外源性硫化氢对脑缺血再灌注损伤大鼠海马气体信号分子的影响

目的 研究外源性硫化氢（H2S）对脑缺血再灌注损伤大鼠海马气体信号分子的影响。方法 雄性Wistar大鼠24只，日龄90-120 d，体重180-220 g，随机分为4组，每组6只：对照组（Ⅰ组）、脑缺血再灌注组（Ⅱ组）、脑缺血再灌注＋50μmol／L NaHS组（Ⅲ组）和脑缺血再灌注＋100μmol／L NaHS组（Ⅳ组）。采用四动脉阻断法制作大鼠全脑缺血再灌注损伤模型，Ⅰ组行假手术，Ⅲ组和Ⅳ组夹闭两侧颈总动脉前30 min分别腹腔注射50μmol／L和100μmol／L NaHS各1 ml，Ⅰ组和Ⅱ组分别腹腔注射1 ml生理盐水，再灌注6 h后处死大鼠取海马，测定海马组织中H2S、NO和Co的含量和胱硫醚β-合酶（CBS）、血红素氧合酶（HO）和诱导型一氧化氮合酶（iNOS）的活性及CBS mRNA、iNOS mRNA和HO-1 mRNA表达的水平;电镜下观察海马神经元的超微结构，计算线粒体变性率。结果 与Ⅰ组比较，Ⅱ组海马组织中H2S、NO、CO、CBS、iNOS、HO、CBS mRNA、iNOS mRNA和HO-1 mRNA水平及线粒体变性率升高（P〈0．05或0．01）;与Ⅱ组比较，Ⅲ组、Ⅳ组海马组织中H2S、CO、HO和HO-1 mRNA水平升高，NO、CBS、iNOS、CBS mRNA和iNOS mRNA水平及线粒体变性率降低（P〈0．05或0．01）。结论 外源性H2S通过抑制iNOS／NO、激活HO-1／CO减轻了大鼠脑缺血再灌注损伤。     

外源性一氧化氮对脑缺血-再灌注损伤大鼠海马气体信号分子的影响

目的 研究外源性一氧化氮(NO)对脑缺血-再灌注(I-R)损伤大鼠海马气体信号分子的影响.方法 24只Wistar大鼠随机均分为四组:脑I-R对照组(Ⅰ组),脑I-R+低浓度硝普钠(SNP)组(Ⅱ组)和脑I-R+高浓度SNP组(Ⅲ组),对照组(Ⅳ组).夹闭两侧颈总动脉制作大鼠全脑I-R模型.颈总动脉夹闭前30 min分别腹腔注射SNP 2 mg/kg(Ⅱ组)或4 mg/kg(Ⅲ组).脑缺血20 min,再灌注6 h后处死大鼠,取脑海马组织,检测硫化氢(H_2S)、NO和CO的量和胱硫醚β-合酶(CBS)、血红素氧合酶-1(HO-1)和诱导型一氧化氮合酶(iNOS)活性,以及CKS mRNA、iNOS mRNA和HO-1-mRNA表达水平.结果 Ⅰ、Ⅱ、Ⅲ组大鼠海马中H_2S、NO和CO的含量和CBS、HO和iNOS的活性均高于Ⅳ组;CBS mRNA、iNOS mRNA和HO-1 mRNA表达增高(P<0.05或P<0.01);Ⅱ、Ⅲ组大鼠海马中的上述指标均高于Ⅰ组(P<0.05或P<0.01).结论 外源性NO能诱导脑I-R后大鼠海马CBS mRNA和HO-1 mRNA表达,激活CBS和HO.在脑I-R损伤过程中存在N0对CBS/H2S和HO-1/CO系统的调节.     

胱硫醚β-合酶/硫化氢和血红素氧合酶-1/一氧化碳体系在大鼠脑缺血再灌注损伤中的作用

目的 研究胱硫醚β-合酶（CBS）／硫化氢（H2S）体系和血红素氧合酶-1（HO-1）／一氧化碳（CO）体系在大鼠脑缺血再灌注损伤中的作用。方法 30只Wistar大鼠随机分为5组（n=6）：对照组（C组）、脑缺血再灌注组（I／R组）、脑缺血再灌注＋锌原卟啉（HO-1抑制剂）组（I／R＋Z组）、脑缺血再灌注＋羟氨（CBS抑制剂）组（I／R＋H组）、脑缺血再灌注＋锌原卟啉＋羟氨组（I／R＋Z＋H组）。采用四血管阻断法建立全脑缺血再灌注损伤模型，I／R＋Z组、I／R＋H组和I／R＋Z＋H组夹闭两侧颈总动脉前30min分别腹腔注射锌原卟啉45／zmol／kg、羟氨5mmol／L、羟氨5mmol／L＋锌原卟啉45／maol／kg1ml，C、I／R组给予等量生理盐水。再灌注6h时处死大鼠，取海马，测定海马组织H2S、CO、还原型谷胱甘肽（GSH）、丙二醛（MDA）、超氧化物歧化酶（SOD）水平及CBSmRNA和HO-1mRNA的表达；电镜下观察海马线粒体变性情况。结果 与C组比较，I／R组海马组织CO、H2S、CBSmRNA和HO-1mRNA、MDA水平及线粒体变性率均升高，海马组织SOD、GSH水平降低（P〈0．01）；与I／R组比较，I／R＋Z组海马组织CO、HO-1mRNA水平降低，海马组织H2S、CBSmRNA、GSH、MDA水平升高，I／R＋H组海马组织CO、HO-1mRNA、MDA水平升高，H2S、CBSmRNA、GSH水平降低；I／R＋Z＋H组海马组织CO、RS、HO-1mRNA和CBSmRNA、SOD、GSH水平降低，线粒体变性率升高（P〈0．05）。结论 CBS／H1S体系和HO-1／CO体系可拮抗大鼠脑缺血再灌注损伤，其作用可相互代偿。     

内源性CO和NO在大鼠脑缺血-再灌注损伤中的作用

目的 研究血红素氧合酶-1(heme oxygenase-1,HO-1)/一氧化碳(CO)体系和诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)/一氧化氮(NO)体系在大鼠脑缺血-再灌注损伤中的相互作用,探讨脑保护策略.方法 24只Wistar大鼠随机均分为四组:脑缺血-再灌注+锌原踮啉组(Z组)、脑缺血-再灌注+氨基胍组(A组)、脑缺血-再灌注组(IR组)、假手术组(C组).Z组和A组夹闭两侧颈总动脉前30 min腹腔分别注射锌原卟啉45 μmol/kg或氨基胍500 mg/kg,C组和IR组腹腔注射等量生理盐水.缺血20 min再灌注6h后处死大鼠取海马,检测大鼠海马组织中CO、NO、SOD、MDA量的变化及HO-1-mRNA和iNOS-mRNA表达水平;电镜观察海马线粒体的变化.结果 与C组相比,IR组CO、NO、MDA的含量增高,SOD降低,HO-1-mRNA和iNOS-mRNA表达增高(P<0.01),电镜观察线粒体受损.与IR组相比,Z组CO和SOD的量降低,NO、MDA的量增高,HO-1-mRNA的表达降低(P<0.01),电镜观察线粒体受损加重;A组NO、MDA的量降低,SOD的量增高,iNOS-mRNA表达降低(P<0.01),电镜观察线粒体受损减轻.结论 脑缺血-再灌注损伤过程中,iNOS/NO体系介导了神经细胞的损伤,而HO-1/CO体系具有抗损伤的作用;iNOS抑制剂在脑缺血-再灌注损伤过程中对神经细胞有保护作用.     

七氟醚预先给药对大鼠心肌缺血再灌注损伤时胱硫醚β-合酶和血红素氧合酶-1表达的影响

目的 评价七氟醚预先给药对大鼠心肌缺血再灌注损伤时胱硫醚β-合酶(CBS)和血红素氧合酶-1(HO-1)表达的影响.方法 健康成年雄性SD大鼠30只,体重180～220 g,采用随机数字表法,将大鼠随机分为3组(n=10):假手术组(S组)、缺血再灌注损伤组(I/R组)和七氟醚组(Sev组).结扎左冠状动脉前降支,缺血30 min,再灌注2h,制备心肌缺血再灌注损伤模型.Sev组于缺血前吸入七氟醚,呼气末浓度1.5％～1.7％,60 min后制备心肌缺血再灌注损伤模型.于再灌注2h时处死大鼠,取心肌组织,测定MDA含量(硫代巴比妥酸法)、SOD活性(黄嘌呤氧化酶法)、GSH含量(荧光法)、H2S含量(分光光度法)、CO含量(分光光度法)、CBS mRNA和HO-1 mRNA表达(RT-PCR法),电镜下观察心肌细胞超微结构.结果 与S组比较,I/R组和Sev组CO、H2S、MDA含量和心肌细胞线粒体变性率升高,CBS mRNA和HO-1 mRNA表达上调,SOD活性及GSH含量降低(P＜0.05);与I/R组比较,Sev组CO、H2S、MDA含量和心肌细胞线粒体变性率降低,CBS mRNA和HO-1 mRNA表达下调,SOD活性和GSH含量升高(P＜0.05).结论 七氟醚预先给药减轻心肌缺血再灌注损伤的机制与下调CBS和HO-1的表达有关.     

七氟醚对内毒素诱导大鼠肺组织氧化应激反应的影响

目的 探讨七氟醚对内毒素（LPS）诱导大鼠肺组织氧化应激反应的影响。方法Wistar大鼠48只，体重200-290g，随机分为4组（n=12）：对照组（C组）、LPS组（L组）、1．0MAC七氟醚组（S1L组）和1．5MAC七氟醚组（S2L组）。各组大鼠腹腔注射异戊巴比妥钠100mg／kg，麻醉后机械通气。维持呼气末二氧化碳分压在35～45mmHg。L组股静脉注射LPS5mg／kg，C组给予生理盐水1．2ml，S1L组、S2L组注射LPS后分别吸入1．0MAC、1．5MAC七氟醚4h。吸入七氟醚后4h处死大鼠，测定肺组织超氧化物超歧化酶（SOD）、丙二醛（MDA）、一氧化氮（NO）、总一氧化氮合酶（tNOS）水平、诱导型一氧化氮合酶（iNOS）活性及iNOS mRNA、蛋白表达。结果 与C组比较，L组肺组织SOD活性下降，MDA、NO、tNOS水平、iNOS活性及iNOS mRNA及蛋白表达均升高（P〈0．01）；与L组比较，S1L组、S2L组肺组织SOD活性升高，MDA、NO、tNOS水平及iNOS mRNA及蛋白表达降低（P〈0．05）；S1L组与S2L组上述各项指标比较差异无统计学意义（P〉0．05）。结论 吸入1．0MAC和1．5MAC七氟醚4h可减轻LPS诱导肺组织氧化应激反应。     

异氟醚对大鼠全脑缺血再灌注时海马ICAM-1 mRNA和外周血中性粒细胞表面CD11b/CD18表达的影响

目的 探讨异氟醚对大鼠全脑缺血再灌注时海马组织ICAM-1 mRNA和外周血中性粒细胞表面CD11b/CD18表达的影响.方法 Wistar大鼠63只,随机分为3组(n=21):假手术组(S组)、缺血再灌注组(I/R组)和异氟醚组(Iso组).采用四血管阻断法制备全脑缺血再灌注模型.Iso组在四血管阻断过程中及再灌注早期吸入1.4%异氟醚.于再灌注6、24、72 h时,采集外周静脉血,采用流式细胞仪测定中性粒细胞表面CD11b/CD18和CD18的表达;RT-PCR法测定海马组织细胞间粘附分子-1(ICAM-1)mRNA和核因子κB(NF-κB)mRNA的表达.结果 与S组比较,I/R组再灌注6 h时CD11b/CD18和CD11b表达上调,再灌注24、72 h时ICAM-1 mRNA表达上调,I/R组和Iso组再灌注24 h时NF-κB mRNA表达上调(P＜0.05或0.01);与I/R组比较,Iso组再灌注6 h时CD11b表达下调,再灌注24 h时ICAM-1 mRNA表达下调(P＜0.05).结论 异氟醚可减轻大鼠全脑缺血再灌注损伤,可能与其抑制海马ICAM-1 mRNA及外周血中性粒细胞表面CD11b/CD18的表达有关.     

七氟醚后处理对大鼠脑缺血-再灌注损伤海马血红素氧合酶-1蛋白表达的影响

目的 探讨七氟醚后处理对大鼠脑缺血-再灌注损伤的保护作用及血红素氧合酶-1(HO-1)在其中的作用.方法 清洁级雄性SD大鼠40只,体重230～270 g,随机均分为五组:假手术组(C组),缺血-再灌注组(IR组),七氟醚组(S组),七氟醚+锌原卟啉Ⅸ(Znpp)组(SZ组)和溶剂对照组(SD组).采用双侧颈总动脉夹闭合并取血降压再回输的方法制备脑缺血-再灌注损伤模型,S组再灌注前5 min气管插管,吸入1MAC七氟醚15 min; SZ组模型制备前腹腔注射Znpp45μmol/kg,溶于二甲基亚砜(DMSO)0.5 ml; SD组模型制备前腹腔注射DMSO 0.5 ml.所有大鼠再灌注24 h后处死,取海马.光镜下观察各组海马病理学变化,检测海马超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量和HO-1蛋白表达.结果 与C组比较,其余四组SOD活性明显降低(P＜0.05),MDA含量明显升高(P＜0.05),SZ组HO-1蛋白表达差异无统计学意义,IR、S和SD组HO-1蛋白表达明显升高(P＜0.05).与IR组比较,S组和SD组SOD活性和HO-1蛋白表达明显升高(P＜0.05),MDA含量明显降低(P＜0.05),SZ组HO-1蛋白表达明显降低(P＜0.05).光镜下S组和SD组海马病理学损伤较IR组和SZ组减轻.结论 七氟醚后处理对大鼠脑缺血-再灌注损伤有保护作用,其作用机制可能与七氟醚上调脑组织中HO-1蛋白表达有关.     

七氟醚预处理对局灶性脑缺血再灌注损伤大鼠海马TREK-1表达的影响

目的 探讨七氟醚预处理对局灶性脑缺血再灌注损伤大鼠海马机械敏感性钾通道TREK-1表达的影响.方法 健康雄性SD大鼠36只,体重240～280 g,随机分为3组(n=12):假手术组(S组)、局灶性脑缺血再灌注组(l/R组)和七氟醚预处理组(Sevo组).结扎右侧颈总动脉、颈外动脉,采用线栓法阻断颈内动脉2 h,再灌注24 h制备大鼠局灶性脑缺血再灌注损伤模型;Sevo组于缺血前1 h经半密闭的吸入箱持续吸入含2.5%七氟醚的02;S组仅分离并结扎右侧颈总动脉、颈外动脉,不置入线栓.各组于再灌注24 h时行神经功能缺陷评分后断头取脑,TIC染色后测定脑梗死体积,采用RT-PCR法测定海马TREK-1 mRNA的表达.结果 与S组相比,I/R组和Sevo组神经功能缺陷评分和脑梗死体积比升高(P<0.01);与I/R组相比,Sevo组神经功能缺陷评分和脑梗死体积比降低,海马TREK-1 mRNA表达上调(P<0.05).结论 七氟醚预处理可通过激活海马TREK-1减轻大鼠局灶性脑缺血再灌注损伤.     

地氟醚对内毒素诱导大鼠肺组织氧化应激反应的影响

目的探讨地氟醚对内毒素（LPS）诱导大鼠肺组织氧化应激反应的影响。方法雄性Wistar大鼠48只,体重200～290 g,随机分为4组（n=12）,对照组（C组）股静脉注射生理盐水1.2ml后机械通气4 h;LPS组（L组）股静脉注射LPS 5mg/kg后机械通气4 h;地氟醚1.0MAC组（D1）和地氟醚1.5 MAC组（D2）组：股静脉注射LPS 5 mg/kg后机械通气,分别吸入地氟醚1.0 MAC和1.5 MAC 4 h,机械通气4 h后处死大鼠,测定肺组织超氧化物歧化酶（SOD）活性、丙二醛（MDA）含量、一氧化氮（NO）含量、总一氧化氮合酶（tNOS）活性、诱导型一氧化氮合酶（iNOS）活性、iNOS mRNA和iNOS表达水平。结果与C组比较,L组SOD活性下降,MDA含量、NO含量、tNOS活性、iNOS活性、iNOS mRNA和iNOS表达升高（P〈0.01）;与L组比较,D1组上述各项指标差异无统计学意义（P〉0.05）,D2组SOD活性下降,MDA含量、iNOS活性、iNOS mRNA和iNOS表达升高（P〈0.05）;与D1组比较,D2组SOD活性下降,MDA含量、iNOS活性、iNOS mRNA和iNOS表达升高（P〈0.05）。结论吸入地氟醚1.5 MAC 4 h可加重LPS诱导大鼠肺组织氧化应激反应,吸入地氟醚1.0 MAC对其无影响。     

Calcium/phosphate/vitamin D homeostasis and bone mass in patients after gastrectomy,vagotomy, and cholecystectomy

Sixty-two outpatients were assessed and divided into the following groups: 20 patients who had had partial gastrectomy (PG group), 22 patients who had had truncal vagotomy and pyloroplasty (TV group) or high selective vagotomy (HSV group), and 20 patients who had had cholecystectomy (CH group). The patients' age ranged from 35 to 64 years (mean 45 years), and the average postoperative period was 9 years. None of the patients evidenced clinical or biochemical symptoms of malnutrition or malabsorption or of diseases affecting vitamin D metabolism. The function of the kidneys and the liver was normal. An age-matched group of volunteers served as a control group. The calcium dietary intake was determined using a standardized questionnaire; and the levels of serum calcium (Ca_s), phosphate (P_s), alkaline phosphatase (AP), and 25-hydroxyvitamin D [25(OH)D] and the excretion of Ca in a sample of fasting urine corrected for concurrent creatine excretion (FuCa/cr) were assessed by means of standard laboratory techniques. The bone mineral density (BMD) of the lumbar spine (L2–4) and femoral neck (neck-L) was determined by means of dual energy x-ray absorptiometry (DXA). The daily Ca dietary intake was lower than recommended (RDA) in 80% of the patients, with most of them ingesting less than 300 mg daily. The mean values of Ca₂, P₂, AP, and FuCa/cr did not differ from these in the controls. Significantly reduced 25(OH) D levels were observed in the PG group (7.0 ng/ml) (p<0.001) and CH group (12.5 ng/ml) (p<0.01) compared with the values in the control group (20.0 ng/ml). The serum 25 (OH)D concentration was correlated with the Ca_s level and postoperative period. The BMD of L2–4 was decreased in all postoperative patients compared to that in the control group (in the PG group the BMD was 80±2%; in the CH group 95±2%; and in the TV or HSV group 94 ±1%) (p<0.05). In both L2–4 and three sites of the femoral neck in was lowest in the PG group (neck 94±1%; Ward's triangle 93±3%; trochanter 95±2%) compared with the CH group (neck 98±1%; Ward's triangle 100±1%; trochanter 98±1%) and with TV or HVS group (100±1%; 100±1%; 98±1%, respectively) (p<0.05). In the postgastrectomy group BMD showed a significant negative correlation with the interval following gastrectomy and Ca excretion in urine but a significant positive correlation with the Ca level and serum 25 (OH)D concentration. The BMD in the CH group showed a positive correlation only with the serum 25(OH)D concentration. Gastrectomy and cholecystectomy without postoperative supplementation of Ca and vitamin D led to insidious disturbances in the calcium-vitamin D homeostasis and osteopenia. Therefore we suggest that immediate supplementation of calcium and vitamin D be initiated as a routine postoperative procedure, particularly in countries where routine fortification of food with Ca and vitamin D is not carried out.

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Resumen Sesenta y dos pacientes ambulatorios fueron valorados y divididos en los siguientes grupos: 20 postgastrectomía (PG), 22 postvagotomia troncular y piloroplastia o vaguectomía altamente selectiva (TA o HSV), 20 postcolecistectomía (CH). Las edades fluctuaron entre 35 y 64 años (media 45) y el período postoperatorio promedio fue de 9 años. Ninguno de los pacientes exhibió evidencia clínica o sítomas bioquímicos de malnutrición o malabsorción ni enfermedades relacionadas con el metabolismo de la vitamina D. La función renal y hepática apareció normal. Se estableció un grupo de voluntarios de similares edades como groupo control. La ingesta de calcio (Ca) en la dieta fue determinado mediante cuestionario estandarizado y los niveles de calcio sérico (Ca_S) fosfato (P_S) y fosfatasa alcalina (AP), 2.5 hidroxivitamina D/25(OH)D/, la excreción de calcion en una muestra de orina en ayunas corregida para el valor concomitante de excreción de creatinina (cr) (FuCa/cr) fueron valorados mediante técnicas rutinarias de laboratorio. La densidad mineral ósea (BMD) de la columna lumbar (L₂–L₄) y del cuello del fémur fucron determinados por absorciometría. La ingesta de Ca dietario apareció menor de lo recomendable (RDA) en 80% de los pacientes, con la mayoría de ellos exhibiendo una ingesta de menos de 300 mg diarios. Los valores medios de Ca_S, P_S, AP, FuCa/cr no resultaron differentes de los obtenidos en los voluntarios del grupo control. Se observaron niveles significativamente reducidos de 25(OH)D en el grupo PG (7.0 ng/ml) (p<0.001) y en el grupo CH (12.5 NG/ML) (p<0.01) en comparación con los valores en el grupo control (20.0 ng/ml). Las concentraciones séricas de 25(OH)D fueron correlacionadas con los niveles ed Ca_S en el período postoperatorio. La densidad mineral de (L₂–L₄) apareció disminuida en todos los pacientes postoperados en comparación conel grupo control (80±2% en el grupo PG; 95±2% en el grupo CH y 94±1% en el grupo HSV o en el TV) p<0.05. La densidad mineral tanto en L₂–L₄ como en tres lugares del cuello femoral apareció más baja en el grupo PG (cuello: 94±1%; triángulo de Ward 93±3%; trocánter 98±1%) y en los grupos HV y HSV (100±1%; 100±1%; 98±1%, respectivamente) p<0.05. En el grupo PG la densidad mineral ósea exhibió significativa correlación negativa con el intervalo luego el la gastrectomía y la excreción de Ca en la orina, con significativa correlación positiva con el nivel de Ca y la concentración sérica de 25(OH)D. La gastrectomía y la colecistectomía sin suplementación postoperatoria de Ca y de vitamina D resultó en alteraciones de la homeostasis del Ca-vitamina D y osteopenia. Por consiguiente. sugerimos la suplementación inmediata de calcio y vitamina D como recomendación rutinaria luego de un procedimiento operatorio, especialmente en países donde no se hace la fortificación rutinaria de los alimentos con Ca y vitamina D.

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Résumé Soixante-deux patients ont été divisés en trois groupes pour analyse: 20 patients ayant eu une gastrectomie partielle (GP), 22 patients ayant eu une vagotomie tronculaire et pyloroplastie (VT) ou vagotomic hypersélective (VHS) et 20 patients ayant eu une cholécystectomie (C). L'âge des patients allait de 35 à 64 (moyen = 45) ans et le suivi moyen a été de 9 ans. Aucun de ces patients n'avaient de symptômes cliniques ou biologiques de malnutrition, de malabsorption ou de maladies du métabolisme vitaminique D. La fonction rénale et hépatique était normale. Un groupe de volontaires, appariés en âge, ont servi de contrôles. L'ingestion de calcium a été déterminée d'après un questionnaire standardisé, et les niveaux de calcium (Ca), de phosphates (Ph), de phosphatases alcalines (PA), de 25-hydroxyvitamine D/25(OH)D, ainsi que l'excrétion de Ca dans les urines corrigée par rapport à la créatinine (FuCa/cr), ont été évaluées. Les densités osseuses minérales (DOM) du rachis lombaire (L2–L4) et du col fémoral (SF) ont été déterminées par l'absorptiométrie aux rayons X (ARX). L'ingestion en Ca était inférieure aux normes chez 80% des patients, inférieure à 300 mg par jour chez la plupart. Les valeurs moyennes de Ca, de P, de PA, et du FuCa/cr ne différaient pas beaucoup des contrôles. Les taux de 25 (OH) D étaient diminués chez les PG (7.0 ng/ml) (p<0.001) et chez les C (12.5 ng/ml) (p<0.01) comparés aux valeurs du groupe contrôle (20.0 ng/ml). Les taux de 25 (OH) D était corrélés avec des taux de Ca et les valeurs postopératoires. La DOM était diminuée chez tous les opérés comparés aux contrôles 80±2% chez les PG, (95±2% chez les C et 94±1% chez les VT ou VHS) (p<0.05). Les taux les plus bas ont été enregistrés chez les PG (94±1% au col fémoral; 93±3% au triangle de Ward et 95±2% au trochanter fémoral) comparé au C (98±1% au col, 100±1% au triangle de Ward, et 98±1% au trochanter) et aux VH ou VHS (100±1%, 100±1% et 98±1%, respectivement) (p<0.05). Dans le groupe post-gastrectomie, la DOM corrélait négativement avec l'intervalle après gastrectomie et l'excrétion du Ca dans les urines, mais corrélait positivement avec des concentrations du Ca et du 25 (OH)D. Chez les C, la DOM corrélait avec les concentration 25 (OH)C seulement. La gastrectomie ou la cholécystectomie sans apport supplémentaire postopératoire en Ca et en vitamine D provoquent des troubles insidieux de l'homéostasie calcium/vitamine D et une ostéopénie. Nous suggérons de donner de façon systématique du Ca et de la Vitamine D en postopératoire, particulièrement dans les pays où ces deux éléments ne sont pas introduits de façon systématique dans l'alimentation.

     

Screening for Gastrointestinal,Hepatic/Biliary,and Renal/Urologic Disease

Narrative ReviewMany organ systems in the body can demonstrate signs and symptoms of impairment that mimic integumentary, musculoskeletal, and/or neuromuscular conditions commonly evaluated and treated by the hand therapist. In this review, diseases and disorders affecting the gastrointestinal (GI), hepatic/biliary, and renal/urologic systems capable of referring pain and other symptoms to the upper quadrant are presented. Specifically, these organ systems can refer pain to the sternum, neck, shoulder, scapulae, and subscapular and interscapular regions. Symptom referral from the viscera to the elbow and hand is extremely rare. Symptoms of carpal tunnel syndrome/paresthesias can occur in renal disorders and with hepatic/biliary problems. Following the screening model proposed by Goodman and Snyder, potential origins from the GI, hepatic/biliary, and renal/urologic systems are discussed. The goal is to identify patients with referred pain patterns and associated signs and symptoms of conditions that require referral to a physician or other appropriate health care professional. The alert hand therapist will recognize red flag histories, clinical presentation, and risk factors suggesting the need for a more thorough examination to ensure that the patient/client has a condition requiring intervention that is within the scope of the therapist's practice. Screening principles and tips for physician referral are offered.Level of Evidence5.     

The Role of RANK/RANKL/OPG Signalling Pathways in Osteoclastogenesis in Odontogenic Keratocysts, Radicular Cysts, and Ameloblastomas

The aim of this study was to evaluate the immunohistochemical expression of molecules involved in osteoclastogenesis, including the receptor activator of nuclear factor kappa B (RANK), RANK ligand (RANKL) and osteoprotegerin (OPG) in odontogenic keratocysts (OKCs), which has been named as a keratocystic odontogenic tumour by the WHO, and compare their expression with radicular cysts and ameloblastomas. RANK is a member of tumour necrosis factor receptor family and it is activated by RANK ligand. OPG binds to RANKL and inactivates it. The imbalance of these factors could cause the differential bone resorption activity in some diseases and tumours. The expression of these molecules was evaluated in ameloblastomas (n = 20), OKCs (n = 20), and radicular cysts (n = 20) by immunohistochemistry. Immunohistochemical reactivity for RANK, RANKL, and OPG was detected in neoplastic and nonneoplastic epithelium and connective tissue cells. RANK showed the greatest expression in OKCs followed by ameloblastomas, with the lowest expression seen in radicular cysts. Expression of RANKL was detected in all lesions and no significant differences were observed between groups. OPG was expressed very low in all groups. In the stroma, the number of RANK positive cells was higher in OKCs when compared with ameloblastomas and radicular cysts but radicular cyst had higher numbers of RANKL positive cells in the stroma than ameloblastomas. The molecular system of RANK/RANKL/OPG is variably expressed in OKCs, radicular cysts, and ameloblastomas and this system may be involved in the osteoclastogenic mechanisms in OKCs and ameloblastomas. Advanced studies could further clarify the role of RANK, RANKL, and OPG in mediating tumour associated bone osteolysis.     

Dental, orthodontic, and oral/maxillofacial evaluation and treatment in Apert syndrome

Although the cause of the midfacial anomalies in Apert syndrome is still elusive, a great experience has accrued in the management of these physically and psychologically handicapping deformities. An interdisciplinary approach that includes input from an orthodontist, pediatric dentist, and oral and maxillofacial surgeon should be an integral part of the management of affected patients. This theme of surgical-orthodontic-dental communication and interaction is stressed and illustrated throughout the article.