0.05). In active SLE, the CD3~+HLA-DR~+, CD4~+HLA-DR~+ and CD8~+ HLA-DR~+ cells of BM were all higher than those of peripheral blood in the control group(P

Animals ; Brain Injuries ; blood ; cerebrospinal fluid ; chemically induced ; Endotoxins ; toxicity ; Female ; Male ; Natriuretic Peptide, C-Type ; analysis ; Neurotensin ; analysis ; Rabbits

Child, Preschool ; Female ; Hand, Foot and Mouth Disease ; complications ; diagnosis ; therapy ; Humans ; Infant ; Male ; Pulmonary Edema ; etiology ; Radiography, Thoracic

Objective To study the possible relationship between the psychological health of children with hematuria and their mothers.Methods Sixty children with hematuria were tested with podiatric symptom checklist(PSC),and the findings were compared with 60 healthy children.The mothers of the patients were assessed by self-rating anxiety scale(SAS),compared with the mothers of healthy children.Results The scores of PSC in patients were higher than those in healthy children(P

Objective It was reported that pretreatment with small dose of lipopolysaccharide (LPS) could protect the animal from lethal dose endotoxin. The purpose of this study was to investigate the effects of pretreatment with small dose of LPS on cardiac function in endotoxemic rats and the possible mechanism. Methods Sixty male Wistar rats weighing 200-280 g were randomly divided into 3 groups: group I normal saline(NS) ( n = 12); group Ⅱ LPS (n = 24) and group Ⅲ LPS-pretreatment ( n = 24). Group Ⅱ and group Ⅲ were further divided into 3 groups: 2 h,4 h and 6 h subgroups based the time when blood sample was taken and the animal was sacrificed. The table shows the LPS given in the 3 groups:groupⅠⅡ Ⅲ0hNSNSLPS 0.25 mg?kg-1ip24 hNSNSLPS0.5mg?kg-1ip96 hNSLPS 10 mg?kg-1 Ⅳ LPS 10 mg?kg-1 TVThe animals were anesthetized with 3 % pentobarbital 30 mg?kg ip and intubated. Right femoral artery and vein were cannulated for MAP monitoring and fluid infusion. Cardiac catheter was placed in the left ventricle for measurement of left ventricular systolic pressure (LVSP) and?dp/dt max. Blood samples were taken 2 h,4 h and 6 h after intravenous LPS (10 mg?kg-1) for determination of plasma levels of L-lactate-dehydrogenase (LDH) and creatine kinase (CK) . The animals were sacrificed right after blood sampling and the heart was removed for determination of myocardial HSP 70 expression using immuno-histochemical staining. Results LVSP and?dp/dt max gradually decreased 1h after intravenous administration of LPS in group Ⅱ (LPS group); while in group DI (pretreatment group) the cardiac contractility was maintained and LVSP,?dp/dt max did not decrease as compared with the baseline value. Plasma LDH concentration and CK activity increased significantly 4 h and 6 h after intravenous IPS in group Ⅱ . The plasma LDH and CK levels were significantly lower in groupⅢthan those in group Ⅱ ( P

Anesthetics are used extensively in surgeries and related procedures to prevent pain. However, there is some concern regarding neuronal degeneration and cognitive deficits arising from regular anesthetic exposure. Recent studies have indicated that brain-derived neurotrophic factor (BDNF) and cyclic AMP response element-binding protein (CREB) are involved in learning and memory processes. Genistein, a plant-derived isoflavone, has been shown to exhibit neuroprotective effects. The present study was performed to examine the protective effect of genistein against isoflurane-induced neurotoxicity in rats. Neonatal rats were exposed to isoflurane (0.75%, 6 hours) on postnatal day 7 (P7). Separate groups of rat pups were orally administered genistein at doses of 20, 40, or 80 mg/kg body weight from P3 to P15 and then exposed to isoflurane anesthesia on P7. Neuronal apoptosis was detected by TUNEL assay and FluoroJade B staining following isoflurane exposure. Genistein significantly reduced apoptosis in the hippocampus, reduced the expression of proapoptotic factors (Bad, Bax, and cleaved caspase-3), and increased the expression of Bcl-2 and Bcl-xL. RT-PCR analysis revealed enhanced BDNF and TrkB mRNA levels. Genistein effectively upregulated cAMP levels and phosphorylation of CREB and TrkB, leading to activation of cAMP/CREB-BDNF-TrkB signaling. PI3K/Akt signaling was also significantly activated. Genistein administration improved general behavior and enhanced learning and memory in the rats. These observations suggest that genistein exerts neuroprotective effects by suppressing isoflurane-induced neuronal apoptosis and by activating cAMP/CREB-BDNF-TrkB-PI3/Akt signaling.
Anesthesia ; Anesthetics ; Animals ; Apoptosis ; Body Weight ; Brain-Derived Neurotrophic Factor ; Cognition Disorders ; Cyclic AMP Response Element-Binding Protein ; Genistein* ; Hippocampus ; In Situ Nick-End Labeling ; Isoflurane ; Learning ; Memory* ; Neurons ; Neuroprotective Agents ; Phosphatidylinositol 3-Kinase ; Phosphorylation ; Rats ; RNA, Messenger ; Spatial Learning*

Objective:To compare the two-dimensional electrophoresis(2-DE) maps of rat spinal cord protein extracted by two different solution systems.Methods: Adult rat spinal cord protein was precipitated with 10% trichloracetic acid in acetone and resuspended in 8 mol/L urea plus 4%CHAPS (A solution) or, 5 mol/L urea, 2 mol/L thiourea, 2%CHAPS plus 2%SB3-10 (B solution). One hundred and fifty micrograms of protein was loaded on 18 cm IPG strip holder and run isoelectric focusing electrophoresis as the first dimension, then horizontal SDS-PAGE as the second dimension. Protein spots were visualized by silver stain.Results:There were 1 059 and 1 023 protein spots in each map, of which 790 spots were matched in two maps. There were 269 and 233 spots exclusively extracted by A and B solutions, respectively. Taken together, 1292 different spots were totally obtained by A and B solutions.Conclusion: Integrating protein spots extracted by different solution systems is beneficial for achieving intact 2-DE map of tissues.

AIM AND METHODSTo study the roles of carbon monoxide on hypoxic pulmonary vasoconstriction (HPV) by investigating the effects of exogenous carbon monoxide and heme oxygenase inhibitor ZnPPIX on hypoxic vasoconstriction reaction of isolated rat pulmonary arterial rings (PAR).

RESULTSHypoxia caused constriction in PAR preconstricted by PE. Both ZnPPIX and carbon monoxide inhibited hypoxic pulmonary constriction significantly by increasing the cGMP level after hypoxia.

CONCLUSIONZnPPIX and exogenous carbon monoxide can inhibit HPV. The reduction of cGMP induced by the decreased of CO may be one of reasons of HPV.

Animals ; Carbon Monoxide ; physiology ; Hypoxia ; In Vitro Techniques ; Male ; Pulmonary Artery ; physiology ; Rats ; Rats, Wistar ; Vasoconstriction ; physiology

OBJECTIVETo investigate regulation function of anodonta glucan HBP-A on chondrocytes through Wnt pathway in vitro.

METHODSRat chondrocytes were cultured and differentiated induced with IL-1beta (10 ng/ml) in vitro. Chondrocytes were divided into five groups:IL-13 group,IL-1beta + IWP-2 (5 microM,Wnt pathway inhibitor) group, IL-1beta + HBP-A (0.3 mg/ml) group and IL-1beta + IWP-2 + HBP-A group. Wnt-3a, beta-catenin (24 h,48 h,72 h) and MMP-13(72 h) genes expression were detected by Rt-PCR, while beta-catenin, MMP-13, Sox-9 and coll-II (48 h) protein expression were measured by Western-blot.

RESULTSAfter induction of IL-1beta, gene expression of Wnt-3a, beta-catenin and MMP-13 were increased,so were the protein expression of beta-catenin and MMP-13. In contrast,protein expression of Sox-9 and Coll-II were declined. Following addition of HBP-A, Wnt-3a, beta-catenin and MMP-13 were shown as induction of IL-1beta, but protein expression of Sox-9 and Coll-II were upgraded. Combining HBP-A with IWP-2 led to the lowest level in Wnt-3a, beta-catenin gene and beta-catenin protein expression and highest expression of Sox-9 protein.

CONCLUSIONHBP-A could not only delay the differentiation of chondrocytes through downgrading the signal expression of Wnt/beta-catenin,but also adjust the expression of Wnt-3a, beta-catenin and Sox-9 when combinated with the Wnt inhibitor.

Animals ; Anodonta ; chemistry ; Cell Differentiation ; drug effects ; Cells, Cultured ; Chondrocytes ; cytology ; drug effects ; metabolism ; Glucans ; pharmacology ; Interleukin-1beta ; metabolism ; Rats ; Wnt Signaling Pathway ; drug effects ; Wnt3A Protein ; genetics ; metabolism ; beta Catenin ; metabolism

The present study investigates the vasodilative action of carbon monoxide on rat pulmonary artery in vitro. After isolation of the pulmonary artery rings (PAR) from Wistar rats, an ACh concentration-response curve was generated; the PARs were incubated with the NOS inhibitor L-NAME (30 micromol/L, n=10) or the heme oxygenase inhibitor ZnPPIX (10 micromol/L)+L-NAME (30 micromol/L, n=10) for 30 min. After that, a second ACh concentration-response curve was elicited. Other isolated PARs were randomly divided into two groups: endothelium-intact group (n=8) and endothelium-denuded group (n=8). The effect of exogenous carbon monoxide (CO) on pulmonary arterial vessel tone was observed. The results showed that ACh induced a concentration-dependent pulmonary vasorelaxation. This relaxation disappeared after endothelium was denuded. The ACh induced relaxation was attenuated after pretreatment with 30 micromol/L L-NAME, and attenuated further after pretreatment with 10 micromol/L ZnPPIX+30 micromol/L L-NAME. Exogenous carbon monoxide relaxed pulmonary artery in both the endothelium-intact group and the endothelium-denuded group. These data suggest that ZnPPIX inhibits ACh induced endothelium-dependent pulmonary artery relaxation and that CO is an endothelium-derived relaxation factor, and exogenous CO can relax pulmonary artery.
Acetylcholine ; pharmacology ; Animals ; Carbon Monoxide ; pharmacology ; Dose-Response Relationship, Drug ; Endothelium, Vascular ; drug effects ; Heme Oxygenase (Decyclizing) ; antagonists & inhibitors ; In Vitro Techniques ; NG-Nitroarginine Methyl Ester ; pharmacology ; Nitric Oxide Synthase ; antagonists & inhibitors ; Protoporphyrins ; pharmacology ; Pulmonary Artery ; drug effects ; Rats ; Rats, Wistar ; Vasodilation ; drug effects