Stan wiedzy studentów pierwszego roku geografii UMCS i UW z zakresu meteorologii i klimatologii

The aim of the study was to compare meteorological and climatological knowledge among first year students of geography at two universities: Maria Curie-Skłodowska University (UMCS) in Lublin and Warsaw University (UW) in Warsaw. Due to the curriculum changes in secondary schools, as well as different conditions of recruiting candidates, the level of knowledge of students in the coming years, as well as in various colleges and universities, may be different. Identical surveys were conducted twice among first year students of first level full-time studies: at the beginning of November 2014 and at the beginning of June 2015, which allowed knowledge changes evaluation at the beginning of the study and after the first year of studying geography.The problem was a matter of self-assessment of knowledge by the respondents, as many of them are not able to correctly identify it. It was found that there was a marginal increase in the level of knowledge of students of Warsaw University and the UMCS.The aim of the study was to compare meteorological and climatological knowledge among first year students of Geography at two universities: UMCS in Lublin and Warsaw University in Warsaw. Due to the curriculum changes in secondary schools, as well as different conditions of recruiting candidates, the level of knowledge of students in the coming years, as well as in various colleges and universities, may be different. Identic surveys were conducted twice among first year students of first level full-time studies: in late November and December 2014 and in the second half of May 2015, what allowed knowledge changes evaluation at the beginning of the study and after the first year of studying geography.The problem was a matter of self-assessment of knowledge by the respondents, as many of them are not able to correctly identify her. It was found that there was a marginal increase in the level of knowledge of students of Warsaw University and the University of Maria Curie-Sklodowsk

Extreme weather and climate phenomena in Polish publications

W opracowaniu przedstawiono stan badań dotyczących zdarzeń (zjawisk) ekstremalnych, w różnych skalach przestrzennych, w polskiej literaturze naukowej (głównie klimatologicznej). Analizą objęto wybrane prace: przedstawiające klasyfikacje zjawisk ekstremalnych, wykorzystujące dotychczasowe klasyfikacje i kryteria wyznaczania zdarzeń ekstremalnych, zawierające charakterystykę przyczyn i skutków ekstremów, prezentujące prognozę na kolejne lata oraz dotyczące wykorzystania wiedzy o zdarzeniach ekstremalnych w praktyce. Przegląd literatury dotyczącej ekstremalnych zdarzeń meteorologicznych i klimatologicznych pozwolił autorom dostrzec wiele problemów, z jakimi związane jest zagadnienie badania ekstremów. Zwrócono głównie uwagę na problemy dotyczące definicji, metod opracowań i prognozy zdarzeń ekstremalnych. Ważnym zagadnieniem są skutki występowania hydrometeorologicznych zdarzeń ekstremalnych.This paper presents the state of research regarding extreme phenomena at different spatial scales in Polish scientific publications (mainly climatological ones). The analysis covered papers concerning: various classifications and criteria for the identification of extreme phenomena, characterising the causes and effects of extreme phenomena, modeling and forecasting of extreme phenomena as well as using the knowledge about extreme phenomena in practice. The review of literature on extreme weather and climate phenomena allowed the authors to see a large number of problems connected with the research upon extreme phenomena. Problems concerning definitions, research methods and extreme phenomena forecasting were mainly dealt with in the paper. The effects of occurrence of hydrometeorological extreme phenomena are an issue of significant importance

Meteorologiczne i klimatologiczne zdarzenia ekstremalne w polskiej literaturze

Extreme weather and climate phenomena in Polish publicationsThis paper presents the state of research regarding extreme phenomena at different spatial scales in Polish scientific publications ( mainly climatological ones ). The analysis covered papers concerning: various classifications and criteria for the identification of extreme phenomena, characterising the causes and effects of extreme phenomena, modeling and forecasting of extreme phenomena as well as using the knowledge about extreme phenomena in practice. The review of literature on extreme weather and climate phenomena allowed the authors to see a large number of problems connected with the research upon extreme phenomena. Problems concerning definitions, research methods and extreme phenomena forecasting were mainly dealt with in the paper. The effects of occurrence of hydrometeorological extreme phenomena are an issue of significant importance

Caspase-11 regulates the tumour suppressor function of STAT1 in a murine model of colitis-associated carcinogenesis

Murine inflammatory caspase-11 has an important role in intestinal epithelial inflammation and barrier function. Activation of the non-canonical inflammasome, mediated by caspase-11, serves as a regulatory pathway for the production of the proinflammatory cytokines IL-1β and IL-18, and has a key role in pyroptotic cell death. We have previously demonstrated a protective role for caspase-11 during dextran sulphate sodium (DSS)-induced colitis, however the importance of caspase-11 during colorectal tumour development remains unclear. Here, we show that Casp11−/− mice are highly susceptible to the azoxymethane (AOM)-DSS model of colitis-associated cancer (CAC), compared to their wild type (WT) littermates. We show that deficient IL-18 production occurs at initial inflammation stages of disease, and that IL-1β production is more significantly impaired in Casp11−/− colons during established CAC. We identify defective STAT1 activation in Casp11−/− colons during disease progression, and show that IL-1β signalling induces caspase-11 expression and STAT1 activation in primary murine macrophages and intestinal epithelial cells. These findings uncover an anti-tumour role for the caspase-11 and the non-canonical inflammasome during CAC, and suggest a critical role for caspase-11, linking IL-1β and STAT1 signalling pathways

The Preoperative Supplementation With Vitamin D Attenuated Pain Intensity and Reduced the Level of Pro-inflammatory Markers in Patients After Posterior Lumbar Interbody Fusion

The aim of this experimental study was to assess whether 5 weeks of preoperative supplementation with vitamin D affects the intensity of pain and the level of inflammatory markers in patients undergoing posterior lumbar interbody fusion (PLIF) followed by rehabilitation. 42 patients were divided, by double-blind randomization, into two groups: supplemented (SUPL) vitamin D (3200 IU dose of vitamin D/day for 5 weeks) and placebo group (PL) treated with vegetable oil. The 10-week program of early rehabilitation (3 times a week) was initiated 4 weeks following PLIF. Measurements of serum 25(OH)D3 and CRP, IL-6, TNF-α, and IL-10 were performed. Pain intensity was measured using VAS. After supplementation with vitamin D serum, the concentration of 25(OH)D3 significantly increased in the SUPL group (∗p < 0.005) and was significantly higher as compared to the PL group (∗p < 0.001). A significant reduction in pain intensity was observed 4 weeks after surgery and after rehabilitation in both groups. In the SUPL group, serum CRP and IL-6 concentration significantly decreased after rehabilitation, compared with the postsurgical level (ap < 0.04). The level of TNF-α was significantly lower after rehabilitation only in the supplemented group (∗p < 0.02). There were no significant changes in the IL-10 level in both groups during the study. Our data indicate that supplementation with vitamin D may reduce systemic inflammation and when combined with surgery and early postsurgical rehabilitation, it may decrease the intensity of pain in LBP patients undergoing PLIF. Data indicate that LBP patients undergoing spine surgery should use vitamin D perioperatively as a supplement

The role of Wnt-5a in cervical carcinoma

Rak szyjki macicy jest trzecim, po raku płuc i piersi, najczęściej występującym nowotworem wśród kobiet na świecie. Obecnie, jako główny czynnik etiologiczny uważa się wirus brodawczaka ludzkiego (HPV). Jednak, jako że tylko niewielka część zainfekowanych komórek ulega transformacji nowotworowej, poszukuje się innych mechanizmów leżących u podłoży nowotworzenia. Wiadomo, iż aktywacja receptora MET, obecnego w dużej ilości na komórkach nowotworowych, przez czynnik wzrostu hepatocytów (HGF) prowadzi do indukcji przejścia epitelialno – mezenchymalnego i tym samym nadaje komórkom cech inwazyjnych. Okazało się jednak, że czynnik ten nie jest wystarczający do zapoczątkowania przerzutowania w początkowych stadiach nowotworu. Drugim niezbędnym składnikiem okazał się Wnt-5a.W eksperymentach została użyta linia komórkowa raka szyjki macicy C-4I.Komórki stymulowano czynnikami, HGF, Wnt-5a lub HGF i Wnt-5a jednocześnie. Po 96 godzinnej inkubacji, określano profile ekspresji genów na poziomie transkryptu za pomocą PCR w czasie rzeczywistym i na poziomie białka za pomocą metody Western Blot. Zdolność do migracji i inwazyjność określono poprzez test zarastania rany i test chemotaksji z użyciem insertów. Zauważono, że synergistyczny efekt HGF i Wnt-5a wpływa na ekspresję markerów charakterystycznych dla przejścia EMT. Zaobserwowano spadek E-kadheryn, i wzrost wimentyn, charakterystyczny dla nabywania cech komórek mezenchymalnych. Sprawdzono również ekspresją białek: SNAIL, SLUG, MMP-1. Kolejne doświadczenia pokazały, że sam Wnt-5a nie wpływa na nabywanie przez komórki zdolności do nieukierunkowanego ruchu. Okazało się, że Wnt-5a jest ważnym czynnikiem chemotaktycznym. Wnt-5a razem z HGF umożliwiały komórkom migrację przez inserty do chemoatraktantów. W obecności HGF komórki nabywały zdolności migracyjnych, ale to Wnt-5a indukował zdolność do ukierunkowanego ruchu. Podsumowując, otrzymane wyniki świadczą o udziale obu białek w procesach nowotworzenia. Stymulacja komórek z HGF i Wnt-5a skutkuje procesami charakterystycznymi dla przejścia epitelialno - mezenchymalnego.Cervical cancer is the third, after lung and breast cancer, leading cause of cancer death among women in Poland. The main etiological factor is human papilloma virus (HPV). It is confirmed that activation of MET receptor by hepatocyte grow factor (HGF) induces epithelial to mesenchymal EMT transition, resulting in tumor cells invasion and metastasis. Previous experiments showed that HGF/MET axis was fully responsible for inducing morphological changes in cervical cancer cells in vitro, however, HGF stimulation was insufficient to enable scattering of cells in early stages of cervical cancer. As investigated, the second factor necessary for cancer metastatic progression was Wnt-5a protein.The aim of this work was to investigate the Wnt5a and HGF influence on C4-I cells which correspond with early stages of cervical cancer. The cells was stimulated for 96 hours with factors: Wnt-5a, HGF or with both of them. We examined the expression of various proteins characteristic for EMT such as: SNAIL, SLUG, vimentin, E-cadherin. We use Real Time PCR and Western Blot for evaluated expression of genes typical for EMT. We also analyze invasion and migration ability by scratch assay and chemotaxis assay. We determined that synergistic effect of Wnt-5a and HGF was crucial for increased Vimentin level and decrease E-cadherin level during epithelial to mesenchymal transition. Also differences in expression of SLUG, SNAIL, MMP-1 was revealed. After stimulation with HGF and Wnt5a changes in protein and RNA expression were typical for EMT. Other experiments show that Wnt-5a does not enhance migratory ability. HGF allow scattering cells and they acquire the capability to invade. It is turned out that Wnt-5a is important chemotactic factor. Wnt-5a together with HGF enable migration of cells, but HGF responds mainly for motility and Wnt-5a is the major chemoattractant.Summarizing, Wnt5a plays important role in cancer invasion and metastasis. This factor, together with HGF, is responsible for implementation of epithelial to mesenchymal transition in cervical cancer

Identification of novel innate immune mechanisms regulating oesophageal adenocarcinoma (OAC) progression and bacterial infection

Inflammation is an essential immune system response to pathogens, damaged cells and stress stimuli and has an essential role in tissue repair and regeneration. The inflammatory response is the coordinated activation of signalling pathway leading to immune cell recruitment into the site of infection and production of inflammatory mediators. In response to the recognition of microorganisms and sterile stressors, a multiprotein complex, called the inflammasome is formed. The inflammasome activates the highly pro-inflammatory cytokines IL-1? and IL-18 and induced programmed cell death-pyroptosis thus inducing inflammation. Despite the undeniable protective role of inflammation, increasing evidence shows that that deregulation in immune response or prolonged inflammation causes and advances many common diseases. Chronic inflammation plays a very important role in oesophageal adenocarcinoma (OAC) and its only known precursor, Barrett?s oesophagus (BO). Recent studies suggest that microbial dysbiosis in oesophagus could contribute to BO and increase the risk of OAC development. TLR2 is involved in the innate immune response to microbial pathogens and host-derived molecules.We assume that TLR2 upregulation will increase the sensitivity of oesophageal cells to bacteria thus leading to chronic inflammation. We show that BO and early-stage OAC cells were responsive to TLR2 stimulation and TLR2 neutralising antibody successfully inhibits TLR2-mediated chemokine production. Factors secreted from TLR2-activated oesophageal cells induce TLR2-mediated differentiation of murine macrophages into M2-like/TAM phenotype. We identify High Mobility Group Box 1 protein (HMGB1) as one of the factors secreted from TLR2-stimulated oesophageal adenocarcinoma cells. We show that extracellular HMGB1 can efficiently prime macrophages for inflammasome activation, upregulating caspase-11 and IL-1B. Findings suggest that HMGB1 is a potential target for early-stage OAC, and that blocking TLR2 signalling may limit HMGB1 release, inflammatory cell infiltration and inflammation during OAC progression. Inflammation is critical for tuberculosis (TB) pathogenesis. Numerous host innate immune responses are induced upon M.tuberculosis (Mtb), although their mechanisms and impact on mycobacterium are not well understood. It is estimated that about one-third of the global population is infected with Mtb. When the infection is not cleared it remains in a latent form for a long time and only 5-10% of infected individuals will develop active disease at some stage of their life. The inhibition of inflammation is the main survival strategy of Mtb. Nitric oxide and IL-1? play an important role in the host resistance to Mtb. Here we investigated the role of caspase-11 in Mtb infection. We first show that STAT1 activation, nitric oxide production and IL-1? expression in macrophages is mediated by caspase-11. The iNOS-induced nitric oxide production is regulated through IFNAR/JAK/STAT1 pathway. We also determined that Caspase-11 is required for restriction of Mtb proliferation in murine macrophages. As nitric oxide is well known to confine the growth of Mtb we hypothesise that Mtb-induced caspase-11 increases iNOS expression and nitric oxide production and is a crucial protein in the innate immune response to TB-induced pathogen. Inhibition of caspase-11 by mycobacteria could be a potential mechanism allowing Mtb proliferation in the host. Peptic ulcers are another example of the inflammation-related condition, caused by the interaction between bacterial and host factors and are often influenced by the presence of Helicobacter pylori infection or use of NSAIDs. This study demonstrates enhanced expression of caspase-4 in peptic ulcer patient biopsies, indicating that pyroptosis and non-canonical inflammasome activity may be processes involved in peptic ulcer disease. We show that primary murine macrophages infected with H. pylori upregulate caspase-11 (the orthologue of human caspase-4), activate caspase-1 and secrete IL-1?. Prostaglandin E2 inhibits caspase-4 mediated and indirectly caspase-1 driven pyroptosis probably through the limitation of DAMPs production. Overall, evidence is provided for a pathological role of caspase-4/11 in peptic ulcer disease and proposes that targeting caspase-4 or inhibiting pyroptosis may have therapeutic potential in the management of peptic ulcers

Meteorologiczne i klimatologiczne zdarzenia ekstremalne w polskiej literaturze

Extreme weather and climate phenomena in Polish publicationsThis paper presents the state of research regarding extreme phenomena at different spatial scales in Polish scientific publications ( mainly climatological ones ). The analysis covered papers concerning: various classifications and criteria for the identification of extreme phenomena, characterising the causes and effects of extreme phenomena, modeling and forecasting of extreme phenomena as well as using the knowledge about extreme phenomena in practice. The review of literature on extreme weather and climate phenomena allowed the authors to see a large number of problems connected with the research upon extreme phenomena. Problems concerning definitions, research methods and extreme phenomena forecasting were mainly dealt with in the paper. The effects of occurrence of hydrometeorological extreme phenomena are an issue of significant importance

Simultaneous Inhibition of BCR-ABL1 Tyrosine Kinase and PAK1/2 Serine/Threonine Kinase Exerts Synergistic Effect against Chronic Myeloid Leukemia Cells

Tyrosine kinase inhibitors (TKIs) revolutionized the treatment of chronic myeloid leukemia in the chronic phase (CML-CP). However, it is unlikely that they can completely “cure” the disease. This might be because some subpopulations of CML-CP cells such as stem and progenitor cells are resistant to chemotherapy, even to the new generation of TKIs. Therefore, it is important to look for new methods of treatment to improve therapeutic outcomes. Previously, we have shown that class I p21-activated serine/threonine kinases (PAKs) remained active in TKI-naive and TKI-treated CML-CP leukemia stem and early progenitor cells. In this study, we aimed to determine if simultaneous inhibition of BCR-ABL1 oncogenic tyrosine kinase and PAK1/2 serine/threonine kinase exert better anti-CML effect than that of individual treatments. PAK1 was inhibited by small-molecule inhibitor IPA-3 (p21-activated kinase inhibitor III), PAK2 was downregulated by specific short hairpin RNA (shRNA), and BCR-ABL1 tyrosine kinase was inhibited by imatinib (IM). The studies were conducted by using (i) primary CML-CP stem/early progenitor cells and normal hematopoietic counterparts isolated from the bone marrow of newly diagnosed patients with CML-CP and from healthy donors, respectively, (ii) CML-blast phase cell lines (K562 and KCL-22), and (iii) from BCR-ABL1-transformed 32Dcl3 cell line. Herein, we show that inhibition of the activity of PAK1 and/or PAK2 enhanced the effect of IM against CML cells without affecting the normal cells. We observed that the combined use of IM with IPA-3 increased the inhibition of growth and apoptosis of leukemia cells. To evaluate the type of interaction between the two drugs, we performed median effect analysis. According to our results, the type and strength of drug interaction depend on the concentration of the drugs tested. Generally, combination of IM with IPA-3 at the 50% of the cell kill level (EC50) generated synergistic effect. Based on our results, we hypothesize that IM, a BCR-ABL1 tyrosine kinase inhibitor, combined with a PAK1/2 inhibitor facilitates eradication of CML-CP cells