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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., Methods: Clinical, morphological, immunohistochemical and ultrastructural analysis was performed. Paraffin sections of cardiac muscle were stained using routine histochemical methods. Frozen sections of skeletal muscle were stained using histochemical methods as well as using monoclonal antisera against N-terminal of dystrophin and antisera against LAMP-2. Ultrastructural examination of both cardiac and skeletal muscle specimens were performed., Results: Cardiac and skeletal muscle revealed an excessive accumulation of early and late autophagic vacuoles containing various cytoplasmic debris. In immunohistochemical analysis the vacuolar membrane seen in skeletal muscle was decorated with antibody against dystrophin and such vacuoles were negative for LAMP-2., Conclusion: Ultrastructural and immunohistochemical analysis of skeletal muscle (less invasive than myocardial biopsy) may be used in diagnosis of Danon disease. Early diagnosis of Danon disease is important for timely cardiac transplantation, the only effective therapeutic option.

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.

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. The correlations between morphological and clinical parameters were evaluated., Methods and Results: During 1999-2004, endomyocardial biopsy was performed in 41 patients hospitalized in our institution due to heart failure of unknown etiology. Amyloid deposits were revealed in 3 patients, in 2 of them the intraoperative specimens were also taken. The deposits were located in myocardial interstitium as well as in the wall of small vessels. One patient showed deposits in the atrial and pericardial walls. Electron microscopy study revealed amyloid fibers adhering to the basement membranes of the myocardial cells and small vessels. Immunohistochemical staining determined two types of amyloid. A woman aged 42 showed transthyretin-related amyloidosis, most probably hereditary. A woman aged 69 exhibited the light chains amyloidosis (AL-lambda). In contrast, diagnosis was not certain (most probably ATTR) in a 35 year old woman. Essential involvement of the pericardium was observed in two younger patients. They underwent pericardiotomy. The survival time (from diagnosis to death) was one year in the patient with amyloidosis ATTR, 17 days in the patient with the AL type, and 2 years in the patient with amyloidosis of undetermined type., Conclusions: Cardiac amyloidosis is associated with poor prognosis. Better recognition of this disease may allow the early diagnosis and institution of modern therapy.

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. Electron microscopic observations revealed the continuity of the muscle cell membrane adjacent to larva surface.

In this study, using scanning and transmission electron microscope, we attempt to evaluate ultrastructural alterations of endothelial cells, macrophages and smooth muscles cells. The inflammatory process has an essential impact on the development of Chlamydia infection. Specimens from human carotid were obtained from patients who underwent endarterectomy. For examination under scanning and transmission electron microscope vessel sections were fixed in paraformaldehyde and glutaraldehyde. We analysed alterations of endothelial cells covering advanced atherosclerotic plaque in carotid using scanning electron microscope. Smooth muscle cells had undergone the heaviest proliferation among the cells on artery wall. In the tested material we detect diversified morphological forms of Chlamydia sp. We found that one of the pathogens that may lead to atherosclerotic lesions is Chlamydia pneumoniae.

Cerebral malaria in man and in animals is the consequence of a cascade of events, involving the patological changes, leading to the amplification of the expression of the receptors for cytoadherence on brain capillary endothelial cells. Sequestration is the process by which erytrocytes infected with the mature forms of the malaria parasite Plasmodium falciparum disappear from circulation and accumulate within venules and capillaries of various organs and tissues. The molecular mechanism in sequestration is one of the most rapidly advancing fields in malaria research. The several specific aspects considered in this paper. Our electron micrographs show cytoadherence in own model of cerebral malaria in rats infected with Plasmodium berghei.

Hypothalamic neurosecretory nuclei of rats in which short-term clinical death was experimentally induced, were examined electron-microscopically. Material for studies was taken two weeks after resuscitation of animals following 5 min cardiac and respiratory arrest. Application of aldehyde fixatives with Alcian blue as well as fixatives containing tannic acid revealed numerous additional ultrastructural features not visualized in routine electron microscopy. The obtained results are indicative that short-term cerebral ischemia in rats results in ultrastructural abnormalities in neurosecretory hypothalamic nuclei, which appear after 2 weeks survival. These are electron microscope exponents of reduced secretory function, increased number of lysosomal structures and changes in cytoskeleton organization. They are accompanied by abnormalities in axoplasm and myelin sheaths. The authors consider those structural abnormalities as exponents of delayed irreversible metabolic changes of nerve cells.

The dynamics of ultrastructural changes in axonal endings were studied after experimental epileptic seizures. Mice and rats from strains with genetically--determined audiogenic epilepsy were used as a model of epilepsy. The animals were divided into 3 groups: in group 1 only one seizure was evoked, in group 2 eight seizures within 4 hours, group 3 served as control. The animals were killed immediately after the last seizure, 30 min. after it or 1 hour after the seizure. Hippocampal gyrus cortex was impregnated with zinc-iodide-osmium tetroxide and synapses were examined under electron microscope. The number of synaptic vesicles showing positive reaction with zinc iodide was calculated in 20 synaptic boutons in each group. A significant correlation was demonstrated between the frequency of seizures and the survival time after the seizure on the one hand, and synaptic changes, on the other. In the control group 97% of synaptic vesicles were filled with neurotransmitter substance giving positive reaction with zinc iodide. Immediately after the single seizure 46% of synaptic vesicles were found emptied, 30 min. later the neurotransmitter substance was demonstrated in 79% of vesicles, 1 hour later 82% of vesicles had normal appearance. Immediately after serial seizures 91% of vesicles were found empty, 30 min. later the neurotransmitter was present in 50% of vesicles, 1 hour later in 78%. In another group of animals seizures were evoked once daily for 40 days (chronic epilepsy model). Synaptic changes were different: the synaptic boutons were swollen, the number of vesicles was reduced, greatly enlarged vesicles and clear membrane-bound vacuoles appeared. They evidenced degenerative character of changes. It is suggested that degenerative synaptic changes may be a substrate of epileptic dementia.