IntroductionRheumatoid arthritis (RA) is characterized by synovial lining hyperplasia, in which there may be an imbalance between the growth and death of fibroblast-like synoviocytes (FLSs). Antibodies against citrullinated proteins are proposed to induce RA. This study aimed to investigate the pathogenic role of citrullinated fibronectin (cFn) in RA.MethodsThe distribution of fibronectin (Fn) and cFn in synovial tissues from RA and osteoarthritis (OA) patients was examined by immunohistochemical and double immunofluorescence analysis. FLSs were isolated from RA and OA patients and treated with Fn or cFn. Apoptosis was detected by flow cytometry and TUNEL assay. The expression of survivin, caspase-3, cyclin-B1, Bcl-2 and Bax was detected by real-time PCR. The secretion of proinflammatory cytokines was measured by ELISA.ResultsFn formed extracellular aggregates that were specifically citrullinated in synovial tissues of RA patients, but no Fn deposits were observed in those of OA patients. Fn induced the apoptosis of RA and OA FLSs while cFn inhibited the apoptosis of RA and OA FLSs. Fn significantly increased the expression of caspase-3 and decreased the expression of survivin and cyclin-B1 in FLSs from RA and OA patients. cFn significantly increased the expression of survivin in RA FLSs. Furthermore, cFn increased the secretion of TNF-α and IL-1 by FLSs.ConclusionscFn plays a potential pathophysiologic role in RA by inhibiting apoptosis and increasing proinflammatory cytokine secretion of FLSs.
Background Soluble growth stimulation expressed gene 2 (sST2) is the receptor of interleukin (IL)-33. We hypothesized the IL-33/ST2 pathway may be closely related to the progression of coronary atherosclerotic lesions. Methods We analyzed 262 patients, including 63 with stable angina pectoris (SAP), 97 with acute coronary syndrome (ACS), and 102 control subjects. Plasma sST2 levels were determined using ELISA. Gensini scores were calculated. Patients with ACS and SAP were further divided according to the complexity of atherosclerotic lesions (simple/complex). Statistical analysis was performed on all data. Results The plasma sST2 levels were significantly higher in patients with coronary artery disease (CAD) than in the control group, and were significantly higher in ACS patients with complex lesions than in those with simple lesions. There were no correlations between plasma sST2 level and both the number of culprit vessels and Gensini score. Multivariate stepwise regression analysis revealed that angiographically detected complex lesions were independently correlated with plasma sST2 level. Logistic regression analyses showed that sST2 was an independent factor of both CAD and the lesion type (simple/complex) of ACS. For the diagnosis of ACS and complex lesions, the area under the receiver operating characteristic curve of sST2 was 0.651. Conclusions The plasma sST2 level was not correlated with the stenosis severity of coronary atherosclerosis. A relationship between the plasma sST2 level and the morphology of complex lesions was found for the first time, especially in ACS patients. It may be a new marker for assessing the stability and complexity of atherosclerotic plaques.
Distant metastasis is one of the leading causes of lung cancer death. Detecting the early-stage molecular alternations in primary tumors, such as gene expression differences, provides a ''prognostic'' value to the precaution of tumor metastasis. The aim of this article is to screen and identify the metastasis-related genes in human squamous cell lung carcinoma. Primary tumor tissues of nine patients with subsequent metastasis and eight patients without metastasis were selected to perform the gene microarray experiment. GO and pathway analyses were used to determine the differentially expressed genes. Two identified genes were further validated by real-time quantitative reverse transcription polymerase chain reaction (PCR) (real-time qRT-PCR). Two hundred and thirty-eight differentially expressed genes were detected in gene chip experiment, including 51 up-regulated genes and 187 down-regulated genes. These genes were involved in several cellular processes, including cell adhesion, cell cycle regulation, and apoptosis. GO analysis showed that the differentially expressed genes participated in a wide ranging of metastasis-related processes, including extracellular region and regulation of liquid surface tension. In addition, pathway analysis demonstrated that the differentially expressed genes were enriched in pathways related to cell cycle and Wnt signaling. Real-time qRT-PCR validation experiment of LCN2 and PDZK1IP1 showed a consistent up-regulation in the metastasis group. The metastasis of human squamous cell lung carcinoma is a complex process that is regulated by multiple gene alternations on the expression levels. The 238 differentially expressed genes identified in this study presumably contain a core set of genes involved in tumor metastasis. The real-time qRT-PCR results of PDZK1IP1 and LCN2 validated the reliability of this gene microarray experiment. Anat Rec,
Objective. To investigate the nutritional risk, malnutrition, severe malnutrition, and malnutrition prevalence of different stages in chronic kidney disease (CKD) patients with and without diabetes mellitus using the Global Leadership Initiative on Malnutrition (GLIM), and to analyze the causes of malnutrition and to improve the clinical outcomes of patients for early intervention. Methods. A total of 683 patients with CKD who were hospitalized in our hospital from January 2020 to January 2021 were enrolled and divided into subgroups 1 to 5 according to whether they were complicated with diabetes and glomerular filtration rate. Using the second step of the malnutrition (GLIM) diagnostic tool and 2 previously commonly used malnutrition assessment methods (body mass index <18.5 kg/m2 with poor general condition, 3 points for nutritional deficiency in nutritional risk screening), combined with clinical research on the main causes of malnutrition, the intervention measures were discussed. Results. The prevalence of malnutrition was 16.7% (114/683) in the patients included in the survey using the diagnostic criteria of malnutrition (GLIM) (excluding whole body muscle mass index). The prevalence of malnutrition in CKD patients with and without diabetes was 23.7% and 12.6%, respectively. The overall prevalence rate of severe malnutrition was 14.2%, and the prevalence rates of those with and without diabetes were 19.0% and 11.4%, respectively; the results of the two methods of malnutrition assessment showed that the prevalence of malnutrition in CKD patients with diabetes was higher than that in the uncombined group. There was no severe malnutrition in patients with CKD stages 1 and 2. From CKD stage 3 onwards, the severe malnutrition in the diabetic group was significantly higher than that in the uncombined group. Conclusion. With the progression of CKD, the incidence of malnutrition also gradually increased, indicating that malnutrition is related to primary diseases and concomitant diseases. Attention should be paid to the malnutrition of CKD patients with diabetes, and clinical medical staff need to pay early attention to various diseases that lead to the progression of CKD, such as diabetes, primary nephropathy, and other factors, to prevent complications and delay the progression of CKD.
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