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Warsaw, Poland

The Medical University of Warsaw was founded in January 1950, building on the University of Warsaw's former Faculty of Medicine, which had been established in the early nineteenth century. The Medical University of Warsaw is the largest medical school in Poland, and one of the most prestigious. Wikipedia.

Agency: Cordis | Branch: H2020 | Program: CSA | Phase: H2020-TWINN-2015 | Award Amount: 1.19M | Year: 2016

In 2013, the Science magazine announced Immunotherapy of cancer as the Breakthrough of the Year. The results of ongoing clinical studies with new cancer immunotherapeutics strongly support this enthusiasm. Following the lead of the top research groups, the Coordinator of the present proposal, Medical University of Warsaw (MUW) displays a predominant ambition of becoming a major player in the thriving area of Immuno-Oncology. MUW is one of the leading centres of competence in the Oncology field in Poland and presents a robust desire for further improvement of its excellence merits. Therefore, the main concept of the STREAM proposal is to bring together the high-level European research organizations with synergistic scientific and innovative expertise in the field of Immuno-Oncology, in order to establish an international, long-term, strategic partnership with MUW. The main model of the STREAM proposal is to foster enhanced scientific dialogue and twinning between MUW and four outstanding research centres via trans-national visits of scientific personnel, joint organization of a summer school and workshops, as well as promoting the active participation of STREAM researchers in the prestigious scientific conferences. Within the duration of the current project we intend to significantly enrich MUWs, regional and national quality profile regarding all of the variables of Composite indicator of Research Excellence in the Immuno-Oncology area. We will also set a new standard for conducting bioresearch and innovative thinking in Poland. We expect that the scale, ambition, and innovative character of the proposed project will bring the MUWs excellence to a new level - internationally recognized and competitive, in order to contribute to the well-being of the society and knowledge-based economy of Poland and EU. Our proposal provides an exceptional occasion to achieve real impact on human health, quality of life and economic status in the new area of enlarged Europe.

Ratajczak M.Z.,University of Louisville | Ratajczak M.Z.,Medical University of Warsaw
Leukemia | Year: 2015

This review presents a novel view and working hypothesis about the hierarchy within the adult bone marrow stem cell compartment and the still-intriguing question of whether adult bone marrow contains primitive stem cells from early embryonic development, such as cells derived from the epiblast, migrating primordial germ cells or yolk sac-derived hemangioblasts. It also presents a novel view of the mechanisms that govern stem cell mobilization and homing, with special emphasis on the role of the complement cascade as a trigger for egress of hematopoietic stem cells from bone marrow into blood as well as the emerging role of novel homing factors and priming mechanisms that support stromal-derived factor 1-mediated homing of hematopoietic stem/progenitor cells after transplantation. © 2015 Macmillan Publishers Limited.

Kaleta B.,Medical University of Warsaw
Archivum Immunologiae et Therapiae Experimentalis | Year: 2014

Systemic lupus erythematosus (SLE) is a multisystemic disease, caused by a variety of factors, which lead to immunological abnormalities. Osteopontin (OPN) is a pleiotropic protein, important in bone remodeling and immune system signaling. OPN, produced by various cells, including immune cells, plays a key role in regulating T-helper 1/T-helper 2 balance, stimulating B lymphocytes to produce antibodies, regulating macrophages, neutrophils and inducing dendritic cells. OPN expression is influenced by genetic polymorphisms of its promoter, hormones and cytokines. Over expression of OPN has been associated with the pathogenesis of immune-mediated diseases. OPN has been implicated in the development of murine model of lupus and in humans with SLE. In this review, I will present current state of research on the role of OPN and OPN gene polymorphisms in pathogenesis and clinical course of SLE. A better understanding of the role of OPN in SLE will contribute to more precise diagnosis and treatment of the disease. © 2014, The Author(s).

Lisowska-Myjak B.,Medical University of Warsaw
Blood Purification | Year: 2010

Acute kidney injury (AKI) is a frequent clinical problem in critically ill patients and the associated mortality is high. Standard serum and urine biomarkers are insensitive and nonspecific for the detection of kidney injury in its early stages which limits the therapeutic options and may compromise the outcome. The study presents new candidates for biochemical markers of AKI, with potentially high sensitivity and specificity, causally related to its pathogenesis and development. Some of these biomarkers measured in serum or urine are well known in laboratory practice but have been used in other tests, while some novel biomarkers have been proposed as a result of experimental and clinical studies. In current clinical practice, identification and classification of AKI is based on elevations in serial serum creatinine concentrations, which are delayed and therefore unreliable in the acute setting. The most promising of the new serum AKI markers are cystatin C, neutrophil gelatinase-associated lipocalin and uric acid. Urinary AKI markers may be classified as enzymes released from damaged tubular cells (alkaline phosphatase, γ-glutamyl transpeptidase, alanine aminopeptidase, isoenzymes of glutathione transferase, N-acetyl-β-D-glucosaminidase), low-molecular-weight proteins (α1-microglobulin, β2-microglobulin, retinol-binding protein, cystatin C) and proteins specifically produced in the kidney and associated with the development of AKI [cysteine-rich protein 61, neutrophil gelatinase-associated lipocalin, kidney injury molecule 1, cytokines and chemokines (Gro-α, IL-18), and structural and functional proteins of renal tubules (F-actin, Na +/H+ exchange isoform 3)]. Based on the different expression of these markers, using a panel of serum and urine markers may potentially help to distinguish between various types of insults, establish the duration and severity of injury, predict the clinical outcome and help to monitor response to treatment in AKI. Copyright © 2010 S. Karger AG, Basel.

Struzycka I.,Medical University of Warsaw
Polish Journal of Microbiology | Year: 2014

Dental caries is one of the most common chronic and multifactorial diseases affecting the human population. The appearance of a caries lesion is determined by the coexistence of three main factors: acidogenic and acidophilic microorganisms, carbohydrates derived from the diet, and host factors. Socio-economic and behavioral factors also play an important role in the etiology of the disease. Caries develops as a result of an ecological imbalance in the stable oral microbiom. Oral microorganisms form dental plaque on the surfaces of teeth, which is the cause of the caries process, and shows features of the classic biofilm. Biofilm formation appears to be influenced by large scale changes in protein expression over time and under genetic control. Cariogenic microorganisms produce lactic, formic, acetic and propionic acids, which are a product of carbohydrate metabolism. Their presence causes a decrease in pH level below 5.5, resulting in demineralization of enamel hydroxyapatite crystals and proteolytic breakdown of the structure of tooth hard tissues. Streptococcus mutans, other streptococci of the so-called non-mutans streptococci group, Actinomyces and Lactobacillus play a key role in this process. Dental biofilm is a dynamic, constantly active metabolically structure. The alternating processes of decrease and increase of biofilm pH occur, which are followed by the respective processes of de- and remineralisation of the tooth surface. In healthy conditions, these processes are in balance and no permanent damage to the tooth enamel surface occurs.

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