Browsing by Author "Lackovic, Vesna (35754725400)"

[No abstract available]

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited adult-onset microangiopathy caused by missense mutations in the Notch3gene on chromosome 19. However, common vascular risk factors may additionally modify clinical expression and progression of the disease. The role of various prothrombotic factors has also been implied. We report a case of a middle-aged man with typical clinical, neuroimaging and histological features of CADASIL, but with notably prolonged activated partial thromboplastin time. Hematological investigations revealed severe clotting Factor XII deficiency. This case illustrates that the occurrence of vascular risk factors should not be overlooked in patients with CADASIL.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited adult-onset microangiopathy caused by missense mutations in the Notch3gene on chromosome 19. However, common vascular risk factors may additionally modify clinical expression and progression of the disease. The role of various prothrombotic factors has also been implied. We report a case of a middle-aged man with typical clinical, neuroimaging and histological features of CADASIL, but with notably prolonged activated partial thromboplastin time. Hematological investigations revealed severe clotting Factor XII deficiency. This case illustrates that the occurrence of vascular risk factors should not be overlooked in patients with CADASIL.

The aim of this study was to examine phenotype status of smooth muscle cells in adult coarctation, their proliferation activity and presence of inflammation in this lesion. We used bioptic material taken from 8 children, in age of 3-10. The tissues were fixed in formalin and embedded in paraffin. Sections 5 micrometers thick were stained by DAKO LSAB+/HRP technique to identify alpha-smooth muscle actin-alpha-SMA, vimentin, desmin, myosin haevy chains-MHC, CD3, CD45, S-100 and Proliferating Cell Nuclear Antigen-PCNA. Our results show significant hypocellularity in subendothelium, especially at posterior wall of aorta, but we conclude that it wasn't due to inflammation, because there wasn't CD3 or CD45 immunoreactivity. These results don't match with literature data, which demonstrate cystic medial necrosis of the base of aortic coarctacion. On the other side, there is thickening in subendothelium with dense elastic fibers. Characteristics of media under this lesion are fragmentation, fenestration and reduplicated elastic lamelae, cysts with mukopolisaharids and dedifferentiation of smooth muscle cells, which summary shows destruction of media began in previous stage of neonatal coarctation.

[No abstract available]

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited vascular disorder caused by Notch3 gene mutations. The main histopathological hallmark is granular osmiophilic material (GOM) deposited in the close vicinity of vascular smooth muscle cells (VSMCs). The authors report the first 7 ultrastructurally and genetically confirmed cases of CADASIL in Serbia. Samples of skin and sural nerve were investigated by transmission electron microscopy. GOM deposits were observed around degenerated VSMCs in all the skin biopsies examined. Sural nerve biopsies revealed severe alterations of nerve fibers, endoneurial blood vessels with GOM deposits, endoneurial fibroblasts, and perineurial myofibroblasts. Total genomic DNA was extracted from peripheral blood leukocytes, and exons 26 of the Notch3 gene were amplified by PCR and subsequently sequenced. Four different mutations in exons 2 (Cys65Tyr), 3 (Gly89Cys and Arg90Cys), and 6 (Ala319Cys), which determine the CADASIL disease, were detected among all described patients. A novel missense mutation Gly89Cys involving exon 3 was detected. Due to the difficulties in the determination of the Notch3 mutations, these data suggest that electron microscopic analysis for GOMs in dermal vessel wall provides a rapid and reliable screening method for this disease. © 2012 Informa Healthcare USA, Inc.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited vascular disorder caused by Notch3 gene mutations. The main histopathological hallmark is granular osmiophilic material (GOM) deposited in the close vicinity of vascular smooth muscle cells (VSMCs). The authors report the first 7 ultrastructurally and genetically confirmed cases of CADASIL in Serbia. Samples of skin and sural nerve were investigated by transmission electron microscopy. GOM deposits were observed around degenerated VSMCs in all the skin biopsies examined. Sural nerve biopsies revealed severe alterations of nerve fibers, endoneurial blood vessels with GOM deposits, endoneurial fibroblasts, and perineurial myofibroblasts. Total genomic DNA was extracted from peripheral blood leukocytes, and exons 26 of the Notch3 gene were amplified by PCR and subsequently sequenced. Four different mutations in exons 2 (Cys65Tyr), 3 (Gly89Cys and Arg90Cys), and 6 (Ala319Cys), which determine the CADASIL disease, were detected among all described patients. A novel missense mutation Gly89Cys involving exon 3 was detected. Due to the difficulties in the determination of the Notch3 mutations, these data suggest that electron microscopic analysis for GOMs in dermal vessel wall provides a rapid and reliable screening method for this disease. © 2012 Informa Healthcare USA, Inc.

Objectives: To determine the phenotypical state of smooth muscle cells during the pathogenesis of an atherosclerotic lesion, and to determine the morphological state of the endothelium and the origin of foam cells. Methods: Twenty-one samples of atherosclerotically changed right coronary arteries, which were divided into six subgroups based on the stage of atherosclerosis, were analyzed. The tissues were fixed in formalin and embedded in paraffin. Sections of 5 μm thickness were stained immunocytochemically using a labelled streptavidin-biotin/horse radish peroxidase kit (Dako, Denmark) for the identification of vimentin, alpha-smooth muscle actin, myosin heavy chains, desmin, S-100 protein, CD3, CD31, CD34, CD45, CD68 and proliferating cell nuclear antigen protein. Results: The present study showed that there is first functional and then morphological damage of the endothelium in the late stages of atherosclerosis. The preatheroma stage revealed the presence of intimal changes of smooth muscle cells, with expression of vimentin and alpha-smooth muscle actin and a lack of expression of desmin, which led to a switch to a synthetic phenotype. The described changes progressed into the later stages of atherosclerosis. Along with these changes, a large number of foam cells of variant origin were observed; some of the foam cells developed from monocyte-macrophage lineage (CD68-immunoreactive) and others originated from smooth muscle cells (vimentin- and S-100-immunoreactive). The late stages of atherosclerosis development, such as the atheroma stage, include intimal changes with the formation of a lipid core (S-100-immunoreactive cells and cell necrosis), while fibrosis in the lipid core and the accumulation of collagen fibres with extreme hypocellularity are characteristics of the fibroatheroma stage. © 2006 Pulsus Group Inc. All rights reserved.

Objectives: To determine the phenotypical state of smooth muscle cells during the pathogenesis of an atherosclerotic lesion, and to determine the morphological state of the endothelium and the origin of foam cells. Methods: Twenty-one samples of atherosclerotically changed right coronary arteries, which were divided into six subgroups based on the stage of atherosclerosis, were analyzed. The tissues were fixed in formalin and embedded in paraffin. Sections of 5 μm thickness were stained immunocytochemically using a labelled streptavidin-biotin/horse radish peroxidase kit (Dako, Denmark) for the identification of vimentin, alpha-smooth muscle actin, myosin heavy chains, desmin, S-100 protein, CD3, CD31, CD34, CD45, CD68 and proliferating cell nuclear antigen protein. Results: The present study showed that there is first functional and then morphological damage of the endothelium in the late stages of atherosclerosis. The preatheroma stage revealed the presence of intimal changes of smooth muscle cells, with expression of vimentin and alpha-smooth muscle actin and a lack of expression of desmin, which led to a switch to a synthetic phenotype. The described changes progressed into the later stages of atherosclerosis. Along with these changes, a large number of foam cells of variant origin were observed; some of the foam cells developed from monocyte-macrophage lineage (CD68-immunoreactive) and others originated from smooth muscle cells (vimentin- and S-100-immunoreactive). The late stages of atherosclerosis development, such as the atheroma stage, include intimal changes with the formation of a lipid core (S-100-immunoreactive cells and cell necrosis), while fibrosis in the lipid core and the accumulation of collagen fibres with extreme hypocellularity are characteristics of the fibroatheroma stage. © 2006 Pulsus Group Inc. All rights reserved.

Classification of the neurons in the human basolateral amygdala is performed on preparations impregnated by the Golgi technique. Three different neuronal types are found in the nuclei of the basolateral amygdala: Type I - Pyramidal cells, with numerous dendritic spines and two subtypes (slender and squat); Type II - Modified pyramidal cells, sparsely spinous with rare dendritic spines and two subtypes (single apical and double apical) and; Type III - Non-pyramidal cells, with few dendritic spines and three subtypes (bipolar, multipolar and gliaform). The analysis of the primary dendritic branches pointed out the occasional presence of dendritic bundles (fascicular dendritic arrangement) with their predomination in the parvicellular division of the basal nucleus and paralaminar nucleus. Additionally, the presence of dendrodendritic contacts, indicated by light microscopy, was also found in the parvicellular division of the basal nucleus and especially in the paralaminar nucleus.

Classification of the neurons in the human basolateral amygdala is performed on preparations impregnated by the Golgi technique. Three different neuronal types are found in the nuclei of the basolateral amygdala: Type I - Pyramidal cells, with numerous dendritic spines and two subtypes (slender and squat); Type II - Modified pyramidal cells, sparsely spinous with rare dendritic spines and two subtypes (single apical and double apical) and; Type III - Non-pyramidal cells, with few dendritic spines and three subtypes (bipolar, multipolar and gliaform). The analysis of the primary dendritic branches pointed out the occasional presence of dendritic bundles (fascicular dendritic arrangement) with their predomination in the parvicellular division of the basal nucleus and paralaminar nucleus. Additionally, the presence of dendrodendritic contacts, indicated by light microscopy, was also found in the parvicellular division of the basal nucleus and especially in the paralaminar nucleus.