Adiponectin (APN) is an insulin sensitizing protein with protective effect secreted by adipose tissue.It has the effects of regulating glucose and lipid metabolism,protecting vascular endothelial function,promoting angiogenesis,and anti-inflammation,etc.It plays an important protective effect in cerebrovascular diseases.This article reviews APN and its effect in ischemic stroke.

Objective To investigate the neuroprotective effect of adiponectin on rats with cerebral ischemic-reperfusion injury and explore its possible mechanism.Methods Sixty-four SD rats were divided into normal group (C) and diabetic group (D) randomly.Type 2 diabetic rats model were made by high-fat diet before the middle cerebral artery occulation model (MCAO) surgery.Each group was divided into two subgroups.CAPNand DAPN groups were given exogenous recombinant globular adiponectin via jugular vein one hour after ischemic-reperfusion injury,C0 and D0 groups were given the same amount of normal saline at the same time.Body weight and blood glucose of the rats were measured before ischemia.We also evaluated the neurological function of rats 24 h after treatment according to Longa criteria and observed the morphological changes of cells in brain area via HE staining.The vascular density in ischemic-reperfusion injury area was detected through 3D confocal image system 2 weeks after the treatment.Results The body weight of diabetic rats was significantly lower than normal rats((284.06 ± 19.85)vs (220.31 ±21.87) g,t =8.634,P =0.000).Blood glucose of diabetic rats before ischemia was significantly higher than normal rats ((4.36±0.13)vs(22.92 ± 1.58) mmol/L,t =11.74,P =0.000).Compared with C0 group,the neurological function score of CAPN group was lower(2.29 ± 0.69 vs 17.0 ± 0.69,t =2.186,P =0.038).Compared with D0 group,the neurological function score of DAPN group was lower(2.89 ± 0.33 vs 2.40 ±0.51,t =2.567,P =0.018),too.HE staining showed that the neuronal injury were milder in CAPN,DAPN group,compared with C0,D0 group,respectively.Adiponectin increased the vascular density of ischemic cortex inC group ((2014.58±61.18)/0.002 mm2 vs(3211.95 ±71.64)/0.002 mm2,t =12.16,P=0.023) and D group ((502.86 ± 30.43)/0.002 mm2 vs (1426.69 ± 97.24)/0.002 mm2,t =25.64,P =0.001).Adiponectin increased the vascular density of ischemic striatum in C group (472.59 ± 4.78)/0.002mm2 vs (736.60 ±104.90) /0.002 mm2,t=7.11,P=0.007) and D group (432.04 ±4.65)/0.002 mm2 vs (1780.75 ± 74.54)/0.002 mm2,t =51.08,P =0.000).Conclusions Adiponectin exerts the neuroprotective effect on cerebral ischemic-reperfusion injury in normal and diabetic rats.And it may protect the brain through promoting angiogenesis.

Objective　To explore the therapeutic effect of treatment of uterine leiomyoma with different dosages of mifepristone and the effects of mifepristone on sex hormones.Methods　The patients of uterine leiomyoma were divided into two groups,group A included 45 patients who were mifepristone orally given neoplasma,25mg per day for 3～6 months,group B included 30 patients who took mifepristone 12.5mg per day for 3～6 months.The size of uterus and uterine leicomyoma were detected with type B sonarography and serum sex hormones level were tested with radioimmunoassay before the treatment.Results　Amenorrhea was found during the treatment of two groups and after tree months' the symptoms were improved,the size of uterine leiomyoma in group A was meanly decreased by 52.56% and 61.69% respectively,after six months' treatment;The size of uterine leiomyoma in group B was averagely decreased by 48.61% after three months' treatment and by 52.12% after six months' treatment.There was no significant difference between A and B group after three months' treatment(P＞0.05),But there was significant difference between the two groups after six months' treatment and it dependent on the time of the treatment.Contents of serum estradiol and progestagen of the two groups were droped dwon significantly after treatment(P＜0.01).Conclusions　Mifepristone applied to treat the uterine leiomyoma have definitve therapeutic effect,and less side effects.Therefore,mifepristone provides a new avenue to treat uterine leiomyoma and suggesting its best dosage is 25mg every day.

Objective: To observe the effect of cooling on systemic and regional oxygen metabolism in febrile critically ill patients. Method: Twenty-five critically ill patients with fever were cooled by ice blankets or by ibuprofen/indomethacin. Oxygen metabolism in whole body and regional organ and hemodynamics were measured. Result: As the temperature was reduced form 38.9?1.1℃ to 37.8?1.5℃,HR,cardiac index (CI),oxygen delivery (DO_2I),and oxygen consumption (VO_2I) decreased significantly,but gastric intramucosal pH increased from 7.26 to 7.37 and the PCO_2 difference between gastric rnucosa and arterial blood decreased markedly. PO_2 and oxygen content in cardiac coronary venous blood and oxygen exrtaction remained unchanged. Conclusion: After cooling the febrile pateints,CI, DO_2I and VO_2I decrease but tissue hypoxia can be improved.

Objective To study the effects of permissive hypercapnia (PHC)on cardiovascular system, oxygen metabolism and gastrointestinal function with acute respiratory distress syndrome(ARDS). Methods In 18 sheep with LPS induced ARDS, hemodynamics, oxygen metabolism and gastrointestinal intramucosal pH(pHi)were observed at different tidal volume(V T).Results PHC was induced by decreasing V T from 16 ml/kg to 4 7ml/kg.Compared with those at V T 16 ml/kg, cardiac index decreased significantly in PHC (P

0 05),But there was significant difference between the two groups after six months' treatment and it dependent on the time of the treatment.Contents of serum estradiol and progestagen of the two groups were droped dwon significantly after treatment(P

Objective To study the effect of endothelial progenitor cells on the behavior of chronic cerebral ischemic rats. Methods Adult rats were treated using the protocol of chronic cerebral ischemic model. Then translated the endothelial progenitor cells in vein to them, and Morris water maze was carried out to test the learning and merrory ability of the rats. The cell proliferation, vascular distribution and the plasma VEGF levels were day of 2nd to 5th of experimental group ( EPC group ) were significantly shorter than the control group ( PBS group), which were(44.45 ±9.44)s,(38.32±1.51)s,(34.95 ±6.76)s,(24.46 ±5.47)s and (52.79±6.47 ) s, ( 43.15 ± 11.21 ) s, ( 50.29 ± 11.41 ) s, ( 53.75 ± 7.35 ) s, (P ＜ 0.01 ) respectively. The time of EPC group spend in the first quadrant were significantly longer than that of the PBS group, which were (26. 76 ±of the EPC group( 26.8 ± 5.76 ) was higher than that of the conrespondering areas in the control group( 12.17 ±ments of capillaries were (P＜0.05) shorter in the PBS groups( (3.4 ±0.24) μm) than in the EPC groups( (2.8± 0.2 )μm) significantly, EPC group could significantly (P ＜ 0.05 ) increased the number of branch points in the boundary regions of ischemia compared with the number in the PBS group (respectively (210. 1 ± 13.80 ) and (164.2 ± 12.3 )). Three-dimensional cerebral vessel surface area in the ipsilateral hemisphere significantly increased in the EPC group compared with the PBS group (respectively (84365 ± 3897 )μm2/0. 002mm3 and group in the plasma VEGF levels ( ( 63.91 ± 6.71 ) pg/ml; ( 21. 81 ± 4.25 ) pg/ml, respectively (P ＜ 0.05, P ＜0.01 ). Conclusion There are positive behavioral effects of endotbelial progenitor cells in chronic cerebral ischemic rats. The possible mechanisns mavbe involve the nerve protection and regeneration of the vascular associated with the VEGF. The endothelial progenitor cells maybe have a great prospect in the therapy of chronic cerebral ischemic disease.

Objective To investigate the effect of autologous bone marrow-derived endothelial progenitor cell (EPC) transplantation on neurological outcomes in cerebral ischernia in rats and its poss le mechanisms.Methods Autologous bone marrow-derived EPC was cultured in vitro and it was labeled with 5-bromodeoxyuridine (BrdU).A middle cerebral artery occlusion (MCAO) model was induced by the intraluminal suture method.The rats in a EPC group transplanted autologous EPC (106/ml/kg) via external jugular veins,those in a control group were injected with phosphate buffered saline (1 ml/kg),and those in a sham operation group (n =15)were not treated.The modified neurological severity score (mNSS) was used to observe the neurological changes of the rats.BrdU immunohistochemical staining was used to evaluate EPC proliferation and differentiation.Three-dimensional confocal image analysis was used to detect the vascular structure and density in cerebral ischemic areas.TUNEL staining was used to detect the apoptotio cells in ischernic brain tissue.Enzyme-linked immunosorbent assay was used to detect the concentration of plasma vascular endothelial growth factor VEGF).Results The mNSS in the EPC group was siginficantly lower than that in the control group (at day 8:6.43 ±0.69 vs.8.86 ±0.95,q =2.673,P=0.035; at day 14:4.55 ±0.89 vs.6.73 ± 1.06,q =5.360,P =0.035).The number of BrdU positive cells in the EPC group was significantly higher than that in the control group (42.2±5.76 vs.25.67±5.49,q=4.020,P=0.030).The capiilary diameter in the EPCgroup was significantly smaller than that in the control group (4.51 ± 0.21 μm vs.6.34 ± 0.24 μm,q =3.980,P =0.003); the density of blood vessels (212.64 ± 8.02/0.002 mm3 vs.153.60 ± 7.21/0.002 mm3; q =9.670,P =0.001 ) and the total surface area of microvessel (92 013 ± 5 132 μm2/0.002 mm3 vs. 71 366 ±4 538 μm2/0.002 mm3; q=4.180,P=0.014) were significantly higher or more than those in the control group.The number of apoptotic cells in the EPC group was significantly less than that in the control group (36.26 ± 6.91 vs.78.34 ± 7.21; t =-4.834,P =0.003).The plasma VEGF concentration in the EPC group was significantly higher than that in the control group (54.91 ± 5.71 pg/ml vs.13.81 ± 4.25 pg/ml,q =12.300,P=0.002).Conclusions Autologous EPC transplantation has a protective effect on ischemic brain tissue in rats.It may be associated with VEGF related angiogenesis and neuroprotection.It has an important application prospect in the treatment of ischemic cerebrovascular disease.

Objective To investigate the correlations of serum adipocyte fatty acid-binding protein (AFABP),adiponectin (APN) and A-FABP/APN ratio with acute ischemic stroke (AIS) and its subtypes.Methods The consecutive patients with AIS (AIS group) of having complete data admitted within 24 hours of onset were enrolled,and at the same time,the healthy subjects of age,sex and body mass index matched with the AIS group were selected as a control group.The demographic characteristics and general clinical data of the AIS group and control group were collected.The serum A-FABP and APN levels were detected by enzymelinked immunosorbent assay.The patients in the AIS group were further divided into large artery atherosclerosis (LAA),small artery occlusion,(SAO),cardioembolism (CE),and stroke of other determined etiology (SOE) according to the TOAST classification criteria.Multivariable logistic regression analysis was used to investigate the relationship between all factors and AIS and its subtypes.Spearman correlation analysis was used to analyze the correlations of the A-FABP and APN levels and the NIHSS scores.Results The serum A-FABP level (P =0.017) and A-FABP/APN ratio (P =0.002) in the AIS group were significantly higher than those in the control group,and the serum APN level was significantly lower than that in the control group (P =0.011).Multivariate logistic regression analysis showed that the increased serum A-FABP level (odds ratio [OR] 1.48,95％ confidence interval [CI] 1.07-1.93; P =0.009) and the A-FABP/APN ratio (OR 1.59,95％ CI 1.10-2.34; P =0.002) as well as the decreased APN level (OR 0.36,95％ CI 0.14-0.65; P =0.011) were independently associated with AIS.And the A-FABP/APN ratio was better than the correlation of both separately.The serum A-FABP level and A-FABP/APN ratio in the LAA,SAO and CE groups were significantly higher than those in other subtype groups (all P ＜0.05),and the APN level was significantly lower than that in other subtype groups (P ＜0.05).Multivariate logistic regression analysis showed that the increased serum A-FABP level and A-FABP/APN ratio as well as the decreased APN level were independently associated with LAA,SAO and CE,and the A-FABP/APN ratio was better than the correlation of both separately.The baseline NIHSS score was positively correlated with the serum A-FABP level (r =0.236,P =0.019),it was negatively correlated with the serum APN level (r =0.307,P =0.002),and the correlation of the serum AFABP/APN ratio was higher than that of A-FABP or APN (r =0.326,P =0.001).Conclusions The increased serum A-FABP level and the decreased APN level may serve as the new risk factors for AIS,especially LAA,SAO and CE subtypes,and they can reflect the severity of AIS.

Objective To explore the effects of granulocyte colony stimulating factor (G-CSF)on chronic cerebral ischemia in rats,and its possible mechanism.Methods Chronic cerebral ischemia (2-VO) model was prepared and bilateral external jugular veins were isolated.A total of 30 rats were divided into 2 groups at random sham group (received no intervention,n=15) and operative group (received G-CSF or PBS through external jugular vein injection,n=15).At 6 weeks after operation,the rats in operative group were divided into G--CSF group (received G-CSF 10 mg/L,1 ml · kg-1 · d-1,1 times every 24 h for,3 times) and PBS control group (received PBS 10 mg/L,1 ml ·kg 1 · d-11,1 times every 24 h for 3 times).At 8 weeks after the operation,morris water maze was carried out to evaluate the learning and memory ability of the rats.The cell proliferation,threedimensional vascular distribution,ischemic neuronal apoptosis,cell morphological changes in ischemic area and the plasma VEGF levels were detected to explore the possible mechanisms.Results In morris water maze,escape latency at the 2rd to 5th day were significantly lower in G-CSF group than the PBS group (all P＜0.05).The swimming time spent in the first quadrant in G-CSF group was significantly longer than the PBS group (P＜0.05).There was a significant difference in the number of BrdU positive cells in the ischemical area between the G-CSF group and the control group [(27.7±4.76) vs.(10.4 ± 3.7),P =0.030).Three-dimensional quantitative measurements of vascular structure showed that the capillary diameters was smaller in the G-CSF group than in the PBS group [(2.90±0.20) μm vs.(3.45±0.26) μm,P=0.020] and the number of branch points in the boundary regions of ischemia had a significant difference in the G-CSF group compared with the control group [(207.82±10.73) /0.002 mm3 vs.(162.10±9.31) /0.002mm3,P=0.005].Threedimensional cerebral vessel surface area in the ipsilateral hemisphere was increased in the G-CSF group compared with the PBS group [(86498±2896) μm2/0.002 mm3vs.(73976±3826) μm2/0.002 mm3,P=0.003].The number of apoptotic cells in G-CSF group was decreased compared with the PBS group [(32.10±6.70) vs.(56.30±11.20),F=11.89,P=0.043].The electron microscope morphological observations showed inflammatory edema in intercellular gap was significantly reduced in the G-CSF group compared with the PBS group.The level of plasma VEGF was significantly increased in the G-CSF group compared with the PBS group [(58.81±6.61) ng/L vs.(20.81±4.35)ng/L,P=0.025].Conclusions G--CSF can improve the learning and memory ability in the chronic cerebral ischemic rats,and its possible mechanism might involve the nerve protection and the vascular regeneration associated with the VEGF.There is a great prospect for G-CSF in the therapy of chronic cerebral ischemic disease.