Extension of the fingers. V. Anatomic approach to lesions of the extensor apparatus]

The physiopathology of the main deformities of the fingers, induced by the injury of the dorsal aponeurosis of the fingers, is caused by an imbalance of forces: proximally between extrinsic and intrinsic muscles; distally between central and collateral structures. The ulna Claw, caused by the whole paralysis of the intrinsic muscles, can be corrected by an interosseous tenodesis on the basis of the finger. The boutoniere is induced by the exaggeration of the action of the collateral structures with respect to this of the central structures. The swan neck is induced by the exaggeration of action of the central structures with respect to this of the collateral structures. The surgical treatment consist to give back those structures their normal lengthening and way, or else to create new detours or shortenings, allowing to give back the balance. So, any structures, spared by the traumatism, will not injure by the surgeon.     

Inhibition of superoxide production and Ca2+ mobilization in human neutrophils by halothane, enflurane, and isoflurane

The inhibitory effects of three inhalation anesthetics, i.e., halothane, enflurane, and isoflurane, on superoxide production and the intracellular mobilization of calcium in human neutrophils were studied. The superoxide production induced by N-formyl-methionyl-leucyl-phenylalanine (FMLP) was inhibited by the anesthetics, but the binding of FML[3H]P to the cells and the superoxide-forming NADPH oxidase of the phagocytic vesicles were not inhibited. The inhibition of the cellular superoxide production was partially reversed by the addition of a calcium ionophore, A23187. The increase in intracellular free calcium monitored by a calcium-sensitive fluorescent probe, quin-2 and the release of calcium from hydrophobic environment monitored by chlortetracycline were inhibited dose dependently by the anesthetics. These observations suggest that decreased mobilization of intracellular Ca2+ is one of the mechanisms by which the anesthetics inhibited the superoxide production of human neutrophils stimulated by FMLP.     

RGD多肽表面修饰生物陶瓷修复骨缺损BMP-2的表达

目的：了解精氨酸-甘氨酸-天冬氨酸（Arg-Gly-Asp,RGD）多肽表面修饰的羟基磷灰石-磷酸三钙（hydroxyapatite-tricalcium phosphate,HA-TCP）修复节段性骨缺损局部骨形态发生蛋白-2（bone morphogenetic protein-2,BMP-2）的表达。方法：以骨髓基质干细胞（marrow stromal cells,MSCs）复合RGD多肽表面修饰的HA-TCP或单纯材料培养制备组织工程骨,选择60只新西兰白兔,制作15mm长的桡骨节段性骨缺损模型,实验根据植入不同的材料分为A、B、C和D组,A组：骨缺损区植入MSCs复合RGD多肽表面修饰的HA-TCP培养制备的组织工程骨;B组：骨缺损区植入MSCs复合HA-TCP培养制备的组织工程骨;C组：骨缺损区植入RGD多肽表面修饰的HA-TCP;D组：骨缺损区植入HA-TCP。术后4周取材,行修复区局部BMP-2免疫组化分析。结果：术后4周各组骨缺损区均有新骨生成,修复区局部BMP-2表达水平依次为：A〉B〉C〉D（P〈0.001,P〈0.05）。结论：RGD多肽表面修饰对以HA-TCP为支架材料组织工程骨的修复作用有明显优化作用。     

Prosthetic metals impair murine immune response and cytokine release in vivo and in vitro

This study was designed to investigate whether prosthetic metals adversely affect immune responses and the release of immunoregulatory cytokines in vivo and in vitro. Titanium and cobalt-chromium alloy were injected into the peritoneal cavity of female mice. At 5, 8, and 12 weeks after the injection, the levels of cobalt and chromium in the blood were significantly increased compared with the levels in control mice; the level of titanium was not significantly changed until 12 weeks. The release of interleukin-2 was significantly inhibited by cobalt-chromium particles after 3 weeks; titanium particles did not have the same effect until 8 and 12 weeks. The release of interleukin-γ was significantly inhibited by cobalt-chromium particles after 3 weeks but was not significantly inhibited by titanium particles until 12 weeks. The release of interferon-y was significantly inhibited by cobalt-chromium particles only at 12 weeks and was not inhibited by titanium particles. The proliferation of T cells was significantly inhibited by cobalt-chromium particles at 3 weeks and by titanium particles at 8 and 12 weeks, and the proliferation of B cells was significantly inhibited by cobalt-chromium particles after 3 weeks but was not inhibited by titanium particles. The production of immunoglobulin by lipopolysaccharide-stimulated B cells was also significantly reduced by cobalt-chromium particles after 3 weeks and by titanium particles at 8 and 12 weeks. The cytokine release by lymphocytes, proliferation of T and B cells, and immunoglobulin production by B cells were also significantly inhibited by titanium and cobalt-chromium particles, as well as by titanium, cobalt, and chromium ions in vitro, whereas these metals are not cytotoxic to murine lymphocytes in vitro. The data indicate that the metal-induced immunosuppression may be another important factor in the development of implant-associated infection in patients with a prosthesis.     

Oxidative stress in atherosclerosis

Oxidative stress is the result of the imbalance between pro-oxidant and antioxidant factors. The participation of oxidative stress in atherosclerosis (ATS) is reflected by lipid peroxidation which is a process initiated and maintained by oxygen reactive species generated by the aterogenic cells themselves. The endothelial aggression in ATS is accompanied by endothelial dysfunction, which is due to the neutralization of nitric oxide by superoxid anion. The key role in the onset and the development of the ATS lesions belongs to oxidated LDL-cholesterol that influence at different levels and by several mechanisms the ATS process. The neutralization of the toxic effects of free radicals is due to the endo and exogen antioxidant systems. It appears that the individual antioxidant status is influenced by environmental factors as well as by a genetic determinant. The antioxidant therapy, which is controversial at the moment, represents an associated therapy in endothelial dysfunction from ATS.     

Smac基因促丝裂霉素诱导膀胱癌细胞凋亡的研究

目的 探讨Smac基因的表达对于丝裂霉素(MMC)诱导膀胱癌细胞凋亡的影响。方法 脂质体介导Smac基因转染膀胱癌T24细胞3d后，用低剂量丝裂霉素诱导凋亡启动，噻唑蓝(MTT)比色分析检测癌细胞生长活性，吖啶橙-溴化乙锭荧光染色法及流式细胞术法检测细胞凋亡；免疫组织化学法和逆转录聚合酶链反应检测Smac基因的表达。结果 T24细胞在低剂量丝裂霉素的诱导下发生凋亡，两种方法检测细胞凋亡率，用0．05g／L丝裂霉素处理的T24细胞凋亡率分别为20，50％和18．84％，而经过转染Smac后用0，05g／L丝裂霉素处理的T24细胞凋亡率分别为36，40％和33．52％，差异有统计学意义(P＜0．05)。结论 促凋亡基因Smac在膀胱癌细胞中的活化表达可以明显增强细胞在刺激信号下的凋亡。     

23例Dieulafoy病的内镜诊断和治疗

目的探讨Dieulafoy病内镜下诊断和治疗的方法。方法回顾分析我科临床诊断明确的23例Dieulafoy病伴消化道出血患者的临床资料。结果急诊胃镜确诊19例,急诊肠镜确诊2例,血管造影检查确诊1例,剖腹探查术确诊1例。19例病变位于近端胃,1例位于胃窦,1例位于十二指肠,2例位于直肠。21例内镜确诊的患者行金属钛夹钳夹成功止血,血管造影确诊的患者经动脉内持续灌注垂体后叶素止血,剖腹探查术确诊的患者行单纯血管缝扎术止血。结论急诊内镜检查是诊断Dieulafoy病的首选方法,内镜下钛夹的合理使用是治疗本病的主要手段。     

阻断ERK2信号转导通路对血小板源生长因子-BB诱导血管平滑肌细胞增殖、迁移和表达转化生长因子-β1的影响

目的 观察ERK2信号转导通路在血小板源生长因子(PDGF-BB)诱导血管平滑肌细胞(VSMC)增殖、迁移和表达转化生长因子(TGF)-β1中的作用.方法 将原代培养的大鼠VSMC分为4组:(1)对照组;(2)PDGF刺激组;(3)Ad-LacZ组;(4)Adanti-ERK2组.用Westernblot检测细胞磷酸化ERK2蛋白水平;噻唑蓝(MTT)比色法测定细胞增殖率;流式细胞仪检测细胞细胞周期;Boyden小室测定细胞的跨膜迁移能力;酶联免疫吸附试验(ELISA)法检测细胞培养液上清中TGF-β1的浓度.结果 Adanti-ERK2组和对照组细胞增殖率、S期细胞百分比及跨膜迁移细胞数目明显低于PDGF刺激组和Ad-LacZ组(细胞增殖率:2.75%、0.00%比64.45%、61.88%;s期细胞百分比:14.18%、13.58%比38.14%、32.99%;跨膜迁移细胞数:8.2±3.2、6.3±2.6比24.8±6.1、23.3±5.8,均P<0.05);(2)Adanti-ERK2组和对照组细胞培养上清液中TGF-β1含量明显低于PDGF刺激组和Ad-LacZ组(P<0.05);而Adanti-ERK2组明显高于对照组(P<0.05).结论 ERK2信号转导通路参与调控PDGF-BB诱导的VSMC增殖、迁移和基因表达.反义ERK2基因预先转染阻断ERK信号转导能显著抑制PDGF-BB刺激的VSMC增殖、迁移,阻断细胞周期由G1期进入S期,并且部分下调TGF-β1的合成分泌.     

Experimental carpal displacement induced by ligamental lesions]

Ligamentous lesions were created experimentally in 40 fresh cadaver wrists. The precise localization of traumatic rupture of the ligaments and the subsequent carpal imbalance were defined by the comparison between the experimental results and the clinical displacements. The displacements may be permanent, sequential or induced by external forces. Lesions of capsular ligaments cause the displacement. There are 3 functional units; the distal scaphoid complex; the palmar ligaments which form a "belt", consisting of the lateral external ligament, the radiocarpal ligaments an the radiate ligament; the medial ligaments, which also form a "belt" consisting of the palmar triquetral ligaments on each side of the triquetrum. The sprains are caused by a lesion of a functional unit. The lateral sprain is characterized by a lesion of the distal scaphoid complex. The scaphoid moves into a horizontal position, causing a dorsal deviation of the lunate and a scapholunate diastasis. The central sprain is induced by a rupture of the palmar "belt", causing an anteroposterior radiocarpal or mediocarpal drawer movement. The medial sprain is induced by the rupture, of different extents, of the medial ligaments. On examination, there is either a click or a palmar deviation of the lunate, sometimes with a lunotriquetral diastasis. The dislocations of the wrist are caused by lesion of several ligamentous units.     

Identification of the sperm antigen interacting with antibodies in serum from an infertile woman

Serum (IS) obtained from an infertile woman induced head-to-head agglutination of human sperm. The immunoglobulin G (IgG) fraction of the IS was prepared by ammonium sulfate fractionation and DEAE cellulose chromatography. The IgG localized to the post-acrosomal region of the sperm, determined by indirect immunofluorescence and interacted with a human sperm protein with an estimated Mr of 80 kDa, determined by immunoblotting. The identity of the interacting sperm antigen was verified by isolating the 80 kDa sperm protein by affinity chromatography. The present results suggest that the anti-80 kDa antibodies may be responsible for the infertility.     

脱细胞软骨支架材料的制备及物理性质

目的 探讨脱细胞软骨生物支架材料(ACM)的制作方法,使其在孔隙率、比表面积、弹性模量等物理性质更加接近天然软骨.方法 猪膝关节软骨冻干加工为粉末,0.25%胰酶消化,1%曲拉通洗脱,蒸馏水洗净冻干,8 W 312 nm紫外线照射(UVI)后成型;扫描电镜观察孔径分布,压汞仪测定孔隙率等参数;INSTRON 5544对ACM进行抗雎弹性模量测定.结果 脱细胞生物支架材料为白色,略微发黄,外表呈多孔疏松网状结构,脆性大并有一定弹性;ACM孔隙率为68.54%,平均孔径为47.13 μm;ACM弹性模量为(1.05±0.38)MPa.结论 ACM在孔隙率、比表面积、平均孔径等方面符合关节软骨支架材料的要求.     

Ketamine and Midazolam Differentially Inhibit Nonadrenergic Noncholinergic Lower Esophageal Sphincter Relaxation in Rabbits: Role of Superoxide Anion and Nitric Oxide Synthase

Background: The authors previously reported that ketamine and midazolam inhibited nitric oxide-mediated nonadrenergic noncholinergic (NANC) lower esophageal sphincter (LES) relaxation via nitric oxide-3',5'-cyclic guanosine monophosphate pathway modulation. The mechanisms inhibiting the NANC relaxation by ketamine and midazolam were investigated.

Methods: The isometric tension of circular distal esophageal muscle strips from Japanese White rabbits was examined. NANC relaxation was induced by KCl (30 mm) in the presence of atropine (3 x 10-6 m) and guanethidine (3 x 10-6 m). Nitric oxide synthase activity in the absence and presence of ketamine and midazolam was analyzed using the biochemical conversion of L-[3H]arginine to L-[3H]citrulline.

Results: The ketamine-induced inhibition of the NANC relaxation was partly reversed by superoxide dismutase (200, 400 U/ml) but not by catalase (100 U/ml). Ketamine concentration-dependently inhibited the relaxation induced by N-ethylethanamine:1,1-diethyl-2-hydroxy-2-nitrosohydrazine (diethylamine NONOate) and S-nitrosoglutathione. The NANC relaxation itself was not affected by superoxide dismutase. The midazolam-induced inhibition of the NANC relaxation was reversed neither by superoxide dismutase nor by catalase, and midazolam did not affect the relaxations induced by nitric oxide donors. The nitric oxide synthase activity was concentration-dependently suppressed by midazolam, but there was no marked effect of ketamine. Pyrogallol, a superoxide generator, inhibited the NANC and the diethylamine NONOate-induced relaxations. The pyrogallol-induced inhibition of the NANC relaxation was reversed by superoxide dismutase.     

Ketamine and midazolam differentially inhibit nonadrenergic noncholinergic lower esophageal sphincter relaxation in rabbits: role of superoxide anion and nitric oxide synthase

BACKGROUND: The authors previously reported that ketamine and midazolam inhibited nitric oxide-mediated nonadrenergic noncholinergic (NANC) lower esophageal sphincter (LES) relaxation nitric oxide-3',5'-cyclic guanosine monophosphate pathway modulation. The mechanisms inhibiting the NANC relaxation by ketamine and midazolam were investigated. METHODS: The isometric tension of circular distal esophageal muscle strips from Japanese White rabbits was examined. NANC relaxation was induced by KCl (30 mm) in the presence of atropine (3 x 10(-6) m) and guanethidine (3 x 10(-6) m). Nitric oxide synthase activity in the absence and presence of ketamine and midazolam was analyzed using the biochemical conversion of L-[3H]arginine to L-[3H]citrulline. RESULTS: The ketamine-induced inhibition of the NANC relaxation was partly reversed by superoxide dismutase (200, 400 U/ml) but not by catalase (100 U/ml). Ketamine concentration-dependently inhibited the relaxation induced by N-ethylethanamine:1,1-diethyl-2-hydroxy-2-nitrosohydrazine (diethylamine NONOate) and S-nitrosoglutathione. The NANC relaxation itself was not affected by superoxide dismutase. The midazolam-induced inhibition of the NANC relaxation was reversed neither by superoxide dismutase nor by catalase, and midazolam did not affect the relaxations induced by nitric oxide donors. The nitric oxide synthase activity was concentration-dependently suppressed by midazolam, but there was no marked effect of ketamine. Pyrogallol, a superoxide generator, inhibited the NANC and the diethylamine NONOate-induced relaxations. The pyrogallol-induced inhibition of the NANC relaxation was reversed by superoxide dismutase. CONCLUSION: These findings suggest that ketamine inhibits NANC LES relaxation by the extracellular production of superoxide anion, and that midazolam inhibits it by the inhibition of nitric oxide synthase activity.     

Quantitative Analysis of Sclerotherapy Results by Using Digital Photography and a Computer Program

BACKGROUND: Despite different telangiectasia treatments in the lower limbs, there is no method standardization for results assessment, making comparison between the existing treatments conflicting. OBJECTIVE: To compare the assessment carried out by a group of specialists with the assessment carried out by a computer program, according to clearance degree of telangiectasias during treatment by sclerotherapy. MATERIALS AND METHODS: Nineteen patients (21 studied areas) with telangiectasias of thighs and popliteal fossa were assessed, with a mean age of 37.5 (21-59) years old, all female. The pre- and posttreatment photos were standardized as per distance, light exposure, and aperture time. The sclerotherapy sessions were performed with 75% glucose. The clearance degree of telangiectasias was judged by a group of six doctors and by a computer program that analyzed the initial and final photos. The results of such assessment were compared according to concordance and correlation. RESULTS: There was no statistical difference between the assessments carried out by the specialists and the assessments carried out by the computer program according to the sclerotherapy results. CONCLUSION: The assessment carried out by the computer program was equivalent to the assessment carried out by the specialists in the judgment of clearance degree of telangiectasias of the lower limbs.     

Changes in the general surgical workload, 1991-1999

HYPOTHESIS: The volume and types of procedures performed by general surgeons have changed from 1991 to 1999.Data Source Medicare data from 1991 through 1999. METHODS: Procedures from the Medicare database were defined as "general surgical" if the yearly volume performed by general surgeons exceeded 1000 cases. These procedures were divided into major and minor procedures. The total volume performed by all surgeons and the volume of cases performed by general surgeons were tabulated for each procedure. Procedures were also grouped into families. For major surgery, representative procedures with the highest volumes were selected for each family. For minor surgery, multiple high-volume procedures within families were selected and analyzed. RESULTS: The volumes for each major surgical family were totaled. Although the volume of representative major general surgical procedures performed by all surgeons rose by 17 544 cases, the volume performed by general surgeons decreased by 8846 cases (1.8%). The total and general surgical volumes for cholecystectomy and appendectomy increased, but the volumes for breast surgery, hernia repair, splenectomy, and colon resection decreased. The total volume increased but the general surgical volume decreased for vascular surgery, pulmonary surgery, and major amputations. CONCLUSIONS: From 1991 to 1999, there has been a decrease in the volume of major procedures performed by general surgeons. Part of this loss relates to reduced general surgical involvement in subspecialty surgery, but there were also reductions in colon surgery, breast surgery, hernia repairs, and splenectomy. The volume of appendectomies and cholecystectomies increased. The volume of minor procedures performed by general surgeons increased slightly, with gains in vascular and endoscopic surgery.     

miR-21在TGF-β1引起的肝卵圆细胞上皮间质转化中的作用

[摘 要] 目的 探讨microRNA-21（miR-21）在TGF-β1引起的肝卵圆细胞（hepatic oval cell,HOC）上皮间质转化（epithelial mesenchymal transition,EMT）中的作用。方法 体外培养大鼠肝卵圆细胞,用10 ng/mL TGF-β1刺激HOC 1、3、5、7 d后,Western blotting检测EMT相关蛋白（E-cadherin、N-cadherin和Vi-mentin）表达情况;用10 ng/mL TGF-β1刺激HOC 5 d后,实时荧光定量PCR检测miR-21的表达情况;分别用miR-21增强和抑制慢病毒转染HOC构建稳定的细胞株,PCR检测miR-21的表达情况;接着用TGF-β1刺激miR-21抑制慢病毒转染的HOC 5 d,Western blotting检测E-cadherin、N-cadherin和Vimentin的表达;用miR-21增强慢病毒转染HOC后,Western blotting检测E-cadherin、N-cadherin和Vimentin的表达。结果 TGF-β1刺激HOC 1、3、5、7 d后,E-cadherin逐渐减低,N-cadherin和Vimentin逐渐升高。TGF-β1刺激HOC 5 d后miR-21的表达增强了4.32倍。分别用增强和抑制慢病毒转染HOC后,miR-21的表达增强了3.82倍和抑制了0.22倍。下调miR-21表达后,TGF-β1致HOC的EMT作用减弱。miR-21过表达后,HOC发生了EMT。结论 抑制miR-21的表达可以减少TGF-β1引起的HOC的EMT作用,从而减轻肝纤维化。     

人端粒酶逆转录酶真核表达质粒转染人成纤维细胞的体外培养及生物学特性研究

目的　　分析人端粒酶逆转录酶 (h TERT)真核表达质粒 p GRN14 5转染人成纤维细胞的生物学特性。方法　体外分离培养小儿包皮成纤维细胞 ,脂质体法将构建的 p GRN14 5转染人成纤维细胞 ,经潮霉素 B筛选 ,扩增培养阳性克隆。 RT- PCR法、TRAP- PCR法分析细胞端粒酶活性。流式细胞术检测细胞增殖周期及细胞凋亡率 ,对转染后细胞行染色体核型分析及免疫组织化学法检测胶原分泌能力。结果　转染后培养的人成纤维细胞形态与转染前相比无明显改变 ,转染细胞稳定地表达端粒酶活性 ,流式细胞术分析转染前后成纤维细胞的增殖周期无明显改变 ,细胞凋亡率较转染前降低。经 p GRN14 5转染的人成纤维细胞保持正常的二倍体核型 ,具有正常分泌 、 型胶原的能力。结论　 p GRN14 5转染的人成纤维细胞稳定地表达端粒酶活性 ,细胞寿命明显延长。初步证实了用这种方法建立组织工程标准化种子细胞系的可行性     

The Stress-Protecting Effect of Metal Plates on the Intact Rabbit Tibia

The purpose of the present study was to find the extent of stress-protection by a steel plate (45 × 5 × 1 mm) on the rabbit tibia. The animals were sacrificed after 6, 12 and 18 weeks. The median strength after plate application was 84, 73 and 72%, respectively. The elastic stiffness of plated bones was also reduced, while the deformation at fracture showed no significant reduction. The mineral content in the bone segment previously covered by a plate was measured by photon absorptiometry; it was reduced after 12 and 18 weeks. The stress-protecting effect caused by this thin steel plate was less pronounced than that previously reported by groups using more rigid plates on rabbit tibiae. The stress-protecting effect increased up to 12 weeks, but subsequently no further increase occurred.     

Effect of activating transcription factor 6 on the apoptosis of podocytes stimulated with palmitic acid

Objective To observe the effect of ATF6 on the apoptosis and proliferation of podocytes induced by palmitic acid (PA). Methods Podocytes were stimulated with different doses of PA for 24 h. The expression of cleaved-caspase3 was detected by Western blotting. The podocyte apoptosis was analyzed by flow cytometry (FCM), and the expression of ATF6 was tested by Western blotting and immunofluorescence staining. After the transfection of adenovirus siRNA against ATF6, the proliferation, the cell cycle and apoptosis of potocytes stimulated with PA were tested by MTT or FCM. Results The levels of cleaved-caspase3 and ATF6 of podocytes stimulated with PA were significantly increased by a dose-dependent manner compared with the control group (P＜0.05). The apoptosis of podocytes stimulated with PA was increased (P＜0.05). Compared with the podocytes stimulated with PA, the apoptosis of podocytes transfected by adenovirus siRNA against ATF6 with PA stimulation was significantly reduced (P＜0.05). The proliferation of podocytes transfected by adenovirus siRNA against ATF6 and stimulated with PA, however, was obviously increased compared with the podocytes stimulated with PA (P＜0.05). Conclusion ATF6 mediated the apoptosis of podocytes induced by palmitate acid.     

人-鼠抗CD4嵌合抗体的生物学效应研究

目的 探讨人－鼠抗ＣＤ４嵌合抗体的生物学效应,方法 观察ＣＤ４人－鼠嵌合抗体和鼠源性单抗对ＣＤ３,植物血凝素（ＰＨＡ）,白细胞－２（ＩＬ－２）及同种异体细胞诱导增殖的影响,以及介导的抗体依赖性细胞介导的细胞毒性（ＡＤＣＣ）作用。结果 提示ＣＤ４嵌合抗体和鼠源性ＣＤ４抗体对以上几种诱导剂诱导的增殖均有抑制作用,且抗体剂量越大,抑制作用越强。