Biomedical subjects

S Kano

Publications and source records attributed to S Kano.

At least 181 records · Page 10Linked to original sources

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

Recombinant interleukin-1 alpha inhibits the growth of rat mesangial cells in culture.

We have investigated the effect of interleukin-1 (IL-1) on the growth of mesangial cells isolated from rat kidney. Recombinant IL-1 alpha inhibited 3H-thymidine uptake by mesangial cells in a dose-dependent manner in the presence of either 0.5% or 5% fetal bovine serum (FBS). In the presence of high concentration of FBS (10%), the effect of IL-1 was not prominent. The inhibitory effect of IL-1 on the growth of mesangial cells was also confirmed by a change in cell numbers and measurements of protein synthesis with 3H-leucine. IL-1-induced inhibition of mesangial cell growth was not affected by indomethacin. IL-1 showed no effects on intracellular Ca2+ levels in mesangial cells. These observations indicate that IL-1 inhibits the growth of mesangial cells, and thus may play a protective role for mesangial cells from abnormal proliferation in some pathophysiological states.

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

Pacing parameters of the canine posterior cricoarytenoid muscle.

The electrical pacing of laryngeal tissue consists of many uncharted parameters. We carried out several acute experiments in the canine model to narrow parametric ranges to serve future research and development in this field. Our findings were as follows. Stimulation intensities greater than 6 V caused tissue damage. Optimum stimulation frequency ranged from 60 to 90 Hz. Optimum pulse duration was 2.0 milliseconds. Biphasic stimulation reduced accumulation of electrical charge at the electrodes.

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↗

PubMed1991

Interaction between dual NADPH-dependent reactions of paraquat in mouse brain microsomes.

Paraquat stimulated NADPH-dependent lipid peroxidation in mouse brain microsomes, while it suppressed lipid peroxidation induced by NADPH plus ascorbate. The stimulation of lipid peroxidation by paraquat was inhibited by N-ethylmaleimide (NEM). However, NEM attenuated the inhibitory effect of paraquat on lipid peroxidation elicited by NADPH in combination with ascorbate. These results suggest that an NADPH-dependent reaction which is susceptible to NEM might share an electron from NADPH with the alternative reaction, lipid peroxidation, in the presence of paraquat in mouse brain microsomes.

Animals↗

PubMed1991

[Effects of physical training on children with bronchial asthma].

Twelve children with exercise-induced bronchospasm (EIB) participated in our physical training program to determine whether it improves physical working capacity and EIB. The effect of physical training on the bronchial reactivity to inhaled 3.6% NaCl was also investigated. The training was performed by bicycle ergometer for four weeks every day at 125% of WBPLA1 (work load at first breaking point of lactic acid). The results obtained were as follows. 1. Heart rate decreased from 188.5 +/- 9.6 bpm before to 178.4 +/- 9.7 bpm after training at 150% of WBPLA1 (p less than 0.05). After training at 175% of WBPLA1 it decreased also from 174.0 +/- 11.9 bpm to 165.6 +/- 11.3 bpm. Maximum oxygen consumption increased from 34.5 +/- 3.5 ml/min/kg to 41.4 +/- 4.0 ml/min/kg after training (p less than 0.001). 2. Max. % fall in FEV1.0 decreased from 27.1 +/- 24.0% before to 18.0 +/- 17.1% after training at 150% of WBPLA1 (p less than 0.05). After training at 175% of WBPLA1 it decreased also from 37.4 +/- 17.4% to 30.0 +/- 22.1%. 3. The mean dose of inhaled 3.6% NaCl inducing 20% fall in FEV1.0 (PD20) was 4.2 +/- 5.9 ml before training. The PD20 was significantly higher after training (8.6 +/- 4.0 ml). There was no significant change in PD20 in the control group. Based on these results, it was concluded that physical training increased physical working capacity and improved EIB and bronchial hyperreactivity to inhaled 3.6% NaCl in asthmatic children.

Adolescent↗

PubMed1990

Identification and gene cloning of a new phosphatidylinositol-linked antigen expressed on mature lymphocytes. Down-regulation by lymphocyte activation.

Lymphocytes are shown to express a limited number of a unique category of membrane Ag, such as Thy-1, Ly-6, Ly-31, and Qa-2, that are covalently linked to the membrane phosphatidylinositol (PI). We have identified a new glycosyl-phosphatidylinositol (GPI)-anchored lymphocyte Ag, B7, by using a mAb and have determined the primary structure by cDNA cloning. B7 Ag was expressed on the majority, if not all, of the mature lymphocytes of both T and B lineages, including strongly CD3+ thymocytes, most splenic T cells, and approximately 60% of splenic IgM+ B cells, whereas the expression of B7 Ag on bone marrow cells was negligible. The expression of B7 Ag was nearly completely abolished with as little as 2 mU of PI-specific phospholipase C per ml, which did not completely eliminate Ly-6C and Thy-1 expression. Unlike the expression of other GPI-linked lymphocyte Ag, the expression of B7 was rapidly down-regulated upon the activation of T cells by mitogens or IL-2 both in vitro and in vivo. Immunoprecipitation analysis revealed that B7 Ag was an approximately 12-kDa protein. With a CDM8 expression vector, a cDNA encoding B7 Ag was cloned, and it was confirmed that the B7 Ag on cDNA-transfected cells was indeed PI-specific phospholipase C sensitive. The B7 cDNA contained an open reading frame of 222 bp including a typical N-terminal leader sequence and a characteristic sequence at the C terminus encoding hydrophobic amino acids. A computer search revealed no significant homology to any known molecule at both DNA and amino acid sequence levels. Northern blot analysis indicated that the B7 transcript was expressed on lymphohematopoietic tissues, including thymus, spleen, and bone marrow, but not on other organs, such as liver, kidney, and brain. The results indicated that B7 Ag is a new member of the GPI-anchored proteins which is selectively expressed on mature resting but not activated lymphocytes.

Amino Acid Sequence↗

PubMed1990

Expression of murine IL-2 receptor beta-chain on thymic and splenic lymphocyte subpopulations as revealed by the IL-2-induced proliferative response in human IL-2 receptor alpha-chain transgenic mice.

Lymphocytes from the human (h) IL-2R alpha chain transgenic mice (TGM) constitutively express high affinity binding sites for hIL-2, consisting of transgenic h-IL-2R alpha and endogenous murine IL-2R beta, and therefore easily proliferate in vitro in response to hIL-2. Our study was undertaken to clarify the hIL-2-responsive lymphocyte subsets in the TGM, which should most likely reflect the normal distribution of m IL-2R beta expression. In both thymus and spleen, the majority of expanded cells by hIL-2 was CD3+CD4-CD8+ TCR alpha beta+ cells. The proliferation of CD4+ cells was not observed at all from either organ despite the expression of transgenic hIL-2R alpha. Potent cellular proliferation was also observed from the thymocytes that had been depleted of CD8+ cells, the expanded cells consisting of CD3- (15-40%) and CD3+ populations (60-85%). Among CD3+ cells, approximately the half portion expressed TCR alpha beta, whereas the other half was suggested to express TCR gamma delta. A variable portion (5-20%) of the CD3+ cells expressed CD8 (Lyt-2) in the absence of Lyt-3, and the CD3+CD8+ cells were confined preferentially to the TCR alpha beta- (TCR gamma delta+) population. In the culture of splenocytes depleted of CD8+ cells, however, the proliferated cells were mostly CD3-CD4-CD8-TCR-Mac1-, whereas a minor portion (10-30%) was CD3+CD4-CD8-TCR alpha beta- (TCR gamma delta+. Analysis of TCR genes at both DNA and mRNA levels confirmed the phenotypical observations. These results strongly suggested that IL-2R beta was constitutively and selectively expressed on the primary murine thymocytes and splenic T and NK cells, except for CD4+ cells in both organs.

Animals↗