Objective To summarize the clinical features of different racial patients with celiac disease (CD) and analyze the disease prevalence,diagnosis and treatment in Chinese population.Methods All the patients were diagnosed as CD and enrolled in Beijing United Family Hospital between January 2005 and July 2015.Clinical data including nationality,age,symptoms,endoscopic and pathological findings,outcome were collected and compared in patients from different countries.Results A total of 87 patients were enrolled including 63 Caucasians,18 Asian patients and 6 Middle East patients.The peak age of disease onset was 40-60 years old.Patients with typical symptoms such as chronic diarrhea and weight loss only accounted for 20.7％ (18/87) and 9.2％ (8/87) respectively.Some patients presented with nonspecific symptoms such as abdominal pain and bloating [32.2％ (28/87)],even constipation [5.7％ (5/87)].13.8％ (12/87) patients were previously diagnosed as irritable bowel syndrome.The incidence of abdominal pain,bloating,diarrhea and constipation between Asians and Caucasians had no statistical significance (P ＞ 0.05);but the proportions of weight loss,growth retardation,iron deficiency anemia and dermatitis herpetiformis in Asian group were significantly higher than that in Caucasian group (P ＜ 0.05).IgA type of anti-gliadin antibody (AGA),endomysium antibody (EMA) and tissue transglutaminase antibody (tTGA) were dominant autoimmune antibodies in patients with CD,which accounted for 58.6％ (51/87),44.8％ (39/87) and 36.8％ (32/87) respectively.The endoscopy showed that the lesion of CD was mainly located in small intestine,with reducing severity from the proximal to the distal small intestine.The lesions of duodenal bulb and descending duodenum appeared more significant in Asian group.Accordingly pathological intestinal atrophy and the degree of intraepithelial lymphocytosis were more severe in Asian patients.All 87 cases took the gluten-free diet (GFD).Eighty-one cases received serological follow up and 8 with endoscopic intestinal biopsy.The celiac disease antibodies in 47 patients turned negative from 6-9 months after GFD treatment,while 34 patients turned negative from 12-18 months after GFD.All patients reported disease remission to some extent.After 1 year GFD treatment,the pathology of endoscopic intestinal biopsy in 8 patients showed significant improvement of villous atrophy and lymphocyte infiltration.Conclusions CD patients with typical clinical manifestations are not the majority.Serological celiac disease antibodies (AGA,EMA and tTGA) have a high diagnostic value.GFD treatment is effective on majority of celiac patients.Clinical manifestations,endoscopy,intestinal pathology,and response to GFD in Chinese patients are not the same as Caucasians.Clinicians need to pay attention to the differential diagnosis.

Objective To investigate whether IL-17 could stimulate the vascular endothelial growth factor (VEGF) production on HaCaT cells alone. We also investigated whether shikonin could inhibited the proinflamation effects of interleukin-17(IL-17) acting on HaCaT cells. MethodsWe examined the expression of VEGF by double antibody sandwich enzyme-linked immunosorbent assay ( ELISA ) and realtime polymerase chain reaction(RT-PCR) in HaCaT cells and the cell supernatant. The viability of HaCaT cells in the drug group was detected by the Cell Counting Kit-8 (CCK-8). ResultsThe expression of VEGF in different time IL-17-stimulated groups on HaCaT cells and the cell supernatant were higher than the control group( P＜0.001 ). The expression of VEGF in different drug treatment groups on HaCaT cells and the cell supematant were lower than the stimulated group by IL-17 ( P＜0. 001 ). The cell viability of different drug treatment groups have no significant difference( P＞0.05 ). ConclusionWe show that IL-17 specifically and time-dependently augmented and induced VEGF expression on HaCaT cells and the cell supernatantThen shikonin markedly inhibited the increase tengency of IL-17 effection on HaCaT cells and the cell supematant level.

Objective To evaluate the CT findings of lymphofollicular thymic hyperplasia in adult myasthenia gravis (MG).Methods The CT findings of thymus area of 134 adult patients with lymphofolficular thymic hyperplasia in MG were reviewed,all of them with surgically and histologically proven diagnosis,and compared with the CT findings of 165 normal subjects.Results In the group of patient,CT showed enlargement of thymus in 31 patients,5 patients had nodule or mass(＜3 cm);thus 36 cases(26.9%)can confirmed diagnose by CT with thymic hyperplasia.CT showed 2 masses(＞3 em) and 9 patients(6.7%)had normal size thymus with soft-tissue density,it can considered with thymic hyperplasia.The spotty or streak shadow showed in other patients,though it could not be certain diagnosed as thymic hyperplasia,but could not be except it.The thymus area tissue complete replacement by fatty density were not found in patient group.The CT findings of patients had marked difference when compared with group of normal subjects(P＜0.01),except the spotty or streak shadows.Conclusion CT scan is an important method in diagnosing thymic lymphofollicular hyperplasia of MG in adult.

OBJECTIVEThis study is aimed to observe the natural draining state of maxillary sinus, to search for the key draining location (KDL) in the natural ostium, to investigate the relation between maxillary sinus draining and sinus inflammation, and to guide the treatment of maxillary sinus opening in endoscopic sinus surgery (ESS).

METHODSMethylene blue was used as tracer agent in this study. Fifteen cases with or without light maxillary sinus inflammation (without any treatment) were selected to observe the natural draining state and the key draining location in maxillary sinus fontanel. Eighty-nine cases with chronic rhinosinusitis, but without nasal polyp, were selected, of which the maxillary sinus mucosa restored well 6 months after ESS, to observe the draining state and modes in maxillary sinus. All patients were followed up for 12 months to evaluate the inflammation state of mucosa, and to analyze the relations between the draining mode and mucosa inflammation.

RESULTSThe KDL for maxillary sinus was located in the posterior-inferior portion of the natural ostium, close to the attachment of caudal end of the uncinate process. The draining flowed along it from maxillary sinus to nasopharynx. After conventional transnasal endoscopic operation, 15 cases showed relatively normal drainage, others displayed abnormal state and mode,including reverse draining (maxillary sinus-ethmoid sinus) , multiphase draining (outflow from front, back and lower wall of natural ostium), draining failure (with cilia transporting function of maxillary epithelium mucosae), cistern like change (maxillary sinus and ethmoid sinus formed one operation cavity, secretion accumulated in maxillary sinus) and mucosa disfunction (loss of cilia transporting function of maxillary epithelium mucosae). Inflammation was observed in 33.7% of the patients 12 months after ESS, especially in those with mucosa disfunction, draining failure and reverse draining.

CONCLUSIONSThe KDL for maxillary sinus may be located in the posterior-inferior portion of the natural ostium, close to the attachment of caudal end of the uncinate process, and the drainage mode is not affected by gravity and posture. The KDL lesion after ESS results in abnormal draining of maxillary sinus, and excessively large maxillary sinus opening may aggravate mucosa inflammation of maxillary sinus. The abnormal draining state and mode may be related with the incidence of mucosa inflammation after operation. Preserving caudal end of uncinate process and avoiding injury of KDL would be beneficial to the restoration of mucosa and lessen the incidence of inflammation recurrence.

Adolescent ; Adult ; Aged ; Endoscopy ; adverse effects ; Female ; Humans ; Inflammation ; Male ; Maxillary Sinusitis ; etiology ; Middle Aged ; Nasal Mucosa ; pathology ; Otorhinolaryngologic Surgical Procedures ; adverse effects ; Young Adult

OBJECTIVETo explore the regulatory effect of arginine on the secretion of hepatic insulin-like growth factor-1 (IGF-I), and the mechanism of enhancing the immune function by arginine.

METHODSWistar rats were randomly divided into normal control (NC), wound control (WC), and wound with arginine (Arg) groups, with 8 rats in each group. The rats in WC and Arg groups were inflicted with soft tissue trauma on the back. The rats in Arg group were fed a diet supplemented with 5% arginine for one week, while those in NC and WC groups were fed with glycine. The serum contents of arginine, ornithine, growth factor (GH), NO and IGF-I were determined 7 days after feeding. T cell proliferation and IGF-I mRNA expression in hepatic tissue were also measured. Meanwhile, the rat hepatocytes were cultured in serum-free medium containing different concentrations of arginine. The supernatant was collected for the determination of IGF-I level.

RESULTS1). There was no obvious difference of the serum level of arginine and ornithine between NC and WC groups (P > 0.05), but the contents of them were obviously higher in the Arg group compared with other two groups (P < 0.01). 2). No difference in the serum GH level was found among all the groups (P > 0.05), but the serum NO content in WC and Arg groups was significantly lower than that in NC group (P < 0.01), and the serum IGF-I content in WC group decreased obviously compared with that in NC group (P < 0.01). 3). The thymocyte proliferation rate in WC group was also markedly lower than that in NC group (P < 0.01), but that in Arg group was improved compared with WC group (P < 0.01). 4). The expression of hepatic IGF-I mRNA: The relative value of IGF-I mRNA was 1.19 +/- 0.06, 1.08 +/- 0.06 and 1.29 +/- 0.06 in NC, WC and Arg, respectively, while the value in WC was lower than that in NC (P < 0.05) group, and that in Arg group was much higher than that in WC group (P < 0.01). 5). The IGF-I level in the supernatant of cultured hepatocytes: When Arg concentration was 0.0750, 0.7500, 7.5000 mmol/L in the culture medium, the IGF-I level in the supernatant of hepatic cell medi-um was obviously higher than that in the medium without arginine (P < 0.01). Although IGF-I level decreased in the culture medium with arginine in the dose of 37.5000 mmol/L, it was still obviously higher than that in the medium without arginine (P < 0.01).

CONCLUSIONArginine could also produce the immune enhancing effect by stimulating hepatic IGF-I secretion.

Animals ; Arginine ; pharmacology ; Enteral Nutrition ; Insulin-Like Growth Factor I ; metabolism ; Liver ; drug effects ; secretion ; Male ; Rats ; Rats, Wistar ; Soft Tissue Injuries ; metabolism ; therapy

Background: High rate of in?stent restenosis (ISR) remained an unsolved clinical problem in clinical practice, especially among patients with diabetes mellitus (DM). Diabetic patients often had hypertriglyceridemia with elevated levels of very low?density lipoprotein cholesterol (VLDL?C). Increasing evidence suggested that VLDL?C was known as a significant risk factor for atherosclerosis and had been recommended as a treatment target by current dyslipidemia guidelines. However, the role of VLDL?C in the occurrence and development of ISR in coronary artery disease (CAD) patients with DM had not been studied. The aim of this study was to evaluate the association between the elevated levels of VLDL?C and the risk of ISR in CAD patients with DM. Methods: A total of 1390 diabetic patients, who underwent coronary drug?eluting stent (DES) implantation at Beijing Anzhen Hospital and followed up by angiography within 6–24 months, were consecutively enrolled. Patients' demographic and clinical characteristics, including age, gender, CAD risk factors, family history, life style, medical history, and coronary angiographic information, were collected carefully at baseline percutaneous coronary intervention and follow?up angiography. Multivariate Cox's proportional hazards regression modeling using the step?wise method (entry, 0.05; removal, 0.05) was used to determine the independent risk associated with ISR in diabetic patients. Results: Finally, 1206 of patients were included in this study. ISR occurred in 132/1206 diabetic patients (10.9%) by follow?up angiography. Patients with ISR had elevated median serum VLDL?C levels compared with those without ISR (0.65 mmol/L vs. 0.52 mmol/L, P = 0.030). The multivariate regression analysis showed that VLDL?C was significantly associated with the risk of ISR in diabetic CAD patients (hazard ratio [HR] = 1.15, 95% confidence interval [CI]: 1.03–1.29, P = 0.017). The HR for the risk of ISR associated with VLDL?C level ≥0.52 mmol/L was 3.01 (95% CI: 1.24–7.34, P = 0.015). Conclusion: The elevated level of serum VLDL?C was a significant and independent risk factor for ISR in diabetic CAD patients after coronary DES implantation.

OBJECTIVE: To investigate the expression of cannabinoid receptor I (CB1R) during mice skin incised wound healing course and time-dependent changes of CB1R in wound age determination. METHODS: The changes of CBIR expression in skin incised wound were detected by immunohistochemistry and Western blotting. RESULTS: The control group showed a low expression of CB1R detected mainly in epidermis, hair follicles, sebaceous gland and dermomuscular layer. CB1R expression was undetectable in neutrophils in the wound specimens from 6h to 12h post-injury. CB1R positive cells were mostly mononuclear cells (MNCs) and fibroblastic cells (FBCs) from 1 d to 5 d post-injury. CB1R positive cells were mostly FBCs from 7 d to 14d post-injury. The ratio of the CB1R positive cells increased gradually in the wound specimens from 6 h to 3 d post-injury, reached peak level at 5 d, and then decreased gradually from 7d to 14 d post-injury. The positive bands of CB1R were observed in all time points of the wound healing course by Western blotting. The expression peak showed at 5 d post-injury. CONCLUSION CB1R is activated during the wound healing course. The expression of CB1R is found in mononuclear cells, which could be involved in inflammation reaction. CBIR is observed in fibroblastic cells, which could participate in the wound healing. CB1R may be a potentially useful marker for determination of wound healing age.
Animals ; Blotting, Western ; Disease Models, Animal ; Fibroblasts/metabolism* ; Forensic Pathology ; Immunohistochemistry ; Male ; Mice ; Monocytes/metabolism* ; Random Allocation ; Receptor, Cannabinoid, CB1/metabolism* ; Skin/metabolism* ; Staining and Labeling ; Time Factors ; Wound Healing ; Wounds and Injuries/pathology*

OBJECTIVETo investigate the expression of 5-hydroxytamine receptors in hepatic stellate cells HSCs and action of 5-hydroxytamine on biological characteristics of HSC.

METHODSLiver ex vivo perfusion of collagenase and density gradient centrifugation were used to isolate hepatic stellate cell. RT-PCR was used to detect the expression of 5-hydroxytamine receptor subtypes 1A, 2A, 2B and 3. Western blot hybridization was used to elucidate the effect of 5-hydroxytamine and its 2A receptor antagonist ketanserin and 3 receptor antagonist ondanosetron on expression of transforming growth factor-beta1 (TGF-beta1) and Smad4 in HSC. HSCs were cultured on silicone membrane. The effect of 5-hydroxytamine, ketanserin and ondanosetron on cell contraction were studied.

RESULTSHSC expressed 5-hydroxytamine receptors subtypes 1A, 2A and 2B. 5-hydroxytamine significantly increased the expression of TGF-beta1 and Smad4 in HSC (P < 0.05). This was antagonized by ketanserin, not by ondanosetron. 5-hydroxytamine induced cell contraction in a dose-dependant manner. Ketanserin antagonized this action, but ondanosetron did not.

CONCLUSIONSHSCs express 5-hydroxytamine receptors. 5-hydroxytamine could affect the biological characteristics of HSC through its receptor mediation, and may play a role in the pathogenesis of liver cirrhosis and portal hypertension.

Animals ; Cells, Cultured ; Hypertension, Portal ; etiology ; Liver ; chemistry ; cytology ; Liver Cirrhosis ; etiology ; Male ; Rats ; Rats, Wistar ; Receptors, Serotonin ; analysis ; physiology ; Serotonin ; pharmacology ; Serotonin Antagonists ; pharmacology ; Transforming Growth Factor beta ; physiology ; Transforming Growth Factor beta1

Measurement of platelet-associated imunoglobulin (PAIg) has frequently been applied for the diagnosis of idiopathic thrombocytopenic purpura (ITP) and other immune thrombocytopenias. In the present study, a flow cytometry (FCM) analysis has been used to detect and characterize PAIg in 47 patients with ITP and Evans' syndrome, 13 patients with non-immune thrombocytopenia, 10 patients with autoimmune hemolytic anemia (AIHA) whose platelet counts were in normal range, and 31 healthy volunteers. With FCM measurement, mean fluorescence intensity (MFI) of platelets from patients with ITP and Evans' syndrome (2.26 +/- 2.29) was significantly higher than those from non-immune thrombocytopenia (0.33 +/- 0.39), AIHA (0.17 +/- 0.07) and control subjects (0.25 +/- 0.15) (P < 0.01). Meanwhile, the percentage of positive platelets of patients with ITP and Evans' syndrome [(44.1 +/- 29.0)%] was also higher than those of non-immune thrombocytopenia [(17.5 +/- 9.4)%], AIHA [(10.7 +/- 7.5)%] and control subjects [(16.6 +/- 8.4)%] (P < 0.01). In addition, some peak shape abnormality appeared (double peaks and peak tail) in the histogram of fluorescence intensity (log) of 11 patients (23.4%) with ITP and Evans' syndrome either alone or accompanied with quantitative alteration of MFI and/or positive platelet percentage. In seven cases, the peak shape abnormality was the unique characteristic that could be detected and have never been seen in normal platelets. This phenotypic alteration perhaps reflects the existence of different platelet populations and could be of diagnostic value. Totally, the positive result of FCM measurement in patients with ITP and Evans' syndrome was 87.2%, slightly higher than 83.0% positive rate with ELISA method, without statistical difference. The correspondent rate of the results of these two analytical settings was 85.1%. This study shows that FCM assay is a rapid and sensitive method for the measurement of PAIg and seems to be suitable as a novel routine diagnostic technique of immune thrombocytopenia.

OBJECTIVERho, a ras homologous gene, encodes a group of GTP-binding proteins. Our previous study suggested that one member of the Rho gene family, RhoC, was related to the progression of human hepatocellular carcinoma (HCC). This study is to elucidate correlation of Rho overexpression with invasion and metastasis of HCC.

METHODSThe expression level of RhoC mRNA and protein in 25 cases of HCC and adjacent non-cancerous liver tissue was examined by RT-PCR and Western blot. Mutation of RhoC gene was examined by PCR-SSCP.

RESULTSThe expression of RhoC mRNA and protein was found in all HCC and adjacent non-cancerous liver tissue. The expression level of RhoC mRNA and protein was significantly higher in tumor tissue than in adjacent non-cancerous liver tissue (1.8 +/- 1.1 vs 1.0 +/- 0.7; 33 992 +/- 10 384 vs 17 342 +/- 9998, P < 0.01). The degree of RhoC overexpression was even more marked in metastatic lesions than in primary tumors (P < 0.01). Overexpression of the rhoC gene was significantly correlated with such clinic-pathological findings as cell differentiation, portal vein invasion, number of primary tumor nodules and metastatic lesions (P < 0.05). Mutation of RhoC gene was found in none of the HCC specimens examined.

CONCLUSIONOverexpression of RhoC gene may play an important role in carcinogenesis and progression of HCC.

Adult ; Aged ; Carcinoma, Hepatocellular ; genetics ; metabolism ; pathology ; Cell Differentiation ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Liver ; metabolism ; Liver Neoplasms ; genetics ; metabolism ; pathology ; Male ; Middle Aged ; Neoplasm Invasiveness ; Portal Vein ; pathology ; RNA, Messenger ; biosynthesis ; genetics ; rho GTP-Binding Proteins ; biosynthesis ; genetics ; rhoC GTP-Binding Protein