肿瘤干细胞表面标记物CD44在胃癌浸润和淋巴结转移中的作用

背景：肿瘤干细胞不仅能启动肿瘤发生,还参与肿瘤细胞的侵袭和转移。对肿瘤干细胞来说,识别其特异性细胞表面标志物已成为研究热点。 目的：探讨肿瘤干细胞表面标记物CD44在胃癌浸润和淋巴结转移中的临床意义。 方法：采用免疫组化 SABC法检测胃癌组织标本CD44蛋白表达,应用Pearsonχ2检验和Cox回归多因素分析,确定CD44表达与胃癌生物学特性及其预后的相关性。 结果与结论：100例胃癌标本中,59例(59.0%)标本CD44蛋白呈阳性表达。CD44蛋白在距胃癌原发灶边缘5 cm以上的正常胃黏膜组织中呈阴性表达。胃癌组织中CD44蛋白广泛表达,主要表达于细胞膜,少量表达于细胞浆。胃癌组织中 CD44蛋白的表达和患者性别、年龄无关(P > 0.05),但与肿瘤分期和淋巴管浸润、组织学分级、肿瘤大小等有关(P < 0.05),其中,肿瘤浸润越深、组织学分级越高、肿瘤直径越大、有淋巴结转移,则CD44蛋白表达阳性率越高,CD44阳性表达是影响患者术后生存的独立预后因素(P < 0.05)。以上结果表明肿瘤干细胞表面标记物CD44在胃癌组织中的表达与胃癌的浸润和淋巴结转移密切相关,表达越高患者预后越差。 中国组织工程研究杂志出版内容重点：干细胞;骨髓干细胞;造血干细胞;脂肪干细胞;肿瘤干细胞;胚胎干细胞;脐带脐血干细胞;干细胞诱导;干细胞分化;组织工程     

VEGF rs3025039和rs3025021多态性与胃癌组织中VEGF、COX-2表达的关系

目的研究血管内皮生长因子(VEGF)基因单核甘酸多态性与安徽地区胃癌易感性关系以及与胃癌临床病理特征和胃癌组织VEGF、环氧化酶-2(COX-2)蛋白表达的关系。方法采用基因测序仪对安徽地区238例胃癌患者及425例正常对照组血样进行VEGF rs3025039和rs3025021的多态性测序,用组织芯片技术及免疫组化法检测相应胃癌组织和30例癌旁组织中VEGF和COX-2的分布。结果与正常对照相比,胃癌患者VEGF rs3025039TT基因型可能增加胃癌风险性(P=0.047,OR=2.86,95%CI=1.01～8.08)。rs3025021CT基因型显著降低胃癌风险性(P=0.032,OR=0.65,95%CI=0.44～0.96)。胃癌组织VEGF和COX-2的阳性率分别为62.6%及61.8%,显著高于癌旁组织的26.7%(P=0.000)和36.7%(P=0.008),并与TNM分期、肿瘤大小、浸润深度、淋巴结转移、临床分期(仅VEGF)及组织学类型(仅COX-2)有关(P=0.001～0.05)。VEGF表达与COX-2呈正相关(rs=0.178,P=0.006)。除VEGF rs3025021与肿瘤大小有关(P=0.026)外,VEGF rs3025039和rs3025021与胃癌临床病理学参数及VEGF及COX-2表达均无关。结论VEGF rs3025039和rs3025021多态性影响安徽地区的胃癌易感性,对胃癌组织VEGF表达无明显影响;VEGF及COX-2表达与胃癌的肿瘤侵袭性密切相关,二者对胃癌的恶化进展可能有一定的协同作用。     

胃癌组织中钙网织蛋白的表达及其与临床病理特征的关系

目的 观察钙网织蛋白(CRT)在胃癌组织中的表达水平及其与临床病理的关系.方法 收集2009年4月至2010年8月本院外科手术切除并经病理确诊的44例新鲜胃癌组织及癌旁正常胃组织,采用实时荧光定量PCR和免疫组织化学方法分别检测44例胃癌及癌旁正常胃组织中CRT的mRNA和蛋白表达水平,分析其表达情况与临床病理学特征之间的关系.结果 胃癌组织中CRT的mRNA表达水平低于正常胃组织[36.50(21.72,71.47)比48.19(20.84,139.20),P=0.031].CRT蛋白主要定位于细胞质中,在胃癌组织中其阳性表达率明显低于正常胃组织[34.09％(15/44)比77.27％ (34/44),P=0.000].胃癌组织中CRT mRNA和蛋白的低表达均与胃癌的分化程度、淋巴结转移等临床病理因素密切相关(均P＜0.05),与患者的年龄、性别、肿瘤大小、TNM分期无关(均P＞0.05).结论 胃癌组织中CRT低表达,且与淋巴结转移、胃癌分化程度密切相关,是一项有潜在价值的肿瘤相关标志物.     

hMLH1和干细胞标志物CD44在胃癌的表达及相互间的关系

目的研究错配修复基因hMLH1和干细胞标志物CD44在胃癌的表达状况、意义及相互间的关系。方法采用免疫组化SP法检测79例胃癌组织和相对应的癌旁组织中错配修复基因hMLH1和干细胞标志物CD44的表达状况,结合临床资料分析这两个指标的表达与肿瘤病理参数间的关系,运用卡方检验分析该两个指标间的相互关系。结果79例胃癌标本中,hMLH1阳性表达的有15例,占19%,,CD44阳性表达的有53例,占67.1%,两者在癌旁正常组织表达的阳性率分别为51%和15.2%,两者差异均有统计学意义(P<0.05);胃癌组织中hMLH1的表达与CD44呈负相关(P<0.05);hMLH1阴性表达、CD44阳性表达与胃癌淋巴结转移、浸润深度、TNM分期及脉管浸润呈正相关(P<0.05)。结论 hMLH1在胃癌的形成过程中起到重要作用,它与胃癌干细胞标志物CD44之间存在拮抗关系。     

胃良恶性病变组织中CD24和CD44v6的表达及其意义

目的： 研究胃良恶性病变组织中癌干细胞标记物CD24、CD44v6的表达并探讨其临床病理意义。方法: 49例胃癌、20例癌旁组织、36例淋巴结转移灶及80例不同类型胃良性病例（浅表性胃炎10例，萎缩性胃炎15例，胃溃疡20例，胃息肉20例，胃腺瘤15例）标本常规制作石蜡包埋切片，CD24和CD44v6染色方法为EnVision免疫组化法。结果: 胃癌病例CD24和CD44v6表达阳性率明显高于癌旁组织和不同类型胃良性病变（P＜0.05或P＜0.01），且阳性表达的良性病例胃黏膜上皮均呈中至重度不典型增生；转移灶CD24和CD44v6表达与相应原发灶呈现高度一致性（P>0.05）；组织学分级Ⅱ级、无淋巴结转移及无远处器官转移胃癌病例CD24和CD44v6表达阳性率明显低于组织学分级Ⅲ或Ⅳ级、淋巴结转移及远处器官转移病例（P＜0.05）。此外，浸润深度T₁-T₂及淋巴结N1站转移病例CD24表达阳性率明显低于浸润深度T₃-T₄和淋巴结N₂、N₃站转移病例（P＜0.05）。结论: CD24和CD44v6表达可能是反映胃癌发生、进展、生物学行为和预后的重要癌干细胞标记物，检测胃良性病例CD24和CD44v6表达水平对预防和早期发现胃癌可能有一定的临床价值。     

CEACAM1和CD34蛋白表达与胃癌侵袭转移的关系

目的探讨癌胚抗原相关黏附分子1(CEACAM1)和CD34蛋白表达与胃癌侵袭转移的关系。方法免疫组化SP法检测90例胃癌组织和30名正常胃黏膜组织中CEACAM1及CD34的表达情况,分析CEACAM1和CD34标记的微血管密度(MVD)与胃癌患者临床病理特征的关系。结果 CEACAM1和CD34蛋白在胃癌中的阳性表达明显高于正常胃黏膜组织(P0.05)。CEACAM1蛋白的表达程度与肿瘤分化、侵袭深度、是否淋巴结转移及病理分期相关(P0.05),胃癌组织中MVD与肿瘤大小、分化、侵袭深度、是否淋巴结转移及病理分期相关(P0.05)。CEACAM1表达程度及CD34标记的MVD在胃癌中的表达呈正相关关系(P0.05)。结论 CEACAM1与CD34参与了胃癌的侵袭和转移,有望成为胃癌发生、发展和预后的预测指标。     

非小细胞肺癌中GPR120、VEGF的表达及临床意义

目的探讨非小细胞肺癌(non-small cell lung cancer, NSCLC)中GPR120、VEGF的表达及与预后的关系。方法应用qPCR及Western blot法检测42例NSCLC新鲜组织(包括癌组织和对应癌旁组织)中GPR120、VEGF mRNA及蛋白表达。免疫组化检测85例NSCLC癌组织及62例癌旁组织石蜡标本中GPR120、VEGF蛋白的表达,并分析其表达与患者生存期的关系。结果 NSCLC组织中GPR120、VEGF的表达明显高于对应癌旁组织(P0.05)。GPR120表达与淋巴结转移、远处转移、TNM分期密切相关(P0.05)。VEGF表达与淋巴结转移、TNM分期密切相关(P0.05)。qPCR及免疫组化结果均提示GPR120与VEGF表达显著相关(r=0.738 6,P0.000 1;r=0.413,P0.001)。NSCLC患者生存期与GPR120低表达、VEGF低表达呈正相关(P0.05)。GPR120蛋白高表达、淋巴结转移、远处转移均为NSCLC患者预后的危险因素(P0.05)。结论 GPR120、VEGF在NSCLC的侵袭、转移中发挥重要作用,并且GPR120可作为NSCLC有价值的预后生物学标志物。     

Ezrin和CD44v6在胃癌中的表达及其临床意义

目的 探讨胃癌组织中Ezrin和CD44v6的表达及其临床病理意义.方法 应用免疫组织化学(SP法)检测73例胃腺癌患者组织标本、15例胃不典型增生组织及12例癌旁胃黏膜组织中Ezrin和CD44v6的表达情况.结果 (1)Ezrin 在正常胃黏膜组、胃不典型增生组和胃癌组中的阳性表达率分别为41.7%、53.3%和83.6%.CD44v6在正常胃黏膜组、胃不典型增生组和胃癌组中的阳性表达率分别为25%、40%和82.2%.(2)Ezrin和CD44v6的表达与淋巴结转移密切相关,有淋巴结转移组Ezrin与CD44v6的阳性率均明显高于无淋巴结转移组(P<0.05);在Ezrin和CD44v6同时表达组中,淋巴结转移率为63%(34/54例)高于两者均为阴性组(1/6例,16.7%)(P＜0.05).结论 联合检测Ezrin和CD44v6的表达有助于预测胃癌的恶性程度和转移潜能.     

胃癌组织中Caspase 3、Caspase 9的表达及其临床意义

目的探讨胃癌组织中Caspase 3和Caspase 9蛋白的表达及其临床意义。方法采用免疫组化SP法检测50例胃癌组织和40例癌旁正常胃黏膜组织中Caspase 3、Caspase9蛋白表达水平,并分析两者表达与胃癌临床病理特征和预后的关系及两者之间的相关性。结果胃癌组织中Caspase3、Caspase 9蛋白表达均低于癌旁正常胃黏膜组织,差异有统计学意义(P0.05);Caspase 3和Caspase 9蛋白表达水平与胃癌组织分化程度、TNM分期、淋巴结转移相关(P0.05),而与浸润深度无相关性(P0.05)。两者在胃癌组织中的表达呈正相关(rs=0.636,P0.05)。结论 Caspase3、Caspase 9的异常表达参与胃癌的发生、发展,两者起正协同作用。Caspase 3、Caspase 9与胃癌临床病理特征密切相关,可作为判断胃癌患者病情进展及预后的生物学标志物,有望成为胃癌未来治疗的新靶点。     

CD44和NANOG在上皮性卵巢癌中的表达及其临床意义

目的:探讨上皮性卵巢癌(epithelial ovarian cancer,EOC)中CD44及转录因子NANOG的表达及其临床意义。方法:用免疫组织化学法检测良性卵巢肿瘤和EOC组织中CD44及NANOG的表达,并对EOC中CD44和NANOG的表达水平做相关性分析。Western blot法检测不同浓度顺铂对卵巢癌SKOV3细胞中CD44及NANOG蛋白表达水平的影响。结果:CD44和NANOG在EOC中的阳性表达率均明显高于良性卵巢肿瘤组织(P0.01);EOC中CD44与NANOG的表达水平呈正相关(r=0.346,P0.01)。CD44在EOC中的阳性表达率与临床分期和淋巴结转移有关(P0.05),而与年龄、病理分级、病理类型和肿瘤位置无关;NANOG在EOC中的阳性表达率与病理分级和临床分期有关(P0.05),而与年龄、病理类型、淋巴结转移和肿瘤位置无关。顺铂可诱导卵巢癌SKOV3细胞中CD44和NANOG表达上调(P0.05)。结论:CD44和NANOG在EOC中高表达,且与EOC发生和发展有关。顺铂可诱导卵巢癌SKOV3细胞中肿瘤干细胞标记物CD44及胚胎干细胞多能性基因产物NANOG表达升高。肿瘤干细胞的产生可能是促进EOC发生、发展及化疗耐药的潜在机制。     

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.