Age-related macular degeneration (AMD) has become a leading cause of irreversible visual loss in senior population with serious influence to their ability of living independently.Epidemiological researches have revealed various risk factors of AMD,some of which are not controllable such as age,heredity and race ;while others are modifiable such as lifestyle,eye conditions and other systemic diseases.However,the awareness of AMD risk factors is alarmingly low in public.Meanwhile,the understanding of AMD risk factors among ophthalmologists is also unsatisfactory.Therefore,the risk factors of AMD are reviewed here in order to improve the understanding of the ophthalmologists and better guide the clinical management of AMD.

Objective To evaluate the clinical value of serum MUC1(sMUC1)in the patients with multiple myeloma.Methods The enzyme linked immunosorbent assay(ELISA)was used to compare the sMUC1 levels in the 12 cases of newly diagnosed multiple myeloma.15 cases of post-chemotherapy and 46 healthy donors.Results The mean concentration of sMUC1 in the newly diagnosed patients with multiple myeloma was 33.44 U/ml(10.86～88.80 U/ml).In the patients of post-chemotherapy the mean concentration was 11.6U/ml(3.92～22.22 U/ml),and in the healthy donors the concentration was 12.81 U/ml(3.84～30.45 U/ml).The level of sMUC1 in the new diagnosed patients was significandy higher than that in the patients of post-chemotherapy(P=0.001)and healthy donors(P=0.000).There was no significant difference between post-chemotherapy and healthy donors(P=0.461).Conclusion sMUC1 may be one of the tumor markers for the diagnosis of multiple myeloma.sMUC1 could also be used as one of the indicators of prognosis and the evaluation of the chemotherapy efficacy.sMUC1 might be a potential target for the immunotherapy to the patients with multiple myeloma.

Objective To construct short hairpin RNA (shRNA) expression plasmids against the inhibitor of differentiation 2 (Id2) gene and establish a suitable cell model for the role of Id2 in proliferation and differentiation of human Ewing sarcoma cell.Methods Three shRNA sequences targeting Id2 gene were designed and inserted into the pGPU6/GFP/Neo (-shRNA-Id2) expression vectors.The recombinant pGPU6/GFP/Neo-shRNA-Id2 plasmids were introduced into Ewing sarcoma RD-ES cells by liposome-mediated transfection.The knock-down efficiency of Id2 in infected RD-ES cells was verified by Western blot assay.The cell growth and cell cycle changes were evaluated by cell counting and flow cytometry between transfected cells and control cells.Results The Id2 expression decreased 54 ％ and 57 ％,respectively,in RD-ES cell line which were transfected with the shRNA-Id2-543 and shRNA-Id2-593 plasmids compared with the control group cells by Western blot analysis.The cell growth assay demonstrated that the cell number in transfected cells was significantly decreased during 6-7 d compared with the control group (P ＜ 0.05).The cells at the S-phase of cell cycle were increased [(36.60±1.53) ％ and (44.89E2.46) ％ vs (29.73±2.03) ％,P ＜ 0.05],and no significant changes at the G2 phase or even reduction in the transfected cells.Conclusions Id2 stable knock-down cell lines are successfully established.The reduced expression of Id2 is related with decreased cell growth and cell cycle arrest in the S-phase.Id2 maybe plays an important role in proliferation of Ewing sarcoma cell.

ObjectiveTo investigate the mental health of freshmen of university.MethodsSymptom Checklist 90 (SCL-90) was used to self evaluate 7763 freshmen of university in Ningbo.Results and ConclusionThe overall level of the mental health of this group was higher than that of the Chinese module, and the prevalence of psychological symptoms was 13.2%. The average level of mental health of female were inferior to male. The difference between the students from cities or towns and from the countryside were distinct. Students who were satisfied with their majority get noticeably higher average score than the ones who were not satisfied.

Objective To investigate that p53 expression in fibroblast-like synoviocytes (FLS) and its effects on CD4+ T lymphocytes from active rheumatoid arthritis (RA) patients. Methods Human FLS was transfected with p53siRNA and cocultured with CD4+ T lymphocytes from active RA patients. The expression of osteoprotegerin and IL-6 secretion was detected in the transfected FLS. In addition, the expressions of IFN-γ, IL-17, IL-4 and CD25 as well as mRNA levels of IFN-γ RORγt, IL-17 and Foxp3 in cocuhured CD4+ T lymphocytes were also measured. Results IL-6 secretion decreased in p53-inhibited FLS while osteopro-tegerin expression was not altered, p53-inhibited FLS could significantly increase IL-17 and IFN-γ expres-sions. It also upregulated Foxp3 expression though had no effect on CD4+CD25high T lymphocytes. Conclusion p53 expression in FLS regulates Th1 and Th17 cells of RA patients, and therefore participate in the pathogenesis of RA.

OBJECTIVETo study the changes of biomarkers in cerebrospinal fluid (CSF) in cerebral amyloid angiopathy (CAA) dementia and Alzheimer(')s disease.

METHODSLevels of amyloid protein β (Aβ42, Aβ40) and phosphorylated Tau-protein (P-tau) in CSF and ratio of Aβ42/Aβ40 were tested in 5 cases with CAA dementia and 20 cases with Alzheimer's disease collected at Peking Union Medical College Hospital from December 2001 to March 2011.

RESULTSThe levels of Aβ42, Aβ40, and P-tau in CSF and ratio of Aβ42/Aβ40 were (660.4 ± 265.2) ng/L, (7111.0 ± 1033.4) ng/L, (71.8 ± 51.5) ng/L, and 0.077 ± 0.033, respectively in CAA dementia and (663.6 ± 365.6) ng/L, (5115.0 ± 2931.1) ng/L, (47.7 ± 38.8) ng/L, and 0.192 ± 0.140, respectively in Alzheimer's disease patients. There were no statistically significant differences between CAA dementia and Alzheimer's disease in terms of these CSF biomarkers (all P>0.05).

CONCLUSIONMeasurements of CSF biomarkers may not be helpful in differential diagnosis of CAA and Alzheimer's disease.

Aged ; Aged, 80 and over ; Amyloid beta-Peptides ; cerebrospinal fluid ; Apolipoproteins E ; genetics ; Biomarkers ; cerebrospinal fluid ; Cerebral Amyloid Angiopathy ; cerebrospinal fluid ; Dementia ; cerebrospinal fluid ; Humans ; Male ; tau Proteins ; cerebrospinal fluid

Objective To establish an animal model of severe blast lung injury in baby rabbits,and to provide a way to study the char-acteristic and treatment of blast lung injury in minors.Methods Randomly selected sixteen 4-weeks old New Zealand white rabbits,and the blast lung injuries were made by BST-Ⅰ biological shock tube with different drive pressure (4.0 MPa and 4.5 MPa)respectively.Then compared the injury severity of the 4.0 Mpa group and the 4.5 MPa group.Selected forty-eight 4-weeks old New Zealand white rabbits and di-vided them into the control group (8 rabbits)and the blast lung injury group (40 rabbits)Rabbits in the blast lung injury group were injured with 4.5 MPa drive pressure.Observed the vital signs,physiological index,gross anatomy of the lung,pathology,and pulmonary water content at the time of injury immediately (0 hour),2 hours,4 hours,6 hours,12 hours,24 hours,48 hours and 72 hours after the injury.Results Rabbits inthe 4.0 Mpa group and the 4.5 MPa group were all alive.The overpressure of blast wave of the 4.0Mpa group was (328.16 ± 4.78)kPa,rate of severe pulmonary defense was 12.5%,and the AIS score was (3.38 ±0.52)points.In the 4.5 MPa group,the overpressure of blast wave was (395.04 ±11.74)kPa,rate of severe pulmonary defense was 87.5%,and the AIS score was (4.13 ±0.64) points.Rabbits in the control group and the blast lung injury group were all alive.The spirits of rabbits were drooping immediately after inju-ry,and it last about 0.5 hour.Then the breathing and heart rate was accelerated,pulmonary water content was increased significantly,and there were extensive hemorrhage and edema in the lung.Most of the rabbits suffered severe lung injury,and the AIS score was (3.98 ±0.55) points.Lung tissue rupture,hemorrhage,edema,and inflammatory cells infiltration were the main pathological manifestations under light microscopy. Conclusion The model of severe blast lung injury in baby rabbits could be established with BST-Ⅰbiological shock tube and drive pressure of 4.5 MPa.It is relatively simple,easily controllable and highly repeatable,which can be used as a feasible model for the study of blast lung injury.

Objective Intercellular adhesion molecule-1 (ICAM-1) plays an important role in mediating pulmonary infiltration of neutrophils .The aim of the study was to observe the expression of ICAM-1 and its potential regulators MK 2/HuR in pulmonary micro-vascular endothelial cells ( PMVEC ) in mice with acute respiratory distress syndrome ( ARDS) induced by lipopolysaccharide ( LPS) . Methods Ten 6-8 weeks old healthy C57BL/6 mice were randomly divided into an LPS and a control group of equal number , the former injected intraperitoneally with LPS diluted in 100 μL PBS while the latter with PBS only , both at 5 mg per kg of the body weight .At 24 hours after injection , all the mice were sacrificed .Real-time PCR was used to determine the mRNA expressions of HuR and ICAM-1 in the PMVECs, Western bolt employed to detect the protein expressions of MK2, HuR and ICAM-1, and flow cytometry adopted to measure the ICAM-1 expression on the surface of the PMVECs and pulmonary infiltration of neutrophils . Results The W/D ratio in the lung tissue of the mice was significantly lower in the LPS than in the control group (3.61 ±0.28 vs 6.16 ±0.40, P<0.05), while the rate of neutrophil infiltration markedly higher in the former than in the latter ([13.92 ±3.23]%vs [3.24 ±1.24]%, P<0.05).The mRNA and protein expressions of ICAM-1 in the PMVECs were significantly elevated in the LPS group as compared with that in the control (P<0.05), and so was the mRNA expression of HuR (P<0.05).No remarkable changes were observed in the expressions of total MK 2 and HuR proteins, but phosphorylated MK2 (p-MK2) and cytoplasmic HuR were increased in the LPS-stimulated mice. Conclusion Specific blockage or reduction of the HuR expression in PMVECs may lower the expression of ICAM-1, reduce neutrophil infiltration , and lessen pathophysiological changes in mice with ARDS .

Objective To evaluate the effect of dexmedetomidine and tramadol on perioperative insulin resistance in patients undergoing radical resection of rectal carcinoma.Methods Sixty ASA I or II patients undergo-ing radical resection of rectal carcinoma were randomly divided into 3 groups(n =20 each):dexmedetomidine group (group D),tramadol group(group T),control group(group C).Group D was given dexmedetomidine intravenously at 1μg/kg 15min before induction of anesthesia followed by a continuous infusion of 0.5μg·kg -1 ·h -1 until the abdo-men was closed,and group T was given tramadol intravenously at 1.5mg/kg 15min before induction of anesthesia fol-lowed by a continuous infusion of 0.5mg·kg -1 ·h -1 until the abdomen was closed,whereas group C received the same volume of normal saline.Venous blood samples were taken at 30min before anesthesia induction(T1 ),1 h after the beginning of the operation(T2 ),1h after operation(T3 ),24h after operation(T4 )for determination of blood con-centrations of glucose(BG),insulin(INS),interleukin -6 (IL -6),tumor necrosis factor -α(TNF -α).Insulin resistance(HOMA -IR)and insulin sensitivity index(QUICKI)were calculated.The numbers of patients with PONV were studied respectively.Results The serum IL -6,TNF -α,BG,INS concentrations and HOMA -IR were signifi-cantly lower while ISI was significantly higher in both group D[t =7.71,3.37,8.78,8.73,11.45,2.82(T2 ),3.04, 2.95,12.75,10.73,16.09,2.92(T3 ),11.26,2.45,11.40,5.10,14.5,2.51(T4 ),all P <0.05]and group T[t =3.02,2.59,2.93,7.76,6.32,2.03(T2 ),8.78,2.27,4.14,8.83,7.68,2.12(T3 ),6.10,2.05,3.71,2.35,7.12, 2.09(T4 ),all P <0.05]at T2 ,T3 and T4 than those in group C.The serum TNF -αconcentration and HOMA -IR were significantly lower while ISI was significantly higher in group D[t =6.68,4.58,2.05 (T2 ),9.01,6.66,2.23 (T3 ),7.54,5.5,2.02(T4 ),all P <0.05]at T2 ,T3 and T4 than those in group T.The numbers of patients with PONV were significantly higher in group T than those in group D and group C (χ2 =26.13,18.75,all P <0.05 ). Conclusion Both dexmedetomidine and tramadol can attenuate perioperative insulin resistance in patients undergo-ing Radical Resection of Rectal Carcinoma,and the decrease the consentrations of IL -6 and TNF -αmay be involved in the mechanism.The roles of prevention of perioperative insulin resistance in dexmedetomidine group are superior to tramadol group.The incidence of PONV is less in a dexmedetomidine group than that in a tramadol group.

Objective: To explore the relationship between expression of tumor necrosis factor-α( TNF-α) and electrophysiological heterogeneity in isolated heart tissues and isolated rat ventricular myocytes.The arrhythmogenic mechanisms of TNF-αwere further studied.Methods:Langendorff perfused heart tissues models were used to verify the arrhythmogenic effects of TNF-α.The monophasic action potentials( MAPs) of the endocardium and epicardium from the isolated heart tissues were recorded by elec-trophysiological experiments.The isolated rat ventricular myocytes were obtained by enzymatic dissociation.K+currents(Ito,IK1)were recorded by using whole cell patch clamp technique.Results: Compared to the control group, the difference in MAPD between endocardium and epicardium dramatically increased with TNF-α( P<0.05 ) .TNF-αcould cause MAP duration ( MAPD ) prolongation, and a single dose of TNF-αdifferentially affected the MAPs of endocardium and epicardium of isolated heart tissues.Compared to the control group,the K+currents(Ito,IK1)were dose-dependently decreased with TNF-αin rat ventricular myocytes(P<0.05).However, etanercept had no effects on the MAPD in the absence of TNF-α.Conclusion:TNF-α-induced heterogeneity of MAPD between the endo-cardium and epicardium may provide the substrate for the onset of ventricular arrhythmias during acute myocardial infarction.The effect might be associated with TNF-αcontribute to re-entrant ventricular arrhythmias which resulted from decreased K+currents(Ito,IK1).