Neutrino oscillations and the anomalous atmospheric neutrino flux.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Honda.
Explore the source record for details and available documents.
The influence of a Mg-deficient diet on blood pressure and various hormonal systems was examined in Wistar rats (WR) and spontaneously hypertensive rats (SHR). The WR and SHR were individually divided into 2 groups. The Mg-deficient diet was given to one group, and a Mg-containing diet was given to the other group for 3 weeks. During this experimental period, the body weight, blood pressure, urine volume, blood and urinary electrolytes, plasma steroid hormones, plasma renin activity (PRA), and urinary hormones [kinin, prostaglandin E2 (PGE2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), and noradrenaline] were examined. Although no significant difference in body weight was observed between the Mg-deficient and Mg-containing diet groups in either the WR or SHR (because the experiments were performed in a pair-fed fashion in both kinds of rat), the blood pressure was increased in the Mg-containing diet group but was unchanged in the Mg-deficient diet group. As regards changes in electrolytes, a decreased urinary excretion of Mg and significantly increased urinary excretion of P were observed in the Mg-deficient diet group in both the WR and SHR. Furthermore, decreased levels of serum Mg and P and increased levels of serum Ca were also noted. In the WR group, the urinary excretion of noradrenaline was significantly increased in the Mg-deficient diet group as compared to the Mg-containing diet group. However, the change was reversed in the SHR group. The plasma steroid hormones and PRA were both significantly low in the Mg-deficient diet group in both the WR and SHR. The urinary excretions of PGE2, 6-keto-PGF1 alpha, and kinin showed no significant differences between the two diet groups. The above results indicate that blood pressure is not affected by the Mg-deficient diet in either the WR or SHR, and the possible participation of the sympathetic nervous system in the mechanism of control of blood pressure may differ somewhat between the WR and SHR. In addition, Mg ion was found to play an important role in the biosynthesis of renin and steroid hormones but to have no such significant role in the urinary excretions of kinin, PGE2, and 6-keto-PGF1 alpha.
Explore the source record for details and available documents.
A very sensitive fluorescence sandwich enzyme-linked immunosorbent assay (FS-ELISA) for the detection of soluble and cell-associated human interleukin-2 receptors (IL-2R) has been developed. For use in this assay system, two anti-human IL-2R monoclonal antibodies, H 48 and biotinylated HA 26, were selected from six monoclonal antibodies directed against different epitopes on the IL-2R molecule. The FS-ELISA specifically detected human IL-2R in both the culture supernatants and cell lysates of human IL-2R-bearing cells and the assay displayed a 10(3)-fold increase in sensitivity over the usual colorimetric IL-2R ELISA. The IL-2R molecules in supernatants and lysates of the PHA-stimulated mononuclear cells were of 50,000 and 60,000 molecular weight, respectively, as estimated by size exclusion high performance liquid chromatography.
Explore the source record for details and available documents.
Monoclonal antibody-drug conjugates were applied as a clinical trial for patients who, based on the experimental study, had colorectal cancer. Monoclonal antibody A7, from a mouse splenocyte immunized against human colon cancer, was used as a drug carrier for colon cancer. The anti-cancer drugs mitomycin C (MMC) and neocarzinostatin (NCS) were bound covalently to A7 to form the conjugates A7-MMC and A7-NCS. The in vitro cytotoxic effects of the conjugates on SW1116 cells were stronger than those on free MMC or NCS. The conjugate A7-NCS, when administered to nude mice, brought about the highest NCS tumor concentration, whereas normal immunoglobulin G (IgG)-NCS distributed evenly in all tissues. The conjugates showed a strong antitumor effect on colon cancer transplanted into nude mice. Forty-one patients with colorectal cancer, including ten patients with postoperative metastasis, were given A7-NCS. The immunoperoxidase and drug concentration studies of the resected specimens showed that NCS was localized specifically in cancer. Patients receiving the conjugate did not experience serious adverse effects. Of the eight patients with postoperative liver metastasis, three showed evidence of tumor reduction on computed tomography (CT) scan and three claimed pain relief. The conjugate did not benefit patients with multiple lung metastasis or peritoneal metastasis.
Spironolactone was administered to spontaneously hypertensive rats (SHRs) in order to examine the urinary excretions of prostaglandin E2 (PGE2) and kinin. Thirteen SHRs were divided into 2 groups, and 0.1 ml of sesame oil was administered to one of 2 groups (spironolactone-untreated group) (n = 6) and 20 mg of spironolactone in 0.1 ml of sesame oil was administered to the other group (spironolactone-treated group) (n = 7) by the subcutaneous route for 10 days in succession, followed by the determination of body weight, blood pressure, urine volume, excretion levels of Na, K, kinin and PGE2 in 24-hour urine. Blood samples were drawn after these animals were killed by decapitation for determining plasma renin activity (PRA). In consequence, decreased blood pressure and increased urinary Na excretion were observed in the spironolactone-treated group. On the other hand, PGE2 excretion level in 24-hour urine markedly decreased immediately after administration of spironolactone (p less than 0.05) and was maintained at lower levels up to the end of experiment. However, 24-hour urinary kinin levels showed similar changes in the spironolactone-treated group and the untreated group with no significant difference between the two groups. These results indicate that spironolactone has a suppressive effect on urinary PGE2 excretion, the activity of which is not mediated by kinin production in the kidneys but produced by a direct action of spironolactone itself.
Single photon emission computed tomography with [123 I] isopropylamphetamine was carried out on a patient with motor neuron disease with dementia. [123 I] uptake was decreased in the frontal lobes. This would reflect the histopathological findings such as neuronal loss and gliosis in the frontal lobes.
In order to examine the role of calcium ion in ACTH-induced steroidogenesis in humans, we carried out infusion of a pharmacological dose of ACTH (4.2 micrograms/kg) and a physiological dose of ACTH (0.0084 microgram/kg) for 120 min, and infusion of dibutyryl cyclic AMP (DBcAMP) [0.33 mg/kg/min] for 20 min, in 22 normal subjects with or without verapamil treatment (360 mg/day, orally) for 5 days. The subjects were pretreated with 1.0 mg of dexamethasone and 5.0 mg of enalapril daily for 2 days before each infusion test to inhibit endogenous ACTH and angiotensin II. Following infusion of 0.0084 microgram/kg of ACTH, plasma levels of corticosterone (P less than 0.02) and cortisol (P less than 0.01) were significantly increased; with chronic verapamil treatment plasma levels of corticosterone (P less than 0.05) and cortisol (P less than 0.02) were significantly lower than those without verapamil. On the other hand, 4.2 micrograms/kg of ACTH for 120 min significantly increased the plasma levels of several steroid hormones, although there were no differences between the infusion with and without verapamil. Infusion of DBcAMP for 20 min significantly increased plasma levels of corticosterone (P less than 0.02) and cortisol (P less than 0.01), but verapamil did not affect the steroidogenic response to the DBcAMP infusion. The present results suggest that steroidogenesis induced by a physiological dose of ACTH differs from that after a pharmacological dose of ACTH or DBcAMP, and is mediated mainly by calcium ion as an intracellular messenger in man.
Explore the source record for details and available documents.
Deficiency of magnesium with cardiovascular effects is thought to be related to alterations in the biosynthesis of prostaglandins (PGs) in the vasculature. Measurements were made of the PGE2, 6-keto-PGF1 alpha and thromboxane B2 (TxB2) outflow from the perfused isolated mesenteric arterial bed and the fatty acid composition of the tissue in rats maintained for 14 weeks on a low magnesium (LMg) diet. The serum Mg levels were significantly decreased and the serum Ca levels were significantly increased in the LMg group as compared to the controls. The arachidonic acid concentration in the triacylglyceride fraction was significantly increased in the LMg group. Long chain polyunsaturates such as 22:4n6 and 22:6n3 were consistently increased in the LMg rats as compared to the controls in both the phospholipid and triglyceride fractions as previously reported in other tissues. The PGE2, 6-keto-PGF1 alpha and TxB2 outflows were significantly increased in the LMg group as compared to the controls. These findings suggest that the biosynthesis of eicosanoids, mainly PGI2, is stimulated in Mg deficiency, and this may provide protection against intracellular Mg depletion and Ca accumulation, so as to counteract to the constricted and hyperreactive state of the vasculature in such a condition.
To evaluate the possible role of somatomedin-C, insulin-like growth factor I, in renal hypertrophy in early diabetes, kidney tissue SmC concentrations were measured in streptozotocin-induced (80 mg/kg ip) diabetic rats. Body weight, liver weight, plasma SmC concentration, and SmC concentration in the liver of diabetic rats were significantly lower than those of controls. Seven days after induction of diabetes, the kidney weight (898 +/- 95 mg) in diabetic rats was significantly greater than that in controls (755 +/- 69 mg), while SmC concentration in the kidney of diabetic rats (1.7 +/- 0.3 U/g kidney) was significantly lower than that of control rats (5.4 +/- 0.6 U/g kidney). These results suggest that renal SmC may not have an important role in renal hypertrophy in early stages of diabetes and that renal production of SmC may be impaired by insulin deficiency in rats.
The effects of elastase on blood pressure (B.P.) and the urinary excretions of prostaglandins (PGs) and catecholamines in the spontaneously hypertensive rat (SHR) were investigated. Male SHRs (n = 20), castrated at 4 weeks of age, were divided into 2 groups. Elastase was then dissolved in saline (5 mg/ml) and injected subcutaneously (10 mg/kg of body weight) into the SHRs of one of the 2 groups (n = 10) at 5 to 13 weeks of age, and the same dose of saline only was injected subcutaneously into the SHRs of the other group (n = 10) as a control during the same period. B.P. was measured by the tail-cuff method every 2 weeks. Urine sampling and measurement of body weight (B.Wt.) were also performed every 2 weeks. The B.P. in the elastase-administered group (184.1 +/- 3.3 mmHg) was found to be significantly lower (p less than 0.02) than that of the control group (198.0. +/- 4.3) at 9 weeks of age. A significant difference (p less than 0.01) in B.P. between the control group (204.0 +/- 4.5) and the elastase-administered group (187.3 +/- 2.7) was also observed at 13 weeks of age. The urinary excretion of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in the control group (5.1 +/- 0.4 ng/day/100 g B.Wt.) at 11 weeks of age was significantly lower (p less than 0.05) than that of the elastase-administered group (10.4 +/- 1.3).(ABSTRACT TRUNCATED AT 250 WORDS)
Spironolactone was administered to spontaneously hypertensive rats (SHRs) in order to examine the urinary excretions of prostaglandin E2 (PGE2) and kinin. Thirteen SHRs were divided into 2 groups: 0.1 ml of sesame oil was administered to one group (the spironolactone-lactone-untreated group, n = 6) and 20 mg of spironolactone in 0.1 ml of sesame oil was administered to the other group (the spironolactone-treated group, n = 7) by the subcutaneous route for 10 days in succession. Determinations were then made of the body weight, blood pressure, urine volume, and excretion levels of Na, K, kinin and PGE2 in the 24-hour urine. After the animals had been killed by decapitation, blood samples were drawn for determination of the plasma renin activity (PRA). The results obtained indicated decreased blood pressure and increased urinary Na excretion in the spironolactone-treated group. On the other hand, the PGE2 excretion level in the 24-hour urine decreased markedly immediately after administration of spironolactone (p less than 0.05) and was maintained at lower levels up to the end of the experiment. However, the 24-hour urinary kinin levels showed similar changes in both the spironolactone-treated group and the untreated group with no significant difference between them. These findings suggest that spironolactone has a suppressive effect on urinary PGE2 excretion, the activity of which is not mediated by kinin production in the kidneys but is the result of a direct action of spironolactone itself.
To determine the effect of maturation on glucose-induced insulin release after starvation, we investigated the insulin release from perfused pancreas of young adult rats after fasting for 18-20 hr. In the rats weighing 300-400 g (12-14 w) and 200-250 g (7-8 w), the glucose-induced insulin secretion from perfused pancreas of starved rats was similar to that of fed rats. While, in the rats weighing 100-150 g (4-5 w), both the first and the second phase of glucose-induced insulin secretion from perfused pancreas of starved rats was markedly decreased compared with that of fed rats. These results suggest that insulin response to glucose is not matured in young below 150 g (5 w).
Explore the source record for details and available documents.
Our study concerned the existence of humoral factor(s) in cardiac hypertrophy arising from experimental perinephritic hypertension in dogs. Hypertension was induced by the method of Page with some modifications. A microassay technique was used on cultured neonatal rat heart cells. Heart extract from the hypertrophied left ventricle of dogs with experimentally induced renal hypertension, but not sham-operated dogs, increased the uptake of 3H-uridine by cultured rat heart cells. At a final heart extract concentration of 5 X 10(-3)% v/v (1-3 micrograms/ml), 3H-uridine was increased by a mean of about 15%, from four experiments. High performance liquid chromatography showed that the heart extract contained at least 16 molecules. Among them, a molecule of approximately 11,200 molecular weight stimulated the uptake of both 3H-uridine and 14C-leucine by cultured rat heart cells. These results indicate that the heart extract from the hypertrophied left ventricle of dogs with experimentally induced renal hypertension contained a factor that might induce and/or modulate myocardial hypertrophy in the model of hypertension.
Explore the source record for details and available documents.