The aim of the present study was to investigate the mechanisms underlying the effects of prednisone on adriamycin-induced nephritic rat kidney damage via the focal adhesion kinase (FAK)/receptor activator of nuclear factor-κB ligand (RANKL)/mitogen-activated protein kinase (MAPK) signaling pathway. An adriamycin-induced nephritic rat model was established to investigate these mechanisms. A total of 30 healthy male Sprague-Dawley rats were randomly assigned to the normal, model or prednisone group. Samples of urine were collected over the course of 24 h at days 7, 14, and 28, and renal cortex tissue samples were harvested at days 14, and 28 following nephritic rat model establishment. The total urinary protein content was measured by biuret colorimetry. Pathological changes in the kidney tissue samples were observed using an electron microscope. The mRNA expressions levels of FAK, RANKL, p38, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and nephrin were then quantified by reverse transcription-quantitative polymerase chain reaction. In addition, the protein expressions levels of FAK, RANKL, p38, ERK, JNK, phosphorylated (p)-FAK, pERK , and p-JNK were quantified by western blotting. As compared with the normal group, the protein expression levels of FAK, RANKL, p-FAK, p38 and pERK in the model group were increased. In the prednisone group, the protein expression levels of pERK decreased, as compared with the normal group. In the prednisone group, the urinary protein levels, the protein expression levels of FAK, RANKL, p38, p-FAK, p-p38 and the mRNA expression levels of FAK, p38, RANKL, ERK, JNK decreased, as compared with the model group. In the prednisone group, the mRNA and protein expression levels of nephrin and the serum expression levels of RANKL increased, the serum expression levels of osteoprotegerin (OPG) were decreased, as compared with the model group. No significant changes in the protein expression levels of JNK were observed among the groups. These results suggested that prednisone is able to protect podocytes from apoptosis, and reduce urinary protein levels by inhibiting the FAK/RANKL/MAPK signaling pathway in kidney tissue samples. Serum prednisone may induce osteoporosis via the OPG/RANK/RANKL signaling pathway.

Background: MicroRNA-130a (miR-130a) regulates angio-cellular dysregulation, atherosclerosis, and cardiocerebral injuries, serving as a biomarker for major adverse cardiovascular and cerebral events (MACCE) in several chronic diseases. However, its clinical application in patients with end-stage renal disease (ESRD) undergoing continuous ambulatory peritoneal dialysis (CAPD), who are at a high risk of developing MACCE, has not been reported. Therefore, this study aimed to explore this aspect.Methods: miR-130a expression in peripheral blood mononuclear cells obtained from 50 healthy controls (HCs) at recruitment and 257 ESRD patients undergoing CAPD at month (M)0, M12, M24, and M36 was determined by reverse transcription-quantitative polymerase chain reaction. ESRD patients undergoing CAPD were followed up until MACCE occurred or M36. Then, MACCE were recorded, and MACCE-free survival was calculated.Results: miR-130a expression was significantly lower in ESRD patients undergoing CAPD than in HCs (p < 0.001). In addition, miR-130a expression significantly decreased from M0 to M36 in ESRD patients undergoing CAPD (p < 0.001). Moreover, miR-130a expression at M0, M12, and M24 was significantly lower in patients with MACCE than in those without MACCE (all p < 0.05). Furthermore, high miR-130a expression at M0, M12, and M36 was significantly correlated with prolonged MACCE-free survival in ESRD patients undergoing CAPD (all p < 0.05), and high miR-130a expression at M0 was an independent factor for improved MACCE-free survival (p = 0.015; hazard ratio (HR) (95% confidential interval): 0.456 (0.243-0.857)). Conclusion: miR-130a expression decreases continuously with disease progression inpatients with ESRD undergoing CAPD. Additionally, this expression is negatively correlated with MACCE risk in these patients.

Tumour revascularization and the consequent radioresistance activated by up–regulating angiogenic pathway after radiation exposure remains major bottleneck for improving the tumoricidal effect of radiotherapy (RT) in hepatocellular carcinoma (HCC). Herein,...

In stage 3-4 CKD patients, B cells and IL-17 participated in the induction of osteoclast activation. YJG could also elevate the level of B cells and decrease their apoptosis, but showed no significant effects on active B cells, IL-17 or osteoclast activity.

IntroductionAvailable patient-reported outcome (PRO) studies are mainly from single institution or of small sample size, and the variations across hospitals and regions were not fully analysed. A multicentre, prospective, patient-reported outcome-reconstruction and oncoplastic cohort (PRO-ROC) will be planned to assess the PROs of Chinese patients with breast cancer who will undergo breast reconstruction (BR) or oncoplastic breast-conserving surgery (OBCS).Methods and analysisThe inclusion criteria are female patients with breast cancer aged >18 years old who will undergo BR or OBCS. This cohort will include at least 10 000 consecutive patients (about 5000 patients who will undergo BR and 5000 patients who will undergo OBCS). The exposures were surgery types: BR and OBCS regardless of the techniques and materials used. The primary endpoint will be PROs, which include BREAST-Q and quality of life (European Organisation for Research and Treatment (EORTC) Quality of Life Questionnaire Core 30 (QLQ-C30) and EORTC QoL Breast Cancer-specific version (QLQ-BR23)). All patients will be followed up to 24 months after operations. All data will be prospectively collected using an app software. Data will be analysed using SPSS and Stata software.Ethics and disseminationThis study follows the Helsinki Declaration. All patients will be asked to sign an informed consent before enrolment. The results of this study will be presented at national and international meetings and published in a scientific peer-reviewed journal.Trial registration numberNCT04030845.