This study was aimed to evaluate levels of neutrophil- (NLR), monocyte- (MLR), eosinophil- (ELR), and basophil-lymphocyte ratio (BLR) and their association with inflammatory markers in systemic autoimmune rheumatic diseases (SARDs). A total of 1139 SARD patients and 170 healthy individuals were enrolled. Clinical and laboratory data were extracted. NLR and MLR were significantly increased, but BLR decreased in most SARD patients (p < 0.05). ELR were significantly decreased in systemic lupus erythematosus (SLE) patients, but increased in those with other SARDs (p < 0.001). In SLE patients, C-reactive protein (CRP) showed positive correlation with NLR, MLR, and BLR. IgG negatively correlated with NLR, and did positively with ELR. IgM negatively correlated with NLR and MLR. In those with rheumatoid arthritis (RA), ankylosing spondylitis (AS), and osteoarthritis (OA), NLR and MLR positively correlated with erythrocyte sedimentation rate (ESR) and CRP. In primary Sjögren's syndrome (pSS) patients, ESR showed positive correlation with NLR and MLR. IgA had positive correlation with BLR. In polymyositis/dermatomyositis (PM/DM) patients, ESR and CRP positively correlated with NLR. Additionally, significant correlations were also found between CRP and BLR, IgG and ELR, IgM and ELR. In systemic sclerosis (SSc) patients, clear correlations were only observed between CRP and NLR or MLR. In mixed connective tissue disease (MCTD) patients, NLR positively correlated with ESR and CRP, while NLR and MLR did negatively with IgM. In polymyalgia rheumatic (PMR) patients, MLR positively correlated with CRP, while ELR did negatively with IgG. This study demonstrated increased NLR and MLR and deceased BLR in most SARDs, decreased ELR in SLE and increased ELR in other SARDs. Furthermore, NLR and MLR may be useful tools to reflect inflammatory status of SARDs.
Soybean isoflavones have been used as a potential preventive agent in anticancer research for many years. Genistein is one of the most active flavonoids in soybeans. Accumulating evidence suggests that genistein alters a variety of biological processes in estrogen-related malignancies, such as breast and prostate cancers. However, the molecular mechanism of genistein in the prevention of human colon cancer remains unclear. Here we attempted to elucidate the anticarcinogenic mechanism of genistein in human colon cancer cells. First we evaluated the growth inhibitory effect of genistein and two other isoflavones, daidzein and biochanin A, on HCT-116 and SW-480 human colon cancer cells. In addition, flow cytometry was performed to observe the morphological changes in HCT-116/SW-480 cells undergoing apoptosis or cell cycle arrest, which had been visualized using Annexin V-FITC and/or propidium iodide staining. Real-time PCR and western blot analyses were also employed to study the changes in expression of several important genes associated with cell cycle regulation. Our data showed that genistein, daidzein and biochanin A exhibited growth inhibitory effects on HCT-116/SW-480 colon cancer cells and promoted apoptosis. Genistein showed a significantly greater effect than the other two compounds, in a time- and dose-dependent manner. In addition, genistein caused cell cycle arrest in the G2/M phase, which was accompanied by activation of ATM/p53, p21waf1/cip1 and GADD45α as well as downregulation of cdc2 and cdc25A demonstrated by q-PCR and immunoblotting assay. Interestingly, genistein induced G2/M cell cycle arrest in a p53-dependent manner. These findings exemplify that isoflavones, especially genistein, could promote colon cancer cell growth inhibition and facilitate apoptosis and cell cycle arrest in the G2/M phase. The ATM/p53-p21 cross-regulatory network may play a crucial role in mediating the anticarcinogenic activities of genistein in colon cancer.
BackgroundThe prevalence of H. pylori is as high as 60–70% in Chinese population. Although duodenal ulcer and gastric cancer are both caused by H. pylori, they are at opposite ends of the spectrum and as such are considered mutually exclusive. Duodenal ulcer promoting (dupA) gene was reported to be associated with duodenal ulcer development. The aim of this study was to determine the prevalence of dupA gene of Helicobacter pylori in patients with various gastroduodenal diseases and to explore the association between the gene and other virulence factors.MethodsH. pylori were isolated from gastric biopsies of patients with chronic gastritis, duodenal ulcer (DU), gastric ulcer (GU), or non-cardia gastric carcinoma. The dupA, cagA, vacA, iceA and babA2 genotypes were determined by polymerase chain reaction. Histological features of gastric mucosal biopsy specimens were graded based on the scoring system proposed by the updated Sydney system. IL-1β polymorphism was investigated using restriction fragment length polymorphism.ResultsIsolates from 360 patients including 133 with chronic gastritis, 101 with DU, 47 with GU, and 79 with non-cardia gastric carcinoma were examined. The dupA gene was detected in 35.3% (127/360) and the prevalence DU patients was significantly greater than that in gastric cancer or GU patients (45.5% vs. 24.1% and 23.4%, P < 0.05). Patients infected with dupA-positive strains had higher scores for chronic inflammation compared to those with dupA-negative strains (2.36 vs. 2.24, p = 0.058). The presence of dupA was not associated with the cagA, vacA, iceA and babA 2 genotypes or with IL-1β polymorphisms.ConclusionIn China the prevalence of dupA gene was highest in DU and inversely related to GU and gastric cancer.
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