Among a number of potential mechanisms we found that VDR deletion from these cells alters the lncRNA profile to a more oncogenic configuration, increasing the expression of well known oncogenic lncRNAs and decreasing the expression of well known tumor suppressor lncRNAs. Subsequent studies in other cancers have found similar associations between VDR and oncogenic lncRNAs with evidence of tumor specificity. To date these studies primarily reveal associations rather than causality, but causal links should be expected as research in this field continues to develop.Ischemia/reperfusion (I/R) injury induces activation of the endoplasmic reticulum stress (ERS) pathway, accompanied by an increase in apoptosis. Multiple microRNAs (miRNAs/miRs) are dysregulated during I/R and contribute to I/R-induced injury. miRNAs act as suppressors of gene expression and negatively regulate gene expression by targeting the protein-coding sequence (CDS) of specific target mRNAs. Seipin is an endoplasmic reticulum protein that has recently been associated with ERS. We previously reported that seipin is the target gene of miR‑187‑3p. Therefore, we explored the involvement of miR-187-3p in I/R-induced ERS via the regulation of seipin. A rat MCAO/R model was established by 1 h of occlusion and 24 h reperfusion. Neurological deficits and infarction area were examined. PC12 cells were exposed to oxygen‑glucose deprivation/reoxygenation (OGD/R) to model I/R. Expression levels of miR-187-3p and proteins related to ERS and apoptosis were measured using RT-PCR, western blotting, immunofluorescence, and immunohistochemistry, respectively. TUNEL staining was used to assay apoptosis. MCAO/R-induced morphological changes were analyzed with Nissl staining and Hematoxylin-eosin staining. I/R-induced ERS was closely associated with an increase in miR-1873p and a decrease in seipin expression. miR-187-3p agomir further activated the ERS pathway and promoted apoptosis but decreased seipin expression levels; these effects were reversed by miR-187-3p antagomir. Moreover, seipin knockdown aggravated ERS in PC12 cells after OGD/R, and this change was rescued by seipin overexpression. miR-187-3p antagomir did not suppress ERS and apoptosis in seipin knockdown PC12 cells after OGD/R. Our findings demonstrate that the inhibition of miR‑187‑3p attenuated I/R‑induced cerebral injury by regulating seipin-mediated ERS.Apoptosis deficiency is one of the most important features observed in neoplastic diseases. The Bcl-2 family is composed of a subset of proteins that act as decisive apoptosis regulators. Research and clinical studies have both demonstrated that the hyperactivation of Bcl-2-related anti-apoptotic effects correlates with cancer occurrence, progression and prognosis, also having a role in facilitating the radio- and chemoresistance of various malignancies. Therefore, targeting Bcl-2 inactivation has provided some compelling therapeutic advantages by enhancing apoptotic sensitivity or reversing drug resistance. Therefore, this pharmacological route turned into one of the most promising routes for cancer treatment. This review discusses some of the well-defined and emerging roles of Bcl-2 as well as its potential clinical value in cancer therapeutics.Giant obscurins (720-870 kDa), encoded by OBSCN, were originally discovered in striated muscles as cytoskeletal proteins with scaffolding and regulatory roles.  https://www.selleckchem.com/products/ly2157299.html  Recently though, they have risen to the spotlight as key players in cancer development and progression. Herein, we provide a timely prudent synopsis of the expanse of OBSCN mutations across 16 cancer types. Given the extensive work on OBSCN's role in breast epithelium, we summarize functional studies implicating obscurins as potent tumor suppressors in breast cancer and delve into an in silico analysis of its mutational profile and epigenetic (de)regulation using different dataset platforms and sophisticated computational tools. Lastly, we formally describe the OBSCN-Antisense-RNA-1 gene, which belongs to the long non-coding RNA family and discuss its potential role in modulating OBSCN expression in breast cancer. Collectively, we highlight the escalating involvement of obscurins in cancer biology and outline novel potential mechanisms of OBSCN (de)regulation that warrant further investigation.
  Contrast-associated acute kidney injury (CA-AKI) is a potential risk associated with the percutaneous coronary interventions (PCI) for chronic total coronary occlusions (CTO). This study should evaluate the incidence of CA-AKI in an era of advanced strategies of recanalization techniques and identify modifiable determinants.
 
  We analysed 1924 consecutive CTO procedures in 1815 patients between 2012 and 2019. All patients were carefully monitored at least up to 48 h after a CTO procedure for changes in renal function.
 
  The incidence of CA-AKI was 5.6%, but there was no relation to the technical approach such as frequency of the retrograde technique, intravascular ultrasound or radial access. Procedures with CA-AKI had longer fluoroscopy times (37.6 vs 46.1 min; p = 0.005). The major determinants of CA-AKI were age, presence of diabetes and reduced ejection fraction, as well as chronic kidney disease stage ≥2, serum haemoglobin, and fluoroscopy time. Contrast volume or contrast volume/GFR ratio were not independent determinants of CA-AKI. Periprocedural perforations were more frequent in CA-AKI patients (11.3 vs 2.3%; p < 0.001), and in-hospital mortality was higher (2.8 vs 0.4%; p < 0.001).
 
  CA-AKI was associated with the risk of in-hospital adverse events. Established patient-related risk factors for CA-AKI (age, diabetes, preexisting chronic kidney disease, low ejection fraction) were confirmed in this study. In addition, the length of the procedure, coronary perforations and low preprocedural serum haemoglobin were risk factors that might be preventable in patients at high risk for CA-AKI.
 CA-AKI was associated with the risk of in-hospital adverse events. Established patient-related risk factors for CA-AKI (age, diabetes, preexisting chronic kidney disease, low ejection fraction) were confirmed in this study. In addition, the length of the procedure, coronary perforations and low preprocedural serum haemoglobin were risk factors that might be preventable in patients at high risk for CA-AKI.