The aquaporins (AQPs) are a group of highly selective water channel protein family. The content of AQP4 in the astrocytes of the brain is the highest. It is the most vital protein in central nerve system. It participates in a series of pathologic processes of cerebrovascular disorders, brain contusion, tumor, and inflammation caused cerebral edema.However, the mechanism of AQP4 in the process of cerebral edema formation remains controversial. Selective modulation of the expression of AQP4 and intervention in part of its role may provide novel ideas and means for the treatment of edema after cerebral ischemia in clinical practice.

Neurogenic pulmonary edema (NPE) is a fatal complication after severe injury of central nervous system. Various cerebrovascular diseases are the common causes of NPE. The mortality of NPE is high. Its pathogenesis involves a variety of factors; however, its exact mechanism remains obscure. This article reviews the advances in pathogenesis and treatment of cerebrovascular diseases complicated with NPE in recent years.

Objective To investigate the significance of the changes of brain natriuretic peptide (BNP) and D-dimer (DD) levels in patients with acute cerebral infarction with different etiological subtypes. Methods One hundred forty-six patients with acute cerebral infarction within 24 hours of onset were divided into four groups according to the TOAST classification:large-artery atherosclerosis (LAA, n =48), small-artery occlusion (SAO, n = 32), cardioembolism (CE, n = 41 ), and cryptogenic cerebral infarction (n = 25 ). Plasma BNP and DD levels were measured in the emergency department, and the correlation between both plasma BNP and DD levels and different subtypes of cerebral infarction, infarct rolume and severity of disease were analyzed. Results The plasma BNP and DD levels in the cardioembolism group were significantly higher than those in all the non-cardioembolism groups (all P ＜0.01). The plasma DD level was also increased significantly (compared to the LAA group, P ＜0. 05; compared to the SAO and cryptogenic cerebral infarction groups, all P ＜ 0. 01 ), while there were no significant differences in plasma BNP and DD levels among all the non-CE groups. The plasma BNP and DD levels in patients of the large infarction group were significantly higher than those of the moderate infarction group (t = 3.766 and 3.029, respectively; P = 0. 013 and 0. 029,respectively), and there was no significant difference between the moderate infarction group and the small infarction group (t= 1.275 and 1.207, respectively; P= 0.258 and 0. 281,respectively). The plasma BNP and DD levels in the National Institutes of Health Stroke Scale (NIHSS) score ≥ 7 group were significantly higher than those in the NIHSS score ＜ 7 group (t = - 3.454 and - 4. 044, respectively; P = 0. 018 and 0. 010, respectively). Conclusions Acute cerebral infarction, particularly the plasma BNP and DD levels were increased significartly in patients with cardioembolism, and the larger the infarct volume, the more serious the disease, and the higher the both levels. Early detection of plasma BNP and DD levels contribute to etiological classification of cerebral infarction, especially for the diagnosis of cardioembolism, as well as the identification of infarct volume and the severity of the disease.

Objective To investigate the effects on brain tissue p38 mitogen-activated protein kinase (MAPK) and aquaporin 4 (AQP4) and neuroprotective effect of edarvone after focal cerebral ischemia and reperfusion in mice.Methods A total of 196 healthy male Kunming mice were randomly divided into four groups:a sham operation group,an ischemia-reperfusion group,a saline control group,and an edaravone group (n =49 in each group).A middle cerebral artery occlusion (MCAO) mothod was used to induce a cerebral ischemia-reperfusion model.At 2 h after ischemia,immediately after reperfusion in the edaravone group and the saline control group,edaravone (5 mg/kg) and the same volume of saline were injected intraperitoneally in mice,then repeated once every 24 h.At 2 h after MCAO,the brain water content and infarct volume at different time points after reperfusion (12 h,24 h,48 h,and 3 d) were measured respectively.At 24 h after MCAO,the expressions of AQP4 and p38 MAPK in the brain tissue of ischemic peripheral cortex were measured by Western blotting.Results The volumes of cerebral infarction (all P ＜ 0.01) and the brain water contents (all P ＜0.05) in the edaravone group were decreased than those in the ischemia-reperfusion group and saline control group at different time points,and they were most significant at 48 h.After 24-h reperfusion,the expression levels of AQP4 (0.985 ± 0.129,1.024 ± 0.117,0.713 ± 0.231) and phospho-p38 MAPK (1.123 ± 0.142,1.214 ± 0.096,0.986 ± 0.087) in the brain tissue of ischemic peripheral cortex in the ischemia-reperfusion group,the saline control group,and the edaravone group were upregulated significantly than those in the sham operation group (AQP4:0.265 ± 0.123;phospho-p38 MAPK:0.465 ±0.023;all P ＜0.01),but edaravone group were significantly lower than the ischemia-reperfusion group and the saline control group (all P ＜ 0.05).Conclusions Edaravone can downregulate the expression level of AQP4 and effectively protect cerebral ischemia reperfusion injury in mice,Its mechanism may be associated with the inhibition of p38 MAPK pathway.

Purpose To study the clinic-pathological features, differential diagnosis and prognosis of extragastrointestinal stromal tumor ( EGIST) arising in the vulva and the rectovaginal septum. Methods Clinical manifestations, pathological features, immunohisto-chemistry, gene mutations, treatment and prognosis were analyzed in 1 case of EGIST arising in the vulva and 2 cases of EGIST arising in the rectovaginal septum with review of related literature. Results Case 1 was a 59-years-old woman who was found to have a 4. 4 cm × 3 cm × 3 cm recurrent mass in the right vulva after 6 months of the first resection. Case 2 was a 58-years-old woman who presen-ted with a 7. 3 cm × 6. 1 cm × 4. 6 cm mass in the rectovaginal septum. Case 3 was a 41-year-old woman who presented with an 8. 6 cm × 7. 4 cm × 6. 7 cm mass in the rectovaginal septum. Histologically, the uniform spindle cells showed the interlacing fascicular, whirl-pool and palisade patterns with high cellular density. Mitotic figures were readily identified. Immunohistochemical evaluation revealed that the tumor cells exhibited strong and diffuse staining for CD117, CD34, NES, H-Caldesmon and DOG-1. Molecular analysis showed the gene mutation of c-Kit exon 11 in all 3 cases. Conclusion EGIST should be considered in the differential diagnosis of the mesenchymal tumors arising in the vulva and the rectovaginal septum. The immunohistochemical evaluation and molecular genetic tes-ting are crucial tools for the differential diagnosis and assessment of the prognosis and targeted therapy of EGIST.

Clinical teaching plays an important role in the education of medical graduate students.In the clinical teaching of the graduate students of burn and plastic surgery,we based it on clinical practice and guided the students in changing their modes of learning and thinking from examination-orientedness to problem solving,from simple vertical to clinical lateral thinking.We made sure that they all acquired innovative ideas and correct methods of clinical research by various academic activities,and cultivated their practical abilities and medical virtues by strict training and moral education.

Objective To investigate the effect of cocaine-amphetamine-regulated transcript peptide (CART) on the content of 4-hydroxy-2-noneral (HNE) and infarct volume after cerebral ischemia/reperfusion in mice.Methods A total of 96 healthy male mice were randomly divided into four groups:ischemia/reperfusion (n =27),CART (n =27),normal saline control (n =27) and sham operation (n =15) groups.A middle cerebral artery occlusion (MCAO) model was induced.Two hours after MCAO,CART 55-102 and equivalent normal saline were injected respectively via the tail veins of mice in the CART group and the normal saline control group,and then they were injected every other 24 hour.The neurological scores,infarct volume and the HNE content of lipid metabolism of oxidative stress were performed and detected respectively at 12,24,48 and 72hours after reperfusion.Results CART could significantly improve the neurological deficit scores (all P ＜0.05) and reduce infarct volume (all P＜0.05) at different time points after ischemia/reperfusion.The content of HNE was upregulated (all P＜0.05) at different points after referfusion.CART could significantly down-regulate the increased HNE levd in brain after ischemia (all P＜0.05).Conclusions CART may protect ischemic brain injury in mice by inhibiting lipid peroxidation.

Objective To assess the safety of early subcutaneous injection of a low-dose low molecular weight heparin (LMWH) nadroparin for prevention of deep vein thrombosis (DVT) in patients with spontaneous intracerebral hemorrhage (sICH).Methods The patients with sICH who early using nadroparin or lower limb intermittent pneumatic compression (IPC) for prevention of DVT were enrolled.A nadroparin group continuously injected nadroparin 0.4 ml/d subcutaneously for 10 days at day 4 after admission and an IPC group used lower limb IPC.Head CT was reexamined and hematoma volume changes were evaluated at day 3,5,and 14 after admission.The hemorrhagic events during the course of treatment were documented,and the lower limb DVT was examined by color Doppler sonography.Results A total of 94 patients with acute sICH (n =41 in the nadroparin group,n =53 in the IPC group) who early use of nadroparin or IPC for prevention of DVT were enrolled.Fourteen patients had lower limb DVT,5 (12.2％) of them were in the nadroparin group and 9 (17.0％) of them were in the IPC group.However,there was no significant difference in the incidence of DVT between the two groups (x2 =0.418; P =0.518).During the treatment,no patient experienced increased intracranial hematoma and rebleeding.Conclusion Early subcutaneous injection of low-dose nadroparin for the prevention of DVT in patients with sICH is safe.

Objective To investigate the effect of cocaine and amphetamine-regulated transcript (CART ) peptides on cortical synaptic plasticity in ischemia-reperfusion (I/R ) injury mice. Methods A total of 288 healthy male specific pathogen free(SPF)grade Kunming mice aged 0 to 12 weeks were selected. They were divided into four groups:I/R group (n =81 ),I/R +CART group (n =81),sham operation group (n=63),and sham operation+CART group (n=63)according to the random number table method. A model of middle cerebral artery occlusion (MCAO)for 2 h and reperfusion was induced. Before reperfusion,the mice of the I/R+CART group were injected CART via tail vein (0. 5μg, 200μl)and the those of the sham operation+CART group were injected equal CART;repeated administration once every 24 hours. 2,3,5-Triphenyl tetrazolium chloride assay was used to detect cerebral infarction volume of the I/R group and the I/R+CART group at different time points (24 h,72 h,and day 7 )after achieving reperfusion. The transmission electron microscope was used to observe the ultrastructural changes of synapses at different time points,and the synaptic morphological parameters were analyzed quantitatively. Western blot was used to observe the expression level of postsynaptic density 95 (PSD-95)proteins in the surrounding area of cortical infarct at 72 h after reperfusion. Results (1 )Compared with the sham operation group,the number of synapses was significantly decreased in the cortical slices in the I/R group (3. 37 ± 0. 38μm2 vs. 7. 04 ± 0. 55μm2 ,2. 89 ± 0. 22μm2 vs. 6. 89 ± 0. 04μm2 ,3. 25 ± 0. 18μm2 vs. 6. 78 ± 0. 42μm2;all P<0. 05). The density of PSD was significantly decreased (24. 4 ± 2. 8 nm vs. 47. 3 ± 6. 1 nm,23. 8 ± 3. 7 nm vs. 46. 5 ± 7. 5 nm,24. 6 ± 2. 2 nm vs. 48. 1 ± 5. 1 nm;all P <0. 05). The width of synaptic cleft was increased (25. 2 ± 2. 1 nm vs. 21. 5 ± 1. 6 nm,25. 2 ± 1. 4 nm vs. 21. 3 ± 1. 0 nm,23. 7 ± 2. 6 nm vs. 21. 6 ± 1. 6 nm;all P<0. 05). The expression level of PSD-95 protein was decreased at 72 h after reperfusion (P<0. 05). (2)Compared with the I/R group,the infarction volume of the I/R+CART group was significantly reduced at 24 h,72 h,and day 7 after reperfusion (29. 0 ± 1. 9% vs. 36. 3 ± 1. 4%,38. 1 ± 1. 4% vs. 47. 6 ± 2. 7%,and 36. 0 ± 2. 8% vs. 42. 5 ± 2. 0%,respectively;all P<0. 05). The number of synapses was significantly increased (4. 32 ± 0. 35 μm2 )and the expression level of PSD-95 protein was increased at 72 h after reperfusion (P<0. 05). The PSD density (33. 8 ± 3. 4,34. 2 ± 4. 6,38. 2 ± 4. 0 nm)was thickened at 24 h,72 h,and day 7 after reperfusion (all P <0. 05),and there were no significant differences in the width of synaptic cleft at each time point(allP>0.05).Conclusion CART can reduce cerebral infarct volume of I/R in mice and improve synaptic plasticity of cortical neurons in mice after ischemic injury.

Objective Toinvestigatetheclinicalsignificanceofplasmamatrixmetalloproteinase9 (MMP-9)intheformationofdelayedcerebraledemaafterintracerebralhemorrhage.Methods The clinical data of 107 patients with spontaneous intracerebral hemorrhage treated with conservative medical treatment were analyzed retrospectively. According to the clinical features and imaging changes,they were divided into either a delayed cerebral edema group (case group n=39)or a non-delayed cerebral edema group (control group n =68 ). The plasma MMP-9 level was detected with enzyme-linked immunosorbent assay within 24 h after onset. The patients performed head CT scan again at day 7 and 14 after admission. The changes of hematoma and edema volume were detected. All the possible factors associated with the formation of delayed cerebral edema were firstly analyzed by the univariate analysis. Univariate analysis showed that the variables with significant differences were enrolled into multiple logistic regression analysis. Results TheplasmaMMP-9levelofthedelayedbrainedemagroupwassignificantlyhigherthanthatof the control group,they were 189 ± 51 and 118 ± 27 mg/L respectively (P<0. 01). The result of univariate analysis showed that age,history of smoking,blood glucose level,baseline hematoma volume,and National Institute of Health stroke scale (NIHSS )score on admission might be associated with the formation of delayed cerebral edema after intracerebral hemorrhage. Logistic regression analysis showed that MMP-9 level (OR,9. 745,95%CI 6. 754-15. 466,P<0. 01),baseline hematoma volume (OR,2. 411,95%CI 1. 190-2. 728,P =0. 018),blood glucose level on admission (OR,1. 327,95%CI 1. 133 -1. 850,P =0.004),and NIHSS score (OR,1. 867,95%CI 1. 272-2. 364,P=0. 020)were the independent risk factorsfortheformationofdelayedcerebraledemaafterintracerebralhemorrhage.Conclusion Theamount of bleeding,NIHSS score,and hyperglycemia are the risk factors for the formation of delayed cerebral edema in patients with spontaneous intracerebral hemorrhage,while high MMP-9 level on admission indicated that the risk of the formation of delayed cerebral edema is high.