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Jarosław Całka

Bio: Jarosław Całka is an academic researcher from University of Warmia and Mazury in Olsztyn. The author has contributed to research in topics: Galanin & Enteric nervous system. The author has an hindex of 19, co-authored 125 publications receiving 1158 citations.


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Journal ArticleDOI
TL;DR: Both colitis and axotomy caused an increase in the number of GAL-LI nerve fibres in the circular muscle and mucosal layers as well as the appearance of a population of Gal-LI cells in the mucosa.
Abstract: This study reports on changes caused by chemically driven inflammation and axotomy in galanin-like immunoreactive (GAL-LI) nerve structures in the porcine descending colon. The distribution pattern of GAL-LI structures was studied using the immunofluorescence technique in the circular muscle layer, the myenteric (MP), outer submucous (OSP) and inner submucous plexuses (ISP), and also in the mucosal layer. Under physiological conditions GAL-LI perikarya were shown to constitute 3.68 ± 0.32%, 7.02 ± 0.93% and 10.99 ± 0.71% in MP, OSP and ISP, respectively. Both colitis and axotomy caused an increase in GAL-like immunoreactivity, which was different in particular parts of the bowel segment studied. The numbers of GAL-LI perikarya increased to 14.16 ± 0.49%, 16.78 ± 1.09% and 37.46 ± 1.18% during colitis and 7.92 ± 0.72%, 10.44 ± 0.71% and 16.20 ± 0.96% after axotomy in MP, OSP and ISP, respectively. Both these processes caused an increase in the number of GAL-LI nerve fibres in the circular muscle and mucosal layers as well as the appearance of a population of GAL-LI cells in the mucosa.

43 citations

Journal Article
TL;DR: An overview of the role of NO in hypothalamic control of LHRH and oxytocin release, aging of the L HRH and Oxytocin neurons and sexual behavior is provided.
Abstract: Nitric oxide (NO) affects reproductive processes both at the level of the brain and reproductive tract and this review is focused on its role as an essential regulator of the hypothalamic control of reproduction. The data gathered indicate that glutamate stimulates noradrenergic neurons which subsequently activate NO-ergic cells via alpha1-adrenergic receptors. The released NO diffuses into luteinizing hormone-releasing hormone (LHRH) terminals where it triggers LHRH secretion by activation of guanylyl cyclase and cyclooxygenase. The NO released by estrogen-stimulated NO-ergic ventromedial neurons plays a crucial role in the regulation of sexual behavior. Furthermore, an increased expression of inducible nitric oxide synthase in the LHRH and oxytocin neurons underlies the destructive action of NO on the aging of the hypothalamic neuroendocrine pathways. Within the hypothalamo-hypophyseal system, NO exerts an inhibitory effect in the control of oxytocin secretion. This action seems to employ an indirect mechanism by which NO may modulate the release of GABA. This review provides an overview of the role of NO in hypothalamic control of LHRH and oxytocin release, aging of the LHRH and oxytocin neurons and sexual behavior.

35 citations

Journal ArticleDOI
TL;DR: Results for the first time show that even low doses of zearalenone can affect the nerve fibers in the digestive tract and the number of nerve fibers immunoreactive to the majority of substances increased in experimental animals.
Abstract: The aim of this study was to investigate, whether low doses (25 % of no observable adverse effect levels values) of zearalenone (ZEN) can affect the expression of active substances in nerve fibers in the muscular layer of porcine ileum. The study was performed on ten immature pigs divided into two groups: experimental group (n = 5), where zearalenone (10 μg/kg body weight) was given for 42 days, and control animals (n = 5), where placebo was administered. Fragments of ileum of all animals were processed for single-labelling immunofluorescence technique using the antibodies against vasoactive intestinal peptide, neuronal form of nitric oxide synthase, cocaine and amphetamine regulatory peptide, galanin, pituitary adenylate cyclase-activating peptide-27 and substance P. The number of nerve fibers immunoreactive to particular substances was evaluated by the counting of nerves per observation field (0.1 mm2). Low doses of zearalenone caused the clear changes in the expression of substances studied. The number of nerve fibers immunoreactive to the majority of substances increased in experimental animals. The exception was only galanin, the expression of which was less after administration of zearalenone. The obtained results for the first time show that even low doses of zearalenone can affect the nerve fibers in the digestive tract.

34 citations

Journal ArticleDOI
TL;DR: Results show that even low doses of T-2 toxin may change the expression of CART in the ENS, one of enteric neuronal factors whose exact functions in the intestines still remain not fully explained.
Abstract: T-2 toxin is a mycotoxin produced by some Fusarium species, which may affect the synthesis of DNA and RNA and causes various pathological processes. Till now, the influence of T-2 toxin on the enteric nervous system (ENS) located in the wall of gastrointestinal tract has not been studied. On the other hand, cocaine- and amphetamine-regulated transcript (CART) is one of enteric neuronal factors, whose exact functions in the intestines still remain not fully explained. The present study describes the influence of low doses of T-2 toxin on CART-positive neuronal structures in porcine stomach, duodenum, and descending colon. Distribution of CART was studied using the double immunofluorescence technique in the plexuses of the ENS, as well as in nerve fibers within the circular muscle and mucosal layers of porcine gastrointestinal tract. Generally, after T-2 toxin administration the greater number of CART-LI structures were studied, but intensity of changes depended on part of the ENS and digestive tract fragment studied. The obtained results show that even low doses of T-2 toxin may change the expression of CART in the ENS.

33 citations

Journal ArticleDOI
TL;DR: The present study reports for the first time a detailed description of the CART distribution pattern within the enteric nervous system (ENS) of the porcine large intestine.
Abstract: The aim of the present study was to investigate the number of cocaine- and amphetamine-regulated transcript-like immunoreactive (CART-LI) nerve structures in the large intestine of juvenile pigs. The distribution pattern of CART-LI structures was studied by immunohistochemistry in the circular muscle layer, myenteric (MP), outer submucous (OSP) and inner submucous plexus (ISP) as well as in the mucosal layer of six regions of the large bowel: caecum, centripetal and centrifugal turns of the proximal colon, transverse colon, descending colon and rectum. CART-LI neural structures were observed in all gut fragments studied. CART-LI nerve fibres were numerous within the circular muscle layer and in the MP of all the regions studied, while they were moderate or few in number in other layers of the intestinal wall. The numbers of CART-LI neurons within the MP amounted to 2.02% in the caecum to 7.92% in the rectum, within the OSP from 2.73% in the centrifugal turns of the proximal colon to 5.70% in the rectum, and within the ISP from 2.23% in the transverse colon to 5.32% in the centrifugal turns of the proximal colon. The present study reports for the first time a detailed description of the CART distribution pattern within the enteric nervous system (ENS) of the porcine large intestine.

30 citations


Cited by
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Journal ArticleDOI
TL;DR: Developmental changes in several neurotransmitter systems controlling pulsatile LHRH release are extensively reviewed and it appears that the reduction in tonic GABA inhibition allows an increase in the release of glutamate as well as other neurotransmitters, which contributes to the increase in pubertal L HRH release.
Abstract: An increase in pulsatile release of LHRH is essential for the onset of puberty. However, the mechanism controlling the pubertal increase in LHRH release is still unclear. In primates the LHRH neurosecretory system is already active during the neonatal period but subsequently enters a dormant state in the juvenile/prepubertal period. Neither gonadal steroid hormones nor the absence of facilitatory neuronal inputs to LHRH neurons is responsible for the low levels of LHRH release before the onset of puberty in primates. Recent studies suggest that during the prepubertal period an inhibitory neuronal system suppresses LHRH release and that during the subsequent maturation of the hypothalamus this prepubertal inhibition is removed, allowing the adult pattern of pulsatile LHRH release. In fact, y-aminobutyric acid (GABA) appears to be an inhibitory neurotransmitter responsible for restricting LHRH release before the onset of puberty in female rhesus monkeys. In addition, it appears that the reduction in tonic GABA inhibition allows an increase in the release of glutamate as well as other neurotransmitters, which contributes to the increase in pubertal LHRH release. In this review, developmental changes in several neurotransmitter systems controlling pulsatile LHRH release are extensively reviewed.

528 citations

Journal ArticleDOI
TL;DR: Recent studies on brain circulation provide quite useful information concerning the physiological roles of NO produced by constitutive isoforms of nitric-oxide synthase and how NO may promote cerebral pathogenesis under certain conditions, including cerebral ischemia/stroke, cerebral vasospasm after subarachnoid hemorrhage, and brain injury.
Abstract: Nitric oxide (NO) is undoubtedly quite an important intercellular messenger in cerebral and peripheral hemodynamics. This molecule, formed by constitutive isomers of NO synthase, endothelial nitric-oxide synthase, and neuronal nitric-oxide synthase, plays pivotal roles in the regulation of cerebral blood flow and cell viability and in the protection of nerve cells or fibers against pathogenic factors associated with cerebral ischemia, trauma, and hemorrhage. Cerebral blood flow is increased and cerebral vascular resistance is decreased by NO derived from endothelial cells, autonomic nitrergic nerves, or brain neurons under resting and stimulated conditions. Somatosensory stimulation also evokes cerebral vasodilatation mediated by neurogenic NO. Oxygen and carbon dioxide alter cerebral blood flow and vascular tone mainly via constitutively formed NO. Endothelial dysfunction impairs cerebral hemodynamics by reducing the bioavailability of NO and increasing the production of reactive oxygen species (ROS). The NO-ROS interaction is an important issue in discussing blood flow and cell viability in the brain. Recent studies on brain circulation provide quite useful information concerning the physiological roles of NO produced by constitutive isoforms of nitric-oxide synthase and how NO may promote cerebral pathogenesis under certain conditions, including cerebral ischemia/stroke, cerebral vasospasm after subarachnoid hemorrhage, and brain injury. This information would contribute to better understanding of cerebral hemodynamic regulation and its dysfunction and to development of novel therapeutic measures to treat diseases of the central nervous system.

343 citations

Journal ArticleDOI
TL;DR: The findings identify a potent mechanism for nervous system regulation of host defense responses in inflammation and immunity and since neuropeptides can be released from peripheral nerve endings into surrounding tissues.
Abstract: Two groups of mediators, the neuropeptides substance P and K and the monocyte-derived cytokines, interact in the neural regulation of immunological and inflammatory responses. Substance P, substance K, and the carboxyl-terminal peptide SP(4-11) induce the release of interleukin-1, tumor necrosis factor-alpha, and interleukin-6 from human blood monocytes. The neuropeptide effects occur at low doses, are specific as shown by inhibition studies with a substance P antagonist, and require de novo protein synthesis. Since monocyte-derived cytokines regulate multiple cellular functions in inflammation and immunity and since neuropeptides can be released from peripheral nerve endings into surrounding tissues, these findings identify a potent mechanism for nervous system regulation of host defense responses.

336 citations

01 Jan 2013
TL;DR: This meta-analytical study reviewed the literature on the short- and long-term release of components from resin-based dental materials, and to determine how much of those components may leach out in the oral cavity.
Abstract: OBJECTIVES Resin-based dental materials are not inert in the oral environment, and may release components, initially due to incomplete polymerization, and later due to degradation. Since there are concerns regarding potential toxicity, more precise knowledge of the actual quantity of released eluates is necessary. However, due to a great variety in analytical methodology employed in different studies and in the presentation of the results, it is still unclear to which quantities of components a patient may be exposed. The objective of this meta-analytical study was to review the literature on the short- and long-term release of components from resin-based dental materials, and to determine how much (order of magnitude) of those components may leach out in the oral cavity. METHODS Out of an initial set of 71 studies, 22 were included. In spite of the large statistical incertitude due to the great variety in methodology and lack of complete information (detection limits were seldom mentioned), a meta-analytical mean for the evaluated eluates was calculated. To relate the amount of potentially released material components with the size of restorations, the mean size of standard composite restorations was estimated using a 3D graphical program. RESULTS While the release of monomers was analyzed in many studies, that of additives, such as initiators, inhibitors and stabilizers, was seldom investigated. Significantly more components were found to be released in organic than in water-based media. Resin-based dental materials might account for the total burden of orally ingested bisphenol A, but they may release even higher amounts of monomers, such as HEMA, TEGDMA, BisGMA and UDMA. Compared to these monomers, similar or even higher amounts of additives may elute, even though composites generally only contain very small amounts of additives. A positive correlation was found between the total quantity of released eluates and the volume of extraction solution. SIGNIFICANCE There is a clear need for more accurate and standardized analytical research to determine the long-term release from resin-based materials. Several guidelines for standardization are proposed.

317 citations

Journal ArticleDOI
01 Sep 2007-Glia
TL;DR: The activation of Ca2+ activated K+ channels in astrocyte endfeet and the efflux of K+ has also been suggested to modify vascular tone by hyperpolarization and relaxation of smooth muscle cells (SMCs), indicating that more work is needed to clarify the contributions ofAstrocytes to vascular dynamics under different cellular conditions.
Abstract: The control of cerebral vessel diameter is of fundamental importance in maintaining healthy brain function because it is critical to match cerebral blood flow (CBF) to the metabolic demand of active neurons. Recent studies have shown that astrocytes are critical players in the regulation of cerebral blood vessel diameter and that there are several molecular pathways through which astrocytes can elicit these changes. Increased intracellular Ca 21 in astrocytes has demonstrated a dichotomy in vasomotor responses by causing the constriction as well as the dilation of neighboring blood vessels. The production of arachidonic acid (AA) in astrocytes by Ca 21 sensitive phospholipase A2 (PLA2) has been shown to be common to both constriction and dilation mechanisms. Constriction results from the conversion of AA to 20-hydroxyeicosatetraenoic acid (20-HETE) and dilation from the production of prostaglandin E2 (PGE2) or epoxyeicosatrienoic acid (EET) and the level of nitric oxide (NO) appears to dictate which of these two pathways is recruited. In addition the activation of Ca 21 activated K 1 channels in astrocyte endfeet and the efflux of K 1 has also been suggested to modify vascular tone by hyperpolarization and relaxation of smooth muscle cells (SMCs). The wide range of putative pathways indicates that more work is needed to clarify the contributions of astrocytes to vascular dynamics under different cellular conditions. Nonetheless it is clear that astrocytes are important albeit complicated regulators of CBF. V C 2007 Wiley-Liss, Inc.

305 citations