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1.
J Natl Med Assoc ; 104(3-4): 179-85, 2012.
Article in English | MEDLINE | ID: mdl-22774385

ABSTRACT

African Americans have higher rates of cardiovascular disease (CVD) and poorer outcomes compared to others. The American Diabetes Association and the National Diabetes Education Program have promoted use of the ABC approach (glycated hemoglobin A1c, blood pressure, cholesterol) for identifying and controlling the leading indicators of CVD risk. In the present study, researchers added a D factor, for depression, because this disorder is common and also predictive of CVD risk and of control of diabetes. Particularly among low-income African Americans, depression is frequently not targeted or treated. The current study tests the effectiveness of recruiting African Americans in churches and training community health workers (CHWs) to educate their peers about CVD and risk reduction. For the intervention group, CHWs participated in a 16-hour training session and delivered a 6-week tailored educational program with counseling sessions and demonstrations. The control group received a weekly lecture by clinical experts. The CHW active-learning intervention was more effective than lectures by clinical experts in increasing the knowledge of CVD risk. The only significant difference in clinical measures reflected a worsening of HbA1c levels in the control group; the CHW intervention group showed a slight improvement. Participants also learned self-management skills, such as taking blood pressure, measuring glucose, and reading labels. Nevertheless, more longitudinal research and a larger sample size are needed to confirm the impact of CHWs in community settings to change factors associated with CVD risk.


Subject(s)
Cardiovascular Diseases/prevention & control , Community Health Workers , Health Education/methods , Health Knowledge, Attitudes, Practice , Black People , Cardiovascular Diseases/etiology , Female , Georgia , Humans , Male , Pilot Projects , Risk Factors
2.
J Hematol Oncol ; 1: 14, 2008 Sep 25.
Article in English | MEDLINE | ID: mdl-18817562

ABSTRACT

BACKGROUND: L-arginine is the common substrate for the two isoforms of arginase. Arginase I, highly expressed in the liver and arginase II mainly expressed in the kidney. Arginase I-producing myeloid derived suppressor cells have been shown to inhibit T-cell function by the depletion of L-arginine. On the other hand, arginase II has been detected in patients with cancer and is thought to metabolize L-arginine to L-ornithine needed to sustain rapid tumor growth; however its role in L-arginine depletion is unclear. Thus, in tumor biology, L-arginine metabolism may play a dual role in tumor growth and in the induction of T cell dysfunction. Therefore, we studied in murine renal cell carcinoma (RCC) cell lines, the effect of arginase II on tumor cell proliferation and L-arginine depletion. The effect of arginase inhibitors on cell proliferation was also tested. METHODS: Three murine renal cell carcinoma (mRCC) cell lines were tested for the presence of arginase. nor-NOHA, an arginase inhibitor was used to substantiate the effect of arginase on cell growth and L-arginine depletion. Amino acid levels were tested by HPLC. RESULTS: Our results show that mRCC cell lines express only arginase II and were able to deplete L-arginine from the medium. Cell growth was independent of the amount of arginase activity expressed by the cells. nor-NOHA significantly (P = 0.01) reduced arginase II activity and suppressed cell growth in cells exhibiting high arginase activity.The depletion of L-arginine by mRCC induced the decrease expression of CD3zeta a key element for T-cell function. CONCLUSION: The results of this study show for the first time that arginase II produced by RCC cell lines depletes L-arginine resulting in decreased expression of CD3zeta. These results indicate that RCC cell lines expressing arginase II can modulate the L-arginine metabolic pathway to regulate both cell growth and T-cell function. Blocking arginase may lead to a decrease in RCC cell growth and aid in restoring immune function by increasing L-arginine availability for T-cell use. Understanding the interplay between arginase II and its interaction with the immune system may provide future therapeutic benefits to treat patients with RCC.


Subject(s)
Arginase/metabolism , Arginine/metabolism , Carcinoma, Renal Cell/enzymology , Cell Proliferation , Animals , Arginase/antagonists & inhibitors , Arginine/analogs & derivatives , Arginine/pharmacology , CD3 Complex/metabolism , Cell Line, Tumor , Humans , Jurkat Cells
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