Serum selenium lipids abnormalities in cirrhotic patients with and without ischemic heart disease

Although the cirrhotic patients are less prone to develop ischemic heart disease [IHD], this study was done to investigate why some and rare cirrhotic patients develop this cardiac disease. Forty male cirrhotic patients of Child's B and C grading were selected twenty of them had only liver cirrhosis [group I] and the other twenty had also IHD [group II]. Liver function tests, serum lipid parameters and serum selenium were done for all subjects. ECG, echo - Doppler study and serum enzymes as CPK and LDH were done additional for patients of group II.Contrary to control, the cirrhotic patients showed highly significant reduction in serum selenium and HDL levels [P<0.01]. They also showed highly significant increases in total lipid, total cholesterol, LDL and triglyceride levels in the serum [P<0.01]. Contrary to the results of group I, serum results of group II showed significant reduction in selenium level, highly significant reduction in HDL and highly Significant increases in total lipids, total cholesterol, LDL and triglyceride levels.In both groups, serum selenium reduction was significant directly correlated with serum albumin level and was highly significant directly correlated with HDL level. However, it was highly significant inversely correlated with serum levels of total lipids, total cholesterol, LDL and triglyceride.It can be concluded that the cirrhotic patients had highly significant reduction in serum selenium and cardioprotective lipoprotein [HDL] levels. Also, they developed highly significant increases in the levels of atherogenesis-induced parameters as total lipids, total cholesterol, LDL and triglyceride. Thus, the highly significant hyperlipidaemia and atherogenesis in patients of group II may be attributed to more significant reduction in their serum selenium

PCR-mediated cloning and expression of the gene for the B-subunit of vibrio cholerae toxin isolated recently in Iran

Knowing the nucleotide sequence of the cholera toxin operon, we designed oligonucleotide primers for its-PCR amplification from local clinical isolates of V. cholerae. The resulting amplification product was cloned in a common pUC18 vector. Subsequently, a part of this operon encoding the cholera toxin B-subunit [CTB] was reamplified and cloned between the BamH 1 and EcoR1 sites of the same vector to create a recombinant plasmid pRI8CTB. Temperature-controlled expression of the target protein was achieved by supplementing pR18CTB with a DNA fragment which contained a strong promoter PR and the gene for a heat-sensitive repressor cI857 of bacteriophage lambda from an expression vector pCQV2. When induced, the constructed plasmid pSCTB18 provided for the production of recombinant CTB secreted into the periplasmic space in a yield of about 3mg per liter of bacterial culture, as revealed by GM 1-ELISA