结合遗传算法和数值模拟,以传热流动综合性能参数PEC作为评价参数,对层流情况下的波节管进行了波形优化.结果表明,优化波形为非对称结构,其波峰对应的水平位置相对于波形段中间位置向下游偏移,波形是雷诺数Re的函数.在同一雷诺数Re下,随着波形段长度增大,优化波节管传热增强、流动阻力减小、PEC增大;随着周期长度增大,优化波节管换热性能略微减弱、流动阻力增加,PEC减小.此外,当雷诺数Re比较小时,本文获得的优化波节管可以在强化传热的同时减小流动阻力.

目的 了解川崎病(KD)患病情况及临床特征,探讨KD冠状动脉损害(CAL)及IVIG耐药的危险因素.方法 回顾性分析华中科技大学同济医学院附属同济医院2012年1月1日至2016年12月31日初诊的KD患儿的临床资料,比较分析KD治疗前后,典型和不完全KD,KD伴或不伴CAL,IVIG敏感或耐药的临床特征,分析CAL发生和IVIG耐药的危险因素.结果 725例KD患儿进入本文分析,男:女为1.61:1,平均年龄(2.7±2.3)岁;不完全KD 206例(28.4％),典型KD 519例;CAL 216例(29.8％),IVIG耐药61例(8.4％);治疗中仅使用阿司匹林者70例(9.6％).KD伴CAL的危险因素为IVIG耐药(OR=5.138,95％CI:1.835～14.836)和氨基末端脑钠肽前体(NT-proBNP)≥1000 pg·mL-1(OR=2.723,95％CI:1.110～6.679).IVIG耐药的危险因素为出现CAL(OR=2.586,95％CI:1.067～6.271).结论 KD患病人数、CAL和IVIG耐药患儿有增加趋势.IVIG耐药和NT-proBNP≥1000 pg·mL-1为KD伴CAL的危险因素,而发生CAL为IVIG耐药的危险因素.

OBJECTIVE:To study the expression of serum cytokines, interleukin-38 (IL-38) and interleukin-1β (IL-1β) in the acute phase of Kawasaki disease (KD) in children and the association of IL-38 and IL-1β with inflammatory response in the acute phase and the development of coronary artery lesion (CAL). METHODS:A total of 40 children with KD who were hospitalized in the hospital between July 2015 and June 2016 were enrolled, with 21 children in the CAL group and 19 in the non-CAL (NCAL) group. Thirty healthy children and 19 children with infection and pyrexia, who were matched for sex and age, were enrolled as healthy control group and pyrexia control group respectively. ELISA was used to measure the serum levels of IL-38 and IL-1β in the 40 children in the acute phase of KD. Spearman's rank correlation analysis was used to investigate the correlations of IL-1β and IL-38 with interleukin-6 (IL-6), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), procalcitonin (PCT), N-terminal pro-brain natriuretic peptide (NT-proBNP), triglyceride (TG), and total cholesterol (TC). RESULTS:The serum level of IL-38 in the children in the acute phase of KD was significantly lower than that in the healthy control group (P<0.05), but significantly higher than that in the pyrexia control group (P<0.05). There was no significant difference in the level of IL-38 between the CAL and NCAL groups (P>0.05). The children in the acute phase of KD had a significantly higher level of IL-1β than the healthy control group (P<0.05), while there was no significant difference between this group and the pyrexia control group (P>0.05). There was also no significant difference in the level of IL-1β between the CAL and NCAL groups (P>0.05). Serum IL-1β and IL-38 levels were not correlated with serum levels of CRP, ESR, PCT, IL-6, and NT-ProBNP or blood lipids (TG and TC) (P>0.05). CONCLUSIONS:IL-38 is involved in an inflammatory response in the acute phase of KD and may exert an anti-inflammatory effect, which is opposite to the effect of IL-1β to promote inflammatory response. However, there is no significant correlation between these two cytokines and the development of CAL in KD.

Objective To evaluate the gene expression of several molecules in Toll-like-receptor-4(TLR4) signal transduction pathway in the monocytes /macrophages after getting stimulated by the serum of Kawasaki disease(KD) patients in the acute phase as well as by γ-globulin,and to investigate the role of TLR4 in endothelial damage of KD and possible mechanism of γ-globulin in the treatment of KD.Methods Forty children with KD and 10 cases age-matched healthy children were studied.The gene expression of several molecules in TLR4 signal transduction pathway in the monocytes macrophages was evaluated after getting stimulated by the serum of KD patients in the acute phase as well as by γ-globulin.Results The expressions of TLR4 mRNA,MyD88 mRNA,TRAF6 mRNA in the human mononuclear macrophage(THP-1) were upregulated in KD serum group than in healthy control group,and γ-globulin could abolish the effect of KD serum group on TLR4 mRNA,MyD88 mRNA,and TRAF6 mRNA expressions;there was no difference in TLR4 mRNA,MyD88 mRNA,TRAF6 mRNA and CD14 mRNA expressions between KD-non coronary artery damage(KD-CAL-) serum group and KD-coronary artery damage(KD-CAL+) serum group.Conclusions It is assumed that TLR4 pathway involves in vascular damage in KD,and blocking the TLR4 pathway may be one of the mechanisms of γ-globulin to treat KD.

Objective: To evaluate potential acylation stimulating protein(ASP) resistance in both adipocytes and preadipocytes under the conditions of insulin resistance induced by testosterone on both receptor level and post-receptor level.Methods: 3T3-L1 preadipocytes were cultured and differentiated,and the adipocytes and preadipocytes were treated with 0(testosterone-free DMEM/F12),10-8,10-7,and 10-6 mol/L testosterone overnight.RT-PCR and flow cytometry were used to detected mRNA and cell surface expression of ASP receptor.Both non-testosterone treated and testosterone treated 3T3-L1 cells were cultured with 5.0 μmol/L ASP for 4 hours.Then the cell proteins were extracted and the expressions of Gβ,Gαq/11,p-PKCα,and p-PKC ζ were measured by Western blot.Results: High dose testosterone suppressed the C5L2 mRNA and protein expression in 3T3-L1 adipocytes but not in preadipocytes.At 10-6 mol/L,testosterone inhibited C5L2 mRNA and cell surface C5L2 expression by 60%(P0.01) and 27%(P0.01),respectively.After overnight incubation with testosterone(in adipocytes and preadipocytes),Gαq/11,Gβ,p-PKCα,and p-PKCζ were downregulated in the presence of ASP treatment to a certain degree.In adipocytes,testosterone effectively blocked the ASP-stimulated Gαq/11,p-PKCα,and p-PKCζ expression by 52%,50% and 57%(P0.05 to P0.01,respectively) at 10-6 mol/L in adipocytes.In preadipocytes,testosterone did not influence the four proteins' expression.Conclusion: Testosterone inhibited ASP-stimulated signal proteins.The ASP resistance mechanism of action involves both changes in expression of C5L2 as well as signaling parameters to some extent.Testosterone-induced ASP resistance may contribute to the physiological abnormalities associated with insulin resistance and some abnormalities related with testosterone such as disorders in polycystic ovarian syndrome and so on.

Objective: To evaluate potential acylation stimulating protein(ASP) resistance in both adipocytes and preadipocytes under the conditions of insulin resistance induced by testosterone on both receptor level and post-receptor level.Methods: 3T3-L1 preadipocytes were cultured and differentiated,and the adipocytes and preadipocytes were treated with 0(testosterone-free DMEM/F12),10-8,10-7,and 10-6 mol/L testosterone overnight.RT-PCR and flow cytometry were used to detected mRNA and cell surface expression of ASP receptor.Both non-testosterone treated and testosterone treated 3T3-L1 cells were cultured with 5.0 μmol/L ASP for 4 hours.Then the cell proteins were extracted and the expressions of Gβ,Gαq/11,p-PKCα,and p-PKC ζ were measured by Western blot.Results: High dose testosterone suppressed the C5L2 mRNA and protein expression in 3T3-L1 adipocytes but not in preadipocytes.At 10-6 mol/L,testosterone inhibited C5L2 mRNA and cell surface C5L2 expression by 60%(P<0.01) and 27%(P<0.01),respectively.After overnight incubation with testosterone(in adipocytes and preadipocytes),Gαq/11,Gβ,p-PKCα,and p-PKCζ were downregulated in the presence of ASP treatment to a certain degree.In adipocytes,testosterone effectively blocked the ASP-stimulated Gαq/11,p-PKCα,and p-PKCζ expression by 52%,50% and 57%(P<0.05 to P<0.01,respectively) at 10-6 mol/L in adipocytes.In preadipocytes,testosterone did not influence the four proteins' expression.Conclusion: Testosterone inhibited ASP-stimulated signal proteins.The ASP resistance mechanism of action involves both changes in expression of C5L2 as well as signaling parameters to some extent.Testosterone-induced ASP resistance may contribute to the physiological abnormalities associated with insulin resistance and some abnormalities related with testosterone such as disorders in polycystic ovarian syndrome and so on.

OBJECTIVE:To evaluate the effects of progesterone on the mRNA expression of acylation stimulating protein (ASP)-receptor C5L2 in adipocytes and preadipocytes and the C5L2 protein expression on the cell surface.METHODS:Preadipocytes of the line 3T3-L1 were cultured and induced to differentiate. Progesterone of the doses 0 - 1 x 10(-6) mol/L was added into the cultured fluid of the mature 3T3-L1 adipocytes and preadipocytes overnight. RT-PCR and flow cytometry were used to detect the mRNA and protein expression of ASP receptor C5L2. Both non-progesterone treated and progesterone-treated 3T3-L1 cells were cultured with 5.0 micromol/L ASP for 4 hours, then the cell protein was extracted and the expressions of G protein (including Galphaq/11 and Gbeta) and phosphated protein kinase C (including p-PKCalpha and p-PKCzeta) were measured by Western blotting.RESULTS:The C5L2 protein expression level of the mature adipocytes stimulated by progesterone 1 x 10(-6) mol/L for 18 h was 36% +/- 15%, significantly downregulated compared with that of the adipocytes stimulated by progesterone 0 mol/L (46% +/- 12%, P < 0.01), with a inhibition rate of 22%. The C5L2 mRNA and protein expression levels of the preadipocytes stimulated by progesterone 1 x 10(-6) mol/L for 18 h were 0.17 +/- 0.11 and 36% +/- 16% respectively, both significantly lower than those of the preadipocytes stimulated by progesterone 0 mol/L (0.50 +/- 0.18 and 51% +/- 20% respectively, P < 0.01 and P < 0.05) with the inhibition rates of 66% and 29%respectively. The ASP-stimulated Galphaq/11, Gbeta, p-PKCalpha, and p-PKCzeta expression levels of the mature adipocytes after overnight exposure to progesterone 1 x 10(-8) and 1 x 10(-6) mol/L were suppressed dose-dependently. For example, the ASP-stimulated Galphaq/11, Gbeta, and p-PKCalpha expression levels of the progesterone 1 x 10(-6) mol/L group were significantly lower than those of the progesterone 0 mol/L group by 41%, 63%, and 49% respectively (P < 0.05 to P < 0.01. In the preadipocytes the reduction of ASP-induced Galphaq/11, Gbeta, and p-PKCzeta expression levels were observed at the concentration of progesterone as low as 1 x 10(-8) mol/L, and all the four proteins were inhibited significantly at the 1 x 10(-6) mol/L progesterone concentration.CONCLUSION:Progesterone induces ASP resistance in adipocytes and preadipocytes. ASP resistance may contribute to the physiological abnormalities associated with insulin resistance induced by progesterone.

Objective:To evaluate the lower urinary tract function in patients received pelvic neoplasm radiotherapy.Methods:Totally 21 patients including 15 cases of cervical cancer, 2 cases of sacral cancer, 4 cases of rectal cancer were included in this study. Maximum flow rate,pressure flow study,urethral pressure profile were measured. The patients were divided into three type based on the main symptom: frequency group, difficulty of urination group and incontinence group, and the causes were analyzed retrospectively. According to the American Urology Association Symptom Score(AUA), the association between voiding dysfunction and score were analyzed.Results:The difference of bladder volume, bladder compliance and maximum detrusor contraction power between radiotherapy group and normal group was significant (P0.05).Among 21 patients, urine incontinence was noted in 6(28.6%), difficulty of urination in 11(52.3%), frequency in 4(14%). There was significant association between voiding dysfunction and AUA score(r=0.43,P0.05).Conclusions:Pelvic neoplasm radiotherapy obviously affects function of bladder and urethra. The application of urodynamics helps to diagnosis complex voiding dysfunction after radiotherapy.

目前认为,新型脂源性激素促酰化蛋白(acylation stimu-lating protein,ASP)具有与胰岛素相似的生物学作用[1].作为一种新型脂源性激素,对阐明ASP信号途径及深入研究ASP调控能量代谢的机制极为重要.

Objective:To study if bladder filling sensations are influenced by the state of rectal fullness.Methods:Bladder filling sensations were evaluated during 2 consecutive cystometric studies in 12 healthy volunteers.The tests were done first with an empty rectum and then with a full rectum.The bladder pressures were recorded at the same time.Results:The state of rectal fullness had very little influences on bladder compliance during filling.Compared with these of the state of rectal empty,the thresholds of first filling sensation,first desire to void and strong desire to void were significantly decreased when the rectum was full.Conclusions:There may exist a nervous reflex pathway between the rectum and bladder that can influence the bladder filling sensations.Before cystometric tests,we should examine the state of rectum in case the state of rectal fullness might influence the bladder filling sensations evaluating.

Aim To evaluate potential acylation stimulating protein (ASP) resistance in both adipocytes and preadipocytes under the conditions which produce insulin resistance by 17β-estradiol on both receptor level and post-receptor level. Methods 3T3-L1 preadipocytes were induced differentiated and 0 mol/L (17β-estradiol-free DMEM/F12), 10-8 mol/L, 10-7 mol/L and 10-6 mol/L 17β-estradiol was added to cultured 3T3-L1 adipocytes and preadipocytes overnight. RT-PCR and flow cytometry were used to detect mRNA and cell surface expression of ASP receptor. Both non-17β-estradiol treated and 17β-estradiol treated 3T3-L1 cells were cultured with 5.0 μmol/L ASP for 4 hours. Then the cell proteins were extracted and the expressions of Gβ, Gαq/11, p-PKCα and p-PKC ζ were measured by Western Blot. Results High dose 17β-estradiol suppressed C5L2 mRNA and protein expression in 3T3-L1 adipocytes but not preadipocytes. At 10-8 mol/L, 17β-estradiol increased C5L2 mRNA and protein expression slightly in both adipocytes and preadipocytes (P>0.05, respectively). At 10-6 mol/L 17β-estradiol inhibited C5L2 mRNA and cell surface C5L2 expression by 40% (P<0.05) and 21% (P<0.05), respectively. After overnight incubation with 17β-estradiol (in adipocytes and preadipocytes), Gαq/11, Gβ, p-PKCα and p-PKCζ were downregulated in the presence of ASP treatment to a certain degree. In adipocytes, at 10-6 mol/L, 17β-estradiol inhibited the ASP-induced Gαq/11, Gβ, p-PKCα and p-PKCζ expression by 17%,23%,15% and 15% (P>0.05, respectively). Whereas high dose 17β-estradiol effectively blocked ASP-stimulated Gαq/11 significantly by 24% (P<0.05) in preadipocytes. However, 17β-estradiol counteracted ASP-stimulated Gαq/11, Gβ, p-PKCα and p-PKCζ to some extent. Conclusion 17β-estradiol induces ASP resistance in adipocytes and preadipocytes. ASP resistance may contribute to the physiological abnormalities associated with insulin resistance induced by 17β-estradiol.

目的探讨颅脑损伤后癫痫持续状态的救治方法。方法对23例颅脑损伤后癫痫持续状态患者的临床资料进行回顾性分析。结果此23例患者中,16例因颅脑损伤接受了手术治疗;23例均接受了抗癫痫药物治疗。根据GOS评分判定疗效,恢复良好18例,重残3例,死亡2例。结论对于颅脑损伤后癫痫持续状态的患者,及时有效地控制发作状态,及时掌握病情变化,可以最大限度提高治疗效果,改善预后及降低死亡率。

OBJECTIVE:To explore the correlation between the parameters of prostate volume (PV) measured by transabdominal ultrasonography and urodynamic results in diagnosing bladder outlet obstruction (BOO).METHODS:112 BPH patients aged 45-85 underwent transabdominal ultrasonography to measure the superior-inferior diameter (R1) anterior-posterior diameter (R2), and left-right diameter (R3). Urodynamic examination was conducted to record the maximum flow rate (Qmax), detrusor pressure at maximum urinary flow rate (Pdet. Qmax), and detrusor pressure at minimum urinary flow rate (Pdet. Qmin), Schafer grading and international prostate symptom score (IPSS) scores were calculated. Correlation analysis was performed.RESULTS:The PV, R1, R2, and R3 were (48 +/- 29) ml, (4.3 +/- 1.0) cm, (3.7 +/- 0.9) cm, and (5.2 +/- 0.8) cm respectively. The Qmax, Pdet. Qmax, Schafer score, and IPSS score were (6.2 +/- 3.2) ml/s, (56 +/- 41) cm H2O, 3.1 +/- 1.8 (0-6) and 23 +/- 2 (15-31) respectively. Logistic regression analysis showed that R1 (OR = 22.662, P = 0.000), PV (OR = 0.946, P = 0.008) , and Qmax (OR = 0.760, P = 0.013) were positively correlated with Schafer grading value.CONCLUSION:The parameters of PV measured by transabdominal ultrasonography are reliable to diagnose BOO due to BPH.

Objective:To study the application of videourodynamic evaluation in patients with lower urinary tract voiding dysfunction.Methods:Clinical data of 64 patients with lower urinary tract voiding dysfunction evaluated by videourodynamic examination were reviewed.Results:In this group,5 patients having vesicoureteral reflux,25 diverticula or trabecula,8 detrusor-sphincter dyssynergia,1 distal urethral stricture.Conclusions:Videourodynamics study should be an essential examination for patients with complicated lower urinary tract voiding dysfunction.