髌骨骨折克氏针内固定导向器的研制及临床应用

目的自行研制一种髌骨骨折克氏针内固定导向器并验证其临床应用的效能。方法髌骨骨折克氏针内固定导向器(专利号:201020575985.8)主体结构由1个带滑动杆的固定爪和1个滑动爪组成。自2010-10—2013-10共52例髌骨骨折符合纳入标准,随机分为试验组(使用髌骨骨折克氏针内固定导向器,29例)及对照组(徒手置入克氏针,23例)。记录手术时间、止血带使用时间、术中出血量、克氏针穿针次数;置针标准性通过下列指标判断比较:CT片测量克氏针与髌骨纵轴的锐角角度α,与髌骨冠状面中轴的锐角角度β,克氏针通过横轴时分别与横轴线上2个3等分点的距离和(a+b),克氏针离关节面的最小距离与5 mm的差值之和(c+d)。结果试验组与对照组术中出血量比较差异无统计学意义(P0.05),但试验组在手术时间、止血带使用时间、穿针次数、置针准确性方面均优于对照组,差异有统计学意义(P0.05)。结论髌骨骨折克氏针导向器设计合理、操作简单,能提高克氏针置针准确性,增强张力带滑动加压性能,充分发挥改良张力带固定髌骨骨折的优点。     

Hepatotoxic effect of ochratoxin A and citrinin,alone and in combination,and protective effect of vitamin E: In vitro study in HepG2 cell

Ochratoxin A (OTA) and citrinin (CTN) are the most commonly co-occurring mycotoxins in a wide variety of food and feed commodities. The major target organ of these toxins is kidney but liver could also be a target organ. The combined toxicity of these two toxins in kidney cells has been studied but not in liver cell. In this study HepG2 cells were exposed to OTA and CTN, alone and in combination, with a view to compare the molecular and cellular mechanisms underlying OTA, CTN and OTA + CTN hepatotoxicity. OTA and CTN alone as well as in combination affected the viability of HepG2 cells in a dose-dependent manner. OTA + CTN, at a dose of 20% of IC₅₀ of each, produced effect almost similar to that produced by either of the toxins at its IC₅₀ concentration, indicating that the two toxins in combination act synergistically. The cytotoxicity of OTA + CTN on hepatocytes is mediated by increased level of intracellular ROS followed/accompanied by DNA strand breaks and mitochondria-mediated intrinsic apoptosis. Co-treatment of vitamin E (Vit E) with OTA, CTN and OTA + CTN reduced the levels of ROS and the cytotoxicity. But the genotoxic effect of OTA and OTA + CTN was not completely alleviated by Vit E treatment whereas the DNA damage as caused by CTN when treated alone was obviated, indicating that OTA induces DNA damage directly whereas CTN induces ROS-mediated DNA damage and OTA + CTN combination induces DNA damage not exclusively relying on but influenced by ROS generation. Taken together, these findings indicate that OTA and CTN in combination affect hepatocytes at very low concentrations and, thereby, pose a potential threat to public and animal health.     

AO微型钢板与克氏针治疗掌指骨骨折临床观察

目的：探讨应用AO微型钢板及克氏针内固定治疗掌指骨骨折的临床疗效。方法：采用AO微型钢板治疗掌指骨骨折40例,克氏针内固定治疗41例,比较两种手术治疗效果。结果：AO微型钢板内固定组的骨折均达解剖复位,悉数愈合,仅1例延迟愈合,平均愈合时长5.1周。克氏针内固定组1例骨折未愈合,其余骨折全部愈合,仅3例延迟愈合,平均愈合时长8.0周。AO微型钢板组优34例,良5例,差1例,优良率为97.5%;克氏针组优者26例,良5例,差10例,优良率75.6%。两组的优良率比较差异有显著性（即P〈0.05）。结论：AO微型钢板质薄、体小、坚强,固定牢靠,能早期功能锻练,其疗效优于克氏针内固定,是掌指骨骨折的一种理想固定方法。     

Dioscin,a natural steroid saponin,induces apoptosis and DNA damage through reactive oxygen species: A potential new drug for treatment of glioblastoma multiforme

Dioscin, a natural product obtained from medicinal plants shows lipid-lowering, anti-cancer and hepatoprotective effects. However, the effect of it on glioblastoma is unclear. In this study, dioscin significantly inhibited proliferation of C6 glioma cells and caused reactive oxygen species (ROS) generation and Ca²⁺ release. ROS accumulation affected levels of malondialdehyde, nitric oxide, glutathione disulfide and glutathione, and caused cell apoptosis. In addition, ROS generation caused mitochondrial damage including structural changes, increased mitochondrial permeability transition and decreased mitochondria membrane potential, which led to the release of cytochrome C, nuclear translation of programmed cell death-5 and increased activities of caspase-3,9. Simultaneously, dioscin down-regulated protein expression of Bcl-2, Bcl-xl, up-regulated expression of Bak, Bax, Bid and cleaved poly (ADP-ribose) polymerase. Also, oxygen stress induced S-phase arrest of cancer cells by way of regulating expression of DNA Topo I, p53, CDK2 and Cyclin A and caused DNA damage. In a rat allograft model, dioscin significantly inhibited tumor size and extended the life cycle of the rats. In conclusion, dioscin shows noteworthy anti-cancer activity on glioblastoma cells by promoting ROS accumulation, inducing DNA damage and activating mitochondrial signal pathways. Ultimately, we believe dioscin has promise as a new therapy for the treatment of glioblastoma.     

Reduced intrathoracic blood volume and left and right ventricular dimensions in patients with severe emphysema: an MRI study

BACKGROUND: Left ventricular (LV) filling is impaired in patients with severe emphysema manifesting in small end-diastolic dimensions. We hypothesized that the hyperinflated lungs of these patients with high intrinsic positive end-expiratory pressure will decrease intrathoracic blood volume (ITBV) and ventricular preload. We therefore measured ITBV, and LV and right ventricular (RV) dimensions and function using MRI techniques in patients with severe emphysema. METHODS: Patients with severe emphysema (n = 13) and matched healthy volunteers (n = 11) were included. The magnetic resonance (MR) examination consisted of three parts: (1) evaluation of RV and LV dimensions and function and interventricular septum curvature using cine MRI; (2) quantification of aortic flow using MR phase velocity mapping; and (3) calculation of the cardiopulmonary peak transit time (PTT) from the pulmonary artery to the ascending aorta using contrast-enhanced, time-resolved, two-dimensional MR angiography. RESULTS: There were no differences between the groups regarding age, height, or weight. In the emphysema patients, ITBV index (- 35%), LV end-diastolic volume index (LVEDVI) [- 21%], RV end-diastolic volume index (- 20%), cardiac index (- 22%), and stroke volume index (SVI) [- 40%] were lower compared to control subjects. LV and RV end-systolic volumes, LV wall mass, septal curvature, and PTT did not differ between the groups. LVEDVI (r = 0.83) as well as SVI (r = 0.82) correlated closely to ITBV index. SVI correlated closely to LVEDVI (r = 0.84). CONCLUSIONS: LV and RV performance is impaired in patients with severe emphysema because of small end-diastolic dimensions. One possible explanation for the decreased biventricular preload in these patients is intrathoracic hypovolemia caused by hyperinflated lungs.     

The AO 8mm solid tibial nail is not defunct

The AO 8mm unreamed tibial nail (UTN) is an established implant that has in some publications been associated with high rate of distal locking screw breakage and failure. Larger reamed nails are now increasingly favoured. We have used the 8mm UTN employing all three available distal screws when appropriate and with a restricted initial weight-bearing regimen. Our experience has been satisfactory with 95% union rate and no adverse effect of distal locking screw breakage. This slender nail requires less frequent reaming which may be an advantage in at least some situations. We suggest that it should be considered an alternative to larger reamed nails and can perform satisfactorily with appropriate application.     

锁骨钩钢板治疗肩锁关节脱位

目的探讨AO锁骨钩铜板（clavicular hook—plate,CHP）内固定治疗严重肩锁关节脱位及锁骨远端骨折的方法及疗效。方法2004年6月～2007年4月用AO锁骨钩钢板内固定治疗严重肩锁关节脱位及锁骨远端骨折23例。男15例,女8例,年龄21-56岁,平均36．1岁。左侧14例,右侧9例,其中新鲜骨折22例,1例10个月后就诊。结果随访23例,时间为12-36月（平均18月）。所有病例均正常愈合,疗效满意。结论应用锁骨钩钢板治疗肩锁关节脱位,具有操作简便、手术时间短、复位固定效果良好、对肩锁关节损伤小,术后可早期功能锻炼,并发症少,肩部活动功能恢复良好,值得临床推广应用。     

Vitamin E protects against the mitochondrial damage caused by cyclosporin A in LLC-PK1 cells

Cyclosporin A (CsA) has nephrotoxic effects known to involve reactive oxygen species (ROS), since antioxidants prevent the kidney damage induced by this drug. Given that mitochondria are among the main sources of intracellular ROS, the aims of our study were to examine the mitochondrial effects of CsA in the porcine renal endothelial cell line LLC-PK1 and the influence of the antioxidant Vitamin E (Vit E).Following the treatment of LLC-PK1 cells with CsA, we assessed the mitochondrial synthesis of superoxide anion, permeability transition pore opening, mitochondrial membrane potential, cardiolipin peroxidation, cytochrome c release and cellular apoptosis, using flow cytometry and confocal microscopy procedures. Similar experiments were done after Vit E preincubation of cells.CsA treatment increased superoxide anion in a dose-dependent way. CsA opened the permeability transition pores, caused Bax migration to mitochondria, and decreased mitochondrial membrane potential and cardiolipin content. Also CsA released cytochrome c into cytosol and provoked cellular apoptosis. Vit E pretreatment inhibited the effects that CsA induced on mitochondrial structure and function in LLC-PK1 cells and avoided apoptosis.CsA modifies mitochondrial LLC-PK1 cell physiology with loss of negative electrochemical gradient across the inner mitochondrial membrane and increased lipid peroxidation. These features are related to apoptosis and can explain the cellular damage that CsA induces. As Vit E inhibited these effects, our results suggest that they were mediated by an increase in ROS production by mitochondria.     

Arsenic moiety in gallium arsenide is responsible for neuronal apoptosis and behavioral alterations in rats

Gallium arsenide (GaAs), an intermetallic semiconductor finds widespread applications in high frequency microwave and millimeter wave, and ultra fast supercomputers. Extensive use of GaAs has led to increased exposure to humans working in semiconductor industry. GaAs has the ability to dissociate into its constitutive moieties at physiological pH and might be responsible for the oxidative stress. The present study was aimed at evaluating, the principle moiety (Ga or As) in GaAs to cause neurological dysfunction based on its ability to cause apoptosis, in vivo and in vitro and if this neuronal dysfunction translated to neurobehavioral changes in chronically exposed rats. Result indicated that arsenic moiety in GaAs was mainly responsible for causing oxidative stress via increased reactive oxygen species (ROS) and nitric oxide (NO) generation, both in vitro and in vivo. Increased ROS further caused apoptosis via mitochondrial driven pathway. Effects of oxidative stress were also confirmed based on alterations in antioxidant enzymes, GPx, GST and SOD in rat brain. We noted that ROS induced oxidative stress caused changes in the brain neurotransmitter levels, Acetylcholinesterase and nitric oxide synthase, leading to loss of memory and learning in rats. The study demonstrates for the first time that the slow release of arsenic moiety from GaAs is mainly responsible for oxidative stress induced apoptosis in neuronal cells causing behavioral changes.     

不同浓度的华蟾素对卵巢癌3AO细胞MMP-2和TIMP-2表达的影响及可行性研究

目的探讨华蟾素对卵巢3AO细胞基质金属蛋白酶（MMP-2）和组织抑制因子（TIMP-2）表达的影响及其,临床意义。方法体外培养卵巢癌3AO细胞,不同浓度的华蟾素干预后,用SABC免疫组化法检测MMP-2和TIMP-2表达。结果卵巢癌3AO细胞可表达MMP-2和TIMP;0．25mg／ml华蟾素对卵巢3AO细胞MMP-2和TIMP-2的表达无显著影响（P〉0．05）;2．5mg／ml华蟾素干预后,卵巢癌3AO细胞MMP-2的表达显著下降,TIMP2的表达显著升高（P〈0．05）;25mg／ml与2．5mg／ml华蟾素对卵巢癌3AO细胞MMP-2和TIMP-2表达影响无统计学差异（P〉0.05）。结论2．5mg／ml华蟾素可显著降调卵巢癌3AO细胞MMP-2的表达,升调TIMP-2的表达,两者的失衡可抑制卵巢癌3AO细胞的侵袭性生长。