In conclusion, we found that ZDV was able to inhibit and change the growth of gingival tissue when the drug was added at either day 0 or day 8 of raft growth. ZDV increased the expression of PCNA, cyclin A and cytokeratin 10. The expression of cytokeratins 5 and 6 and involucrin was decreased in ZDV-treated rafts. Together these results
indicate that ZDV deregulated the growth, differentiation and proliferation profiles in human gingival raft tissue. These results are consistent with the finding of oral complications in patients undergoing long-term HAART. Additional studies will be needed to determine the exact mechanism by which ZDV is exerting its effect. We thank Lynn Budgeon for technical assistance in preparing selleck chemical histological slides. This work was supported by NIDCR grant DE018305 to CM. “
“HIV status has commonly been found to affect the serum lipid profile. The aim of this study was to determine the effect of HIV infection on lipid metabolism; such information may be used to improve the management of HIV-infected patients. Samples were collected from December 2005 to May 2006 at Yaounde University Teaching Hospital, Yaounde, Cameroon. Lipid parameters were obtained using colorimetric AZD6244 mw enzyme assays, while low-density lipoprotein cholesterol (LDLC) values were calculated using the formula of Friedewald et al. (1972) and atherogenicity index by total cholesterol
(TC)/high-density lipoprotein cholesterol (HDLC) and LDLC/HDLC ratios. HIV infection was most prevalent in subjects aged 31 to 49 years. Most of the HIV-positive patients belonged to Centers for Disease Control and Prevention categories
B (43.0%) and C (30.23%). Compared with control subjects, patients with CD4 counts<50 cells/μL had significantly lower TC (P<0.0001) and LDLC (P<0.0001) but significantly higher triglyceride (TG) values (P<0.001) and a higher atherogenicity index for TC/HDLC (P<0.01) and HDLC/LDLC (P=0.02); patients with CD4 counts of 50–199 cells/μL had significantly lower TC (P<0.001) and significantly higher TG values (P<0.001); patients with CD4 counts of 200–350 cells/μL had significantly higher TG (P=0.003) and a higher atherogenicity index for TC/HDLC (P<0.0002) and HDLC/LDLC (P=0.04); and those with CD4 counts >350 cells/μL had a higher atherogenicity index Ribose-5-phosphate isomerase for TC/HDLC (P<0.0001) and HDLC/LDLC (P<0.001). HDLC was significantly lower in HIV-positive patients irrespective of the CD4 cell count. Lipid parameters were also influenced by the presence of opportunistic infections (OIs). HIV infection is associated with dyslipidaemia, and becomes increasingly debilitating as immunodeficiency progresses. HDLC was found to be lower than in controls in the early stages of HIV infection, while TG and the atherogenicity index increased and TC and LDLC decreased in the advanced stages of immunodeficiency. HIV infection is a major public health problem worldwide. It affects 33.2 million people globally, of whom 24.5 million are in Africa [1].