Publications
Department of Medicine faculty members published more than 3,600 peer-reviewed articles in 2024.
2010
2010
Statin treatment has been shown to reduce graft-versus-host disease while preserving graft-versus-tumor effect in allogeneic stem cell transplantation. Herein, we investigated whether lovastatin treatment affects the function of human cytolytic T lymphocytes (CTLs). Upon T-cell receptor stimulation, lovastatin significantly inhibited the proliferation of both CD4+ and CD8+ T cells from healthy donors whereas their intracellular cytokine production including interferon-γ and tumor necrosis factor-α remained the same with a slight decrease of interleukin-2. Moreover, the specific lysis of target cells by CTL lines derived from patients and normal donors specific for Epstein-Barr virus-encoded antigen latent membrane protein-2 or cytomegalovirus-encoded antigen pp65 was uncompromised in the presence of lovastatin. In addition, we evaluated the effect of lovastatin on the proliferation and effector function of the CD8+ tumor-infiltrating lymphocytes (TILs) derived from melanoma patients specific for MART-1 antigen. Lovastatin significantly reduced the expansion of antigen-specific TILs upon MART-1 stimulation. However, the effector function of TILs, including the specific lysis of target cells and secretion of cytokine interferon-γ, remained intact with lovastatin treatment. Taken together, these data demonstrated that lovastatin inhibits the proliferation of Epstein-Barr virus, cytomegalovirus, and MART-1-specific CTLs without affecting cytolytic capacity. The differential effect of lovastatin on the proliferation versus cytotoxicity of CTLs might shed some light on elucidating the possible mechanisms of graft-versus-host disease and graft-versus-tumor effect elicited by alloimmune responses.
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2010
2010
2010
Experimental research on sexual decision making is limited, despite the public health importance of such work. We describe formative work conducted in advance of an experimental study designed to evaluate the effects of alcohol intoxication and sexual arousal on risky sexual decision making among men who have sex with men. In Study 1, we describe the procedures for selecting and validating erotic film clips (to be used for the experimental manipulation of arousal). In Study 2, we describe the tailoring of two interactive role-play videos to be used to measure risk perception and communication skills in an analog risky sex situation. Together, these studies illustrate a method for creating experimental stimuli to investigate sexual decision making in a laboratory setting. Research using this approach will support experimental research that affords a stronger basis for drawing causal inferences regarding sexual decision making.
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PURPOSE OF REVIEW
The purpose of this review is to present recent results on biomarkers and risk of cardiovascular disease (CVD) in the general population and to review studies of biomarkers among individuals with HIV infection.
RECENT FINDINGS
Several inflammatory as well as lipid biomarkers are associated with risk of CVD. Biomarkers associated with inflammation such as C-reactive protein and interleukin-6 have been suggested to improve risk stratification among intermediate-risk persons; however, their routine use is not recommended in the general population. Both biomarkers have recently been reported elevated in patients with HIV. Additionally, interleukin-6 and D-dimer have been reported to predict overall mortality among individuals with HIV. However, the utility of other biomarkers to predict CVD among individuals with HIV infection is not clear.
SUMMARY
The risk of CVD is increasing in the HIV-infected population and will increase as this population continues to age. Identification of intermediate-risk individuals using biomarkers will be an important tool for clinicians in the future to be able to treat HIV-infected individuals aggressively. Future studies of biomarkers among individuals with HIV will be needed to help determine the utility of specific markers in predicting CVD risk as well as the mechanism underlying increased CVD risk in the setting of HIV infection.
View on PubMed2010