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Chest. 2005 Oct;128(4):2794-803.Effect of moderate-intensity exercise, whole-body periodic acceleration, and passive cycling on nitric oxide release into circulation.Sackner MA, Gummels E, Adams JA.Division of Pulmonary Disease and Critical Medicine, Mount Sinai Medical Center, Miami Beach, FL, USA. [email protected] OBJECTIVE: To determine if a 3-min bout of moderately intensive supine bicycle exercise, whole-body periodic acceleration (pGz), and passive motorized cycling cause nitric oxide (NO) release into the circulation, as detected by dicrotic notch descent on the diastolic limb of a finger pulse wave. PARTICIPANTS: Fourteen healthy adults underwent two levels of supine bicycle ergometry that caused heart rate to rise to 56% (light moderate exercise) and 67% (heavy moderate exercise) of maximum predicted heart rate, and a single bout of pGz. Several months later, 9 of the 14 subjects underwent passive motorized cycling. METHODS: The ECG and finger pulse wave were recorded. The dicrotic notch position was computed from the amplitude of the digital pulse wave ( a) divided by the height of the dicrotic notch above the end-diastolic level ( b) and designated the a/b ratio. Increase of the a/b ratio due to dicrotic notch descent reflects the vasodilator action of NO on resistance vessels. The last 30 s of baseline, exercise or pGz, and recovery periods were analyzed. RESULTS: Compared to baseline, light moderate exercise produced a nonsignificant rise of the a/b ratio. Both heavy moderate exercise and pGz produced statistically significant rises of peak and mean a/b ratios over baseline. Heavy moderate exercise produced a greater mean a/b ratio than pGz, but the peak a/b ratio did not differ between the two. Episodic rises and falls of a/b ratios were more common during pGz than exercise. Passive motorized cycling did not alter the a/b ratio. CONCLUSIONS: Dicrotic notch descent occurs during a brief bout of moderate cycling exercise, consistent with NO release into circulation. pGz produces comparable descent, but passive motorized cycling does not. In terms of the beneficial effects of NO, this suggests that pGz might serve as a substitute in subjects who are physically incapable of exercising.PMID: 16236957－－－－－－－－－－－－－－－－－－－－－－－－－－－－－－－－－闲来无事，将这份摘要大概译了一下，大家可以和楼下 乔80119 战友译的接合起来看。研究目的：研究时间为 3min 的中等强度蹬车运动引起NO释放后进入循环系统的影响。三种形式 a. 仰卧蹬车 b.全身周期性加速 c. 被动的牵引 。判断则是据手指脉搏波（finger pulse wave 翻译见 > 3. Acta Physiologica is part of the OnlineEarly service (Article-by-article publishing online, ahead of print issues, with articles in final edited form and citable by their unique DOI number) 4. Average time from submission to decision is just 35 days 5. Acta Physiologica has a rising impact factor of 2.086 6. You can submit your paper online at mc.manuscriptcentral.com/aph 大家自己看吧，不多说了。1889 年创刊的一本科研journal（periodical？）历史如果peking university 一样的久远。在新的一年要更名了，预示着什么呢，北欧人的作风是很严谨的。且其刊物影响因子不算低（在本专业内，其口碑一直不错的），拭目以待吧…… 0000.pdf (24.47k)第三篇尝试翻译完毕，因为自觉无法完成第二篇，所以跳过了，yangt兄和乔战友翻译的都不错，但是乔战友的术语方面应重视．第四篇尚未细看，如有可能，继续领养！杂志，年，卷，期，页码：Acta Physiol Scand. 2005 Oct;185(2):123-31标题:Exhaled nitric oxide during normoxic and hypoxic exercise in endurance athletes.作者及联系方式:Verges S, Flore P, Favre-Juvin A, Levy P, Wuyam B.Laboratoire HP2, Faculte de Medecine, Universite Joseph Fourier, 38700 La Tronche, France.摘要:Aim: Endogenous nitric oxide (NO) through its relaxing effect on smooth muscle cells may be involved in pulmonary gas exchange as well as in the modulation of the hypoxic pulmonary vasoconstriction. As athletes with exercise-induced hypoxaemia (EIH) present pulmonary gas exchange abnormalities in normoxia that could be even greater in hypoxia, we hypothesized that pulmonary NO may be lower in such athletes with EIH. METHODS: Eleven athletes with EIH [decrease in arterial oxygen blood partial pressure (PaO2) > 12 mmHg] and 9 without EIH (NEIH) exercised at 40%, 60% (10 min) and 90% (5 min) of normoxic maximal power output (Pmax) in normoxia, and at 40% and 60% (10 min) of Pmax in hypoxia (FiO2 = 15%). Exhaled NO concentration during a constant flow exhalation (FENO(0.170)) and arterialized blood gases were measured at every power output. RESULTS: FENO(0.170) decreased from rest to exercise both in normoxia (-27.8 +/- 22.8% at 90% Pmax, P < 0.001) and hypoxia (-23.8 +/- 17.5% at 60% Pmax, P < 0.001). At 90% Pmax in normoxia, EIH athletes showed lower PaO2 (76.7 +/- 5.4 vs. 82.8 +/- 4.4 mmHg, P = 0.013) and greater FENO(0.170) decrement (-37.0 +/- 24.7% vs. -16.6 +/- 14.6%, P = 0.042) than NEIH athletes. During hypoxic exercise, P(a )O(2) and FENO(0.170) decreases were similar in both groups (P > 0.05). CONCLUSION: The present study shows lower pulmonary NO in athletes with gas exchange abnormalities during intense exercise in normoxia, while EIH and NEIH athletes have similar decreases in blood gases and pulmonary NO during hypoxic exercise. Decreased pulmonary NO in such conditions may contribute to ventilation-perfusion inequality and/or increase pulmonary vascular tone in athletes.PMID: 16168006 －－－－－－－－－－－－－－－－－－－－－－－－－－－－－－－Title:耐力性运动员常氧及缺氧运动中呼出气一氧化氮（eNO）的研究Abstract:目的：内源性一氧化氮可能通过其舒张平滑肌细胞作用介入肺气交换及缺氧性肺血管收缩反应（HPV）的调节。患运动性低氧血症（EIH）的运动员在常氧情况下表现出肺气交换反常，在缺氧情况下则更是明显，我们猜测这些患EIH的运动员肺一氧化氮水平相对较低。方法：患EIH运动员11例[动脉血氧分压（PaO2 ）下降超过12毫米汞柱]及无EIH（NEIH）运动员9例在常氧状态下进行40%、60%（运动时间均为10分钟）、90%（运动时间5分钟）最大输出功率（Pmax）强度运动，在缺氧情况下则以40%、60%（运动时间均为10分钟）Pmax强度进行运动（吸氧浓度为15%）。持续气流呼吸中的呼出气一氧化氮（FENO）浓度（FENO0.170）及动脉化血液中的气体量在各功率输出强度均有测量。结果：常氧情况下从静息到运动，FENO(0.170)下降（以90% Pmax强度运动时变化为-27.8 +/- 22.8%, P < 0.001）缺氧情况下以60% Pmax强度运动时下降幅度则为-23.8 +/- 17.5%（P < 0.001）。常氧状态下以90% Pmax运动时，患EIH运动员与NEIH运动员相比氧气分压较低（76.7 +/- 5.4 vs. 82.8 +/- 4.4 毫米汞柱, P = 0.013）而FENO(0.170)消耗则更大（-37.0 +/- 24.7% vs. -16.6 +/- 14.6%, P = 0.042）。缺氧运动时，各组间氧分压及FENO(0.170)减少情况相似（P > 0.05，无统计学意义）。结论：此研究显示，常氧状态下从事剧烈运动时，存在气体交换反常的运动员肺一氧化氮水平较低，而进行缺氧运动时患EIH运动员和NEIH运动员血气及肺一氧化氮减少情况相似。上述情况下一氧化氮的减少可能导致运动员肺泡通气/血流比值不均和（或）血管紧张度增加。_____________________________________________________________________哈哈!今天版块好是冷清!我来跟进第四篇吧!杂志，年，卷，期:Med Hypotheses. 2006 Jan 9标题:Reduced tolerance of exercise in fibromyalgia may be a consequence of impaired microcirculation initiated by deficient action of nitric oxide.作者及联系方式:Kasikcioglu E, Dinler M, Berker E.Department of Sports Medicine, Istanbul University, Istanbul Faculty of Medicine, Istanbul, Turkey.摘要:Although the underlying mechanism responsible for muscular fatigue and exercise intolerance remains to be elucidated, it is reported two major mechanisms, central and peripheral hypothesis. As a peripheral mechanism, there are few reports on abnormalities of the microcirculation in patients with fibromyalgia. The key point to note is that ischemia associated with a modest decline in tissue oxygen causes muscle fatigue. It has been shown that have been found low muscle levels of phosphates and abnormalities in microcirculation in fibromyalgia. Based on several novel data, production abnormalities of nitric oxide level might lead to symptoms of fatigue as a long term effect. There a vicious cycle concerning impairment of microcirculation in FM. The cycle is firstly initiated decrease of production of nitric oxide in the endothelial level by some trigger factors. Changed level of nitric oxide may cause microcirculation abnormalities in the tissue levels, muscular region. At the end of these phases, muscular fatigue and exercise intolerance may progressively develop in the FM. It is possible that this theory appears to provide a physiopathological explanation for decreased exercise capacity in patients with fibromyalgia. This paper describes a plausible mechanism for the development of exercise intolerance on microcirculation abnormalities.PMID: 16412581 －－－－－－－－－－－－－－－－－－－－－－－－－－－－－－－Title:纤维肌痛患者运动耐力下降可能是由一氧化氮不足引发的微循环损伤所致Abstract:尽管造成肌肉疲劳和运动不耐受的潜在机制仍有待阐明，但有两种主要机制已见报道，即中枢和外周假说。对于外周机制，已有少数研究报道了纤维肌痛患者微循环异常，其中关键的一点就是缺血与组织氧水平的适度下降共同引起肌肉疲劳。已有研究显示，纤维肌痛患者具有低肌肉磷酸盐水平以及微循环异常。一些新数据表明，一氧化氮水平的生成异常可能作为一种长期影响导致疲劳症状的发生。纤维肌痛患者存在一个与微循环损伤有关的恶性循环，这个循环首先通过一些触发因素引起内皮水平一氧化氮的生成减少，而一氧化氮水平的改变则可能导致各组织水平和肌肉区的微循环异常。最后，便是纤维肌痛患者肌肉疲劳和运动不耐受的逐渐发展。这一学说可能为纤维肌痛患者的运动能力下降作出了一个病理生理学诠释。本文则为微循环异常相关的运动不耐受提供了一个比较可能理解的机制。J Physiol. 2005 Sep 15;567(Pt 3):815-28. Epub 2005 Jul 1. Nitric oxide synthase inhibition affects sarcoplasmic reticulum Ca2+ release in skeletal muscle fibres from mouse.Pouvreau S, Jacquemond V.Physiologie Integrative Cellulaire et Moleculaire, Universite Claude Bernard - Lyon 1, UMR CNRS 5123, Villeurbanne, France.Nitric oxide (NO) generated by skeletal muscle is believed to regulate force production but how this is achieved remains poorly understood. In the present work we tested the effects of NO synthase (NOs) inhibitors on membrane current and intracellular calcium in isolated skeletal muscle fibres from mouse, under voltage-clamp conditions. Resting [Ca(2+)] and [Ca(2+)] transients evoked by large depolarizations exhibited similar properties in control fibres and in fibres loaded with tenth millimolar levels of the NOs inhibitor N-nitro-L-arginine (L-NNA). Yet the voltage dependence of calcium release was found to be shifted by approximately 15 mV towards negative values in the presence of L-NNA. This effect could be reproduced by the other NOs inhibitor S-methyl-L-thiocitrulline (L-SMT). Separate experiments showed that the voltage dependence of charge movement and of the slow calcium current were unaffected by the presence of L-NNA, ruling out an effect on the voltage sensor. A negative shift in the voltage dependence of calcium release with no concurrent alteration in the properties of charge movement was also observed in fibres exposed to the oxidant H(2)O(2) (1 mM). Conversely the reducing agent dithiothreitol (10 mM) had no obvious effect on Ca(2+) release. Overall, the results indicate that physiological levels of NO exert a tonic inhibitory control on the activation of the calcium release channels. Changes in the voltage dependence of Ca(2+) release activation may be a ubiquitous physiological consequence of redox-related modifications of the ryanodine receptor.PMID: 15994183＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝＝本摘要（文）已由 summer027 兄搞定！！>Investigational medicinal products should be produced in accordance with the principles and the detailed guidelines of Good Manufacturing Practice for Medicinal Products (The Rules Governing Medicinal Products in The European Community, Volume IV). Other guidelines published by the European Commission should be taken into account where relevant and as appropriate to the stage of development of the product. Procedures need to be flexible to provide for changes as knowledge of the process increases, and appropriate to the stage of development of the product.In clinical trials there may be added risk to participating subjects compared to patients treated with marketed products. The application of GMP to the manufacture of investigational medicinal products is intended to ensure that trial subjects are not placed at risk, and that the results of clinical trials are unaffected by inadequate safety, quality or efficacy arising from unsatisfactory manufacture. Equally, it is intended to ensure that there is consistency between batches of the same investigational medicinal product used in the same or different clinical trials, and that changes during the development of an investigational medicinalproduct are adequately documented and justified.The production of investigational medicinal products involves added complexity incomparison to marketed products by virtue of the lack of fixed routines, variety of clinical trial designs, consequent packaging designs, the need, often, for randomisation and blinding and increased risk of product cross-contamination and mix up. Furthermore, there may be incomplete knowledge of the potency and toxicity of the product and a lack of full process validation, or, marketed products may be used which have been re-packaged or modified insome way.These challenges require personnel with a thorough understanding of, and training in, theapplication of GMP to investigational medicinal products. Co-operation is required with trial sponsors who undertake the ultimate responsibility for all aspects of the clinical trial including the quality of investigational medicinal products.The increased complexity in manufacturing operations requires a highly effective qualitysystem.The annex also includes guidance on ordering, shipping, and returning clinical supplies,which are at the interface with, and complementary to, guidelines on Good Clinical Practice.研究性药物产品应该以GMP(管理药品的欧洲共同体的规则；4卷)为原则与指南。由欧洲委员会出版的其它药品生产指南应该在与产品发展的阶段有关的地方考虑进去。为了工序的改变与适合于产品发展的阶段，操作应灵活多变。在临床试验中，与服用以售药品的患者相比，受试者将会受到更多的危险。GMP的应用于研究性药物产品的生产目的是为了确保：临床受试者不会有危险，以及不会因受到由于不合理的生产所导致的安全性问题影响临床试验结果。同样地，它能保证用于同一或不同的临床试验的研究性药品间有一致性；以及能适当地证明研究性药物产品发展中的变化。以已售药品相比，研究性药物产品的生产包括不断增加地复杂性，因为固定程序的缺乏，临床试验和包装设计的多样性，随机抽样的需要以及产品交叉性污染的增加。而且，关于药品的效能与毒性仍有不完善的地方，全过程缺乏合法性，或者，经过重新包装的产品或者稍加改变的产品仍在使用。而完成这些挑战的人应该具备这样的素质：能彻底明白如何将GMP应用于研究性药物产品中。整个合作需要这样的试验领导：能担负包括研究性药品质量的临床试验各方面的责任。制造业操作的日益复杂性需要高效的质量体系。该附件同时也包括临床辅助材料的定购、运输和回复指南，而临床辅助材料是GCP指南的界面与补充yangt1193兄：您好，借此宝地锻炼一下自己的专业英语，可能与你专题不一样，望见量。 乔兄，欢迎之至！！！－－yangt1193如果专题差的太远，您可以新建一个您的翻译专题，你的帖子我会帮您挪到您的专题下事成，贵在恒。NOTEProducts other than the test product, placebo or comparator may be supplied tosubjects participating in a trial. Such products may be used as support or escapemedication for preventative, diagnostic or therapeutic reasons and/or needed toensure that adequate medical care is provided for the subject. They may also beused in accordance with the protocol to induce a physiological response. Theseproducts do not fall within the definition of investigational medicinal products and may be supplied by the sponsor, or the investigator. The sponsor should ensure that they are in accordance with the notification/request for authorisation to conduct the trial and that they are of appropriate quality for the purposes of the trial taking into account the source of the materials, whether or not they are the subject of a marketing authorisation and whether they have been repackaged. The advice and involvement of a Qualified Person is recommended in this task.GLOSSARYBlindingA procedure in which one or more parties to the trial are kept unaware of the treatmentassignment(s). Single-blinding usually refers to the subject(s) being unaware, and doubleblinding usually refers to the subject(s), investigator(s), monitor, and, in some cases, data analyst(s) being unaware of the treatment assignment(s). In relation to an investigational medicinal product, blinding shall mean the deliberate disguising of the identity of the product in accordance with the instructions of the sponsor. Unblinding shall mean the disclosure of the identity of blinded products.Clinical trialAny investigation in human subjects intended to discover or verify the clinical,pharmacological and/or other pharmacodynamic effects of an investigational product(s)and/or to identify any adverse reactions to an investigational product(s), and/or to studyabsorption, distribution, metabolism, and excretion of one or more investigational medicinal product(s) with the object of ascertaining its/their safety and/or efficacy.Comparator productAn investigational or marketed product (i.e. active control), or placebo, used as a reference in a clinical trial.Investigational medicinal productA pharmaceutical form of an active substance or placebo being tested or used as a reference in a clinical trial, including a product with a marketing authorisation when used or assembled (formulated or packaged) in a way different from the authorised form, or when used for an unauthorised indication, or when used to gain further information about the authorised form.Immediate packagingThe container or other form of packaging immediately in contact with the medicinal or investigational medicinal product.InvestigatorA person responsible for the conduct of the clinical trial at a trial site. If a trial is conducted by a team of individuals at a trial site, the investigator is the responsible leader of the team and may be called the principal investigator.Manufacturer/importer of Investigational Medicinal ProductsAny holder of the authorisation to manufacture/import referred to in Article 13.1 ofDirective 2001/20/EC.OrderInstruction to process, package and/or ship a certain number of units of investigationalmedicinal product(s).Outer packagingThe packaging into which the immediate container is placed.希望有兴趣的同志们多多参与，共同学习学习。您在发贴子的时候请务必贴出相关来源，以便我据您翻译材料的权威性评分。也更有利于其他战友的相互学习。－－您的朋友：yangtDiabetes. 2003 Sep;52(9):2205-12. Effect of exercise intensity on skeletal muscle AMPK signaling in humans.Chen ZP, Stephens TJ, Murthy S, Canny BJ, Hargreaves M, Witters LA, Kemp BE, McConell GK.St. Vincent's Institute of Medical Research, University of Melbourne, Fitzroy, Victoria, Australia.The effect of exercise intensity on skeletal muscle AMP-activated protein kinase (AMPK) signaling and substrate metabolism was examined in eight men cycling for 20 min at each of three sequential intensities: low (40 +/- 2% VO(2) peak), medium (59 +/- 1% VO(2) peak), and high (79 +/- 1% VO(2) peak). Muscle free AMP/ATP ratio only increased at the two higher exercise intensities (P < 0.05). AMPK alpha 1 (1.5-fold) and AMPK alpha 2 (5-fold) activities increased from low to medium intensity, with AMPK alpha 2 activity increasing further from medium to high intensity. The upstream AMPK kinase activity was substantial at rest and only increased 50% with exercise, indicating that, initially, signaling through AMPK did not require AMPK kinase posttranslational modification. Acetyl-CoA carboxylase (ACC)-beta phosphorylation was sensitive to exercise, increasing threefold from rest to low intensity, whereas neuronal NO synthase (nNOS) micro phosphorylation was only observed at the higher exercise intensities. Glucose disappearance (tracer) did not increase from rest to low intensity, but increased sequentially from low to medium to high intensity. Calculated fat oxidation increased from rest to low intensity in parallel with ACC beta phosphorylation, then declined during high intensity. These results indicate that ACC beta phosphorylation is especially sensitive to exercise and tightly coupled to AMPK signaling and that AMPK activation does not depend on AMPK kinase activation during exercise.PMID: 12941758Exerc Immunol Rev. 2005;11:53-63Fiber type specific expression of TNF-alpha, IL-6 and IL-18 in human skeletal musclesPlomgaard P, Penkowa M, Pedersen BK.Centre of Inflammation and Metabolism at The Department of Infectious Diseases and The Copenhagen Muscle Research Centre, Rigshospitalet, The Faculty of Health Sciences, University of Copenhagen, Denmark. [email protected] muscle is now recognized as an endocrine organ with the capacity to produce signal peptides in response to muscle contractions. Here we demonstrate that resting healthy human muscles express cytokines in a fiber type specific manner. Human muscle biopsies from seven healthy young males were obtained from m. triceps, m. quadriceps vastus lateralis and m. soleus. Type I fibers contributed (mean +/- SE) 24.0 +/- 2.5% in triceps of total fibers, 51.3 +/- 2.4% in vastus and 84.9 +/- 22% in soleus. As expected, differences in the fiber type composition were accompanied by marked differences between the three muscles with regard to MHC I and MHC IIa mRNA expression. Immunohistochemistry demonstrated that tumor necrosis factor (TNF)-alpha and interleukin (IL)-18 were solely expressed by type II fibers, whereas the expression of IL-6 was more prominent in type I compared to type II fibers. The fiber type specificity was found in triceps, vastus and soleus indicating that the level of daily muscle activity did not influence basal cytokine expression. The specificity of cytokine expression in different muscle fiber types in healthy young males suggests that cytokines may play specific regulatory roles in normal physiology.PMID: 16385844 [PubMed - in process] --------------------------------------------------------------------------------Exerc Immunol Rev. 2004;10:107-28.The missing links in exercise effects on mucosal immunity.Gleeson M, Pyne DB, Callister R.School of Biomedical Sciences, Faculty of Health, University of Newcastle, Callaghan NSW 2308, Australia. [email protected] review highlights research limitations within the existing exercise immunology literature and summarises unanswered questions to assist researchers and clinicians interested in exploring relationships between exercise, training and mucosal immunity. The primary limitations of the existing literature include: inadequate descriptions of training stimuli, age, gender and physical activity of subjects; failing to account for the influence of these factors and the underlying fitness and health status of subjects; methodological differences in assessments of mucosal immunity; limited understanding of the sources of biological variability in mucosal immunity; limited clinical and laboratory diagnosis of respiratory illness; and neglect of psychological, environmental, nutritional and pharmacological influences. Despite a considerable volume of research on mucosal immunity the unanswered research questions include: whether athletes are really more prone to illness; whether illness impacts on athletic performance; identifying subject or training characteristics that influence the mucosal immune responses to exercise; defining how exercise influences the acute mucosal immune response; assessing whether moderate exercise can enhance mucosal immune status; defining more clearly the treatment and management strategies for the athlete suffering recurrent illness, overtraining or long-term fatigue; and the effectiveness of dietary and therapeutic interventions. Answers to these questions should define future research strategies and assist clinicians seeking guidance on the assessment, treatment and management of athletes suffering from respiratory illness, particularly those with recurrent illness, long-term post-viral fatigue or suspected of being overtrained.PMID: 15633590Exerc Immunol Rev. 2004;10:56-65.Chronic heart failure and proinflammatory cytokines: possible role of physical exercise.Fuchs M, Drexler H.Medical University of Hannover, Germany.PMID: 15633586 可惜啊可惜，缺了任何一篇（哪怕是摘要），心里都欠着。暂且记下吧～～Exerc Immunol Rev. 2004;10:6-41.Reversing age-associated immunosenescence via exercise.Kohut ML, Senchina DS.HHP/Immunobiology, Iowa State University, Ames, 50011, USA. [email protected] in immune responsiveness with age are thought to contribute to the increased incidence and severity of infectious disease among the elderly. Several interventions, including exercise, have been proposed to restore immune function in older populations. The findings from some, but not all studies, support the possibility that exercise may attenuate immunosenescence. In recent years, the role of exercise in modulating immune response has been examined using models that may have clinical relevance, such as the response to vaccines and novel antigens. Taken together, the accumulated data suggest that exercise may be an efficacious therapy for restoring immune function in the elderly. In general, long term exercise interventions appear to show the most promise. Exercise related improvements have been reported with respect to antibody titre, T cell function, macrophage response, alterations of the T(H)1/T(H)2 cytokine balance, the level of pro-inflammatory cytokines, and changes in naive/memory cell ratio. However, current data is minimal, and many questions remain including: the mechanisms that are involved, the potential clinical impact, the appropriate type or dose of exercise, and whether the benefits extend to all populations including frail, older adults. This review summarizes the major findings of these studies and proposes directions for future exploration.PMID: 15633584