Publications by authors named "Katarzyna Zalewska"

15 Publications

  • Page 1 of 1

Stercoral perforation requiring a total colectomy: a challenging and extreme case.

ANZ J Surg 2021 Jan 6. Epub 2021 Jan 6.

General Surgery Department, Rockhampton Hospital, Rockhampton, Queensland, Australia.

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http://dx.doi.org/10.1111/ans.16556DOI Listing
January 2021

The interaction between cuticle free fatty acids (FFAs) of the cockroaches Blattella germanica and Blatta orientalis  and hydrolases produced by the entomopathogenic fungus Conidiobolus coronatus.

PLoS One 2020 9;15(7):e0235785. Epub 2020 Jul 9.

National Institute of Public Health-National Institute of Hygiene, Warsaw, Poland.

The interactions between entomopathogenic fungi and insects serve a classic example of a co-evolutionary arms race between pathogens and their target host. The cuticle, site of the first contact between insects and entomopathogenic fungus, is an important defensive barrier against pathogens. It is covered by a layer of lipids that appears to play a key role in these processes and cuticular free fatty acid (FFA) profiles are consider as a determinant of susceptibility, or resistance, to fungal infections. These profiles are species-specific. The cockroaches Blattella germanica (Blattodea: Blattidae) and Blatta orientalis (Blattodea: Ectobiidae) are unsusceptible to the soil fungus Conidiobolus coronatus (Entomophthorales: Ancylistaceae) infection, therefore we studied the profiles of FFAs in order to understand the defensive capabilities of the cockroaches. The fungus was cultivated for three weeks in minimal medium. Cell-free filtrate was obtained, assayed for elastase, N-acetylglucosaminidase, chitobiosidase and lipase activity, and then used for in vitro hydrolysis of the cuticle from wings and thoraces of adults and oothecae. The amounts of amino acids, N-glucosamine and FFAs released from the hydrolysed cuticle samples were measured after eight hours of incubation. The FFA profiles of the cuticle of adults, and the wings, thoraces and oothecae of both species were established using GC-MS and the results were correlated with the effectiveness of fungal proteases, chitinases and lipases in the hydrolyzation of cuticle samples. Positive correlations would suggest the existence of compounds used by the fungus as nutrients, whereas negative correlations may indicate that these compounds could be engaged in insect defence.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0235785PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7347226PMC
September 2020

Aerobic exercise and consecutive task-specific training (AExaCTT) for upper limb recovery after stroke: A randomized controlled pilot study.

Physiother Res Int 2019 Jul 3;24(3):e1775. Epub 2019 Apr 3.

Priority Research Centre for Physical Activity and Nutrition, University of Newcastle, Callaghan, NSW, Australia.

Objective: This study examined the feasibility of a parallel-group assessor-blinded randomized controlled trial investigating whether task-specific training preceded by aerobic exercise (AEX + TST) improves upper limb function more than task-specific training (TST) alone.

Methods: People with upper limb motor dysfunction after stroke were allocated to TST or AEX + TST. Both groups were prescribed 60 hr of TST over 10 weeks (3 × 1-hr sessions with a therapist per week and 3 × 1 hr of home-based self-practice per week). The AEX + TST group performed 30 minutes of aerobic exercise immediately prior to the 1 hr of TST with the therapist. Recruitment, adherence, retention, participant acceptability, and adverse events were recorded. Clinical measures were performed prerandomization at baseline, on completion of the intervention, and at 1- and 6-month follow-up.

Results: Fifty-nine persons after stroke were screened, 42 met the eligibility criteria, and 20 (11 male; mean [SD] age: 55.4 [16.0] years; time since stroke: 71.7 [91.2] months) were recruited over 17 months. The mean Wolf Motor Function Test Functional Ability Score at baseline was 27.4 (max = 75) and the mean Action Research Arm Test score was 11.2 (max = 57). Nine were randomized to AEX + TST and 11 to TST. There were no adverse events, but there was one drop out. Retention at 1- and 6-month follow-up was 80% and 85%, respectively. Attendance was 93% (6) for the AEX + TST group, and 89% (9) for the TST group. AEX + TST was perceived as acceptable (100%) and beneficial (87.5%). Exertional fatigue (visual analogue scale) prior to TST was worse in the AEX + TST group (3.5 [0.7] out of 10) than the TST group (1.7 [1.4] out of 10). The TST group performed 31% more repetitions per session than the AEX + TST group.

Conclusion: A subsequent Phase III study is feasible, but modifications to eligibility criteria, outcome measures, and intervention delivery are recommended.
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http://dx.doi.org/10.1002/pri.1775DOI Listing
July 2019

Low oxygen post conditioning prevents thalamic secondary neuronal loss caused by excitotoxicity after cortical stroke.

Sci Rep 2019 03 19;9(1):4841. Epub 2019 Mar 19.

School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, Australia.

In the current study, we were interested in investigating whether Low oxygen post-conditioning (LOPC) was capable of limiting the severity of stroke-induced secondary neurodegeneration (SND). To investigate the effect of LOPC we exposed adult male C57/BL6 mice to photothrombotic occlusion (PTO) of the motor and somatosensory cortex. This is known to induce progressive neurodegeneration in the thalamus within two weeks of infarction. Two days after PTO induction mice were randomly assigned to one of four groups: (i) LOPC-15 day exposure group; (ii) a LOPC 15 day exposure followed by a 15 day exposure to normal atmosphere; (iii) normal atmosphere for 15 days and (iv) normal atmosphere for 30 days (n = 20/group). We observed that LOPC reduced the extent of neuronal loss, as indicated by assessment of both area of loss and NeuN cell counts, within the thalamus. Additionally, we identified that LOPC reduced microglial activity and decreased activity within the excitotoxic signalling pathway of the NMDAR axis. Together, these findings suggest that LOPC limits neuronal death caused by excitotoxicity in sites of secondary damage and promotes neuronal survival. In conclusion, this work supports the potential of utilising LOPC to intervene in the sub-acute phase post-stroke to restrict the severity of SND.
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http://dx.doi.org/10.1038/s41598-019-39493-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6425023PMC
March 2019

Spatiotemporal analysis of impaired microglia process movement at sites of secondary neurodegeneration post-stroke.

J Cereb Blood Flow Metab 2019 12 11;39(12):2456-2470. Epub 2018 Sep 11.

School of Biomedical Sciences and Pharmacy and the Priority Research Centre for Stroke and Brain Injury, University of Newcastle, Callaghan, NSW, Australia.

It has recently been identified that after motor cortex stroke, the ability of microglia processes to respond to local damage cues is lost from the thalamus, a major site of secondary neurodegeneration (SND). In this study, we combine a photothrombotic stroke model in mice, acute slice and fluorescent imaging to analyse the loss of microglia process responsiveness. The peri-infarct territories and thalamic areas of SND were investigated at time-points 3, 7, 14, 28 and 56 days after stroke. We confirmed the highly specific nature of non-responsive microglia processes to sites of SND. Non-responsiveness was at no time observed at the peri-infarct but started in the thalamus seven days post-stroke and persisted for 56 days. Loss of directed process extension is not a reflection of general functional paralysis as phagocytic function continued to increase over time. Additionally, we identified that somal PY was present on non-responsive microglia in the first two weeks after stroke but not at later time points. Finally, both classical microglia activation and loss of process extension are highly correlated with neuronal damage. Our findings highlight the importance of microglia, specifically microglia dynamic functions, to the progression of SND post-stroke, and their potential relevance as modulators or therapeutic targets during stroke recovery.
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http://dx.doi.org/10.1177/0271678X18797346DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6893987PMC
December 2019

Low Oxygen Post Conditioning as an Efficient Non-pharmacological Strategy to Promote Motor Function After Stroke.

Transl Stroke Res 2019 08 28;10(4):402-412. Epub 2018 Aug 28.

School of Biomedical Sciences and Pharmacy and Priority Research Centre for Stroke and Brain Injury, University of Newcastle, Callaghan, 2308, NSW, Australia.

Low oxygen post conditioning (LOPC) has shown promising results in terms of neuroprotection after stroke, but the effects on motor function have not been considered. Cortical stroke targeting the motor and sensory cortex was induced by photothrombotic occlusion and after 48 h allocated to LOPC (11% O) for 2 weeks. Motor impairment was assessed using the cylinder and grid walk tests during the exposure period and for two further weeks upon completion of the intervention. Neuroprotection was evaluated by histological and molecular analysis at two time points. Two weeks of LOPC was sufficient to significantly reduce motor deficits and tissue loss after stroke. This functional improvement was associated with increased capillary density, enhanced levels of BDNF, decreased neuronal loss and decreased microglia activation. These improvements, in most instances, were maintained up to 2 weeks after the end of the treatment. To our knowledge, this is the first study to demonstrate that LOPC induces a persistent improvement in motor function and neuroprotection after stroke, and in doing so provides evidence to support a case for considering taking LOPC forward to early stage clinical research.
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http://dx.doi.org/10.1007/s12975-018-0656-5DOI Listing
August 2019

Growth Hormone Improves Cognitive Function After Experimental Stroke.

Stroke 2018 05 10;49(5):1257-1266. Epub 2018 Apr 10.

From the Priority Research Centre for Stroke and Brain Injury (L.K.O., F.R.W., M.N., J.I.)

Background And Purpose: Cognitive impairment is a common outcome for stroke survivors. Growth hormone (GH) could represent a potential therapeutic option as this peptide hormone has been shown to improve cognition in various clinical conditions. In this study, we evaluated the effects of peripheral administration of GH at 48 hours poststroke for 28 days on cognitive function and the underlying mechanisms.

Methods: Experimental stroke was induced by photothrombotic occlusion in young adult mice. We assessed the associative memory cognitive domain using mouse touchscreen platform for paired-associate learning task. We also evaluated neural tissue loss, neurotrophic factors, and markers of neuroplasticity and cerebrovascular remodeling using biochemical and histology analyses.

Results: Our results show that GH-treated stroked mice made a significant improvement on the paired-associate learning task relative to non-GH-treated mice at the end of the study. Furthermore, we observed reduction of neural tissue loss in GH-treated stroked mice. We identified that GH treatment resulted in significantly higher levels of neurotrophic factors (IGF-1 [insulin-like growth factor-1] and VEGF [vascular endothelial growth factor]) in both the circulatory and peri-infarct regions. GH treatment in stroked mice not only promoted protein levels and density of presynaptic marker (SYN-1 [synapsin-1]) and marker of myelination (MBP [myelin basic protein]) but also increased the density and area coverage of 2 major vasculature markers (CD31 and collagen-IV), within the peri-infarct region.

Conclusions: These findings provide compelling preclinical evidence for the usage of GH as a potential therapeutic tool in the recovery phase of patients after stroke.
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http://dx.doi.org/10.1161/STROKEAHA.117.020557DOI Listing
May 2018

Cuticular fatty acids of Galleria mellonella (Lepidoptera) inhibit fungal enzymatic activities of pathogenic Conidiobolus coronatus.

PLoS One 2018 8;13(3):e0192715. Epub 2018 Mar 8.

BIOMIBO, Warsaw, Poland.

The entomopathogenic fungus Conidiobolus coronatus produces enzymes that may hydrolyze the cuticle of Galleria mellonella. Of these enzymes, elastase activity was the highest: this figure being 24 times higher than NAGase activity 553 times higher than chitinase activity and 1844 times higher than lipase activity. The present work examines the differences in the hydrolysis of cuticles taken from larvae, pupae and adults (thorax and wings), by C. coronatus enzymes. The cuticles of the larvae and adult thorax were the most susceptible to digestion by proteases and lipases. Moreover, the maximum concentration of free N-glucosamine was in the hydrolysis of G. mellonella thorax. These differences in the digestion of the various types of cuticle may result from differences in their composition. GC-MS analysis of the cuticular fatty acids isolated from pupae of G. mellonella confirmed the presence of C 8:0, C 9:0, C 12:0, C 14:0, C 15:0, C 16:1, C 16:0, C 17:0, C 18:1, C 18:0, with C 16:0 and C 18:0 being present in the highest concentrations. Additional fatty acids were found in extracts from G. mellonella imagines: C 10:0, C 13:0, C 20:0 and C 20:1, with a considerable dominance of C 16:0 and C 18:1. In larvae, C 16:0 and C 18:1 predominated. Statistically significant differences in concentration (p≤0.05) were found between the larvae, pupae and imago for each fatty acid. The qualitative and quantitative differences in the fatty acid composition of G. mellonella cuticle occurring throughout normal development might be responsible for the varied efficiency of fungal enzymes in degrading larval, pupal and adult cuticles.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0192715PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5843172PMC
June 2018

Sustained administration of corticosterone at stress-like levels after stroke suppressed glial reactivity at sites of thalamic secondary neurodegeneration.

Brain Behav Immun 2018 03 21;69:210-222. Epub 2017 Nov 21.

School of Biomedical Sciences and Pharmacy and the Priority Research Centre for Stroke and Brain Injury, University of Newcastle, Callaghan, NSW, Australia; Hunter Medical Research Institute, Newcastle, NSW, Australia; NHMRC Centre of Research Excellence Stroke Rehabilitation and Brain Recovery, Australia.

Secondary neurodegeneration (SND) is an insidious and progressive condition involving the death of neurons in regions of the brain that were connected to but undamaged by the initial stroke. Our group have published compelling evidence that exposure to psychological stress can significantly exacerbate the severity SND, a finding that has considerable clinical implications given that stroke-survivors often report experiencing high and unremitting levels of psychological stress. It may be possible to use one or more targeted pharmacological approaches to limit the negative effects of stress on the recovery process but in order to move forward with this approach the most critical stress signals have to be identified. Accordingly, in the current study we have directed our attention to examining the potential effects of corticosterone, delivered orally at stress-like levels. Our interest is to determine how similar the effects of corticosterone are to stress on repair and remodelling that is known to occur after stroke. The study involved 4 groups, sham and stroke, either administered corticosterone or normal drinking water. The functional impact was assessed using the cylinder task for paw asymmetry, grid walk for sensorimotor function, inverted grid for muscle strength and coordination and open field for anxiety-like behaviour. Biochemically and histologically, we considered disturbances in main cellular elements of the neurovascular unit, including microglia, astrocytes, neurons and blood vessels using both immunohistochemistry and western blotting. In short, we identified that corticosterone delivery after stroke results in significant suppression of key microglial and astroglial markers. No changes were observed on the vasculature and in neuronal specific markers. No changes were identified for sensorimotor function or anxiety-like behaviour. We did, however, observe a significant change in motor function as assessed using the inverted grid walk test. Collectively, these results suggest that pharmacologically targeting corticosterone levels in the future may be warranted but that such an approach is unlikely to limit all the negative effects associated with exposure to chronic stress.
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http://dx.doi.org/10.1016/j.bbi.2017.11.014DOI Listing
March 2018

Microsatellite Mutation Rate in Atlantic Sturgeon (Acipenser oxyrinchus).

J Hered 2017 Sep;108(6):686-692

Museum and Institute of Zoology, Polish Academy of Sciences, Warsaw, Poland; Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw, Poland; Department of Wildlife Ecology and Conservation, University of Florida, Gainesville, FL 32611; Program in Fisheries and Aquatic Sciences, School of Forest Resources and Conservation, University of Florida, Gainesville, FL 32611; Institute of Genetics and Biotechnology, Department of Biology, University of Warsaw, Warsaw, Poland; University of Newcastle, Callaghan, Australia; Centre of New Technologies, University of Warsaw, Warsaw, Poland.

Understanding mutation rates can greatly extend the utility of population and conservation genetic analyses. Herein, we present an estimate of genome-wide microsatellite mutation rate in Atlantic sturgeon (Acipenser oxyrinchus) based on parent-offspring transmission patterns. We screened 307 individuals for parentage and mutation-rate analysis applying 43 variable markers. Out of 13228 allele transfers, 11 mutations were detected, producing a mutation rate of 8.3 × 10-4 per locus per generation (95% confidence interval: 1.48 × 10-3, 4.15 × 10-4). Single-step mutations predominated and there were trends toward mutations in loci with greater polymorphism and allele length. Two of the detected mutations were most probably cluster mutations, being identified in 12 and 28 sibs, respectively. Finally, we observed evidences of polyploidy based on the sporadic presence of 3 or 4 alleles per locus in the genotyped individuals, supporting previous reports of incomplete diploidization in Atlantic sturgeon.
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http://dx.doi.org/10.1093/jhered/esx057DOI Listing
September 2017

Oral administration of corticosterone at stress-like levels drives microglial but not vascular disturbances post-stroke.

Neuroscience 2017 06 11;352:30-38. Epub 2017 Mar 11.

School of Biomedical Sciences and Pharmacy and the Priority Research Centre for Stroke and Brain Injury, University of Newcastle, Callaghan, NSW, Australia; Hunter Medical Research Institute, Newcastle, NSW, Australia; NHMRC Centre of Research Excellence Stroke Rehabilitation and Brain Recovery, Heidelberg, VIC, Australia. Electronic address:

Exposure to chronic stress following stroke has been shown, both clinically and pre-clinically, to impact negatively on the recovery process. While this phenomenon is well established, the specific mechanisms involved have remained largely unexplored. One obvious signaling pathway through which chronic stress may impact on the recovery process is via corticosterone, and its effects on microglial activity and vascular remodeling. In the current study, we were interested in examining how orally delivered corticosterone at a stress-like concentration impacted on microglial activity and vascular remodeling after stroke. We identified that corticosterone administration for two weeks following stroke significantly increased tissue loss and decreased the weight of the spleen and thymus. We also identified that corticosterone administration significantly altered the expression of the key microglial complement receptor, CD11b after stroke. Corticosterone administration did not alter the expression of the vessel basement membrane protein, Collagen IV after stroke. Together, these results suggest that corticosterone is likely to represent only one of the major stress signals responsible for driving the negative impacts of chronic stress on recovery.
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http://dx.doi.org/10.1016/j.neuroscience.2017.03.005DOI Listing
June 2017

Reconsidering the role of glial cells in chronic stress-induced dopaminergic neurons loss within the substantia nigra? Friend or foe?

Brain Behav Immun 2017 Feb 4;60:117-125. Epub 2016 Oct 4.

School of Biomedical Sciences and Pharmacy and the Priority Research Centre for Stroke and Brain Injury, University of Newcastle, Callaghan, NSW, Australia; Hunter Medical Research Institute, Newcastle, NSW, Australia; NHMRC Centre of Research Excellence Stroke Rehabilitation and Brain Recovery, Heidelberg, VIC, Australia. Electronic address:

Exposure to psychological stress is known to seriously disrupt the operation of the substantia nigra (SN) and may in fact initiate the loss of dopaminergic neurons within the SN. In this study, we aimed to investigate how chronic stress modified the SN in adult male mice. Using a paradigm of repeated restraint stress (an average of 20h per week for 6weeks), we examined changes within the SN using western blotting and immunohistochemistry. We demonstrated that chronic stress was associated with a clear loss of dopaminergic neurons within the SN. The loss of dopaminergic neurons was accompanied by higher levels of oxidative stress damage, indexed by levels of protein carbonylation and strong suppression of both microglial and astrocytic responses. In addition, we demonstrated for the first time, that chronic stress alone enhanced the aggregation of α-synuclein into the insoluble protein fraction. These results indicate that chronic stress triggered loss of dopaminergic neurons by increasing oxidative stress, suppressing glial neuroprotective functions and enhancing the aggregation of the neurotoxic protein, α-synuclein. Collectively, these results reinforce the negative effects of chronic stress on the viability of dopaminergic cells within the SN.
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http://dx.doi.org/10.1016/j.bbi.2016.10.001DOI Listing
February 2017

Management of esophageal atresia and tracheoesophageal fistula in North Queensland.

Int Surg 2014 May-Jun;99(3):276-9

Department of Surgery, The Townsville Hospital, Townsville, Queensland, Australia.

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http://dx.doi.org/10.9738/INTSURG-D-13-00253.1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4027913PMC
September 2015

[Nurses and doctors--prognosis for the future].

Przegl Lek 2009 ;66(8):469-70

Instytut Pielegniarstwa i Połoznictwa Wydziału Medycznego Uniwersytetu Rzeszowskiego w Rzeszowie.

Mutual cooperation between medical doctor and nurses are presented, while analizing new trends in the European Union. Nurse family practice and specialist training are discussed as well as new specializations, i.e. Study nurse trained for participation in clinical trials.
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February 2010

In vivo effect of diallyl sulfide and cimetidine on phenacetin metabolism and bioavailability in rat.

Acta Biochim Pol 2002 ;49(1):249-56

Department of Toxicology, The Medical University of Warsaw, Warszawa, Poland.

Numerous cytochrome P450 inhibitors have been described as effective modulators of cytochrome P450 isoforms activity in vitro. Their inhibitory efficiency may be considerably modified after in vivo application. The aim of this study was to examine the effect of oral administration of diallyl sulfide--a cytochrome P450 2E1 inhibitor and cimetidine--a cytochrome P450 2C6 and 2C11 inhibitor on rat serum concentration of phenacetin and its metabolite acetaminophen. Both inhibitors increased area under the curve (AUC(0-4 h)) for phenacetin by 50%. Only cimetidine reduced AUC(0-4 h) for acetaminophen indicating inhibition of O-deethylation activity. Quinidine--a cytochrome P450 2D subfamily and P-glycoprotein inhibitor did not change significantly phenacetin bioavailability. These results suggest that diallyl sulfide inhibits the deacetylation pathway catalysed by arylamine N-acetyl transferase. Beside cytochrome P450 1A2 other cytochrome P450 isoforms (2A6 and/or 2C11) are involved in phenacetin O-deethylation in rat.
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January 2003