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Clinical efficacy of aspirin combined with clopidogrel in treating cerebral infarction and its influence on serum high-sensitivity C-reactive protein (hs-CRP), soluble intercellular adhesion molecule-1 (sICAM-1) and tumor necrosis factor-α (TNF-α) were explored. Ninety patients with acute cerebral infarction treated in Yidu Central Hospital of Weifang were analyzed, and those treated with aspirin alone were group A (n=40) and those treated with aspirin and clopidogrel were group B (n=50) according to the different treatment plans. The NIHSS score, total effective rate and incidence rate of adverse reactions after treatment and admission were compared between the two groups. The expression level of hs-CRP was detected by enzyme-linked immunosorbent assay, and the expression levels of sICAM-1 and TNF-α were analyzed by radioimmunoassay before treatment and three weeks after surgery, respectively, and they were analyzed and compared. After treatment, the total effective rate of patients in group B was significantly higher than that of group A (P<0.05). The general clinical baseline information, NIHSS score, and the expression levels of hs-CRP, sICAM-1, and TNF-α of patients in group B were significantly improved after treatment compared with those before treatment (P<0.05), and the NIHSS score and the expression levels of serum hs-CRP, sICAM-1, and TNF-α of those in group B were significantly lower than those in group A (P<0.05). Combination therapy of aspirin and clopidogrel can improve cerebral infarction effectively, and inhibit the expression levels of hs-CRP, sICAM-1 and TNF-α more effectively than aspirin alone. [ABSTRACT FROM AUTHOR]

Transplantation of olfactory ensheathing cells (OECs) has potential for treating spinal cord and brain injury. However, they are void of an extracellular matrix to support cell growth and migration. Engineering of tissue to mimic the extracellular matrix is a potential solution for neural repair. Tussah silk fibroin (TSF) has good biocompatibility and an Arg-Gly-Asp tripeptide sequence. A small number of studies have assessed the effect of the diameter of TSF nanofibers on cell adhesion, growth and migration. In the present study, TSF nanofibers with a diameter of 400 and 1,200 nm were prepared using electrospinning technology; these were then used as scaffolds for OECs. The structure and morphology of the TSF nanofibers were characterized by scanning electron microscopy (SEM) and Fourier-transform infrared spectroscopy. An inverted-phase contrast microscope and SEM were used to observe the morphology of OECs on the TSF nanofibers. The effect on the adhesion of the cells was observed following crystal violet staining. The phenotype of the cells and the maximum axon length on the scaffolds were evaluated by immunostaining for nerve growth factor receptor p75. Cell proliferation and viability were assessed by an MTT assay and a Live/Dead reagent kit. The migration efficiency of OECs was observed using live-cell microscopy. The results indicated that a 400-nm TSF fiber scaffold was more conducive to OEC adhesion, growth and migration compared with a 1,200-nm TSF scaffold. The phenotype of the OECs was normal, and no difference in OEC phenotype was observe when comparing those on TSF nanofibers to those on PLL. The present study may provide guidance regarding the preparation of tissue-engineered materials for neural repair. [ABSTRACT FROM AUTHOR]

Mast cells have been demonstrated to accumulate around and within solid tumors of numerous types, and express a number of pro-angiogenic compounds, including tryptase. They may serve an early role in angiogenesis within developing tumors. In the present study, the role and mechanism of tryptase in the activation of endothelial progenitor cells (EPCs) in breast cancer angiogenesis were evaluated. Human umbilical cord blood EPCs were isolated and cultured. MB-MDA-231 breast cancer cells were then pretreated with tryptase, and the conditioned medium was collected. The effects of tryptase on the migratory and angiogenesis abilities of EPCs were determined using wound-healing and tube formation assays, respectively. The effect of tryptase on the proliferation of EPCs was detected using a Cell Counting Kit-8 assay. Alterations in proteinase activated receptor (PAR)-2, phosphorylated (p)-protein kinase B (AKT), p-extracellular signal-regulated kinase (p-ERK) and vascular endothelial growth factor receptor (VEGFR)-2 expression were analyzed, in tryptase or conditioned medium-treated EPCs, by western blot analysis and reverse transcription-quantitative polymerase chain reaction. It was confirmed that the EPCs expressed PAR-2; and that tryptase treatment promoted the migration and tube formation of EPCs. Treatment with a PAR-2 agonist had a similar effect to tryptase, whereas treatment with a tryptase inhibitor, APC366, or a PAR-2 inhibitor, SAM 11, inhibited the effect of tryptase treatment. Tryptase and PAR-2 agonists did not affect the rate of EPC proliferation. MB-MDA-231 cells also expressed PAR-2. Treatment with tryptase or conditioned medium increased the expression of PAR-2, p-AKT, p-ERK and VEGFR-2 in EPCs. In conclusion, tryptase activated EPCs via PAR-2-mediated AKT and ERK signaling pathway activation, thereby enhancing angiogenesis in breast cancer. [ABSTRACT FROM AUTHOR]

Pulmonary tuberculosis (TB) is a chronic respiratory infectious disease. Certain microRNAs (miRNAs or miRs) are reported to be involved in regulating TB progression. The present study aimed to evaluate the diagnostic potential of miR-125b in pulmonary TB. The expression levels of miR-125b and Raf1 proto-oncogene serine/threonine protein kinase (RAF1) were analyzed via reverse transcription-quantitative (RT-q)PCR in patients with TB. The correlation between miR-125b and the clinical indicators was investigated, and a receiver operating characteristic (ROC) curve was used to evaluate the diagnostic value of miR-125b. The relationship between miR-125b and RAF1 was examined using the dual luciferase reporter gene assay. IL-6, TNF-α, NF-κB and IFN-γ levels were detected using ELISA kits, and then the correlation between miR-125b expression and the levels of IL-6, TNF-α, NF-κB, IFN-γ and RAF1 in peripheral blood mononuclear cells (PBMCs) was analyzed. Moreover, RAF1 mRNA and protein expression levels were detected via RT-qPCR and western blotting. The results demonstrated that miR-125b expression was decreased in patients with TB, while RAF1 expression was increased. Furthermore, miR-125b expression was associated with sputum acid-fast bacillus smear. The area under the ROC curve of miR-125b was 0.9413, and the sensitivity and specificity of miR-125b expression for TB were 90 and 92.5%, respectively. IL-6, TNF-α, NF-κB and IFN-γ levels were negatively correlated with miR-125b expression, and were inhibited by miR-125b in PBMCs. Moreover, miR-125b targeted RAF1 to negatively regulate its expression levels. RAF1 reversed the role of miR-125b in attenuating IL-6, TNF-α, NF-κB and IFN-γ levels in PBMCs. The present study demonstrated that the levels of IL-6, TNF-α, NF-κB and IFN-γ were negatively correlated with miR-125b expression in PBMCs. Thus, it was suggested that miR-125b served important roles in the occurrence and development of TB by decreasing the levels of IL-6, TNF-α, NF-κB and IFN-γ by inhibiting RAF1. [ABSTRACT FROM AUTHOR]