不同周龄大鼠心肌细胞收缩/舒张功能的研究

目的研究不同周龄对大鼠心肌细胞收缩/舒张功能的影响。方法SD大鼠分为三个周龄组:A组(12~15周)、B组(36~41周)和C组(51~55周),并以常规酶解法分离成年大鼠心肌细胞,观察分离即刻(D时间点)、复钙1h后(E时间点)和电刺激10min后(F时间点)心肌细胞成活率,采用IonOptix单细胞动缘探测系统同步检测心肌细胞的收缩幅度、收缩/舒张速度和钙瞬变等,这些指标均由计算机自动实时采集并记录。结果复钙1h后和电刺激10min后心肌细胞成活率降低均有统计学意义(P<0.05或P<0.01),周龄越大越明显,随着周龄的增大,心肌细胞收缩幅度(峰值高度,ph)、心肌细胞收缩幅度/单个心肌细胞的长度百分比(ph/bl%)、最大收缩速率(maxi mal velocity of contraction, dL/dt)、最大舒张速率(maxi mal velocity of relaxation,-dL/dt)和钙瞬变幅度(FFI)降低,ph在A组、B组和C组分别为(0.14±0.06),(0.12±0.05),(0.11±0.05)μm;ph/bl%分别为(9.17±3.54)%、(7.14±2.58)%和(6.56±2.36)%; dL/dt分别为(2.01±0.74),(1.82±0.51),(1.51±0.56)μm/s;-dL/dt分别为(2.10±0.75),(1.70±0.62),(1.41±0.52)μm/s;FFI分别为(0.38±0.05),(0.35±0.04),(0.25±0.05)。其中C组ph/bl%、 dL/dt、-dL/dt和FFI均较A组显著降低(P<0.05),降低幅度分别为27%,26%,33%和31%。结论随着周龄的增大,分离大鼠心肌细胞的成活率下降,大鼠心肌细胞的收缩/舒张功能降低,钙瞬变幅度减小。     

血管钠肽抑制异丙肾上腺素对心肌细胞收缩的增强作用

目的 :研究血管钠肽 （VNP）对心肌细胞收缩的作用及其机制 ,观察 HS- 14 2 - 1、8- Br- c GMP和镁蓝 （methyleneblue,MB）对心肌细胞收缩的影响。方法 :采用单心肌细胞动缘探测技术检测细胞收缩的幅度。结果 :10 - 1 0、10 - 9、10 - 8、10 - 7、10 - 6 m ol/L Iso可剂量依赖性地引起心肌细胞收缩增强 ,与对照组相比较分别增强 （13± 3） %、（2 6± 2 ）%、 （6 0± 5 ） %、（15 3± 4 ） %和 （312± 7） %。此效应可被普萘洛尔 （10 - 6 mol/L ）所阻断。 10 - 1 0 、10 - 9、10 - 8、10 - 7、10 - 6 m ol/L VNP可剂量依赖性地抑制 Iso（10 - 8mol/L）引起的心肌细胞收缩幅度的升高 ,与 Iso（10 - 8mol/L）相比较分别减弱 （99± 3） %、（95± 2 ） %、（84± 6 ） %、（6 6± 3） %和 （6 1± 3） %。 8- Br- c GMP（10 - 7～ 10 - 3m ol/L）也可剂量依赖性地抑制 Iso（10 - 8mol/L）引起心肌细胞收缩的增强。钠尿肽鸟苷酸环化酶 （guanylate cyclase,GC）受体的特异性阻断剂 HS- 14 2 - 1（2× 10 - 5mol/L）使 VNP的作用几乎完全消失。MB是 GC的抑制剂 ,10 - 5mol/L MB不但使VNP的作用完全消失 ,而且增强心肌细胞收缩的效应。VNP和 HS- 14 2 - 1本身对心肌细胞收缩无显著影响。而 MB使心肌细胞收缩幅度升高。结论 :VNP作用于心肌细?     

性别对成年小鼠心肌细胞收缩力的影响

目的研究性别对成年C57BL/6小鼠心肌细胞收缩力和钙瞬变的影响。方法采用Langendorff逆行灌流、Ⅱ型胶原酶消化方法分离不同性别成年C57BL/6小鼠心肌细胞,比较两组心肌细胞的形态学差异;运用Ion Optix细胞收缩及离子浓度同步测量系统,同步记录不同性别小鼠心肌细胞肌节长度及钙瞬变随电刺激的变化,比较两组间心肌细胞收缩力(肌节缩短幅度、肌节缩短率、肌节最大收缩速度和最大舒张速度)和心肌细胞钙瞬变(钙瞬变峰值、钙瞬变幅度和钙离子消除时间常数)的差异。结果成年雄性C57BL/6小鼠心肌细胞收缩力指标:肌节缩短幅度[(0.14±0.02)μm比(0.08±0.01)μm]、肌节缩短率(7.47%±0.93%比4.60%±0.59%)、肌节最大收缩速度[(-3.25±0.37)μm/s比(-2.11±0.38)μm/s]和肌节最大舒张速度[(2.45±0.29)μm/s比(1.57±0.31)μm/s]明显高于雌性小鼠(均为P<0.05)。此外,成年雄性C57BL/6小鼠心肌细胞钙瞬变指标钙瞬变峰值和钙瞬变幅度亦显著高于雌性小鼠(均为P<0.05),而雄性小鼠心肌细胞钙离子消除时间常数低于雌性小鼠[(122.40±22.99)ms比(189.20±19.54)ms,P<0.05]。结论成年雄性C57BL/6小鼠的心肌细胞收缩力及钙瞬变均高于雌性小鼠。     

拉西地平对CTGF诱导大鼠心肌细胞肥大的影响及其与ERK1/2的关系

目的 观察拉西地平对结缔组织生长因子（CTGF）诱导大鼠心肌细胞肥大的作用，探讨其作用与细胞外信号调节激酶1/2（ERK1/2）的关系。方法 以培养的新生SD大鼠的心肌细胞为实验模型，用图象分析法、3H-亮氨酸掺入法、考马斯亮蓝染色、蛋白免疫印迹法（Western blot）等，评价拉西地平对CTGF诱导心肌细胞肥大的抑制作用及其与ERK1/2的关系。结果 ①以50 ng/L的CTGF作用24 h后，心肌细胞表面积为（1 812.52±168.73）μm2，与对照组（689.31±96.58）μm2比较显著增加（P<0.01）；5、10、25及50 μmol/L拉西地平干预组的心肌细胞表面积分别为（1 476.52±156.73）μm2、（1 120.39±149.68）μm2、（926.10±101.44）μm2及（739.81±91.55）μm2，与CTGF组比较呈浓度依赖性降低（P<0.01）。②以50 ng/L的CTGF作用24 h后，心肌细胞的3H-亮氨酸掺入率为（2 368.72±122.45）cpm/孔，与对照组（950.26±89.43）cpm/孔比较显著增加（P<0.01）。 5、10、25及50 μmol/L拉西地平干预组的心肌细胞的3H-亮氨酸掺入率，分别为（2023.12±106.15）cpm/孔、（1629.15±103.46）cpm/孔、（1302.19±98.53）cpm/孔及（1 055.72±90.96）cpm/孔，与CTGF组比较呈浓度依赖性降低（P<0.01）。③以50 ng/L的CTGF作用24 h后，心肌细胞蛋白的含量为（1.692±0.203）ng/细胞,与对照组（0.622±0.068）ng/细胞比较显著增加（P<0.01）;5、10、25及50 μmol/L拉西地平干预组的心肌细胞蛋白的含量分别为（1.269±0.167）ng/细胞、（0.923±0.119）ng/细胞、（0.766±0.085）ng/细胞及（0.682±0.063）ng/细胞，与CTGF组比较呈浓度依赖性降低（P<0.01）。④50 ng/L CTGF组的心肌细胞p-ERK1/2表达强度明显高于对照组，5 μmol/L、10 μmol/L、25 μmol/L、50 μmol/L拉西地平干预组心肌细胞p-ERK1/2的表达强度与CTGF组比较呈浓度依赖性降低。心肌细胞t-ERK1/2的表达在各组之间没有明显的差异。结论 拉西地平可抑制CTGF诱导的心肌细胞肥大，其作用机制可能与ERK1/2磷酸化有关。     

不同剂量脂多糖对缺血再灌注大鼠心肌功能损害的实验研究

目的:探讨脂多糖(LPS)对缺血再灌注大鼠心肌功能的影响。方法:应用不同剂量的LPS腹腔注射建立大鼠败血症模型,通过对大鼠心脏左前降支阻塞40min建立心肌缺血再灌注损伤模型。STNFaR注射阻断LPS对心肌的效应。结果:心肌收缩功能指标dp/dt在缺血期从(4 831±213)mmHg/s降至(2 265±114)mmHg/s,心肌舒张功能指标-dp/dt由(4 119±179)mmHg/s降至(2 056±109)mmHg/s。低剂量LPS(1μg)对缺血心肌的收缩功能dp/dt和舒张功能-dp/dt没有影响,高浓度的LPS能够抑制心肌收缩和舒张功能。心肌缺血后血清肌钙蛋白I浓度升至(9.6±2.5)ng/dl,伴随着LPS注射浓度增加而升高。阻断肿瘤坏死因子-α(TNF-α)效应后并不能改善缺血心肌收缩和舒张功能,但能减轻LPS所致心肌细胞损伤。结论:低剂量的LPS对缺血再灌注大鼠心肌功能没有明显影响,而高剂量LPS导致心功能功能障碍和心肌损伤加重。     

内皮素-1对新生大鼠心肌细胞的影响及机制

目的:研究内皮素-1（ET-1）诱导心肌肥大的机制及对抗的药物。方法:在培养新生大鼠心肌细胞中,采用L-型钙通道阻滞剂拉西地平（larc id ip ine）和MN9202、钙激活氯通道阻断剂尼氟灭酸（n iflum ic ac id,NFA）、蛋白激酶C（prote in k inase C,PKC）通路的阻断剂白屈菜季氨碱（chelerythrine,che）和ERK通路阻断剂PD98059（PD）观察内皮素-1在诱导心肌蛋白质合成中的影响。结果:对照组（DMEM）蛋白质含量为273±20μg/m l,ET-1组为312±30μg/m l,较对照组升高14%。ET-1+NFA组、ET-1+che组、ET-1+MN9202组、ET-1+larc id ip ine组、ET-1+PD98059组分别为280±10μg/m l、283±10μg/m l、285±27μg/m l、275±22μg/m l、293±33μg/m l;与ET-1组比较分别降低10%、9%、8.6%、13.1%、6.1%。结论:ET-1刺激引起的心肌细胞蛋白合成与钙激活氯通道和L-型钙通道有关,PKC和ERK通路在ET-1诱导心肌肥大的信号转导通路中起重要作用。     

金属硫蛋白对败血症小鼠心功能不全及氧化应激作用的研究

目的 探讨抗氧化剂金属硫蛋白(metallothionein,MT)对败血症小鼠心功能不全的保护作用及其抗氧化应激作用.方法 将年龄与体重配对的雄性FVB小鼠与心脏特异性过表达MT小鼠分为四组:FVB小鼠对照组(FVB组),FVB小鼠脂多糖(Lipopolysaccharide,LPS)处理组(FVB-LPS组),MT转基因小鼠对照组(MT组)和MT小鼠LPS处理组(MT-LPS组).LPS处理组小鼠腹腔注射LPS,剂量为4 mg/kg.6 h后应用心脏超声及单心肌细胞机械功能测定技术测定小鼠心脏整体功能及单个细胞收缩舒张功能.M型超声心动图测定心率、左心室舒张末期及左心室收缩末期内径(LVEDD、LVESD),计算左心室射血分数(EF)及左心室短轴缩短率(FS),细胞收缩和舒张通过收缩峰值、最大收缩和舒张速率积分(±dl/dt)、到达收缩峰值的时间、90%舒张时间进行评估.细胞内Ca2+浓度的变化通过在360/380两个波长下fura-2荧光强度比来推断,细胞内Ca2+的清除率用荧光延迟时间来衡量,如适合程序的单指数曲线或双指数曲线.通过对细胞内活性氧含量测定和谷胱甘肽/氧化型谷胱甘肽比率的测定来观察MT抗氧化应激作用.结果 心脏超声结果表明,与自身对照相比,腹腔注射LPS后小鼠心率增快及LVESD增加(P＜0.05).但LVEDD、EF及FS明显减小(P＜0.05),MT-LPS组小鼠心脏功能较FVB-LPS组有明显改善:心率、LVEDD、EF、FS比分别为(528±72)次/min与(557±69)次/min、(2.7±0.7)mm与(2.3±0.6)mm、(66±14)%与(42±10)%、(46±11)%与(30±10)%,P＜0.05.FVB-LPS组小鼠单个心肌细胞收缩峰值及±dl/dt均较MT-LPS组降低[(5±1.1)%与(7.2±0.8)%,(160±15)μm/s与(212±36)μm/s,(175±32)μm/s与(208±29)μm/s]并且90%舒张时间延长[(0.24±0.03)s与(0.19±0.02)s,P＜0.05].细胞内Ca2+浓度的变化及Ca2+的清除率的变化规律也同上述,心脏特异性过表达MT可改善由LPS诱导的单心肌细胞收缩、舒张功能不全与细胞内Ca2+处理能力的减低.心脏特异性过表达MT减轻了细胞内活性氧的含量[(0.35±0.08)A值/μg蛋白与(0.24±0.03)A值/μg蛋白,P＜0.05],提高了谷胱甘肽/氧化型谷胱甘肽的比率(2.1±0.2与2.6±0.4,P＜0.05).结论 研究表明,心脏特异性过表达MT改善了LPS引起的心脏收缩、舒张功能障碍,维持了胞内Ca2+的稳态和减轻了氧化应激,可以改善败血症引起的小鼠心功能不全.

Abstract：

Objective This study was designed to examine the impact of the antioxidant metallothionein (MT) on cardiac contractile, intracellular Ca2+ function and oxidative stress in lipopolysaccharide (LPS)-treated mice. Methods Weight and age matched adult male FVB and cardiacspecific MT-overexpressing transgenic mice were injected intraperitoneally with 4 mg/kg Escherichia Coli LPS dissolved in sterile saline or an equivalent volume of pathogen-free saline ( control groups). Six hours following LPS or saline injection, cardiac geometry and function were evaluated in anesthetized mice using the 2-D guided M-mode echocardiography. Mechanical and intracellular Ca2+ properties were examined in hearts. Cell shortening and relengthening were assessed using the following indices: peak shortening (PS)-indicative of the amplitude a cell can shorten during contraction; maximal velocities of cell shortening and relengthening ( ± dl/dt) -indicative of peak ventricular contractility; time-to-PS (TPS) -indicative of systolic duration; time-to-90% relengthening ( TR90 )-indicative of diastolic duration ( 90% rather 100%relengthening was used to avoid noisy signal at baseline concentration). The 360 nm excitation scan was repeated at the end of the protocol and qualitative changes in intracellular Ca2+ concentration were inferred from the ratio of fura-2 fluorescence intensity (FFI) at two wavelengths (360/380). Fluorescence decay time was measured as an indicator of the intracellular Ca2+ clearing rate. Glutathione/glutathione disulfide ratio and ROS generation were detected as the markers of oxidative stress. Results Heart rate was increased while EF was reduced in LPS-FVB mice and heart rate was reduced and EF increased in MT-LPS transgenic mice [(528 ±72) beats/min vs (557 ±69) beats/min, (66 ± 14)% vs (42 ± 10)%, P ＜0.05].Cardiomyocytes from the LPS treated FVB mice displayed significantly reduced peak shortening (PS) and maximal velocity of shortening/relengthening ( ± dl/dt ) associated with prolonged time-to-90%relengthening (TR90), these effects were attenuated in cardiomyocytes from the MT-LPS mice [PS (5 ±1.1 )% vs (7.2 ± 0. 8)%, dl/dt (160 ± 15) μm/s vs (212 ± 36) μm/s, - dl/dt (175 ± 32) μm/s vs (208 ±29)μm/s, TR90 (0.24 ±0.03)s vs (0.19 ±0.02) s, P ＜0.05].LPS treated mice showedsignificantly reduced peak intracellular Ca2 + and electrically- stimulated rise in intracellular Ca2 + as well as prolonged intracellular Ca2+ decay rate without affecting the basal intracellular Ca2+ levels, again, these effects were significantly attenuated in MT-LPS transgenic mice. Metallothionein overexpression also ablated oxidative stress [reduced ROS generation and increased glutathione/glutathione disulfide ratio, ROS(0. 35 ±0.08)A/μg protein vs (0.24 ±0.03) A/μg protein] . GSH/GSSG 2.1 ±0.2 vs 2.6 ±0.4, P ＜0. 05. Conclusion MT overexpression improved cardiac function and ablated oxidative stress in LPS treated mice.     

腺苷A1受体与к阿片肽受体激活对异丙肾上腺素诱导的心肌细胞肥大的交互作用

目的观察腺苷A1受体与κ阿片肽受体(κ-OR)激活对异丙肾上腺素(Iso)诱导的心肌细胞肥大的交互作用及机制。方法体外培养大鼠乳鼠心肌细胞,以Iso 10μmol/L诱导心肌细胞肥大,观察腺苷A1受体激动剂R(-)-N6-(2-phenylIsopropyl)adenosine(R-PIA)1μmol/L和κ-OR激动剂U50,488H1μmol/L对其作用,进一步探讨腺苷A1受体拮抗剂8-cyclopentyl-1,3-dipropylxanthine(CPDPX)0.1μmol/L存在时κ-OR的激活对细胞肥大的影响和κ-OR拮抗剂nor-binaltorphimine(NOR-BNI)1μmol/L存在时腺苷A1受体的激活对心肌细胞肥大的影响。通过Lowry法测心肌细胞蛋白含量;消化分离法及计算机图像分析系统测细胞体积;以Fluo-3/AM为荧光探针,共聚焦显微镜下测量心肌细胞内[Ca2+]i变化;RT-PCR法检测心肌细胞心房钠尿肽(ANP)的mRNA表达。结果 10μmol/LIso可以诱导心肌细胞肥大,1μmol/L的R-PIA(腺苷A1受体激动剂)可以明显抑制Iso诱导的心肌细胞蛋白合成增加、体积增大、ANPmRNA表达增加、心肌细胞内[Ca2+]i荧光强度增大,该抑制作用可以被1μmol/Lκ-OR拮抗剂NOR-BNI部分阻断;κ-OR激动剂U50,488H1μmol/L可以明显抑制Iso诱导的心肌细胞蛋白合成增加、体积增大、ANPmRNA表达增加、心肌细胞内[Ca2+]i荧光强度增大,该抑制作用可以被腺苷A1受体拮抗剂CPDPX部分阻断。结论腺苷可通过激动A1受体、阿片肽可通过激动κ受体抑制Iso诱导的心肌肥大,二者可以通过影响心肌细胞内[Ca2+]i浓度的增大而交互抑制Iso诱导的心肌肥大。     

α烯醇化酶靶向RNA干扰对原代培养乳鼠心肌细胞能量代谢及收缩功能的影响

目的 采用RNA干扰技术抑制培养大鼠心肌细胞α烯醇化酶的表达,探讨α烯醇化酶对心肌细胞能量产生和收缩功能的影响.方法 针对α烯醇化酶基因,化学合成3对小片段干扰RNA(siRNA)(分别为针对α烯醇化酶mRNA 406～425位点的序列1,针对α烯醇化酶mRNA 656～675位点的序列2及针对α烯醇化酶mRNA754～773位点的序列3)并转染原代培养的WKY大鼠心肌细胞.采用Real-time RT-PCR和Western blot技术分别在mRNA和蛋白水平检测α烯醇化酶的表达情况,筛选其中沉默效应最好的序列(序列1)转染心肌细胞,即RNA干扰实验组,以未转染siRNA的心肌细胞为对照组,荧光素荧光素酶法检测细胞ATP水平,视频跟踪计算机测定系统测定细胞收缩反应,参数包括最大收缩幅度(dL),最大收缩速度(dL/dtmax).结果 针对α烯醇化酶mR-NA 406～425位点的siRNA显著下调α烯醇化酶mRNA和蛋白的表达,并且呈剂量和时间依赖关系,200 nmol/L可达到最大沉默效应,其下调α烯醇化酶mRNA和蛋白表达的最大效应分别出现在转染后24 h和48 h.α烯醇化酶沉默后细胞ATP产生减少(3.55×10-7 nmol/mg蛋白),dL[(0.82±0.02)μm]和dL/dtmax[(2.7±0.3)μm/s]下降.结论 应用siRNA技术靶向α烯醇化酶mRNA 406～425位点可有效下调心肌细胞α烯醇化酶的表达,使细胞产能减少,收缩功能下降.     

氨吡酮对离体灌流鼠心收缩与舒张功能的作用

在离体等容收缩与舒张的灌流鼠心,观察了氨吡酮对心脏收缩与舒张功能的作用.结果表明,低浓度氨吡酮(Inmol/L,100nmol/L)不能明显增加左室发生压(LVDP)、最大左室压力上升速度(dp/dt max)及下降速度(-dp/dt max),也不能明显缩短时间常数(t);高浓度氨吡酮(1μmol/L明显降低了LVDP(p<0.01)、dp/dt max(p<0.01)、-dp/dt max(p<0.01),并且显著地延长了t值(p<0.05).此表明、氨吡酮并无直接的正性肌力与改善舒张功能的作用,相反,高浓度时反抑制心脏的收缩与舒张功能.     

Pathogenesis of carcinoma of the papilla of Vater

Most adenomas and carcinomas of the small intestine and extrahepatic bile ducts arise in the region of the papilla of Vater. In familial adenomatous polyposis (FAP) it is the main location for carcinomas after proctocolectomy. In many cases symptoms due to stenosis lead to diagnosis at an early tumor stage. In about 80%, curative intended resection is possible. Operability is the most relevant prognostic factor. Most ampullary carcinomas resp. carcinomas of the papilla of Vater develop from adenomatous or flat dysplastic precursor lesions. They can be sited in the ampulloduodenal part of the papilla of Vater, which is lined by intestinal mucosa. They also can develop in deeper parts of the ampulla, which are lined by pancreaticobiliary duct mucosa. Intestinal-type adenocarcinoma and pancreaticobiliary-type adenocarcinoma represent the main histological types of ampullary carcinoma. Furthermore, there exist unusual types and undifferentiated carcinomas. Many carcinomas of intestinal type express the immunohistochemical marker profile of intestinal mucosa (keratin 7?, keratin 20+, MUC2+). Carcinomas of pancreaticobiliary type usually show the immunohistochemical profile of pancreaticobiliary duct mucosa (keratin 7+, keratin 20?, MUC2?). Even poorly differentiated carcinomas, as well as unusual histological types, may conserve the marker profile of the mucosa they developed from. These findings underline the concept of histogenetically different carcinomas of the papilla of Vater which develop either from intestinal- or from pancreaticobiliary-type mucosa of the papilla of Vater. Molecular alterations in ampullary carcinomas are similar to those of colorectal as well as pancreatic carcinomas, although they appear at different frequencies. In future studies, molecular alterations in ampullary carcinomas should be correlated closely with the different histologic tumor types. Consequently, the histologic classification should reflect the histogenesis of ampullary tumors from the two different types of papillary mucosa.     

Demonstration of the mechanism of action of biguanides

Summary Palmitic acid oxidation in rat diaphragm homogenate is depressed by biguanide concentrations that are still incapable of inhibiting oxidative phosphorylation. Glucose oxidation is not directly effected by the same biguanide concentrations: however, the inhibitory effect of palmitic acid on glucose oxidation is partly removed by biguanides. Inhibition of fatty acid oxidation, which accounts for most of the metabolic effects caused by these drugs, can be regarded as the fundamental mechanism of action of biguanides. There is some evidence suggesting that these drugs might interact with carnitine, thus preventing long-chain fatty acids from being transported across the mitochondrial membrane to the site of oxidation. Traduzione a cura degli AA.     

胰岛素瘤的解剖分布特点分析

目的胰岛素瘤是最常见的胰腺神经内分泌肿瘤，因其临床表现多样，导致诊断困难。影像学诊断尤其是超声内镜(EUS)在胰岛素瘤的诊断中起着重要作用，拥有较高的敏感性和特异性。本研究拟通过明确胰岛素瘤的解剖分布特点，以期有助于提高影像学的诊断准确率和降低漏诊率，尤其是在教育和培训实践中对于EUS的学习者更具有指导价值。 方法回顾性分析解放军总医院第一医学中心病案资料数据库1993年1月至2019年11月经外科手术、病理确诊为胰岛素瘤的患者的临床资料，检索方法采取搜索术后病理诊断为"胰岛素瘤"的病例，通过查阅病例的方法，提取出胰岛素瘤的大小和解剖分布等数据，进一步分析其特点。 结果共检索到确诊为胰岛素瘤的患者116例，其中，男45例、女71例，年龄13～76岁，平均年龄(44.4±14.85)岁。胰岛素瘤单发110例(94.8%)、多发6例(5.2%)。位置分布：头颈部46例(39.7%)，单发45例、多发1例；体尾部68例(58.6%)，单发65例、多发3例；全胰腺多发2例(1.7%)。病变大小特点：最大径0.4～3.4 cm，平均大小(1.53±0.58)cm。≤1 cm 29例、>1 cm而≤1.5 cm41例、>1.5 cm而≤2.0 cm28例，≤3 cm 15例，>3 cm 3例。年龄与肿瘤的大小相关，≤44岁患者肿瘤平均大小为(1.36±0.51)cm、>44岁患者肿瘤平均大小为(1.70±0.60)cm，P<0.05。头颈部的肿瘤大于体尾部的肿瘤，头颈部肿瘤平均大小(1.66±0.63)cm，体尾部(1.42±0.52)cm，P<0.05。 结论胰岛素瘤在胰腺体尾部较头颈部更好发；绝大多数单发，但可以全胰腺多发；多数小于1.5 cm，肿瘤的大小与患者年龄和肿瘤的解剖分布相关。     

氯硝柳胺悬浮剂的毒性评价

目的评价氯硝柳胺悬浮剂的毒性，为现场大规模应用灭螺提供依据。方法按照中华人民共和国国家标准GB 15670-1995《农药登记毒理学试验方法》和鱼类毒性试验方法进行。结果经口、经皮肤的LDso雌、雄性大鼠均>5 000 mg/kg，经呼吸道的LCso雌、雄性大鼠均>5 000mg/m3，该药经口、经皮肤、经呼吸道毒性均属微毒类药物；兔眼用药后，观察期内无不良反应，对眼无刺激性；皮肤用药后对皮肤无刺激性。与氯硝柳胺原药、氯硝柳胺乙醇胺盐原药和氯硝柳胺乙醇胺盐可湿性粉剂相比，氯硝柳胺悬浮剂对鱼急性毒性最低。结论氯硝柳胺悬浮剂属微毒类药物，对鱼的毒性低于其乙醇胺盐可湿性粉剂，适合于现场应用。     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.     

血吸虫童虫生长发育及其机制的研究进展

血吸虫童虫是宿主免疫系统攻击的重要靶标,包括皮肤型、肺型和肝门型童虫。宿主分子对童虫生长发育具有重要作用。童虫生长发育机制包括免疫调节、信号转导、性别发育及凋亡等。肌动蛋白、组织蛋白酶、烯醇化酶和葡萄糖基转移酶等分子为血吸虫童虫生长发育的重要分子。本文对血吸虫童虫生长发育及其机制的研究进展做一综述。     

124例耐多药结核分枝杆菌基因突变特征分析

目的对临床分离的耐多药结核分枝杆菌相关基因的突变特征进行分析。方法对124例耐多药结核分枝杆菌以及50株敏感株的耐药相关基因(包括异烟肼inh A、kat G、oxyR-ahp C间隔区以及利福平rpo B)进行序列测定,分析其基因突变情况。结果异烟肼耐药inh A基因突变率为14.5%;kat G基因突变率为70.2%(87/124),主要位于315位;oxyR-ahp C间隔区突变率为15.3%;inh A、kat G两种基因同时突变率75.0%,三种基因同时突变率为89.5%。利福平rpo B基因突变的检出率高达95.2%,突变主要发生在531、526、516位点。结论我省耐多药菌异烟肼耐药相关基因最常见突变为kat G 315、inh A C-T(-15)、axyR-ahp C间隔区(-10)C-T,利福平为rpo B531、526、516。结合MDR-TB耐药相关基因的特征分析,可以建立一种快速、准确、特异的适合于我省的检测结核菌耐多药性的新方法。     

Assessment of quality of life of parents of children with juvenile chronic arthritis

The aim of the study was to assess the quality of life (QOL) and the psychological status of parents of children with juvenile chronic arthritis (JCA). The QOL, anxiety and depression of the parents of 28 children with JCA were evaluated and compared to those of the parents of 28 healthy children. Mothers of JCA children and mothers of healthy children reported similar QOL. The reported anxiety and depression levels were similar for mothers and fathers in both groups. The parents of children with pauciarticular-type JCA reported lower QOL and higher levels of anxiety and depression than the parents of children with other types, namely polyarticular and systemic JCA. These findings may be explained by the fact that the pauciarticular patients had shorter disease duration and were less frequently seen in the outpatient clinic. The QOL of mothers of children with JCA was found to be slightly impaired in the group of children with pauciarticular JCA. Future larger studies are needed to confirm these results, as the number of subjects in the three groups was rather low. Received: 26 September 2001 / Accepted: 8 February 2002     

CagA-Hp抗体IgG与胃炎的组织学分析

研究幽门螺杆菌(Hp)感染与胃炎的关系。方法对204例慢性胃炎患者胃粘膜进行观察分析,并测定其中137例Hp阳性患者血清CagA-Hp抗体IgG水平,与组织学对照。结果慢性萎缩性胃炎伴肠上皮化生患者血清CagA抗体IgG明显高于对照组(P＜0.01);其他类型胃炎患者血清CagA抗体IgG水平无明显增高(P＞0.05)。结论CagA-Hp可能是导致慢性萎缩性胃炎伴肠上皮化生的因素之一,对这类患者应密切随访观察。     

慢阻肺急性加重期患者预后的影响因素分析

目的探讨慢性阻塞性肺病急性加重期(AECOPD)患者预后的相关危险因素。方法回顾性调查、收集58例AECOPD患者可能影响其预后的相关因素,并对其分别进行单因素分析。并进行Logistic多元逐步回归进行多因素分析,筛选影响AECOPD患者预后的独立危险因素。结果单因素分析后将结果 P0.1的因素纳入多因素Logistic回归,分析发现是否合并呼吸衰竭、气促程度、白细胞计数、APACHEⅡ、应用抗氧化剂、慢阻肺治疗依从性为影响AECOPD患者预后不佳的独立因素(P0.05)。结论根据AECOPD患者预后的独立危险因素,及早判断,选择合适的后续治疗方案,对提高其生存率及生存质量具有重要意义。