Objective To explore the resilience characteristics of the traumatic fracture patients and its influence on acute stress disorder(ASD),and provide the basis for improving the population's ability to cope with stressful events and resilience level for clinic.Methods 440 cases of traumatic fracture patients hospitalized in Tangshan Second Hospital were selected in this study.All subjects were assessed with SAS-RQ,CD-RISC,AIS-ISS,VAS and the general condition of investigations.Results The resilience level of traumatic fracture patients was at the middle,the resilience total score was(51.13±14.81) points,and lower than that of the national norm(t=-20.217,P＜0.01).Sex,age,personality and injury severity had the impact on resilience (P＜0.05).Resilience dimensions and total scores had negative correlation with SASRQ dimen sions and its total score (r=-0.587--0.739,P＜0.01).High-leveled resilience patients have lower ASD scores and lighter symptoms(P＜ 0.05).The multivariate analysis appeaed that resilience and the degree of pain were the main factors affecting ASD (P＜ 0.05).Conclusion The resilience level of the traumatic frac ture patients should be further improved and the construction of resilience should be strengthened in order to prevent the occurrence of ASD.

Objective To explore and analyze the executive function of patients with traumatic brain injury in recovery phase and reveal its influential factors.Methods Behavioral Assessment of Dysexecutive Syndrome (BADS) was conducted in 104 patients with brain injury at 5 ～ 6 months after discharging and matched healthy comparison subjects in this study.Basic information in patients with the clinical data were collected by self-designed questionnaire to analyze the relevant factors.Results BADS findings showed that the individual scores and total standard scores of brain injury patients( 12.05 ± 2.54 ) were significantly lower than those of health population ( 19.02 ± 3.77 ) (P ＜ 0.05 ).Action program test, temporal judgment test, modified six elements test and total sub-standard scores ( 14.83 ±3.86)in junior high school education level and below group were significantly lower than that in high school and higher education group ( 17.67 ± 4.10 ).The individual scores and total standard scores ( 10.13 ± 3.86 )in heavier group were significantly lower than that in the lighter group ( 15.68 ± 4.10 ).The group without complication' action program test, key search test, zoo map test, modified six elements test were significantly lower than the group with complication.The BADS scores were related to education, illness condition,and complication (hypertension, hyperglykemia, hyperlipemia) (P＜0.05).Conclusion There is executive dysfunction in traumatic brain injury patients.The executive dysfunction is mainly correlated with education, illnesscondition and complication.Medical staff should provide pertinent intervention and treatment according to the above aspects, in order to obtain better effects of rehabilitation therapy .

Objective To study the utility of sleep intervention combined with memory training for alleviating dysmnesia in the elderly and provide a basis for improving memory function. Methods A total of 647 community-dwelling elderly people were evaluated using the Pittsburgh Sleep Quality Index (PSQI) and the Rivermead behavioral memory test ( RBMT). One hundred and fifty elderly persons with sleep disorders and dysmnesia were divided into three groups; the control group, the memory intervention group, and the sleep plus memory training group. Sleep quality and dysmnesia were evaluated again after 3 months of intervention. Results Among the 647 elderly people, the incidence of sleep disorders was 38. 8% , and of dysmnesia was 78. 4%. Dysmnesia was significantly more prevalent among subjects who also had sleep disorders. After three months of intervention, instant recall scores had declined in the control group while scores on 7 kinds of memory function had improved significantly in the memory intervention group. Scores on 10 measures of memory and sleep quality improved in the sleep plus memory intervention group. Compared to the control group, scores on 9 kinds of memory improved significantly in the memory intervention group and scores on 11 kinds of memory improved in the sleep plus memory intervention group. Compared to the memory intervention group, scores on 5 kinds of memory had improved significantly in the sleep plus memory intervention group. Conclusions The occurrence of dysmnesia in elderly people is influenced by sleep quality. Memory training can improve their memory function, but sleep intervention combined with memory training is even more effective.

Objective To investigate the effects of Edaravone (Ed) on p38mitogen-activated protein kinases/Caspase-3 (p38MAPK/Caspase-3) pathway following the diffuse injury of brain (DIB) in rats, as well as the protective effects of Edaravone on traumatic injury of brain (TIB). Method The TIB models were established by using Marmarou's method in adult male Spraque-Dawlley rats. A total of 250 rats were divided (random number)9nto control group, model group, low-dose Edaravone treatment group and high-dose Edaravone treatment group.The rats were sacrificed separately 1, 6, 24, 48 and 72 hours after DIB and the brain tissues of rats were taken.The morphological changes of neuron in hippocampus region were observed by using Nissl staining. The levels of phosphorylated p38MAPK and Caspase-3 were detected by using immunohistochemistry and Western blot. The learning and memory functions were determined with Morris water maze test from the 3rd to 7th day after injury.Results Compared with control group, some neurons displayed histopathological changes of necrosis and apoptosis in rats of model group. The levels of phosphorylated p38MAPK significantly increased in 1, 6, 24, and 48 hours after injury in rats of model group ( P ＜ 0.05), but there was no statistic significance in increase 72 hours later ( P＞ 0.05). The levels of Caspase-3 significantly increased in 6, 24, 48 and 72 hours after injury in rats of model group ( P ＜ 0.05), but there was no significant difference in increase in one hour after injury (0.59±0.29 vs.0.40±0.17, P ＞0.05).In the Morris water maze test from the 3rd to 6th day, the latency to find the platform significantly prolonged in rats of model group ( P ＜ 0.05), and the numbers of passing the platform by rats decreased on the 7th day (2.28 ± 1.18 vs. 8.20 ± 1.52, P ＜ 0.05). Compared with model group, the levels of phosphorylated p38MAPK in 6, 24 and 48 hours after injury in low-dose Edaravone group were lower (P ＜0.05), but there was no statistical difference in one hour after injury ( P ＞ 0.05). The levels of Caspase-3 in 6,24, 48 and 72 hours after injury in rats of low-dose Edaravone group were lower than those of model group ( P ＜0.05). The latency to find the platform significantly shortened ( P ＜ 0.05) and the numbers of passing the platform by rats increased (4.17 ± 1.15 vs. 2.28 ± 1.18, P ＜ 0.05) in low-dose Edaravone group. The above variables changed more prominently in high-dose Edaravone group. Conclusions Edaravone attenuates p38MAPK pathway activation, lowers the level of Caspase-3 following DIB and protects the rats against the traumatic injury of brain.

Objective To explore the effects of hypoxic post-conditioning on cognitive function and the expression of silent information regulator 1 (SIRT1) in hippocampal CA1 of rats with cerebral ischemia. Methods Sixty Sprague-Dawley rats were randomly divided into sham operation group, model group and treatment group with 20 cases in each group. Each group was divided into one day, two days, three days, seven days subgroups according to the time of ischemia reperfusion. Global cerebral ischemia reperfusion was induced with modified Pulsinelli′4-vessel occlusion. The treatment group received 8%oxygen for two hours after ischemia. The cognitive function was assessed with Morris water maze test. Morphological changes of the hippocampal CA1 region were observed by HE staining. The expression of SIRT1 in the hippocampal CA1 region was detected with immunohistochemical assay and Western blotting. Results Compared with the model group, the escape latency significantly shortened (P<0.05), the number of times crossing the platform increased (P<0.05), the speed and the percentage of time spent in the platform quadrant increased (P<0.05), and the total distance decreased (P<0.05);the expression of SIRT1 in hippocampal CA1 increased (P<0.05) and the number of normal neurons increased (P<0.05) in the treatment group. Conclusion Hypoxic post-conditioning can improve the cognitive function of rats with global cerebral ischemia, which may relate with up-regulating SIRT1 in hippocampus.

Objective To explore the mechanism of ischemic postconditioning in relieving cerebral ischemia reperfusion (IR) by regulating autophagy through P38MAPK pathway.Methods Cerebral ischemia reperfusion model was established by using modified Pulsinelli four-vessel occlusion (4-VO).Totally 128 male SD rats were divided into 4 groups randomly:control group (sham),cerebral ischemia reperfusion model group (CIR),cerebral ischemic postconditioning group (CIP),and cerebral ischemic postconditioning + P38MAPK inhibitor group (SB203580 group).Each group was subdivided into four time points:6 h,24 h,48 h,and 72 h.The morphological changes of the hippocampus CA1 area neurons at each time point and the number of surviving nerve cells were detected with HE staining.The expression of the hippocampus CA1 area phosphorylated P38MAPK and the autophagy-related genes of Beclin-1 and LC3-Ⅱ were detected with immunohistochemistry.The protein content of the hippocampus phosphorylated P38MAPK and autophagy-related genes of Beclin-1 and LC3-Ⅱ were detected with Western blotting.Results Compared with those in sham group,the damage of rats' hippocampal neuron structure and the survival rate of neurons at each time point decreased in CIR group,the expressions of p-P38MAPK,LC3-Ⅱ and Beclin-1 increased.Compared with those in CIR group,in CIP and SB203580 groups the structure of rats hippocampal neurons was improved,the survival rate of neurons increased,the expression of p-P38MAPK decreased and the expressions of LC3-Ⅱ and Beclin-1 increased at each time point.Compared with CIP group,SB203580 grouphad improved structure of rats' hippocampal neurons,increased survival rate of neurons,decreased expression of p-P38MAPK,and increased expressions of LC3-Ⅱ and Beclin-1 at each time point.Conclusion Cerebral ischemic postconditioning through inhibiting P38MAPK pathway can regulate autophagy and exert its nerve-protective effect.

Objective To study the effects of mindfulness behavior training on coping style and illness uncertainty in patients of shoulder hand syndrome (SHS) after ischemic stroke.Methods 65 cases with SHS were randomly divided into two groups by digit method: the control group (n=32) and experimental group (n=33).Patients in control group only received routine rehabilitation, while patients in experimental group also received mindfulness behavior training.The daily life, medical coping style, illness uncertainty and mindfulness were evaluated respectively by Barthel Index (BI) , Medical Coping Style Questionnaire (MCMQ) , Illness Uncertainty Scale (IUS) and Mindful Attention Awareness Scale (MAAS).Results Before training, there were no significant difference in BI,MCMQ,IUS and MAAS (P＞0.05).After treatment, scores in BI improved significantly in the experimental group than that in the control group(72.4± 11.6 vs 62.9±10.1) ,scores in IUS improved significantly in the experimental group than that in the control group(69.3±9.3 vs 86.9±7.2) and scores in MCMQ and MAAS improved significantly in the experimental group than that in the control group(P＜0.05).26 cases whose Barthel index was more than 60 points in experimental group after treatment were found while 17 cases whose Barthel index was more than 60 points in control group were done after treatment (x2 =6.415, P＜0.05).Conclusion Mindfulness behavior training can regulate the patient coping style and weaken illness uncertainty,and improve functions rehabilitation.

Objective To understand the anxiety among gerontal patients with osteoporosis,and to analyze the correlated factors of the anxiety.Methods The social information of the gerontal patients with osteoporosis were investigated,as well as by SAS for the anxiety,and by NRS,PSQI,AHSMSRS for their pain level,sleep quality and healthy management.Results The incidence rate of anxiety was 20.3%,and the average score was (41 .1 4 ± 9.71 )points.Some factors had influence upon the rate,which included sex,month income,sleep quality,self -care ability,pain level,self -management and exercise.Multivariate logistic regression analysis showed that exercise and pain level were the major risk factors.The differences were statistically significant(t =3.033,2.727,P =0.003, 0.007).Conclusion It's higher that the incidence rate of anxiety among gerontal patients with osteoporosis maybe influenced by species of factors,and the quality of life among them needs to be improved by intervention clinically implicated in those factors.

Objective To investigate the changes in the expression of phosphatidylinositol 3?kinase(PI3?K),mammalian target of rapamycin (mTOR)and Beclin?1 in the hippocampus of normal rats and intermittent hypoxia rats with cerebral ischemia/reperfusion ,so as to explore the role of PI3K/mTOR/autophagy pathway in global cerebral ischemia/reperfusion injury aggravated by intermittent hypoxia. Methods A total of 80 healthy male Wistar rats were randomly divided into sham operation group(SO group,n=20),merely ischemia/reperfusion group(I/R group,n=20),intermittent hypoxia for 7?day ischemia/reperfusion group(IH7+I/R group,n=20),and intermittent hypoxia for 21?day ischemia/reperfusion group(IH21+I/R group,n=20). IH7+I/R group and IH21+I/R group were respectively given intermittent hypoxia for 7 days and 21 days before ischemia/reperfusion. The cerebral ischemia/reperfusion model was established by modified Pulsinelli four?vessel occlusion method. The morpholog?ical changes of nerve cells in hippocampal CA1 region were observed by HE staining and electron microscope. The protein expressions of PI3?K, mTOR and Beclin?1 of nerve cells in hippocampal CA1 region were detected by immunohistochemical staining and RT?PCR. The learning memory capacity of rats were assessed by the Morris water maze test. Results Compared with SO group,I/R group increased the never cells morphology damages,reduced the number of survival neurons,and declined the ability of learning and memory(P<0.05). Immunohistochemistry showed that the number of PI3?K immunoreactive cell,mTOR immunoreactive cell and Beclin?1 immunoreactive cell increased in I/R group compared with S0 group(P<0.05). RT?PCR showed that the expressions of PI3?K,mTOR and Beclin?1 increased in I/R group compared with S0 group(P<0.05). Compared with I/R group,intermittent hypoxia groups increased the never cells morphology damages,decreased the number of survival neu?rons,and declined the ability of learning and memory(P<0.05). Immunohistochemistry showed that the number of PI3?K immunoreactive cell, mTOR immunoreactive cell and Beclin?1 immunoreactive cell increased in IH7+I/R and IH21+I/R groups compared with I/R group(P<0.05). RT?PCR showed that the expressions of PI3?K,mTOR and Beclin?1 increased in IH7+I/R and IH21+I/R groups compared with I/R group(P<0.05),and the changes were more significant in IH21+I/R group(P<0.05). Conclusion Intermittent hypoxia can aggravate neurological injury after ischemia,which is related to PI3K/mTOR/autophagy pathway activation.

Objective To study the effects of 3-n-butylphthalide (NBP) on motor function and learning and memory ability in rats with diffuse brain injury (DBI). Methods 128 male Sprague-Dawley rats were randomly divided into sham operation group, traumatic group,low-dose NBP treatment group and high-dose NBP treatment group with 32 rats in each group. Every group was divided into 24 h, 48 h and 72 h subgroups. DBI rat model was established according to the description of Marmarou's diffused brain injury. The histopathologic changes of cerebral tissue (0.2 cm bilateralis coronal line) were observed by light and electron microscope at 24 h, 48 h and 72 h after injury. Morris water maze and rolling test were performed daily at 24, 48 and 72 h (time points). Results Compared with the model group, the damage of brain tissue decreased, and the survival nerve cells increased (P<0.01). The behavioral tests showed that the latency to find the platform shortened (P<0.01) and the frequency of crossing the platform increased in the 72 h subgroup (P<0.01). The general movement ability enhanced in NBP groups (P<0.05). All the indexes were more significant in high-dose NBP treatment group. Conclusion NBP can improve neurological function and learning and memory function after brain injury and the molecular mechanisms is related to the decrease of the nerve cells lose and traumatic cerebral ultrastructure damage.