Preferencje help
Polish version English version Język
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 15

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
1

Badania nad właściwościami szczepów laseczki larwy (Bacillus larvae White) występujących na terenie woj. opolskiego

100%
Mika J.
Medycyna Weterynaryjna
|
1968
|
tom 24
|
nr 07
2
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Glej - wróg czy przyjaciel?

100%
Mika J.
Wszechświat
|
2014
|
tom 115
|
nr 01-03
3

Teoria wiotkich budowli piętrzących

100%
Mika J.
Zeszyty Naukowe Akademii Rolniczej we Wrocławiu. Melioracja
|
1991
|
nr 39
4

Spinal microglia activation-importance for chronic pain

100%
Mika J.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr Suppl.1
Pain may now be considered a neuro-immune disorder, since it is known that the activation of immune and immune-like glial cells in the dorsal root ganglia and spinal cord results in the release of both pro- and anti-inflammatory cytokines, as well as algesic and analgesic mediators. Our studies underline an important role of cytokines (IL-1alfa, IL-1beta, IL-4, IL-6, IL-10, IL-18, fractalkine and CCL2); complement components (C1q); metaloproteinases (MMP-2, -9) and many other factors, which become activated under neuropathic pain. Another novel approach for controlling neuropathic pain can be pharmacological attenuation of glial and immune cell activation. It has been found that propentofylline, pentoxifylline, fluorocitrate and minocycline suppress the development of neuropathic pain. The other way of pain control can be inhibition of transcription factor synthesis (NF-kappaB); kinase synthesis (p38MAPK) and protease activation (MMP9). Additionally, since it is known that the opioid-induced glial activation opposes opioid analgesia, some glial inhibitors, which are safe and clinically well tolerated, are proposed as potential useful ko-analgesic agents for opioid treatment of neuropathic pain. Our results support the idea that targeting microglial activation represents a novel and clinically promising method for enhancing analgesic effects of opioids in neuropathic pain. Acknowledgments: Supported by grant 2011/03/B/NZ4/00042 and statutory funds.
5

Eksperymentalne badania wiotkich budowli piętrzących

63%
Mika J., Woloszyn J.
Zeszyty Naukowe Akademii Rolniczej we Wrocławiu. Melioracja
|
1990
|
nr 37
6

Changes of plant water defiit under various environmental factors

51%
Kostrej A., Danko J., Mika J.
Acta Physiologiae Plantarum
|
1998
|
tom 20
|
nr 1 suppl.
7

Effect of reserpine or 6-OHDA on NPY and CRF expression and synthesis in rat amygdala

51%
Smialowska M., Bajkowska M., Mika J., Przewlocka B.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
8

The influence of alkylresorcinols on phospholipase A2 activity

51%
Czajkowska D., Mika J., Stasiuk M., Kozubek A.
Cellular and Molecular Biology Letters
|
2005
|
tom 10
|
nr Suppl.
9

Involvement of endogenous opiold systems in neuropathic pain

45%
Mika J., Schafer M. K.-H., Przewlocki R., Weihe E., Przewlocka B.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
10

The role of microglia cells activation in the effects of opioids

39%
Popiolek-Barczyk K., Rojewska E., Zychowska M., Makuch V., Przewlocka B., Mika J.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Development of neuropathic pain is accompanied by many changes in immune and glial cells. These changes correspond to activation of immune and glial cells that have been shown to influence the opioid effectiveness and can be modulated by minocycline (a potent inhibitor of microglial activation). In earlier study we have demonstrated that function of opioidergic neurons may be modulated by the immune system. These changes have been shown to be responsible for the efficacy of opioids. The aim of our study was to examine the effect of the minocycline-triggered inhibition of microglia activation on the injury-induced changes and the efficacy of mu and delta opioid receptor ligands in a rat model of neuropathic pain (chronic constriction injury to the sciatic nerve). In cell culture studies, we examined the influence of opioids (morphine, DAMGO, DPDPE, deltorphin II) on activated primary cultured rat microglia by using MTT and/or NO assays. All experiments were performed according to the IASP recommendations and were approved by a local Bioethics Committee. On the spinal cord level the injury to the sciatic nerve induced an up-regulation of IL-1beta, IL-6 expression, CX3CR1 and C1q (marker of microglia, macrophage and leukocyte activation). Chronic administration of minocycline not only diminished neuropathic pain-related behavior and C1q-positive cell activation, but also attenuate the changes in proinflammatory factors like IL1beta, IL-6 and CX3CR1 in the spinal cord and DRG. In in vivo experiments, the analgesic effects of mu-opioid (morphine and DAMGO), but not delta-opioid (DPDPE, deltorphin II) receptor ligands were lower in the rats under neuropathic pain. Moreover, the analgesic effects of morphine and DAMGO, but not DPDPE and deltorphin II were significantly potentiated by minocycline chronic administration. Our in vitro findings that non-stimulated microglia cells respond differently to opioids in comparisons with stimulated cells as measured by MTT and/or NO assays, corresponded well with the results of in vivo studies. Our study underlined that inhibition of microglial activation could differently influence analgesic effects of mu- but not delta-opioid ligands in injury-induced pathologies, which may influence the effect of various opioid drugs used in chronic pain therapy.
11

Hanges of genes expression in the nucleus accumbens during neuropathic pain in mouse brain

39%
Wawrzczak-Bargiela A., Ziołkowska B., Bilecki W., Rojewska E., Mika J., Przewlocka B., Przewlocki R.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
12

Minocycline affects neuropathic pain by regulation of kynurenic pathway – role of microglial cells

39%
Rojewska E., Piotrowska A., Jurga A. M., Makuch W., Przewlocka B., Mika J.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
The participation of kynurenine system in the pathology of neurodegenerative and autoimmune diseases was studied, but the significance of this pathway in neuropathic pain have been poorly studied. The kynurenine pathway has already been shown to exist mainly in macrophages and microglia. Growing evidence suggests that spinal microglia are crucial in the neuropathic pain. Minocycline, a microglial inhibitor, is a substances with diverse mechanisms of action that modulate the neuroimmune system have been shown to relieve neuropathic pain. The aim of our study was to examine the role of kynurenine 3-monooxygenase (Kmo) in a rat model of neuropathy. Chronic constriction injury (CCI) of the sciatic nerve was performed according to Bennett and Xie (1988). Behavioral studies consisted of the tactile and thermal hypersensitivity measurements, biochemical studies comprised the RT-PCR and/or Western blot analysis in the tissue (spinal cord, DRG) and primary glia cultures. The experiments were carried out according to IASP rules. Using microarray and qRT-PCR methods, we showed that intraperitoneal administration of minocycline decreased neuropathic pain in rats and in parallel the spinal 3-monooxygenase kynurenine expression (Kmo). Further, minocycline administration diminished the lipopolysaccharide (LPS)-induced upregulation of Kmo mRNA in primary microglial cell cultures. Moreover, we verified that not only indirect inhibition of Kmo using minocycline but also direct inhibition using Kmo inhibitors (JM6,Ro61-6048) decreased neuropathic pain intensity. Ro61-6048 administration reduced in the spinal cord and/or the DRG the protein levels of IBA-1, IL-6, IL-1beta and NOS2. Interestingly, Kmo inhibitors potentiated the analgesic properties of morphine. Summing up, our results suggest that the kynurenine pathway is an important mediator of neuropathic pain pathology. FINANCIAL SUPPORT: Supported by National Science Centre grant-Sonata 2015/17/D/NZ4/02284 and statutory funds. AP is a scholarship holder from the KNOW sponsored by Ministry of Science and Higher Education, Republic of Poland.
13

Changes of genes expression in the nucleus accumbens during neuropathic pain in mouse brain

39%
Wawrzczak-Bargiela A., Ziołkowska B., Bilecki W., Rojewska E., Mika J., Przewlocka B., Przewlocki R.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: The nucleus accumbens (NAc), which is known to be an important component of the mesolimbic dopaminergic reward system also plays a role in pain, however the molecular mechanisms of this involvement are not known. In the present study we explored molecular pathways involved in the neuropathic pain. Understanding of this process would allow us brain mapping and find biomarkers for pain transmission. AIM(S): The aim of this study was to investigate the alterations in genes expression after CCI in the NAc. METHOD(S): Neuropathic pain was induced by applying a Chronic Constriction Injury (CCI) model in C57BL/6J mice. Two behavioral tests for neuropathic pain were used: the von Frey’s test and the cold plate test. In our biochemical researches we used qRT-PCR. RESULTS: We found that nerve injury produced a significant increase in the expression of opioid genes (PDYN, PENK), opioid kappa and delta receptors genes (KOR, DOR) and calcium/calmodulin - dependent protein kinase kinase 1 (CAMKK1) in the nucleus accumbens. Furthermore, we observed that neuropathic pain augmented the expression of stress – and inflammatory response genes coding for the glucocorticoid receptor (GR), FK506 binding protein5 (FKBP5), and interleukins IL1 beta and IL6 in the nucleus accumbens. Moreover, elevated levels of GFAP (astrocyte marker) but not C1q (microglia marker) mRNAs were detected. CONCLUSIONS: Our results demonstrate that CCI produces lasting biochemical changes in the NAc.Taking into account the well-known roles of opioid systems in pain transmission and emotional processes, the observed changes in the expression of the opioid propeptides and receptors genes may contribute to changes in pain sensitivity and in affective response to nociceptive stimulation. Furhermore, increased expression of GFAP, GR, FKBP5, Il6 and Il1beta genes suggests that cellular stress and inflammatory processes are involved in this type of pain not only on the level of the spinal cord but also in the brain. FINANCIAL SUPPORT: Research supported by HEALTH-F2-2013-602891 NEUROPAIN.
14
Content available remote

Comparison of gene expression profiles in neuropathic and inflammatory pain

39%
Rodriguez Parkitna J., Korostynski M., Kaminska-Chowaniec D., Obara I., Mika J., Przewlocka B., Przewlocki R.
Journal of Physiology and Pharmacology
|
2006
|
tom 57
|
nr 3
Molecular mechanisms underlying the differences between chronic neuropathic and inflammatory pain are still poorly understood. Identifying those differences should provide insight into the molecular mechanism underlying features unique for neuropathic pain, such as allodynia. We have performed screening for differentially expressed genes in the spinal cord in the rat models of neuropathic and inflammatory pain. Using BD Atlas Rat 4K arrays we found several differences in expression of secretion-related genes between inflammatory and neuropathic pain. Development of the latter was characterized by up-regulated expression of genes associated with immune response and microglia activation and also, to a lesser extent, with cytoskeleton rearrangement. The relative increase in abundance of four genes, intercellular adhesion molecule 1 (ICAM-1), calcitonin gene related peptide (CGRP), tissue inhibitor of metalloproteinase 1 (TIMP-1), chemokine-like receptor 1 was confirmed by reverse transcription Real-Time PCR (qPCR) validation in the spinal cord in neuropathic pain. Levels of transcripts corresponding to ICAM-1 and TIMP-1 were also increased in the dorsal root ganglia (DRG) of neuropathic rats. Our data point at the importance of immune response- and microglia activation-related genes in the development of chronic neuropathic pain, and suggest that expression of CGRP gene in the dorsal horn of the spinal cord could be involved in persistence of its symptoms.
15

Involvement of FosB protein in various behavior

33%
Solecki W., Krowka T., Kubik J., Osikowicz M., Mika J., Wozniak G., Kaczmarek L., Przewlocka B., Przewlocki R.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.