Objective To analyze the gene expression profiles in relation to the migration ability of adult human bone marrow-derived neural stem cells (Md-NSCs), and identify the genetic basis of the high migration potential of Md-NSCs in the central nervous system (CNS). Methods Adult human bone marrow stromal celIs(BMSCs) obtained from adult healthy volunteers were induced to differentiate into Md-NSCs in vitro, and the expressions of the genes related to cell invasiveness and metastasis were investigated by microarray analysis. Quantitative real-time PCR (RT-PCR) was used to verify the microarray results. Results The results of microarray analysis revealed significant overexpressions of the genes MMP1, MMP2, MMP17, ITGA3, RhoB, RhoC and RhoD in the Md-NSCs as compared with the expressions in fresh normal human adult bone marrow cells depleted of red blood cells. Quantitative RT-PCR verified the overexpression ofMMP2 gene by 2.84×100 folds, ITGA3 gene by 2.22×102folds, and RhoC gene by 4.92×100 folds. Conclusion The high migration potential of the Md-NSCs in the CNS is probably associated with the overexpression of the genes that promote cell invasiveness and metastasis. These overexpressed genes are also important oncogenes, and therefore the tumorigenicity of the Md-NSCs warrants further investigation.

Objective To observe the effect of acidic fibroblastic growth factor (aFGF) on traumatic brain edema. Methods Recombinant human aFGF (10mg/ml) was continuously injected into the intraventricle for 12 h before brain traumatic injury in rats, and the brain water content was determined and the histological and ultrastructural changes in the brain tissue observed. Results Brain edema and neuronal damage were reduced remarkably by the administration of aFGF. Conclusion aFGF can obviously alleviate brain edema and neuronal damage.

Objective To observe the effect of acidic fibroblastic growth factor (aFGF) on traumatic brain edema. Methods Recombinant human aFGF (10mg/ml) was continuously injected into the intraventricle for 12 h before brain traumatic injury in rats, and the brain water content was determined and the histological and ultrastructural changes in the brain tissue observed. Results Brain edema and neuronal damage were reduced remarkably by the administration of aFGF. Conclusion aFGF can obviously alleviate brain edema and neuronal damage.

Objective To investigate the changes in mitoehondrial membrane potential of the rat neurons after acute brain contusion and laceration injuries. Methods Seventy Sprague-Dawley (SD)rats were randomized into the sham injury group(n=10)and brain injury group.The brain injury group was divided into 6 subgroups(n=10)for observation at 1,6,and 24 h and 2,3,and 7 days after acutebrain contusion and laceration injury,which was induced by impact of the brain with a flee-falling object.In the brain slices labeled with fluorescent JC-l staining,the changes in the mitoehondrial membrane potential of the neurons were observed under confocal laser scanning microscopy at the indicated time points.The neuronal apoptosis Was detected using Hoehesd3342 staining and TUNEL assay,and the number of apoptotic neurons was determined under optical microscope.The ultrastructural alterations of the neurons were observed with transmission electron microscopy. Results Compared with that of the sham injury group,the mitoehondrial membrane potential of the neurons decreased significantly 1 h alterthe brain injury(P<0.01),reachingthe lowestlevel at 24 h,and maintained the low level aRerwards.Apoptotie neurons were identified in the brain slices with Hochest33342 staining.One hour after the brain injury,TUNEL assay revealed a small number of positive neurons,which increased significantly at 6 h(P<0.01)and reached the highest level at 48 h.The alteration pattern of the number of the positive neurons showed a 24-h delay in compariSOIl witll that of the mitochondrial membrane potential aRer the brain trauma.Under electronmicroscope.the mitocbondria of the neurons exhibited only slight swelling at l h. and obvious morphological changes of the mitochondria occurred 6 h after the brain trauma,accompanied by chromatin fragmentation,presence of marginal nuclei and broadened nuclear membrane;nuclear condensation and chromatolysis were observed in the neurons 24 h after the brain trauma.Conclusion In rats with acute brain contusion and laceration injuries,the mitochondrial membrane potential of the neurons decreases early(<1h)after the brain injury,which induces apoptosis of the neurons.

Objective In order to study the localization of NMDA receptor protein on the neuron membrane, a new immunocytochemistry method to visualize and quantify 3D earmark the membrane protein in nanometer scale has been achieved by atomic force microscope (AFM) with labeled colloid gold particle. Methods First step, the distribution of the anti-NMDAR1 IgG-SPA-gold complexes molecule on the surface of mica had been scanned by AFM and the characteristic 3D conformation was analyzed by particle software. Then the 3D conformation was contrasted with the IgG-SPA-gold complexes molecules combined with the neuron membrane surface and that were compared with the results of light microscope, laser confocal microscope and scanning electron microscope. Results The 3D conformation of IgG-SPA-gold scanned through mica surface shows the average diameter of globe particles is 49 nm. The neuron membrane NMDA receptor protein combined with IgG-SPA-gold immunocomplexes are globe or cosh shapes . Its average diameter is 53 nm. The long axis section is a typical two apexes structure. Conclusion AFM could determine the situation and 3D conformation of NMDAR protein on neuron membrane surface in nanometer scale. NMDAR single molecule could combine with one or two colloidal gold particles. Colloidal gold particle scanned by AFM in situ is a new detecting method of immunocytochemistry.

OBJECTIVETo explore clinical efficacy of closed reduction and external fixation under local anesthesia for the treatment of high-risk elderly patients with intertrochanteric fracture.

METHODSFrom March 2013 to March 2015, 10 patients with intertrochanteric fractures treated with closing reduction and external fixator under local anesthesia were analyszed, including 4 males and 6 females, aged from 69 to 88 years old with an average of 75.2 years old. All fractures were caused by injury and classified to type I (5 cases), II (3 cases), and V (2 cases) according to Evans classification. According to American Society of Anesthesiologists (ASA), 6 cases were type III and 4 cases were type IV. Blood loss,operative time,hospital stays, postoperative complications, ambulation time and fracture healing time were observed, and Harris scoring were used to evaluate hip joint function.

RESULTSAll patients were followed up from 3 to 23 months with an average of 13.1 months. One patient with chronic obstructive pulmonary disease died for non-operation reason at 4 months after operation, the other fractures were healed at stage I, the mean fracture healing time was 5.6 months. There were no coxa vara, lower limb venous thrombosis, loosen and remove of needle passage. The average operative time was 46 min, blood loss was (35.00 ± 8.46) ml without blood transfusion. One patient was occurred pulmonary infection and stent-tract infection on the 2 nd and 3 rd day after operation, and improved with active anti-infection and dressing change; the other patients gone to ground activity at 4.2 d after operation. The patients stayed hospital for 10.6 d on average. According to Harris scoring at final following-up, the total score was 83.42 ± 3.27, 3 cases obtained excellent results, 5 cases good and 1 case poor.

CONCLUSIONClosed reduction and external fixation under local anesthesia in treating high-risk elderly patients with intertrochanteric fracture,which has advantages of shorter operative time, less blood loss, good recovery of postoperative function, is a safe, stable and economic method.

Aged ; Aged, 80 and over ; Anesthesia, Local ; Bone Nails ; Female ; Follow-Up Studies ; Fracture Fixation, Internal ; Fracture Fixation, Intramedullary ; Fractures, Closed ; surgery ; Hip Fractures ; surgery ; Humans ; Male ; Treatment Outcome

BACKGROUND:Hand-foot-mouth disease has become a major public health issue in children in China. In the present prospective study we investigated the clinical characteristics and emergency management of children with severe encephalitis associated with NPE caused by enterovirus 71. METHODS:The study was conducted in 2 pediatric intensive care units (PICUs) over a 2-month period. Clinical records were reviewed of critically ill children with severe encephalitis associated with NPE caused by EV71 who were admitted to PICUs during the period of May to June 2008 in Fuyang. RESULTS:We reviewed the complete records of 36 children, of whom 23 (63.9％) were male and 13 (36.1％) female. Their age ranged from 4 to 48 months, with an average of 15.8 months. Al children except one were under 3 years of age. The overal mortality in these children was 19.4％. The average duration of critical life threatening signs and symptoms was 2.1 days (12 hours-5 days). Nervous system diseases included brainstem encephalitis in 27 children (75％), brainstem encephalitis associated with myelitis in 6 children (16.7％), and general encephalitis in 3 chidren (8.3％), respectively. In 12 patients of NPE (33.3％) pink or bloody bubble sputum and asymmetric pulmonary edema or hemorrhage was the primary manifestation but no typical exanthema was observed. Five children died of acute onset of NPE and / or pulmonary hemorrhage with rapid progression of cardiopulmonary failure within hours after admission. Therapeutic management consisted of mechanical ventilation and administration of mannitol, methylprednisolone, intravenous immunoglobulin (IVIG) and vasoactive drugs, associated with the need of fluid volume resuscitation in 9 (25％) of the 36 children. CONCLUSIONS:In children less than 3 years of age found to be affected by severe EV71 encephalitis associated with NPE, one fifth may die. The major organ systems infected by severe EV71 include the central nervous system, the respiratory system, and the cardiovascular system. Early diagnosis and evaluation, respiratory support, treatment of intracranial hypertension, and mainttenance of function of the cardiovascular system are the most important therapeutic measures.

Abstract?AIM: To investigate mechanism of bradykinin ( BK) on inflammations of retinal pigment epithelium ( RPE) cells.?METHODS: ARPE -19 cells were cultured in vitro, stimulated by 100nM BK for 24h. Cell morphology changes were observed by microscope, and BK receptor localization was detected through cell immunofluorescence. Changes of Ca2+in BK and BR antagonist stimuli were detected by laser scanning confocal microscopy.The expressions of COX-1, COX-2, eNOS and iNOS protein in control group and BK group were detected by Western Blot.?RESULTS: After the stimulation of BK, there was no significant changes of ARPE-19 cells in morphology.Kinin B1 receptors ( B1R ) and B2 receptors ( B2R ) could be detected in ARPE-19 cells.Compared with control group, Ca2+concentrations significantly increased in BK group; in B1R antagonist group and B2R antagonist group Ca2+concentrations increased less than BK group; B1R and B2R antagonist group showed no obvious changes in Ca2+concentrations.Compared with control group, COX-2 and iNOS protein concentrations were significantly increased in BK group (P<0.001).?CONCLUSION:BK induces the increasing expression of COX-2 and iNOS in the cultured ARPE cells through binding with either B1R or B2R.

Fluorescence imaging is a noninvasive and dynamic real-time imaging technique;however,it exhibits poor spatial resolution in centimeter-deep tissues because biological tissues are highly scattering media for optical radiation.The recently developed ultrasound-controlled fluorescence(UCF)imaging is a novel imaging technique that can overcome this bottleneck.Previous studies suggest that the effective contrast agent and sensitive imaging system are the two pivotal factors for generating high-resolution UCF images ex vivo and/or in vivo.Here,this review highlights the recent advances(2015-2020)in the design and synthesis of contrast agents and the improvement of imaging systems to realize high-resolution UCF imaging of deep tissues.The imaging performances of various UCF systems,including the signal-to-noise ratio,imaging resolution,and imaging depth,are specifically discussed.In addition,the challenges and prospects are highlighted.With continuously increasing research interest in this field and emerging multidisciplinary applications,UCF imaging with higher spatial resolution and larger imaging depth may be developed shortly,which is expected to have a far-reaching impact on disease surveillance and/or therapy.

Objective To study the changes of cytochrome C (CtyC) and apoptosis-induced factor (AIF) in the brain and effects of them on neuronal cells in rats after traumatic brain injury (TBI). Methods Seventy Sprague-Dawley (SD) rats were randomly divided into sham-injury group (n=10) and brain injury group. The brain injury group was divided into 6 subgroups according to 1, 6, 24, 48, 72, 168 h after traumatic brain injury (n=10). Rat models with contusion and laceration of brain were established by Feeney's impact with flee falling. Fluorescence intensity of CtyC and AIF were observed by immnnofluorescence and confocal laser scanning microscopy at different time points. The effects of CtyC and AIF on neuronal cells were observed by double-labeled immunofluorescence. Results (1)The changes of CtyC in the brain after TBI: at 1, 6, 24 and 48 h following TBL CtyC was 1.89±0.03, 2.69±0.07, 2.99±0.06 and 3.05±0.05 in the cortex and 1.34±0.04, 1.87±0.03, 2.60±0.03 and 2.80±0.06 in the hippocampus, respectively, being significantly higher than that of sham-injury group (P<0.05); at 72 h, CtyC declined to 1.94±0.05 in the cortex and to 1.12±0.04 in the hippocampus, respectively, being significantly higher than that of sham-injury group (P<0.05); at 168 h, CtyC recovered to the normal level in the cortex and hippocampus, being not significantly different between injury group and sham-injury group. (2) The changes of AIF in the brain after TBI: at 1, 6, 24 and 48 h following TBI, AIF was 1.82± 0.16, 2.16±0.34, 2.75±0.22, 2.87±0.12 in the cortex and 1.27±0.06, 2.01±0.05, 2.49±0.02, 2.62±0.05 in the hippocampus, respectively, being significantly higher than that of sham-injury group (P<0.05); at 72h, AIF declined to 1.35±0.09 in the cortex and to 1.32±0.05 in the hippocampus, respectively, being significantly higher than that of sham-in jury group (P<0.05); at 168 h, AIF recovered to the normal level in the cortex and hippocampus, being not significantly different between injury group and sham-injury group (P<0.05). (3) CtyC and AIF triggered neuronal cell apoptosis. Conclusion CtyC and AIF might release from mitochondria after TBI, and can induce neuronal cell apoptosis as apoptosis-inducing factors.