In order to determine whether the cAMP is a central madiator and participates in the mechanism of the ET-induced fever, in the following experiments, we have compared the cAMP levels in csf, plasma to the cAMP levels in tissues of hypothalamus, brain-stem and brain-cortex during the ET-induced fever. The results obtained demonstrate: the cAMP Ievels in tissues of hypothalamus and in csf are increased markedly during the fever Compared with the normal control. These changes of the cAMP levels are paralleled and correlated apparently with the body temperature. However, there isn't any obvious change of the cAMP levels in the tissues of brain-stem, brain-cortex and in plasma during the fever. This demonstrats that the cAMP increased in csf may indirectly reflect cAMP level in hypothalamus during the fever in rabbits and the main source of cAMP increased in csf may be synthesized and released by hypothalamus.

This paper showed that levels of cAMP, PGE_2 in plasma and cAMP in spleen tissue and abdominal cavity macrophages in burned rats are increased (cAMP levels in plasma of the control groups were 24.65?4.59pmol/ml; PGE_2 levels were 309.38?77.64Pg/ml. cAMP levels in plasma of burned groups were 36.58?2.74pmol/ml: PGE_2 levels were 937.50+102.91Pg/ml; P

The purpose of this study was to investigate the effects of gypsum on LP-induced fever and the CSF levels of cAMP and cGMP in rabbits. It was found that gypsum could inhibit the rise of body temperature caused by LP injection, (△T of gypsum +LP group is 0.40?0.08℃, TRI_3 2.55; LP group 0.91?0.06℃, TRI_3 4.99 P

AIM: To investigate the anti-apoptotic effect of nerve growth factor (NGF) on PC12 cells and to observe the mechanism of signal transduction of JNK pathway. METHODS: PC12 cells were treated with 6-hydroxydopamine (6-OHDA) to induce cell apoptosis. NGF and SP600125, the c-Jun N-terminal kinase inhibitors, were added respectively in order to study the relationship between the activity of c-Jun N-terminal kinase and apoptosis of PC12 cells. The cells were divided into control group, 6- OHDA group, NGF group, 6-OHDA plus NGF group, NGF plus SP600125 group. The apoptotic rates of PC12 cells with different treatments were detected by flow cytometry and activities of JNK in PC12 cells were determined by Western blotting. RESULTS: 6-OHDA increased the apoptotic rate and activity of JNK1 in PC12 cells. Incubation with SP600125 or NGF for 15 min before adding 6-OHDA decreased the apoptotic rate of PC12 cells and activity of JNK1 in PC12 cells.CONCLUSION: Activity of JNK is involved in the pro-apoptotic effect of 6-OHDA on PC12 cells. Anti-apoptotic effect of NGF on PC12 cells affected by 6-OHDA is related to the decrease in the activity of JNK1.

When the fever was induced by leukocytic pyrogen(LP)on rabbits, we observed the effects of acupuncture on the main point of "Du Channel". At the same time measured the changes of cAMP and cGMP levels in CSF of the animals.It was found that cAMP levels increased (cAMP levels of normal group 18.60?1.56 pmol/ml and experimental group 25.30?1.14pmol/ml,P

AIM: To investigate the role of NF-κB in diabetic neuropathy.METHODS: The diabetic rats were induced by intraperitoneal injection of streptozocin ( STZ) .The pain behavior test was used to detect the mechanical and thermal withdraw threshold of the rats’ bilateral hind paws.The protein levels of p-NF-κB and t-NF-κB in the rats’ L4 and L5 dorsal root ganglions ( DRG) were determined by Western blotting.The expression of Nav1.7 in DRG of diabetic neuropathy rats with or without NF-κB inhibitor PDTC was detected by the method of immunohistochemistry.RESULTS:The mechanical and thermal withdraw threshold of bilateral hind paws in the diabetic rats was decreased from 4 weeks to 12 weeks after injection of STZ.The protein levels of p-NF-κB in L4 and L5 DRG were significantly increased in the rats with diabetic neuropathy.Intrathecal administration of NF-κB inhibitor PDTC attenuated the increase in p-NF-κB and Nav1.7 in L4 and L5 DRG.Pain behaviors were also alleviated by PDTC.CONCLUSION:The increase in p-NF-κB is closely rela-ted to the generation of diabetic neuropathy.Inhibition of NF-κB blocks pain behaviors and the over-expression of Nav1.7 in DRG.

BACKGROUND:Tai Chi exercise can relieve the decreasing lung function and increase exercise tolerance in patients with chronic obstructive pulmonary disease, but some studies found that Tai Chi exercise did not achieve the desired improvement effect in patients. OBJECTIVE:To objectively evaluate the rehabilitation effects in lung function and exercise endurance of Tai Chi exercise on old patients with stable chronic obstructive pulmonary disease. METHODS:A computer-based online retrieval of PubMed, EMBASE, Web of Science, The Cochrane Library, CNKI, VIP and WanFang databases between January 1980 and July 2014 were searched. Randomized control ed trials of Tai Chi intervening in old patients with chronic obstructive pulmonary disease were col ected, including Tai Chi exercise intervention group and drug or physical education control group. RESULTS AND CONCLUSION:A total of 6 randomized control ed trials were included, with 406 patients. The results of Meta-analyses showed that, compared with the control group, Tai Chi exercise obviously improved the percentage of forced expiratory volume in one second/forced vital capacity (MD=4.62, 95%CI:0.73-8.51, P=0.02), the percentage of forced expiratory volume in one second to the prediction value (MD=4.95, 95%CI:0.33-9.57, P=0.04) and 6-minutes walking distance (MD=33.81, 95%CI:6.00-61.62, P=0.02) in patients with chronic obstructive pulmonary disease. Forced expiratory volume in one second showed no significant difference between Tai Chi exercise intervention group and control group (MD=0.02, 95%CI:-0.10, 0.14, P=0.76). Tai Chi exercise could improve the lung function and exercise endurance in old patients with stable chronic obstructive pulmonary disease, and has positive rehabilitation effects.

AIM:To observe the effects of Sini decoction against pulmonary injury induced by ex vivo ischemia-reperfusion in rats. METHODS: The model of ischemia-reperfusion was established. Twenty-four Sprague-Dawley rats were randomly divided into Sham, I/R, and SND groups. Wet to dry lung weight ratio (W/D), mean pulmonary artery pressure (MPAP), SOD activity and MDA contents in pulmonary perfusate and tissue, NOS activity and NO contents in pulmonary tissue were detected. The pathologic changes in pulmonary tissue were also observed by light microscope. RESULTS: The morphological changes of pulmonary injury were alleviated in SND group. Wet/dry ratio, MPAP and MDA contents in pulmonary perfusate and tissue were significantly lower in SND group after ischemic/reperfusion. SOD activity in pulmonary perfusate and tissue, and NO contents in pulmonary tissue were significantly higher in SND group than those in I/R group. No significant difference in NOS activity in pulmonary tissue among three groups was observed. CONCLUSION: These results indicate that SND may have a protective effect on ischemia-reperfusion injured lung by its antioxidant activity and by adjusting NO level.

Objective To investigate the risk factors of severe hemolysis during extracorporeal membrane oxygenation (ECMO). Methods The clinical data of adult patients undergoing ECMO after cardiac surgery admitted to Fuwai Hospital from December 2010 to October 2015 were retrospectively analyzed. Demographic characteristics, renal function, primary disease, operation data, ECMO related data and outcomes were recorded. Patients were divided into normal free hemoglobin (FHB) group (FHB ≤ 500 mg/L) and severe hemolysis group (FHB > 500 mg/L) according to the FHB level during ECMO support. The parameters before and after ECMO support were compared between the two groups. Logistic regression was used to identify the independent risk factors of severe hemolysis. Results A total of 81 patients including 19 patients with severe hemolysis was enrolled, and 62 in normal FHB group. There was no difference in cardiopulmonary bypass (CPB) time, clamping time, lactate level before ECMO, cardiopulmonary resuscitation, intra-aortic balloon pump use and central catheter insertion between two groups. The maximums of serum creatinine (SCr) and FHB levels were higher in severe hemolysis group as compared with those in normal FHB group [maximal SCr (μmol/L): 281.02±164.11 vs. 196.67±87.31, maximal FHB (mg/L): 600 (600, 700) vs. 200 (100, 300)], the incidence of clots in circuit or oxygenator, infection, and hemofiltration in severe hemolysis group was increased [26.3% (5/19) vs. 4.8% (3/62), 31.6% (6/19) vs. 12.9% (8/62), 36.8% (7/19) vs. 14.5% (9/62), all P < 0.1]. As well as outcomes including the rate of site of surgery or intubation bleeding and acute renal failure [ARF, 57.9 % (11/19) vs. 30.6% (19/62), 94.7% (18/19) vs. 41.9% (26/62)], and the survival rate was lowered [10.5% (2/19) vs. 51.6% (32/62), all P < 0.05]. As result of univariate analysis, clots in circuit or oxygenator, infection and hemofiltration were associated with severe hemolysis. It was showed by logistic regression analysis that the clots in circuit or oxygenator was a risk factor of severe hemolysis during ECMO [odds ratio (OR) = 6.262, 95% confidence interval (95%CI) = 1.244-31.515, P = 0.026]. Conclusions The clots in circuit or oxygenator were independent risk factors of severe hemolysis during ECMO. Severe hemolysis can induce the increase of the rate of bleeding in the operation site or intubation and the rate of ARF, and decrease of the survival rate.

Objective To investigate the dynamic expression of the drug resistance protein P-glycoprotein (P-gp) within 72 hours in the pentylenetetrazol (PTZ)-induced status epilepticus (SE) model, and to identify the optimal detection time to inhibit P-gp. Methods mRNA and protein expressions of P-gp in rats hippocampal tissue were detected by using immunohistochemistry , RT-qPCR and Western blot at different time points after modeling (0, 3, 6, 12, 24, 48, 72 h). Results The mean density of P-gp protein in the hippocampus of status epilepticus model was 0.325 1 ± 0.008 2 at 24 h, and was 0.396 3 ± 0.016 8 at 48 h, which were consistently higher than those of the control group (P < 0.05, P < 0.01, respectively). Results of qRT-PCR showed that MDR1a expression was significantly upregulated at 24 h and at 48 h (P < 0.05, P < 0.01, respectively). Western blot assay revealed that P-gp protein was also significantly increased at 48 h after seizures (P < 0.05). Conclusions The upregulation of P-gp after SE peaked at 48 h, which maybe the optimal detection time to detect drug resistant after SE.