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Mccall Burks posted an update 6 months, 3 weeks ago
Various parameters reflecting right heart size, right ventricular function and capacitance have been shown to be prognostically important in patients with pulmonary hypertension (PH). In the advanced disease, patients suffer from right heart failure, which is a main reason for an impaired prognosis. Right heart size has shown to be associated with right ventricular function and reserve and is correlated with prognosis in patients with PH. Right ventricular reserve, defined as the ability of the ventricle to adjust to exercise or pharmacologic stress, is expressed by various parameters, which may be determined invasively by right heart catheterization or by stress-Doppler-echocardiography as a noninvasive approach. As the term “right ventricular contractile reserve” may be misleading, “right ventricular output reserve” seems desirable as a preferred term of increase in cardiac output during exercise. Both right heart size and right ventricular reserve have been shown to be of prognostic importance and may therefore be useful for risk assessment in patients with pulmonary hypertension. In this article we aim to display different aspects of right heart size and right ventricular reserve and their prognostic role in PH.Neuropathic pain exerts a global burden caused by the lesions in the somatosensory nerve system, including the central and peripheral nervous systems. The mechanisms of nerve injury-induced neuropathic pain involve multiple mechanisms, various signaling pathways, and molecules. Currently, poor efficacy is the major limitation of medications for treating neuropathic pain. Thus, understanding the detailed molecular mechanisms should shed light on the development of new therapeutic strategies for neuropathic pain. Several well-established in vivo pain models were used to investigate the detail mechanisms of peripheral neuropathic pain. Molecular mediators of pain are regulated differentially in various forms of neuropathic pain models; these regulators include purinergic receptors, transient receptor potential receptor channels, and voltage-gated sodium and calcium channels. Meanwhile, post-translational modification and transcriptional regulation are also altered in these pain models and have been reported to mediate several pain related molecules. In this review, we focus on molecular mechanisms and mediators of neuropathic pain with their corresponding transcriptional regulation and post-translational modification underlying peripheral sensitization in the dorsal root ganglia. Taken together, these molecular mediators and their modification and regulations provide excellent targets for neuropathic pain treatment.Background and objectives Identifying the factors affecting the Quality of Work Life (QWL) of cancer survivor female nurses is important and necessary to overcome the various challenges experienced by these professionals upon returning to work following recovery from the disease. Therefore, this study aimed to identify the factors affecting the level of nurses’ QWL. Materials and Methods A cross-sectional survey was conducted among 115 registered female nurses who had survived cancer, in general hospitals and clinics in South Korea. SPSS statistics version 21 was used for ordinary least squares, and Stata version 12.0 was used for quantile regression analysis. Results Workplace spirituality affected all quantiles of QWL except the 90% quantile; fatigue was an affecting factor in the 20%, 30%, and 70% quantiles; and job stress in the 20%, 30%, 40%, and 60%, 70%, 80% quantiles. For workplace spirituality, the effect size was 0.33 (p less then 0.001) in the 10% quantile, increasing to 0.45 (p less then 0.001) in the 80% quantile. Conclusions Based on the results of this study, suggestions for clinical practice include providing the mediating strategies and programs to manage fatigue and job stress as well as workplace spirituality. Job-related factors such as shift work should also be considered.Advanced glycation end-products (AGE) can promote chronic kidney disease (CKD) progression and CKD-related morbidities. The soluble receptor for AGE (sRAGE) is a potential biomarker of inflammation and oxidative stress. Here, we explored the role of AGE, glycated albumin, sRAGE and its different forms, cRAGE and esRAGE, as prognostic factors for mortality in 111 advanced CKD patients. The median follow-up time was 39 months. AGE were quantified by fluorescence, sRAGE and its forms by ELISA. Malnutrition was screened by the Malnutrition Inflammation Score (MIS). The Cox proportional hazards regression model was used to assess the association of variables with all-cause mortality. Mean levels of sRAGE, esRAGE and cRAGE were 2318 ± 1224, 649 ± 454 and 1669 ± 901 pg/mL. The mean value of cRAGE/esRAGE was 2.82 ± 0.96. AGE were 3026 ± 766 AU and MIS 6.0 ± 4.7. eGFR correlated negatively with AGE, sRAGE, esRAGE and cRAGE, but not with cRAGE/esRAGE. Twenty-eight patients died. No difference was observed between diabetic and non-diabetic patients. Starting dialysis was not associated with enhanced risk of death. selleck compound AGE, esRAGE and cRAGE/esRAGE were independently associated with all-cause mortality. AGE, esRAGE and cRAGE/esRAGE may help to stratify overall mortality risk. Implementing the clinical evaluation of CKD patients by quantifying these biomarkers can help to improve patient outcomes.The crosstalk between cancer cells and adipocytes is critical for breast cancer progression. However, the molecular mechanisms underlying these interactions have not been fully characterized. In the present study, plasminogen activator inhibitor-1 (PAI-1) was found to be a critical effector of the metastatic behavior of breast cancer cells upon adipocyte coculture. Loss-of-function studies indicated that silencing PAI-1 suppressed cancer cell migration. Furthermore, we found that PAI-1 was closely related to the epithelial-mesenchymal transition (EMT) process in breast cancer patients. A loss-of-function study and a mammary orthotopic implantation metastasis model showed that PAI-1 promoted breast cancer metastasis by affecting the EMT process. In addition, we revealed that leptin/OBR mediated the regulation of PAI-1 through the interactions between adipocytes and breast cancer cells. Mechanistically, we elucidated that leptin/OBR further activated STAT3 to promote PAI-1 expression via miR-34a-dependent and miR-34a-independent mechanisms in breast cancer cells.