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Biomedical subjects

K Uchida

Publications and source records attributed to K Uchida.

At least 1,513 records · Page 84Linked to original sources
PubMed1979

Should the ruptured renal allograft be removed?

During a 16-month period when 93 renal transplants were performed, eight kidney graft ruptures were detected within 18 days of transplantation, without evidence of venous obstruction. Six grafts were removed at the time of an exploratory operation for rupture and only one showed signs of probable irreversible rejection when examined by microscopy. Two graft ruptures were repaired and one of these grafts has had good long-term function 22 months later. These observations suggest that if bleeding at the site of grafts has had good long-term function 22 months later. These observations suggest that if bleeding at the site of graft rupture can be securely controlled and if the conditions of the patient and of the graft are favorable except for the rupture, it may be possible to save more than one of eight grafts.

Adolescent↗
PubMed1979

Rat stomach kallikrein: its purification and properties.

From rat stomach, kallikrein was purified by chromatographies on columns of p-aminobenzamidine-Sepharose, DEAE-Sephadex A-50 and Sephadex G-150 and by isoelectric focusing, measuring its activities to hydrolyse prolylphenylalanyl-arginine-4-methyl-coumarine amide (Pro-Phe-Arg-MCA) and to release kinin from rat heated-plasma. The purified stomach kallikrein showed a single band on Disc electrophoresis at pH 7.0. The molecular weight of the kallikrein was calculated to be 29,000 by gel-filtration on a column of Sephadex G-50. The kallikrein was stable between pH 6 and 11 and hydrolysed Pro-Phe-Arg-MCA optimally at pH 11.0. The Pro-Phe-Arg-MCA hydrolysing activity of rat stomach kallikrein was inhibited by DFP and Trasylol, but not by trypsin inhibitors from soyabean, limabean and ovomucoid. These properties of rat stomach kallikrein was clearly distinguishable from those of partially purified rat plasma kallikrein, but similar properties to other glandular kallikreins from other species. From these results, it was concluded that kallikrein is present in rat stomach, which can be classified into glandular kallikrein.

Animals↗
PubMed1979

The surface connected canalicular system of carp (Cyprinus carpio) thrombocytes: its fine structure and three-dimensional architecture.

The presence and the three dimensional distribution of the surface connected canalicular system (SCCS) in thrombocytes of a teleost, Cyprinus carpio, were studied using a transmission electron microscope, a high voltage electron microscope and a scanning electron microscope. When the specimens were fixed routinely in glutaraldehyde followed by osmium tetroxide, numerous electron lucent vesicles and canaliculi were distributed throughout the cytoplasm. As ruthenium red-positive reaction product was observed on the inner surface of the vesicles and canaliculi, these are defined as the SCCS of carp thrombocytes. In the stereo-pair of the photographs of thick sectioned specimens and the plastic reconstruction of serially sectioned thrombocytes, we succeeded in finding the whole structure of the SCCS which is composed of numerous anastomosing canaliculi. Scanning electron micrographs revealed many crater-like depressions throughout the cell surface which seem to be the openings of the SCCS.

Animals↗
PubMed1979

Fine structural distribution of the surface-connected canalicular system in frog thrombocytes.

The existence of the surface-connected canalicular system (SCCS) has been demonstrated in semithick sections of the frog thrombocytes by the use of a high voltage electron microscope. The SCCS of the thrombocytes in Rana catesbeiana and Rana nigromaculata consists of numerous canaliculi and vesicles with a diameter of 250 nm, which join with one another to make a complex network throughout the cytoplasm. Although the SCCS of Xenopus laevis fits well into the pattern described in Rana catebeiana, the diameter of the canaliculi of the SCCS is about 500 nm. The results of this study suggest that the SCCS is a specific organelle of the thrombocyte system common to submammals and mammals.

Animals↗
PubMed1979

Degradation of rat cardiac myofibrils and myofibrillar proteins by a myosin-cleaving protease.

The degradation of rat cardiac myofibrils and their constituent proteins with a myosin-cleaving protease was studied. Electrophoretograms of the digestion products of myofibrils showed that myosin,M-protein, C-protein, and troponin were degraded, but actin and tropomyosin were not. Degradation of these constituents resulted in losses of the Mg2+-ATPase activity and its Ca2+-sensitivity of myofibrils. Incubation of myofibrils with the protease induced the release of alpha-actinin without degradation. Susceptibilities of myosin, actin, troponin, and alpha-actinin purified from rat and pig hearts to the protease were essentially identical to those of the assembled forms in myofibrils. Although the purified tropomyosin was readily degraded into five fragments with the protease, the tropomyosin assembled in myofibrils and actin-tropomyosin complex were insusceptible to the protease. Digestion of myosin in the filamentous state with the protease resulted in the disappearance of myosin heavy chain and light chain 2, producing two fragments having molecular weights of 130,000 and 94,000 which originated from the degradation of heavy chain. The Ca2+- and EDTA-ATPase activities of the degradation products remained unchanged during incubation for 22 h. The actin-activated ATPase activity of myosin was reduced by 30% during incubation for 6 h, and recovered to the original level on adding actin to give a ratio of actin to myosin of 2:1. The pH optima for degradation of myosin in the soluble and filamentous states were 8.5 and 7.0, respectively. The results indicate that cardiac myosin in the filamentous state was more readily degraded with the protease than the myosin in the soluble state.

Actinin↗
PubMed1979

Reduced response of plasma aldosterone to acute ACTH stimulation during long-term treatment with spironolactone in essential hypertension.

The response of plasma aldosterone (PA) to ACTH administration (250 micrograms alpha 1-24 ACTH i.m.) before and during treatment with spironolactone (Sp, 75--100 mg/day) for at least 8 months was studied in 11 patients with essential hypertension. These responses were compared with those before and during prolonged treatment with hydrochlorothiazide (Th, 50--75 mg/day), with or without potassium supplement, in 14 hypertensives. PA and plasma cortisol (PC) were determined by radioimmunoassay in which Sp showed minimal cross-reactivity. Both Sp and Th treatments caused similar increases in plasma renin activity accompanied by nearly identical decreases in blood pressure and body weight. PA was also increased by both treatments, but to a significantly greater extent in the Sp-treated group. Serum potassium concentration was increased only by Sp treatment. The response of PA, but not of PC, to acute ACTH stimulation was blunted in the Sp-treated group. That is, the maximal increment of PA above the baseline level was significantly lower during Sp treatment than either before Sp treatment of during Th treatment. These results demonstrate that long-term treatment with Sp can inhibit aldosterone production by acute ACTH stimulation in patients with essential hypertension.

Adrenocorticotropic Hormone↗
PubMed1979

Selective hypoaldosteronism with hyperreninemia in a diabetic patient.

A 62-yr-old diabetic woman exhibited low plasma and urinary aldosterone levels in the face of markedly elevated PRA during the course of nonketoacidotic hyperglycemic precoma with dehydration, hyponatremia, and hyperkalemia, for which she was hospitalized. Studies performed after her recovery from precoma revealed hyperreninemic hypoaldosteronism with normal adrenoglucocorticoid function. While the patient was supine, PRA on a 256-meq sodium intake was at or above the upper limit of the normal range for a 200-meq sodium intake; furthermore, after sodium depletion with furosemide and 4 h of ambulation, PRA markedly increased. No increases in plasma inactive renin were found. Plasma renin substrate concentration was normal. Plasma levels and urinary excretion of aldosterone were low and increased slightly during sodium restriction with insulin treatment, accompanied by hyperkalemia and sodium loss, despite markedly elevated PRA. Repository ACTH administration induced sodium retention and potassium loss with a normal increase in urinary 17-hydroxycorticosteroids. Plasma levels of deoxycorticosterone, corticosterone, and 18-hydroxycorticosterone were normal, while plasma aldosterone was low. Levels of these mineralocorticoids remained unchanged during angiotensin II infusion on both 256-meq and 100-meq sodium intakes. Rapid ACTH administration produced normal increases in plasma deoxycorticosterone and corticosterone but caused a subnormal increase in plasma aldosterone. These results suggest adrenal insensitivity to angiotensin II, possibly a defect in adrenal angiotensin II receptors, as the cause of hypoldosteronism with hyperreninemia in this patient.

Aldosterone↗
PubMed1979

Altered bile acid metabolism in alloxan diabetic rats.

Changes of cholesterol, phospholipid, triglyceride or bile acid levels in serum liver, bile and feces after the treatment with alloxan were examined in Wistar strain male rats. Serum cholesterol, phospholipid and triglyceride levels and liver cholesterol level markedly increased but liver phospholipid and triglyceride levels remained unchanged. The lipid levels in serum very low density and low density lipoproteins were elevated but those in high density lipoprotein were not. Bile flow was not changed but biliary secretion of cholesterol, phospholipid and bile acids markedly increased. Among the biliary bile acid components, cholic acid markedly increased but the amount of chenodeoxycholic acid was similar to that of normal rats. Fecal excretion of deoxycholic acid increased but that of lithocholic and hyodeoxycholic acids decreased, and alpha, beta- and omega-muricholic acids did not change, thus, the total amount of fecal bile acids remained unchanged. Hepatic cholesterol synthesis was markedly depressed, while cholesterol 7 alpha-hydroxylase activity did not change and cytochrome P-450 content was elevated by about 40%. From such evidence, it was apparent that synthesis of cholic acid increased while that of chenodeoxycholic acid decreased and the total amount of bile acids synthesized did not change in the diabetic rats. Furthermore, marked increase of the pool size of cholic acid and hepatic secretion of cholic acid stimulated the absorption of lipids and produced a hyperlipidemia in the diabetic rats.

Alloxan↗
PubMed1979

Prolonged pseudoaldosteronism induced by glycyrrhizin.

We describe the natural recovery from the aggravated hypertension, hypokalemia and suppression of the renin-aldosterone axis after the glycyrrhizin discontinuation in two mild hypertensive women aged 71 and 68 years, who had been administered 273 to 546 mg glycyrrhizin daily for 1.5 and 6 months, respectively, for the treatment of liver disease. About one month after the glycyrrhizin discontinuation, acceleration of hypertension, hypokalemia and suppression of the renin-aldosterone system still continued in both patients. At this stage, sodium restriction resulted in the normalization of blood pressure with weight loss and the subsequent sodium repletion produced a rapid increase in blood pressure to hypertensive levels observed before sodium restriction, with weight gain. Plasma renin activity and plasma aldosterone were low and did not respond to sodium restriction. Inappropriately excessive amounts of potassium were also excreted in the presence of hypokalemia. About one and a half months later, the improvements of aggravated hypertension, hypokalemia and suppressed renin-aldosterone system gradually occurred in both patients. Sodium restriction performed about three months later in case 2 no longer produced the changes in blood pressure and body weight. Plasma renin activity and plasma aldosterone responded subnormally to sodium restriction. These results demonstrate that both patients had a prolongation of the syndrome resembling primary aldosteronism except the low plasma aldosterone level about one month after the glycyrrhizin discontinuation. The possible mechanisms by which this prolongation was caused are discussed.

Aged↗
PubMed1979

An analysis of follow-up results of 1000 intracranial saccular aneurysms with definitive surgical treatment.

The authors report a follow-up review of 1000 cases of intracranial definitive surgery for saccular aneurysms. The prognosis for such surgical cases is discussed. Postoperative results at least 6 months after discharge from the hospital were analyzed in 876 (93.3%) of the 939 surviving patients. The longest follow-up period was 14 years and 5 months, with an average of 3 years and 7 months. At the time of discharge, there were 543 excellent results, 186 good, 117 fair, 93 poor, and 61 deaths. The chief findings were as follows: 1) Most of the patients determined as "excellent" or "good" at discharge were able to return to normal life; most of the deaths or instances of worsened condition found in the follow-up study were due to new lesions. 2) Fully 62% of the cases determined as "fair" at discharge were found in an improved state at the follow-up study, having returned to normal life. 3) Only 19% of cases determined as "poor" at discharge had improved to the point where a return to normal life was possible, the majority having died or remaining in poor condition.

Adolescent↗
PubMed1979

Bile acid metabolism in benign recurrent intrahepatic cholestasis. Comparative studies on the icteric and anicteric phases of a single case.

Bile acid compositions in the serum, urine, bile, and feces were examined in a typical case of benign recurrent intrahepatic cholestasis for a period of 3 yr. The serum cholesterol level remained almost constant. The serum and urinary levels of total bile acids increased markedly during the icteric phase but returned to normal toward the anicteric phase. Daily fecal excretion of bile acids in the anicteric phase was about three times the normal value. Bile acids in the bile and feces, and in the serum and urine, mainly consisted of chenodeoxycholic and cholic acids, with little deoxycholic acid even in the anicteric phase. Scarcely any coprostanol was found in the feces. These observations suggest that metabolism by intestinal bacteria was altered in this patient. The ratio of cholic acid/chenodeoxycholic acid in the serum was above 2.0 in the icteric phase but was reduced to 0.9 in the anicteric phase. At least three unusual bile acids, designated as peak 7a, 11, and 13, were detected in the feces. The amount of bile acid in peak 7a reached about 10% of the total in the anicteric phase.

Adult↗
PubMed1979

[Two cases of azygos anterior cerebral artery aneurysm (author's transl)].

Two cases with azygos anterior cerebral artery were reported from an analysis of 37 cases of distal anterior cerebral artery aneurysm. Case 1 was a 57-year-old woman. She had an attack of subarachnoid hemorrhage two months before admission to our clinic. The anterior cerebral artery was not demonstrated on the right carotid angiogram, and an azygos anterior cerebral artery was visualized on the left carotid angiogram. The aneurysm was situated at the distal end of the azygos artery. Case 2 was a 71-year-old hypertensive woman. Subarachnoid hemorrhage occurred 6 days before admission to our clinic. The left carotid angiography with contraleteral compression revealed an azygos artery and an aneurysm in its middle part. The azygos arteries in both cases were confirmed at operation and aneurysmal necks were managed without any serious deficit. The distal anterior cerebral artery aneurysm is frequently accompanied by azygos artery. This vascular anomaly may cause a hemodynamic change and may be one of the factors of aneurysmal formation at this part.

Aged↗