Cryptosporidium infection in undernourished children with HIV/AIDS in Jos, Nigeria

Background: AIDS and Protein energy malnutrition (PEM) severely impair the immune system Cryptosporidium has over the last two decades emerged as a life threatening disease. The study attempts to determine the prevalence of Cryptosporidium infection in malnourished children with HIV/AIDS. Method: Blood and stool samples of 52 HIV-seropositive children and another 52 HIV-sero-negative children aged 0-5 years were collected and screened for HIV and Cryptosporidium oocysts respectively. The sera were screened by double ELISA and the stool by the modified Ziehl-Neelsen method. Results: Out of the 52 HIV-seropositive undernourished, under-five children, none (0%) excreted Cryptosporidium oocyst in their stools while 2 (3.8%) of the control group excreted the oocyst. Conclusion: Cryptosporidium infection seems to be uncommon among undernourished under five children with HIV/AIDS in Jos. Key Words: Cryptosporidium, children, HIV/AIDS, undernutrition Annals of African Medicine Vol.3(2) 2004: 80-8

Lysophosphatidic Acid Induces MDA-MB-231 Breast Cancer Cells Migration through Activation of PI3K/PAK1/ERK Signaling

Enhanced motility of cancer cells is a critical step in promoting tumor metastasis. Lysophosphatidic acid (LPA), representing the major mitogenic activity in serum, stimulates migration in various types of cancer cells. However, the underlying signaling mechanisms for LPA-induced motility of cancer cells remain to be elucidated.In this study, we found that LPA dose-dependently stimulated migration of MDA-MB-231 breast cancer cells, with 10 µM being the most effective. LPA also increased ERK activity and the MEK inhibitor U0126 could block LPA-induced ERK activity and cell migration. In addition, LPA induced PAK1 activation while ERK activation and cell migration were inhibited by ectopic expression of an inactive mutant form of PAK1 in MDA-MB-231 cells. Furthermore, LPA increased PI3K activity, and the PI3K inhibitor LY294002 inhibited both LPA-induced PAK1/ERK activation and cell migration. Moreover, in the breast cancer cell, LPA treatment resulted in remarkable production of reactive oxygen species (ROS), while LPA-induced ROS generation, PI3K/PAK1/ERK activation and cell migration could be inhibited by N-acetyl-L-Cysteine, a scavenger of ROS.Taken together, this study identifies a PI3K/PAK1/ERK signaling pathway for LPA-stimulated breast cancer cell migration. These data also suggest that ROS generation plays an essential role in the activation of LPA-stimulated PI3K/PAK1/ERK signaling and breast cancer cell migration. These findings may provide a basis for designing future therapeutic strategy for blocking breast cancer metastasis