Objective To study the protective role of pre-resolving mediator lipoxin A4(LXA4) in the NA+ -K+-ATPase in alveolar type Ⅱ (AT Ⅱ ) epithelial cells of rats exposed to lipopolysaccharide (LPS). Method The AT Ⅱ cells were isolated and purified, and divided randomly into control group (PBS), vehiculum (alcohol 0.7 μL/mL) group, LPS (1 μg/mL) group, LXA4(1/10 mol/mL) group and LPS (1 μg/mL LPS) + LXA4(1/10 mol/mL) group. After exposure to LPS and/or LXA4 for4 hours, NA+-K+ -ATPase and β1-subunits mRNA in AT Ⅱ epithelial cells were detected by using RT-PCR, and ATP, ADP, AMP, total adenine nucleotides (TAN) and energy charge (EC) were measured by using high performance liquid chromatography (HPLC), and then the activities of Na+-K+-ATPase were calculated accordingly. Results The NA+-K+-ATPase α-subunit and β-subunit mRNA were significantly decreased in LPS group ( P ＜ 0.05 vs. control group). However, the expressions of NA+ -K+-ATPase mRNA were significantly enhanced by application of LXA4 to AT Ⅱ epithelial cells exposed to LPS (P ＜0.05 vs. LPS group). The activities of NA+ -K+ -ATPase were enhanced in LPS group (P ＜0.05 vs. control group). Compared with control group and LPS group, the activities of NA+-K+-ATpase in LPS + LXA4 group were significantly increased (P ＜0.01 vs. control group; P ＜0.05 vs. LPS group). The EC of AT Ⅱ epithelial cells were higher in LPS group ( P ＜ 0.01 vs. control group). There were no significant differences in EC between control group and LPS + LXA4group(P ＞0.05). Conclusions The pro-resolving mediator LXA4 can enhance the expressions of NA + -K + -ATPase α-subunit and β-subunit mRNA, and the activities of NA + -K + -ATPase in AT Ⅱ epithelial cells or rats exposed to LPS, and ca also balance the metabolism of AT Ⅱ epithelial cells. These findings suggest that LXA4 plays an important role in lung edema clearance in lung injury induced by endotoxin, and the role is likely associated with the enhancement of the expressions of Na+ -K+ -AT-Pase α-subunit and β-subunit, and the activities of Na+ -K* -ATPase, maintaining the balance of metabolism of AT Ⅱ epithelial cells.

This paper is to show a way of acqusition of the variable region gene of rabbit osteoprotegerin (OPG) and to analyse series. Total RNA was extracted from rabbit tibia, transcripted reversely into cDNA with random primers. The variable region of the OPG gene ampliflied using 5'RACE. Sequencing was confirmed by agarose gel electrophoresis and sequencing analysis. Full length of OPG gene was 1540bp that encoding 400 amino acids. It shared 89% identity with human OPG in whole amino acid sequence and about 85% with rattus norvegicus and other mammal. The OPG sequence of rabbit was obtained by 5'RACE, which could provide a good basis for OPG functional study.
Animals ; Base Sequence ; Molecular Sequence Data ; Osteoprotegerin ; genetics ; Rabbits ; Sequence Homology, Amino Acid

The finite element model of the intact lumbar spine (L1-L5) was set up to study the biomechanical changes of three different pairs of the lumbar laminectomy. The three-dimensional finite elements model of L1-L5 vertebrae structure was constructed by the combination of self-compiled software and Hyper Mesh. The finite element model was compared with the experimental data in vitro. The finite element model was modified of stenosis at L3-L4 and L4-L5 with the same boundary conditions and physical loads to study the motion and loading in the annulus changes at the surgical site as a result of surgical alteration. The study suggested that the removal of posterior lumbar spinal elements for the treatment of stenosis at L3-L4 and L4-L5 produced a graded increase in motion at the surgical site, with the greatest changes occurring in flexion-extension and axial rotation and that during lateral bending the amount of resection was only slightly affected. The data showed that for flexion-extension and axial rotation the increases in motion were correlated to the extent of posterior element removal. It is necessary to retain the greatest degree of posterior lumbar structures in thorough decompression, which can further reduce the postoperative intervertebral disc, facet degeneration.
Adult ; Biomechanical Phenomena ; Computer Simulation ; Finite Element Analysis ; Humans ; Laminectomy ; methods ; Lumbar Vertebrae ; diagnostic imaging ; surgery ; Male ; Models, Biological ; Spinal Stenosis ; diagnostic imaging ; surgery ; Tomography, Spiral Computed

Objective To investigate the influential factors for the outcome of the first 131I therapy in patients with PTC after total thyroidectomy.Methods One hundred and fifty-nine patients (45 males,114 females,average age (43.4± 12.2) years) with PTC after total thyroidectomy who underwent 131I therapy from July 2014 to December 2015 were retrospectively analyzed.Curative efficacy was evaluated 6 months after 131I therapy.Therapeutic outcome was evaluated according to TSH stimulated Tg (sTg) level,Dx-WBS and evidences of other imaging modalities.Twelve possible factors affecting therapeutic outcome of 131I therapy,including patients' age,gender,time interval between thyroidectomy and 131I therapy,primary tumors size and extrathyroidal extension,number and range of primary tumor lesions,lymph node metastases in surgery,status of thyroid remnant in 99TcmO4-imaging,pre-treatment laboratory measurements (TSH,sTg and TgAb),131I therapeutic dose,results of Rx-WBS and SPECT after 131I therapy,were analyzed with univariate and multivariate logistic regression.ROC curve and diagnostic critical point were analyzed to evaluate the predictive value of influential factors for the outcome of 131I therapy.Results The cure rate of the first 131I therapy was 64.2％ (102/159).Univariate logistic regression analysis showed that age,gender,lymph node metastases,sTg and 131I therapeutic dose (all P＜0.01) were the influential factors for the outcome of 131I therapy.Multivariate logistic regression analysis showed that lymph node metastases (regression coefficient:1.118) and sTg (regression coefficient:0.314) were influential factors (both P＜0.05).The regression equation was:Logit P =-4.155+ 1.118×lymph node metastases+0.314×sTg (x2 =93.7,P＜0.001).Taking sTg as a predictive factor for the outcome of 131I therapy,the AUC of ROC curve was 0.926 (95％ CI:0.888-0.963).The cut-off value of sTg was 2.97 μg/L with a sensitivity of 94.7％ (54/57) and a specificity of 76.5％ (78/102).Conclusions PTC patients with low sTg levels and few lymph node metastases after total thyroidectomy are more likely to be cured in the first 131I therapy.

BACKGROUND: Epidemiological studies have suggested that noise exposure may increase the risk of type 2 diabetes mellitus (T2DM), and experimental studies have demonstrated that noise exposure can induce insulin resistance in rodents. The aim of the present study was to explore noise-induced processes underlying impaired insulin sensitivity in mice. METHODS: Male ICR mice were randomly divided into four groups: a control group without noise exposure and three noise groups exposed to white noise at a 95-dB sound pressure level for 4 h/day for 1, 10, or 20 days (N1D, N10D, and N20D, respectively). Systemic insulin sensitivity was evaluated at 1 day, 1 week, and 1 month post-noise exposure (1DPN, 1WPN, and 1MPN) via insulin tolerance tests (ITTs). Several insulin-related processes, including the phosphorylation of Akt, IRS1, and JNK in the animals' skeletal muscles, were examined using standard immunoblots. Biomarkers of inflammation (circulating levels of TNF-α and IL-6) and oxidative stress (SOD and CAT activities and MDA levels in skeletal muscles) were measured via chemical analyses. RESULTS: The data obtained in this study showed the following: (1) The impairment of systemic insulin sensitivity was transient in the N1D group but prolonged in the N10D and N20D groups. (2) Noise exposure led to enhanced JNK phosphorylation and IRS1 serine phosphorylation as well as reduced Akt phosphorylation in skeletal muscles in response to exogenous insulin stimulation. (3) Plasma levels of TNF-α and IL-6, CAT activity, and MDA concentrations in skeletal muscles were elevated after 20 days of noise exposure. CONCLUSIONS Impaired insulin sensitivity in noise-exposed mice might be mediated by an enhancement of the JNK/IRS1 pathway. Inflammation and oxidative stress might contribute to insulin resistance after chronic noise exposure.
Animals ; Biomarkers ; metabolism ; Inflammation ; physiopathology ; Insulin Receptor Substrate Proteins ; genetics ; metabolism ; Insulin Resistance ; genetics ; immunology ; MAP Kinase Signaling System ; physiology ; Male ; Mice ; Mice, Inbred ICR ; Mitogen-Activated Protein Kinase 8 ; genetics ; metabolism ; Noise ; adverse effects ; Oxidative Stress ; physiology ; Proto-Oncogene Proteins c-akt ; genetics ; metabolism ; Random Allocation ; Time Factors