Objective To explore the changes of plasma brain natriuretic peptide(BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP)of sepsis combined with myocardial injury in newborns.Methods According to neonatal sepsis treatment program,45 cases of sepsis newborns in NICU of the Second Hospital in Lanzhou University from Jul.2007 to Jun.2008 were collected.According to the myocardial injury diagnostic criteria,45 cases neonatal sepsis were divided into myocardial injury group(n=22) and non-myocardial injury group(n=23).Myocardial injury group was also divided into congenital heart disease group and non-congenital heart disease group accor-ding to echocardiography.At the same time,30 healthy newborns were collected as healthy control group.Every newborns were tested the level of plasma BNP,NT-proBNP,creatine kinase-MB(CK-MB) and cardiac-troponin I (cTnI).Results There were significant difference between myocardial injury group,non-myocardial injury group and healthy control group in the levels of plasma BNP,NT-proBNP,CK-MB and cTnI,those in congenital heart disease group were higher than those in non-myocardial injury group and the healthy control group(Pa0.05).Conclusions BNP and NT-proBNP can be early used to diagnose myocardial injury and heart failure of neonatal sepsis associated with CK-MB and cTnI.In NICU,infants with sepsis should normally test BNP and NT-proBNP in order to early diagnose myocardial injury of neonatal sepsis.

Adolescent ; Adult ; Aged ; China ; epidemiology ; Female ; Genes, Viral ; Genotype ; Hepacivirus ; genetics ; Hepatitis C, Chronic ; epidemiology ; Humans ; Male ; Middle Aged ; Young Adult

OBJECTIVETo investigate the inhibitory effects of OMT on TGF-β1-induced CFBs proliferation, and then explore the mechanism.

METHODThe experiment was randomly divided into 6 groups as following: control group (serum free DMEM), model group (20 μg x L(-1) TGF-β1), OMT low dose group (1.89 x 10(-4) mol x L(-1) + 20 μg x L(-1) TGF-β1), OMT medium dose group (3.78 x 10(-4) mol x L(-1) + 20 μg x L(-1) TGF-β1), OMT high dose group (7.56 x 10(-4) mol x L(-1) + 20 μg x L(-1) TGF-β1), SB203580 group (p38MAPK blocking agent, 1 x 10(-5) mol x L(-1) + 20 μg x L(-1) TGF-β1). Vimentin of CFBs was identified by immunocytochemical methods, α-SMA of myFBs as well. Inhibitory effects of OMT on CFBs proliferation was detected by the MTT assay. Picric acid Sirius red staining was analyzed collagen type I and collagen type III deposition. Western blot was determined the expression of p38MAPK, p-p38MAPK, collagen type I and collagen type III.

RESULTMTT results showed that OMT significantly inhibited CFBs proliferation induced by TGF-β1 (P < 0.01) α-SMA immunocytochemical experiments suggested that OMT could protect against the CFBs proliferation. OMT could significantly decrease the deposition of collagen type I and collagen type III by Western bloting and picric acid Sirius red staining. Western blot results showed that TGF-β1 enhanced p38MAPK phosphorylation, however OMT attenuated the phosphorylation of p38MAPK induced by TGF-β1 (P < 0.01).

CONCLUSIONOMT can inhibit the CFBs proliferation induced by TGF-β1, and its mechanism may be involved in inhibiting p38MAPK phosphorylation.

Alkaloids ; pharmacology ; Animals ; Cell Proliferation ; drug effects ; Collagen ; metabolism ; Down-Regulation ; Female ; Fibroblasts ; drug effects ; Heart ; drug effects ; In Vitro Techniques ; Male ; Phosphorylation ; Quinolizines ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Transforming Growth Factor beta1 ; antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases ; antagonists & inhibitors ; metabolism

Objectives:To analyze the statistics of nursing errors of nursing staff in the top three hospital during last year,and the relationship between nursing staff's job satisfaction and job. Methods:From February 2017 to Au-gust 2017,a cluster randomized sampling method was used to select 320 cases of standard nursing staff in the top three hospitals. The questionnaires for general information, questionnaires for nursing job errors, job satisfaction questionnaire,and job burnout survey questionnaire for nursing staff were used to investigate and analyze,and to ex-plore the relevance of nursing work errors, job satisfaction and job burnout. Results:The incidence of nursing error rate was 65.61%. Statistical analysis shows that the occurrence of nursing work errors was related to job satisfaction and job burnout. Among them, nursing staff's personal sense of achievement, personality and overload work, work not recognized, lack of management, unclear responsibility, and low welfare benefits easily led to nursing errors. Conclusions:Based on the impact of job satisfaction and job burnout on the work of nursing staff,improving the nurs-ing staff satisfaction,alleviating the job burnout would reduce the occurrence of nursing errors through the optimiza-tion of scheduling,welfare,management communication and other development opportunities.

OBJECTIVESTo investigate the mechanical properties of bilateral atlantoaxial trans-articular screws and atlas laminar hooks instrumentation with finite element method.

METHODSThere was a volunteer with age of 28 years old, body height 172 cm, body weight of 60 kg and without cervical deformity by X rays. The ligamentous, nonlinear, three-dimensional finite element models of normal upper cervical spine (C0-3) was developed and validated. The destabilized model with bilateral atlantoaxial trans-articular screws and atlas laminar hooks was evaluated for quasistatic loading.

RESULTSThe finite element model of upper cervical spine consists of 229,047 nodes and 152,475 elements, and correlated well with experimental data for all load cases and could be used for experiment. The finite model with bilateral atlantoaxial trans-articular screws and atlas-laminar hooks predicted that the maximum Von Mises Stress was in the region in which screws penetrated the atlantoaxial articular facet. The novel instrumentation resulted in sufficient stability.

CONCLUSIONThe bilateral atlantoaxial trans-articular screws and atlas laminar hooks instrumentation is useful and effective for atlantoaxial arthrodesis.

Atlanto-Axial Joint ; surgery ; Biomechanical Phenomena ; Bone Screws ; Cervical Vertebrae ; diagnostic imaging ; Finite Element Analysis ; Humans ; Imaging, Three-Dimensional ; Internal Fixators ; Joint Instability ; surgery ; Male ; Radiography ; Spinal Fusion ; instrumentation ; methods

BACKGROUNDPulmonary artery smooth muscle cell (PASMC) proliferation plays an important role in pulmonary vessel structural remodelling. At present, the mechanisms related to proliferation of PASMCs are not clear. Focal adhesion kinase (FAK) is a widely expressed nonreceptor protein tyrosine kinase. Recent research indicates that FAK is implicated in signalling pathways which regulate cytoskeletal organization, adhesion, migration, survival and proliferation of cells. Furthermore, there are no reports about the role of FAK in human pulmonary artery smooth muscle cells (HPASMCs). We investigated whether FAK takes part in the intracellular signalling pathway involved in HPASMCs proliferation and apoptosis, by using antisense oligodeoxynucleotides (ODNs) to selectively suppress the expression of FAK protein.

METHODSCultured HPASMCs stimulated by fibronectin (40 microg/ml) were passively transfected with ODNs, sense FAK, mismatch sense and antisense-FAK respectively. Expression of FAK, Jun NH2-terminal kinase (JNK), cyclin-dependent kinase 2 (CDK 2) and caspase-3 proteins were detected by immunoprecipitation and Western blots. Cell cycle and cell apoptosis were analysed by flow cytometry. In addition, cytoplasmic FAK expression was detected by immunocytochemical staining.

RESULTSWhen compared with mismatch sense group, the protein expressions of FAK, JNK and CDK 2 in HPASMCs decreased in antisense-FAK ODNs group and increased in sense-FAK ODNs group significantly. Caspase-3 expression upregulated in HPASMCs when treated with antisense ODNs and downregulated when treated with sense ODNs. When compared with mismatch sense ODNs group, the proportion of cells at G1 phase decreased significantly in sense ODNs group, while the proportion of cells at S phase increased significantly. In contrast, compared with mismatch sense ODNs group, the proportion of cells at G1 phase was increased significantly in antisense-FAK ODNs group. The level of cell apoptosis in antisense-FAK group was higher than in the mismatch sense group and the latter was higher than sense-FAK group. In addition, the sense-FAK ODNs group was strongly stained by immunocytochemistry, whereas the antisense-FAK ODNs group was weakly stained.

CONCLUSIONSThe results suggest that FAK relates to the proliferation of HPASMCs. Antisense-FAK ODNs inhibit HPASMCs proliferation and facilitate their apoptosis. It is possible that FAK via JNK, CDK 2 signalling pathways enhances HPASMCs proliferation and via caspase-3 inhibits HPASMCs apoptosis.

Apoptosis ; CDC2-CDC28 Kinases ; analysis ; Caspase 3 ; Caspases ; analysis ; Cell Cycle ; Cell Proliferation ; drug effects ; Cells, Cultured ; Cyclin-Dependent Kinase 2 ; Focal Adhesion Kinase 1 ; Focal Adhesion Protein-Tyrosine Kinases ; Humans ; Immunohistochemistry ; JNK Mitogen-Activated Protein Kinases ; analysis ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; physiology ; Oligodeoxyribonucleotides, Antisense ; pharmacology ; Protein-Tyrosine Kinases ; analysis ; physiology ; Pulmonary Artery ; cytology

OBJECTIVETo investigate the clinical characteristics of children with critical hand-foot-mouth disease (HFMD) who were treated with mechanical ventilation and to explore the risk factors for poor prognosis.

METHODSThe clinical data of 63 children with critical HFMD who were admitted to the pediatric intensive care unit between April 2012 and September 2013 and needed mechanical ventilation were retrospectively analyzed.

RESULTSAmong the 63 children, 43 were boys and 20 were girls, and their mean age was 25 ± 18 months, with 81% under 3 years old. The four death cases were all under three years old. Compared with the cured cases, the death cases had a significantly lower mean age (8 ± 3 months vs 25 ± 18 months; P<0.05). Poor peripheral circulation above the elbow or knee joint, pulmonary edema involving at least two thirds of the lung field, and pulmonary hemorrhage were all closely related to death (P<0.01). The death cases and cured cases had significantly different peripheral white blood cell counts, blood lactic acid, and blood glucose (24 ± 11× 10⁹/L vs 12 ± 5×10⁹/L; 6.6 ± 1.8 mmol/L vs 3.6 ± 1.7 mmol/L; 16.4 ± 2.5 mmol/L vs 10.0 ± 3.0 mmol/L). The cases with critical illness score <90 had a significantly higher death risk (P<0.01).

CONCLUSIONSChildren with critical HFMD are mainly under 3 years old. The children face extremely high risk of death when they suffer from poor peripheral circulation above the elbow or knee joint, pulmonary edema involving at least two thirds of the lung field, and pulmonary hemorrhage. Significant increases in peripheral white blood cell counts, blood lactic acid, and blood glucose are risk factors for poor prognosis. Critical illness score is also related to poor prognosis.

Blood Glucose ; analysis ; Child ; Child, Preschool ; Female ; Hand, Foot and Mouth Disease ; blood ; mortality ; therapy ; Humans ; Infant ; Lactic Acid ; blood ; Leukocyte Count ; Male ; Prognosis ; Respiration, Artificial ; Retrospective Studies

Objective:To explore the mechanism of EV71 antagonizing IFN signaling pathway.Methods: RD cells were infected or un-infected with EV71.Then the cells were treated with or without IFN-β.The four groups (the control group,the EV71 group,the IFN-β group,the EV71+IFN-β group) were detected by molecular biology techniques.The expression of interferon stimulated genes (ISGs) were detected by Real-time PCR,while the protein levels of STAT1 and IRF9 were examined by Western blot assay.By preparing the cytosolic and nuclear fractions,the translocation of p-STAT1 was monitored through Western blot assay.Results:Compared with the IFN-β group,the mRNA level of OAS1,MX1 and ISG54 in the EV71+IFN-β group was down regulated by 47%, 50% and 48%,respectively,indicating that EV71 inhibited the expression of ISGs.The results also showed that EV71 did not effect the protein level and phosphorylation of STAT1.Moreover,we found that p-STAT1 was translocated into neuclear in IFN-β group,while p-STAT1 was located in the cytoplasm in the EV71+IFN-β group.And the expression of IRF9 was boviously down regulated in EV71+IFN-β group compared with that in IFN-β group,suggesting that EV71 blocked the expression of IRF9 induced by IFN-β.Conclusion:EV71 inhibited the IFN signaling pathway by downregulating the expression of IRF9 induced by IFN-β.

BACKGROUNDGreat advances have been made in the diagnosis, molecular pathogenesis and treatment of acute lymphoblastic leukemia (ALL) in the past decade. Due to the lack of large population-based studies, the recent trends in the incidence and geographic variations of ALL in Shanghai, China have not been well documented. To better understand the incidence and epidemiological features of ALL in Shanghai, we conducted a retrospective survey based on the database from the Shanghai Center for Disease Control and Prevention (CDC) and the medical records in all large-scale hospitals in Shanghai, especially those 30 major hospitals with hematology department.

METHODSAccording to the data from Shanghai CDC, 544 patients, with a median age of 32 years (ranging 1.2 - 89 years), were diagnosed as de novo ALL from January 1, 2002 to December 31, 2006, and they were followed up until December 31, 2007.

RESULTSThe average annual incidence of ALL in Shanghai was 0.81/100 000. The incidence in men (0.86/100 000) was slightly higher than that in women (0.75/100 000). The age-stratified incidence showed that the incidence was 2.31/100 000 in patients ≥ 17 years old, 0.54/100 000 in those 18 - 34 years old, 0.46/100 000 in those 35 - 59 years old, and 0.94/100 000 in those ≥ 60 years old. Moreover, there were substantial geographic variations in the incidence of ALL, with the incidence in Chongming county, an island in the east of Shanghai city being 0.60/100 000, much lower than those of other districts. Both French-American-British (FAB) and World Health Organization (WHO) classification systems were applied in the present study. Eighty-eight patients were diagnosed as L1 (26.2%), 193 L2 (57.4%), and 55 L3 (16.4%). For 302 patients with immunophenotypic results, 242 were identified as B cell origin (80.1%), 59 as T cell origin (19.5%), and 1 as biphenotype (0.4%). The leukemia cells in 61 patients co-expressed one or two myeloid antigen (20.2%). For 269 patients with cytogenetic results, the incidences of t(9;22) in patients aged < 10, 11 - 17, 18 - 44, 45 - 59 and ≥ 60 years old were 4.2%, 11.4%, 19.2%, 23.1% and 5.3%, respectively.

CONCLUSIONCompared with the previous data, the incidence of ALL is increased in Shanghai, and has a geographic distribution characteristic.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; China ; epidemiology ; Data Collection ; Female ; Humans ; Incidence ; Male ; Middle Aged ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; epidemiology ; Young Adult

OBJECTIVETo investigate the expression of angiotensin converting enzyme 2 (ACE2) and the changes treated with angiotensin converting enzyme inhibitor (ACEI), and its signal transduction pathway.

METHODSAtrial tissues were obtained from 47 patients with RHD undergoing cardiac surgery. The mRNA of ACE2 and ACE were semi-qualified by RT-PCR and normalized to the gene beta-actin. Western blot analysis was employed to examine the expressions of ACE2, ACE, ERK1/2 and phosphorylated ERK (pERK1/2). The atrial tissue angiotensin II (Ang II) content was determined by radioimmunoassay detection.

RESULTSThe expression of ACE2 was significantly decreased (P < 0.05), the expression of ACE and pERK1/2 were significantly increased (P < 0.05), and the level of atrial tissue Ang II was significantly increased in patients with chronic atrial fibrillation group (CAF) compared with sinus rhythm group (SR) (P < 0.05). Compared with CAF patients treated without ACEI, the expression of ACE2 significantly increased (P < 0.01), and the relative activity of ERK1/2 significantly decreased (P < 0.05), whereas the expression of ACE and the level of atrial tissue Ang II remained unchanged in CAF patients treated with ACEI.

CONCLUSIONSThe study suggested that the dysequilibrium of ACE/ACE2 might play an important role in the process of atrial fibrillation, which may be related to the activation of ERK1/2 pathway. The clinical effect of long-term treatment of ACEI maybe associated with elevated ACE2 expression but not ACE expression.

Adult ; Aged ; Angiotensin-Converting Enzyme Inhibitors ; therapeutic use ; Atrial Fibrillation ; drug therapy ; metabolism ; Female ; Heart Atria ; metabolism ; Humans ; Male ; Middle Aged ; Mitogen-Activated Protein Kinase 1 ; metabolism ; Mitogen-Activated Protein Kinase 3 ; metabolism ; Peptidyl-Dipeptidase A ; metabolism ; RNA, Messenger ; metabolism ; Signal Transduction