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 know the prevalence tendency of Keshan disease(KSD) under control after 10 years in Shaanxi Province, the factors that causes or relative to the disease, to provide scientific reference for disease's prevention and control. Methods Through stratified cluster sampling, based on the severity of KSD in endemic area of Shaanxi Province, 12 villages from 6 counties were randomly selected as investigation points in 2006. The people older than 3 year-old were chosen to do clinical check up and electrocardiogram tracing. Among them, suspicious or abnormal cases were asked to take chest X-ray and cardiac ultrasound. Maize and rice, hair and whole blood were randomly collected to test the selenium content, the activity of Glutathione peroxidase (GSH-Px). Results The total detection rate of potential or chronic KSD was 2.44%(139/5694), the detection rate of abnormal ECG was 9.19% (523/5692), the detection rate of cardiac enlargement from chest X-ray and cardiac ultrasound were 45.6%(72/158) and 34.5%(59/171) respectively. The average content of selenium in staple foods(wheat and corn) were[(0.045±0.036), (0.035±0.025)mg/kg, respectively]. The level of hair selenium in patients and healthy people were [(0.376±0.091), (0.384±0.077)mg/kg, respectively], with non-significant different (u=0.77, P>0.05). There were significant differences in whole blood selenium of patients, healthy people in KSD areas and healthy people in non-KSD areas[(0.071±0.017), (0.077±0.017), (0.090±0.016)mg/L, respectively; F=4.55, P<0.05), the whole blood selenium in patients lower than in healthy people in KSD areas (P<0.05), in healthy people in KSD areas lower than in non-KSD areas (P<0.05). Conclusions After the KSD condition being controlled, the situation in Shaanxi Province has become stable and exhibited a decreasing tendency. The selenium level of both internal and external environment in the endemic area increased significantly, that is the main factors of controlling disease.

Objective To explore the status of Keshan disease in Shaanxi province to provide a scientific basis for decision-making of prevention and control of Keshan disease. Methods Nineteen infected villages were randomly selected in 19 infected counties in the range of Keshan disease infected area in Shaanxi province in 2008 as the investigation sites. Clinical examination and electrocardiography were performed in the chosen people at every spots, chest X-ray of posteroanterior position film in 2-meter distance was taken in suspicious cardiac patients, and determining the selenium contents was also determined in the collected grain samples of the investigators. Results Of the 10 228 investigated residents in the endemic area, 110 Keshan disease patients were detected, the total detection rate was 1.08% (110/10 228). Among the 110 patients, 92 were potential Keshan disease, which accounted 0.90%(92/10 228); 18 chronic Keshan disease formed a detection rate of 0.18%( 18/10 228); no acute and sub-acute type of Keshan disease had been inspected. Potential Keshan disease patients often showed electrocardiogram abnormality of complete fight bundle branch block [48.57%(51/105)], ST-T change[ 19.05% ( 20/105 ) ], frequent premature ventricular contraction [ 10.48 % ( 11/105 ) ], left ventricular hypertrophy [ 5.71% (6/105) ], block in the anterosuperior division of the left branch[5.71%(6/105)]; Chronic of Keshan patients mostly presented atrial fibrillation [ 24.00% (6/25) ], left ventricular hypertrophy [ 20.00% (5/25) ], complete right bundle branch block [ 20.00% (5/25)]. The increase rate of cardiothoracie ratio was 18.08% (32/177). Food samples of wheat, corn, millet and rice in infected area residents were of selenium content, being (0.096± 0.028), (0.089 ±0.029), (0.087 ± 0.016), (0.047 ± 0.016)mg/kg, respectively. Conclusions Keshan disease in Shaanxi province is steadily declining, potential and chronic Keshan diseases are currently the main clinical types. Selenium content of food in endemic area has reached the level of the non-endemic area.

Objective To investigate the effects ofkallikrein gene transfer on microvascularproliferation around the cerebral infarct and on the recovery of regional cerebral blood flow (rCBF)following ischemia/reperfusion injury in rats. Methods The rats with cerebral ischemia/reperfusioninjury induced by middle cerebral artery occlusion (MCAO) were randomly assigned into blank controlgroup, saline group, and pAdCMV-HTK treatment group and received corresponding injections into thetissues around the infarct area. Each group was divided into 3 subgroups (n=10) for observation at 12, 24and 72 h after the treatment. The neurological deficits of the rats before and after the treatment wereevaluated using neurological severity scores (NSS), and the expressions of exogenous human tissuekallikrein (HTK) and vascular endothelial growth factor (VEGF) in the brain tissues were detectedimmunohistochemically. TIC staining was performed to measure the changes in the infarct size.14C-iodoantipyrine tracing technique was used to define the rCBF in the rats. Results Compared tothe blank control group, the cerebral infarct size was significantly reduced in pAdCMV-HTK group 24 hafter the treatment, and was further reduced at 72 h (P<0.05). At 24 h after the treatment, the NSS inpAdCMV-HTK group was significantly lower than that in the blank euntrol and saline groups (P<0.05),and was further reduced at 72 h (P<0.01). After MCAO, the VEGF-positive cells were found mostly inthe cortex and the white matter around the infarct area. The expression of VEGF in pAdCMV-HTK groupwas markedly higher than that in the other two groups at 12, 24, and 72 h after the treatment (P<0.05). Inall the 3 groups, the rCBF around the infarct was slightly decreased as compared to that in thecontralateral hemisphere, pAdCMV-HTK slightly increased the rCBF 12 h after the injection (P>0.05),and significant increase in the rCBF occurred 24 h and 72 h after the injection (P<0.05). ConclusionKallikrein gene transfer following cerebral ischemia/reperfusion injury promotes vascular proliferationaround the infarct and increases the rCBF to reduce the infarct volume and attenuate neurological deficitsin rats.

Objective To investigate the metabolic effects of glucose dependent insulinotropic peptide receptor antagomst pro3 (GIP) in induced diabetes mice about blood glucose,triglyceride,cholesterol,leptin and fatty issue.Methods 27 C57 mice were randomly divided into normal group and diabetes mice group,and the mice in diabetes group were fed with high fat food and intraperitoneal injected streptozocin.Then 1 mouse that random blood giucose lower than 16.9 mmol/L was deleted in diabetes group.The rest mice in diabetes group were divided into two groups,diabetes control group,pro3 (GIP) group.Pro3 (GIP) group was given drug pro3 (GIP).The bloodglucose and glucose tolerance were measured.After treatment for 6 weeks,all mice were sacrificed and fatty tissues were collected.Results After 6 weeks,the blood glucose of the pro3 (GIP) group was obviously lower than diabetes control group (t=8.43,P＜0.01),and insulin levers in 0,30,60 and 120 min were obviously lower than diabetes control group (t =3.90,2.60,6.88 and 3.33,P＜0.05).There was significant difference between pro3 (GIP) group and diabetes control group about inflammatory cells.Moreover,leptin in pro3 (GIP) group was obviously lower than in diabetes control group (t =5.04,P＜0.01),but triglyceride,cholesterol,and adiponectin had no significant difference between two groups.Conclusion Pro3 (GIP) can significantly reduce blood glucose,insulin level,leptin of diabetes mice,and attenuate the inflammatory cells infiltration in fatty issue.