Objective This study investigates the relationship of serum irfflammatory cytokine levels with intracranial pressure (ICP) in patients with severe traumatic brain injury (TBI) after surgery.Methods A total of 32 cases with severe TBI and placement of ICP monitor were prospectively enrolled.Serum was collected before surgery and every 12 h after surgery.Cytokines levels of interleukin (IL)-1β,IL-8,and tumor necrosis factor (TNF)-α were analyzed and compared with outcome of patients.Hourly values of ICP were recorded.The degree of ICP above treatment threshold (20 mm Hg) were calculated every 12 h as pressure times time dose(PTD-ICP20),which was compared with serum cytokine levels before (Pre) and after (Post) the 12-hour time period using linear regression method.Results Serum IL-1β (P＜0.05),IL-8 (P＜0.01) and TNF-a (P＜0.01) levels elevated dramatically after severe TBI and were significantly associated with outcome of patients.Mean PTD-ICP20 was (42.9 ± 60.2)mm Hg/h and was correlated with increased Pre-IL-8 (r=0.554,P＜0.001),Pre-TNF-α (r=0.597,P＜0.001),Post-IL-8 (r=0.629,P＜0.001) and Post-TNF-α (r=0.538,P＜0.001) levels.Conclusion Serum IL-8 and TNF-α demonstrated the most promising candidate bio.rnarkers of impending ICP elevation in this study.These findings indicate a feasible way of monitoring patients with severe TBI.

Objective To investigate the preventive effect of inactive schistosome ova on trinitrobenzesulfonic acid(TNBS)-induced colitis in mice and its mechanism.Methods Murine colitis was induced by administration of 3 mg of TNBS.Sixty mice were divided into control group(n=20),treatment group(n=20)and model group(n=20).Ten thousand frozen inactive schistosome ova were intraperitoneal injected at 14th and third day before TNBS induction in treatment group.The mice in model group were intraperitoneaUy injected with saline. All survival mice were killed at 7th day and mortality rate was calculated and morphological and pathological changes were eveluated.Expression of interleukin-10 and interferon-γ at colon tissue and serum were measured by real-time PCR and ELISA,respectively.Results The mortality rate in treatment group was lower than that in model group(20%vs 50%,P＜0.05)and the colonic inflammation alleviated(Ameho-criteria score:1.58±0.5 vs 4.18±0.8,P＜0.05)compared with the model group.Meanwhile,compared with model group,the expression of interferon-γ was decreased[serum:(48.33±16.59)pg/ml vs(29.79±6.97)pg/ml,colon tissue:2.31±1.08 vs 7.23±3.52 P＜0.05]and interleukin-10 was increased significantly[serum:(28.87±5.74)pg/ml vs(38.22±9.96)pg/ml,colon tissue:3.68±1.58 vs 7.44±3.04 P＜0.05]in treatment group.Conclusions IntraDeritonealy injection of inactive schistosome ova can alleviate inflammation of TNBS-induced colitis in mice,which may be the result of increased IL-10 and decreased IFN-γ expression in colon and serum.

Objective To evaluate the clinical value of multiple tumor marker protein chip in diagno-sis and detection of postoperative recurrence of breast cancer.Methods The serum levels of 12 tumor makers (CA199,NSE,CEA, CA2A2,Ferritin,β-HCG,AFP,f-PSA,PSA,CA125,CA153 and HGH)were measured in 70 preoperative breast cancer patients, 32 recurrence patients,52 non-recurrence patients and 76 normal con-trois.Results ①The breast cancer group had significantly higher positive rate than that of the controls (P<0.05).The positive rates and serum levels of CA199,CEA,CA242,Ferritin,CAI25 and CA153 in breast cancer patients had those of control significant differences compared with groups (P<0.05).②The recurrence group had significantly higher positive rate than that of non-recurrence group (P<0.05).The positive rates and se-rum levels of CA199, CEA, Ferritin, CA125 and CA153 in the recurrence patients had significant differences compared with those of non-recurrence patients(P<0.05).③The positive rate of recurrence group had signif-icant difference compared with that of breast cancer group(P<0.05).Moreover,The positive rate and serum level of Ferritin in the recurrence patients had significant difference compared with that of breast cancer pa-tients.Conclusion The multiple tumor marker protein chip detective system has valid value of clinical appli-cation in the diagnosis and detection of postoperative recurrence of breast cancer.The combination detection of CA199, CEA, Ferritin ,CA125 and CA153 may be the economical and effective in the diagnosis and detection of postoperative recurrence of breast cancer.

BACKGROUND:MATLAB has capabilities of large numerical calculation, mathematical drawing and simple finite element analysis. It can establish models rapidly and can be able to identify the grayscale with BMP and JPG
format, and it can directly transform the identified data into ANSYS finite element software-readable format, thus avoiding personal error produced by the repositioning and secondary treatment in the Autocad software.
OBJECTIVE:To find a simple, convenient and accurate method to construct the model of lumber fusion and to analyze the biomechanics of lumbar motion segment after lumbar fusion.
METHODS:Lamel ar CT and Matlab (Matrix Laboratory) scientific computing software combining Ansys finite
element software was used to construct the models of lumber fusion. Then the models were loaded to analyze the biomechanical change of the fusion model.
RESULTS AND CONCLUSION:The established models were loaded with axial, bending and stretching loads, and the biomechanical analysis showed that interbody fusion had the best stability among al the fusion models. Combined with joint fusion, the axial displacements of interbody, rear side and rear fusion models were
decreased by 5%, 1%and 4%than that of simple interbody fusion, posterolateral fusion and posterior fusion models. Under the stretch-buckling load conditions, the rotation angles were reduced by 23%, 11%and 45%. Stress concentration to the fusion parts showed fusion block could increase the load displacement. The
technology of lamel ar CT, Matlab software and Ansys finite element software can accelerate the construction of lumber fusion model and make the model more accurate. Facet joint fusion combined with interbody fusion,
posterolateral fusion and posterior fusion can get better lumbar stability, and this increased stability is more significant in the rear fusion. Stress distribution of posterior fusion is more reasonable.

Objectives To investigate the infection and colonization of Mycoplasma genitalium and Ureaplasma urealyticum in different male populations, to explore the association of M. genitalium and U. urealyticum with nongonococcal urethritis (NGU) respectively. Methods A case-controlled, cross sectional study of four different male populations was performed, namely: NGU patients (G1), non-NGU subjects attending STD clinic (G2), men who had sex with men participating in a health education program (G3), and healthy volunteers (G4). Nested PCR and culture were used to detect U. urealyticum. Nested PCR and PCR product sequencing were applied to detect M. genitalium. Results The prevalence rates of M. genitalium in the four study populations were 25.0%(25/100), 6.4%(6/94), 5.5%(6/110) and 0% respectively. Significant difference was found between each two groups except G2～G3 with a p value of 0.80. By multivariate regression analysis, controlling for the age of first sex, new sexual partners, urethritis and condom use in the previous 3 months, M. genitalium was only associated with urethritis (P= 0.004, OR = 6.754, 95% CI 1.833～24.893). The direct sequencing of PCR products showed gene mutations, in comparison with the reference sequence in GenBank, in 3 samples. The prevalence rates of U. urealyticum by PCR in 4 groups were 40.0%, 44.7%, 22.7% and 46.9% respectively, and there was no significant difference between G1～G2, G1～G4 or G2～G4 with a p value of 0.419, 0.325, 0.868 respectively, but the prevalence rate of U. urealyticum in G3 was significantly lower than that in other groups. Conclusions M. genitalium is strongly associated with NGU and the prevalence rate is significantly higher in groups with high risk sexual behaviors than that in general population. There is no association between the colonization of U. urealyticum and NGU.

Objective To investigate the mechanism related to reduced antibiotic sensitivity of Acinetobacter baumannii inducted by meropenem in vitro.Methods Three strains of clinically isolated carbapenems-sensitive Acinetobacter baumannii were induced by meropenem in vitro, and the mutant strains (MS1, MS2 and MS3) were obtained.Minimal inhibitory concentrations (MICs) of antimicrobial agents to strains before and after induction were determined by automatic drug sensitivity analyzer .The homology of strains was analyzed by Enterobacterial repetitive intergenic consensus -polymerase chain reaction ( ERIC-PCR).Modified Hodge test and EDTA-Na2-double disk synergy test were used to detect carbapenemase and metallo-β-lactamase (MBL), respectively.Main carbapenemase genes were detected by PCR and followed by DNA sequencing.Expressions of adeB and outer membrane proteins in strains before and after induction were detected with fluorescence quantitative PCR and SDS -polyacrylamide gel electrophoresis , respectively.t test was used for data analysis .Results The sensitivity of mutant Acinetobacter baumannii strains to meropenem and most antibiotics was reduced , except to imipenem, amikacin and polymyxin; and the reduced sensitivity to meropenem in MS2 and MS3 was of genetic stability.ERIC-PCR showed 100%homology between the mutant strains and parental strains .Both carbapenemase and metallo -β-lactamase were negative in mutant strains and parental strains , and only OXA-51 gene was found.The expressions of adeB gene in mutant strains were 24.26 ±0.91, while those in parental strains were 22.81 ±0.38, and the difference was not significant (t =2.534, P >0.05).Outer membrane protein with molecular weight 54 000 was missing in MS1, while that with molecular weight 47 000 was missing in MS2 and MS3.Conclusion Reduced antibiotics sensitivity in meropenem -induced Acinetobacter baumannii may be correlated with the deficiency of outer membrane protein with molecular weight 47 000.

Objective: To explore the phenotypic and genotypic characteristics in Chinese children with classic pantothenate kinase-associated neurodegeneration (PKAN). Method: The clinical, radiographic and genetic data of all PKAN patients diagnosed at pediatric department of Peking University First Hospital from November 2006 to December 2016 were retrospectively collected and analyzed. Result: Twenty patients with classic PKAN were included in the study. The median age at onset was 3.5 years (ranging from 1.0 to 10.0 years), and the most common initial symptom was gait disturbance (16 cases). At the last evaluation, the clinical features were limbs dystonia (20 cases), dysarthria (16 cases), dysphagia (11 cases), pyramidal sign (7 cases), mental regression (3 cases) and pigmentary retinopathy (5 cases). For those classic PKAN patients, the median time from onset of disease to loss of independent ambulation was 6.9 years (ranging from 2.0 to 12.0 years). Imaging data showed, except "eye of tiger" in MRI (19 cases), globus pallidus calcification in CT was also found in four patients. In gene testing, 26 different mutations in PANK2 gene were identified, and 16 of 26 were novel mutations. Moreover, c. 1502T>C (p.Ile501Asn) was the most common mutation (4 cases). Conclusion Dystonia is the major neurologic feature of classic PKAN. Disease progression is rapid, with loss of independent ambulation within 10 years after onset. Except "eye of tiger" in MRI, globus pallidus calcification in CT may be another imaging feature of PKAN.Sixteen novel mutations of PANK2 gene were identified in the study.

Drug-associated reward memories are conducive to intense craving and often trigger relapse. Simvastatin has been shown to regulate lipids that are involved in memory formation but its influence on other cognitive processes is elusive. Here, we used a mass spectrometry-based lipidomic method to evaluate the impact of simvastatin on the mouse brain in a cocaine-induced reinstatement paradigm. We found that simvastatin blocked the reinstatement of cocaine-induced conditioned place preference (CPP) without affecting CPP acquisition. Specifically, only simvastatin administered during extinction prevented cocaine-primed reinstatement. Global lipidome analysis showed that the nucleus accumbens was the region with the greatest degree of change caused by simvastatin. The metabolism of fatty-acids, phospholipids, and triacylglycerol was profoundly affected. Simvastatin reversed most of the effects on phospholipids induced by cocaine. The correlation matrix showed that cocaine and simvastatin significantly reshaped the lipid metabolic pathways in specific brain regions. Furthermore, simvastatin almost reversed all changes in the fatty acyl profile and unsaturation caused by cocaine. In summary, pre-extinction treatment with simvastatin facilitates cocaine extinction and prevents cocaine relapse with brain lipidome remodeling.
Animals ; Brain ; Cocaine ; Conditioning, Operant ; Extinction, Psychological ; Lipidomics ; Male ; Mice ; Simvastatin/therapeutic use*

Drug-associated reward memories are conducive to intense craving and often trigger relapse. Simvastatin has been shown to regulate lipids that are involved in memory formation but its influence on other cognitive processes is elusive. Here, we used a mass spectrometry-based lipidomic method to evaluate the impact of simvastatin on the mouse brain in a cocaine-induced reinstatement paradigm. We found that simvastatin blocked the reinstatement of cocaine-induced conditioned place preference (CPP) without affecting CPP acquisition. Specifically, only simvastatin administered during extinction prevented cocaine-primed reinstatement. Global lipidome analysis showed that the nucleus accumbens was the region with the greatest degree of change caused by simvastatin. The metabolism of fatty-acids, phospholipids, and triacylglycerol was profoundly affected. Simvastatin reversed most of the effects on phospholipids induced by cocaine. The correlation matrix showed that cocaine and simvastatin significantly reshaped the lipid metabolic pathways in specific brain regions. Furthermore, simvastatin almost reversed all changes in the fatty acyl profile and unsaturation caused by cocaine. In summary, pre-extinction treatment with simvastatin facilitates cocaine extinction and prevents cocaine relapse with brain lipidome remodeling.