In observing temperature changes in 100 cases of art ificial joint replacement,we discovered that the temperature curves p resented a “double peak” phenomenon.Accordingly,we analyzed the reasons for th is phenomenon and dealt with them,improving our nursing quality.

Adult ; Female ; Humans ; Lung Neoplasms ; complications ; microbiology ; Lymphoma ; complications ; microbiology ; Tuberculosis, Pulmonary ; complications

Humans ; Membrane Proteins ; metabolism ; Myelodysplastic Syndromes ; metabolism ; Receptors, Colony-Stimulating Factor ; metabolism ; Signal Transduction

0.05). The level of serum IL-8 and expression of TNF ? in the colonic mucosa decreased at the 7th day ( P

Objective To investigate the signal pathway of platelet activation in acute respiratory distress syndrome (ARDS). Methods Thirty healthy Sprague-Dawley (SD) rats were randomly divided into control group (n = 6) and model group (n = 24). The model of ARDS was reproduced by intravenous injection of oleic acid (0.25 mL/kg), and the rats in control group were injected with the same amount of normal saline. The blood of abdominal aorta was collected at 2, 6, 24, and 72 hours after model reproduction, the platelets were separated, and c-Jun N-terminal kinase phosphorylation (pJNK) levels which was one of major protein kinases in the mitogen-activated protein kinases (MAPKs) signal pathway was determined by Western Blot. The rats were sacrificed, the lung tissues were harvested, and lung coefficient (lung weight/body weight ×100%) and lung wet/dry (W/D) ratio were calculated. Pathological changes in the lung tissue were observed with hematoxylin-eosin (HE) staining in light microscope. Results Comp ared with the control group, platelet pJNK level in ARDS model group was significantly increased at 2 hours after model reproduction (gray value: 0.72±0.09 vs. 0.22±0.01), and peaked at 6 hours (gray value: 0.91±0.03 vs. 0.22±0.01), then it was decreased gradually. It was also significantly higher than that of control group till 72 hours after model reproduction (gray value: 0.39±0.06 vs. 0.22±0.01, all P < 0.05). Lung coefficient and lung W/D ratio in ARDS model group were significantly increased at 2 hours after model reproduction as compared with those of control group [(1.30±0.20)% vs. (0.60±0.10)%, 6.00±0.60 vs. 3.30±0.30], then they were decreased gradually. They were also significantly higher than those of control group till 72 hours after model reproduction [(0.90±0.10)% vs. (0.60±0.10)%, 4.80±0.70 vs. 3.30±0.30, all P < 0.05]. It was showed by light microscopy that lung tissue of rats in the control group had no significant pathological changes. At 2 hours after model reproduction in model group, clearly visible alveolar edema and interstitial edema, interstitial lung infiltration of inflammatory cells, small blood vessels dilation and congestion were found, and the re were a lot of protein exudates. The lesions of lung peaked at 24 hours. At 72 hours, absorption of most of fluid leaking in alveolar, alveolar space narrow, alveolar septum thickening, the reduction of inflammatory cells infiltration, fibrous tissue proliferation, and micro thrombosis formation were found. Conclusion In ARDS, in addition to pathological changes in the lung tissue, platelet activation occurs, and its activation process is related to the priming of JNK signal transduction pathways.

Adult ; Anemia, Hemolytic ; Female ; Humans

Acupuncture Therapy ; Adult ; Aged ; Female ; Gastroesophageal Reflux ; therapy ; Humans ; Male ; Middle Aged ; Treatment Outcome

Dust ; Humans ; Occupational Exposure ; prevention & control ; Pneumoconiosis ; prevention & control

3200 mg?L~(-1)),and could suppress HBeAg and HBsAg secretion and lower the HBV-DNA level cultured in HepG2 2.2.15 cell line in a dose and time-dependent manner.Conclusion Some of the mechanisms of PSP against HSV-1 and HSV-2 may be explained by the considerable inhibition of virus absorption and virus replication in cells.Some of the mechanisms of PSP against HBV may be explained by inhibition of the secretion of HBV-antigen and the replication of HBV-DNA.

Objective:To study the expression of P selectin in the colonic mucosa and on surfaces of platelets in circulation, and determine its association with IL 8 and TNF ? in trinitrobenzene sulphonic acid (TNBS) induced colitis in rat, in order to investigate the effects of P selectin on inflammation and thrombosis in inflammatory bowel disease Methods:TNBS was instilled into the colon of the rats to induce colitis Animals were sacrificed at the 24th hour, the 1st and the 2nd week after production Blood and colonic tissues were obtained P selectin on the platelets were detected by radioimmunoassay IL 8 in serum was detected by ELISA method Expression of P selectin and TNF ? in colonic mucosa were assessed with immunohistochemistry Results:P selectin in mucosa was increased in different time points compared with control group The positive expression was above 50% P selectin on the platelets wasn't increased at the 24th hour, but increased at the 1st and 2nd week (P