Long-term ultrastructural indices of lead intoxication in pulmonary tissue of the rat.

In the present research long-term pulmonary toxicity of lead was investigated in rats treated by intraperitoneal administration of lead acetate for three consecutive days (25 mg/kg per day). Five weeks after treatment average lead content in the whole blood was 0.41 μg/dL ± 0.

Functional alterations in endothelial NO, PGI₂ and EDHF pathways in aorta in ApoE/LDLR-/- mice.

Adequate endothelial production of nitric oxide (NO), endothelium-derived hyperpolarizing factor (EDHF), and prostacyclin (PGI₂) is critical to the maintenance of vascular homeostasis. However, it is not clear whether alterations in each of these vasodilatory pathways contribute to the impaired endothelial function in murine atherosclerosis. In the present study, we analyze the alterations in NO-, EDHF- and PGI₂-dependent endothelial function in the thoracic aorta in relation to the development of atherosclerotic plaques in apoE/LDLR⁻/⁻ mice.

Ultrastructural changes in lung tissue after acute lead intoxication in the rat.

Pulmonary toxicity of lead was studied in rats after an intraperitoneal administration of lead acetate at a dose of 25 mg/kg. Three consecutive days of treatment increased lead content in the whole blood to 2.1 µg/dl and in lung homogenate it attained 9.

Genetic and ultrastructural studies in dilated cardiomyopathy patients: a large deletion in the lamin A/C gene is associated with cardiomyocyte nuclear envelope disruption.

Major nuclear envelope abnormalities, such as disruption and/or presence of intranuclear organelles, have rarely been described in cardiomyocytes from dilated cardiomyopathy (DCM) patients. In this study, we screened a series of 25 unrelated DCM patient samples for (a) cardiomyocyte nuclear abnormalities and (b) mutations in LMNA and TMPO as they are two DCM-causing genes that encode proteins involved in maintaining nuclear envelope architecture. Among the 25 heart samples investigated, we identified major cardiomyocyte nuclear abnormalities in 8 patients.

MMP2 and MMP9 in immature endothelial cells following surgical injury of rat cerebral cortex--a preliminary study.

Matrix metalloproteinases (MMPs) are zinc-dependent endopeptidases capable of extracellular matrix remodeling. They have been implicated in various physiological and pathological phenomena involving neurovascular unit elements (neurons, astrocytes and capillary vessels). Surgical injury of the fronto-temporal region of rat cerebral cortex induces massive neurodegeneration and cell death accompanied by astrogliosis.

Ultrastructural and immunochemical studies of glial scar formation in diabetic rats.

We explored the rebuilding of the brain parenchyma after surgical injury due to reactive astrogliosis. In the present study, we investigated the initial stages of rebuilding in the perilesional cortex of streptozotocin-induced diabetic rats. Our methods utilized ultrastructural and immunohistochemical studies as well as Western blot analysis of glial fibrillary acidic protein (GFAP) and vimentin.

Staphylococcal cysteine protease staphopain B (SspB) induces rapid engulfment of human neutrophils and monocytes by macrophages.

Abstract Circulating neutrophils and monocytes constitute the first line of antibacterial defence, which is responsible for the phagocytosis and killing of microorganisms. Previously, we have described that the staphylococcal cysteine proteinase staphopain B (SspB) cleaves CD11b on peripheral blood phagocytes, inducing the rapid development of features of atypical cell death in protease-treated cells. Here, we report that exposure of phagocytes to SspB critically impairs their antibacterial functions.

Apoptotic death of cortical neurons following surgical brain injury.

Unilateral surgical brain injury of the rat is a model of surgery-related brain damage of humans. Our preliminary experiments showed two phenomena within the damaged cortical region of rat brain. Those were: degeneration and death of neurons and massive gliosis.

[Ultrastructural features of normal and dysfunctional endothelium of the blood vessels].

Endothelium of the blood vessels plays a very important role in blood circulation, inflammation, atherosclerosis and cancer progression. We describe the ultrastructural morphology, function of endothelium and its participation in vessel formation during regenerative or inflammatory processes in adults. Transmission and scanning electron microscopic studies indicate on endothelial cell function in atherosclerotic plaque formation.

Obliteration of cardiomyocyte nuclear architecture in a patient with LMNA gene mutation.

Objective: The aim of our study was to perform an immunohistochemical and ultrastructural analysis of the nuclear architecture of cardiomyocytes from an end-stage DCM patient with a missense point mutation in the exon 3 of the LMNA gene which is predicted to result in a D192G substitution.

Methods: We studied endomyocardial biopsy samples taken from the right ventricle by immunostaining using antibodies against the lamins A and C and by electron microscopy. The cardiomyocyte ultrastructure was analysed, with particular attention to the nuclear architecture.

Detection of mitochondrial dysfunction by EPR technique in mouse model of dilated cardiomyopathy.

Tgalphaq44 mice with targeted overexpression of activated Galphaq protein in cardiomyocytes mimic many of the phenotypic characteristics of dilated cardiomyopathy in humans. However, it is not known whether the phenotype of Tgalphaq44 mice would also involve dysfunction of cardiac mitochondria. The aim of the present work was to examine changes in EPR signals of semiquinones and iron in Fe-S clusters, as compared to classical biochemical indices of mitochondrial function in hearts from Tgalphaq44 mice in relation to the progression of heart failure.

[Morphological and clinical aspects of Danon disease].

Background: Danon disease, an X-linked hypertrophic cardiomyopathy, is caused by primary deficiency of lysosome-associated membrane protein (LAMP-2). The pathological hallmark of the disease is the appearance of intracytoplasmic vacuoles containing autophagic material and the absence of LAMP-2 activity in the muscle.

Aim: To define the LAMP-2 protein deficiency we investigated cardiac and skeletal muscle of a 19-year-old man with hypertrophic cardiomyopathy without clinically apparent skeletal myopathy or mental impairment, whose mother died suddenly at 46 years of age.

The immature endothelial cell in human glioma. Ultrastructural features of blood capillary vessels.

New vessel formation is a prerequisite for the growth of a tumour mass. Growing evidence suggests that endothelial progenitor cells circulate in the blood and participate in that process. The purpose of the present study was ultrastructural and electron microscopic immunocytochemical examination of capillary blood vessels in human glioma.

Abnormal chaperone-mediated autophagy (CMA) in cardiomyocytes of a boy with Danon disease.

Ultrastructural analysis of the cardiomyocyte structure in Danon disease reveals dramatic accumulation of abnormal late autophagic vacuoles (AVd) suggestive of primary lysosomal defect. Moreover, the accumulation of AVd in cardiomyocytes is consistent with a decreased rate of autophagic to lysosomal trafficking. These results suggest that the loss of the LAMP-2 protein strongly inhibits uptake of proteins into lysosomes for degeneration.

Dilated cardiomyopathy caused by LMNA mutations. Clinical and morphological studies.

Background: Dilated cardiomyopathy (DCM) is familial in about 20-35% of patients. The most frequently encountered mutations associated with DCM are found in LMNA.

Aim: To define the frequency of LMNA mutations in a series of consecutive DCM patients and to evaluate the phenotype of mutation carriers.

The immature endothelial cell in new vessel formation following surgical injury in rat brain.

Objectives: We investigated neovasculatization in the cerebral cortex of the adult rat after surgical brain injury by ultrastructural, immunocytochemical and immunochemical means. Previously we described endothelial-like cell that participates in new vessel formation on plasma proteins that served as a provisional matrix in the region immediately adjacent to the traumatic injury. In the present study we describe new vessel formation in the multistep process with the alterations in endothelial-like cell immunophenotype.

Application of the lithium and magnesium initiators for the synthesis of glycolide, lactide, and epsilon-caprolactone copolymers biocompatible with brain tissue.

The subject of this work is new method of the synthesis of biodegradable copolymers compatible with brain tissue. Copolymerization of glycolide with lactide was conducted in solution or in bulk in the presence of LiBu, LiAcac, MgBu(2), Mg(acac)(2) as initiators. In all cases, copolymers with molecular weight of 20000-40000 were obtained, which enables to use them as drug carriers.

[Ultrastructural analysis of capsule and nurse-cell morphology examined seven months after Trichinella spiralis mouse infection].

Ultrastructural changes in muscles cells of mice infected with T. spiralis larvae in 220 day of infection were evaluated. The object of study was in the region of the "nurse-cell" being in direct contact with the larva wall.

Involvement of immature endothelial cells in vascular alterations in Alzheimer's disease.

The aim of the present study was to investigate ultrastructural features of cerebral capillaries and the pattern of new vessel formation in a patient with Alzheimer's disease (AD). Recent neuropathological studies have demonstrated that patients with AD have cerebrovascular pathology. Using electron microscopy, we showed that alterations of the capillaries are a common finding both in vascular disease and in AD, suggesting that vascular factors may also play a role in the pathogenesis of AD.

Inhibition of poly(ADP-ribose) polymerase activity protects hippocampal cells against morphological and ultrastructural alteration evoked by ischemia-reperfusion injury.

Poly(ADP-ribose) polymerase 1 (PARP-1 EC 2.4.2.

Calcification of Trichinella spiralis larval capsule.

Trichinella spiralis larvae were examined in TEM to identify calcareous corpuscles in the outer part of parasite capsule. The microroentgenographic analysis of calcareous corpuscles mainly demonstrated the presence of phosphorus and calcium. The physiological importance of calcareous corpuscles, as well as their significance in decay of T.

Cardiac amyloidosis diagnosed by endomyocardial biopsy. Clinical, histopathological, immunohistochemical and ultrastructural studies.

Background: The heart is often involved by primary (AL) and familial transthyretin-related (ATTR) amyloidosis. Endomyocardial biopsy is a valuable diagnostic method, useful in detection and recognition of the type of amyloid.

Aim: The aim of the study was to determine the type of amyloid deposits found in endomyocardial biopsies, using histochemical, immunohistochemical and ultrastructural methods.

2-deoxyglucose induces beta-APP overexpression, tau hyperphosphorylation and expansion of the trans-part of the Golgi complex in rat cerebral cortex.

The effects of a single intraperitoneal injection of a non-metabolizable glucose analog 2-deoxyglucose (2-DG, 500 mg/kg) on the levels of beta-APP expression, and phosphorylated and unphosphorylated tau protein in the rat cerebral cortex were investigated. The effects of 2-DG on the ultrastructure of cortical neurons with particular emphasis on the morphology of the Golgi apparatus, and on brain bioenergetics assessed by in vivo 31P-MRS technique were also evaluated. Seven and a half hours after injection of 2-deoxyglucose a significant increase in brain cortex beta-APP expression, increased tau phosphorylation, and a marked relative expansion of the trans- part of the Golgi intracellular secretory pathway in cortical neurons has been found.

Expansion of the Golgi apparatus in rat cerebral cortex following intracerebroventricular injections of streptozotocin.

Streptozotocin (STZ) is a bacterial toxin which selectively damages both insulin-producing cells and insulin receptors. Injections of STZ into the cerebral ventricles of experimental animals are followed by sustained biochemical, metabolic and behavioral effects resembling those which are found in human brains afflicted by Alzheimer's disease. The aim of the present study was to assess the effects of double intracerebroventricular application of STZ on the ultrastructure of rat frontoparietal cortical neurons.

Matrix metalloproteases activity and ultrastructural changes in the early phase of experimental allergic encephalomyelitis. The effect of oral treatment with spinal cord hydrolysate [correction of hydrolisate] proteins in Lewis rat. The pilot study.

Matrix metalloproteinases (MMPs) are a family of genes of the neutral proteinases that are important to normal development and to a variety of pathological processes including neuroinflammation. In the central nervous system (CNS), MMPs degrade components of the basal lamina, leading to disruption of the blood-brain barrier (BBB), and contribute to the neuroinflammatory responses. Their concentration in experimental allergic encephalomyelitis (EAE) increases a few folds and is accompanied by a thinner basal membrane in the early phase of EAE.