AB

Bibliografia publikacji pracowników
Państwowej Szkoły Wyższej w Białej Podlaskiej

Baza tworzona przez Bibliotekę Akademii Bialskiej im. Jana Pawła II.


Zapytanie: SACHARCZUK MARIUSZ
Liczba odnalezionych rekordów: 15



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1/15
Autorzy: , , , .
Tytuł pracy:
Tytuł pracy w innym języku: MickaelSacharczukoriginal-articleF000.00993999009994.1001422-0067003Susceptibility to Pentylenetetrazole-Induced Seizures in Mice with Distinct Activity of the Endogenous Opioid SystemInternational Journal of Molecular Sciences20241422-00672023/202410.3390/ijms25136978Paszkiewicz, Justynaendogenous opioid systemFINAL_PUBLISHEDCurrently, pharmacotherapy provides successful seizure control in around 70% of patients with epilepsy; however, around 30% of cases are still resistant to available treatment. Therefore, effective anti-epileptic therapy still remains a challenge. In our study, we utilized two mouse lines selected for low (LA) and high (HA) endogenous opioid system activity to investigate the relationship between down- or upregulation of the opioid system and susceptibility to seizures. Pentylenetetrazole (PTZ) is a compound commonly used for kindling of generalized tonic-clonic convulsions in animal models. Our experiments revealed that in the LA mice, PTZ produced seizures of greater intensity and shorter latency than in HA mice. This observation suggests that proper opioid system tone is crucial for preventing the onset of generalized tonic-clonic seizures. Moreover, a combination of an opioid receptor antagonist-naloxone-and a GABA receptor agonist-diazepam (DZP)-facilitates a significant DZP-sparing effect. This is particularly important for the pharmacotherapy of neurological patients, since benzodiazepines display high addiction risk. In conclusion, our study shows a meaningful, protective role of the endogenous opioid system in the prevention of epileptic seizures and that disturbances in that balance may facilitate seizure occurrence.epilepsyseizures : Michel-Edward : Mariusz : Oryginalny artykuł naukowy : publikacja bezkosztowa : 998599140.0000140.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR140.000PUNKTACJA UWM : 009859.000 : Q : 003 : Vol. 25 : CC-BY
Charakterystyka formalna:
Język publikacji: 0184AOartykuł oryginalny naukowyPUBLIKACJAPEŁNA PUBLIKACJAAAartykuł w czasopiśmie z IF (wykaz MNiSW)AFILIACJA PODANAENGhttps://www.mdpi.com/1422-0067/25/13/6978100^a1422-0067^bQ^iX^jXY^kQ009159^a003^b003^c2024-07-08, 13:53^d2024-07-08, 13:54^e3023968886^f3023968885^aSusceptibility to Pentylenetetrazole-Induced Seizures in Mice with Distinct Activity of the Endogenous Opioid System^aInternational Journal of Molecular Sciences^a2024^bVol. 25^cissue 13^darticle number 6978^a1422-0067^a2023/2024^a10.3390/ijms25136978^aPaszkiewicz, Justyna^cy^aendogenous opioid system^aFINAL_PUBLISHED^bCC-BY^cAT_PUBLICATION^eOPEN_JOURNAL^aCurrently, pharmacotherapy provides successful seizure control in around 70% of patients with epilepsy; however, around 30% of cases are still resistant to available treatment. Therefore, effective anti-epileptic therapy still remains a challenge. In our study, we utilized two mouse lines selected for low (LA) and high (HA) endogenous opioid system activity to investigate the relationship between down- or upregulation of the opioid system and susceptibility to seizures. Pentylenetetrazole (PTZ) is a compound commonly used for kindling of generalized tonic-clonic convulsions in animal models. Our experiments revealed that in the LA mice, PTZ produced seizures of greater intensity and shorter latency than in HA mice. This observation suggests that proper opioid system tone is crucial for preventing the onset of generalized tonic-clonic seizures. Moreover, a combination of an opioid receptor antagonist-naloxone-and a GABA receptor agonist-diazepam (DZP)-facilitates a significant DZP-sparing effect. This is particularly important for the pharmacotherapy of neurological patients, since benzodiazepines display high addiction risk. In conclusion, our study shows a meaningful, protective role of the endogenous opioid system in the prevention of epileptic seizures and that disturbances in that balance may facilitate seizure occurrence.^aepilepsy^aseizures
Streszczenie:

2/15
Nr opisu: ga Piotr^bPiotr^c^d^e^f^g^h^i ^m_^n_^oReliga Piotr^pReliga Piotr^rReliga^sPiotr^u^t^qReliga P^w^x0000026524^zReliga Piotr^aThornetr^rReliga^sPiotr^u^t^qReliga P^w^x0000026524^zReliga Piotr^aThorne
Autorzy: , , .
Tytuł czasopisma:
Charakterystyka merytoryczna:
Język publikacji:
Wskaźnik Impact Factor ISI: artykuł w czasopiśmie z IF (wykaz MNiSW)AFILIACJA PODANAENGhttps://link.springer.com/article/10.1007/s12026-024-09514-4100^a0257-277X^bQ^e1559-0755^iX^jXY^kQ008122^a003^b003^c2024-08-08, 14:37^d2025-01-09, 14:44^e3022968802^f2929958795^aThe impact of BDNF and CD4 + T cell crosstalk on depression^aImmunologic Research^a2024^bVol. 72^cissue 5^dp.883--894^a0257-277X^b1559-0755^a2024/2025^a10.1007/s12026-024-09514-4^aPaszkiewicz, Justyna^cy^abrain-derived neurotrophic factor's (BDNF)^aKopia dostępna w Sekcji Bibliometrii.^aDepression represents a prevalent health concern since it affects approximately 350 million people of all ages worldwide [1, 2]. Both genders suffer from depression, albeit women are disproportionally affected by it more than men [3]. Notably, depression has the potential to impact individuals across various phases of their lifespan. Around 15% of adolescents aged 14 to 18 will encounter at least a single significant depressive episode [4]. Depression continues to be a concern within the elderly community. Namely, approximately 7% of individuals aged 60 and above experience symptoms of depression [5, 6]. These observations highlight that depression is pervasive in our society. Brain-derived neurotrophic factor's (BDNF) role in depression is highly affected by various factors [7,8,9]. BDNF is a neurotrophin known for its roles in synaptic plasticity, dendritic spine morphology, cognitive function, and mood regulation [10,11,12,13,14]. BDNF polymorphisms, such as Val66met, can significantly influence an individual's predisposition to depression [15,16,17,18,19,20]. Epigenetic alterations of BDNF, such as increase/decrease in DNA methylation at specific CpG sites, have recently emerged as relevant mechanisms promoting susceptibility to the development of depressive-like symptoms [21, 22]. These genetic and epigenetic factors are deeply intertwined with environmental influences, such as early-life experiences, social support, and exposure to stressors. Together, they contribute to the role of BDNF in the onset and progression of depression [23,24,25]. Recently, CD4 + T cells, a fundamental constituent of the adaptive immune system, have come under the attention of various research groups for their potential involvement in mediating neuroinflammatory processes that influence mood and cognition [26,27,28]. CD4 + T cells are a heterogeneous group of cells that include both pro- (e.g., Th1 and Th17) and anti-inflammatory cell types (e.g., Treg). CD4 + T cells can influence depression onset and development in various ways, including direct effects on neurons, astrocytes, and microglia through the production of cytokines and expressing receptors for molecules produced by brain cells [29,30,31,32,33]. BDNF seems to have a positive effect on CD4 + T cell proliferation and differentiation. However, our understanding of BDNF's effects on each cell type remains limited. Surprisingly, IL-17, which is produced by pro-inflammatory Th17 cells, and IL-4, which is produced by anti-inflammatory Tregs, both seem to increase BDNF production by astrocytes. The reason behind this counterintuitive phenomenon remains unknown. This review aims to investigate the mechanisms of interaction between CD4 + T cells and BDNF in the context of depression to acquire a deeper understanding of depression and the development of more effective therapies. Therefore, we first cover the role of BDNF in depression, followed by discussing what is currently known about the role of C^aCD4 + T cells^adepression
Punktacja ministerstwa:
Praca recenzowana
Słowa kluczowe ang.: ;
kuł w czasopiśmie z IF (wykaz MNiSW)AFILIACJA PODANAENGhttps://link.springer.com/article/10.1007/s12026-024-09514-4100^a0257-277X^bQ^e1559-0755^iX^jXY^kQ008122^a003^b003^c2024-08-08, 14:37^d2025-01-09, 14:44^e3022968802^f2929958795^aThe impact of BDNF and CD4 + T cell crosstalk on depression^aImmunologic Research^a2024^bVol. 72^cissue 5^dp.883--894^a0257-277X^b1559-0755^a2024/2025^a10.1007/s12026-024-09514-4^aPaszkiewicz, Justyna^cy^abrain-derived neurotrophic factor's (BDNF)^aKopia dostępna w Sekcji Bibliometrii.^aDepression represents a prevalent health concern since it affects approximately 350 million people of all ages worldwide [1, 2]. Both genders suffer from depression, albeit women are disproportionally affected by it more than men [3]. Notably, depression has the potential to impact individuals across various phases of their lifespan. Around 15% of adolescents aged 14 to 18 will encounter at least a single significant depressive episode [4]. Depression continues to be a concern within the elderly community. Namely, approximately 7% of individuals aged 60 and above experience symptoms of depression [5, 6]. These observations highlight that depression is pervasive in our society. Brain-derived neurotrophic factor's (BDNF) role in depression is highly affected by various factors [7,8,9]. BDNF is a neurotrophin known for its roles in synaptic plasticity, dendritic spine morphology, cognitive function, and mood regulation [10,11,12,13,14]. BDNF polymorphisms, such as Val66met, can significantly influence an individual's predisposition to depression [15,16,17,18,19,20]. Epigenetic alterations of BDNF, such as increase/decrease in DNA methylation at specific CpG sites, have recently emerged as relevant mechanisms promoting susceptibility to the development of depressive-like symptoms [21, 22]. These genetic and epigenetic factors are deeply intertwined with environmental influences, such as early-life experiences, social support, and exposure to stressors. Together, they contribute to the role of BDNF in the onset and progression of depression [23,24,25]. Recently, CD4 + T cells, a fundamental constituent of the adaptive immune system, have come under the attention of various research groups for their potential involvement in mediating neuroinflammatory processes that influence mood and cognition [26,27,28]. CD4 + T cells are a heterogeneous group of cells that include both pro- (e.g., Th1 and Th17) and anti-inflammatory cell types (e.g., Treg). CD4 + T cells can influence depression onset and development in various ways, including direct effects on neurons, astrocytes, and microglia through the production of cytokines and expressing receptors for molecules produced by brain cells [29,30,31,32,33]. BDNF seems to have a positive effect on CD4 + T cell proliferation and differentiation. However, our understanding of BDNF's effects on each cell type remains limited. Surprisingly, IL-17, which is produced by pro-inflammatory Th17 cells, and IL-4, which is produced by anti-inflammatory Tregs, both seem to increase BDNF production by astrocytes. The reason behind this counterintuitive phenomenon remains unknown. This review aims to investigate the mechanisms of interaction between CD4 + T cells and BDNF in the context of depression to acquire a deeper understanding of depression and the development of more effective therapies. Therefore, we first cover the role of BDNF in depression, followed by discussing what is currently known about the role of C^aCD4 + T cells^adepression

3/15
Nr opisu: cek^sTomas^u^t^qVanecek T^w^x0000036941^zVanecek Tomas^aPaszkiewicz
Autorzy: , , , Justyna Mariusz Piotr Oryginalny artykuł naukowy publikacja bezkosztowa 99929970.0000070.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR70.000PUNKTACJA UWM 009929.000 Q 003 Vol. 46 CC-BY PaszkiewiczSacharczukReligaoriginal-articleF000.00996100009996.2001467-3037003Using Copy Number Variation Data and Neural Networks to Predict Cancer Metastasis Origin Achieves High Area under the Curve Value with a Trade-Off in PrecisionCurrent Issues in Molecular Biology20241467-30452023/2024https://doi.org/10.3390/cimb46080490Paszkiewicz, JustynaaiFINAL_PUBLISHEDThe accurate identification of the primary tumor origin in metastatic cancer cases is crucial for guiding treatment decisions and improving patient outcomes. Copy number alterations (CNAs) and copy number variation (CNV) have emerged as valuable genomic markers for predicting the origin of metastases. However, current models that predict cancer type based on CNV or CNA suffer from low AUC values. To address this challenge, we employed a cutting-edge neural network approach utilizing a dataset comprising CNA profiles from twenty different cancer types. We developed two workflows: the first evaluated the performance of two deep neural networks-one ReLU-based and the other a 2D convolutional network. In the second workflow, we stratified cancer types based on anatomical and physiological classifications, constructing shallow neural networks to differentiate between cancer types within the same cluster. Both approaches demonstrated high AUC values, with deep neural networks achieving a precision of 60%, suggesting a mathematical relationship between CNV type, location, and cancer type. Our findings highlight the potential of using CNA/CNV to aid pathologists in accurately identifying cancer origins with accessible clinical tests.cancerclinical testcopy number variantgenomic markersmetastasisneural network, Justyna Mariusz Piotr Oryginalny artykuł naukowy publikacja bezkosztowa 99929970.0000070.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR70.000PUNKTACJA UWM 009929.000 Q 003 Vol. 46 CC-BY PaszkiewiczSacharczukReligaoriginal-articleF000.00996100009996.2001467-3037003Using Copy Number Variation Data and Neural Networks to Predict Cancer Metastasis Origin Achieves High Area under the Curve Value with a Trade-Off in PrecisionCurrent Issues in Molecular Biology20241467-30452023/2024https://doi.org/10.3390/cimb46080490Paszkiewicz, JustynaaiFINAL_PUBLISHEDThe accurate identification of the primary tumor origin in metastatic cancer cases is crucial for guiding treatment decisions and improving patient outcomes. Copy number alterations (CNAs) and copy number variation (CNV) have emerged as valuable genomic markers for predicting the origin of metastases. However, current models that predict cancer type based on CNV or CNA suffer from low AUC values. To address this challenge, we employed a cutting-edge neural network approach utilizing a dataset comprising CNA profiles from twenty different cancer types. We developed two workflows: the first evaluated the performance of two deep neural networks-one ReLU-based and the other a 2D convolutional network. In the second workflow, we stratified cancer types based on anatomical and physiological classifications, constructing shallow neural networks to differentiate between cancer types within the same cluster. Both approaches demonstrated high AUC values, with deep neural networks achieving a precision of 60%, suggesting a mathematical relationship between CNV type, location, and cancer type. Our findings highlight the potential of using CNA/CNV to aid pathologists in accurately identifying cancer origins with accessible clinical tests.cancerclinical testcopy number variantgenomic markersmetastasisneural network.
Tytuł równoległy: SacharczukReligaoriginal-articleF000.00996100009996.2001467-3037003Using Copy Number Variation Data and Neural Networks to Predict Cancer Metastasis Origin Achieves High Area under the Curve Value with a Trade-Off in PrecisionCurrent Issues in Molecular Biology20241467-30452023/2024https://doi.org/10.3390/cimb46080490Paszkiewicz, JustynaaiFINAL_PUBLISHEDThe accurate identification of the primary tumor origin in metastatic cancer cases is crucial for guiding treatment decisions and improving patient outcomes. Copy number alterations (CNAs) and copy number variation (CNV) have emerged as valuable genomic markers for predicting the origin of metastases. However, current models that predict cancer type based on CNV or CNA suffer from low AUC values. To address this challenge, we employed a cutting-edge neural network approach utilizing a dataset comprising CNA profiles from twenty different cancer types. We developed two workflows: the first evaluated the performance of two deep neural networks-one ReLU-based and the other a 2D convolutional network. In the second workflow, we stratified cancer types based on anatomical and physiological classifications, constructing shallow neural networks to differentiate between cancer types within the same cluster. Both approaches demonstrated high AUC values, with deep neural networks achieving a precision of 60%, suggesting a mathematical relationship between CNV type, location, and cancer type. Our findings highlight the potential of using CNA/CNV to aid pathologists in accurately identifying cancer origins with accessible clinical tests.cancerclinical testcopy number variantgenomic markersmetastasisneural network : Justyna : Mariusz : Piotr : Oryginalny artykuł naukowy : publikacja bezkosztowa : 99929970.0000070.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR70.000PUNKTACJA UWM : 009929.000 : Q : 003 : Vol. 46 : CC-BY
Tytuł czasopisma:
Charakterystyka merytoryczna:
Język publikacji:
Wskaźnik Impact Factor ISI:
Punktacja ministerstwa:
Praca recenzowana
Słowa kluczowe ang.: TACJA UWM^a009996.200^b009929.000^c009999.000^d009929.000202420242024Using Copy Number Variation Data and Neural Networks to Predict Cancer Metastasis Origin Achieves00000481150000000208AOartykuł oryginalny naukowyPUBLIKACJAPEŁNA PUBLIKACJAAAartykuł w czasopiśmie z IF (wykaz MNiSW)AFILIACJA PODANAENGhttps://www.mdpi.com/1467-3045/46/8/490100^a1467-3037^bQ^e1467-3045^iX^jXY^kQ004712^a003^b003^c2024-10-02, 10:59^d2024-11-22, 14:12^e3021029180^f3019828827^aUsing Copy Number Variation Data and Neural Networks to Predict Cancer Metastasis Origin Achieves High Area under the Curve Value with a Trade-Off in Precision^aCurrent Issues in Molecular Biology^a2024^bVol. 46^cissue 8^dp. 8301--8319^a1467-3045^a2023/2024^ahttps://doi.org/10.3390/cimb46080490^aPaszkiewicz, Justyna^cy^aai^aFINAL_PUBLISHED^bCC-BY^cAT_PUBLICATION^eOPEN_JOURNAL^aThe accurate identification of the primary tumor origin in metastatic cancer cases is crucial for guiding treatment decisions and improving patient outcomes. Copy number alterations (CNAs) and copy number variation (CNV) have emerged as valuable genomic markers for predicting the origin of metastases. However, current models that predict cancer type based on CNV or CNA suffer from low AUC values. To address this challenge, we employed a cutting-edge neural network approach utilizing a dataset comprising CNA profiles from twenty different cancer types. We developed two workflows: the first evaluated the performance of two deep neural networks-one ReLU-based and the other a 2D convolutional network. In the second workflow, we stratified cancer types based on anatomical and physiological classifications, constructing shallow neural networks to differentiate between cancer types within the same cluster. Both approaches demonstrated high AUC values, with deep neural networks achieving a precision of 60%, suggesting a mathematical relationship between CNV type, location, and cancer type. Our findings highlight the potential of using CNA/CNV to aid pathologists in accurately identifying cancer origins with accessible clinical tests.^acancer^aclinical test^acopy number variant^agenomic markers^ametastasis^aneural network
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4/15
Autorzy: , , .
Szczegóły:
Tytuł pracy w innym języku: PlewikGrudniewskiSacharczukoriginal-article997999009998.1000860-4037003Assessment of nanomechanical properties of Candida albicans as an element of the oral mycobiota in healthy subj : Dorota : Tomasz Marek : Mariusz : Oryginalny artykuł naukowyACPartykuł w czasopiśmie polskim0.900IF : 998999100.0000100.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR100.000PUNKTACJA UWM : 009899.000 : Q : 003
Charakterystyka wg MNiSW:
Słowa kluczowe ang.:

DOI:

5/15
Nr opisu:
Autorzy: , , .
Strony zajęte przez pracę:
Tytuł pracy w innym języku: TeodorowiczTokarska-RodakMichalukZarębskaPlewikGrudniewskiSacharczuk : Patrycja : Małgorzata : Estera : Marta : Dorota : Tomasz Marek : Mariusz
Charakterystyka formalna:
Charakterystyka merytoryczna:
Język publikacji:
Słowa kluczowe: k Dorota^bDorota^c017^dWNZS0101^eWNOZ^f0000000294^g^h^i*^j_^k_^lPlewik Dorota^pPlewik Dorota^rPLEWIK^sDOROTA^u^tZakład Pielęgniarstwa^qPlewik D^w^x0000017125^zPlewik Dorota^aGrudniewski
Słowa kluczowe ang.: ;

6/15
Autorzy: , , .
Tytuł pracy:
Tytuł pracy w innym języku: F018328.00993999009994.1001422-0067003Investigation of Mutated in Colorectal Cancer (MCC) Gene Family Evolution History Indicates a Putative Role in Th17/Treg DifferentiationInternational Journal of Molecular Sciences20231422-00672022/202310.3390/ijms241511940Paszkiewicz, Justynacolorectal cancerWpływ endogennego rozszczelnienia bariery krew-mózg w patogenezie zróżnicowanej podatności na inokulowanego czerniaka u linii myszy selekcjonowanych w kierunku wysokiej i niskiej analgezji postresowejFINAL_PUBLISHEDThe MCC family of genes plays a role in colorectal cancer development through various immunological pathways, including the Th17/Treg axis. We have previously shown that MCC1 but not MCC2 plays a role in Treg differentiation. Our understanding of the genetic divergence patterns and evolutionary history of the MCC family in relation to its function, in general, and the Th17/Treg axis, in particular, remains incomplete. In this investigation, we explored 12 species' genomes to study the phylogenetic origin, structure, and functional specificity of this family. In vertebrates, both MCC1 and MCC2 homologs have been discovered, while invertebrates have a single MCC homolog. We found MCC homologs as early as Cnidarians and Trichoplax, suggesting that the MCC family first appeared 741 million years ago (Ma), whereas MCC divergence into the MCC1 and MCC2 families occurred at 540 Ma. In general, we did not detect significant positive selection regulating MCC evolution. Our investigation, based on MCC1 structural similarity, suggests that they may play a role in the evolutionary changes in Tregs' emergence towards complexity, including the ability to utilize calcium for differentiation through the use of the EFH calcium-binding domain. We also found that the motif NPSTGE was highly conserved in MCC1, but not in MCC2. The NPSTGE motif binds KEAP1 with high affinity, suggesting an Nrf2-mediated function for MCC1. In the case of MCC2, we found that the "modifier of rudimentary" motif is highly conserved. This motif contributes to the regulation of alternative splicing. Overall, our study sheds light on how the evolution of the MCC family is connected to its function in regulating the Th17/Treg axis.differentiationevolutionTh17Treg : Oryginalny artykuł naukowy : utrzymanie i rozwój potencjału badawczego - art. 365 pkt 2 ustawy : 998599140.0000140.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR140.000PUNKTACJA UWM : 009859.000 : Q : 003 : Vol. 24 : Akademia Bialska im. Jana Pawła II w ramach Regulaminu wsparcia rozwoju zawodowego pracowników uczelni : CC-BY
Strony: F018328.00993999009994.1001422-0067003Investigation of Mutated in Colorectal Cancer (MCC) Gene Family Evolution History Indicates a Putative Role in Th17/Treg DifferentiationInternational Journal of Molecular Sciences20231422-00672022/202310.3390/ijms241511940Paszkiewicz, Justynacolorectal cancerWpływ endogennego rozszczelnienia bariery krew-mózg w patogenezie zróżnicowanej podatności na inokulowanego czerniaka u linii myszy selekcjonowanych w kierunku wysokiej i niskiej analgezji postresowejFINAL_PUBLISHEDThe MCC family of genes plays a role in colorectal cancer development through various immunological pathways, including the Th17/Treg axis. We have previously shown that MCC1 but not MCC2 plays a role in Treg differentiation. Our understanding of the genetic divergence patterns and evolutionary history of the MCC family in relation to its function, in general, and the Th17/Treg axis, in particular, remains incomplete. In this investigation, we explored 12 species' genomes to study the phylogenetic origin, structure, and functional specificity of this family. In vertebrates, both MCC1 and MCC2 homologs have bee, Oryginalny artykuł naukowy, utrzymanie i rozwój potencjału badawczego - art. 365 pkt 2 ustawy, 998599140.0000140.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR140.000PUNKTACJA UWM, 009859.000, Q, 003, Vol. 24, Akademia Bialska im. Jana Pawła II w ramach Regulaminu wsparcia rozwoju zawodowego pracowników uczelni, CC-BY, 009999.000, 2023-09-29, 13:32, issue 15, y, PB/5/2022, AT_PUBLICATION, 009859.000202320232023Investigation of Mutated in Colorectal Cancer (MCC) Gene Family Evolution History Indicates a Put00000464160000000342AOartykuł oryginalny naukowyPUBLIKACJAPEŁNA PUBLIKACJAAAartykuł w czasopiśmie z IF (wykaz MNiSW)AFILIACJA PODANAENGhttps://www.mdpi.com/1422-0067/24/15/11940100, 2024-06-25, 14:13, article number 11940
Seria: 8328.00993999009994.1001422-0067003, 998599140.0000140.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR140.000PUNKTACJA UWM, 009859.000, Q, 003, 009999.000, 2023-09-29, 13: ; 009859.000202320232023Investigation of Mutated in Colorectal Cancer (MCC) Gene Family Evolution History Indicates a Put00000464160000000342AOartykuł oryginalny naukowyPUBLIKACJAPEŁNA PUBLIKACJAAAartykuł w czasopiśmie z IF (wykaz MNiSW)AFILIACJA PODANAENGhttps://www.mdpi.com/1422-0067/24/15/11940100
Charakterystyka formalna: 22-0067^a2022/2023^a10.3390/ijms241511940^aPaszkiewicz, Justyna^cy^acolorectal cancer^aWpływ endogennego rozszczelnienia bariery krew-mózg w patogenezie zróżnicowanej podatności na inokulowanego czerniaka u linii myszy selekcjonowanych w kierunku wysokiej i niskiej analgezji postresowej^bAkademia Bialska im. Jana Pawła II w ramach Regulaminu wsparcia rozwoju zawodowego pracowników uczelni^cPB/5/2022^aFINAL_PUBLISHED^bCC-BY^cAT_PUBLICATION^eOPEN_JOURNAL^aThe MCC family of genes plays a role in colorectal cancer development through various immunological pathways, including the Th17/Treg axis. We have previously shown that MCC1 but not MCC2 plays a role in Treg differentiation. Our understanding of the genetic divergence patterns and evolutionary history of the MCC family in relation to its function, in general, and the Th17/Treg axis, in particular, remains incomplete. In this investigation, we explored 12 species' genomes to study the phylogenetic origin, structure, and functional specificity of this family. In vertebrates, both MCC1 and MCC2 homologs have been discovered, while invertebrates have a single MCC homolog. We found MCC homologs as early as Cnidarians and Trichoplax, suggesting that the MCC family first appeared 741 million years ago (Ma), whereas MCC divergence into the MCC1 and MCC2 families occurred at 540 Ma. In general, we did not detect significant positive selection regulating MCC evolution. Our investigation, based on MCC1 structural similarity, suggests that they may play a role in the evolutionary changes in Tregs' emergence towards complexity, including the ability to utilize calcium for differentiation through the use of the EFH calcium-binding domain. We also found that the motif NPSTGE was highly conserved in MCC1, but not in MCC2. The NPSTGE motif binds KEAP1 with high affinity, suggesting an Nrf2-mediated function for MCC1. In the case of MCC2, we found that the "modifier of rudimentary" motif is highly conserved. This motif contributes to the regulation of alternative splicing. Overall, our study sheds light on how the evolution of the MCC family is connected to its function in regulating the Th17/Treg axis.^adifferentiation^aevolution^aTh17^aTreg
Język publikacji: a2022/2023^a10.3390/ijms241511940^aPaszkiewicz, Justyna^cy^acolorectal cancer^aWpływ endogennego rozszczelnienia bariery krew-mózg w patogenezie zróżnicowanej podatności na inokulowanego czerniaka u linii myszy selekcjonowanych w kierunku wysokiej i niskiej analgezji postresowej^bAkademia Bialska im. Jana Pawła II w ramach Regulaminu wsparcia rozwoju zawodowego pracowników uczelni^cPB/5/2022^aFINAL_PUBLISHED^bCC-BY^cAT_PUBLICATION^eOPEN_JOURNAL^aThe MCC family of genes plays a role in colorectal cancer development through various immunological pathways, including the Th17/Treg axis. We have previously shown that MCC1 but not MCC2 plays a role in Treg differentiation. Our understanding of the genetic divergence patterns and evolutionary history of the MCC family in relation to its function, in general, and the Th17/Treg axis, in particular, remains incomplete. In this investigation, we explored 12 species' genomes to study the phylogenetic origin, structure, and functional specificity of this family. In vertebrates, both MCC1 and MCC2 homologs have been discovered, while invertebrates have a single MCC homolog. We found MCC homologs as early as Cnidarians and Trichoplax, suggesting that the MCC family first appeared 741 million years ago (Ma), whereas MCC divergence into the MCC1 and MCC2 families occurred at 540 Ma. In general, we did not detect significant positive selection regulating MCC evolution. Our investigation, based on MCC1 structural similarity, suggests that they may play a role in the evolutionary changes in Tregs' emergence towards complexity, including the ability to utilize calcium for differentiation through the use of the EFH calcium-binding domain. We also found that the motif NPSTGE was highly conserved in MCC1, but not in MCC2. The NPSTGE motif binds KEAP1 with high affinity, suggesting an Nrf2-mediated function for MCC1. In the case of MCC2, we found that the "modifier of rudimentary" motif is highly conserved. This motif contributes to the regulation of alternative splicing. Overall, our study sheds light on how the evolution of the MCC family is connected to its function in regulating the Th17/Treg axis.^adifferentiation^aevolution^aTh17^aTreg
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7/15
Nr opisu: na^pPaszkiewicz Justyna^rPASZKIEWICZ^sJUSTYNA^u^tZakład Pielęgniarstwa^qPaszkiewicz J^w930593^x0000013936^zPaszkiewicz Justyna^aTeodorowicz
Autorzy: , , , , Patrycja Tomasz Jarosław Olav Gina Mariusz Michel-Edwar Oryginalny artykuł naukowyACZartykuł w czasopiśmie zagranicznym2.800IF 99929970.0000070.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR70.000PUNKTACJA UWM 009929.000 Q 003 Vol. 45 CC-BY TeodorowiczKockiHorbańczukMandaSacharczukMickaeloriginal-article996100009996.2001467-3037003Investigation of the Molecular Evolution of Treg Suppresion Mechanisms Indicates a Covergent OriginCurrent Issues in Molecular Biology20231467-30452022/202310.3390/cimb45010042aiFINAL_PUBLISHEDRegulatory T cell (Treg) suppression of conventional T cells is a central mechanism that ensures immune system homeostasis. The exact time point of Treg emergence is still disputed. Furthermore, the time of Treg-mediated suppression mechanisms' emergence has not been identified. It is not yet known whether Treg suppression mechanisms diverged from a single pathway or converged from several sources. We investigated the evolutionary history of Treg suppression pathways using various phylogenetic analysis tools. To ensure the conservation of function for investigated proteins, we augmented our study using nonhomology-based methods to predict protein functions among various investigated species and mined the literature for experimental evidence of functional convergence. Our results indicate that a minority of Treg suppressor mechanisms could be homologs of ancient conserved pathways. For example, CD73, an enzymatic pathway known to play an essential role in invertebrates, is highly conserved between invertebrates and vertebrates, with no evidence of positive selection (w = 0.48, p-value < 0.00001). Our findings indicate that Tregs utilize homologs of proteins that diverged in early vertebrates. However, our findings do not exclude the possibility of a more evolutionary pattern following the duplication degeneration-complementation (DDC) model. Ancestral sequence reconstruction showed that Treg suppression mechanism proteins do not belong to one family; rather, their emergence seems to follow a convergent evolutionary pattern.evolutionmolecular evolutiontregs, Patrycja Tomasz Jarosław Olav Gina Mariusz Michel-Edwar Oryginalny artykuł naukowyACZartykuł w czasopiśmie zagranicznym2.800IF 99929970.0000070.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR70.000PUNKTACJA UWM 009929.000 Q 003 Vol. 45 CC-BY TeodorowiczKockiHorbańczukMandaSacharczukMickaeloriginal-article996100009996.2001467-3037003Investigation of the Molecular Evolution of Treg Suppresion Mechanisms Indicates a Covergent OriginCurrent Issues in Molecular Biology20231467-30452022/202310.3390/cimb45010042aiFINAL_PUBLISHEDRegulatory T cell (Treg) suppression of conventional T cells is a central mechanism that ensures immune system homeostasis. The exact time point of Treg emergence is still disputed. Furthermore, the time of Treg-mediated suppression mechanisms' emergence has not been identified. It is not yet known whether Treg suppression mechanisms diverged from a single pathway or converged from several sources. We investigated the evolutionary history of Treg suppression pathways using various phylogenetic analysis tools. To ensure the conservation of function for investigated proteins, we augmented our study using nonhomology-based methods to predict protein functions among various investigated species and mined the literature for experimental evidence of functional convergence. Our results indicate that a minority of Treg suppressor mechanisms could be homologs of ancient conserved pathways. For example, CD73, an enzymatic pathway known to play an essential role in invertebrates, is highly conserved between invertebrates and vertebrates, with no evidence of positive selection (w = 0.48, p-value < 0.00001). Our findings indicate that Tregs utilize homologs of proteins that diverged in early vertebrates. However, our findings do not exclude the possibility of a more evolutionary pattern following the duplication degeneration-complementation (DDC) model. Ancestral sequence reconstruction showed that Treg suppression mechanism proteins do not belong to one family; rather, their emergence seems to follow a convergent evolutionary pattern.evolutionmolecular evolutiontregs.
Tytuł czasopisma:
Charakterystyka formalna: Mariusz^u^t^qSacharczuk M^w^x0000026532^zSacharczuk Mariusz^aMickael
Charakterystyka merytoryczna:
Język publikacji:
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Punktacja ministerstwa:
Praca recenzowana
Słowa kluczowe ang.:

8/15
Autorzy: , , , .
Tytuł pracy:
Strony: RadziszewskiFraczekWolińskaPaszkiewiczReligaSacharczukF014101.00993999009994.1001422-0067003The Journey of Cancer Cells to the BrainInternational Journal of Molecular Sciences20231422-00672022/202310.3390/ijms24043854Paszkiewicz, JustynabraineFINAL_PUBLISHEDCancer metastases into the brain constitute one of the most severe, but not uncommon, manifestations of cancer progression. Several factors control how cancer cells interact with the brain to establish metastasis. These factors include mediators of signaling pathways participating in migration, infiltration of the blood-brain barrier, interaction with host cells (e.g., neurons, astrocytes), and the immune system. Development of novel therapies offers a glimpse of hope for increasing the diminutive life expectancy currently forecasted for patients suffering from brain metastasis. However, applying these treatment strategies has not been sufficiently effective. Therefore, there is a need for a better , Jakub, Karolina, Renata, Justyna, Piotr, Mariusz, utrzymanie i rozwój potencjału badawczego - art. 365 pkt 2 ustawy, 998599140.0000140.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR140.000PUNKTACJA UWM, 009859.000, Q, 003, Challenges and Opportunities, Vol. 24, CC-BY, , , , 017, , , 009999.000, 2023-03-15, 10:29, issue 4, y, AT_PUBLICATION, , , , WNZS0101, , , 009859.000202320232023Journey of Cancer Cells to the Brain Challenges and Opportunities00000450840000000466AOartykuł oryginalny naukowyPUBLIKACJAPEŁNA PUBLIKACJAAAartykuł w czasopiśmie z IF (wykaz MNiSW)AFILIACJA PODANAENGhttps://www.mdpi.com/1422-0067/24/4/3854100, 2024-06-25, 14:23, article number 3854
ISBN: Radziszewski
Charakterystyka formalna:
Język publikacji: arczuk Mariusz^bMariusz^c^d^e^f^g^h^i ^m_^n_^oSacharczuk Mariusz^pSacharczuk Mariusz^rSacharczuk^sMariusz^u^t^qSacharczuk M^w^x0000026532^zSacharczuk MariuszŁazarczyk Marzena Mickael Michel Edward Skiba Dominik Kurzejamska Ewa Ławiński Michał Horbańczuk Jarosław Olav^aF01^butrzymanie i rozwój potencjału badawczego - art. 365 pkt 2 ustawy^a4101.00^11ACZartykuł w czasopiśmie zagranicznym4.900IF^a993999^b998599140.0000140.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR140.000PUNKTACJA UWM^a009994.100^b009859.000^c009999.000^d009859.000202320232023Journey of Cancer Cells to the Brain Challenges and Opportunities00000450840000000466AOartykuł oryginalny naukowyPUBLIKACJAPEŁNA PUBLIKACJAAAartykuł w czasopiśmie z IF (wykaz MNiSW)AFILIACJA PODANAENGhttps://www.mdpi.com/1422-0067/24/4/3854100^a1422-0067^bQ^iX^jXY^kQ009159^a003^b003^c2023-03-15, 10:29^d2024-06-25, 14:23^e3127899210^f3024798816^aThe Journey of Cancer Cells to the Brain^bChallenges and Opportunities^aInternational Journal of Molecular Sciences^a2023^bVol. 24^cissue 4^darticle number 3854^a1422-0067^a2022/2023^a10.3390/ijms24043854^aPaszkiewicz, Justyna^cy^abraine^aFINAL_PUBLISHED^bCC-BY^cAT_PUBLICATION^eOPEN_JOURNAL^aCancer metastases into the brain constitute one of the most severe, but not uncommon, manifestations of cancer progression. Several factors control how cancer cells interact with the brain to establish metastasis. These factors include mediators of signaling pathways participating in migration, infiltration of the blood-brain barrier, interaction with host cells (e.g., neurons, astrocytes), and the immune system. Development of novel therapies offers a glimpse of hope for increasing the diminutive life expectancy currently forecasted for patients suffering from brain metastasis. However, applying these treatment strategies has not been sufficiently effective. Therefore, there is a need for a better understanding of the metastasis process to uncover novel therapeutic targets. In this review, we follow the journey of various cancer cells from their primary location through the diverse processes that they undergo to colonize the brain. These processes include EMT, intravasation, extravasation, and infiltration of the blood-brain barrier, ending up with colonization and angiogenesis. In each phase, we focus on the pathways engaging molecules that potentially could be drug target candidates.^acancer^aimmune cells^ametastasis
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Streszczenie:

9/15
Nr opisu: z^bMariusz^c^d^e^f^g^h^i ^m_^n_^oSacharczuk Mariusz^pSacharczuk Mariusz^rSacharczuk^sMariusz^u^t^qSacharczuk M^w^x0000026532^zSacharczuk MariuszLazarczyk Marzena Duda Kamil Mickael Michel Edward AK Onurhan Paszkiewicz Justyna Kowalczyk Agnieszka^aoriginal-article^bOryginalny artykuł naukowy^aF01^butrzymanie i rozwój potencjału badawczego - art. 365 pkt 2 ustawy^a1247.77^11ACZartykuł w czasopiśmie zagranicznym4.600IF^a994300^b998599140.0000140.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR140.000PUNKTACJA UWM^a009994.400^b009859.000^c009999.000^d009859.000202220222022Adera 2.0. A Drug Repurposing Workflow for Neuroimmunological Investigations Using Neural Network00000442170000000549AOartykuł oryginalny naukowyPUBLIKACJAPEŁNA PUBLIKACJAAAartykuł w czasopiśmie z IF (wykaz MNiSW)AFILIACJA PODANAENGhttps://www.mdpi.com/1420-3049/27/19/6453100^a1420-3049^bQ^iX^jXY^kQ014587^a003^b003^c2022-10-10, 13:28^d2024-04-17, 10:03^e3220948911^f3026879236^aAdera 2.0. A Drug Repurposing Workflow for Neuroimmunological Investigations Using Neural Networks^aMolecules^a2022^bVol. 27^cissue 19^darticle number 6453^a1420-3049^a2021/2022^a10.3390/molecules27196453^aPaszkiewicz, Justyna^cy^adeep neural network^aFINAL_PUBLISHED^bCC-BY^cAT_PUBLICATION^eOPEN_JOURNAL^aDrug repurposing in the context of neuroimmunological (NI) investigations is still in its primary stages. Drug repurposing is an important method that bypasses lengthy drug discovery procedures and focuses on discovering new usages for known medications. Neuroimmunological diseases, such as Alzheimer's, Parkinson's, multiple sclerosis, and depression, include various pathologies that result from the interaction between the central nervous system and the immune system. However, the repurposing of NI medications is hindered by the vast amount of information that needs mining. We previously presented Adera1.0, which was capable of text mining PubMed for answering query-based questions. However, Adera1.0 was not able to automatically identify chemical compounds within relevant sentences. To challenge the need for repurposing known medications for neuroimmunological diseases, we built a deep neural network named Adera2.0 to perform drug repurposing. The workflow uses three deep learning networks. The first network is an encoder and its main task is to embed text into matrices. The second network uses a mean squared error (MSE) loss function to predict answers in the form of embedded matrices. The third network, which constitutes the main novelty in our updated workflow, also uses a MSE loss function. Its main usage is to extract compound names from relevant sentences resulting from the previous network. To optimize the network function, we compared eight different designs. We found that a deep neural network consisting of an RNN neural network and a leaky ReLU could achieve 0.0001 loss and 67% sensitivity. Additionally, we validated Adera2.0's ability to predict NI drug usage against the DRUG Repurposing Hub database. These results establish the ability of Adera2.0 to repurpose drug candidates that can shorten the development of the drug cycle. The workflow could be download online.^adrug repu
Autorzy: , .
Tytuł pracy w innym języku: original-articleF011247.77994300009994.4001420-3049003Adera 2.0. A Drug Repurposing Workflow for Neuroimmunological Investigations Using Neural NetworksMolecules20221420-30492021/202210.3390/molecules27196453Paszkiewicz, Justynadeep neural networkFINAL_PUBLISHEDDrug repurposing in the context of neuroimmunological (NI) investigations is still in its primary stages. Drug repurposing is an important method that bypasses lengthy drug discovery procedures and focuses on discovering new usages for known medications. Neuroimmunological diseases, such as Alzheimer's, Parkinson's, multiple sclerosis, and depression, include various pathologies that result from the interaction between the central nervous system and the immune system. However, the repurposing of NI medications is hindered by the vast amount of information that needs mining. We previously presented Adera1.0, which was capable of text mining PubMed for answering query-based questions. However, Adera1.0 was not able to automatically identify chemical compounds within relevant sentences. To challenge the need for repurposing known medications for neuroimmunological diseases, we built a deep neural network named Adera2.0 to perform drug repurposing. The workflow uses three deep learning networks. The first network is an encoder and its main task is to embed text into matrices. The second network uses a mean squared error (MSE) loss function to predict answers in the form of embedded matrices. The third network, which constitutes the main novelty in our updated workflow, also uses a MSE loss function. Its main usage is to extract compound names from relevant sentences resulting from the previous network. To optimize the network function, we compared eight different designs. We found that a deep neural network consisting of an RNN neural network and a leaky ReLU could achieve 0.0001 loss and 67% sensitivity. Additionally, we validated Adera2.0's ability to predict NI drug usage against the DRUG Repurposing Hub data : Oryginalny artykuł naukowy : utrzymanie i rozwój potencjału badawczego - art. 365 pkt 2 ustawy : 998599140.0000140.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR140.000PUNKTACJA UWM : 009859.000 : Q : 003 : Vol. 27 : CC-BY
Tytuł czasopisma:
ISBN: Sacharczuk
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Praca recenzowana
Słowa kluczowe: 4-04-17, 10:03^e3220948911^f3026879236^aAdera 2.0. A Drug Repurposing Workflow for Neuroimmunological Investigations Using Neural Networks^aMolecules^a2022^bVol. 27^cissue 19^darticle number 6453^a1420-3049^a2021/2022^a10.3390/molecules27196453^aPaszkiewicz, Justyna^cy^adeep neural network^aFINAL_PUBLISHED^bCC-BY^cAT_PUBLICATION^eOPEN_JOURNAL^aDrug repurposing in the context of neuroimmunological (NI) investigations is still in its primary stages. Drug repurposing is an important method that bypasses lengthy drug discovery procedures and focuses on discovering new usages for known medications. Neuroimmunological diseases, such as Alzheimer's, Parkinson's, multiple sclerosis, and depression, include various pathologies that result from the interaction between the central nervous system and the immune system. However, the repurposing of NI medications is hindered by the vast amount of information that needs mining. We previously presented Adera1.0, which was capable of text mining PubMed for answering query-based questions. However, Adera1.0 was not able to automatically identify chemical compounds within relevant sentences. To challenge the need for repurposing known medications for neuroimmunological diseases, we built a deep neural network named Adera2.0 to perform drug repurposing. The workflow uses three deep learning networks. The first network is an encoder and its main task is to embed text into matrices. The second network uses a mean squared error (MSE) loss function to predict answers in the form of embedded matrices. The third network, which constitutes the main novelty in our updated workflow, also uses a MSE loss function. Its main usage is to extract compound names from relevant sentences resulting from the previous network. To optimize the network function, we compared eight different designs. We found that a deep neural network consisting of an RNN neural network and a leaky ReLU could achieve 0.0001 loss and 67% sensitivity. Additionally, we validated Adera2.0's ability to predict NI drug usage against the DRUG Repurposing Hub database. These results establish the ability of Adera2.0 to repurpose drug candidates that can shorten the development of the drug cycle. The workflow could be download online.^adrug repurposing^aneuro-immunology
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10/15
Nr opisu:
Autorzy: , .
Charakterystyka formalna:
Język publikacji: wnik projektu^aZakład Pielęgniarstwa, Wydział Nauk o Zdrowiu ABNS w Białej Podlaskiej; Zakład Farkamodynamiki -Warszawski Uniwersytet Medyczny; Zakład Genomiki Eksperymentalnej - Instytut Genetyki i Biotechnologii Zwierząt Polskiej Akademii Nauk w Jastrzębcu^aJednym z problemów przewlekłego przyjmowania opioidów w terapii bólu (szczególnie bólu nowotworowego) są zjawiska tolerancji i hiperalgezji poopioidowej. Wystąpienie tych niekorzystnych zjawisk jest najczęściej związane ze stosowaniem zbyt wysokich dawek preparatów o niezmodyfikowanym uwalnianiu, gdzie aktywacja mechanizmów molekularnych prowadzących do rozwoju tolerancji może wystąpić nawet po kilku dniach podawania leku. Przedmiotem badań jest identyfikacja potencjalnego mechanizmu stojącego za osłabieniem zjawiska tolerancji morfinowej przez disulfiram. Zgodnie z wynikami badań z ostatnich lat, disulfiram podawany jako koanalgetyk w przewlekłej terapii morfiną u zwierząt doświadczalnych całkowicie i długotrwale zahamował rozwój tolerancji morfinowej a także osłabił objawy odstawienne. Podobne działanie, zaobserwowano także u pacjentów poddawanych stymulacji kluczowej w hamowaniu bólu struktury nadrdzeniowej - istoty szarej okołowodociągowej. Jednakże, mechanizm zjawiska istotnego i długotrwałego hamowania tolerancji morfinowej przez disulfiram nie jest znany a większość dostępnych w literaturze hipotez znajduje się albo w sferze spekulacji albo nie zostało potwierdzonych.^adisulfiram^a35 000,00 zł^aAkademia Bialska Nauk Stosowanych im. Jana Pawła II w Białej Podlaskiej^cRegulamin wsparcia rozwoju zawodowego pracowników uczelni^adr hab. Anna Leśniak (Warszawski Uniwersytet Medyczny), wykonawca projektu^aośrodkowy układ nerwowy^aprof. dr hab. Mariusz Sacharczuk (Warszawski Uniwersytet Medyczny), wykonawca projektu^areceptor opioidowy^amgr Patrycja Teodorowicz, wykonawca projektu

11/15
Nr opisu:
Autorzy: , , dr Justyna Paszkiewicz, wykonawca projektuZakład Pielęgniarstwa, Wydział Nauk o Zdrowiu ABNS w Białej Podlaskiej; Zakład Farkamodynamiki -Warszawski Uniwersytet Medyczny; Zakład Genomiki Eksperymentalnej - Instytut Genetyki i Biotechnologii Zwierząt Polskiej Akademii Nauk w JastrzębcuPrzedstawiony projekt porusza słabo poznane procesy dotyczące mechanizmów przeciwdziałających neurodegeneracji i zaburzeniom neuroplastyczności wywołanymi urazem fizycznym, w szczególności roli w tym procesie układu opioiodowego. Uzyskane wyniki mogą stworzyć podstawy do opracowania skutecznych metod leczenia w przypadkach urazów ośrodkowego układu nerwowego wywołanych wypadkami komunikacyjnymi, działaniami terrorystycznymi czy wojennymi, kiedy dochodzi do indukcji chronicznych procesów neurodegeneracji oraz towarzyszących im procesom nieprawidłowej plastyczności. Celem projektu jest określenie różnic w ekspresji genów receptorów opioidowych w korze mózgu oraz hipokampie po wywołaniu łagodnego, urazowego uszkodzenia mózgu u myszy linii selekcjonowanych, w kierunku wysokiej (HA - high analgesia) i niskiej (LA - low analgesia) analgezji postresowej (SIA - stress-induced analgesia).Bdnf30 000,00 złAkademia Bialska Nauk Stosowanych im. Jana Pawła II w Białej Podlaskiejprof. dr hab. Mariusz Sacharczuk (Warszawski Uniwersytet Medyczny), wykonawca projektuneurotrofinydr hab. Anna Leśniak (Warszawski Uniwersytet Medyczny), wykonawca projektuNgfośrodkowy układ nerwowyreceptor opioidowy.
Charakterystyka formalna:
3.07.01^amgr Patrycja Teodorowicz, kierownik projektu^adr Justyna Paszkiewicz, wykonawca projektu^aZakład Pielęgniarstwa, Wydział Nauk o Zdrowiu ABNS w Białej Podlaskiej; Zakład Farkamodynamiki -Warszawski Uniwersytet Medyczny; Zakład Genomiki Eksperymentalnej - Instytut Genetyki i Biotechnologii Zwierząt Polskiej Akademii Nauk w Jastrzębcu^aPrzedstawiony projekt porusza słabo poznane procesy dotyczące mechanizmów przeciwdziałających neurodegeneracji i zaburzeniom neuroplastyczności wywołanymi urazem fizycznym, w szczególności roli w tym procesie układu opioiodowego. Uzyskane wyniki mogą stworzyć podstawy do opracowania skutecznych metod leczenia w przypadkach urazów ośrodkowego układu nerwowego wywołanych wypadkami komunikacyjnymi, działaniami terrorystycznymi czy wojennymi, kiedy dochodzi do indukcji chronicznych procesów neurodegeneracji oraz towarzyszących im procesom nieprawidłowej plastyczności. Celem projektu jest określenie różnic w ekspresji genów receptorów opioidowych w korze mózgu oraz hipokampie po wywołaniu łagodnego, urazowego uszkodzenia mózgu u myszy linii selekcjonowanych, w kierunku wysokiej (HA - high analgesia) i niskiej (LA - low analgesia) analgezji postresowej (SIA - stress-induced analgesia).^aBdnf^a30 000,00 zł^aAkademia Bialska Nauk Stosowanych im. Jana Pawła II w Białej Podlaskiej^cRegulamin wsparcia rozwoju zawodowego pracowników uczelni^aprof. dr hab. Mariusz Sacharczuk (Warszawski Uniwersytet Medyczny), wykonawca projektu^aneurotrofiny^adr hab. Anna Leśniak (Warszawski Uniwersytet Medyczny), wykonawca projektu^aNgf^aośrodkowy układ nerwowy^areceptor opioidowy

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13/15
Nr opisu: was designed to investigate the possibility that disturbances in G-protein signaling could explain the divergent response to opioid agonists. Supraspinal and spinal opioid sensitivity was assessed in vivo with intraperitoneal morphine and subsequent thermal stimulus exposure. The level of opioid receptor-mediated G-protein activation was investigated by means of DAMGO and morphine-stimulated [35S]GTPγS assay in the brain and spinal cord homogenates from HA and LA mice. Morphine (3-249 ľmol/kg, i.p) was over 6 - and 3 - times more potent in HA than LA mice in the hot plate and tail-flick assays, respectively. Additionally, HA mice showed elevated ß - endorphin levels in the brain. Enhanced efficacy of agonist-stimulated [35S]GTPγS binding was detected in opioid receptor-rich limbic regions of HA mice like the hypothalamus and hippocampus. Increased G-protein activity also emerged in the thalamus, periaqueductal gray matter and prefrontal cortex. In conclusion, the magnitude of the antinociceptive response to opioids in HA and LA mice is correlated with alterations in G-protein activation in brain regions responsible for integration and descending modulation of nociceptive information as well as at sites governing the emotional response to stressful stimuli.^aopioid system^aHA and LA mice^aG-protein activation
Autorzy: .
Tytuł pracy:
Uwagi: 0028-3908003Bidirectional selection for high and low stress-induced analgesia affects G-protein activityNeuropharmacology20190028-39082018/201910.1016/j.neuropharm.2018.10.014Strzemecka, JoannaantinociceptionKopia do
Miejsce:
Charakterystyka formalna:
Charakterystyka wg MNiSW: asopiśmie z IF (wykaz MNiSW)AFILIACJA PODANAENGPRACA RECENZOWANA100^a0028-3908^bQ^e1873-7064^iX^jXY^kQ014977^a003^b003^c2019-01-09, 09:28^d2020-06-30, 11:28^e3529959311^f3424749111^aBidirectional selection for high and low stress-induced analgesia affects G-protein activity^aNeuropharmacology^a2019^bVol. 144^cJanuary 2019^dp. 37--42^a0028-3908^b1873-7064^a2018/2019^a10.1016/j.neuropharm.2018.10.014^aStrzemecka, Joanna^cy^aantinociception^aKopia dostępna w Sekcji Bibliometrii.^aMice selected for high (HA) and low (LA) swim stress-induced analgesia (SSIA) are a unique model for studying the genetic background of this phenomenon. HA and LA miceshow substantial differences in the magnitude of the antinociceptive response to stress and when treated with exogenous opioids. However, the direct cause underplaying this distinctive feature has not yet been identified. The current study was designed to investigate the possibility that disturbances in G-protein signaling could explain the divergent response to opioid agonists. Supraspinal and spinal opioid sensitivity was assessed in vivo with intraperitoneal morphine and subsequent thermal stimulus exposure. The level of opioid receptor-mediated G-protein activation was investigated by means of DAMGO and morphine-stimulated [35S]GTPγS assay in the brain and spinal cord homogenates from HA and LA mice. Morphine (3-249 ľmol/kg, i.p) was over 6 - and 3 - times more potent in HA than LA mice in the hot plate and tail-flick assays, respectively. Additionally, HA mice showed elevated ß - endorphin levels in the brain. Enhanced efficacy of agonist-stimulated [35S]GTPγS binding was detected in opioid receptor-rich limbic regions of HA mice like the hypothalamus and hippocampus. Increased G-protein activity also emerged in the thalamus, periaqueductal gray matter and prefrontal cortex. In conclusion, the magnitude of the antinociceptive response to opioids in HA and LA mice is correlated with alterations in G-protein activation in brain regions responsible for integration and descending modulation of nociceptive information as well as at sites governing the emotional response to stressful stimuli.^aopioid system^aHA and LA mice^aG-protein activation
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Nr opisu: DELFIJSKAIMPACT FACTOR140.000PUNKTACJA UWM^a009995.944^b009859.000^c009999.000^d009859.000201920192019Divergent Response to Cannabinoid Receptor Stimulation in High and Low Stress-Induced Analgesia M00000367950000001238AOartykuł oryginalny naukowyPUBLIKACJAPEŁNA PUBLIKACJAAAartykuł w czasopiśmie z IF (wykaz MNiSW)AFILIACJA PODANAENGhttps://www.sciencedirect.com/science/article/abs/pii/S0306452219301174PRACA RECENZOWANA100^a0306-4522^bQ^e1873-7544^iX^jXY^kQ014996^a003^b003^c2019-02-25, 12:54^d2020-07-03, 14:26^e3528798985^f3424018813^aDivergent Response to Cannabinoid Receptor Stimulation in High and Low Stress-Induced Analgesia Mouse Lines Is Associated with Differential G-Protein Activation^aNeuroscience^a2019^bVol. 404^dp. 246--258^a0306-4522^a2018/2019^a10.1016/j.neuroscience.2019.02.015^aStrzemecka, Joanna^cy^acannabinoid system^aKopia dostępna w Sekcji Bibliometrii.^aBidirectional selection of mice for high (HA) and low (LA) swim stress-induced analgesia (SSIA) is associated with a divergent response to opioids. In the current study, we investigated whether the genetic divergence in opioid system activity between HA and LA mice also affects cannabinoid sensitivity. Additionally, we also investigated whether the endocannabinoid system mediates SSIA in these lines. Numerous reports support the existence of pharmacological and molecular interactions between the opioid and cannabinoid systems along the pain pathways, as both systems utilize the same G-protein subtype for signal transduction. Mice from both lines were treated with a non-selective CB1/CB2 agonist, WIN55,212-2 and their behavior was evaluated according to the tetrad paradigm assessing antinociception, catalepsy, hypothermia and locomotor activity. Surprisingly, the engagement of CB1 receptors in SSIA was not confirmed. G-protein activation was studied in different brain regions and the spinal cord in the [35S]GTP?S assay. It was shown that WIN55,212-2 produced more potent antinociception in HA than in LA mice. Also, HA mice displayed stronger cannabinoid-induced catalepsy in the bar test. However, LA mice were more sensitive to the hypothermic effect of WIN55,212-2. The intensity of behavioral responses to WIN55,212-2 was correlated with increased G-protein activation in the periaqueductal gray matter, frontal cortex, striatum and thalamus in HA mice. A weak response to WIN55,212-2 in LA mice could depend on impaired CB2 receptor signaling. In conclusion, differences in both opioid and cannabinoid sensitivity between HA and LA mice could s
Autorzy: , .
Tytuł pracy:
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Praca recenzowana
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Nr opisu: s-induced analgesia^aPrzegląd badań nad uzależnieniem od alkoholu w modelu myszy selekcjonowanych w kierunku wysokiej i niskiej analgezji postresowej^aHealth Problems of Civilization^a2018^bVol. 12^cissue 3^dp. 217--222^a2353-6942^b2354-0265^a10.5114/hpc.2018.76747^aStrzemecka, Joanna^cx^auzależnienie od alkoholu^aalcohol abuse^aFINAL_PUBLISHED^bCC-BY-NC-SA^cBEFORE_PUBLICATION^d1^eOPEN_JOURNAL^aDecades of studies on alcohol dependence showed that it is a very complex and multifactorial disorder. Several receptor systems are involved in development and susceptibility to alcohol abuse; however, there are some which play a crucial role in its pathogenesis, e.g. dopaminergic or opioid system. In this paper, an effort is made to explain the role of endogenous opioid system activity in alcohol dependence. To achieve the goal, we use a unique model is used which shows mice lines that are divergently selected for high (HA) and low (LA) stress-induced analgesia. This process allowed for selecting individuals characterised by hyperactive (HA) or hypoactive (LA) opioid system. Basing on the performed experiments, we proved that delta opioid receptors play a critical role in the development of addiction. The most notable achievement is an unspecific reaction of mice with the hyperactive opioid system to naloxone - an unspecific opioid system antagonist, which is currently approved in the pharmacotherapy of dependent patients.^aselekcjonowane linie myszy^aselected mouse lines^aUzależnienie od alkoholu jest chorobą wieloczynnikową, za której etiologię odpowiedzialnych jest kilka mechanizmów. Wieloletnie badania pozwoliły na zidentyfikowanie kilku układów receptorowych, które są zaangażowane w rozwój
Autorzy: , .
Tytuł pracy w innym języku: Przegląd badań nad uzależnieniem od alkoholu w modelu myszy selekcjonowanych w kierunku wysokiej i niskiej analgezji postresowejHealth Problems of Civilization20182353-694210.5114/hpc.2018.76747Strzemecka, Joannauzależnienie od alkoholualcohol abuseFINAL_PUBLISHEDDecades of studies on alcohol dependence showed that it is a very complex and multifactorial disorder. Several receptor systems are involved in development and susceptibility to alcohol abuse; however, there are some which play a crucial role in its pathogenesis, e.g. dopaminergic or opioid system. In this paper, an effort is made to explain the role of endogenous opioid system activity in alcohol dependence. To achieve the goal, we use a unique model is used which shows mice lines that are divergently selected for high (HA) and low (LA) stress-induced analgesia. This process allowed for selecting individuals characterised by hyperactive (HA) or hypoactive (LA) opioid system. Basing on the performed experiments, we proved that delta opioid receptors play a critical role in the development of addiction. The most notable achievement is an unspecific reaction of mice with the hyperactive opioid system to naloxone - an unspecific opioid system antagonist, which is currently approved in the pharmacotherapy of dependent patients.selekcjonowane linie myszyselected mouse linesUzależnienie od alkoholu jest chorobą wieloczynnikową, za której etiologię odpowiedzialnych jest kilka mechanizmów. Wieloletnie badania pozwoliły na zidentyfikowanie kilku układów receptorowych, które są zaangażowane w rozwój oraz podatność do uzależnienia od alkoholu, jednakże niektóre z nich odgrywają krytyczną rolę w jego patogenezie : Vol. 12 : 2354-0265 : CC-BY-NC-SA
Tytuł czasopisma:
Seria: Przegląd badań nad uzależnieniem od alkoholu w modelu myszy selekcjonowanych w kierunku wysokiej i niskiej analgezji postresowejHealth Problems of Civilization20182353-694210.5114/hpc.2018.76747Strzemecka, Joannauzależnienie od alkoholualcohol abuseFINAL_PUBLISHEDDecades of studies on alcohol dependence showed that it is a very complex and multifactorial disorder. Several receptor systems are involved in development and susceptibility to alcohol abuse; however, there are some which play a crucial role in its pathogenesis, e.g. dopaminergic or opioid system. In this paper, an effort is made to explain the role of endogenous opioid system activity in alcohol dependence. To achieve the goal, we use a unique model is used which shows mice lines that are divergentl, Vol. 12, 2354-0265, CC-BY-NC-SA, issue 3, x, BEFORE_PUBLICATION ; p. 217--222 ; 1, OPEN_JOURNAL
Wskaźnik Impact Factor ISI: that are divergently selected for high (HA) and low (LA) stress-induced analgesia. This process allowed for selecting individuals characterised by hyperactive (HA) or hypoactive (LA) opioid system. Basing on the performed experiments, we proved that delta opioid receptors play a critical role in the development of addiction. The most notable achievement is an unspecific reaction of mice with the hyperactive opioid system to naloxone - an unspecific opioid system antagonist, which is currently approved in the pharmacotherapy of dependent patients.^aselekcjonowane linie myszy^aselected mouse lines^aUzależnienie od alkoholu jest chorobą wieloczynnikową, za której etiologię odpowiedzialnych jest kilka mechanizmów. Wieloletnie badania pozwoliły na zidentyfikowanie kilku układów receptorowych, które są zaangażowane w rozwój oraz podatność do uzależnienia od alkoholu, jednakże niektóre z nich odgrywają krytyczną rolę w jego patogenezie np. układ dopaminergiczny lub opioidowy. W niniejszym artykule przedstawiamy wyniki badań, których celem było określenie roli endogennej aktywności układu opioidowego w uzależnieniu od alkoholu. Do realizacji tego celu wykorzystano unikalny model myszy selekcjonowanych w kierunku wysokiej (HA) oraz niskiej (LA) analgezji postresowej. Proces selekcji pozwolił na wybranie osobników charakteryzujących się wysoką (HA) oraz niską (LA) aktywnością układu opioidowego. Na podstawie przeprowadzonych eksperymentów, udowodniliśmy krytyczną rolę receptorów opioidowych typu delta w rozwoju uzależnienia od alkoholu. Godnym uwagi osiągnięciem było wykazanie niespecyficznej reakcji myszy o wysokiej aktywności układu opioidowego na nalokson - niespecyficznego antagonistę receptorów opioidowych, który jest aktualnie używany w farmakoterapii uzależnionych pacjentów.^aukład opioidowy^aopioid system
Punktacja ministerstwa: ^aPrzegląd badań nad uzależnieniem od alkoholu w modelu myszy selekcjonowanych w kierunku wysokiej i niskiej analgezji postresowej^aHealth Problems of Civilization^a2018^bVol. 12^cissue 3^dp. 217--222^a2353-6942^b2354-0265^a10.5114/hpc.2018.76747^aStrzemecka, Joanna^cx^auzależnienie od alkoholu^aalcohol abuse^aFINAL_PUBLISHED^bCC-BY-NC-SA^cBEFORE_PUBLICATION^d1^eOPEN_JOURNAL^aDecades of studies on alcohol dependence showed that it is a very complex and multifactorial disorder. Several receptor systems are involved in development and susceptibility to alcohol abuse; however, there are some which play a crucial role in its pathogenesis, e.g. dopaminergic or opioid system. In this paper, an effort is made to explain the role of endogenous opioid system activity in alcohol dependence. To achieve the goal, we use a unique model is used which shows mice lines that are divergently selected for high (HA) and low (LA) stress-induced analgesia. This process allowed for selecting individuals characterised by hyperactive (HA) or hypoactive (LA) opioid system. Basing on the performed experiments, we proved that delta opioid receptors play a critical role in the development of addiction. The most notable achievement is an unspecific reaction of mice with the hyperactive opioid system to naloxone - an unspecific opioid system antagonist, which is currently approved in the pharmacotherapy of dependent patients.^aselekcjonowane linie myszy^aselected mouse lines^aUzależnienie od alkoholu jest chorobą wieloczynnikową, za której etiologię odpowiedzialnych jest kilka mechanizmów. Wieloletnie badania pozwoliły na zidentyfikowanie kilku układów receptorowych, które są zaangażowane w rozwój oraz podatność do uzależnienia od alkoholu, jednakże niektóre z nich odgrywają krytyczną rolę w jego patogenezie np. układ dopaminergiczny lub opioidowy. W niniejszym artykule przedstawiamy wyniki badań, których celem było określenie roli endogennej aktywności układu opioidowego w uzależnieniu od alkoholu. Do realizacji tego celu wykorzystano unikalny model myszy selekcjonowanych w kierunku wysokiej (HA) oraz niskiej (LA) analgezji postresowej. Proces selekcji pozwolił na wybranie osobników charakteryzujących się wysoką (HA) oraz niską (LA) aktywnością układu opioidowego. Na podstawie przeprowadzonych eksperymentów, udowodniliśmy krytyczną rolę receptorów opioidowych typu delta w rozwoju uzależnienia od alkoholu. Godnym uwagi osiągnięciem było wykazanie niespecyficznej reakcji myszy o wysokiej aktywności układu opioidowego na nalokson - niespecyficznego antagonistę receptorów
Praca recenzowana
Słowa kluczowe ang.: selected for high and low stress-induced analgesia^aPrzegląd badań nad uzależnieniem od alkoholu w modelu myszy selekcjonowanych w kierunku wysokiej i niskiej analgezji postresowej^aHealth Problems of Civilization^a2018^bVol. 12^cissue 3^dp. 217--222^a2353-6942^b2354-0265^a10.5114/hpc.2018.76747^aStrzemecka, Joanna^cx^auzależnienie od alkoholu^aalcohol abuse^aFINAL_PUBLISHED^bCC-BY-NC-SA^cBEFORE_PUBLICATION^d1^eOPEN_JOURNAL^aDecades of studies on alcohol dependence showed that it is a very complex and multifactorial disorder. Several receptor systems are involved in development and susceptibility to alcohol abuse; however, there are some which play a crucial role in its pathogenesis, e.g. dopaminergic or opioid system. In this paper, an effort is made to explain the role of endogenous opioid system activity in alcohol dependence. To achieve the goal, we use a unique model is used which shows mice lines that are divergently selected for high (HA) and low (LA) stress-induced analgesia. This process allowed for selecting individuals characterised by hyperactive (HA) or hypoactive (LA) opioid system. Basing on the performed experiments, we proved that delta opioid receptors play a critical role in the development of addiction. The most notable achievement is an unspecific reaction of mice with the hyperactive opioid system to naloxone - an unspecific opioid system antagonist, which is currently approved in the pharmacotherapy of dependent patients.^aselekcjonowane linie myszy^aselected mouse lines^aUzależnienie od alkoholu jest chorobą wieloczynnikową, za której etiologię odpowiedzialnych jest kilka mechanizmów. Wieloletnie badania pozwoliły na zidentyfikowanie kilku układów receptorowych, które są zaangażowane w rozwój oraz podatność do uzależnienia od alkoholu, jednakże niektóre z nich odgrywają krytyczną rolę w jego patogenezie np. układ dopaminergiczny lub opioidowy. W niniejszym artykule przedstawiamy wyniki badań, których celem było określenie roli endogennej aktywności układu opioidowego w uzależnieniu od alkoholu. Do realizacji tego celu wykorzystano unikalny model myszy selekcjonowanych w kierunku wysokiej (HA) oraz niskiej (LA) analgezji postres ; divergently selected for high (HA) and low (LA) stress-induced analgesia. This process allowed for selecting individuals characterised by hyperactive (HA) or hypoactive (LA) opioid system. Basing on the performed experiments, we proved that delta opioid receptors play a critical role in the development of addiction. The most notable achievement is an unspecific reaction of mice with the hyperactive opioid system to naloxone - an unspecific opioid system antagonist, which is currently approved in the pharmacotherapy of dependent patients.^aselekcjonowane linie myszy^aselected mouse lines^aUzależnienie od alkoholu jest chorobą wieloczynnikową, za której etiologię odpowiedzialnych jest kilka mechanizmów. Wieloletnie badania pozwoliły na zidentyfikowanie kilku układów receptorowych, które są zaangażowane w rozwój oraz podatność do uzależnienia od alkoholu, jednakże niektóre z nich odgrywają krytyczną rolę w jego patogenezie np. układ dopaminergiczny lub opioidowy. W niniejszym artykule przedstawiamy wyniki badań, których celem było określenie roli endogennej aktywności układu opioidowego w uzależnieniu od alkoholu. Do realizacji tego celu wykorzystano unikalny model myszy selekcjonowanych w kierunku wysokiej (HA) oraz niskiej (LA) analgezji postresowej. Proces selekcji pozwolił na wybranie osobników charakteryzujących się wysoką (HA) oraz niską (LA) aktywnością układu opioidowego. Na podstawie przeprowadzonych eksperymentów, udowodniliśmy krytyczną rolę receptorów opioidowych typu delta w rozwoju uzależnienia od alkoholu. Godnym uwagi osiągnięciem było wykazanie niespecyficznej reakcji myszy o wysokiej aktywności układu opioidowego na nalokson - niespecyficznego antagonistę receptorów opioidowych, który jest aktualnie używany w farmakoterapii uzależnionych pacjentów.^aukład opioidowy^aopioid system
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