Objective To analyze the expression of excision repair cross-complementation group 1 (ERCC1),MutS protein homolog 2 (MSH2) and poly ADP-ribose polymerase 1 (PARP1) in non-small cell lung cancer (NSCLC) and their prognostic value for patients receiving platinum-based postoperative adjuvant chemotherapy.Methods Immunohistochemistry was applied to detect the expression of ERCC1,MSH2 and PARP1 in 111 cases of NSCLC paraffin embedded surgical specimens.Through OG-Rank survival analysis,the prognostic value of the ERCC1,MSH2,PARP1 and the related clinic pathological factors were evaluated.Cox regression analysis was used to determine whether ERCC1,MSH2 and PARP1 were independent prognostic factors or not.Results Among the 111 NSCLC patients,the positive expression rates of ERCC1,MSH2 and RARP1 were 33.3 ％(37/111),36.9 ％(41/111) and 55.9 ％(62/111),respectively.Besides,a total of 72 patients who received platinum-based chemotherapy had complete follow-up data.ERCC1 (P＜ 0.001) and PARP1 (P=0.033) were found to be correlated with the survival time while there was no correlation for MSH2 (P =0.298).Patients with both ERCC1 and PARP1 negative had significant longer survival time than those with ERCC1 (P=0.042) or PARP1 (P=0.027) positive alone.Similarly,the survival time of patients with both ERCC1 and PARP1 positive was shorter than those with ERCC1 (P=0.048) or PARP1 (P=0.010) positive alone.Conclusions The NSCLC patients with ERCC1 and (or) PARP1 negative may benefit from platinumbased postoperative adjuvant chemotherapy.The detection of ERCC1 and PARP1 can be used as an important method to assess the prognosis of patients with NSCLC.

Objective To study the relationship of serum pulmonary surfactant protein and vascular endothelial growth factor re‐lated indexes to lung cancer .Methods Totally 56 patients with lung cancer in our hospital from September 2014 to December 2015 were selected as the observation group ,56 healthy personnel at the same period were selected as the control group ,then the serum pulmonary surfactant protein and vascular endothelial growth factor related indexes of control group and observation group ,obser‐vation group with different stages and pathological classifications were compared ,and the relationship between serum pulmonary surfactant protein and vascular endothelial growth factor related indexes and lung cancer were satisfacted with Logistic analysis .Re‐sults The serum pulmonary surfactant protein and vascular endothelial growth factor related indexes of observation group were all higher than those of control group ,and the serum pulmonary surfactant protein and vascular endothelial grow th factor related inde‐xes of observation group with higher stages were all higher than those of patients with lower stages ,and the levels of patients with adenocarcinoma were all higher than those of patients with squamous cell carcinoma ,and the serum pulmonary surfactant protein and vascular endothelial growth factor related indexes all had close relationship to the lung cancer (all P<0 .05) .Conclusion The serum pulmonary surfactant protein and vascular endothelial growth factor related indexes all have close relationship to the lung cancer ,and those indexes of patients with lung cancer should be paid more attention .

Objectives To investigate the risk factors of acute renal injury (acute kidney injury) in patients with acute left heart failure.Methods Clinical data of 188 patients with acute left heart failure who were admitted to our hospital were retrospectively analyzed.Logistic regression analysis was used to assess the risk factors for AKI.Results Among 188 patients with acute left heart failure,incidence of acute kidney injury was 33.51％.Univariate and Multivariable logistic regression analyses showed that the independent predictors of acute kidney injury were lower baseline eGFR (OR=4.294,P ＜ 0.001) and anemia (OR=3.573,P=0.006).Conclusions The incidence of acute left heart failure complicated with AKI was high.Basic state of renal function and anemia were the independent risk factors for AKI.

OBJECTIVE: To investigation the further inquiry the reasons of cerebral palsy child's hearing lose, and giving the hearing lose children of cerebral palsy overall medical treatments in time, this paper has given the academic comprehensive analysis of the reasons of this synthetic symptom above. METHOD: By the means of the medical checks of ABR, OAE and acoustic immittance measurements, we have investigated the reasons, and analyzed the types of all cerebral palsy children in our hospital from January to December in 2005. RESULT: The result of medical checks in 484 cerebral palsy children showed that there were 160 abnormal cases (33.06%), and we marked OAE medical check to the 92 abnormal cerebral palsy children, there are 36.90% passing rates. among which the passing rate of slight hearing lose (72.00%) is obviously higher than that of the serious hearing lose (4.20%). CONCLUSION The symptoms of serious suffocation, premature delivery, and jaundice are not only the main factors given rise to the cerebral palsy, but also are the main reasons led to cerebral palsy child's hearing lose.
Cerebral Palsy ; physiopathology ; Child ; Child, Preschool ; Female ; Hearing Loss ; diagnosis ; etiology ; Humans ; Infant ; Male

Objective To follow up the long-term prognosis of acute kidney injury (AKI) patients with normal basic renal function,and to further identify the clinical features as well as risk factors associated with the prognosis of AKI patients.Methods Clinical date of 166 patients who occurred AKI episode during hospitalization from Jan 1 2011 to Dec 31 2014 in The First Affiliated Hospital of Fujian Medical University were retrospectively analyzed.All these patients had normal basic renal function and had follow-up of more than two years after discharge.According to their renal function after two years,patients were divided into recover and non-recover group.The clinical features and risk factors associated with the prognosis of AKI patients were identified using multivariate logistic regression,and the proportion of renal function progression was calculated during follow-up period.Results One hundred and sixty-six patients were enrolled in this observational study,including 114 male,52 female with an average age of 58.1± 16.6.Eighty-seven patients were AKI stage 1,39 AKI stage 2,and 40 AKI stage 3.Thirty-seven patients were caused by pre-renal factors,113 patients by renal causes and 16 patients by post-renal causes.Renal function when discharged (P=0.002,OR=2.980) and infection (P=0.003,OR=2.786) were the risk factors of failing to restore after two years.Eighty-four patients' renal function returned to normal when discharged,but the number of patients whose renal function progressed to CKD 3 stage and even worse 1 year and two years later were 12 (14.3％) and 20 (23.8％) respectively.Fifty-four patients were diagnosed as partial recovery and 28 patients as non-recovery when discharged.One year later 22 (40.7％) and 12 (42.9％) patients' renal function progressed to CKD 3 stage and more,while those numbers became 28 (51.9％) and 16 (57.1％) two years later.Conclusions The risk factors of AKI long-term outcome include unrecovered renal function when discharged and infection.After AKI episode,even with fully recovered renal function,patients are still possible to progress to CKD,highlighting the importance of follow-up observation.

Objective To investigate the effect of complement C3a on mouse podocytes phenotype transformation.Methods Purified C3a recombinant protein was used to stimulate mature mouse podocytes.The expression of the mature podocyte markers synaptopodin,podocin,nephrin,CD2-associated protein (CD2AP) and the mesenchymal cell markers fibroblast specific protein 1 (FSP-1),α-smooth muscle actin (α-SMA) were detected by RT-PCR,Western blotting,immunochemistry and immunofluorescence,respectively.Some podocytes were transfected with integrin-linked kinase (ILK) siRNA before the administration of C3a,the expression of nephrin and α-SMA were accessed by Western blotting,and the expression of Snail and α-actinin 4 were accessed by Western blotting and immunochemical method.The migration ability of podocytes was observed by scratch test.Results Immunocytochemistry and immunofluorescence analysis showed that synaptopodin,podocin,nephrin,CD2AP were highly expressed by mature mouse podocytes.The expression of these podocyte markers could be markedly inhibited after 24 h of C3a (0.1 μmol/L) treatment,and accompanied by the induction of mesenchymal markers FSP-1 and α-SMA.Compared with control group,the mRNA levels of synaptopodin,podocin,CD2AP and nephrin were significantly repressed by the administration of C3a in a dose-dependent manner,whereas the transcription of FSP-1 and α-SMA were remarkably up-regulated by C3a treatment (P ＜ 0.05,respectively).Western blotting analysis also confirmed the decrease of synaptopodin,podocin,nephrin and CD2AP protein and the increase of FSP-1 and α-SMA protein were closely depend on the C3a concentration (P ＜ 0.05,respectively).To further assess the downstream of C3a,some podocytes were transfected with ILK siRNA before the administration of C3a.Compared with C3a group,the protein levels of nephrin and α-SMA were significantly changed by the administration of ILK siRNA (P ＜ 0.05,respectively).The expression of α-actinin 4 and Snail induced by C3a were inhibited by ILK knockdown (P ＜ 0.05,respectively),accompanied by a decline of cell migration potency.Conclusion Complement fragment C3a can induce transformation of mouse podocytes to mesenehymal cells,and ILK signaling pathway is involved in this cell type transformation.

Objective: To construct a Tat-dependent MazF expression vector pcDNA3.1-GFP-HA-MazF-U3TAR. Methods: HIV-1 U3TAR and MazF gene were amplified from pCR2.1-U3TAR and pET28a-MazF, respectively. Two gene fragments were linked together to form U3TAR-MazF by an overlapping PCR, and then cloned into pMD18T. An N-terminal HA tag was added to MazF to form U3TAR-MazF-HA. After double enzyme digestion using EcoR I and Hind Ⅲ, U3TAR-MazF-HA was reversely inserted into pcDNA 3.1 to form pcDNA3.1-HA-MazF-U3TAR. Then, a fluorescent reporter gene GFP was inserted into the downstream of U3TAR to form pcDNA3.1-GFP-HA-MazF-U3TAR. Results: The co-transfection experiments with pcDNA3.1-tat-flag showed that pcDNA3.1-GFP-HA-MazF-U3TAR is Tat dependent. MazF was expressed only under the presence of Tat. In addition, compared with the cells transfected with pcDNA3.1-GFP-HA-MazF-U3TAR, less green fluorescent signal was observed in the cells co-transfected with pcDNA3.1-GFP-HA-MazF-U3TAR and pcDNA3.1-tat-flag, indicating that expressed MazF down-regulated the expression of GFP. Conclusions The expression vector pcDNA3.1-GFP-HA-MazF-U3TAR will provide an important tool for the development of MazF-based AIDS gene therapy strategies.