Cimetidine and immunoreactivity.
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Cimetidine↗
Biomedical subjects
W Sato
Publications and source records attributed to W Sato.
Double balloon catheter for concomitant augmentation of abdominal organ perfusion during intraaortic balloon counterpulsation.
A newly devised double balloon catheter to augment abdominal organ perfusion concomitant with original cardiac assist during intraaortic balloon counterpulsation provided satisfactory hemodynamics and urinary output around cardiac surgical procedures in 2 patients with coronary artery disease. Some optional advantages in clinical application and problems arising in the catheter design which need to be investigated are discussed.
Acetylglucosaminidase↗
[Surgical treatment for ischemic cardiomyopathy].
From June 1970 to Aug. 1995. We were experienced 2,235 coronary surgical patients at the Heart Institute of Japan. Among them, the ischemic cardiomyopathy (ICM) was defined as the elective, isolated CABG with the EF of less than 20%. Among the 1,640 cases of elective, isolated CABG, the cases with the EF of less than 20% were 29, 1.8% of the total. The hospital mortality was 2 cases (6.9%). The late mortality was 2 cases. The graft patency rate was 96.6%. An actuarial survival rates at 1 year, 3 years and 5 years were 93%, 93 and 87%. Operative mortality and 5-year survival rate of CABG for ICM are acceptable, and appear comparable to that achieved in similar patients after transplantation.
Adult↗
[Effect of sevoflurane on release of TNF-alpha and IL-1 beta from human monocytes].
Although isoflurane inhibits TNF-alpha and IL-1 beta release from human monocytes stimulated by LPS in dose dependent fashion, it is unclear whether sevoflurane has the same effects. Therefore, we investigated whether sevoflurane could inhibit TNF-alpha and IL-1 beta secretions from human monocytes stimulated by LPS in dose dependent fashion in vitro. Human monocytes stimulated by LPS were cultured for 3 h in the presence of sevoflurane 1% or 5%. Another group of human monocytes were cultured in the absence of sevoflurane. TNF-alpha and IL-1 beta increased after stimulation of LPS and these increases were not inhibited by sevoflurane in a dose dependent fashion. We conclude that sevoflurane does not inhibit TNF-alpha and IL-1 beta release from monocytes stimulated by LPS.
Anesthetics, Inhalation↗
[Emergency coronary artery bypass in an 84-year-old patient with severe left main disease and cardiogenic shock].
An 84-year-old male was admitted to pur hospital because of unstable angina. The patient presented in cardiogenic shock with a cardiac index of 1.3 l/min/m2 associated with hypotension (systolic blood pressure < 80 mmHg) and oliguria, and in ventricular fibrillation after an acute broad anterolateral infarction due to severe left main coronary disease. The patient received an intra-aortic balloon pumping (IABP) and underwent emergency CABG. After completion of CABG, left ventricular contractility was markedly diminished to maintain systemic circulation. Because the patient could not be weaned from cardio-pulmonary bypass (CPB) in spite of IABP and high-dose of catecholamines, we decided to continue CPB. It was continued for 163 minutes and the patient was successfully weaned from CPB. In spite of the high risk of operative mortality with CABG for left main shock syndrome in elderly patients, CABG could be performed safely. The patient ran an uneventful postoperative course and is now doing well.
Aged↗
Relationship between multidrug resistant gene expression and multidrug resistant-reversing effect of MS-209 in various tumor cells.
MS-209 is a novel quinoline compound which can overcome multidrug resistance (MDR) both in vitro and in vivo, while having a low level of side effects, and is now being evaluated in a clinical phase II study. Reverse transcription-polymerase chain reaction (RT-PCR) was used to quantitate the expression levels of MDR genes in various mouse and human tumor cell lines. The MDR gene and the beta actin gene, as the internal reference standard, were coamplified separately, and the relative expression of the MDR gene was represented by the MDR/beta actin ratio. The in vitro MDR-reversing effect of MS-209 was then compared with the MDR gene expression (MDR/beta actin ratio). We found a significant correlation between these two parameters. Moreover, a significant correlation was also observed between the level of expression of the MDR1 gene and that of P-glycoprotein in human cell lines. Therefore, the efficacy of MS-209 seems to specifically depend on the level of MDR gene expression (P-glycoprotein). From these observations, it is suggested that RT-PCR assays of MDR1 gene in tumor biopsy specimens might be an effective means to predict the response of tumor cells to combination therapy with MS-209.
Animals↗
Reversal of multidrug resistance by a novel quinoline derivative, MS-209.
MS-209, a novel quinoline derivative, was examined for its reversing effect on multidrug-resistant tumor cells. MS-209 at 1-10 microM completely reversed resistance against vincristine (VCR) in vitro in multidrug-resistant variants of mouse leukemia P388 cells (VCR-resistant P388/VCR and Adriamycin (ADM)-resistant P388/ADM) and human leukemia K562 cells (VCR-resistant K562/VCR and ADM-resistant K562/ADM). MS-209 at 1-10 microM also completely reversed resistance against ADM in vitro in P388/VCR cells, K562/VCR cells, and K562/ADM cells. In ADM-resistant P388 (P388/ADM) cells, however, ADM resistance was only partially reversed at the MS-209 concentrations tested. MS-209 enhanced the chemotherapeutic effect of VCR in P388/VCR-bearing mice. When MS-209 was given p.o. at 80 mg/kg twice a day (total dose, 160 mg/kg per day) with 100 micrograms/kg VCR, a treated/control (T/C) value of 155% was obtained. MS-209 also enhanced the chemotherapeutic effect of ADM in P388/ADM-bearing mice. The most prominent effects were obtained when MS-209 was given with 2 mg/kg ADM, yielding T/C values of 150%-194% for the combined treatment at an MS-209 dose of 200-450 mg/kg. MS-209 inhibited [3H]-azidopine photolabeling of P-glycoprotein efficiently. Furthermore, the accumulation of ADM in K562/ADM cells was increased more efficiently by MS-209 than by verapamil. These results indicate that MS-209, like verapamil, directly interacts with P-glycoprotein and inhibits the active efflux of antitumor agents, thus overcoming multidrug resistance in vitro and in vivo.
ATP Binding Cassette Transporter, Subfamily B, Mem↗
Detection of neoplastic clone in the hypoplastic and recovery phases preceding acute lymphoblastic leukemia by in vitro amplification of rearranged T-cell receptor delta chain gene.
This study assessed the clonality of hypoplastic and subsequent recovery phases before the development of overt leukemia by molecular genetic analysis. We describe a boy who had transient granulocytopenia and anemia before the development of acute lymphoblastic leukemia (ALL). Initially, his bone marrow was hypocellular with 23.6% of lymphoblastic cells, whereas subsequent marrow after the administration of granulocyte colony-stimulating factor (G-CSF) appeared almost normal without any lymphoblasts. At diagnosis, we found the rearrangement of T cell receptor (TCR) delta gene in the leukemic cell DNA by Southern blot hybridization. The junctional sequence of the V delta 2-D delta 3 recombination of leukemic cells obtained by polymerase chain reaction (PCR) was used for a clonospecific probe. Using the probe, the presence of leukemic clone in the materials before and after diagnosis was examined. We found that the clonospecific probe could detect one leukemic cell in 10,000 normal cells, and we demonstrated the presence of the leukemic clone at the initial hypoplastic and the subsequent recovery phase. The PCR method is very useful to confirm the presence of leukemic clone even in a retrospective analysis using low-quality materials and may be helpful to understand the pathogenesis of a smoldering preleukemic phase.
Bone Marrow↗
Identification and expression of a missense mutation (Y446C) in the acid sphingomyelinase gene from a Japanese patient with type A Niemann-Pick disease.
Types A and B Niemann-Pick disease (NPD), an autosomal recessive lysosomal storage disorder, are caused by deficiency of acid sphingomyelinase (ASM). The recent identification of mutations in ASM gene causing types A and B NPD has led to the investigation of the phenotypic heterogeneity and the ethnic distribution of this disease, especially in Ashkenazi Jewish population. To characterize the mutations causing NPD in Japanese population, we analyzed the genomic sequence of ASM from a Japanese patient with type A NPD by PCR amplification and sequencing. A new mutation, Y446C, was identified. The authenticity of this lesion was demonstrated by the expression of the Y446C allele in COS-1 cells. No residual ASM activity was detected from the expression of the Y446C.
Amino Acid Sequence↗
Isolation of cDNA encoding the human liver phosphorylase kinase alpha subunit (PHKA2) and identification of a missense mutation of the PHKA2 gene in a family with liver phosphorylase kinase deficiency.
X-linked liver glycogenosis (XLG) due to liver phosphorylase kinase (PHK) deficiency is the most frequent liver glycogen storage disease. The affected patients present in early childhood with hepatomegaly and growth retardation. We isolated and determined the structure of human liver alpha subunit of PHK (PHKA2) cDNA. The 3705 base pair open reading frame encodes a polypeptide of 1235 amino acid residues, and the deduced amino acid sequence shows 93 and 68% homology to that of rabbit liver alpha subunit of PHK and human muscle alpha subunit of PHK, respectively. We identified a missense mutation, a valine substitution for glycine at amino acid 193, in the PHKA2 gene of a family with XLG.
Amino Acid Sequence↗
[Milrinone suppresses TNF-alpha and IL-1 beta release in mouse peritoneal macrophages].
Tumor necrosis factor-alpha (TNF-alpha) exerts a wide spectrum of biological activities and contributes to the pathophysiology of septic shock. We studied whether milrinone suppresses TNF-alpha and IL-1 beta releases from mouse peritoneal macrophages. Mouse peritoneal macrophages were stimulated for 18 hr with lipopolysaccharide and different doses of milrinone. TNF-alpha release was suppressed in a dose-dependent fashion with milrinone, reaching half-maximal inhibition at 30 microM. Release of IL-1 beta was not suppressed with 25 microM of milrinone, but it was suppressed with 250 microM of milrinone. We conclude that TNF-alpha release is suppressed by therapeutically administered milrinone.
Animals↗
[The effect of isoflurane on the secretion of TNF-alpha and IL-1 beta from LPS-stimulated human peripheral blood monocytes].
The cytokines such as tumor necrosis factor and interleukin-1 secreted from macrophages/monocytes proved to play important roles in the pathogenesis of endotoxemia, severe pancreatitis and other surgical injuries. However, it is still unclear how inhalational anesthetic agents influence the secretion of these cytokines from macrophages/monocytes. We investigated the effects of isoflurane on TNF-alpha and IL-1 beta secretions from human peripheral blood monocytes stimulated by lipopolysaccharide. TNF-alpha and IL-1 beta secretions increased after LPS stimulation and this increase was inhibited by isoflurane in dose-dependent fashion. The inhibitory action of isoflurane disappeared between 1 and 3 hours after stopping isoflurane inhalation. We concluded that isoflurane could inhibit TNF-alpha and IL-1 beta secretions from peripheral blood monocytes stimulated by LPS in a dose-dependent fashion and that the inhibitory action of isoflurane was reversible.
Anesthesia, Inhalation↗
A T-to-C substitution at nucleotide 12311 in tRNA(Leu(CUN)) gene may be a mtDNA polymorphism.
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Humans↗
Cardiomyopathy and angiopathy in patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes.
In four patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS) in which mutated mitochondrial deoxyribonucleic acid was seen, hypertrophic cardiomyopathy and angiopathy was demonstrated by echocardiography, dipyridamole stress scintigraphy, and cardiac catheterization. On stress scintigraphy with dipyridamole, three patients showed hypoperfusion in the early image and a "filling-in" pattern in the late image. However, coronary angiography did not demonstrate narrowing of the large vessels in these patients. Light and electron microscopy of endomyocardial biopsy specimens indicated abnormal mitochondria, with marked increase in the number and size of mitochondria in endothelium. Modified Gomori's trichrome staining in biopsied endomyocardial specimens revealed a red-purple deposit similar in appearance of the ragged-red fibers in skeletal muscle, a characteristic finding of mitochondrial disease. Deterioration of complex I in the mitochondrial electron transfer system, which is widely observed in various mitochondrial diseases, appeared in biopsied skeletal muscle of our patients, indicating deficiency of some subunits of complex I. These results indicate that mitochondrial diseases such as MELAS show not only cardiomyopathy but also angiopathy. We speculate that proliferation of mitochondria leads to narrowing of the lumen of arterioles, which might be responsible for the ischemic findings observed scintigraphically.
Adolescent↗
A mitochondrial tRNA(Leu)(UUR) mutation at 3,256 associated with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS).
Enzymatic and molecular analyses were conducted on the muscular tissue of a patient with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). Significant decreases in activity of complexes I and IV were found and three nucleotide substitutions in the mitochondrial tRNA genes were detected. Two of the substitutions were detected in unaffected members of the family and in some healthy controls. A C-to-T transition mutation at the nucleotide position 3,256 in the mitochondrial tRNA(Leu)(UUR) gene was detected only in the patient and not in unaffected members of the family or 100 healthy controls. The data strongly suggest that this mutation at nucleotide position 3,256 in the mitochondrial tRNA(Leu)(UUR) gene is associated with MELAS.
Adult↗
[Prostaglandin E1 does not inhibit production of TNF and IL-1 by mononuclear cells after head-neck surgery].
We studied whether human blood mononuclear cells could produce tumor necrosis factor (TNF) and interleukin 1 (IL-1) by surgical stimuli, and if so, prostaglandin E1 (PGE1) could inhibit their increases before and following operation in patients undergoing head-neck surgery. The patients were randomly allocated into 2 groups; no PGE1 infusion group (control group, n = 6) and PGE1 infusion group (PGE1 group, n = 6). PGE1 group was infused intravenously with PGE1 at a rate of 30 ng.kg-1 x min-1 during surgery and at a rate of 10-30 ng.kg-1 x min-1 after surgery. Peripheral blood was withdrawn into heparinized syringes from these patients immediately before surgery and on the 1st postoperative day. Production of TNF on the 1st postoperative day increased 1.5 fold in control group and 1.4 fold in PGE1 group compared with those before surgery. Production of IL-1 on the 1st postoperative day increased 1.7 fold in control group and 1.1 fold in PGE1 group compared with those before surgery. Also, there were no significant differences between 2 groups in both productions of TNF and IL-1. These data indicate that human blood mononuclear cells would produce TNF and IL-1 by surgical stimuli and PGE1 could inhibit their production by surgical stimuli. It also provides evidence that PGE1 does not inhibit the body's defense response to surgical stimuli.
Aged↗
[Prostaglandin E1 suppresses hypersecretion of antidiuretic hormone induced by surgical stress].
We studied the effects of prostaglandin E1 (PGE1) on decrease in urine output during surgery in patients for radical total hysterectomy under general anesthesia. The patients were randomly allocated into two groups. Five patients (control group) were given no PGE1 and served as control. Seven patients (PGE1 group) were given continuous infusion of PGE1 at a rate of 50 ng.kg-1 x min-1 after first measurement (baseline). Urine output in control group decreased by 68%, but in PGE1 group it did not change from the baseline. Urine sodium and fractional sodium excretion in control group decreased, but in PGE1 group they increased. Creatinine clearance increased from the baseline in both groups. Antidiuretic hormone in control group increased by 30%, but in PGE1 group decreased by 53%. Plasma renin activity, angiotensin I, angiotensin II in both groups increased, and those in the control group were higher than those in PGE1 group. However, aldosterone in the control group was lower than that in PGE1. These results indicate that diuretic effect of PGE1 could be mediated by suppression of antidiuretic hypersecretion induced by surgical stress, inhibition of the action of antidiuretic hormone, and suppression of sodium and water reabsorption in proximal and distal tubules. Also, PGE1 did not directly stimulate renin-angiotensin system.
Adult↗
Tissue distribution of mutant mitochondrial DNA in mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS).
We analysed the distribution of mutant mitochondrial DNA (mtDNA) with A-to-G substitution mutation of tRNA(Leu)(UUR) in various autopsied tissues from a patient with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). There was no significant difference in the proportion (76-86%) of mutant mtDNA in many tissues, except in the lung and spleen. Unequal partitioning of mtDNA in somatic cells appears less prominent than that in germ cells.
Adult↗