Mechanism by Which Tong Xie Yao Fang Heals the Intestinal Mucosa of Rats with Ulcerative Colitis through the Hippo Pathway.

OBJECTIVE: Tong Xie Yao Fang (TXYF) is a classic and effective prescription in traditional Chinese medicine which is used to treat ulcerative colitis (UC). Our study investigated the effect of TXYF on Hippo pathway activation in UC-induced intestinal mucosa injury and explored the possible mechanism. METHOD: After ulcerative colitis was successfully induced by trinitrobenzene sulfonic acid (TNBS), 48 Sprague Dawley (SD) rats were randomly divided into a control group, model group, TXYF group, and sulfasalazine group and treated with the corresponding drugs for 28 days. The parameters including body weight, colon length, spleen index, and disease activity index (DAI) and histopathological characteristics were assessed. The myeloperoxidase (MPO) activity and IL-6 level in the colon mucosa were determined with the corresponding commercial kits. The expressions of the Hippo pathway components YAP1, TAZ, P-YAP, and LATS1 were detected in the colon mucosa of each group on different stages by quantitative real-time PCR (qRT-PCR) and western blotting. Immunohistochemical staining was used to evaluate the growth and apoptosis of the colon epithelium. RESULT: TXYF significantly improved the weight loss, colonic shortening, DAI, spleen enlargement, and histopathological score of the rats with TNBS-induced UC. TXYF also reduced the MPO activity and expression of IL-6 in the colon mucosa. Furthermore, treatment with TXYF significantly increased YAP1 expression in the early stage (3-7 days) and significantly decreased YAP1 expression in the late stage (14-28 days). In the early stage, TXYF inhibited Hippo pathway activity, which promoted proliferation and regeneration of the intestinal mucosa. In the late stage, the Hippo pathway was activated, thereby inhibiting apoptosis and promoting intestinal mucosal differentiation. CONCLUSION: TXYF alleviated the inflammatory response and promoted mucosal healing in rats with UC, which was probably achieved through the Hippo pathway. These results indicated that TXYF was a potential therapy for treating UC.

Detachable string magnetically controlled capsule endoscopy for complete observation of the upper gastrointestinal tract.

BACKGROUND: Wireless magnetically controlled capsule endoscopy (WMCCE) was feasible, well tolerated, highly acceptable, and had high consistency in diagnosis of gastric diseases with esophagogastroduodenoscopy (EGD). But WMCCE is not suitable for inspection of the esophagus. We developed detachable string magnetically controlled capsule endoscopy (DS-MCCE) to observe gastroesophageal diseases. METHODS: A total of 60 volunteers were enrolled. Thirty participants underwent DS-MCCE, and the other 30 underwent WMCCE. The primary outcome measures included swallowing time, esophageal transit time, the whole examination time, grade of air-bubble interference on esophageal, gastric preparation, visualization of Z-line and gastric mucosa, and discomfort scores. RESULTS: The esophageal time (222.53 ± 107.53 s vs. 49.50 ± 34.90 s, P < 0.001) and the whole examination time (26.53 ± 6.33 min vs. 15.97±4.90 min, P < 0.001) in DS-MCCE group were longer than in WMCCE group. DS-MCCE had a significantly better visualization of Z-line visualization. Visualization of the gastric mucosa was assessed as good in 24 (80%) participants for DS-MCCE and 26 (86.6%) for WMCCE, moderate in 6 (20%) with DS-MCCE as compared with 4 (13.3%) with WMCCE. The visualization of gastric cardia for DS-MCCE was better than for WMCCE (100 vs 80%, P = 0.024). The visualization of gastric angle, antrum, and pylorus in DS-MCCE group was not as good as in WMCCE group (80 vs. 100%, 80 vs. 100%, 83.3 vs. 100%, P = 0.024). CONCLUSIONS: DS-MCCE is feasible and well tolerated in the diagnosis of gastroesophageal diseases. For people who cannot stand conventional EGD or with contraindication of EGD, DS-MCCE may be an excellent alternative screening modality.

Silencing long non-coding RNA CASC9 inhibits colorectal cancer cell proliferation by acting as a competing endogenous RNA of miR-576-5p to regulate AKT3.

Increasing studies have shown that long non-coding RNAs (lncRNAs) are regarded as important regulators in the occurrence and development of colorectal cancer (CRC). Although lncRNA CASC9 has been studied in CRC, the detailed regulatory mechanism of CASC9 in CRC is still unclear. In this study, we found that CASC9 was significantly upregulated in CRC tissues and cell lines compared to normal controls and that aberrant expression was associated with the tumor-node-metastasis (TNM) stage of CRC. Functionally, CASC9 depletion efficiently inhibited the proliferation of CRC cells and induced cell apoptosis in vitro. Mechanistically, CASC9 was mainly enriched in the cytoplasm of CRC cells and interacted directly with miR-576-5p. Downregulation of miR-576-5p reversed the inhibitory effect of CASC9 siRNA on CRC cell progression. Furthermore, AKT3 has been identified as a downstream target of miR-576-5p. Spearman's correlation analysis revealed that AKT3 was negatively correlated with miR-576-5p but positively correlated with CASC9. Downregulation of miR-576-5p restored the effect of CASC9 silencing on AKT3 expression. Therefore, silencing CASC9 could downregulate the expression of AKT3 by reducing the competitive binding of CASC9 to miR-576-5p, thus suppressing CRC cell proliferation and promoting cell apoptosis. In summary, we identified CASC9 as an oncogenic lncRNA in CRC and defined the CASC9/miR-576-5p/AKT3 axis, which might be considered a potential therapeutic target for CRC patients, as a novel molecular mechanism implicated in the proliferation and apoptosis of CRC.

The mechanism and role of intracellular α-ketoglutarate reduction in hepatic stellate cell activation.

BACKGROUND: The activation of hepatic stellate cells (HSCs) plays a central role in liver fibrosis. α-ketoglutarate is a natural metabolite and previous studies have shown that increase in intracellular α-ketoglutarate can inhibit HSC activation. AIM: The aim of the present study is to determine the changes and role of intracellular α-ketoglutarate in HSC activation and clarify its mechanism of action. METHODS: A human HSC cell line (LX-2) and the primary mouse HSC were used in the present study. We detected the changes of intracellular α-ketoglutarate levels and the expression of enzymes involved in the metabolic processes during HSC activation. We used siRNA to determine the role of intracellular α-ketoglutarate in HSC activation and elucidate the mechanism of the metabolic changes. RESULTS: Our results demonstrated that intracellular α-ketoglutarate levels decreased with an HSC cell line and primary mouse HSC activation, as well as the expression of isocitrate dehydrogenase 2 (IDH2), an enzyme that catalyzes the production of α-ketoglutarate. In addition, knockdown of IDH2 efficiently promoted the activation of HSCs, which was able to be reversed by introduction of an α-ketoglutarate analogue. Furthermore, we demonstrated that α-ketoglutarate regulated HSC activation is independent of transforming growth factor-ß1 (TGF-ß1). CONCLUSIONS: Our findings demonstrated that decrease in IDH2 expression limits the production of α-ketoglutarate during HSC activation and in turn promotes the activation of HSCs through a TGF-ß1 independent pathway. The present study suggests that IDH2 and α-ketoglutarate may be potential new targets for the prevention and treatment of liver fibrosis.

Comparing about three types of endoscopic therapy methods for upper gastrointestinal submucosal tumors originating from the muscularis propria layer.

Background: Endoscopic submucosal excavation (ESE), endoscopic full-thickness resection (EFTR) and submucosal tunneling endoscopic resection (STER) have been widely applied to upper gastrointestinal submucosal tumors (SMTs) originating from the muscularis propria (MP) layer in recent years. But until now, there are few studies that comparing the efficacy and safety of three endoscopic therapy methods.Method: From January 2013 to August 2018, a total of 218 patients with SMTs who underwent ESE, EFTR or STER were enrolled in this retrospective study. Clinicopathological characteristics, endoscopic features, complication and follow-up data were analyzed.Result: There were 114 patients underwent ESE, 61 underwent EFTR and 43 underwent STER, respectively. The en bloc and complete resection rates in STER group (83.7% and 90.0%) were significantly lower and postoperative complication rate (62.8%) was significantly higher than those of the other 2 methods. Furthermore, for lesions <40 mm, no significant differences were found in the en bloc rate, complete rate and postoperative complication rate among 3 methods. The perforation rate decreased in the order of EFTR (100%), ESE (23.7%), STER (7.0%). The median number of clips, fasting time and hospital stay were lowest in ESE group (5, 2 days, and 7 days). And the cost was highest in EFTR group ($4993.1). There were no differences in the bleeding and recurrence rates among three groups.Conclusion: For SMTs <40 mm, the efficacy among 3 ER methods are comparative. The choice of ER methods mainly based on the comprehensive consideration of lesion size, location, growth pattern and clinical experience of endoscopists. For benign SMTs ≥40 mm in stomach, ESE and EFTR becomes alternative choices.

Knockdown of lncRNA H19 inhibits abnormal differentiation of small intestinal epithelial cells in diabetic mice.

Diabetes mellitus (DM) comprises a group of metabolic diseases characterized by insulin deficiency or resistance and hyperglycemia. We previously reported the presence of abnormal differentiation of small intestinal epithelial cells (IECs) in diabetic mice, but the exact mechanism of this phenomenon has not been thoroughly elucidated to date. In this study, we found that H19 was markedly upregulated in IECs of DM mice. H19 knockdown significantly inhibited abnormal differentiation of IECs in DM mice. Bioinformatics analysis identified miR-141-3p as a candidate for H19. Based on luciferase reporter assays, we found that miR-141-3p directly targeted H19. Luciferase reporter assays also showed that miR-141-3p could directly target ß-catenin. Furthermore, H19 might act as an endogenous "sponge" by competing for miR-141-3p binding to regulate miRNA targets in vitro and in vivo. In summary, our findings provide the first evidence supporting the role of H19 in IECs of DM mice, and miR-141-3p targets not only protein-coding genes but also the lncRNA H19.

The lncRNA ZEB1-AS1 sponges miR-181a-5p to promote colorectal cancer cell proliferation by regulating Wnt/ß-catenin signaling.

Long noncoding RNAs (lncRNAs) are important regulators of the biological functions and underlying molecular mechanisms of colorectal cancer (CRC). However, the role of the lncRNA ZEB1-AS1 in CRC is not thoroughly understood. In this study, we found that ZEB1-AS1 was markedly upregulated in CRC. ZEB1-AS1 knockdown significantly suppressed CRC cell proliferation and induced apoptosis, whereas enhanced expression of ZEB1-AS1 had the opposite effect. Bioinformatics analysis identified miR-181a-5p as a candidate target of ZEB1-AS1. Moreover, we found an inverse correlation between ZEB1-AS1 and miR-181a-5p expression in CRC tissue. Inhibition of miR-181a-5p significantly upregulated ZEB1-AS1, whereas overexpression of miR-181a-5p had the opposite effect, suggesting that ZEB1-AS1 is negatively regulated by miR-181a-5p. Using luciferase reporter and RIP assays, we found that miR-181a-5p directly targets ZEB1-AS1. Importantly, ZEB1-AS1 may act as an endogenous 'sponge' to regulate miRNA targets by competing for miR-181a-5p binding. In summary, our findings provide the evidence supporting the role of ZEB1-AS1 as an oncogene in CRC. Our study also demonstrates that miR-181a-5p targets not only protein-coding genes but also the lncRNA ZEB1-AS1.

MicroRNA-185 suppresses pancreatic cell proliferation by targeting transcriptional coactivator with PDZ-binding motif in pancreatic cancer.

The aim of the present study was to compare the expression of transcriptional coactivator with the PDZ-binding motif (TAZ) in pancreatic cancer (PC) patients, and to investigate the regulation mechanisms of TAZ in the proliferation of PC. PC tissues and matched peritumoral tissues, pancreatic juice and serum were collected from PC patients who underwent pancreatectomy between June 2012 and December 2015 at the Affiliated Hospital of Qingdao University (Qingdao, China). Pancreatic juice and serum were collected from patients with chronic pancreatitis as a control. The levels of taz mRNA expression in the samples were examined by reverse-transcription quantitative polymerase chain reaction, and the protein expression of TAZ was assessed by western blot analysis and ELISA. MicroRNAs (miRNAs) that regulate TAZ expression were also predicted by bioinformatics analysis and validated by dual luciferase reporter and rescue assays. In addition, the proliferation of PC cells was evaluated after transfection with TAZ small interfering RNA (siRNA) or its upstream miRNA agomir. Expression of TAZ was significantly increased in the PC tissues, pancreatic juice and serum of PC patients at the mRNA and protein levels compared with controls (P<0.05). Furthermore, TAZ was predicted and verified to be a target of miRNA (miR)-185, and miR-185 and TAZ were inversely expressed in samples from PC patients (P<0.05). In addition, TAZ siRNA or agomiR-185 transfection significantly inhibited human pancreatic adenocarcinoma cell proliferation (P<0.05). However, overexpression of TAZ in the agomiR-185 group rescued the inhibition (P<0.05). Finally, the expression of TAZ effector proteins, namely ankyrin repeat domain-containing protein and cysteine-rich 61, were upregulated in PC tissues (P<0.05), but repressed following transfection of PC cells with agomiR-185 (P<0.05). Thus, miR-185 may regulate the proliferation of PC by targeting TAZ, making it a promising diagnostic marker for PC.

Association of polymorphisms in key Th-17 immune response genes with HBeAg-positive chronic hepatitis B susceptibility and response to PEG-IFNa-2α.

This study aims to investigate effects of polymorphisms in key Th-17 immune response genes on the susceptibility to HBeAg-positive (HBeAg+) chronic hepatitis B (CHB) and response to PEG-IFNa-2α. A total of 139 patients with HBeAg+ CHB treated with PEG-IFNa-2α and 145 healthy controls were enrolled to explore the association between IL-17A, IL-17F, IL-21 and IL-23R polymorphisms and HBeAg+ CHB susceptibility, as well as treatment efficacies. Genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and DNA sequencing. IL-17A rs4711998 and IL-17F rs763780 may affect susceptibility to HBeAg+ CHB and response to PEG-IFNa-2α treatment. The T allele of IL-21 rs12508721 may lower HBeAg+ CHB susceptibility but enhance PEG-IFNa-2α response, and the GA genotype and the A allele of IL-23R rs11209026 may reduce the susceptibility to HBeAg+ CHB. Th17-related gene polymorphisms were linked to HBeAg+ CHB susceptibility, and rs4711998, rs763780 and rs12508721 were associated with sustained responses to PEG-IFNa-2α.

Cervical lymph node thyroglobulin measurement in washout of fine-needle aspirates for diagnosis of papillary thyroid cancer metastases.

BACKGROUND: Patients with papillary thyroid cancer (PTC) and enlarged cervical lymph nodes (CLNs) are usually assessed by fine-needle aspiration biopsy cytology (FNAB-C). Thyroglobulin (Tg) is frequently detected in washout of fine-needle aspirates (FNA) of these lymph nodes. The aim of this study was to evaluate the accuracy of the measurement of FNAB-Tg in the washout of FNAB in combination with FNAB-C to detect CLN metastases in PTC. METHODS: We retrospectively evaluated 163 surgically proven CLNs. Ultrasound-guided FNAB-C and FNAB-Tg measurements were performed and the ultrasound features were evaluated. RESULTS: The sensitivity, specificity and accuracy of FNAB-C, FNAB-Tg and FNAB-C/FNAB-Tg in diagnosis of metastatic CLNs were 85.7, 87.8 and 71.6%, were 80.5, 87 and 82.8% and were 97.1, 96.3 and 95.7%, respectively. The diagnostic sensitivity, specificity and accuracy of FNAB-C/FNAB-Tg for metastatic CLNs was significantly higher than that of FNAB-C or FNAB-Tg alone (p < 0.01). CONCLUSION: Combined US-guided FNAB-C and FNAB-Tg can improve the accuracy for diagnosis of metastatic CLNs in patients with PTC.

Fine needle aspiration cytology for lymph nodes: a three-year study.

BACKGROUND AND AIMS: The cytologic patterns of lymph node fine needle aspirations (FNAs) exhibit a wide variation in different diseases and in different ethnic groups in various geographical locations. Knowledge of lymphadenopathy patterns in a given geographical region is essential for making a confident diagnosis of suspected disease in that location. In the present study, we assessed the cytologic patterns of lymph node aspirations in patients in the Huangdao region of China. METHODS: A three-year retrospective study design was conducted on FNA cytology samples from the lymph nodes of patients in our hospital between January 2011 and December 2014. RESULTS: A total of 2136 lymph nodes were aspirated during the study period. Cytologic analysis of the lymph nodes revealed the following: malignancy, 53.6%; chronic non-specific lymphadenitis, 15.2%; reactive lymph node, 7.5%; pyogenic abscess, 2.9%; tuberculosis lymphadenitis, 8.7%; Hodgkin lymphoma, 4.8%; and non-Hodgkin lymphoma, 7.16%. The 30-50 year age group was the most affected age group, while lymphadenopathy in the >60 year age group was less frequent. Cervical lymph nodes were the most frequent site for lymphadenopathy in women (31.4%, p < 0.001) and men (49.1%, p < 0.001). CONCLUSIONS: Lymphadenopathy is associated with a wide range of disorders; however, metastatic lymph nodes of malignancies are the most common cause for enlarged lymph nodes.

Hydrogen sulfide from a NaHS source attenuates dextran sulfate sodium (DSS)-induced inflammation via inhibiting nuclear factor-κB.

This study investigated the alleviating effects of hydrogen sulfide (H2S), derived from sodium hydrosulfide (NaHS), on inflammation induced by dextran sulfate sodium (DSS) in both in vivo and in vitro models. We found that NaHS injection markedly decreased rectal bleeding, diarrhea, and histological injury in DSS-challenged mice. NaHS (20 µmol/L) reversed DSS-induced inhibition in cell viability in Caco-2 cells and alleviated pro-inflammation cytokine expression in vivo and in vitro, indicating an anti-inflammatory function for H2S. It was also found that H2S may regulate cytokine expression by inhibiting the nuclear factor-κB (NF-κB) signaling pathway. In conclusion, our results demonstrated that H2S alleviated DSS-induced inflammation in vivo and in vitro and that the signal mechanism might be associated with the NF-κB signaling pathway.

In-depth analysis of the critical genes and pathways in colorectal cancer.

The present study aimed to investigate the molecular targets for colorectal cancer (CRC). Differentially expressed genes (DEGs) were screened between CRC and matched adjacent noncancerous samples. GENETIC_ASSOIATION_DB_DISEASE analysis was performed to identify CRC genes from the identified DEGs using the Database for Annotation, Visualization and Integrated Discovery, followed by Gene Οntology (GO) and Kyoto Encyclopedia of Genes and Genomes analysis for the CRC genes. A protein­protein interaction (PPI) network was constructed for the CRC genes, followed by determination and analysis of the hub genes, in terms of the protein domains and spatial structure. In total, 35 CRC genes were determined, including 19 upregulated and 16 downregulated genes. Downregulated N­acetyltransferase (NAT)1 and NAT2 were enriched in the caffeine metabolism pathway. The downregulated and upregulated genes were enriched in a number of GO terms and pathways, respectively. Cyclin D1 (CCND1) and proliferating cell nuclear antigen (PCNA) were identified as the hub genes in the PPI network. The C­terminal and N­terminal domains were similar in PCNA, but different in CCND1. The results suggested PCNA, CCND1, NAT1 and NAT2 for use as biomarkers to enable early diagnosis and monitoring of CRC. These results form a basis for developing therapies, which target the unique protein domains of PCNA and CCND1.

Dissecting the mechanism of colorectal tumorigenesis based on RNA-sequencing data.

OBJECTIVE: This study aimed to identify the differentially expressed genes (DEGs), mutated genes and fusion genes in colorectal cancer. MATERIALS AND METHODS: RNA-sequencing data (ID: SRP009386) from cancerous, paracancerous non-tumor and distant normal tissue from one Chinese patient with stage III colorectal cancer were downloaded from Sequence Read Archive. Quality control was checked using FastQC, followed by sequence alignment against the hg19 reference genome using TopHat v1.3.3. The expression levels were quantified using Cufflinks, followed by DEGs screening using NOISeq. Enrichment analysis was performed using DAVID. Transcription factors were screened using TRANSFA. Mutated loci were identified using SAMTools and VCFTools. Gene fusion events were detected by TopHat-fusion. RESULTS: In total 2440, 1887 and 834 DEGs were respectively detected in cancerous vs. normal tissue, cancerous vs. paracancerous tissue and paracancerous vs. normal tissue. The up-regulated genes from cancerous and paracancerous tissue compared with normal tissue were enriched in "extracellular matrix receptor interaction" and "focal adhesion pathway" as well as some biological processes except for "negative regulation of programmed cell death" uniquely presenting in cancer. Dysregulated transcription factors including SOX4, BCL6, CEBPB and MSX2 were enriched in the unique biological process. Trp53 was identified with one mutated locus 7577142 (C → T) on chromosome 17. BCL6 also experienced missense mutation. Additionally, COL1A1-PPP2R2C and EXPH5-COL1A2 were observed fusion genes in cancer tissue. CONCLUSIONS: The unique biological process in cancer tissue may be the cause for colorectal carcinogenesis. The screened transcription factors, mutated genes and fusion genes may contribute to the progression of colorectal cancer.

Expression of Beclin1 in the colonic mucosa tissues of patients with ulcerative colitis.

To investigate the expression of Beclin1 in the colonic mucosa tissue of patients with ulcerative colitis (UC), which acts as a regulator of autophagy and might play a part in the disease progression potentially. A total of 112 patients were selected from September 2013 to November 2014, and their colonic mucosal tissues were collected as the subject of study. Among them, 75 cases were diagnosed with ulcerative colitis (UC), 37 cases were diagnosed with irritable bowel syndrome (IRS) during the same time, which was set as the control group. The mucosal tissues were processed with ELISA and IHCA to measure the expression level of Beclin1, and correlation analysis was performed to demonstrate its role in the disease progression. The expression level pf Beclin1 was significantly higher in the UC patients compared with the control group (P<0.05). Meanwhile, it's positively correlated with the severity of disease, the endoscopic classification and the pathologic staging results, which has statistical significance (P<0.05). Beclin1 was expressed at a higher level in UC patients, and correlated with the severity of the disease, indicating the abnormal regulation of autophagy in the disease progression.

Study on the diversity of Bacteroides and Clostridium in patients with primary gout.

To analyze the diversity of both Bacteroides and Clostridium in patients with primary gout and the difference from that of normal individuals. And to investigate the relationship between the primary gout and the intestinal flora. Fecal samples of 90 cases with the primary gout and 94 cases normal comparison group were selected, together with the cases that match the filter criteria. The DNA is extracted from the feces. 16S rRNA specific primers of both Bacteroides and Clostridium were adopted for the PCR amplification. The molecular fingerprints of Bacteroides and Clostridium in both the primary gout group and the normal control group were obtained through DGGE and subjected for further analysis on both the diversity and the similarity. Compared with normal individuals, the number of bands and Shannon-Weaver (H') of Bacteroides in patients with primary gout was not reduced, but significantly decreased in Clostridium. Furthermore, the intra-group and inter-group similarity of both Bacteroides and Clostridium were lower. The primary gout has caused the structural change of both Bacteroides and Clostridium, inducing the low similarity, especially for Clostridium. It has statistic significance. The gut predominant flora may play an important role in the development of primary gout.

Construction and Antiapoptosis Activities of Recombinant Adenoviral Expression Vector Carrying EBV Latent Membrane Protein 2A.

To evaluate the possible effects of LMP2A (EBV latent membrane protein 2A) on human gastric cancer cell line SGC-7901, LMP2A coding gene was subcloned into shuttle plasmid pAdTrackCMV to form transfer plasmid pAdTrackCMV-2A, which was linearized with PmeI and cotransformed into E.coli BJ5183 with adenovirus genomic plasmid of pAdeasy-1. The identified recombinant adenovirus plasmid DNA was digested with PacI and transfected into 293 cells to package recombinant adenovirus particles named vAd-2A. Then the expression and antiapoptosis activities of LMP2A on SGC-7901 infected with vAd-2A were analyzed. The vAd-2A was successfully constructed and identified by PCR, restriction digestion, and sequencing. LMP2A expression in SGC was identified by strong green fluorescence expression with fluorescence microscopic photograph and Southern blotting. The growth of LMP2A expressing SGC cells was apparently improved. Both cyclin E expression and S phase ratio in LMP2A expressing SGC cells were upregulated by cell cycle analysis and confocal microscopic analysis respectively. The replication-deficient recombinant adenovirus vector can express LMP2A antigen in SGC cells and inhibit their apoptosis. The results indicate that LMP2A might play an important role in pathogenesis of EBV-associated gastric cancer (EBVaGC). This study establishes a foundation for further study on EBVaGC and its gene therapy.

[The clinical characteristics of postinfectious irritable bowel syndrome in Qingdao].

OBJECTIVE: To investigate the clinical characteristics of postinfectious irritable bowel syndrome (PI-IBS) in Qingdao. METHODS: Two hundred and four PI-IBS and 2068 non-PI-IBS patients were investigated with questionnaire including general information, symptoms and quality of life scores with microecological study before and after therapy. RESULTS: (1) The morbidity rate of PI-IBS in female was 2. 2 times of that in male, which was similar to that in non-PI-IBS. (2) Brain work labors dominated in both PI-IBS and non-PI-IBS patients. (3) As to the simultaneous presence of extra-gastrointestinal symptoms, there was no statistical difference between the rate of physical symptoms in PI-IBS and non-PI-IBS patients (chi2 =10.5, P > 0.05), but the rate of mental symptoms was higher in PI-IBS than in non-PI-IBS patients, and the difference was significant (chi2 = 28.7, P < 0.05). (4) The alteration of intestinal microflora rate in PI-IBS was obviously higher than that in non-PI-IBS patients. (5) The quality of life scores in PI-IBS was improved after treatment with Birid Triple Viable , and there was significant difference (t = 3.8, P < 0.01), but there was no statistical difference in non-PI-IBS (t = 1.5, P > 0.05). CONCLUSION: There was some difference in certain clinical characteristics between PI-IBS and non-PI-IBS patients in Qingdao.

Effects of Zhaoyangwan on chronic hepatitis B and posthepatic cirrhosis.

AIM: To study the therapeutic effects of zhaoyangwan (ZYW) on chronic hepatitis B and hepatic cirrhosis and the anti-virus, anti-fibrosis and immunoregulatory mechanisms of ZYW. METHODS: Fifty cases of chronic hepatitis B and posthepatic cirrhosis with positive serum HBsAg, HBeAg, anti-Hbc and HBV-DNA were divided randomly and single-blindly into the treatment group (treated with ZYW) and the control group (treated with interferon). After 3 month treatment, the effects of the treatment group and the control group were evaluated. RESULTS: The serum ALT normalization was 83.3% (30/36) in the treatment group and 85.7% (12/14) in the control group, with no significant difference (chi2=0.043, P>0.05). After the course, the negative expression rates of the serum HBV-DNA and HBeAg were 44.4% (16/36) and 50% (18/36) in the treatment group, and 50% (7/14) and 50% (7/14) in the control group, respectively, with no significant difference (chi2=0.125, chi2=0.00, both P>0.05). Negative HBsAg and positive HBsAb appeared in 4 cases of the treatment group and 1 case of the control group. Serum anti-HBc turned negative in 6 cases of the treatment group and 1 case of the control group, respectively. After the ZYW treatment, serum CD3+, CD4+, CD8+, CD4+/CD8+ and NK cell activation were significantly increased. Only serum CD3+ and NK cell activation were significantly increased in the control group with a significant difference between the two groups. The serum C4, C1q, C3, B and C9 were significantly increased in the treatment group. In the control group only the serum C4 was increased. The concentration of serum interferon had no change after treatment with ZYW, while it was significantly increased in the control group after treatment with interferon. The ultrastructure of the liver restored, which helped effectively to reduce the degeneration and necrosis of hepatic cells,infiltration of inflammatory cells and hepatic cirrhosis. CONCLUSION: ZYW is a pure Chinese herbal medicine. It can exert potent therapeutic effects on chronic hepatitis B and posthepatic cirrhosis. ZYW has similar therapeutic effects to those of interferon. It is cheap and easily administered with no obvious side-effects. It can be widely used in clinical practice.