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目的:报告1例罕见异位中肾管囊肿合并异位睾丸恶变病例,提高对本病的诊治水平。方法:回顾分析异位中肾管囊肿合并异位睾丸恶变的病例的临床资料,结合国内外相关文献,探讨异位中肾管囊肿合并异位睾丸恶变的发病机制、诊断及治疗。结果:经腹切除巨大囊肿及右侧异位恶变睾丸,左侧隐睾行下降固定,病理示"右异位中肾管囊肿,右侧异位睾丸精原细胞瘤",随访1年无转移。结论:异位中肾管囊肿合并异位睾丸恶变极为罕见,影像学检查可协助诊断,但最终需病理确诊,应早期行手术切除。后续治疗取决于隐睾恶变的病理类型及分期。 相似文献
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Multiparametric whole‐body anatomic,functional, and metabolic imaging characteristics of peripheral lesions in patients with schwannomatosis
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Integration of vascular biology and magnetic resonance imaging in the understanding of atherothrombosis and acute coronary syndromes 总被引:2,自引:0,他引:2
V. Fuster R. Corti † Z. A. Fayad J. Schwitter† J. J. Badimon 《Journal of thrombosis and haemostasis》2003,1(7):1410-1421
Summary. The interaction between the vulnerable atherosclerotic plaque prone to disruption and thrombus formation is the cornerstone of acute coronary syndrome (ACS). Although distinct from one another, the atherosclerotic and thrombotic processes appear to be interdependent, hence the term atherothrombosis. Inflammation is a crucial common pathophysiological mechanism. Overall, the association of plaque vulnerability and ACS has been well documented. Given the multifactorial origin of atherothrombosis the best preventive approach should be aggressive management of all the risk factors. New interventions should be directed toward decreasing vulnerability of the lesions thereby decreasing the risk of ACS. 相似文献
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Jordi Ochando Zahi A. Fayad Joren C. Madsen Mihai G. Netea Willem J. M. Mulder 《American journal of transplantation》2020,20(1):10-18
Consistent induction of donor‐specific unresponsiveness in the absence of continuous immunosuppressive therapy and toxic effects remains a difficult task in clinical organ transplantation. Transplant immunologists have developed numerous experimental treatments that target antigen‐presentation (signal 1), costimulation (signal 2), and cytokine production (signal 3) to establish transplantation tolerance. While promising results have been obtained using therapeutic approaches that predominantly target the adaptive immune response, the long‐term graft survival rates remain suboptimal. This suggests the existence of unrecognized allograft rejection mechanisms that contribute to organ failure. We postulate that trained immunity stimulatory pathways are critical to the immune response that mediates graft loss. Trained immunity is a recently discovered functional program of the innate immune system, which is characterized by nonpermanent epigenetic and metabolic reprogramming of macrophages. Since trained macrophages upregulate costimulatory molecules (signal 2) and produce pro‐inflammatory cytokines (signal 3), they contribute to potent graft reactive immune responses and organ transplant rejection. In this review, we summarize the detrimental effects of trained immunity in the context of organ transplantation and describe pathways that induce macrophage training associated with graft rejection. 相似文献
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Naghavi M Libby P Falk E Casscells SW Litovsky S Rumberger J Badimon JJ Stefanadis C Moreno P Pasterkamp G Fayad Z Stone PH Waxman S Raggi P Madjid M Zarrabi A Burke A Yuan C Fitzgerald PJ Siscovick DS de Korte CL Aikawa M Airaksinen KE Assmann G Becker CR Chesebro JH Farb A Galis ZS Jackson C Jang IK Koenig W Lodder RA March K Demirovic J Navab M Priori SG Rekhter MD Bahr R Grundy SM Mehran R Colombo A Boerwinkle E Ballantyne C Insull W Schwartz RS Vogel R Serruys PW Hansson GK Faxon DP Kaul S 《Circulation》2003,108(15):1772-1778
Atherosclerotic cardiovascular disease results in >19 million deaths annually, and coronary heart disease accounts for the majority of this toll. Despite major advances in treatment of coronary heart disease patients, a large number of victims of the disease who are apparently healthy die suddenly without prior symptoms. Available screening and diagnostic methods are insufficient to identify the victims before the event occurs. The recognition of the role of the vulnerable plaque has opened new avenues of opportunity in the field of cardiovascular medicine. This consensus document concludes the following. (1) Rupture-prone plaques are not the only vulnerable plaques. All types of atherosclerotic plaques with high likelihood of thrombotic complications and rapid progression should be considered as vulnerable plaques. We propose a classification for clinical as well as pathological evaluation of vulnerable plaques. (2) Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis) and vulnerable myocardium (prone to fatal arrhythmia) play an important role in the outcome. Therefore, the term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future. (3) A quantitative method for cumulative risk assessment of vulnerable patients needs to be developed that may include variables based on plaque, blood, and myocardial vulnerability. In Part I of this consensus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable patients. Part II of this consensus document will focus on vulnerable blood and vulnerable myocardium and provide an outline of overall risk assessment of vulnerable patients. Parts I and II are meant to provide a general consensus and overviews the new field of vulnerable patient. Recently developed assays (eg, C-reactive protein), imaging techniques (eg, CT and MRI), noninvasive electrophysiological tests (for vulnerable myocardium), and emerging catheters (to localize and characterize vulnerable plaque) in combination with future genomic and proteomic techniques will guide us in the search for vulnerable patients. It will also lead to the development and deployment of new therapies and ultimately to reduce the incidence of acute coronary syndromes and sudden cardiac death. We encourage healthcare policy makers to promote translational research for screening and treatment of vulnerable patients. 相似文献