Child, Preschool ; Humans ; Influenza A Virus, H1N1 Subtype ; Influenza, Human ; complications ; virology ; Male ; Mediastinal Emphysema ; etiology ; Subcutaneous Emphysema ; etiology

Antineoplastic Agents ; therapeutic use ; Colorectal Neoplasms ; drug therapy ; genetics ; metabolism ; Genes, ras ; genetics ; Humans ; Lung Neoplasms ; drug therapy ; genetics ; metabolism ; Molecular Targeted Therapy ; methods ; Mutation ; Neoplasms ; drug therapy ; genetics ; metabolism ; Pancreatic Neoplasms ; drug therapy ; genetics ; metabolism ; Proto-Oncogene Proteins ; genetics ; metabolism ; Proto-Oncogene Proteins p21(ras) ; Receptor, Epidermal Growth Factor ; drug effects ; metabolism ; Signal Transduction ; ras Proteins ; genetics ; metabolism

Objective To investigate the neuroprotective effect of adiponectin on rats with cerebral ischemic-reperfusion injury and explore its possible mechanism.Methods Sixty-four SD rats were divided into normal group (C) and diabetic group (D) randomly.Type 2 diabetic rats model were made by high-fat diet before the middle cerebral artery occulation model (MCAO) surgery.Each group was divided into two subgroups.CAPNand DAPN groups were given exogenous recombinant globular adiponectin via jugular vein one hour after ischemic-reperfusion injury,C0 and D0 groups were given the same amount of normal saline at the same time.Body weight and blood glucose of the rats were measured before ischemia.We also evaluated the neurological function of rats 24 h after treatment according to Longa criteria and observed the morphological changes of cells in brain area via HE staining.The vascular density in ischemic-reperfusion injury area was detected through 3D confocal image system 2 weeks after the treatment.Results The body weight of diabetic rats was significantly lower than normal rats((284.06 ± 19.85)vs (220.31 ±21.87) g,t =8.634,P =0.000).Blood glucose of diabetic rats before ischemia was significantly higher than normal rats ((4.36±0.13)vs(22.92 ± 1.58) mmol/L,t =11.74,P =0.000).Compared with C0 group,the neurological function score of CAPN group was lower(2.29 ± 0.69 vs 17.0 ± 0.69,t =2.186,P =0.038).Compared with D0 group,the neurological function score of DAPN group was lower(2.89 ± 0.33 vs 2.40 ±0.51,t =2.567,P =0.018),too.HE staining showed that the neuronal injury were milder in CAPN,DAPN group,compared with C0,D0 group,respectively.Adiponectin increased the vascular density of ischemic cortex inC group ((2014.58±61.18)/0.002 mm2 vs(3211.95 ±71.64)/0.002 mm2,t =12.16,P=0.023) and D group ((502.86 ± 30.43)/0.002 mm2 vs (1426.69 ± 97.24)/0.002 mm2,t =25.64,P =0.001).Adiponectin increased the vascular density of ischemic striatum in C group (472.59 ± 4.78)/0.002mm2 vs (736.60 ±104.90) /0.002 mm2,t=7.11,P=0.007) and D group (432.04 ±4.65)/0.002 mm2 vs (1780.75 ± 74.54)/0.002 mm2,t =51.08,P =0.000).Conclusions Adiponectin exerts the neuroprotective effect on cerebral ischemic-reperfusion injury in normal and diabetic rats.And it may protect the brain through promoting angiogenesis.

0.05).61 patients received no sedatives nor analgesics showed significantly higher incidence of SUE compared with those patients received either sedatives or analgesics(73.8% vs 37.3%,P

Objective To evaluate the migrating regulation and ultrastructure of the corneal epithelial stem cells in human fetuses. Methods We examined the corneal cryosections of 14-38 weeks of gestation. Hematoxylin-eosin staining showed the stratified corneal epithelium and the corneal epithelial stem cells were localized by mouse monocolonal antibody against human 64-kilodalton keratin (mAE5), and the ultrastructure of the corneal epithelial stem cells was observed. Results At 14 weeks of gestation, the corneal epithelium was composed of a single basal cells layer and 1-2 superficial squamous cells layers. Some superficial squamous cells were mAE5 positive in the limbus as well as the central and peripheral cornea. At 17-29 weeks of gestation, the limbus epithelium developed from 3 to 5 cells layers and the central region from 2 to 3 cells layers. mAE5 positive cells were found in the suprabasal layers of all 3 regions examined but not in the basal layer. At 33-38 weeks of gestation, the corneal epithelium consisting of 4-6 cells layers was morphologically mature. mAE5 immunoreaction showed the negative cells were confined to limbus basal layer. The ultrastructure of basal layer cells showed they had more heterochromatin in the nucleus, less organells in the cytoplasm and less desmosomes among them. Conclusion The migration of corneal epithelial stem cells in the human fetuses was from the whole layers to basal layer and confined to limbus region finally, and their ultrastructure was immature.

Objective To assess the effectiveness of different concentration of iodized salt for preventing iodine deficiency disorders. Methods Using the principle and method of systematic review, we searched Cochrane Library(from 1994 to Mar. 2007), Medline(from 1966 to Mar. 2007), BA(from 1969 to Mar. 2007), PubMed(from 1950 to Mar. 2007), OC1D(from 1950 to Mar. 2007), ISI Web of Knowledge(from 1966 to Mar. 2007), Vip (from 1989 to Mar. 2007), Wanfang(from 1997 to Mar. 2007), CBMDisc(from 1978 to Mar. 2007) and CNKI(1994 to Mar. 2007) and hand searched 6 relevant Chinese journals, including Chinese Journal of Preventive Medicine, Chinese Journal of Endemiology, Chinese Journal of Epidemiology, Chinese Journal of Control of Endemic Disease, Endemic Diseases Bulletin and Modern Preventive Medicine. We screened the for eligible studies according to the inclusion and exclusion criteria to be rigorously evealuatecl descriptly and qualitatively. Results Thirteen studies were included, of which, the first six were intervention trials with comparison, including two community intervention trials, which classified all objects into different groups, using iodized salt at different concentration as intervention, four were RCTs with different intervention methods, compare the iodized salt with other intervention measures. Seven were cross-sectional studies, which analyzed the iodine nutrition of people after the concentration of iodized salt was lowered down. Because of different interventions in control groups and different outcome measures, it was difficult to perform recta-analysis, a descriptive analysis of the results was presented. Most studies showed that urinary iodine level decreased as the concentration of iodized salt went down gradually. When the concentration of iodized salt went down to the best level recommended, goiter rate decreased obviously. Conclusions Iodized salt was considered as the hest method of iodine supply to prevent iodine deficiency disorders. But effectiveness of preventing iodine deficiency disorders with various concentration of iodized salt is different. To lower the concentration of iodized salt properly can not only prevent iodine deficiency disorders but also reduce the side effect of excess iodine intake to the minimum. And it can also save a lot of iodine resource. Well-designed community-based intervention trials with large sample size are needed to confirm the effect of different concentration of iodized salt on preventing iodine deficiency disorder.

To observe the effect of oxidized low density lipoprotein (OxLDL) on arterial endothelial cells apoptosis in vivo, we established a model in which Sprague-Dawley rats were given intraperitoneal and intravenous injection of unmodified LDL (8 mg/kg every day) via the tail vein. Seven days after the injection, the aortic endothelial cells specimens were prepared by an en face preparation of rat aorta. The apoptotic cells were identified and counted by in situ nick and labelling (TUNEL) method and light microscopy. The numbers of the apoptotic cells were 12.52 +/- 4.71/field in the intraperitoneal injection control group, 11.41 +/- 2.94/field in the intravenous injection control group, 22.98 +/- 8.01/field in the intraperitoneal injection LDL group and 103.8 +/- 11.5/field in the intravenous injection LDL group, respectively. The difference was significant between injection LDL group and control (P < 0.01), and the difference was also significant between two LDL injection groups (P < 0.01). These findings suggest that injection of LDL can induce apoptosis in arterial endothelial cells and the effect is especially significant with intravenous injection LDL. After injection, oxidative modification of LDL may occur in local arteries and causes injury to the endothelial cells.
Aorta ; Apoptosis/*drug effects ; Endothelium, Vascular/*pathology ; In Situ Nick-End Labeling ; Injections, Intraperitoneal ; Injections, Intravenous ; Lipoproteins, LDL/*metabolism ; Lipoproteins, LDL/*pharmacology ; Oxidation-Reduction ; Random Allocation ; Rats, Sprague-Dawley

To compare the clinical effect of Qianliekang and finasteride in the treatment of benign prostatic hyperplasia to explore the effectiveness of traditional Chinese medicine for the therapy of benign prostatic hyperplasia. Methods:Totally 36 Wistar rats were selected, and then divided into 3 groups randomly with 12 ones in each, namely Qianliekang group, finasteride group and the control group. After 14 days of castration, the three groups were all treated with subcutaneous injection of 5 mg kg-1 testosterone propi-onate, and Qianliekang group was additionally treated with intragastric administration at 10-fold adult dose, finasteride group was trea-ted with intragastric administration at the dose of 0. 1 mg·kg-1 , and the control group was treated with the same amount of distilled water. The rats were sacrificed after the 21-day treatment, and the wet weight of prostate was determined, the prostate volume was measured and the pathological changes in prostate tissue were observed under a light microscope. Results:The wet weight of prostate in Qianliekang group and finasteride group was (0. 467 ± 0. 061) g and(0. 408 ± 0. 058) g, respectively, the prostate volume was (0. 371 ± 0. 059)ml and(0. 365 ± 0. 054)ml, respectively, and the above indicators were significantly lower than those in the control group(P<0. 05). Conclusion:Qianliekang can effectively inhibit benign prostatic hyperplasia in the model rats, and the mechanism may be related to the proliferation inhibition of prostate cells.

Objective To investigate the effects of rosiglitazone on the proliferation,connective tissue growth factor and Smad expression in cultured cardiac fibroblasts induced by advanced glycosylation end-products (AGEs).Methods After being treated with various amounts of rosiglitazone,the cultured neonatal rat cardiac fibroblasts were incubated with AGEs.The status of cardiac fibroblasts proliferation and cell cycle were detected by 3-(4,5-dimethyhhiazol-2-yl) -2,5-diphenyl tetrazolium bromide (MTI) assay and flow cytometry.Furthermore,ELISA technique was applied to identify the level of TGF-β1.The protein expressions of CTGF and Smad in cardiac fibroblasts of neonatal SD rats were detected with Western blotting.Results The exposure of cardiac fibroblasts to AGEs at doses of 0-200 mg/L induced a dose-dependent increase in cell proliferation.At the concentration of rosiglitazooe (0.1,1,and 10 μmol/L),the cell proliferation was reduced compared with 200 mg/L AGEs group by O.823±0.072,0.785±0.060,0.601±0.081 vs 0.981±0.049,respectively (P < 0.05).The increased levels of TGF-β1 in supematants of cultured cardiac fibroblasts stimulated by AGEs were inhibited by rosiglitazone at the concentrations of 0.1,1,10μmol/L by 257.77±9.09,230.29±6.56,200.84±10.26 vs 300.68±8.56,respectively (vs 200 mg/L AGEs,P<0.01).Western blot indicated that pretreatment with rosiglitazone (0.1,1,and 10 μmol/L) inhibited CTGF protein production in a dose-dependent by 0.769±0.108,0.590±0.095,0.534±0.115 vs 1.021±0.113,respectively (vs 200 mg/L AGEs,P<0.01).It was also demonstrated that pretreatment with rosiglitazone (1 and 10 μmol/L) inhibited Smad2 protein production by 0.424±0.059,0.396±O.080 vs 0.572±0.073,respectively (vs 200 mg/L AGEs,P < 0.05 or P < 0.01).Meanwhile pretreatment with rosiglitazone (1 and 10 μmol/L) inhibited Smad4 protein production by 0.580±0.063,0.556±0.051 vs 0.672±0.059,respectively (vs 200 mg/L AGEs,P < 0.05 or P < 0.01).Conclusions The findings suggest that AGEs promote the proliferation of cardiac fibroblasts and stimulate the protein production of Smad and CTGF of cardiac fibroblasts.Rosiglitazone inhibits the above reaction.These results indicate that CTGF/Smad pathway may play an important role in the protective effect of rosiglitazone on myocardial fibrosis.

Objective To analyse the therapeutic effect of methylprednisolone combined with anterior decompression and internal fixation in the treatment of cervical spine hyperextension injury. Methods 42 patients who were diagnosed with cervical hyperextension injury in orthopaedics department of the First Hospital of Jiaxing were collected.All patients were randomly divided into experimental group and control group, 21 cases in each group.Patients in control group received anterior cervical decompression and internal fixation only , patients in experimental group received methylprednisolone combined with anterior decompression and internal fixation, after treatment, the serum levels of TNF-α, SOD and American Spinal Injury Association (ASIA) score were detected in all patients.Results After treatment, compared with control group, the serum levels of TNF-αwas lower, SOD was higher and ASIA score was higher in experimental group, and the differences were statistically significant (P<0.05).Conclusion The methylprednisolone combined with anterior decompression and internal fixation could significantly reduce the serum level of TNF-α, and increase the serum level of SOD and ASIA score in patients with cervical spine hyperextension injury, could reduce the inflammatory damage, improve the antioxidant capacity, which has a good clinical effect.