Characteristics of early gastric tumors with different differentiation and predictors of long-term outcomes after endoscopic submucosal dissection.

BACKGROUND: Gastric cancer is a common malignant tumor of the digestive tract, and endoscopic submucosal dissection (ESD) is the preferred treatment for early-stage gastric cancer. The analysis of the epidemiological characteristics of gastric mucosal tumors with different differentiation degrees and the influencing factors of long-term ESD efficacy may have certain significance for revealing the development of gastric cancer and ESD. AIM: To analyze the features of gastric mucosal tumors at different differentiation levels, and to explore the prognostic factors of ESD. METHODS: We retrospectively studied 301 lesions in 285 patients at The Second Affiliated Hospital of Xi'an Jiaotong University from 2014 to 2021, according to the latest Japanese guidelines (sixth edition), and divided them into low-grade intraepithelial neoplasia (LGIN), high-grade intraepithelial neoplasia (HGIN), and differentiated and undifferentiated early carcinoma. They are followed up by endoscopy, chest and abdominal computed tomography at 3, 6 and 12 months after ESD. We compared clinicopathologic characteristics, ESD efficacy, and complications with different degrees of differentiation, and analyzed the related factors associated with ESD. RESULTS: HGIN and differentiated carcinoma patients were significantly older compared with LGIN patients (P < 0.001) and accounted for more 0-IIc (P < 0.001), atrophic gastritis was common (P < 0.001), and irregular microvascular patterns (IMVPs) and demarcation lines (DLs) were more obvious (P < 0.001). There was more infiltration in the undifferentiated carcinoma tissue (P < 0.001), more abnormal folds and poorer mucosal peristalsis (P < 0.001), and more obvious IMVPs, irregular microsurface patterns and DLs (P < 0.05) than in the LGIN and HGIN tissues. The disease-free survival rates at 2, 5, and 8 years after ESD were 95.0%, 90.1%, and 86.9%, respectively. Undifferentiated lesions (HR 5.066), white moss (HR 7.187), incomplete resection (HR 3.658), and multiple primary cancers (HR 2.462) were significantly associated with poor prognosis. CONCLUSION: Differentiations of gastric mucosal tumors have different epidemiological and endoscopic characteristics, which are closely related to the safety and efficacy of ESD.

Non-acid reflux and esophageal dysmotility is associated with early esophageal squamous cell carcinoma.

BACKGROUND: Studies have demonstrated that non-acid reflux (NAR) is associated with esophageal squamous cell carcinoma (ESCC). Esophageal dysmotility is associated with NAR but few studies have focused on the esophageal motility of ESCC patients. We explored the relationship between ESCC, NAR and esophageal dysmotility with the aid of multichannel intraluminal impedance and pH (MII-pH) and high-resolution manometry (HRM). METHODS: From Jan 2021 to Oct 2022, 20 patients with superficial ESCC were enrolled as the ESCC group, while 20 age and gender matched individuals without gastroesophageal reflux disease (GERD) symptoms and 20 age and gender matched patients with GERD symptoms were recruited as the control groups. Patients received 24 h MII-pH and HRM procedure before endoscopic submucosal dissection (ESD), and the data were then collected to identify the type of reflux and esophageal dysmotility. RESULTS: Prevalence of esophageal dysmotility was significantly different among the three groups, 75.0% in the ESCC group, 35.0% in the non-GERD group and 70.0% in the GERD group (P = 0.029). NAR episodes at 15 cm above the lower esophageal sphincter (LES) in the ESCC group were significantly higher than that in the non-GERD group (6.5 (3.5-9.3) vs 1.0 (0.8-4.0), P = 0.001) and were similar with that in the GERD group (6.5 (3.5-9.3) vs 5.5 (3.0-10.5), P > 0.05). NAR episodes at 5 cm above LES was significantly higher in the ESCC group than that in the non-GERD group (38.0 (27.0-60.0) vs 18.0 (11.8-25.8), P = 0.001) and was significantly higher than that in the GERD group (38.0 (27.0-60.0) vs 20.0 (9.8-30.5)), P = 0.010). Prevalence of pathologic non-acid reflux was significantly different among the three groups, 30.0% in the ESCC group, 0.0% in the non-GERD group and 10.0% in the GERD group (P < 0.001). CONCLUSION: Our study found NAR and esophageal dysfunction frequently occur in ESCC patients. NAR and esophageal dysmotility may be associated with ESCC. CLINICAL TRIAL REGISTRATION NUMBER: ChiCTR2200061456.

Transmembrane Protein 100 Inhibits the Progression of Colorectal Cancer by Promoting the Ubiquitin/Proteasome Degradation of HIF-1α.

Transmembrane protein 100 (TMEM100) is involved in embryonic cardiovascular system development. However, the biological role of TMEM100 in human cancers, particularly colorectal cancer (CRC), is unclear. In this study, tissue microarrays were stained using immunohistochemistry methods to evaluate the association between TMEM100 levels and clinic-pathological features for CRC. Kaplan-Meier and log-rank tests revealed that decreased levels of TMEM100 correlated with shorter overall survival. Cox regression revealed that reduced levels of TMEM100 was an independent prognostic factor for detrimental survival in CRC. A lentiviral vector was used to overexpress TMEM100 in HCT116 cells, and small interfering RNA was used to knockdown TMEM100 in SW480 cells. The CCK-8 assay, colony formation analysis, cell cycle analysis, cell migration assay, mouse xenograft model and mouse lung metastasis model showed that TMEM100 suppressed CRC cell proliferation and migration in vitro and in vivo. IHC scores of TMEM100 and HIF-1α were significantly negatively correlated. A half-time determination analysis in which cells were treated with cycloheximide revealed that TMEM100 shortened the HIF-1α half-life. Further immunoprecipitation experimental results showed that TMEM100 promoted the ubiquitination of HIF-1α, which caused HIF-1α degradation via the 26S proteasome pathway. Angiogenesis assay and migration assay results revealed that TMEM100 suppressed the migration and angiogenesis induction capacities of HCT116 cells, but this inhibitory effect was abolished when HIF-1α degradation was blocked by MG132 treatment. These results indicated that TMEM100 inhibited the migration and the angiogenesis induction capacities of CRC cells by enhancing HIF-1α degradation via ubiquitination/proteasome pathway.

Suppression of rhomboid domain-containing 1 produces anticancer effects in pancreatic adenocarcinoma through affection of the AKT/GSK-3ß/ß-catenin pathway.

The protumor role of rhomboid domain-containing 1 (RHBDD1) has been observed in multiple cancers. However, the relationship between RHBDD1 and pancreatic adenocarcinoma has not been addressed. This project focused on the potential relevance of RHBDD1 in pancreatic adenocarcinoma. Bioinformatic analysis by publicly available data revealed that RHBDD1 was abundantly expressed in pancreatic adenocarcinoma. We further verified that RHBDD1 was expressed highly in clinical specimens of pancreatic adenocarcinoma. The Kaplan-Meier curve demonstrated that high-RHBDD1 expression was associated with poor prognosis in pancreatic adenocarcinoma patients. The functional studies revealed that depletion of RHBDD1 produced in vitro anticancer effects in pancreatic adenocarcinoma cells, including retardation of proliferation, reduction of metastatic potential, and induction of cell-cycle arrest at the G0/G1 phase and apoptosis. Mechanistic studies indicated that loss of RHBDD1 affected the activation of ß-catenin via regulation of AKT. Forced expression of ß-catenin reversed the RHBDD1-loss-induced anticancer effects in pancreatic adenocarcinoma cells. Crucially, depletion of RHBDD1 retarded the growth of pancreatic adenocarcinoma xenografts in vivo, a phenomenon associated with the AKT/ß-catenin pathway. Collectively, these findings delineated that restraint of RHBDD1 displayed remarkable anticancer effects in pancreatic adenocarcinoma by affecting the AKT/ß-catenin pathway. Our work unveils a pivotal role of RHBDD1 in pancreatic adenocarcinoma and proposes it as a novel candidate target for anticancer therapy of pancreatic adenocarcinoma.

Knockdown of TRIM15 inhibits the proliferation, migration and invasion of esophageal squamous cell carcinoma cells through inactivation of the Wnt/ß-catenin signaling pathway.

TRIM15 is a member of tripartite motif-containing protein (TRIM) protein family, which plays important roles in several cancers. The aim of the present study was to evaluate the role of TRIM15 in esophageal squamous cell carcinoma (ESCC). Our results showed that TRIM15 was upregulated in human ESCC tissues and cell lines. In vitro studies showed that knockdown of TRIM15 significantly inhibited the proliferation, migration, and invasion of ESCC cells. Knockdown of TRIM15 caused a significant increase in E-cadherin expression, as well as decreases in expression of N-cadherin and Vimentin proteins. Moreover, in vivo assay proved that tumor growth was suppressed by knockdown of TRIM15. Furthermore, the protein expression levels of ß-catenin, C-myc, and CyclinD1 were markedly decreased in sh-TRIM15-infected ESCC cells. Additionally, treatment with LiCl reversed the inhibitory effects of TRIM15 knockdown on ESCC cells. In conclusion, these findings indicated that knockdown of TRIM15 blocked the growth and metastasis of ESCC in part through inhibiting the Wnt/ß-catenin signaling pathway. Thus, TRIM15 might serve as a promising therapeutic target for ESCC.

Accuracy of Endoscopic Diagnosis of Helicobacter pylori Based on the Kyoto Classification of Gastritis: A Multicenter Study.

BACKGROUND: There is lack of clinical evidence supporting the value of the Kyoto classification of gastritis for the diagnosis of Helicobacter pylori (H. pylori) infection in Chinese patients, and there aren't enough specific features for the endoscopic diagnosis of past infections, which is of special significance for the prevention of early gastric cancer (GC). METHODS: This was a prospective and multicenter study with 650 Chinese patients. The H. pylori status and gastric mucosal features, including 17 characteristics based on the Kyoto classification and two newly-defined features unclear atrophy boundary (UAB) and RAC reappearance in atrophic mucosa (RAC reappearance) were recorded in a blind fashion. The clinical characteristics of the subjects were analyzed, and the diagnostic odds ratio (DOR), sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), area under the receiver operating characteristics curve (ROC/AUC), and 95% confidence intervals were calculated for the different features, individually, and in combination. RESULTS: For past infection, the DOR of UAB was 7.69 (95%CI:3.11-19.1), second only to map-like redness (7.78 (95%CI: 3.43-17.7)). RAC reappearance showed the highest ROC/AUC (0.583). In cases in which at least one of these three specific features of past infection was considered positive, the ROC/AUC reached 0.643. For current infection, nodularity showed the highest DOR (11.7 (95%CI: 2.65-51.2)), followed by diffuse redness (10.5 (95%CI: 4.87-22.6)). Mucosal swelling showed the highest ROC/AUC (0.726). Regular arrangement of collecting venules (RAC) was specific for no infection. CONCLUSIONS: This study provides evidence of the clinical accuracy and robustness of the Kyoto classification of gastritis for the diagnosis of H. pylori in Chinese patients, and confirms UAB and RAC reappearance partly supplement it for the diagnosis of past infections, which is of great benefit to the early prevention of GC.

Decreased expression of DEAD-Box helicase 5 inhibits esophageal squamous cell carcinomas by regulating endoplasmic reticulum stress and autophagy.

DEAD-Box Helicase 5(DDX5), also known as P68, is one of the founding members of the DEAD-Box helicase superfamily and it plays a key role in RNA metabolism. Several studies have reported that DDX5 is involved in many types of tumors through abnormal expression, but the detailed mechanism of DDX5 in esophageal squamous cell carcinoma (ESCC) has not been elucidated. In this study, we demonstrate that the level of DDX5 is a negative prognostic factor for ESCC. The obtained results indicated that decreased expression of DDX5 inhibits ESCC cell proliferation and metastasis. Further experiments suggested that CDK2, Cyclin D1 and Vimentin were downregulated, while E-cadherin was upregulated after DDX5 was knocked down. In addition, DDX5 was positively correlated with the expression of BIP, phospho-eIF2α, phospho-PERK and P62, suggesting that knockdown of DDX5 can inhibit endoplasmic reticulum(ER) stress and promote the recovery of autophagy flux. Therefore, this study demonstrates that the downregulation of DDX5 in ESSC correlates to lower malignancy and presents a novel target for the development of new treatment strategies.

[Effect of L-cysteine on colonic motility and the underlying mechanism].

The purpose of the present study is to investigate the effect of L-cysteine on colonic motility and the underlying mechanism. Immunohistochemical staining and Western blot were used to detect the localization of the H2S-generating enzymes cystathionine-ß-synthase (CBS) and cystathionine-γ-lyase (CSE). Organ bath system was used to observe the muscle contractile activities. Whole-cell patch-clamp technique was applied to record ionic channels currents in colonic smooth muscle cells. The results showed that both CBS and CSE were localized in mucosa, longitudinal and circular muscle and enteric neurons. L-cysteine had a dual effect on colonic contraction, and the excitatory effect was blocked by pretreatment with CBS inhibitor aminooxyacetate acid (AOAA) and CSE inhibitor propargylglycine (PAG); L-cysteine concentration-dependently inhibited L-type calcium channel current (ICa,L) without changing the characteristic of L-type calcium channel (P < 0.01); In contrast, the exogenous H2S donor NaHS increased ICa,L at concentration of 100 µmol/L, but inhibited ICa,L and modified the channel characteristics at concentration of 300 µmol/L (P < 0.05); Furthermore, L-cysteine had no effect on large conductance calcium channel current (IBKCa), but NaHS significantly inhibited IBKCa (P < 0.05). These results suggest that L-cysteine has a potential dual effect on colonic smooth muscle and the inhibitory effect might be directly mediated by L-type calcium channel while the excitatory effect might be mediated by endogenous H2S.

CREB1-induced lncRNA LEF1-AS1 contributes to colorectal cancer progression via the miR-489/DIAPH1 axis.

Long non-coding RNAs (lncRNAs) have been identified as new regulatory factors in tumor progression. Lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1) was a recently identified lncRNA. This research aimed to investigate the roles and mechanisms of LEF1-AS1 in colorectal cancer (CRC). We firstly showed that LEF1-AS1 expression was upregulated in human CRC tissues and cell lines. LEF1-AS1 upregulation was demonstrated to be induced by CREB1. Clinical study revealed that high LEF1-AS1 expression was positively associated with histological grade, lymph nodes metastasis, and decreased survivals of CRC patients. Functionally, down-regulation of LEF1-AS1 using si-LEF1-AS1 decreased cell growth, migration and invasion, as well as increased apoptosis in CRC cells. Mechanically, LEF1-AS1 functioned as competing endogenous RNA (ceRNA) for miR-489 to positively recover DIAPH1, thus playing an oncogenic role in CRC pathogenesis. Overall, our observations identified a novel CRC-related lncRNA LEF1-AS1 and discovered a critical role for this lncRNA as a ceRNA in CRC pathogenesis, suggesting that it may serve as a novel biomarker for prognosis and act as a therapeutic target for CRC treatment.

p62 functions as an oncogene in colorectal cancer through inhibiting apoptosis and promoting cell proliferation by interacting with the vitamin D receptor.

OBJECTIVES: The role of p62 in cancer is controversial. Evidence has shown that p62 is upregulated in different cancers and promotes tumour growth, such as in liver cancer and lung cancer. However, a recent study showed that the downregulation of p62 in hepatic stellate cells (HSCs) promotes hepatocellular carcinoma (HCC) development. How p62 is regulated in colorectal cancer (CRC) remains largely unknown. In this study, we aimed to investigate the roles and molecular mechanisms of p62 in CRC. MATERIALS AND METHODS: The expression levels of p62 in CRC tissues and adjacent non-tumour tissues were determined by immunohistochemistry (IHC). Stable p62-overexpression HCT116 cells and p62-knockdown SW480 cells were established with lentiviral vectors. The role of p62 in CRC was investigated in in vitro and in vivo functional studies. The relationship between p62 and the vitamin D receptor (VDR) was investigated by coimmunoprecipitation (Co-IP) assays. RESULTS: p62 was significantly upregulated in CRC, and a high p62 level was an independent risk factor for a poor prognosis in CRC patients. p62 promoted CRC migration and invasion by inhibiting apoptosis and promoting cell proliferation in vitro, and p62 aggravated tumour growth and metastasis in vivo. Co-IP assays indicated that p62 interacts with the VDR and may target the NRF2-NQO1 axis. CONCLUSIONS: Our study suggested that p62 functions as an oncogene in CRC through inhibiting apoptosis and promoting cell proliferation by interacting with the VDR.

Weighted gene co-expression network analysis and connectivity map identifies lovastatin as a treatment option of gastric cancer by inhibiting HDAC2.

OBJECTIVE: This study aimed to identifying and validating therapeutic compounds which might have positive effects on patients with gastric cancer (GC) based on weighted gene co-expression network analysis (WGCNA) and connectivity map (CMap). METHODS: We performed WGCNA to gain insights into the molecular aspects of GC. Raw microarray datasets (including 132 samples) were downloaded from the Gene Expression Omnibus (GEO) website. We utilized the WGCNA to identify the coexpressed genes (modules) and modular hub genes after non-specific filtering. Furthermore, these differentially expressed genes were submitted to CMap analysis to identify candidate therapeutic compounds for GC. In experimental part, cell growth inhibition was evaluated by Cell Counting Kit-8 (CCK-8) and colony formation assays. Tumor growth was assessed using nude mice with xenografts established in vivo. QRT-PCR and western blot were used for determination of HDAC2 expression level and immunohistochemistry was performed to quantify HDAC2 in gastric tumor samples. RESULTS: Through WGCNA and CMap analysis, we found two potential therapeutic compounds, the valproic acid (VPA), which is the histone deacetylase (HDAC) inhibitor and lovastatin. HDAC2 was overexpressed in gastric cancer cell lines including AGS, BGC-823, NCI-N87 and MKN28. Dose-dependent inhibition of gastric cancer cells by VPA and lovastatin was verified in vitro. Apoptosis of GC cells was induced after treatment with VPA and lovastatin through suppressing HDAC2 expression. Furthermore, the inhibition of VPA with cisplatin and lovastatin with cisplatin were also dose-dependent and cisplatin exhibited synergistic effects. In the xenografts, similar results were found. CONCLUSION: WGCNA was able to identify significant groups of genes associated with cancer prognosis. Moreover, analysis of gene expression signature using CMap is a powerful way to explore potential therapeutics for human diseases. For treating GC, lovastatin may be a potential drug.

LncRNA CASC11 promoted gastric cancer cell proliferation, migration and invasion in vitro by regulating cell cycle pathway.

In this study, we aimed to investigate the effects of lncRNA CASC11 on gastric cancer (GC) cell progression through regulating miR-340-5p and cell cycle pathway. Expressions of lncRNA CASC11 in gastric cancer tissues and cell lines were determined by qRT-PCR. Differentially expressed lncRNAs, mRNAs and miRNAs were screened through microarray analysis. The relationship among CASC11, CDK1 and miR-340-5p was predicted by TargetScan and validated through dual luciferase reporter assay. Western blot assay examined the protein level of CDK1 and several cell cycle regulatory proteins. GO functional analysis and KEGG pathway analysis were used to predict the association between functions and related pathways. Cell proliferation was determined by CCK-8 assays. Cell apoptosis and cell cycle were detected by flow cytometry assay. CASC11 was highly expressed in GC tissues and cell lines. Knockdown of CASC11 inhibited GC cell proliferation, promoted cell apoptosis and blocked cell cycle. KEGG further indicated an enriched cell cycle pathway involving CDK1. QRT-PCR showed that miR-340-5p was down-regulated in GC cells tissues, while CDK1 was up-regulated. Furthermore, CASC11 acted as a sponge of miR-340-5p which directly targeted CDK1. Meanwhile, miR-340-5p overexpression promoted GC cell apoptosis and induced cell cycle arrest, while CDK1 overexpression inhibited cell apoptosis and accelerated cell cycle. Our study revealed the mechanism of CASC11/miR-340-5p/CDK1 network in GC cell line, and suggested that CASC11 was a novel facilitator that exerted a biological effect by activating the cell cycle signaling pathway. This finding provides a potential therapeutic target for GC.

A giant and extensive solitary Peutz-Jeghers-type polyp in the antrum of stomach: Case report.

RATIONALE: A solitary Peutz-Jeghers-type polyp is a hamartomatous polyp which without either mucocutaneous pigmentation or a family history of Peutz-Jeghers syndrome (PJS). It can occur in all of the gastrointestinal tract, but it is extremely rare in the stomach. PATIENT CONCERNS: A 53-year-old man was admitted to the local hospital with left upper abdominal pain lasting 2 weeks. A gastroscopy showed a giant and extensive bulging lesion on the greater curvature and posterior and anterior walls of the gastric antrum, involving three-quarters of the gastric wall. Endoscopic ultrasonography showed a muscularis mucosa lesion. DIAGNOSES: A solitary Peutz-Jeghers-type polyp in the antrum of stomach. INTERVENTIONS: The patient underwent an endoscopic submucosal dissection (ESD). OUTCOMES: The patient recovered quickly, without any complications. LESSONS: This is the second largest gastric solitary Peutz-Jeghers-polyp reported until now, and the largest gastric solitary Peutz-Jeghers type-polyp treated by endoscope.

[Camostat mesilate, a protease inhibitor, inhibits visceral sensitivity and spinal c-fos expression in rats with acute restraint stress].

OBJECTIVE: To observe the effect of gut protease activity on visceral hypersensitivity in rats with acute restraint stress. METHODS: Sprague-Dawley rats were given 30, 100 or 300 mg/kg camostat mesilate (CM), a protease inhibitor, or saline intragastrically 30 min before acute restraint stress induced by wrapping the fore shoulders, upper forelimbs and thoracic trunk for 2 h. Visceral perception of the rats was quantified as the visceral motor response with an electromyography, and the rectal mucosa and feces protease activity and spinal c-fos expression were measured. RESULTS: CM dose-dependently reduced visceral sensitization elicited by rectal distension, but these doses did not completely inhibit stress-induced visceral sensitization. In normal rats, c-fos expression was found mainly in the superal spinal cord dorsal horn, and after the administration the CM, c-fos-positive cells decreased significantly in all dose groups (P<0.05). In 30 mg/kg CM group, fecal and rectal mucosal protease activity significantly decreased as compared with that in the stress group (P<0.05), and as CM dose increased to 100 and 300 mg/kg, the protease activity decreased even further (P<0.01). CONCLUSION: The gut protease is involved in acute stress-induced visceral hypersensitivity, and CM can lower the visceral sensitivity and spinal c-fos expression in rats.

Effects of serum containing Chinese medicine Sanpi Pingwei () formula on proliferation and apoptosis of human SGC-7901 cells.

OBJECTIVE: To investigate the effects of serum containing Chinese medicine (CM) Sanpi Pingwei (, SPPW) formula on the proliferation and apoptosis of human SGC-7901 cells and the possible mechanism. METHODS: Serum containing CM SPPW formula (SPPW serum) was prepared by a serum pharmacology method. Human SGC-7901 cells were incubated with SPPW serum at three different concentrations and with the anticancer drug 5-fluorouracil (5-FU), respectively. Cell proliferation was assessed by MTT assay, and cell apoptosis was detected by flow cytometry assay. Real-time quantitative polymerase chain reaction (RT-PCR) and Western blot assay were employed to confirm the expressions of Bcl-2, Bax and p53 in SGC-7901 cells at mRNA and protein levels, respectively. RESULTS: SPPW serum suppressed the proliferation of SGC-7901 cells in a time- and dose-dependent manner. The colony forming rate of negative control was 48.2%, while those in the three SPPW serum groups and the 5-FU group decreased significantly (P<0.01). The number of colony forming units in the SPPW high dosage group was significantly smaller than that in the 5-FU group (P<0.01). MTT assay showed that SPPW serum restrained the proliferation of SGC-7901 cells, and the inhibition rate increased significantly in a dose-dependent manner. Annexin V/PI Assay suggested that SPPW serum induced the apoptosis of SGC-7901 cells significantly. RT-PCR and western blot assay indicated that SPPW serum upregulated the protein and mRNA expression levels of Bax and p53 in SGC-7901 cells, but downregulated the protein and mRNA expressions of Bcl-2. CONCLUSIONS: SPPW formula inhibits the proliferation of SGC-7901 cells in vitro and induces the cell apoptosis. It plays an anticancer role by regulating the expressions of Bax, p53 and Bcl-2 in SGC-7901 cells.

[A research of migrating motor complex in patients with irritable bowel syndrome].

OBJECTIVES: To compare the migrating motor complex (MMC) in irritable bowel syndrome (IBS) patients with that in healthy controls. To explore whether discrete clustered contractions (DCC) are connected with abdominal pain in IBS patients. To improve the method of measuring gastroenteric motility (esp. jejunum). METHODS: By using 16-channel water-perfused catheter and manometry instruments, MMC in 16 cases of IBS with constipation (IBS-C), 18 cases of IBS with diarrhea (IBS-D) and 18 cases of healthy controls were monitored. RESULTS: The MMC durations of IBS-C and IBS-D patients were (127.5 +/- 25.5) min and (74.5 +/- 18.7) min, respectively. Comparision with those in the control group [(87.5 +/- 24.2) min] showed significant differences (P < 0.001). The contraction amplitudes of stage III in different sites of IBS-C patients decreased significantly as compared with those in the controls [jejunum, (39.8 +/- 11.7) mm Hg vs. (61.1 +/- 14.1) mm Hg, P < 0.001, 1 mm Hg = 0.133 kPa]. The propagation velocities of stage III in different sites of IBS-C patients also decreased significantly as compared with those in the controls [jejunum, (1.8 +/- 0.9) cm/min vs. (2.6 +/- 0.8) cm/min, P < 0.01]. The contraction amplitudes of stage III in different sites of IBS-D patients increased significantly as compared with those in the controls [jejunum, (69.7 +/- 20.5) mm Hg vs. (61.1 +/- 14.1) mm Hg, P < 0.01]. The propagation velocities of stage III in different sites of IBS-D patients also increased significantly as compared with those in the controls [jejunum, (4.1 +/- 2.5) cm/min vs. (2.6 +/- 0.8) cm/min, P < 0.01]. DCC incidences of IBS-C and IBS-D were 87.5% and 88.8%, respectively. Comparision with those in the normal group (83.3%) did not show significant difference (P > 0.05). The prevalences of abnormal stage III contractions (include disturbances and interferences of stage III contractions) in IBS-C and IBS-D patients were 68.8% and 66.7%, respectively; there were no significant differences between the two groups (P > 0.05). However abnormal stage III contractions did not exist in healthy controls. CONCLUSIONS: (1) The MMC of IBS-C and IBS-D patients are changed, as compared with that in healthy people; this implies that small intestinal motility dysfunction is one of the pathogenetic factors of IBS. The abnormal stage III contractions in jejunum may be a predominant change in IBS gastroenteric motility. (2) No apparent connection is found between DCC and pain in IBS. (3) By using 16-channel water-perfused catheter, we first carried out the method of monitoring jejunum contractions in China. Parameters of MMC in Chinese healthy people were investigated, esp. those of jejunum.

[Effect of ghrelin on duodenal myoelectric activity in conscious rats].

OBJECTIVE: To explore the effect of ghrelin on the duodenal myoelectrical activity during the feeding state and the fasting state in rats. METHODS: One pair of bipolar silver electrodes were chronically implanted in the duodenal serosa of rats for electromyography. The myoelectrical activity was recorded when ghrelin was injected intravenously into rats during the feeding state or the fasting state. Some rats were pretreated with atropine, phentolamine, propranolol, L-arginine, and (D-Lys3)GHRP-6 respectively to explore the mechanism of ghrelin. RESULTS: Duodenal migrating myoelectrical complex (MMC) could be induced by ghrelin in the feeding state. Ghrelin could shorten the length of duodenal MMC cycle and increase the amplitude and frequency of phase III during the fasting state. The percentage of phase III in the MMC cycle did not change. These effects were inhibited by atropine and L-arginine (D-Lys3)GHRP-6, but not by propranolol and phentolamine. CONCLUSION: Ghrelin seems to be closely related to the duodenal motility. The excitatory effect of ghrelin on duodenal MMC might rely on the cholinergic pathway, and have a close relationship with NO. The receptor of ghrelin can regulate its activity.

Effect of Mexican tea herb and pilular adina herb on concrescence of gastric mucosa in experimental gastric ulcer rats.

OBJECTIVE: To study the effect and mechanism of mexican tea herb and pilular adina herb (abbreviated to MP) on concrescence of gastric mucosa in experimental gastric ulcer rats by observing the changes of epidermal growth factor (EGF), nitrogen monoxidum (NO) and expression of epidermal growth factor receptor (EGFR). METHODS: The rat ulcer model was established by 100% glacial acetic injection into the subserosa. The ulcer index (UI) was measured by sliding caliper. The levels of NO and EGF in tissue and serum were measured by the nitrate reductase method and enzyme-linked immunosorbent assay, respectively. The expression of EGFR in the mucosa around the ulcer was detected by the immunohistochemical assay and microimage analysis system. RESULTS: (1) Compared with the model group, UI of MP groups (10, 15 and 20 mg.kg(-1).d(-1)) and ranitidine group was lower (P<0.05 or P<0.01), the levels of NO and EGF in the tissue and serum were higher (P<0.05), the thickness of regenerated mucous membrane increased, and the width loss of lamina muscularis mucosa decreased (all P<0.05). (2) The expression of EGFR is weakly positive in gastric mucosa cells in the normal group, mainly in the cytoplasm and cytomembrane. In the model group, the expression of EGFR was mainly in epithelial cells in cervical part and basilar part of gastric gland around the ulcer margin, and the number of cells with EGFR weakly positive expression was more than that in the normal group. Compared with that in the normal and model groups, the number of cells with EGFR positive in MP groups and ranitidine group increased (all P<0.05), with weakly positive expression. CONCLUSION: MP can protect gastric mucosa, cure gastric ulcer, restrain the secretion of gastric acid, and boost multiplication, differentiation, migration and repair of the endothelial cell by promoting the secretion of NO and EGF, and increasing the expression of EGFR of gastric mucosa epithelial cells.

[Investigation on the health-related quality of life among 411 patients with irritable bowel syndrome].

OBJECTIVE: To evaluate and compare the health-related quality of life (HRQOL) on patients with irritable bowel syndrome (IBS). METHODS: Following the Rome III Criteria, 411 IBS patients and 430 healthy people were selected as subjects,who were outpatients in Department of Gastroenterology, 2nd Hospital of Xi' an Jiaotong University and Shaanxi Provincial People's Hospital from July 2006 to April 2007. Using the 36-Item Short-Form Health Survey (SF-36). This study compared the SF-36 scale scores of IBS patients with the healthy people. RESULTS: On all of the 8 SF-36 scales, patients with IBS scored significantly lower than healthy people (P < 0.001). Decrements in HRQOL were most predominant in general health perception and role limitations caused by emotional health problem, with scores of 33.5 + 16.9, 40.8 +/- 25.1 respectively. The emotional well-being and energy/fatigue scale scores were also quite low (42.2 +/- 19.3,43.1 +/- 20.2,respectively). They also scored significantly lower on both physical summary. and mental summary scores (P < 0.001). IBS patients were classified into IBS with constipation,IBS with diarrhea, mixed IBS and unsubtyped IBS subgroups, with percentages as 25.3%, 50.1%, 11.2% and 13.4% respectively. CONCLUSION: IBS patients experienced great impairment in HRQOL. These data offered further insight into the impact of IBS on patient functional status and well-being.