胰岛素强化治疗拮抗烫伤大鼠心肌细胞凋亡的机制研究

目的 探讨大鼠重度烫伤后胰岛素强化治疗拮抗心肌细胞凋亡的作用及机制.方法 将18只SD大鼠按随机数字表法分为假伤组、烫伤组和胰岛素强化治疗组(强化治疗组),每组6只.制作30％总体表面积(TBSA)Ⅱ度烫伤模型及胰岛素强化治疗模型.伤后6h取大鼠左室心肌组织,采用原位末端缺刻标记法(TUNEL)检测心肌细胞凋亡,用免疫组化和蛋白质免疫印迹法(Western blotting)分别观察3种凋亡相关基因天冬氨酸特异性半胱氨酸蛋白酶3(caspase-3)、Bax和Bcl-2的蛋白表达.结果 与假伤组比较,烫伤后心肌凋亡细胞明显增多[(13.1±3.4)％比(0.6±0.4)％,P＜0.01];caspase-3、Bax的蛋白表达明显增高(免疫组化caspase-3:13.72±4.13比1.36±0.95,Bax:29.64±5.42比2.24±1.04; Western blotting caspase-3:5.72±2.13比1,Bax:4.64±1.42比1),而Bcl-2表达水平显著降低(免疫组化:3.39±1.52比8.01±2.56;Western blotting:0.69±0.42比1,均P＜0.01).经胰岛素强化治疗后,心肌细胞的凋亡率较烫伤组明显降低[(6.7±1.8)％比(13.1±3.4)％,P＜0.01],3种凋亡相关基因的蛋白表达水平正好与烫伤组的变化相反(免疫组化caspase-3:8.88±3.36比13.72±4.13,Bax:14.43±3.69比29.64±5.42,Bcl-2:8.61±3.72比3.39±1.52;Western blotting caspase-3:2.18±0.86比5.72±2.13,Bax:2.87±1.35比4.64±1.42,Bcl-2:3.57±1.70比0.69±0.42,P＜0.05或P＜0.01).结论胰岛素强化治疗可能通过调节caspase-3、Bax和Bcl-2 3种细胞凋亡相关基因的表达,对烫伤后心肌细胞发挥抗凋亡作用.     

缺血后处理对心肌缺血再灌注损伤过程中内质网应激的影响

目的探讨缺血后处理对心肌缺血再灌注损伤(myocardial ischemia-reperfusion injury,MIRI)中细胞凋亡及特异性内质网应激损伤相关蛋白葡萄糖调节蛋白78(glucose regulated protein 78,GRP78)和半胱氨酸蛋白酶12(cysterine protease-12,caspase-12)表达水平的影响和意义。方法 Wistar大鼠24只随机分为假手术组、缺血再灌注组和缺血后处理组,每组8只。采用改良Pferfer MA推管法制备大鼠缺血再灌注模型,假手术组于左冠状动脉前降支下穿线、套管,不结扎,旷置220min;缺血再灌注组结扎左冠状动脉40min后完全开放,再灌注180min;缺血后处理组结扎左冠状动脉40min后,再灌注缺血开始前连续实施3个循环的30s/30s的缺血再灌注后处理,随后完全开放左冠状动脉再灌注180min。采用Evans blue与TTC双染法测定心肌梗死面积百分比和缺血区面积百分比,采用TUNEL法检测心肌细胞凋亡指数,采用Western blot法检测心肌组织caspase-12、GRP78蛋白表达水平。结果假手术组心肌缺血区面积百分比(0)和梗死区面积百分比(0)明显低于缺血后处理组[(46.46±2.13)%、(41.02±2.93)%]和缺血再灌注组[(53.31±3.87)%、(52.19±3.44)%](P0.01),心肌细胞凋亡指数[(6.70±2.25)%]、心肌组织caspase-12蛋白(0.11±0.01)和GRP78蛋白(0.13±0.03)表达水平明显低于缺血后处理组[(20.54±3.05)%、0.35±0.06、1.17±0.14]和缺血再灌注组[(26.92±1.91)%、0.41±0.06、1.04±0.16](P0.01);缺血后处理组心肌缺血区面积百分比、梗死区面积百分比、心肌凋亡指数、心肌组织caspase-12蛋白表达水平低于缺血再灌注组(P0.01),心肌组织GRP78蛋白表达水平高于缺血再灌注组(P0.05)。结论缺血后处理可减轻心肌细胞凋亡,而内质网应激激活参与了大鼠MIRI过程,推测缺血后处理在大鼠MIRI过程中可能通过调节内质网应激途径抑制细胞凋亡,改善MIRI。     

促红细胞生成素对心肺复苏后心肌功能的影响

目的 探讨促红细胞生成素(EPO)对窒息性心搏骤停大鼠心肺复苏(CPR)后心功能不全的心肌保护作用.方法 经夹闭气管8 min建立窒息性心搏骤停-CPR动物模型.按随机数字表法将24只SD大鼠分为3组,每组8只.CPR组窒息致心搏骤停后8 min予胸外按压和机械通气进行复苏;EPO组于自主循环恢复(ROSC)后3 min股静脉注射EPO 5 kU/kg;正常对照组不予任何处理.持续监测左心室收缩压(LVSP)、左心室舒张期末压(LVEDP)、左心室内压上升或下降最大速率(±dp/dt max)等血流动力学指标.于观察终点(ROSC后120 min)处死大鼠,采血测定血清心肌肌钙蛋白Ⅰ(cTnI)含量;光镜和透射电镜下观察心肌组织病理改变;原位末端缺刻标记法(TUNEL)检测心肌细胞凋亡.结果 CPR组和EPO组ROSC后30、60、90、120 min时LVSP、+dp/dt max和- dp/dt max绝对值均较基线水平明显下降.与正常对照组比较,CPR组和EPO组ROSC 30 min时LVSP(mm Hg,1 mm Hg=0.133 kPa)、+dp/dt max(mm Hg/s)、- dp/dt max绝对值(mm Hg/s)即明显下降(LVSP:119.52±12.68、134.32±15.78比165.82土7.05; +dp/dt max:4 457.14±826.22、6 019.85±1 192.19比10 325.93±773.09; - dp/dt max:-3 956.04±952.37、-4 957.22±838.60比-8 421.33±886.65,均P＜0.01),并持续至ROSC 120 min(LVSP:124.62±8.07、145.61±16.70比162.34±7.63; +dp/dt max:4 977.67±350.40、7 471.62±998.32比9 999.39±727.96;- dp/dt max:-4 145.51±729.77、-5 895.64±787.30比-8 089.75±981.52,均P＜0.01);经EPO处理后ROSC各时间点LVSP、+dp/dtmax和- dp/dtmax绝对值均较CPR组显著升高(均P＜0.05).CPR组和EPO组ROSC 120 min LVEDP(mm Hg/s)均较正常对照组明显升高(22.94±3.94、11.18±2.58比2.89±0.70,均P＜0.01),EPO组LVEDP则较CPR组明显下降(P＜0.05).光镜和电镜下观察,CPR组心肌细胞坏死、炎性细胞浸润,心肌细胞胞膜完整性丧失、线粒体肿胀,心肌细胞凋亡增加[凋亡细胞数(个):314.1±30.7比165.2±45.9,P＜0.01];经EPO干预后心肌病理损伤减轻,心肌细胞凋亡较CPR组减少(凋亡细胞数:242.1±20.0比314.1±30.7,P＜0.05).CPR组和EPO组ROSC 120 min血清cTnI (μg/L)均较正常对照组明显升高(20.70土5.96、16.98±3.81比2.60±0.86,均P＜0.01),而CPR组和EPO组比较无差异.结论 EPO可以改善窒息性心搏骤停大鼠CPR后的心功能,减轻心肌损伤,其机制可能与减少线粒体损伤和心肌细胞凋亡有关.     

生长激素对大鼠心肌缺血/再灌注后心肌细胞凋亡及凋亡相关基因Caspase-3 Cleaved caspase-3蛋白表达的影响

目的 研究生长激素(Growth hormone, GH)对大鼠心肌缺血/再灌注(ischemia reperfusion,I/R) 后心肌细胞凋亡及相关基因Caspase-3、Cleaved caspase-3蛋白表达的影响.方法 24只大鼠随机分为三组,假手术组(sham-operated group,n=8,仅手术24 h)、心肌缺血/再灌注(I/R)组(n=8)、GH组(n=8),后两组均缺血30 min,再灌注24 h,GH组于建立模型前7 d每天给予人重组生长激素(reconbination human growth hormone,rhGH)针剂皮下注射(1 U/kg体质量),其他二组等量生理盐水注射.以TUNEL法检测心肌细胞凋亡情况, DAB免疫组化法检测心肌细胞Caspase-3、Cleaved caspase-3蛋白表达并进行心肌组织病理学检查.结果 大鼠心肌I/R 24 h后心肌细胞凋亡指数明显上升(对照于假手术组,P<0.05),心肌细胞Caspase-3、Cleaved caspase-3蛋白表达呈阳性染色指数明显升高(P<0.05),心肌病理检查见心肌缺血区呈大小不一的坏死灶,缺血心肌间有炎症细胞浸润,心肌排列不整齐(HE染色),而GH组心肌细胞凋亡率及心肌细胞Caspase-3、Cleaved caspase-3蛋白表达呈阳性染色指数明显好于I/R组(P<0.05),心肌细胞炎症细胞也明显减少,坏死灶也少于I/R组.结论 GH可以减少心肌I/R后心肌细胞凋亡及细胞Caspase-3、Cleaved caspase-3染色阳性指数,说明GH对I/R后的心肌具有保护作用.     

慢性高原病患者骨髓造血细胞凋亡及caspase-8和caspase-9表达研究

目的 探讨慢性高原病( CMS)患者骨髓造血细胞凋亡指数及caspase-8和caspase-9mRNA表达变化的意义.方法 选取18例CMS患者,采用末端脱氧核苷酸转移酶介导的dUTP缺口标记(TUNEL)技术定量研究骨髓单个核细胞(BMMNC)凋亡指数,同时采用RT-PCR半定量方法检测BMMNC caspase-8和caspase-9 mRNA的表达.以16例骨科单纯骨折患者为对照.结果 ①CMS患者BMMNC凋亡指数[(8.51±3.35)％]明显低于对照组[(16.00±4.28)％](P＜0.01).②CMS患者caspase-8和caspase-9 mRNA的相对表达水平分别为0.28 ±0.07和0.23±0.08,对照组分别为0.45±0.09和0.41±0.09,CMS组均明显低于对照组(P值均＜0.01).③CMS患者caspase-8和caspase-9mRNA表达水平与血红蛋白浓度呈负相关(r值分别为-0.520及-0.610,P值均＜0.05),与凋亡指数均未发现明显相关性(P值均＞0.05),CMS患者凋亡指数与血红蛋白浓度呈负相关(r=-0.890,P＜0.01).结论 CMS患者BMMNC凋亡指数及caspase-8和caspase-9表达水平均降低,提示CMS患者骨髓造血细胞凋亡减少,caspase-8和caspase-9均参与CMS骨髓造血细胞凋亡异常机制.     

乌司他丁对内毒素血症心肌损伤大鼠线粒体通路介导细胞凋亡的影响

目的探讨线粒体通路介导的细胞凋亡在内毒素血症大鼠心肌损伤中的机制及乌司他丁对该通路的影响。方法将24只雄性Wistar大鼠分为三组:对照组、内毒素组及乌司他丁组,每组各8只大鼠。内毒素组与乌司他丁组大鼠腹腔注射脂多糖10 mg/kg,乌司他丁组大鼠1 h后再次腹腔注射乌司他丁20 000 U/kg,对照组大鼠于同一时间点注射同等剂量的等渗NaCl溶液。观察各组大鼠心肌组织病理变化,采用酶联免疫吸附试验测定血清中心肌肌钙蛋白T(cTnT)、脑钠肽(BNP),并计算心肌细胞凋亡指数。同时,采用免疫组织化学法检测心肌细胞中Bcl-2、Bax、CytC、Caspases-3的表达。结果内毒素组大鼠心肌组织损伤严重,乌司他丁组大鼠心肌组织虽然有损伤,但病变较内毒素组轻。三组大鼠cTnT、BNP水平比较,差异均有统计学意义(F=69.217、18.250,P均0.05),内毒素组与乌司他丁组大鼠cTnT[(20.3±1.0)、(18.7±1.3)、(12.2±1.0)μg/L]、BNP[(26.6±1.4)、(23.0±2.4)、(17.0±1.6)μg/L]水平显著高于对照组,且内毒素组更高(P均0.05)。乌司他丁组大鼠凋亡指数明显低于内毒素组[(19.8±1.7)%vs.(22.6±1.2)%,t=3.675,P=0.020]。同时,内毒素组及乌司他丁组大鼠Bcl-2的表达显著高于对照组[(80.3±3.8)、(76.6±2.90)、(49.6±3.9)],且内毒素组大鼠更高(P均0.05),而Bax[(70.8±1.7)、(80.0±4.8)、(99.7±5.6)]、CytC[(120±5)、(132±3)、(151±7)]、Caspases-3[(108.8±4.0)、(113.9±5.2)、(157.2±2.5)]蛋白表达在内毒素组及乌司他丁组均显著低于对照组,且内毒素组更低(P均0.05)。结论乌司他丁可能通过抑制线粒体通路的激活,减少心肌细胞凋亡的发生,对内毒素血症心肌损伤起到了一定的保护作用。     

葡萄糖转运蛋白3在子痫前期胎盘中的表达及意义

目的探讨葡萄糖转运蛋白3(GLUT3)在子痫前期(PE)胎盘中的表达及意义。方法选取2014年9月至2018年1月海南医学院第二附属医院产科住院治疗的50例PE患者作为PE组,同期选取50例正常妊娠健康孕妇作为对照组进行前瞻性研究。比较两组孕妇的胎盘GLUT3、半胱天冬氨酸蛋白酶(caspase)-3 mRNA、caspase-8 mRNA、caspase-9 mRNA、滋养细胞凋亡指数,并比较轻度和重度PE患者胎盘GLUT3、可溶性血管内皮生长因子受体1(sFlt-1)、血管内皮生长因子(VEGF)表达,采用Pearson相关性分析评价GLUT3与caspase-3、caspase-8、caspase-9、滋养细胞凋亡指数、sFlt-1、VEGF的相关性,以Logistic多元回归方程分析GLUT3、sFlt-1、VEGF与PE病情的相关性。结果PE组孕妇的免疫组化胎盘GLUT3阳性率(90.00%)及GLUT3 mRNA表达(1.16±0.15)均高于对照组(22.00%,0.74±0.10),差异具有统计学意义(P 0.05); PE组孕妇的caspase-3 mRNA(1.56±0.12)、caspase-8 mRNA(1.45±0.10)、caspase-9 mRNA(1.34±0.13)、滋养细胞凋亡指数(0.15±0.03)均高于对照组(0.92±0.06,0.94±0.05,0.91±0.04,0.08±0.02),差异具有统计学意义(P 0.05); GLUT3均与caspase-3(r=0.573)、caspase-8(r=0.529)、caspase-9(r=0.441)、滋养细胞凋亡指数(r=0.607)呈正相关(P 0.05);重度患者胎盘GLUT3 mRNA、sFlt-1 mRNA高于轻度患者,VEGF mRNA低于对照组,差异具有统计学意义(P 0.05); GLUT3与sFlt-1 (r=0.496)呈正相关,与VEGF(r=-0.416)呈负相关(P 0.05)。结论 GLUT3在PE患者胎盘中呈高表达,其水平与滋养细胞凋亡、内皮功能障碍显著相关,并能反映病情的严重程度。     

液体复苏对创伤致严重脓毒症和脓毒性休克患者心肌损伤的影响

目的 观察液体复苏对创伤致严重脓毒症和脓毒性休克患者心肌损伤的影响,以及心肌损伤标志物对液体复苏的指导作用.方法 78例复合伤致严重脓毒症和脓毒性休克患者,急性生理学与慢性健康状况评分系统Ⅱ(APACHEⅡ)评分18 ～ 35分;记录治疗前及治疗3d、5d血清心肌肌钙蛋白Ⅰ(cTnI)、N末端-心室利钠肽前体(NT-proBNP)及血流动力学参数,并进行相关性分析.结果 62.8％(49/78)的严重脓毒症和脓毒性休克患者出现血清cTnI升高,73.5％(36/49)升高值大于界限值的2倍以上,30.6％( 15/49)超过界限值的4倍以上.入院时血清NT-proBNP升高者占46.2％(36/78),经液体复苏后继续升高者达74.4％(58/78).存活组(55例)治疗后血清cTnI、NT-proBNP、肺动脉楔压(PAWP)及心排血指数(CI)均明显改善;死亡组(23例)各指标无明显变化,且死亡组血清cTnI(μg/L)和NT-proBNP(ng/L)水平显著高于存活组(cTnI 3 d:2.09±1.00比1.57±0.93,5 d:1.78±0.67比0.72±0.51;NT-proBNP 3 d:3.52±0.73比3.16±0.65,5 d:3.21±0.66比2.66±0.58),CI( ml· s-1· m-2)明显低于存活组(3 d:57.6±6.2比68.3±5.6,5 d:40.5±4.7比80.7±6.8,均P＜0.05).46例液体复苏达目标值的患者cTnI水平(μg/L)低于32例未达标者(1.16±0.62比1.97±0.76,P＜0.05),且CI(ml ·s-1 ·m-2)明显增加(61.2±6.4比49.3±6.1,P＜0.05),液体复苏是否达到目标值与血清NT-proBNP、PAWP无关.血清cTnI与NT-proBNP呈正相关(r=0.865,Y=2.069+ 0.695X,P＜0.01),NT-proBNP与PAWP呈正相关(r=0.762,Y=1.125+ 4.929X,P＜0.01),cTnI与CI呈负相关(r=-0.891,Y=50.623 -6.114X,P＜0.01).结论 创伤致严重脓毒症和脓毒性休克患者有明显的心肌损伤,液体复苏可改善心肌损伤;血清cTnI和NT-proBNP与患者预后有关,NT-proBNP用于指导液体复苏的意义尚不能确定.     

美托洛尔对脓毒症大鼠心肌细胞凋亡的影响

目的:探讨美托洛尔对脓毒症大鼠心肌细胞凋亡的抑制作用及机制。方法:72只大鼠随机分为对照组(n=24)、脓毒症组(n=24)及治疗组[n=24,脓毒症模型基础上美托洛尔0.05mg冲击量后0.2mg/(kg·h)静脉泵入]。于术后3、6、12、24h测定血清肿瘤坏死因子-α(TNF-α),心肌髓过氧化物酶(MPO)和半胱氨酸天冬氨酸酶-3(caspase-3)活性,TUNEL法检测心肌细胞凋亡,光镜下观察心肌组织病理改变。结果:脓毒症组和治疗组大鼠各时点血浆TNF-α,心肌MPO、caspase-3活性、心肌细胞凋亡指数均较对照组显著升高(P<0.05),以术后12h最显著。应用美托洛尔后,上述指标与脓毒症组各时点相比均有不同程度降低,其中血浆TNF-α和心肌MPO活性在12、24h有统计学差异(P<0.05),心肌caspase-3活性和心肌细胞凋亡指数在6、12和24h有统计学差异(P<0.05),且心肌损害病理改变较脓毒症组显著减轻。结论:美托洛尔具有对抗脓毒症大鼠心肌细胞凋亡的作用,可能与抑制细胞因子、减轻心肌炎症反应、降低caspase-3活性有关。     

氯沙坦对心力衰竭大鼠心肌细胞凋亡和Ca2+变化的影响

目的:从细胞凋亡和细胞内钙调节的角度探讨血管紧张素ⅡⅠ型受体阻断剂--氯沙坦治疗心力衰竭(简称:心衰)的机制.方法:采用阿霉素腹腔注射造心衰模型,分为心衰组与治疗组,治疗组给予氯沙坦干预.同期选择8只正常大鼠为对照组.透射电镜观察心肌超微结构改变,检测血清中CPK、CK-MB及LDH的含量.检测大鼠心肌细胞凋亡及心肌组织匀浆中Ca2+的变化.结果:心衰组与治疗组相比,心肌细胞损伤明显,并可见凋亡小体.心肌组织中CPK、CK-MB和LDH活力降低.心肌细胞凋亡指数明显增加(P＜0.01).与对照组相比,心衰组心肌组织中的Ca2+含量升高(P＜0.01):治疗组与心衰组相比Ca2=显著降低(P＜0.01).结论:心力衰竭过程中发生了心肌细胞凋亡,氯沙坦可有效抑制心肌细胞凋亡,使心肌超微结构受损减轻,心肌酶外漏减少.心衰时心肌组织匀浆中Ca2+增加,可能是肌浆网钙泵活性受损.氯沙坦可抑制心肌细胞凋亡及Ca2+超载有积极逆转心肌受损,改善心衰进程作用.     

Guns and Knives in New Mexico: Patterns of Penetrating Trauma, 1978–1993

Objective: To identify patterns of nonfatal and fatal penetrating trauma among children and adults in New Mexico using ED and medical examiner data.
Methods: The authors retrospectively sampled in 5-year intervals all victims of penetrating trauma who presented to either the state Level-1 trauma center or the state medical examiner from a 16-year period (1978–1993). Rates of nonfatal and fatal firearm and stabbing injury were compared for children and adults.
Results: Rates of nonfatal injury were similar (firearm, 34.3 per 100,000 person-years; stabbing, 35.1). However, rates of fatal injury were significantly different (firearm, 21.9; stabbing, 2.7; relative risk: 8.2; 95% confidence interval: 5.4, 12.5). From 1978 to 1993, nonfatal injury rates increased for children (p = 0.0043) and adults (p < 0.0001), while fatal penetrating injury remained constant. The increase in nonfatal injury in children resulted from increased firearm injury rates. In adults, both stabbing and firearm nonfatal injury rates increased.
Conclusions: Nonfatal injury data suggest that nonfatal violence has increased; fatal injury data suggest that violent death rates have remained constant. Injury patterns vary by age, mechanism of trauma, and data source. These results suggest that ED and medical examiner data differ and that both are needed to guide injury prevention programs.     

Dissociable correlates of two classes of retrieval processing in prefrontal cortex

Although substantial evidence suggests that the prefrontal cortex (PFC) implements processes that are critical for accurate episodic memory judgments, the specific roles of different PFC subregions remain unclear. Here, we used event-related functional magnetic resonance imaging to distinguish between prefrontal activity related to operations that (1) influence processing of retrieval cues based on current task demands, or (2) are involved in monitoring the outputs of retrieval. Fourteen participants studied auditory words spoken by a male or female speaker and completed memory tests in which the stimuli were unstudied foil words and studied words spoken by either the same speaker at study, or the alternate speaker. On "general" test trials, participants were to determine whether each word was studied, regardless of the voice of the speaker, whereas on "specific" test trials, participants were to additionally distinguish between studied words that were spoken in the same voice or a different voice at study. Thus, on specific test trials, participants were explicitly required to attend to voice information in order to evaluate each test item. Anterior (right BA 10), dorsolateral prefrontal (right BA 46), and inferior frontal (bilateral BA 47/12) regions were more active during specific than during general trials. Activation in anterior and dorsolateral PFC was enhanced during specific test trials even in response to unstudied items, suggesting that activation in these regions was related to the differential processing of retrieval cues in the two tasks. In contrast, differences between specific and general test trials in inferior frontal regions (bilateral BA 47/12) were seen only for studied items, suggesting a role for these regions in post-retrieval monitoring processes. Results from this study are consistent with the idea that different PFC subregions implement distinct, but complementary processes that collectively support accurate episodic memory judgments.     

Interprofessional approaches to creating safe,high quality health care

Three supplementary perspectives are presented arguing that interprofessional collaboration is both necessary and desirable. Nonetheless, there are often too many serious intra-professional barriers and obstacles to interprofessional collaboration to make it successful. Some of these barriers, it is argued and illustrated, are found in the multiple ways in which professional identity is tacitly acquired and embodied in the practitioners' habitual, everyday practice. The paper then explores ways in which reflection, especially Second order reflection, can help to elucidate and overcome these obstacles, as well as increasing professional adaptability and competence.     

Systematic Reviews Published in the January 2011 Issue of The Cochrane Library

ABSTRACT

The Cochrane Library of Systematic Reviews is published quarterly as a DVD and monthly online. The January 2011 issue (first quarterly DVD for 2011) contains 4515 complete reviews, 1985 protocols for reviews in production, and 13,521 one-page summaries of systematic reviews published in the general medical literature. In addition, there are citations of 641,000 randomized controlled trials, and 14,018 cited papers in the Cochrane methodology register. The health technology assessment database contains over 9300 citations. One hundred and seven new reviews have been published in the last 3 months, of which five have potential relevance for practitioners in pain and palliative medicine.     

Modified micro-superior percutaneously-assisted total hip: early experiences & case reports

Because of the extensile nature and familiarity of the standard posterior-lateral approach to the hip, a family of "micro-posterior" approaches has been developed. This family includes the Percutaneously-Assisted Total Hip (PATH) approach, the Supercapsular (SuperCap) approach and a newer hybrid approach, the Supercapsular Percutaneously-Assisted Total Hip (SuperPATH) approach. Such approaches should ideally provide a continuum for the surgeon: from a "micro" (external rotator sparing) posterior approach, to a "mini" (external rotator sacrificing) posterior approach, to a standard posterior approach. This could keep a surgeon within his comfort zone during the learning curve of the procedure, while leaving options for complicated reconstructions for the more practiced micro-posterior surgeons. This paper details one author's experiences utilizing this combined approach, as well as permutations of this entire micro-posterior family of approaches as applied to more complex hip reconstructions.     

Determination of creatine kinase isoenzyme MB activity in serum using immunological inhibition of creatine kinase M subunit activity. Activity kinetics and diagnostic significance in myocardial infarction.

This is a new method for the determination of creatine kinase isoenzyme MB activity in serum. The method uses direct activity measurement of creatine kinase B subunit activity after blocking of CK-M subunit activity by inhibiting antibodies. The test takes no longer than 15 min. The method yields an intra-serial C.V. of 2.0-12.9%, and a C.V. from day to day of 5.5%. The detection limit is 3.4 U/l creatine kinase MB. In the 95 cases with proven myocardial infarction several types of creatine kinase MB activity kinetics could be determined. The percentage of creatine kinase MB of peak CK-total is 6-25%, with a mean of 11.1%. The amount of creatine kinase MB with respect to total CK activity after reinfarction is higher than the amount after initial infarction.     

Structure and function of "metalloantibiotics"

Although most antibiotics do not need metal ions for their biological activities, there are a number of antibiotics that require metal ions to function properly, such as bleomycin (BLM), streptonigrin (SN), and bacitracin. The coordinated metal ions in these antibiotics play an important role in maintaining proper structure and/or function of these antibiotics. Removal of the metal ions from these antibiotics can cause changes in structure and/or function of these antibiotics. Similar to the case of "metalloproteins," these antibiotics are dubbed "metalloantibiotics" which are the title subjects of this review. Metalloantibiotics can interact with several different kinds of biomolecules, including DNA, RNA, proteins, receptors, and lipids, rendering their unique and specific bioactivities. In addition to the microbial-originated metalloantibiotics, many metalloantibiotic derivatives and metal complexes of synthetic ligands also show antibacterial, antiviral, and anti-neoplastic activities which are also briefly discussed to provide a broad sense of the term "metalloantibiotics."