Experimcnts showed that the nest of Macrotermes annandalei (Silvestri ) had the activity of relieving co gh, eliminating phlegm, and bacteriostasis. It coild also promote the phagocytosis of macrophages, enhance the transformation of T-cell of lymphocyte and rasiethe ratio of ANAE cell of lymphocyte in mice.

Objective:To discuss the variation of parameters in ambulatory blood pressure for neurally mediated syncope(NMS) in children,and to analyze the diagnostic value of ambulatory blood pressure pattern in children with NMS.Methods: Forty-seven children with NMS [20 males and 27 females,mean age(11.7?2.8) years] who came from Peking University First Hospital from July,2007 to March,2008 were included in the study.Twenty-three healthy children [12 males and 11 females,mean age(11.0?3.2) years] were recruited as control group.And the hemodynamic patterns of NMS were detected.Based on the hemodynamic patterns,they were divided into vasovagal syncope(VVS) group [16 children in total,7 males and 9 females,mean age(11.5?2.8) years] and postural tachycardia syndrome(POTS) group [31 children in total,13 males and 18 females,mean age(11.7?2.9) years].Parameters of children with different hemodynamic patterns in ambulatory blood pressure and diagnostic value of ambulatory blood pressure pattern were analyzed.SPSS 10.0 software was used for the statistical analysis of these data.Results: Mean diastolic pressure of the whole day,mean diastolic pressure in the day-time and mean systolic pressure at night in POTS group were higher than those of the control group,reapectively(P0.05).The systolic pressure differences in the day-time and at night in VVS group and POTS group were lower than those of the control group,respectively(P0.05).The non-spoon pattern rate of fluctuation curve of ambulatory blood pressure in VVS group and POTS group was higher than that of the control group(68.8% vs 17.4%,64.5% vs 17.4%,P0.05).The sensitivity,specificity and diagnostic coincidence of ambulatory blood pressure pattern to NMS was 66.0%,82.6% and 71.4%,respectively.Conclusion: There was autonomic nerve adjustment imbalance in children with NMS.And the diagnostic value of ambulatory blood pressure pattern to children with NMS was high.

Objective To observe the changes of plasma ghrelin in patients with severe sepsis and to explore the correlation of the plasma ghrelin and cytokines with sepsis.Methods Choose the healthy volunteer(n=10)as control group,and measure the plasma ghrelin(by ELISA),TNF-?,IL-1?,PCT(procalcitonin)and CRP at the 1st day,3rd day and 10th day in sepsis group(n=26).Results The plasma ghrelin level in sepsis group increased significantly compared with control group(P

Objective:To investigate the role of endogenous hydrogen sulfide(H2S)in patients with asthma.Methods:Levels of serum H2S,lung function and cell differential count in induced sputum were studied in 44 patients with acute exacerbation of asthma,33 patients with stable asthma and 12 health subjects.Of the 33 patients with stable asthma,3 failed to achieve induced sputum.Results:The serum H2S level was(75.2?13.0)?mol/L in controls(12 cases),(55.8?13.6)?mol/L in patients with stable asthma(33 cases),(57.8?6.3)?mol/L in patients with mild of acute exacerbation asthma(9 cases),(40.8?5.1)?mol/L in that with moderate of acute exacerbation asthma(13 cases),and(31.3?2.9)?mol/L in that with severe of acute exacerbation asthma(22 cases,F=44.592,P

Objective: To determine the role of cross-talk between calcineurin-dependent signal transduction pathway and protein kinase C (PKC), mitogen-activated protein kinase (MAPK) and protein kinase A (PKA) in airway remodeling in asthma. Methods: Male guinea pigs were sensitized with intraperitoneal injections of ovabumin (OVA), then treated with cyclosporin A (CsA,5 mg/kg), an inhibitor of calcineurin, then inhaled OVA for 2 weeks 14 days later. Activities of calcineurin, PKC, MAPK, and PKA were was analyzed by phosphorylation and dephosphorylation. In primary cultures of rat airway smooth muscle cells (ASMC), activities of calcineurin, PKC, MAPK, and cross-talk induced by urotensin Ⅱ (UⅡ), a recently identified strong mitogen, were measured. Results: (1) The activities of calcineurin, MAPK and PKC increased by 19% (P0.05). (4) CsA 10 -6 mol/L inhibited UⅡ-stimulated PKC activity by 14% (P0.05). Conclusion:The signal transduction pathways between calcineurin and other protein kinases such as PKC, MAPK and PKA have cross-talk in airway remodeling in asthma.

AIM and METHOD:To determine the production of nitric oxide(NO) and change of NO synthase(NOS) activity in mitochondria isolated from the rat brains of the ischemia/reperfusion rat model produced by transient occlusion of middle cerebral artery on the following the points: 2 h after occlusion of artery and 30 min, 2h, 4h after reperfusion. RESULTS: After the occlusion of middle cerebral artery, the respiratory control rate(RCR) of mitochondria significantly decreased and slightly increased at 4h after reperfusion. Meantime, the production of NO in mitochondria increased significantly. But with the increase of perfusion, production of NO gradually decreased and reached normal level as in the control group. It also shows that cerebral ischemia increased NOS's activity significantly in the mitochondria and still kept a higher level than the control group although it decreased gradually after reperfusion. But the iNOS's activity did not show obvious change. The change of total NOS's activity depends on the change of cNOS's activity. CONCLUSION: The activation of NO/NOS system in the mitochondria might play an important role in the reperfusion injury during reperfusion of ischemic brain.

Objective: To explore the effects of hydrogen sulfide (H 2S) on hypoxic pulmonary vascular smooth muscle cell (VSMC) apoptosis in rats. Methods: Twenty four Wistar rats were divided into 3 groups: control group ( n =8), hypoxia group ( n =8), and hypoxia +NaHS group ( n =8). The plasma level of H 2S was determined by methylene blue spectrophotometric method. VSMC apoptosis was measured by terminal deoxynucleotidyl transferase biotin nick end labeling (TUNEL). The protein expressions of Bcl 2, Fas and caspase 3 in pulmonary arteries were detected by immunohistochemical technique. Results: Compared with rats in the control group, the plasma level of H 2S decreased by 36% in rats of hypoxic group . The apoptotic rate per area in VSMCs detected with TUNEL was significantly decreased by 52.9% in rats of hypoxic group . The expressing integral score of Bcl 2 of VSMCs was increased by 123.9%,while Fas protein expression of VSMCs was decreased by 45% and caspase 3 protein expression of VSMCs was not significantly changed in rats of hypoxia group. But compared with rats in the hypoxia group, the plasma level of H 2S increased by 65% in rats of hypoxia+NaHS group. The apoptotic rate in VSMCs of TUNEL was significantly increased by 62.5% in rats of hypoxia+NaHS group. The Bcl 2 protein expression of VSMCs was decreased by 36.4% in rats of hypoxia+NaHS group. The expressing integral scores of Fas and caspase 3 were significantly higher in rats of hypoxia+NaHS group than in those of hypoxia group. Conclusion: Hypoxia decreased the pulmonary artery smooth muscle cell apoptosis. H 2S inhibited Bcl 2 protein expression of VSMCs and activated Fas and caspase-3 protein expressions of VSMCs, and therefore promoted the pulmonary artery smooth muscle cell apoptosis.

AIM:To study lipopolysaccharide (LPS)-stimulated secretion of endothelin-1 (ET-1) and adrenomedullin (Adm) from human vascular endothelial cells (HVEC) and its mechanism. METHODS:In cultured HVEC, LPS was used to stimulate ET-1 and Adm secretion from HVEC. The contents of ET-1 and Adm in medium were determined by radioimmunoassay. RESULTS:LPS stimulated secretion of ET-1 and Adm from HVEC in time-dependent and concentration-dependent manner. The ratio of secreted ET-1 to Adm was not changed compared with the control group. The increase of ET-1 could be inhibited by inhibitor of extracellular signal-regulated protein kinases (PD098059) and inhibitor of P38 kinase (SB202190)（P＜0.01）, while the increase of Adm could only be inhibited by SB202190（P＜0.05）, both had no response to inhibitor of protein kinase C (H7), inhibitor of calmodulin (W7), inhibitor of calcineurin (cyclosporin A) and inhibitor of Ca2+ (nicardipine)（P＞0.05）.CONCLUSION:ERKs and P38 signal pathways may play an important role in the secretion of ET-1 from LPS -stimulated HVEC, while only P38 kinase signal pathway is invovled in the secretion of Adm.

AIM: To investigate the effect of endothelin (ET), angiotensin II (AngII) and homocysteine (Hcy) on C-type natriuretic peptide (CNP) synthesis and release. METHODS: Human endothelial cell was cultured; CNP was measured by radioimmunoassay method. RESULTS: ET and AngII could augment CNP synthesis in human endothelial cells. Compared with control group, 10-9,10-8,10-7 mol/L ET and Ang II increased CNP content of endothelial cells by 1%(P＞0.05), 49%(P＜0.05),117%(P＜0.01) and 137% (P＜0.01),165%(P＜0.01),201%(P＜0.01),respectively. A great dose of ET and Ang II also stimulated CNP release from cultured human endothelial cells. Hcy had no effect on CNP synthesis, but 10-9，10-8,10-7 mol/L Hcy enhanced CNP release from cultured human endothelial cells by 17%(P＞0.05),84%(P＜0.01) and 555%(P＜0.01), respectively. CONCLUSION: ET, AngII and Hcy might be involved in the synthesis and release of human endothelial cell CNP.

Aim To investigate the effect of urotensin Ⅱ on vascular calcification.Methods Calcified VSMCs of rat in vitro were induced by β-glycerophosphate.Cellular calcium content,ALP activities,~(45)Ca accumulation and osteocalcin content were measured.Results Compared with those of control group,calcium content,ALP activities,~(45)Ca uptake and osteocalcin in calcified VSMCs increased greatly(P<0.01).Calcium content,ALP activities,~(45)Ca uptake and osteocalcin of calcified VSMCs stimulated by urotensin Ⅱ (10~(-10)、10~(-9) and 10~(-8) mol·L~(-1))were greatly increased in a concentration-dependent manner as compared with those of calcified group(P<0.01).Conclusion UrotensinⅡ aggravates the calcification of VSMCs induced by β-glycerophosphate.