Objective:To study the size difference of bilateral axillary vein in adults, and to provide basis for the design of interventional surgical treatment.Methods:From December 2017 to December 2018, 145 inpatients (117 cases of hypertension, 28 cases of heart failure) and 87 healthy volunteers were selected from the Second People's Hospital of Lianyungang as study objects.The size of bilateral axillary vein of each study object was measured and the difference was statistically analyzed.Results:Among the 232 subjects, the dominant hand was the right hand, accounting for 95.7% (222/232). There were no statistically significant differences in the size of left and right axillary veins (all P>0.05). There were no statistically significant differences in the other indicators except age between the two groups (all P>0.05). The diameter of axillary vein was (0.67±0.15)cm in male and (0.53±0.13)cm in female, the difference is statistically significant( P=0.000). In the healthy control group, the dominant, non-dominant and large cross-sectional areas were (0.54±0.17)mm 2, (0.54±0.15)mm 2, (0.60±0.16)mm 2, respectively, which in the hypertension group were (0.55±0.14)mm 2, (0.54±0.14)mm 2, (0.59±0.14)mm 2, respectively, which in the heart failure group were (0.54±0.16)mm 2, (0.56±0.19)mm 2, (0.59±0.1)mm 2, respectively, there were no statistically significant differences among the three groups (all P>0.05). Conclusion:The difference is not obvious in the size of bilateral axillary vein, and there is no correlation between the size of bilateral axillary vein and dominant hand.The size of axillary vein in adults of different genders is different, and the size of axillary vein can be estimated by the gender of subjects, but not by the dominant hand or other data.

Objective To investigate the reduce of experimental autoirnmune encephalomyelitis(EAE) susceptivity after lipopolysaccharide (LPS) exposure in neonatal rats and its relation with inhibition of macrophage immune function.Methods Litter male neonatal rats were divided into blank control group (n=1 1),phosphate buffer (PBS) group (n=12) and LPS group (n=12);rats in the LPS group were performed intraperitoneal injection of 50 μL LPS on postpartum day 3 and 5.Rats in the PBS group and LPS group were established EAE models by immune induce of spinal cord homogenate of guinea pig with complete Freund's adjuvant at 12 weeks old,while rats in the blank control group were given immune induce of complete Freund's adjuvant.Since the day of induce,the behavioral scale scores of all the rats were assessed.On the 20th d,all rats were sacrificed and paraffin sections were cut and stained with HE to detect inflammatory cell infiltration.The number of infiltrating macrophages and the expressions of CD86,CD80,MHC-Ⅱ were determined by flow cytometry.The transcriptional levels of C-C chemokine receptor type 2 (CCR2),interleukin (IL)-1β and tumor necrosis factor (TNF)-α in macrophages were determined by real-time fluorogenic quantitative PCR.Results As compared with the PBS group,LPS group had significantly lower EAE incidence (11/12 vs.5/12) and higher EAE latency ([10.50±0.71] d vs.[12.17± 1.17] d),and statistically decreased cumulative clinic scores and peak clinic scores (20.00±9.13 vs.5.58±7.12;2.58±1.08 vs.1.03±0.83,P＜0.05).The inflammation in the spinal cord of the PBS group was severer than that in the LPS group (2.83±0.75 vs.1.17±1.17,P＜0.05).The number of infiltrating macrophages of the PBS group was significantly larger than that in the LPS group ([202.70 ±81.89] × 103 cells vs.[92.58 ±42.65] × 103 cells,P＜0.05).The expressions of CD80 and MHC-Ⅱ,and mRNA levels of CCR2,IL-1β and TNF-α in the PBS group were significantly higher than those in the LPS group (P＜0.05).Conclusion Neonatal LPS exposure reduces the severity of EAE,which may relate to impaired macrophage immune function.

[ ABSTRACT ] AIM: To study the effect of idazoxan on the permeability of inflammatory blood-brain barrier ( BBB) model in vitro and the expression of tight junction protein ZO-1.METHODS:In vitro BBB model was established by murine brain endothelial cell line bEnd.3 incubated for 7 d.The cells were treated with TNF-α(10 nmol/L) for addi-tional 24 h to establish the inflammatory BBB model, which was pretreated with IDA at doses of 50, 100 and 200μmol/L, respectively.The permeability was measured using fluorescein isothiocyanate-conjugated dextran (FD-40, MW 40,000), the expression of ZO-1 was detected by Western blot analysis, the distribution of ZO-1 was observed by immunofluores-cence, and the mRNA expression of MMP-9/TIMP-1 was measured by RT-PCR.RESULTS:After incubated for 7 d, b. End3 cells converged to be confluent monolayer with low permeability.The inflammatory BBB model induced by TNF-αtreatment displayed much higher permeability with decreased expression of tight junction protein ZO-1, destroyed distribu-tion of ZO-1 and increased mRNA expression of MMP-9.When pretreated with IDA, the permeability was greatly de-creased, the expression of ZO-1 was greatly increased, the abnormal distribution of ZO-1 was greatly ameliorated and the mRNA expression of MMP-9 was obviously reduced.The effect was most significant in IDA ( 200 μmol/L )-pretreated group (P<0.01).CONCLUSION:IDA directly acts on brain endothelial cells to reduce the expression of MMP-9, in-crease the expression of tight junction protein ZO-1 and ameliorate the destroyed distribution of ZO-1 in the inflammatory BBB, thus reversing the abnormally elevated permeability in a inflammatory BBB model in vitro induced by TNF-α.

Objective To investigate the effects of valproic acid ( VPA ) on SD rats with experimental autoimmune encephalomyelitis ( EAE) and its possible immunomodulatory mechanism .Meth-ods Fifty female Sprague-Dawley ( SD) rats were randomly divided into five groups by random digit table , including control group (n=10), EAE group(n=10), low dose VPA treated group (100 mg/kg, n=10), median dose VPA treated group (300 mg/kg, n=10) and high dose VPA treated group (600 mg/kg, n=10).The SD rat model of EAE was induced by immunizing with a guinea pigs′spinal cord homogenate (GPSCH).Normal saline and various doses of VPA were given to rats in according groups twice a day from day 0 to day 19 ( close to the peak stage of EAE ) .The severity of EAE was scored according to the signs and symptoms.Pathological changes were observed through Hematoxylin-Eosin staining, and then the degrees of inflammatory infiltration were evaluated .The numbers of activated neuroglia that expressed Iba-1 in cerebral and lumber cords were counted by immunohistochemistry .The expression of IFN-γ, IL-17 and IL-10 in cer-ebral and lumber cords were measured by ELISA .Results Compared with EAE group , rats in the low, me-dian and high dose VPA treated groups had lower incidence of EAE and prolonged latency , but only the me-dian dose treated group showed significant alleviation in clinical symptoms (P<0.05).Both the median and the high dose treated group showed decreased inflammatory cell infiltration in CNS (P<0.05).Immunohisto-chemistry results showed that the numbers of activated microglia were significantly inhibited in rats treated with median and high dose of VPA in comparison with those in EAE group (P<0.05).Results of ELISA demonstrated that the expression of IFN-γand IL-17 in both median and high dose VPA treated groups were significantly decreased compared with those in EAE group (P<0.05), but only the median dose treated group showed a remarkably increased expression of IL-10 (P<0.05).Conclusion VPA, especially medi-um dose of VPA ( 300 mg/kg ) , had neuroprotective effects on rats with EAE .The possible mechanism might be associated with the inhibited activation of microglia and the increased percentage of anti -inflammato-ry cytokines .

[ ABSTRACT] AIM:To study the effect of idazoxan ( IDA) on the permeability of blood-brain barrier ( BBB) and the expression of matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) in mouse ex-perimental autoimmune encephalomyelitis (EAE).METHODS: Female C57BL/6 mice (n=36) were randomly divided into control group, EAE group and IDA group, with 12 mice in each group.EAE was induced by myelin oligodendrocyte glycoprotein 35-55 ( MOG35-55 ) .IDA (2 mg/kg, ip, bid) was administered for 15 d after immunization.The neurological defects of the mice were observed daily and scored.The pathological changes were observed under microscope with HE stai-ning and LFB myelin staining.The BBB permeability was detected by Evans blue extravasation.The expression of MMP-9 and TIMP-1 in the brain of EAE mice was determined by Western blotting.RESULTS: Compared with EAE group, the score of neurological defects in IDA group was decreased, the inflammation was relieved, the BBB permeability was re-duced, and the expression MMP-9 and the ratio of MMP-9/TIMP-1 were decreased ( P<0.05 ) .CONCLUSION: The neuroprotective effect of IDA on mouse EAE might be related to the down-regulation of MMP-9 and the ratio of MMP-9/TIMP-1, thus reducing the degradation of BBB and the permeability of BBB, and ameliorating the pathologic process of EAE.

Objective To investigate the effects of chronic treatment with levamisole (LMS) on imidazoline I2 receptor (I2R) in rats with experimental autoimmune encephalomyelitis (EAE).Methods Thirty female Wistar rats were randomly divided into three groups:control group (n=8),EAE model group (n=10),EAE+LMS treatment group (n=12); the rat models of EAE were induced by immunizing with guinea pigs spinal cord homogenate.Subcutaneous injection of 0.5 mL of normal saline+complete Freund's adjuvant (CFA) emulsion was performed to rats in the control group,and 0 and 24 h after the that,intraperitoneal injection of 0.4 mL of saline twice daily was performed; subcutaneous injection of 0.5 mL of homogenate+CFA emulsion was performed to rats in the EAE model group; subcutaneous injection of 0.5 mL of homogenate+CFA emulsion was performed to rats in the EAE+LMS treatment group,and 0 and 24 hafter the that,intraperitoneal injection of LMS (10 mg/kg) twice daily was performed.The severity of EAE was scored according to the signs and symptoms.Pathological changes were observed through hematoxylin-eosin staining and Luxol-Fast blue dyeing,and the degrees of inflammatory infiltration were evaluated.The maximal binding capacity (Bmax) and dissociation content (Kd) of I2R were measured by radioligand binding assay.Results As compared with rats in the EAE model group,rats in the EAE+LMS treatment group had lower incidence of EAE,alleviated clinical symptoms,prolonged latency and decreased central nervous system inflammation.Radioligand binding assay showed that both the Bmax values and Kd constant of I2R (266.1 ±28.13 fmol/mg and 5.307 ± 1.107) in the EAE model group were increased as compared with those in the control group (177.5±26.10 fmol/mg and 3.586±1.053,respectively),with statistically significant differences (P＜0.05).As compared with those in the EAE model group,the I2R Bmax values in the EAE+LMS treatment group (496.1±52.31 fmol/mg) were markedly increased (P＜0.05),but there were no significantly differences in Kd values of I2R between these two groups (P＞0.05).Conclusion Chronic treatment with LMS has beneficial neuroprotective effect on rats with EAE,and its mechanism might be related to the regulation of I2R.

Objective To explore the immunomodulatory mechanism of 2-(-2-benzofuranyl )-2-imidazoline(2-BFI) in rat model of experimental autoimmune encephalomyelitis (EAE).Methods Fifty fe-male Sprague-Dawley(SD) rats were randomly divided into five groups by random digit table , including con-trol group(n=10), EAE model group(n=10), low dose 2-BFI group(1.5 mg/kg, n=10), median dose 2-BFI group (3 mg/kg, n=10) and high dose 2-BFI group (6 mg/kg, n=10).The SD rat model of EAE was induced by immunizing with a guinea pigs′spinal cord homogenate ( GPSCH ) .The severity of EAE was scored according to the signs and symptoms .Pathological changes were observed through Hematoxylin-eosin staining, and then the degrees of inflammatory infiltration were evaluated .The number of activated neuroglia that expressed GFAP and iba 1 in lumbar cords was counted by immunohistochemistry .The expressions of IL-1β, IFN-γ, IL-4 and IL-10 in cervical cords were measured by ELISA .Results Compared with EAE group, rats in the low, median and high dose 2-BFI treatment group had lower incidence of EAE , prolonged latency and decreased CNS inflammation , but only the median dose group showed significant alleviation in clinical symptoms and decrease in CNS inflammatory cell infiltration (P<0.05).Immunohistochemical re-sults showed that the numbers of activated microglia were significantly inhibited ,but the numbers of activated astroglia were increased in the rats treated with median dose of 2-BFI in comparison with the EAE group ( P<0.05).Results of ELISA demonstrated that expressions of IL-1βand IFN-γin 3 mg/kg 2-BFI treated group were significantly decreased compared with that in the EAE group (P<0.05), but expressions of IL-4 and IL-10 were remarkably increased(P<0.05).Conclusion 2-BFI at median dose of 3 mg/kg has a benefi-cial neuroprotective effect on rats with EAE , and its mechanism might be related to immunodulation .

Objective To investigate the event-based prospective memory (EBPM) and time-based prospective memory (TBPM) in temporal lobe epilepsy patients,and test the hypothcsis that temporal lobe is involved in the prospective memory network. Methods Sixty-two patients with temporal lobe epilepsy (TLE) and 30 age- and education level-matched healthy adults were examed with the neuropsychological battery of tests including EBPM and TRPM tasks. Results In comparison with the controls,the TLE patients were impaired on MMSE,DS and VFT.Compared with the healthy adults ( EBPM:6.83± 1.34,TBPM:5.00 ± 1.70),the patients with temporal lobe epilepsy had a significant loss in EBPM (3.95 ±2.77,t =6.72,P ＜0.01 ) and TBPM (3.08 ±2.42,t =4.39,P ＜0.01).There was no difference in the performance of EBPM (3.82 ± 2.70,4.10 ± 2.90 ; t =- 0.40,P ＞ 0.05 ) and TBPM (2.55 ± 2.20,3.69± 2.55; t =-1.90,P ＞0.05 ) between the patients with taking antiepileptic drugs and those without antiepileptic drugs. Conclusions These results suggest that patients with temporal lobe epilepsy may experience general difficulties with prospective memory.It is possible that temporal lobe is involved in the prospective memory network.The passages of TBPM need more self-initiated processes.

Objective To investigate the relationship between blood pressure(BP) and prognosis in three different ischemic stroke subtypes.Methods The consecutive patients with a brain infarction proven on diffusion-weighted MRI who were hospitalized within 48 hours after stroke onset between April 2007 and April 2008 were registered.All subjects with acute ischemic stroke consecutively admitted to the neurological wards of the First Affiliated Hospital of Wenzhou Medical College,were registered in the Wenzhou Stroke Registry Program.Data were collected and coded at primary registration.The BP levels were studied during the initial 7 hospital days.Survival and dependency were assessed at 3 months.Outcomes were adjusted age,consciousness level,admission NIHSS score,the decline level of systolic BP,the decline level of diastolic BP,complication and so on. Logistic regression model was used to estimate the relationship between BP and prognosis.Results A U-shaped effect was observed in each subgroup between BP and prognosis.In the subgroups of atherothrombosis,cardioembolism and small artery disease,those who had a BP of 150/95 mm Hg(1 mm Hg=0.133 kPa)on admission,140/90 mm Hg on day 1-7 would have a better prognosis.In the subgroups of atherothrombosis and cardioembolism,the decrease of BP during the first 24 hours was the independent predictor of the death and disability at 3-month.In the atherothrombosis group,when the decrease of systolic BP during the first 24 hours was greater than 20 mm Hg,the risk of the death and disability at 3-month increased 4.44 times(OR 4.44,95%CI 1.70-11.59,P=0.002).In the atherothrombosis group,when the decrease of diastolic BP during the first 24 hours was greater than 10 mm Hg,the risk of the death/disability at 3-month increased 3.70 times(OR 3.70,95%CI 1.54-8.90.P=0.00).In the cardioembolism group,the risk increased respectively 7.98 times(OR 7.98,95%CI 1.34-47.66.P=0.026)and 6.68 times(OR 6.68.95%CI 1.55-28.79,P=0.01).In the subgroups of small artery disease,the decrease of BP during the first 24 hours was not the independent predictor of the death and disability at 3-month.Conclusions A U-shaped effect is observed in each subgroup between BP and prognosis.In the subgroups of atherothrombosis and cardioembolism,the decrease of BP during the first 24 hours is the independent predictor of the death and disability at 3-month.

Objective:To observe the change of periphery and centra lymphocyte subsets at the crest-time of MOG_(35-55) induced EAE disease in mice,and to explore the alteration of cellular immunity and humoral immunity in the invasion process in EAE.Methods:MOG_(35-55) was used to establish EAE model in femina C57BL/6 mice.The behavioral changes and the histological scores were recorded after the mice were immuned .The changes of CD3~+CD4~+,CD3~+CD8~+,CD4~+CD25~+ and B220~+ on periphery and centra lymphocytes in spleen,brain and spinal cord were analyzed by flow cytometry.Results:The CD3~+CD4~+,CD3~+CD8~+,CD4~+CD25~+ and B220~+ lymphocytes were detected in the brain and spinal cord of EAE group mice,but they were not detected in CFA control group.The CD3~+CD4~+ and CD3+CD8+lymphocytes in the spleen of EAE crest-time group were lower than those in CFA control group(P＜0.05).The B220~+ lymphocytes were obviously higher than in the CFA control group (P＜0.01).And CD4~+CD25~+ lymphocytes were slight higher than the CFA control group.Conclusion:At the crest-time during EAE,the CD3~+CD4~+,CD3~+CD8~+lymphocytes of spleen reduced obviously,B220~+ lymphocytes increased markedly,and the CD4~+CD25~+ lymphocytes just have the increasing trend.It indicates that cellular immunity and humoral immunity coregulated the patho-process at the crest-time of EAE,T lymphocytes and B lymphocytes all played important roles in the pathogenesy of EAE.