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

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

Adult ; Anemia, Hemolytic ; Female ; Humans

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

Objective To study the killing effect of focused ultrasound activated-hematoporphyrin on H-22 and its optimum exposure time.Methods The distribution of hematoporphyrin in H-22 cells was measured by a fluorescence photometer,the uhrastructure changes were evaluated at different time with a scanning electron micro- scope after treatment with focused ultrasound at the frequency of 1.43 MHz and intensity of 1.0 W/cm~2, 2.0 W/cm~2,3.0 W/cm~2,respectively,in combination with HpD.Results The concentration of HpD in the H-22 cells reached its peak after being added to H-22 tumor cells for 45 minutes,which will produce the hest anti-tumor effect when activated by ultrasound.Morphological observation showed that HpD alone had a slight influence on H-22 cells;ULtrasound alone showed an anti-tumor effect on tumor cells,which was dosage-dependent.Ultrasound dia- thermy in combination with HpD has more effective in terms of its antitumor effect when compared with uhrasound dia- thermy alone.Conclusion The killing effect on H-22 tumor cells of sonodynamic treatment was dependent on the intensity of uhrasound and the content of HpD in the cells,as well as on the time of action of both uhrasound and HpD.

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 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.