BACKGROUND: The coating induced by conventional simulated body fluid (SBF) and 1.5-folds SBF as biomimetic method has the shortcomings of slowly growth with weeks or months growth cycle. OBJECTIVE: To evaluate Ti-6Al-4V alloy surface deposition of hydroxyapatite coating induced by 3-folds SBF. DESIGN, TIME AND SETTING: In vitro biological analysis. The experiment was performed at the Institute of Metal Research, Chinese Academy of Sciences from November 2008 to March 2009. MATERIALS: Ti-6A1-4V alloy was supported by Boda Metel Materials Co., Ltd. METHODS: The pretreated Ti-6Al-4V alloy was immersed in 37 'C 3-folds SBF. The SBF was replaced every 24 hours for 3 days. MAIN OUTCOME MEASURES: The morphology, phase and elemental composition of calcium phosphate coating were analyzed by scanning electron microscopy, X-ray diffraction and infrared spectroscopy analysis. RESULTS: The scanning electron microscopy exhibited that the surface of Ti-6A1 -4V alloy was covered with deposited film with granular crystal on local areas at day 1 after immersion. The deposited film covered surface of Ti-6A1-4V alloy at day 3 after immersion, and granular or scale-shaped crystal could be seen. The crystal deposition displayed sustained growth with certain area as center. The product comprised Ca, P, O, C elements without Al, V. X-ray diffraction and infrared spectroscopy analysis revealed that the main component of the coating was hydroxyapatite. CONCLUSION: The 3-folds SBF can accelerate the deposition as well as shorten formation duration of hydroxyapatite coating on Ti-6A1-4V alloy.

Objective To investigate the effect of desflurane anesthesia on the autonomic nervous system in patients at high risk for coronary artery disease.Methods Thirty patients at high risk for coronary artery disease scheduled for elective abdominal operation were selected. Heart rate variability (HRV) was assessed at preoperation, inhalation of 05,10,15 and 20 MAC of desflurane with Holter electrocardiography Results Low-frequency component increased markedly inhaling low concentration of desflurane. With the increase of the concentration of desflurane, both the high-frequency and low-frequency components decreased significantly (P0 05).Conclusions Desflurane balanced anesthesia dose not increase the activity of sympathetic nervous system.

Plastic bronchitis(PB) is an uncommon respiratory disease characterized by formation of casts in tracheobronchial tree.It can lead to airway obstruction, difficulty of breathing and even respiratory failure.PB in children is commonly associated with lower airway infection, cyanotic congenital heart disease and asthma or atopic diseases.It can also be found in children with sickle cell anemia, thalassemia and cystic fibrosis and so no.There are three main mechanisms for the formation of casts: airway inflammation results in mucus hypersecretion; inflammatory insults lead to necrosis and abscission of the airway epithelium, mucosal edema, and finally cause airway clearance impairment; leakage of chyle from lung lymphatic circulation into airway.But the etiology of this disease is various, pathogenesis is complex.Further research is required to elucidate the pathogenesis.

BACKGROUND: Drug treatment has unsatisfactory effect on Alzheimer disease, while many studies have indicated that the transplantation of bone marrow stromal cells (MSCs) is effective on Parkinson disease, cerebral ischemia, etc., but the mechanism is still unclear.OBJECTIVE: To imitate transplantation environment by co-culture of amyloid β1-40 (Aβ1-40) damaged PC12 cells and MSCs, observe the effect of bi-directional information feedback in the microenvironment on the transdifferentiation of MSCs to nerve cells, and observe its protective effect on the apoptosis of damaged PC12 cells.DESTGN: A comparative observation.SETTING: Department of Neurology, China Medical University.MATERIALS: SD rats of 2-3 weeks after birth either male or female were used. PC12 cell lines were purchased from the Institute of Cell Biology, Chinese Academy of Sciences; neuro-specific enolase (1:50, Boster, Wuhan);Methyl-thiazol-tetrazolium (MTT) 15 μL (terminal concentration of 0.5 g/L).METHODS: The experiment was carried out in the Experimental Center (provincial experimental animal center) of China Medical University from June to July in 2004. Bilateral femurs were aseptically removed from 1 SD rat, and MSCs were identified using CD44 antibody immunofiuorescently. PC12 was used to replace nerve cells. The PC12 cells were stimulated by Aβ1-40 then transferred by Transwell. There were 5 groups: Group A: normally cultured PC12 co-cultured with MSCs; Group B: Aβ1-40 stimulated PC12 co-cultured with MSCs; Group C: normal PC12 supernatant+MSCs; Group D: damaged PC12 supernatant+MSCs; Group E: MSCs cultured with common medium 1640.MAIN OUTCOME MEASURES:Routine immunohistochemical staining was performed. NSE positive cells were observed under inverted fluorescence microscope, 10 visual fields (200×) were randomly selected to count the positive cells. MTT metabolic rate was used to detect the proliferation of MSCs in each group. The differences of measurement data were compared using the one-way analysis of variance.fluorescent and bright fields, NSE positive cells appeared as red fluorescence, MSCs were bipolar, multipolar and cone shapes, and appeared as neuron-like forms with dendrite-like structure, and there were extensive connections among some neuron-like cells. The NSE positive rates was obviously higher in group B than groups A, C, D and E (P ＜ 0.01 ).in groups A, C, D and E (F=9.713, P＜ 0.01).

BACKGROUND: The primary pathophysiology of Alzheimer disease (AD) is linked to β-amyloid (Aβ)protein. Neural progenitor cells (NPCs), which have the ability of multipotency, self-renewal and repair,have been detected in the central nerve system (CNS) of adult rat recently. But effective function of these neural progenitor cells are not seen in the AD brain ,which mechanism is unclear.It is unclear if Aβ1-40protein is compromised by the signal pathway of c-Jun N-termial kinase associated with the neurotoxicity to the progenitor cells on the cortex of embryonic rats.OBJECTIVE: To investigate the mechanism of c-Jun N-terminal kinase signal transduction pathway of Aβ1-40 protein, which has neuronal toxicity to progenitor cells(CPC)on the cortex of embryonic rats . To detect the neuroprotective effects of c-Jun N-termial kinase inhibitor (SP600125) against Aβ1-40-induced neuronal toxicity to the cortical progenitor cells on the cortex of embryonic rats.DESIGN: A randomized and controlled trial with cells as objects.SETTING: Department of Neurology, First Hospital Affiliated to China Medical UniversityMATERIALS: This experiment was carried out at the Central Laboratory,China Medical University from May to October 2005. Embryos at age of 14 days from Wistar rats were used in this experiment.METHODS: Cortical progenitor cells harvested from Wistar embryonic rats were cultured in vitro, passaged and identified. Embryonic rat cortical progenitor cells of rats with good growth state were randomly divided into 4groups:Aβ1-40 group (10 nmol/L Aβ1-40 in each well);SP600125+Aβ1-40group (10 μmol/L SP600125 for 30 minutes and then with 10 nmol/L Aβ1-40 in each well); SP600125 group ( 10 μmol/L SP600125 in each well); Normal saline group (same volume of normal saline). The incubated durations were 0,2 hours, 4 hours, 6 hours, 12 hours, 24 hours respectively,8 wells for each time point. The cell survival rate was measured by MTF assay (The concentration of cortical progenitor cells on the cortex was 1×10s L-1 in each group), the apoptosis rate was detected by flow cytometer (The concentration of cortical progenitor cells on the cortex was 1 ×1010 L-1in each group) and the expression of c-Jun N-termial kinase and p-c-Jun N-termial kinase, c-Jun,p-c-Jun were measured by Western Blot(The concentration of cortical progenitor cells on the cortex was 1×1013 L-1 in each group). t test was adopted for the comparison of difference in measurement data.sion of c-Jun N-terminal kinase, p-c-Jun N-termial kinase ,c-Jun and p-c-Jun of embryonic rat CPC .ture time in Aβ group and SP600125 +Aβ group, decreased obviously at 4hours; cellular survival rate in Aβ1-40 group was lower obviously than that in the other 3 groups at 0,2,4,6,12,24 hours (P ＜ 0.01); Cellular survival rate in SP60025 +Aβ1-40 group was lower obviously than that in SP600125 group and normal saline group at 2,4,6,12,24 hours (P ＜ 0.01);Compared with normal saline group, the difference of cell survival rate was not significant without time-dependent manner in SP600125 group (P＞ 0.05).amyloid protein group and SP600125 +Aβ group, increased obviously at 4hours; cell apoptosis rate in Aβ1-40 group was higher obviously than that of the other 3 groups at 0,2,4,6,12,24 hours(P ＜ 0.01); Cellular apoptosis rate in SP60025+Aβ1-40 group was higher obviously than that in the SP600125 group and normal saline group at 2,4,6,12,24 hours (P ＜ 0.01);Compared with normal saline group, the difference of cellular apoptosis rate was not significant without time-dependent manner in SP600125 group 12,24 hours without changes in Aβ1-40 group; the expression of p-c-Jun N-terminal kinase and p-c-Jun in Aβ1-40 group were seen at 0hour ,increased gradually, reached to the peak at hour 4 and decreased gradually.CONCLUSION: Aβ1-40 could inhibit the cell activity of CPC , reduce cellular survival rate and induce cellular apoptosis. c-Jun N-terminal kinase signal transduction pathway may mediate the Aβ1-40 inducd neurnal apoptosis in AD which may be one reason for unseen rescue mechanism in AD. SP600125 (c-Jun N-terminal kinase inhibitor) could inhibit the activation of c-Jun N-terminal kinase and c-Jun and protect the embryonic rats CPC from the Aβ1-40-induced neurotoxicity.

Objective To discuss the efficacy and safety of sodium tanshinone ⅡA combined with edaravone in treatment of acute cerebral infarction.Methods 100 cases of acute cerebral infarction were randomly divided into two groups.The control group (50 cases) was treated with edaravone.The observation group (50 cases) was treated with sodium tanshinone ⅡA combined with edaravone.The efficacy of sodium tanshinone ⅡA combined with edaravone in treatment of acute cerebral infarction was evaluated by the efficacy at 1 month after treatment,ESS scores,SF-36 scores before and after treatment and adverse reaction during treatment.Results After treatment,the effective rate of observation group was 90.0％ and control group was 72.0％.The effective rate of observation group was higher than that of the control group (P ＜ 0.05).Compared with the value before treatment,the ESS scores of two groups were increased after treatment (P ＜ 0.05).3 d,7 d,14 d after treatment,the ESS scores of observation group was higher than that of the control group (P ＜ 0.05).Before treatment,there were no statistical significance on SF-36 between two groups.After treatment,the SF-36 scores were increased in two groups (P ＜ 0.05).During treatment,there were no statistical significance on adverse reaction between two groups.Conclusion Sodium tanshinone ⅡA combined with edaravone had a good therapeutic effect on acute cerebral infarction.It could improve the quality of life and neurological function with high safety.It was worthy of clinical application.

Theinnate immunity system of human body has more and more attention for its antibacterial, antiviral, maintainingimmunehemostasis and promoting tissue damage and repair and other physiological functions.As members of NOD-like receptors(NLRs), NOD1 and NOD2 receptors are identified as intracellular pattern recognition receptors(PRRs), can be identified with molecular damage endogenous(damage-associated molecular patterns, DAMPs)and exogenous injury-molecular pathogen associated molecular(pathogen-associated molecular patterns, PAMPs), and initiation of innate and specific immune response, maintain the steady balance of body.Recently, a bunch of evidence have demonstrated that the importance of NOD1 receptor and NOD2 receptor is not limited in field of anti-infection, and the insulin resistance, kidney and liver damage recovery, cardiovascular disease and tumorigenesis are also closely related with these two receptors.So the aim of this article is to interpret the NOD1 and NOD2 general structure and function, and summarize the link between these two PRRs and tumorigenesis and finally make a clue for cancer immunotherapy.

Objective To evaluate the efficacy of quadriceps femoris fasciculation induced by lowcurrent nerve stimulation when used to assist ultrasound-guided lumbar plexus block.Methods One hundred patients of both sexes,aged 18-45 yr,of American Society of Anesthesiologists physical status Ⅰ or Ⅱ,weighing 50-85 kg,scheduled for elective unilateral knee arthroscopy,were selected and randomly divided into 2 groups (n =50 each) using a random number table:ultrasound assisted by nerve stimulator group (group SU) and ultrasound group (group U).The shamrock method was used to perform the ultrasound-guided lumbar plexus block in two groups.In group SU,the nerve stimulator with current 0.35 mA and frequency 1 Hz was used in the process of puncture,and 0.5％ ropivacaine 0.4 ml/kg was administrated when quadriceps femoris fasciculation was induced.In group U,when the tip of the nerve stimulating needle was located around the lumbar plexus,which was confirmed by ultrasound,0.5％ ropivacaine 0.4 ml/kg was administrated.The time of puncture,depth of needle insertion,onset time of block and effective block were recorded.Motor block was assessed using the modified knee score,and the development of complications was recorded within 24 h after block.Results Compared with group U,the onset time of block was significantly shortened,the rate of effective block was increased,the degree of motor block was aggravated (P＜0.05),and no significant change was found in the time of puncture or depth of needle insertion in group SU (P＞0.05).No complications were observed in two groups.Conclusion Low-current (0.35 mA) nerve stimulation-induced quadriceps femoris fasciculation when used to assist location can improve the efficacy of ultrasound-guided lumbar plexus block.

Objective:To study the prevalence of mild cognitive impairment (MCI) among elderly people and associated factors to it.Method:A sample of 1865 elderly people aged 60 or above living in Beijing metropolitan area was investigated by a two-stage survey.In the first stage, a door-to-door visit to the subjects was performed by a trained interviewer to conduct general questionnaire including activity daily living assessment, memory and cognitive test.On the second stage, neurologists examined all screened subjects to collect family history and to finish general and neurological examination as well as neuropsychological testing.MCI was diagnosed by the consensus of 2 neurologists.Result:Among the 1865 subjects visited, 217 (11.6%) were defined to have MCI.After adjusted for age and gender the standardized prevalence reaches 8%.Within the people with MCI 22.6% was classified as vascular MCI.The prevalence of MCI was higher in people living in rural area, in people with lower educational attainment, and in people who were labor workers.The prevalence increased with age advancing.Conclusion:Similar to dementia, people with advance aged, with low education and living in rural area are those at high risk of developing MCI.

Aim To study the inhibitory and apoptosis-inducing effects of aspisol on proliferation of B16 melanoma in vitro and in vivo. Methods The effect of aspisol on the proliferation of B16 cells was analyzed by MTT assay; its effect on cell apoptosis was measured by flow cytometry. The suspension of melanoma cells was injected subcutaneously into forelimb axillas of C57BL/6J mice to establish xenograft models. From the next day, the mice received intraperitoneal injection of aspisol in different concentrations once a day for 28 days; the mice received injection of dacarbazine (DTIC) were used as positive controls,and received injection of normal saline (NS) were used as negative controls. The inhibition rate of tumor growth was calculated .The apoptosis rate was detected by TUNEL assay. The expression of Survivin and C-erbB-2 was detected by immunohistochemistry. Results Aspisol inhibited the proliferation of B16 cells, with the inhibition rate up to (68.78?1.27)%, and induced the apoptosis with the highest apoptosis rate up to 15.8%.The inhibition rate of tumor growth was 15.0% in 200 mg?kg-1 aspisol group, 32.3% in 400 mg?kg-1 aspisol group, 49.4% in 800 mg?kg-1 aspisol group,and 51.4% in 40 mg?kg-1 DTIC group. Typical apoptotic morphologic changes were seen in the 4 groups. Survivin and C-erbB-2 expression was significantly lower in aspisol groups than in NS group. Conclusion Aspisol could inhibit proliferation and induce apoptosis of B16 melanoma cells in vitro and in vivo, which may be correlated to down-regulation of Survivin and C-erbB-2.