Objective To explore the clinical effect of restructuring human brain natriuretic peptide in treatment of heart failure associated with severe acute myocarditis.Methods Fifty cases of heart failure associated with severe acute myocarditis were divided into experimental group and control group according random number table method,each group 25 cases.The patients in control group were given conventional treatment,and the patients in experimental group were given restructuring human brain natriuretic peptide on the basis of conventional treatment.The clinical effects of two groups were observed.Results The level of N terminal brain natriuretic peptide,left ventricular ejection fraction,urine volume,creatinine in two groups had no significant difference before treatment (P ＞ 0.05).After treatment,these index in experimental group were better than those in control group [(7 785 ± 432) ng/L vs.(10 022 ± 447) ng/L,(45.28 ± 2.67)％ vs.(41.34 ±3.11)％,(1 833 ±49) ml/24 h vs.(1 456 ±47) ml/24 h,(109.34 ± 10.77) μmol/L vs.(125.44 ± 11.00) μ mol/L] (P ＜ 0.05).The rate of clinical symptoms improving in experimental group was significantly higher than that in control group [71.4％ (55/77) vs.26.0％ (20/77)] (P ＜0.01).Conclusion Restructuring human brain natriuretic peptide with conventional treatment can effectively improve heart failure associated with severe clinical symptoms of acute myocarditis,improve the clinical therapeutic effect.

OBJECTIVE:To explore the effects of bioactive compounds from entomogenous fungi(BCEF0083)on hip-pocampus neurons and mRNA expression of BDNF in chronic stress depression rat models.METHODS:The selected rats were randomly divided into control group,model group,moclobemide20mg/kg group,and BCEF0083100,50,25mg/kg groups.The change in hippocampus neuron numbers were observed by HE staining and mRNA expression of BDNF was detected with RT-PCR.RESULTS:BCEF0083could increase the neuron numbers and up-regulate the expression of BDNF mRNA in hippocampus.CONCLUSION:The antidepressant effect of BCEF0083in chronic stress depression rat models is probably re-lated to the increase in hippocampus neuron numbers and up-regulation of expression of BDNF mRNA in hippocampus.

Pender′s health promotion model explains the factors influencing health behaviors, which provides a framework for nursing practice and research. Functional exercise compliance in postoperative patients with breast cancer was in a low level, this article reviewed factors influencing functional exercise among breast cancer survivors through three aspects based on health promotion model and made some suggestions on nursing intervention, to promote the rehabilitation of this population.

Objective To investigate the expression of Circulating tumor cells ( CTCs ) in peripheral blood cells of patients with different stages of Small-Cell Lung Cancer ( SCLC) ,and to evaluate its significance in early diagnosis of lung cancer metastasis.Methods Thirty-five patients with SCLC ( 12 in limited stage and 23 in extensive stage ) and 25 patients with benign lung disease were recruited at the Shanghai Changhai Hospital from April 2011 to April 2013.Samples were prepared from 7.5 ml peripheral venous blood and collected in CellSave tubes.The CTC counts were determined using CellTracks AutoPrep fluorescence scanning system according to the manufacturers′instructions.The expression of CTCs in peripheral blood of SCLC patients and benign lung disease patients were analyzed.The expression of CTCs in different stages of SCLC was measured and compared.Furthermore, samples were prepared from 2 ml peripheral venous blood by centrifugation.The serum levels of NSE Neuron specific enolase were measured.The relationship between the expression of CTC and NSE was analyzed.Results CTCs positive rates in SCLC were significantly higher than in benign lung disease controls [ Positive rates of CTC≥1 were 80.0%and 12.0%(χ2 =27.003,P<0.000 1),CTC≥5 were 51.4%and 0 (χ2 =18.367,P<0.000 1), CTC≥10 were 34.3%and 0(χ2 =10.714,P<0.001),CTC≥50 were 17.1 and 0(P=0.036,P<0.05), respectively ].CTCs positive rates in SCLC extensive stage were significantly higher than limited-stage [Positive rates of CTC≥1 were 58.3% and 91.3%(P=0.033,P<0.05), CTC≥5 were 65.2% and 25.0%(P=0.035,P<0.05), respectively].The expression of CTCs was significantly correlated with NSE (r=0.743 7, P<0.000 1).Conclusion The expression of CTC in SCLC patients is significantly higher than those in control group , and is closely related to clinical stages , which may provide new clues to early predicting of SCLC metastasis and deterioration.

Objective To evaluate the role of c-Jun N-terminal kinase (JNK) in lipopolysaccharide (LPS)-induced acute lung injury ( ALI) in rats.Methods Eighty male SD rats weighing 250-300 g were randomly divided into 4 groups ( n = 20 each) : control group (group C) ; ALI group; LPS + SP600125 (JNK inhibitor)group (group S) and LPS+ DMSO (the solvent) group (group DMSO) . ALI was induced by intravenous LPS 5mg/kg. In S and DMSO groups, SP600125 30 mg/kg and DMSO 0.2 ml were injected intravenously after LPS administration respectively. Ten animals were sacrificed by exsanguinafions at 4 h after LPS administration in each group. The broncho-alveolar lavage fluid (BALF) was colleted. The TNF-α and IL-1β concentrations in BALF were measured. The lungs were removed for microscopic examination and determination of W/D lung weight ratio. The other 10 animals in each group were observed for 48 h survival rate. Results Intravenous LPS significantly increased TNF-α and IL-1β concentrations in BALF and W/D lung weight ratio, decreased 48 h survival rate and induced histologic damage. Intravenous SP600125 30 mg/kg significantly attenuated the above-mentioned LPS-induced changes. Conclusion Activation of JNK is involved in the development of endotoxin-induced ALI in rats.

Human enterovirus 71 (EV71) is one of the major etiological agents for the hand, foot, and month disease (HFMD) and is causing frequent, widespread occurrence in the mainland of China. The single positive-stranded RNA genome of EV71 is translated into a single polyprotein which is autocleavaged into structural and nonstructural proteins. The functions of many nonstructural proteins characterized in the life cycle of virus are potential targets for blocking viral replication. This article reviews the studies of the structures and functions of nonstructural proteins of EV71 and the anti-enterovirus 71 drugs targeting on these nonstructural proteins.

Objective To evaluate the role of JNK signal pathway in brain injury after resuscitation in a rat model of asphyxia cardiac arrest.Methods Forty healthy male SD rats 'weighing 300-350 g were randomly divided into 4 groups ( n =10 each):sham operation group (group SH) ; cardiac arrest group (group CA) ; group SP600125-JNK inhibitor (group SP) and dimethyl sulfexide (DMSO) group.The rats were anesthetized with intraperitoneal pentobarbital 45 mg/kg,tracheostomized and mechanically ventilated.PETCO2 was maintained at 35-45 mm Hg.Femoral artery and vein were cannulated for BP monitoring and fluid infusion.Cardiac arrest was induced by clamping tracheal tube until ECG activity disappeared and MAP ＜ 10 mm Hg.Resuscitation was started at 3 min after cardiac arrest.MAP ＞ 60 mm Hg and HR ＞ 250 bpm were considered to be signs of successful resuscitation.SP600125 20 mg/kg and DMSO 0.2 ml were injected iv as soon as chest compression was started in groups SP and DMSO respectively.The animals were sacrificed at 5 h after successful resuscitation and their brains were removed for determination of wet/dry (W/D) weight ratio and microscopic examination of hippocampus.Neuronal apoptosis was detected by TUNEL.Results Cardiac arrest significantly increased W/D ratio and the number of apoptotic cells in group CA.SP600125 iv significantly attenuated the cardiac arrest-induced increase in W/D ratio and the number of apoptotic cells but DMSO did not.Conclusion JNK signal pathway is involved in the brain injury after resuscitation in a rat model of asphyxia cardiac arrest.

OBJECTIVETo observe the mucosal immune mechanism of anti-tumor action of Ganoderma lucidum polysaccharides (GLP).

METHODSThe concentration of H22 cells in suspension were adjusted to 1 x 10(9)/ L, and 0.2 mL of the cell suspension was injected subcutaneously in the right oxter of Kunming mice. Then the H22 bearing mice were randomly divided into 4 groups: the GLP group, the Cytoxan (CTX) group, the CTX + GLP group and the untreated model group, 8 mice in each group. Besides, a blank control group was set up. Starting from the 2nd day of modeling, GLP, at the dose of 1.02 g/kg was given to GLP group and GLP + CTX group by gastrogavage once a day for 12 successive days; CTX at the dose of 100 mg/kg was administered via peritoneal injection to the CTX group and the GLP + CTX group on the 1st day and the 6th day of the experimental course; but to the model group and the blank group, only equal volume of distilled water was given. All mice were sacrificed on the 14th day, the ileum at 1 cm upper to cecum was taken, through 4% paraform fixation and paraffin section, it was used for immunohistochemical detecting expressions of immunoglobulin A (IgA), tumor necrosis factor-alpha (TNF-alpha), interleukin-2 (IL-2) and interleukin-10 (IL-10) in ileum. Besides, the lymphocyte subsets in the intraepithelial lymphocyte (IEL), lamina propria lymphocytes (LPL), and Peyer's patch lymphocytes (PPL) were analyzed by immune fluorescence technique and flow cytometry.

RESULTSCompared with the blank control group, the phenotype of lymphocytes and the expression of cytokines in ileum in the model group changed significantly; and the phenotype was variant in different regions. Compared with the model group, both indexes were adjusted in the GLP, CTX and GLP + CTX group to different degrees.

CONCLUSIONThe adjustment of GLP on intestinal mucosal immune is probably another path for its anti-tumor action.

Animals ; Antineoplastic Agents, Phytogenic ; pharmacology ; Drugs, Chinese Herbal ; pharmacology ; Immunoglobulin A ; metabolism ; Interleukin-2 ; metabolism ; Intestinal Mucosa ; immunology ; Liver Neoplasms, Experimental ; immunology ; Male ; Mice ; Mice, Inbred Strains ; Polysaccharides ; isolation & purification ; pharmacology ; Random Allocation ; Reishi ; chemistry ; Tumor Necrosis Factor-alpha ; metabolism

Objective:To investigate the effects of methylprednisolone(MP)on pneumocyte apoptosis during lung ischemia/reperfusion injury in rats and to study the possible role of MP in pneumocyte apoptosis.Methods:Forty-two male Sprague-Dawley rats used for unilateral lung ischemia/reperfusion model were randomly divided into three groups:sham operation group(Sh group),ischemia/reperfusion group(I/R group),and methylprednisolone group(MP group).Each group has two subgroups of three hours and six hours.Apoptosis rate in lung tissue was detected by the way of Annexin-V-PI in flow cytometer.Expression of I?B-? in lung was observed by immunohistochemical stain.The index of quantitative assessment of histological lung injury(IQA),the wet to dry weight ratio(W/D),the pathological and ultrastructure changes of lung tissue were measured.Results:Apoptosis rate,W/D,IQA of lung tissue were significantly higher in I/R group than which in Sh group(P

Aim To study the antidepressant effects of bioactive compounds from entomogenous fungi(BCEF) in mouse models of depression. Methods The antidepressant effects of Bioactive compounds from entomogenous fungi was examined on the chronic unpredictable stress test, yohimbine induced lethality test, and 5-HTP induced head-twitches test. Results BCEF(50 mg?kg~-1 , ig, qd?21 d)could significantly increase the crossing and rearing score in open-field test. After administration yohimbine 1 h, BCEF 100 mg?kg~-1 group mice mortality rate rising rapidly; BCEF(50,100 mg?kg~-1 ) could distinctly increase the head-twitch number in the 5-HTP induced head-twitches test. Conclusion BCEF has antidepressant effects in depression mouse models. The mechanisms of its antidepressant effects may be related with the reinforcement of central monoamine neurotransmitter especially to 5-HT and NE nerves system.