Post-traumatic stress disorder(PTSD),as a mental disorder disease,can seriously damage the physical and mental health and social functioning of patients.Physical therapy is increasingly being used in research on the treatment of PTSD due to its ability to directly target specific brain regions and improve the core symptoms of PTSD.This review categorizes on physical therapy for PTSD into two categories:non-invasive physical therapy and invasive physical therapy.Non-invasive physical therapy methods included electroconvulsive therapy,transcranial direct current stimulation,transcranial magnetic stimulation,and the Flexyx neurotherapy system.Non-invasive physical therapy had the advantages of safety,convenience,and simple operation.However,their stimulation accuracy was limited.Invasive physical therapy methods included deep brain stimulation and stellate ganglion block.Invasive physical therapy had the advantages of precise stimulation,fewer adverse reactions.However,there were surgical risks,high operational difficulty,and high treatment costs.In addition,potential physical therapy methods included transcranial alternating current stimulation,magnetic seizure therapy,and vagus nerve stimulation,which were currently in the theoretical research stage.This study discussed the mechanism of action,therapeutic parameters,clinical efficacy,adverse effects and the latest forms of technology of the above physical therapy methods,so as to provide reference for the treatment of PTSD.

Objective:To observation the application of multimedia combined with health education manuals in asthma children.Methods:A total of 192 asthma children who were admitted to Haikou Hospital of the Maternal and Child Health between January and December 2019 were enrolled. They were divided into observation group and control group by random number table method, 96 cases in each group. The control group was given routine health education based on oral education, while observation group was additionally given multimedia intervention. Both groups were continuously intervened for 4 weeks. After intervention, treatment compliance was evaluated. The health behaviors and quality of life before and after intervention in both groups were recorded. Both groups were followed up after 6 months of intervention. The number of cases with acute asthma attacks, and number of re-admission and hospitalization cases due to asthma in both groups were statistically analyzed.Results:The compliance of observation group was significantly better than that of control group in terms of quantitative medication on time, inhaler usage and recording asthma diary ( Z values were 9.809, 10.082, 10.287, P<0.05). After intervention, health behaviors such as keeping away from allergens, medication following doctor's advice, paying attention to keep warm, diet control, exercise training and inhaler usage in observation group were significantly higher than those in control group ( χ 2 values were 5.169-19.006, P<0.05). After intervention, scores of symptoms, activities and emotion, and total score of Pediatric Asthma Quality of Life Questionnaire (PAQLQ) in observation group were (48.52±7.46), (25.16±4.83) (110.32±20.64) and (36.57±5.64) points, significantly higher than (42.17±7.12), (18.65±3.72), (29.86±5.48) and (85.06±16.23) points in control group ( t values were 6.146-10.463, P<0.05). During follow-up, the incidence rates of acute asthma attack, re-admission and re-hospitalization due to asthma in observation group were 21.89% (20/91), 15.38% (14/91), 9.89% (9/91), which were lower than 39.33% (35/89), 23.58% (29/89), 25.84% (23/89) in control group ( χ 2 values were 6.381, 7.321, 7.833, P<0.05). Conclusion:The multimedia combined health education manuals can effectively improve treatment compliance, health behaviors and quality of life in asthma children, and reduce incidence of asthma related events.

Objective:To study the protective role of ischemic precondition in brain cells and its mechanism in rats after cerebral infarction.Methods:According to random number table method, 120 SD rats were divided into ischemic precondition group ( n=50), cerebral infarction group ( n=50), sham-operated group ( n=10), and normal control group ( n=10); cerebral infarction models of middle cerebral artery occlusion (MCAO) in the former two groups were induced by modified Longa thread method; precondition (blood flow in the middle cerebral artery was blocked for 15 min before model making) was given to the ischemic precondition group; rats in the sham-operated group were performed sham ischemic precondition and sham occlusion of middle cerebral artery blood; rats in the normal control group did not receive any treatment. At 24 h after model making, rats in the normal control group (n=10) and sham-operated group (n=10) were sacrificed, and 2, 6, 12, 24, and 48 h after model making, rats in the ischemic precondition group (n=10) and the cerebral infarction group (n=10) were sacrificed; the Caspase-3 expression in the ischemic penumbra was detected by immunohistochemistry, and the apoptosis rate in the ischemic penumbra was determined by TUNEL. Real-time PCR and Western blotting were used to detect the mRNA and protein expressions of arginyl-tRNA synthetase (ArgRS). Results:As compared with those in the normal control group and sham-operated group, the apoptosis rate, positive expression rate of Caspase-3, and ArgRs mRNA and protein expressions in the ischemic penomere zone of the rats in the cerebral infarction group were significantly increased at different time points after modeling ( P<0.05). As compared with those in the cerebral infarction group, the apoptosis rate, positive expression rate of Caspase-3, and ArgRs mRNA and protein expressions in the ischemic penomere zone at different time points after modeling in the ischemic precondition group were significantly decreased ( P<0.05). Conclusion:Cerebral ischemic precondition can inhibit the mRNA and protein expressions of ArgRS and Caspase-3 expression, reduce the apoptosis of brain cells, and thus play a neuroprotective role in brain tissues.

Objective To investigate any effects of carbamylated erythropoietin (CEPO) on the expression of LINGO-1,growth-associated protein-43 (GAP-43) and the infarcted volume after cerebral ischemia,so as to explore the effect of CEPO on neural regeneration after cerebral ischemia.Methods Forty-eight Sprague-Dawley rats were randomly divided into a sham operation group,an ischemia control group and a CEPO treatment group,each of 16.Middle cerebral artery occlusion (MCAO) was used to simulate focal cerebral ischemia in all except the rats in the sham operation group.Then the CEPO group was injected with 0.5 ml of CEPO,while the other two groups were given a 0.5 ml injection of normal saline daily for 7 days before they were sacrificed to prepare slices of brain tissue.Western blotting was used to detect the expression of LINGO-1 and activated caspase-3.Immunohistochemical staining was applied to observe the expression of GAP-43.The slices of brain tissue were stained with cresyl violet and the volume of infarction and edema were quantified with the Image J software.Results The average expression of LINGO1 in the sham operation group,the ischemia control group and the CEPO treatment group were (0.25±0.02),(1.22±0.06) and (0.66±0.05) respectively,with significant differences among the 3 groups.There was no expression of activated caspase-3 in the sham operation group.However,the expression of activated caspase-3 increased significantly (to 86.6±10.2)％ in the ischemia control group and increased significantly less (to 40.3±8.7)％ in the CEPO treatment group.The average positive expression of GAP-43 in the sham operation group,the ischemia control group and the CEPO treatment group were 0,(55.02± 1.62) and (72.11±3.23)/HP,respectively,with significant differences among them.Moreover,the average volumes of cerebral infarction and brain edema in the CEPO treatment group were significantly lower than those in the ischemia control group.Conclusions CEPO can inhibit the expression of LINGO-1 and activated caspase-3,promote the expression of GAP-43,reduce infarct volume and limit cerebral edema so as to promote neural regeneration after cerebral ischemia,at least in rats.

Objective Calreticulin (CRT)is a multifunctional protein of endoplasmic reticulum implicated in the pathogenesis of rheumatoid arthritis(RA). The present study was undertaken to determine whether CRT was involved in an?giogenesis events in RA. Methods Serum CRT levels were measured by enzyme-linked immnuosorbent assay(ELISA)in 106 patients with established RA, 75 osteoarthritis(OA)and 80 healthy controls(HC). CRT levels in synovial fluid were al?so measured in 25 RA and 22 OA patients. The expression of CRT in synovial tissue was examined by immunohistology. In order to investigate the role of CRT on angiogenesis, human umbilical vein endothelial cells(HUVECs)were isolated and cultured for in vitro experiments. The proliferation, migration and tube formation of HUVECs following CRT stimulation were examined in vitro by MTT assay, scratch wound healing assay and tube formation assay. Results Our results showed a sig?nificantly higher concentration of CRT in serum [(6.4±3.1) μg/L] of RA patients compared to that of OA [(3.7±0.9) μg/L, P<0.01] and HC [(3.4±1.0) μg/L, P<0.01];and significantly higher CRT in synovial fluid [(6.9±3.4) μg/L] of RA vs OA [(3.9± 0.7) μg/L, P<0.01]. Increased CRT expression predominantly localized to vascular endothelial cells, inflammatory cells and perivascular areas in both the lining and sublining layers of RA synovial tissue. Furthermore, CRT significantly promoted the proliferation, migration and tube formation of HUVECs, as showed by MTT assay, scratch wound healing assay and tube for?mation assay. Conclusion These findings suggested that CRT may be involved in synovitis and pannus formation events via promoting angiogenesis in RA.

Objective To explore the clinical character,diagnosis and treatment principals of pyeloureteritis glandularis and cystitis glandularis.Methods The clinical manifestation,character of imageology and endoscopy images of the case for one year follow-up were analyzed and the relevant literatures were reviewed.Results During one year follow-up,there was no clinical symptoms and any progress on imageology.The patient is still in close following-up.Conclusions According to literatures,cystitis glandularis is not common in clinical,and it should be paid more attention by clinicians.There were a few reports about the ureteritis glandularis.Pelvis,ureter and bladder have the same epithelial tissue,pyelitis glandularis is very rare,up to now there is no efficient treatment ways.

Objective To study the protection and its mechanism of carbamylated erythropoietin (CEPO) on ischemic brain injury and to compare its function with erythropoietin (EPO).Methods Focal cerebral ischemia/reperfusion was induced by occlusion of the middle cerebral artery (MCAO) using the intraluminal filament technique.The expression of endothelial NO synthase (eNOS) and activated caspase-3 were detected with Western blot.The inducible NO synthase (iNOS) positive cells were detected by immunohistochemistry staining.The apoptotic cell was detected by TUNEL staining.Results The expression of eNOS, iNOS and activated caspase-3 in cerebral cortex significantly increased after MCAO.The influence of CEPO and EPO on eNOS in ischemic cortex were not significantly different.However, the expression of activated caspase-3 markedly dropped from 95.4%±16.7% in group NS to 43.5%±13.1% in group CEPO and 45.1%±11.2% in group EPO (t=5.99 and 6.13,P<0.01).Immunohistochemistry staining revealed iNOS positive cells in ischemic cortex was (3.1±1.9) cells/square, CEPO and EPO remarkably reduced them to (0.7±0.2) cells/square and (0.8±0.2) cells/square, respectively (t=3.08 and 2.95, P < 0.05).The apoptotic cells in ischemic cortex fell from (94.2±15.2) cells/square in group NS to (40.5±9.8) cells/square in group CEPO (t=7.27, P < 0.01), the anti-apoptosis by EPO was similar to CEPO.Conclusion CEPO and EPO have the similar function of anti-apoptosis by inhibiting expression of activated caspase-3 and iNOS.

OBJECTIVE To study the expression of matrix metalloproteinase 2 (MMP-2) and its correlation with microvascular density(MVD) and tumor metastasis in nasopharyngeal carcinoma. METHODS The expression of MMP-2 and MVD were detected in the specimens of 50 cases with nasopharyngeal carcinoma and 15 cases with nasopharyngeal inflammation by immunohistochemical technique. RESULTS The MVD in nasopharyngeal carcinoma(21.92?7.80) was significantly higher than that in inflammation nasopharyngeal tissues (9.23? 1.84, P

To study the protective effect of rosuvastatin on ischemic brain injury and its mechanism, focal cerebral ischemia/reperfusion was induced by occlusion of the middle cerebral artery (MCA) using the intra-luminal filament technique. The cerebral blood flow was monitored with laser-Doppler flowmetry (LDF). The slices of brain tissue were stained with cresyl-violet. The cerebral volume of infarction and edema were quantified with ImageJ software. The expressions of endothelial NO synthase (eNOS) and activated caspase-3 were detected with Western blot. The inducible NO synthase (iNOS) positive cells were immunohistochemically observed. The results demonstrated that rosuvastatin (20 mg/kg) could remarkably decrease infarct volume and cerebral edema after MCAO 90 min/reperfusion 24 h. Western blots showed that the expression of eNOS in cerebral cortex before and after ischemia was (100+/-43.3) %, (1668.9+/-112.2) % respectively (P<0.001), rosuvastatin significantly up-regulated the expression of eNOS in non-ischemic cortex (P<0.001), whereas in ischemic cortex of rosuvastatin group the expression of eNOS was (1678.8+/-121.3) %. There was no expression of activated caspase-3 in non-ischemic cortex, nonetheless the expression of activated caspase-3 increased after ischemia, and rosuvastatin significantly diminished it (P<0.01). Immunohistochemistry revealed no iNOS-positive cells in non-ischemic brain area, while in ischemic brain area the number of iNOS positive cells went up, and rosuvastatin could significantly reduced them. Consequently, the mechanisms of rosuvastatin's neural protection on ischemic brain injury are to enhance expression of eNOS, to inhibit expression of iNOS and activated caspase-3.

To study the protective effect of rosuvastatin on ischemic brain injury and its mechanism,in on ischemic brain injury and its mechanism,focal cerebral ischemia/reperfusion was induced by occlusion of the middle cerebral artery (MCA)-luminal filament technique. The cerebral blood flow was monitored with laser-Doppler flowmetry (LDF). The slices of brain tissue were stained with cresyl-violet. The cerebral e quantified with ImageJ software. The expressions of endothelial NO synthase (eNOS) and activated caspase-3 were detected with Western blot. The inducible NO were immunohistochemically observed. The results demonstrated that rosuvastatin (20 mg/kg) could remarkably decrease infarct volume and cerebral edema after MCAO ots showed that the expression of eNOS in cerebral cortex before and after ischemia was (100±43.3) %, (1668.9±112.2) % respectively (P＜0.001), rosuvastatin gulated the expression of eNOS in non-ischemic cortex (P＜0.001), whereas in ischemic cortex of rosuvastatin group the expression of eNOS was (1678.8±121.3) %. There was no hemic cortex, nonetheless the expression of activated caspase-3 increased after ischemia, and rosuvastatin significantly diminished it (P＜0.01). Immunoaled no iNOS-positive cells in non-ischemic brain area, while in ischemic brain area the number of iNOS positive cells went up, and rosuvastatin could significantly reduced them.'s neural protection on ischemic brain injury are to enhance expression of eNOS, to inhibit expression of iNOS and activated caspase-3.mia/reperfusion; NOS; caspase-3