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71.
72.
Background
The effect of the changes in the femoral posterior condylar offset (PCO) on anterior–posterior (AP) translation and internal–external (IE) rotation in cruciate-retaining (CR) and posterior-stabilized (PS) total knee arthroplasty (TKA) remains unknown. The purpose of this study was to compare the kinematics in CR and PS TKA with respect to the difference in prosthetic design and PCO change through a computational simulation.Methods
We developed three-dimensional finite element models with the different PCOs of ± 1, ± 2 and ± 3?mm in the posterior direction using CR and PS TKA. We performed the simulation with different PCOs under a deep knee bend condition and evaluated the kinematics for the AP and IE in CR and PS TKA.Results
The more tibiofemoral (TF) translation in the posterior direction was found as PCO translated in posterior direction for both CR and PS TKA compared to the neutral position. However, the change of the AP translation with respect to the PCO change in CR TKA was greater than PS TKA. The more TF external rotation was found as PCO translated in the anterior direction for both CR and PS TKA compared to the neutral position. However, unlike the TF translation, the TF rotation was not influenced by the PCO change in both CR and PS TKA.Conclusion
The PCO magnitude was influenced by a postoperative change in the kinematics in CR TKA although a relatively smaller effect was observed in PS TKA. Hence, surgeons should be aware of the PCO change, especially for CR TKA. 相似文献73.
明胶-聚乳酸载药纳米微球的制备及其体外释药研究 总被引:21,自引:0,他引:21
采用复合乳液—溶剂挥发法制得明胶—聚乳酸载五氟脲嘧啶(5—Fu)微球,以混合型乳化剂Tween—80:Span—80=5:1—作为初乳乳化剂,O—羧甲基壳聚糖作为复乳乳化剂,考察了明胶—聚乳酸载药微球的制备条件对微球的成球性、药物包封率及体外释药的影响。结果表明乳化剂的选择、内部水相药物浓度和PLA分子量等均对载药微球的结构与性能产生影响,经优化条件得到了成球性和体外释放都比较好的载药微球。 相似文献
74.
门静脉的体表定位及其临床意义 总被引:3,自引:0,他引:3
目的:为超声波检查门静脉或经皮经肝门静脉穿刺提供解剖学基础。方法:在40例成人尸体标本上观测了门静脉的行程及其分叉位置的体表投影。结果:门静脉肝外段与身体的垂线呈约40°角;门静脉分叉位置在经右半胸宽中点的垂线与右锁骨中线上肝高中点的水平线的交点附近;门静脉右支分为前、后支的位置在剑突尖平面下方约2cm,右锁骨中线上肝高的中点附近;门静脉左支分出第1外侧支的位置在剑突尖稍下方的右侧约2cm。结论:在右腋中线剑突尖平面下方约2cm经皮经肝穿刺至锁骨中线,导管即可进入门静脉右支内 相似文献
75.
Gao HZ Kobayashi K Tabata A Tsuge H Iijima M Yasuda T Kalkanoglu HS Dursun A Tokatli A Coskun T Trefz FK Skladal D Mandel H Seidel J Kodama S Shirane S Ichida T Makino S Yoshino M Kang JH Mizuguchi M Barshop BA Fuchinoue S Seneca S Zeesman S Knerr I Rodés M Wasant P Yoshida I De Meirleir L Abdul Jalil M Begum L Horiuchi M Katunuma N Nakagawa S Saheki T 《Human mutation》2003,22(1):24-34
Classical citrullinemia (CTLN1), a rare autosomal recessive disorder, is caused by mutations of the argininosuccinate synthetase (ASS) gene, localized on chromosome 9q34.1. ASS functions as a rate-limiting enzyme in the urea cycle. Previously, we identified 32 mutations in the ASS gene of CTLN1 patients mainly in Japan and the United States, and to date 34 different mutations have been described in 50 families worldwide. In the present study, we report ASS mutations detected in 35 additional CTLN1 families from 11 countries. By analyzing the entire coding sequence and the intron-exon boundaries of the ASS gene using RT-PCR and/or genomic DNA-PCR, we have identified 16 novel mutations (two different 1-bp deletions, a 67-bp insertion, and 13 missense) and have detected 12 known mutations. Altogether, 50 different mutations (seven deletion, three splice site, one duplication, two nonsense, and 37 missense) in 85 CTLN1 families were identified. On the basis of primary sequence comparisons with the crystal structure of E. coli ASS protein, it may be concluded that any of the 37 missense mutations found at 30 different positions led to structural and functional impairments of the human ASS protein. It has been found that three mutations are particularly frequent: IVS6-2A>G in 23 families (Japan: 20 and Korea: three), G390R in 18 families (Turkey: six, U.S.: five, Spain: three, Israel: one, Austria: one, Canada: one, and Bolivia: one), and R304W in 10 families (Japan: nine and Turkey: one). Most mutations of the ASS gene are "private" and are distributed throughout the gene, except for exons 5 and 12-14. It seems that the clinical course of the patients with truncated mutations or the G390R mutation is early-onset/severe. The phenotype of the patients with certain missense mutations (G362V or W179R) is more late-onset/mild. Eight patients with R86H, A118T, R265H, or K310R mutations were adult/late-onset and four of them showed severe symptoms during pregnancy or postpartum. However, it is still difficult to prove the genotype-phenotype correlation, because many patients were compound heterozygotes (with two different mutations), lived in different environments at the time of diagnosis, and/or had several treatment regimes or various knowledge of the disease. 相似文献
76.
77.
Trichoplusia ni immune genes up-regulated in response to bacterial infection have been isolated using differential display polymerase chain reaction. Here we report the cloning and characterisation of a gut-specific immune gene encoding an azurocidin-like protein. The deduced protein is 317 amino acid residues long with a hydrophobic C-terminus and a predicted 17-residue signal peptide. The mature T. ni protein shows 30% identity to human azurocidin, an antibacterial protein. Like azurocidin, the T. ni protein contains two amino acid substitutions in the active site triad normally present in serine proteases. The T. ni protein was synthesised with a six-histidine C-terminal extension using the baculovirus expression system. Sequencing of the recombinant azurocidin-like protein confirmed the predicted cleavage of the signal peptide. Northern blots show that T. ni azurocidin-like protein is expressed solely in the larval gut and that expression is up-regulated by injecting or feeding bacteria. Expression reaches its highest level at 10 h after bacteria injection. 相似文献
78.
三个常染色体隐性遗传早发型帕金森病家系的PARKIN基因研究 总被引:1,自引:0,他引:1
目的 探讨PARKIN基因与中国人常染色体隐性遗传早发型帕金森病(autosomal recessive early-onset Parkinson’s disease,AREP)家系的关系。方法 对3个AREP家系的6例患者和23位成员进行系统的临床检查并进行PARKIN基因PCR扩增,产物通过变性高压液相色谱(denaturing high—performance liquid chmnatogmphy,DHPLC)进行突变检测,阳性结果标本进行基因测序。结果 所有研究对象的PARKIN基因外显子均扩增成功。DHPLC检测和基因测序发现一个家系中存在PARKIN基因杂合Gly284Arg突变,另一个家系中存在PARKIN基因Ser167Asn多态性,且患者均有环境毒物接触史。结论 PARKIN基因杂合Gly284Arg突变在环境因素的协同作用下可能导致发病。PARKIN基因Ser167Asn多态性是帕金森病的易感因素,汞中毒与其共同作用可能导致发病。 相似文献
79.
Detection of YMDD motif mutants by oligonucleotide chips in lamivudine-untreated patients with chronic hepatitis B virus infection 总被引:9,自引:0,他引:9
Heo J Cho M Kim HH Shin YM Jang HJ Park HK Kim CM Kim GH Kang DH Song GA Yang US 《Journal of Korean medical science》2004,19(4):541-546
Lamivudine, a nucleoside analogue, has been used widely as an effective antiviral agent for the treatment of patients with chronic hepatitis B virus (HBV) infection. However, the YMDD motif mutation of HBV polymerase resistant to lamivudine occurs very frequently after long term therapy. We developed an oligonucleotide chip for the detection of YMDD motif mutants resistant to lamivudine and investigated the prevalence of the mutants in patients with chronic HBV infection who had not been treated by lamivudine before. Forty patients who had not been treated with lamivudine were included in this study. Serum samples were tested by the oligonucleotide chips designed for detection of wild-type YMDD motif, M552V and M552I. Samples were confirmed by restriction fragment length polymorphism (RFLP) and direct sequencing. M552I mutants were detected by the oligonucleotide chips in 7.5% (3/40) of chronic HBV infected patients (2 chronic hepatitis and 1 cirrhosis). The results were in accordance with those of RFLP. YMDD motif mutants occur as natural genome variabilities in patients with chronic HBV infection who had not been treated with lamivudine before. Oligonucleotide chip technology is a reliable and useful diagnostic tool for the detection of mutants resistant to antiviral therapy in chronic HBV infection. 相似文献
80.
Peyer's patches (PPs) and/or mesenteric lymph nodes (MLNs) are thought to be essential for immunoglobulin A (IgA) production. We found that the severe IgA deficiency in lymphotoxin-deficient (LT(-/-)) mice could be fully reversed by reconstitution with LT-expressing bone marrow, despite the absence of both LNs and PPs. The number of IgA precursors from LT(-/-) mice was not reduced, and they were able to migrate into the lamina propria (LP) of wild-type mice but not of LTbetaR(-/-) mice. Consistently, lymphoid tissue chemokines and adhesion molecules were reduced within the LP of LTalpha(-/-) and LTbetaR(-/-) mice. IgA deficiency in LTalpha(-/-) mice was reversed by the transplantation of a segment of RAG-1 (recombination-activating gene 1) deficient intestine, which confirmed the dispensability of the MLNs and PPs and the sufficiency of the LT-mediated gut microenvironment for IgA production. 相似文献