Abstract: Background: Fibromascular dysplasia of internal carotid arteries (ICA) leading to their pathological deformities is one of the causes of cerebral vascular insufficiency. The structural changes of the artery wall and their causes remain poorly understood. Materials and Methods: We investigated the expression of elastin, collagen types I and III, smooth muscle cells, gelatinases degrading elastin (matrix metalloproteinases 2 and 9 (MMP2 and MMP9) and tissue inhibitors of matrix metalloproteinases 1 and 2 (TIMP1 and TIMP2) on formalin-fixed surgical samples with the methods of immunohistochemistry and confocal laser scanning microscopy. Results: We revealed the fragmentation of elastic fibers (100% of patients) and some reduction of smooth muscle cells (p <0.05) in the tunica media of ICA. There were no changes in collagen types I and III and TIMP2 expression. The study of the ratio of the expression of MMPs and TIMPs revealed the statistically significant predominance of high MMP2 and -9 and low TIMP1 content in ICA with pathological deformities. With the use of confocal microscopy, we showed the decrease of elastin expression with a high MMP9 activity which correlated with low expression of TIMP-1 in the group of ICA with pathological deformities. While in the control group there was a high level of elastin expression and a low level of MMP9 expression that correlated with the low TIMP-1 amount (p >0.05). Conclusion: Our data demonstrate that the main feature of fibromuscular dysplasia underlying the pathological deformities of ICA –fragmentation of elastic fibers – is caused by the disturbance of balance between gelatinases and their inhibitors.Abstract: Background: Fibromascular dysplasia of internal carotid arteries (ICA) leading to their pathological deformities is one of the causes of cerebral vascular insufficiency. The structural changes of the artery wall and their causes remain poorly understood. Materials and Methods: We investigated the expression of elastin, collagen types I and III, smo...Show More
Abstract: Asthma-Chronic obstructive pulmonary disease overlap syndrome (ACOS) or ASCOS is a frequently encountered clinical syndrome. It is identified by the clinical features that it shares with asthma and COPD. There is no clear consensus definition yet for this medical syndrome. ACOS has not been extensively studied partly because of the absence of clarity of its clinical significance and because of the lack of a clear definition for this syndrome. ACOS is characterized by persistent airflow limitation with several features usually associated with asthma and several features usually associated with chronic obstructive pulmonary disease (COPD). It has been described and named differently by different authors. Some of the commonly encountered names are asthmatic bronchitis, asthma of the elderly, patients with COPD and a prominent asthmatic component, asthma that complicates COPD, asthma with permanent obstruction, COPD with a reversible component and asthma-COPD overlap syndrome. In most obstructive lung disease trials patients with overlap syndrome are excluded because they are not strictly asthmatic per the study inclusion criteria or they are not strictly chronic obstructive pulmonary disease patients. With no clear consensus on the definition and few studies on its genetics or pathophysiology, it is difficult to create management guidelines for this group of patients. Patients with ACOS have been found to have higher risk not only for exacerbations, but also for hospitalizations. Global Initiative for Chronic Obstructive Lung Disease (Gold) and the Global Initiative for Asthma (GINA) have suggested a stepwise diagnostic and management criteria for patients with ACOS.Abstract: Asthma-Chronic obstructive pulmonary disease overlap syndrome (ACOS) or ASCOS is a frequently encountered clinical syndrome. It is identified by the clinical features that it shares with asthma and COPD. There is no clear consensus definition yet for this medical syndrome. ACOS has not been extensively studied partly because of the absence of clari...Show More