外科植入物用钛合金研究进展和标准化现状

介绍了外科植入物用钛的研究：（1）纯钛，Ti-6Al-4V合金；（2）Ti-6Al-7Nb合金；（3）新型β钛合金（Ti-13Nb-13Zr,Ti-12Mo-6Zr-2Fe,Ti-15Mo-2.8Nb-0.2Si合金）；（4）Ti-Ni合金，概述了其研究进展，这些合金的性能特点，应用和标准化现状。     

退火态Ti?6Al?3Nb?2Zr?1Mo钛合金的组织和力学性能

采用模锻工艺及980℃退火工艺制备了Ti-6Al-3Nb-2Zr-1Mo合金,通过扫描电子显微镜(scanning electron microscope,SEM)观察和电子背向散射衍射(electron back-scattered diffraction,EBSD)分析等方法研究了退火态合金不同截面上的微观组织与力学性能。结果表明:与锻态合金比较,退火态Ti-6Al-3Nb-2Zr-1Mo合金的α相含量减少,亚稳态的β相增多。在空气冷却的过程中,合金的亚稳态β相又转化为次生α相和少量β相。退火态Ti-6Al-3Nb-2Zr-1Mo合金中α-Ti呈现出RD//[ī2ī0]、FD//[0001]的织构类型(FD为锻件压缩方向(锻造方向),RD为锻件自由延伸方向)。退火态Ti-6Al-3Nb-2Zr-1Mo合金的三个方向拉伸断裂主要是韧性断裂,并且断裂方式呈现出微孔聚集断裂。沿RD方向拉伸时韧窝尺寸较大,对应的延伸率也优于其他方向。     

短时高温钛合金热变形行为研究

采用热模拟试验机对铸态Ti-6Al-4Sn-8Zr-0.8Mo-1.5Nb-1W-0.25Si短时高温钛合金进行热模拟试验，研究了其高温变形行为。试验结果表明：该高温钛合金热变形对温度和变形速率敏感，随着应变速率降低和变形温度升高，真应力显著降低。利用高温压缩应力应变数据绘制了热加工图，分析结果显示：(α+β)相区的900～960℃、0.035～0.368 s^-1和960～1 010℃、0.165～0.577 s^-1;β相区的1 010～1 020℃、0.165～1 s^-1为最适合加工的区域。经计算，(α+β)两相区的热变形激活能为316.229 kJ/mol，并构建了该相区内的本构方程。     

Ti-6Al-4V-0.1B合金热压缩过程中温度和应变速率对变形行为和组织演化的影响

Tamirisakandala等报道了通过在Ti-6Al-4V合金中添加0.1%硼,使合金的β晶粒尺寸由1 700μm减小为200μm。然而截至目前,对于添加硼的Ti-6Al-4V合金在热机械加工过程中的变形行为和显微组织演化还不是很清楚。为此,印度学者ShibayanRoy等人对添加硼的Ti-6Al-4V合金进行了热压缩试验,研究了变形温度和应变速率对变形行为和组织     

Ti-25Al-14Nb-2Mo-1Fe合金热压缩变形流变应力行为与微观组织演变的研究

在Gleeble-3500热模拟试验机上对Ti-25Al-14Nb-2Mo-1Fe合金进行了等温恒应变速率压缩试验,研究了在变形温度为950~1 100℃,应变速率为0.001~1 s-1,最大变形程度为50%的条件下合金的热压缩变形流变应力行为与微观组织演变。结果表明:Ti-25Al-14Nb-2Mo-1Fe合金的流变应力对变形温度和应变速率均较为敏感,其流变应力曲线具有应力峰值、流变软化和稳态流变的特征。在变形温度为950℃,应变速率为0.001~0.1 s-1的条件下,Ti-25Al-14Nb-2Mo-1Fe合金的热变形特性为片层组织球化,其热变形机制可用晶界分离球化模型进行解释说明;在变形温度为1 000~1 100℃,应变速率为1 s-1的条件下,材料只发生了动态回复现象;在变形温度为1 050~1 100℃,应变速率为0.001~0.1 s-1的条件下,材料发生了动态再结晶现象。     

钛合金发动机阀门

钛合金发动机阀门上有一层由硬质陶瓷或金属化合物弥散于钛中而涂于阀门表面上的硬质涂层。本工艺的特殊之处在于其硬质陶瓷是碳化物、氧化物或氮化物,例如碳化钛、碳化硅、碳化铬或碳化钨。用于阀门的钛合金有Ti-6Al-4V、Ti-6Al-6V-2 Sn、Ti-6Al-2Sn-4Zr-2Mo、Ti-6Al-2Sn-4Zr--6Mo、Ti-10V-2Fe-3Al、Ti-5Al-2.5Sn、Ti-8Al-1Mo-1V、Ti-13V-11Cr-3Al、Ti-8Mo-8V-2Fe-     

退火温度对Ti-6Al-3Nb-2Zr-1Mo合金组织及力学性能的影响

研究了退火温度对Ti-6Al-3Nb-2Zr-1Mo合金组织和力学性能的影响。结果表明:随着退火温度升高,初生α相含量降低,2°～15°小角度晶界逐渐减少;退火温度较高时,退火过程中发生了α相→β相→α相的相变,<0001>//横向织构消失。随着退火温度升高,Ti-6Al-3Nb-2Zr-1Mo合金屈服强度逐渐降低,抗拉强度、延伸率先升高后降低。退火温度升高后,片层组织比例升高,裂纹扩展功占冲击吸收功的比例增大,材料韧性提升。     

单相亚稳β组织的Ti-5Al-5V-5Mo-3Cr合金的热变形机制

<正>Ti-5Al-5V-5Mo-3Cr合金是一种高强近β型钛合金,该合金兼具良好的加工性能和力学性能,已被用于制造大型航空部件。日本研究人员基于组织演变和加工图技术,对原始组织为单相β等轴晶的Ti-5Al-5V-5Mo-3Cr合金的热变形机制进行了研究。实验温度分别为600、700、800、900、1 000、1 100℃,应变速率分别为0.001、0.01、0.1、1、     

β相稳定元素对TiAl合金高温变形行为的影响

利用Gleeble-1500D热模拟试验机研究了Ti-44Al、Ti-44Al-6Nb和Ti-44Al-6Nb-1Cr-2V合金在1 100～1 250℃和0. 01 s-1条件下的热变形行为。研究结果表明,添加β相稳定元素可降低TiAl合金的流变应力,在相同变形条件下Ti-44Al-6Nb-1Cr-2V合金具有更低的峰值应力。高温变形时,TiAl合金主要发生片层弯曲和拉长协调变形,以及片层团晶界处动态再结晶和B2相协调变形。动态再结晶程度随着变形温度的升高以及β相稳定元素含量的提高而增加,B2相协调变形和促进动态再结晶是TiAl合金的主要软化方式。添加β相稳定元素和控制B2相含量能有效改善TiAl合金热加工性能。     

热等静压对Ti-6Al-4V粉末冶金件组织和性能的影响

以Ti-6Al-4V合金棒材为原料,采用等离子旋转电极雾化法(PREP)制备出高品质球形钛粉,再通过热等静压近净成形工艺将粉末压制成块,并对Ti-6Al-4V合金块体的组织和性能进行研究。结果表明:Ti-6Al-4V合金粉末经热等静压后,组织主要由等轴α相+片条α相以及少量β相组成。升温升压速率较快时,粉末颗粒内部主要以片条状的α相为主,且同一束域内的α相彼此平行,规则排列成同一取向,颗粒边界处以等轴α相为主,其力学性能超过锻件;升温升压速率较慢时,冶金件组织发生明显粗化,力学性能介于锻件和铸件之间。     

The S1(1A1)-S0(1A1) Electronic Transition of Jet-Cooled o-Difluorobenzene

Retinal pigment epithelium transplantation has been proposed as adjunctive treatment for age-related macular degeneration following surgical excision of choroidal neovascular membranes. The goal of this study was to develop a model to evaluate retinal pigment epithelium transplantation onto human Bruch's membrane in vitro. We investigated the ability of cultured fetal human retinal pigment epithelium to colonize human cadaver Bruch's membrane, determined the incubation time needed to form a monolayer and to exhibit apical microvilli and tight junctions, and assessed the production of basement membrane. Freshly enucleated (less than 48 hours old) human eyes were cut through the pars plana, and the anterior segment, vitreous, and retina were removed. The native retinal pigment epithelium was debrided with a surgical sponge. Bruch's membrane and choroid at the macula were trephined with a 7.0 mm diameter trephine and then incubated with 1/2 ml of Dulbecco's modified Eagle's medium +15% fetal calf serum+basic fibroblast growth factor (1 ng ml-1), and fetal human retinal pigment epithelium at a concentration of 242,000 cells ml-1. Specimens were incubated for 1, 4, 6, 8, 12, or 24 hours. The specimens were fixed in half strength Karnovsky's fixative, processed, and analysed with scanning and transmission electron microscopy. The retinal pigment epithelium covered the debrided macular specimens to different degrees at different incubation times. After 1 hour, the cells started to attach and flatten (median percent coverage: 78%). The extent of Bruch's membrane coverage by fetal retinal pigment epithelium varied greatly between specimens. After 4-6 hours, the cells covered the entire debrided surface in a monolayer (median percent coverage: 97.2% at 4 hours, 99.8% at 6 hours). Tight junctions were observed, and the cells had few apical microvilli. The lateral cell borders were obliquely oriented with respect to Bruch's membrane, and the nuclei were elongated, exhibited prominent nucleoli, and were oriented parallel to Bruch's membrane. After 6-8 hours, cells started to become hexagonal (median percent coverage at 8 hours: 99.97%). Cells attached to the inner collagenous layer tended to be flatter than cells attached to residual native basement membrane. At 12 and 24 hours, expression of hexagonal shape, tight junctions, and apical microvilli were observed more frequently (median percent coverage: 99.87% at 12 and 100% at 24 hours). No newly formed basement membrane was observed at these time points. In separate experiments comparing attachment in the presence and absence of native RPE basement membrane, the presence of native retinal pigment epithelial basement membrane promoted the early attachment of the cells and more rapid expression of normal morphology. This in vitro system provides a reproducible way to study the adherence of retinal pigment epithelium to normal and diseased human Bruch's membrane.     

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NF1 (neurofibromatosis type 1)

Several distinct Ras GTPase activating proteins (GAPs) from mammals, including Ras GAP of 120 kDa (GAP1) and NF1, stimulate the intrinsic GTPase activity of normal Ras, but not oncogenic Ras mutants (Trahey and McCormick, 1987). That is the reason why normal Ras remains predominantly in the inactive GDP-bound form (D-Ras), whereas oncogenic Ras remains constitutively in the active GTP-bound form (T-Ras). NF1 is a tumor suppressor of 2818 amino acids whose disruption or deletion causes brain tumors called neurofibromatosis type 1 by elevating the T-Ras level. T-Ras activates several distinct oncogenic effectors, including Ser/Thr kinase Raf, GAP1, P1-3 kinase, PKC-zeta and Ra1 GDS. Interestingly, the binding of T-Ras to either GAPs or these oncogenic effectors requires the same effector domain I (residues 32-40) of T-Ras molecule. In other words, these GAPs and effectors compete for binding to T-Ras. Using a series of N- and C-terminal deletion mutants of NF1, we identified a 78 amino acid fragment (NF78, residues 1441-1518) as the minimum GAP domain, and a 56 amino acid fragment (NF 56, residues 1441-1496) as the minimum Ras-binding domain. Furthermore, we identified the Raf fragment of 81 amino acids (Raf81, residues, 51-131) as the minimum Ras-binding domain with a high affinity. We found that (i) these NF1 fragments and Raf81 compete for binding to T-Ras, and that (ii) over-expression of these NF1 or Raf fragments strongly suppresses the malignant transformation caused by oncogenic Ras mutants. Thus, these agents offer a unique opportunity to control the proliferation of T-Ras-associated tumors that represent more than 30% of all human carcinomas including neurofibromatosis type 1.     

Modulation of JunD.AP-1 DNA binding activity by AP-1-associated factor 1 (AF-1)

AP-1-associated factor 1 (AF-1), is a novel protein complex that dramatically enhances the assembly of JunD-containing dimers onto AP-1 consensus sites. We describe the partial purification of AF-1 from nuclear extracts of the T-cell line MLA 144 by ionic, hydrophobic and gel filtration chromatography. AF-1 is a DNA-binding protein composed of low molecular mass polypeptides of 7-17 kDa that exists in solution as a 34-kDa complex. JunD interactions with DNA are accelerated in the presence of AF-1 through the formation of a true tri-molecular complex with JunD dimers and DNA that assembles much more rapidly on DNA than JunD alone. DNA binding analysis of AF-1 interaction with JunD.AP-1 and DNA shows that AF-1 increases the DNA binding affinity of JunD for AP-1 sites over 100-fold. DNA cleavage footprint analysis of isolated AF-1.JunD DNA complexes shows that the ternary complex makes nearly twice as many contacts with DNA than JunD dimers alone. AF-1 interacts readily, but differentially with Jun homodimers and Jun.Fos heterodimers. These findings distinguish AF-1 as a significant protein-specific modulator of AP-1.JunD in T-cells.