Search PubMed⌕ Search

Biomedical subjects

K Kosaka

Publications and source records attributed to K Kosaka.

At least 307 records · Page 17Linked to original sources
PubMed1983

A computed tomography study of Alzheimer's disease.

Computed tomography (CT) was used to study cerebral atrophy in 18 patients with clinically diagnosed Alzheimer's disease of presenile type and in 14 healthy age-matched subjects as controls. Using the computerized planimetric method, Subarachnoid Space Volume Index and Ventricle Volume Index were calculated as the measure of cortical atrophy and ventricular dilatation respectively. From the results the following conclusions were drawn: 1. The cerebral atrophy in Alzheimer patients could be attributable to the disease processes rather than to physiological aging of the brain. 2. The degree of atrophy increases in parallel with the progress of the clinical stage, and the cortical atrophy is already apparent at an early stage, whereas the ventricular dilatation becomes pronounced at later stages. 3. CT could be one of the most useful clinical tests available for the diagnosis of Alzheimer's disease.

Age Factors↗
PubMed1983

Reduction of C-peptide secretion in noninsulin-dependent diabetic patients with long duration of insulin treatment.

We examined the responses of serum free C-peptide immunoreactivity (CPR) during a 100 g oral glucose tolerance test (OGTT) on diabetic patients undergoing different kinds and durations of treatment. None of the patients were ketosis-prone or had any history of nephropathy and they all developed diabetes when over the age of 30. The sigma serum free CPR (the sum of serum free CPR values during OGTT) of group A (duration of insulin treatment was less than 5 years, N = 10) was found to be higher than that of group B (duration of insulin treatment was 5 years or more, N = 10) (p less than 0.005). On the other hand, the sigma serum free CPR of group C (treatment with an oral hypoglycemic agent for less than 5 years, N = 9) was not statistically different from that of group D (treatment with an oral hypoglycemic agent for 5 years or more, N = 11). There were no statistical differences between group A and group B in age at onset, duration of diabetes, daily insulin dose, relative body weight index, serum creatinine or sigma BG (the sum of blood glucose values during OGTT). Just before the start of insulin treatment, there were no significant differences between the two groups in the following: 1. fasting blood glucose values (all 10 patients measured in group A and 9 patients in group B) 2. blood glucose and plasma immunoreactive insulin (IRI) responses (7 patients measured in group A and 6 in group B). Among those with plasma IRI measured on the previous occasion, sigma serum free CPR was found to be higher in group A than in group B (p less than 0.025) at the time of the present study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

On the pathogenesis of type II diabetes with special reference to diminished insulin response and obesity: a 5-12 year follow-up study of subjects with borderline glucose tolerance.

In a 5-12 year follow-up study of 288 subjects with borderline glucose tolerance, 56 of them worsened to overt noninsulin dependent diabetes mellitus (NIDDM). Multivariate analysis indicated that a high level of fasting and 2-hour blood glucose values at the initial 100 g oral glucose tolerance test, a large maximal body weight index (Max. BWI) and a diminished insulin response to glucose load were significant independent risk factors for worsening to diabetes. Deterioration to diabetes was observed 4.5 times, 6.1 times and 2.1 times more frequently in subjects with fasting blood glucose greater than or equal to 100 mg/100 ml, 2-hour blood glucose greater than or equal to 180 mg/100 ml and Max. BWI greater than or equal to 130%, respectively, as compared with those having lower values of each variable. Diabetes developed almost exclusively from low insulin responders in 253 non- or mildly obese subjects, while in 35 severely obese subjects a certain number of 'normal or high' insulin responders did develop diabetes. In conclusion, the majority of cases of NIDDM develop on the basis of low insulin secretion, with an additional precipitating factor of obesity, and, in some with higher insulin responses diabetes develops when extreme obesity exists, though these cases form a minor group in Japan today.

Blood Glucose↗
PubMed1983

Islet-cell antibodies in IDDM and NIDDM in a Japanese population.

Islet-cell antibodies (ICA) were studied in 538 Japanese diabetics with insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). The overall prevalence of ICA was 17% (16/93), 4% (7/164), 2% (2/90) and 3% (5/191) in IDDM, NIDDM treated with insulin, NIDDM treated with oral hypoglycemic agents, and NIDDM treated by diet alone, respectively. ICA were detected in 58% (11/19) of patients with IDDM in the first year of the disease. The prevalence of ICA decreased drastically with prolongation of the disease. We could not find any ICA-positive IDDM in subjects with a clinical course of more than 10 years. The level of thyroid microsomal antibodies was not significantly higher in either type of diabetes when compared to nondiabetic controls. These results suggest that Japanese diabetics may have a weaker autoimmune predisposition than Caucasians.

Adult↗
PubMed1983

Blood groups and diabetes mellitus: a possible tool in the analysis of the hereditary background of diabetes mellitus.

Blood groups ABO, MN, P1, Lewis and KIDD, were examined in 64 adult and 53 child diabetics. Patients were classified into 4 groups, NIDDM (n = 30), Insulin less than 20 U (n = 13) and Insulin greater than or equal to 20 U (n = 21) in adults and IDDM in children (n = 53). ABO blood group was found to have some association with Insulin greater than or equal to 20 U and IDDM. P1(+) was significantly rarer in the Insulin greater than or equal to 20 U group in adults, while this difference was not observed in IDDM in children. MN, Lewis and KIDD blood groups did not show any association with diabetes mellitus in our study. Further studies are needed to clarify the association of blood groups with diabetes mellitus.

Adult↗
PubMed1983

The features of causes of death in Japanese diabetics during the period 1971-1980.

The principal causes of death among 9,737 diabetics who died in 280 hospitals all over Japan during the period 1971-1980 have been analyzed retrospectively in this study. The main cause of death in Japanese diabetics was vascular complications. The mortality from vascular complications was 41.5%, 37.9% for males and 46.8% for females, increasing with the duration of diabetes and with age. The most interesting findings were of cardiovascular disease which was the cause of death in 12.3% of the subjects in our study as compared to 54.6% of the Joslin Clinic patients (1971). However, our incidence rate was almost twice that reported in Japan in 1967 by Goto (Japan). In contrast, cerebrovascular disease and nephropathy are much more common in Japanese than in American diabetics. Recently cancer has become more common in Japanese diabetics and 25.3% of the deaths have been assigned to it. In contrast, diabetic coma due to hyperglycemia accounted for only 4.1% of deaths. The average life span of Japanese diabetics is still over 10 years shorter than that of non-diabetics.

Adult↗
PubMed1983

The pharmacokinetics of insulin after continuous subcutaneous infusion or bolus subcutaneous injection in diabetic patients.

Pharmacokinetic models of insulin were examined in order to describe a plasma concentration-time profile after subcutaneous (s.c.) administration of insulin to the patients with insulin-dependent diabetes mellitus (IDDM) or non-insulin-dependent diabetes mellitus (NIDDM). Diabetic subjects were restricted to those with fasting plasma insulin levels around the lowest limit for insulin assay (5 microU/ml). A one-compartment open model with first-order absorption and elimination was appropriate for estimating the plasma concentration-time profile of insulin injected or infused subcutaneously. In the case of continuous s.c. insulin infusion (CSII) for 1 h at the rate of 3 ml/h (2--3 U/ml), the absorption rate constant (Ka), elimination rate constant (Ke), and distribution volume (Vd) were 0.026 +/- 0.001 min-1 (mean +/- SEM; absorption half-life: 27 min), 0.013 +/- 0.005 min-1 (elimination half-life: 53 min), and 1.99 +/- 0.49 L/kg body wt, respectively. These values did not differ significantly from those generated by single bolus s.c. injection of undiluted insulin (40 U/ml). The calculated areas under the plasma insulin concentration-time curves from time zero to infinity ([AUC] 0 infinity) did not differ after each mode of administration, while the [AUC] 0 infinity after CSII was about 32% of that following intravenous bolus injection (P less than 0.01). The following conclusions can be drawn from these results: (1) the plasma concentration-time profile of insulin after CSII or bolus s.c. injection can be analyzed by pharmacokinetic modeling, (2) the absorption kinetics of insulin did ot differ significantly between two modes of s.c. insulin administration in the patients with IDDM or NIDDM, and (3) the insulin after CSII or single bolus s.c. injection seems to be degraded at the s.c. site to the same extent.

Adult↗
PubMed1983

Long-term and dependent growth of human leukemic blast cells with granulocyte-macrophage differentiation in vitro.

A clonal growth of leukemic cells from the bone marrow of a patient with acute myeloid leukemia was observed in vitro for more than 20 months. Cytochemical and electron microscopic studies of the cells growing in vitro demonstrated that they were blast cells, differentiated granulocytes, and macrophages. They showed complete dependence on granulocyte-macrophage colony-stimulating factor for colony formation in agar. In addition to the presence of granulocytic colonies, some showed granulocyte-macrophage characteristics, suggesting that bipotential cells were also involved in long-term growth. Initially, they showed localized proliferation on or around giant fibroblast-like cells. Even after constant growth was established, attempts to transfer these cells were unsuccessful, and their growth was confined to the original flasks. These observations seen to indicate that their growth was not autonomous but dependent on the adherent cells in the flasks. This was also supported by a coculture experiment in which the cells were demonstrated to proliferate for 4 months only in the presence of normal bone marrow particles and bone marrow particle-derived feeder layers. These results suggest that, in some cases, long-term growth of leukemic cells can be induced in vitro by the cocultivation of bone marrow stromal cells.

Adult↗
PubMed1983

Association of hypercalcemia with tumors producing colony-stimulating factor(s).

Two human malignant tumors, which we previously reported to produce colony-stimulating factors (CSFs), were found to be accompanied by remarkable hypercalcemia. A patient with a CSF-producing lower jaw cancer (squamous cell carcinoma) developed a marked granulocytosis (150,000/microliters) and hypercalcemia (more than 215 mg/dl). The tumor was successfully transplanted into nude mice, which developed marked granulocytosis (300,000/microliters) and hypercalcemia (20 mg/dl). White blood cell and serum calcium concentrations of these mice decreased promptly to normal levels when the tumor was excised. Treatment with prednisolone (1.5 mg/kg) or indomethacin (5 mg/kg) had no effect on the serum calcium level of these mice. Parathyroid hormone or prostaglandin E was not increased in the serum of the mice or in the tumor tissue. However, the mice bearing the tumor excreted extremely large amounts of calcium in their urine, and their bony tissues contained less calcium and phosphorus than controls. Moreover, histology of bony tissues of these nude mice clearly demonstrated the decrease in trabecular tissues and cortical thickness as well as remarkable activation of osteoclasts. Another patient with a CSF-producing bronchogenic squamous cell carcinoma showed mild granulocytosis and hypercalcemia. The biopsied tumor tissue was transplanted into nude mice, which developed marked granulocytosis (300,000/microliters) and also severe hypercalcemia (18 mg/dl). These results suggest the presence of a new syndrome of granulocytosis and hypercalcemia associated with CSF-producing tumors. The causal mechanism of the hypercalcemia was shown to be some humoral factor which activates osteoclasts other than parathyroid hormone. Neither prostaglandins nor osteoclast-activating factor seemed to be the cause of the hypercalcemia.

Adult↗
PubMed1983

Hereditary multisystemic degeneration with unusual combination of cerebellipetal, dentato-rubral, and nigro-subthalamo-pallidal degenerations.

An autopsy case of a 51-year-old housewife with dominantly inherited ataxia is reported. Pathologic examination revealed an unusual combination of systemic degenerations: spinocerebellar tracts, pontine basis and middle cerebellar peduncles, dentato-rubral and nigro-subthalamo-pallidal systems, upper and lower motor neurons, ascending sensory system, and optic tracts. The inferior olive and cerebellar cortex showed only a slight change. The combination of the dentato-rubral with nigro-subthalamo-pallidal degenerations in a case with cerebellipetal systemic degeneration was particularly striking. Furthermore, combined degeneration of the ocular motor nuclei, vestibular nuclear group, perihypoglossal nuclei, fastigial nucleus, medial longitudinal fasciculus, and vestibulospinal tracts occurred. According to recent experimental results, these lesions were restricted precisely to the anatomophysiologically interrelated system for the control of eye movement. The present case is considered an example of systemic degeneration as a pathologic basis for ophthalmoplegia.

Brain Diseases↗
PubMed1983

Changes in aminolevulinate synthase and aminolevulinate dehydratase activity in cirrhotic liver.

Delta-Aminolevulinate synthase and delta-aminolevulinate dehydratase activities were determined in liver biopsy specimens obtained from 12 patients with hepatic cirrhosis. Delta-Aminolevulinate synthase activity was determined by the incorporation of [1,4-14C]succinyl coenzyme A into delta-aminolevulinate. The mean activity of delta-aminolevulinate synthase was significantly higher in cirrhotic liver specimens (mean +/- SE, 193.7 +/- 34.5 picomoles delta-aminolevulinate per milligram protein per 30 minutes) than in controls with minimal histologic changes (32.7 +/- 13.6, p less than 0.01). Furthermore, the mean activity of delta-aminolevulinate synthase was higher in micronodular cirrhosis (281.6 +/- 58.8) than in the other types of cirrhosis (131.0 +/- 23.1, p less than 0.05). Levels of indocyanine green retention at 15 min correlated with the activity of hepatic delta-aminolevulinate synthase (p less than 0.05). The mean activity of delta-aminolevulinate dehydratase, in contrast, was significantly lower in cirrhotic liver specimens (9.4 +/- 1.3 nanomoles porphobilinogen per milligram protein per hour) than in controls (22.0 +/- 2.6, p less than 0.05). These results suggest that the extent of liver injury or the degree of portosystemic shunting, or both, influence the rate of hepatic heme biosynthesis.

5-Aminolevulinate Synthetase↗