Chromosome Disorders ; Chromosomes, Human, Pair 13 ; Humans ; Infant ; Male ; Trisomy ; Trisomy 13 Syndrome

Objective　To survey about the health status, the activity of daily living conditions and their influencing factors among the elderly in Anhui province, to provide the reference for the current health service system reform of China. Methods　1 424 older persons were selected by Cluster sampling and random sampling methods. The chronic diseases prevalence rate, the damage of ADL among the elderly were investigated. The main influencing factors related to the damage of ADL was analyzed by single and multiple variable logistic regression model. Results　The older persons with aging, lose fare or divorce, multiple chronic disease and smoking habit were at high risk to ADL damage, but physical exercise, high income and well health knowledge may be protective factors which can reduce the ADL damage rate. Different kind of chronic diseases played the different role in the ADL damage among the elderly. Conclusion　The conditions of ADL damage remains serious among the elderly and there are a lot of affected factors. How to find the effective preventive intervention for the elderly and put it into practice, improve their quality of health living are new social problems in china.

Objoctive:To investigate the expression of transforming growth factor-β(TGF-β)isoforms in colonic mucosa of ulcerative colitis(UC),and its role in the incidence of UC thereof.Methods:The expression of TGF-β isoforms was detected in colonic mucosa by immunohistochemical Envision method in UC patients,and the patients with irritable bowel syndrome (IBS)were used as controls.The relationship was analyzed between the expression of TGF-β isoforms and the degree of severity and extent of the disease.Results:There were statistical differences in the expression of TGF-β1 and TGF-β2 between the active stage UC,remission stage UC and IBS groups(P ＜ 0.01).The expression was significantly higher in active stage UC group than that in remission stage UC and 1BS groups(P＜ 0.01).The expression was significantly higher in remission stage UC group than that in IBS group(P ＜ 0.01).However,there was no statistical difference in the expression of TGF-β3 between active stage UC,remission stage UC and IBS groups(P＞ 0.05).The expression of TGF-β1 and TGF-β2 had positive correlation with the degree of sevefity(P ＜ 0.05).However,the expression of TGF-β3 had no linear correlation with the degree of severity(P ＞ 0.05).There was no linear correlation on the expressions of TGF-β1,TGF-β2 and TGF-β3 with extent of the disease(P ＞ 0.05).The degree of severity had positive correlation with extent of the disease(P ＜ 0.05).Conclusion:The expressions of TGF-β1 and TGF-β2 were enhanced in colonic mucosa of UC,and were correlated with the pathogenesis of UC.The expressions of TGFβ1 and TGF-β2 may serve as markers for assessing disease activity of UC.

Humans ; Monitoring, Intraoperative ; methods ; Perioperative Care ; Sleep Apnea, Obstructive ; nursing ; therapy

Objective To investigate the effect of angiotenisn ⅡI (Ang Ⅱ) on RIN-m β-cell,and to explore the mechanism of β-cell function impairment caused by Ang Ⅱ.Methods RIN-m cells were cultured with various concentrations of AngⅡ (0.1,1,10,100 nmol/L).After incubation for 24 hours,the basal(3.3 mmol/L) and glucose-stimulated(16.7 mmol/L) insulin secretion(GSIS)were detected by radioimmunoassay,mRNA and protein expressions of uncoupling protein 2(UCP2)were determined by RT-PCR and Western blot,respectively.The intracellular ATP content was measured by luciferase bioluminescence.The mitochondrial membrane potential and cellular Ca~(2+) concentration were detected by flow cytometry.Results (1) Various concentrations of Ang Ⅱ had no significant influence on the basal insulin secrection of RIN-m cell(F=0.644,P = 0.634).Except for 0.1 nmol/L AngⅡ,the other concentrations of Ang Ⅱ markedly reduced GSIS of RIN-m cells(F= 118.528,P = 0.000).(2) Compared with the control group,Ang Ⅱ significantly increased mRNA and protein expression of UCP2(F= 1 370,P = 0.000;F=675.175,P = 0.000).(3)Except for 0.1 nmol/L Ang Ⅱ,the other concentrations of Ang Ⅱ significantly decreased the mitochondrial membrane potential,cellular ATP content,and cellular Ca2+ concentration of RIN-m cell(F=4.035,P=0.008;F=3.353,P = 0.013;F=5.867,P = 0.001).Conclusion Ang Ⅱ impairs GSIS of p-cell,the mechanism of impairment may be interpreted that Ang Ⅱ can increase the expression of UCP2,furthermore,it can reduce mitochondrial membrane potential,decrease the content of cellular ATP and the concentration of cellular Ca~(2+),can finally impair the function of β-cell.

Corneal transplantation has been considered a primary method for treatment of keratopathy. Corneal transptantation would bring immunological rejection although cornea belongs to an immune-privileged tissue owing to no vessels and lymphatic vessels. Immunological rejection is highly likely to occur in keratopathy patients who undergo large sizes of corneal transplantation or present with newly formed vessels in the center of implant. Many patients have to replace other implants because of immunological rejection. But severer immunological rejection caused by several corneal transplantations as well as rare donor source can not satisfy patients' requirement. Therefore, much attention has been paid to studies regarding drugs for immunologic protection following surgery. There have been many clinical studies confirming that the principle drugs against immunologic rejection, such as glucocorticoid and ciclosporin A, can not acquire satisfactory curative effects and concomitantly bring many adverse reactions. For this reason, many new immunosuppressive agents should be investigated. The method of drug combination has become an important research project for keratopathy physicians.

BACKGROUND:The rapidly developed transplantation of peripheral blood stem cells have been successfully used to substitute bone marrow transplantation and become the first choice method for transplantation of hemopoietic stem cells.It is relatively difficult to collect peripheral blood stem cells from young age and low body mass infants.OBJECTIVE:To investigate the safety and adverse effects of peripheral blood stem cell collection from young age and low body mass through the use of blood cell separator.METHODS:Two type 1 diabetes mellitus infants,aged younger than 2 years old and with body mass less than 15 kg,were treated using autologous hemopoietic stem cell transplantation.The two infants were adequately comforted to lesion the fear of collection.At 1 week prior to collection,calcium agent was orally taken to reduce the incidences of low calcium.Within 24 hours prior to collection,oily food was forbidden,and on the day of collection,milk was forbidden,to avoid chylemia,which influences blood collection.Prior to collection,200 mL 25 Gy y-ray radiated red blood cells suspension was injected into the tube,which was routinely placed in the subclavian vein,to avoid hypovolaemic syndrome and the effects on hematocrit.Individualized collection parameters were set,During collection,blood circulation volume was 3,4 times of systemic blood circulation to ensure sufficient total circulation volume.During isolation,the ratio of ACD to whole blood was kept between 1:11 and 1:13 to prevent sodium citrate poisoning.RESULTS AND CONCLUSION:Peripheral blood stem cells were successfully collected during first intention in each infant.During collection,stable vital signs but no adverse effects were observed.After collection,mononuclear cells weighted 14.71×108/kg and 18.82×108/kg respectively,and CD34+ cells were about 34.13×108/kg and 32.38×106/kg,respectively in each infant.Therefore,it is feasible to collect peripheral blood stem cells from infants of young age and low body mass under sufficient psychological preparation.

Breast Neoplasms ; genetics ; pathology ; Chromosome Aberrations ; Comparative Genomic Hybridization ; methods ; DNA, Neoplasm ; genetics ; Female ; Gene Dosage ; Humans ; Prognosis

DEDD is a member of the death-effector domain protein family. DEDD inhibits the Smad3 mediated transcriptional activity and participates in the regulation of apoptosis. In this study, how the death-effector domain of DEDD participates in the regulation of Smad3 activity and apoptosis has been further investigated. Immunoblotting, immunofluorescence and immunoprecipitation had been used to detect the effects of the full length DEDD and its two truncated mutants, N-DEDD and C-DEDD on Smad3 subcellular distribution, phosphorylation, and interaction between Smad4. The effects of the full length DEDD and its two truncated mutants on cell apoptosis and proliferation had also been explored by flow cytometry and MTT assay. It showed that DEDD and N-DEDD inhibit TGF-beta1 induced Smad3 nuclear translocation and the formation of Smad3-Samd4 complex. DEDD and its two mutants can induce cell apoptosis and inhibit cell proliferation. These results suggested that DEDD inhibits the activity of Smad3 through its death-effector domain. Both the two truncated mutants of DEDD participate in the regulation of apoptosis and cell proliferation.

TLR2 activity plays an important role in the pathogenesis of autoimmune diseases, tumor carcinogenesis and cardio-cerebrovascular diseases. To establish a TLR2 receptor-based cell screening model, NF-kappaB promoter-driven luciferase reporter plasmids were transfected into human embryonic kidney cells (HEK293) stably expressing human TLR2 and co-receptors CD14, TLR1 and TLR6. Single clones were then isolated and characterized. Using this screening system, a human TLR2-binding peptide C8 was obtained from the Ph.D.-7 Phage Display Peptide Library through biopanning and rapid analysis of selective interactive ligands (BRASIL). The binding characteristic of C8 with human TLR2 was evaluated by ELISA, flow cytometry and immunofluorescence. The NF-kappaB luciferase activity assay showed that C8 could activate the TLR2/TLR1 signaling pathway and induce the production of cytokines TNF-alpha and IL-6. In conclusion, the TLR2 receptor-based cell screening system is successfully established and a new TLR2-binding peptide is identified by using this system.