[A case of coronary spasm angina induced by anaphylactic shock].
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Biomedical subjects
Publications and source records attributed to C Matsumoto.
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Serum samples with lower temperature-dependent antibody with low avidity to C100-3 (HCV) antigen were found in 0.19% of 23,197 voluntary blood donors at this blood center. They showed positive C100-3 antibody activity at 24 C but not at 37 C. The antibody activity bound to C100-3 antigen at lower temperature disappeared after incubation for 60 min at 37 C or treatment with 8 M urea. Other markers of hepatitis C virus infection, especially the presence of HCV-RNA were demonstrated in some of these serum samples and the importance of this phenomenon is discussed with regard to virus screening of blood donors for hepatitis C.
Human T-cell leukemia virus type I (HTLV-I) provirus DNA from the cultured cell line HUT 102 and from peripheral mononuclear cells (PBMC) of anti-HTLV-I antibody-positive Japanese blood donors was detected by the nested double polymerase chain reaction (PCR) method. This procedure consists of a first amplification and a second amplification with the products of the first amplification and primers interior to the first primers. Using this method, we demonstrated that it is possible to detect single-template DNA. Polyacrylamide gel electrophoresis of the nested double PCR products, with our primers, revealed three bands with excess amounts of template DNA, two bands with moderate amounts, and a single band with limited amounts. The amount of provirus in PBMC was roughly estimated from the results of the nested double PCR. Particle agglutination (PA) assays and indirect immunofluorescence testing (IF) with mixed MT-2 cells and Molt-4 cells as targets to detect anti-HTLV-I antibody were performed, and the results were compared with those of the nested double PCR of the pX region. None of the 101 PA-negative samples were positive in either the IF or PCR test. Of the 155 samples that were antibody positive by the PA assay, 57 were positive by both PCR and IF. Furthermore, the results of the IF and PCR tests coincided completely. It was therefore concluded that the IF method is most appropriate for confirmation of the PA assay currently used in most diagnostic laboratories and blood centers.
PURPOSE: Evaluate the lytic state (LS) expressed by the level of plasmatic fibrinogen (PF) after rt-PA "in bolus" infusion for acute myocardial infarction (MI) and its relation to coronary reperfusion. PATIENTS AND METHODS: Fifty-one patients (38 men, mean age of 53.0 +/- 9.8 years) with demonstrated occlusion of the infarct related artery (IRA) received an intravenous bolus infusion of 70 mg of rt-PA, PF was assessed before and 90 minutes after the treatment and the levels were compared in patients with (group 1) and without (group 2) reperfusion of the IRA. RESULTS: Basal levels of PF were within the normal range in all patients. There was a decrement of 35.1% in the PF dosed at 90 minutes, from 276.8 +/- 55.5 mg/dl to 168.0 +/- 68.2 mg/dl. Both groups were similar in the levels of PF 90 after treatment (145.1 +/- 95.7 mg/dl in group 1 versus 187.0 +/- 53.7 mg/dl in group 2). CONCLUSION: "In bolus" rt-PA treatment for MI significantly reduces the PF, but the LS obtained was similar in patients with or without reperfusion of the IRA.
Nizatidine, a new H2-receptor antagonist for treatment of duodenal ulcer disease, was evaluated in a unique two-phase, placebo-controlled, randomized, double-blind, multicenter clinical trial. Patients received either 150 mg nizatidine twice daily or placebo for 4 weeks (phase I). If ulcer healing did not occur during phase I, patients were randomly reallocated to receive either 150 mg nizatidine twice daily or placebo for an additional 4 weeks (phase II). Patients with a healed ulcer continued on the same therapy. All patients were endoscoped at week 8. Healing rates at week 2 were 93 of 265 (35%) nizatidine-treated patients and 55 of 260 (21%) placebo-treated patients (p less than 0.001); at week 4, healing rates were 198 of 259 (76%) nizatidine-treated patients and 95 of 243 (39%) placebo-treated patients (p less than 0.001). In phase II, ulcer healing occurred in 46 of 86 (53%) nizatidine-treated patients and in 23 of 90 (26%) placebo-treated patients (p = 0.002). In patients who had a healed ulcer at previous endoscopies, 18 of 178 (10%) nizatidine-treated patients and 10 of 81 (12%) placebo-treated patients had a recurrence of duodenal ulcer. Smokers who had histories of previous ulcers were more likely to have an early recurrence.
Nizatidine was studied in six high-acid-secretor (basal secretion, greater than or equal to 5 mEq/hr) male volunteers in a randomized, double-blind, nonbalanced, cross-over, placebo and standard drug-controlled study. Doses of 75 mg, 150 mg, and 300 mg bid were compared with placebo and cimetidine 300 mg qid. Nocturnal acid output was significantly reduced (P less than .01) by all doses of nizatidine (36 +/- 22, 36 +/- 31, and 26 +/- 20 mEq) with 75 mg, 150 mg and 300 mg, respectively, and also by cimetidine (43 +/- 39 mEq) as compared with placebo (101 +/- 61 mEq). Nizatidine also significantly reduced meal-stimulated acid secretion at breakfast (14 +/- 9, 9 +/- 7, and 5 +/- 6 mEq/2 hours with 75 mg, 150 mg, and 300 mg, respectively, P less than .01), at lunch (50 +/- 22, 57 +/- 22 and 50 +/- 35 mEq/2 hours, P less than .05) but did not have any effect at dinner (65 +/- 16, 78 +/- 24, and 71 +/- 17 mEq/2 hours) whereas cimetidine, given every 6 hours, significantly (P less than .01) reduced meal-stimulated acid secretion (25 +/- 16, 27 +/- 20 and 31 +/- 15 mEq/2 hours, breakfast, lunch, and dinner, respectively) as compared with placebo (81 +/- 30, 76 +/- 25, and 66 +/- 16 mEq/2 hours, breakfast, lunch, and dinner, respectively). Both drugs have a similar pharmacokinetic profile. Nizatidine seems to be a promising H2 antagonist, more potent than cimetidine (on an mg/mg basis), and efficacy studies on gastric acid disorders should be performed.
Nizatidine, a new H2-receptor antagonist for the treatment of duodenal ulcer disease, was compared with placebo in a dose-response, double-blind, parallel, multicenter clinical trial. Patients were randomly allocated to receive either nizatidine (25 mg b.i.d., 150 mg b.i.d., or 300 mg at bedtime) or placebo. At the end of 4 weeks, patients whose ulcer had not healed were randomly reallocated to receive either the nizatidine 150 mg b.i.d. dosage regime or placebo for an additional 4 weeks. Nizatidine doses of 300 mg at bedtime and 150 mg b.i.d. demonstrated similar healing frequencies. Both of these doses were statistically significantly superior in ulcer healing to the nizatidine 25 mg b.i.d. dose and to placebo at the end of 4 weeks. Patients randomly reallocated to receive nizatidine had significantly greater healing rates than patients randomly reallocated to receive placebo. In summary, nizatidine given as a single evening dose of 300 mg or as 150 mg b.i.d. proved to be equally safe and effective in the healing of active duodenal ulcers.
A new H2-receptor antagonist, nizatidine (150 mg h.s.), was compared with placebo as maintenance therapy in a randomized, parallel, double-blind, one-year study of 513 patients with recently healed duodenal ulcer. Endoscopies were performed at 0, 3, 6, and 12 months and at unscheduled times if symptoms of active peptic ulcer disease were present. Cumulative ulcer recurrence rates for nizatidine and placebo were 13 versus 40% at 3 months, 24 versus 57% at 6 months, and 34 versus 64% at 12 months. The differences were significant (p less than 0.001) at each treatment period. Smokers in both treatment groups had significantly greater recurrence rates than non-smokers. Symptoms of peptic ulcer disease were significantly less in nizatidine-treated patients in the first 3 months of treatment. Adverse events, including those related to peptic ulcer disease, occurred more frequently in placebo-treated patients. Nizatidine proved to be safe and effective in preventing recurrences of duodenal ulcer.
To examine the effects of transient hyperprolactinemia on in vitro fertilization and embryo transfer, 61 cycles in 50 euprolactinemic ovulatory women with irreparable tubal diseases were stimulated with clomiphene (CC) alone or CC and human menopausal gonadotropin followed by human chorionic gonadotropin (hCG). Serum prolactin (PRL) increased after hCG administration with peak values of 45.4 +/- 4.2 ng/ml on the day of laparoscopic oocyte aspiration. The highest serum estradiol (E2) concentration was found on the day before PRL peak and serum progesterone (P) began to increase after hCG injection concomitant with the PRL rise. The group having 50 ng/ml or more of PRL (34 cycles) had significantly higher levels of E2 during preovulatory and early luteal phase compared to those of the group having less than 50 ng/ml of PRL (27 cycles) but there was no significant difference between the P levels in the two groups. In the higher PRL group 72 (62.1%) of 116 collected oocytes were fertilized and 6 (20.0%) conceived. In the lower PRL group 45 oocytes (58.4%) of 77 were fertilized and 3 (12.5%) became pregnant. These data suggest that elevated serum PRL concentrations may have no effect on fertilization of oocytes in vitro or embryonic development.
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In a program for in vitro fertilization and embryo transfer, laparoscopies for oocyte aspiration were performed in 40 cycles in 36 normally menstruating women with irreparable tubal diseases (IVF patients) who received clomiphene citrate (CC) and human menopausal gonadotropin (hMG). An intramuscular injection of human chorionic gonadotropin (hCG) was given to all patients after completion of follicular maturation. Fourteen cycles in 13 spontaneously ovulating women (control patients), also stimulated with CC and hMG, were adequately monitored to identify the appearance of the spontaneous luteinizing hormone (LH) surge. The follicular maturation was followed by daily ovarian ultrasonographic examination and serum estradiol estimations. Just before the LH surge the diameter of the leading follicle was 20.2 +/- 0.7 (mean +/- S.E.) mm and the serum estradiol concentration per follicle was 384.1 +/- 16.3pg/ml in the control patients. In the IVF patients the former was 20.6 +/- 0.3mm and the latter was 305.8 +/- 13.3pg/ml prior to hCG administration. When the relationship of follicular size to the rates of oocytes recovery, maturation, fertilization and cleavage was examined, larger follicles (3ml less than or equal to follicular fluid volume) showed good results. Of the 152 oocytes that were recovered from these IVF patients, 96 (63.2%) were fertilized and 79 (52.0%) cleaved. Three pregnancies resulted from 35 embryo transfers.
The activities of S-adenosylmethionine synthetase isozymes in liver were measured after rats received a diet containing excess methionine. The activity of the alpha-form increased with increasing methionine content in the diet, and reached 4-5 fold after 6 days on a 3% methionine diet. However, the activity of the beta-form showed only a 1.5 fold increase. The activity of the gamma-form in kidney showed no significance change.
Treatment of rats with an ethionine plus adenine or a methionine diet leads not only to a marked increase of the alpha-form isozyme of S-adenosylmethionine synthetase in liver, but also to the accumulation of comparable amounts of S-adenosylethionine and S-adenosylmethionine in liver. Transplantation of ascites tumor cells into mice leads to a marked increase only of the beta-form isozyme in the host liver, but the levels of S-adenosylmethionine do not significantly change in liver.
An assay method has been developed for the measurement of tissue levels of S-adenosylmethionine based upon the ability of this compound to activate tripolyphosphatase associated with S-adenosylmethionine synthetase beta prepared from rat liver. The method has been used to measure S-adenosylmethionine levels in rat liver after feeding rats on various concentrations of methionine in the diet. The results obtained by this method agree well with those measured by the spectrophotometric method. The limit of sensitivity of the assay was about 0.1 nmol of S-adenosylmethionine in an incubation volume of 0.1 ml (10(-6) M).
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