PVC一次性输液器中DEHP和TOTM增塑剂溶出量对比

目的偏苯三酸三辛酯(trioctyl trimellitate,TOTM)被认为是可替代邻苯二甲酸二乙基乙酯[bis(2-ethylhexyl)phthalate,DEHP],提高医用输血输液器中聚氯乙烯(polyvinyl chloride,PVC)管路使用安全性的新型医用增塑剂。本实验对比两种增塑剂的溶出量,考察TOTM的安全性。方法采用硝酸甘油、单硝酸异山梨酯两种药物及45%乙醇水模拟药液,模拟临床使用。药液经过输液器后采用HPLC进行测试,测量两种药物及模拟药液中的TOTM和DEHP,考察采用上述两种增塑剂的输液器中增塑剂的溶出情况。结果两种药物中均未检出两种增塑剂。在乙醇水模拟药液中,检出两种增塑剂,且TOTM的溶出量较DEHP高。结论模拟药液评价增塑剂的溶出性能存在局限性,因此,需要医疗器械生产企业和医疗器械监管机构协同合作,模拟临床实际使用进行检测,确保医疗器械的安全性。     

一次性使用聚氯乙烯输液器中邻苯二甲酸二乙基乙酯和偏苯三酸三辛酯溶出量对比研究

本研究通过对比研究邻苯二甲酸二乙基乙酯(phthalic acid diethyl ethyl ester,DEHP)和偏苯三酸三辛酯(rimellitic acid three dioctyl,TOTM)在不同药液中的溶出量,为安全使用DEHP或TOTM增塑的一次性使用聚氯乙烯(polyvinyl chloride,PVC)输液器提供依据。选用氯化钠注射液、单硝酸异山梨酯注射液、紫杉醇注射液、乙醇水溶液模拟临床滴注,分别收集通过两种输液器后的药液,采用高效液相色谱法(HPLC)检测药液中DEHP或TOTM的溶出量。结果显示,在氯化钠注射液、单硝酸异山梨酯注射液中未检出DEHP,在紫杉醇注射液、乙醇水溶液中有检出。在氯化钠注射液、单硝酸异山梨酯注射液和紫杉醇注射液中未检出TOTM,在乙醇水溶液中有少量检出。说明在临床上输注药物,选择合适材质的一次性使用PVC输液器非常有必要。     

PVC输液器输注青霉素钠的相容性研究

通过模拟临床使用一次性输液器输注青霉素钠注射液,对一次性使用输液器中可沥滤物进行分析。研究中使用了两个不同厂家A、B两种型号的一次性使用输液器,通过高效液相色谱分析发现在输注青霉素钠时并未发生药物吸附,且对有关物质研究也证实没有迁移出新的物质。但通过气相色谱-质谱分析,流经A、B两种型号输液器的药液中均检出环己酮和DEHP,A型输液器中还检出了少量的异辛醇。这些可沥滤物主要是由输液器的生产过程中引入的,且其含量均远低于人体安全摄入量,因此,本研究表明临床治疗中使用一次性输液器输注青霉素钠存在较低风险     

一次性使用避光延长管中增塑剂DEHP向模拟药液迁移情况

因一次性使用避光延长管中聚乙烯粒料中加入了一定比例的邻苯二甲酸二辛酯（DEHP）,过量的DEHP进入人体可能会有一定的影响。本实验使用水和不同浓度乙醇溶液来模拟不同极性的药物通过一次性避光延长管,并模拟临床输液情况,从而动态制备相应的模拟溶液。根据增塑剂在不同溶剂中溶解度的大小,分别采取浓缩或稀释的手段将DEHP转移至甲醇溶液中,采用气相色谱法进行试验。以保留时间定性,以外标法定量。经一系列方法学验证,说明该方法准确可靠,且操作简单,大量减少有机溶剂的使用,安全、环保、有效。从模拟试验数据可见随着溶剂极性的降低,一次性使用避光延长管中DEHP向溶液的迁移量逐渐递增,因此在输液过程中,使用极性小的药物时应尽量避免使用此类物质。     

一种新型体外血浆脂类吸附过滤器的性能评价

目的对一种新型体外血浆脂类吸附过滤器JX—DELP进行性能评价。方法①通过体外静态吸附实验检验过滤器滤膜对血脂的吸附效果。②模拟过滤器产品结构组成，设计并加工了小型血浆过滤装置。使用该装置模拟临床应用条件，考察了血浆用量、过滤速度和时间对过滤吸附效果的影响；考察了循环过滤方式对高脂血症患者血浆的综合过滤吸附效果。③考察滤膜与全血直接接触条件下材料的血液相容性。结果过滤器的滤膜在体外对血脂的清除率分别为：总胆固醇（TC）16．7％，甘油三酯（TG）9．7％，低密度脂蛋白（LDL）13．5％。在体外循环实验中，在一定的血浆处理体积、过滤速度和时间内，对TC、TG和LDL的清除率分别为52．0％、50．1％和38．4％。血浆其他组分的浓度变化不显著。过滤器滤膜对全血各组分无显著破坏作用，溶血率仅为0．19％，具有良好的血液相容性。结论体外血浆脂类吸附过滤装置，JX—DELP，能快速有效地去除高脂血症患者血浆中含量过高的血脂，而不会对血液其他组分产生破坏作用，同时滤膜本身有很好的血液相容性。该装置可用于降低血脂和血黏度，临床治疗某些高血脂相关疾病。     

盐酸戊乙奎醚对原位肝移植后急性肺损伤的保护效应

背景：盐酸戊乙奎醚具有抗炎、细胞保护等作用,其对于肝移植后急性肺损伤的治疗效果尚不明确。 目的：验证盐酸戊乙奎醚对原位肝移植后急性肺损伤的保护效应。 方法：纳入原位肝移植后急性肺损伤患者35例,随机分为盐酸戊乙奎醚组和安慰剂对照组,双盲法连续3 d每隔24 h在常规综合治疗的基础上静脉给予盐酸戊乙奎醚0.05 mg/kg或等量生理盐水注射液。以酶联免疫吸附法观察两组治疗前,治疗后24,72 h血清白细胞介素8,10的质量浓度,根据动脉血气计算氧合指数,记录呼吸机的使用时间。 结果与结论：与对照组相比,盐酸戊乙奎醚组患者治疗后24 h和72 h的白细胞介素8质量浓度降低,白细胞介素10质量浓度升高,氧合指数升高,呼吸机使用时间缩短(P均 < 0.05)。提示盐酸戊乙奎醚能调控肝移植后急性肺损伤患者炎性因子的水平,改善动脉氧合,缩短呼吸机的使用时间。     

胰岛素在多腔袋肠外营养液中的稳定性研究

目的探讨胰岛素在多腔袋肠外营养液中的稳定性。 方法2018年1月至3月于北京医院国家老年医学中心进行胰岛素体外对照实验研究，分为3组：多腔袋组、院内配置组、葡萄糖组。多腔袋组使用工业化多腔袋肠外营养制剂[脂肪乳氨基酸(17)葡萄糖(10%)注射液，每袋均含葡萄糖97 g，大豆油长链甘油三酯51 g，氨基酸34 g，液体总量1 440 mL，乙烯-醋酸乙烯共聚物(EVA)袋]；院内配置组为自配型肠外营养液(总量1 500 mL，含20%长链脂肪乳剂250 mL，8.6%复方18种氨基酸500 mL，50%葡萄糖溶液250 mL，0.9%氯化钠溶液500 mL等，EVA袋)；葡萄糖组为10%葡萄糖注射液1 000 mL，使用苯乙烯、乙烯、丁烯共聚物(SEB)袋，加入15%氯化钾1.5 g；每组各10袋。分别加入精蛋白生物合成人胰岛素10、20、30、40、50 IU，混匀后静置30 min，模拟临床应用模式体外匀速输注12 h，分别测定混匀后即刻，输注前，输注2、4、6、8、10、12 h肠外营养液中胰岛素浓度；计算加入胰岛素10、50 IU 3组不同时相点胰岛素浓度变化值与变化幅度。 结果标准操作规范下，添加胰岛素剂量10 IU，多腔袋组混匀后即刻，输注前，输注2、4、6、8、10、12 h肠外营混合液中胰岛素浓度分别为1 375、1 355、1 290、1 215、1 260、1 270、1 310、1 275 μU/mL；添加胰岛素量50 IU，多腔袋组混匀后即刻，输注前，输注2、4、6、8、10、12 h肠外营养混合液中胰岛素浓度分别为4 710、4 675、4 915、4 525、4 805、4 575、4 805、4 570 μU/mL。加入胰岛素10 IU，多腔袋组输注前，输注2、4、6、8、10、12 h对应的胰岛素浓度变化值分别为－20、－85、－160、－115、－65、－100 μU/mL；加入胰岛素50 IU，多腔袋组输注前，输注2、4、6、8、10、12 h对应的胰岛素浓度变化值分别为－35、205、－185、95、－135、95、－140 μU/mL。加入胰岛素10 IU，多腔袋组输注前，输注2、4、6、8、10、12 h对应的的胰岛素浓度变化幅度分别为1.5%、6.2%、11.6%、8.4%、7.6%、4.7%、7.3%；加入胰岛素50 IU，多腔袋组输注前，输注2、4、6、8、10、12 h对应的胰岛素浓度变化幅度分别为0.7%、4.4%、3.9%、2.0%、2.9%、2.0%、3.0%。多腔袋组不同时相点胰岛素浓度较为稳定，不受胰岛素加入剂量和使用时间的影响；院内配置组胰岛素浓度变化趋势与多腔袋组相似；葡萄糖组胰岛素浓度稳定性尚好，但相对浓度低于前2者水平。 结论胰岛素在多腔袋肠外营养制剂中稳定性较好，不受浓度和时间影响。     

黄芪诱导骨髓间充质干细胞向神经干细胞分化

目的:观察黄芪注射液诱导大鼠骨髓间充质于细胞(BMSCs)分化的特点以及黄芪对BMSCs活性的影响。方法:分别使用浓度为20、50、100、200μl/ml的黄芪注射液诱导BMSCs,分别在1、5、24 h光镜观察细胞形态变化,免疫细胞化学方法观察巢蛋白、神经元特异性烯醇化酶(NSE)、胶质纤维酸性蛋白(GFAP)、微管相关蛋白2(MAP-2)的表达,MTT方法检测黄芪对BMSCs活性的影响。结果:诱导后细胞体积增大,胞核固缩,核质比减小,有细长突起形成,部分细胞间可见网络状连接。巢蛋白阳性细胞在100μl/ml浓度诱导24 h组染色最强,而NSE和GFAP阳性细胞在200μl/ml浓度诱导24 h组阳性细胞数量最多,染色最强,MAP-2抗体染色只在100μl/ml浓度诱导24 h组和200μl/ml浓度诱导24 h组出现少量阳性细胞。不同浓度的黄芪注射液以及作用不同时间均对BMSCs的活性产生影响。结论:在黄芪作用下,BMSCs表达神经干细胞特异标志物,随着时间的延长,进一步表达神经元特异标志物和胶质细胞特异标志物。     

温敏性壳聚糖水凝胶对大鼠成骨细胞的毒性

背景：温敏性壳聚糖与多种细胞相容性良好,是组织工程中不可多得的优良载体,但其对成骨细胞毒性研究相对缺乏。 目的：验证温敏性壳聚糖水凝胶对成骨细胞的毒性。 方法：成骨细胞在温敏性壳聚糖水凝胶中进行培养,显微镜下观察细胞形态及扩增情况,同时,SD大鼠成骨细胞在不同浓度的温敏性壳聚糖水凝胶浸提液中体外培养24,48,72,96 h,MTT法测定细胞相对增殖率,判断细胞毒性的级别。 结果与结论：SD大鼠成骨细胞在温敏性壳聚糖水凝胶中培养24 h内镜下观察呈圆形,48 h后开始伸出触角并扩增;温敏性壳聚糖水凝胶浸提液中培养的各组细胞在不同时间点相对增殖率在92%~112%之间,各浓度的温敏性壳聚糖水凝胶材料浸提液的细胞毒性均为0级或1级,完全符合生物材料的安全评价标准。     

MDA-MB-231乳腺癌细胞两种低氧模型的建立与比较分析

目的:由于实体瘤内的肿瘤细胞常处于低氧环境,本实验拟探究两种常用低氧模型对乳腺癌细胞影响的差异。方法:以不同浓度(0~300μmol/L)CoCl2处理人乳腺癌MDA-MB-231细胞不同时间(24 h、48 h和72 h)建立化学低氧模型,以不同程度低氧(1%、2%和5%O2)处理MDA-MB-231细胞不同时间(4 h、16 h和24 h)建立物理低氧模型。采用CCK-8法检测细胞活力,Western blot检测低氧诱导因子1α(HIF-1α)、Bcl-2及基质金属蛋白酶2(MMP-2)的蛋白表达;流式细胞术检测细胞凋亡;Transwell和划痕实验检测细胞的侵袭及迁移能力。结果:综合不同时间和浓度的HIF-1α蛋白表达结果,最终以100μmol/L CoCl2处理24 h建立化学低氧模型,以2%O 2处理24 h建立物理低氧模型;物理低氧细胞的HIF-1α蛋白表达明显高于化学低氧,且物理低氧细胞处于复氧环境后HIF-1α蛋白快速降解;物理低氧细胞凋亡增加,抗凋亡蛋白Bcl-2表达降低,而化学低氧细胞无明显变化;两种低氧细胞的MMP-2蛋白表达均升高,且化学低氧细胞的侵袭及迁移能力增强。结论:两种低氧细胞模型构建成功,并且两种低氧细胞在HIF-1α蛋白表达与稳定性、细胞活力、凋亡、侵袭及迁移等方面均存在差异。这些差异可为低氧模型的选择和研究低氧环境下的肿瘤细胞特性提供参考。     

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.