Study of association between sickle cell trait and renal dysfunction among young adults in South-west Nigeria.

BACKGROUND: Although sickle cell disease has become a recognized etiology of chronic kidney disease (CKD), the sickle cell trait (SCT) variant was until recently believed to be a benign carrier state with little or no effect on the health of affected individuals. However, recent studies now appear to suggest an association between SCT and CKD. OBJECTIVE: The objective of the study is to determine the association between SCT (hemoglobin AS) and renal dysfunction among young Nigerian adults. METHODOLOGY: This was a cross-sectional, descriptive study among apparently healthy undergraduates of Adeyemi College of Education, Ondo, southwest Nigeria. Their hemoglobin genotypes were determined using standard alkaline electrophoresis; their blood pressure, anthropometry, serum total cholesterol (TC), creatinine, and estimated glomerular filtration rate (eGFR) were determined. Data analyzed using Statistical Package for Social Sciences (SPSS) 20 were significant at P < 0.05. RESULTS: Six hundred and two subjects with HbAS (SCT, n = 465) and HbAA (non-SCT, n = 137) were studied. Their age range was 18-30 years with male-to-female ratio 1:3.8. There was no difference in the prevalence of renal dysfunction between SCT and non-SCT subjects (5.1% vs. 5.2%, P = 0.591). There was no increased risk of CKD among subjects with SCT (PR, 0.99 at 95% CI [0.417-2.348]). CONCLUSION: SCT was not associated with increased risk of renal dysfunction among young adults in Nigeria. Further studies are needed to clarify the controversy, especially in Nigeria, with a relatively higher prevalence of SCT.

Silencing of stathmin induces tumor-suppressor function in breast cancer cell lines harboring mutant p53.

Cancers harboring dominant-negative p53 mutations are often aggressive and difficult to treat. Direct attempts to restore wild-type p53 function have produced little clinical benefit. We investigated whether targeting a p53-target gene could induce certain tumor-suppressor characteristics. We found that inhibition of stathmin, a microtubule regulator that can be transcriptionally repressed by wild-type p53, restored certain wild-type functions to cancer cells with mutant p53. Silencing of stathmin by small interfering RNA (siRNA) in mutant p53 cell lines lowered expression to that observed following activation of wild-type p53 by DNA damage in wild-type p53 cell lines. siRNA-induced repression of stathmin decreased cell proliferation, viability and clonogenicity in mutant p53 cell lines. Furthermore, knockdown of stathmin partially restored cell-cycle regulation and activation of apoptosis. Therefore, targeting stathmin, a gene product that is overexpressed in the presence of mutant p53, may represent a novel approach to treating cancers with aberrant p53 function.

[Ultrasonic examination of the status of the ovaries and endometrium after the treatment of tubal and peritoneal infertility]. / Sostoianie iaichnikov i éndometriia po dannym UZI v protsesse terapii posle likvidatsii trubnogo i peritoneal'nogo besplodiia.

The authors analyze the usefulness of ultrasonic examination for the assessment of ovarian and endometrial status in 84 patients operated on for tubal and peritoneal sterility. After surgery the patients were recommended nootropic agents and cyclic vitamin therapy for 3 months. In cases with concomitant diseases (endometriosis, small pelvis varicose veins) synthetic estrogen-gestagen drugs, anticoagulants, disaggregants were prescribed. If the treatment did not result in pregnancy in 2 months, ovulation stimulants (clostilbegit, choriogonin) were prescribed. Drug therapy had a favorable effect on ovarian and endometrial function. Ultrasonic examination may be recommended for monitoring ovarian and endometrial status.