Impact of an intervention to improve contraceptive use through follow-up phone calls to female adolescent clinic patients.

Context: Adolescent females often have questions or concerns about their contraceptive methods, and they may discontinue use if these questions are not answered. Little evidence exists on whether follow-up phone calls to address young women's concerns can help sustain contraceptive use.

Methods: Between 2005 and 2007, a total of 805 females aged 14-18 attending a reproductive health clinic in San Francisco were randomly assigned to receive either regular clinic services or regular clinic services plus nine follow-up phone calls over 12 months.

Zebrafish-encoded 3-O-sulfotransferase-3 isoform mediates herpes simplex virus type 1 entry and spread.

Heparan sulfate proteoglycans modified by human glucosaminyl 3-O-sulfotransferase-3 (3-OST-3) isoform generates the cellular receptor for herpes simplex virus type 1 (HSV-1). Interestingly, the ability of zebrafish (ZF)-encoded 3-OST-3 isoform to modify heparan sulfate to mediate HSV-1 entry and cell-cell fusion has not been determined although it is predominantly expressed in ZF, a popular model organism to study viral infections. Here, we demonstrate that expression of ZF-encoded 3-OST-3 isoform renders the resistant Chinese hamster ovary (CHO-K1) cells to become susceptible for HSV-1 entry.

An unusual dependence of human herpesvirus-8 glycoproteins-induced cell-to-cell fusion on heparan sulfate.

Human herpesvirus-8 (HHV-8) is known to interact with cell surface heparan sulfate (HS) for entry into a target cell. Here we investigated the role of HS during HHV-8 glycoproteins-induced cell fusion. Interestingly, the observed fusion demonstrated an unusual dependence on HS as evident from following lines of evidence: (1) a significant reduction in cell-to-cell fusion occurred when target cells were treated with heparinase; (2) in a competition assay, when the effector cells expressing HHV-8 glycoproteins were challenged with soluble HS, cell-to-cell fusion was reduced; and, (3) co-expression of HHV-8 glycoproteins gH-gL on target cells resulted in inhibition of cell surface HS expression.

Utilization of the least shrew as a rapid and selective screening model for the antiemetic potential and brain penetration of substance P and NK1 receptor antagonists.

Substance P (SP) is thought to play a cardinal role in emesis via the activation of central tachykinin NK1 receptors during the delayed phase of vomiting produced by chemotherapeutics. Although the existing supportive evidence is significant, due to lack of an appropriate animal model, the evidence is indirect. As yet, no study has confirmed that emesis produced by SP or a selective NK1 receptor agonist is sensitive to brain penetrating antagonists of either NK1, NK2, or NK3 receptors.

Predictors of HIV transmission among migrant and marginally housed Latinos.

This study examined predictors of HIV-related sexual risk taking in a high risk and understudied convenience sample of 366 predominantly Mexican, migrant adults without stable housing. The sample included 27% men who have sex with men, 28% injectors of illegal drugs, and 21% sex workers. Hierarchical regression analysis showed that sexual risk taking was predicted by low condom self-efficacy, high-risk behavior, and being female.

Cancer dormancy. VII. A regulatory role for CD8+ T cells and IFN-gamma in establishing and maintaining the tumor-dormant state.

Dormant tumor cells resistant to ablative cancer therapy represent a significant clinical obstacle due to later relapse. Experimentally, the murine B cell lymphoma (BCL1) is used as a model of tumor dormancy in mice vaccinated with the BCL1 Ig. Here, we used this model to explore the cellular mechanisms underlying dormancy.

Immunotoxins: an update.

The use of immunotoxins (ITs) in the therapy of cancer, graft-vs-host disease (GvHD), autoimmune diseases, and AIDS has been ongoing for the past two decades. ITs contain a targeting moiety for delivery and a toxic moiety for cytotoxicity. Theoretically, one molecule of a toxin, routed to the appropriate cellular compartment, will be lethal to a cell.

Staphylococcal enterotoxin B induces the expression of activation markers on murine memory T cells in the absence of proliferation or lymphokine secretion.

Superantigens have been used to study peripheral tolerance in CD4+ T cells. The superantigen SEB induces T cell anergy by promoting the differentiation of SEB-activated virgin T cells into anergic memory T cells. Memory T cells from SEB or antigen-primed mice do not proliferate when they are cultured with SEB.

Loss of myb expression in an aggressive SJL/J B-cell lymphoma.

SJL mice spontaneously develop B-cell lymphomas that can be propagated by transplantation into syngeneic mice. These tumors usually have an indolent phenotype and require at least several weeks to produce morbidity following transplantation. However an aggressive lymphoma (RCS5) has been found that produces morbidity within days of transplantation.

CD8 suppressor cell activity and its effect on CD4 helper cell-dependent growth of SJL/J B-cell lymphomas.

CD8 cells, flow cytometrically sorted from the lymph nodes of tumor-bearing and normal SJL/J mice, suppressed in vitro proliferation of syngeneic CD4 cells in response to concanavalin A, two independent SJL/J lymphomas, and LPS-activated syngeneic B-cell blasts. The data confirm earlier reports that nonspecific suppressor cells are generated as a consequence of SJL/J lymphoma-stimulated T-cell proliferation. Earlier reports are extended, in that the suppressor cell is identified as expressing CD8, and the suppressor activity is shown to decrease the tumor-stimulated CD4 cell proliferation which is essential to growth of these CD4-dependent murine B-cell lymphomas.

Progression of transplanted SJL/J lymphomas attributed to a single aggressive H-2Ds-negative lymphoma.

Spontaneously arising, H-2Ds-positive SJL/J lymphomas have been reported to become irreversibly more aggressive and H-2Ds-negative upon successive transplantation in syngeneic mice. In an effort to determine whether this process was one of tumor progression, we sought to: (a) establish whether a clonal relationship exists between readily transplantable aggressive SJL/J lymphomas and their respective indolent predecessors; and (b) identify genetic events critical to the process of acquisition of increased malignancy. Examination of putatively distinct, aggressive, H-2Ds-negative lymphomas, including the long term transplantable line RCS5, revealed them to have the same heavy and light immunoglobulin chain gene rearrangement patterns, a characteristic karyotype marked by nine chromosomal abnormalities, and approximately ten newly acquired ecotropic murine leukemia proviruses at similar genomic sites.

The CD4 cell dependency of SJL/J B-cell lymphomas as a target for cyclophosphamide therapy.

SJL/J B-cell lymphomas induce proliferation of syngeneic CD4 cells, on which the tumors are dependent for growth. We sought to determine whether cyclophosphamide (CY) treatment of tumor-bearing mice would be successful through effects on tumor cells, CD4 cells, or both. The markedly increased survival of treated mice derived predominantly from reduced proliferation of CD4 cells in response to tumor.