Objective To investigate therapeutic effects of endoscopic mucosal resection( EMR) on gastric polyps and colorectal polyps.Methods 172 cases of elderly patients with early gastric and colorectal polyps were col-lected.They were divided into the observation group and control group by random number table,each group 86 cases. The observation group were treated with EMR,the control group were received conventional treatment for surgery.The clinical efficacy and adverse events were compared.Results The total effective rate of the observation group was 96.51%,significantly higher than 70.93% in the control group (χ2 =15.73,P<0.05);the postoperative adverse reactions in the observation group was 22.09%,significantly lower than 47.67% in the control group (χ2 =31.65, P<0.05).Conclusion For patients with pre-senile and senile stomach and colon polyps,the application of endo-scopic mucosal resection in the treatment not only can achieve better clinical efficacy, but also lower incidence of adverse reactions.

Objective To study clinical diagnosis value of using magnifying endoscopy with narrow-band imaging(NBI-ME) in the CEA positive cases of microvascular parting to gastric cancer and colorectal cancer .Methods 873 cases in our hospital from 2012~2013 ,who had serum CEA positive were choosen ,the 114 patients who first diagnosis for suspected gastric cancer ,35 pa-tients who first diagnosis forsuspected colorectal cancer were included in this study .Using NBI-ME to check and the pathology bi-opsy .NBI-M E check key observation microvascular properties and classification :rules ,slightly irregular ,irregular ,disappeared ,the microvascular parting situation compared with pathological findings .Results 13 patients diagnosed with cancer by pathology ,the positive rate was 8 .72% ;intraepithelial neoplasia in 10 cases ,the positive rate was 6 .71% .No cases of cancer were regular and slightly irregular type ,all cancer cases in the disappearance .The sensitivity of type of disappeared was 100 .00% ,and the sensitivity of irregular type of canceration possibility intestinal large atrophy and high grade intraepithelial neoplasia was 87 .50% ,the differ-ence was statistically significant(P<0 .05) .Conclusion Using NBI-ME microvascular classification diagnosis could help observa-tion CEA positive cases in the screening of gastric cancer and colorectal cancer .

Objective To evaluate the feasibility and clinical efficacy of minimally invasive surgery combined with sentinel lymph node (SLN) biopsy for early gastric cancer (EGC).Methods The clinical data of 39 EGC patients undergoing minimally invasive surgery combined with sentinel lymph node biopsy from December 2008 to January 2014 were analyzed retrospectively.Results 36 SLN negative EGC patients received endoscopic submucosal dissection (ESD), and 3 SLN positive EGC patients underwent laparoscopic distal gastrectomy with D2 dissection.The mean number of SLN was (2.8 ± 1.0).The SLN detection rate and accuracy of determination of lymph node (LN) status were both 100％.The rate of LN metastasis in patients with EGC was 8％ with no false negative rate.In ESD group, local recurrence and liver metastasis developed in one each cases.Meanwhile 1 patient in laparoscopic group sufferd postoperative liver and lung metastasis.Total disease free survival was 95％.Conclusions Minimally invasive surgery combined with sentinel lymph node biopsy for EGC is both safe and feasible.

Objective To investigate the correlation between single nucleotide polymorphisms (SNP) of gene interleukin-23 receptor (IL-23R) rs1004819, rs1495965, rs1884444, rs2201841,rs6677188, rs7517847, rs7530511, rs10489629, rs10889677 and rs11209026 with susceptibility of inflammatory bowel disease (IBD) in Han population of Jiangsu province in China. Methods The gene polymorphism in 134 healthy volunteers, 135 cases of ulcerative colitis(UC) and 43 cases of Crohn's disease(CD) were detected with SNaPshot. Experimental data were analyzed with SPSS 17.0 software. Results In UC, genotype frequency of CC and CT on rs7530511 was 99.26％ (134/135)and 0.74％(1/135), allele frequency of C and T was 99.63％(269/270)and 0. 37％(1/270). While in normal controls, which were 94.03％(126/134), 5.97％(8/134), 97.01 ％(260/268)and 2.99％(8/268)respectively. Compared genotype frequency of these two group, P value was 0. 040 (OR＝0.118、95％CI:0.014～0.953). Compared allele frequency of these two group, P value was 0. 043 (OR＝0.121、95％CI:0.015～0.973). In wild type and mutation type UC patients, the age distribution was different, more young patients in mutation type while more middle-aged patients in wild type, P value was 0.032 and 0.001 respectively. Most UC patients of rs6677188 AT type were in remission under endoscope (P＝0.032). Conclusion The mutation of IL-23R rs7530511 may be a protective factor of UC. The polymorphism of rs6677188 was associated with the age of patients and the remission under endoscope.

ObjectiveTo investigate the possible association of interleukin-23 receptor(IL-23R) polymorphisms with the susceptibility and phenotype of inflammatory bowel diseases (IBD) in Jiangsu Han population.MethodsWe genotyped 178 IBD patients including 135 patients with ulcerative colitis ( UC),43 patients with Crohn's disease (CD),and 134 headthy controls for rs11805303,rs1343151,rs11465804,rs11209032,rs17375018,rs11465788.ResultsComparing with the controls (50.4％ ),there was a significant increase in the carriage of the T allele of rs11805303 in UC (60.4％) ( P =0.020).In genotypephenotype correlation of rs17375018 in UC,clinical severity(UCDAI) was associated with the prevalence of the G allele showed a trend to mild activity.Genotype polymorphisms of rs17375018A was observed more in younger than 25 in the genotype-phenotype correlation in CD(41.7％ vs 22.0％,P =0.050,OR =2.532,95％ CI 0.988-6.494),while rs11805303 was associated with age at diagnose and disease lesion (P =O.039 and 0.044).The risk of extra intestinal manifestation in rs17375018A allele carriers was lower (23.1％ vs46.7％,P=0.040,OR =2.917,95％CI 1.027-8.283).ConclusionsWe confirmed the susceptibility of rs11805303polymorphisms with UC and first demonstrated the genotype-phenot correlation of rs11805303,rs17375018 with UC,CD in Jiangsu Han population.

Objective The primary aim of this study was to examine the proportion and natural history of Helicobacter pylori (Hp) negative bleeding peptic ulcers. Methods The study was designed as a multiple-center, case-control study conducted in 14 endoscopy centers in China from April 2006 to March 2007. Each center was expected to recruit 30 peptic ulcer patients with bleeding ( PUB group) and 30 without (PU group). All screened patients with upper gastrointestinal bleeding received endoscopy within 24 hours of admission. Biopsy specimens were taken from the antrum to determine Hp infection by rapid urease test and pathology. Patients with negative Hp infection at first examination were asked to receive urease breathe test (UBT) one month later. Results A total of 617 patients were enrolled with 263 in PUB group and 354 in PU group. There is no significant difference in demographic characters between 2 groups ( P ＞0. 05). The rate of Hp infection in PUB group ( 161/263, 61.2% ) was significantly lower than that in PUgroup (311/354, 87. 9%, P ＜0. 001 ). The incidence of complex ulcer in Hp positive PUB patients was 7.5% ( 12/161 ), which is significantly higher than that in Hp negative PUB patients ( 1/102, 1.0% , P =0. 018). In PUB group, no significant differences were found between Hp positive and negative patients in regarding of age, sex, rates of haematemesis, duodenal ulcer and gastric ulcer, and size of ulcer ( P ＞0. 05 ). Among 102 Hp negative cases in PUB, no positive case was found in UBT one month later. Conclusion We have demonstrated a rise in the incidence of Hp negative bleeding ulcers in China. The idiopathic ulcer was not rare, and might have a higher tendency to cause bleed.

ObjectiveThe antitumor activity of sesquiterpenoid M36 isolated from Myrrha against human hepatoma HepG2 cells was investigated in this study. MethodHepG2 cells were treated with M36 at different concentrations （0， 2， 4， 6， 8， 10 μmol·L^-1）. Firstly， the effects of M36 on the proliferation of human hepatoma HepG2 cells were detected by methyl thiazolyl tetrazolium （MTT）， colony formation assay， and EdU proliferation assay. Hoechst staining， flow cytometry analysis， and Western blot were used to explore the effect of M36 on the apoptosis of human hepatoma HepG2 cells. Acridine orange staining and western blotting were used to examine the effect of M36 on autophagy in HepG2 cells. Finally， Western blot was used to detect protein expression of cancer-related signaling pathways. ResultCompared with the blank group， M36 treatment significantly inhibited the proliferation of human hepatoma HepG2 cells （P<0.01）， and the half inhibitory concentration （IC₅₀） value of M36 for 48 h was 5.03 μmol·L^-1， in a dose- and time-dependent manner. M36 was also able to induce apoptosis and autophagy in human hepatoma HepG2 cells. After treatment with 8 μmol·L^-1 M36 for 48 hours， the apoptosis rate of HepG2 cells was （42.03±9.65）% （P<0.01）. Compared with the blank group， HepG2 cells treated with 4 and 8 μmol·L^-1 M36 for 48 h had a significant increase in cleaved poly ADP-ribose polymerase （cleaved-PARP） protein levels （P<0.01）. Acridine orange staining showed that autophagy was significantly activated in HepG2 cells treated with 4 and 8 μmol·L^-1 M36 for 48 h compared with the blank group （P<0.01）， which was further verified by the up-regulation of microtubule-associated protein 1 light chain 3 Ⅱ （LC3 Ⅱ）. Western blot results showed that compared with the blank group， the levels of phosphorylated extracellular regulated protein kinase （p-ERK）， phosphorylated p38 mitogen-activated protein kinase （p-p38 MAPK）， phosphorylated c-Jun N-terminal kinase （p-JNK）， and its downstream nuclear transcription factors c-Jun and p-c-Jun protein were significantly increased in M36 group （P<0.05， P<0.01）. The mechanism may be related to the up-regulation of MAPK signaling pathway. ConclusionThe sesquiterpenoid M36 isolated from Myrrha inhibits the proliferation of human hepatoma HepG2 cells and promotes apoptosis and autophagy， which may be related to the activation of the MAPK signaling pathway.

The prevalence and mortality of cancer have been on the rise， and it has been the global leading cause of death. The causes of cancer are diverse， such as heredity， radiation， and carcinogens. The abnormality of cell cycle regulation is also one of the causes. Cell cycle is a complex sequence of events through which a cell duplicates its contents and divides. Cell cycle is highly organized to ensure the integrity of genetic material. This process involves many regulatory genes and proteins. Cell cycle will be dysregulated when these proteins and genes change， resulting in the loss of control of cell proliferation， the inhibition of apoptosis， and finally the occurrence of tumor. At the moment， the therapies for cancer include traditional surgical resection， radiotherapy， chemical therapy， and targeted therapy. Chinese medicine has a wide range of sources and little side effect， which is worthy of further research and development. More and more studies have revealed that a variety of Chinese medicines play an anti-tumor role by inducing cell cycle arrest， so as to improve the quality of life and prolong the survival time of patients with advanced tumors. This article first introduces the characteristics and related regulatory factors of each phase of cell cycle， and enumerates the clinical and experimental examples of tumorigenesis caused by abnormal cell cycle. Then， we summarize the hot anti-tumor drugs targeting cell cycle in China and abroad， such as Cyclin-dependent kinase （CDK） inhibitors， cell division cycle 25 （CDC25） inhibitors， ataxia-telangiectasia-mutated-and-Rad3-related kinase （ATR） inhibitors， and checkpoint kinase 1 （CHK1） inhibitors. Finally， this article summarizes the recent research on the anti-tumor effect of Chinese medicine by inducing cell cycle arrest from the three aspects of cell cycle G₀/G₁ phase， S phase and G₂/M phase， in order to provide some reference for the research on the anti-tumor effect of Chinese medicine.

In vitro studies have established the prevalent theory that the mitochondrial kinase PINK1 protects neurodegeneration by removing damaged mitochondria in Parkinson's disease (PD). However, difficulty in detecting endogenous PINK1 protein in rodent brains and cell lines has prevented the rigorous investigation of the in vivo role of PINK1. Here we report that PINK1 kinase form is selectively expressed in the human and monkey brains. CRISPR/Cas9-mediated deficiency of PINK1 causes similar neurodegeneration in the brains of fetal and adult monkeys as well as cultured monkey neurons without affecting mitochondrial protein expression and morphology. Importantly, PINK1 mutations in the primate brain and human cells reduce protein phosphorylation that is important for neuronal function and survival. Our findings suggest that PINK1 kinase activity rather than its mitochondrial function is essential for the neuronal survival in the primate brains and that its kinase dysfunction could be involved in the pathogenesis of PD.