ObjectiveTo explore the theory and methods of the development and standardization of ICF-based measurement in rehabilitation medicine.MethodsICF and psychometric theories and approaches were applied.ResultsOn the basis of ICF theory of functioning, disability and health, the approaches of the development of ICF-based measurement had been proposed as well as the approaches and procedures of standardization of ICF-based measurement had been advised in rehabilitation medicine. One case study of the development of ICF Core-sets had been discussed.ConclusionThe approach and procedures had been proposed for the ICF-based standardized measurement in rehabilitation medicine.

0.05). Postoperative cataract incidence was higher in the patients without IOL implantation than that in the patients with IOL implantation. Postoperative cataract appeared 6 months after operation in the patients without IOL implantation, while it appeared 14 months after operation in the patients with IOL implantation. There was no significant difference in the postoperative complications between group A and group B. Conclusions Combined surgery is effective and safe for the selected patients of primary retinal detachment accompanied with cataract.

AIM: To observe the effects of some component of Chinese herbs for external use on proliferation of human umbilical vein endothelial cells (HUVEC) and investigate the mechanism of promoting tissue repair. METHODS: The method of MTT was used to examine the effects of Rg1, Rh1, perlolyrine, cinnamyl aldehyde, muscone, astragalus polysaccharin (APS), velver antler polypeptide (VAP) and soluble extract of boswellia carterii birdw (BCB) on proliferation of HUVEC. RESULTS: APS did not promote proliferation of HUVEC at 9.75 mg/L-2.5 g/L; Rh1 promoted proliferation of HUVEC at 1.94 mg/L-0.5 g/L (P

Objective:Based on the model of human umbilical vein endothelial cell(HUVEC) treated by tumor necrosis factor-alfa(TNF),We investigate the effects of muscone on polymophonulear leukocytes(PMN)-HUVEC adhesion and its adhesion molecules(CAMs) expression.Methods:Confocal system was used for identifying cultured HUVEC,MTT assay for its activity,Rose Bengal Staining for PMN-HUVEC adhesion,and fluorescent-immunocytochemistry techniques for CAMs expression.Results:After HUVEC treated by TNF,the adhesion between PMN and HUVEC increased dramatically(P

AIM: To investigate the effects of Astragalus polysacharin(APS) on human fibroblast and human umbilical vein endothelia cell (HUVEC) proliferation, as well as its acts on adhesion between white cells and HUVECs. METHODS: Human fibroblasts from distal and proximal skin away the ulcer were cultured as normal fibroblasts(NF) and wounded fibroblasts(WF). MTT assay was used for detecting cell proliferation, Rose Bengal staining and fluorescence immunohistology assay were used for examining the adhesion of human polymorpho-nuclear cell(PMN) and TPH-1 to HUVECs. RESULTS: 2 44-156 mg/L APS promoted WF proliferation, and 2 44-39 mg/L APS also promoted NF proliferation, but it did not show any proliferating effect on HUVECs. APS inhibited the adhesion of PMN or TPH-1 to HUVECs induced by tumor necrosis factor(TNF). At 25-100 mg/L, it also inhibited both VCAM-1 and ICAM-1 expression in HUVECs induced by TNF. Treatment with APS for 12 h also inhibited CD44 expression in HUVECs. CONCLUSION: APS shows mitogenic activity on both human normal and wounded fibroblasts. It also exerts anti-inflammation effects by inhibiting adhesion molecule expression and adhesion of white cells to HUVECs. [

Objective To explore the danger of lead exposure in newborns who accepted the blood stored in blood bank for blood change treatment.Methods The lead level of blood was examined before and after blood change treatment for 37 neonates with hyperbilirubinemia who accepted 53 cases blood stored in blood bank during Jun.to Dec.2006.The level of blood lead was measured by graphite stove atom absorb spectrum method.Results The average lead level of 53 cases blood stored in blood bank was 101.02 ?g/L,which had attained the level of lead poisoning.There were 15 cases(28.5%) whose blood lead levels was very high(≥100 ?g/L),3 cases whose blood lead level ≥200 ?g/L.After blood change treatment,the percentage of the blood lead level ≥100 ?g/L rose from 2.9% to 19.0%.The average level of blood lead after blood change treatment was higher than before(P

AIM:To investigate peripapillary vessel density and its relationship with other ocular parameters in highly myopic eyes with peripapillary intrachoroidal cavitation (PICC), and to analyze risk factors for PICC.METHODS:Cross-sectional study.A total of 35 highly myopic eyes with PICC, 40 highly myopic eyes without PICC and 35 normal eyes were included in this study.All participants underwent fundus photography and spectral-domain optical coherence tomography (SD-OCT).OCT angiography was also performed to image the retinal vasculature in the peripapillary areas of different sectors, including the radial peripapillary capillaries (RPC) and optic nerve head (ONH) layer.The difference of morphology changes in optic disc and peripapillary vessel density between these three groups were compared.Correlations between peripapillary vessel density and PICC and risk factors for the presence of PICC were analyzed.RESULTS: Significant differences were found among the three groups in spherical equivalent refraction (SER), best-corrected visual acuity (BCVA), axial length, peripapillary atrophy β-zone (β-PPA) area, retinal nerve fiber layer (RNFL) thickness and the presence of tilted optic disc, posterior staphyloma and myopic maculopathy (MMD) (P<0.05).There were significant differences among the three groups in the peripapillary vessel density both in RPC (54.34±5.58, 57.54±7.44, 64.42±3.50) and ONH (51.24±7.43, 52.75±9.96, 61.25±4.15) layers (P<0.001).In highly myopic eyes, vessel density was significantly lower in eyes with PICC than in those without in inferotemporal area both in the RPC (56.76±6.62,63.84±6.02,67.52±4.78) and ONH (56.47±5.79,60.38±4.72,64.18±4.37) layers.The vessel density was significantly correlated with the presence of MMD, β-PPA area and RNFL thickness in the RPC layer, whereas correlated with the presence of MMD, PICC and RNFL thickness in the ONH layer (P<0.05).Tilted optic disc and posterior staphyloma were independent risk factors for the presence of PICC (OR=8.007, 95%CI: 2.045-31.348;OR=7.558, 95%CI: 1.398-50.026).CONCLUSION:Highly myopic eyes with PICC had relatively lower peripapillary vessel densities, especially in the temporal area, than those without.Tilted optic disc and posterior staphyloma were independent risk factors for the presence of PICC.

OBJECTIVETo study the protective effect of rosmarinic acid (Ros A) on the primary cardiomyocyte hypoxia/reoxygenation (H/R) injury.

METHODPrimary cardiomyocytes of rats were cultured in vitro to establish the H/R injury of cardiomyocytes and observe the changes in the cell viability and LDH leakage. The changes in ATP content and ROS in cardiomyocytes were measured by using chemiluminescence and fluorescent probe technique. The effects of rosmarinic acid on the apoptosis of cardiomyocytes, cleaved-caspase 3, Akt and p-Akt protein expression were further detected by flow cytometry and western blot analysis.

RESULTAccording to the experimental results, Ros A at doses of 25, 50, 100 mg x L(-1) could inhibit the decrease in H/R-induced cell viability, LDH leakage and excessive ROS generation, and maintain the ATP level in cells. Ros A at doses of 50, 100 mg x L(-1) could remarkably inhibit the H/R-induced cardiomyocyte apoptosis and down-regulate the expression of cleaved caspase-3. Moreover, Ros A at doses of 100 mg x L(-1) could significantly up-regulate the expression of p-Akt.

CONCLUSIONRos A has the significant effect in resisting the cardiomyocyte H/R injury, improve cardiomyocyte energy metabolism and reduce cell apoptosis, which is related to the activation of Akt pathway.

Adenosine Triphosphate ; metabolism ; Animals ; Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Cell Hypoxia ; drug effects ; Cell Survival ; drug effects ; Cells, Cultured ; Cinnamates ; pharmacology ; Depsides ; pharmacology ; Humans ; Hypoxia ; genetics ; metabolism ; physiopathology ; prevention & control ; Male ; Myocytes, Cardiac ; cytology ; drug effects ; metabolism ; Oxygen ; metabolism ; Plant Extracts ; pharmacology ; Protective Agents ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species ; metabolism ; Rosmarinus ; chemistry

OBJECTIVE To determine the functional role of hydrogen sulfide (H2S) in protecting against mitochondrial dysfunction in heart failure through the inhibition of Ca2 +/calmodulin-dependent protein kinaseⅡ (CaMKⅡ) using wild type and CSE knockout mouse models. METHODS Continuous subcutaneous injection isoprenaline (7.5 mg·kg-1·d-1), once a day for 4 weeks to induce heart failure in Male C57BL/6 (6-8 weeks old) mice and CSE-/- mice. 150 μmol·L-1 H2O2 was used to induce oxidative stress in H9c2 cells. Echocardiograph was used to detect cardiac parameters. H&E stain and Masson stain was to observation histopathological changes. Western blot was used to detect protein expression and activity. The siRNA was used to silence protein expression. HPLC was used to detect H2S level. Biotin assay was used to detect the level of S- sulfhydration protein. RESULTS Treatment with S-propyl-L-cysteine (SPRC) or sodium hydrosulfide (NaHS), modulators of blood H2S levels, attenuated the development of heart failure in animals, reduced lipid peroxidation, and preserved mitochondrial function. The inhibition CaMKⅡ phosphorylation by SPRC and NaHS as demonstrated using both in vivo and in vitro models corresponded with the cardioprotective effects of these compounds. Interestingly, CaMKⅡ activity was found to be elevated in CSE-/- mice as compared to wild type animals and the phosphorylation status of CaMKⅡ appeared to relate to the severity of heart failure. Importantly, in wild type mice SPRC was found to promote S-sulfhydration of CaMKII leading to reduced activity of this protein however, in CSE-/- mice S-sulfhydration was abolished following SPRC treatment. CONCLUSION A novel mechanism depicting a role of S-sulfhydration in the regulation of CaMKⅡ is presented. SPRC mediated S-sulfhydration of CaMKII was found to inhibit CaMKⅡ activity and to preserve cardiovascular homeostasis.

OBJECTIVE To determine the functional role of hydrogen sulfide (H2S) in protecting against mitochondrial dysfunction in heart failure through the inhibition of Ca2 +/calmodulin-dependent protein kinaseⅡ (CaMKⅡ) using wild type and CSE knockout mouse models. METHODS Continuous subcutaneous injection isoprenaline (7.5 mg·kg-1 per day), once a day for 4 weeks to induce heart failure in male C57BL/6 (6-8 weeks old) mice and CSE-/- mice. 150 μmol·L-1 H2O2 was used to induce oxidative stress in H9c2 cells. Echocardiograph was used to detect cardiac parameters. H&E stain and Masson stain was to observation histopathological changes. Western blot was used to detect protein expression and activity. The siRNA was used to silence protein expression. HPLC was used to detect H2S level. Biotin assay was used to detect the level of S-sulfhydration protein. RESULTS Treatment with S-propyl-L-cysteine (SPRC) or sodium hydrosulfide (NaHS), modulators of blood H2S levels, attenuated the development of heart failure in animals, reduced lipid peroxidation, and preserved mitochondrial function. The inhibition CaMKⅡ phosphorylation by SPRC and NaHS as demonstrated using both in vivo and in vitro models corresponded with the cardioprotective effects of these compounds. Interestingly, CaMKⅡ activity was found to be elevated in CSE-/- mice as compared to wild type animals and the phosphorylation status of CaMK Ⅱ appeared to relate to the severity of heart failure. Importantly, in wild type mice SPRC was found to promote S-sulfhydration of CaMKⅡ leading to reduced activity of this protein however, in CSE-/- mice S-sulfhydration was abolished following SPRC treatment. CONCLUSION A novel mechanism depicting a role of S-sulfhydration in the regulation of CaMKⅡ is presented. SPRC mediated S-sulfhydration of CaMKⅡ was found to inhibit CaMKⅡ activity and to preserve cardiovascular homeostasis.