Hoodkejser4936

5% (14 of 85 patients). Therefore, the incidence of long-term cardiotoxicity was 15%. Of these 14 patients with AC, 12 had asymptomatic systolic dysfunction, 1 had heart failure and 1 suffered sudden death. Fifteen percent developed systolic dysfunction during follow-up. An early decline in strain was observed in patients who developed long-term AC. CONCLUSIONS The incidence of long-term cardiotoxicity in patients treated with low-cumulative dose of anthracyclines is high, 16.5% at 4.5 years. This was observed in almost all cases after the first year of follow-up. Therefore, long-term monitoring may be advisable.BACKGROUND Hyperlipidemia is one of the major risk factors for developing a cardiovascular disease (CVD) and it is a frequent post-transplant complication, occurring in up to 60% of the renal transplant recipients (RTRs). Lipid lowering therapy with HMG-CoA reductase inhibitors (statins) is generally recommended and may reduce the overall cardiovascular risk. The aim of this study was to evaluate the lipid profile, statin administration and their relationship with arterial stiffness parameters in renal transplant recipients. METHODS Three hundred and forty-four stable RTRs (62.5% male) transplanted between 1994 and 2018 were randomly enrolled to the study. The following parameters of arterial stiffness was measured in each patient carotid femoral pulse wave velocity (baPWV left and right, cfPWV) and pulse pressure (PP right and left). The study group was divided based on the use statins 143 (41.6%) and 201 (58.4%). RTRs were qualified to the statin (+) and the statin (-) group, respectively. RESULTS In the statin (+) as compared to statin (-) group there were more patients with a CVD (32.9% vs. 14.9%) and diabetes (25.2% vs. 14.4%). Bimiralisib In the whole study group, CVD was associated with a significant increase of both baPWV and cfPWV as well as PP (8.5 mmHg). There were significant differences in arterial stiffness parameters (baPWV, cfPWV, PP) between the statin (+) and the statin (-) group. CONCLUSIONS Arterial stiffness was increased in RTRs with CVD and hyperlipidemia. The control of hyperlipidemia was poor in RTRs.BACKGROUND Cardiac fibroblasts (CFs) are principal extracellular matrix-producing cells. In response to injury, CFs transdifferentiate into myofibroblasts. Intracellular calcium (Ca2+) signaling, involved in fibroblast proliferation and differentiation, is activated in fibroblasts through transient receptor potential (TRP) channels, but the function of these channels has not been investigated in human ventricular CFs. Under evaluation in this study, was the role of TRP channels in the differentiation of human ventricular CFs induced by transforming the growth factor beta (TGF-β), a pro-fibrotic cytokine. METHODS Human ventricular CFs were used in this study. The differentiation of CFs into myofibroblast was induced with TGF-β and was identified by the expression of smooth muscle actin. RESULTS Results indicate that Ca2+ signaling was an essential component of ventricular CF differentiation. CFs treated with TGF-β demonstrated increased expression of a TRP channel, TRPV4, both at the mRNA and protein levels, which corresponded with CF-myofibroblast trans-differentiation, as evidenced by the upregulation of α-smooth muscle actin, a myofibroblast marker, and plasminogen activator inhibitor-1, which are fibrogenesis markers. An agonist of TRPV4 induced the conversion of CFs into myofibroblasts, whereas it's antagonist as well a Ca2+ chelating agent reduced it, indicating that the Ca2+ influx throughTRPV4 is required for CF trans-differentiation. Overall, these results demonstrate that TRPV4-mediated Ca2+ influx participates in regulating the differentiation of human ventricular CFs into myofibroblasts through the MAPK/ERK pathway. CONCLUSIONS Overall, these results demonstrate that TRPV4-mediated Ca2+ influx participates in regulating the differentiation of human ventricular CFs into myofibroblasts through the MAPK/ERK pathway.Wide-reaching health promotion interventions are needed in influential, accessible community settings to address African American (AA) diabetes and CVD disparities. Most AAs are overweight/obese, which is a primary clinical risk factor for diabetes/CVD. Using a faith-community-engaged approach, this study examined feasibility and outcomes of Project Faith Influencing Transformation (FIT), a diabetes/CVD screening, prevention, and linkage to care pilot intervention to increase weight loss in AA church-populations at 8 months. Six churches were matched and randomized to multilevel FIT intervention or standard education control arms. Key multilevel religiously tailored FIT intervention components included (a) individual self-help materials (e.g., risk checklists, pledge cards); (b) YMCA-facilitated weekly group Diabetes Prevention Program (DPP) weight loss classes; (c) church service activities (e.g., sermons, responsive readings); and (d) church-community text/voice messages to promote healthy eating and physical activity. Health screenings (e.g., weight, blood pressure, blood glucose) were held during church services to identify participants with diabetes/CVD risks and refer them to their church's DPP class and linkage to care services. Participants (N = 352 church members and community members using churches' outreach ministries) were primarily female (67%) and overweight/obese (87%). Overall, FIT intervention participants were significantly more likely to achieve a > 5 lb weight loss (OR = 1.6; CI = 1.24, 2.01) than controls. Odds of intervention FIT-DPP participants achieving a > 5 lb weight loss were 3.6 times more than controls (p  5 lb. weight loss. AA churches can feasibly assist in increasing reach and impact of diabetes/CVD risk reduction interventions with intensive weight loss components among at risk AA church-populations.Endometriosis has several distinguishing features in the ectopic endometrium, including chronic inflammation and fibrosis. According to the retrograde menstruation theory, endometriotic cells are derived from eutopic endometrial cells, and adhesion of endometrial cells to the extracellular matrix can be the initial step in the development of endometriosis. Therefore, we hypothesized that cell adhesion, which mediates a sequence of events in the development of endometriosis triggering inflammatory responses and tissue fibrosis could be a possible therapeutic target for endometriosis. We found co-upregulation of focal adhesion kinase (FAK) and monocyte chemoattractant protein-1 (MCP-1) in the endometriotic tissues compared with that in the normal endometrium. MCP-1 secretion was significantly higher in the endometriotic stromal cells than in the eutopic endometrial stromal cells. Furthermore, co-culture of U937 cells and endometriotic stromal cells upregulated secretion of transforming growth factor-β1 (TGF-β1).