慢性氟中毒大鼠大脑皮质NOS阳性神经元的变化

目的　探讨慢性氟中毒对大鼠大脑皮质一氧化氮合酶（NOS）阳性神经元的影响。方法　采用NADPH-黄递酶（NADPH-d）组织化学方法，标记大脑皮质NOS阳性神经元，对慢性氟中毒大鼠大脑皮质NOS阳性神经元变化进行计数。结果　慢性氟中毒大鼠皮质NOS阳性神经元数明显少于对照组（P<0.01）。结论　慢性氟中毒大鼠脑内皮质NOS阳性神经元的改变可能是氟中毒影响脑功能的重要原因之一。     

氟对大鼠脑髓鞘碱性蛋白及髓鞘磷脂质损伤的研究

目的：研究氟对大鼠脑有髓神经髓鞘形态及化学组份的影响，进一步探讨氟对大脑髓鞘碱性蛋白（MBP）及髓鞘磷脂质损伤机理。方法：取饮用含F^－150mg/L水7个月大鼠的脑组织，应用Anti-MBP-HRP免疫组化法标记大脑髓鞘碱性蛋白分布，用组织化学法观察大脑髓鞘脂质改变,MBP－ELISA法分析血清中MBP含量。结果：免疫组化显示，氟中毒大鼠大脑髓鞘染色变浅，髓鞘结构解紊乱和均质化，证明髓鞘MPB缺失或溶解，组化法显示，氟组大鼠大脑髓鞘磷脂溶解，成空泡状或状样变，且染色变浅，说明高氟对髓鞘磷脂产生了破坏作用，实验组动物血清中MBP含量显著升高与对照组比较差异有显著意义，个体间MBP含量高低与免疫组化结果呈相关关系。结论：氟中毒可造成大鼠大脑中枢有髓神经鞘直接损伤，髓鞘MBP缺失，髓鞘脂质解，髓鞘结构被破坏。     

氟中毒与红细胞

就近年来有关氟中毒对红细胞三磷酸腺苷酶（ATPase）活性、唾液酸（SA）含量、抗氧化功能、免疫功能和红细胞形态影响的研究进行了较为详尽的综述，为进一步研究氟中毒引起贫血的机理和生产实践中防治氟中毒提供参考。     

慢性氟中毒、砷中毒及氟砷联合中毒大鼠脊髓神经丝蛋白免疫组织化学比较研究

用神经丝（ＮＦ）免疫组织化学方法研究了大鼠氟、砷及氟砷联合中毒后３５天、３个月和６个月脊髓神经元的病理性改变。结果：中毒３５天氟砷联合中毒组ＮＦ免疫组织化学反应阴性（－），３个月以后反应增强，呈（）。而氟中毒或砷中毒组中毒３５天反应即呈强阳性（），３个月以后反应减弱，呈（），且随中毒时间延长，反应进一步减弱，呈（＋）。从结果推测中毒早期氟与砷之间有协同作用，中毒晚期有拮抗作用。     

慢性氟中毒哺乳期大鼠脑干5-羟色胺神经元的免疫细胞化学研究

目的：探讨慢性氟中毒哺乳期大鼠脑干5－羟色胺（5－HT）神经元的病理变化。方法：以饮用含氟水的方法复制哺乳期大鼠慢性氟中毒模型，对脑干中缝核群5－羟色胺神经元进行免疫细胞化学定性、定量研究。结果：慢性氟中毒大鼠脑干中缝核群5－HT神经元减少，胞质内5－HT阳性反应颗粒减少且界限不清，显微图象分析仪定量检测神经元内5－HT含量降低。结论：高氟对中枢神经系统有直接损害。     

氟对人胎腺上皮细胞超微结构的影响

目的观察氟病区胎儿肝、肾上腺、甲状腺上皮细胞的超微结构变化，为研究氟对细胞损伤机理提供实验依据。方法收集氟病区胎儿１０例，其母亲均有氟斑牙，尿氟含量为（４．３７±２．９４）ｍｇ／Ｌ。非氟病区胎儿１０例，其母亲无氟斑牙，尿氟含量为（１．６７±０．８２）ｍｇ／Ｌ。用氟电极法测定胎儿骨氟含量。取胎儿肝脏、肾上腺、甲状腺组织作电镜检查。结果病区胎儿骨氟含量（２．７７±０．２５）ｍｇ／ｋｇ，与非病区胎儿骨氟（２．５０±０．１１）ｍｇ／ｋｇ相比，差异有显著性（ Ｐ<０． ０１）。电镜观察结果：细胞膜的主要变化是微绒毛变短、变少，甚至消失。细胞间连接松解，结构紊乱。病变严重者有髓鞘样结构形成。线粒体的主要变化为：线粒体肿胀、体积增大，甚至嵴消失，呈空泡状。内质网的主要病变为粗面内质同扩张呈囊状，网上核蛋白体部分脱失。细胞核的主要病变为核膜的双层结构破坏，呈囊状扩张。有的细胞浆内出现巨大包涵体或异常电子致密度较高的颗粒。结论氟对细胞结构的破坏是多方面的。氟中毒时细胞膜、线粒体、粗面内质网及核膜均可受到损伤。     

慢性氟中毒大鼠垂体生长激素细胞及下丘脑生长抑素神经元…

本实验对慢性氟中毒大鼠垂体生长激素（ＧＨ）细胞及下丘脑生长抑素（ＳＳ）神经元分析了免疫细胞化学染色，并用图像分析仪对ＧＨ及ＳＳ进行了半定量分析，结果表明：同对照组相比，氟中毒垂体ＧＨ细胞中的阳性反应颗粒细小并弥散地分布，半定量分析表明其ＧＨ含量明显低于对照组，未见下丘脑ＳＳ神经元及其ＳＳ含量有明显改变，本研究结果提示高氟可直接作用于垂体ＧＨ细胞影响其合成分泌功能。     

实验性氟中毒大鼠中缝背核神经元超微结构研究

以喂饲高氟（１００ｍｇ／Ｌ）水的方法制造了雄性大鼠慢性中毒模型，透射电子显微镜下观察了大鼠中缝背核（ＮＲＤ）神经元的超微结构变化。结果表明，氟中毒大鼠ＮＲＤ神经元出现超微结构改变。主要表现为神经元的核浆比值增大，核内异染色质增多且边集，线粒体扩张，嵴断裂或消失，粗面内质网池，高尔基复合体扁平囊亦扩张。神经元胞体，尤其是突起中脂褐素明显增多，并有较多的自噬体出现。个别神经元固缩。神经纤维有髓鞘松散及     

实验性氟中毒大鼠关节滑膜细胞的体视学研究

为探讨氟中毒对关节滑膜的损伤，用１２只Ｗｉｓｔａｒ大鼠随机分为对照组和实验组。实验大鼠饲以５０ｍｇ／Ｌ含氟水１２０ｄ后，取关节滑膜进行超微结构体视学检查。结果显示：氟中毒大鼠关节滑膜细胞体积缩小，线粒体肿胀、增生，与对照组比较，差异有显著性（Ｐ＜０．０５）。表明过量氟对滑膜细胞有损伤作用。     

慢性氟、砷及联合中毒对小鼠大脑脂质过氧化功能的影响

目的 探讨慢性氟、砷及联合中毒对小鼠大脑脂质过氧化损害程度。方法 昆明种小白鼠120只．随机分成对照、氟中毒、砷中毒和氟砷联合中毒4组．分别自由饲用普通、高氟、高砷和高氟高砷饲料。饲养6和12个月。分别检测小鼠大脑LPO和GSH含量、脑SOD、GSH—Px、SDHase和G-6-Pase活性。结果 3种中毒均可引起小鼠大脑LPO含量显著升高，脑GSH含量，SOD、GSH-Px、SDHase和G-6-Pase活性显著降低。但3种中毒对这些指标的影响程度是不同的。结论 慢性氟、砷和联合中毒均能引起小鼠大脑发生脂质过氧化损害作用．可能损害脑细胞的线粒体和微粒体，氟、砷对这一损害作用存在一定的相互影响。     

Biliary microlithiasis,sludge,crystals,microcrystallization,and usefulness of assessment of nucleation time

BACKGROUND:The process of microcrystallization,its sequel and the assessment of nucleation time is ignored.This systematic review aimed to highlight the importance of biliary microlithiasis,sludge,and crystals,and their association with gallstones,unexplained biliary pain,idiopathic pancreatitis, and sphincter of Oddi dysfunction.DATA SOURCES:Three reviewers performed a literature search of the PubMed database.Key words used were"biliary microlithiasis","biliary sludge","bile crystals","cholesterol crystallisation","bile microscopy","microcrystal formation of bile","cholesterol monohydrate crystals","nucleation time of cholesterol","gallstone formation","sphincter of Oddi dysfunction"and"idiopathic pancreatitis".Additional articles were sourced from references within the studies from the PubMed search.RESULTS:We found that biliary microcrystals account for almost all patients with gallstone disease,7%to 79%with idiopathic pancreatitis,83%with unexplained biliary pain, and 25%to 60%with altered biliary and pancreatic sphincter function.Overall,the detection of biliary microcrystals in gallstone disease has a sensitivity ranging from 55%to 87%and a specificity of 100%.In idiopathic pancreatitis,the presence of microcrystals ranges from 47%to 90%.A nucleation time less than 10 days in hepatic bile or ultra-filtered gallbladder bile has a specificity of 100%for cholesterol gallstone disease.CONCLUSIONS:Biliary crystals are associated with gallstone disease,idiopathic pancreatitis,sphincter of Oddi dysfunction, unexplained biliary pain,and post-cholecystectomy biliary pain.Pathways of cholesterol super-saturation,crystallisation, and gallstone formation have been described with scientificsupport.Bile microscopy is a useful method to detect microcrystals and the assessment of nucleation time is a good method of predicting the risk of cholesterol crystallisation.     

Antibacterial activity of cefpodoxime in comparison with cefixime,cefdinir, cefetamet,ceftibuten, loracarbef,cefprozil, BAY 3522, cefuroxime,cefaclor and cefadroxil

Summary The new oral cephalosporins cefpodoxime, cefixime, cefdinir, cefetamet and ceftibuten demonstrate enhanced activity against Enterobacteriaceae susceptible to the established compounds as well (e.g. cefuroxime, cefaclor, cefadroxil). In addition, cefpodoxime, cefixime, cefdinir, cefetamet and ceftibuten include in their spectrum species hitherto resistant to oral cephalosporins (Proteus vulgaris, Providencia spp.,Yersinia enterocolitica). Besides, the majority of these compounds demonstrate relevant activity (MIC₅₀ equal to or below 2 mg/l) againstEnterobacter spp.,Citrobacter freundii, Serratia spp. andMorganella morganii. Ceftibuten is the most potent oral cephalosporin against most of the Enterobacteriaceae. Non-fermentative bacilli (Acinetobacter spp.,Pseudomonas spp.) remain completely resistant to oral cephalosporins (except someAcinetobacter species against cefdinir andPseudomonas cepacia against ceftibuten). Antistaphylococcal activity for oral cephalosporins is highest for cefdinir followed by BAY 3522, cefprozil, cefuroxime and cefpodoxime. Loracarbef, cefaclor and cefadroxil are about equally active, while the other compounds are only weakly active (cefixime) or inactive (cefetamet, ceftibuten). Enterococci are insensitive to new generation oral cephalosporins as they have been to established compounds. The most active oral cephalosporins against hemolytic streptococci are cefdinir and cefprozil.Streptococcus pneumoniae, Streptococcus milleri andStreptococcus mitior are most susceptible to cefpodoxime, cefdinir, cefuroxime and BAY 3522. Penicillin resistant pneumococci have to be regarded as resistant to all oral cephalosporins. Fastidious pathogens likeHaemophilus spp.,Moraxella catarrhalis andNeisseria gonorrhoeae are more susceptible to cefpodoxime, cefixime, cefdinir, cefetamet and ceftibuten than to the other oral cephalosporins. The activity of oral cephalosporins is only weak againstListeria spp.,Helicobacter pylori and anaerobic pathogens (except BAY 3522).Bordetella pertussis remains resistant to all absorbable cephalosporins. Progress in antibacterial activity of oral cephalosporins was mainly achieved by cefpodoxime, cefixime, cefdinir, cefetamet and ceftibuten against Enterobacteriaceae and the fastidious pathogens and against staphylococci and the nonenterococcal streptococci by cefdinir, BAY 3522, cefprozil and cefpodoxime.

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Antibakterielle Aktivität von Cefpodoxim im Vergleich mit anderen oralen Cephalosporinen

Zusammenfassung Die neuen oralen Cephalosporine Cefpodoxim, Cefixim, Cefdinir, Cefetamet und Ceftibuten zeigen eine verstärkte Aktivität auch gegen solche Enterobacteriaceae, die gegen etablierte Substanzen empfindlich sind (z.B. Cefuroxim, Cefaclor, Cefadroxil). Zusätzlich schließt das Spektrum von Cefpodoxim, Cefixim, Cefdinir, Cefetamet und Ceftibuten Spezies ein, die gegen die bisherigen oralen Cephalosporine resistent waren (Proteus vulgaris, Providencia spp.,Yersinia enterocolitica). Daneben zeigt die Mehrheit der neuen Substanzen erhöhte Aktivität (MHK₅₀<2 mg/l) gegenEnterobacter spp.,Citrobacter freundii, Serratia spp. undMorganella morganii. Gegen die meisten Enterobacteriaceae ist Ceftibuten das wirksamste orale Cephalosporin. Non-Fermenter (Acinetobacter spp.,Pseudomonas spp.) bleiben gegenüber oralen Cephalosporinen vollständig resistent (mit Ausnahme einigerAcinetobacter-Spezies gegen Cefdinir undPseudomonas cepacia gegen Ceftibuten). Die Antistaphylokokken-Aktivität oraler Cephalosporine ist am höchsten bei Cefdinir, gefolgt von BAY 3522, Cefprozil, Cefuroxim und Cefpodoxim. Loracarbef, Cefaclor und Cefadroxil sind etwa gleich aktiv, während die anderen Substanzen nur schwach aktiv (Cefixim) oder inaktiv sind (Cefetamet, Ceftibuten). Enterokokken sind gegenüber der neuen Generation oraler Cephalosporine ebenso unempfindlich wie gegenüber den etablierten Substanzen. Die aktivsten oralen Cephalosporine gegen hämolysierende Streptokokken sind Cefdinir und Cefprozil.Streptococcus pneumoniae, Streptococcus milleri undStreptococcus mitior sind am empfindlichsten gegen Cefpodoxim, Cefdinir, Cefuroxim und BAY 3522. Penicillin-resistente Pneumokokken müssen als resistent gegenüber allen oralen Cephalosporinen betrachtet werden. Anspruchsvolle Erreger wieHaemophilus spp.,Moraxella catarrhalis undNeisseria gonorrhoeae sind gegen Cefpodoxim, Cefixim, Cefdinir, Cefetamet und Ceftibuten empfindlicher als gegen die anderen oralen Cephalosporine. Die Aktivität oraler Cephalosporine gegenListeria spp.,Helicobacter pylori und Anaerobier (Ausnahme BAY 3522) ist nur schwach.Bordetella pertussis bleibt gegen alle resorbierbaren Cephalosporine resistent. Der Fortschritt in der antibakteriellen Aktivität oraler Cephalosporine wurde gegen Enterobacteriaceae und anspruchsvolle Erreger hauptsächlich durch Cefpodoxim, Cefixim, Cefdinir, Cefetamet und Ceftibuten erlangt, gegen Staphylokokken und Streptokokken (außer Enterokokken) durch Cefdinir, BAY 3522, Cefprozil und Cefpodoxim.

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Supported by Luitpold-Werk, a company of the Sankyo group.     

Electrochemical Recovery and Behaviors of Rare Earth (La,Ce, Pr,Nd, Sm,Eu, Gd,Tb, Dy,Ho, Er,Tm, and Yb) Ions on Ni Sheets

The electrochemical behaviors of rare earth (RE) ions have extensively been studied because of their high potential applications to the reprocessing of used nuclear fuels and RE-containing materials. In the present study, we fully investigated the electrochemical behaviors of RE(III) (La, Ce, Pr, Nd, Sm, Eu, Gd, Tb, Dy, Ho, Er, Tm, and Yb) ions over a Ni sheet electrode in 0.1 M NaClO₄ electrolyte solution by cyclic voltammetry between +0.5 and −1.5 V (vs. Ag/AgCl). Amperometry electrodeposition experiments were performed between −1.2 and −0.9 V to recover RE elements over the Ni sheet. The successfully RE-recovered Ni sheets were fully characterized by scanning electron microscopy, energy dispersive X-ray spectroscopy, Fourier transform infrared spectroscopy, X-ray photoelectron spectroscopy, and photoluminescence spectroscopy. The newly reported recovery data for RE(III) ions over a metal electrode provide valuable information on the development of the treatment methods of RE elements.     

Clinical trials update: highlights of the scientific sessions of The American College of Cardiology 2002: LIFE,DANAMI 2, MADIT-2, MIRACLE-ICD,OVERTURE, OCTAVE,ENABLE 1 & 2, CHRISTMAS,AFFIRM, RACE,WIZARD, AZACS,REMATCH, BNP trial and HARDBALL

This article continues a series of reports updating recent research developments of particular interest to personnel involved in the treatment and management of patients with heart failure. This is a summary of selected presentations made at the American College of Cardiology 51st Annual Scientific Session held in Atlanta on 17-20 March 2002. Reports of the following clinical studies are included: LIFE, DANAMI 2, MADIT-2, MIRACLE-ICD, OVERTURE, OCTAVE, ENABLE 1 & 2, CHRISTMAS, AFFIRM, RACE, WIZARD, AZACS, REMATCH, BNP trial and HARDBALL.