Objective To study the impact of personality and coping style on postpartum depression.Methods 273 cases of postpartum women were estimated by Edinburgh Postnatal Depression Scale ( EPDS),NEO Five-Factor Inventory (NEO-FFI) and Trait Coping Style Questionnaire (TCSQ). With the SPSS11.5,t-test,correlation analysis and regression analysis were carried out for the collected data. Results 23. 1% of postpartum women suffered from depression. There were significant differences in personality traits and coping styles between postpartum depression group and normal group(P＜ 0. 01 ). There was a significant correlation in depression of postpartum and neuroticism, extraversion ( r = - 0. 409 ～ 0. 824 ), agreeableness of personality traits, coping styles.The personality traits was related to coping styles ( r = 0.260, - 0.445, - 0. 234,0. 375 , - 0.431 ). The extraversion, agreeableness of personality traits, negative coping style and positive coping style entered the regression equation of depression and can explain the 32.9% percent variance. Conclusion The extraversion, agreeableness of personality traits, negative coping style and positive coping style are important factors for postpartum depression.

Objective To investigate the effects of thymoquinone (TQ) on the levels of proteins involved in oxidative stress and cytokine in the brain of rats with type 2 diabetes mellitus.Methods Wistar rats (n=48) were randomly divided into 3 groups:normal control group,model group and TQ treatment group (n =16).The normal control group was fed with clean grade ordinary feed.The model group and TQ treatment group rats were fed with high-glucose and high-fat diet.After 6 weeks' feeding,model group and TQ treatment group rats were administered streptozocin (STZ) (35 mg/kg) to establish type 2 diabetic model by intraperitoneal injection.Then,the model group and TQ treatment group rats were fed with high-glucose and high-fat diet for another 6 weeks.After that,TQ treatment group rats were administered TQ (5 mg/kg) by intraperitoneal injection every other day.The model group rats were injected with an equal dose of ethanol.Six weeks later,all the rats were sacrificed to obtain the hippocampal tissue for the protein extract.The protein levels of nuclear factor erythroid 2-related factor 2 (Nrf2),heme oxygenase-1 (HO-1) and cyclo-oxygenase 2 (COX-2) in the hippocampal tissue were measured by Western blot.Superoxide dismutase (SOD) activity was determined by SOD kit.Blood-glucose meter was used to assess the blood glucose before the rats were sacrificed and after the model was successfully established.All the measurement data was described by the x ± s,measurement data were compared among groups using One Way ANOVA.Results The results by Western blots showed that the levels of the Nrf2 and HO-1 protein were significantly decreased in the model group compared with the normal control group,the levels of the Nrf2 and HO-1 proteins were increased in the TQ treatment group in comparison with the model group (P＜ 0.05).Meanwhile,compared with the normal control group,the SOD activity of the hippocampus in model group was significantly lower (P＜ 0.05);by contrast with the model group,the SOD activity in the TQ treatment group was considerably increased (P＜0.05).By contrast,the COX-2 level in the model group was substantially higher than that in the normal control (P＜0.05),and the COX-2 level in the TQ treatment group was lower than that in the model group (P＜0.05).Conclusions TQ might inhibit inflammation and improve oxidative stress of the brain tissue in the rats with type 2 diabetes mellitus.

Objective To investigate the changes in cortisol (COR) secretion in the acute phase of traumatic brain injury (TBI) .Method Seventy-five patients admitted to the hospital at 2-24 h after TBI were divided into 3 groups based on the Glasgow Coma Scale score: mild TBI group (group TBI1, n = 30), moderate TBI group (group TBI2, n = 12) and severe TBI group (TBI3, n = 33). Thirteen patients with cervical spondylosis or osteoma of the skull (admitted to the hospital at the same period) were regarded as control group (group C). Venous blood samples were taken on the first day after admission to measure the serum concentrations of total COR, adrenocorticotropin (ACTH) and corticosteroid-binding globulin (CBG). Free COR concentrations and free COR index were calculated. High blood COR was recorded. Result Compared with group C, the serum concentrations of total COR and ACTH, free COR levels and free COR index were significantly increased in TBI1, TBI2 and TBI3groups (P ＜ 0.05). The parameters mentioned above were significantly higher in TBI2 and TBI3 groups than in TBI1 group ( P ＜0.05). There was no significant difference in serum CBG concentrations among the four groups.The incidence of high blood COR was significantly higher in TBI1, TBI2 and TBI3 groups than in C group, and in TBI3 group thanin TBI1 and TBI2 groups (P ＜0.05). Conclusion COR secretion is increased in the acute phase of TBI and the level of COR secretion is related to the severity of brain damage.

China ; Hepatitis B ; epidemiology ; Humans ; Seroepidemiologic Studies

Objective: To investigate the effects of hydrogen on the lung damage of mice at early stage of severe burn. Methods: One hundred and sixty ICR mice were divided into sham injury, hydrogen, pure burn, and burn+ hydrogen groups according to the random number table, with 40 mice in each group. Mice in pure burn group and burn+ hydrogen group were inflicted with 40% total body surface area full-thickness scald (hereafter referred to as burn) on the back, while mice in sham injury group and hydrogen group were sham injured. Mice in hydrogen group and burn+ hydrogen group inhaled 2% hydrogen for 1 h at post injury hour (PIH) 1 and 6, respectively, while mice in sham injury group and pure burn group inhaled air for 1 h. At PIH 24, lung tissue of six mice in each group was harvested, and then pathological changes of lung tissue were observed by HE staining and the lung tissue injury pathological score was calculated. Inferior vena cava blood and lung tissue of other eight mice in each group were obtained, and then content of high mobility group box 1 (HMGB1) and interleukin-6 (IL-6) in serum and lung tissue was determined by enzyme-linked immunosorbent assay. Activity of superoxide dismutase (SOD) in serum and lung tissue was detected by spectrophotometry. After arterial blood of other six mice in each group was collected for detection of arterial partial pressure of oxygen (PaO₂), the wet and dry weight of lung tissue were weighted to calculate lung wet to dry weight ratio. The survival rates of the other twenty mice in each group during post injury days 7 were calculated. Data were processed with one-way analysis of variance, LSD test and log-rank test. Results: (1) At PIH 24, lung tissue of mice in sham injury group and hydrogen group showed no abnormality. Mice in pure burn group were with pulmonary interstitial edema, serious rupture of alveolar capillary wall, and infiltration of a large number of inflammatory cells. Mice in burn+ hydrogen group were with mild pulmonary interstitial edema, alveolar capillary congestion accompanied by slight rupture and bleeding, and the number of infiltration of inflammatory cells was smaller than that in pure burn group. The lung tissue injury pathological scores of mice in sham injury group, hydrogen group, pure burn group, and burn+ hydrogen group were (0.7±0.5), (0.8±0.5), (6.1±1.0), and (2.8±0.8) points, respectively. The lung tissue injury pathological score of mice in pure burn group was significantly higher than that in sham injury group (P<0.001). The lung tissue injury pathological score of mice in burn+ hydrogen group was significantly lower than that in pure burn group (P<0.001). (2) At PIH 24, the content of HMGB1 and IL-6 in serum and lung tissue of mice in hydrogen group was close to that in sham injury group (with P values above 0.05). The content of HMGB1 and IL-6 in serum and lung tissue of mice in pure burn group was significantly higher than that in sham injury group (with P values below 0.001). The content of HMGB1 and IL-6 in serum and lung tissue of mice in burn+ hydrogen group was significantly lower than that in pure burn group (with P values below 0.001). (3) At PIH 24, the activity of SOD in serum and lung tissue of mice in hydrogen group was close to that in sham injury group (with P values above 0.05). The activity of SOD in serum and lung tissue of mice in pure burn group was significantly lower than that in sham injury group (with P values below 0.001). The activity of SOD in serum and lung tissue of mice in burn+ hydrogen group was significantly higher than that in pure burn group (with P values below 0.001). (4) At PIH 24, there was no statistically significant difference in PaO₂ among the mice in four groups (F=0.04, P>0.05). (5) At PIH 24, the ratios of lung wet to dry weight of mice in sham injury, hydrogen, pure burn, and burn+ hydrogen groups were 3.52±0.22, 3.61±0.24, 7.24±0.32, and 5.21±0.41, respectively. The ratio of lung wet to dry weight of mice in pure burn group was significantly higher than that in sham injury group (P<0.001). The ratio of lung wet to dry weight of mice in burn+ hydrogen group was significantly lower than that in pure burn group (P<0.001). (6) The survival rates of mice in sham injury group and hydrogen group during post injury days 7 were 100%. Compared with those in sham injury group, survival rates of mice in pure burn group from post injury days 3 to 7 were significantly decreased (with P values below 0.05). Compared with those in pure burn group, survival rates of mice in burn+ hydrogen group from post injury days 5 to 7 were significantly increased (with P values below 0.05). Conclusions Hydrogen can significantly alleviate the infiltration of inflammatory cells and improve the pathological lesions of lung tissue of mice with severe burn. It has the effects of reducing inflammatory reaction and inhibiting oxidative stress, further showing the protective effect on the lung of burn mice.

Objective To evaluate the effect of hydrogen on autophagy during inflammatory responses following lung injury in burned mice.Methods Ninety-six clean-grade healthy male ICR mice,aged 6 weeks,weighing 20-25 g,were divided into 4 groups (n=24 each) using a random number table:sham operation group (SH group),H2 group (H2 group),burn group (B group) and burn plus H2 group (B+H2 group).Forty percent of the total body surface was shaved with 80 g/L sodium sulfide and then exposed to a 92 ℃ scald device for 18 s in B and B+H2 groups.Forty percent of the total body surface was shaved with 80 g/L sodium sulfide and then exposed to a scald device of skin temperature for 18 s in SH and H2 groups.Mice inhaled 2％ H2 for 1 h starting from 1 and 6 h after burn in H2 and B+H2 groups.The animals were sacrificed at 24 h after burn and lungs were removed for determination of wet/dry weight ratio (W/D rario),expression of autophagy-related microtubule-associated protein 1 light chain 3 (LC3) (by Western blot),activity of myeloperoxidase (MPO),and contents of interleukin-6 (IL-6) and high mobility group box 1 (HMGBI) (by enzyme-linked immunosorbent assay).The ratio of LC3-Ⅱ to LC3-Ⅰ expression (LC3-Ⅱ/LC3-Ⅰ) was calculated.The bronchoalveolar lavage fluid (BALF) was collected at 24 h after burn to detect the concentrations of IL-6 and HMGB1 and to count neutrophil.Results Compared with group SH,the W/D ratio,levels of LC3-Ⅱ/LC3-Ⅰ,MPO,IL-6 and HMGB1,concentrations of IL-6 and HMGB1 in BALF and neutrophil count were significantly increased at 24 h after scald in B and B+H2 groups (P＜0.05).Compared with group B,the W/D ratio,levels of LC3-Ⅱ/LC3-Ⅰ,MPO,IL-6 and HMGB1,concentrations of IL-6 and HMGBl in BALF and neutrophil count were significantly decreased at 24 h after scald in group B+H2 (P＜0.05).Conclusion Hydrogen can alleviate the lung injury in burned mice,and the mechanism is related to enhancing autophagy.

Objective To evaluate the effect of hydrogen on blood brain barrier of mice with sepsisassociated encephalopathy (SAE).Methods A total of 100 adult male ICR mice,aged 6-8 weeks,weighing 20-25 g,were divided into 4 groups (n =25 each) using a random number table method:sham operation group (group Sham),sham operation plus hydrogen group (group Sham+H),group SAE and SAE plus hydrogen group (group SAE+ H).Sepsis was induced by cecal ligation and puncture (CLP).Sham+H and SAE+H groups inhaled 2％ hydrogen for 1 h starting from 1 and 6 h after CLP,respectively.At 24 h after CLP,Evans blue (EB) was injected via the caudal vein,and then the mice were sacrificed and brain tissues were removed for measuring the EB and water contents,for examining the pathological changes of hippocampi (with a light microscope) and for detecting the expression of occludin and VE-cadherin (by Western blot).Morris water maze test was performed at days 10-16 after CLP.Results Compared with group Sham,the contents of EB and water in brain tissues were significantly increased,the expression of occludin and VE-cadherin was down-regulated,the escape latency was prolonged,and the number of crossing the original platform was reduced in SAE and SAE+H groups (P＜0.05).Compared with group SAE,the contents of EB and water in brain tissues were significantly decreased,the expression of occludin and VE-cadherin was up-regulated,the escape latency was shortened,the number of crossing the original platform was increased (P＜0.05),and the pathological changes of hippocampi were significantly attenuated in group SAE+H.Conclusion The mechanism by which hydrogen mitigates SAE may be related to reducing the damage to blood brain barrier of mice.

Objective To investigate the changes in FUNDC1/microtubule-associated protein 1 light chain 3 Ⅱ (LC3 Ⅱ) signaling pathway during sepsis-induced liver injury in mice.Methods Tbirtytwo clean-grade healthy male C57BL/6 mice,aged 6 weeks,weighing 20-25 g,were divided into sham operation group (n =8) and sepsis group (n =24) using a random number table method.Sepsis was induced by cecal ligation and puncture.Blood samples were obtained at 24 h after operation in sham operation group and at 6,12 and 24 h after establishing the model in sepsis group for determination of concentrations of alanine aminotransferase and aspartate aminotransferase in serum.Mice were then sacrificed,and the right lobe of livers was removed for examination of the pathological changes and for determination of the expression of FUNDC1 and LC3 Ⅱ by Western blot.The mitochondria in the right lobe of livers were isolated to measure the respiratory function,and respiratory control rate was calculated.Results Compared with sham operation group,the concentrations of alanine aminotransferase and aspartate aminotransferase in serum and pathological scores were significantly increased,the respiratory control rate of mitochondria was decreased,the expression of FUNDC1 was down-regulated,and the expression of LC3 Ⅱ was up-regulated at each time point after establishing the model in sepsis group (P＜0.05).Conclusion The mechanism by which sepsis induces liver injury may be related to inhibiting activation of FUNDC1/LC3 Ⅱ signaling pathway in mice.

Objective To evaluate the effect of dexmedetomidine on expression of hypoxia-inducible factor-1α (HIF-1α) during endotoxin-caused apoptosis in macrophages of mice.Methods Mouse macrophage cell line RAW264.7 cultured in vitro were seeded in 6-well or 96-well plates and divided into 4 groups (n=16 each) when cell confluence reached 60％-70％ using a random number table method:control group (group Con),dexmedetomidine group (group Dex),lipopolysaccharide (LPS) group,and LPS plus dexmedetomidine group (group LPS+Dex).Phosphate buffer solution was added in group Con.Dexmedetomidine 1 μmol/L was added in group Dex.LPS 1 μg/ml was added in LPS and LPS+Dex groups.Dexmedetomidine 1 μmol/L was added immediately after adding LPS in group LPS+Dex.Cells were then cultured for 24 h in each group.Cell apoptosis was measured using TUNEL,mitochondrial membrane potential using JC-1,reactive oxygen species (ROS) content by ROS kit,and ATP content by ATP kit.The apoptosis rate was calculated.The expression of HIF-1α,cytochrome C (Cyt-c),caspase-9 and cleaved caspase-3 was detected by Western blot.Results Compared with group Con,the apoptosis rate and ROS content were significantly increased,ATP content and mitochondrial membrane potential were decreased,the expression of HIF-1α,Cyt-c,caspase-9 and cleaved caspase-3 was up-regulated in group LPS (P＜ 0.05),and no significant change was found in the parameters mentioned above in group Dex (P＞0.05).Compared with group LPS,the apoptosis rate and ROS content were significantly decreased,ATP content and mitochondrial membrane potential were increased,the expression of HIF-1α was up-regulated,and the expression of Cyt-c,caspase-9 and cleaved caspase-3 was down-regulated in group LPS + Dex (P＜0.05).Conclusion Dexmedetomidine can reduce endotoxin-caused oxidative stress injury to macrophages,improve mitochondrial function and inhibit mitochondrial apoptosis,and the mechanism may be related to upregulating the expression of HIF-1α in mice.

Objective To evaluate the role of autophagy in dexmedetomidine-induced reduction of lipopolysaccharide ( LPS)-caused inflammatory responses in macrophages of mice. Methods Mouse mac-rophage cell line RAW264. 7 cultured in vitro were seeded in 6-well or 96-well plates and divided into 4 groups ( n=20 each ) when cell confluence reached 60％ using a random number table method: control group (group Con), LPS group, LPS plus dexmedetomidine group (group LPS+DEX), and LPS plus dexmedetomidine plus autophagy inhibitor 3-MA group (group LPS+DEX+3-MA). PBS was added and cells were cultured for 12 h in group Con. LPS at the final concentration of 1000 ng∕ml was added and cells were incubated for 12 h in group LPS. LPS at the final concentration of 1000 ng∕ml was added, and then dexmedetomidine at the final concentration of 1 μmol∕L was immediately added, and cells were incubated for 12 h in group LPS+Dex. In group LPS+Dex+3-MA, 3-MA at the final concentration of 2 mmol∕L was added and cells were incubated for 1 h, LPS at the final concentration of 1000 ng∕ml was added, and then dexmedetomidine at the final concentration of 1 μmol∕L was immediately added, and cells were incubated for 12 h. Cell viability was detected by CCK-8 assay, and the concentrations of nitrous oxide ( NO) , tumor necrosis factor-alpha ( TNF-α) and interleukin-1beta ( IL-1β) in the supernatant were determined by en-zyme-linked immunosorbent assay, and the expression of microtubule-associated protein 1 light chain 3 Ⅰ( LC3 Ⅰ) , LC3Ⅱ, P62 and Bcelin-1 was detected by Western blot. LC3Ⅱ∕LC3Ⅰ ratio was calculated. Results Compared with group Con, the cell viability was significantly decreased, the concentrations of TNF-α, IL-1β and NO and LC3Ⅱ∕LC3Ⅰratio were increased, and the expression of P62 and Beclin1 was up-regulated in group LPS (P<0. 05). Compared with group LPS, the cell viability was significantly in-creased, the concentrations of TNF-α, IL-1βand NO were decreased, LC3Ⅱ∕LC3Ⅰratio was increased, the expression of P62 was down-regulated, and the expression of Beclin1 was up-regulated in group LPS+DEX ( P<0. 05) . Compared with group LPS+Dex, the cell viability was significantly decreased, the con-centrations of TNF-α, IL-1β and NO were increased, LC3Ⅱ∕LC3Ⅰ ratio was decreased, the expression of P62 was up-regulated, and the expression of Beclin1 was down-regulated in group LPS+Dex+3-MA ( P<0. 05) . Conclusion Enhanced autophagy is involved in dexmedetomidine-induced reduction of LPS-caused inflammatory responses in macrophages of mice.