The method of flying through the air is a qi-promoting and qi-circulating technique commonly used in clinical acupuncture. It includes four methods: the blue dragon wagging its tail, the white tiger shaking its head, the green turtle probing the cave and the red phoenix winging to the source and functions to circulate bodily meridian qi. The method of flying through the air was firstrecorded in Golden needle Fu. Later and modern doctors developed it on the basis of Golden needle Fu. This article straightens up the historical origin and development of four methods of flying through the air.

Objective To study the effect of the long-term administration of hemocoagulasein vitro and in vivo,whether it may cause hypofibrinogenemia and changes of cytokine interleukin-6(IL-6) expression level which related to fibrinogen synthesis.Methods Totally 50 healthy subjects pooled plasma was chose in vitro experiments,which was divided into 7 groups.After that,added various of dilutions of injection hemocoagulase and incubated at 37 ℃,detected FIB concentration every 12 h.In vivo experiments,80 rats with six-week old were randomly divided into 4 groups:negative control group,high-dose group,middle-dose group,low-dose group,After 3 weeks administration,the serum level of Ⅴfactor,Ⅷ factor,PT,activated partial thromboplastin time (APTT),FIB,IL-6 was detected.Results Hemocoagulase in vitro had a strong role to reduce fibrin,and showed a significant dose-dependent and time-dependent;Hemocoagulase prolonged low-dose use might reduce the concentration of FIB in mice,but theⅤfactor,Ⅷ factor,PT,APTT,TT were not significantly affected.Compared with the negative control group,FIB and IL-6 concentration decreased in high-dose group,middle-dose group,low-dose group and had statistically significant differences (P<0.05);The level of FIB among the groups had statistically significant differences (P<0.05).The APTT of the middle and high dose groups was slightly prolonged,which was significantly different from that of the negative control group (P<0.05).Conclusion Hemocoagulase has a strong effect to reduce the concentration of fibrin,when there is a long-term medication,fibrin concentration of the patient should be closely monitored,hemocoagulase not only directly decomposed fibrin,but also may affect the synthesis of IL-6,the specific mechanism needs further study.

Objective To explore the relationship between serum adiponectin (APN) concentration and insulin resistance(IR) in elderly pregnancy patients(GDM) with gestational diabetes mellitus.Methods Data of 120 cases of elderly pregnancy patients with gestational diabetes mellitus admitted from Jan.2011 to Dec.2016 were retrospective analyzed.The relationship between serum APN concentration and IR was assayed.Healthy subjects and normal pregnancy patients in our Department were taken as the control.Results The concentration of APN was lower while the CysC,BNP,IGF1,IGF2 and IGFIR were higher in elderly pregnancy patients with gestational diabetes mellitus than those in the control group with a significant difference (P＜0.05).At the same time,Spearman analysis results showed that the serum APN was negatively related with IR while CysC,BNP,IGF1,IGF2 and IGFIR were positively related with IR (P＜0.05).Conclusion Theserumconcentrationofadiponectin and visfatin were negatively related with insulin resistance in elderly pregnancy patients with GDM.

Objective: To study the mechanism of inhibitory ef fect of ginsenoside Rg3 on tumor growth. Methods: The chick chor ioallantoic membrane(CAM) test and Lewis lung carcinoma model were used to inves tigate the inhibitory effect of Rg3 on tumor angiogenesis. Results: Rg3(0.1 or 0.5 mmol/L) obviously inhibited angiogenesis in the CAM. Treatmen t with Rg3 in vivo obviously inhibited Lewis lung carcinoma growth with the inhibition ratio from 23% to about 47%. We also observed that the angiogenesis in implanted Lewis lung carcinoma tissue decreased obviously after treated wit h Rg3 (5, 10, 20 mg/kg). Conclusion: Rg3 can obviously inhibit t he growth of Lewis lung cancer, the inhibitory effect partially due to the effec t of Rg3 inhibiting neovascularization induced by malignant tumor.

Purpose To Investigate the effect of diet-induced hyperchole sterolemia on the kidney ofWistar rats. Methods Male Wistar rats were fed with normal chow supplemented with 5 % cholesteroland observed biochemical changes in plasma lipid concentration, urinary microalbumin excretion, renalfunction, lipid component in renal cortices and morphological changes at 30,60 and 90 days. ResultsTotal plasma cholesterol (TCh) and low density lipoprotein (LDL) concentration were significantly elevatedin the group E (P＜0.05)at 30 days, and progressively increased thereafter, but during the entire study,there ere no differences in plasma urea nitrogen(BUN),creatinine(Cr), and endogenous creatinine clearance(Ccr) between the two groups. Quantitative urinary microalbumin excration was markely elevated in group E( P ＜ 0.05 ). Cholesterol (Ch), phosphatidylcholine(PC) and phosphatidylethanolamine(PE) levels of t he renalcortices were sigificantly increased in the group E at 12 weeks. Progressive development in mesangialhypercellulary, increased mesangial matrix, glomerular capillaries collapes were observed in the group E. Noelectron dense deposits were observed in any of the glomeruli examined. There was a siginificant positivecorrelation for the urinary microalbumin, Ch in the renal corticres, and glomerular size with plasma TCh andLDL concentration. Conclusions The diet-induced hypercholesterolemia may cause lipid nephrotoxicity inWistar rats.

Objective To study the changes in interleukin-32 (IL-32) in rats with Klebsiella bacillus pneumonia and approach its significance. Methods Seventy-two Sprague-Dawley(SD)rats were divide into control group,model group and experimental group by the method of random digits table,then the experimental group was subdivided into 4 hours and 1,3 and 5 days experimental subgroups(each n=6). The rat model of Klebsiella bacillus pneumonia was established by injection of 0.3 mL Klebsiella bacterial suspension into the trachea. Before the establishment of the model in the experimental group,IL-32 inhibitory agent,protease activated receptor-2(PAR2) was injected into the abdominal cavity. After model establishment,at different time points,blood was collected via tail vein to observe the changes in serum levels of IL-32,tumor necrosis factor-α(TNF-α),IL-6 and IL-8 in all the groups. The lungs were removed and stained with hematoxylin-eosin(HE)method to investigate the histopathological changes of the lung tissues under the light microscope. Results Compared to the control group, with the prolongation of time the levels of IL-32,TNF-α,IL-8 and IL-6 were increased gradually in the model group,and reached their peaks at 3 days〔IL-32(ng/L):84.40±28.24 vs. 18.57±3.86,t=5.544,P=0.002;TNF-α(ng/L):79.27±14.64 vs. 17.82±3.86, t=9.994, P=0.000;IL-8(ng/L):55.85±10.90 vs. 16.66±3.76,t=8.544, P=0.000;IL-6(ng/L):56.65±2.57 vs. 28.48±2.11,t=19.693,P=0.000〕;PAR2 could inhibit above indexes significantly,there was statistical difference at 3 days compared with the model group〔IL-32(ng/L):54.13±6.68 vs. 84.40±28.24,t=2.560,P=0.046;TNF-α(ng/L):49.12±3.56 vs. 79.27±14.64,t=4.901,P=0.003;IL-8 (ng/L):22.95±2.52 vs. 55.85±10.90,t=7.204,P=0.000;IL-6(ng/L):36.49±2.63 vs. 56.65±2.57,t=13.443, P=0.000〕. Under the light microscope,the inflammatory changes in the lung tissue in experimental group were milder than those in the model group. Conclusion As a pro-inflammatory cytokine,IL-32 can induce the production of TNF-α,IL-6 and IL-8,and the inhibition of IL-32 production may play a role in suppression of the development of Klebsiella bacillus pneumonia.

Objective Hypertension is a leading modifiable risk factor for cardiovascular disease .However , a lot of hyper-tension patients hold inactive attitudes to hypertension treatment .The purpose of this study was to investigate the relationship between previous treatment of hypertension and stroke severity in acute ischemic stroke . Methods We retrospectively analyzed the clinical data of 653 in-hospital ischemic stroke patients with hypertension between January 2011 and December 2014 .According to the National Institutes of Health Stroke Scale (NIHSS) at admission, the stroke patients were divided into a mild group (NIHSS≤3) and a severe group (NIHSS >3) and, based on their history of hypertension treatment , allocated to a regular treatment, an irregular treatment, a non-treatment , and an unawareness group .We studied the relationship of previous hypertension treatment with stroke severity by Spearman correlation analysis and identified the potential factors associated with stroke severity by multivariate logistic regression anal-ysis. Results Previous treatment of hypertension was positively correlated with stroke severity (r=0.146, P=0.000 2).Compared with the patients of the regular treatment group , those in the irregular treatment group (OR: 2.21; 95%CI:1.39 -3.52; P =0.001), non-treatment group ( OR: 2.18; 95%CI: 1.41 -3.36; P =0.0004) and unawareness group (OR:1.80;95%CI:1.12-2.88; P=0.015) tended to have more severe stroke. Conclusion Previous treatment of hypertension is closely related to the severity of ischemic stroke .

Objective To explore the effects and mechanisms of prenatal hypoxia on vasomotor functions of fetal rats.Methods Sixteen pregnant Sprague-Dawley rats were randomly divided into two groups:control and hypoxia groups (eight in each group).Rats in the hypoxia group were provided with 10.5％ of oxygen from gestation day 5 to 21,while those in the control group were exposed to normoxic condition.Fetuses were removed from the pregnant rats by cesarean section on gestational day 21.Fetal body weight,blood gas and electrolyte levels were measured.Thoracic aorta rings were separated from fetal rats and used in different vascular function tests.Effects of hypoxia during pregnancy on angiotensin Ⅱ (Ang Ⅱ)-mediated vasoconstrictions and acetylcholine (Ach)-mediated vasodilatations in fetal thoracic aortas were measured.Changes in vasomotor functions were observed after both endothelial nitric oxide synthase (eNOS) inhibitor NG-nitro-L-arginine methyl ester (L-Name) and L-type calcium channel (LTCC) inhibitor nifedipine were administered.T-test and two-way analysis of variance were used for statistical analysis.Results (1) Compared with the control group,fetal body weight [(4.40±0.23) vs (3.33±0.42) g,t=2.871],blood partial pressure of oxygen [(50.64±2.17) vs (42.50-±-2.32) mmHg (1 mmHg=0.133 kPa),t=-2.618] and blood oxygen saturation [(58.95±1.97)％ vs (47.73±2.24)％,t=3.564] in the hypoxia group were significantly reduced (all P＜0.05).(2) Compared with the control group,Ang Ⅱ-mediated vasoconstrictions increased,but Ach-mediated vasodilatations in fetal thoracic aortas decreased in the hypoxia group (both P＜0.05).L Name induced stronger Ang Ⅱ-mediated contractions in thoracic aortas in the control group than that in the hypoxia group (P＜0.05).However,nifedipine decreased Ang Ⅱ-induced contractions,especially in the hypoxia group (P＜0.05).Conclusions Maternal hypoxia during pregnancy not only affects the growth and development of fetuses but also changes their blood vessel functions,which may be related to the change of LTCC and the impairment of eNOS.

Objective To investigate the roles of SENP1 in regulation of biological characteristics of NK cells.Methods Lentivirus-mediated-Senp1-small-hairpinRNA (shRNA) transduction was applied to NK92 cells.The expression of SENP1 in NK92 cells was determined by real-time PCR and Western blot.The proliferation of NK92 cells was detected by CCK-8 assay.The apoptosis of NK92 cells was determined by Annexin Ⅴ and PI labeling.The cytotoxicity of NK92 cells against K562 cells was evaluated by luciferase reporter assay.Results Treatment of NK92 cells with IL-21 resulted in SENP1 upregulation.Lentivirus mediated SENP1 knockdown reduced proliferation and increased apoptosis in NK-92 cells,but SENP1 inhibition had slight impact on the cytotoxic ability of NK92 cells to kill K562 cells.Conclusion SENP1 mediates the regulatory effect of IL-21 on the proliferation and survival of NK92 cells.