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This publication presents the analysis of communal urban planning documents for the Pagory Chelmskie area with regards to their contents on the protection and development of the landscape. It pays special attention to the issue of agricultural landscape protection and the aesthetic values of the main elevations. The results of the conducted analyses prove that this subject is rarely researched and treated very generally, even in the studies of conditions and communal development plans. The idea of a landscape only shows up in the context of natural qualities and listed monuments, which is why recommendations regarding landscape protection and development are sometimes conflicting and often contribute to the decay of aesthetic values. The publication includes also, in addition to the assessment of studies and local plans, a proposal of changes in the way of preparing urban planning documents for this area. Select ways of landscape protection and development of the most valuable hills have also been specified.
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Molecular mechanism of emotional fever - the role of nitric oxide

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The purpose of these studies was to assess the involvement of nNOS and iNOS inhibitors on stress fever caused by exposure to an open field in freely moving biotelemetered rats. Vinyl-L-NIO (N5 - (1-Imino-3-butenyl) - ornithine, a neural nitric oxide synthase (nNOS) inhibitor, and aminoguanidine, an inducible nitric oxide synthase (iNOS) inhibitor, were injected into the lateral ventricle (icv) at a dose of 5 µg and 10 µg, respectively, and then immediately exposed to open field for 30 min. After exposure to the open field, rats not treated with NOS inhibitors responded with a rapid rise in Tb and it was accompanied with an increase of motor activity. Both inhibitors significantly suppressed the stress fever. vL-NIO did not influence stress-induced rise in locomotor activity as well as did not change Tb in unstressed rats. Since aminoguanidine caused a transient fall in Tb below the baseline in rats exposed or not to open field and because this inhibitor suppressed stress-induced rise in locomotor activity, we concluded that nNOS expression inside the brain is critically involved in the rise in Tb due to exposure to psychological stress.
Nitric oxide (NO) has been shown to be an important mediator of febrile response to lipopolisaccharide (LPS). To clarify the role of different isoforms of NO synthase (NOS) in febrile response to immune challenge, effects of selective iNOS and nNOS inhibitors on fever to LPS were examined in freely moving biotelemetered rats. Vinyl-L-NIO (N5 - (1-Imino-3-butenyl) - ornithine (vL-NIO), a neuronal nitric oxide synthase (nNOS) inhibitor, and aminoguanidine hydrochloride, an inducible nitric oxide synthase (iNOS) inhibitor, were injected intracerebroventricularly at a dose of 10 µg/rat just before intraperitoneal injection of LPS at a dose of 50 µg/kg. Both inhibitors injected at a selected doses had no effect on normal day-time body temperature (Tb) and normal night-time Tb. vinyl-L-NIO and aminoguanidine injected intracerebroventricularly at a dose of 10 µg/animal suppressed the LPS-induced fever in rats. The fever index calculated for rats pretreated with v-LNIO or with aminoguanidine and injected with LPS was reduced by 43% and 72%, respectively, compared to that calculated for water-pretreated and LPS-injected rats. Whereas vL-NIO partly attenuated both phases of febrile rise in Tb, administration of aminoguanidine into the brain completely prevented fever induced by LPS. These data indicate that activation of iNOS inside the brain is not only responsible for triggering but also for maintaining of LPS-induced fever in rats. It is, therefore, reasonable to hypothesize that, activation of iNOS inside the brain is more important in fever development than activation of nNOS.
The purpose of this study was to investigate the role of neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS) in the brain during development of fever in response to localized tissue inflammation caused by injection of turpentine in freely moving biotelemetered rats. To determine the role of both NOSs in turpentine-induced fever, we injected vinyl-L-NIO (N5 – (1-Imino-3-butenyl) – ornithine (vL-NIO), a selective nNOS inhibitor, and aminoguanidine hydrochloride, a selective iNOS inhibitor, intracerebroventricularly (i.c.v.) 5 h after turpentine injection. Rats responded with fever to intramuscular injection of 20 µl of turpentine that commenced about 5 - 6 h after injection and reached peak value between 9 - 11 h post-turpentine. The inhibition of nNOS as well as iNOS in the brain did not affect fever induced by turpentine. Fevers in control rats (treated i.c.v. with pyrogen-free water) and iNOS or nNOS inhibitor-i.c.v. treated rats injected with turpentine were essentially the same. Furthermore, on the basis of these data, we concluded that iNOS and nNOS inside the brain do not participate in generation of fever to turpentine in rats.
The aim of the study was to investigate changes of internal temperature and locomotor activity of birds in conditions of endotoxin fever, pyrogenic tolerance and its suppression. The experiment was performed in pigeons (n = 12). On the first day of the experiment a state of endotoxin fever was evoked. The pigeons were categorized into two groups: experimental and control. The first group of the animals (n = 8) received Escherichia coli LPS intravenously once at the dose of 10 µg/kg b.w. whereas the control pigeons (n = 4) were administered in the apyrogenic saline intravenously once at the dose of 1 ml/kg b.w. On the second and third day of the experiment the state of pyrogenic tolerance was induced in the pigeons and their internal temperature and locomotor activity were investigated. To this end the experimental group of birds received E. coli LPS intravenously twice at 24 h intervals at a dose of 10 µg/kg b.w. Conversely, the control pigeons were twice treated with saline (1 ml/kg b.w.). On the fourth day of the study an attempt of pyrogenic tolerance suppression in the pigeons was carried out. The experimental birds with the stable state of pyrogenic tolerance were then categorized into two subgroups. The first subgroup (n = 4) received Salmonella Abortusequi LPS intravenously at the dose of 10 µg/kg b.w., whereas the second one (n = 4) - E. coli LPS at a double amount of the pyrogen (20 µg/kg b.w.). The control pigeons were administered S. Abortusequi LPS in an analogical dose as the first experimental subgroup. Results of the study indicated the occurrence of endotoxin fever and depression of locomotor activity of the pigeons in response to the first injection of E. coli LPS. The third administration of the pyrogen stabilized the state of pyrogenic tolerance, manifested by the reduction of the increased internal temperature and the stimulation of pigeon locomotor activity. Whereas in the state of stable pyrogenic tolerance in pigeons the intravenous injection of the other exogenous pyrogen, i.e. S. Abortusequi LPS, and also the double dose of E. coli pyrogen caused the suppression of the tolerance and the restoration of endotoxin fever in the birds.
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