Polymorphism of the angiotensin I-converting enzyme gene in diabetic nephropathy in type II diabetic patients with proliferative retinopathy.

Recently, deletion (D)/insertion (I) polymorphism in the Angiotensin I-converting enzyme (ACE) gene has been suggested to be related to the development of diabetic nephropathy in type I diabetes mellitus. This hypothesis, however, remains controversial. Differences in clinical states between patients, especially in glycemic control or duration of diabetes, could be responsible for these contradictory results. In this study we examined the relationship between D/I polymorphism of the ACE gene and diabetic nephropathy in type II diabetic patients who had already developed proliferative retinopathy (n = 45), and were thought to have been in a hyperglycemic state for long enough to develop microangiopathy. The patients were divided into two subgroups: 24 with nephropathy (albumin excretion rate: AER > or = 20 micrograms/min) and 21 without (AER < 20 micrograms/min). There was no difference in the duration of diabetes, HbA1c levels or average blood pressure over the previous year between these subgroups and other clinical characteristics were comparable. Patients without nephropathy exhibited allele I more often than those with nephropathy (p = .025). AER was lowest in genotype II and highest in genotype DD patients but the difference was not statistically significant (p = .07). From these findings, it was concluded that genotype II for the ACE gene could be a marker for reduced risk of diabetic nephropathy.

[Thoracoabdominal aneurysm complicated with disseminated intravascular coagulopathy--a case of surgical treatment following heparin pretreatment].

This article reports a case of a thoracoabdominal aneurysm complicated with disseminated intravascular coagulopathy (DIC). The thoracoabdominal aneurysm was successfully replaced with a prosthetic graft following the short terms of heparin pretreatment. Although heparin pretreatment had been effective for the temporal remission of DIC, a large amount of blood transfusion was necessary because of prolonged bleeding from surgical wound. However, hematological evidence of DIC and bleeding tendency were dramatically arrested in the immediate postoperative period. It was concluded that the definitive treatment for DIC was removal of the aneurysm. Heparin was usefull for the preservation of coagulation factors and platelet, but it did not lessen operative bleeding.

[Surgical treatment of aortic root aneurysm associating with infectious endocarditis].

From 1979 to 1989, aortic root aneurysms were encountered in 6 of the 30 patients who underwent surgical treatment for infectious endocarditis. Four patients underwent aortic valve replacement and direct or patch closure of the orifice of aortic root aneurysm. In additional 2 patients with infected aneurysm of right coronary sinus of Valsalva rupturing into the right ventricle, the aneurysm and infected tissue in the right ventricular outflow tract were completely resected and the defect of aortic sinus and VSD were closed with double Teflon fabric patches. All patients survived postoperatively, however, one patients died 1.5 months after the operation probably due to rupture of mycotic aneurysm of cerebral artery. Another late death seemed to be concerned with recurrent aortic root aneurysm, in which case direct closure of aneurysm had been performed. We believe that even if the aneurysm seems to be small, its orifice should be closed with the use of a fabric patch to prevent recurrent aneurysm formation.

Cysteine biosynthesis in Saccharomyces cerevisiae: mutation that confers cystathionine beta-synthase deficiency.

The cys2-1 mutation of Saccharomyces cerevisiae was originally thought to confer cysteine dependence through a serine O-acetyltransferase deficiency. In this study, we show that cys2-1 strains lack not only serine O-acetyltransferase but also cystathionine beta-synthase. However, a prototrophic strain was found to be serine O-acetyltransferase deficient because of a mutation allelic to cys2-1. Moreover, revertants obtained from cys2-1 strains had serine O-acetyltransferase but not cystathionine beta-synthase, whereas transformants obtained by treating a cys2-1 strain with an S. cerevisiae genomic library had cystathionine beta-synthase but not serine O-acetyltransferase. From these observations, we conclude that cys2-1 (serine O-acetyltransferase deficiency) accompanies a very closely linked mutation that causes cystathionine beta-synthase deficiency and that these mutations together confer cysteine dependence. This newly identified mutation is named cys4-1. These results not only support our previous hypothesis that S. cerevisiae has two functional cysteine biosynthetic pathways but also reveal an interesting gene arrangement of the cysteine biosynthetic system.