膀胱尿路上皮癌中碳酸酐酶Ⅸ的表达及意义

目的探讨碳酸酐酶Ⅸ(carbonic anhydraseⅨ,CAⅨ)在膀胱尿路上皮癌中的表达,及CAⅨ在膀胱尿路上皮癌中的诊断价值及临床意义。方法应用免疫组化EnV ision法检测70例(低级别尿路上皮癌30例,高级别尿路上皮癌40例)和10例膀胱黏膜慢性炎中CAⅨ的表达。结果CAⅨ在膀胱尿路上皮癌中的阳性率为67.1%(47/70),而在膀胱慢性炎中均阴性,差异有统计学意义(P0.01)。CAⅨ在低级别尿路上皮癌中的表达高于高级别尿路上皮癌,差异有统计学意义(P0.05)。CAⅨ在膀胱pT 0期尿路上皮癌中的阳性表达高于pT 1及以上分期,但差异无统计学意义(P0.05)。结论CAⅨ免疫组化检测可有助于膀胱尿路上皮癌的诊断。膀胱尿路上皮癌中CAⅨ低表达可能会预测膀胱癌的生物学行为。     

RIN1在人膀胱尿路上皮癌中的表达

目的研究RIN1在人膀胱尿路上皮癌中的表达。方法分别应用免疫蛋白印迹技术和实时定量PCR技术检测RIN1蛋白和RIN1 m RNA在人膀胱尿路上皮癌及癌旁组织中的表达。结果 Real-time PCR结果发现,在15对新鲜的膀胱尿路上皮癌及癌旁组织中,有12对的癌组织中RIN1表达高于癌旁组织。在膀胱尿路上皮癌组织中,RIN1的m RNA表达平均倍数为10.61±5.42,癌旁组织中,RIN1的m RNA平均倍数为4.31±1.77,P0.05。Western blot法结果认证了RIN1在膀胱尿路上皮癌组织中的表达是升高的。结论 RIN1在膀胱尿路上皮癌组织中的m RNA和蛋白的表达水平高于癌旁组织。     

具有内翻生长特征的尿路上皮增生性病变的临床病理学研究

目的 研究伴内翻生长特征的尿路上皮增生性病变的临床病理特征,探讨免疫组织化学和多点荧光原位杂交在其鉴别诊断中的作用.方法 收集具有内翻生长特征的尿路上皮病变41例,分为内翻乳头状瘤、内翻生长型尿路上皮癌、旺炽型von Brunn细胞巢,用多点荧光原位杂交方法检测其3、7、17号染色体获得和9p21缺失;免疫组织化学EnVision法标记p53、CK20和Ki-67;并对12例进行随访.结果 (1)内翻乳头状瘤12例,平均1.2 cm,由互相连接的细胞索或巢在固有膜内生长,细胞索相对较细而宽窄一致,细胞巢外呈栅栏状、内为流水状排列,可见鳞状分化,无细胞学上的异型性,无或偶见核分裂象,4例可见少量表面外生乳头,被覆少于6层的正常尿路上皮.(2)内翻生长型尿路上皮癌24例,平均2.1 cm,结构似内翻乳头状瘤,但细胞索较粗并宽窄不一,细胞巢粗大并不规则状,可形成实体结构,瘤细胞轻至中度异形,核分裂象1～8个/10 HPF,3例表面均未见外生性乳头,但表层尿路上皮有明显异型增生,有少量外生乳头者外生成分形态符合低级别或低度恶性潜能.(3)旺炽型yon Brunn细胞巢5例,平均0.9 cm,表面被覆正常或增厚的黏膜组织,固有膜内见巢状分布、大小不等、排列紧密的尿路上皮团伴有囊腔形成,细胞均无异型性,无或偶见核分裂象.多点荧光原位杂交:79.1%(19/24)的内翻生长型尿路上皮癌存在染色体异常阳性,而内翻乳头状瘤和旺炽型von Brunn细胞巢无阳性染色体异常.免疫组织化学:CK20仅在2例内翻生长型尿路上皮癌中弱表达,内翻乳头状瘤和旺炽型von Brunn细胞巢均为阴性;16例内翻生长型尿路上皮癌和1例内翻乳头状瘤中有5%～50%的瘤细胞弱表达p53;内翻生长型尿路上皮癌中1%～5%表达Ki-67,内翻乳头状瘤和旺炽型von Brunn细胞巢均低于1%.随访:2例内翻生长型尿路上皮癌经多次复发后为浸润性癌,行全膀胱切除后仍发生远处转移.内翻乳头状瘤无复发.结论 伴内翻生长特征的尿路上皮增生性病变在良恶性病变中存在形态学上的重叠,但内翻生长型尿路上皮癌在形态及免疫组织化学上有独特特征.多点荧光原位杂交在鉴别诊断中有辅助作用.     

卵巢成熟性囊性畸胎瘤癌变为小细胞癌混合鳞状细胞癌1例

卵巢成熟性囊性畸胎瘤癌变(malignant transformation of ovarian mature cystic teratoma, MCT)较罕见。本文报道1例卵巢成熟性囊性畸胎瘤, 灶区伴小细胞神经内分泌癌混合鳞状细胞癌变(小细胞癌约占60%, 鳞状细胞癌约占40%)。本例小细胞癌区域CD56、突触素阳性以及Ki-67阳性指数高表达至80%, p40、细胞角蛋白(CK)5/6阴性, 提示神经内分泌癌分化;鳞状细胞癌癌变区域p40、CK5/6阳性, CD56、突触素阴性;两种癌变区域p53及p16均阴性。该疾病主要与宫颈或阴道的鳞状细胞癌、胃肠道低分化腺癌、泌尿系统的尿路上皮癌、呼吸道及胃肠道小细胞癌转移、卵巢粒层细胞瘤相鉴别。此病以手术全切除为主, 术后辅以系统性放、化疗。     

P504S在前列腺癌、肾细胞癌和膀胱尿路上皮癌中的表达及临床意义

目的：探讨肿瘤标记物P504S在前列腺癌(prostate cancer,Pca)、肾细胞癌(renal cell carcinoma, RCC)和膀胱尿路上皮癌(bladder transitional cell carcinoma,BTCC)组织中的表达及临床意义。方法：采用免疫组织化学标记菌葡萄聚糖聚合物法(labeled dextran polymer,LDP),检测P504S在前列腺癌、肾细胞癌和膀胱尿路上皮癌组织中的表达情况,探讨其在前列腺增生(benign prostatic hyperplasia,BPH)组织、正常肾组织和正常膀胱组织中的表达并作相应比较。结果：P504S在Pca、RCC和BTCC组织中阳性表达率分别为93.10%、65.28%和46.07%,而在BPH、正常肾组织和正常膀胱组织分别为0%、6.67%和6.25%,各组间差异均有统计学意义(P<0.01);P504S阳性表达水平与Pca、RCC及BTCC病理分级和临床分期均呈正相关(P<0.05),与肿瘤的预后也密切相关。结论：P504S的表达水平可较好地反映前列腺癌、肾细胞癌和膀胱尿路上皮癌生物学行为,可作为判断肿瘤侵袭、病情发展及预后指标之一。     

p21 Ras和表皮生长因子受体蛋白在喉鳞状细胞癌组织中的表达

目的探讨p21 Ras及表皮生长因子受体在喉鳞状细胞癌发病机制中的表达及相关性分析。方法选取50例喉鳞状细胞癌组织(实验组)及10例正常喉黏膜组织(对照组),应用免疫组织化学方法检测两组组织中p21 Ras和表皮生长因子受体的蛋白表达,并进行统计学分析。结果与对照组相比,p21 Ras蛋白在喉鳞状细胞癌组织中的阳性表达率显著升高(分别为40.0%和72.0%,P0.05),且与喉鳞状细胞癌临床分期、分化程度及淋巴结转移密切相关(P0.05);与对照组相比,EGFR在喉鳞状细胞癌组织中的表达显著升高(分别为20.0%和76.0%,P0.05),且与喉鳞状细胞癌淋巴结转移密切相关(P0.05),而与性别、肿瘤发生部位、分化程度、临床分期无关(P0.05)。相关性分析结果显示,EGFR与p21 Ras表达呈正相关(r=0.81,P0.05)。结论 p21 Ras和EGFR在喉鳞状细胞癌组织中的高阳性率可作为喉鳞状细胞癌发生的预测指标,在伴有淋巴结转移组的强阳性表达提示二者在喉鳞状细胞癌发展过程中起重要作用。     

膀胱尿路上皮癌MMP-2表达及其与FAK、p53、bcl-2、Ki-67的关系

目的 比较不同分化和浸润程度膀胱尿路上皮癌MMP—2表达及其与FAK、p53、bcl—2和Ki—67的关系。方法 采用免疫组化EnVision法对83例膀胱尿路上皮癌和68例非肿瘤尿路上皮，进行MMP—2、FAK、p53、bcl—2和Ki—67的表达检测。结果 MMP—2在肿瘤组织中的表达显著高于非肿瘤性移行上皮，其表达强度随肿瘤分化程度降低和浸润深度增加而显著增强。分化差和浸润性膀胱癌中FAK和p53表达增强，并与MMP—2表达呈正相关；分化差膀胱癌中Ki—67表达增强而bcl—2表达丢失，Ki—67与MMP—2表达呈正相关。结论 在膀胱尿路上皮癌的进展和分化过程中，肿瘤分化程度越低，肿瘤细胞分泌MMP—2越多，其浸润和转移的能力也越强。FAK、p53、Ki—67和bcl—2不但与肿瘤细胞的生长密切相关，还可能直接或间接地参与了MMP—2的调控。     

膀胱尿路上皮癌中IDO和Bin1的表达及其临床意义

目的探讨吲哚胺2,3-二氧化酶(indoleamine-2,3-dioxygenase,IDO)和桥接整合因子1 (bridging integrator 1,Bin1)在膀胱尿路上皮癌中的表达及其与临床病理特征的关系。方法收集2016年11月～2017年8月昆明医科大学第三附属医院行膀胱肿瘤切除并经病理确诊为膀胱尿路上皮癌及癌旁新鲜标本21例,采用Real-time q PCR检测IDO和Bin1的m RNA表达。结果在21例膀胱尿路上皮癌组织中,IDO m RNA明显高于癌旁组织(Z=-4. 084,P 0. 001); Bin1 m RNA明显低于癌旁组织(Z=-4. 508,P 0. 001)。膀胱尿路上皮癌组织中IDO表达强度与Bin1表达呈负相关(r=-0. 588,P 0. 05)。IDO及Bin1的表达与患者组织学分类、组织分级和TNM分期均有相关性(P 0. 05);与患者性别、年龄、肿瘤大小均无相关性(P 0. 05)。结论在膀胱尿路上皮癌中IDO高表达、Bin1低表达或表达缺失,两者有望成为膀胱尿路上皮癌预后评估和治疗的新靶点。     

膀胱尿路上皮癌组织中miR-133b的表达水平与其化疗敏感性的关系分析

目的 探讨膀胱尿路上皮癌组织中miR-133b的表达水平与其化疗敏感性的关系分析.方法 回顾性分析2011年2月至2012年2月于本院确诊为膀胱尿路上皮癌患者65例,根据癌组织中miR-133b表达水平将其分为高表达组(n=25)和低表达组(n=40),采用茎环实时荧光逆转录聚合酶链反应(stem-loop real-time,RT-PCR)检测膀胱尿路上皮癌组织和癌旁正常组织中 mi R-133b的表达水平,随访5年,统计分析所有患者化疗效果、5年存活情况.结果 膀胱尿路上皮癌组织中miR-133b的表达量(U6标准化后的) 低于癌旁正常组织,差异有统计学意义(P<0.05);高表达组患者化疗有效率高于低表达组,差异有统计学意义(P<0.05);所有患者随访0.5~5年,平均随访时间3.86年,最终有45例存活5年以上,高表达组患者5年存活率(88.00%)高于低表达组(57.25%),差异有统计学意义(P<0.05);存活组患者膀胱尿路上皮癌组织中miR-133b水平高于死亡组,差异有统计学意义(P<0.05).结论 与癌旁正常组织比较,膀胱尿路上皮癌组织中miR-133b呈明显低表达,且与术后化疗敏感性、预后有密切关系,有可能作为预测化疗疗效和判断预后的指标之一.     

MGMT基因启动子甲基化与膀胱尿路上皮癌生物学行为关系的研究

目的 检测膀胱尿路上皮癌组织中O6-甲基鸟嘌呤-DNA甲基转移酶(MGMT)基因启动子甲基化状态,探讨MGMT甲基化与其蛋白表达水平以及肿瘤生物学行为之间的关系.方法 应用免疫组织化学SP法和甲基化特异性PCR(MSP)分别检测60例膀胱尿路上皮癌及15例正常膀胱黏膜组织中MGMT蛋白表达情况和MGMT基因启动子甲基化状态.结果 膀胱癌组织中MGMT蛋白阳性表达率为35.0 %(21/60),低于正常膀胱组织(86.7 %,13/15,P<0.01).膀胱癌组织中MGMT甲基化阳性率为45.0 %(27/60),明显高于正常膀胱组织(0.0 %,0/15,P<0.01);MGMT启动子甲基化与其蛋白表达呈负相关(r = -0.453,P<0.01);并且高级别膀胱癌中MGMT甲基化阳性率(70.6 %,12/17)要比低级别膀胱癌高(34.9 %,15/43),(P<0.05),而MGMT甲基化与膀胱癌临床分期无明显关系.结论 MGMT启动子甲基化可能参与了膀胱尿路上皮癌的发生和肿瘤分化,MGMT启动子甲基化有望成为预判膀胱癌预后的重要标记.     

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.