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ABSTRACT: Nodular regenerative hyperplasia (NRH) of liver may be one of the leading causes of non-cirrhotic intrahepatic portal hypertension (NCIPH), although the exact relationship is currently unknown. Diagnosis of NRH is relatively difficult and involves surgical pathology, and thus it is necessary to improve the preoperative recognition of NRH. Here, we analyze 15 cases of NRH to better understand this disease. All the liver specimens were microscopically examined by hematoxylin-eosin staining and reticulin and Masson trichrome staining. Diagnoses of NRH were confirmed by pathological examination. Clinically, NRH presents as diffused liver lesions with mildly increased liver enzymes. Portal hypertension is the most common clinical manifestation presenting prominently as splenomegaly, hypersplenism, and esophageal varices bleeding. NRH is often associated with autoimmune or collagen vascular diseases, and such patients often present with a variety of positive autoantibodies and increased erythrocyte sedimentation rate (ESR), Ig and γ %. Pathological examination of the liver showed diffuse small regenerative nodules without fibrous septa and obstructive portal venopathy. For those patients with portal hypertension of unknown cause and preserved liver function, especially, those combined with autoimmune diseases, NRH should be considered.
Cell biochemistry and biophysics 06/2012; 64(2):115-21. · 3.34 Impact Factor
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12/2011; , ISBN: 978-953-51-0410-0
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ABSTRACT: To prospectively assess the utility of multidetector row computed tomography angiography (MDCTA) in the diagnosis of active gastrointestinal bleeding (GIB).
MDCTA is a relatively recent advance in CT scanning technology enabling excellent vascular visualization and detection of various vascular abnormalities. However, there is no prospective study with a large population evaluating the role of MDCTA in the diagnosis of active GIB.
From January 2006 to January 2011, 113 consecutive patients with clinical signs of active GIB underwent MDCTA (16-slice, 64-slice, or dual-source). The criteria for positive CT findings included active extravasation of contrast material within bowel lumen, abnormal bowel mucosal enhancement, vascular malformation, abnormally enhancing polyp or diverticulum, or tumor. Two radiologists reviewed the images and assessed CT findings in consensus. The standards of reference included digital subtraction angiography, endoscopy, surgery, or final pathology reports. Sensitivity, specificity, positive and negative predictive values, and accuracy of MDCTA for detection of active GIB were evaluated.
Positive CT findings for active GIB were identified in 80 of 113 patients (70.8%), all of which were confirmed by 1 or more reference standard. Negative MDCTA results were obtained in 33 patients (29.2%). Of these, 27 patients did not require any further intervention and were discharged without incident. The overall sensitivity, specificity, positive and negative predictive values, and accuracy of MDCTA was 86.0%, 100%, 100%, 60.6%, and 88.5%, respectively.
MDCTA is an accurate first-line screening method for detection and localization of GIB and can guide triage in patients with active GIB.
Journal of clinical gastroenterology 11/2011; 46(1):31-41. · 2.21 Impact Factor
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Jihua Shi,
Lu Zhou,
Alexandra Zhernakova, Jiaming Qian,
Feng Zhu,
Gang Sun,
Liming Zhu,
Xuejun Ma,
Gerard Dijkstra,
Cisca Wijmenga,
Klaas Nico Faber,
Xinghua Lu,
Rinse K Weersma
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ABSTRACT: The incidence of ulcerative colitis (UC) varies between Western and Eastern ethnicities. A distinct genetic background may play a role in the differences. Until now, very little was known of the UC genetics in Asian populations. Here we performed a haplotype-based analysis of six known UC susceptibility loci in Han Chinese patients.
In all, 245 UC patients and 300 healthy controls of Han Chinese descent were genotyped for 27 single nucleotide polymorphisms (SNPs), which cover the major haplotypes of the chromosome regions containing IL10, IL2/IL21, MYO9B, ECM1, MST1, and IL23R in Han Chinese.
In contrast to the tight linkage disequilibrium (LD) block of the IL2/IL21 region in Caucasians, IL2 and IL21 reside in two independent LD blocks in Han Chinese. The IL2 SNP rs2069762 (P = 7.0 × 10(-4) , odds ratio [OR] = 1.54, 95% confidence interval [CI] 1.20-1.99) and the IL21 SNP rs2055979 (P = 1.2 × 10(-4) , OR = 1.50, 95% CI 1.17-1.92) were independently associated with UC. We identified one risk haplotype in IL2 and another independent risk haplotype in IL21. In addition to the IL2/IL21 locus, we observed association of the TT genotype of SNP rs1545620 in MYO9B with UC (P = 0.0169; OR = 0.29, 95% CI 0.11-0.78) and association of rs17375018 in IL23R with pancolitis in Chinese UC patients (P = 0.002; OR = 2.38, 95% CI 1.41-4.02).
Our study confirmed the association of the IL2/IL21 region with UC in Han Chinese patients, and further implied both IL2 and IL21 as genetic risk factors for UC. Han Chinese UC patients share part of their genetic susceptibility with Caucasian patients.
Inflammatory Bowel Diseases 06/2011; 17(12):2472-9. · 4.86 Impact Factor
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Zhanju Liu,
Praveen K Yadav,
Xiaorong Xu,
Jingling Su,
Chi Chen,
Maochun Tang,
Hui Lin,
Jifeng Yu, Jiaming Qian,
Ping-Chang Yang,
Xingpeng Wang
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ABSTRACT: This study analyzed IL-23p19 expression in inflamed mucosa of IBD and the role in the induction of IEL and NK cell activation as well as Th17 cell differentiation. Expression of IL-23p19 was performed by immunohistochemistry and quantitative real-time PCR. Expression of IL-23R was assessed by flow cytometry. Cytolytic activities of IEL and NK cells by IL-23 were determined by a standard (51)Cr-release assay. Cytokine levels were analyzed by ELISA and quantitative real-time PCR. Expression of IL-23p19 was increased significantly in inflamed mucosa of CD compared with that in UC and healthy controls. Double-staining confirmed that IL-23p19(+) cells were mainly CD68(+) macrophages/DCs. IL-23R(+) cells were increased significantly in PB- and LP-CD4(+) and -CD8(+) T and NK cells. IL-23 markedly promoted IBD IEL and NK cell activation and cytotoxicity and triggered IBD PB- and LP-T cells to secrete significantly higher levels of IFN-γ, TNF, IL-2, and IL-17A compared with controls. Importantly, IL-23 promoted IBD PB- or LP-CD4(+) T cells to differentiate into Th17 cells, characterized by increased expression of IL-17A and RORC. Anti-TNF treatment could markedly reduce IL-23 expression and Th17 cell infiltration in inflamed mucosa of CD patients. These data indicate that IL-23 is highly expressed in inflamed mucosa of IBD and plays an important role in the induction of IEL, NK, and T cell activation, proinflammatory cytokine secretion, and Th17 cell differentiation. Targeted therapy directed against IL-23p19 may have a therapeutic role in treatment of IBD.
Journal of leukocyte biology 01/2011; 89(4):597-606. · 4.99 Impact Factor
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ABSTRACT: To evaluate the association of the IBD5 locus to the predisposition of inflammatory bowel diseases (IBDs), a series of meta-analyses between five IBD5 variants (OCTN1 C1672T, OCTN2 G-207C, OCTN1/2 TC haplotype, IGR2096a_1, IGR2198a_1 and IGR2230a_1) and Crohn's disease (CD) and ulcerative colitis (UC) were performed, which included a total of 26 studies. Overall, five IBD5 variants in a per-allele model of inheritance were significantly associated with elevated CD risk (for OCTN1: OR = 1.23, 95% CI = 1.16-1.30, P < 0.001; for OCTN2: OR = 1.20, 95% CI = 1.11-1.30, P < 0.001; for IGR2096a_1: OR = 1.36, 95% CI = 1.24-1.46, P < 0.001; for IGR2198a_1: OR = 1.34, 95% CI = 1.24-1.46, P < 0.001; for IGR2230a_1: OR = 1.35, 95% CI = 1.23-1.48, P < 0.001) and OCTN1/2 TC haplotype (OR = 1.32, 95% CI = 1.22-1.43, P < 0.001). In the subgroup analysis, the statistically significant associations were also observed in adult- and pediatric-onset CD and in Caucasians for five IBD5 variants and the OCTN1/2 TC haplotype. A statistically significant increase in the risk of UC was detected in a recessive model of inheritances for OCTN1 (OR = 1.23, 95% CI = 1.08-1.40, P < 0.001), OCTN2 (OR = 1.18, 95% CI = 1.05-1.33, P = 0.006), IGR2096a_1 (OR = 1.37, 95% CI = 1.15-1.62, P < 0.001) and IGR2198a_1 (OR = 1.35, 95% CI = 1.10-1.66, P = 0.004); the increased risks of UC were maintained in the adult and Caucasian subgroups, but not the pediatric subgroup. In summary, our results suggested that the IBD5 locus contributes to the susceptibility of CD in a per-allele manner in adults, children and Caucasians, and the locus contributes to the susceptibility of UC in a recessive manner in adult and Caucasian populations.
Human Genetics 01/2011; 129(6):597-609. · 5.07 Impact Factor
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ABSTRACT: A Ras homologue member I (ARHI) is an imprinted tumor suppressor gene whose expression is frequently lost in pancreatic cancers. This small GTP-binding protein is a member of the Ras superfamily with significant homology to Ras. In contrast to the Ras oncogene, ARHI has been shown to have anti-proliferative effects, but the mechanisms by which it inhibits pancreatic cancer cell proliferation and induces cell cycle arrest remain unclear. By generating stable transfectants, ARHI was reexpressed in pancreatic cancer cells that had lost its expression. Flow cytometry analysis indicated that ARHI blocked cell cycle progression at the G1 phase in pancreatic cancer cells. In ARHI transfectants, phosphorylated AKT protein expression decreased compared to that of vector transfectants. Reexpression of ARHI increased the expression of the cyclin-dependent kinase (CDK) inhibitor (CKI) p21WAF1, through the accumulation of p53 protein by the inhibition of PI-3K/AKT signaling. In addition, ARHI enhances expression of CKI p27kip1 through the inhibition of PI-3K/AKT signaling. The expression of cyclins A and D1 decreased, while cyclin E was not affected under the same conditions. The activities of cyclin-dependent kinases 2 (CDK2) and 4 (CDK4) were reduced in ARHI transfectants. These results suggest that the PI-3K/AKT pathway plays a pivotal role in the pathogenesis of pancreatic cancer and ARHI exerts its growth-inhibitory effects through modulation of several key G1 regulatory proteins, such as p21WAF1, p27kip1, CDK2, CDK4 and cyclins A and D1. ARHI represents a modulator of cancer cell proliferation and may play an important role in the development of pancreatic cancer.
Oncology Reports 10/2009; 22(3):635-40. · 1.84 Impact Factor
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ABSTRACT: The role of the brain-gut axis interaction in the pathogenesis of irritable bowel syndrome (IBS) is not well understood. To examine this possibility, a novel rat model of IBS subjected to both chronic and acute stress (CAS) was established. G proteins play a crucial role in the pathophysiology of depression. The alpha 2A adrenoceptor (alpha(2A)-AR) and the norepinephrine reuptake transporter (NET) determine the sympathetic signal activity. It is conceivable that stress may induce brain G proteins, colonic alpha(2A)-ARs, and NET abnormal expression, which may be responsible for the abnormalities in IBS. Colonic motility, visceral sensation, and secretion were assessed by counting fecal pellets, abdominal muscle contractions in response to colorectal balloon distension (CRD), and short-circuit current study, respectively. Western blot analysis was used to investigate the expression of G proteins, alpha(2A)-ARs, and NET. Compared with control animals, the colonic epithelial secretion, fecal pellets, and numbers of abdominal muscle contraction induced by CRD were significantly higher in both acute stress only (AS) and CAS rats. However, the G proteins, alpha(2A)-AR, and NET expression changed differently in AS and CAS rats. We showed that exposure to either AS or CAS would cause the increase of secretion, motility, and sensation, but the change of protein expression in brain-gut axis was different. It may be responsible for the pathogenesis of IBS.
Translational Research 01/2009; 152(6):283-9. · 2.99 Impact Factor
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ABSTRACT: This study was designed to evaluate the antiangiogenic properties of emodin and its ability to inhibit tyrosine-kinase-mediated phosphorylation of vascular endothelial growth factor (VEGF) receptors in colon cancer cells.
The effects of emodin on VEGF-receptor (VEGFR) phosphorylation were determined by assaying the tyrosine kinase activity and by Western blot analysis. The antiproliferative and proapoptotic activities of emodin were evaluated by soft agar colony formation, flow cytometric analysis of cell cycle, and by apoptotic assay.
Emodin causes a dose-dependent inhibition of VEGFR phosphorylation in colon cancer cells. Treatment with 40 muM of emodin decreased the relative activity of VEGFR-1 to 22.4%, when compared to the control group (assigned a value of 100%); VEGFR-2 and -3 showed a similar reduction in relative activity at 58.5% and 31.6%, respectively (p < 0.01, in each case). Treatment with emodin reduced VEGFR phosphorylation, as evidenced by Western blot analysis. Flow cytometric analysis showed that, upon treatment with emodin, the HCT116 cell cycle was blocked at the G2/M phase. Emodin also increased the apoptosis of HCT116 cells in a dose-dependent manner; treatment with 40 muM emodin increased the apoptotic rate from 8.1% +/- 2.7% in the control group to 27.8% +/- 10.9% in the treated group (p < 0.01).
These studies demonstrate that emodin may inhibit cancer-cell growth by blocking VEGFR signaling and indicate that emodin can be used as a potential inhibitor for tumor angiogenesis.
Cancer Biotherapy & Radiopharmaceuticals 04/2008; 23(2):222-8. · 1.44 Impact Factor
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Digestive Diseases and Sciences 07/2007; 52(6):1444-7. · 2.12 Impact Factor
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ABSTRACT: To explore new methods for the early diagnosis of pancreatic cancer through detection of K-ras and p53 mutations in pancreatic juice and stool.
201 patients in PUMC Hospital from 1994 - 2000 and 60 control individuals were enrolled in this study. K-ras point mutation was detected by PCR-RFLP while p53 mutation was detected by PCR-SSCP.
K-ras mutation was found in pancreatic juice in 87.8% (36/41) of pancreatic cancer patients and 23.5% (4/17) of benign pancreatic disease patients. In 261 stool specimens, amplification found mutations successfully in 235 patients (90%). K-ras mutation was found in stool in 88% (66/75) of pancreatic cancer patients, 51.1% (24/47) of benign pancreatic disease patients and 19.6% (9/46) of normal individuals. p53 mutation was found in pancreatic juice in 47.4% (18/38) of pancreatic cancer patients and 12.5% (2/16) of benign pancreatic disease patients. p53 mutation was found in stool in 37.1% (23/62) and 19.1% (4/21) of chronic pancreatitis patients.
K-ras mutation in pancreatic juice has higher diagnosis sensitivity and specificity, and therefore may be used as a supplement in the diagnosis of pancreatic cancer. Detection of K-ras mutation combined with p53 mutation in stool can aid in the screening of pancreatic cancer.
Chinese medical journal 12/2002; 115(11):1632-6. · 0.86 Impact Factor
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ABSTRACT: To probe the relationship between location and extent of ulcerative colitis (UC) by analyzing its extra-intestinal manifestations.
392 UC cases in Peking Union Medical College Hospital from 1976 to 2000 were reviewed retrospectively. Chi-square test was used to test the difference between groups.
82 of 392 patients (20.9%) with UC had extra-intestinal manifestations, 34 (8.7%) of these patients had more than one extra-colonic organ involvement; It shows that the extensive colitis has highest incidence of extra-intestinal manifestations with UC than that of the left-sided colitis did, while the proctitis had the lowest incidence. There were no significant difference (P > 0.05) between the group of extensive colitis and that of left-side colitis; The incidence of extra-intestinal manifestations in severe cases was significantly greater than that in mild cases. There was a trend of increasing incidence from severe to moderate to mild type (P < 0.05); Most of the extra-intestinal manifestations were associated with active UC, except for AS, PSC, healed during SASP and/or steroid treatment.
Extra-intestinal manifestations had a high incidence in UC. The most frequently involved organs were joints, hepatobiliary system, skin, mouth and eyes. The majority of them were associated with the active UC. The incidence of extra-intestinal manifestations with UC was closely related with the extent and severity of the lesions, and the most of the extra-intestinal manifestations occurred in the active phase of UC. But the incidence of extra-intestinal manifestations was not related to prognosis.
Zhonghua nei ke za zhi [Chinese journal of internal medicine] 10/2002; 41(10):675-7.
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ABSTRACT: To investigate the procedure and tactics used in the cognitive therapy for patients with irritable bowel syndrome (IBS), and to evaluate the efficacy of cognitive therapy in the treatment of refractory IBS.
A self-control study on the cognitive therapy for 22 patients with refractory IBS symptoms (according to Rome II criteria) was performed. The procedure of cognitive therapy included five steps, namely health education, patients' questioning, relaxing training, dissensitization training, and patients' homework for enforcing the effect of former four steps. The effects of cognitive therapy for IBS were evaluated by improvement of symptom-related-anxiety, index of symptom, quality of life specific for IBS and coping.
All 22 cases completed cognitive therapy and first follow-up unit (FFU), at the end of FFU, clinical symptoms in all patients improved (P < 0.05), of them, 81.8% improved significantly (P < 0.001); at 12-months-follow-up, complete remission of clinical symptoms occurred in 72.7% (8/11) patients. Comparison of the scores of symptom-related-anxiety, index of symptom, quality of life specific IBS and coping at the end of 1st follow-up unit with that at basal level, the scores of symptom-anxiety, indexes of severity and frequency of symptoms decreased significantly (P < 0.001, respectively); the scores of depression and anxiety in SCL-90 also decreased significantly (P < 0.001). The scores of active coping rose significantly (P = 0.000). IBS-QOL improved significantly (P < 0.05), of them, dysphoria, body image, food avoidence improved very significantly (P < 0.001, respectively).
Cognitive therapy for patients with refractory IBS is rational and effective. During cognitive therapy, we should follow the therapeutic procedure and the principle of individuation.
Zhonghua nei ke za zhi [Chinese journal of internal medicine] 03/2002; 41(3):156-9.
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ABSTRACT: To investigate the features of selective attention in patients with irritable bowel syndrome (IBS) and the effect of psychological hint on visceral sensation in IBS patients.
A set of 36 modified investigation cards originally developed for depression patients and including 12 cards describing gastrointestinal (GI) symptoms, 12 cards describing respiratory symptoms, and 12 cards with neutral terms, was used to investigate selective attention. 36 patients with diagnosis of IBS based on Rome II criteria, 23 patients with asthma, and 26 healthy volunteers, all without hemorrhoid, were asked to select one card from the set and put it in an envelop. A rectal balloon was inserted into the rectum of the examinees, then the balloon was inflated by pumping air so as to distend the rectum and the thresholds of initial filling sensation, evacuation sensation, urgent evacuation sensation, and utmost tolerance sensation were recorded. The examinees were asked to talk about something so as to divert their attention, and then examination of thresholds of rectal sensation and the time needed for diverting attention were recorded. After a rest for 5 approximately 10 minutes, the examinees were asked to fill the contents of selective attention they still remembered in a recording card. Then pictures of anatomy and pathology of colon were shown and conversation about gastrointestinal diseases was made to the examinees (as malignant stimuli) the changes of thresholds were recorded again.
More terms about GI diseases were selectively recalled by the IBS patients than by asthma patients and healthy controls (all P < 0.001). During rectal distention, IBS patients had lower thresholds of initial sensation (21 +/- 5 mm Hg), evacuation sensation (36 +/- 9 mm Hg), urgent evacuation sensation (51.3 +/- 14.2 mm Hg), and utmost tolerance sensation (67 +/- 17 mm Hg) in comparison with the other two groups (both P < 0.001). After diverting the examinees' attention by talking and reading, the thresholds of the above mentioned different kinds of sensation in different groups increased significantly as compared with the basic values (all P < 0.05), in particular, the threshold of initial sensation in IBS patients increased markedly (P < 0.01). Focusing the examinees' attention on GI stimuli by reading pictures of malignant gastrointestinal diseases significantly decreased the sensation thresholds in IBS patients (P < 0.05). However, no remarkable change in the thresholds was recorded in the nonpatients.
Selective attention of GI symptoms is the cognitive-behavioral characteristic of patients with IBS. Diverting the examinees' attention may decrease their response to stimuli. Psychological hint exerts significant influence on the rectal pain sensitivity of IBS patients. Psychotherapy may be helpful in treatment of IBS.
Zhonghua yi xue za zhi 03/2002; 82(5):308-11.
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ABSTRACT: Aplesia Ras homologue member I (ARHI, DIRAS3) is a Ras-related imprinted growth inhibitory gene whose expression is down-regulated in the majority of breast and ovarian cancers. This study investigated the inhibitory function of ARHI in pancreatic cancer. Six pancreatic cancer cell lines, tumor xenografts in nude mice and 20 pancreatic cancer tissue sections were analyzed. ARHI is widely expressed in ductal and acinar cells of normal pancreatic tissue, but is down-regulated or lost in approximately 50% of pancreatic cancers. Aberrant methylation of the ARHI locus was found in five pancreatic cancer cell lines, which exhibited down-regulation or loss of ARHI expression. Hypermethylation was detected in five cell lines (5/5, 100%) at CpG island I, in two cell lines (2/5, 40%) at CpG island II and in four cell lines (4/5, 80%) at CpG island III. Re-expression of ARHI significantly inhibited the growth of pancreatic cancer cells. This inhibition was associated with the induction of apoptosis. Treatment with the demethylating agent 5-aza-2'deoxycytidine (5-aza-dC) restored ARHI mRNA expression, inhibited cell growth and induced apoptosis in PANC-1 and P3 human pancreatic cancer cells in culture. In nu/nu mice, 5-aza-dC also inhibited the growth of PANC-1 xenografts and induced apoptosis, as observed by TUNEL staining. These effects were associated with the re-expression of ARHI protein. Therefore, ARHI may serve as a growth inhibitory gene in a significant fraction of pancreatic cancers. Re-expression of ARHI significantly induced the apoptosis of pancreatic cancer cells. A demethylation agent reduced human pancreatic cancer cell line growth in conjunction with ARHI re-expression.
Molecular Medicine Reports 3(4):581-7. · 0.42 Impact Factor
