A Novel Method for the Object Detection and Weight Prediction of Chinese Softshell Turtles Based on Computer Vision and Deep Learning.

With the rapid development of the turtle breeding industry in China, the demand for automated turtle sorting is increasing. The automatic sorting of Chinese softshell turtles mainly consists of three parts: visual recognition, weight prediction, and individual sorting. This paper focuses on two aspects, i.e., visual recognition and weight prediction, and a novel method for the object detection and weight prediction of Chinese softshell turtles is proposed. In the individual sorting process, computer vision technology is used to estimate the weight of Chinese softshell turtles and classify them by weight. For the visual recognition of the body parts of Chinese softshell turtles, a color space model is proposed in this paper to separate the turtles from the background effectively. By applying multiple linear regression analysis for modeling, the relationship between the weight and morphological parameters of Chinese softshell turtles is obtained, which can be used to estimate the weight of turtles well. An improved deep learning object detection network is used to extract the features of the plastron and carapace of the Chinese softshell turtles, achieving excellent detection results. The mAP of the improved network reached 96.23%, which can meet the requirements for the accurate identification of the body parts of Chinese softshell turtles.

Targeting the chromatin structural changes of antitumor immunity.

Epigenomic imbalance drives abnormal transcriptional processes, promoting the onset and progression of cancer. Although defective gene regulation generally affects carcinogenesis and tumor suppression networks, tumor immunogenicity and immune cells involved in antitumor responses may also be affected by epigenomic changes, which may have significant implications for the development and application of epigenetic therapy, cancer immunotherapy, and their combinations. Herein, we focus on the impact of epigenetic regulation on tumor immune cell function and the role of key abnormal epigenetic processes, DNA methylation, histone post-translational modification, and chromatin structure in tumor immunogenicity, and introduce these epigenetic research methods. We emphasize the value of small-molecule inhibitors of epigenetic modulators in enhancing antitumor immune responses and discuss the challenges of developing treatment plans that combine epigenetic therapy and immunotherapy through the complex interaction between cancer epigenetics and cancer immunology.

Developing a Flying Explorer for Autonomous Digital Modelling in Wild Unknowns.

Digital modelling stands as a pivotal step in the realm of Digital Twinning. The future trend of Digital Twinning involves automated exploration and environmental modelling in complex scenes. In our study, we propose an innovative solution for robot odometry, path planning, and exploration in unknown outdoor environments, with a focus on Digital modelling. The approach uses a minimum cost formulation with pseudo-randomly generated objectives, integrating multi-path planning and evaluation, with emphasis on full coverage of unknown maps based on feasible boundaries of interest. The approach allows for dynamic changes to expected targets and behaviours. The evaluation is conducted on a robotic platform with a lightweight 3D LiDAR sensor model. The robustness of different types of odometry is compared, and the impact of parameters on motion planning is explored. The consistency and efficiency of exploring completely unknown areas are assessed in both indoor and outdoor scenarios. The experiment shows that the method proposed in this article can complete autonomous exploration and environmental modelling tasks in complex indoor and outdoor scenes. Finally, the study concludes by summarizing the reasons for exploration failures and outlining future focuses in this domain.

Cadmium (Cd) and 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) co-exposure induces acute kidney injury through oxidative stress and RIPK3-dependent necroptosis.

Environmental pollution is complex, and co-exposure can accurately reflect the true environmental conditions that are important for assessment of human health. Cadmium (Cd) is a widespread toxicant that can cause acute kidney injury (AKI), while its combined effect with 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) is not fully understood. Thus, we used an in vivo model where C57BL/6J mice were treated with low dietary intake of Cd (5 mg/kg/day) and/or BDE-47 (1 mg/kg/day) for 28 days to examine AKI, and in vitro experiments to investigate the possible mechanism. Results showed that Cd or BDE-47 caused pathological kidney damage, accompanied by elevated urea nitrogen (BUN) and urinary creatinine, as well as increased interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α), and reduced IL-10 in kidney tissues. In vitro Cd or BDE-47 exposure decreased cell viability and induced cell swelling and blebbing of human embryonic kidney 293 (HEK-293) and renal tubular epithelial cell lines (HKCs), and changes in co-exposure was larger than that in Cd and BDE-47 treatment. Oxidative stress indicators of the reactive oxygen species (ROS) and malondialdehyde (MDA) were elevated, while the antioxidant superoxide dismutase (SOD) was decreased. Necrosis occurred with increased lactate dehydrogenase (LDH) release and propidium iodide (PI) staining, which was attenuated by the ROS scavenger N-acetyl-L-cysteine (NAC). Furthermore, necroptotic genes of receptor-interacting protein kinase-3 (RIPK3), classical mixed lineage kinase domain-like protein-dependent (MLKL), IL-1ß and TNF-α were up-regulated, whereas RIPK1 was down-regulated, which was attenuated by the RIPK3 inhibitor GSK872. These findings demonstrate that Cd or BDE-47 alone produces kidney toxicities, and co-exposure poses an additive effect, resulting in AKI via inducing oxidative stress and regulating RIPK3-dependent necroptosis, which offers a further mechanistic understanding for kidney damage, and the combined effect of environmental pollutants should be noticed.

Morphology Optimization of the Photoactive Layer through Crystallinity and Miscibility Regulation for High-performance Polymer Solar Cells.

On the premise of strongly crystalline materials involved, it is a challenge to control the phase separation of bulk-heterojunction donor/acceptor active layer to fabricate high-performance polymer solar cells (PSCs). Herein, we develop a molecular design strategy of the third component to synthesize three guest materials (namely BTPT, BTP-Th, and BTP-2Th) to address this issue. We investigate and reveal the effect of crystallinity and miscibility of the third component in controlling the phase separation of Y6-derivatives-based blend film. As a result, a remarkable power-conversion efficiency of 18.53 % is obtained in the ternary PSC based on PTQ10 : m-BTP-PhC6 with BTP-Th as the third component, which is a significant improvement with regard to the efficiency of 17.22 % for the control binary device. Our study offers a molecular design strategy to develop a third component for building ternary PSCs in terms of crystallinity and miscibility regulation.

Intra-industry peer effect in corporate environmental information disclosure: Evidence from China.

Corporate environmental information disclosure is an important way for stakeholders to understand the performance of corporate environmental responsibilities. To explore the group relevance of corporate environmental information disclosure, this paper empirically tests the intra-industry peer effect of corporate environmental information disclosure using a panel fixed-effects model based on data of Chinese heavily polluted listed companies from 2015 to 2019 and studies its formation mechanism and impact path. The results show that there is an intra-industry peer effect in corporate environmental information disclosure; this effect exists in corporations of different ownership; social learning mechanism and environmental pressure mechanism are the channels to form the intra-industry peer effect of corporate environmental information disclosure; there are both intra-group imitation and inter-group imitation in the intra-industry peer effect of corporate environmental information disclosure. Based on the research results, the government can select corporations in various industries with excellent quality of environmental information disclosure as benchmarks to provide learning templates for corporations with inferior information. At the same time, the government can impose appropriate environmental protection pressure to promote learning and imitation among corporations. It is important to note that when selecting benchmarking companies, priority should be given to large and high-performing corporations.

Percutaneous transhepatic cholangiography and drainage and endoscopic retrograde cholangiopancreatograph for hilar cholangiocarcinoma: which one is preferred?

INTRODUCTION: both percutaneous transhepatic cholangiography and drainage (PTCD) and endoscopic retrograde cholangiopancreatography (ERCP) with SEMS implantation have been used for unresectable hilar cholangiocarcinoma (HC) in the clinic for many years. However, which one is preferred is still unknown. OBJECTIVE: to study the effects of biliary drainage of self-expanding metal stents (SEMS) implantation under PTCD or ERCP to treat HC. METHODS: the clinical data of 82 patients with HC from January 2006 to January 2015 were recorded retrospectively. Patients were treated with biliary implantation of self-expanding metal stents (SEMS) under PTCD (PTCD group, 40 patients) or ERCP (ERCP group, 42 patients). Clinical data, including total bilirubin concentrations, complications and survival time were analyzed. RESULTS: the remission of jaundice was similar in both groups (p > 0.05). The median survival time of the ERCP group and PTCD group were 237 d and 252 d respectively, with no significant differences (p > 0.05). The biliary infection rates under ERCP and PTCD procedure were 52.4 % and 20.0 % respectively, with a significant statistical difference (p < 0.05). For those HC patients of Bismuth III/IV, the infection rates under ERCP and PTCD procedure were 58.3 % and 14.3 %, respectively (p < 0.05). CONCLUSIONS: both PTCD and ERCP with SEMS implantation were effective to prolong the survival time of HC patients. The biliary infection rates were higher in the ERCP group, especially for Bismuth III/IV HC patients.

LIN28B-AS1-IGF2BP1 binding promotes hepatocellular carcinoma cell progression.

IGF2BP1 overexpression promotes hepatocellular carcinoma (HCC) progression. Long non-coding RNA LIN28B-AS1 directly binds to IGF2BP1. In the present study, LIN28B-AS1 and IGF2BP1 expression and their potential functions in HCC cells were tested. Genetic strategies were applied to interfere their expression, and cell survival, proliferation and apoptosis were analyzed. We show that LIN28B-AS1 is expressed in established/primary human HCC cells and HCC tissues. RNA-immunoprecipitation (RIP) and RNA pull-down results confirmed that LIN28B-AS1 directly associated with IGF2BP1 protein in HCC cells. LIN28B-AS1 silencing (by targeted siRNAs) or knockout (KO, by CRISPR-Cas9 method) depleted IGF2BP1-dependent mRNAs (IGF2, Gli1, and Myc), inhibiting HCC cell growth, proliferation, migration, and invasion. Conversely, ectopic overexpression of LIN28B-AS1 upregulated IGF2BP1-dependent mRNAs and promoted HCC cell progression in vitro. Importantly, ectopic IGF2BP1 overexpression failed to rescue LIN28B-AS1-KO HepG2 cells. LIN28B-AS1 siRNA and overexpression were ineffective in IGF2BP1-KO HepG2 cells. In vivo, LIN28B-AS1 KO-HepG2 xenograft tumors grew significantly slower than the control tumors in the nude mice. Taken together, we conclude that LIN28B-AS1 associates with IGF2BP1 to promote human HCC cell progression in vitro and in vivo.

Location matters: cooperativity of catalytic partners in porous organic polymers for enhanced CO2 transformation.

Herein, we show that by following molecular engineering of the inter-site distance between the two functionalities in porous organic materials, it is possible to enable them to work in a concerted manner. Specifically, the activity can be amplified by the placement of the hydroxyl group in the meta position of the phosphonium salts in the representative cycloaddition of epoxides and CO2.

EndoClot®SIS Polysaccharide Injection as a Submucosal Fluid Cushion for Endoscopic Mucosal Therapies: Results of Ex Vivo and In Vivo Studies.

BACKGROUND: There are many studies on submucosal injection materials, but their clinical use is restricted for various reasons. The objective of this study was to compare the feasibility and safety of injected EndoClot®SIS polysaccharide as a submucosal injection material (SFC) in ESD in the pig stomach to that of injected sigMAVisc™ or Eleview™. METHODS: Four pig stomachs were used for the ex vivo study. Eighteen pigs were used for the in vivo study. In the ex vivo study, four injections were made in the gastric submucosa to induce submucosal uplift and extend its duration. Tissue change was observed. The in vivo study was performed in 2 steps. First, 3 injections were made in the esophageal mucosa to induce submucosal uplift and extend its duration. Histological change was observed. Second, ESD was performed in the stomach by injecting EndoClot®SIS polysaccharide, sigMAVisc™, or Eleview™ (each, n = 6) as an SFC. The effects of these agents on wound healing were examined. We evaluated the efficacy and safety of endoscopic surgery after EndoClot®SIS polysaccharide injection. RESULTS: EndoClot®SIS polysaccharide produced a longer-lasting elevation with clearer margins than was achieved by sigMAVisc™, Eleview™, or 0.9% NaCl and thereby enabled precise ESD without complications, such as bleeding and perforation. No obvious histopathological damage was observed at the injection site on endoscopy and histology. CONCLUSION: Submucosally injected EndoClot®SIS polysaccharide increased the effective separation of the mucosa and submucosa and reduced surgical complications. Hence, EndoClot®SIS polysaccharide injection is a safe and effective submucosal injection material.

KDM5D inhibit epithelial-mesenchymal transition of gastric cancer through demethylation in the promoter of Cul4A in male.

Gastric cancer is one of the top causes of cancer-related death around the world, and poor prognosis of gastric cancer is due to the lack of early detection and effective treatment especially in male. Here, we first revealed the role of histone lysine-specific demethylase 5D (KDM5D) in gastric cancer in male. KDM5D was associated with the metastasis of gastric cancer because of its critical role in the epithelial-mesenchymal transition of gastric cancer cells. Downregulation of KDM5D in gastric cancer cells significantly increase the number of migrated or invaded cells due to the increasing expressions of mesenchymal markers. Downregulation of KDM5D also promotes tumor formation of gastric cancer cell in vivo. For mechanism, downregulation of KDM5D could inhibit the demethylation in the promoter of CUL4A, which lead to the increasing expression of ZEB1 and decreasing expressions of p21 and p53. Collectively, KDM5D performed its role in metastasis of gastric cancer through demethylation in the promoter of CUL4A, and it suggested us a novel target in gastric cancer treatment in male.

A MnO2-[Ru(dpp)3]Cl2 system for colorimetric and fluorimetric dual-readout detection of H2O2.

Two-dimensional (2D) MnO2 nanosheets were synthesized by a template-free and one-step route, and the dye [Ru(dpp)3]Cl2 was linked onto the MnO2 nanosheet surface via electrostatic interaction. The formed MnO2-[Ru(dpp)3]Cl2 hybrid was used for a dual optical detection for H2O2, an important reactive oxygen species (ROS). Upon addition of H2O2, the reaction of MnO2 with H2O2 results in the dissolution of MnO2 nanosheets and simultaneous generation of O2. The fading of the solution and simultaneous fluorescence change of [Ru(dpp)3]Cl2, sensitive to O2, enables colorimetric and fluorimetric dual-mode detection of H2O2. The dual-output assay in a single probe provides a good sensitivity with a detection limit of 0.18 µM H2O2. The dual-signal strategy can efficiently overcome the shortcoming of the single detection mode, and improve the detection accuracy by an additional correction of output signals from each other. Moreover, the successful determination of H2O2 in the serum samples demonstrates the potential applicability of the MnO2-[Ru(dpp)3]Cl2 based probe in biosensing and bioanalysis.

Luteolin Ameliorates Experimental Chronic Pancreatitis Induced by Trinitrobenzenesulfonic Acid in Rats.

OBJECTIVES: The purpose of this study is to assess the effect and possible mechanism of luteolin on chronic pancreatitis (CP). METHODS: Trinitrobenzenesulfonic acid-induced CP was used as CP models in vivo. After the intervention of luteolin for 28 days, chronic pancreatic injury was assessed by serum hydroxyproline and pancreatic histology. α-Smooth muscle actin (α-SMA) expression was performed to detect the activation of pancreatic stellate cells (PSCs). Pancreatic stellate cells were also isolated and cultured in vitro, and the effect of luteolin on PSCs was evaluated. Transforming growth factor ß (TGF-ß1) signaling and its regulated mRNA expression was tested by Western blot and quantitative real-time polymerase chain reaction, respectively. RESULTS: The protective role of luteolin on CP was confirmed by increased pancreas/body weight ratio, decreased pancreas hydroxyproline level, and reduced fibrosis. α-SMA expressions in PSCs were significantly decreased both in vitro and in vivo after the management of luteolin. Pancreas TGF-ß1 expression was significantly decreased by luteolin. Luteolin inhibited the proliferation and activation of PSCs in a dose-dependent manner. CONCLUSIONS: Luteolin played a protective role in CP in many aspects, partly by regulating release of inflammatory cytokines through TGF-ß1 signaling pathway.

Increased expression of tight junction protein occludin is associated with the protective effect of mosapride against aspirin-induced gastric injury.

Mosapride is known to affect gastric motility, however whether mosapride has anti-ulcergenic effects in gastric mucosal injury is unclear. The aim of the present study was to investigate the effects of mosapride on aspirin-induced gastric injuries. GES-1 cells were cultured and divided into 5 groups: Control group, aspirin injury group (treated with 18.2 mmol/l aspirin) and mosapride pretreatment groups (treated with 0.4, 0.5, or 0.6 µmol/l mosapride). Cell proliferation was evaluated via MTT assay and cell apoptosis was investigated via flow cytometry. The expression of occludin was determined by western blot analysis. A total of 40 male Sprague-Dawley rats were randomized into five groups: Control group, aspirin injury group (150 mg/kg) and mosapride pretreatment groups (0.25, 0.50 or 0.75 mg/kg). Gastric mucosal lesions were induced by administering 200 mg/kg aspirin daily for 4 days. Rats in the mosapride groups were pretreated with mosapride 1 h prior to aspirin administration. Histological changes were evaluated under a light microscope and gastric epithelial TJs were observed via transmission electron microscopy. The results revealed that cell apoptosis was significantly increased in the aspirin injury group compared with the control (P<0.05), whereas apoptosis was significantly decreased in the mosapride pretreatment groups compared with the aspirin group (P<0.05). Cell viability was significantly increased in the mosapride pretreatment groups compared with the aspirin injury group (P<0.05), and that of the aspirin injury group was significantly decreased compared with the control group (P<0.05). Compared with the aspirin injury group, occludin expression was significantly increased in the three mosapride pre-treatment groups (all P<0.05). It was also demonstrated that gastric damage was significantly attenuated in the mosapride pretreatment groups compared with the aspirin injury group (P<0.05). Impaired TJ integrity was observed in aspirin injury group, whereas TJs in the mosapride groups were almost intact. In conclusion, the results of the present study suggest that mosapride exerts a gastroprotective action on aspirin-induced gastric mucosal injury at least in part via attenuating cell apoptosis and increasing occludin expression.

Enhancement of Proliferation and Invasion of Gastric Cancer Cell by KDM5C Via Decrease in p53 Expression.

Gastric cancer is a malignancy with high incidence and the second leading cause of cancer death worldwide. Development of efficient therapies against gastric cancer is urgent. Until now, the mechanisms of gastric cancer genesis remain elusive. The KDM5C is a histone demethylase that promotes cancer cell growth and is enriched in drug-resistant cancer cells. But the pathogenic breadth and mechanistic aspects of this effect relative to gastric cancer have not been defined. In present study, we found that KDM5C was overexpressed in gastric cancer cell lines and gastric cancer tissues but not in normal gastric tissues. The proliferation and invasive potential of gastric cancer cells was significantly increased by ectopic expression of KDM5C. Contrarily, RNA interference targeting KDM5C in gastric cancer cells significantly decreased the proliferation and invasive potential of cells. Moreover, we also found that the expression of p53 was modulated by KDM5C. Cells with overexpression of KDM5C exhibited greatly decreased p53 expression, whereas silencing of KDM5C expression dramatically increased p53 expression at both the messenger RNA and protein levels. Inhibition of p53 by small-interfering RNA reversed the shKDM5C-induced proliferation and invasion. Our results collectively suggested that KDM5C played a role in gastric cancer cells proliferation and invasion, which may be partly associated with the p53 expression.

Halitosis and helicobacter pylori infection: A meta-analysis.

BACKGROUND: Halitosis is used to describe any disagreeable odor of expired air regardless of its origin. Numerous trials published have investigated the relation between Helicobacter pylori (H pylori) infection and halitosis, and even some regimes of H pylori eradication have been prescribed to those patients with halitosis in the clinic. We conducted a meta-analysis to define the correlation between H pylori infection and halitosis. OBJECTIVES: To evaluate whether there is a real correlation between H pylori infection and halitosis, and whether H pylori eradication therapy will help relieve halitosis. METHODS: We searched several electronic databases (The Cochrane Library, MEDLINE, EMBASE, PubMed, Web of Science, and Wanfangdata) up to December 2015. Studies published in English and Chinese were considered in this review. After a final set of studies was identified, the list of references reported in the included reports was reviewed to identify additional studies. Screening of titles and abstracts, data extraction and quality assessment was undertaken independently and in duplicate. All analyses were done using Review Manager 5.2 software. RESULTS: A total of 115 articles were identified, 21 of which met the inclusion criteria and presented data that could be used in the analysis. The results showed that the OR of H pylori infection in the stomach between halitosis-positive patients and halitosis-negative patients was 4.03 (95% CI: 1.41-11.50; P = 0.009). The OR of halitosis between H pylori-positive patients and H pylori-negative patients was 2.85 (95% CI: 1.40-5.83; P = 0.004); The RR of halitosis after successful H pylori eradication in those H pylori-infected halitosis-positive patients was 0.17 (95% CI: 0.08-0.39; P <0.0001), compared with those patients without successful H pylori eradication. And the RR of halitosis before successful H pylori eradication therapy was 4.78 (95% CI: 1.45-15.80; P = 0.01), compared with after successful H pylori eradication therapy. CONCLUSIONS: There is clear evidence that H pylori infection correlates with halitosis. H pylori infection might be important in the pathophysiological mechanism of halitosis, and H pylori eradication therapy may be helpful in those patients with refractory halitosis.

miRNA-223 inhibits epithelial-mesenchymal transition in gastric carcinoma cells via Sp1.

Sp1 plays critical roles in epithelial-mesenchymal transition (EMT) of certain cancer. However, few studies have indicated whether Sp1 is involved in the EMT of gastric cancer, and whether abnormal expression of Sp1 in gastric cancer EMT is regulated in a post-transcriptional manner, and the involvement of miRNAs in this regulation. In this study, we selected 20 cases of gastric cancers, their liver metastases and para-carcinoma tissues to examine the levels of Sp1 protein and mRNA by immunohistochemistry and fluorescent PCR, which showed that Sp1 was increased in gastric cancers and their metastases compared with adjacent tissues, but there was no difference in Sp1 mRNA between these three groups, suggesting changes in Sp1 may be attributed to inactivation of post-transcriptional regulation. We verified by a luciferase reporter system that miRNA-223 binds to 3'-UTR of Sp1 gene and inhibits its translation, in agreement with negative correlation between miRNA-223 and Sp1 protein levels in gastric cancer cells. By employing TGF-ß1 to induce MGC-803, BGC-823 and SGC-7901, we successfully built cellular EMT model. Then, we overexpressed miRNA-223 in the model by using a lentiviral system, which diminished EMT indicators and suppressed proliferation and invasion ability, and induced apoptosis. Finally, we verified the specificity of the regulation pathway miRNA-223/Sp1/EMT. These findings suggest that low expression of miRNA-223 in gastric cancer cells is an important cause for EMT. miRNA-223 specifically regulates the EMT process of gastric cancer cells through its target gene Sp1. Overexpression of miRNA-223 in these cells inhibits EMT via the miRNA-223/Sp1/EMT pathway.

Increased endoplasmic reticulum stress response is involved in clopidogrel-induced apoptosis of gastric epithelial cells.

BACKGROUND: The widespread use of clopidogrel alone or in combination with aspirin may result in gastrointestinal mucosal injury, clinically represented as recurrent ulceration and bleeding complications. Our recent work suggested that clopidogrel significantly induced human gastric epithelial cell (GES-1) apoptosis and disrupted gastric mucosal barrier, and that a p38 MAPK inhibitor could attenuate such injury. However, their exact mechanisms are largely unknown. METHODS: The GES-1 cells were used as a model system, the effects of clopidogrel on the whole gene expression profile were evaluated by human gene expression microarray and gene ontology analysis, changes of the mRNA and protein expression were determined by real-time PCR and Western blot analysis, and cell viability and apoptosis were measured by MTT assay and flow cytometry analysis, respectively. RESULTS: Gene microarray analysis identified 79 genes that were differentially expressed (P<0.05 and fold-change >3) when cells were treated with or without clopidogrel. Gene ontology analysis revealed that response to stress and cell apoptosis dysfunction were ranked in the top 10 cellular events being affected, and that the major components of endoplasmic reticulum stress-mediated apoptosis pathway - CHOP and TRIB3- were up-regulated in a concentration- and time-dependent manner when cells were treated with clopidogrel. Pathway analysis demonstrated that multiple MAPK kinases were phosphorylated in clopidogrel-treated GES-1 cells, but that only SB-203580 (a p38-specific MAPK inhibitor) attenuated cell apoptosis and CHOP over-expression, both of which were induced by clopidogrel. CONCLUSIONS: Increased endoplasmic reticulum stress response is involved in clopidogrel-induced gastric mucosal injury, acting through p38 MAPK activation.

Proton-pump inhibitors can decrease gastrointestinal bleeding after percutaneous coronary intervention.

BACKGROUND: Current medical therapies for patients who have an acute coronary syndrome (ACS) focus on the coagulation cascade and platelet inhibition. These, coupled with early use of cardiac catheterization and revascularization, have decreased morbidity and mortality rates in patients who have acute ischemic heart disease with risk of bleeding. OBJECTIVE: The study aimed to determine the incidence of gastrointestinal bleeding after percutaneous coronary intervention (PCI). The effect of proton-pump inhibitor (PPI) treatment was also analyzed. METHODS: This case-control study evaluated gastrointestinal bleeding within a year of PCI for stable angina and acute coronary syndromes at Nanjing First Hospital between 2008 and 2011. Cases were identified and outcomes assessed using linkage analysis of data from cardiology and gastroenterology department databases. Analysis of the case and control groups for both risk and protective factors was performed using independent two-sample Student's t-test with Fisher's exact P value and logistic regression. RESULTS: The incidence of gastrointestinal bleeding following PCI was 1.3% (35/2680 patients). The risk factors for gastrointestinal bleeding were advanced age, female gender, smoking, drinking, previous peptic ulcer and previous gastrointestinal bleeding. PPI use after PCI (P=0.000) was accompanied by a lower risk of gastrointestinal bleeding, with only a few cases of gastrointestinal bleeding events reported. CONCLUSION: The incidence of gastrointestinal bleeding associated with the combination of aspirin and clopidogrel therapy was estimated to be 1.3%. Advanced age, being female, smokers, drinkers, previous peptic ulcer and previous gastrointestinal bleeding were significant independent risk factors. PPI for the prevention and treatment of gastrointestinal bleeding induced by the combination of aspirin and clopidogrel in patients after PCI was safe and effective.