0.05).Conclusions Serum NT-proBNP level is sensitive and specific for the diagnosis of pneumonia complicated with CHF and CHD complicated with CHF. There is an increasing tendency of NT-proBNP level companied increasing pulmonary pressure.

OBJECTIVETo investigate the effects of serotonin (5-HTIA) receptors in the hippocampal dentate gyrus (DG) on active avoidance learning in rats.

METHODSTotally 36 SD rats were randomly divided into control group, antagonist group and agonist group(n = 12). Active avoidance learning ability of rats was assessed by the shuttle box. The extracellular concentrations of 5-HT in the DG during active avoidance conditioned reflex were measured by microdialysis and high performance liquid chromatography (HPLC) techniques. Then the antagonist (WAY-100635) or agonist (8-OH-DPAT) of the 5-HT1A receptors were microinjected into the DG region, and the active avoidance learning was measured.

RESULTS(1) During the active avoidance learning, the concentration of 5-HT in the hippocampal DG was significantly increased in the extinction but not establishment in the conditioned reflex, which reached 164.90% ± 26.07% (P <0.05) of basal level. (2) The microinjection of WAY-100635 (an antagonist of 5-HT1A receptor) into the DG did not significantly affect the active avoidance learning. (3) The microinjection of 8-OH-DPAT(an agonist of 5-HT1A receptor) into the DG significantly facilitated the establishment process and inhibited the extinction process during active avoidance conditioned reflex.

CONCLUSIONThe data suggest that activation of 5-HT1A receptors in hipocampal DG may facilitate active avoidance learning and memory in rats.

8-Hydroxy-2-(di-n-propylamino)tetralin ; pharmacology ; Animals ; Avoidance Learning ; Dentate Gyrus ; physiology ; Piperazines ; pharmacology ; Pyridines ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptor, Serotonin, 5-HT1A ; physiology ; Serotonin ; physiology ; Serotonin Receptor Agonists ; pharmacology

Objective To investigate the clinical significance of procalcitonin(PCT) in early diagnosis of neonatal infections.Methods Rapid hemi-quantitative immunoassay was used to measure PCT levels in 196 hospitalized neonates, who were divided into sepsis group,(local-)infection group, virus-infection group and non-infection group.Results If plasma PCT≥0.5 ?g/L was taken as positive,the positive rates in sepsis group,local-infection,virus-infection,non-infection group were 87.87%,41.66 %,12.0%,11.11%,respectively.The positive rate of sepsis group was significantly higher than that of the other 3 groups(all P

Chemotherapy, Adjuvant ; Gastrectomy ; Humans ; Microsatellite Repeats ; Neoadjuvant Therapy ; Stomach Neoplasms/pathology*

In this study, cardiotonic and cardiotoxic effects of Buthus martensi Karsch (BmK) I, a modulator of voltage-gated sodium channels, were investigated on the isolated rat hearts. The results showed that BmK I evoked complex effects characterized by a change in both cardiac mechanical and electrical activity. Langendorff perfusion showed that: (1) maximal left ventricular developed pressure (LVDP(max)) and dp/dt(max) were markedly increased by BmK I (0.5-10 micromol/L) in a dose-dependent manner (n=6, P<0.05), positive chronotropic effects were also induced by BmK I (n=6, P<0.05); (2) negative inotropic action and bradycardia could be elicited at a larger dose of BmK I (20 micromol/L); (3) the coronary flow varied inversely with the positive inotropic effects, coronary flow reduced during positive inotropic effects from 14.5 to 8.6 ml/min after administration of 500 nmol/L BmK I (n=6, P<0.05). In addition, tachycardia and complex cardiac arrhythmias were induced by BmK I (0.5-10 micromol/L). The modulating of BmK I on the heart mechanical, electrical activity could be partially recovered after washing. As propranolol was applied to block the release of catecholamines before administration of BmK I, suggesting that the changes in cardiac mechanical and electrical activity induced by BmK I might not due to catecholamine release from the nerve terminal and subsequent stimulation of the beta-adrenoceptor but attributable to the modulation of BmK I on cardiac voltage-gated sodium channels.
Action Potentials ; drug effects ; Animals ; Electrophysiology ; In Vitro Techniques ; Insect Proteins ; Male ; Myocardial Contraction ; drug effects ; NAV1.5 Voltage-Gated Sodium Channel ; Neurotoxins ; pharmacology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Scorpion Venoms ; pharmacology ; Sodium Channel Blockers ; pharmacology ; Sodium Channels ; drug effects

Histocytochemistry ; methods ; Humans ; Pathology, Clinical ; methods ; Specimen Handling ; methods ; Staining and Labeling ; methods

Animals ; Brain-Derived Neurotrophic Factor ; metabolism ; Hypothalamus ; metabolism ; Male ; Physical Conditioning, Animal ; physiology ; Rats ; Rats, Sprague-Dawley

Objective To investigate the clinical manifestations and treatment regiment of children with juvenile dermatomyositis(JDM).Methods The clinical manifestation,changes of serum muscale enzyme,myopathic laboratory examination,treatment and prognosis of 15 children with JDM retrospectively admitted from Jan.1990 to Jan.2004 were analyzed.Results All of the children had symmetrical weakness of the proximal muscles.The most frequent features were heliotrope and Gottron's papules.Elevated muscle enzymes were noted in all cases.Electromyography revealed typical change of myopathic type and muscle biopsy was compalible with myositis in all cases.Most of patients achieved normal muscle enzymes within 1 month and had improved muscle strength with 2.5 monthes of the initiation of corticosteroid therapy.Conclusion It is very important to know the clinical features of JDM,and prompt diagnosis and treatment will result in an improved prognosis.

AIMTo investigate the inclusion of coenzyme Q10 with beta-cyclodextrin (beta-CD).

METHODSThe inclusion of the electroactive guest molecule coenzyme Q10 with the host molecule beta-CD was studied by the polarography. The change of the reduction peak current of the inclusion complex with time and the change of the peak potential of the inclusion complex with beta-CD concentration were examined. In order to study the photostability, the change of the reduction peak current of both coenzyme Q10 and coenzyme Q10-beta-CD inclusion complex with time were also examined under light, separately.

RESULTSIn 0.1 mol x L(-1) HAc/NaAc (pH 4.7) buffer-ethanol/water (60:40) medium, coenzyme Q10 was included with p-CD to form an 1:1 inclusion complex. The formation constant Kf was 1.26 x 10(4) L x mol(-1) the apparent formation rate constant was 6.64 x 10(-2) min(-1). The photodegradation apparent rate constant of coenzyme Q10 as 7.77 x 10(-3) min(-1) and that of the coenzyme Q10-beta-CD inclusion complex was 3.38 x 10(-3) min(-1).

CONCLUSIONThe inclusion of coenzyme Q10 with beta-CD took place. The stability of coenzyme Q10 to lights was improved in a certain degree due to the formation of the inclusion complex.

Coenzymes ; chemistry ; Drug Compounding ; methods ; Light ; Oxidation-Reduction ; radiation effects ; Polarography ; methods ; Ubiquinone ; analogs & derivatives ; chemistry ; beta-Cyclodextrins ; chemistry

OBJECTIVETo study the effects of oxaliplatin combined with low-molecular-weight citrus pectin (LCP) on cell proliferation and apoptosis in human colon carcinoma cell line HT29 in vitro.

METHODSEffects of oxaliplatin alone and oxaliplatin combined with LCP on HT29 cells proliferation were determined by MTT. Coefficient of drug interaction (CDI) was calculated. Influence of oxaliplatin alone and oxaliplatin combined with LCP on HT29 cell apoptosis was determined by fluorescence activated cell sorting (FACS). Protein expression change of procaspase-3, 8, 9, PARP was examined by Western blotting.

RESULTSBoth oxaliplatin alone and oxaliplatin combined with LCP could suppress HT29 cell proliferation in both dose- and time-dependent manner. The inhibitory effect of oxaliplatin combined with LCP on HT29 cell proliferation was more significant (P<0.01) with a CDI less than 1. FACS analysis showed that oxaliplatin alone and combination therapy could increase the apoptosis proportion of HT29 cells. After the drug treatment for 6, 24, and 48 hours, the apoptosis rate of oxaliplatin alone group was (9.76±0.47)%, (20.45±0.74)%, (28.70±3.29)%, and apoptotic rate of the combination group was (20.63±0.69)%, (34.35±1.02)%, (49.47±3.04)%, respectively, which was significantly higher as compared to oxaliplatin alone (P<0.01). Both oxaliplatin alone and combination therapy down-regulated expressions of procaspase-3, 9, and PARP protein. Procaspase-3, 9, PARP protein expression in combination group decreased more significantly, while procaspase-8 expression was not significantly different between the two groups.

CONCLUSIONLCP can enhance the ability of oxaliplatin to inhibit cell proliferation and induce apoptosis, which may be associated with the activation of mitochondrial apoptosis pathway.

Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Colonic Neoplasms ; pathology ; HT29 Cells ; Humans ; Organoplatinum Compounds ; pharmacology ; Pectins ; pharmacology