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Volume 101 (1993)
- Issue 6 Pages 349-
- Issue 5 Pages 289-
- Issue 4 Pages 197-
- Issue 3 Pages 101-
- Issue 2 Pages 59-
- Issue 1 Pages 1-
Volume 101, Issue 2
Displaying 1-4 of 4 articles from this issue
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Takeo ASAKAWA, Keiichi ENOMOTO, Masako TAKANO1993 Volume 101 Issue 2 Pages 59-68
Published: 1993
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSAdenylate cyclase is a key enzyme that couples with both the stimulatory and inhibitory G proteins (Gs and Gi). The cyclase has been purified and shown to be a glycoprotein of molecular weight 115, 000-180, 000. Cloning of cDNAs for adenylate cyclase showed that the cyclase is a member of a large family consisting of a variety of subtypes of the enzyme. These subtypes show different responses to calmodulin and G protein βγ subunits, and their distributions in tissues and organs are also different. This suggests that each subtype is involved in a particular physiological function. The general structure of adenylate cyclase is composed of two cytoplasmic domains and two membrane-spanning domains, each of which contains 6 transmembrane spans (12 spans in a molecule). The amino acid sequence of each cytoplasmic domain, which is thought to contain a nucleotide (ATP) binding site, is well-conserved among the various subtypes. This review also focuses on the regulation of adenylate cyclase activity by G protein subunits, particularly on several models for adenylate cyclase inhibition by Gi. As one of these mechanisms, direct inhibition of adenylate cyclase by the βγ subunits recently demonstrated by us will be discussed.View full abstractDownload PDF (20561K) -
Yasushi YAMAZOE, Kiyoshi NAGATA1993 Volume 101 Issue 2 Pages 69-77
Published: 1993
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSDuring the last decade, the influences of genetic factors on individual drug metabolizing capacity in humans have been characterized in fairly great detail at the molecular level. Debrisoquine/sparteine and mephenytoin polymorphisms are now known to be derived from defects in the human liver of specific forms of microsomal CYP (P450 or previously termed cytochrome P-450), CYP2D6 and CYP2C9 (2C18), respectively. In these polymorphisms, clear ethnic differences are observed in the incidence of poor metabolizers (PM). Although debrisoquine PM is detected in high incidence (5-10%) in Caucasians, little was found in Japanese. In contrast, mephenytoin PM is detected in higher percentages in Japanese (15-25%) than in Caucasians (3-7%). In this mini-review, current understanding of the molecular mechanism of both types of polymorphism and structural relationships of CYP2D6 and CYP2C9 substrates are shown. Relationships between specific phenotypes and cancer risks or disease are also discussed.View full abstractDownload PDF (18944K) -
Hideaki KIDO, Yoshiji KUBO, Satoru INOUE, Kazutaka HAYASHI, Yuji NARIT ...1993 Volume 101 Issue 2 Pages 79-91
Published: 1993
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSThe thrombolytic effects and changes in left ventricular function after intravenous administration of nasaruplase were examined in a canine thrombus model of acute myocardial infarction. When 8 U/kg/min of nasaruplase was intravenously administered after 30 min of coronary arterial occlusion, coronary recanalization was achieved in 78.6% (11/14) of the animals with little change in plasma fibrinogen concentration. There was no further decrease in cardiac output, left ventricular ejection fraction or regional wall motion immediately after reperfusion, compared with 30 min after coronary arterial occlusion. However, all these parameters returned to pre-occlusion levels one week after reperfusion. Nasaruplase markedly reduced infarct size as well as cardiac hypertrophy following coronary arterial occlusion, demonstrating suppression of the development of ischemic myocardial damage. These results indicate that coronary thrombolytic therapy with intravenous administration of nasaruplase is useful for the treatment of acute myocardial infarction.View full abstractDownload PDF (30224K) -
Itaru OHOI, Naomi OZAWA, Keita NAKAMURA1993 Volume 101 Issue 2 Pages 93-99
Published: 1993
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSUsing anesthetized rats, we performed a dose-response study of the ability of r-h-SOD to reduce the mortality caused by reperfusion-induced irreversible arrhythmia. The hearts were subjected to regional ischemia by the occlusion of the left coronary artery for 4 min followed by reperfusion for 7 min. First, the relation between the anti-arrhythmic effect of r-h-SOD and the size of the ischemic zone was examined. The protective effect of r-h-SOD was easily detected in rats with an ischemic zone size of 40 - 55% of the total heart weight, but not in rats with other zone sizes. Intravenous infusion of r-h-SOD at rates of 430 to 130, 000 U/kg/min beginning 1 min after regional ischemia significantly reduced the mortality after reperfusion. R-h-SOD at the doses used did not affect the blood pressure, heart rate or arrhythmia during the ischemic period. R-h-SOD at rates of 130 to 130, 000 U/kg/min was intravenously infused into anesthetized rats, and its plasma level was measured at 3 min after the beginning of the infusion. The plasma level of r-h-SOD increased dose-dependently (8.5 to 6, 600 U/ml). In conclusion, r-h-SOD reduced mortality after reperfusion over a wide range of doses and its effective plasma level was estimated to be 28 to 6, 600 U/ml in this model.View full abstractDownload PDF (16184K)
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