14 research outputs found

    A TIME-MOTION ANALYSIS OF THE FOOTBALL WORLD CUP IN RUSSIA 2018

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    The focus of the research is the motion characteristics of the teams which participated in the World cup 2018 in Russia. For the purpose of the research we collected the data from all the matches in the knock out phase of the tournament. We divided the results for every position during the halves and calculated the total distance covered. This way we could get an idea of the intensity and the profile of elite soccer players. In the analyses we included 273 players that played in the knock out phase. As a result of the research, we found that the goalkeeper had total distance covered of 4061,59 meters; defenders had a 9352 meters; midfielders had a 10708 meters and strikers had a 9731 meters. It is interesting that the total distance covered during the second half is greater than in the first one. Conclusion of the research is that the total distance covered is different for all of the researched positions which is a predisposition for disclosing the motor profile of the players. From the study of motor activity in football at world championships we can draw the following conclusions:1) The results are confirmation that even at a World Cup the performance characteristics are greatly influenced by position of play; 2) The higher total distance covered during the second half suggests extremely high aerobic capabilities of elite football players

    Diabetes Mellitus in the Transplanted Kidney

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    Diabetes mellitus (DM) is the most common cause of chronic kidney disease (CKD) and end stage renal disease (ESRD). New onset diabetes mellitus after transplant (NODAT) has been described in approximately 30 percent of non-diabetic kidney transplant recipients many years post transplantation. DM in patients with kidney transplantation constitutes a major comorbidity, and has significant impact on the patients and allografts’ outcome. In addition to the major comorbidity and mortality that result from cardiovascular and other DM complications, long standing DM after kidney transplant has significant pathological injury to the allograft, which results in lowering the allografts and the patients’ survivals. In spite of the cumulative body of data on diabetic nephropathy (DN) in the native kidney, there has been very limited data on the DN in the transplanted kidney. In this review, we will shed the light on the risk factors that lead to the development of NODAT. We will also describe the impact of DM on the transplanted kidney, and the outcome of kidney transplant recipients with NODAT. Additionally, we will present the most acceptable data on management of NODAT

    Unwinding focal segmental glomerulosclerosis [version 1; referees: 3 approved]

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    Focal segmental glomerulosclerosis (FSGS) represents the most common primary glomerular disease responsible for the development of end-stage renal disease (ESRD) in the United States (US). The disease progresses from podocyte injury to chronic kidney disease (CKD), ultimately leading to total nephron degeneration. Extensive basic science research has been conducted to unwind the mechanisms of FSGS and, with those insights, understand major contributors of CKD in general. As a result, several putative molecules and pathways have been studied, all implicated in the disease; some serve, in addition, as early biomarkers. The ongoing research is currently focusing on understanding how these molecules and pathways can interplay and be utilized as potential diagnostic and therapeutic targets. Among these molecules, the soluble urokinase plasminogen activating receptor (suPAR) has been studied in detail, both clinically and from a basic science perspective. By now, it has emerged as the earliest and most robust marker of future CKD. Other circulating factors harming podocytes include anti-CD40 auto-antibody and possibly cardiotrophin-like cytokine factor-1. Understanding these factors will aid our efforts to ultimately cure FSGS and possibly treat a larger portion of CKD patients much more effectively

    Dyslipidemia, malnutrition, inflammation, cardiovascular disease and mortality in chronic kidney disease

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    Dyslipidemia, malnutrition and inflammation are common in patients with chronic kidney disease (CKD) and are strongly associated with cardiovascular disease (CVD) and increased mortality. The epidemiology of dyslipidemia and its interactions with malnutrition and inflammation in CKD patients have been the subject of much interest in the past decade. Recent clinical trials have explored the effects of statins on CVD specifically in CKD patients. Whereas the risk relationship between total cholesterol level and CVD morbidity and mortality is direct, strong and progressive in CKD patients without malnutrition and inflammation, it is inconsistent and often paradoxical in those with malnutrition and inflammation. Accumulating evidence demonstrates that statins reduce significantly the risk of CVD in CKD patients before the initiation of dialysis. However, the beneficial effect of statins in CKD patients on dialysis is uncertain. In CKD patients on dialysis, malnutrition and inflammation pose a higher risk for CVD than dyslipidemia. In CKD patients, the risk of CVD associated to dyslipidemia is complex and is modified by malnutrition and inflammation

    CD2AP in mouse and human podocytes controls a proteolytic program that regulates cytoskeletal structure and cellular survival

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    Kidney podocytes are highly differentiated epithelial cells that form interdigitating foot processes with bridging slit diaphragms (SDs) that regulate renal ultrafiltration. Podocyte injury results in proteinuric kidney disease, and genetic deletion of SD-associated CD2-associated protein (CD2AP) leads to progressive renal failure in mice and humans. Here, we have shown that CD2AP regulates the TGF-β1–dependent translocation of dendrin from the SD to the nucleus. Nuclear dendrin acted as a transcription factor to promote expression of cytosolic cathepsin L (CatL). CatL proteolyzed the regulatory GTPase dynamin and the actin-associated adapter synaptopodin, leading to a reorganization of the podocyte microfilament system and consequent proteinuria. CD2AP itself was proteolyzed by CatL, promoting sustained expression of the protease during podocyte injury, and in turn increasing the apoptotic susceptibility of podocytes to TGF-β1. Our study identifies CD2AP as the gatekeeper of the podocyte TGF-β response through its regulation of CatL expression and defines a molecular mechanism underlying proteinuric kidney disease
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