PubMed Health⌕ Search

Biomedical subjects

H Fushimi

Publications and source records attributed to H Fushimi.

At least 73 records · Page 4Linked to original sources
PubMed1989

[Evaluation of a radioimmunoassay of alpha 1-microglobulin (alpha 1-m) with simplified procedures].

A newly established double antibody radioimmunoassay (RIA) was fundamentally and clinically evaluated. Original procedures were partially modified as follows: Sample volume for serum and urine was changed to 25 microliters, and thus 200 mg/l of alpha 1-m standard was prepared using 50 microliters of original standard solution (100 mg/l). The results were satisfactory in sensitivity (0.3 mg/l obtained from -2SD method), intra-assay precision with its coefficient variation (CV) ranging from 3.0 to 7.4%, interassay precision with its CV ranging from 3.0 to 10.7%, and recovery with the mean value of 102.4% in serum and 108.2% in urine respectively. There were no changes about alpha 1-m value between diluted (2 times) and undiluted with high concentration samples. Normal levels of alpha 1-m were less than 25 mg/l in serum and less than 10 mg/l in urine. The present results indicate that the determination of alpha 1-m could be very simple and useful for the most sensitive screening test for the evaluation of renal function.

Alpha-Globulins↗
PubMed1988

Impaired catecholamine secretion as a cause of diabetic autonomic neuropathy.

Human and animal studies were performed to investigate the causes of diabetic autonomic neuropathy. Human diabetics, with and without autonomic neuropathy, were measured for plasma catecholamine response to insulin hypoglycemia and for urinary catecholamine excretion. In streptozotocin-diabetic rats, plasma catecholamine response and tissue catecholamine concentrations were measured at various stages of the disease. As the duration of the diabetic state lengthens in rats, there is a time-proportional stepwise decrease in plasma catecholamine response. This is similar to the clinical course observed in human diabetics, which also includes a reduction of catecholamine excretion after the appearance of autonomic neuropathy. After 6 weeks of diabetes, rat tissue is found to have an increased concentration of catecholamines; this may represent a compensatory reaction to the difficulties of secretion. At 13 weeks of diabetes, tissue catecholamine concentrations return to almost normal, when plasma responses have disappeared. These results suggest that the impaired secretion of catecholamines in diabetics may be a cause of diabetic autonomic neuropathy.

Animals↗
PubMed1987

Leydig cells within the aspermatogenic seminiferous tubules.

Cells identical to Leydig cells were found within a peritubular boundary layer and even inside a basal lamina of seminiferous tubules in three male patients (two with inguinal cryptorchism and one with infertility). The seminiferous tubules of all patients showed a moderate to marked thickening of the boundary layer and a complete loss of spermatogenic cells. The "ectopic Leydig cells" were characterized by the presence of Reinke crystals or an extensively developed smooth endoplasmic reticulum. These cells were believed to have differentiated in situ from myoid cells within the boundary layer and also to have invaded from the interstitial tissue in the form of mature Leydig cells. The occurrence of ectopic Leydig cells appeared to parallel the extent of loss of the Sertoli cells and also that of the thickening of the boundary layer. The functional significance of the ectopic occurrence might be implicated in the impaired spermatogenesis.

Adult↗
PubMed1986

Morphological changes in autonomic ganglionic cells of the heart in diabetic patients.

To clarify the histological changes of the cardiac autonomic nervous system in diabetes mellitus, ganglionic cells of the hearts of autopsy cases were examined light microscopically. In 7 severely diabetic patients, the ganglionic neurons showed cellular contraction, cytoplasmic condensation and poor staining of Nissl substance. As neuronal alterations were obvious neither in the mild diabetic patients nor in the non-diabetic patients, these alterations therefore seemed to correlate with diabetes mellitus. The neuronal changes did not seem to correlate with major coronary arterial atherosclerotic narrowing.

Aged↗
PubMed1985

A new index of autonomic neuropathy in diabetes mellitus: heat stimulated thermographic patterns.

Autonomic neuropathy, especially sympathicopathy, a life-threatening complication of diabetes mellitus, has been difficult to evaluate, and remains undetermined. We studied the thermographic patterns of 62 patients (50-69 years old), revealing the vasodilated activities of one leg by immersing the other leg in a warm water bath, for the detection of sympathetic neuropathy, using Thermoviewer MDJTG-MD. The normal pattern shows an increase in skin temperature, while the flat pattern shows no rise or even a paradoxical decrease. The latter had a significantly longer duration of diabetes and poor blood sugar control. The thermographic pattern is closely related to microangiopathy, R-R interval variation and motor nerve conduction velocity. However, R-R interval variation is often abnormal in patients with normal thermographic patterns, showing vasosympathetic abnormalities appearing far later in the development of diabetic neuropathy. The flat pattern develops slowly after at least several years of poor blood sugar control. Change in the pattern is also gradual and slow. The reproducibility of the pattern is excellent and requires relatively simple and noninvasive techniques. Thermography is one of the most reliable, reproducible and noninvasive indexes for finding and following diabetic sympathetic abnormalities.

Aged↗
PubMed1984

Abnormalities in plasma catecholamine response and tissue catecholamine accumulation in streptozotocin diabetic rats: a possible role for diabetic autonomic neuropathy.

Plasma catecholamine levels, determined by high performance liquid chromatography, were elevated in response to blood withdrawal in normal rats. Such a response was also observed in streptozotocin diabetic rats 2 and 6 weeks after disease onset, but was no longer seen at 13 weeks. Tissue (adrenal, heart, skin, kidney) catecholamine levels in diabetic rats were increased at 6 weeks as well as at 13 weeks. These abnormalities were corrected by insulin treatment in at least a part of diabetic rats. The present data suggest that there might be a catecholamine accumulation, which is later accompanied with an impairment of catecholamine secretion, in diabetic rats, and they gave a basis for an inference that similar changes might play some role in the pathogenesis of diabetic autonomic neuropathy in man.

Adrenal Glands↗
PubMed1982

Increased norepinephrine content in diabetic rat heart.

In an attempt to clarify the mechanism of cardiac neuropathy in diabetes mellitus, Wister male rats were made diabetic by streptozotocin injection for 11 to 13 weeks, and catecholamine concentrations of hearts were determined by high performance liquid chromatography. No apparent histological changes were found in hearts and kidneys of any group of rats. Controls used were age-matched normal rats and Goldblatt-hypertensive rats, because streptozotocin induced diabetic rats appeared to be significantly hypertensive. Heart norepinephrine concentrations of diabetic rats and diabetic-Goldblatt-hypertensive rats were markedly higher (8,380 +/- 300 pmol/g tissue and 6,980 +/- 390, respectively) compared with those of controls and Goldblatt-hypertensive rats (2,700 +/- 470 and 2,010 +/- 300, respectively). These results suggest some disturbances in catecholamine secretion in diabetic hearts before typical microangiopathic changes take place.

Animals↗
PubMed1982

Decreased response of plasma catecholamine to stress in diabetic rats.

Previously we reported that the heart norepinephrine concentration was markedly increased in diabetic rats. To further study the relationship between a disturbance in the autonomic nervous system and catecholamine metabolism in diabetes mellitus, the plasma catecholamine response to stress and catecholamine concentration of heart and adrenals were measured. Wistar male rats were made diabetic by streptozotocin and kept for 13 weeks. A silicon catheter was placed in the superior V. cava 1 week prior to the experiment. Insulin was injected subcutaneously for 3 days once daily. After an overnight fast and without anesthesia, 1 ml of blood, a control sample, was obtained and then the animals were exsanguinated. The blood was mixed with 1 mM EGTA at a final concentration and centrifuged. The tissue was homogenized with 0.4 N perchloric acid containing 1 mM EGTA and centrifuged at 10,000 x g for 20 minutes. Catecholamines were determined by high performance liquid chromatography. Normal rats responded to blood withdrawal stress, and plasma catecholamines were markedly increased, but almost no increase or an actual decrease was observed in diabetic rats. These abnormal responses were improved by insulin treatment. Heart norepinephrine was increased significantly in the diabetic rats compared with the control rats and was reduced significantly by insulin injections. Adrenal epinephrine was also significantly increased in the diabetic rats compared with the control rats, but was not significantly reduced by insulin. These result suggest a possible disturbance of catecholamine secretion in the diabetic rats.

Adrenal Glands↗
PubMed1980

The effects of parabiosis on serum and kidney glycosidase activities in spontaneously diabetic mice.

Spontaneously diabetic non-obese mice of the ICR strain were newly inbred in Shionogi laboratory, Japan. Animals became diabetic suddenly, more frequently and severely in females. Blood glucose levels were 452 +/- 73 mg/100 ml with serum insulin levels of less than 1.0 microU/ml in the fed state. Parabiosis with normal control ICR mice for 2 weeks decreased the blood glucose level to 260 +/- 51 mg/100 ml (P less than 0.01) and resulted in serum insulin levels of 46.0 +/- 18.0 microU/ml (P less than 0.01). Kidney homogenate beta-N-acetylglucosaminidase and beta-galactosidase activities were reduced in diabetic mice (42% and 44% decreases respectively) (P less than 0.025 and P less than 0.001), and restored almost to normal after 2 weeks of parabiosis. Renal alpha-mannosidase activity was decreased 43% (P less than 0.001) in the diabetic mice but unaffected by parabiosis. Serum beta-N-acetylglucosaminidase, beta-galactosidase and alpha-glucosidase activities were significantly increased in diabetic mice (179%; 233% and 58% increase respectively) (P less than 0.005, P less than 0.001 and P less than 0.001), and returned to normal with parabiosis.

Animals↗
PubMed1980

Glycosidase activities in the liver and kidney of hereditary diabetic mice.

Hereditary diabetic mice (NSY) were inbred from original streptozotocin diabetic ICR mice for 8-9 generations using hyperglycemia as an index. The normoglycemic ICR mice were used as controls for the NSY line. The nonfasting blood sugar level of the NSY mice was 305 +/- 14 mg/100ml, while their immunoreactive insulin level was 30 +/- 4 microU/ml (the values of the controls were 165 +/- 12 mg/100 ml and 79 +/- 14 microU/ml, respectively). beta-N-Acetylglucosaminidase [EC 3.2.1.29], beta-galactosidase [EC 3.2.1.23], alpha-glucosidase [EC 3.2.1.21], and alpha-mannosidase [EC 3.2.1.24] activities were determined in the 1,000 X g supernatant of the liver and the kidney of control and streptozotocin diabetic ICR mice and their NSY line. In the kidneys of the insulinopenic NSY mice, the beta-galactosidase and alpha-mannosidase activities were significantly decreased. No significant changes were found in liver enzyme activities. Insulin treatment increased the kidney beta-galactosidase activity signficantly. The insulinopenic state, which caused a decrease in the glycosidase activities in the kidney, could induce retarded breakdown of glycoprotein.

Animals↗
PubMed1980

A case of insulin autoimmune syndrome associated with small insulinomas and rheumatoid arthritis.

Twenty five cases of insulin autoimmune syndrome including this case has been reported so far without having the pathogenesis clarified. This paper describes a case which suggests one aspect of pathogenesis. The patient, a housewife concurrently had insulinoma and severe rheumatoid arthritis, complaining of hypoglycemic syncope attacks. During the attacks her blood sugar levels ranged from 19 to 22 mg%. Her serum extractable immunoreactive insulin (IRI) and insulin binding antibody levels were 557 microunits/ml and 0.390 mU/ml, respectively. gamma-Globulin-bound insulin was also measured electrophoretically. Bio-Gel P 10 column chromatography eluted almost all IRI at the void volume at pH 7.4 and a smaller but significant IRI peak also at pH 3.0. Selective angiography revealed a tumor-like staining in the pancreas body. Pancreatectomy relieved her of hypoglycemic attacks. Histology disclosed two small insulinomas. Insulinoma, rheumatoid arthritis and insulin autoimmune syndrome coexisted in this case, suggesting some causal relationship among them.

Adenoma, Islet Cell↗
PubMed1980

An approach to the genesis of idiopathic cardiomyopathy.

The turnover of cholesterol of red blood cells in healthy hamsters was faster than that in cardiomyopathic hamsters. The uptake of 2-deoxy-D-glucose by heart cells was more rapid in the diseased hamsters compared with that of the healthy ones. Freeze-etch study of heart cells disclosed a difference of membrane structure between the two groups. Results of lactate content in hearts with nonexercised and exercised hamsters of both the diseased and healthy groups revealed the retention of lactate in the diseased hearts, even in a nonexercised state. Electron microscopic findings confirmed that an increased hypoxic condition caused by exercise aggravates the diseaes in the cardiomyopathic hamsters. These two conditions, membrane abnormality and hypoxia, probably play a role fundamental to the genesis of the disease, because hypoxia in the cellular level may well be caused by membrane abnormality.

Animals↗