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Systemic inflammation plays an important role in cancer cachexia. However, among the systemic inflammatory biomarkers, it is unclear which has optimal prognostic value for cancer cachexia.The Kaplan-Meier method was used and the log-rank analysis was performed to estimate survival differences between groups. Cox proportional hazard regression analyses were conducted to assess independent risk factors for all-cause mortality.The C-reactive protein-to-albumin ratio (CAR) was the optimal prognostic assessment tool for patients with cancer cachexia, with 1-, 3-, and 5-year predictive powers of 0.650, 0.658, and 0.605, respectively. Patients with a high CAR had significantly lower survival rates than those with a low CAR. Moreover, CAR can differentiate the prognoses of patients with the same pathological stage. Cox proportional risk regression analyses showed that a high CAR was an independent risk factor for cancer cachexia. For every standard deviation increase in CAR, the risk of poor prognosis for patients with cancer cachexia was increased by 20% (hazard ratio = 1.200, 95% confidence interval = 1.132-1.273, P 0.001).CAR is an effective representative of systemic inflammation and a powerful factor for predicting the life function and clinical outcome of patients with cancer cachexia.

Systemic inflammation is the most representative host-tumor interaction in cancer. This study aimed to develop a novel inflammatory burden index (IBI) to assess the inflammatory burden of different cancers and predict the prognosis of patients with cancer.A total of 6359 cancer patients admitted to multiple centers from 2012 through 2019 were included in this study. The IBI was formulated as C-reaction protein × neutrophil/lymphocyte. Survival differences between the groups were compared using the Kaplan-Meier method. Cox proportional hazard regression analysis was used to estimate the hazard ratio (HR) and 95% confidence interval (CI). Logistic regression analysis was used to assess the association between the inflammatory burden index and outcomes.Cancers assessed by the IBI could be classified as high, moderate, or low inflammatory burden and had different prognostic stratification effects (46.5% vs 61.0% vs 83.0%; P .001). Compared with other systemic inflammation biomarkers, the IBI had the highest accuracy in predicting survival. Patients with a high IBI had significantly lower survival rates than those with a low IBI (45.7% vs 69.1%; P .001). For every standard deviation increase in the IBI, the risk of poor prognosis for patients with cancer increased by 10.3% (HR, 1.103; 95% CI, 1.072-1.136; P .001). The IBI could be used as a useful prognostic supplement in the pathological stage. A high IBI was an independent high-risk factor that affected patient's physical condition, malnutrition, cachexia, and short-term outcomes and an independent risk factor for patients with cancer in both validation cohorts a (hazard ratio, 1.114; 95% confidence interval, 1.072-1.157; P .001) and b (hazard ratio, 1.125; 95% confidence interval, 1.060-1.193; P .001).The IBI, as a novel indicator of systemic inflammation, is a feasible and promising predictive biomarker in patients with cancer and can be used to assess the inflammatory burden of different cancers.

The cachexia index is a useful predictor for cancer cachexia and prognostic assessment. However, its use is limited because of high testing costs and complicated testing procedures. Thus, in this study, we aimed to develop a hand grip strength (HGS)-based cancer cachexia index (H-CXI) as a potential predictor of cancer cachexia and prognosis in patients with cancer.Here, 14 682 patients with cancer were studied, including the discovery (6592), internal validation (2820) and external validation (5270) cohorts. The H-CXI was calculated as [HGS (kg)/height (m)There was a significant non-linear relationship between the H-CXI and OS in all cohorts. Patients with a low H-CXI had significantly lower OS than those with a high H-CXI in the discovery cohort (6-year survival percentage: 55.72% vs. 76.70%, log-rank P 0.001), internal validation cohort (6-year survival percentage: 55.81% vs. 76.70%, log-rank P 0.001), external validation cohort (6-year survival percentage: 56.05% vs. 75.48%, log-rank P 0.001) and total cohort (6-year survival percentage: 55.86% vs. 76.27%, log-rank P 0.001). Notably, the prognostic stratification effect of the H-CXI in patients with advanced-stage disease was more significant than that in patients with early-stage disease. The multivariate Cox proportional risk regression model confirmed that a low H-CXI negatively affected the prognosis of patients with cancer in the discovery cohort [hazard ratio (HR) 0.75, 95% confidence interval (CI) 0.71-0.80, P 0.001], internal validation cohort (HR 0.79, 95 %CI 0.72-0.86, P 0.001), external validation cohort (HR 0.84, 95% CI 0.79-0.89, P 0.001) and total cohort (HR 0.80, 95% CI 0.77-0.83, P 0.001). Multivariate logistic regression models showed that a low H-CXI was an independent risk factor predicting adverse short-term outcomes and cancer cachexia in patients with cancer.The simple and practical H-CXI is a promising predictor for cancer cachexia and prognosis in patients with cancer.

Albicanol is a natural terpenoid derived from Dryopteris fragrans. Herein, we assessed the ability of Albicanol to protect against oxidative stress-induced senescence. Using a murine model of D-galactose (D-gal)-induced aging, we determined that Albicanol treatment can reverse D-gal-mediated learning impairments and behavioral changes, while also remediating brain tissue damage in treated mice. We found that serum SOD, CAT, GSH-Px, and T-AOC levels were significantly decreased in aging mice, and that Albicanol treatment significantly increased the serum levels of these antioxidant enzymes. We additionally evaluated the impact of Albicanol treatment on the Keap1/Nrf2/ARE signaling pathway, and found that it was able to decrease Keap1 expression while increasing the expression of Nrf2, thereby activating this signaling pathway, suppressing oxidative damage, and enhancing the expression of downstream target genes including SOD, GSH, GST, HO-1, and NQO1 in this murine aging model system. Albicanol treatment also inhibited the secretion of inflammatory TNF-a and IL-1b. Together, these data indicated that Albicanol can activate Nrf2 pathway-related genes, thereby inhibition of delayed aging by alleviating oxidative stress-induced damage.

The body's immune-nutrition status affects prognosis in patients with lung cancer. The Controlling Nutritional Status (CONUT) score is an immune-nutrition-related index associated with prognosis in other tumors. We aimed to assess the value of CONUT scores in predicting prognosis in patients with lung cancer.In this retrospective, multicenter study, 1339 patients with lung cancer were divided into low and high CONUT score groups. The relationship between CONUT scores and overall survival (OS) was assessed by survival curves and Cox proportional hazards regression modeling. A nomogram, including CONUT scores and other clinical variables, was established.There were 659 (49.2%; mean age, 59.91 years) low and 680 (50.8%; mean age, 62.23 years) high CONUT score patients. OS was significantly worse in patients with high than in those with low CONUT scores (P0.001), even after stratification by pathological types (non-small-cell lung cancer and small-cell lung cancer) and Tumor, Node, Metastasis (TNM) stages. A high CONUT score independently predicted risk in patients with lung cancer (adjusted hazard ratio, 1.48; 95% CI, 1.26-1.73; P0.001). The CONUT-based nomogram could predict prognosis well (C-index, 0.701), with better resolution and accuracy than TNM staging for predicting OS at 1, 2, and 3 years (area under the receiver operating characteristic curve, 0.735 vs 0.678, 0.742 vs 0.696, and 0.768 vs 0.743, respectively).The CONUT score can predict prognosis in patients with lung cancer. A CONUT-based nomogram can improve the accuracy of survival prediction in such patients.

Cancer cachexia is a systemic paraneoplastic phenomenon involving multiple organs, including the liver. Total bilirubin (TBIL) is an easily obtained blood biomarker that reflects liver homeostasis. The aim of this study was to evaluate the prognostic value of serum TBIL in patients with cancer cachexia.This study included 2282 patients from a multicenter research database who were diagnosed with cancer cachexia between June 2012 and December 2019. The hazard ratio (HR) for all-cause mortality was analyzed using Cox proportional hazards regression models. The association of serum TBIL with all-cause mortality was modeled with restricted cubic splines. The optimal cutoff value for TBIL was calculated with maximally selected rank statistics.Of the participants, there were 1327 (58.2%) men and 955 (41.8%) women. The mean patient age was 60.4 ± 1.5 y. The 12-mo all-cause mortality rate for patients with cancer cachexia was 29.5% (95% confidence interval [CI], 27.6%-31.3%), resulting in a rate of 209.58 events per 1000 patient-years. An inverted L-shaped association between TBIL and all-cause mortality was observed. The cutoff point for TBIL for the prediction of the time to mortality was21.7 µmol/L. A high TBIL level but not the direct bilirubin or indirect bilirubin level was identified as an independent prognostic factor (HR, 1.60; 95% CI, 1.32-1.93). For patients with digestive system tumors, a high serum TBIL level (≥21.7 µmol/L) was significantly associated with mortality.High TBIL levels are associated with increased all-cause mortality in patients and might be a promising prognostic indicator in patients with cancer cachexia.

Background/objectives The assessment of nutritional status and the quality of life in patients with gastric cancer has become one of the important goals of current clinical treatment. The purpose of this study was to assess the nutritional status in hospitalized gastric cancer patients by using patient-generated subjective global assessment (PG-SGA) and to analyze the influence of nutritional status on the patients’ quality of life (QOL). Methods We reviewed the pathological diagnosis of gastric cancer for 2322 hospitalized patients using PG-SGA to assess their nutritional status and collected data on clinical symptoms, the anthropometric parameters (height, weight, body mass index (BMI), mid-arm circumference (MAC), triceps skin-fold thickness (TSF), and hand-grip strength (HGS). We also collected laboratory data (prealbumin, albumin, hemoglobin) within 48 h after the patient was admitted to the hospital. The 30-item European Organization for Research and Treatment of Cancer Core Quality of Life Questionnaire (EORTC QLQ-C30) was used for QOL assessment in all patients. Results By using PG-SGA, we found 80.4% of the patients were malnourished (score ≥ 4) and 45.1% of the patients required urgent nutritional support (score ≥ 9). In univariate analysis, old age (> 65 years, p

Background Completing Patient‐Generated Subjective Global Assessment (PG‐SGA) questionnaires is time consuming. This study aimed to develop and validate an easy‐to‐use modified PG‐SGA (mPG‐SGA) for cancer patients. Methods Seventy professionals assessed the content validity, comprehensibility, and difficulty of the full PG‐SGA. A survey including the PG‐SGA and other questionnaires was completed by 34 071 adult hospitalized cancer patients with first cancer diagnosis or recurrent disease with any tumour comorbidities from the INSCOC study. Among them, 1558 patients were followed for 5 years after admission. Reliability and rank correlation were estimated to assess the consistency between PG‐SGA items and to select mPG‐SGA items. The external and internal validity, test–retest reliability, and predictive validity were tested for the mPG‐SGA via comparison with both the PG‐SGA and abridged PG‐SGA (abPG‐SGA). Results After deleting items that more than 50% of professionals considered difficult to evaluate (Worksheet 4) and items with an item‐total correlation

BackgroundColorectal cancer (CRC) is a common malignancy with high incidence of malnutrition. Increasing evidence showed that nutritional status could be a prognostic indicator of cancer survival. However, there were few prognostic models involving nutrition-related indicators in CRC. This study aimed to develop a nutrition-related prognostic model for CRC survival.MethodsThis multicenter retrospectively primary cohort data included 1,373 CRC patients, and the external validation cohort enrolled other 108 CRC patients. LASSO and multivariate regression analyses were used to select prognostic indicators and develop the nomogram. We performed C-index, calibration curves, and DCA to assess the discrimination, calibration, and applicability. Finally, the indicators of the nomogram model were used as adjustment factors. Multivariate Cox survival analyses were performed to investigate the benefit of the Patient-Generated Subjective Global Assessment (PG-SGA) and Global Leadership Initiative on Malnutrition (GLIM) malnutrition criteria to CRC prognosis.ResultsFive prognostic indicators (TNM stage, radical resection, reduced food intake, activities and function decline, and low albumin) were chosen to develop the nomogram. C-index of the nomogram was 0.74 (95% CI 0.72-0.77) and 0.72 (95% CI 0.62-0.81) in the primary cohort and validation cohort, which were higher than other models. Calibration plots and DCA showed that the nomogram model has a good consistency and clinical benefit in predicting CRC survival. Multivariate Cox survival analysis suggested moderate (PPP>0.05). Finally, stratified analysis suggested that malnourished CRC patients with low albumin synergistically increased the death risk of CRC OS both in PG-SGA and GLIM. (P for interaction = 0.007 and 0.004, respectively)ConclusionThis study established a prospective model to predict the OS in CRC patients using nutrition-related indicators. Moreover, we also found that PG-SGA had a better prognostic and predictive efficiency in CRC than GLIM. These findings grant further verification.

Oral anatomy and physiology is the main course in the basic learning stage of stomatology which not only provides a solid theoretical knowledge for clinical subjects but also a basis subject for students to learn the following courses. Improving the quality of oral anatomy and physiology will have a profound impact on the students who major in stomatology. In the teaching practice, we try to combine the modern PBL (Problem-based learning) teaching method with the traditional LBL (Lecture-based learning) teaching method to improve the initiative and enthusiasm of students to study this course, thereby improving the teaching effectiveness of the Oral anatomy and physiology and lays the foundation for the study of other medical courses.

Esophageal squamous cell carcinoma (ESCC) is one of the most common cancers in China with very low 5-year survival rate mostly due to the paucity of effective early diagnostic methods. Serum autoantibodies against 9 tumor-associated antigens (TAAs) from ESCC patients and healthy controls were detected by enzyme-linked immunosorbent assay to evaluate their performances in the immunodiagnosis of ESCC. Logistic regression models were generated to predict the probability of individuals being diagnosed with ESCC in training cohort (648 participants) and further validated in another independent cohort (372 participants). Finally, a panel of four TAAs showed high diagnostic accuracy with areas under the receiver operating characteristic curve of 0.838 in training cohort and 0.872 in validation cohort, respectively. The percentages of individuals correctly classified were 77.01 % in training cohort and 78.49 % in validation cohort, respectively. This model could discriminate early-stage (AJCC stage 0, I and II) ESCC patients from normal controls, with true-positive rate (TPR) of 67.57 % in training cohort and TPR of 63.33 % in validation cohort, and the overall TPR for early-stage ESCC was 66.85 % when the two cohorts were combined. The diagnostic performance of this model showed no significant difference between early-stage and late-stage (AJCC stage III and IV) ESCC patients. In summary, the optimized model with 4 TAAs has a high diagnostic performance for ESCC detection, especially for early-stage ESCC.

The level of the systemic inflammatory marker C-reactive protein (CRP) is elevated in many patients with malignant disease and may be related to nutritional status.To analyze the association between serum CRP levels in patients with malignant tumors and their nutritional status.A total of 3,692 cases were analyzed and the serum CRP levels were determined using an immunometric assay. Nutritional status was assessed by using patient-generated subjective global assessment (PG-SGA). The biochemical evaluation of prealbumin (PA), albumin (ALB), cholesterol (CHOL), and triglycerides (TG) were assayed within 48 h admission to the hospital. The association between serum CRP concentration and the nutritional status, the stage of the tumor and other factors was analyzed by univariate and multivariate logistic regression analysis.Elevated serum CRP was observed in 47.6% (1,548/3,269) of patients compared with the reference value, and the median CRP concentration was 18.29 mg/l. Patient serum CRP concentrations in the malnourished group (PG-SGA B + C) were higher than in the well-nourished (PG-SGA A) patients (P 0.05). The serum CRP level was related to the patients' age, gender, tumor stage, and was affected by hepatitis, liver cirrhosis, diabetes, but it has no effect on hypertension. The CRP high patients had lower PA and ALB levels, lower Karnofsky performance status scores, and higher PG-SGA scores (P 0.05), and there was no relationship with CHOL and TG levels. Weight loss in the previous 1 mo was seen with CRP positive patients (P 0.05).Almost 50% of malignant tumor patients had elevated serum CRP levels indicating a systemic inflammatory state. The nutritional status was worse in cancer patients with higher concentrations of serum CRP. The level of CRP was associated with the tumor stage, and, as stage is a prognostic factor, so can CRP be used as a prognostic maker in malignant tumors patients.

Helicobacter pylori, a risk factor of cancer and chronic diseases, remains highly prevalent in China. This review aims to systematically evaluate the H. pylori-attributable burden for gastric cancer (GC), coronary heart disease (CHD), and ischemic stroke (IS) in the Chinese population. Helicobacter pylori prevalence was updated by pooling the results reported in studies across China. The population attributable fraction (PAF) was calculated based on the H. pylori prevalence 10 years ago and relative risks of specific disease by reviewing the prospective studies published from 2000 through 2015. In China, the nationwide average prevalence of H. pylori was estimated to be 42.06 % in the general population during 2009-2013. The fixed effects pooled relative risk (RR) of 1.89 [95 % confidence interval (CI): 1.57-2.26] was obtained for gastric cancer and H. pylori infection. Helicobacter pylori infection was responsible for around 37.38 % of noncardia GC, corresponding to about 105,536 cases in 2012. As for extra-gastric disorders, H. pylori infections had higher risk of CHD (RR = 1.55, 95 % CI: 1.37-1.76) and IS (RR = 1.54, 95 % CI: 1.42-1.66). About 23.15 % of CHD and 22.29 % of IS were attributable to H. pylori infection. The estimates of H. pylori-attributable burden reveal a great potential of reducing H. pylori-related chronic disease burden by H. pylori eradication. Large prospective studies are warranted to identify which H. pylori strains, which subtypes of the disease, and which subgroups of the population have the greatest risk of relevant diseases and the effect of H. pylori eradication on the prevention of H. pylori-related diseases.

Cervical cancer is a cause of cancer death, making it as the one of the most common cause for death among women globally. Though many studies before have explored a lot for cervical cancer prevention and treatment, there are still a lot far from to know based on the molecular mechanisms. Janus kinase 2 (JAK2) has been reported to play an essential role in the progression of apoptosis, autophagy and proliferation for cells. We loaded gold-quercetin into poly (dl-lactide-co-glycolide) nanoparticles to cervical cancer cells due to the propertities of quercetin in ameliorating cellular processes and the easier absorbance of nanoparticles. Here, in our study, quercetin nanoparticles (NQ) were administrated to cells to investigate the underlying mechanism by which the cervical cancer was regulated. First, JAK2-inhibited carvical cancer cell lines were involved for our experiments in vitro and in vivo. Western blotting, quantitative RT-PCR (qRT-PCR), ELISA, Immunohistochemistry, and flow-cytometric analysis were used to determine the key signaling pathway regulated by JAK2 for cervical cancer progression. And the role of quercetin nanoparticles was determined during the process. Data here indicated that JAK2, indeed, expressed highly in cancer cell lines compared to the normal cervical cells. And apoptosis and autophagy were found in JAK2-inhibited cancer cells through activating Caspase-3, and suppressing Cyclin-D1 and mTOR regulated by Signal Transducer and Activator of Transcription (STAT) 3/5 and phosphatidylinositide 3-kinase/protein kinases (PI3K/AKT) signaling pathway. The cervical cancer cells proliferation was inhibited. Further, tumor size and weight were reduced by inhibition of JAK2 in vivo experiments. Notably, administration with quercetin nanoparticles displayed similar role with JAK2 suppression, which could inhibit cervical cancer cells proliferation, invasion and migration. In addition, autophogy and apoptosis were induced, promoting cervical cancer cell death. To our knowledge, it was the first time to evaluate the role of quercetin nanoparticles in improving cervical cancer from apoptosis, autophagy and proliferation, which could be a potential target for future therapeutic approach clinically.

Esophageal cancer is the sixth leading cause of cancer-associated death worldwide. Phospholipase C epsilon 1 (PLCE1) gene was found to be associated with the risk of esophageal squamous cell carcinoma (ESCC) by three large-scale genome-wide association studies (GWAS) in Chinese populations. To evaluate the association between the single nucleotide polymorphisms (SNPs) in PLCE1 gene and ESCC risk, a case-control study including 550 patients with ESCC and 550 age, gender-matched controls was carried out to investigate the genetic susceptibility of three SNPs (rs3765524 C/T and two unreported potentially functional SNPs rs10882379 G/A and rs829232 G/A) as well as the interactions of gene-gene and gene-environment in the development of ESCC. And the results showed that GA genotype of rs10882379 was significantly associated with reduced ESCC risk compared with GG genotype (adjusted OR [95% CI]: 0.66 [0.51, 0.86]), while AA genotype of rs829232 was significantly associated with increased ESCC risk compared with GG genotype (adjusted OR [95% CI]: 1.37 [1.12, 1.67]). The haplotype analysis showed increased ESCC risk in Grs10882379Crs3765524Ars829232 and Grs10882379Trs3765524Ars829232 haplotypes with OR (95% CI) of 1.40 (1.13, 1.73) and 1.66 (1.18, 2.34), respectively and inversely reduced ESCC risk in Ars10882379Crs3765524Grs829232 haplotype with OR (95% CI) of 0.74 (0.61, 0.91). The gene-environment interaction analysis emerged a best model consisted of four factors (rs10882379, rs3765524, rs829232 and family history of ESCC) that could increase the ESCC risk in the 'high risk group' with 4.45-fold (OR [95% CI]: 5.45 [4.13, 7.19]), compared to the 'low risk group.' Our results further validate that the SNPs in PLCE1 gene may contribute to the ESCC susceptibility in Chinese Han population. Also the gene-gene and gene-environment interactions play a certain crucial role in the ESCC progression.

Background and aims Epithelial barrier dysfunction plays a critical role in the pathogenesis of allergic diseases; the mechanism is to be further understood. The ubiquitin E3 ligase A20 (A20) plays a role in the endocytic protein degradation in the cells. This study aims to elucidate the role of A20 in the maintenance of gut epithelial barrier function. Methods Gut epithelial cell line, HT-29 cell, was cultured into monolayers to evaluate the barrier function in transwells. RNA interference was employed to knock down the A20 gene in HT-29 cells to test the role of A20 in the maintenance of epithelial barrier function. Probiotic derived proteins were extracted from the culture supernatants using to enhance the expression of A20 in HT-29 cells. Results The results showed that the knockdown of A20 compromised the epithelial barrier function in HT-29 monolayers, mainly increased the intracellular permeability. The fusion of endosome/lysosome was disturbed in the A20-deficient HT-29 cells. Allergens collected from the transwell basal chambers of A20-deficient HT-29 monolayers still conserved functional antigenicity. Treating with probiotic derived proteins increased the expression of A20 in HT-29 cells and promote the barrier function. Conclusion A20 plays an important role in the maintenance of epithelial barrier function as shown by HT-29 monolayer. Probiotic derived protein increases the expression of A20 and promote the HT-29 monolayer barrier function.

A set of accurate, effective and operable methodology can ensure the normalization, standardization and transparency of each operating link in the process of emission trading. On the basis of introducing the fundamental thought of emission trading, this paper summarizes the research achievements and methods of emission trading mechanism methodology, and indicates that the innovative research of emissions trading mechanism methodology provides significant technical support for the implementation of emission trading in China.

Background and aims Epithelial barrier dysfunction plays a critical role in the initiation of a number of immune diseases; the causative factors are not fully understood. The present study aimed to elucidate the mechanism by which the eosinophil-derived interferon (IFN)-lambda induced the gut epithelial barrier dysfunction. Methods The duodenal biopsies were obtained from patients with or without food allergies. The eosinophils and IFNλ expression were observed by immune staining. Intestinal epithelial cell line, T84 cells, and a mouse model were employed to observe the effect of IFNλ on the epithelial barrier function and the initiation of skewed T helper (Th)2 polarization in the mouse intestine. Results IFNλ expression was observed in over 80% human eosinophils of the subjects with or without food allergies. Exposure to microbial products, lipopolysaccharide or peptidoglycan, could induce eosinophils to release IFNλ. Exposure to IFNλ could induce intestinal epithelial barrier dysfunction via inducing the epithelial cell apoptosis. Concurrent exposure to microbial products and food antigens could induce aberrant antigen specific Th2 polarization and Th2 pattern inflammation in the intestine. Conclusions Eosinophils express IFNλ that can induce intestinal epithelial barrier dysfunction and promotes the initiation of the aberrant Th2 polarization in the intestine.

Molecular dynamics simulation is used to study the decomposition and stability of SII hydrogen and hydrogen/tetrahydrofuran (THF) hydrates at 150 K, 220 K and 100 bar. The modelling of the microscopic decomposition process of hydrogen hydrate indicates that the decomposition of hydrogen hydrate is led by the diffusive behaviour of H(2) molecules. The hydrogen/THF hydrate presents higher stability, by comparing the distributions of the tetrahedral angle of H(2)O molecules, radial distribution functions of H(2)O molecules and mean square displacements or diffusion coefficients of H(2)O and H(2) molecules in hydrogen hydrate with those in hydrogen/THF hydrate. It is also found that the resistance of the diffusion behaviour of H(2)O and H(2) molecules can be enhanced by encaging THF molecules in the (5(12)6(4)) cavities. Additionally, the motion of THF molecules is restricted due to its high interaction energy barrier. Accordingly, THF, as a stabiliser, is helpful in increasing the stability of hydrogen hydrate.

Dynamics model on abrasive particles and workpieces during the centrifugal barrel surface finishing process was built by Discrete Element Method (DEM). The motion status of abrasive particles and workpieces was visually simulated and some important process parameters were numerically studied. The influence of fill ratio on finishing efficiency was analyzed, and finishing efficiency was the highest as the fill ratio is 65%. the simulation results are basically coincident to the experimental results. Both results have proved that filling ratio is the main parameter that changes medium motion laws, which provides an very efficient way to further optimize design parameters and process parameters, as well as to improve production efficiency.

Dynamics model on abrasive particles and workpieces during the centrifugal barrel surface finishing process was built by Discrete Element Method (DEM). The motion status of abrasive particles and workpieces was visually simulated and some important process parameters were numerically studied. The influence of planetary transmission ratio on finishing efficiency was analyzed, and finishing efficiency was the highest as the transmission ratio is -1. Finally, the conclusion was validated by experiments. Such economical and precise method could replace lots of finishing tests to optimize process parameters, which would provide theoretic basis for experimental research and efficient means for the finishing mechanism analysis of centrifugal barrel finishing.

Thin films of B-site substituted Bi4Ti3O12 (BTO) by Zr, Bi4Ti3−xZrxO12 (BTZx, x=0.2, 0.5, 1.0 and 1.5), were fabricated on Pt/Ti/SiO2/Si substrates by pulsed laser deposition. Structures and properties of the films were studied as functions of Zr composition. Structure characterization was conducted by X-ray diffraction, scanning electron microscopy, and Raman spectroscopy. The Zr substitution does not change the layered structures of the BTZx. However, with increasing x from 0.2 to 1.5, the vibration modes of the TiO6 octahedra weaken greatly, which is responsible for the corresponding weakening ferroelectricity the remnant polarizations are 14.8, 11.2, 2.4, and 1.4 μC/cm2, respectively. Additionally, the Zr substitution cannot improve the fatigue-resistance of BTZx significantly. After 7.22×109 switching cycles, the nonvolatile polarization decreases by 30.3 and 64.9% of the initial values for x=0.2, and 0.5, respectively. The dielectric properties of these films are also investigated briefly. The relationship between the structures and properties is established experimentally.

Sera of cancer patients may contain antibodies that react with a unique group of autologous cellular antigens called tumor-associated antigens (TAAs). The present study aimed to determine whether a mini-array of multiple TAAs would enhance antibody detection and be a useful approach in esophageal cancer detection and diagnosis. Our mini-array of multiple TAAs consisted of eleven antigens, p53, pl6, Impl, CyclinB1, C-myc, RalA, p62, Survivin, Koc, CyclinD1 and CyclinE full-length recombinant proteins. Enzyme-linked immunosorbent assays (ELISA) were used to detect autoantibodies against eleven selected TAAs in 174 sera from patients with esophageal cancer, as well as 242 sera from normal individuals. In addition, positive results of ELISA were confirmed by Western blotting. In a parallel screening trial, with the successive addition of antigen to a final total of eleven TAAs, there was a stepwise increase in positive antibody reactions. The eleven TAAs were the best parallel combination, and the sensitivity and specificity in diagnosing esophageal cancer was 75.3% and 81.0%, respectively. The positive and negative predictive values were 74.0% and 82.0%, respectively, indicating that the parallel assay of eleven TAAs raised the diagnostic precision significantly. In addition, the levels of antibodies to seven antigens, comprising p53, Impl, C-myc, RalA, p62, Survivin, and CyclinD1, were significantly different in various stages of esophageal cancer, which showed that autoantibodies may be involved in the pathogenesis and progression of esophageal cancer. All in all, this study further supports our previous hypothesis that a combination of antibodies might acquire higher sensitivity for the diagnosis of certain types of cancer. A customized mini-array of multiple carefully-selected TAAs is able to enhance autoantibody detection in the immunodiagnosis of esophageal cancer and autoantibodies to TAAs might be reference indicators of clinical stage.

Polymorphisms in miRNA binding sites have been shown to affect miRNA binding to target genes, resulting in differential mRNA and protein expression and susceptibility to common diseases. Our purpose was to predict SNPs (single nucleotide polymorphisms) within miRNA binding sites of inflammatory genes in relation to gastric cancer. A complete list of SNPs in the 3’UTR regions of all inflammatory genes associated with gastric cancer was obtained from Pubmed. miRNA target prediction databases (MirSNP, Targetscan Human 6.2, PolymiRTS 3.0, miRNASNP 2.0, and Patrocles) were used to predict miRNA target sites. There were 99 SNPs with MAF>0.05 within the miRNA binding sites of 41 genes among 72 inflammation-related genes associated with gastric cancer. NF-κB and JAK-STAT are the two most important signaling pathways. 47 SNPs of 25 genes with 95 miRNAs were predicted. CCL2 and IL1F5 were found to be the shared target genes of hsa-miRNA-624-3p. Bioinformatic methods could identify a set of SNPs within miRNA binding sites of inflammatory genes, and provide data and direction for subsequent functional verification research.

Methylenetetrahydrofolate reductase (MTHFR) plays a central role in folate metabolism. This study with 381 esophageal cancer patients and 432 healthy controls was conducted to examine the association of MTHFR C677T and A1298C polymorphisms with susceptibility to esophageal cancer (EC) in a Chinese population. Compared with the CC genotype of MTHFR C677T, subjects carrying homozygote TT and variant genotypes (CT+TT) demonstrated reduced risk of EC with adjusted ORs (95% CI) of 0.44 (0.28-0.71) and 0.57 (0.37-0.88), respectively. However, no association was found between the MTHFR A1298C polymorphism and the risk of EC. Comparing to haplotype CA, haplotypes TA and TC could reduce the susceptibility to EC with adjusted ORs (95% CI) of 0.61(0.47-0.79) and 0.06 (0.01-0.43), respectively. In conclusion, the present study suggested that the MTHFR C677T polymorphism can markedly influence the risk of EC in Chinese.

UNLABELLED Meta-analyses have shown that microRNA polymorphisms have variable effects in different population. Yet, no meta-analysis investigated the association of two common polymorphisms of miRNA, mir-499 rs3746444 polymorphism and mir-149 rs2292832 polymorphism, with cancer risk in the Chinese population. We searched the PubMed, Web of Knowledge, MEDLINE, CNKI databases, as well as Cochrane library, updated on December 31, 2012 for assays regarding cancer risk association with these two common polymorphisms in the present meta-analysis. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were used to explore the strength of associations. The results showed that rs3746444 polymorphism was associated with increased cancer risk (dominant model: GG/AG vs. AA: OR = 1.43, 95% CI: 1.14-1.80; recessive model: GG vs. AG/AA OR = 1.54, 95% CI: 1.04-2.30; homozygote model: GG vs. AA: OR = 1.69, 95% CI: 1.10-2.60; heterozygote model: AG vs. AA: OR = 1. 35, 95% CI: 1.09-1.67), and rs3746444 was associated with liver cancer in the subgroup of cancer types. For the rs2292832 polymorphism, the results showed no significant risk association in both overall pooled analysis and subgroup of cancer types, smoking status, gender and tea drinking status in the Chinese population. This meta-analysis suggested that the rs3746444 GG genotype is associated with increased cancer risk, especially liver cancer, while the rs2292832 polymorphism showed no association with cancer risk in Chinese.

This study aimed to understand the correlation between tag single nucleotide polymorphisms (tSNP) of microRNA regulatory genes and the gentic susceptibility of primary liver cancer.1:1 case-control study was applied in this research. A total of 532 primary liver cancer patients in 2 teaching hospitals in Zhengzhou city were enrolled as case group.532 healthy individuals were enrolled as control group. The subjects were surveyed by a face-to-face interview and 5 ml of peripheral venous blood were collected. Candidate tSNP were screened from DICER1, RAN and GEMIN4 gene, respectively. PCR-RFLP or Allele specific PCR was applied for genotyping of the subjects. Conditional logistic regression model and Multifactor-Dimensionality Reduction method were applied for analyzing the correlation between tSNP of above genes and gentic susceptibility of primary liver cancer. The gene-environment interaction was also analyzed.The frequencies of genotype CC, CT, TT in rs14035 locus were 67.29% (358/532), 28.20% (150/532), 4.51% (24/532) in case group, and 70.30% (374/532), 28.20% (150/532), 1.50% (8/532) in control group, respectively (χ2=8.35, P0.05). The frequencies of genotype GG, GA, AA in rs1045491 locus were 71.05% (378/532), 26.69% (142/532), 2.26% (12/532) in case group, and 80.45% (428/532), 18.42% (98/532), 1.13% (6/532) in control group, respectively (χ2=13.17, P0.01); the frequencies of genetype GG, GT, TT in rs2291778 locus were 53.38% (284/532), 40.23% (214/532), 6.39% (34/532) in case group, and were 25.94% (138/532), 63.91% (340/532), 10.15% (54/532) in control group (χ2=83.71, P0.01). TT genotype in rs14035 locus (OR=2.54, 95%CI: 1.19-6.32) and GA genetype in rs1045491 locus (OR=1.74, 95%CI: 1.08-2.66) were susceptible genotype of primary liver cancer, whereas GT (OR=0.52, 95%CI: 0.43-0.75) and TT genotype (OR=0.62, 95%CI: 0.46-0.86) in rs2291778 locus were protective genotype. Haplotype analysis showed that haplotype 3 (AACTGGGT) (OR=1.42, 95%CI: 1.10-1.82) and haplotype 5 (AGCCAGCC) increased the risk of occurrence of primary liver cancer (OR=1.36, 95%CI: 1.02-1.80), whereas haplotype 2 (AACTATCC) (OR=0.69, 95%CI: 0.52-0.91) and haplotype 6 (AACTGTGT)(OR=0.61, 95%CI: 0.45-0.81) decreased the risk. Subjects exposed to allele A of rs1045491, allele T of rs14035 and HBV infection intend to be the high risk population of primary liver cancer (OR = 3.72, 95%CI: 2.38 - 5.56).Genotypes of TT in rs14035 locus, and GA in rs1045491 locus may be susceptible genotypes of liver cancer carcinogenesis. T allele in rs2291778 locus is a non-susceptible allele of primary liver cancer. Combined effects of multigene alleles and multi-locus genotype may have a synergistic role in the carcinogenesis of liver cancer.

This paper defines the industrial symbiosis (IS) networks, points the factors that influence the development of IS networks in Industrial Parks, and discusses the mold that the networks can exist. Finally, the paper emphasizes that the factors should be coordination in industrial parks so as to make such networks stabilization and development step by step.

Parking demand forecast is the important part of static traffic issues. In this paper, fully considering the main influencing factors of parking demand, a parking demand forecasting model based on principal component analysis and BP neural network is established. In this model, the parking demand forecasting influencing factors are obtained by principal component analysis. The parking demand forecasting model is established based on BP neural network. Finally, the model is verified by an example.

Polyposis is an end form of chronic mucosal inflammation in a number of disorders and has an important impact on patient's life quality. Thymic stromal lymphopoietin (TSLP) is involved in many inflammatory processes such as asthma and allergic rhinitis (AR). The aim of this study is to elucidate the role of TSLP in the pathogenesis of polyposis.Ninety-four patients with nasal polyposis (NP) and/or allergic rhinitis (AR) were treated with inferior turbinectomy and polyp resection. Levels of TSLP in the nasal epithelial layer were measured; expression of TSLP receptor and OX40 ligand (OX40L) was assessed in isolated nasal mucosal dendritic cells (DC); tumor necrosis factor (TNF), interleukin (IL)-4 and interferon (IFN)-γ expressions were determined in isolated nasal mucosal CD4(+) T cells.The levels of TSLP in nasal epithelial layer were higher in the NP group than in the non-NP group. Higher expression of TSLP receptor and OX40L were detected in DCs of NP nasal mucosa. TNF-α(+) IL-4(+)CD4(+) T cells were detected in NP/AR nasal mucosa; TNF(+) IFN-γ(+) CD4(+) T cells were identified in NP/non-AR nasal mucosa. TSLP-primed DCs drove naive CD4(+) T cells to become TNF(+) IL-4(+) CD4(+) T cells, whereas TSLP/lipopolysaccharide-primed DCs induced naive CD4(+) T cells to become TNF(+) IFN-γ(+) T cells.The data indicate that TSLP is involved in the pathogenesis of polyposis.

To explore the risk factors of esophageal cancer (EC) in the high-incidence regions, so as to provide scientific evidence for taking effective prevention measures.A population based case-control family study was carried out. 1711 case family members in 505 families in which one of the couple or their first degree relatives suffered from EC were selected from high incidence in Henan province. Control families without neoplasm were selected from the same villages in matching conditions of age, sex, and family members. All information of case and control families was collected by Questionnaire of Life and Health of Inhabitant. The data were analyzed with logistic regression model.Compared with the control families,it was shown that hobby for smoked food [2.10% (36/1711), 0.82% (14/1711); chi2 = 9.82, P = 0.00; OR = 2.61, 95% CI: 1.40 - 4.85], hobby for fried food [7.17% (66/921), 3.91% (35/894) ; chi2 = 9.13, P = 0.00; OR = 1.90, 95% CI: 1.24 -2.89], hobby for raw and hard food [13.36% (123/921), 8.95% (80/894); chi2 = 8.87, P =0.03; OR =1.57, 95% CI: 1.16 - 2.11], and hobby for hot food [20.05% (343/1711), 15.20% (260/1711); chi2 = 13.87, P= 0.00; OR= 1.40, 95% CI: 1.17 - 1.67], the history with mental stimulated [6.72% (115/1711), 3.10% (53/1711); chi2 = 24.06, P = 0.00; OR = 2.25, 95% CI: 1.62 -3.14], upper digestive symptom history [19.40% (332/1711), 12.74% (218/ 1711); chi2 = 28.15, P = 0.00; OR= 1.65, 95% CI: 1.37 - 1.99] entered the last model, and were responsible for the higher risk of EC. Eating fast was shown to be a protective factor [20.85% (192/921), 25.14% (225/895); chi2 = 4.73, P =0.03; OR = 0.78, 95% CI: 0.63 - 0.98].EC is a kind of malignant tumor caused by multiple factors. Prevention and control of EC should be initiated from environmental factors, life style, genetic factors and social-psychological factors comprehensively.

AIM: To determine if disruption of the cagA gene of Helicobacter pylori (H pylori) has an effect on the expression of other proteins at proteome level. METHODS: Construction of a cagA knock out mutant Hp27_ΔcagA (cagA-) via homologous recombination with the wild-type strain Hp27 (cagA+) as a recipient was performed. The method of sonication-urea-CHAPS-DTT was employed to extract bacterial proteins from both strains. Soluble proteins were analyzed by two-dimensional electrophoresis (2-DE). Images of 2-DE gels were digitalized and analyzed. Only spots that had a statistical significance in differential expression were selected and analyzed by matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF-MS). Biological information was used to search protein database and identify the biological function of proteins. RESULTS: The proteome expressions between wild-type strain and isogenic mutant with the cagA gene knocked-out were compared. Five protein spots with high abundance in bacteria proteins of wild-type strains, down-regulated or absently expressed in bacteria proteins of mutants, were identified and analyzed. From a quantitative point of view, the identified proteins are related to the cagA gene and important antioxidant proteins of H pylori, including alkyl hydroperoxide reductase (Ahp), superoxide dismutase (SOD) and modulator of drug activity (Mda66), respectively, suggesting that cagA is important to maintain the normal activity of antioxidative stress and ensure H pylori persistent colonization in the host. CONCLUSION: cagA gene is relevant to the expressions of antioxidant proteins of H pylori, which may be a novel mechanism involved in H pylori cagA pathogenesis.