0.05). In stratified studies, risk of asthma in individuals with null genotype of GSTM1 is 2.667 times of that with wild genotype after exposure to light air pollution. Risk of asthma in individuals living in heavy air pollution area is 2.125 time of that in light pollution area for all wild genotype of GSTM1 individuals, but without statistical significance. Conclusion It was not found that the relationship between GSTM1, GSTT1 polymorphism and asthma. Synergism of genotype of GSTM1, GSTT1 and air pollution was not also seen in this study.

Background Several cytokines,especially interleukin-1β (IL-β) involve in the breakdown of blood-retina barrier,and the signal of cytokine is transduced through protein tyrosine kinase (PTK) pathway.Objective This study was to investigate the effects of PTK inhibitor,Genistein,on IL-1β-induced blood-retinal barrier breakdown and possible mechanism.Methods The animal models of blood-retinal barrier breakdown were induced through intravitreal injection of IL-1β(10ng) in 24 clean healthy SD rats and assigned to IL-1β group and Genistein group.5μl IL-1β+1μl Genistein with 0.2,1,5μg were intravitreally injected in 12 model rats and 5μl IL-1β (2mg/L)+1μl DMSO was used at the same way in other 12 models.Evans Blue was injected in rats via jugular vein in 1 hour before sacrifice of animals and the arterial blood was collected for the detect of serum Evans Blue.The retinas of the rats were obtained in 4 and 48 hours after injection of vitreous cavity to assay the content of Evans Blue in retina.The changes of vessels and infiltration of inflammatory cells were observed with hematoxylin-eosin stain.RT-PCR was employed to determine the expression of IL-8 and MCP-1mRNA in neuroretina after intravitreal injection.Expression of MCP-1 protein was localized by immunohistochemistry.Results The ratio of retinal Evans Blue and plasma Evans Blue was significantly decreased after intravitreal injection of different doses of Genistein among Genistein groups and IL-8 group with a statistical difference (4 hours:F=7.510,P=0.010;48 hours:F=5.960,P=0.019).With the increase of time after injection of Evans Blue,the ratio of retinal Evans Blue and plasma Evans Blue was gradually reduced in comparison to IL-1β group (P＜0.05).After injection of IL-1β,the dilation of retinal vessel and adhesion of leukocyte to vessel wall were seen under the light microscope,but infiltration of less inflammatory cells was found in Genistein group.The expressions of IL-8 and MCP-1mRNA were obviously declined in retina of rats in Genistein groups compared with IL-8 group (P＜0.05).Immunochemistry indicated that the expression of MCP-1 protein in neuroretina tissue was weaker in Genistein group compared with IL-8 group.Conclusion PTK inhibitor,Genistein,can decrease IL-1β-induced permeability of vessel and maintain the integrity of blood-retinal barrier by downregulating the expression of chemokines and infiltration of leukostasis in retinal vessels.This study imply that PTK pathway plays an important role in IL-1β-induced blood-retinal barrier breakdown.

Objective To investigate the changes of growth arrest and DNA damage inducible gene ?(GADD45?)expression during 3T3-L1 preadipocyte differentiation and analyze the regulative role of tumor necrosis factor-alpha(TNF-?) on GADD45? gene expression in matured 3T3-L1 adipocytes.Methods 3T3-L1 preadipocytes were cultured in vitro and differentiated into the matured adipocytes.TNF-? in different concentrations(0.1,1.0,10.0 ?g/L) was added into the culture medium of fully differentiated adipocytes(day 10) for various times(0.5,2,6,12,24 h).The levels of GADD45? gene mRNA expression were evaluated by reverse transcription polymerase chain reaction(RT-PCR).Results With the 3T3-L1 preadipocytes being differentiated into the matured adipocytes,the level of GADD45? gene mRNA expression was downregulated and reached the lower level in fully differentiated adipocytes.There was a significant difference between any 2 detected phases in the levels of GADD45? gene mRNA expression(P0.05).Treatment of day 10(3T3-L1) adipocytes with TNF-? of different concentrations resulted in a significant increase in the level of GADD45? gene mRNA expression.The induction effect of TNF? on GADD45? gene mRNA expression generally tended to be reinforced with the elongation of time course.Conclusions GADD45? gene may be involved in adipocyte differentiation and adipogenesis.TNF-? can upregulate the mRNA expression of GADD45? gene in matured adipocytes.The induction effect of TNF-? on GADD45? gene expression is generally(time-)correlated.

Objective:To investigate the relationship of etiology and complications of rhabdomyolysis with its prognosis in the elderly.Methods:Patients with rhabdomyolysis at the emergency department of our hospital from January 1, 2018 to December 31, 2019 were retrospectively analyzed.Based on age, patients were divided into the non-elderly group(<65 years old)and the elderly group(≥65 years old). The frequency distribution of etiological factors, concurrent acute kidney injury, and their association with prognosis were analyzed.Results:The number of patients with rhabdomyolysis caused by 2 or more etiologies was higher in the elderly group than in the non-elderly group(40.3% or 48/119 vs.17.0% or 16/94, χ2=13.582, P=0.000). The frequency distribution of etiological factors was different between the two groups.The top-five etiologies were infection, muscle ischemia/hypoxia, endocrine metabolic abnormalities, trauma and muscle fatigue in the elderly group and muscle fatigue, infection, endocrine metabolic abnormalities, drugs/toxicants and trauma in the non-elderly group.Compared with the non-elderly group, the elderly group had fewer patients with typical clinical manifestations(32.8% or 39/119 vs.48.9% or 46/94, χ2=5.067, P=0.024). In contrast, patients who newly presented with disturbance of consciousness were more likely to be found in the elderly group than in the non-elderly group(40.3% or 48/119 vs.21.3% or 20/94)( χ2=7.923, P=0.005). There were 37 patients with AKI(38.9% or 37/95)in the elderly group and 13 of them died(35.1%), and there were 17 patients with AKI in the non-elderly group(19.3% or 17/88)and 4 died(23.5%), indicating the elderly were prone to AKI( χ2=7.545, P=0.006). There was a significant correlation between AKI and prognosis in the non-elderly group( χ2=7.196, P=0.007). Conclusions:Rhabdomyolysis caused by multiple etiologies is more common in elderly patients than in non-elderly patients.The etiological classification of rhabdomyolysis in the elderly is different from that in the non-elderly.Elderly patients are less likely to have typical clinical manifestations and are more prone to AKI.Elderly patients with rhabdomyolysis combined with AKI have a poor prognosis.

Child ; Cochlear Implantation ; Cochlear Implants ; Evoked Potentials, Auditory, Brain Stem ; Hearing Loss, Central ; physiopathology ; Humans ; Vestibulocochlear Nerve Diseases ; physiopathology

OBJECTIVETo observe the effect of Hydroxy Safflower Yellow A (HSYA) on the expression of osteogenic markers, such as alkaline phosphatase, Cbf(alpha)l and type I collagen, and explore the mechanism of HSYA in the prevention and treatment of glucocorticoid-induced ischemic necrosis of femoral head.

METHODSFifteen healthy and adult New Zealand white rabbits were collected and weighted 0.9 to 1.3 kg. The rabbits were injected abdominally with anesthetic drugs, then received marrow cavity puncture of tibia and anterior superior iliac spine to get bone marrow blood. Rabbits bone marrow mesenchymal stem cells (BMSCs) were separated from the bone marrow blood, cultured in vitro and passaged. The 3rd generation of BMSCs which had good growth condition were randomly divided into blank group, model group and HSYA groups with different doses. The BMSCs in model group were treated with high dose of dexamethasone to induce adipogenic differentiation of cells cultured in vitro, and inhibit osteogenic differentiation. The BMSCs in HSYA groups received high dose of dexamethasone and different concentrations of HSYA simultaneously. The blank group received not any special handling. After a week,the expressions of alkaline phosphatase, Cbf(alpha)l and type I collagen mRNA were detected.

RESULTSThe alkaline phosphatase activity was significantly decreased in BMSCs of the model group as compared with the blank group (P < 0.01), and the expression of Cbf(alpha)l and type I collagen mRNA were also decreased significantly (P<0.01). The alkaline phosphatase activity was significantly increased in BMSCs of each HSYA group as compared with the model group (P < 0.05 or P < 0.01), and the expression of Cbf(alpha)l and type I collagen mRNA were also increased significantly (P < 0.05 or P < 0.01).

CONCLUSIONThe mechanism of HSYA may be related to the effect of antagonism to the reduced osteogenic differentiation induced by glucocorticoid.

Alkaline Phosphatase ; genetics ; metabolism ; Animals ; Bone Marrow Cells ; cytology ; drug effects ; metabolism ; Cell Differentiation ; drug effects ; Cells, Cultured ; Chalcone ; analogs & derivatives ; chemistry ; pharmacology ; Collagen Type I ; genetics ; metabolism ; Core Binding Factor alpha Subunits ; genetics ; metabolism ; Drugs, Chinese Herbal ; chemistry ; pharmacology ; Female ; Glucocorticoids ; pharmacology ; Male ; Mesenchymal Stromal Cells ; cytology ; drug effects ; metabolism ; Osteogenesis ; drug effects ; Rabbits

Adult ; Female ; Heart Diseases ; etiology ; Humans ; Male ; Mitochondrial Diseases ; complications ; Young Adult

Objective To investigate the risk factors of type 2 diabetes mellitus(T2DM) in patients with nonalcoholic fatty liver disease (NAFLD) and correlations with carotid atherosclerosis.Methods The clinical data of 51 cases of N AFLD with T2DM (NAFLD with T2DM group),43 cases of NAFLD(NAFLD group) and 45 healthy objects (control group) were collected.The clinical biochemical features,carotid intima-media thickness (IMT) were observed.Results The BMI and smoking rate in NAFLD with T2DM group and NAFLD group were significandy higher than those in control group [(27.25 ±3.16),(26.31 ± 2.63) kg/m2 vs.(23.12 ±3.44) kg/m2,43.1％(22/51),37.2％(16/43) vs.13.3％(6/45)](P＜0.05).The ratio of family history of T2DM in NAFLD with T2DM group was significantly higher than that in NAFLD group and control group[66.7％(34/51)vs.32.6％(14/43),8.9％(4/45)](P ＜ 0.05).Compared with control group,the level of total cholesterol (TC),trigalloyl glycerol (TG),low density lipoprotein cholesterol (LDL-C),alanine transaminase(ALT),aspartic transaminase(AST),IMT in NAFLD with T2DM group and NAFLD group were significantly higher [(5.39 ± 0.85),(5.12 ± 0.77) mmol/L vs.(4.11 ± 0.64) mmol/L,(2.77 ± 1.11),(2.32 + 1.04) mmol/L vs.(1.21 ± 0.52) mmol/L,(2.98 ±0.93),(2.76 +0.78) mmol/L vs.(2.15 ±0.57) mtmol/L,(48.4 ± 18.9),(43.3 ± 16.5) U/L vs.(21.4 ± 13.6) U/L,(46.2 ± 16.7),(42.1 ± 17.5) U/L vs.(20.5 ± 12.6) U/L,(1.95 ±0.93),(1.26±0.51) mmvs.(0.71 ±0.22) mm](P＜ 0.05),while the level of high density lipoprotein cholesterol (HDL-C) was significantly lower [(1.01 ± 0.35),(1.13 + 0.22) mmol/L vs.(1.31 ± 0.26) mmol/L] (P ＜ 0.05).The level of above mentioned index,there were no significant difference between NAFLD with T2DM group and NAFLD group (P ＞ 0.05).The level of fasting blood glucose (FBG),2-hour postprandial blood glucose (2 h PBG),glycosylated hemoglobin (HbA1c),fasting insulin (FINS),2-hour postprandial insulin (2 h PINS) and insulin resistance index of HOMA (HOMA-IR) in NAFLD with T2DM group were significantly higher than those in NAFLD group and control group [(8.15 ± 1.48) mmol/L vs.(5.10 ± 1.32),(5.62 ± 0.88) mmol/L,(13.67 ± 1.59) mmol/L vs.(7.31 ± 1.25),(8.64± 1.35) mmol/L,(7.03 ±0.84)％ vs.(5.16 ±0.72)％,(5.53 ±0.61)％,(13.32 ±4.55) mU/L vs.(6.06 ±3.11),(9.13 ±4.37) mU/L,(106.37 ±21.45) mU/L vs.(33.21 ± 18.87),(46.34 ± 16.39) mU/L,3.88 + 2.14 vs.1.13 ± 0.36,2.23 ± 1.15] (P ＜ 0.05).Carotid IMT,the incidence of carotid plaque and Crouse scores of plaque in NAFLD with T2DM group were significandy higher than those in NAFLD group [(1.95 ±0.93) mm vs.(1.26 ±0.51) mm,64.7％(33/51) vs.30.2％(13/43),(3.11 ±0.57) nn vs.(1.35 ± 0.49) mm] (P ＜ 0.05).The regression analysis showed that family history of T2DM,FBG,2 h PBG,FINS,2 h PINS were independently associated with T2DM.Conclusions Family history of T2DM,FBG,2 h PBG,FINS,2 h PINS are the main risk factors for the onset of T2DM in NAFLD.The risk of carotid atherosclerosis is increased in patients of NAFLD with T2DM.

BACKGROUND:Human femur medul ary cavity has torsional anatomic structure. If the femur medul ary cavity’s torsional structure is copied to the stem of the prosthesis, the prosthesis wil transform the force loaded to torque between femur medul ary cavity and prosthesis stem, and the torque is transmitted to the proximal femur when the prosthesis is inserted in the medul ary cavity and load force on the prosthesis. OBJECTIVE:To optimize the force transmission of the proximal femur, and to avoid the stress shielding at the proximal end of the prosthesis. METHODS:We reconstructed a three-dimensional (3D) model of the femoral canal with the CT images of specimen femur and took the 3D model as the design model for prosthesis stem. The customized stem model and the proximal model of standard prosthesis could be put together to form customized prosthesis. We took advantage of robot grinding technology to manufacture the customized prosthesis, and matched it with specimen femur canal. Finite element analysis simulation and experimental methods were used to analyze the relationship between the loading force on the prosthesis and the micromotion of proximal end of the prosthesis. RESULTS AND CONCLUSION:The simulation and experimental results showed that the torsional structure matching by femoral canal and stem could effectively transmit the force on the prosthesis to the proximal end of the prosthesis in the form of torque. The torsional fretting of the proximal end of the prosthesis was related to the movement of the handle body. However, stem micromotion can be control ed by varying the matching size between stem and medul ary cavity.

AIM: To investigate the inhibitory effect of Chinese medicine Jinan injection(JA) on Lewis lung cancer (LLC) in mice. METHODS: The C 57 BL/6J mice with Lewis lung cancer(LLC) were divided into normal saline(NS), Jinan high dose (JAH), Jinan middle dose (JAM), Jinan low dose (JAL) and cyclophosphamide(CTX) groups. The body weight changes and inhibitory rate of LLC in each group were observed. In addition, flow cytometry and TUNEL were used to detect the anticancer mechanism of Jinan. RESULTS: The body weights were increased significantly in JA-treated groups vs CTX and the resistant rate was 45.79%, 40.90%, 32.48% and 98.96%, respectively. The apoptotic rate was 24.19%, 14.95% and 13.93% in JAH, JAM and JAL, respectively, and the Jinan induced apoptosis of LIC in a dose-dependent manner.CONCLUSION: Jinan injection inhibites the growth of LLC, and the apoptosis induction may be one of mechanisms that Jinan treates LLC in mice.