Objective To investigate the protective effect of Vitamin D (VitD) on diabetic rats,and whether the protective mechanism is associated with the expression of nuclear factor kappa B (NF-κB) and insulin resistance (IR).Methods Diabetic Wistar rats were established by intraperitoneal injection of streptozotocin,and randomly divided into diabetic group,VitD treatment group (treatment group).Normal rats were served as normal control group.Treatment group was treated with VitD for 8 weeks.The levels of 24 h urinary protein (24 h UP),fasting plasma glucose (FPG),plasma insulin (p-Ins),plasma adiponectin (p-Adi),plasma glucagon (p-Gln) were measured.Tumor necrosis factor alpha (TNF-α),monocyte chemotactic protein 1 (MCP-1),interleukin-6 (IL-6) were determinated in renal cortical homogenate.The activity of NF-κB was evaluated by electrophoretic mobility shift assay.The mRNA expressions of glucose transporter protein 1 (GLUT1) and GLUT4 in renal cortex were detected by reverse transcriptase (RT)-PCR.Western blot analysis was performed to measure the phosphorylation of NF-κB and its inhibitor I kappa Balpha (IκBα),insulin receptor substrate protein 1 (IRS1),phosphatidylinositol 3 kinase (PI3K),p38 mitogen activated protein kinase (p38MAPK).Results Compared with the normal control group,24 h UP,FPG,p-Ins,p-Gln were significantly increased,and inflammatory markers and the expression of GLUT1 elevated in renal cortex in DM group,there were significant differences(all P ＜0.01).The activity of NF-κB (P ＜0.01) and the phosphorylation of NF-κB p65 and p38MAPK were elevated (all P ＜ 0.01),and phosphorylation of IκBα,IRS1,PI3K were decreased (all P ＜ 0.05,0.01) in diabetic group compared with those of normal control group.VitD treatment could ameliorate urine protein,increase p-Adi,reduce inflammatory markers and NF-κB activity (P ＜ 0.01),maintain GLUT1 expression,but had no effect on GLUT4 expression in renal cortical,attenuate NF-κB p65,p38MAPK phosphorylation (all P ＜ 0.05),partly restore IκBα,IRS1,PI3 K phosphorylation in diabetic rats (all P ＜ 0.05,0.01).Conclusions Protective role of VitD is associated with inhibiting the expression of NF-κB and reducing the insulin resistance in diabetes.

OBJECTIVE: To evaluate the therapeutic effect of multi-plane operations in treating obstructive sleep apnea-hypopnea syndrome (OSAHS). METHOD: One hundred and fifteen patients with OSAHS diagnosed by polysomnography were treated with uvuplopalatopharyngoplasty. Eighteen of them were treated combining with nasal septal construction. Twenty six patients also received nasal septal construction and partial inferior turbinectomy. One patients also received Genioglossus advancement and partial resection of corpus linguae. Five patients also received partial resection of corpus linguae. Some patients with the nasal disease and/or the lingual hypertrophy; AHI > 40 and/or BMI > 30 are received tracheotomy before general anaesthesia. RESULT: According to the postoperative follow-up 43 patients, were cured, 46 patients were improved, 26 patients were invalid, the effective power was 77.4%. CONCLUSION The operative effective power were increased by multi-plane operations in OSAHS patients. The serious complication were prevented through tracheotomy before general anaesthesia in multi-plane operations of severe OSAHS.
Adult ; Aged ; Female ; Humans ; Male ; Middle Aged ; Retrospective Studies ; Sleep Apnea, Obstructive ; surgery ; Treatment Outcome

Objective:To investigate the baseline levels of 25-hydroxy-vitamin D [25-(OH) D] in 3340 hospitalized children, analyze the 25-( OH) D levels in children with different diseases, age and gender in different seasons, and study the correlation between the 25-( OH) D levels and the clinical indicators. Methods:Totally 3340 hospitalized children were randomly selected, the 25-( OH) D levels were detected by an ELISA method, and Pearson correlation analysis of 25-( OH) D levels and clinical indicators such as liver function, myocardial enzymes, immunoglobulins, lymphocyte subtypes and thyroid function was performed. Results: The serum 25-(OH) D level in 3340 cases (1850 male, 1490 female) was (33. 00 ± 13. 42) ng·m1 -1, and that in those with neonatal diseases was the lowest followed by those with primary nephrotic syndrome, Henoch-schordeinpurpura and juvenile idiopathic arthritis. The ser-um 25-( OH) D levels in the premature was higher than that in full term infant. Except the newborn, the level of serum 25-( OH) D gradually reduced along with the age increase, while the percentage of insufficiency gradually increased. The serum 25-( OH) D level between the male and the female had no significant difference. The 25-( OH) D levels of hospitalized children were the highest in sum-mer. The serum level of 25-( OH) D was positively correlated with body mass index ( BMI) , alanine transaminase ( ALT) , aspartate transaminase (AST), creatine kinase (CK), creatine-phosphokinase (CK-MB), lactate dehydrogenase(LDH), free T4 (FT4) and free T3 (FT3), and negative correlation with alkaline phosphatase(ALP), immunoglobulin E (IgE) and immunoglobulin M (IgM). Conclusion:The incidence of vitamin D insufficiency is high in hospitalized children. The level of vitamin D is different among various diseases. The level of serum 25-( OH) D may have certain relevance with BMI, allergies, myocardial damage and thyroid function.

Objective To test the effects of Vitamin D (VitD) on endothelial nitric oxide(NO) production and to study the signal pathway leading to NO release.Methods In vitro cultured human umbilical vein endothelial cells (HUVEC) were treated with various concentrations of VitD(0 mmol/L,0.01 mmol/L,0.10 mmol/L,1.00 mmol/L,10.00 mmol/L) for 60 min,and VitD at concentration of 1.00 mmol/L at different time points (30 min,60 min,90 min,120 min).The effect of VitD on NO production in presence of VitD receptor(VDR) agonist(ZK191784) or antagonist(ZK159222) for 60 min were examined in cell culture supernatant with kit for the detection of nitric oxide fluorescent probe(DAF-FM DA).HUVEC was cultured with VitD in presence of VDR agonist or antagonist for 60 min,and the effect of VitD on NO production with DAF-FM DA and the protein expression and phosphorylation of Caveolin-1 and endothelial nitric oxide synthase(eNOS) were detected by Western blot,respectively.Results VitD caused a concentration-dependent increase in NO production.The maximum effect was observed at a concentration of 1.0 mmol/L and the optimal time of stimulation was 60 min.Effects induced by VitD were enhanced by VDR agonist,and abolished by antagonist.VitD and VDR agonist maintained the expression of Caveolin-1 at the same low phosphorylation level the same as normal,increased the phosphorylated level of eNOS.However,VDR antagonist increased the phosphorylation of caveolin-l,but reduced the level of eNOS phosphorylation,respectively.Conclusions VitD can induce a significant increase in endothelial NO production through VDR.VitD interaction with VDR causes the low phosphorylation of caveolin-1 leading to eNOS activation and NO production.

Objectives To study the protective effects of vitamin D (VitD) on podocyte insulin resistance and its mecha-nisms. Methods Immortalized mouse podocytes in vitro were randomly divided into 4 groups:podocytes+5 mmol/L glucose group (group A);podocytes+5 mmol/L glucose+1 nmol/L propylene glycol group (group B);podocytes+30 mmol/L glucose+1 nmol/L propylene glycol group (group C); podocytes+30 mmol/L glucose+1 nmol/L propylene glycol+1 nmol/L VitD group (group D). The percentage of podocyte apoptosis was determined after 48 h of incubation. Podocyte viability was assessed by MTT assay. The mRNA expressions of vitamin D receptor (VDR) and insulin receptor substrate protein 1 (IRS1) in podocyte were detected by RT-PCR. Western blot analysis was performed to measure the protein levels of p-IRS1/IRS, p-Akt/Akt and p-ERK1/2/ERK1/2. Results There were significant differences in apoptosis percentage, viability and the expression of VDR, IRS1, p-ERK1/2 of podoctyes(P<0.05)among 4 groups. There was no difference in p-Akt/Akt expression among 4 groups(P>0.05). Compared with group A, B , and D, the percentage of podocyte apoptosis in group C was significantly increased, the cell viabi-lity was decreased, the expressions of VDR and IRS1 mRNA and p-IRS1 and p-Akt proteins were down-regulated, whereas p-ERK1/2 was up-regulated in group C. The levels of p-IRS1/IRS1, p-Akt/Akt, p-ERK1/2/ERK1/2 had no statistical differences in group A, B, and D (P>0.05). Conclusions VitD-VDR system alleviates podocyte apoptosis induced by high glucose, and acti-vates insulin signaling pathway and counteracts insulin resistance signal to improve podocyte insulin resistance.

Objective To investigate the expression of thyroid cancer-1 (TC1) and β-catenin in cervical carcinoma and precancerous lesions and their significance. Methods Immunohistochemical methods were used to examine the expression of TC1 and β-catenin in80 cervical squamous cell carcinoma (CSCC) tissues, 40 high-grade squamous intraepithelial lesions (HSIL), 40 low-grade squamous intraepithelial lesions (LSIL), and 30 normal cervical tissues. Results Although TC1 expression in CSCC was significantly higher than that in LSIL (P = 0.002) and normal cervical tissues (P ＜ 0.001), it was similar to that in HSIL (P = 0.576). TC1 expression was positively correlated with poor differentiation (P = 0.005) and advanced FIGO stage (P = 0.004) in CSCC. β-catenin expression in CSCC was significantly higher than that in LSIL (P ＜ 0.001) and normal cervical tissues (P ＜ 0.001), but was similar to that in HSIL (P = 0.907). The abnormal β-catenin expression was also correlated with poor differentiation (P = 0.025) and advanced FIGO stage (P = 0.001) in CSCC. TC1 expression was positively correlated with the abnormal β-catenin expression in CSCC (r = 0.294, P = 0.008) and cervical squamous intraepithelial lesions (r = 0.549, P ＜ 0.001). Conclusion TC1 and β-catenin expression in CSCC and HSIL was significantly higher than that in LSIL and normal cervical tissues. TC1 expression correlated with the abnormal β-catenin expression, and with poor differentiation and advanced FIGO stage of CSCC.

OBJECTIVE：To provide reference for constructing a patent linking system in line with international standards and balancing the interest conflict between original drug enterprises and generic drug enterprises. METHODS ：The relevant supporting systems of patent link in the United States were introduced ；combined with the development status and relevant systems of drug patent protection at home and abroad ，the existing problems of China ’s drug patent management system were analyzed to put forward suggestions for improvement. RESULTS & CONCLUSIONS ：The United States patent linking system included Orange book system ，generic drug patent declaration system ，generic drug approval waiting period and market monopoly period system of the first generic drug. The innovation and accessibility in the field of pharmaceutical products were facing the dilemma of “commons tragedy ”and“anti commons tragedy ”. There were many problems in China ’s drug patent protection ，such as insufficient R&D and innovation ability inhibited the development of the pharmaceutical industry ，imperfect laws and regulations were not conducive to the settlement of medical professional disputes. It is suggested to establish a digital information database of patented drugs ，standardize the existing generic drug patent declaration system ，promote the coordination between patent litigation cycle and approval waiting period ，increase the independent innovation ability of the pharmaceutical industry ，promote the coordination between pharmaceutical innovation and drug accessibility ，and jointly promote the improvement of intellectual property legislation and the development of medical and health undertakings.

Fibrosis is a common pathological change in clinical end-stage diseases,which can occur in any organ and is also a major burden of global health care.Persistent fibrosis can lead to organ failure and seri-ously threaten the life and health of patients,but its mechanism is still unclear.With the deepening of the re-search on fibrosis in modern science,the application of single cell genomics has brought new insights into the exploration of fibrosis tissue biology and disease mechanism in clinic.Since the discovery of autophagy,more and more studies at home and abroad have confirmed that autophagy is involved in the occurrence and develop-ment of fibrosis,which provides a new direction for the treatment of organ fibrosis.This article summarizes the effects of autophagy on organs such as lung and uterus,and summarizes the research progress of autoph-agy pathway in organ fibrosis in recent years,in order to provide new ideas for the treatment of organ fibrosis.