Objective To investigate the effect and mechanism of Clara cell secretory protein (CC16 ) on lung injury of traumatic shock rats.Methods Thirty SD male rats were randomly assigned to three groups:sham-operation group,control group and CC16-treatment group.The rat model of traumatic shock was used in this study.Rats of sham-operation group were operated,but not treated by depletion and recovery.Rats of control group inhaled the physiological saline before fluid resuscitation.Rats of CC16-treatment group inhaled 0.1 μg/mL of recombinant human Clara cell secretory protein (rh-CCSP)before fluid resuscitation.Arterial blood gas analysis and wet/dry weight were detected in each group.The contents of malondialdehyde (MDA),myeloperoxidase (MPO)of lung tissues and lung tissue pathology changes were also studied. Results Compared with control group,pH and PaO2 value in CC16-treatment group increased significantly.Meanwhile,BE value and lung wet/dry weight ratio also decreased significantly (P<0.05).Compared with control group,contents of MDA and MPO in CC16-treatment group decreased significantly (P<0.05).Lung tissue pathology improved in the CC16 group compared with that of control group (P <0.05 ).Conclusion Inhaled Rh-CCSP may have potential protective effect on lung injury tissues of traumatic shock rats model through its antioxidative effect.

Objective To discuss the effective nursing method of severe erythema multiforma exudativum children patients complicated with bronchopneumonia.Methods Two cases of erythema multiforma exudativum were reviewed,and the nursing methods were summarized,including protective isolation,care of wound surface,care of intravenous infusions,psychological care,oral care,eyes care,perineal care,care of fever,and discharge instructions.Results Two children patients were both cured.Conclusions For severe erythema multiforma exudativum children patients complicated with bronchopneumonia,proper nursing method and careful observation can decrease the complications and help patients to cure quickly.

ObjectiveTo evaluate the role of Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway in attenuation of myocardial ischemia-reperfusion (I/R) injury by tetramethylpyrazine in rats.MethodsSixty-four healthy male Wistar rats weighing 250-300 g were randomly divided into 4 groups( n ＝ 16 each):sham operation group (group S),myocardial I/R group(group I/R),teramethylpyrazine group (group T) and AG,490( a JAK2 inhibitor) group (group AG).Myocardial I/R was induced by 30 min occlusion of left anterior desecending coronary artery (LAD) followed by 120 min reperfusion in groups I/R,T and A.In groups T and A teramethylpyrazine 20 mg/kg was injected iv 20 min before LAD occlusion.In group A AG490 3 tμg/g was injected iv at 5 min before reperfusion.Blood samples were then taken from inferior vena cava at 120 min of reperfusion for measurement of serum creatine phosphokinase (CK) and lactose dehydrogenase (LDH) activities.Myocardial infarct size was then measured and myocardial tissue was obtained for microscopic examination.ResultsSerum CK and LDH activities were significantly higher in group I/R than in group S.Pretreatment with tetramethylpyrazine significantly decreased myocardial infarct size and I/R-induced increase in serum CK and LDH activities and histologic damage.The protective effect of tetramethylpyrazine against myocardial 1/R injury was attenuated by postconditioning with AG490.ConclusionJAK2/STAT3 signaling pathway is involved in attenuation of myocardial I/R injury by tetramethyl pyrazine in rats.

Summary: The effect of rosiglitazone as the ligand of peroxisome proliferator-activated receptorγ (PPARγ) inhibiting the TLR4 expression in ischemic lobes in partial hepatic ischemia/reperfusion injury (IRI) in BABL/C mice and the action of rosiglitazone inhibiting the TLR4 receptor-mediated inherent immune response were investigated. The model of the mouse partial hepatic ischemia/reperfusion injury was established. All the animals were randomly divided into 3 groups: rosiglitazone group, vehicle (dimethylsulphoxide, DMSO) group and sham operation group. The hepatic samples were collected when mice were sacrificed 0, 2, 4 and 6 h after reperfusion following 1h ischemia to analyze the acute phase of hepatic IRJ. The dynamic expression of TIR4 mRNA was detected quantitatively by real-time-PCR, and the levels of TNF-α, IL-10 and ALT in portal vein were determined in all groups. After restoration of blood supply, the expression of TLR4 mRNA in ischemic lobes was detected in 0, 2, 4 and 6h after reperfusion following 1h ischemia in rosiglitazone group and vehicle group. The most intensive expression of TLR4 mRNA was present at 4 h after reperfusion in ischemic lobes in vehicle group. As compared with vehicle group, the expression of TLR4 mRNA in ischemic lobes in rosiglitazone group was significantly decreased at 4h after reperfusion. The level of IL-10 in portal vein was markedly up-regulated in rosiglitazone group as compared with vehicle group. Contrarily, the levels of TNF-α and ALT in portal vein were markedly down-regulated in rosiglitazone group as compared with vehicle group at every time point in mouse partial hepatic IRI model. Rosiglitazone could alleviate the hepatic IRI by inhibiting TLR4 receptor-mediated inherent immune response.