The bipartite tarsal navicular bone: Radiographic and computed tomography findings

Two cases of bipartite tarsal navicular bone are presented. The radiographic and computed tomography (CT) findings of this anatomical variant are described. Correct recognition of this entity is important, both because it may be the cause of symptoms perse, and because it may be misdiagnosed as a fracture. When plain films are not diagnostic, CT scanning is helpful in distinguishing between a fracture and this variant.     

Rupture of the posterior tibial tendon: CT and surgical findings

Computed tomography (CT) was performed in 42 patients with 49 clinically suspected tears of the posterior tibial tendon. Twenty-eight of the 49 suspected tears were subsequently surgically explored and repaired. Three patterns of tendon abnormalities were recognized on CT scans: type I-intact, hypertrophied, heterogeneous tendon; type II-attenuated tendon; and type III-absence of a portion of a tendon. Types I and II correlated with partial rupture seen during surgery, and type III correlated with complete rupture of the tendon. CT findings were accurate in 96% of the patients who underwent surgery. In four cases (14%), tendon rupture was seen on CT scans, but the extent of the injury was underestimated and the rupture was misclassified. Reactive periostitis of the distal tibia was seen in 71% of diseased tendons and may represent an important factor in the diagnosis of tendon rupture.     

拉米夫定抗乙型肝炎病毒治疗中耐药突变的后续治疗

拉米夫定(lamivudine)抗乙型肝炎病毒治疗中耐药突变发生率高,文献报道在拉米夫定治疗1,2,3,4,5a时分别为14%,38%,49%,66%,69%.耐药突变可导致血清HBVDNA水平阳转或明显上升,肝功能严重受损,甚至病情恶化死亡.关于拉米夫定抗乙型肝炎病毒治疗中耐药突变的后续治疗目前国内外尚无统一用药方案,单药治疗(如:继续使用拉米夫定、阿德福韦、恩替卡韦)在临床使用中已经取得了一定疗效,联合抗病毒治疗和中医药治疗是今后研究的方向.     

From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part II

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.     

Distribution of endogenous apoprotein B-containing lipoproteins in normal and injured aortas of normocholesterolemic rabbits.

The distribution of endogenous apolipoprotein B (apo B) was studied in both normal and balloon catheter-injured aortas of standard fed rabbits. Using light and electron microscopy, the distribution within entire aortic walls and individual tissue compartments was investigated by immunocytochemistry using an antibody raised against rabbit apo B. The concentration of apo B across the vessel wall dropped sharply from the luminal front towards the media of the normal aortas. The strong superficial reaction was mainly due to a heavy, yet specific, labelling of endothelial cells. Significant concentrations of apo B were also detected within the innermost regions of the extracellular space. The characteristics associated with the labelling of the intimal layer suggested an intense uptake and transcellular transport of apo B by endothelial cells. In contradistinction, normal smooth muscle cells did not appear to be labelled. In the previously injured aortas, the same features of strong superficial apo B labelling were present in the areas covered by regenerated endothelial cells, but not in those persistently deendothelialized. The smooth muscle cells of these regions appeared to show a low uptake of apo B. The increased concentrations of apo B in deeper interstitial areas of injured aortas, indicated the contribution of the extracellular matrix to apo B accumulation. This was especially prominent in the advanced lesions, selectively developed within neointima covered by regenerated endothelium. A rather uniform labelling pattern accompanying small lipid particle deposits, suggested a direct extracellular accumulation of circulating lipoproteins. Intensely labelled foam cells and irregularly distributed apo B within areas of cellular necrosis were detected as well. Injury-mediated responses of the cellular and extracellular aortic components can trigger the development of lipoprotein accumulations characteristic of atherosclerosis within aortas of normocholesterolemic animals.