Effect of Risk-Focused Diversified Safety Management Mode in Patients with Major Artery Stent Implantation.

Background: Intracranial atherosclerotic stenosis (ICAS) causes a series of neurological symptoms, such as vertigo, impaired consciousness, limb weakness, ataxia, dysphagia, ocular motility disorders, and visual impairment. With the improvement of people's living standards, there are higher requirements for nursing care. Nursing, as an indispensable part of medical care, is closely related to achieving the goal of patient's safety and the overall quality of nurses, quality of care, and nursing management methods. Objective: To explore the effect of risk-centered diversified safety management in patients undergoing aortic stenting. Methods: Eighty patients with cerebral infarction were selected and treated with percutaneous transluminal angioplasty and stent implantation (PTAS). Then they were divided into a control group (40 cases) with routine monitoring and an experimental group (40 cases) with risk-focused intervention of a diversified safety management model according to the mode of care. Patient satisfaction and blood index test results were compared after the intervention. Results: Patients in the experimental group had 6 falls, 3 bed falls, 3 phlebitis, 4 tube slips, and 10 deep vein thrombosis, all significantly fewer than those in the control group. Thirty-eight patients in the experimental group expressed satisfaction with safe management, which was substantially better than the control group (P < 0.05). The levels of tissue plasminogen activator (tPA), plasminogen activator inhibitor-1 (PA1-1), and von Willebrand factor (vWF) in the experimental group were (13.5 ± 1.3) ng/mL, (60.1 ± 9.9) ng/mL, and (2.1 ± 0.2), respectively, which were substantially lower than those in the control group ((14.6 ± 2.4) ng/mL, (64.2 ± 10.7) ng/mL, and (2.8 ± 0.3)), respectively (P < 0.05). Conclusion: The risk-centered diversified safety management model can effectively reduce the probability of adverse events in patients, improve patient satisfaction with nursing services, and promote faster postoperative recovery, which has clinical application value.

Circ-Klhl8 overexpression increased the therapeutic effect of EPCs in diabetic wound healing via the miR-212-3p/SIRT5 axis.

Previous studies found that hypoxic pretreatment of endothelial progenitor cells (EPCs) prior to transplantation had a greater therapeutic effect than untreated EPCs in promoting diabetic wound healing. However, the exact mechanism is uncertain. Here, circRNA expression in EPCs after hypoxic treatment was investigated. High-throughput sequencing was used to assess abnormal expression by EPCs of circular RNAs (circRNAs) following hypoxic pretreatment. Additionally, an in vivo full-thickness skin defect mouse model was used to assess the effects of transplanted EPCs on diabetic wound closure. Subsequently, the regulatory mechanism and targets were studied. The results showed that circ-Klhl8 overexpression suppressed hyper glucose-induced endothelial cell damage by activating autophagy. MiR-212-3p and SIRT5 were identified as the downstream targets of circ-Klhl8. Circ-Klhl8 overexpression promoted skin wound healing by regulating SIRT5-mediated autophagy. In conclusion, the study found that circ-Klhl8 overexpression increased the EPC therapeutic effect in promoting diabetic wound healing by targeting the miR-212-3p/SIRT5 axis.

MicroRNA­93 regulates angiogenesis in peripheral arterial disease by targeting CDKN1A.

MicroRNAs (miRNAs) are considered to be critical mediators of gene expression with respect to tumor progression, although their role in ischemia­induced angiogenesis is poorly characterized, including in peripheral arterial disease (PAD). Furthermore, the underlying mechanism of action of specific miRNAs in PAD remains unknown. Reverse transcription­quantitative polymerase chain reaction analysis revealed that microRNA­93 (miR­93) was significantly upregulated in patients with PAD and in the EA.hy926 endothelial cells in response to hypoxia. Additionally, miRNA (miR)­93 promoted angiogenesis by enhancing proliferation, migration and tube formation. Cyclin dependent kinase inhibitor 1A (CDKN1A), verified as a potential target gene of miR­93, was inhibited by overexpressed miR­93 at the protein and mRNA expression levels. Furthermore, a hind­limb ischemia model served to evaluate the role of miR­93 in angiogenesis in vivo, and the results demonstrated that miR­93 overexpression enhanced capillary density and perfusion recovery from hind­limb ischemia. Taken together, miR­93 was indicated to be a promising target for pharmacological regulation to promote angiogenesis, and the miR­93/CDKN1A pathway may function as a novel therapeutic approach in PAD.

EndMT: A promising and controversial field.

The endothelial to mesenchymal transition (EndMT) is the process by which endothelial cells lose a portion of their cellular features and obtain certain characteristics of mesenchymal cells, including loss of tight junctions, increased motility, and increased secretion of extracellular matrix proteins. EndMT is involved in cardiac development and a variety of diseases processes, such as vascular or tissue fibrosis and tumor. However, its role in specific diseases remains under debate. This review summarizes EndMT-related diseases, existing controversies, different types of EndMT, and molecules and signaling pathways associated with the process.

High expression of PFTK1 in cancer cells predicts poor prognosis in colorectal cancer.

The serine/threonine-protein kinase PFTAIRE 1 (PFTK1) is a member of the cyclin­dependent kinase family that is highly expressed in several malignant tumors, including hepatocellular carcinoma, esophageal, breast and gastric cancers, and glioma. It contributes to tumor progression and influences tumor prognosis. However, the expression and clinicopathological significance of PFTK1 in human colorectal cancer (CRC) remain to be elucidated. The present study aimed to examine the expression of PFTK1 and to evaluate the clinical significance of its expression in human CRC. Reverse transcription­quantitative polymerase chain reaction was performed on 10 fresh CRC and 10 surrounding normal tissue samples to detect and compare the expression of PFTK1 mRNA in CRC and normal colorectal tissues. Immunohistochemistry was performed on 179 CRC tissue specimens and 47 control samples of normal colorectal lesions to characterize the expression of PFTK1 protein. Kaplan­Meier overall survival (OS) rate and Cox regression analyses were performed to evaluate the prognosis of patients with CRC. The expression of PFTK1 mRNA in CRC tissues (1.433±0.168) was significantly higher compared with normal tissues (0.853±0.107; t=1.97 ('t' was the value obtained from quantification of the mRNA data, following a paired t­test), P=0.008). High PFTK1 expression in cancerous cells was detected in 92 of the CRC specimens (51.40%), and high levels of PFTK1 were associated with tumor node metastasis (TNM) stage (P=0.042), tumor classification (P=0.022) and preoperative carcinoembryonic antigen (CEA) level (P<0.001). Kaplan­Meier OS rate and Cox regression analysis revealed that high PFTK1 expression level (hazard ratio (HR)=1.999; P=0.019) was an independent prognostic factor of CRC patients. The degree of differentiation (HR, 0.368, P=0.003), TNM classification (HR, 2.118, P=0.001) and preoperative CEA level (HR, 2.302, P=0.003) were also predictors of the prognosis of patients with CRC. The present study suggested that PFTK1 may be a potential anticancer target and prognostic marker in patients with CRC.