Public Relations in the Perspective of the Catholic Church in Poland

The issue of the use of marketing tools by religious organisations is a research problem because for moral reasons, churches declare that they do not use marketing communication explicitly. In religious circles, marketing tends to be associated with unethical practices, especially public relations, which in practice can be associated with propaganda. A careful analysis of the activities carried out by churches shows that many marketing communication methods and tools are used by religious organisations. To be successful, companies must identify the basic elements determining customer satisfaction and meet them more effectively than their competitors. At the same time, it is not about one-off transactions, but about building long-term relationships. This model is also slowly finding acceptance in religious circles, despite arguments that satisfying individual needs will be at the expense of church doctrine or will result in long-standing church traditions being abandoned and replaced by pop-cultural attitudes. The article discusses the specificity of building the brand image of the Catholic Church in Poland and the use of modern marketing tools in this process. It also presents the results of the authors’ research, which leads to the final conclusions verifying the research hypotheses set out in the research methodology. The article aims to initiate a wider discussion on the controversial topic of implementing commercial marketing tools into the image management processes of the Catholic Church. The conducted research results indicate the need for a change in the perception of the Catholic Church in Poland of the communication processes leading to the building and strengthening of its image. A major challenge for the Catholic Church in Poland seems to be changing the attitudes of non-believers towards the Catholic Church

Endoplasmic Reticulum Stress Underlies Nanosilver-Induced Neurotoxicity in Immature Rat Brain

The growing production of silver nanoparticles (AgNPs), and their widespread use in medical and consumer products, poses a potential threat to the environment and raises questions about biosafety. Immature organisms are particularly susceptible to various insults during development. The biological characteristics of immature organisms are different from those of adults, and dictate the consequences of exposure to various toxic substances, including AgNPs. Nanoparticles are highly reactive and can easily cross the blood–brain barrier (BBB) to accumulate in brain tissues. It is therefore important to investigate the molecular mechanisms of AgNP-induced neurotoxicity in the developing brain. Immature 2-week-old rats were exposed to a low dose of AgNPs (0.2 mg/kg b.w.) over a long period. Subsequently, brain tissues of the animals were subjected to ultrastructural and molecular analyses to determine endoplasmic reticulum (ER) stress. Ultrastructural markers of ER stress, such as pathological alterations in the ER and elongated forms of mitochondria accompanied by autophagy structures, were confirmed to be present in AgNP-exposed rat brain. Evidence for induction of ER stress in neurons was also provided by molecular markers. Upregulation of genes related to the ER-stress-induced unfolded protein response (UPR) pathway, such as GRP78, PERK, and CHOP ATF-6, was observed at the transcriptional and translational levels. The results show that prolonged exposure of immature rats to a low dose of AgNPs during the developmental period leads to induction of ER stress in the neurons of the developing brain. Simultaneously, in response to AgNP-induced ER stress, neurons promote protective mechanisms that partially compensate for ER stress by regulating the biodynamic processes of mitochondria and autophagy

Memantine Modulates Oxidative Stress in the Rat Brain following Experimental Autoimmune Encephalomyelitis

Experimental autoimmune encephalomyelitis (EAE) is an animal model most commonly used in research on the pathomechanisms of multiple sclerosis (MS). The inflammatory processes, glutamate excitotoxicity, and oxidative stress have been proposed as determinants accompanying demyelination and neuronal degeneration during the course of MS/EAE. The aim of the current study was to characterize the role of NMDA receptors in the induction of oxidative stress during the course of EAE. The effect of memantine, the uncompetitive NMDA receptor antagonist, on modulation of neurological deficits and oxidative stress in EAE rats was analyzed using several experimental approaches. We demonstrated that the expression of antioxidative enzymes (superoxide dismutases SOD1 and SOD2) were elevated in EAE rat brains. Under the same experimental conditions, we observed alterations in oxidative stress markers such as increased levels of malondialdehyde (MDA) and decreased levels of sulfhydryl (-SH) groups, both protein and non-protein (indicating protein damage), and a decline in reduced glutathione. Importantly, pharmacological inhibition of ionotropic NMDA glutamate receptors by their antagonist memantine improved the physical activity of EAE rats, alleviated neurological deficits such as paralysis of tail and hind limbs, and modulated oxidative stress parameters (MDA, -SH groups, SOD’s). Furthermore, the current therapy aiming to suppress NMDAR-induced oxidative stress was partially effective when NMDAR’s antagonist was administered at an early (asymptomatic) stage of EAE

Early and Delayed Impact of Nanosilver on the Glutamatergic NMDA Receptor Complex in Immature Rat Brain

Silver nanoparticles (AgNPs) are the one of the most extensively used nanomaterials. The strong antimicrobial properties of AgNPs have led to their use in a wide range of medical and consumer products. Although the neurotoxicity of AgNPs has been confirmed, the molecular mechanisms have not been extensively studied, particularly in immature organisms. Based on information gained from previous in vitro studies, in the present work, we examine whether ionotropic NMDA glutamate receptors contribute to AgNP-induced neurotoxicity in an animal model of exposure. In brains of immature rats subjected to a low dose of AgNPs, we identified ultrastructural and molecular alterations in the postsynaptic region of synapses where NMDA receptors are localized as a multiprotein complex. We revealed decreased expression of several NMDA receptor complex-related proteins, such as GluN1 and GluN2B subunits, scaffolding proteins PSD95 and SynGAP, as well as neuronal nitric oxide synthase (nNOS). Elucidating the changes in NMDA receptor-mediated molecular mechanisms induced by AgNPs, we also identified downregulation of the GluN2B-PSD95-nNOS-cGMP signaling pathway which maintains LTP/LTD processes underlying learning and memory formation during development. This observation is accompanied by decreased density of NMDA receptors, as assessed by a radioligand binding assay. The observed effects are reversible over the post-exposure time. This investigation reveals that NMDA receptors in immature rats are a target of AgNPs, thereby indicating the potential health hazard for children and infants resulting from the extensive use of products containing AgNPs

Characterization of the EAE animal model and the clinical parameters of EAE rats prior to and after treatment with antagonists of glutamatergic receptors.

<p>The values represent the means ± SD. *P<0.05 indicates significant differences compared with the EAE rats. Combined administration of LY 367385 or MPEP in combination with the NMDAR antagonists (amantadine and memantine) did not influence the neurological deficits or the condition of the experimental rats during the course of the disease. The neurological deficits and condition of the examined animals were the same as in the case of treatment with amantadine or memantine exclusively (data not presented). CI – cumulative index.</p><p>Characterization of the EAE animal model and the clinical parameters of EAE rats prior to and after treatment with antagonists of glutamatergic receptors.</p

Glutamate release from synaptosomes (A) and GPV fraction (B) obtained from control, EAE, EAE+amantadine, EAE+memantine, EAE+LY367385, and EAE+MPEP rat brains during the acute phase of the disease (12 d.p.i.).

<p>Bars present total radioactivity in pellet (KCl no added), radioactivity remaining in pellet after depolarization by KCl (pellet radioactivity), and released of [³H] glutamate radioactivity from pellet after depolarization by KCl. Membranes were depolarized with 50 mM KCl at a maximum of the uptake curves (6 min), and radioactivity was assayed after 6 min. Results represent the means ± SD from five separate experiments performed in triplicate; * P<0.05 significantly different from the spontaneous release control group; # P<0.05 vs. EAE rats not subjected to therapy (Student's t-test).</p