Objective To explore the mechanism of neurotoxic effects of neuron nitric oxide synthase(nNOS)and inducible nitric oxide synthase(iNOS),and the therapeutic effects of 7-nitroindazole(7-NI)and aminoguanidine(AG),in traumatic brain injury(TBI)rats.Methods Two hundred and fifty adult male Wistar rats were randomly divided into 5 groups:sham operation group,traumatic group,AG group,7-NI group and AG+7-NI group.Animals in each group were divided into 8 subgroups according to the time after trauma(1,3,6,12 hours and 1,3,7,14 days).Severe diffused brain injury model was made with Marmarou method.Expressions of nNOS and iNOS in hippocampus CA1 region were determined by immunohistochemistry,nerve cells apoptosis in hippocampus CA1 region was observed by TUNEL methods,and the relationship between apoptosis and NOS was observed by double staining.Results In trauma group,the expression of nNOS in hippocampus CA1 region peaked at 6h post-trauma,the expression of iNOS and apoptosis of nerve cells in hippocampus CA1 region both peaked at 3d post-trauma,while the apoptosis was alleviated in AG group,7-NI group and AG+7-NI group.The number of both TUNEL staining and nNOS immunostaining positive cells increased at 6h post-trauma in trauma group,significantly higher than that in 7-NI group.The number of both TUNEL staining and iNOS immunostaining positive cells increased at 3d post-trauma in trauma group,significantly higher than that in AG group.Conclusions The over-expression of nNOS and iNOS has toxic effects to neural tissues of brain,serves as one of the factors inducing nerve cell apoptosis in hippocampus CA1 region.7-NI and AG can inhibit the expression of nNOS and iNOS,reduce the nerve cell apoptosis,and play an important role in neuroprotective effect.

Objective To study the mechanism of interaction between neuronal nitric oxide syn-thase (nNOS) and inducible nitric oxide synthase (iNOS) following traumatic brain injury (TBI) in rats. Methods A total of 250 male Wistar rats were randomly divided into five groups, ie, sham oper-ation group, trauma group, 7-nitroindazole (7-NI) treatment group, aminoguanidine (AG) treatment group and combined AG and 7-NI treatment group. Severe closed TBI was made by using Marmarou meth-od. Protein expressions of nNOS and iNOS in hippocampus CAI were detected by means of immunohisto-chemical staining at 1,3, 6, 12 hours and at days 1,3, 7 and 14 after TBI. Results The expression of nNOS reached a peak at 6 hour after injury in all groups, with no statistical difference between groups (P > 0. 05), when there was no statistical difference between 7-NI treatment group and trauma group (P > 0. 05) but statistical difference in AG treatment group and combined AG and 7-NI treatment group compared with trauma group at 12 hours after TBI (P <0.05). The expression of iNOS reached maximal level at day 3 after TBI, with lower level in 7-NI group, AG treatment group and combined AG and 7-NI treatment group compared with trauma group (P < 0.05). Conclusions After TBI, nNOS interacts with iNOS by means of the feedback of nitric oxide. The enhanced expression of nNOS is initial factor for increase of iNOS expression, which can down regulate the expression of iNOS.

Objective To investigate the effect of low dose of BDE209 on thyroid hormone and thyroid hormone metabolism enzyme-iodothyroninedeiodinases Ⅱ(D2) in off spring mice after pregnancy exposure .Methods Total 64 adult SPF female Kun-ming mice were randomly divided into 4 groups ,which treated with oral gavage of 0 ,50 ,100 ,300 μg · kg -1 · d-1 dose of BDE209 after successful pregnancy ,the exposure continue to 21 days after delivery .10 mice was randomly selected in each offspring group and get the peripheral blood and brain sample ,the serum thyroid hormones level ,oxidative damage and the expression of D2 mRNA in brain were detected .Results Compared with the control group(0μg · kg -1 · d-1 dose of BDE209) ,the TT4 ,TT3 ,FT4 and FT3 levels of offspring mice increased significantly in every exposure group (P< 0 .05);antioxidant enzyme glutathione-S transferees (GST) ,superoxide dismutase (SOD) activity decreased with the BDE209 dose increase (P<0 .05) ,and malondialdehyde (MDA) level increased (P<0 .05);the D2 mRNA relative expression of brain in middle(100μg · kg -1 · d-1 dose of BDE209) and high(300μg · kg -1 · d-1 dose of BDE209) dose group decreased when compared with control group (P< 0 .05) .Conclusion Low level of BDE209 exposure in pregnancy resulted in the increasing of thyroid hormone levels in offspring mice ,which may cause oxidative damage and decrease expression of D2 mRNA in the brain .

OBJECTIVE: To observe the effects of maternal low-level decabromodiphenyl( BDE209) exposure on nervous system and secretion of thyroid hormones in offspring mice. METHODS: Sixty-four specific pathogen free female,aged 4 weeks Kunming mice were used. These mice were randomly divided into control group and low,medium and high exposure groups after successful mating was confirmed. The rats of control group were fed with 0. 01 L/kg body mass of peanut oil.The maternal mice in the experimental groups were given BDE209 at doses of 50,100 and 300 μg/kg body mass by oral gavage once per day. Continuous exposure was given until 21 days after birth of offspring,the exposure model from gestation to lactation was established. At the end of the exposure,10 mice of each group including half female and half male were randomly selected and the body mass and growth development status were observed. Morris water maze was used to examine the learning and memory ability in offspring mice. The serum levels of total triiodothyronine( TT3),free triiodothyronine( FT3), total tetraiodothyronine( TT4) and free tetraiodothyronine( FT4) were measured by chemiluminescence immunoassay. The levels of glutathione transferase( GST), superoxide dismutase( SOD) and malondialdehyde( MDA) level in hippocampus were measured by colorimetry. RESULTS: The escape latency of the medium exposure group was longer than that of the control group( P < 0. 05). The escape latency of high exposure group was longer than that of control group,low exposure group and medium exposure group( P < 0. 05). The time of quadrant movement and number of crossing the platform in offspring rats in high exposure group were less than that of the control group and the low and medium exposure groups( P < 0. 05). The serum levels of TT3,FT3,TT4 and FT4 increased,the activities of GST and SOD in hippocampus tissue decreased,the MDA level increased with the increasing exposure dose( P < 0. 05).CONCLUSION: Maternal low-level BDE209 exposure can result in decrease the learning and memory ability of offspring mice. It also can increase the serum thyroid hormone level and induce oxidative stress injury in hippocampus in a dose dependent manner in offspring mice.

Objective:To explore the current situation of nursing human caring in hospital wards and analyze its influencing factors, so as to facilitate the development of nursing human caring practice.Methods:From July to November 2022, a total of 107 hospitals were surveyed through stratified convenience sampling method, and 4 072 ward nursing managers were recruited to finish the general information questionnaire and the ward nursing human caring status questionnaire. The general information included the region, class and type of the hospital, etc. The ward nursing human caring status questionnaire included 38 items in 5 dimensions of nursing human caring system and process, humanistic quality and training of nursing staff, humanistic environment and facilities, human caring procedures and measures, and human caring quality evaluation and improvement, with a full score of 190 points. Descriptive statistics were used to analyze the general data, independent samples t-test, ANOVA and correlation analysis were used to analyze the factors influencing the current status of nursing human caring in the ward, while multiple linear regression analysis was used to conduct a multivariate analysis. Results:The score of nursing human caring in hospital wards was 156.91±27.78. Whether the hospital had carried out nursing human caring pilot(demonstration) wards, whether the ward had previously been a hospital nursing human caring pilot(demonstration) nursing unit, the type of ward, and whether nursing managers had participated in human caring training were the influencing factors of the implication of nursing humanistic caring in wards( P<0.05). Conclusions:The practice of nursing human caring in hospital wards is at a good level, but needs to be further strengthened. Nursing managers should take systematically strategies to promote the development of nursing human caring practice.