Background Clinical studies indicated that the pathogenesis of most corneal dystrophy is associated with the mutation of the transforming growth factor beta-induced (TGFBI) gene.However,the molecular mechanism of mutated TGFBI gene in corneal dystrophy is unclear. Objective The present study was to investigate the expression of the TGFBI gene in human corneal tissue and cells in vitro.MethodsHuman corneal epithelial cells and keratocytes were cultured and passaged,and donor corneal tissue was obtained for the section preparation.RT-PCR was used to detect the expression of TGFBI mRNA in human corneal tissue and cells.Immunofluorescence was used to test the expression of the TGFBI protein in the human corneal tissue,and immunohistochemistry was used to test the expression of the TGFBI protein in human corneal epithelial cells and corneal stromal cells.ResultsRT-PCR analysis showed that TGFBI mRNA could be detected as a 1274 bp band in human corneal tissue and corneal stromal cells,but no TGFBI mRNA was observed in corneal epithelial cells.Immunofluorescence assay revealed that corneal stromal cells were positive ly expressed for the TGFBI protein,but the corneal epithelial cells did not express the TGFBI protein.Immunohistochemistry indicated that the expression of TGFBI was detected the red fluoressence in the cytoplasm of corneal stromal cells;however,no positive response was found in corneal epithelial cells.ConclusionsThe expression of the TGFBI gene occurs in human corneal stromal cells but not in the corneal epithelial cells.This result might be of helpful for studying the function and role of TGFBI gene in pathogenesis of corneal dystrophy.

Objective To investigate the relationship between coagulation factor ⅩⅢ deficiency and delayed intracranial hematoma after craniotomy. Methods The clinical data of 2 cases with delayed intracranial hematoma induced by coagulation factor ⅩⅢ after craniotomy were analyzed and compared with the data of 58 cases with delayed intracranial hematoma induced by other causes during the same period, so as to find out the clinical characteristics of the disease induced by coagulation factor ⅩⅢ. Results The delayed intracranial hematoma induced by the deficiency in coagulation factor ⅩⅢ was commonly located in the operative regions after surgery, and the process was insidiousand fast. Conclusion When the delayed intracranial hematoma is confirmed after craniotomy, the deficiency in coagulation factor ⅩⅢ should be taken into consideration. The prognosis will be satisfying if the diagnosis and treatment are in time.

The external medicine is an indispensable treatment of traditional Chinese medicine (TCM) surgery.The application of Hg is one of the characteristics of TCM surgery medicine for external use.This paper analyzes the present situation of clinical application of Hg and summarizes the common adverse reactions in the literature.The focus of the research on the development of new drugs containing Hg in traditional Chinese medicine is discussed.

Background Researches demonstrated that avastin-assisted vitrectomy for serious proliferative diabetic retinopathy can decrease intra-operation complication and bring down difficulty of surgery.It is speculated that this is associated with suppression of avastin on neovascularization.However,the evidence of its pathology is lack.Objective The aim of this study was to evaluate the application and mechanism of avastin in vitrectomy for severe proliferative diabetic retinopathy. Methods Twenty-four eyes from consecutive 24 patients with vitrectomy for severe proliferative diabetic retinopathy were enrolled in this study.Fourteen eyes received all intravitreal injection of 0.06 ml avastin(1.5 mg)14 days prior to vitrectomy。And the other 10 eyes underwent only vitrectomy without avastin injection as controls,Preretinal membranes were collected during vitrectomy for histopathologic examination by hemotoxylin and eosin staining.The differences in the density of the neovessels and micro-neovessels between the two groups were observed by detecting the expression of CD34 in vesse]endothelial cells using immunohistochemistry.Written informed consent was obtained from each patient before surgery. Results No statistically significant differences were found in the demography and eye manifestations between only vitreetomy group and avastin+vitrectomy group(P＞0.05).The neovessels with grade three was in 10 eyes in only vitrectomy group and 1 eye in avastin+vitrectomy group(P＜0.01).More capillary-like neovascularization with single vascular endothelial cells,obvious hemorrhage and inflammatory cells infiltration were observed on preretinal membranes in vitrectomy group.However,there were less hemorrhage,ceUular components and few capillary-like neovascularization but more hyaline degeneration of fibrous tissue were observed in avastin+vitrectomy group under the light microscope.Immunochemistry revealed that CD34 was positively expressed in vascular endothelial cells on preretinal membrane in both two groups.The neovessels density and miero-neovessels density were 15.40±7.42/field and 1.88±1.70/field in avastin+vitrectomy group and those in vitreetomy group were 18.00±3.80/field and 0.45±0.56/field respectively,showing significant differences between these two groups(neovessels density:Z=-4.102,P＜0.01;micro-neovessels density:Z=-4.137,P＜0.01).Conclusion As an adjunct drug during the vitrectomy for proliferative diabetic retinopathy, avastin can improve the successful rate of surgery by inhibiting the neovascular formation and alleviating retinal edema.

Objective To investigate the effect of exogenous kallikrein on apoptosis of the neurons aroundthe cerebralinfarctareain rats. Methods Thirty rats wjth cerebral infarction induced by middle cerebral artery occlusion(MCAO)were assigned randomly into 3 groups(n=10),namely the blank control group,saline group,and pAdCMV-HTK group.In the pAdCMV-HTK group,kallikrein gene was delivered into the cerebral ischemie lesion via a replication-defective adenovims using stereotaetic injection technique, and the expression of exogenous kallikrein was detected immunohistoehemically.TUNEL staining was performed to evaluate the neuronal apoptosis around the infarct area,and RT-PCR used to detect the mRNA expressions ofbcl-2,bax and caspase-3 in the brain tissues. Results At 24 h aftertreatment there were some HTK expressed cells found in group C and peal(at 72 h after treatment.While compare with group B and group C,there existed significant difference(112±6.1,68±4.2,59±3.9,P<0.05).At 72 h after treatment,the NSS of group C was significantly lower than that ofgruop B and A(6.70±0.16,8.13±0.16,7.93±0.20,P<0.05);7 days after the treatment,the difference was more significant(5.14±0.18,7.82±0.14,7.91±0.10,P<0.01).Apoptotic cells were mostly seen around the infarct area.The ratsinpAdCMV-HTK group showed significantly reduced number of cells positive for TUNEL staining as compared to those in the saline and blank control groups at 3 days(10.1±0.9,16.7±1.1,and 20.4±0.8,respectively)and 7 days after the treatment(15.2±1.2,33.6±1.3,and 28.8±1.7,respectively)(P<0.05).The mRNA levels ofbc1-2.bax and caspasc-3 were elevated in all the groups at 24 h,peaked at 72 h,and decreased gradually till 7 days alter the treatment.Compared with those in the other two groups，bcl-2 mRNA level in the pAdCMV-HTK group increased slightly P>0.05) while bax and caspase-3 mRNA levels decreased markedly(P<0.05) 72 h and 7 days after the treatment.Conclusion Kallikrein can inhibit neuronal apoptosis around the cerebral infarct and improve the neurological fimction of rats following cerebral infarction probably by reducing the expressions of such apoptotic factors as bax and caspase-3.

Objective To offered some prophase works by preparing Neurocan protein, antiserum, and assaying their characteristics, in order to construct the isopropy-β-D-thiogalactoside (IPTG)-participated DNA vaccine, which can neutralize the inhibitors in the injured CNS following the immune administration and then promote the nerve regeneration. Methods Neurocan gene was syntbetized with HisTag label in beginning and enzyme-cut sites at amphi- of the sequence. The prokaryotic expression plasmid, PET30a-Neurocan, was constructed as usual, converted into the Escherichia coli, and induced by IPTG to express positively. The interest protein was identified by SDS-PAGE and Western blot respectively. The preimmune serum was as the negative control during the ELISA assay of antiserum valency. The immune serum was as the first antibody, and the goat-anti-rabbit labeling with alkaline phosphatase (AP) was employed as the second one. Coloration was with NBT/BCIP method. Results The correct sequence of the synthetic Neurocan gene was clearly showed by identification with enzyme-cut, PCR and sequencing. The Neurocan protein expressed by prokaryotic showed its molecular weigh as 55 000 following the SDS-PAGE identification, and it could specifically bind with anti-HisTag, which implied the interesting protein just as the expression product of Neurocan gene. The valency of antiserum was shown by ELISA as 1:1 000 000, the purpose strap of which was confirmed by Western blot. Conclusions Neurocan protein could be successfully expressed in prokaryotic, the antibody of which could be specifically obtained by immune administration to the rabbit. The Neuroncan antibody could bind with the Neurocan protein specifically.

Oxazolidinones are a potent class of synthetic antimicrobial agents with activity mainly against Gram-positive strains.In this review,we summarize the mechanism of action and resistance,as well as the safety from clinical experience of oxazolidinones.The structural modifications and structure-activity relationships of oxazolidinones derivatives will also be presented.

To assess the normal value of left ventricular twist (LVtw) and examine the changeswith normal aging by 2-dimensional ultrasound speckle-tracking imaging (STI), 121 healthy volunteers were divided into three age groups: a youth group (19-45 y old), a middle-age group (46-64 y old ) and an old-age group (≥65 y old). Basal and apical short-axis images of left ventricular were ac- quired to analyse LV rotation (LVrot) and LVrot velocity. LVtw and LVtw velocity was defined as apical LVrot and LVrot velocity relative to the base. Peak twist (Ptw), twist at aortic valve closure (AVCtw), twist at mitral valve opening (MVOtw), untwisting rate (UntwR), half time of untwisting (HTU), peak twist velocity (PTV), time to peak twist velocity (TPTV), peak untwisting velocity (PUV), time to peak untwisting velocity (TPUV) were separately measured. The results showed that the normal LV performs a wringing motion with a clockwise rotation at the base and a counterclock- wise rotation at the apex (as seen from the apex). The LVtw velocity showed a systolic counterclock- wise twist followed by a diastolic clockwise twist. Peak twist develops near the end of systole (96%±4.2% of systole). With aging, Ptw, AVCtw, MVOtw, HTU and PUV increased significantly (P<0.05) and UntwR decreased significantly (P<0.05). However, no significant differences in TPUV, PTV and TPTV were noted among the 3 groups (P0.05). It is concluded that LV twist can be meas- ured non-invasively by 2-dimensional ultrasound STI imaging. The age-related changes of LVtw should be fully taken into consideration in the assessment of LV function.

Objective To systematically evaluate the association between frailty and risk of postoperative delirium.Methods Systematic review of literature was conducted using eight electronic databases:PubMed,Embase,CENTRAL,Web of Science,CNKI,CBM,VIP and Wanfang Data,and prospective cohort studies about association between frailty and postoperative delirium published before March 2017 were included.Two authors independently screened the literature,extracted the data,and assessed the quality using NOS Scale,and meta-analysis was conducted by RevMan 5.3 software.Results A total of eight studies involving 846 patients were included in this review.Meta-analysis showed that:frailty was associated with higher risk of postoperative delirium [OR=3.63,95％CI (2.06,6.40),P＜0.001].Subgroup analysis showed that:①Frailty assessment tool:Fried frailty criteria and other frailty assessment were associated with increased risk of postoperative delirium[OR=5.81,95％CI(3.54,9.77),P＜0.001],[OR=1.76,95％CI(1.06,2.92),P=0.03].②Age:frailty patients aged 60～74 had increased risk of postoperative delirium [OR=5.05,95％CI (3.14,8.12),P＜0.001],but for patients aged ≥ 75,frailty wasn't associated with postoperative delirium [0R=1.73,95％CI (0.99,3.00),P=0.05].③Type of surgery:for cardiovascular and non-cardiovascular surgery patients,frailty was associated with increased risk of postoperative delirium [OR=3.40,95％CI (1.64,7.05),P＜0.001],[OR=4.95,95％CI (2.41,10.16),P＜0.001].Conclusion Frailty can increase the risk of postoperative delirium.In consideration of quantity and quality of included studies,the conclusion needs to be validated by multi-centered prospective cohort studies with large sample size.