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T Hidaka

Publications and source records attributed to T Hidaka.

At least 181 records · Page 10Linked to original sources
PubMed1992

[An autopsy case of malignant rheumatoid arthritis (MRA) which was difficult to distinguish from polyarteritis nodosa (PN)].

We encountered a patient who was diagnosed as rheumatoid arthritis (RA) at 15 years old and developed malignant RA (MRA) within one year. He suffered from mononeuritis multiplex and cutaneous infarction. Despite of treatment including steroid pulse therapy, neuritis progressed. Lung infiltration, pancreatitis and intestinal bleeding were accompanied. He died of disseminated intravascular coagulation on 153 days after admission. Autopsy revealed systemic rheumatoid vasculitis in coronary artery, pancreas, liver, small and large intestine, kidney and lung. These severe vasculitis occurred in young RA patient are rare case and it is important to consider the therapy and prognosis.

Adolescent↗
PubMed1992

Spontaneous reflex sympathetic dystrophy (Sudeck's atrophy) syndrome associated with idiopathic thrombocytopenia.

A 37-year-old woman developed reflex sympathetic dystrophy (RSD) (Sudeck's atrophy) syndrome in the right foot. Simultaneously, she had idiopathic thrombocytopenia. There was no history of injury or bone fracture before onset of RSD. Spontaneous RSD associated with idiopathic thrombocytopenia has rarely been described. A possible relationship between the 2 conditions is discussed.

Adult↗
PubMed1992

Relationship among cardiac sympathetic nerve activity, blood pressure and heart rate during infusion of carperitide in rats.

The effect of the infusion of carperitide (alpha-human atrial natriuretic peptide; alpha-hANP) on cardiac sympathetic nerve activity, blood pressure and heart rate was studied in anesthetized rats. Intravenous infusion of carperitide (0.1 and 1.0 micrograms/kg/min) produced mild and dose-related decreases in mean arterial pressure without significant changes in cardiac sympathetic nerve activity or heart rate. In debuffered rats, carperitide (1.0 micrograms/kg/min) also produced a mild decrease in mean arterial pressure. No significant changes in cardiac sympathetic nerve activity or heart rate were observed. A significant correlation between changes in heart rate and cardiac sympathetic nerve activity was noted during infusion of carperitide and deafferentation did not alter this relationship. In contrast, no significant correlation was observed between changes in cardiac sympathetic nerve activity and blood pressure during infusion of carperitide in either buffer nerve intact or debuffered rats. These results suggest that the reduction of blood pressure induced by intravenous infusion of carperitide may not trigger the baroreceptor-mediated cardiac sympathoexcitation and this inhibition of baroreflex may be responsible for the anti-tachycardic effect of carperitide.

Animals↗
PubMed1992

Bactericidal action at low doses of a new rifamycin derivative, 3'-hydroxy-5'-(4-isobutyl-1-piperazinyl) benzoxazinorifamycin (KRM-1648) on Mycobacterium leprae inoculated into footpads of nude mice.

Among a series of newly-synthesized benzoxazinorifamycins, 2 of the 3'-hydroxy-5'-(4-alkyl-1-piperazinyl) derivatives, named KRM-1648 and KRM-2312, whose respective alkyl residues are isobutyl and isopropyl, were examined for efficacy against nude mouse-model leprosy. KRM-1648 completely inhibited the growth of leprosy bacilli inoculated into nude mouse footpads, even 6 months after the medication had been stopped, when given orally at a daily dose of 0.6 mg/kg, 5 or 6 times weekly, during 3-5 months postinoculation. In comparison, the growth inhibition by KRM-2312 was incomplete under the same conditions, though it was still stronger than that by rifampicin. Complete growth inhibition by KRM-1648 was also observed when it was given orally at a dose of 1 or 3 mg/kg twice weekly during the same period. In contrast, the growth inhibition by rifampicin was only slight at 1 mg/kg and partial at 3 mg/kg under the same condition.

Animals↗
PubMed1991

Electron spin resonance studies on the mechanism of adriamycin-induced heart mitochondrial damages.

Rats were given i.p. injections of Adriamycin (4 mg/kg body weight) for 6 consecutive days. Electron spin resonance spectrometry with spin labeling and a trapping technique was applied to heart mitochondria obtained from treated and control animals, in order to examine the physical response of heart mitochondrial membrane affected by Adriamycin. The Adriamycin treatment resulted in a decrease of membrane fluidity (and an increase in order parameter S), with concomitant dysfunction of respiratory responses. The generation of hydroxyl radicals from mitochondria was enhanced in the Adriamycin-treated group. In addition, superoxide dismutase activity in the mitochondrial matrix was found to decrease. The heart mitochondria of Adriamycin-treated animals contained a large amount of lipid peroxide. These results suggest that the enhancement of hydroxyl radical formation in mitochondria affected by Adriamycin is one of the factors involved in Adriamycin-induced cardiotoxicity.

Animals↗
PubMed1991

Reduction of chromium(VI) in Chinese hamster V-79 cells.

The cellular reduction of chromate(VI) was studied by electron spin resonance spectrometry. Incubation of Chinese hamster V-79 cells with Na2CrO4 resulted in the formation of both chromium(V) and chromium(III) complex in a manner dependent on time (30 min-2 h) and concentration (50-500 microM). Following removal of extracellular chromate, the level of chromium(V) complex decreased quickly during the first hour but more slowly for the next hour, whereas the level of chromium(III) remained unchanged, indicating that chromium(III) is the ultimate ion of this metal in cells. Alkaline elution studies demonstrated that treatment of cells with Na2CrO4 induced DNA single-strand breaks that decreased quickly and DNA-protein crosslinks that persisted for 2 h after removal of this metal. These results suggest that the cellular levels of chromium(V) and chromium(III) may be associated with the formation of DNA damage induced by chromium (VI).

Animals↗
PubMed1991

Prevention of 4-pentenoic acid-induced liver injury in rats by 16,16-dimethyl PGE2.

16,16-Dimethyl PGE2 (dmPGE2) is known to protect against cellular damage in various tissues. Histological and biochemical approaches were used to examine the effect of this prostaglandin on hepatocellular damage in an experimental Reye's syndrome model produced in rats by 4-pentenoic acid. Chronic intraperitoneal administration of 4-pentenoic acid induced an accumulation of fatty droplets throughout the hepatic lobules along with mitochondrial abnormalities including swelling, disappearance of christae, and heterogeneity of matrix. These abnormalities were more intense in the marginal zone and successively decreased nearer to the central vein. Such hepatic abnormalities were markedly reduced by the combined administration of dmPGE2 with 4-pentenoic acid. Biochemical examination confirmed that dmPGE2 was able to inhibit the accumulation of hepatic triglyceride seen after the treatment with 4-pentenoic acid alone. These results indicated that dmPGE2 can prevent characteristic hepatocellular damage in this experimental Reye's syndrome model, suggesting that the involvement of prostaglandins should be taken into account in discussing the etiology and management of this syndrome.

16,16-Dimethylprostaglandin E2↗
PubMed1991

Generation of leukotrienes and hydroxyeicosatetraenoic acids in peritoneal macrophages of tumor-bearing mice.

To examine the potential role of lipoxygenase products in the pathophysiology observed after experimental tumor implantation, we examined the generation of leukotrienes (LTs) and hydroxyeicosatetraenoic acids (HETEs) in peritoneal macrophages. C57BL/6 mice were given subcutaneous inoculations of B16 melanoma cells, and peritoneal macrophages were isolated various days after the inoculation. Macrophages were incubated for 1 h at 37 degrees C in serum-free RPM11640 containing 10 microM calcium ionophore A23187, 10 microM exogenous arachidonic acid (AA), 5 mM cysteine hydrochloride and 1 mM reduced glutathione. LTs and HETEs were separately extracted, passed through Sep-Pak cartridges, then identified and quantitated with a HPLC system using UV absorbance. The B16 melanoma-cell-treated/untreated macrophages were found to produce substantial amounts of 15-HETE, 12-HETE and 5-HETE and LTC4 by enzymatic mechanisms. Thus, when determined under various conditions, the production of HETEs was dependent on substrate-concentration, incubation-time and cell-number. The production of LTC4 was dependent on incubation-time and cell number but not substrate-concentration, indicating utilization of endogenous AA stores. Of these products, 12-HETE and LTC4 showed a significant increase on the fourth day after the tumor cell inoculation and returned to the control level by the 11th day after the same treatment. These results suggest that in vivo tumor cell implantation may induce a transient increase of 12-HETE and LTC4 production in macrophages.

Animals↗
PubMed1991

Interleukin 5 up-regulates high-affinity interleukin 2 receptor expression by human resting peripheral T cells: a comparison with the effect of interleukin 4 on B cells.

The separate regulation mechanisms of cytokines on two classes of interleukin 2 receptors (IL-2R) on human peripheral T and B cells were analyzed by a flow cytometer using a double stain with IL-2R alpha (55 kilodalton Tac) and IL-2R beta (75 kilodalton mik beta 1, mik beta 3). Although the expression of IL-2R alpha by T cells was slightly enhanced by IL-2 and IL-4, expression of the beta chain was diminished by both cytokines. IL-5 by itself did not alter the expression of either IL-2R alpha or beta, but preculturing with IL-2 for 24 h followed by IL-5 for another 24 h induced an increase in IL-2R alpha expression and in simultaneous alpha/beta chain expression. Increased numbers of high-affinity IL-2R were confirmed by 125I binding assays. On B cells, IL-4 increased alpha, beta, and simultaneous alpha/beta chain expression, but IL-4-treated B cells did not show an increased number of high-affinity IL-2R.

B-Lymphocytes↗
PubMed1991

Involvement of active oxygen in lipid peroxide radical reaction of epidermal homogenate following ultraviolet light exposure.

To elucidate the radical mechanism of lipid peroxidation induced by ultraviolet light (UV) irradiation, an electron spin resonance (ESR) study was made on epidermal homogenate prepared from albino rat skin. The exposure of the homogenate to UV light resulted in an increase in lipid peroxide content, which was proportional to the time of UV exposure. Using ESR spin trapping (dimethyl-1-pyrroline-N-oxide, DMPO), the DMPO spin adduct spectrum of lipid radicals (L.) was measured following UV exposure (DMPO-L.:aN = 15.5 G, aH = 22.7 G), as was the spectrum of DMPO-hydroxyl radical (DMPO-OH, aN = aH = 15.5 G). In the presence of superoxide dismutase, the DMPO spin adduct spectrum of lipid radicals was found to be reduced remarkably. Therefore, it was shown that the generation of the lipid radicals partially involves superoxide anion radicals, in addition to hydroxyl radicals. In the ESR free-radical experiment, an ESR signal appeared at g = 2.0064 when the ESR tube filled with homogenate was exposed to UV light at -150 degrees C. The temperature-dependent change in the ESR free radical signal of homogenate exposed to UV light was observed at temperatures varying from -150 degrees C to room temperature. By using degassed samples, it was confirmed that oxygen is involved in the formation of the lipid peroxide radicals (LOO.) from the lipid radicals (L.).

Animals↗
PubMed1991

In vitro antimycobacterial activities of newly synthesized benzoxazinorifamycins.

Newly synthesized rifamycin derivatives, KRM-1648, KRM-1657, KRM-1668, KRM-1686, and KRM-1687, having the chemical structures of 3'-hydroxy-5'-(4-alkylpiperazinyl)-benzoxazinorifamycins (alkyl residues: isobutyl, propyl, sec-butyl, sec-butyl [R configuration], and sec-butyl [S configuration], respectively), were studied for their in vitro antimycobacterial activities. Representative (KRM-1648) MICs for 90% of the strains tested, determined by the agar dilution method on 7H11 medium, of various pathogenic mycobacteria (9 species, 174 strains) were as follows (in micrograms per milliliter): Mycobacterium tuberculosis (rifampin [RMP]-susceptible strains), less than or equal to 0.0125; M. tuberculosis (RMP-resistant strains), 12.5; M. kansasii, 0.05; M. marinum, less than or equal to 0.0125; M. scrofulaceum, 0.1; M. avium, 1.56; M. intracellulare, 0.1; M. fortuitum, greater than 100; and M. chelonae subsp. abscessus and M. chelonae subsp. chelonae, greater than 100. These values are more than 64 times lower than those of RMP, except for the values against RMP-resistant M. tuberculosis (8 times lower) and those against rapid growers, including M. fortuitum and M. chelonae (the same as those of RMP). The other derivatives had similar levels of in vitro activity against these mycobacteria. When murine peritoneal macrophages in which M. intracellulare was phagocytosed in vitro were cultured in the presence of the benzoxazinorifamycins (1 microgram/ml), much more rapid killing of the organisms ingested in the macrophages was seen compared with when the same amount of RMP was added to the medium. The addition of benzoxazinorifamycins at the concentration of 0.05 micrograms/ml caused more marked suppression of intracellular growth of the organisms compared with addition of RMP. KRM-1648 and KRM-1657 inhibited intracellular growth of M. tuberculosis, and their efficacies were much greater than that of RMP.

Animals↗
PubMed1991

Reciprocal responses to exercise in hepatic ketogenesis and lipid secretion in the rat.

The effects of 4 weeks of voluntary exercise (rotating wheel) on serum and liver lipid levels were studied in 6-week-old male Wistar rats. The hypotriglyceridemic effect of exercise was not influenced by the dietary fat levels (4.5 and 14.5%), whereas the hypocholesterolemic effect was higher in a low-fat diet than in a high-fat diet. Although the serum cholesterol-lowering effect of exercise was marginal, the beneficial effect on hepatic lipids was observed only in rats fed a high-cholesterol diet. The hepatic contribution to the serum lipid-lowering action of exercise was examined in the isolated perfused livers of rats fed a low fat diet. The reduction (34%) of serum triglyceride by exercise corresponded to the decrease (32%) in the hepatic triglyceride secretion rate, indicating a significant role of the liver in the hypotriglyceridemic effect of exercise. In contrast, the decrease (31%) in serum total cholesterol was considerably greater than that (23%) in the hepatic secretion, suggesting an extra-hepatic contribution. On the other hand, the hepatic production of ketone body was increased by exercise. These results indicate that the altered hepatic partition of long-chain free fatty acids between esterification and oxidation is one of the causative factors for the serum lipid-lowering effect of exercise.

Animals↗
PubMed1991

Arachidonate metabolism in bovine gallbladder mucosa.

Incubation of [1-14C] arachidonicacid (AA) with homogenates of bovine gallbladder mucosa in the presence or absence of reduced glutathione (GSH) generated large amounts of products that cochromatographed with PGE2 and 6-keto-PGF1 alpha and small amounts of products comigrating with PGF2 alpha, TxB2 and PGD2. In the presence of GSH PGE2-like material was predominantly produced while in the absence of GSH 6-keto-PGF1 alpha-like material was a major product. Identification of PGE2 was performed by its chemical conversion with NaBH4 or KOH treatments and by gas chromatography-mass spectrometry. Identification of 6-keto-PGF1 alpha was confirmed by gas chromatography-mass spectrometry. Gallbladder muscle produced predominantly 6-keto-PGF1 alpha in the presence or absence of GSH. The total amount of cyclooxygenase products was approximately 2 times higher in the mucosa than in the muscle. These results indicate that bovine gallbladder mucosa contains higher levels of fatty acid cyclooxygenase, and PGE2 isomerase and PGI2 synthetase in a proportion different from that in the muscle.

Animals↗
PubMed1991

Riboflavin deficiency caused by treatment with adriamycin.

The present study was undertaken to determine whether administration of adriamycin causes the depletion of riboflavin content. Rats received intraperitoneal injections of adriamycin (4 mg per kg body weight) for 6 consecutive days. Urinary riboflavin excretion began to increase after 2 days of treatment with adriamycin. Erythrocyte FAD levels decreased gradually and plasma lipid peroxide contents increased markedly at the 6th day. The activity coefficient of erythrocyte glutathione reductase showed a significant increase before the decrease of flavin content and the elevation of lipid peroxide level. Therefore, the value of this coefficient obtained from erythrocyte appears to be a reliable index of riboflavin deficiency, particularly during the early stage.

Animals↗
PubMed1991

Does atrial appendectomy aggravate secretory function of atrial natriuretic polypeptide?

The present study was designed to clarify how atrial appendectomy affects hemodynamics and secretory function of atrial natriuretic polypeptide in the failing heart. Eleven mongrel dogs were prepared for the experimental model of high-output heart failure by creation of arteriovenous fistulas between femoral arteries and veins. Two months after the first operation, effects of bilateral atrial appendectomies on basal and pacing-induced secretions of atrial natriuretic polypeptide were investigated in five dogs with simultaneous measurement of various hemodynamic indices. In the remaining six dogs, used as a control group, pacing-induced secretion of atrial natriuretic polypeptide was examined in the same way as in the appendectomy group. After excision of the atrial appendages, neither systolic blood pressure nor either atrial pressure changed, but plasma atrial natriuretic polypeptide level was decreased (292 +/- 54 to 188 +/- 47 pg/ml, p less than 0.01) and cardiac output fell (3.7 +/- 0.9 to 3.0 +/- 0.8 L/min, p less than 0.01). During pacing-induced tachycardia, the peak level of plasma atrial natriuretic polypeptide was lower in the appendectomy group than in the control groups (593 +/- 213 versus 1170 +/- 324 pg/ml, p less than 0.05), despite similar left atrial pressures in the two groups. The excised appendages contained approximately 30% of the total amount of atrial natriuretic polypeptide. These results demonstrate that atrial appendectomy decreases secretory function of atrial natriuretic polypeptide and reduces cardiac output in dogs with experimental high-output heart failure.

Animals↗
PubMed1991

[A case of pregnant woman with lupus anticoagulant positive systemic lupus erythematosus complicated with intrauterine fetal death, eclampsia, and brainstem vascular damage].

A 28-year-old female patient with SLE was found to have complications from intrauterine fetal death, eclampsia, and brainstem vascular damage during pregnancy. These symptoms were associated with lupus anticoagulant (LAC). An LAC positive SLE case with accompanying cerebrovascular disease and fetal loss at the same time has rarely been reported. The first brain CT scan revealed the presence of multiple middle pons infarction. Ten days after onset, a brain MRI showed the change into hemorrhagic infarction in the same region, suggesting disseminated intravascular coagulation (DIC) caused by severe obstetric complications. Although the severity of the brain damage implied poor prognosis, her symptoms were alleviated by intensive care with a large amount of steroid therapy and active rehabilitation. LAC-positive SLE patients are apt to encounter obstetric complications in pregnancy. Therefore they must be treated by medical specialists in cooperation with gynecologists. When they also have accompanying with cerebrovascular diseases, active therapy for SLE is necessary for a good prognosis.

Adult↗