[Cardiovascular disease and reactive oxygen toxicity--analysis by site-directed-SOD derivatives].
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Albumins↗
Biomedical subjects
N Watanabe
Publications and source records attributed to N Watanabe.
[Have the results of mitral valve replacement improved?].
The operative mortality following valvular surgery remains substantial for specific high risk groups despite recent improvement in surgical techniques, anesthetic managements, and postoperative care. To test the contention that the results of valvular surgery are better in recent years, we examined patients undergoing isolated or combined mitral valve replacement in an earlier era (1980-1984; n = 68) and a later era (1985-1989; n = 106). There were no significant differences concerning the clinical characteristics between an earlier era and a later era, although patients in an earlier era were more seriously in hemodynamics, and in a later era were older, a higher prevalence of reoperations and a combined tricuspid valve surgery. The operative mortality was 10.3% in an earlier era, 6.6% in a later era, and so it is not significantly improved in a recent 5 years, however the incidence of premature death (death within 30 days) except valve re-replacement was significantly improved. Using univariate multiple logistic model, the predictors for operative death after mitral valve replacement in an earlier era were advanced NYHA functional class, larger CTR, higher systolic pulmonary pressure and pulmonary capillary wedge pressure, associated preoperative organ dysfunction and heart lung machine time. In a later era, these were advanced NYHA functional class, higher right atrial mean pressure, associated preoperative organ dysfunction, valve re-replacement, heart lung machine time and aortic cross clamp time. Multivariate analysis including these significant factors could not demonstrated the most independent predictors of operative mortality after mitral valve replacement in both an earlier era and a later era.(ABSTRACT TRUNCATED AT 250 WORDS)
Female↗
[Acute megakaryoblastic leukemia with complex chromosomal aberrations].
A case of acute megakaryoblastic leukemia with complex chromosomal aberrations is reported. A 63-year-old man was admitted to our hospital because of pancytopenia. Bone marrow aspiration resulted in a dry tap and biopsy showed hypoplastic marrow with fibrosis. Blast cells in the peripheral blood were identified as megakaryoblasts because they were positive for electron microscopic platelet peroxidase (PPO). In addition, monoclonal antibody, TP80, to platelet glycoprotein II b-III a reacted with in about 26% of the blast cells. Chromosomal analysis of the peripheral blood revealed a mosaic pattern of a normal karyotype and abnormal ones, including 44, XY, -5, -7, -18, 10q-, +marker.
Chromosome Aberrations↗
[Assessment of myocardial viability by resting 201Tl SPECT image].
The aim of this study was to assess whether resting 201Tl scintigraphy is superior in detecting viable myocardium than previous conventional methods. We performed not only stress 201Tl SPECT but also resting 201Tl SPECT within one month in 65 patients with coronary artery disease. Resting 201Tl images were quantitatively compared with 4 hour late images of stress study using a polar map. In stress study, redistribution was recognized on 83% (25/30) of non-MI SEGs with perfusion defect in the stress 201Tl image, and on 39% (18/46) of infarcted SEGs. The agreement of resting 201Tl study with 4 hour late images of stress study was shown on 93% (28/30) of non-MI SEGs and on 52% (24/46) of MI SEGs. The increased uptake of 201Tl in resting study, however, was found on 13 (46%) of 28 MI SEGs showing fixed defects in stress study. In stress delayed image with fixed defect, the %Tl uptake of improved SEGs was higher than that of unchanged SEGs (59 +/- 10% vs 48 +/- 11%; p greater than 0.05). There was no viable myocardium which had %Tl uptake less than 40% at stress delayed image. In conclusion, the resting 201Tl imaging will give an important information as for the myocardial viability showing fixed defects, if more than 40% Tl uptake is observed.
Aged↗
[Estimation of I-123 metaiodobenzylguanidine (MIBG) myocardial washout].
A crosstalk from I-123 to Tl-201 (Tl) window was 35 +/- 30% (mean +/- SD) and 30 +/- 10% in a myocardial phantom and the images of 6 patients respectively. However, the crosstalk from Tl to I-123 was approximately 1% in each. I-123 MIBG (MIBG) and Tl myocardial SPECT images were recorded in 3 normal volunteers (N), 10 patients with myocardial infarction (MI), and 4 with dilated cardiomyopathy (DCM). The MIBG and Tl imagings were performed on the other day to avoid the crosstalk. Myocardial washout rates (WR) of Tl and MIBG were derived from 15 min and 4 hour images. WR of Tl was approximately 36% in each group. On the other hand, WR of MIBG in DCM (52 +/- 7%) and MI (41 +/- 14%) groups were statistically higher than in N (24 +/- 7%) group. Thus WR of MIBG would be useful to detect abnormalities in adrenergic nervous system.
3-Iodobenzylguanidine↗
[Sudden cardiac arrest during percutaneous nephrostolithotomy (PNL) under epidural anesthesia].
There have been few major complications of percutaneous nephrostolithotomy (PNL) reported. We recently experienced cardiac arrest during PNL under epidural anesthesia. The patient was a 52 year old man weighing 64 kg who had been suffering from right renal pelvic stone for years. He was scheduled for PLN under epidural anesthesia. Analgesia was obtained to the level of Th6. The operation proceeded uneventfully for about 60 min. By this time, he suddenly complained nausea, and hypotension with bradycardia occurred. Blood pressure and pulse rate returned immediately to the normal level by IV atropine and ephedrine. But after three minutes, blood pressure and pulse rate went down again. This hypotension with bradycardia was unresponsive to epinephrine, calcium chloride and sodium bicarbonate. This was followed by asystole. Resuscitation was successful with the addition of epinephrine, calcium chloride, and sodium bicarbonate about 15 min after cardiac massage had started. The patient was, on the fifth postoperative day, with no evidence of impairment of renal, cardiac and respiratory functions but a slight impairment of neurologic function. Several possible causes for this cardiac arrest and anesthetic management of percutaneous nephrostolithotomy are discussed.
Anesthesia, Epidural↗
Factitious proteinuria in a young girl.
A 16-year-old girl showed waxing and waning proteinuria and fat globules in urine for three years. There were no other abnormal findings except for the urinalysis. The renal biopsy findings did not indicate glomerular disease. Electrophoresis of the urinary protein showed two abnormal fractions at the alpha and beta globulins. Immunoelectrophoresis demonstrated that these abnormal proteins were not derived from human serum proteins, but were egg proteins. It appears that the proteinuria was factitious and that egg proteins were injected into the bladder, as they were also present in the bladder urine.
Adolescent↗
[The relationship between preoperative status and postoperative exercise tolerance after mitral valve replacement].
Treadmill exercise test was performed for the evaluation of exercise tolerance after mitral valve replacement. The duration of maximum exercise tolerance in TR free group had no significant difference as compared with TR combined group. Preoperative RV function in TR combined group was kept relatively good as shown in cardiac index, pulmonary arterial and right atrial pressure. As hemodynamics was improved by TAP (TVR), it may not occur the difference in exercise tolerance between the groups. The duration of maximum exercise tolerance with MS group showed shorter tolerance than that of MR group. This difference in MS group might be considered due to the limitation of LV dilatation by rheumatic cardiac damage. Exercise tolerance after MVR was significantly lowered by atrial fibrillation, cardio-thoracic ratio over 60% and pulmonary vascular resistance over 3.0 Runits.m2.
Exercise Tolerance↗
Presence of glucagon-(1-21)-Like immunoreactive substance in the dog small intestinal mucosa.
By using an antiserum (K291) specifically directed to the C-terminal of glucagon-(1-21)-peptide, we demonstrated the presence of glucagon-(1-21)-like immunoreactivity (G21-IR) in the dog intestine. G21-IR was found to be widely distributed throughout the small intestine and colon in parallel with the distribution of glucagon-like immunoreactivity (GLI), measured by N-terminal glucagon antiserum (OAL196). The subsequent analyses by gel filtration and three HPLC columns (reverse phase, ion exchange and further reverse phase columns) showed that G21-IR consisted of three main peaks, and the smallest molecular form of G21-IR is identical to glucagon-(1-21)-peptide.
Amino Acid Sequence↗
Liquid chromatographic-atmospheric pressure ionization mass spectrometric analysis of toremifene metabolites in human urine.
A liquid chromatographic-atmospheric pressure ionization mass spectrometric method has been developed for the analysis of toremifene metabolites in human urine after oral administration. This ionization source is a useful device for studying metabolites of toremifene because the total effluent from high-performance liquid chromatography is fed through an interface with a direct heating nebulizer and vaporizer at atmospheric pressure. To obtain good sensitivity the use of the right mobile phase is very important: ammonium acetate in methanol in the case of toremifene and its metabolites. Four unconjugated and three glucuronide-conjugated metabolites were detected in human urine. The majority of these were new and distinguishable from known metabolites.
Antineoplastic Agents↗
Specific proteolysis of the c-mos proto-oncogene product by calpain on fertilization of Xenopus eggs.
The Xenopus c-mos proto-oncogene product, pp39mos, accumulates in the unfertilized egg during maturation, is hyperphosphorylated and exhibits protein kinase activity. On fertilization, or soon after the completion of meiosis, the accumulated pp39mos undergoes selective proteolysis. Using an in vitro protease assay system, we show here that this specific proteolysis is caused by the calcium-dependent cysteine protease, calpain.
Animals↗
The c-mos proto-oncogene product is a cytostatic factor responsible for meiotic arrest in vertebrate eggs.
The c-mos proto-oncogene product, pp39mos, is present in unfertilized Xenopus eggs, and disappears on fertilization. Microinjection of synthetic mos RNA into two-cell embryos induces cleavage arrest at metaphase. By contrast, egg cytosol extracts, when immunodepleted of endogenous pp39mos, lose their cleavage-arresting activity in injected embryos. These results demonstrate that Mos protein is the cytostatic factor CSF, long known as an endogenous meiotic inhibitor in vertebrate eggs.
Animals↗
Inhibition of postischemic reperfusion arrhythmias by an SOD derivative that circulates bound to albumin with prolonged in vivo half-life.
Intravenously administered superoxide dismutase (SOD) rapidly disappeared from the circulation and often failed to prevent oxidative tissue injury. Thus, although superoxide radicals have been postulated to play an important role in the pathogenesis of postischemic reflow-induced tissue injury, conclusive evidence supporting this concept is lacking. We have synthesized an SOD derivative (SM-SOD) that circulated bound to albumin and accumulated in injured tissues whose local pH was decreased. Transient occlusion followed by reperfusion of the coronary artery elicited severe ventricular arrhythmias in rats. Intravenous administration of SM-SOD markedly inhibited the reflow-induced arrhythmias. SOD did not show such inhibitory effect. Kinetic analysis revealed that SM-SOD accumulated in the acidic lesion of the injured heart soon after reflow and returned to the circulation thereafter. These and other results suggest that superoxide radical and/or its metabolites would play a critical role in the pathogenesis of reperfusion arrhythmias and that SM-SOD may be useful for protecting acute myocardial injury induced by such hazardous oxygen metabolites.
Animals↗
Sulphotransferase-mediated activation of the carcinogen 5-hydroxymethyl-chrysene. Species and sex differences in tissue distribution of the enzyme activity and a possible participation of hydroxysteroid sulphotransferases.
Sulphation of the carcinogen 5-hydroxymethyl-chrysene (5-HCR) to the active metabolite 5-HCR sulphate occurred at significant rates in all of hepatic cytosols prepared from the male and female experimental animals, rats, mice, guinea-pigs and hamsters. The 5-HCR-sulphating activity was also found in kidney cytosols of all the experimental animals used, while their activities were much less than those of hepatic cytosols. In the male mice, the enzyme activity of testis was higher than any other examined tissue. Small intestine and adrenal of male and female guinea-pigs had relatively high enzyme activities. Small enzyme activities were also found in a variety of extrahepatic tissues of some of these animals. Marked species and sex differences (female much greater than male in the rat and mouse) were observed in the hepatic enzyme activity. In the female rat liver which showed the highest 5-HCR-sulphating activity among the examined tissues of all the animals, a typical hydroxysteroid sulphotransferase inhibitor, dehydroepiandrosterone (DHA) sulphate (1 mM), potently and competitively inhibited the sulphation of 5-HCR as well as that of DHA, a typical substrate for hydroxysteroid sulphotransferases. On the contrary, the phenol sulphotransferase inhibitors, pentachlorophenol and 2,6-dichloro-4-nitrophenol, had only a little effect on these enzyme activities even at a concentration of 50 microM that showed a potent inhibition of the phenol sulphotransferase activity. These results suggest that 5-HCR be sulphated in the female rat liver by hydroxysteroid sulphotransferases, but not by phenol sulphotransferases.
Animals↗
Synthesis of a superoxide dismutase derivative that circulates bound to albumin and accumulates in tissues whose pH is decreased.
Protection of tissues from oxidative stress is one of the major prerequisites for aerobic life. Since intravenously injected Cu2+/Zn2+-type superoxide dismutase (SOD) disappears from the circulation with a short half-life of 5 min, its clinical use as a scavenger for superoxide radical is limited. We synthesized a human erythrocyte type SOD derivative (SM-SOD) by linking 2 mol of hydrophobic organic anion, alpha-4-[( 6-(N-maleimido)hexanoyloxymethyl]cumyl]half-butyl-esterified poly(styrene-co-maleic acid) (SM), to the cysteinyl residues of the dimeric enzyme without decreasing enzymic activity. SM-SOD, but not SOD, bound to an albumin-Sepharose column; the bound SM-SOD was eluted by a buffer solution containing 0.5% sodium dodecyl sulfate or 10 mM warfarin, suggesting that SM-SOD reversibly binds to the warfarin site on albumin. Due to the amphipathic nature of the SMI moiety, SM-SOD bound also to cell membranes particularly when the pH was decreased. In vivo analysis in the rat revealed that intravenously injected SM-SOD circulated bound to albumin with a half-life of 6 h. Postischemic reperfusion arrhythmias were almost completely prevented by a single dose of SM-SOD, but not SOD. Thus, the prolonged half-life of SM-SOD in the circulation and its preferential accumulation in an injured site with decreased pH appeared to be responsible for preventing myocardial injury. These results suggest that superoxide radical and/or its metabolite(s) would play an important role in the pathogenesis of postischemic reperfusion arrhythmias and that SM-SOD may be useful for decreasing tissue injury in ischemic heart disease.
Animals↗
Intracellular hydroxyl radical production induced by recombinant human tumor necrosis factor and its implication in the killing of tumor cells in vitro.
This study investigated the effect of recombinant human tumor necrosis factor (rhTNF) on hydroxyl radical production by established cell lines in vitro, and its implication in the killing of tumor cells by rhTNF. During incubation of TNF sensitive mouse tumorigenic fibroblast L-M cells (2 X 10(7) cells) in the presence of rhTNF (100 U), hydroxyl radical production as detected by the evolution of methane gas from dimethyl sulfoxide increased gradually, at 18 h reaching 1.8 times that in the absence of rhTNF. This increase was dependent on the concentration of rhTNF and was effectively prevented by the simultaneous addition of anti-rhTNF monoclonal antibody III 2F3, which inhibited both the binding of rhTNF to its receptor and the cytotoxic activity of rhTNF. The addition of iron chelator 2,2'-bipyridine, which inhibits iron-catalized Fenton reaction and so inhibits hydroxyl radical generation, suppressed both the increase of hydroxyl radical production and the cytotoxicity induced by rhTNF. A similar increase in hydroxyl radical production in the presence of rhTNF was also detected with TNF-sensitive human myosarcoma-derived KYM cells, but no such increase was detected with TNF insensitive human embryonic lung fibroblast HEL cells. The results show that rhTNF induces increased hydroxyl radical production in TNF-sensitive cells, and suggest that this plays an important role in the mechanism of tumor cell killing by rhTNF.
2,2'-Dipyridyl↗
High performance liquid chromatography of biological polyamines using immobilized enzyme as post-column reactor followed by electrochemical detection.
A novel analytical method for biological polyamines (putrescine, spermidine and spermine) was developed. Polyamines were separated by ion-pair reversed phase chromatography using a polymer-based octadecyl bonded column. A polyamine oxidase immobilized column worked effectively as a post-column reactor to convert polyamines to hydrogen peroxide which was eventually detected by electrochemical oxidation on platinum electrode. This method required neither tedious derivatization nor gradient elution, permitting us to perform simple and rapid analysis of polyamines. The detection limits were 0.3, 0.6, and 4 pmol injected for putrescine, spermidine, and spermine, respectively with a linear range of two to three orders of magnitude. Chromatograms obtained with samples from human urine and rat brain homogenates demonstrated the high sensitivity and selectivity of the method.
Animals↗
Cachectin/TNF kills or inhibits the differentiation of 3T3-L1 cells according to developmental stage.
The effects of cachectin/tumor necrosis factor (TNF) on growth and differentiation of 3T3-L1 cells were examined. This fibroblastic cell line can be induced to differentiate into a mature cell type having the biochemical and morphological characteristics of normal adipocytes. At various stages of growth and differentiation, 3T3-L1 cells were exposed to 2.5 x 10(-16) to 2.5 x 10(-8) M (4.2 fg/ml to 420 ng/ml = ca. 1.2 x 10(-14) to 1.2 x 10(-16) U/ml) recombinant human cachectin/TNF for 24 hr, after which cytotoxicity or differentiation was evaluated. During log-phase cell growth, cachectin/TNF had no significant effect on cell viability, and the preadipocytic cells were also resistant to the cytotoxic effect of cachectin/TNF at the contact-inhibited confluent stage. However, when cachectin/TNF was added to the cells during induced differentiation, only 20% of the cells survived. After differentiation into adipocytes, cells regained their resistance to cachectin/TNF-induced cytotoxicity. Cachectin/TNF also markedly affected the differentiation of 3T3-L1 cells into adipocytes. When cells in the confluent phase of growth were exposed to cachectin/TNF for 24 hr, their subsequent hormone-induced differentiation to adipocytes was inhibited. Like cachectin/TNF, IL-1 also induces suppression of lipoprotein lipase and enhances lipolysis in differentiated 3T3-L1 adipocytes; however, in contrast to cachectin/TNF, IL-1 had no effect on the viability or differentiation of pre-adipocyte 3T3-L1 cells. These results indicate that the cytotoxic action of cachectin/TNF varies in the same cell type depending on the stage of growth or differentiation. The results also imply that cachectin/TNF may play a normal role in controlling the differentiation of certain types of cells in vivo including adipocyte lineages.
Animals↗