Skyrme model and strong-coupling model.
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Biomedical subjects
Publications and source records attributed to Y Hara.
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Freezing has been shown to damage pancreatic islets and to disrupt their insulin release, probably because of intracellular ice formation. We compared frozen islets with fresh ones and with others stored at temperatures above freezing from a standpoint of insulin release response to glucose and transplantation. Group A islets, isolated from rats and immersed in 10% dimethyl sulfoxide in RPMI 1640, were stored at -2 degrees C, and group B islets at -196 degrees C, for 7 days. As for group B, the islets were cooled at 1 degree C/min from room temperature to -40 degrees C, subsequently at 3 degrees C/min to -80 degrees C and then put into liquid nitrogen to be rapidly frozen to -196 degrees C. The control islets were fresh. In vitro, basal release at 3.3 mM glucose was similar in group A to that in the controls, but was higher in group B than group A. Stimulated release against 16.7 mM glucose was lower in group A than group B. However, insulin responsiveness, i.e., the ratio of insulin release at 16.7 mM glucose to that at 3.3 mM glucose, was lost in group B. Freezing also caused damage to the group B cells visible under the light and electron microscopes, while group A islets were largely intact. In vivo, after 600 islets were transplanted into streptozotocin-induced diabetic rats, group A was better able to lower fasting blood glucose than was group B, and remained so for 4 weeks. Above sub-zero preservation in the non-frozen state thus seems adequate for the short-term storage for 7 days.
The conventional method for rat islet isolation was improved by injection of collagenase solution (1.3 mg/ml) into the bile duct and the concomitant dissection of the inferior vena cava, static incubation of the removed distended pancreas for 15 min at 37 degrees C and filtration of the digested tissue through two different meshes of 1190 and 590 micron in pore size. This new technique led to about 2.5 times higher yield of viable islets than the conventional method.
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A patient with a somatostatin (SRIH)-secreting islet cell tumor, whose only symptoms were dyspepsia and anemia, is described. The diagnosis of somatostatinoma was based on high plasma SRIH concentrations and immunocytochemical findings. The pancreatic exocrine response to secretin was decreased, whereas the insulin and/or glucagon responses to glucose and arginine were normal. Although the basal plasma GH concentration was normal, the plasma GH response to GHRH was subnormal. Gel permeation chromatography studies indicated that SRIH-14 was the predominant form of SRIH in plasma as well as in tumor tissue.
Inhibitory effects of terazosin on the compensatory blood pressure responses to tilting were studied in conscious rabbits and spontaneously hypertensive rats (SHR). In rabbits, doses which reduced the mean blood pressure by 15 mmHg were 330 micrograms/kg, i.v., for terazosin and 42 micrograms/kg, i.v., for prazosin, while those which depressed the blood pressure responses to tilting by 30 mmHg were 180 micrograms/kg, i.v., for terazosin and 54 micrograms/kg, i.v., for prazosin. In SHR, almost equal decreases in the mean blood pressure (about 30%) were observed by 1 mg/kg prazosin, p.o., 20 mg/kg hexamethonium, i.p., 3 mg/kg hydralazine, p.o., or 3 mg/kg nicardipine, p.o. In these conditions, prazosin and hexamethonium markedly depressed the blood pressure responses to tilting, whereas hydralazine and nicardipine showed little effect. The results with these antihypertensive drugs closely paralleled the established orthostatic profiles seen clinically. In this SHR tilting model, when the mean blood pressure was reduced by 15%, prazosin significantly depressed the tilting reflexes; however, terazosin produced no depression. Considering the dose ratio of terazosin to prazosin for antihypertensive effects and inhibitory effects on the tilting reflexes, the orthostatic liability of terazosin was about 3 times as low as that of prazosin. On the basis of these results, it is expected that terazosin causes less orthostatic hypotension than prazosin in clinical use.
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To study the factors involved in the low thyroid hormone levels in patients with chronic renal failure (CRF), we investigated thyroid functions just before and after hemodialyses (HD) in 32 such patients who were on maintenance HD. In addition, we measured serum thyroid hormone binding inhibitor activities (THBI) in another set of 37 patients. None of the patients had been suspected of having thyroid diseases. HD duration and aging did not have a significant effect on the results of the thyroid function tests. Before each HD, the serum concentrations of T3, T4, FT3, FT4, rT3, PBI, FT3I, FT4I, FT3/T3, FT4/T4, T4/TBG, T4/TSH and FT4/TSH were lower, and those of TSH, TBG, and thyroglobulin (Tg) were higher in the patients than in normal controls. The thyroid hormone concentrations were negatively correlated with the BUN and creatinine levels. The Tg levels were positively correlated with the BUN levels. After each HD, almost all the thyroid function tests including T4/TBG ratio showed improvements, which indicated that hemodilution and a decrease in the T4-binding affinity of TBG with thyroid hormones were the major factors in the low thyroid hormone levels in CRF patients. However, even after HD, T3, FT3, rT3, T4/TSH and FT4/TSH were still lower and TSH and Tg were still higher in the patients. These data suggested that the CRF patients were in a subclinical hypothyroid state. THBI was high in patients with CRF and did not change following HD. NEFA did not seem to contribute to the high THBI before HD, because they were in the normal range. However, as NEFA became very high after HD and possessed THBI, we calculated the corrected THBI (C-THBI) by subtracting the effect of NEFA from total THBI. C-THBI was high before HD and decreased after HD. Therefore, it was suggested that this C-THBI contributed to the abnormalities in the affinity of TBG with thyroid hormones. From these studies, it is concluded that (1) the patients with CRF may be in a subclinical hypothyroid state, although hemodilution was seen to have a strong effect on the thyroid hormone concentrations, and (2) C-THBI may have an effect on the affinity of TBG with thyroid hormones and play an additional role in low thyroid hormone levels in these patients. The mechanisms of hypothyroidism and the nature of C-THBI remain to be clarified.
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A newly established monoclonal radioimmunoassay system (kit II) for carcinoembryonic antigen (CEA) was evaluated in comparison to a conventional polyclonal system (kit I). Among 619 unselected serum samples, approximately 15% were CEA positive with kit I, whereas 27% were positive with kit II; consequently, approximately 12% showed dissociated CEA values to be positive only with kit II. More than 75% of patients with the dissociated values were found to have a malignant disease. Positive rates in normal individuals (266 samples) were less than 5% with both the kit I and kit II and, in those with benign disease were 11.9% with kit II, except for liver cirrhosis in which a quite high positive rate (58%) was obtained. In contrast, a definitely increased positive rate in malignant disease (381 samples) was obtained with kit II (61.4%) in comparison to that with kit I (42.3%). The assessment of technical qualities, such as reproducibility, recovery and dilution tests, demonstrated the excellent performance of kit II.
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The cDNA encoding the third type of alpha-subunit of NaK-ATPase was found in rat brain cDNA library. The deduced amino acid sequence was very similar to those of alpha- and alpha plus-subunits. The third one was suggested to be highly ouabain-sensitive from its aminoacid sequence. From Northern blot analysis the third type of the subunit was not expressed in adult rat kidney and heart.
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