Role of cholesterol phospholipid cholic acid and mucoprotein in the crystallization of gallbladder stone / 生物医学工程学杂志

Normal feed and stone-leading feed were used respectively to raise guinea pigs in the control group and stone-causing group. The dynamic changes of total cholesterol, mucoprotein, total phospholipid and total cholic acid were measured during various raising periods. The formation of crystal nucleus and the growth of gallstone were studied under polarzing microscope. It was found that the contents of total cholesterol, mucoprotein, total phospholipid and total cholic acid in the gallbladder bile of control group were nearly the same during the whole feeding process, and no shaped stone crystal was formed. In the stone-causing group, however, the contents of total cholesterol and mucoprotein gradually went up and the contents of total phospholipid and total cholic acid gradually went down. After 10 days' feeding, significant difference was seen,and after 25 days' feeding, highly significant difference was noted. With the increase of feeding days, the liquid crystal vesicles in the bile increased, became bigger, gathered in strings, and then formed liquid crystal cells. The stone crystal growth along these nuclei of bile liquid crystal cells spread out rapidly, and the micro-crystal grains formed further in number. It was shown that, during the process of gallbladder stone formation, bile liquid crystal cells form a basic kind of nucleus, and the gathering and merging of bile liquid crystal vesicles be the key to crystal growth. So cholesterol and mucoprotein play the role of nucleation-leading factors in enhancing the gathering and merging of liquid crystal vesicles, and phospholipid and cholate play the role of anti-nucleation during the formation of gallbladder stone.

Mitochondrial DNA 3243, 3316 point mutations and type 2 diabetes mellitus / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To investigate the prevalence of mitochondrial DNA (mtDNA) mutation at position 3243(A/G) and 3316(G/A) in Chinese patients with type 2 diabetes mellitus.</p><p><b>METHODS</b>Two hundred and twenty-five unrelated Chinese patients with type 2 diabetes and 195 nondiabetic control individuals without family history of diabetes in Yunnan were examined. The presence of mt 3243 and 3316 mutations was determined by polymerase chain reaction amplification and restriction fragment length polymorphism (PCR/RFLP). Finally, mutant mtDNA was confirmed by DNA sequencing.</p><p><b>RESULTS</b>The mitochondrial DNA mutation at position 3316 was found in 5 of 225 (2.22%) patients with type 2 diabetes, and this mutation was found in 2 of 195 (1.03%) control individuals. There was no significant difference in respect to the frequency of the mutation between patients and controls. The mitochondrial DNA mutation at position 3243 was not found in any of the patients and controls.</p><p><b>CONCLUSION</b>The results suggest that the prevalence of the mitochondrial tRNA (Leu(UUR))gene at position 3243(A/G) mutation is so low that it may not be a major cause of type 2 diabetes mellitus in patients of Yunnan, China, and the mitochondrial ND1 gene at position 3316(G/A) mutation may be a polymorphism unrelated to diabetes in Chinese. The role of other genetic, environmental and intrauterine factors needs further investigation.</p>

Changes of protein tyrosine phosphorylation in erythrocyte band 3 glucose-6-phosphate dehydrogenase deficiency / 中华血液学杂志

<p><b>OBJECTIVE</b>To explore the hemolytic mechanism of glucose-6-phosphate dehydrogenase (G6PD) deficient erythrocytes in the view of phosphorylation of membrane protein.</p><p><b>METHODS</b>The alternation of membrane protein phosphorylation and the effect of dithiothreitol (DTT) on protein phosphorylation were analysed by Western blot technique. The activity of phosphotyrosine phosphatase (PTPs) was determined by using p-nitrophenyl phosphate as substrate.</p><p><b>RESULTS</b>Tyrosine phosphorylation of band 3 protein was obviously enhanced in G6PD-deficient erythrocytes. The activity of PTPs was low compared to the normal erythrocytes. The level of phosphotyrosine in G6PD-deficient erythrocytes incubated with DTT was almost the same as in those without DTT. The results were consistent with the activity of PTPs.</p><p><b>CONCLUSIONS</b>PTPs activity reduction and tyrosine phosphorylation enhancement induced by oxidation in G6PD deficiency play an important role in erythrocytes hemolysis. However, the alternation of thiol group is not the only factor affecting the activity of PTPs in G6PD-deficient erythrocytes.</p>

Study on Na~+-K~+ ATPase and Ca~(2+) -Mg~(2+) ATPase activities of human erythrocyte membrane in G6PD deficient individuals / 中国病理生理杂志

By using Person's separating blood ghost method basically, Na~+-K~+ ATP ase and Ca~(2+)-Mg~(2+) ATPase activties of human erythrocyte membrane were studied. The comparison was made between 11 G6PD deficient subjects and 11 healthy control persons. The results showed that both enzyme activities as well as ouabain inhibition rate were decreased in G6PD deficient individuals (P