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The identification of high recurrence risk stage II colon cancer patients was critical to adjuvant chemotherapy decision. However, current definition of high-risk features remains inadequate. This study aimed to construct a model for predicting recurrence risk based on tumor enhancement ratio (TER) on abdominal contrast-enhanced CT scan.282 stage II colon cancer patients were included and randomly divided into training and validation sets in the ratio of 7:3. TER was calculated using maximum tumor attenuation value in contrast-enhanced CT scan divided by the minimum. Kaplan-Meier survival analyses were adopted to evaluate the prognostic value of variables. A model based on TER was built to predict recurrence risk through the LASSO Cox model. The recurrence risk score of patients was calculated based on this model.The optimal cut-off value of TER was 1.83 derived from the time-dependent ROC (tdROC) curve. Patients with high-TER showed increasingly poorer disease-free survival (DFS) in both training (p 0.001) and validation (p 0.001) sets. A model was built based on TER demonstrated satisfactory performance to recurrence risk prediction (C-index: 0.784 in the training set and 0.725 in the validation set). Patients were regrouped into modified high-risk and non-high risk according to recurrence risk score (cut-off value: 1.75) and a significant DFS difference was observed (training set: p 0.001; validation set: p 0.001).TER can serve as a high-risk feature of stage II colon cancer. And a model based on TER provided a new approach to assess recurrence risk of stage II disease.

An O2 self-evolving core-shell theranostic nanohybrid was developed by encapsulating a nanoenzyme cerium oxide (CeOx) in a metal-organic framework (MOF). The hybrid reveals a 9-fold higher apoptotic percentage than bare CeOx in a harsh hypoxic microenvironment through tandem homogenous catalysis. Simultaneously, the oxygen-promoted therapeutic efficiency was self-monitored by the hybrid with caspase-3 activation, paving the way for MOF-functionalized nanoenzymes in theranostics.

Intensive applications of toxic malathion pesticides bring a vital threat to the environment and health. Hence, a credible and sensitive strategy is urgently needed for the respective detection of malathion. In this work, an aptamer-based nonenzymatic autonomous DNA walking machine was fabricated for monitoring trace malathion contamination in cells and foods. Along with the machine walking driven by malathion-triggered reaction entropy, multiple fluorescent signal outputs were thermodynamically generated for signal amplification. The proposed stable DNA nanomachine achieved satisfactory results with a detection limit of 81.9 pg L

Purpose Cervical cancer metastasis results in poor prognosis and increased mortality, which is not separated from inflammatory reactions accumulated by prostaglandin E2 (PGE2). As a specific G-protein coupled PGE2 receptor, EP3 is demonstrated as a negative prognosticator of cervical malignancy. Now, we aimed to investigate the pathological mechanism of EP3 in modulating cervical cancer carcinogenesis. Methods Bioinformatics analysis was used to identify PAI-1 and uPAR correlations with EP3 expression, as well as the prognosis of cervical cancer patients. In vitro analyses were carried out to investigate the role of EP3 on cervical cancer proliferation and migration. Results In vitro studies showed that sulprostone (an EP3 agonist) enhanced the proliferation and migration of cervical cancer cells, whereas silencing of EP3 inhibited their proliferation and migration. Furthermore, EP3 knockdown increased the expression of plasminogen activator inhibitor type 1 (PAI-1), urokinase-type plasminogen activator receptor (uPAR), and phosphorylated extracellular signal-regulated kinases 1/2 (p-ERK1/2), but decreased p53 expression. Bioinformatics analysis showed that both PAI-1 and uPAR were correlated with EP3 expression, as well as the prognosis of cervical cancer patients. The survival analysis further showed that uPAR overexpression (IRS≥2) was correlated with a lower overall survival rate of cervical cancer patients with advanced stages (FIGO III-IV). Conclusion These results indicated that EP3 signaling pathway might facilitate the migration of cervical cancer cells through modulating uPAR expression. Therefore, EP3 and uPAR could represent novel therapeutic targets in the treatment of cervical cancer in advantaged stages.

Unexplained recurrent pregnancy loss (uRPL) is associated with macrophage polarization, which can be modulated by prostaglandin E2 (PGE2). Our previous study demonstrated that PGE2 receptor 3 (EP3) signaling is induced in the first-trimester placentas of uRPL patients compared with its expression in healthy controls. However, whether EP3 plays a role in macrophage polarization at the maternal-fetal interface of uRPL women remains unknown. The positive expression of EP3 in decidual macrophages was confirmed by double immunofluorescence staining in the first-trimester placentas collected from uRPL patients and healthy controls. Antibodies CD68, iNOS, and CD163 were used as immunofluorescence marker for decidual macrophages, M1, and M2 macrophages. To clarify the effects of EP3 on macrophage polarization, THP-1 monocyte cells were applied as M0 macrophages after phorbol 12-myristate 13-acetate (PMA) treatment for in vitro study. The mRNA levels of representative M1 markers (interleukin-1β and interleukin-6) and M2 markers (interleukin-10 and arginase-1) were quantified with qPCR in M0 macrophages being stimulated with sulprostone (an EP3 agonist) or L-798,106 (an EP3 antagonist). We found that EP3 expression was upregulated in the decidual macrophages of first-trimester placentas from uRPL patients compared with healthy controls. Furthermore, EP3 expression was increased in M1 macrophages compared with that in M2 macrophages in first-trimester placentas of uRPL patients. Sulprostone intensified the mRNA levels of IL-6 together with interferon-γ, whereas L-798,106 stimulated the mRNA expression of IL-10 and Arg-1 in a dose-dependent manner.

Andrographis paniculata (A. paniculata) is a traditional herbal medicine that has been widely used in Asian countries for hundreds of years. Andrographolide (AG) is a diterpene lactone extracted from A. paniculata. Owing to the in-depth study of pharmacological mechanisms, the therapeutic potential of AG, including its anti-inflammatory, anti-tumor, and immunoregulatory attributes, has attracted the attention of many researchers. Studies testing the therapeutic effects of AG have demonstrated desirable results in the treatment of a variety of clinical diseases. With high safety and various biological functions, AG might be a promising candidate for the treatment of musculoskeletal disorders. Here, we review all available literatures to summarize the pharmacological effects of AG and facilitate further researches on musculoskeletal diseases.

Obesity is a major epigenetic cause for colorectal cancer (CRC). Leptin is implicated in obesity-associated CRC, but the underlying mechanism remains unclear. The current study identified over-expression of metallopanstimulin-1 (MPS-1) in CRC patients through microarray and histological analysis, especially in obese CRC patients. MPS-1 was correlated with advanced tumor stage, suggesting its association with CRC progression. In addition, MPS-1 over-expression was associated with poor overall survival (OS) in obese CRC patients, but not in their non-obese counterparts, suggesting its potential as a prognostic marker of obese CRC patients. MPS-1 expression was positively associated with circulating leptin levels in CRC patients, especially in obese cases. Functional experiments demonstrated that MPS-1 silencing inhibited tumor proliferation and colony formation, and induced apoptosis of CRC cells in vitro. Converse results were obtained from the experiments with MPS-1 over-expression. Mechanistically, MPS-1 executed its action through induction of c-Jun N-terminal kinase (JNK)/c-Jun pathway. Moreover, the promotion effect of MPS-1 on CRC progression was modulated by leptin. In vivo studies demonstrated that MPS-1 silencing suppressed tumor growth of CRC via inhibiting JNK/c-Jun signaling. Collectively, this study indicates that MPS-1 promotes leptin-induced CRC via activating JNK/c-Jun pathway. MPS-1 might represent a potent candidate for the treatment and prognostic prediction of obesity-associated CRC.

Human liver cancers, including hepatocellular carcinomas and intra-hepatic cholangiocarcinomas, are often diagnosed late with poor prognosis. A better understanding of cancer initiation could provide potential preventive therapies and increase survival. Models for studying human liver cancer initiation are largely missing. Here, using directly reprogrammed human hepatocytes (hiHeps) and inactivation of p53 and RB, we established organoids possessing liver architecture and function. HiHep organoids were genetically engineered to model the initial alterations in human liver cancers. Bona fide hepatocellular carcinomas were developed by overexpressing c-Myc. Excessive mitochondrion-endoplasmic reticulum coupling induced by c-Myc facilitated hepatocellular carcinoma initiation and seemed to be a target of preventive treatment. Furthermore, through the analysis of human intra-hepatic cholangiocarcinoma-enriched mutations, we demonstrate that the RAS-induced lineage conversion from hepatocytes to intra-hepatic cholangiocarcinoma cells can be prevented by the combined inhibition of Notch and JAK-STAT. Together, hiHep organoids represent a system that can be genetically manipulated to model cancer initiation and identify potential preventive therapies.

Background We recently demonstrated the increased abundance of anti-trophoblast antibodies (ATAB) in sera of patients with unexplained recurrent miscarriages (uRM). Further, the ATAB-positive sera bound to JEG-3 human choriocarcinoma cells in vitro, resulting in decreased productions of β-human chorionic gonadotropin (β-hCG) and progesterone in these cells. However, the specific antigenic epitopes of ATAB have remained unknown. Therefore, it was the aim of this study to determine specific targets of ATAB in uRM patients. Methods Potential targets of ATAB were analyzed by 2-dimensional difference gel electrophoresis (2D-DIGE) and mass spectrometry, and thereby identifying α-Enolase (ENO1). ATAB targeting of ENO1 was further confirmed in a competitive binding assay. Levels of anti-ENO1 antibodies as well as β-hCG and progesterone were quantified with enzyme-linked immunosorbent assay (ELISA). Additionally, expression of ENO1 was analyzed in first trimester placentas by immunohistochemistry and immunofluorescence analysis. Findings We here identified ENO1 as a prominent target of ATAB. Serum levels of anti-ENO1 antibodies were increased in ATAB-positive compared to ATAB-negative patients. Further, increased expression of ENO1 and its co-expression with β-arrestin was found in the extra villous trophoblasts of uRM patients in first trimester placentas. In vitro, anti-ENO1 antibodies decreased the secretion of β-hCG and progesterone in JEG-3 and primary human villous trophoblast cells. Interpretation Serum anti-ENO1 antibodies might be an autoimmune biomarker for uRM. Targeting the formation of anti-ENO1 antibodies or inhibition of ENO1 expression could potentially represent therapeutic strategies for these patients. Fund All authors declare no conflict of interest. Yao Ye was supported by the China Scholarship Council. Hellen Ishikawa-Ankerhold and Christian Schulz were supported by the SFB914, projects Z01 and A10. None of the rest authors has any conflict of interest to declare.

The incidence of combined hepatocellular carcinoma-intrahepatic cholangiocarcinoma (cHCC-ICC) is relatively low, and the knowledge about the prognosis of cHCC-ICC remains obscure. In the study, we aimed to screen existing primary liver cancer staging systems and shed light on the prognosis and risk factors for cHCC-ICC.We retrospectively reviewed 206 cHCC-ICC patients who received curative surgical resection from April 1999 to March 2017. The correlation of survival measures with the histological types or with tumor staging systems was determined and predictive values of tumor staging systems with cHCC-ICC prognosis were compared.The histological type was not associated with overall survival (OS) (P = 0.338) or disease-free survival (DFS) (P = 0.843) of patients after curative surgical resection. BCLC, TNM for HCC, and TNM for ICC stages correlated with both OS and DFS in cHCC-ICC (all P 0.05). The predictive values of TNM for HCC and TNM for ICC stages were similar in terms of predicting postoperative OS (P = 0.798) and DFS (P = 0.191) in cHCC-ICC. TNM for HCC was superior to BCLC for predicting postoperative OS (P = 0.022) in cHCC-ICC.The TNM for HCC staging system should be prioritized for clinical applications in predicting cHCC-ICC prognosis.

Purpose Nonsteroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors (COXibs) inhibit the progression of endometrial cancer, ovarian cancer and cervical cancer. However, concerning the adverse effects of NSAIDs and COXibs, it is still urgent and necessary to explore novel and specific anti-inflammation targets for potential chemoprevention. The signaling of cyclooxygenase 2-prostaglandin E2-prostaglandin E2 receptors (COX-2-PGE2-EPs) is the central inflammatory pathway involved in the gynecological carcinogenesis. Methods Literature searches were performed to the function of COX-2-PGE2-EPs in gynecological malignancies. Results This review provides an overview of the current knowledge of COX-2-PGE2-EPs signaling in endometrial cancer, ovarian cancer and cervical cancer. Many studies demonstrated the upregulated expression of the whole signaling pathway in gynecological malignancies and some focused on the function of COX-2 and cAMP-linked EP2/EP4 and EP3 signaling pathway in gynecological cancer. By contrast, roles of EP1 and the exact pathological mechanisms have not been completely clarified. The studies concerning EP receptors in gynecological cancers highlight the potential advantage of combining COX enzyme inhibitors with EP receptor antagonists as therapeutic agents in gynecological cancers. Conclusion EPs represent promising anti-inflammation biomarkers for gynecological cancer and may be novel treatment targets in the near future.

Autophagy is an essential cellular process that is closely implicated in diverse pathophysiological processes and a variety of human diseases, especially tumors. Autophagy is regarded as not only an anti-cancer process in tumorigenesis but also a pro-tumor process in progression and metastasis according to current research. It means the role of autophagy in tumor is considered to be complex, controversial and context dependent. Hence, a comprehensive database is of great significance to obtain an in-depth understanding of such complex correlations between autophagy and tumor. To achieve this objective, here we developed the Autophagy and Tumor Database (named as ATdb, http://www.bigzju.com/ATdb/#/) to compile the published information concerning autophagy and tumor research. ATdb connected 25 types of tumors with 137 genes required for autophagy-related pathways, containing 219 population filters, 2650 hazard ratio trend plots, 658 interacting microRNAs, 266 interacting long non-coding RNAs, 155 post-translational modifications, 298 DNA methylation records, 331 animal models and 70 clinical trials. ATdb could enable users to search, browse, download and carry out efficient online analysis. For instance, users can make prediction of autophagy gene regulators in a context-dependent manner and in a precise subpopulation and tumor subtypes. Also, it is feasible in ATdb to cluster tumors into distinguished groups based on the gene-related long non-coding RNAs to gain novel insights into their potential functional implications. Thus, ATdb offers a powerful online database for the autophagy community to explore the complex world of autophagy and tumor. Database URL: http://www.bigzju.com/ATdb/#/

Background Meningioma, a neoplasm of the meninges, is usually a benign localized tumor. Extraneural metastasis is an extremely rare complication of meningiomas, and only a few cases have been reported to date. The present study reports a case of scalp metastasis of an atypical meningioma and discusses the types of atypical meningiomas and their management options. Case Description A 69-year-old man presented with scalp metastasis of an atypical meningioma. Six years after the right frontoparietal meningioma lesion was completely resected, an isolated subcutaneous metastasis developed at the right frontal region of the scalp, originating at the scar left by the first surgery. Postoperative histologic examination of the subcutaneous tumor revealed the features of an atypical meningioma. Conclusions This study highlights that resection of meningiomas is still associated with a risk of iatrogenic metastasis. Surgeons should carefully wash out the operative field and change surgical tools frequently to avoid the potential risk of metastasis.

Implantation consists of a complex process based on coordinated crosstalk between the endometrium and trophoblast. Furthermore, it is known that the microenvironment of this fetal–maternal interface plays an important role in the development of extravillous trophoblast cells. This is mainly due to the fact that tissues mediate embryonic signaling biologicals, among other molecules, prostaglandins. Prostaglandins influence tissue through several cell processes including differentiation, proliferation, and promotion of maternal immune tolerance. The aim of this study is to investigate the potential pathological mechanism of the prostaglandin E2 receptor 4 (EP4) in modulating extravillous trophoblast cells (EVTs) in unexplained recurrent marriage (uRM). Our results indicated that the expression of EP4 in EVTs was decreased in women experiencing uRM. Furthermore, silencing of EP4 showed an inhibition of the proliferation and induced apoptosis in vitro. In addition, our results demonstrated reductions in β- human chorionic gonadotropin (hCG), progesterone, and interleukin (IL)-6, which is likely a result from the activation of the cyclic adenosine monophosphate (cAMP)- cAMP-dependent protein kinase A (PKA)-phosphorylating CREB (pCREB) pathway. Our data might provide insight into the mechanisms of EP4 linked to trophoblast function. These findings help build a more comprehensive understanding of the effects of EP4 on the trophoblast at the fetal–maternal interface in the first trimester of pregnancy.

Recently our study identified EP3 receptor and galectin-3 as prognosticators of cervical cancer. The aim of the present study was the analysis of EP2 as a novel marker and its association to EP3, galectin-3, clinical pathological parameters and the overall survival rate of cervical cancer patients. Cervical cancer tissues (n = 250), as also used in our previous study, were stained with anti-EP2 antibodies employing a standardized immunohistochemistry protocol. Staining results were analyzed by the IRS scores and evaluated for its association with clinical-pathological parameters. H-test of EP2 percent-score showed significantly different expression in FIGO I-IV stages and tumor stages. Kaplan-Meier survival analyses indicated that EP3-negative/EP2-high staining patients (EP2 IRS score ≥2) had a significantly higher survival rate than the EP3-negative/EP2-low staining cases (p = 0.049). In the subgroup of high galectin-3 expressing patients, the group with high EP2 levels (IRS ≥2) had significantly better survival rates compared to EP2-low expressing group (IRS

Preeclampsia (PE) is characterized by hypertension and proteinuria. It affects about 5% to 8% of pregnancies and causes maternal and perinatal mortality and morbidity. The immune imbalance and excessive inflammatory response play vital roles in the pathogenesis of PE. In this study, we performed a case-control study to investigate the levels of cytokines, chemokines and adhesion molecules in serum and placenta of normal pregnant and PE women by Bio-Plex multiplex immunoassay and immunohistochemistry. In addition, we explored the phenotypes of monocyte and macrophage in peripheral blood and placentas in 2 groups by using flow cytometry analysis and immunohistochemistry. Our results show that pro-inflammatory factors, including interleukin-1β (IL-1β), IL-6, IL-7, IL-8, IL-17a, monocyte chemotactic protein 1 (MCP -1), and macrophage inflammatory protein 1β (MIP-1β) were significantly increased in serum of women with PE compared with controls. In addition, we detected that IL-1β, IL-6, and MCP-1 were also increased in placentas of women with PE. We further revealed that peripheral blood monocytes showed a pro-inflammatory M1-like phenotype in women with PE. Consistently, M1 macrophage infiltration was increased in placenta of women with PE compared to that of normal pregnant women. Our results demonstrated that immune imbalance promotes an inflammatory state during PE and it may be a potential therapeutic possibility for the management of PE.

The design of DNA-based logic circuits has become an active research field in DNA nanotechnology and holds great potential in intelligent bioanalysis. To date, although many DNA-based logic systems have been realized, the implementation of advanced logic functions is still challenging, especially with simple and homogeneous compositions. Herein, by integrating two DNA tetraplex structures (G-quadruplex and i-motif), a completely label-free logic platform with high scalability was established, with which a series of advanced functions were realized, including arithmetic (adders and subtractors) and nonarithmetic ones (majority and dual-transfer gates). Furthermore, the platform was also applied as an intelligent biosensor to coanalyze two cancer-related micro-RNAs with high sensitivities and specificities. Considering the excellent versatility, expandability, and biocompatibility, the platform may promote the development of DNA computing and hold great potential in multiparameter sensing and medical diagnosis.

Peroxisome proliferator-activated receptors (PPARα, PPARβ/δ, and PPARγ) belong to the transcription factor family, and they are highly expressed in all types of trophoblast during pregnancy. The present review discusses currently published papers that are related to the regulation of PPARs via lipid metabolism, glucose metabolism, and amino acid metabolism to affect trophoblast physiological conditions, including differentiation, maturation, secretion, fusion, proliferation, migration, and invasion. Recent pieces of evidence have proven that the dysfunctions of PPARs in trophoblast lead to several related pregnancy diseases such as recurrent miscarriage, preeclampsia, intrauterine growth restriction, and gestational diabetes mellitus. Moreover, the underlying mechanisms of PPARs in the control of these processes have been discussed as well. Finally, this review’s purposes are to provide more knowledge about the role of PPARs in normal and disturbed pregnancy with trophoblast, so as to find PPAR ligands as a potential therapeutic target in the treatment and prevention of adverse pregnancy outcomes.

Backgroud Prostaglandin E2 (PGE2), an inflammatory mediator, modulates cytokines, regulates immune responses in reproductive processes and stimulates inflammatory reactions via the prostaglandin E2 receptor 2 (EP2). However, the regulatory effects of EP2 signaling on trophoblasts and its role in unexplained recurrent miscarriage (uRM) remains unclear. Patients and methods A total of 19 placentas from patients with a history of more than two consecutive pregnancy losses of unknown cause (uRM group) and placentas of 19 healthy patients following a legal termination of their pregnancy were used for PGE2 receptor (EP1, EP2 and EP4) expression analyses via immunohistochemistry. Double immunofluorescence was also used to identify EP2 expressing cells in the decidua. Finally, HTR-8/SVneo cells were used to clarify the role of EP2 in in vitro experiments. Results The expression of EP2 and EP4 was found to be reduced in the syncytiotrophoblast and decidua of uRM patients. A selective EP2 receptor antagonist (PF-04,418,948) reduced the proliferation and secretion of s-hCG, inhibited interleukin -6 (IL-6) and interleukin-8 (IL-8) and up-regulated the production of the tumor necrosis factor-α (TNF-α) and plasminogen activator inhibitor type 1 (PAI-1) in HTR-8/SVneo cells in vitro. Conclusion PGE2-EP2 signaling pathway may represent a novel therapy option for uRM. The involvement of EP2 in uRM acts perhaps via inflammatory cytokines and indicates that the PGE2-EP2 signaling pathway might represent an unexplored etiology for uRM.

The proteins BAFF, ST6GALNAC2, C1GALT1, and COSMC in peripheral blood mononuclear cells (PBMCs) and plasma levels of IgA1 and galactose-deficient IgA1 (Gd-IgA1) are potential biomarkers for IgAN nephropathy. In this study, we comparatively studied the changes of those biomarkers before and after tonsillectomy.Peripheral blood samples were obtained from 16 IgAN patients with pre- and post-tonsillectomy. IgAN was diagnosed based on results from analysis of percutaneous renal biopsy tissue. Peripheral blood samples from three patients without renal diseases (non-IgAN), before and after tonsillectomy, and 16 healthy controls were also examined. BAFF, ST6GALNAC2, C1GALT1, and COSMC mRNA levels in PBMCs were detected using real-time PCR. Plasma IgA1 content was measured by ELISA. Gd-IgA1 levels were determined using the VV lectin-ELISA method.BAFF, ST6GALNAC2, C1GALT1, and COSMC mRNA levels and the plasma concentrations of IgA1 and Gd-IgA1 in IgAN patients before tonsillectomy were significantly higher than those in healthy controls (P 0.05). Tonsillectomy significantly increased the expression of BAFF and ST6GALNAC2, and plasma IgA1 level, while it downregulated that of C1GALT1 and COSMC (P 0.05). However, in non-IgAN patients, tonsillectomy did not affect the mRNA levels of BAFF, ST6GALNAC2, C1GALT1, and COSMC, plasma IgA1 content and Gd-IgA1 level. Positive correlations were established between BAFF and IgA1 (r = 0.604, P 0.01) and between ST6GALNAC2 and Gd-IgA1 (r = 0.623, P 0.01).Tonsillectomy changes the mRNA levels of BAFF, ST6GALNAC2, C1GALT1, and COSMC in PBMCs, as well as the plasma IgA1 level in IgAN patients. BAFF and ST6GALNAC2 might regulate IgA1 secretion and O-glycosylation.

Rab3D belongs to Rab protein family. Previous reports showed that the expression of Rab3D was dysregulated in various types of cancer. Rab3D belongsRab3D belongs. However, little is known about the role of Rab3D in carcinogenesis and progression of colorectal cancer (CRC). Here, we first evaluated the expression of Rab3D in 32 fresh CRC and matched normal tissues and found Rab3D was dramatically increased in CRC tissues compared to normal tissues (p

By evaluating extent of tumour enhancement on preoperative contrast-enhanced MDCT, we aimed to establish an imaging-based model to predict cancer-specific survival in stage I–III colon cancer. A total of 548 stage I–III colon cancer patients who underwent curative resection from 2007 to 2013 were retrospectively included and divided into primary cohort and validation cohort according to admission time. The attenuation coefficient of each colon cancer was measured on the workstation by drawing the ROI in CT images. The enhancement ratio was calculated using maximum tumour attenuation value in triphasic MDCT scanning divided by the minimum. Patients were divided into low/high-enhancement groups according to the optimal cut-off value derived from time-dependent ROC curve. Kaplan–Meier method and COX regression analysis were adopted to evaluate prognostic value of variables. A nomogram for prognosis was conducted on the basis of a multivariate Cox proportional hazard model. No significant differences were observed in age, sex, pTNM stage, perioperative chemoradiotherapy, serum CEA, tumour size, tumour localisation and histologic type between low- and high-enhancement groups. The high-enhancement group had a significantly shorter cancer-specific survival rate (69.5%) than the low-enhancement group (85.9%) (p < 0.001). Subgroup analysis indicated that high-enhancement state was closely associated with increased risk of colon cancer mortality in stage I (p = 0.033), stage II (p = 0.002) and stage III (p = 0.014). Cox regression analysis indicated the extent of enhancement was an independent prognostic factor (HR 2.258, 95% CI 1.476–3.455; p < 0.001). The extent of tumour enhancement on MDCT can serve as a potential risk factor for stage I–III colon cancer. • Survival rates of stage I–III colon cancer vary widely even within the same stage. • Prognostic value of the extent of tumour enhancement on MDCT was assessed. • The high-enhancement group had a significantly shorter cancer-specific survival rate.

summary Background & aims: The association between dietary vitamin A, retinol intake and blood retinol level and gastric cancer risk has been investigated by many studies. However, the results of these studies were controversial. The aim of our study was to systematically assess this issue. Methods: PUBMED and EMBASE were searched, supplemented with manual-screening for relevant publications. Meta-analyses were performed to evaluate the association between vitamin A, retinol dietary intake or blood retinol level and gastric cancer risk. Results: Thirty-one studies were included in this meta-analysis. Comparing the highest with the lowest categories, vitamin A intake significantly reduced gastric cancer risk (pooled RR ¼ 0.66, 95% CI: 0.52 e0.84), whereas a marginally inverse association was found between retinol intake (pooled RR ¼ 0.94, 95% CI: 0.87e1.03) or blood retinol level (pooled RR ¼ 0.87, 95% CI: 0.73e1.05) and gastric cancer risk. Interestingly, the results of subgroup analysis indicated that high vitamin A intake and blood retinol level were associated with reduced gastric cancer risk in Western countries, while a marginally inverse association was found between retinol and gastric cancer risk in Western countries. Conclusions: Vitamin A intake was inversely associated with gastric cancer risk, while no significant association was found with retinol intake or blood retinol level.

Background: We aimed to systematically summarize the diagnostic and prognostic value of circulating/tissue miR21 in patients with colorectal cancer. Methods: An original study was conducted to explore the potential value of circulating miR21 in colorectal cancer diagnosis and tissue miR21 in colorectal cancer prognosis. PUBMED and EMBASE were searched (to August, 2013) to identify eligible studies. To explore the diagnostic performance of circulating miR21, meta-analysis methods were used to pool sensitivity, specificity, positive and negative likelihood ratio, diagnostic OR and to construct a summary ROC curve. For prognostic meta-analysis, study-specific HRs of tissue miR21 for survival were summarized. Subgroup and sensitivity analyses were applied to explore heterogeneity. Results: Finally, 14 studies (including our study) were included in the meta-analyses. The pooled sensitivity, specificity, and AUC of circulating miR21 were 0.76 [95% confidence interval (CI), 0.59–0.88], 0.81 (95% CI, 0.76–0.85), and 0.81 (95% CI, 0.78–0.85) in diagnosing colorectal cancer. Patients with higher expression of tissue miR21 had significant inferior overall survival (OS; pooled HR, 1.56; 95% CI, 1.16–2.11) and disease-free survival (DFS; pooled HR, 1.35; 95% CI, 1.08–1.69). The individual participant data (IPD) meta-analysis demonstrated that tissue miR21 level was independently associated with worse colorectal cancer OS (HR, 1.69; 95% CI, 1.07–2.67; P = 0.023), whereas this association seems to be confined to males (P = 0.007) but not for females (P = 0.845). Conclusions: Circulating miR21 level has potential value for colorectal cancer early detection, whereas high tissue miR21 level is associated with adverse colorectal cancer prognosis. Impact: miR21 is a promising biomarker for early detection and prognosis of colorectal cancer. Cancer Epidemiol Biomarkers Prev; 23(12); 2783–92. ©2014 AACR.

In recent years, a vast amount of studies have centered on the role of vitamin D in the pathogenesis of certain types of cancers such as breast, colorectal and lung cancer. Increasing evidence suggests that vitamin D and its receptor play a crucial role in the development of gynecological cancers. In this review, we systematically analyzed the effect of vitamin D and the vitamin D receptor on endometrial, ovarian, cervical, vulvar and vaginal cancer. Our literature research shows that vitamin D levels and vitamin-D-related pathways affect the risk of gynecological cancers. Numerous ecological studies give evidence on the inverse relationship between UVB exposure and gynecological cancer risk. However, epidemiologic research is still inconclusive for endometrial and ovarian cancer and insufficient for rarer types of gynecological cancers. The vitamin D receptor (VDR) is upregulated in all gynecological cancers, indicating its influence on cancer etiology. The VDR polymorphism FokI (rs2228570) seems to increase the risk of ovarian cancer. Other nuclear receptors, such as the RXR, also influence gynecological cancers. Although there is limited knowledge on the role of the VDR/RXR on the survival of endometrial, cervical, vulvar or vaginal cancer patients, some studies showed that both receptors influence survival. Therefore, we suggest that further studies should focus on the vitamin D- and its hetero dimer receptor RXR in gynecological cancers.

Purpose To investigate the impact of ovarian stimulation and hormone replacement treatment on key regulatory cytokines in endometrial secretion during endometrium implantation window. Methods Fifty-six patients undergoing ovarian stimulation (OS) with gonadotropin releasing hormone antagonist and frozen embryo transfer with hormone replacement treatment (HRT) were recruited. Endometrial secretion aspiration was performed repeatedly during implantation window in natural, OS and HRT cycles of every patient. The concentrations of 17 mediators, known to be involved in human embryo implantation, were assessed by multiplex immunoassay. Results Compared with natural cycle (NC), the concentration of IFN-γ, G-CSF and IL-8 within endometrium were almost the same following OS and HRT. Furthermore, increased MCP-1 levels were observed following HRT and OS. In addition, an increase in IL-1b, IL-7, IL-17, IL-6, TNF-a, IL-12, IL-4, IL-13, IL-10, IL-5, VEGF and MIP-1b concentrations were found in OS cycle only. The level of GM-CSF was lower in HRT cycle and higher in OS cycle, when compared with NC. Among all 17 cytokines, no correlation was found between cytokine concentrations and serum estradiol and progesterone, while only IL-7 concentration has a low correlation with serum LH level. Conclusion Compared to natural and hormone replacement cycle, patients’ endometrium cytokine profiles present an increased inflammatory response following ovarian stimulation.

Normal pregnancy is a state of hypercoagulability with diminishing fibrinolytic activity, which is mainly caused by an increase of plasminogen activator inhibitor type 1 (PAI-1). PAI-1 is the main inhibitor of plasminogen activators, including tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA). In human placentas, PAI-1 is expressed in extravillous interstitial trophoblasts and vascular trophoblasts. During implantation and placentation, PAI-1 is responsible for inhibiting extra cellular matrix (ECM) degradation, thereby causing an inhibition of trophoblasts invasion. In the present study, we have reviewed the literature of various reproductive diseases where PAI-1 plays a role. PAI-1 levels are increased in patients with recurrent pregnancy losses (RPL), preeclampsia, intrauterine growth restriction (IUGR), gestational diabetes mellitus (GDM) in the previous pregnancy, endometriosis and polycystic ovary syndrome (PCOS). In general, an increased expression of PAI-1 in the blood is associated with an increased risk for infertility and a worse pregnancy outcome. GDM and PCOS are related to the genetic role of the 4G/5G polymorphism of PAI-1. This review provides an overview of the current knowledge of the role of PAI-1 in reproductive diseases. PAI-1 represents a promising monitoring biomarker for reproductive diseases and may be a treatment target in the near future.

To study the effects of ultrasound guided inter-scalene brachial plexus block and patient-controlled infraclavicular brachial plexus block for postoperative pain and surgical efficacy in patients with terrible tyriad of the elbow.From March 2015 to August 2016, 60 patients with terrible tyriad of the elbows were treated in Ningbo No.6 Hospital with ASA I to II internal fixation. There were 32 males and 28 females, ranging in age from 16 to 70 years old, with a mean age of (55.6±18.2) years old. All the patients were divided into two groups(30 cases in each group): controlled intermuscular groove brachial plexus block (group C), infraclavicular brachial plexus block(group I). All catheters were placed using ultra-sound visualization and injected 0.33% ropivacaine 30 ml preoperatively. After regaining consciousness, all patients connected the electronic pump. The solution contained 0.2% ropiva-caine and the pump was setup to deliver a 5 ml bolus dose, with a 15 min lock out interval and background infusion at 5 ml/h. Both analgesia lasted until 5 d after operation. The patients underwent rehabilitation exercise everyday for 5 consecutive days starting from 24 h after operation.VAS score was recorded at 24 h, 48 h, 72 h and 4 d, 5 d after operation during rest and rehabilitation exercise time. The elbow articular range of motion and Mayo elbow performance score (MEPS) were recorded at 6 d after operation. Catheter-related adversereactions (such as oozing from the insertion site, obstruction, prolapse) were recorded.The success rate of blockade was 100% during insertion in both groups. Compared with group C, the VAS score at 3 d during rest time and 3, 4, 5 d after operation during rehabili-tation exercise were decreased(2.5±0.5 vs. 3.8±1.1, 3.0±0.4 vs. 5.0±0.9, 2.5±0.4 vs. 4.5±1.2, 2.1±0.3 vs. 4.1±1.0,Patient-controlled infraclavieular brachial plexus block can be effectively used for postoperative pain after fixation for terrible tyriad of the elbows, and it can increase surgical outcome.

The objective of the present study was to systematically assess the association between dioxin/2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and cancer incidence and mortality. Systematic literature searches were conducted until July 2015 in Pubmed, Embase and Cochrane library to identify relevant studies. A random-effects model was applied to estimate the pooled odds ratio (OR), risk ratio (RR), standard incidence ratio (SIR) or standard mortality ratio (SMR) for cancer incidence or mortality. In addition, dose-response, meta-regression, subgroup, and publication bias analyses were conducted. Thirty-one studies involving 29,605 cancer cases and 3,478,748 participants were included. Higher external exposure level of TCDD was significantly associated with all cancer mortality (pooled SMR = 1.09, 95% CI: 1.01–1.19, p = 0.04), but not all cancer incidence (pooled RR = 1.01, 95% CI: 0.97–1.06, p = 0.49). Higher blood level of TCDD was both significantly associated with all cancer incidence (pooled RR = 1.57, 95% CI: 1.21–2.04, p = 0.001) and all cancer mortality (pooled SMR = 1.45, 95% CI: 1.25–1.69, p

To provide insights into the correlation among lipid metabolism, cytokine profiles in the follicular fluid (FF) and embryo quality of women with Polycystic Ovary Syndrome (PCOS) with metabolic syndrome (MS).Ninety women undergoing in vitro fertilization (IVF) treatment were recruited, including 60 PCOS patients (PCOS non MS and PCOS MS) and 30 age-matched controls. Individual FF samples were analyzed using the cytometric multiplex immunoassay.In the FF, the PCOS MS group was associated with higher, total cholesterol (TC), triglyceride (TG) and lower high-density lipoprotein (HDL) concentrations compared with that in the control group (P0.05). The FF tumor necrosis factor-α (TNF-α) level in the PCOS MS group was 3.89±1.18ng/mL, which was significantly higher compared with the control (2.94±1.02ng/mL) and PCOS non-MS groups (3.05±1.21ng/mL) (P=0.002), while the granulocyte colony-stimulating factor (G-CSF) level in the PCOS MS group (4.18±1.33ng/mL) was lower compared with the control (5.61±1.82ng/mL) and PCOS non-MS groups (5.32±1.91ng/mL) (P=0.004). The FF G-CSF showed a trend toward negative relationship with TG and TC; TNF-α concentration was positively associated with TG. The percentage of top-quality embryo decreased in the PCOS MS group than in the other two groups (20% vs. 38.4% and 34.6%).In conclusion, there was an elevated lipolysis condition within the FF of PCOS MS patients and the TNF-α and G-CSF levels in FF were associated with top-quality embryo percentage. TNF-α and G-CSF may be the key cytokines involved in the mechanism of decreased embryo development potential in PCOS MS patients.

Objectives Independent epidemiological studies have evaluated the association between markers of glucose metabolism (including fasting glucose, fasting insulin, homeostasis model of risk assessment-insulin resistance (HOMA-IR), glycated haemoglobin (HbA1c) and C peptide) and the risk of colorectal cancer (CRC). However, such associations have not been systematically analysed and no clear conclusions have been drawn. Therefore, we addressed this issue using a meta-analysis approach. Design Systematic review and meta-analysis. Data sources PubMed and EMBASE were searched up to May 2015. Primary and secondary outcome measures Either a fixed-effects or random-effects model was adopted to estimate overall ORs for the association between markers of glucose metabolism and the risk of CRC. In addition, dose–response, meta-regression, subgroup and publication bias analyses were conducted. Results 35 studies involving 25 566 patients and 5 706 361 participants were included. Higher levels of fasting glucose, fasting insulin, HOMA-IR, HbA1c and C peptide were all significantly associated with increased risk of CRC (fasting glucose, pooled OR=1.12, 95% CI 1.06 to 1.18; fasting insulin, pooled OR=1.42, 95% CI 1.19 to 1.69; HOMA-IR, pooled OR=1.47, 95% CI 1.24 to 1.74; HbA1c, pooled OR=1.22, 95% CI 1.02 to 1.47 (with borderline significance); C peptide, pooled OR=1.27, 95% CI 1.08 to 1.49). Subgroup analysis suggested that a higher HOMA-IR value was significantly associated with CRC risk in all subgroups, including gender, study design and geographic region. For the relative long-term markers, the association was significant for HbA1c in case–control studies, while C peptide was significantly associated with CRC risk in both the male group and colon cancer. Conclusions The real-time composite index HOMA-IR is a better indicator for CRC risk than are fasting glucose and fasting insulin. The relative long-term markers, HbA1c and C peptide, are also valid predictors for CRC risk. Considering the included case–control studies in the current analysis, more cohort studies are warranted to enhance future analysis.

The purpose of this double-blind, randomised trial was to compare the clinical performance of a hybrid composite (Clearfil AP-X, Kuraray, Tokyo) and a nanocomposite (Filtek Z350, 3M ESPE, St. Paul, MN) over a period of 2 years in non-carious class V lesions using a modified US Public Health Service (USPHS) system.Forty-six patients with at least one pair of equivalent non-carious cervical lesions under occlusion and a mean age of 44.1 years (range 27-66 years; median 45 years) were enrolled in this study. A total of 116 restorations (58 with each material) were placed according to manufacturer's instructions by two calibrated operators. The restorations were evaluated at baseline and at 6, 12 and 24 months after placement using the USPHS criteria for retention, colour match, marginal discolouration, marginal adaptation, anatomic form, surface texture and secondary caries. Statistical analysis was conducted using the Cochran and the McNemar tests at a significance level of 5% (P 0.05).No surface texture changes or secondary caries were detected in association with any restorations. The retention rates for Clearfil AP-X (100%) and for Filtek Z350 (91.38%) did not differ significantly (P 0.05). Two Z350 restorations were completely lost after 2 years. No significant differences were observed in the colour match, marginal discolouration, marginal adaptation or anatomic form.There were no significant differences in the clinical performances between the materials.Both restorative materials exhibited acceptable clinical performance in class V non-carious lesions 2 years post-restoration.

Aims/Introduction Type 2 diabetes is a metabolic disease characterized by insulin resistance, and is associated with the effects of genetic and environmental factors. The present study aimed to not only analyze the influence of a single factor for type 2 diabetes, but also to investigate the interaction effects between risk factors. Materials and Methods A total of 6,660 individuals selected by the method of cluster random sampling accepted a cross-sectional survey (questionnaire investigation, physical measurement, laboratory examination and liver ultrasound examination). The classification tree was used to analyze the risk factors and their interactions in type 2 diabetes. The clinical and metabolic characteristics were compared between type 2 diabetes patients and controls, and the non-conditional logistic regression model was used to quantitatively analyze the interactions. Results A total of 338 participants were classified as type 2 diabetes (217 men and 121 women), the classification tree model showed three variables with close associations with type 2 diabetes: age, triglycerides (TG) and non-alcoholic fatty liver disease (NAFLD). Type 2 diabetes patients had higher age and incidences of high TG, NAFLD, hypertension, high body mass index, high uric acid, high total cholesterol, high low-density lipoprotein cholesterol and low high-density lipoprotein cholesterol. The multivariate logistic regression analysis showed that the following factors had interactions in type2 diabetes: high TG × advanced age (odds ratio 2.499, 95% confidence interval 1.868–3.344, P = 0.000), NAFLD × advanced age (odds ratio 1.250, 95% confidence interval 1.048–1.491, P = 0.013) and NAFLD × high TG (odds ratio 1.349, 95% confidence interval 1.144–1.590, P = 0.000). Conclusions The present study showed that type 2 diabetes resulted from the interactions of many factors; the interactions among age, TG and NAFLD are important risk factors for type 2 diabetes.

Vitamin D, besides its classical role in bone metabolism, plays a distinct role in multiple pathways of the feto-maternal unit. Calcitriol is the major active ligand of the nuclear vitamin D receptor (VDR). The vitamin D receptor (VDR) is expressed in different uteroplacental parts and exerts a variety of functions in physiologic pregnancy. It regulates decidualisation and implantation, influences hormone secretion and placental immune modulations. This review highlights the role of the vitamin D receptor in physiologic and disturbed pregnancy, as preeclampsia, fetal growth restriction, gestational diabetes and preterm birth. We discuss the existing literature regarding common VDR polymorphisms in these pregnancy disorders.

We previously demonstrated that the detection of circulating cancer cells (CCC) expressing survivin mRNA could provide valuable information for predicting metastasis and recurrence in breast cancer. The objective of this study was to investigate the significance of detecting survivin-expressing CCC on the clinical outcomes of patients with non-small cell lung cancer (NSCLC). Peripheral blood samples collected from 143 NSCLC patients and 177 healthy volunteers were quantitatively evaluated using a technique developed in our laboratory that detected reverse transcription-polymerase chain reaction (RT-PCR) products based on a hybridisation-enzyme linked immunosorbant essay (ELISA), which we called RT-PCR ELISA. The presence of survivin-expressing CCC was detected in 63 cancer patients (44.1%) and was significantly associated with pathological T classification, nodal status, and disease stages (all P < 0.001). During a follow-up period of 36 months, patients who had positive survivin expressions at the time of the initial assay test had a higher relapse rate and shorter survival time when compared to those who had negative survivin expressions (all P < 0.001). Through multivariate analysis, the detection of survivin-expressing CCC was found to be an independent predictor for cancer recurrence (HR = 43.5; 95% CI = 2.67–70.9; P = 0.008) and survival (HR = 1.35; 95% CI = 1.02–4.31; P = 0.049). Thus, detection of survivin-expressing CCC could be used in the prediction of disease recurrence as well as in the prognosis of NSCLC.

The association between dietary carbohydrate intake, glycemic index (GI) and glycemic load (GL), and risk of gastric cancer (GC) has been investigated by many studies. However, the results of these studies were controversial. The aim of our study was to systematically assess this issue. PUBMED and EMBASE were searched up to March 2015, and either a fixed- or a random-effects model was adopted to estimate overall relative risks (RRs). Dose–response, meta-regression, subgroup, and publication bias analyses were applied. Twenty-six studies with approximately 540,000 participants were finally included in this meta-analysis. High level of dietary carbohydrate intake (pooled RR 1.17, 95 % CI 0.91–1.50), GI (pooled RR 1.17, 95 % CI 0.80–1.69), and GL (pooled RR 1.06, 95 % CI 0.90–1.26) were all nonsignificantly associated with incidence of GC. In addition, no significant dose–response relationship was observed between carbohydrate intake, GI and GL, and the risk of GC. However, further subgroup analyses based on gender and geographic region suggested a significant association between higher carbohydrate intake (pooled RR 1.52, 95 % CI 1.10–2.08), GL (pooled RR 1.41, 95 % CI 1.04–1.92), and GC risk in males subgroup, and between higher carbohydrate intake (pooled RR 1.69, 95 % CI 1.36–2.09) and GC risk in Asian studies. No significant association was found between dietary carbohydrate intake, GI and GL, and risk of GC. However, significantly positive association was observed in the males subgroup and Asian studies.

We know that one of the main risk factors for cervical cancer is an infection with high-risk human papillomavirus (HR-HPV). Prostaglandins and their receptors are very important for the tumour growth and tumour-associated angiogenesis. Little is known about the expression of the Prostaglandin E receptor type 3 (EP3) or the Prostaglandin (PG)E2-EP3 signalling in cervical cancer, so the aim of the study was to analyse the expression of the EP3 receptor in cervical cancer and find prognostic factors in relation to survival; EP3 immunohistological staining of 250 cervical cancer slides was performed and analysed with a semi-quantitative score. The statistical evaluation was performed with Statistical Package for the Social Sciences (SPSS) to evaluate the staining results and the survival analyses of the cervical cancer cases. A significant difference was observed in EP3 expression in Fédération Internationale de Gynécologie et d’Obstétrique (FIGO) stadium I versus FIGO stadium II–IV cases. High expression of EP3 (IRS ≥ 1.5) in cervical cancer patients was correlated with poor prognosis in overall survival rates. Survival in adenocarcinoma (AC) of the cervix was lower than in squamous cell carcinoma (SCC). Cox regression analysis shows that EP3 is an independent prognosticator. In this study we could show that the membrane-bound prostaglandin receptor EP3 is an independent prognosticator for cervical cancer patient survival. Targeting the EP3 receptor seems to be an interesting candidate for endocrine therapy. Therefore, more research is needed on the influence of the receptor system and its influence on cervical cancer growth.

Objective The objective of this meta-analysis was to systematically assess the survival benefit of aspirin use before or after diagnosis for patients with colorectal cancer (CRC). Design Relevant studies were identified through searching PubMed, Embase and Cochrane databases before May 2014. Two investigators extracted data independently for baseline characteristics and outcomes from the included studies. Either a fixed-effects or a random-effects model was derived to composite the pooled HR for overall mortality and CRC-specific mortality of CRC. Results Seven studies on postdiagnosis aspirin therapy and seven studies on prediagnosis aspirin use were finally included in this meta-analysis. The overall survival benefit associated with postdiagnosis aspirin use represented an HR of 0.84 (95% CI 0.75 to 0.94). This effect was observed both in colon cancer (HR=0.78, 95% CI 0.64 to 0.96) and in rectal cancer (HR=0.90, 95% CI 0.83 to 0.98). Besides, the survival benefit of postdiagnosis aspirin use appeared to be confined to those patients with positive prostaglandin endoperoxide synthase 2 (PTGS2, also known as cyclooxygenase-2, COX-2) expression (HR=0.65, 95% CI 0.50 to 0.85) and with mutated PIK3CA tumours (HR=0.58, 95% CI 0.37 to 0.90). Aspirin use postdiagnosis was not associated with CRC-specific mortality (HR=0.77, 95% CI 0.52 to 1.14). We observed no evidence of an association between prediagnosis aspirin use and CRC overall mortality (HR=1.01, 95% CI 0.96 to 1.06) or CRC-specific mortality (HR=0.93, 95% CI 0.82 to 1.05). Conclusions These findings provide further indication that postdiagnosis aspirin therapy improved CRC overall survival, especially for patients with positive PTGS2 (COX-2) expression and mutated PIK3CA tumours.

Summary Background & aims Association between zinc intake and digestive tract cancers risk has been reported in several epidemiological studies, while the results were controversial. The aim of our study was to get a systemic review of this issue. Methods PUBMED and EMBASE were searched up to April 2013, supplemented with manual-screening for relevant articles. Two independent reviewers independently extracted data from eligible studies, risk ratio (RR) or odds ratio (OR) with 95% CIs for the highest versus lowest categories of zinc intake was adopted. Either a fixed- or a random-effects model was adopted to estimate overall odds ratios. Besides, dose–response, subgroup, and publication bias analyses were applied. Results Nineteen studies with approximately 400,000 participants were included in this meta-analysis. The pooled relative risk (RR) of overall digestive tract cancers for the highest versus lowest categories of zinc intake was 0.82 (95% CI: 0.70–0.96; p = 0.013). Comparing the highest with lowest categories, higher zinc intake was significantly associated with reduced colorectal cancer risk (pooled RR = 0.80, 95% CI: 0.70–0.92; p = 0.002), while zinc intake was not statistically associated with gastric cancer risk (pooled RR = 0.91, 95% CI: 0.64–1.29; p = 0.581) or esophageal cancer risk (pooled RR = 0.72, 95% CI: 0.44–1.17; p = 0.187). However, subgroup analyses showed that zinc intake was significantly associated with esophageal cancer risk and gastric cancer risk in Asia, but not in America and Europe. Conclusions Dietary zinc intake was inversely associated with digestive tract cancers, especially colorectal cancer risk in this study.

Background A generally acceptable definition and a severity grading system for anastomotic leakages (ALs) following rectal resection were not available until 2010, when the International Study Group of Rectal Cancer (ISGRC) proposed a definition and a grading system for AL. Methods A search for published data was performed using the MEDLINE database (2000 to December 5, 2012) to perform a systematic review of the studies that described AL, grade AL according to the grading system, pool data, and determine the average rate of AL for each grade after anterior resection (AR) for rectal cancer. Results A total of 930 abstracts were retrieved; 40 articles on AR, 25 articles on low AR (LAR), and 5 articles on ultralow AR (ULAR) were included in the review and analysis. The pooled overall AL rate of AR was 8.58% (2,085/24,288); the rate of the asymptomatic leakage (Grade A) was 2.57%, that of AL that required active intervention without relaparotomy (Grade B) was 2.37%, and that of AL that required relaparotomy (Grade C) was 5.40%. The pooled rate of AL that required relaparotomy was higher in AR (5.40%) than in LAR (4.70%) and in ULAR (1.81%), which could be attributed to the higher rate of protective defunctioning stoma in LAR (40.72%) and ULAR (63.44%) compared with that in AR (30.11%). Conclusions The new grading system is simple that the ALs of each grade can be easily extracted from past publications, therefore likely to be accepted and applied in future studies.

Supplemental Digital Content is available in the text, The application of serum interleukin-6 (IL-6) in the diagnosis and prognosis of colorectal cancer (CRC) has been evaluated in many studies, whereas the results were contradictive. The aim of this study was to systematically evaluate this issue. An original study was conducted to explore the diagnostic value of serum IL-6 in CRC. Pubmed, Embase, and Cochrane library databases were searched for eligible studies. For diagnostic meta-analysis, aggregate data (AD) and individual participant data (IPD) meta-analyses were both adopted. The sensitivity and specificity were pooled and a summary receiver-operating characteristic (ROC) curve was constructed. For prognostic meta-analysis, study-specific hazard ratios (HRs) of IL-6 for survival were summarized. Secondary analysis of survival data was performed to synthesize the Kaplan–Meier curves. Total 17 studies (including our study) were included in this meta-analysis. The pooled sensitivity, specificity, and area under curve (AUC) of serum IL-6 were 0.72 (95% CI: 0.46–0.88), 0.74 (95% CI: 0.56–0.86), and 0.79 (95% CI: 0.75–0.82) in CRC diagnosis, respectively. Further, IPD meta-analysis strengthened the diagnostic value of serum IL-6 (the AUC, sensitivity, and specificity were 0.794, 0.606, and 0.839, respectively). For prognostic analysis, the high serum level of IL-6 was inversely associated with overall survival (OS) (pooled HR = 1.76, 95% CI: 1.42–2.19, P

Survivin mRNA expression was detected in 69.2%-93.8% of primary breast carcinomas, but is rarely expressed in normal breast tissues and hematopoietic cells. The objective of this study was to investigate the significance that the detection of Survinin-expressing circulating breast cancer cells in the peripheral blood has on clinical outcomes. The detection method was based on a RT-PCR ELISA technique developed in our laboratory. Sixty-seven breast cancer patients in various stages and 135 normal healthy women were investigated. Survivin-expressing circulating cancer cells were detected in the peripheral blood samples from 34 (50.7%) out of 67 breast cancer patients, but not in the healthy women that were used as controls. The presence of Survivin-expressing circulating breast cancer cells was found to be significantly associated with various clinicopathological parameters such as vessel infiltration, histological grade, tumor size, nodal status, ER/PgR status, Her-2 status and clinical stages of the disease (P < 0.01). During a follow-up period of 36 months, 9 out of 11 (81.8%) breast cancer patients that had a positive Survivin-expressing at the time of the initial assay test suffered a relapse of the disease, whereas recurrence was only found in 2 out of 6 (33.3%) breast cancer patients that had a negative Survivin-expression. Thus, the detection of circulating cancer cells expressing Survivin mRNA could provide valuable information for the prediction of metastasis and recurrence of breast cancer.

To study the effect of DTB against HIV-1, for developing anti-HIV drugs.Different concentration of DTB was added to cell culture system after viral inoculation, MTT staining method for viable cells (MTT assay) and p24 (ELISA) were used as markers to monitor the viral replication.The inhibition rates of DTB at concentrations 160, 80, and 40mg/ml were 93.0%, 56.2% and 18.1%, respectively.DTB could effectively inhibit HIV-1 in vitro.

To investigate the effects of emergent preoperative self-expandable metallic stent (SEMS) vs emergent surgery for acute left-sided malignant colonic obstruction.Two investigators independently searched the MEDLINE, EMBASE and Cochrane Central Register of Controlled Trials, as well as references of included studies to identify randomized controlled trials (RCTs) that compared two or more surgical approaches for acute colonic obstruction. Summary risk ratios (RR) and 95% CI for colonic stenting and emergent surgery were calculated.Eight studies met the selection criteria, involving 444 patients, of whom 219 underwent SEMS and 225 underwent emergent surgery. Seven studies reported difference of the one-stage stoma rates between the two groups (RR, 0.60; 95% CI: 0.48-0.76; P0.0001). Only three RCTs described the follow-up stoma rates, which showed no significant difference between the two groups (RR, 0.80; 95% CI: 0.59-1.08; P = 0.14). Difference was not significant in the mortality between the two groups (RR, 0.91; 95% CI: 0.50-1.66; P = 0.77), but there was significant difference (RR, 0.57; 95% CI: 0.44-0.74; P0.0001) in the overall morbidity. There were no significant differences between the two groups in the anastomotic leak rate (RR, 0.60; 95% CI: 0.28-1.28; P = 0.19), occurrence of abscesses, including peristomal abscess, intraperitoneal abscess and parietal abscess (RR, 0.83; 95% CI: 0.36-1.95; P = 0.68), and other abdominal complications (RR: 0.67; 95% CI: 0.40-1.12; P = 0.13).SEMS is not obviously more advantageous than emergent surgery for patients with acute left-sided malignant colonic obstruction.