Background Despite current advances in gastric cancer treatment, disease metastasis and chemo-resistance remain as major hurdles against better overall prognosis. Previous studies indicated that IGHG1 as well as -Catenin serve as important regulators of tumor cellular malignancy. Therefore, understanding detailed molecular mechanism and identifying druggable target will be of great potentials in future therapeutic development. Methods Surgical tissues and gastric cancer cell lines were retrieved to evaluate IGHG1 expression for patients with or without lymph node/distal organ metastasis. Functional assays including CCK8 assay, Edu assay, sphere formation assay and transwell assay, wound healing assay, etc. were subsequently performed to evaluate the impact of IGHG1/-catenin axis on tumor cell proliferation, migration and chemo-resistance. Results Gastric cancer tissues and tumor cell lines demonstrated significantly higher level of IGHG1. Functional study further demonstrated that IGHG1 promoted proliferative and migration as well as chemo-resistance of gastric cancer tumor cells. Further experiments indicated that IGHG1 activated AKT/GSK-3/-Catenin axis, which played crucial role in regulation of proliferative and chemo-resistance of gastric cancer cells. Conclusion This study provided novel evidences that IGHG1 acted as oncogene by promotion of gastric cancer cellular proliferation, migration and chemo-resistance. Our research further suggested that IGHG1/AKT/GSK-3β/β-Catenin axis acted as novel pathway which regulated gastric cancer cellular malignant behavior. Our research might inspire future therapy development to promote overall prognosis of gastric cancer patients.
Aim of the study was to determine the characteristics and prognosis, and to identify the risk factors for mortality in patients with primary Sjögren syndrome (pSS) with interstitial lung disease (pSS-ILD). A total of 1422 patients with SS were screened and 178 patients with pSS-ILD were recruited. The medical records and outcomes were retrospectively reviewed. Overall survival and case control study were performed to explore the predictors of death. Among 178 pSS-ILD patients, 87.1% were women. Mean age was 61.59 ± 11.69-year-old. Median disease duration was 72.0 (24.0, 156.0) months. Nonspecific interstitial pneumonia was the predominant high-resolution computed tomography pattern (44.9%). Impairment in diffusion capacity was the most common abnormality of pulmonary function test (75.8%) and the most severe consequence. Type 1 respiratory failure and hypoxia were observed in 15.0% and 30.0% patients, respectively. Mean survival time after confirmation of pSS-ILD diagnosis was 9.0 (6.8, 13.0) years. The 10-year survival rate for all patients with pSS-ILD was 81.7%. Forty-four (24.7%) of 178 patients died during the follow-up period. The most predominant cause of death was respiratory failure (n = 27). Twenty-seven patients died of ILD and formed study group. The 78 patients who survived formed control group. Age and smoking were risk factors for mortality in patients with pSS-ILD. In addition, severity of ILD, as reflected by high-resolution computed tomography, pulmonary function test, and arterial blood gas, was an independent risk factor. However, inflammation status (erythrocyte sedimentation rate, C-reactive protein) and anti-Sjögren syndrome–related antigen A and anti-Sjögren syndrome–related antigen B were not. ILD is a severe complication of pSS. Age, smoking, and severity of lung involvement are more critical for prognosis rather than inflammation status and autoantibodies.
To determine the expression of Semaphorin3A (Sema3A) in rheumatoid arthritis (RA) patients, and analyze the correlation between serum Sema3A and the pathogenesis of RA. The concentration of serum Sema3A and its mRNA expression level were detected in RA patients. The association of serum Sema3A level with clinical and laboratory features of RA were analyzed. Serum Sema3A of 130 RA patients (15.89 ± 8.58 ng/ml) was significantly higher than that of 150 HC (6.96 ± 2.62 ng/ml) and 215 patients with other rheumatic diseases (P < 0.05). Consistent with the serum level, the Sema3A mRNA level was also higher in RA patients' PBMC than that in HC (1.8-fold increase, P < 0.01). The serum level of Sema3A was correlated with platelet counts (r = 0.229), ESR (r = 0.172), RF (r = 0.230), IgM (r = 0.254) and Sharp score (r = 0.254), and bone mineral density (BMD) of lumbar spine (r = 0.263). Serum Sema3A was also fundamentally higher in AKA-, APF-, anti-CCP-positive groups compared with negative groups (P < 0.05). The ROC curve showed that the optimum diagnostic cutoff value for Sema3A was 10.881 ng/ml. RF level and antibodies (anti-CCP, APF, AKA, and GPI) positive rates were significantly higher in Sema3A positive group. Sharp score was also higher, although without significance. The expression of Sema3A is significantly elevated in RA patients. The level of serum Sema3A is positively correlated with inflammatory factors (including ESR, IgM, and RF) and is associated with auto-antibody production and bone destruction.
Background: We studied early poor postoperative prognosis in acute Stanford type A aortic dissection (ATAAD) patients and investigated the predictive effect of interleukin-6 (IL-6) combined with D-dimer in the early poor postoperative prognosis after ATAAD. Methods: Data on 141 ATAAD patients, who underwent emergency surgery between January 2018 and December 2018 at our hospital, were studied. We analyzed early postoperative prognosis using two patient groups. Patients with good prognosis were included in group A and those with poor prognosis were in group B. Univariate logistic and multivariable logistic regression analysis were performed for poor early postoperative prognosis. Results: Preoperative IL-6 level was lower (57.8 ± 39.0 vs 211.0 ± 153.7 pg/mL, p < 0.001) and the D-dimer was also lower (7.3 ± 6.1 vs. 16.7 ± 5.8 μg/mL, p < 0.001) in group A than in B. The cutoff points, determined by the ROC curve, were preoperative IL-6 > 108 pg/mL (area under the curve: AUC = 0.901) and D-dimer > 14.0 μg/mL (AUC = 0.817). Univariate logistic regression analysis showed that IL-6 > 108 pg/mL, D-dimer > 14.0 μg/mL, prothrombin time > 15 s, creatinine > 135 mmol/mL, and operation time > 306 min for ATAAD appeared to be early postoperative risk factors of poor prognosis. Multivariable logistic regression analysis showed that IL-6 > 108 pg/mL and D-dimer > 14.0 μg/mL were early postoperative risk factors for poor prognosis after ATAAD, and the odds ratios (ORs) of IL-6 > 108 pg/mL and D-dimer > 14.0 μg/mL were 24.937 (6.837, 90.931) and 18.757 (5.094, 69.075), respectively. When IL-6 was > 108 pg/mL (AUC = 0.901), the sensitivity and specificity of predicting early postoperative prognosis after ATAAD were 79.4 and 89.7%, respectively (95% confidence interval [CI] 0.839 to 0.963). When D-dimer was > 14.0 g/mL (AUC = 0.817), the sensitivity and specificity were 82.4 and 84.1%, respectively (95% CI 0.731 to 0.903). When combined with D-dimer (AUC = 0.936) (95% CI 0.793 to 0.979), the AUC values were more predictive than those for the individual marker.
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