Diagnostic and prognostic value of magnetic resonance imaging in the detection of tumor depth of invasion and bone invasion in patients with oral cavity cancer

La radiologia medica - To evaluate the accuracy of preoperative contrast-enhanced magnetic resonance imaging (MRI) in the assessment of radiological depth of invasion (rDOI) and bone invasion in...     

Microenvironment and tumor cell plasticity: An easy way out

Cancer cells undergo genetic changes allowing their adaptation to environmental changes, thereby obtaining an advantage during the long metastatic route, disseminated of several changes in the surrounding environment. In particular, plasticity in cell motility, mainly due to epigenetic regulation of cancer cells by environmental insults, engage adaptive strategies aimed essentially to survive in hostile milieu, thereby escaping adverse sites. This review is focused on tumor microenvironment as a collection of structural and cellular elements promoting plasticity and adaptive programs. We analyze the role of extracellular matrix stiffness, hypoxia, nutrient deprivation, acidity, as well as different cell populations of tumor microenvironment.     

Advanced glycation end products and vascular inflammation: implications for accelerated atherosclerosis in diabetes

The formation of advanced glycation end products (AGEs) is an important biochemical abnormality that accompanies diabetes mellitus and, likely, inflammation in general. Here we summarize and discuss recent studies indicating that the effects of AGEs on vessel wall homeostasis may account for the rapidly progressive atherosclerosis associated with diabetes mellitus. Driven by hyperglycemia and oxidant stress, AGEs form to a greatly accelerated degree in diabetes. Within the vessel wall, collagen-linked AGEs may "trap" plasma proteins, quench nitric oxide (NO) activity and interact with specific receptors to modulate a large number of cellular properties. On plasma low density lipoproteins (LDL), AGEs initiate oxidative reactions that promote the formation of oxidized LDL. Interaction of AGEs with endothelial cells as well as with other cells accumulating within the atherosclerotic plaque, such as mononuclear phagocytes and smooth muscle cells (SMCs), provides a mechanism to augment vascular dysfunction. Specifically, the interaction of AGEs with vessel wall components increases vascular permeability, the expression of procoagulant activity and the generation of reactive oxygen species (ROS), resulting in increased endothelial expression of endothelial leukocyte adhesion molecules. AGEs potently modulate initiating steps in atherogenesis involving blood-vessel wall interactions, triggering an inflammatory-proliferative process and, furthermore, critically contribute to propagation of inflammation and vascular perturbation in established disease. Thus, a better understanding of the biochemical mechanisms by which AGEs contribute to such processes in the vessel wall could be relevant to devise preventive and therapeutic strategies for diabetic atherosclerosis.     

Predictors of cognitive improvement after reality orientation in Alzheimer's disease

BACKGROUND: there is increasing evidence to support the efficacy of reality orientation in cognitive deficits in patients with Alzheimer's disease. The clinical characteristics of patients who respond to reality orientation are poorly understood; this knowledge could be important, given that the provision of reality orientation therapy is labour-intensive and may provoke emotional distress. AIM: to evaluate retrospectively which demographic and clinical characteristics of Alzheimer's patients predict cognitive outcomes. METHOD: we analysed 38 mild-to-moderately demented outpatients who regularly attended a one-month formal reality orientation programme. The mini mental state examination score changes from baseline-and immediately after-reality orientation were correlated with demographic and pre-treatment clinical characteristics by a linear regression analysis. RESULTS: short-term responsiveness to reality orientation was significantly predicted by a lower level of cognitive functioning (as measured by the mini mental state examination) at baseline and by the absence of euphoria, accounting together for 57.6% of variance. CONCLUSION: a lower mini mental state examination and the absence of euphoric behaviour in patients with mild-to-moderate Alzheimer's disease may predict a good cognitive outcome of reality orientation therapy.     

Segmental dyskinesia in Wolff-Parkinson-White syndrome: a possible cause of dilatative cardiomyopathy

Wolff-Parkinson-White (WPW) is a syndrome characterized by the presence of an accessory pathway that skipping A-V node may lead the electrical stimulus from the atrium directly to the ventricle. Some studies reported the finding of myocardial dyskinesia in the segments precociously activated by the accessory pathway, at echocardiogram and at nuclear cardiac study. Soria et al. reported, in 1985, an increased incidence of dilative cardiomyopathy in patients with WPW. The pathophysiological pathway that leads to ventricular dilation may be due to the increase of end-diastolic pressure secondary to a tachycardia-induced cardiomyopathy. Tachycardia-induced cardiomyopathy is usually secondary to frequent and prolonged tachycardia episodes. In this paper we report the cases of three patients affected by WPW who developed dilative cardiomyopathy during the follow-up. Particularly dyskinetic segments, working such as a functional aneurysm, could induce deep modifications of intraventricular haemodynamics, leading to remodelling and progressive ventricular dilation. This hypothesis could have important empirical consequences because it could imply the necessity of a precocious ablative therapy in this kind of patients.     

A novel silent beta-thalassemia mutation in the distal CACCC box affects the binding and responsiveness to EKLF

The silent beta-thalassemia mutation, beta(+)-101C-->T, is the only mutation currently described in the distal beta-globin CACCC box. We present a novel mutation, a C-->G transversion, in the same position. Expression analysis in heterozygous subjects demonstrated that the mutation determines a 20% reduction in the output of the beta-globin gene. DNA-protein interaction and transactivation analysis correlated the decrease in the beta-globin synthesis with the reduced binding and transactivation of EKLF to the mutant promoter. These data predict that the beta-101C-->G mutation will display a silent thalassemia phenotype similar to that of the beta-101C-->T mutation.