Public Health Ophthalmology is a population-,region-or country-based as a whole object,and is committed to improving the eye health of the whole population.Epidemiological investigation of the eye was named to the region from a single disease to variation of diseases from cross-sectional survey to a longitudinal cohort study.Epidemiological investigations is the most important way which can reflect the pathogenic factors for public health policy-making,early diagnosis and prevention and treatment of eye disease,and Research to Prevent Blindness.Imaging Diagnosis,quality control,improve the reliability of the epidemiological investigation,and to strengthen the study of disease,race,and molecular levels and create a unique epidemiological study.

Objective To investigate the mechanism of 5′adenosine monophosphate-activated pro-tein kinase ( AMPK) in the regulation of LPS-induced secretion of inflammatory cytokines in mouse alveolar macrophages.Methods Alveolar macrophages were isolated from wild type and AMPKα1-/-C57BL/6J mice.ELISA was used to measure the concentrations of IL-1βand TNF-αin the culture supernatants of LPS treated alveolar macrophages with or without 5-amino-1-β-D-ribofuranosyl-imidazole-4-carboxamide ( AICAR ) stimulation.Western blot assay was performed to analyze the expression of AMPKα1 and AMPKα2 in alveolar macrophages isolated from wild type and AMPKα1-/-mice as well as the LPS-induced changes of p-AMPKαactivity in wild type mice.Results The LPS-induced secretion of inflammatory cyto-kines in alveolar macrophages isolated from AMPKα1-/-mice were significantly higher than that of wild type mice.The activities of p-AMPKαin wild type mice were suppressed by LPS treatment.Treatment of AICAR inhibited the LPS-induced secretion of TNF-αand IL-1β.Conclusion The LPS-induced secretion of in-flammatory cytokines was enhanced in AMPKα1-deficient mice, but could be suppressed upon the treatment of AICAR, an agonist of AMPK.AMPK was involved in the regulation of LPS-induced secretion of inflamma-tory cytokines by alveolar macrophages in mice.

Objective The purpose of this study was to research the expression of Twist in cervical cancer tissues and the relationship between its expression and clinicopathologic characteristic, and to investigate the role of twist in cervical cancer invasion, metastasis and progress. Methods Immunohistochemistry was used to detect the expression of the Twist in 78 cases of middle and advanced stages cervical cancer tissue microarray chip. The relationship between its expression and clinicopathological characteristic was analyzed. Results (1) The positive expression of twist in cervical cancer was 56/78 (71.8%);(2) The expression of Twist in cervical cancer was significantly related to tumor histology type, FIGO stage, lymph node metastasis and differentiation degree. With the increase of FIGO stage, the emergence of lymph node metastasis and the decrease of differentiation degree, the expression of Twist increased gradually ( <0.05) . Conclusion The expression of Twist may be closely related to the invasion, metastasis and progress of cervial cancer.

The intracellular signal transduction pathways play an important role in the occurrence and development of thyroid cancer.Mitogen activated protein kinase (MAPK) signal transduction pathway,phosphatidylinositol 3-kinase (PI3K)-AKT pathway,NF-κB pathway and RASSF1-MST1-FOXO3 pathway affect the occurrence and development of thyroid cancer by modulating the activity and expression of specifical proteins,and determine the growth and apoptosis of thyroid cancer cells.

Clinical practice is an important process for the formation of the clinical skills and decent medical ethics of medical students.This paper clarifies various issues arising in the current medical ethics education,and proposes relevant countermeasures from the perspectives of medical colleges,training hospitals,guidance teachers,and so on.

Objective To explore the molecular mechanism of inhibition of LPS-induced inflammation by fenoterol, a β2 adrenoceptor agonist in monocyte. Methods Concentrations of interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α) and MCP-1 from cell supernatants from THP-1 cells and wild type or MyD88- / - mice peritoneal macrophages stimulated by LPS in the presence or absence of fenoterol were determined by use of an ELISA system. Expression of MyD88 (myeloid differentiation factor 88) stimulated by LPS in the presence or absence of fenoterol were determined by Western blot. Results Fenoterol inhibited LPS-induced activation of MyD88 and secretion of inflammatory cytokines (TNF-α, MCP-1, and IL-1β). The reaction of MyD88- / - mice peritoneal macrophages to LPS was much lower than that of the wild type mice peritoneal macrophages. Conclusions MyD88 plays an important role in inflammation induced by LPS. The inhibition of LPS-induced expression of MyD88 by fenoterol is associated with its anti-inflammatory effect.

The core-shell nanopaticles of Au@polyvinyl-pyrrolidone ( PVP) with uniform size and controllabe shell-thickness were prepared by hydrothermal method. The core-shell nanoparticles could be assembled to be the monolayer array on Si substrate relying on the dispersion of core-shell nanoparticles arising from PVP shell. The malachite green ( MG ) absorbed by H-bond could be detected on the array under the electromagnetic enhancement of inner-core Au nanoparticles. Under the conditions of the optimum shell-thickness of Au@PVP and the appropriate absorbed time of MG, the detection of MG could be realized in the linear range from 1 × 10-10 mol/L to 1 × 10-5 mol/L with the correlation coefficient ( R2 ) of 0. 98. The detection limit was 10-12 mol/L. This method was applied to the determination of MG in tilapia fish fillets of Xiagang market. No MG was found in this real sample. The spiked recoveries of the sample ranged from 70. 8% to 126. 0%. This method is simple and accurate, and can be used for detection of MG in the fish.

ObjectiveTo investigate the effect of SalB on bone marrow-derived mesenchymal stem cells (BMSCs) apoptosis induced by hypoxia and serum deprivation (hypoxia/SD) in the vitro. Methods BMSCs were cultured in the vitro and randomly divided into control group, hypoxia/SD group and SalB group.SalB group was composed by four groups and were pretreated by complete medium with 0.1、 1、 10、 100 mg/L SalB for 1 hour. And after that they were washed with phosphate buffer for 2 times, added by IMDM with 0.1、1、 10、 100 mg/L SalB and cultured with hypoxia/SD group together in the same condition of hypoxia/SD for 6hours. The control group was cultured for 6 hours in the condition of aerobic and enough serum. Apoptosis was detected by Hoechst33342 staining with inverted phase contrast, fluorescence microscope and Annexin V/PI dual-color flow cytometry. Results Significant apoptosis of BMSCs was induced by hypoxia/SD in the vitro.The early apoptosis of BMSCs induced by hypoxia/SD was significantly decreased by SalB of 0.1、 1、 10 mg/L(P＜0.05) . Conclusion0.1、 1、 10 mg/L SalB can decrease the early apoptosis of BMSCs induced by hypoxia/SD.

Objective To investigate the expression of CD14/CD16 by monocytes and the anti-inflammatory effects of hypertonic saline plus dextran (HSD) in adult blunt trauma patients in hemonhagic shock. Method A total of 30 adult patients were eligible for inclusion in the study if they sustained blunt trauma from March to October 2007 and had at least one recorded episode of hypotension (systolic blood pressure ≤ 90 mm Hg) with clear evidence of blood loss (external or internal including the thorax, abdomen or retroperitoneum). Patients were excluded if they refused to participate, were admitted ≥ 6 hours after injury, were pregnant, or had chronic disease. The enrolled patients were randomly divided in a double-blinded manner into an HSD group which was administered 7.5% Nad plus 6% dextran - 70, and a control group which was administered 0.9% NaCl. A single 250 ml dose of either HSD or NaO was immediately administered to the patients in each of the two groups while they were in the emergency room. The primary outcomes were to measure the changes in CD4/CD16 expression by monocytes and the levels of anti-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-lra and IL-10. Patient demographics, fluid requirements, organ dysfunction, infection and death were recorded. Results A total of 28 patients were enrolled with no significant differences in their clinical measurements. Hyperosmolarity was modest and transient. HSD altered the shock-induced monocyte redistribution pattern by reducing the drop in the "classic" CD14 ++ subset and remarkably affecting the expansion of the "pro-inflammatory" CD14+CD16+ subsets. In parallel, HSD significamly reduced pro-inflammatory TNF-α production while increasing anti-inflammatory IL-lra and IL-10 production. Conclusions This human trial demonstrates that HSD has anti-inflammatory and immunologic properties for trauma patients in hemorrhagic shock. HSD exerts profound immunomodulatory effects, promoting more balanced pro-/anti-inflammatory responses and reducing post-traumatic complications. Therefore, it could be useful in attenuating post-trauma multiorgan dysfunction (MOD).