PubMed Health⌕ Search

Biomedical subjects

S Kano

Publications and source records attributed to S Kano.

At least 19 recordsLinked to original sources
PubMed1992

CD3+4-8- alpha beta T cell population with biased T cell receptor V gene usage. Presence in bone marrow and possible involvement of IL-3 for their extrathymic development.

Analysis of TCR of a series of CD4-8- (double negative; DN) alpha beta T cell lines induced with IL-3 revealed that their V gene usage was biased for V alpha 4 and V beta 2. This has been confirmed in the primary short-term cultures. Thus, IL-3 induced the generation of DN alpha beta T cells with predominant V beta 2 gene expression from the CD4+/CD8+ T cell-depleted spleen or bone marrow (BM) cells of both normal and nude BALB/c mice within 10 days. It was further indicated that the V beta 2+ beta-chain genes contained few junctional N regions in both IL-3-induced primary DN alpha beta T cells and continuous lines. Search for the in vivo counterpart of in vitro IL-3-induced DN alpha beta T cells revealed that BM, but not spleens, of normal BALB/c and B6 mice did contain a significant proportion of DN alpha beta T cells, and that the majority of them expressed V beta 2+ beta-chain genes with few junctional N regions. The presence of V beta 2+ DN alpha beta T cells was similarly observed in the BM of BALB/c nude mice, but their proportion varied markedly among various strains of mice, which was not linked to H-2 haplotypes. The results indicated that V beta 2+ DN alpha beta T cells in the BM represented one of the thymus-independent T cell populations, whose development was under the major histocompatibility Ag complex-unlinked genetic control. TCR of these T cells were shown to be functional as judged by the proliferative response to anti-V beta 2 antibody. Taken together, present results suggested that IL-3 could induce differentiation and/or proliferation of DN alpha beta T cells with uniquely limited repertoire, which existed preferentially in BM in vivo, and implied the possible involvement of extrathymic endogenous ligands as a positive selection force.

Animals↗
PubMed1992

Soybean phospholipid dependent reductions in triacylglycerol concentration and synthesis in the liver of fasted-refed rats.

The effect of dietary soybean phospholipid on the activities of hepatic triacylglycerol-synthesizing enzymes was compared with soybean oil in fasted-refed rats. Soybean oil at the dietary level corresponding to 20% but not at 5% fatty acid level (21.2 and 5.3% on weight bases, respectively) significantly decreased liver microsomal diacylglycerol acyltransferase activities measured with the endogenous diacylglycerol substrate. Dietary soybean phospholipid even at the dietary level corresponding to 2% fatty acids (3.4% on weight base) significantly decreased the acyltransferase activities measured with endogenous substrate. The dietary phospholipid further decreased the parameter as the dietary level increased, and at the 5% fatty acid level, it was lower than that obtained with soybean oil at 20% fatty acid level. Soybean oil and phospholipid decreased the diacylglycerol acyltransferase activities measured with the saturating concentration of exogenous dioleoylglycerol substrate only when the activities were expressed in terms of total activity (mumol/min per liver) but to much lesser extents. Dietary phospholipid compared to the oil profoundly decreased not only hepatic triacylglycerol but also microsomal diacylglycerol levels. It was indicated that the availability of microsomal diacylglycerol as the substrate for diacylglycerol transferase is the critical determinant in regulating hepatic triacylglycerol synthesis and concentration in this experimental situation. Alterations in the activities of microsomal glycerol 3-phosphate acyltransferase and of the enzymes in fatty acid synthesis could account for the phospholipid-dependent decrease in the microsomal concentration of this intermediate in triacylglycerol synthesis.

Acyltransferases↗
PubMed1992

Interleukin 6 gene transcripts are expressed in atherosclerotic lesions of genetically hyperlipidemic rabbits.

We have investigated the involvement of interleukin 6 (IL-6), a growth-regulatory molecule for vascular smooth muscle cells (SMC), in the development of atherosclerotic lesions of Watanabe heritable hyperlipidemic (WHHL) rabbits. In in situ hybridization analysis, quite low levels of IL-6 mRNA were expressed in 'quiescent' SMC cultured from WHHL rabbits; however, high levels of IL-6 mRNA were induced in SMC exposed to 10% fetal bovine serum (FBS), suggesting that growth-stimulated SMC themselves can synthesize IL-6. In in vivo WHHL aortae, transcripts for the IL-6 gene were clearly observed in the fibrous plaques. These findings support the premise that IL-6 is an important autocrine and/or paracrine regulator of SMC proliferation and of pathogenesis of atherosclerosis in this animal model.

Animals↗
PubMed1992

Renal potassium wasting in distal renal tubular acidosis: role of aldosterone.

The pathogenesis of renal potassium wasting and hypokalemia in classic renal tubular acidosis (type 1 RTA) remains uncertain. The prevailing theory is that K(+)-Na+ exchange is stimulated due to an inability of the distal tubule to establish a normal steep lumen-peritubular H+ gradient. We encountered a 42-year-old woman with type 1 RTA associated with Sjögren's syndrome, in whom renal potassium wasting and hypokalemia persisted despite sustained correction of systemic acidosis with alkali therapy and increased intake of potassium. In addition, plasma renin activity was markedly increased and the serum aldosterone level was upper-normal despite the hypokalemia. Increased intake of sodium resulted in suppression on the serum aldosterone and correction of renal potassium wasting and hypokalemia. This case shows that secondary hyperaldosteronism, possibly due to an impairment of sodium conservation in the distal tubule, may contribute to the loss of potassium from the distal tubule even after the correction of acidosis.

Acidosis, Renal Tubular↗
PubMed1992

[False positive reaction in measurement of allergen-specific IgE--comparison of 3M IgE FAST-Plus Test using polystyrene well as adsorbent with Phadezym RAST].

Irrelevant IgE binding to cellulose discs is known to give false positive results in Phadezym RAST (Pharmacia) for the estimation of allergen-specific IgE in serum. We investigated FAST-Plus Test (3M Diagnostic Systems), an enzyme-linked sandwich type Fluoro-Allergo-Sorbent Test in which a particular allergen was coated to polystyrene well. Phadezym RAST and CAP RAST (Pharmacia) using cellulose-derivative discs as adsorbent were used as reference methods. Patients' sera which gave negative blank reactions to uncoated filter paper disc in the Phadezym RAST system were assayed for specific IgE to 6 allergens using FAST-Plus Test, CAP RAST and Phadezym RAST, and the results of the former two were compared with those of Phadezym RAST using a comparable class system. FAST-Plus Test showed variable correlations with Phadezym RAST, the correlation coefficients ranged from 0.41 to 0.97 (r = 0.462 in house dust 1, r = 0.713 in house dust 2, r = 0.412 in Candida albicans, r = 0.952 in Dermatophagoides peteronyssinus, r = 0.969 in Dermatophagoides farinae and r = 0.682 in Japanese cedar), although most of the results were within one class difference. Similar correlations were obtained between CAP RAST and Phadezym RAST. Of 3004 patients' sera tested in the past two years using Phadezym RAST, 132 (96 cases) displayed positive blank reactions to the uncoated filter paper disc. Of the 96 cases, 80 sera were assayed for binding of IgE to the uncoated cellulose-derivative disc in the CAP RAST system. 18 showed positive results up to 7 IU/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Allergens↗
PubMed1992

[An emergency coronary artery bypass for failed percutaneous transluminal coronary angioplasty with intractable ventricular tachycardia and fibrillation].

A 73-year-old man with effort angina after myocardial infarction is admitted for percutaneous transluminal coronary angioplasty (PTCA). During PTCA, the left anterior descending artery (LAD) was completely occluded. He was suffered from severe cardiogenic shock with systemic cyanosis and loss of consciousness. Under assist of intraaortic balloon pump (IABP) and cardiac massage, he was transferred to an operating room. Before the start of operation, cardioversion were required 13 times because of repeat attacks of ventricular tachycardia and fibrillation. Coronary artery bypass was completed in 177 minutes after total occlusion of the LAD. At the 5th postoperative day, IABP could be discontinued, and at the 8th postoperative day, the patient was weaned from mechanical ventilation. He was transferred to the prior hospital for rehabilitation on the 65 days after operation. We must try to perform CABG for salvage of myocardium, even if a patient falls in severe cardiogenic shock presenting intractable ventricular tachycardia and fibrillation.

Aged↗
PubMed1992

[A systemic lupus erythematosus patient with multiple aseptic bone necroses, thrombosis of superior mesenteric artery and anti-phospholipid antibody].

A 38 year old woman with systemic lupus erythematosus (SLE) was admitted because of epigastralgia and fever. The diagnosis of SLE was made 22 years ago based on Raynaud's phenomenon, butterfly rash, hair loss, photosensitivity and positive antinuclear antibody. She had episodes of consciousness disturbance, transient visual disturbance of the left eye, and a necrosis of the left big toe. She underwent artificial arthroplasty of bilateral femoral heads 11 years ago, when multiple aseptic necroses of thirteen bones were found, and when anti-cardiolipin (CL) antibody was found to be positive. An echogram of abdomen suggested an obstruction of superior mesenteric artery (SMA) when she was admitted. Selective angiography revealed a complete obstruction of SMA and splenic artery, and incomplete obstruction of celiac artery. Conservative treatment with urokinase infusion and prednisolone 50 mg/day was not effective, and small intestine and right colon were resected on the 23rd hospital day. The pathological examination showed thrombosis of SMA. There was no evidence of arteritis or atherosclerosis. Anti-CL antibody and lupus anticoagulant were positive on admission, but the level of both anti-DNA antibody and complement was normal. Therefore, it was suggested that the thrombosis was related with anti-phospholipid antibody. The characteristic clinical feature were multiple aseptic bone necroses and thromboses of several arteries. We discussed the relationship of thrombosis and the etiology of multiple bone necrosis in this case with anti-phospholipid antibody.

Adult↗
PubMed1992

Recombinant interleukin-6 inhibits the growth of rat mesangial cells in culture.

Murine recombinant interleukin-6 (IL-6) inhibited [3H]thymidine uptake by cultured rat mesangial cells in a dose-dependent manner in the presence of 0.5% fetal bovine serum (FBS). The inhibitory effect of IL-6 on the growth of mesangial cells was also confirmed by a change in cell numbers. In the presence of increased concentrations of FBS (5% or 10%), the effect of IL-6 was not prominent. IL-6 showed no effects on intracellular Ca2+ levels of mesangial cells. IL-6 gene expression was rapidly induced in the "quiescent" mesangial cells by exposure to 20% FBS. These observations support the premise that IL-6 is synthesized in mesangial cells and inhibits the growth of mesangial cells in an autocrine manner.

Animals↗
PubMed1992

[Studies on clinical subsets and severity of systemic lupus erythematosus based on a 1987 questionnaire conducted in Japan--clinical analysis of the outcome and treatments in clinical subsets].

A 1987 questionnaire sponsored by the Health and Welfare Ministry concerning the clinical subsets and severity of systemic lupus erythematosus (SLE) was distributed to 93 medial facilities. A clinical analysis of the outcome and treatments was accomplished on one thousand six hundred and fourteen SLE patients fulfilling ARA criteria. The outcome was evaluated into 6 categories, namely; complete remission, incomplete remission, no change, gradual worsening, rapid worsening and unknown. Treatments included (1) anti-inflammatory drugs, (2) initial dose of prednisolone (PSL) below 29 mg/day, (3) initial dose of PSL from 30 to 59 mg/day, (4) initial dose of PSL above 60 mg/day, (5) pulse therapy, (6) immunosuppressants, (7) plasmapheresis, and (8) hemodialysis. Statistical significances were determined with ridit analysis. The severity of the disease for 1,614 SLE patients was evaluated by the judgement of each medical facility independently, separating it into 3 grades. As a result, 16.8% was evaluated as severe, 54.6% was evaluated as moderate, and 28.6% was evaluated as mild. Clinical subsets were divided into 3 categories according to the outcome; (1) those with high complete remission rates (serositis, convulsion, oral ulcers, unconsciousness, hemolytic anemia and so on), (2) those with high incomplete remission rates (lupus nephritis, digital gangrene, hypertension, peripheral neuropathy, erythema, Raynaud's phenomenon and so on), and (3) those with high rates of no change or worsening (aseptic bone necrosis, pulmonary hypertension, pneumonitis, chronic renal failure and so on). SLE patients with persistent proteinuria below 3.4 g/day, pulmonary hypertension, or pneumonitis treated with large doses of PSL such as an initial dose of PSL above 60 mg/day and/or pulse therapy had a significantly higher remission rate than those treated with small dosages of PSL. Hereafter, the establishment of modes of treatments for increasing the remission rates of intractable clinical subsets in highly desired.

Adolescent↗
PubMed1992

Antioxidant effect of calmodulin antagonists in rat brain homogenate.

Several calmodulin antagonists, W-7, amitriptyline, trifluoperazine, chlorpromazine, dibucaine, prenylamine, calmidazolium, and compound 48/80, inhibited lipid peroxidation induced non-enzymatically in rat brain homogenate by ascorbate and Fe2+. Suggestions of involvement of calmodulin in various oxidative cellular responses, based on experiments using calmodulin antagonists, may need to be re-evaluated.

Animals↗
PubMed1991

Posterior cricoarytenoid muscle denervation.

Vocal fold paralysis most commonly results from injury to the recurrent laryngeal nerve. The length of time required for denervation atrophy would be useful in planning reinnervation procedures. Given the absence of long-term data on the status of the canine posterior cricoarytenoid muscle following denervation, this study was undertaken. The results indicate that muscle atrophy does not occur for at least 1 year following denervation.

Animals↗
PubMed1991

Effects of MPTP, MPP+, and paraquat on NADPH-dependent lipid peroxidation in mouse brain and lung microsomes.

Both MPTP and MPP+ inhibited the NADPH-dependent microsomal LPO in mouse brain and lung. On the other hand, PQ significantly stimulated the LPO in brain microsomes in a dose-dependent manner. The herbicide, however, stimulated lung microsomal LPO only in a narrow concentration range, despite much higher P450 reductase activity in lung microsomes than that in brain microsomes. These findings suggest that the effect of PQ on microsomal LPO is different from those of the analogous neurotoxins, MPTP and MPP+, and is not uniform in brain and lung.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1991

Interleukin-1 suppresses mesangial cell growth via inhibition of Ca2+ entry.

We have investigated the effect of interleukin-1 (IL-1) on the cell growth and Ca2+ homeostasis of rat mesangial cells in culture. DNA synthesis measured by [3H]thymidine uptake by mesangial cells was significantly inhibited by IL-1 (10 U/ml) and the calcium channel antagonist nicardipine (5 x 10(-6) M). 45Ca2+ uptake by mesangial cells was also significantly inhibited by IL-1 and nicardipine. The above observations support the premise that IL-1 suppresses the growth of mesangial cells via inhibition of extracellular Ca2+ entry to the cytosol.

Angiotensin II↗
PubMed1991

Different effects of paraquat on microsomal lipid peroxidation in mouse brain, lung and liver.

Paraquat stimulates NADPH-Fe(2+)-dependent microsomal lipid peroxidation in mouse brain and strongly inhibits it in the liver. In lung microsomes, the lipid peroxidation was stimulated by paraquat at 10(-4) M, but not at higher doses. An antioxidant action of paraquat seemed to account, at least in part, for the lack of stimulation in lung microsomes, but it was inappropriate to explain the result in hepatic microsomes. There was no apparent correlation between the effects of paraquat on the lipid peroxidation and on the activity of NADPH-cytochrome P-450 reductase, the enzyme which initiates redox cycling of paraquat, resulting in generation of active oxygen species. In fact, the effect of paraquat on the lipid peroxidation was independent of paraquat radical production, an intermediate in the cycle. However, the inhibitory potency of N-ethylmaleimide on NADPH-cytochrome P-450 reductase activity paralleled that on the lipid peroxidation stimulated by paraquat in brain and lung. These findings indicate that the effect of paraquat on microsomal lipid peroxidation differs among the organs and that other factors, besides NADPH-cytochrome P-450 reductase, might be involved in the stimulation of lipid peroxidation by paraquat.

Animals↗
PubMed1991

Mechanism of paraquat-stimulated lipid peroxidation in mouse brain and pulmonary microsomes.

Paraquat-stimulated NADPH-dependent lipid peroxidation in mouse brain and pulmonary microsomes was inhibited by superoxide dismutase and singlet oxygen quenchers, but not by catalase or hydroxyl radical scavengers. MnCl2, which might form a salt with unsaturated lipid, inhibited the lipid peroxidation in brain microsomes, but not that in pulmonary microsomes. These findings suggest that activated oxygen species, especially superoxide and singlet oxygen, may play a major role in the stimulation of microsomal lipid peroxidation by paraquat in both brain and lung, and that the nature of the lipids exposed to peroxidative attack may be different in microsomes of the two organs.

Animals↗
PubMed1991

Interleukin 6 stimulates growth of vascular smooth muscle cells in a PDGF-dependent manner.

We have investigated the effect of interleukin 6 (IL-6) on the growth of vascular smooth muscle cells (VSMC) isolated from rat aortas. Murine recombinant IL-6 significantly increased the number of VSMC and stimulated tritiated thymidine incorporation into VSMC in a dose-dependent manner. The IL-6-induced thymidine incorporation into VSMC was totally inhibited by the Ca2+ channel blocker verapamil; however, IL-6 showed no effects on the intracellular Ca2+ level ([Ca2+]i) in VSMC. Antibody against platelet-derived growth factor (PDGF) also totally inhibited the IL-6-induced thymidine uptake. PDGF caused a significant increase in the [Ca2+]i, which was totally inhibited by verapamil. IL-6 mRNA was not detected in unstimulated "quiescent" VSMC, but its expression was stimulated by exposure of VSMC to 10% fetal bovine serum. Immunohistochemical study using anti-PDGF antibody showed that IL-6 stimulated PDGF production in VSMC. These results support the premise that IL-6 is released by VSMC in an autocrine manner and promotes the growth of VSMC via induction of endogenous PDGF production.

Animals↗
PubMed1991

[A case of primary Sjögren's syndrome presenting as osteomalacia secondary to renal tubular acidosis].

We report a 43-year-old female with primary Sjögren's syndrome (SjS) who presented as osteomalacia due to distal renal tubular acidosis (RTA). Osteomalacia was thought to be a rare complication of RTA in SjS, although it had been often described in association with RTA in general. In 1979, she presented with dry mouth, parotid gland swelling and leg purpura. A diagnosis of primary SjS and hyperglobulinemic purpura was made on the basis of positive staining with Rose Bengal stain, sialography of the parotid gland and histological examination of the salivary gland of the lip. She was admitted to Jichi Medical School Hospital in March 1988 with chest pain. X-ray films revealed pseudofractures of bilateral ribs. Bone scanning showed abnormal multiple accumulation of RI on the same parts. Laboratory studies on admission revealed: GOT 50 IU/ml, GPT 9 IU/ml, ALP 190 IU/ml, LDH 301 IU/ml, BUN 11.0 mg/dl, creatinine 1.0 mg/dl, uric acid 2.7 mg/dl, total protein 7.4 g/dl (gamma globulin 22.3%), sodium 141 mEq/l, potassium 3.7 mEq/l, chloride 106 mEq/l, calcium 8.9 mg/dl, and phosphorus 2.4 mg/dl. Arterial blood gas studies on room air showed: PO2 96.7mmHg, PCO2 35.5mmHg, HCO3-19.1 mEq/l, PH 7.347 and base excess -5.4 mEq/l. The urinalysis showed: specific gravity 1.008, PH 7.0, and no protein and glucose. Immunologically, antinuclear antibody was positive at 1:640 with a speckled pattern. Anti-DNA antibody was negative. Antibodies to SS.A and SS.B were 1:64 and 1:32 respectively. Distal RTA was confirmed by the sodium bicarbonate and NH4Cl loading test.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗