Objective To evaluate the characteristics and safety of capsule endoscopy for elderly patients.Methods The clinical data of 376 patients who underwent capsule endoscopy between May 2002 and September 2007 were retrospectively analyzed,and patients were divided into geriatric group(≥60 years old,n=134)and control group(

Objective To construct the recombinant X-linked inhibitor of apoptosis protein(XIAP) gene 3′untranslational region (3′UTR)-luciferase reporter vector ,and analyze the microRNA(miRNA) which possibly regulate the expression of XIAP gene . Methods Polymerase chain reaction (PCR) was employed to amplify X IA P-3′UTR sequences from human cDNA ,in which luciferase reporter vector pGL3-Ctrl was inserted ,and the recombinant vector pGL3-Ctrl/XIAP was gained .Target Scan 6 .2 soft-ware was adopted to predict the miRNA which possibly combined with the X IA P-3′UTR .pGL3-Ctrl/XIAP recombinant plasmids and the miRNA were co-transfected into A549 cells ,and the X IA P-3′UTR-luciferase activity was measured .Results Confirmed by digestion and DNA sequencing ,the X IA P-3′UTR-luciferase reporter recombinant was successfully constructed .Prediction of miRNA target sites indicated that X IA P gene may be the target of miR-200b ,miR-200c and miR-429 .Compared with miRNA mim-ic ctrl group ,miR-200b ,miR-200c and miR-429 significantly reduced the luciferase activity of pGL 3-Ctrl/XIAP with statistically significant difference(P<0 .05) .Conclusion X IA P-3′UTR-luciferase reporter vector is successfully constructed .miR-200b ,miR-200c and miR-429 can obviously decrease the luciferase activity .

Objective To established cardiac-specific transgenic mice of the cTnC D145E and cTnCG159D and compare the HCM and the DCM.Methods The cTnCD145E and cTnCG159D were generated by site-directed mutagenesis and the transgenic plasmids were constructed by insertion of the mutant genes under the control of α-MHC, which is a myocardium specific promoter.The transgenic mice were generated by microinjection and were all maintained on a C57BL/6J genetic backgroud .The cardiac structure and function of the transgenic mice were compared and analysized by echocardiographic and pathological observation at different ages .Results The cTnCD145E and cTnCG159D transgenic mice were established and developed to HCM and DCM, respectively, with aging.The left ventricular end-systolic volume (ESV) and left ventricular end-diastolic volume ( EDV) decreased and ejection fraction ( EF) and left ventricular end-systolic posterior wall thickness (ESPWT) increased in the cTnCD145E transgenic mice, while EDV and ESV increased and EF and ESPWT decreased in the cTnCG159D transgenic mice at 12 months of age.Conclusions Cardiac-specific human cTnCD145E transgenic mice showed HCM phenotypes , and cardiac-specific human cTnC G159D transgenic mice showed DCM phenotypes , which can be used as different models for comparative study of the pathogenesis of cardiomyopathy .

Objectiye To observe the prevalence of prolonged seizures and the changes of biochemical markers of myocardial injury in patients with prolonged seizures after modified electroconvulsive therapy(MECT).Methods Patients treated with MECT or simulated ECT were divided into three groups.Group Ⅰ , 26 patients,experienced at least one prolonged seizure after MECT;group Ⅱ,41 selected patients, had not prolonged seizures at all during a course of MECT treatments and group Ⅲ, 31 patients, received simulated ECT.Biochemical markers of myocardial injury, including phosphocreatine kinase (CK), MR isoenzyme of phosphocreatine kinase (CK-MB), lactate dehydrogenase ( LDH ), α-hydroxybutyrate dehydrogenase ( α-HBDH ) and cardiac troponin (cTnT) ,were measured immediately, 3 hours later and on the following day after the first prolonged seizure for group Ⅰ ,the same time points as group Ⅰ after the first treatment of MECT for group Ⅱ , immediately after simulated ECT for group Ⅲ.These indexes were compared between the patients of three groups.Results The positive rate ofcTnT was 30.8%(8/26) and 17.1% (7/41)in group Ⅰ and Ⅱ respectively, but no difference was found(P＞0.05 ).CK measured immediately after MECT in patients of group Ⅰ was significantly higher than that of group Ⅲ(P ＜ 0.05 ).CK-MB (immediately), LDH ( immediately and 3 hours later) and α-HBDH ( immediately, 3 hours later and on the following day) in patients of group Ⅰ were significantly higher than those of group Ⅱ and Ⅲ measured after MECT or simulated ECT(P＜0.05 ).Conclusion More attention should be paid that absolute or relative hypoxemia may lead to minor myocardial injury.

BackgroundGlaucoma is an optic neuropathy caused by structural damage of the optic nerve,and its early diagnosis is critical for arresting the irreversible damage of visual function. Optical coherence tomography (OCT) allows an early diagnosis of glaucoma by the measurements of the optic disc and retinal nerve fiber parameters. Objective This study was carried out to evaluate the effects of optic disc tomography and the measurement of the retinal nerve fiber layer (RNFL)thickness by spectral-domain OCT on the diagnosis of glaucomatous eye. MethodsIt was a noninterventional, cross-sectionalstudy. The optic disctopographic parameters and total and regional RNFL thickness were measured by RTVue OCT in 62 normal eyes and 67 glaucomatous eyes. The area under the receiver operating characteristic curve( ROC ) was used to assess the ability to differentiate glaucoma eyes from normal eyes of each testing parameter. This trial complied with the Helsinki Declaration and was approved by the Clinical Trial Ethic Committee of Beijing TongrenHospital. All of the participants signed the written informed consent before any medical examination. Results In the comparison of demography ,the ages of patients, the mean deficiency( MD ) and pattern standard difference( PSD ) of perimetry were obviously larger in the glaucoma group, primary open angle glaucoma ( POAG ) group and primary closure-angle glaucoma(PACG) group than those of normal controls( P＜0. 01 ). No significant differences were found in the disc area between a total glaucoma group, POAG group or PACG group and normal group ( P =0. 101,0. 741 and 0. 652, respectively) ;however, the average RNFL thickness between normal eyes and glaucomatous eyes were significantly different( 109. 758 μm versus 79. 539 μm, P＜0. 01 ). Among the eight regions around the optic disc, the thickest RNFL located at the inferotemporal( 150. 109 μm) and superotemporal( 146. 105 μm) regions in normal eyes,and at the superotemporal( 104. 354 μm) and inferotemporal( 102. 436 μm) regions in glaucomatous eyes. Both in normal and glaucomatous eyes,the thinnest RNFL located at the nasal(NU+NL) and temporal(TU + TL) regions. For optic disc topographic parameters,the highest ROC were observed in rim volume( ROC--0. 850,0. 841 and 0. 862 in total glaucoma,POAG and PACG, respectively) and vertical cup/disc ratio( ROC =0. 840,0. 849 and 0. 830 in total glaucoma,POAG and PACG,respectively), and the sensitivities for specificity cutoff set at 80％ were 73.1％ and 76. 1％ in total glaucoma,73.0％ and 81.1％ in POAG and 73.3％ and 70.0％ in PACG, respectively. For RNFL thickness ,the highest ROC was observed in average RNFL( ROC =0. 925,0. 910 and 0. 942 in total glaucoma, POAG and PACG,respectively) ,and the sensitivities for specificity cutoff set at 80％ were 89. 6％ ,89.2％ and 90. 0％ in total glaucoma,POAG and PACG, respectively. Among the eight regions around the optic disc, RNFL thickness of region IT achieved the highest ROC, RNFL thickness of region TU and TL had the lowest ROC. Conclusions RTVue OCT appears to be of fair discriminating ability in distinguishing normal from glaucomatous eyes. RTVue OCT shows promise for the diagnosis of glaucoma.

Objective To develop a model that could copy the pathological development of psoriasis, the triple-transgenic mice that harboring Plasminogen activator, urokinase ( PLAU) ,PLAU receptor ( PLAUR) and signal transducer and activator of transcription 3 ( STAT3 ) were generated.They are the important genes involved in the pathological development of psoriasis.Methods The transgenic plasmid was constructed by insertion of the PLAU, PLAUR and STAT3 into the downstream bovine keratin 5 promoter respectively.The transgenic mouse was produced by microinjection and the genotyping was detected by PCR.The expression level of the transgenic gene was determined by Western blotting.The pathological changes were observed by HE staining.Results One mouse line was selected with over expression of the PLAU, PLAUR and STAT3 in the tissue of skin.The transgenic mice showed decreased dermal layer, a hyperkeratinized cuticular layer and increased stratum spinosum.The number of hair follicle was reduced and developed abnormally in the transgenic mice.The Munro abscess in the dermal layer and the increased inflammatory cell infiltrates in dermal layer were also observed in the transgenic mice.Conclusions A transgenic mouse line was produced and passage stably, which expressed the PLAU, PLAUR and STAT3 in the tissue of skin and developed the psoriasis progressively.All of our results suggested that the transgenic mice were a useful animal model for psoriasis.

Parkinson's disease (PD) is the second major neurodegenerative disease.The pathogenesis of PI) is still unclear.It is generally believed that neural damage, mitochondrial dysfunction, inflammation, oxidative stress and autophagy dysfunction caused by the transmission and aggregation of a- synuclein play an important role in the occurrence and development of PD.More and more research show- that metabolic disorder is one of the pathogenesis of PD.We examined whether overexpression of a- synuclein could induce metabolic disorder in mice and the possible mechanisms.Mice were divided into two groups: Thyl-aSYN transgenic mice (TG) and the control wild-type (WT) group.The rotarod test was used to analyze motor function in mice.We detected the body weight, plasma insulin content, glucose tolerance and insulin tolerance in the two group mice.The morphology of islets in the two groups were observed by hematoxylin eosin (HE) staining, and the islets were isolated to detect the glucose- stimulated insulin secretion (GSIS).The results showed that compared with the WT group, exercise tolerance of 12-month-old TG group decreased by 23.1% (P < 0.05) , body weight increased by 7% (P < 0.01), glucose tolerance decreased (P < 0.05), insulin tolerance decreased (P < 0.05), and insulin contents in the peripheral blood decreased by 20% (P < 0.05).Compared with the WT group, the levels of ce -syn proteins in the pancreas of the TG group increased by 1.32 times (P < 0.05) , the area of islets in the TG group decreased (P < 0.05 ) , the number of islets decreased (P < 0.01) , and the insulin secretion function decreased (P< 0.01).This study showed that the role of a-synuclein in PD is not limited to the damage of dopaminergic neurons, it also can affect metabolism and the morphology and function of peripheral organs, which provides a new theoretical basis for the pathogenesis of PD.

Objective To investigate the association of the tumor necrosis factor ligand superfamily member(TNFSF)4 gene polymorphisms rs3861950 and cerebral infaretion in Hunan area.Methods The frequencies of the genotypes of rs3861950 were detected utilizing real-time fluorescent PCR method based on TaqMan probe.Subiects examined were composed of 287 patients and 285 healthy individuals.Results There were significant differences in TNFSF4 gene rs3861950 C→T site polymorphism and allele frequency between the subjects and the controls,the distribution of CC genotype was significantly higher in the former (7.7%)than in the later(2.1%,X2=9.553,P=0.008),so was the frequencies of C allele(0.190 vs 0.137,X2=5.887,P=0.015).Moreover,there were significant differences in the distribution of genotype and the frequencies of allele between the subgroup of cerebral thrombosis and control group ( for the distribution of genotype X2=9.396 P=0.009,for the frequencies of allele X2=6.134,P=0.013).Logistic regression analysis showed that the risk factor of CC genotype was 3.7 times higherthan others(P=0.002.OR 3.706).Conclusions TNFSF4 gene SNP rs3861950 is associated with cerebral infarction and C allele is considered to be one of independent risk factors in the Han population in Hunan Province.

Background:Mutations in the isocitrate dehydrogenase 1 (IDH1) and IDH2 genes are important for both the integrated diagnosis and the prognosis of diffuse gliomas.The p.R132H mutation of IDH1 is the most frequently observed IDH mutation,while IDH2 mutations were relatively rarely studied.The aim of the study was to determine the pathological and genetic characteristics of lowergrade gliomas that carry IDH2 mutations.Methods:Data from 238 adult patients with lower-grade gliomas were retrospectively analyzed.The status of IDH1/2 gene mutations,telomerase reverse transcriptase (TERT) promoter mutations,O6-methylguanine-DNA-methyltransferase (MGMT) promoter methylation,1p/19q co-deletion and the expressions of IDH1 R132H,alpha-thalassemia X-linked mental retardation,and p53 were evaluated.Progression-free survival (PFS) and overall survival (OS) were calculated via Kaplan-Meier estimation using the log-rank test.Results:Totally,71％ (169/238) of patients were positive for IDH mutations,including 12 patients harboring mutations in IDH2.Among the 12 patients with IDH2 mutations,ten patients harbored the R172K mutation,one patient harbored the R172S mutation and one harbored the R172W mutation.Of these,11 tumors occurred in the frontal lobe and showed morphology typical of oligodendroglioma.The proportion of grade Ⅱ tumors was higher than that of grade Ⅲ tumors in IDH2 mutant-gliomas.IDH2 mutations were frequently associated with TERT promoter mutations,1p/19q co-deletion and MGMT promoter methylation.IDH2 mutations were associated with better outcomes compared with IDH wild-type gliomas (P ＜ 0.05).However,the PFS and OS did not differ from that of IDH1 mutant patients (P =0.95 and P =0.60,respectively).Conclusions:IDH2 mutations are more frequent in oligodendrogliomas and associated with a better prognosis.IDH2 mutations may segregate in distinct clinico-pathological and genetic subtypes of gliomas,and therefore may merit routine investigation.

OBJECTIVETo study the morphologic features, immunophenotype, differential diagnosis and prognosis of nodal marginal zone B-cell lymphoma (NMZL).

METHODSLight microscopic examination and immunohistochemical study were carried out in 10 cases of NMZL. Seven of which had follow-up information available.

RESULTSAll cases presented with good performance status at the time of diagnosis. Amongst the 7 cases with follow-up information available, most (6/7) were in advanced clinical stage (stage II to III). The one-year survival rate was 67%. A vaguely nodular growth pattern was observed in most cases of NMZL (5/10). The lymphoma was composed predominantly of atypical lymphoid cells resembling centrocytes (7/10). A predominance of monocytoid B-cell (2/10) or small lymphocytic (1/10) morphology was rare. Instead, the presence of a minor component of monocytoid B cells was not uncommon (5/10). Plasmacytoid or plasmacytic cells were also frequently found (8/10). The proliferation index ranged from 5% to 50%. Follicular dendritic cells appeared atrophic in 7 cases and variably hyperplasic in 3 cases.

CONCLUSIONSPrimary NMZL is rare. It has a unique growth pattern and most cases are composed predominantly of cells resembling centrocytes. Differential diagnosis includes lymphoplasmacytic lymphoma, lymph node involvement by extranodal marginal zone B-cell lymphoma and T-zone hyperplasia. The clinical stage is often high at presentation, with systemic dissemination. The prognosis of NMZL is thus relatively poor.

Adult ; Aged ; Diagnosis, Differential ; Female ; Follow-Up Studies ; Humans ; Lymph Nodes ; pathology ; Lymphoma, B-Cell, Marginal Zone ; drug therapy ; metabolism ; pathology ; Male ; Middle Aged ; Neoplasm Staging ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Remission Induction ; Survival Rate ; Waldenstrom Macroglobulinemia ; pathology