Acute lung injury occurs mostly in the very low birth weight and extremely low birth weight infants. The pathological process leading to acute lung injury includes immature and/or diseased lung that experienced oxidative stress, inflammation and mechanical insult with the bronchial, alveolar and capillary injuries and cell death. It may be the first step to the subsequent development of chronic lung disease of prematurity or bronchopulmonary dysplasia. The mechanisms of lung injury are extensively investigated in the experimental models and clinical studies, mostly performed on the adult patients. At present, the explanations of the mechanism(s) leading to lung tissue injury in tiny premature babies are just derived from these studies. Acute lung injury seems to be rather a syndrome than a well-defined nosological unit and is of multifactorial etiology. The purpose of this review is to discuss the main factors contributing to the development of acute lung injury in the very low or extremely low birth weight infants - lung immaturity, mechanical injury, oxidative stress and inflammation. Nevertheless, numerous other factors may influence the status of immature lung after delivery., P. Zoban, M. Černý., and Obsahuje bibliografii
Elevated levels of insulin have been reported to induce both an arterial vasodilation mediated by nitric oxide (NO), and vasoconstriction mediated by endothelin and reactive oxygen radicals. Metformin, used to control blood glucose levels in type 2 diabetes, has also been shown to cause NO-mediated dilation of conduit arteries. It is possible that these contradictory vascular effects are due to a non-direct action on arteries. Therefore, the direct effect of high levels of insulin and metformin infusion on resistance artery diameter was evaluated. Experiments were carried out on the anesthetized pig; blood flow and pressure were measured in the iliac artery. An adjustable snare was applied to the iliac above the pressure and flow measurement site to induce step decreases (3-4 occlusions at 5 min intervals were performed for each infusion) in blood flow, and hence iliac pressure, and the conductance (Δflow / Δpressure) calculated. Saline, insulin (20 and 40 mUSP/l/min), and metformin (1 μg/ml/min) were infused separately downstream of the adjustable snare and their effect on arterial conductance assessed. Insulin at both infusion rates and metformin caused a significant reduction in peripheral vascular conductance. In conclusion, hyperinsulinemia and metformin infusion constrict resistance arterial vessels in vivo., F. Markos, C. M. Shortt, D. Edge, T. Ruane-O'Hora, M. I. M. Noble., and Obsahuje bibliografii
Host responses against skin inhabiting monogeneans are commonly obserÇetHtflfthe responsible immune mechanisms in the fish skin are insufficiently described. Based on recent knowledge of fish immunity and skin response mechanisms in mammals a model for the skin immunity in fish to monogcnean infections is proposed. Important cellular components of the model are the epithelial cells, the mucous cells and leucocytes. The release of cytokines, e.g. IL-1, following mechanical or chemical injury of the epithelial cells, initiates a series of events leading to decrease of the ectoparasite population. Cytokines (e.g. IL-1, TNF, INF) are suggested to affect secretions from mucous cell and attract neutrophils and macrophages. Leukotrienes are probably involved in the inflammatory reactions. The subsequent production of humoral substances (among others complement factors and peptides) could be responsible for the antiparasitic response in the later stages of infection. Although non-specific factors dominate the response, the involvement of specific antibodies and lymphocytes cannot be excluded.
Immunity plays an important role in the reactivity of the organism and, in this context, is an essential factor in the pathogenesis of many diseases. Basically, there is no system or organ in the body, whose dysfunction is not related to immunity consequences. In addition, there are also multisystem diseases simultaneously involving multiple body systems. They are not always caused by weak immunity, but also often by modified immune reactions known as overshooting. The essence of all these diseases is a change in the reactivity of the organism where immunity plays an important role. The immunity as such is then part of the systems of neuroendocrine-immune regulation, which have common mediators and receptors. The establishment of psychoneuroimmunology, a relatively new discipline in neuroscience, contributed to a detailed understanding of these mechanisms between central and peripheral nervous system, the endocrine system and the immune system. This research enabled the uncovering of the nature of stress-diseases and impact of other regulatory disturbances on the function of various body organs and systems of the organism as a whole. The aim of this short review is to show complex interconnections of these relationships to better understand the human health and disease., F. Vožeh., and Seznam literatury
Ribulose 1,5-bisphosphate carboxylase/oxygenase (RuBPCO) and RuBPCO binding protein (BP) were isolated from barley leaves. RuBPCO was dissociated into subunits under denaturing conditions. Polyclonal antibodies against RuBPCO, RuBPCOBP and RuBPCO large subunit (LS) were raised. Inununoblotting analyses showed that anti-RuBPCO antibodies did not cross-react with BP. Anti-BP antibodies cross-reacted with RuBPCO smáli subunit (SS) and reacted but more slightly with RuBPCO LS.
M1-muscarinic acetylcholine (ACh) receptors (M1R) were directly demonstrated immunocytochemic ally in electronmicroscopic images of rat diaphragm neuromus cular junctions (NMJ). Specific electron-dense granules were located at presynaptic nerve ending membranes and in the sa rcolemma in the depths of postsynaptic folds. This first visualization of M1R on both sides of the NMJ is in agreement with previous pharmacological data on the regulatory role of M1R in quantal and non-quantal ACh release. and Obsahuje bibliografii a bibliografické odkazy
Insect peptidyl-dipeptidase A [angiotensin I - converting enzyme (ACE)] is a soluble single-domain peptidyl-dipeptidase that has many properties in common with the C-domain of mammalian somatic ACE and with the single-domain mammalian ACE. In agreement with a variety of insects, immunocytochemical studies reveal the presence of an ACE-like protein in Locusta migratoria. ACE-like immunoreactivity is present in neurosecretory cells of the pars intercerebralis. These cells have axons projecting into the nervus corporis cardiaci I and into the storage part of the corpus cardiacum, a neuroendocrine organ directly releasing into the aorta. The localisation of ACE in neurosecretory cells is consistent with its proposed role as a processing enzyme that is involved in the generation of active peptide hormones., Dirk Veelaert, Liliane Scoofs, Nathalie Macours, Anick Vandingenen, Arnold De Loof, Elwyn Isaac, Michel Salzet, Roger Huybrechts, and Lit