Anna Leja-Szpak

Dr. Anna Leja-Szpak


Research Focus & Metrics

Academic Career Length

24Years (2003-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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Verified
Journal Article
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JJJolanta Jaworek
Jolanta Jaworek
ALAnna Leja-Szpak
Anna Leja-Szpak
KNKatarzyna Nawrot-Porąbka
Katarzyna Nawrot-Porąbka
JSJoanna Szklarczyk
Joanna Szklarczyk
MKMiroslawa Kot
Miroslawa Kot
JBJoanna Bonior
Joanna Bonior
Melatonin is an indoleamine produced from the amino acid l-tryptophan, whereas metabolites of melatonin are known as kynuramines. One of the best-known kynuramines is N1-acetyl-N1-formyl-5-methoxykynuramine (AFMK). Melatonin has attracted scientific attention as a potent antioxidant and protector of tissue against oxidative stress. l-Tryptophan and kynuramines share common beneficial features with melatonin. Melatonin was originally discovered as a pineal product, has been detected in the gastrointestinal tract, and its receptors have been identified in the pancreas. The role of melatonin in the pancreatic gland is not explained, however several arguments support the opinion that melatonin is probably implicated in the physiology and pathophysiology of the pancreas. (1) Melatonin stimulates pancreatic enzyme secretion through the activation of entero-pancreatic reflex and cholecystokinin (CCK) release. l-Tryptophan and AFMK are less effective than melatonin in the stimulation of pancreatic exocrine function; (2) Melatonin is a successful pancreatic protector, which prevents the pancreas from developing of acute pancreatitis and reduces pancreatic damage. This effect is related to its direct and indirect antioxidant action, to the strengthening of immune defense, and to the modulation of apoptosis. Like melatonin, its precursor and AFMK are able to mimic its protective effect, and it is commonly accepted that all these substances create an antioxidant cascade to intensify the pancreatic protection and acinar cells viability; (3) In pancreatic cancer cells, melatonin and AFMK activated a signal transduction pathway for apoptosis and stimulated heat shock proteins. The role of melatonin and AFMK in pancreatic tumorigenesis remains to be elucidated.

Verified
Journal Article
Open access
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JBJoanna Bonior
Joanna Bonior
ZWZygmunt Warzecha
Zygmunt Warzecha
Piotr CeranowiczPiotr Ceranowicz
Piotr Ceranowicz
RGRyszard Gajdosz
Ryszard Gajdosz
PPPiotr Pierzchalski
Piotr Pierzchalski
JJJolanta Jaworek
Jolanta Jaworek
Ghrelin was shown to exhibit protective and therapeutic effect in the gut. Aim of the study was to investigate the role of sensory nerves (SN) in the protective effect of ghrelin in acute pancreatitis (AP). Studies were performed on male Wistar rats or isolated pancreatic acinar cells. After capsaicin deactivation of sensory nerves (CDSN) or treatment with saline, rats were pretreated intraperitoneally with ghrelin or saline. In those rats, AP was induced by cerulein or pancreases were used for isolation of pancreatic acinar cells. Pancreatic acinar cells were incubated in cerulein-free or cerulein containing solution. In rats with intact SN, pretreatment with ghrelin led to a reversal of the cerulein-induced increase in pancreatic weight, plasma activity of lipase and plasma concentration of tumor necrosis factor-α (TNF-α). These effects were associated with an increase in plasma interleukin-4 concentration and reduction in histological signs of pancreatic damage. CDSN tended to increase the severity of AP and abolished the protective effect of ghrelin. Exposure of pancreatic acinar cells to cerulein led to increase in cellular expression of mRNA for TNF-α and cellular synthesis of this cytokine. Pretreatment with ghrelin reduced this alteration, but this effect was only observed in acinar cells obtained from rats with intact SN. Moreover, CDSN inhibited the cerulein- and ghrelin-induced increase in gene expression and synthesis of heat shock protein 70 (HSP70) in those cells. Ghrelin exhibits the protective effect in cerulein-induced AP on the organ and pancreatic acinar cell level. Sensory nerves ablation abolishes this effect.

1 December 2018 in Pharmacological Reports
Verified
Journal Article
Closed access
ALAnna Leja-Szpak
Anna Leja-Szpak
KNKatarzyna Nawrot-Porąbka
Katarzyna Nawrot-Porąbka
MGMarta Góralska
Marta Góralska
MJMartyna Jastrzębska
Martyna Jastrzębska
PLPaweł Link-Lenczowski
Paweł Link-Lenczowski
JJJolanta Jaworek
Jolanta Jaworek

1 April 2019 in Pancreatology
Verified
Journal Article
Closed access
JJJolanta Jaworek
Jolanta Jaworek
JSJoanna Szklarczyk
Joanna Szklarczyk
MKMichalina Kot
Michalina Kot
MGMarta Góralska
Marta Góralska
AJAndrzej Jaworek
Andrzej Jaworek
PPPiotr Pierzchalski
Piotr Pierzchalski

GPGrazyna Puto
Grazyna Puto
MJMaria Jurzec
Maria Jurzec
ALAnna Leja-Szpak
Anna Leja-Szpak
JBJoanna Bonior
Joanna Bonior
MMMarta Muszalik
Marta Muszalik
AGAgnieszka Gniadek
Agnieszka Gniadek
Introduction: Working during the COVID-19 pandemic is a particular challenge for nurses because, while performing their daily routines, they are exposed to physical and social consequences of the SARS-CoV-2 virus, which is accompanied by intensified stress. The aim of this study was to assess the intensity of stress and coping strategies applied by nurses working with both infected and non-infected patients with SARS-CoV-2 virus during the COVID-19 pandemic. Materials and Methods: The study was conducted between January and March 2021. Due to the epidemiological situation, the questionnaire was posted on Facebook in nurses’ groups and sent out via the “Messenger” and “WhatsApp” applications. Stress intensity was assessed by means of the Perceived Stress Scale (PSS-10), whereas coping strategies were assessed using the Mini-COPE stress coping inventory. Results: Among 151 surveyed nurses, more than half (52.3%) worked with infected patients and the remaining ones (47.7%) worked with non-infected patients. The level of stress perceived by nurses working with infected patients was higher than among nurses working with patients without SARS-CoV-2 infection (22.22 ± 5.94 vs. 20.21 ± 5.68, p = 0.03). The nurses working with infected patients were most likely to choose coping strategies focused on the problem (2.00 ± 0.62) and emotions (2.01 ± 0.69), whereas those working with non-infected patients usually chose strategies focused only on the problem (2.11 ± 0.58). Conclusions: During the COVID-19 pandemic, nurses working with SARS-CoV-2 patients experienced more intense stress than those working with non-infected patients. Nurses working with SARS-CoV-2 patients tended to cope with stress using strategies focused on the problem and on emotions, while those working with non-infected patients were more likely to choose strategies focused only on the problem.

Verified
Journal Article
Open access
PDF file
JBJoanna Bonior
Joanna Bonior
Piotr CeranowiczPiotr Ceranowicz
Piotr Ceranowicz
RGRyszard Gajdosz
Ryszard Gajdosz
Beata Kuśnierz-CabalaBeata Kuśnierz-Cabala
Beata Kuśnierz-Cabala
PPPiotr Pierzchalski
Piotr Pierzchalski
JJJolanta Jaworek
Jolanta Jaworek
Ghrelin (GHRL) is an endogenous ligand for the growth hormone secretagogue receptor (GHS-R). Experimental studies showed that GHRL protects the stomach and pancreas against acute damage, but the effect of GHRL on pancreatic acinar cells was still undetermined. Aim: To investigate the effect of GHRL and caerulein on the functional ghrelin system in pancreatic acinar cells taking into account the role of sensory nerves (SN). Methods: Experiments were carried out on isolated pancreatic acinar cells and AR42J cells. Before acinar cells isolation, GHRL was administered intraperitoneally at a dose of 50 µg/kg to rats with intact SN or with capsaicin deactivation of SN (CDSN). After isolation, pancreatic acinar cells were incubated in caerulein-free or caerulein containing solution. AR42J cells were incubated under basal conditions and stimulated with caerulein, GHRL or a combination of the above. Results: Incubation of isolated acinar cells with caerulein inhibited GHS-R and GHRL expression at the level of mRNA and protein in those cells. Either in rats with intact SN or with CDSN, administration of GHRL before isolation of acinar cells increased expression of GHRL and GHS-R in those cells and reversed the caerulein-induced reduction in expression of those parameters. Similar upregulation of GHS-R and GHRL was observed after administration of GHRL in AR42J cells. Conclusions: GHRL stimulates its own expression and expression of its receptor in isolated pancreatic acinar cells and AR42J cells on the positive feedback pathway. This mechanism seems to participate in the pancreatoprotective effect of GHRL in the course of acute pancreatitis.