骶骨S2椎弓根外进钉固定的生物力学分析

背景：模拟骶骨骨折S2椎弓根钉外进钉固定拔出力与在拔出椎弓钉时的应变电测分析鲜有报道。 目的：测量S2椎弓根外进钉固定拔出力与骶骨应变分布,为临床提供生物力学参数。 方法：取正常国人新鲜尸体骶骨标本,以椎弓根钉外进钉方法固定于S2椎弓根,以小型力传感器与椎弓根钉固定装置连接测量椎弓根钉的拔出力,同时以动静态电阻应变仪,对预先粘贴在4个椎弓根螺栓固定边缘部位和骶骨不同部位的应变片进行应变电测量。1号进钉点位置为左侧第1骶后孔下缘最低点,2号进钉点位置为右侧第1骶后孔下缘最低点,3号进钉点为左侧第1骶后孔连线与骶外侧嵴的交点,4号进钉点为右侧第1骶后孔连线与骶外侧嵴的交点。测量椎弓根螺钉最大拔出力和骶骨各测点应变值。 结果与结论：外进钉1号螺钉拔出力为(399.0±7.2) N,2号螺钉拔出力为(281.0±5.2) N,3号螺钉拔出力为(196.0±4.3) N,4号螺钉拔出力为(220.1±4.6) N。应变电测量最小应变发生在2号螺钉8号测点,应变为(13.5±1.1) με;最大应变发生在1号螺钉1号测点,应变为(96.8±6.5) με。提示S2椎弓根钉外进钉固定方法符合生物力学原理。     

骶二椎弓根钉外进钉固定拧紧力与骶骨应变分布规律的研揪

研究骶二椎弓根钉固定拧紧力与骶骨应变分布,为临床骶二椎弓根钉固定术提供生物力学参数.取正常国人新鲜尸体骶骨标本,以椎弓根钉内进钉法固定于骶二椎弓根,以小型力传感器与椎弓根钉固定装置连接,测量椎弓根钉的拧紧力,同时以动静态电阻应变仪对预先粘贴在四个椎弓根螺栓固定边缘部位和骶骨不同部位的应变片进行应变电测量.得出了椎弓根钉的最大拧紧力和S1椎体、S2椎体、S3椎体正中线左侧和右侧应变值,还得出了S1左侧、S1右侧上关节突关节面部位及S1、2左侧,S1、2右侧骶后孔连线与骶中间嵴交点处应变值.说明骶二椎弓根钉术式符合生物力学原理.     

骶二椎弓根钉外进钉固定拧紧力与骶骨应变分布规律的研究

研究骶二椎弓根钉固定拧紧力与骶骨应变分布,为临床骶二椎弓根钉固定术提供生物力学参数。取正常国人新鲜尸体骶骨标本,以椎弓根钉内进钉法固定于骶二椎弓根,以小型力传感器与椎弓根钉固定装置连接,测量椎弓根钉的拧紧力,同时以动静态电阻应变仪对预先粘贴在四个椎弓根螺栓固定边缘部位和骶骨不同部位的应变片进行应变电测量。得出了椎弓根钉的最大拧紧力和S1,椎体、S2椎体、S3椎体正中线左侧和右侧应变值,还得出了s,左侧、S,右侧上关节突关节面部位及S1、2左侧,S1、2右侧骶后孔连线与骶中间嵴交点处应变值。说明骶二椎弓根钉术式符合生物力学原理。     

骶二椎弓根钉内进钉固定拔出力与骶骨应变分布规律的实验研究

目的研究骶二椎弓根钉固定拔出力与骶骨应变分布规律,为临床骶二椎弓根钉固定术提供生物力学参数。方法取正常人新鲜尸体骶骨标本,以椎弓根钉内进钉方法固定于骶二椎弓根,于电子万能试验机上进行相应力学测试,并利用动静态电阻应变仪对预先粘贴在四个椎弓根螺栓固定边缘部位和骶骨不同部位的应变片进行测量。结果得出了椎弓根钉的最大拔出力为（514．5±9．4）N,发生在2号钉位置;最大应变发生在1号钉,其最大应变为（168．5±5．8）X10一。结论骶二椎弓根钉内进钉固定应变分布合理,有利于平衡和稳定。     

下颈椎经椎弓根内固定应用解剖学研究

目的：为经椎弓根螺钉在颈椎的应用提供解剖学基础。方法：用游标卡尺和Ｘ线摄片测量方法，对５４具成年Ｃ３～Ｃ７段干燥颈椎标本椎弓根的高度、宽度、长度、椎弓根轴线的角度及进钉点定位等作了三维形态学观测。结果：颈椎椎弓根的宽度可以接受３．０～４．５ｍｍ的螺钉，进钉深度在２５ｍｍ，进钉方向与上终板平行，并且在Ｃ３～Ｃ６与矢状线的夹角约为４０°～４５°；Ｃ７为３０°～４０°。进钉点定位：Ｃ３～Ｃ６位于颈椎侧块背面的中上１／４水平平分线与中外１／４垂直平分线的交点，Ｃ７位于侧块中垂线与中上１／４水平平分线的交点偏上处。结论：根据不同节段颈椎椎弓根的解剖特点，合理设计椎弓根螺钉的直径和长度，准确选择相应的进钉点和进钉方向，可以保证椎弓根螺钉内固定在下颈椎的安全应用     

CT辅助导航经皮骶髂螺钉内固定路径

目的:探讨CT辅助导航经皮骶髂螺钉内同定术的定位和路径.方法:60个成年健康志愿者行S1～3多层螺旋CT扫描,由计算机重构图像后测量通过椎弓根狭窄处中心点与正中推辞矢状面之间的角度、椎弓根高度和宽度等参数,根据这些数据确定体表进钉点、进钉角度和螺钉长度,结果:S1进针点距离后正中线(91.03±10.62)mm,同侧髂嵴后部(41.16±8.80)mm,位于通过髂后上棘连线的骶骨层面头侧(11.29±5.87)mm,进钉方向与水平而夹角(30.76±5.34)°,欠状而(48.76±9.43)°,最佳长度(84.59q±5.29)mm.S2体表进针点距离后正中线(127.82±15.63)mm,同侧髂嵴后部(59.34±9.03)mm,位于通过髂后上棘连线的骶骨层而尾侧(15.35±5.50)mm,进钉方向与水平面夹角(30.76±5.34)°,矢状面(61.15±8.38)°,最佳长度(64.04±6.65)mm.仰卧位和俯卧位骶骨倾斜度差别无统计学意义(P＞0.05),结论:(1)经多层螺旋CT扫描图像分析确、上的体表进钉点、进钉角度和螺钉长度可直接引导经皮骶髂螺钉内固定术;(2)分析确立的由CT扫描导航经皮骶髂螺钉内固定手术定位和路径为临床骶髂关节修复手术提供了一种快速、准确、安全的方法.     

寰椎前路侧块双螺钉固定的定量解剖学研究及可行性分析

目的:验证寰椎前路侧块双螺钉固定是否具有可行性。方法:对干性寰椎标本进行加密薄层螺旋CT扫描和三维重建,通过Mimics软件对相关解剖学指标进行测量,包括寰椎侧块有效宽度等内容,并进行统计学分析。根据解剖研究结果,将2枚直径为3.5 mm的寰椎侧块螺钉在干性寰椎标本上行置钉实验,置钉后行X线检查,观察螺钉在寰椎侧块中的位置。结果:测得寰椎前路侧块双螺钉固定中的螺钉存横断面上的外倾角度平均为20.46°,在矢状面上的上倾角度为0°;寰椎前路侧块双螺钉固定中的内侧螺钉理想进钉点平均为寰椎前结节巾点旁开9.80 mm,与下关节面前缘以上4.69 mm的交点,外侧螺钉理想进钉点平均为寰椎前结节中点旁开16.73 mm,与下关节面前缘以上10.99 mm的交点。寰椎前路侧块双螺钉固定中的2枚螺钉均位于侧块内,X线检查显示2枚螺钉在侧块位置佳。结论:寰椎前路侧块双螺钉固定具有解剖学可行性,可以避开横突孔、椎动脉沟、椎管等重要解剖结构。     

寰椎椎弓根解剖和CT测量在椎弓根螺钉固定中的意义

目的：确定寰椎后路椎弓根钉的进钉点和验证螺钉在寰椎侧块中的位置。方法：用40副干燥寰枢椎标本测量进钉点的最佳位置和相关数据，临床应用该置钉技术，CT测量6例术后病人钉在寰椎侧块中的位置和螺钉长度。结果：寰椎椎弓根平均宽度为7．78mm，进钉点在寰椎椎弓根中线外缘2．2mm，即枢椎下关节突中点的矢状线，CT测量螺钉均位于寰椎侧块内，螺钉长度为28--30mm。结论：寰椎椎弓根钉进钉点可用枢椎下关节突中点的矢状延长线来确定，螺钉长度28--30mm。     

寰椎后路两种螺钉固定的解剖学测量和生物力学测试的对比研究

目的　对寰椎椎弓根螺钉和寰椎侧块螺钉两种固定方法进行解剖测量和生物力学测试的对比研究，为临床选择寰椎螺钉的固定方式提供依据。方法　用电子游标卡尺和量角器测量16套正常成年人寰椎新鲜标本的相关参数，包括寰椎侧块螺钉的最大进钉长度(L1)、侧块螺钉进钉点到寰椎后弓后缘的长度(L2)、椎弓根螺钉在寰椎侧块内部分的长度(L3)、椎弓根螺钉在寰椎后弓内的长度(L4)、寰椎椎弓根螺钉的最大进钉长度(L3+L4)、椎弓根螺钉和侧块螺钉的外倾角(αo)和上斜角(βo)等14项内容。进行寰椎单皮质和双皮质的椎弓根螺钉或侧块螺钉固定，测试比较其螺钉拔出强度和钉道长度。结果　L1为(25.01±0.23)mm、L2为(9.85±1.31)mm、L3为(19.58±1.63)mm、L4为(10.47±1.51)mm、L3+L4为(29.81±1.27)mm、椎弓根螺钉和侧块螺钉的外倾角(αo)和上斜角(βo)分别为10o、5o和15o、20o。双皮质寰椎椎弓根螺钉的最大拔出力为(1686.0±425.3)N，单皮质寰椎椎弓根螺钉为(1082.5±292.7)N；双皮质寰椎侧块螺钉最大拔出力为(1127.2±367.1)N，与单皮质寰椎椎弓根螺钉无明显差异，单皮质寰椎侧块螺钉最小，为(785.2±402.7)N。结论　由于寰椎椎弓根螺钉和寰椎侧块螺钉进钉点的位置不同，使得寰椎椎弓根螺钉的长度较寰椎侧块螺钉要长。寰椎侧块螺钉的长度大于寰椎椎弓根螺钉在寰椎侧块内部分的长度，是因为寰椎侧块螺钉的上斜角度和外倾角度均较大之故。在同时适用寰椎椎弓根螺钉和寰椎侧块螺钉固定的患者，从手术操作和螺钉固定强度考虑，宜首先选择寰椎椎弓根螺钉固定，次选寰椎侧块螺钉固定。     

后凸成形和传统钉道骨水泥强化对骶骨钉松动的生物力学作用

背景：后凸成形骨水泥强化可应用于骨质疏松患者的腰椎椎弓根钉固定。 目的：评价松动的骶骨钉经后凸成形和传统钉道骨水泥强化后的固定强度。 方法：纳入9具骨质疏松症患者的新鲜尸体标本。在同一骶骨标本上,分别测试单皮质和双皮质骶骨椎弓根钉最大拔出力后,分别建立传统钉道骨水泥强化与后凸成形骨水泥强化椎弓根钉固定模型。在MTS材料试验机上,对螺钉尾部施加2 000次周期性压力载荷后,进行螺钉最大拔出力测试。 结果与结论：9个标本的骨密度均值为  0.71 g/cm²(0.61~0.77 g/cm²)。4种骶骨钉固定技术单皮质、双皮质、传统钉道骨水泥强化和后凸成形骨水泥强化骶骨钉的平均最大拔出力分别为203,325,437及565 N。双皮质骶骨钉的拔出力显著高于单皮质钉(P < 0.05);但此2固定均显著低于骨水泥强化组(P < 0.05)。后凸成形骨水泥强化组的拔出力显著高于传统钉道骨水泥强化组(P < 0.05)。此外,4种骶骨钉固定技术的最大拔出力与骨密度值均呈现显著的正相关(P < 0.05)。结果证实,传统钉道骨水泥强化技术和后凸成形骨水泥强化技术均可做为骶骨椎弓根钉松动的补救手段,但后凸成形骨水泥强化可获得更为坚强的锚定。     

Opportunities and challenges in the prevention and control of cancer and other chronic diseases: children's diet and nutrition and weight and physical activity

OBJECTIVE: The purpose of this article is to review the role of behavioral research in disease prevention and control, with a particular emphasis on lifestyle- and behavior-related cancer and chronic disease risk factors--specifically, relationships among diet and nutrition and weight and physical activity with adult cancer, and tracking developmental origins of these health-promoting and health-compromising behaviors from childhood into adulthood. METHOD: After reviewing the background of the field of cancer prevention and control and establishing plausibility for the role of child health behavior in adult cancer risk, studies selected from the pediatric published literature are reviewed. Articles were retrieved, selected, and summarized to illustrate that results from separate but related fields of study are combinable to yield insights into the prevention and control of cancer and other chronic diseases in adulthood through the conduct of nonintervention and intervention research with children in clinical, public health, and other contexts. RESULTS: As illustrated by the evidence presented in this review, there are numerous reasons (biological, psychological, and social), opportunities (school and community, health care, and family settings), and approaches (nonintervention and intervention) to understand and impact behavior change in children's diet and nutrition and weight and physical activity. CONCLUSIONS: Further development and evaluation of behavioral science intervention protocols conducted with children are necessary to understand the efficacy of these approaches and their public health impact on proximal and distal cancer, cancer-related, and chronic disease outcomes before diffusion. It is clear that more attention should be paid to early life and early developmental phases in cancer prevention.     

Beta-endorphin and drug-induced reward and reinforcement

Although drugs of abuse have different acute mechanisms of action, their brain pathways of reward exhibit common functional effects upon both acute and chronic administration. Long known for its analgesic effect, the opioid beta-endorphin is now shown to induce euphoria, and to have rewarding and reinforcing properties. In this review, we will summarize the present neurobiological and behavioral evidences that support involvement of beta-endorphin in drug-induced reward and reinforcement. Currently, evidence supports a prominent role for beta-endorphin in the reward pathways of cocaine and alcohol. The existing information indicating the importance of beta-endorphin neurotransmission in mediating the reward pathways of nicotine and THC, is thus far circumstantial. The studies described herein employed diverse techniques, such as biochemical measurements of beta-endorphin in various brain sites and plasma, and behavioral measurements, conducted following elimination (via administration of anti-beta-endorphin antibodies or using mutant mice) or augmentation (by intracerebral administration) of beta-endorphin. We suggest that the reward pathways for different addictive drugs converge to a common pathway in which beta-endorphin is a modulating element. beta-Endorphin is involved also with distress. However, reviewing the data collected so far implies a discrete role, beyond that of a stress response, for beta-endorphin in mediating the substance of abuse reward pathway. This may occur via interacting with the mesolimbic dopaminergic system and also by its interesting effects on learning and memory. The functional meaning of beta-endorphin in the process of drug-seeking behavior is discussed.     

PTEN与信号转导及肿瘤

ＴＥＮ[1] (ｐｈｏｓｐｈａｔａｓｅａｎｄｔｅｎｓｉｎｈｏｍｏｌｏｇｙｄｅｌｅｔｅｄｏｎｃｈｒｏｍｏｓｏｍｅｔｅｎ)又名ＭＭＡＣ1 [2 ] (ｍｕｔａｔｅｄｉｎｍｕｔｉｐｌｙａｄａｎｃｅｄｃａｎｃｅｒ 1 )和ＴＥＰ1 [3 ] (ＴＧＦ -βｒｅｇｕｌａｔｅｄａｎｄｅｐｉｔｈｅｌｉａｌｃｅｌｌ -ｒｉｃｈｅｄｐｈｏｓｐｈａｔａｓｅ 1 ) (以下均称为ＰＴＥＮ) ,是 1 997年由 3个研究小组先后发现的一个具有双特异磷酸酶活性的抑癌基因。ＰＴＥＮ基因异常广泛存在于人类多种恶性肿瘤 ,如恶性神经胶质瘤、前列腺癌、子宫内膜癌、黑色素瘤等…     

Tobacco and alcohol and the risk of head and neck cancer

Summary We carried out two case-control studies on the relative risk of head and neck cancer in association with tobacco and alcohol consumption. The first study carried out at the ENT Department of the University hospitals of Heidelberg and Giessen (FRG) comprised 200 male patients with squamous cell cancer of the head and neck and 800 control subjects matched for sex, age, and residential area (1:4 matching design). Of the tumour patients, 4.5% had never smoked, in contrast to 29.5% of the control group. The average tobacco and alcohol consumption of the patients was approximately twice as high as in the control subjects. The highest alcohol and tobacco consumption was observed in patients suffering from oropharyngeal cancer. Tobacco and alcohol increased the risk of head and neck cancer in a dose-dependent fashion and acted as independent risk factors. In heavy smokers (> 60 pack-years) a relative risk of 23.4 (alcohol adjusted) was calculated. Combined alcohol and tobacco consumption showed a synergistic effect. The risk ratio increased more in a multiplicative than in an additive manner. Oral and laryngeal cancer were associated with the highest tobacco-associated risk values. The highest ethanol-associated risk values were associated with oropharyngeal and laryngeal cancer. The second study was carried out at the ENT Department of the University of Heidelberg on 164 males with squamous cell carcinoma of the larynx and 656 control subjects matched for sex, age and residential area (1:4 matching design). Of the cases, 4.2% had never smoked, compared with 28.5% of the control subjects. The risk of laryngeal cancer by tobacco consumption was dose dependent, reaching a maximum value of 9.1 (adjusted for alcohol) for a consumption of more than 50 tobacco-years (TY). The relative risk of laryngeal cancer associated with alcohol intake was also dose dependent, reaching a value of 9.0 (adjusted for tobacco) for a mean daily consumption of more than 75 g alcohol. An analysis of subsite specific risks showed that heavy smokers (> 50 TY) carried a nearly ten times higher risk of supraglottic cancer than of glottic cancer. The risk of supraglottic cancer from alcohol consumption was also higher than that of glottic cancer.     

Postinfectious immunodeficiency and autoimmunity: pathogenic and clinical values and implications

Autoimmunity is still a mystery of clinical immunology and medicine as a whole. The etiology and pathogenesis of autoimmune disorders remain unclear and, thus, are assessed as a balance between hereditary predisposition, triggering factors and the appearance of autoantibodies and/or self-reactive T cells. Among the immunological armamentarium, molecular mimicry, based on self-reactive T- and B-cell activation by cross-reactive epitopes of infectious agents, is of special value. Hypotheses regarding the possible involvement of molecular mimicry in the development of postinfectious autoimmunity are currently very intriguing. They provide new approaches for identifying etiological agents that are associated with postinfectious autoimmunity, paired microbial- and tissue-linked epitopes targeted for autoimmune reaction determination, postinfectious autoimmunity pathogenesis recognition and specific prevention, and therapy for autoimmune disorder development.     

Pain and Effusion and Quadriceps Activation and Strength

Context:

Quadriceps dysfunction is a common consequence of knee joint injury and disease, yet its causes remain elusive.

Objective:

To determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion affect the magnitude of quadriceps dysfunction.

Design:

Crossover study.

Setting:

University research laboratory.

Patients or Other Participants:

Fourteen (8 men, 6 women; age = 23.6 ± 4.8 years, height = 170.3 ± 9.16 cm, mass = 72.9 ± 11.84 kg) healthy volunteers.

Intervention(s):

All participants were tested under 4 randomized conditions: normal knee, effused knee, painful knee, and effused and painful knee.

Main Outcome Measure(s):

Quadriceps strength (Nm/kg) and activation (central activation ratio) were assessed after each condition was induced.

Results:

Quadriceps strength and activation were highest under the normal knee condition and differed from the 3 experimental knee conditions (P < .05). No differences were noted among the 3 experimental knee conditions for either variable (P > .05).

Conclusions:

Both pain and effusion led to quadriceps dysfunction, but the interaction of the 2 stimuli did not increase the magnitude of the strength or activation deficits. Therefore, pain and effusion can be considered equally potent in eliciting quadriceps inhibition. Given that pain and effusion accompany numerous knee conditions, the prevalence of quadriceps dysfunction is likely high.Key Words: arthrogenic muscle inhibition, central activation failure, voluntary activation, muscles

Key Points

• Knee pain and effusion resulted in arthrogenic muscle inhibition and weakness of the quadriceps.
• The simultaneous presence of pain and effusion did not increase the magnitude of quadriceps dysfunction.
• To reduce arthrogenic muscle inhibition and improve muscle strength, clinicians should employ interventions that target removing both pain and effusion.

Quadriceps weakness is a common consequence of traumatic knee joint injury^1,2 and chronic degenerative knee joint conditions.^3,4 Arthrogenic muscle inhibition (AMI), a neurologic decline in muscle activation, results in quadriceps weakness and hinders rehabilitation by preventing gains in strength.⁵ The inability to reverse AMI and restore muscle function can lead to decreased physical abilities,⁶ biomechanical deficits,⁷ and possibly reinjury.⁵ Furthermore, researchers^8,9 have suggested that quadriceps weakness resulting from AMI may place patients at risk for developing osteoarthritis in the knee. In light of the substantial influence of quadriceps AMI on these clinically relevant outcomes, we need to improve our understanding of the factors that contribute to this neurologic decline in muscle activity so efforts to target and reverse it can be implemented and gains in strength can be achieved more easily.Joint injury and disease are accompanied by numerous sequelae (ie, pain, swelling, tissue damage, inflammation), so ascertaining which one ultimately leads to neurologic muscle dysfunction is difficult. Whereas a joint effusion can result in AMI,^10–12 the effects of pain are less understood despite many clinicians attributing AMI to pain. Using techniques that introduce knee pain without accompanying injury may provide insights into the role of pain in eliciting AMI.The degree of knee joint damage may play a role in the quantity of AMI that manifests. Hurley et al^13,14 demonstrated that quadriceps AMI, measured using an interpolated-twitch technique, was greater in patients with extensive traumatic knee injury (eg, fractured tibial plateau, ruptured medial collateral ligament, and medial meniscectomy) than patients with isolated joint trauma (ie, isolated anterior cruciate ligament [ACL] rupture). Similarly, patients with more knee joint symptoms (ie, greater number of symptoms and increased severity of symptoms) may present with greater magnitudes of quadriceps inhibition. Recently, investigators¹⁵ have suggested that patients with more pain display less quadriceps strength, supporting this tenet. Given that effusion and pain often present simultaneously with joint injuries and diseases, such as ACL injury and osteoarthritis, examining both the isolated and cumulative effects of these sequelae appears warranted to determine if they influence the magnitude of muscle inhibition.Experimental joint-effusion and pain models are safe and effective experimental methods that allow for the isolated examination of their effects on muscle function. The effusion model, whereby sterile saline is injected directly into the knee joint capsule,⁷ produces a clinically relevant magnitude of the joint effusion that may be present with traumatic injury. Effusion is thought to activate group II afferents responding to stretch or pressure,^16–18 which in turn may facilitate group Ib interneurons and result in quadriceps AMI.⁵ The pain model involves injecting hypertonic saline into the infrapatellar fat pad to produce anteromedial knee pain similar to that described in patients with patellofemoral pain syndrome.¹⁹ Pain is considered to initiate AMI through activation of group III and IV afferents that act as nocioceptors to signal damage or potential damage to joint structures.^16–18 The firing of these afferents then may lead to facilitation of group Ib interneurons, the flexion reflex, or the gamma loop, ultimately resulting in quadriceps inhibition.²⁰ Thus, these models allow us to create symptoms that are associated with knee injury and have the added benefit of providing a way to examine their effects in isolation.Therefore, the purpose of our study was to determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion would affect the magnitude of quadriceps dysfunction. We hypothesized that pain alone would result in quadriceps inhibition and that the magnitude of inhibition would be greater when effusion and pain were present simultaneously.     

类赖氨酰氧化酶2与肿瘤转移和发生

类赖氨酰氧化酶2(lysyl oxidase-like 2,LOXL2)是赖氨酰氧化酶(lysyl oxidase,LOX)基因家族的成员之一,其表达产物能促进胶原沉积.LOXL2的过表达能促进纤维化,并与肿瘤侵袭、转移及不良预后有关.目前大部分学者认为LOXL2是一种转移促进基因,也有实验支持其是一种肿瘤抑制基因.研究发现LOXL2可以通过激活Snail/Ecadherin通路或Src/FAK通路促进转移.LOXL2有望作为肿瘤生物标志物,用于预后判断,成为一个新的治疗靶点.