Aim To study the interfering effects of picroside Ⅱ on the expressions of nuclear transcription factor kappaB(NF-?B)and inhibitor of NF-?B(I-?B) after cerebral ischemic reperfusion in rats. Methods Intraluminal thread methods were applied to establish the middle cerebral artery occlusion reperfusion models in rats. PicrosideⅡ(10 mg?kg-1) and salvianic acid A sodium(10 mg?kg-1 ) were injected from the tail vein for treatment. TUNEL positive cells were counted by immunofluorescence assay. The expressions of NF-?B and I-?B were determined by immunohistochemical assay,and the concentration of NF-?B and I-?B in brain tissue was determined by ELISA. Results The exprssions of NF-?B and I-?B were weakly and the apoptotic cells were scattering at cortex,striatum and hip-pocampus in the sham operative group. In the negative control group,the number of TUNEL positive cells and the expressions of NF-?B and I-?B increased,the absorption(A) values and the concentration were significantly higher than those in the sham operative group(P0.05 ). Conclusion Picroside Ⅱ might downregulate the expressions of NF-?B and I-?B to inhibit neuronal apoptosis induced by inflammation after cerebral ischemia reperfusion injury in rats.

Aim To study the interfering effects of picrosideⅡ on the expressions of nuclear transcription factor kappaB(NF-κB)and inhibitor of NF-κB(I-κB)after cerebral ischemic reperfusion in rats.Methods Intraluminal thread methods were applied to establish the middle cerebral artery occlusion reperfusion models in rats.PicrosideⅡ(10 mg·kg~(-1))and salvianic acid A sodium(10 mg·kg~(-1))were injected from the tail vein for treatment.TUNEL positive cells were counted by immunofluorescence assay.The expressions of NF-κB and I-κB were determined by immunohistochemical assay,and the concentration of NF-κB and I-κB in brain tissue was determined by ELISA.Results The exprssions of NF-κB and I-κB were weakly and the apoptotic cells were scattering at cortex,striatum and hippocampus in the sham operative group.In the negative control group,the number of TUNEL positive cells and the expressions of NF-κB and I-κB increased,the absorption(A)values and the concentration were significantly higher than those in the sham operative group(P<0.05).While in the positive control and picroside groups,the expressions(A values)and concentration of NF-κB and I-κB and the number of TUNEL positive cells were significantly lower than those in the negative control group(P<0.05).There was no significant difference between the positive control group and picroside group(P>0.05).Conclusion Picroside Ⅱ might downregulate the expressions of NF-κB and I-κB to inhibit neuronal apoptosis induced by inflammation after cerebral ischemia reperfusion injury in rats.

Objective To present the intraoperative nursing of laparoscopic radical prostatectomy performed through extraperitoneal transumbilical single-port.Methods The cooperation experience for 11 cases receiving extraperitoneal transumbilical single-port laparoscopic radical prostatectomy were summarized.The measures included:full preoperative preparation and various inspection,mastering of cooperative main points by participated nurses,familiar with property and handling of apparatuses,cooperating with doctor during operation,closely monitoring of patients' condition,and perfect various intraoperative care.Results The operations were successful,no intraoperative complications occurred and the patients recovered very well postoperatively.Conclusions The success of this operation requires not only complicate surgical techniques and special instruments,but also perfect intraoperative nursing.

Objective To discuss the clinical manifestations,imaging features and prognosis of children with mild encephalitis/encephalopathy with a reversible splenial lesion(MERS).Methods Twenty-five patients with MERS admitted to Beijing Children′s Hospital,Capital Medical University,between November 2013 and March 2016 were enrolled and their clinical and imaging data were retrospectively analyzed.Ages of onset of these 25 cases were from 6 months to 13 years old.Because of different clinical manifestations in different onset ages,these 25 cases were divided into 2 groups:≤6 years old group (20 cases),with the onset age of 6 months to 3 years and 9 months old(average 2 years and 2 months);>6 years old group(5 cases),with the onset age of 9 years 3 months to 13 years old (average 10 years and 10 months).Results Nineteen cases among the 25 patients had infection history before onset,including 10 cases of digestive tract infection(all were ≤6 years old children),9 cases of respiratory tract infection(6 children ≤6 years old and 3 children >6 years old).The main clinical manifestations included convulsion (18/25 cases,72.0%),fever (17/25 cases,68.0%),vomiting (11/25 cases,44.0%),and disturbance of consciousness (11/25 cases,44.0%).The main clinical manifestation of ≤6 years old group was convulsion (18/20 cases,90.0%),while the main clinical manifestations of the>6 years old group were fever(3/5 cases,60.0%),headache and dizziness(2/5 cases,40.0%),and none of the patients in >6 years old group had convulsion.Eight cases had liver function injury,myocardial enzymes increased in 10 cases,and hyponatremia occurred in 9 cases.Magnetic resonance imaging (MRI) showed 21 cases were type Ⅰ MERS(only involving corpus callosum),and 4 cases of type Ⅱ MERS which involved corpus callosum as well as deep brain white matter,subcortical white matter (centrum semiovale).MRI lesions disappeared after 8-56 days (average 16.5 days) of anti-infection and reducing intracranial pressure treatment.Conclusion MERS is more common in ≤6 years old children,and digestive tract infection is common in ≤6 years old children,while respiratory tract infection is common in >6 years old children.The symptoms in children are mainly manifested as fever,convulsion,vomiting,conscious disturbance,and so on.Infection and hyponatremia are the main causes of MERS in children.MRI is the first choice of imaging examination methods.

The incidence of nonalcoholic fatty liver disease (NAFLD) is increasing worldwide and the age of onset gradually gets younger. However, specific therapeutic interventions are lacking. The exact mechanism of NAFLD has not yet been well elucidated. Recent studies indicate that adiponectin (APN) is an adipokine with anti-inflammatory activity and is considered a hepatic protector, which plays a central role in the pathogenesis of NAFLD. Research on APN actions in NAFLD is popular around the world. This article summarizes the mechanism of APN actions in NAFLD, briefly describes the relationship of APN with nonalcoholic steatohepatitis and NAFLD-related hepatic fibrosis, and reviews related clinical studies. It is suggested that APN holds promise as a novel therapeutic target in the treatment of NAFLD and further research into the signaling pathway of APN would lead to a better understanding of its action mechanism and can provide a novel strategy for the treatment of NAFLD.

Objective To investigate the effects of IL-12 coexpression level on antigen expression and immune responses induced by HBsAg DNA vaccination. Methods DNA vaccine plasmid pHBV carrying codon-optimized preS2-S gene of reference sequence CHN-HBV07-C in China was constructed. Three DNA vaccine plasmids pHBV-12i, pHBV-12l and pHBV-12h were also constructed by subcloning three different IL-12 expression cassettes with various expression strengths to plasmid pHBV, respectively. Expression levels of IL-12 and HBsAg in vaccine plasmid-tranfected 293T cells were measured by quantitative ELISA. DNA vaccines were administered intramuscularly to BALB/c mice and HBsAg-specific cellular immune responses were determined by IFN-γ ELISPOT. HBsAg-specific antibodies were tested by Chemiluminescence Quantitative Immunoassay. Results The HBsAg expression level in 293T cells was 70 ng/ml when transfected by plasmid pHBV without IL-12 expression cassette, and the HBsAg level was 18 ng/ml when transfected by plasmid pHBV-12l carrying low-level IL-12 expression cassette, whereas the HBsAg level was only 6 ng/ml when transfected by plasmid pHBV-12h carrying high-level IL-12 expression cassette.Results of DNA vaccination revealed that HBsAg-specific humoral and cellular immune responses were significantly decreased in mice administering vaccine pHBV-12h carrying high-level IL-12 expression cassette. Although HBsAg-specific antibody responses in mice inoculated with pHBV-12l were also decreased when compared with those in pHBV-vaccinated mice without IL-12 expression, the HBsAg-specific cellular immune responses were significantly increased. Conclusion High-level coexpression of IL-12 may suppress the expression of HBsAg, Whereas modest coexpression of IL-12 significantly enhanced the HBsAg-specific T cell responses induced by DNA vaccination. Therefore, it is so important to balance the expression between adjuvant and antigen to enhance the immune response.

Objective To study the intrinsic relationships between the binding energy of the antibody light and heavy chains and the conformational characteristics , physical and chemical properties , and to establish a corresponding mathemat-ical model and evaluate the thermal stability of the antibody molecules , which contribute to the antibody design , optimiza-tion and affinity maturation .Methods Based on bioinformatics and computational biology methods , the antibody′s structur-al information with the crystal diffraction data was analyzed .The conformational character of the variable domain of the antibody was studied using distance geometry and computer graphics technology .With the aid of the intermolecular hydrogen bond formation theory and the reaction free energy theory , the dynamic structure and energy characteristics be-tween the heavy and light chain variable regions of the antibody were studied .Furthermore , using nonlinear fitting and regression analysis, a mathematical model was set up .Results According to simulation and statistic analysis , there was a linear relationship between the binding energy and the number of the intermolecular hydrogen bonding , Van der Waals interaction of the heavy and light chains of the antibody .There was polynomial correlation between the binding energy and the physicochemical properties of the antibody .Using the frequency of amino acid position and the established model , the humanized anti-ricin antibody , which could not obtain the stable engineering cell line , was evaluated and optimized .The stable engineering cell line of the humanized anti-ricin antibody was obtained in the experiment .Conclusion The self structure of the antibody variable region ( conformation and physicochemical properties ) has much effect on its stability . The antibody stability can be improved by structural optimization .

Background: Aberrant Bcl-2 transcription is closely related with nodal diffuse large B-cell lymphoma (DLBCL), however, the relationship between Bcl-2 and primary gastrointestinal DLBCL (PGI-DLBCL) was not fully studied.Aims: To investigate the relationship between Bcl-2 gene amplification and protein expression and clinicopathological characteristics, immunophenotype and prognosis of PGI-DLBCL.Methods: Clinical data was collected from 136 PGI-DLBCL patients receiving surgical treatment, and a telephone interview was conducted for survival information.Bcl-2 gene amplification and protein expression in tumor tissue were determined by fluorescence in situ hybridization and immuno-histochemistry, respectively, and relationships between Bcl-2 and clinicopathological characteristics, immunophenotype and prognosis of PGI-DLBCL were analyzed.Results: Among 136 PGI-DLBCL patients, 33 (24.3%) showing gene amplification and 90 (66.2%) showing protein expression of Bcl-2;gene amplification was correlated with primary tumor location, Ann Arbor stage, serum lactate dehydrogenase level, B symptom and International Prognostic Index (IPI) score (P<0.05), while protein expression was correlated with primary tumor location and immunophenotype (P<0.05).5-year overall survival (OS) in patients positive for Bcl-2 gene amplification and patients with non-GCB immunophenotype and positive for Bcl-2 protein expression were inferior to those negative ones (41.5%vs.71.5%, P<0.05;54.6% vs.84.6%, P<0.05).In Bcl-2 gene amplification or protein expression positive patients, 5-year OS of CHOP chemotherapy was inferior to that of rituximab combined with CHOP chemotherapy (48.6%vs.80.3%, P<0.05;66.4%vs.83.4%, P<0.05).Conclusions: Detection of Bcl-2 gene amplification is useful for prediction of prognosis in PGI-DLBCL.Both patients with Bcl-2 gene amplification and non-GCB patients with Bcl-2 protein expression have a poorer prognosis.Rituximab may improve the prognosis in patients with Bcl-2 gene amplification or protein expression.

Objective: To investigate the clinical manifestations, laboratory findings, treatment and outcome of anti-GQ1b antibody syndrome. Method: The clinical manifestations, laboratory examination, diagnosis, treatment and prognosis of (4 patients 4 male patients, from 4 to 12 years) with anti-GQ1b syndrome in Beijing Children's Hospital affiliated to Capital Medical University from 2015 to 2016 were retrospectively analyzed. Result: All 4 children presented with ataxia. Case 1 showed impaired speech, ptosis and weakness of arms; case 2 and 3 had external ophthalmoplegia, weakness of limbs; case 4 presented hypersomnia, irritability and hallucinations. Serum anti-GQ1b-IgG antibody was positive in all cases. Case 1-3 received lumber puncture at the course of 1-2 weeks, CSF presented albuminocytological dissociation, case 4 had CSF pleocytosis and increased protein level. Brain MRI of Case 1-2 were normal; Case 3 showed long T1 and T2 signal in cerebellar dentate nucleus, pons and corpus callosum; Case 4 showed long T1 and T2 signal in bilateral centrum semiovale, basal ganglia, external capsule, insula and cerebellum. Electromyograms of case 1-3 showed peripheral axonal lesion. All children were treated with IVIG. After treatment, condition of all patients were improved. According to the clinical manifestation, laboratory examination, and outcome after treatment, case 1 was diagnosed as anti-GQ1b antibody syndrome (Pharyngeal-Cervical-Brachial weakness overlapped with Miller Fisher syndrome), case 2 and 3 were diagnosed as anti-GQ1b antibody syndrome (Miller Fisher syndrome overlapped with Guillain Barré syndrome) and case 4 was diagnosed as anti-GQ1b antibody syndrome (acute ataxia hypersomnolence). Conclusion When patients with the presence of prodromic infections, monophasic course, drowsiness, ataxia, ophthalmoplegia, weakness and the symptoms/signs are relatively symmetric, anti-GQ1b antibody syndrome should be considered. Anti-GQ1b antibody has important significance for diagnosis. Most children have a good prognosis. Early correct diagnosis can avoid unnecessary examinations and guide appropriate use of immunotherapy.

Objective: To investigate the clinically and genetic characteristics of children with Leigh syndrome. Method: Patients with clinically diagnosed Leigh syndrome(LS)in the department of Neurology, Beijing Children′s Hospital from January 2013 to February 2016 underwent the mitochondrial DNA (mtDNA) and nuclear DNA (nDNA) detecting with next generation sequencing (NGS) technology. The clinical data of gene confirmed cases were retrospectively collected and analyzed. The differences in the onset age, clinical manifestations, lactic acid level and MRI results between the mtDNA variation and nDNA variation were compared and analyzed.t test, Chi-square test and Fisher′s exact test were used for statistical analysis. Result: Thirty-five cases were diagnosed by gene detection, including 20 males and 15 females. The median onset age was 1 year (ranging from the neonatal period to 4.4 years old). The age of onset within 2 years accounted for 74%(26 cases). The onset age of initial symptoms, including developmental delay, developmental regression, and seizures, were 6 (4, 12) months, 12 (8, 14) months, and 6 (1, 23) months respectively. The onset age of ptosis, extrapyramidal symptoms and ataxia were 26 (18, 44) months, 28 (23, 40) months and 28 (19, 35) months, respectively. There were significant differences in the onset age between the three groups (H=21.919, P=0.01). Within the 35 cases, 29 were manifested with developmental delay (83%), 26 with dystonia (74%), 18 with growth retardation, 15 with myasthenia, 13 with developmental regression, 11 with dysphagia, 10 with feeding difficulties, 4 with skeletal dysplasia, and 2 with digestive tract symptoms; nystagmus and respiratory abnormalities were observed in 9 cases respectively; extrapyramidal symptoms, peripheral nerve injury, ptosis, seizures were observed in 8 cases respectively; and ataxia, ophthalmoplegia and hypertrichiasis were found in 5 cases respectively.The blood lactic acid was measured in 32 LS patients, within which 23 cases (72%) had increased results; 8 out of 11 cases who underwent were cerebrospinal fluid lactic acid test had increased results. The results of neuroimaging revealed that all the patients were involved in the brainstem and (or) basal ganglia, of whom 27 (77%) had brainstem involvement, 24 (69%) had basal ganglia involvement. Thirteen out of 14 patients who had medulla oblongata involvement had nDNA variation; while 7 out of 8 patients with cerebellar involvement had nDNA variation. Genetic etiology was confirmed in all patients, among whom there were 17 cases (49%) with mtDNA mutation, including 8993T>C/G (n=5), 14487T>C (n=4), 13513G>A (n=2), 9176T>C, 10158T>C, 3697G>A, 10191T>C, 14459A>G and 11777C>A (n=1) respectively. Remaining 18 cases(51%) had nDNA mutation, including SURF1 gene(n=10), PDHA1 gene(n=3) and one case each of NDUFV1, NDUFAF6, NDUFAF5, NDUFS1 and COQ7 genes. In this study, 27 types of mutations were founded, 15 of which had not been previously reported. Respiratory chain gene mutations have been found in 31 cases(89%); 3 cases had PDHc gene mutations, and 1 case had other mutation. Conclusion LS usually occurs in infants. The most common primary symptoms are age-dependent abnormal movements, ocular symptoms, and seizures. Respiratory chain defects is the most common causes of LS.SURF1 is the most common variation, followed by 8993T>C/G, 14487 T>C and 13513G>A mutation.