Men’s pathways to risky sexual behavior: Role of co-occurring childhood sexual abuse,posttraumatic stress disorder,and depression histories

Recent reports of sexually transmitted infection-rate increases among men indicate the need for renewed study of male sexual risk behavior to aid development of updated and novel risk reduction interventions. Men who have childhood sexual abuse (CSA) histories consistently report frequent sexual risk behavior. The objective of this sturdy is to explore whether posttraumatic stress disorder (PTSD) and depression are moderators and/or mediators of the association between CSA and sexual risk in adult men. A cross-sectional survey study employing random digit dial recruitment was administered to men aged 18–49 years from Philadelphia County. Two bundred ninety eight men were recruited and screened for CSA history, administered items from the Posttraumatic Stress Diagnostic Scale (PDS) and Center for Epidemiologic Studies—Depression (CES-D), and asked to estimate their number of lifetime sexual partners (LSPs). Effects of sociodemographic characteristics, CSA, PTSD, and depression on the number of LSPs were modeled using Poisson regression. Results show that 197 (66%) men participated; 43 (22%) had CSA histories. CSA was significantly associated with PTSD/depression (P=.03). Four sociodemographic variables (age, race, sexual identity, and education), CSA (incidence rate ratio, IRR=1.47, P<.001), PTSD (IRR=1.19, P=.04), depression (IRR=1.29, P=.001), all 2-way interactions, and the 3-way CSA/PTSD/depression interaction (IRR=11.00, P<.001) were associated with the number of LSPs (R²=0.27). In conclusion, sexual partnership patterns unique to men with CSA histories and comorbid PTSD/depression appear to lead to substantially higher numbers of LSPs. Estimates of this relationship may have been biased toward the null by underreporting that can occur with phone surveys. Cross-sectional studies do not support causal inferences; however, the identification of a moderating and mediating influence of PTSD/depression on the relationship between CSA and sexual risk behavior is important and suggests the need for future studies with larger samples that examine trajectories for CSA, psychiatric illness, and sexual partnerships.     

Tumorigenicity and tumour-graft rejection of polyoma virus-transformed fibroblast-T-lymphocyte hybrids.

In anticipation of the use of functional T-lymphocyte hybrids in adoptive immunotherapy, the differentiation and tumorigenicity of hybrid clones generated by fusion of a T lymphocyte derived from F1 (DBA/J2 x AKR) mouse spleen, and a polyoma virus-transformed fibroblast initiated from C3H mouse cells, were studied. The hybrid cells grew in suspension and had an appearance (by transmission and scanning electron microscopy) very similar to that of the lymphocytic line. The hybrid and the different clones could induce tumour grafts. Malignancy was dominant in newborn mice where tumours were obtained in all mouse strains (allogeneic or semi-allogeneic) inoculated. In adult mice, the hybrid cells were tumorigenic in C3H and F1 (DBA/J2 x AKR), whereas there was complete tumour rejection in allogeneic (C57/BL6) or semi-allogeneic (DBA/J2 and AKR) mice. The role played by major histocompatibility antigens in the graft rejection is discussed. The histology of the tumour grafts was intermediate between fibrosarcoma and lymphosarcoma.     

Differential effect of Serratia protease on platelet surface glycoproteins Ib and V

The effect of a zinc metalloprotease from Serratia marcescens on platelet surface glycoproteins (GP) Ib and V was analyzed. Increasing protease treatments caused progressive loss of GP Ib with appearance of the major fragment, glycocalicin, in the supernatant solution. No GP V was detected in the supernatant solution, and protease-pretreated platelets had the same capacity as control platelets to release fragment 1 of GP V in response to thrombin. The Serratia protease- pretreated platelets did show the lag before thrombin-induced dense granule secretion, characteristic of platelets modified by pretreatment with other nonstimulating proteases. Treatment with Serratia protease gives the only demonstrated selective loss of GP Ib without apparent effect on GP V. It suggests that GP V (1) does not depend on GP Ib for its association with platelets and (2) is not the substrate for protease modification of platelet function.     

Monoclonal antibody OKT17 recognizes most cases of T-cell malignancy

Membrane phenotype analysis with monoclonal antibodies (McAb) has demonstrated great heterogeneity within the T-cell malignancies. We describe here the reactivity with an anti-T cell McAb, OKT17, in 80 leukaemia samples. Cells from all types of T-cell leukaemia (48 cases), except from the small group of pre-T-ALL, strongly expressed the antigen identified by OKT17 whereas none of the 32 non-T leukaemias were OKT17 positive. When the reactivity of OKT17 was compared with that of other pan-T markers, OKT17 was positive in a larger number of T-cell leukaemias: 87% of cases compared with 74% with E-rosettes and 73% with the McAb 3A1. In the mature or post-thymic proliferations OKT17 was positive in 96% of cases, compared with 77% with E-rosettes and 61% with 3A1. The latter reagent, on the other hand, was better than OKT17 for detecting leukaemias with a thymic phenotype, 100% and 68% of positive cases respectively. The combined use of OKT17, 3A1 and terminal transferase permits a more precise classification of all the T-cell leukaemias according to the main stages of T-cell differentiation.     

Interleukin 2 does not promote the in vitro and in vivo proliferation and growth of human acute leukaemia cells of myeloid and lymphoid origin

The effect of recombinant interleukin 2 (IL2) on the in vitro and in vivo proliferation and growth of human acute leukaemia cells of both myeloid and lymphoid origin was investigated. In none of the 25 primary samples tested could a continuously in vitro growing cell line be obtained by adding IL2 to the culture medium. Although IL2 induced a proliferative signal in three of the 31 acute leukaemias analysed, the overall 3H-thymidine uptake of the neoplastic cells was significantly reduced (P less than 0.05) in the presence of IL2. The unlikelihood of an important proliferative signal triggered by IL2 was confirmed in a semisolid clonogenic assay, which failed to document an increased colony growth in the 26 samples studied. Furthermore, using a colorimetric assay as a test for cell proliferation and survival, in seven of the 11 fresh acute leukaemia samples tested a 22-40% reduction in viability was observed in the presence of IL2, while in the remaining four, IL2 was ineffective. In order to investigate the effect of IL2 in an in vivo setting, an experimental model in heavily immunosuppressed nu/nu mice was established. In no case did IL2 promote the in vivo proliferation and growth of human myeloid and lymphoid acute leukaemia cells injected in the mice. On the contrary, with seven of the eight leukaemic cell lines which gave rise spontaneously to leukaemic masses, this could be prevented when the mice received locally 300 U of IL2 three times daily for 90 d. IL2 also blocked the growth in vivo of three fresh acute leukaemia samples (two myeloid and one lymphoid). Co-culture experiments using leukaemic cell lines and increasing numbers of normal lymphocytes suggest that the inhibitory effect of IL2 is probably exerted via an indirect mechanism. These findings, coupled to the well-documented ability of IL2 to generate lymphokine activated killer cells cytolytic against leukaemic blasts, further point to the potential role of immunotherapy with IL2 in the management of patients with haematological malignancies.