PUBLIC HEALTH ACHIEVEMENTS AND CHALLENGES: SYMPOSIUM OF THE UNIVERSITY OF MOSTAR FACULTY OF HEALTH STUDIES

Public health is an important area of health care that reflects the readiness of the state and society to provide the welfare of all citizens through the promotion of health and the preservation of a healthy environment - factors that directly affect the health of the population. The field of public health is very broad and its concept is changing over time, being defined in a narrower and wider sense. In short, public health is a science and practice that aims at ensuring the conditions in which people can preserve and improve their health and prevent health damage. The third millennium brings its specifics, needs and priorities according to challenges public health is faced by in the twenty-first century: the economic crisis, rising inequality, population aging, rising rates of chronic diseases, migration, urbanization, ecosystem change, climate change, etc. The role of public health is to protect, improve health, prevent diseases and injuries. Such a public health approach implies a multisectoral work focusing on "wider health determinants", and within this activity experts from various medical and non-medical profiles, whose field of public health is concerned, can be found. The development of inter-departmental co-operation skills contributes to a better understanding of health professionals and professionals of other profiles, and facilitates common, synergistic actions in addressing public health problems in the community. Symposium on Public Health Achievements and Challenges organized by the University of Mostar Faculty of Health Studies is just another indication of the obligation, the need and the desire for professional and scientific contribution to the fight for better health. Our faculty has so far organized other numerous symposia, and the aim of this symposium is to present public health achievements and challenges in our surrounding in order to protect, improve health, prevent diseases and injuries in a modern way

The effects of valsartan on cardiac function and pro-oxidative parameters in the streptozotocin-induced diabetic rat heart

© 2020, University of Kragujevac, Faculty of Science. All rights reserved. Diabetes mellitus is a major risk factor for cardiovascular diseases, while cardiovascular diseases are a leading cause of morbidity and mortality worldwide. The renin–angiotensin– aldosterone system controls renal, cardiovascular, adrenal function and regulates fluid and electrolyte balance as well as blood pressure. Because of his role, inhibition of renin-angiotensin-aldosteron system is another therapy approach that reduces the risk of diabetes and cardiovascular disease. In this study, our goal was to evaluate effect of valsartan,as inhibitor of angiotensin II receptor type 1, on cardiac tissue and function, with focus on cardiodynamic and oxidative stress. The present study was carried out on 20 adult male Wistar albino rats (8 week old and with body masses of 180-200 g). Rats were divided randomly into 2 groups (10 animals per group). Healthy animals treated with 1 μM of valsartan and streptozotocin-induced diabetic animals perfused with 1 μM of valsartan 4 weeks after the induction of diabetes. Our results demonstrated that acute application of valsartan has different effect on cardiodynamics in rat heart of diabetic and healthy animals but did not improve cardiac function in hy-perglycemia-induced changes. A challenge for further investi-gations are studies with chronic or acute administration, alone or in combination with other angiotensin-converting-enzyme inhibitor in various models of diabetes

Allosteric inhibitor of β-catenin selectively targets oncogenic Wnt signaling in colon cancer.

Abnormal regulation of β-catenin initiates an oncogenic program that serves as a main driver of many cancers. Albeit challenging, β-catenin is an attractive drug target due to its role in maintenance of cancer stem cells and potential to eliminate cancer relapse. We have identified C2, a novel β-catenin inhibitor, which is a small molecule that binds to a novel allosteric site on the surface of β-catenin. C2 selectively inhibits β-catenin, lowers its cellular load and significantly reduces viability of β-catenin-driven cancer cells. Through direct binding to β-catenin, C2 renders the target inactive that eventually activates proteasome system for its removal. Here we report a novel pharmacologic approach for selective inhibition of β-catenin via targeting a cryptic allosteric modulation site. Our findings may provide a new perspective for therapeutic targeting of β-catenin

IRE1α and IGF signaling predict resistance to an endoplasmic reticulum stress-inducing drug in glioblastoma cells.

To date current therapies of glioblastoma multiforme (GBM) are largely ineffective. The induction of apoptosis by an unresolvable unfolded protein response (UPR) represents a potential new therapeutic strategy. Here we tested 12ADT, a sarcoendoplasmic reticulum Ca2+ ATPase (SERCA) inhibitor, on a panel of unselected patient-derived neurosphere-forming cells and found that GBM cells can be distinguished into "responder" and "non-responder". By RNASeq analysis we found that the non-responder phenotype is significantly linked with the expression of UPR genes, and in particular ERN1 (IRE1) and ATF4. We also identified two additional genes selectively overexpressed among non-responders, IGFBP3 and IGFBP5. CRISPR-mediated deletion of the ERN1, IGFBP3, IGFBP5 signature genes in the U251 human GBM cell line increased responsiveness to 12ADT. Remarkably, >65% of GBM cases in The Cancer Genome Atlas express the non-responder (ERN1, IGFBP3, IGFBP5) gene signature. Thus, elevated levels of IRE1α and IGFBPs predict a poor response to drugs inducing unresolvable UPR and possibly other forms of chemotherapy helping in a better stratification GBM patients

KP-LAB Knowledge Practices Laboratory -- External release of end-user applications

deliverablesThis deliverable describes the M24 release of the End user applications for knowledge practices software v2.0.0. The deliverable includes the technical development performed until M24 (January 2008) within WP6 according to Description of Work 2.1 and D6.4 M21 specification of end-user applications. The current release is comprised of two set of tools: 1. Shared Space Tool The shared space and the accompanying support material can be found on the Internet at: http://2d.mobile.evtek.fi:8080/shared-space 2. Map-It. The installer program for Map-It v2.0.0 is available at: http://www.kp-lab.org/intranet/testable-tools/kp-lab-tools/map-it/map-it-2-0.0 Please consult the "Getting Started" Note before installing and using Map-It: http://www.kp-lab.org/intranet/testable-tools/kp-lab-tools/map-it/getting-started-with-map-it 3. Change Laboratory tools The release targeted for the end users participating in the trials planned to be conducted in the CL Working Knot can be accessed via the following link: http://2d.mobile.evtek.fi:8080/shared-space/cl.html Anyone who wishes to try the software out but is not participating in the Change Laboratory trials should use the development deployment on: http://mielikki.mobile.evtek.fi/shared-space/cl.html The M24 release of Semantic Multimedia Annotation tools is still delayed. The release of CASS Memo Client has been postponed to be included in the M28 release in DoW3

Antimicrobial resistance monitoring and surveillance in the meat chain: A report from five countries in the European Union and European Economic Area

Background The emergence of antimicrobial resistance (AMR) in zoonotic foodborne pathogens (Salmonella, Campylobacter) and indicator microorganisms (E. coli, enterococci) is a major public health risk. Zoonotic bacteria, resistant to antimicrobials, are of special concern because they might compromise the effective treatment of infections in humans. Scope and approach In this review, the AMR monitoring and surveillance programmes in five selected countries within European Union (EU) and European Economic Area (EEA) are described. The sampling schemes, susceptibility testing for AMR identification, clinical breakpoints (clinical resistance) and epidemiological cut-off values (microbiological resistance) were considered to reflect on the most important variations between and within food-producing animal species, between countries, and to identify the most effective approach to tackle and manage the antimicrobial resistance in the food chain. Key findings and conclusions The science-based monitoring of AMR should encompass the whole food chain, supported with public health surveillance and should be conducted in accordance with ‘Zoonoses Directive’ (99/2003/EC). Such approach encompasses the integrated AMR monitoring in food animals, food and humans in the whole food (meat) chain continuum, e.g. pre-harvest (on-farm), harvest (in abattoir) and post-harvest (at retail). The information on AMR in critically important antimicrobials (CIA) for human medicine should be of particular importance

Proceedings of the 12th International Conference on Kinanthropology

Proceedings of the 12th Conference of Sport and Quality of Life 2019 gatheres submissions of participants of the conference. Every submission is the result of positive evaluation by reviewers from the corresponding field. Conference is divided into sections – Analysis of human movement; Sport training, nutrition and regeneration; Sport and social sciences; Active ageing and sarcopenia; Strength and conditioning training; section for PhD students

Oncogenic EGFR Signaling Activates an mTORC2-NF- B Pathway That Promotes Chemotherapy Resistance

Although it is known that mTOR complex 2 (mTORC2) functions upstream of Akt, the role of this protein kinase complex in cancer is not well understood. Through an integrated analysis of cell lines, in vivo models and clinical samples, we demonstrate that mTORC2 is frequently activated in glioblastoma (GBM), the most common malignant primary brain tumor of adults. We show that the common activating epidermal growth factor receptor (EGFR) mutation (EGFRvIII) stimulates mTORC2 kinase activity, which is partially suppressed by PTEN. mTORC2 signaling promotes GBM growth and survival, and activates NF-κB. Importantly, this mTORC2-NF-κB pathway renders GBM cells and tumors resistant to chemotherapy in a manner independent of Akt. These results highlight the critical role of mTORC2 in GBM pathogenesis, including through activation of NF-κB downstream of mutant EGFR, leading to a previously unrecognized function in cancer chemotherapy resistance. These findings suggest that therapeutic strategies targeting mTORC2, alone or in combination with chemotherapy, will be effective in cancer