Induction of a functional subset of HIV-specific CD4+ T cells that is resistant to HIV infection could enhance immune protection and decrease the rate of HIV disease progression. CMV-specific CD4+ T cells, which are less frequently infected than HIV-specific CD4+ T cells, are a model for such an effect. To determine the mechanism of this protection, we compared the functional response of HIV gag-specific and CMV pp65-specific CD4+ T cells in individuals co-infected with CMV and HIV. We found that CMV-specific CD4+ T cells rapidly up-regulated production of MIP-1α and MIP-1β mRNA, resulting in a rapid increase in production of MIP-1α and MIP-1β after cognate antigen stimulation. Production of β-chemokines was associated with maturational phenotype and was rarely seen in HIV-specific CD4+ T cells. To test whether production of β-chemokines by CD4+ T cells lowers their susceptibility to HIV infection, we measured cell-associated Gag DNA to assess the in vivo infection history of CMV-specific CD4+ T cells. We found that CMV-specific CD4+ T cells which produced MIP-1β contained 10 times less Gag DNA than did those which failed to produce MIP-1β. These data suggest that CD4+ T cells which produce MIP-1α and MIP-1β bind these chemokines in an autocrine fashion which decreases the risk of in vivo HIV infection.

Background Medication errors during hospitalization are a major patient safety concern. Medication reconciliation is an effective tool to reduce medication errors, yet internal medicine residents rarely receive formal education on the process.

Breast cancer (BC) is the most common cancer for females, and its incidence tends to increase year by year. Currently, the backbone of therapy for BC is mainly chemotherapy; however, its toxicity in normal cells and acquired tumor resistance to the drug users are considered the main barriers. Therefore, there is still an urgent need for the development of more effective and safer anti-BC agents. Based on previous reference documents in recent years, this review covers the work reported on the anti-BC compounds classified according to the structures. This review summarized significant anti-BC compounds organized by functional groups according to the animal model data, although there would be some limitations. This review highlights the properties of new compounds having promising anti-BC properties, which may be proven to be more effective and selective, and possibly free of unwanted side effects. The reviewed compounds represent an interesting possibility of overcoming BC and reducing the percentage of patients with an inadequate response to drug therapy.

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