular calcium as its effect was attenuated or lost when extracellular calcium was deleted. Its action was also dependent on intracellular calcium since preincubation of cells in low, normal, or high calcium to diminish, maintain, or increase intracellular calcium, followed by incubation with veratridine in the absence of calcium, altered the secretory responses of both glucagon and insulin. Ouabain (0.5 mM) stimulated glucagon and insulin secretion, although its effect was less than that of veratridine (50 microM). These results suggest that a common releasing mechanism, dependent on extra- and intracellular calcium, is involved in both endocrine cells.

Animals↗
PubMed1981

Inappropriate secretion of antidiuretic hormone in nude mice bearing a human bronchogenic oat cell carcinoma.

A 58-year-old man with bronchogenic oat cell carcinoma developed a typical syndrome of inappropriate secretion of antidiuretic hormone. The tumor tissue obtained at autopsy had been serially transplanted in nude mice for more than four years with 20 passages. The levels of vasopressin were remarkably increased in the plasma of nude mice bearing this tumor [24.4 +/- 18.3 (S.D.) pg/ml, n = 3] as well as in the tumor tissues ]134.3 +/- 72.2 ng/g, n = 3]. Furthermore, human nicotine-stimulated neurophysin was detected in both plasma and tumor tissues (7.4 +/- 3.7 ng/ml, n = 3, and 2.28 +/- 0.90 micrograms/g, n = 3, respectively). On ad libitum intake of water, nude mice bearing this tumor excreted significantly less urine with higher sodium concentration than did controls, but serum sodium concentrations did not differ from those of controls. When tumor-bearing mice were hydrated with 2 ml of water twice a day i.p., their diuretic response was found to be suppressed in parallel with the tumor size. However, these mice did not become hyponatremic because they drank less water. When a larger amount of water was loaded which could not be compensated by restriction of water drinking, serum sodium concentrations were markedly decreased. On the basis of these results, the lung cancer, when transplanted into nude mice, produced and secreted its own antidiuretic hormone, which induced inappropriate secretion of antidiuretic hormone in the mice. These mice may provide a useful experimental model for the study of excessive secretion of antidiuretic hormone and associated pathophysiological disorders.

Animals↗