Background-Immunosuppressive medication non-adherence is one of the most prevalent but preventable causes of poor outcomes in adult renal transplant recipients, yet there is a paucity of studies testing interventions in this area.
This project examined patterns, predictors, and outcomes of medication adherence in a convenience sample of 37 renal transplant recipients aged 55 years or older in a Mid-Southern U.S. facility using an exploratory, descriptive, longitudinal design. Electronic monitoring was conducted for 12 months using the Medication Event Monitoring System. An alarming 86% of the participants were nonadherent with medications. Four clusters of medication taking and timing patterns were identified with evening doses presenting particular challenges. Depression, self-efficacy, social support, and medication side effects did not predict medication adherence. There was no significant difference in medication adherence scores between those with and without infections. Medication adherence pattern data from electronic monitoring provides an opportunity for health care professionals to move away from blaming the patient by attempting to identify predictors for medication nonadherence. Medication dose taking and timing patterns could be explored with patients so that medication adherence interventions could target specific patient patterns.
IL-33 is a member of the IL-1 family of cytokines, and no study has been performed to address its direct anti-tumor effect. This study is designed to investigate whether IL-33 has any direct effect on pancreatic cancer. Clonogenic survival assay, immunohistochemistry, TUNEL staining, proliferation, caspase-3 activity kits and RT-PCR were used to evaluate the effects of IL-33 on cell survival, proliferation and apoptosis of a pancreatic cancer cell line, MIA PaCa-2. We found that the percentage of colonies of MIA PaCa-2 cells, PCNA+ cells and the OD value of cancer cells were all decreased in the presence of IL-33. TUNEL+ cells and the relative caspase-3 activity in cancer cells were increased in the presence of IL-33. We further found that its anti-proliferative effect on cancer cells correlated with downregulation of pro-proliferative molecules cdk2 and cdk4 and upregulation of anti-proliferative molecules p15, p21 and p53. Its pro-apoptotic effect correlated with downregulation of anti-apoptotic molecule FLIP and upregulation of pro-apoptotic molecule TRAIL. These results suggest that IL-33 presents significant anti-tumor effects by inhibition of proliferation and induction of apoptosis of MIA PaCa-2 pancreatic cancer cells. Thus, strength of IL-33/ST2 signal pathway might be a promising way to treat pancreatic cancer.
This study evaluates the technical efficiency of federal hospitals in the United States using a variable returns to scale, input-oriented, data envelopment analysis (DEA) methodology. Hospital executives, health care policy-makers, taxpayers, and other stakeholders, benefit from studies that improve the efficiency of federal hospitals. Data for 280 federal hospitals in 1998 and 245 in 2001 were analyzed using DEA to measure hospital efficiency. Results indicate overall efficiency in federal hospitals improved from 68% in 1998 to 79% in 2001. However, based upon 2001 spending of $42.5 billion for federal hospitals potential savings of $2.0 billion annually are possible through more efficient management of resources. From a policy perspective, this study highlights the importance of establishing more specific policies to address inefficiency in the federal health care industry.
Prostate cancer (PCA) is the most common malignancy in men in USA, and the role of Trichomonas vaginalis (T. vag) in the development of PCA is still controversial. Clonogenic assay, PCNA staining, TUNEL staining and caspase-3 activity assay were used to investigate the in vitro role of T. vag in human prostate cancer. We further investigated the possible molecular mechanisms using RT-PCR and immunohistochemical staining. Culture supernatant of T. vag inhibits growth of PC-3 prostate cancer cells, and this correlated with upregulation of p21. Culture supernatant of T. vag induced apoptosis of PC-3 cells, and this correlated with downregulation of Bcl-2. The growth inhibition effect of culture supernatant of T. vag is also demonstrated in another prostate cancer cell line DU145, suggesting that its effect is not specific to one prostate cancer cell line. Culture supernatant of T. vag inhibits growth of prostate cancer by inhibition of proliferation and promotion of apoptosis. Such a study might be helpful to address the association between PCA and infection of T. vag.
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