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

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

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

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

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

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

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.

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

OBJECTIVETo observe the effects and mechanisms of endotoxin pretreatment on the rat lung in endotoxemia.

METHODSEighty-four male Wistar rats were divided into seven groups (each group containing 12 rats): saline control and lipopolysaccharide (LPS)-treated 2 h, 4 h, 6 h groups and LPS-pretreated 2 h, 4 h, 6 h groups. LPS-pretreated rats were administrated with intraperitoneal injection of 0.25 mg/kg LPS. After 24 hours, they were injected with 0.5 mg/kg of LPS. Saline control and LPS-treated rats received an equivalent amount of saline. After 72 hours, LPS-treated and LPS-pretreated rats were intravenously injected with 10 mg/kg of LPS. An equivalent amount of saline was injected in the control rats. Blood was drawn from the carotid artery in LPS-treated and LPS-pretreated rats and sacrificed after intravenous injection of LPS 2, 4, 6 hours. Following saline injection of control rats, blood was drawn from the carotid artery after 6 hours. Arterial blood was drawn for blood gas analysis. The lungs were removed for detecting the mRNA levels of intercellular adhesion molecule-1 (ICAM-1) by reverse transcription polymerase chain reaction and the protein levels of inhibitor kappa B-alpha (I kappa B-alpha) by immunohistochemical staining. Bronchoalveolar lavage was performed in the right lung. Cell counts were evaluated with a light microscopy. The supernatant of bronchoalveolar lavage fluid (BALF) was assayed for the level of protein. The whole lung was weighed and the value was used to determine the lung-body index. The tissue was homogenized and centrifuged for the determination of myeloperoxidase enzyme (MPO) activity.

RESULTSThe rats exposed to LPS alone demonstrated an increase in lung-body index, protein in BALF, and MPO activity in the lung tissue. In contrast, the rats exposed to LPS pretreatment exhibited a significant decrease in lung-body index, protein in BALF, and MPO activity. There was a significant decrease in the level of arterial bicarbonate in the LPS-treated rats in comparison with saline-treated and LPS-pretreated animals at 2 hours to 6 hours after LPS administration. The decrease of arterial bicarbonate was compensated by alveolar hyperventilation in LPS-treated animals, with a significant decrease in partial pressure of carbon dioxide. At the same time, partial pressure of oxygen decreased significantly compared with saline control animals and LPS-pretreated animals. LPS-treated rats showed a significant gradually increase in ICAM-1mRNA in the lung in comparison with the saline group. In contrast, ICAM-1mRNA levels in rats pretreated with LPS was lower than that in LPS-treated rats. In LPS-treated animals, LPS caused a decrease of I kappa B-alpha protein expression at 2 hours, returned to control level at 4 hours, and remained at 6 hours. There was no decrease of I kappa B-alpha protein expression in LPS-pretreated animals.

CONCLUSIONThe results in this study showed that administration of a small dose of LPS 72 hours before endotoxemia caused a attenuation effect on lung injury, which may be correlated to I kappa B-alpha expression induced by LPS pretreatment.

Animals ; Carbon Dioxide ; blood ; Endotoxemia ; metabolism ; I-kappa B Proteins ; analysis ; metabolism ; Immunohistochemistry ; Intercellular Adhesion Molecule-1 ; genetics ; Lipopolysaccharides ; pharmacology ; Lung ; metabolism ; pathology ; Male ; NF-KappaB Inhibitor alpha ; Oxygen ; blood ; Peroxidase ; metabolism ; RNA, Messenger ; analysis ; Rats ; Rats, Wistar