The launch of Expedition 1 to the International Space Station (ISS) opened a new era in the history of human space flight, so far fourteen Expeditions had been achieved. But the astronauts were exposed to abnormal environment such as microgravity, radiation, isolation, confinement, and misalignment of circadian rhythm during space flight. In order to reduce health risks incurred by living in space, the 59 projects have been or will be studied aboard ISS. Those researches has elucidated the rate of subregional bone loss and its recovery, characteristics of atrophy and reduced contraction function in antigravity skeletal muscle, decrease in spinal cord excitability, and relationship between reduced immune function and reactivation of some viruses. The psychological and behavior changes in a prolonged isolation and confinement condition, as well as the fast circadian rhythm inducing sleep disruption has been observed. It has been found exposure to radiation not only causing cataracts and cancers, but also damaging the reproductive organs and nervous system, and inducing genetic damage. The efficacy of countermeasures of medicine, nutrition and vibration have been validated aboard the ISS. The effective countermeasures on different systems were checked further. All of those studies and observations have made a solid foundation for developing novel countermeasures which will be more effective.

At present, immune checkpoint inhibitors (ICIs) are widely used in clinical, and the common adverse reactions include adverse reactions of skin, gastrointestinal tract, endocrine and liver. Adverse reactions to the lungs and heart are relatively rare, but can be fatal. Systemic steroid therapy is the main treatment for immune related adverse events (irAEs). If there is no response to steroid therapy, an immunomodulator may be considered. Understanding the incidence, pathogenesis, common types and treatment strategies of irAEs can provide theoretical basis for the safe application of ICIs in clinical practice.

Endothelial Cells ; metabolism ; pathology ; Humans ; Sepsis ; metabolism ; physiopathology

Background The pathogenesis of myopia is currently unclear. Studies showed that retinoic acid regulates the development of myopia. Whether IRBP, a retinoid transport proteins, participates in the development of myopia or not is unknown. Objective The aim of this study was to investigate the expression of interphotoreceptor retinoid-binding protein (IRBP) in the retina of guinea pig with lens-induced myopia and study the relationship between IRBP expression and experimental myopia. Methods Fifty guinea pigs were randomized into the normal controls(n=10) ,defocus Ⅰ group (n=20) and defocus Ⅱ group (n=20). Guinea pigs in the defocus Ⅰ groups wore -10. 00 D lenses on the right eyes for 14 days and the defocus Ⅱ group for 28 days. The left eyes of both defocus groups did not wear any lens served as self-control. The refraction diopter and axial length were measured before and after wearing lenses. The protein expression of IRBP in the retina was detected by immunohistochemisty and Western blot. RT-PCR was used to observe the level of IRBP mRNA in the retina. Result Compared with the control eyes,the right eyes in the defocus Ⅰ and Ⅱ groups developed to ( -5. 53±1.93) D and (-8.69±2.46) D, and the ocular axial length elongated to (0. 31±0. 15 ) mm and (0.41 ±0. 13 ) mm, showing statistically significant differences between them ( group Ⅰ: t= 12. 57,29.63 ,P＜0.05 ;group Ⅱ :t= 15.82,44.35 ,P＜0.05 ) ,and the degree of myopia was lower and axial length was shorter in group Ⅰ than the eyes of group Ⅱ ( P＜0.05 ). There was no statistically significant differences found between the left eyes of defocus group Ⅰ and defocus group Ⅱ or eyes of the control group in diopter and axial length (P＞0.05). Immunochemistry revealed that the mean gray value of IRBP protein expression was 165.62t4. 93 and 171.00±4. 25 in defocus Ⅰ group and defocus Ⅱ group and was significantly higher than that of the self-control eyes and the normal control group ( 156. 31±4.00,155.26 ±3.49 and 158.61 ±4. 58 ) ( P＜0.05 ). Western blot demonstrated that the expressios of IRBP protein were down-regulated and RT-PCR showed the IRBP mRNA level of IRBP was significantly lower in defocusIgroup and defocusⅡgroup,compared with the self-control eyes and the normal control group (P＜0. 05). Conclusion Expression of IRBP in guinea pig may play a role in lens-induced myopia.

AlM: To evaluate the effectiveness of Spot Vision Screener on vision screening of children without cycloplegia.METHODS:A total of 87 children (174 eyes) aged from 2~9 years old were examined with Spot Vision Screener and optometrist before cycloplegia.RESULTS: Statistical analysis demonstrated that the cylinder diopter and axis, the equivalent spherical diopter in both eyes, and the spherical diaopter in left eye had no significant change ( P>0. 05 ). However, the spherical diaopter in right eye had statistical significance. CONCLUSlON: Spot Vision Screener is a suitable instrument in vision screening of children without cycloplegia.

Acquired Immunodeficiency Syndrome ; prevention & control ; Adult ; Burnout, Professional ; Chi-Square Distribution ; Female ; Humans ; Male ; Medical Staff ; Middle Aged ; Rural Population ; Surveys and Questionnaires ; Young Adult

Chemokine CXCL9/Mig (monokine induced by IFN-?) belongs to the subfamily of chemotactic cytokines known as CXC-chemokines. In vivo CXCL9 is mainly induced by IFN-? in macrophages and primary glial cells. In vitro, CXCL9 can be secreted by cells such as macrophages, microvascular endothelial cells and neutrophils, in response to the synergy of IFN-? and TLR(toll-like receptor) ligands. CXCL9 is a chemoattractant for activated T lymphocytes, tumor-infiltrating T-lymphocytes, but not for neutrophils or monocytes. The receptor specific for CXCL9 is CXCR3, a G protein-coupled protein which has seven transmembrane domain. The structure and the chemical characterization of CXCL9, as well as its effects on autoimmune deseases, allograft rejection, cancer therapy were reviewed.

Objective To investigate the role of antisense RNA of plasminogen activator inhibitor 1 (PAI 1) in regulating the expression of PAI 1 and vascular endothelial growth factor (VEGF) in aorta endothelial cells (EC) cultured in vitro. Methods The second extron of PAI 1 was amplified by polymerase chain reaction(PCR) and the product was inserted into eukaryotic cell expression vector pcDNA3.1(-) to construct PAI 1 antisence RNA recombinant plasmid. The recombinant plasmid was transfected into EC and the PAI 1 expression was detected by immunohistochemistry, Westernblot and ELISA. The effects of PAI 1 variation on VEGF were examined by immunofluorescence method. Results PAI 1 antigen was the lowest (0 017 ng/ml) in cells and the immunofluorescence representing the expression of VEGF in the cytoplasm showed the weakest at the third day after transfection. At the fifth day, PAI 1 antigen increased to 0 093 ng/ml with VEGF expression increased correspondingly. At the seventh day, PAI 1 antigen(0 143 ng/ml) and VEGF increased closed to normal level. Conclusions PAI 1 antisense RNA blocked the translation of PAI 1 proteins effectively and inhibited the expression of VEGF in aorta endothelial cells.

Objective To investigate the action of inorganic arsenic in the induction of DNA strand breaks in primary cultured human skin fibroblasts. Methods Sodium arsenate and sodium arsenite were used as test inorganic arsenics. DNA strand breaks were assessed by single cell gel electrophoresis assay (SCGE). Results Arsenate at 1～10 ?mol/L dose_dependently induced DNA strand breaks in cells. Arsenate at lower concentrations induced mainly degree I DNA strand breaks, while the proportion of cells with degree Ⅱ DNA strand breaks increased to 50% when treated with 10?mol/L arsenate,but no cells with degree ⅢDNA strand breaks were observed.Cells treated with 1?mol/L arsenite showed no significant increase in DNA strand breaks. At the concentration of 10?mol/L, however, arsenite induced DNA strand breaks with different degrees, and the apoptotic type DNA strand breaks were the major type. Conclusion Sodium arsenate mainly induced general type DNA strand breaks and sodium arsenite induced apoptotic type,beside general type of DNA strand breaks in primary cultured human skin fibroblasts. This could be explained by their different reaction modes with DNA, and further studies were needed.

ObjectiveTo investigate the influence of nateglinide treatment of newly diagnosed patients with type 2 diabetes on the state of inflammatory response. MethodsThe clinical data of 74 newly diagnosed patients with type 2 diabetes were retrospectively reviewed,and treated with nateglinide,before and after treatment,the fasting blood glucose (FBG), postprandial blood glucose 0.5h ( 0.5 hPG), 1 h postprandial blood glucose ( 1 hPG) ,2h postprandial blood glucose(2hPG) ,fasting insulin(FINS) ,0.5h postprandial insulin(0. 5hINS) ,postprandial 1h insulin( 1 bINS),2h postprandial insulin(2hINS),interleulin-2(IL-2) and C-reactive protein(CRP) levels were observed. ResultsAfter treatment,the FBG,0. 5hPG, 1hPG,2hPG, FINS,0. 5hINS, 1hINS,2hINS, IL-2 and CRP of patients were ( 8.0 ± 1.5) mmol/L,(12.0±1.8)mmol/L,(10.2 ± 1.3) mmol/L,(10.5 ±1.2) mmol/L,(168.2 ±11.5) pmol/L,(213.5±23.5) pmol/L,(197.0 ±21.5) pmol/L,(189.5 ±12.0) pmol/L,(14.0 ±1.5) μg/L, (13.5 ±1.5) mg/L,compared with( 10. 5 ± 1.0) mmol/L, ( 14. 5 ± 1.5) mmol/L, ( 12. 5 ± 1.4) mmol/L, ( 11.6 ±2.0) mmol/L,(180.7 ±12.0) pmol/L,(229.8 ±26.0) pmol/L,(218.5 ±23.0) pmol/L, (197.0± 14.5) pmol/L,(12.5 ±2.0) μg/L, (22.8 ±2.0) mg/L before treatment decreased significantly(t =11. 9293,9. 1785,10. 3561,4. 1115,6. 4696,4.0009,5. 8744,3. 4279,5. 2307,32.0006, all P ＜0. 05). There was no serious adverse events in treatment process. ConclusionNateglinide treatment of newly diagnosed patients with type 2 diabetes could significantly improve the patient's inflammatory response state,and there was no serious adverse events in treatment process.