The metabolic hypothesis is more likely than the epileptogenic hypothesis to explain stroke-like lesions

Stroke-like episodes (SLEs) are a hallmark of mitochondrial encephalopathy, lactic acidosis, and stroke-like episode (MELAS) syndrome but occur in other mitochondrial disorders (MIDs) as well. The morphological equivalent of the SLE is the stroke-like lesion (SLL) on magnetic resonance imaging (MRI). The pathophysiology of SLLs is under debate, but several hypotheses have been raised to explain the phenomenon. Of these, the metabolic, epileptogenic, and vascular hypotheses are the most frequently discussed. There are several arguments for and against these hypotheses, but a consensus has not been reached which of them provides the correct explanation. A recent consensus statement generated by a panel of experts applying the Delphi method, favoured the epileptogenic hypothesis and recommended treatment of SLEs with antiepileptic drugs, irrespective if the patient presented with a seizure or epileptiform discharges on electroencephalography (EEG) or not. We disagree with this general procedure and provide the following arguments against the epileptogenic hypothesis: 1. not each SLE is associated with seizures. 2. epileptiform discharges may be absent on EEG during a SLE. 3. SLLs are not restricted to the cortex. 4. antiseizure-drugs (ASDs) may not prevent the progression or recurrence of a SLL. 5. ASDs may terminate seizures but no other phenotypic feature of a SLE. 6. patients already under ASDs are not immune from developing a SLL. 7. SLLs usually last longer than seizures. 8. no animal model supports the epileptogenic hypothesis. The strongest arguments for the metabolic hypothesis are that SLLs are not confined to a vascular territory, that the oxygen-extraction fraction within a SLL is reduced, and that there is hypometabolism within a SLL on FDG-PET. SLLs may respond to antioxidants, NO-precursors, steroids, or the ketogenic diet. ASDs should be applied only if there is clinical or electrophysiological evidence of seizure-activity.

The metabolic hypothesis is more likely than the epileptogenic hypothesis to explain stroke-like lesions

Stroke-like episodes (SLEs) are a hallmark of mitochondrial encephalopathy, lactic acidosis, and stroke-like episode (MELAS) syndrome but occur in other mitochondrial disorders (MIDs) as well. The morphological equivalent of the SLE is the stroke-like lesion (SLL) on magnetic resonance imaging (MRI). The pathophysiology of SLLs is under debate, but several hypotheses have been raised to explain the phenomenon. Of these, the metabolic, epileptogenic, and vascular hypotheses are the most frequently discussed. There are several arguments for and against these hypotheses, but a consensus has not been reached which of them provides the correct explanation. A recent consensus statement generated by a panel of experts applying the Delphi method, favoured the epileptogenic hypothesis and recommended treatment of SLEs with antiepileptic drugs, irrespective if the patient presented with a seizure or epileptiform discharges on electroencephalography (EEG) or not. We disagree with this general procedure and provide the following arguments against the epileptogenic hypothesis: 1. not each SLE is associated with seizures. 2. epileptiform discharges may be absent on EEG during a SLE. 3. SLLs are not restricted to the cortex. 4. antiseizure-drugs (ASDs) may not prevent the progression or recurrence of a SLL. 5. ASDs may terminate seizures but no other phenotypic feature of a SLE. 6. patients already under ASDs are not immune from developing a SLL. 7. SLLs usually last longer than seizures. 8. no animal model supports the epileptogenic hypothesis. The strongest arguments for the metabolic hypothesis are that SLLs are not confined to a vascular territory, that the oxygen-extraction fraction within a SLL is reduced, and that there is hypometabolism within a SLL on FDG-PET. SLLs may respond to antioxidants, NO-precursors, steroids, or the ketogenic diet. ASDs should be applied only if there is clinical or electrophysiological evidence of seizure-activity.

MORPHOLOGICAL GROUNDS FOR PLASTIC SURGERY IN THE MASTOID AREA

This article presents the data on the structural peculiarities of the mastoid region, the dependency between the thickness of the epidermis, dermis, subcutaneous fat, and size of the structural elements of the skin at various stages of its deformation that allows us to determine the digital indices for the depth of skin peeling and skin amount dissected when planning plastic and reconstructive operations skin that is carved. In order to achieve the optimal result of plastic operations, and, in particularly, of cosmetic otoplasty and lower rhytidectomy, and to minimize the development of postoperative complications, the manual skills of the surgeon are not sufficient. It is essential to know exactly morphofunctional characteristics of layered structure of certain topographic and anatomical sites, especially within mastoid area, where the main incisions are made when performing on the above-mentioned surgical interventions. After stretching the test samples of the skin taken from the mastoid region within 5 mm, we observed subtle differences between them even in the state of physiological rest. The study of the structure of the skin-fat flap samples after stretching within 15 mm demonstrated the occurrence of pathological processes in the skin epithelium and dermis. The morphological picture indicated the development of balloon dystrophy that is known as the morphological equivalent of focal necrosis. Investigation of microslides of the skin taken from and exposed to stretching within 20 mm made it possible to reveal the intensification of the previously described changes and the development of qualitatively new pathological changes both in the epidermis and in the dermis. The results obtained enable us to conclude that during operations in the mastoid area, the biomechanical properties of the skin-fat flaps should be taken into account. When the skin was stretched within 5 – 10 mm, irreversible changes did not occur, and these are optimal indicators during surgical interventions. With a flap deformation within 15-20 mm, pathological changes were observed, in some cases they were classified as irreversible that led to necrosis in the postoperative period.

STRUCTURAL ASSESSMENT OF VIOLATIONS OF THE ADAPTIVE MECHANISMS OF ADRENAL CALVESIN THE ACUTE COURSE OF CRYPTOSPORIDIOSIS

The study was the first to assess the adaptation mechanisms disorders of the adrenals of calves in acute cryptosporidiosis. The cryptosporidiosis in patients with symptoms of diarrhea in the farms of the Republic of Tatarstan was diagnosed through formalin-ether sedimentation and following staining of infectious agents by Ziehl-Neelsen acid fast staining method. For specific identification of cryptosporidium in the feces of calves, an enzyme immunoassay kit, “H&R Crypto Rapid Test”, was used to detect cryptosporidium in feces. The agents of cryptosporidiosis of the genus Cryptosporidium were determined in pathological material taken from sick and dead at the age of 5 to 10 days calves. Histological examination of the organs and tissues of calves with the cryptosporidiosis were carried out using generally accepted method of staining of histological sections with hematoxylin and eosin. Structural studies of adrenal cortex and medulla of calves with the cryptosporidiosis revealed significant changes in synthesized hormonal products profiles. The characteristics of intense glucocorticoid biosynthesis were found in the adrenal cortex at the height of disease, as shown by a sharp expansion in zona fasciculate of the cortex, numerous small and large vacuoles in the cytoplasm of spongiocytes and enhanced profiles of capillary net. Intense excretion of glucocorticoids in hemocirculation maximally activated the catabolic processes in the organisms of sick calves. Small number of adrenocorticocytes, the predominance of small hyperchromic nuclei in them and the absence of characteristics of mitotic activity were not edinzona glomerulosa of the cortex that corresponded to the morphological equivalent of retardation of mineralcorticodes biosynthesis. There had been a dramatic increase in cells with characteristics of apotosis among adrenocorticocytes in all zones of the cortex, including the small in width reticular zone. The small catecholamine-synthesizing cells in the medullary area were represented predominantly by small with sharply clarified cytoplasm and small rounded adrenocytes nuclei and by significantly smaller amount of larger noradrenocytes. The found pathological changes in the cortex and medulla of the adrenals characterized the increase of catabolic processes, vascular, metabolic disorders in organisms of calves with the cryptosporidiosis. In view of disorders of adaptation mechanisms and limited plastic resources, a fast death was observed in newborn calves.

Morphofunctional Transformations in the Lungs of Rats Under the Long-Term Exposure to Sodium Tetraborate

The aim of the study was to identify reactive and adaptive changes in the lungs of rats under the longterm exposure to sodium tetraborate.Material and methods. The study included male rats which were administered sodium tetraborate in dosage of 1/30 LD50, intraperitoneally, daily. The study samples (lung fragments) were selected for histological examination in 7, 14, 21 and 30 days from the beginning of the experiment.Results. Long-term exposure to sodium tetraborate resulted in a complex of destructive changes in the air-conducting and respiratory parts of the lung. Leukocyte infiltration in the connective tissue and epithelium of the bronchial and alveoli wall, focal destruction of the bronchial epithelium and alveoli, growth of the connective tissue in the organ interstitial were observed with underlying edema, stasis of blood corpuscles in capillaries, focal destruction of the capillary wall. The study revealed alveolocyte wall thickening and growth and sclerosing of the connective tissue in the interalveolar spaces; this appears to be the morphological equivalent of the increased thickness of the aero-hematic barrier and deterioration of the gas exchange in the alveoli. The increased proportion of the bronchi-associated lymphoid tissue mainly presented by the lymphoid tissue of the diffuse character and less rarely by the lymphoid follicles was registered in the wall of the medium bronchi.Conclusion. The results have proven the negative impact of sodium tetraborate on lung structures and demonstrated the adaptive capacity of the lungs, their ability to maintain the necessary structural-functional characteristics under the extreme destabilizing factors effect.

Early and long-term neuroendocrine effects of prenatal stress in male and female rats

The effect of maternal stress or so-called prenatal stress (PS) on the neuroendocrine regulation of reproduction and stress reactivity of the progeny was studied. Prenatal stress prevented the formation of sex dimorphism of catecholamine content and aromatase and androgen 5a-reductase activities in the preoptic region of the brain and mediobasal hypothalamus of 10-day-old rats. Leveling of sex-specific differences in the size of the neurocyte nuclei in the suprachiasmatic nucleus was the morphological equivalent of functional disorders induced by PS. Stress and adrenergic reactivity of the hypothalamo-pituitary-adrenal system was changed in prenatally stressed males and females. Remote effects of PS are regarded as a manifestation of disorders in the hormone neurotransmitter imprinting of the neuroendocrine system.

Calycophoran siphonophore muscle fibres without any sarcoplasmic reticulum but with tubular invaginations morphologically analogous to a T-system

Different marine invertebrates have different tubular or vesicular systems within their locomotor muscle fibres. The siphonophores Chelophyes, Abylopsis and Muggeia have invaginated tubules which are the morphological equivalent of the vertebrate invaginated tubular system, but lack a sarcoplasmic reticulum. In Chelophyes the previous suggestion that Ca2+ channels in the extensive invaginated tubule system allow ingress of Ca2+ is shown to be incorrect. Contraction of the swimming muscles in Chelophyes is not blocked by 20 μM ryanodine, nor is it induced by 10 mM caffeine, hence intracellular Ca2+ stores appear absent. Contraction is, however, maintained by replacement of the greater part of the usual external Na+ by Li+ or by or N-methyl-D-glucamine, although action potentials can still be evoked. Hence we conclude that following contraction, internal Ca2+ is reduced by a Na/Ca2+ exchange mechanism.

Demonstration of Aquaporin-Chip in Peritoneal Tissue of Uremic and Capd Patients

Aquaporin-CHIP is a 28 kD channel forming integral membrane protein. It acts as an osmotically driven, water-selective pore. The presence of aquaporin-CHIP has been demonstrated in the proximal tubule in the kidney and in the pleura, as well as in other tissues. During peritoneal dialysis a dissociation between the transport of water and sodium using hyperosmolar solutions has been reported, suggesting the presence of ultrasmall pores. Water channels, like aquaporin-CHIP, could be the morphological equivalent of these pores. We investigated the possible presence of aquaporinCHIP in cryo-sections of peritoneal tissue using affinity purified human anti-CHIP IgG (P. Agre, Baltimore, MD). Peritoneal biopsies (omenta) were obtained at catheter insertion in 2 uremic patients with end-stage renal disease, and at catheter reimplantation of 1 patient treated with continuous ambulatory peritoneal dialysis (CAPD) for two years. Peritoneal tissue obtained at autopsy from 1 patient who had been on CAPD for four years, but in whom CAPD had been discontinued for five months, was also studied. Aquaporin-CHIP antiserum specific staining was found in the endothelial cells of the peritoneal capillaries in all patients. No obvious difference in the intensity of staining was seen between uremic and CAPD patients. This demonstration of aquaporin-CHIP in human peritoneal endothelial cells supports the hypothesis of the existence of ultrasmall pores within the peritoneal membrane. These water channels facilitate the transcellular transport of water, induced by an osmotic gradient, in the absence of sodium transport. It may be the explanation for the dissociation of water and sodium transport that occurs during hyperosmolar solutions. Aquaporin-CHIP is present in human peritoneal endothelial cells in both uremic and CAPD patients. Aquaporin-CHIP may be the morphological equivalent of the ultrasmall pores within the peritoneal membrane.