Molecular medicine reports
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An impulse oscillometry system (IOS) assesses pulmonary resistance and reactance. The present study investigated which IOS measurement is correlated with airflow obstruction, airway conductance and lung volume in chronic obstructive pulmonary disease (COPD). A total of 180 patients with COPD were selected and 95 agreed to follow‑up 1 year after the initial tests. ⋯ Similarly, the changes in X5, Fres and R5 were significantly correlated with the changes in RV and the correlation coefficients were ‑0.264, 0.287 and 0.318, respectively. In the COPD patients, the IOS reactance measurements were more closely correlated with other pulmonary function measurements rather than with resistance measurements. The IOS reactance measurements, particularly X5, appear to indicate changes in pulmonary compliance caused by airflow obstruction.
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The aim of the present study was to investigate the correlations and possible synergy among the urokinase‑type plasminogen activator receptor (uPAR) isomer D1D2 and integrin α5β1 expression levels, malignant transformation in hepatic cells and the occurrence of liver cancer. The expression site and concentration of uPAR (D1D2) were analyzed using polymerase chain reaction and in situ hybridization at the gene level in 60 samples of hepatocellular carcinoma (HCC) tissues, 60 samples of para‑carcinoma tissues and 25 samples of normal liver tissues. The mRNA levels of uPAR (D1D2) and integrin α5β1 were markedly increased para‑carcinoma tissue and liver cancer tissue as compared with those in normal tissue. ⋯ In situ hybridization revealed that the expression levels of uPAR (D1D2) and integrin α5β1 in the cytoplasm and the positive rate of the two molecules in the HCC tissue were significantly higher than those in the para-carcinoma and normal liver tissues, and the expression levels were positively correlated (rs1=0.257, P<0.05; rs2=0.261, P<0.05). The results suggested that uPAR (D1D2) mRNA overexpression may be due to changes in the conformation of the uPAR isomer. Synergy of uPAR (D1D2) mRNA and integrin α5β1 interaction may result in abnormal signal transduction in liver cells and ultimately liver cell abnormal clonal hyperplasia and malignant transformation.
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Accumulating evidence has implicated that liraglutide, one of the human glucagon‑like peptide‑1 (GLP‑1) analogues, elicits protective effects on diabetic nephropathy; however, the mechanism has yet to be fully elucidated. The present study aimed to assess the effect and underlying mechanisms of liraglutide in diabetic nephropathy. Wistar rats with streptozotocin‑induced diabetes mellitus were subcutaneously injected with liraglutide or phosphate buffer for 12 weeks at a dose of 0.3 mg/kg/12 h. ⋯ Liraglutide also reduced the expression of NF‑κB at mRNA and protein levels; the expression of tumor necrosis factor‑α, interferon‑γ, interleukin‑6 and monocyte chemoattractant protein‑1 were also reduced. By contrast, eNOS phosphorylation, eNOS activity and NO production appeared to have increased. Liraglutide may have a direct beneficial effect on diabetic nephropathy by improving eNOS activity by inhibiting the NF‑κB pathway without eliciting a glucose lowering effect.
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Severe acute pancreatitis (SAP) is an acute inflammatory disease of the pancreas that involves various distant tissues and organs. This study aimed to investigate post-tissue injury repair by mesenchymal stem cells (MSCs) in a rat model of SAP. A total of 54 pathogen-free adult male SD rats were randomly assigned to the groups SAP, SAP + MSCs and sham-operated (SO). ⋯ The intestinal expression of AQP-1 was increased at 12 and 24 h post-MSC transplantation compared to the SO group. Rats of the SAP + MSCs group displayed higher pathological scores compared to the SAP group at all time points. Overall, these data showed that MSCs can inhibit systemic inflammation and reduce TNF-α release in a rat model of SAP-induced intestinal injury, suggesting that MSCs exert protective effects on the intestinal barrier during SAP.
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Mutations in the SCN5A gene encoding the Nav1.5 channel α-subunit are known to be risk factors of arrhythmia, including Brugada Syndrome and Long QT syndrome subtype 3. The present study focused on the role of SCN5A variants in the development of ventricular fibrillation (VF) during acute myocardial infarction (AMI). Since VF during AMI is the major cause of sudden death in the Western world, SCN5A mutations represent genetic risk factors for sudden death. ⋯ In conclusion, the majority of AMI/VF+ patients demonstrated a wild type sequence or common SNPs in SCN5A. Only two out of 46 (4.3%) AMI/VF+ patients revealed mutations that may be involved in Nav1.5 dysfunction and VF. However, this requires further functional validation.