Relevant bibliographies by topics / Uremic toxin

Academic literature on the topic 'Uremic toxin'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Uremic toxin"

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Popkov, Vasily A., Anastasia A. Zharikova, Evgenia A. Demchenko, Nadezda V. Andrianova, Dmitry B. Zorov, and Egor Y. Plotnikov. "Gut Microbiota as a Source of Uremic Toxins." International Journal of Molecular Sciences 23, no. 1 (January 1, 2022): 483. http://dx.doi.org/10.3390/ijms23010483.

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Uremic retention solutes are the compounds that accumulate in the blood when kidney excretory function is impaired. Some of these compounds are toxic at high concentrations and are usually known as “uremic toxins”. The cumulative detrimental effect of uremic toxins results in numerous health problems and eventually mortality during acute or chronic uremia, especially in end-stage renal disease. More than 100 different solutes increase during uremia; however, the exact origin for most of them is still debatable. There are three main sources for such compounds: exogenous ones are consumed with food, whereas endogenous ones are produced by the host metabolism or by symbiotic microbiota metabolism. In this article, we identify uremic retention solutes presumably of gut microbiota origin. We used database analysis to obtain data on the enzymatic reactions in bacteria and human organisms that potentially yield uremic retention solutes and hence to determine what toxins could be synthesized in bacteria residing in the human gut. We selected biochemical pathways resulting in uremic retention solutes synthesis related to specific bacterial strains and revealed links between toxin concentration in uremia and the proportion of different bacteria species which can synthesize the toxin. The detected bacterial species essential for the synthesis of uremic retention solutes were then verified using the Human Microbiome Project database. Moreover, we defined the relative abundance of human toxin-generating enzymes as well as the possibility of the synthesis of a particular toxin by the human metabolism. Our study presents a novel bioinformatics approach for the elucidation of the origin of both uremic retention solutes and uremic toxins and for searching for the most likely human microbiome producers of toxins that can be targeted and used for the therapy of adverse consequences of uremia.
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Popkov, Vasily A., Denis N. Silachev, Arthur O. Zalevsky, Dmitry B. Zorov, and Egor Y. Plotnikov. "Mitochondria as a Source and a Target for Uremic Toxins." International Journal of Molecular Sciences 20, no. 12 (June 25, 2019): 3094. http://dx.doi.org/10.3390/ijms20123094.

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Elucidation of molecular and cellular mechanisms of the uremic syndrome is a very challenging task. More than 130 substances are now considered to be “uremic toxins” and represent a very diverse group of molecules. The toxicity of these molecules affects many cellular processes, and expectably, some of them are able to disrupt mitochondrial functioning. However, mitochondria can be the source of uremic toxins as well, as the mitochondrion can be the site of complete synthesis of the toxin, whereas in some scenarios only some enzymes of the pathway of toxin synthesis are localized here. In this review, we discuss the role of mitochondria as both the target and source of pathological processes and toxic compounds during uremia. Our analysis revealed about 30 toxins closely related to mitochondria. Moreover, since mitochondria are key regulators of cellular redox homeostasis, their functioning might directly affect the production of uremic toxins, especially those that are products of oxidation or peroxidation of cellular components, such as aldehydes, advanced glycation end-products, advanced lipoxidation end-products, and reactive carbonyl species. Additionally, as a number of metabolic products can be degraded in the mitochondria, mitochondrial dysfunction would therefore be expected to cause accumulation of such toxins in the organism. Alternatively, many uremic toxins (both made with the participation of mitochondria, and originated from other sources including exogenous) are damaging to mitochondrial components, especially respiratory complexes. As a result, a positive feedback loop emerges, leading to the amplification of the accumulation of uremic solutes. Therefore, uremia leads to the appearance of mitochondria-damaging compounds, and consecutive mitochondrial damage causes a further rise of uremic toxins, whose synthesis is associated with mitochondria. All this makes mitochondrion an important player in the pathogenesis of uremia and draws attention to the possibility of reducing the pathological consequences of uremia by protecting mitochondria and reducing their role in the production of uremic toxins.
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Castillo-Rodriguez, Esmeralda, Raul Fernandez-Prado, Raquel Esteras, Maria Perez-Gomez, Carolina Gracia-Iguacel, Beatriz Fernandez-Fernandez, Mehmet Kanbay, et al. "Impact of Altered Intestinal Microbiota on Chronic Kidney Disease Progression." Toxins 10, no. 7 (July 19, 2018): 300. http://dx.doi.org/10.3390/toxins10070300.

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In chronic kidney disease (CKD), accumulation of uremic toxins is associated with an increased risk of CKD progression. Some uremic toxins result from nutrient processing by gut microbiota, yielding precursors of uremic toxins or uremic toxins themselves, such as trimethylamine N-Oxide (TMAO), p-cresyl sulphate, indoxyl sulphate and indole-3 acetic acid. Increased intake of some nutrients may modify the gut microbiota, increasing the number of bacteria that process them to yield uremic toxins. Circulating levels of nutrient-derived uremic toxins are associated to increased risk of CKD progression. This offers the opportunity for therapeutic intervention by either modifying the diet, modifying the microbiota, decreasing uremic toxin production by microbiota, increasing toxin excretion or targeting specific uremic toxins. We now review the link between nutrients, microbiota and uremic toxin with CKD progression. Specific focus will be placed on the generation specific uremic toxins with nephrotoxic potential, the decreased availability of bacteria-derived metabolites with nephroprotective potential, such as vitamin K and butyrate and the cellular and molecular mechanisms linking these toxins and protective factors to kidney diseases. This information provides a conceptual framework that allows the development of novel therapeutic approaches.
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Kiss, István. "The uremic toxin indoxyl sulfate reflects cardio-renal risk and intestinal-renal relationship." Orvosi Hetilap 152, no. 43 (October 2011): 1724–30. http://dx.doi.org/10.1556/oh.2011.29223.

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Uremic syndrome and condition is primarily a result of kidney failure in which uremic toxins are accumulated. More and more attention is paid to possibilities for removal of uremic toxins, which not only means dialysis, but also takes into account special dietary considerations and treatments, which aim to absorb the toxins or reduce their production. These uremic toxins, which also increase the cardiovascular risks, play a major part in morbidity and mortality of patients suffering from chronic renal failure and those receiving renal replacement therapy. One of them is a member of the indol group, the indoxyl sulfate. This toxin is difficult to remove with dialysis and is an endogenous protein-bound uremic toxin. Today we know that indoxyl sulfate is a vascular-nephrotoxic agent, which is able to enhance progression of cardiovascular and renal diseases. It is of particular importance that because of its redox potency, this toxin causes oxidative stress and antioxidant effects at the same time and, on top of that, it is formed in the intestinal system. Its serum concentration depends on the nutrition and the tubular function and, therefore, it can also signal the progression of chronic renal failure independently of glomerular filtration rate. Successful removal of indoxyl sulfate reduces the morbidity and mortality and improves survival. Therefore, it could be a possible target or area to facilitate the reduction of uremia in chronic renal failure. The use of probiotics and prebiotics with oral adsorbents may prove to be a promising opportunity to reduce indoxyl sulfate accumulation. Orv. Hetil., 2011, 152, 1724–1730.
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Chen, Jia-Huang, and Chih-Kang Chiang. "Uremic Toxins and Protein-Bound Therapeutics in AKI and CKD: Up-to-Date Evidence." Toxins 14, no. 1 (December 23, 2021): 8. http://dx.doi.org/10.3390/toxins14010008.

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Uremic toxins are defined as harmful metabolites that accumulate in the human body of patients whose renal function declines, especially chronic kidney disease (CKD) patients. Growing evidence demonstrates the deteriorating effect of uremic toxins on CKD progression and CKD-related complications, and removing uremic toxins in CKD has become the conventional treatment in the clinic. However, studies rarely pay attention to uremic toxin clearance in the early stage of acute kidney injury (AKI) to prevent progression to CKD despite increasing reports demonstrating that uremic toxins are correlated with the severity of injury or mortality. This review highlights the current evidence of uremic toxin accumulation in AKI and the therapeutic value to prevent CKD progression specific to protein-bound uremic toxins (PBUTs).
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Jansen, Jitske, Joachim Jankowski, Prathibha R. Gajjala, Jack F. M. Wetzels, and Rosalinde Masereeuw. "Disposition and clinical implications of protein-bound uremic toxins." Clinical Science 131, no. 14 (June 30, 2017): 1631–47. http://dx.doi.org/10.1042/cs20160191.

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In patients with chronic kidney disease (CKD), adequate renal clearance is compromised, resulting in the accumulation of a plethora of uremic solutes. These uremic retention solutes, also named uremic toxins, are a heterogeneous group of organic compounds with intrinsic biological activities, many of which are too large to be filtered and/or are protein bound. The renal excretion of protein-bound toxins depends largely on active tubular secretion, which shifts the binding and allows for active secretion of the free fraction. To facilitate this process, renal proximal tubule cells are equipped with a range of transporters that co-operate in basolateral uptake and luminal excretion. Many of these transporters have been characterized as mediators of drug disposition, but have recently been recognized for their importance in the proximal renal tubular transport of uremic toxins as well. This also indicates that during uremia, drug disposition may be severely affected as a result of drug–uremic toxin interaction. In addition, CKD patients receive various drugs to treat their complications potentially resulting in drug–drug interactions (DDIs), also for drugs that are non-renally excreted. This review discusses the current knowledge on formation, disposition and removal of protein-bound uremic toxins. Furthermore, implications associated with drug treatment in kidney failure, as well as innovative renal replacement therapies targetting the protein-bound uremic toxins are being discussed. It will become clear that the complex problems associated with uremia warrant a transdisciplinary approach that unites research experts in the area of fundamental biomedical research with their colleagues in clinical nephrology.
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Chao, Chia-Ter, and Shih-Hua Lin. "Uremic Vascular Calcification: The Pathogenic Roles and Gastrointestinal Decontamination of Uremic Toxins." Toxins 12, no. 12 (December 21, 2020): 812. http://dx.doi.org/10.3390/toxins12120812.

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Uremic vascular calcification (VC) commonly occurs during advanced chronic kidney disease (CKD) and significantly increases cardiovascular morbidity and mortality. Uremic toxins are integral within VC pathogenesis, as they exhibit adverse vascular influences ranging from atherosclerosis, vascular inflammation, to VC. Experimental removal of these toxins, including small molecular (phosphate, trimethylamine-N-oxide), large molecular (fibroblast growth factor-23, cytokines), and protein-bound ones (indoxyl sulfate, p-cresyl sulfate), ameliorates VC. As most uremic toxins share a gut origin, interventions through gastrointestinal tract are expected to demonstrate particular efficacy. The “gastrointestinal decontamination” through the removal of toxin in situ or impediment of toxin absorption within the gastrointestinal tract is a practical and potential strategy to reduce uremic toxins. First and foremost, the modulation of gut microbiota through optimizing dietary composition, the use of prebiotics or probiotics, can be implemented. Other promising strategies such as reducing calcium load, minimizing intestinal phosphate absorption through the optimization of phosphate binders and the inhibition of gut luminal phosphate transporters, the administration of magnesium, and the use of oral toxin adsorbent for protein-bound uremic toxins may potentially counteract uremic VC. Novel agents such as tenapanor have been actively tested in clinical trials for their potential vascular benefits. Further advanced studies are still warranted to validate the beneficial effects of gastrointestinal decontamination in the retardation and treatment of uremic VC.
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Sato, Toshihiro, Hiroaki Yamaguchi, Takuma Kogawa, Takaaki Abe, and Nariyasu Mano. "Organic Anion Transporting Polypeptides 1B1 and 1B3 Play an Important Role in Uremic Toxin Handling and Drug-Uremic Toxin Interactions in the Liver." Journal of Pharmacy & Pharmaceutical Sciences 17, no. 4 (October 27, 2014): 475. http://dx.doi.org/10.18433/j3m89q.

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PURPOSE. Organic anion-transporting polypeptide (OATP) 1B1 and OATP1B3 contribute to hepatic uptake of numerous drugs. Thus, reduced OATP1B1 and OATP1B3 activity in chronic kidney disease (CKD) may have a major impact on the hepatic clearance of drugs. The effect of drug-uremic toxin interactions on OATP1B1 and OATP1B3 has not been well studied. In the present study, we examine the inhibitory effects of uremic toxins on OATP1B1 and OATP1B3 transport activity to evaluate the interactions between drugs and uremic toxins in patients with chronic kidney disease. METHODS. [3H]Estron-3-sulfate, [3H]taurocholate uptake and [3H]methotrexate by OATP1B1 and OATP1B3 expressing HEK293 cells were performed to evaluate the inhibitory effect of uremic toxins. To clarify whether the uremic toxins that interact with OATP1B1 and/or OATP1B3 were substrates for these transporters, we performed uptake studies. RESULTS. Four uremic toxins, kynurenic acid, indole-3-acetic acid, indoxyl sulfate, and p-cresol, inhibited OATP1B1- and OATP1B3-mediated transport in a concentration-dependent manner, with IC50 values of 180, 770, 2700, and 4600 µM, respectively, for OATP1B1 and 180, 1100, 1300, and 1700 µM, respectively, for OATP1B3. [3H]Methotrexate uptake by OATPs was also inhibited by the four uremic toxins in a dose-dependent manner. Uptake studies revealed that kynurenic acid is a substrate for both the OATP1B1 and OATP1B3. Moreover, OATP1B3 was involved in the transport of indoxyl sulfate. Indole-3-acetic acid and p-cresol were not significantly transported by OATP1B1 and OATP1B3. CONCLUSIONS. We showed that some uremic toxins inhibit OATP-mediated uptake in a concentration-dependent manner, and clarified OATPs contribution to uremic toxin handling in the liver. Thus, we provided basic information to estimate the inhibitory effects of uremic toxins on OATPs in CKD patients. These data suggest that the dose of drugs excreted via renal and non-renal pathways should be carefully adjusted in CKD patients.This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.
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Yamagami, Fumi, Kazuko Tajiri, Dai Yumino, and Masaki Ieda. "Uremic Toxins and Atrial Fibrillation: Mechanisms and Therapeutic Implications." Toxins 11, no. 10 (October 13, 2019): 597. http://dx.doi.org/10.3390/toxins11100597.

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Atrial fibrillation (AF) is the most prevalent arrhythmia in the general population. There is a close association between chronic kidney disease (CKD) and AF. In recent years, attention has been focused on the relationship between AF and uremic toxins, including indoxyl sulfate (IS). Several animal studies have shown that IS promotes the development and progression of AF. IS has been shown to cause fibrosis and inflammation in the myocardium and exacerbate AF by causing oxidative stress and reducing antioxidative defense. Administration of AST-120, an absorbent of uremic toxins, decreases uremic toxin-induced AF in rodents. We have recently reported that patients with a higher serum IS level exhibit a higher rate of AF recurrence after catheter ablation, with serum IS being a significant predictor of AF recurrence. In this review, we discuss the possible mechanisms behind the AF-promoting effects of uremic toxins and summarize the reported clinical studies of uremic toxin-induced AF.
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Masereeuw, Rosalinde. "The Dual Roles of Protein-Bound Solutes as Toxins and Signaling Molecules in Uremia." Toxins 14, no. 6 (June 11, 2022): 402. http://dx.doi.org/10.3390/toxins14060402.

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In patients with severe kidney disease, renal clearance is compromised, resulting in the accumulation of a plethora of endogenous waste molecules that cannot be removed by current dialysis techniques, the most often applied treatment. These uremic retention solutes, also named uremic toxins, are a heterogeneous group of organic compounds of which many are too large to be filtered and/or are protein-bound. Their renal excretion depends largely on renal tubular secretion, by which the binding is shifted towards the free fraction that can be eliminated. To facilitate this process, kidney proximal tubule cells are equipped with a range of transport proteins that cooperate in cellular uptake and urinary excretion. In recent years, innovations in dialysis techniques to advance uremic toxin removal, as well as treatments with drugs and/or dietary supplements that limit uremic toxin production, have provided some clinical improvements or are still in progress. This review gives an overview of these developments. Furthermore, the role protein-bound uremic toxins play in inter-organ communication, in particular between the gut (the side where toxins are produced) and the kidney (the side of their removal), is discussed.
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Dissertations / Theses on the topic "Uremic toxin"

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Bollinger, Laurie M. "Factors affecting prevalence of Shiga toxin-producing Escherichia coli in cattle /." abstract and full text PDF (UNR users only), 2008. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3329564.

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Morigi, Marina. "Unravelling molecular and biochemical dysfunction by Shiga toxin: implication for thrombotic microangiopathy in Hemolytic Uremic Syndrome." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 2006. http://arno.unimaas.nl/show.cgi?fid=7590.

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Karpman, Diana O. "Studies of the pathogenesis of hemolytic uremic syndrome and thrombotic thrombocytopenic purpura." Lund : Lund University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/68945090.html.

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Leeper, Molly Maitland. "Trends in Toxin Profiles of Human Shiga Toxin-Producing Escherichia Coli (STEC) O157 Strains, United States, 1996-2008." Atlanta, Ga. : Georgia State University, 2009. http://digitalarchive.gsu.edu/iph_theses/57/.

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Thesis (M.P.H.)--Georgia State University, 2009.
Title from file title page (Digital Archive@GSU, viewed June 16, 2010) Karen Giseker, committee chair; Peter Gerner-Smidt, committee member. Includes bibliographical references (p. 101-105).
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Gomes, Priscila Aparecida Dal Pozo. "Desenvolvimento de uma nova estratégia vacinal contra síndrome hemolítica urêmica utilizando linhagens geneticamente modificadas de Bacillus subtilis capazes de expressar a toxina Stx2 de EHEC." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/42/42132/tde-04062008-102629/.

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A Síndrome Hemolítica Urêmica (SHU) é a principal doença associada à infecção com linhagens de Escherichia coli produtoras de toxina de Shiga (Stx), doença para qual não há uma vacina ou tratamento específico. A toxina Stx é formada por uma subunidade A enzimaticamente ativa e uma B pentamérica responsável pela ligação da toxina na célula hospedeira. Neste trabalho propomos o uso de Bacillus subtilis, uma bactéria não patogênica e formadora de esporos, como veículo vacinal para a expressão de formas atóxicas da Stx2, sob o controle de um promotor induzível por estresse (PgsiB). Camundongos BALB/c imunizados com células vegetativas ou esporos das linhagens vacinais de B. subtilis, por diferentes vias, induziram baixos níveis de anticorpos anti-Stx em soro (IgG) e fezes (IgA). Avaliamos também o potencial imunogênico da Stx gerada em linhagens recombinates de E. coli, mas os anticorpos gerados não foram capazes de neutralizar a toxina nativa. Os resultados indicam que formas alternativas de expressão e/ou o uso de adjuvantes são necessárias para gerar formulações vacinais eficazes contra a SHU.
The Hemolytic Uremic Syndrome (HUS) is the main disease associated with infections with Shiga toxin (Stx) - producing Escherichia coli strain and no effective vaccine or treatment exist. The Stx toxin consist of an enzymatically active A subunit and a pentameric B subunit responsible toxin binding to host cells. In this work we propose the use of Bacillus subtilis, a harmless spore form bacteria as a vaccine vehicle for the expression atoxic forms of Stx2, under the control of stress inducible (PgsiB) promoter. BALB/c mice immunized with vegetative cells and spores of the B. subtilis vaccine strain using different immunization routes elicited low specific antibody levels at serum (IgG) or fecal extracts (IgA). We also investigated the immunogenic potencial of StxB purified from recombinant E. coli strain, but the induced anti-StxB antibodies did not neutralize the native toxin. The results indicate that alternative expression system or the incorporation of the adjuvants are required for the generation of vaccine formulation active against HUS.
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McGannon, Colleen M. "Antibiotic Therapy in the Treatment of E. coli O157:H7." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1230919332.

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Fogo, Verônica Simões. "Prevalência e caracterização de Escherichia coli O157:H7 e outras cepas produtoras de toxina de Shiga (STEC) na linha de abate de carne bovina destinada à exportação." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/9/9131/tde-27012017-123850/.

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Escherichia coli é um microrganismo presente no trato intestinal do homem e de animais de sangue quente, fazendo parte da microbiota, coexistindo sem causar danos ao hospedeiro. No entanto, algumas linhagens desse microrganismo podem ser patogênicas e causar doenças tanto ao homem como aos animais. E. coli produtoras de toxina de Shiga (STEC), consideradas patógenos de origem alimentar, podem causar desde diarréias brandas até severas e sanguinolentas a complicações graves, como colite hemorrágica (HC), síndrome urêmica hemolítica (HUS) e púrpura trombótica trombocitopênica (TTP). O gado é considerado um importante reservatório deste patógeno e a contaminação de seres humanos ocorre, na maioria das vezes, através do consumo de alimentos ou água contaminados. O presente trabalho teve como objetivos avaliar a ocorrência de E. coli O157:H7 e outras STEC em amostras de couro de animais bovinos e de suas respectivas carcaças, na etapa de pré-evisceração, e meia-carcaças, na etapa de pós-evisceração; identificar os genes que codificam para os fatores de virulência (stx1 , stx2, eaeA e ehxA) dos isolados obtidos; evidenciar cepas de E. coli O157:H7 através da pesquisa do gene uidA; identificar os sorotipos dos isolados; verificar a citotoxicidade dos isolados de STEC em células Vero e avaliar a sensibilidade a diferentes antibióticos. De 198 animais amostrados, sete (3,5%) apresentaram cepas de STEC. Em seis (3%) destes, STEC foi detectada no couro e em um (0,5%) foi isolada de meia-carcaça, não tendo sido detectada em amostras de carcaça. As 23 cepas isoladas do couro apresentaram o perfil stx2, eaeA, uidA e ehxA, podendo ser consideradas E. coli enterohemorrágica (EHEC), e a isolada de meia carcaça apresentou o perfil stx2, uidA e ehxA. Das 24 cepas isoladas, 13 (54,2%) pertenciam ao sorotipo O157:H7. Além deste sorotipo, foram isoladas cepas de outros sorotipos previamente descritos e associados a doenças humanas severas no Brasil e em outros países, como O174:H21, O6:H49, ONT:H7, ONT:H8 e OR:H10. Dos sete animais com cepas positivas para stx2e ehxA, cinco (71,4%) apresentaram cepas com atividade citotóxica em células Vero e um (14,2%) apresentou cepas positivas na avaliação da produção de entero-hemolisina. Com relação ao teste com antibióticos, quatro (16,7%) das 24 cepas testadas apresentaram resistência a um ou mais antibióticos, sendo três (12,5%) a estreptomicina e uma (4,2%) a estreptomicina e ampicilina. Diante destes resultados, pode-se dizer que a produção de entero-hemolisina e a pesquisa dos genes ehxA e uidA não demonstraram ser bons marcadores na pesquisa do sorotipo O157:H7. A presença de cepa de STEC na meia-carcaça alerta para a necessidade de vigilância da presença destes microrganismos, uma vez que eles poderiam contaminar o produto final, colocando em risco a saúde do consumidor.
Escherichia coli is a microorganism present in the intestinal tract of humans and warm-blood animals, being part of the normal microbiota and harmless to the host. However, some strains are able to cause human and animal infections. Shiga toxin-producing E. coli (STEC), regarded as foodborne pathogens, can cause since mild or severe and bloody diarrhea to major complications, such as hemorrhagic colitis (HC), hemolytic-uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP). Cattle are considered the main reservoir of this pathogen and the transmission to humans happens, most of the times, due to the consumption of contaminated food or water. The aim of the present research was to determine the prevalence of E. coli O157:H7 and other STEC on hide samples of beef cattle and on their corresponding carcasses, sampled prior to evisceration, and half-carcasses, sampled after evisceration; identity the genes that code for the virulence factors (stx1, stx2, eaeA e ehxA) of the isolates; detect E. coli O157:H7 strains using the gene uidA as epidemiological marker; identify the serotypes of the STEC isolates; verify the citotoxicity of the isolates in Vero cells and evaluate their resistance to different antibiotics. From 198 animals sampled, seven (3.5%) carried STEC strains. In six (3%) of them, STEC was detected on hide and in one (0.5%) it was isolated from half-carcass. The 23 strains isolated from hide presented the profile stx2, eaeA, uidA e ehxA, and were regarded as enterohemorrhagic Escherichia coli (EHEC), and the one isolated from half-carcass presented the profile stx2, uidA e ehxA. From the 24 isolated strains, 13 (54.2%) belonged to the serotype O157:H7. Besides this serotype, other strains belonging to serotypes that have been previously described and associated with severe human infections in Brazil and other countries, such as O174:H21 , O6:H49, ONT:H7, ONT:H8 and OR:H10, were isolated. From seven animals with strains harboring stx2, and ehxA, five (71.4%) presented verocytotoxigenic strains and one (14.2%) presented enterohemolisin producing strains. Regarding the antibiotics tested, four (16.7%) of the 24 isolated strains were resistant to some antibiotic, being three (12.5%) to streptomycin and one (4.2%) to streptomycin and ampicilin. Faced with these results, the production of enterohemolisin and the search of the genes ehxA and uidA can not be considered good epidemiological markers for the serotype O157:H7. The isolation of STEC strain from the half-carcass alerts for the need of surveillance on the presence of these microorganisms, since they may contaminate the final product, representing a risk to consumers health.
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ASTORI, EMANUELA. "IN VITRO AND IN VIVO APPROACHES TO STUDY OXIDATIVE STRESS, ANEMIA AND DYSBIOSIS IN CHRONIC KIDNEY DISEASE." Doctoral thesis, Università degli Studi di Milano, 2021. http://hdl.handle.net/2434/818976.

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CKD is diagnosed when there’s a decreased kidney function shown by a GFR less than 60 ml / min (established for a reference man with 1.73 m² body surface area), or markers of kidney damage, or both, of at least 3 months duration. The severity of complications increases in parallel with the GFR decline. We focused on three comorbidities extremely common in CKD patients: oxidative stress and inflammation; anemia and dysbiosis. We investigated these CKD comorbidities both with in vitro and in vivo approaches. More in detail, regarding in vivo studies, we measured oxidative stress biomarkers in a population of ESRD patients before and after the hemodialysis treatment, comparing the results with a population of healthy subjects; we evaluated oxidative stress biomarkers in the plasma of HD patients before, during and after two type of iron treatments (intravenous and sucrosomial iron). Regarding in vitro experiments, we focused on two uremic toxins, urea and indoxyl sulphate, and we evaluated their effects on a human endothelial cell line (Human Microvascular Endothelial Cells 1, HMEC-1).
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Loganathan, Narasimhan. "Adsorption of protein bound uremic toxins in zeolites : a molecular simulation study." Aix-Marseille 1, 2010. http://www.theses.fr/2010AIX11120.

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Le paracrésol sous sa forme libre est une toxine urémique causant des dommages cellulaires très importants qui peuvent conduire E1 des arrêts cardiaques. Le traitement de l'insuffisance rénale repose principalement sur l‘utilisation de la dialyse. Il s'avère cependant que ce procédé ne permet pas une élimination efficace de la toxine. Une alternative serait d'utiliser des zéolithes afin de piéger la molécule pour ensuite l'éliminer. Ce travail de thèse présente une étude théorique de l‘adsorption du paracrésol et de l'eau dans les zéolithes silicalite-1 et faujasites NaY. Les simulations ont été réalisées par la technique Monte Carlo dans les ensembles grand-canonique et canonique à une température de 37°C (310 K). Les résultats montrent qu‘un effet coopératif interviendrait entre les deux molécules lors de la coadsorption dans la silicalite-1. L‘étude détaillée des interactions énergétiques intermoléculaires semble confirmer cette hypothèse. Les simulations montrent que le mécanisme d'adsorption dans la faujasite est quelque peu différent
The paracresol as a free molecule is a uremic toxin that may cause critical cell damages which can eventually lead to heart failures. The treatment of renal insufficiency is essentially based on the utilisation of the dialysis techniques. However, it appears that, this process does not allow the effective elimination of the molecule. A possible alternative would be to use zeolites to sequestrate the molecule in order to eliminate it. This PhD thesis presents a theoretical investigation of the adsorption of paracresol and water in the silicalite-1 and faujasite NaX and NaY zeolites. The computer simulations were performed using the Monte Carlo technique in both the grand-canonical and canonical ensembles at a temperature of 98. 6° (310 K). The results show that, a cooperative effect could appear between both molecules during the coadsorption in silicalite-1. The detailed study of the energetic intermolecular interactions seems to confirm this hypothesis. The simulations show that, the mechanism of adsorption in the faujasite zeolites is somewhat different
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Yi, Dan. "Contribution to the study of uremic toxins in the context of chronic kidney disease." Thesis, Lyon, 2018. http://www.theses.fr/2018LYSEI054.

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L'insuffisance rénale chronique (IRC) est une affection caractérisée par une perte progressive de la fonction rénale. L’IRC est associée à l'accumulation de diverses toxines urémiques. Les toxines urémiques ou solutés de rétention de l'urémie sont des composés qui s'accumulent chez les patients atteints d'IRC en raison d'un défaut de clairance rénale et qui exercent des effets biologiques délétères. Les hémodialyses éliminent mal les toxines urémiques liées aux protéines (PBUT), en raison de leur liaison aux protéines plasmatiques, en particulier la sérumalbumine humaine. En conséquence, les toxines urémiques liées aux protéines s'accumulent chez les patients atteints d'IRC et leur concentration ne peut que difficilement être diminuée chez les patients atteints d'insuffisance rénale terminale (IRT). Mes travaux sont principalement centrés sur les toxines urémiques, en particulier les toxines urémiques liées aux protéines, comme l’indoxyl-sulfate (IS), l'acide phénylacétique (PAA) et le p-crésyl-glucuronide (p-CG); et la zinc-alpha2-glycoprotéine (ZAG) qui est une « middle molécule ». Nous avons étudié le rôle de l'IS dans le développement de la résistance à l'insuline et d'autres troubles métaboliques associés à l'IRC, ainsi que ses effets sur l'inflammation et le stress oxydant. Nous avons exploré les propriétés de liaison du PAA et du p-CG à la sérumalbumine, qui est la plus abondante protéine dans le plasma humain. Enfin, nous avons essayé de développer une nouvelle stratégie d'élimination des PBUT, à l’aide de déplaceurs/compétiteurs chimique
Chronic kidney disease (CKD) is a condition characterized by progressive loss of kidney function. CKD is associated with the accumulation of various uremic toxins. Uremic toxins or uremic retention solutes are compounds that accumulate in patients with CKD due to impaired renal clearance and exert deleterious biological effects. Protein-bound uremic toxins (PBUT) is poorly removed by hemodialysis because of its binding to plasma proteins, particularly human serum albumin. As a result, protein-bound uremic toxins accumulate in patients with CKD and their concentration can hardly be reduced in patients with end-stage renal disease (ESRD). My work focuses mainly on uremic toxins, particularly protein-bound uremic toxins such as indoxyl-sulfate (IS), phenylacetic acid (PAA) and p-cresyl-glucuronide (p-CG); and zinc-alpha2-glycoprotein (ZAG) which is a "middle molecule". We investigated the role of IS in the development of insulin resistance and other metabolic disorders associated with CKD, as well as its effects on inflammation and oxidative stress. We have investigated the binding properties of PAA and p-CG to serum albumin, which is the most abundant protein in human plasma. Finally, we tried to develop a new strategy to eliminate PBUTs, using chemical displacers / competitors
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Books on the topic "Uremic toxin"

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Ringoir, Severin, Raymond Vanholder, and Shaul G. Massry, eds. Uremic Toxins. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5445-1.

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Niwa, Toshimitsu, ed. Uremic Toxins. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118424032.

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Niwa, Toshimitsu. Uremic toxins. Hoboken, N.J: John Wiley & Sons, 2012.

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Ghent Symposium on Uremic Toxins (1986). Uremic toxins. New York: Plenum Press, 1987.

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Saito, Hideyuki, and Takaaki Abe, eds. Uremic Toxins and Organ Failure. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-7793-2.

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Enterohemorrhagic Escherichia coli and Other Shiga Toxin-Producing E. coli. ASM Press, 2015.

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Escherichia coli O157:H7 and other shiga toxin-producing E. coli strains. Washington, DC: ASM Press, 1998.

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Niwa, Toshimitsu. Uremic Toxins. Wiley & Sons, Incorporated, John, 2012.

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Niwa, Toshimitsu. Uremic Toxins. Wiley & Sons, Incorporated, John, 2012.

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Niwa, Toshimitsu. Uremic Toxins. Wiley & Sons, Incorporated, John, 2012.

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Book chapters on the topic "Uremic toxin"

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D’Haese, Patrick C., Frank L. Van de Vyver, Ludwig V. Lamberts, and Marc E. De Broe. "Aluminum an Uremic Toxin." In Advances in Experimental Medicine and Biology, 89–96. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5445-1_12.

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Yamamoto, Suguru. "Uremic Toxin-Related Systemic Disorders." In Uremic Toxins and Organ Failure, 53–67. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-7793-2_4.

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Massry, Shaul G. "Parathyroid Hormone: A Uremic Toxin." In Advances in Experimental Medicine and Biology, 1–17. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5445-1_1.

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Ouchi, Haruki, Yosuke Hirakawa, and Reiko Inagi. "D-serine as a Novel Uremic Toxin." In Uremic Toxins and Organ Failure, 115–29. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-7793-2_8.

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Vo, Victoria, and Stuart M. Sprague. "Parathyroid Hormone as a Uremic Toxin." In Parathyroid Glands in Chronic Kidney Disease, 143–49. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43769-5_9.

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Fujimori, Akira. "Beta-2-Microglobulin as a Uremic Toxin: the Japanese Experience." In Contributions to Nephrology, 129–33. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000321751.

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Shintani, H., A. B. Wojcik, R. Tawa, and S. Uchiyama. "Uremic toxin analysis with pre- and post-column immobilized enzyme reactors." In Analytical Applications of Immobilized Enzyme Reactors, 131–73. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1310-6_4.

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Vanholder, R., N. Meert, E. Schepers, and G. Glorieux. "From Uremic Toxin Retention to Removal by Convection: Do We Know Enough?" In Hemodialysis - From Basic Research to Clinical Trials, 125–31. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000130657.

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Glassock, Richard J., and Shaul G. Massry. "Uremic Toxins: An Integrated Overview of Definition and Classification." In Uremic Toxins, 1–12. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118424032.ch1.

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Teplan, Vladimír, and Jaroslav Racek. "Asymmetric Dimethylarginine." In Uremic Toxins, 143–61. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118424032.ch10.

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Conference papers on the topic "Uremic toxin"

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Kanzelmeyer, N. K., C. Lerch, D. Hohmann, C. Junge, L. Neubert, A. Fieguth, P. Beerbaum, D. Haffner, L. Pape, and M. Böhne. "Cardiac Involvement in Shiga Toxin-Producing Escherichia coli–Induced Hemolytic Uremic Syndrome." In The 54th Annual Meeting of the German Society for Pediatric Cardiology (DGPK). Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1742975.

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Holmar, Jana, Fredrik Uhlin, Rain Ferenets, Kai Lauri, Risto Tanner, Jurgen Arund, Merike Luman, and Ivo Fridolin. "Estimation of removed uremic toxin indoxyl sulphate during hemodialysis by using optical data of the spent dialysate." In 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6611095.

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Schiefer, Elberth M., Andressa F. Santos, Marcia Muller, Andrea E. M. Stinghen, Lucas H. Negri, and Jose L. Fabris. "Study of Interferents of a Plasmonic Sensor for Uremic Toxins." In 2022 SBFoton International Optics and Photonics Conference (SBFoton IOPC). IEEE, 2022. http://dx.doi.org/10.1109/sbfotoniopc54450.2022.9992542.

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Leboucher, A., M. Rath, and A. Kleinridders. "Increased uremic toxins in cerebrospinal fluid of obese mice cause insulin resistance." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641817.

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Zoja, C., L. Furci, F. Ghilardi, P. Zilio, A. Benigni, and G. Remuzzi. "CYCLOSPORIN A (CyA) INDUCED ENDOTHELIAL CELL INJURY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644123.

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The chronic administration of CyA to animals and humans to prevent graft rejection may induce renal arteriolar damage resembling hemolytic uremic syndrome (HUS). This is a syndrome of vascular damage with thrombotic occlusions of the microcirculation. Endothelial damage is considered the first event in the pathogenetic cascade leading to HUS. We have used bovine aortic endothelial cells in culture to address the issue of CyA-induced arteriolar damage. CyA-induced a time (1-24 hours) and dose (1-50 μM) dependent cell damage. CyA-induced injury was characterized by an early cell detachment followed by lysis as documented by the increase in LDH and Cr release. 1 μM CyA did not induce cell detachment and lysis was evident only after prolonged incubations. 10 and 50 μM CyA both induced marked cell detachment and lysis: lysis started 3 hours after incubation of endothelial cells with CyA and was maximal at the end of 24 hour incubation (LDH release, percent specific increase over control values: 10 μM CyA, 47%; 50 μM CyA, 70%; 51 Cr release, percent specific increase over control values: 10 μM CyA, 28%; 50 μM CyA, 34%). CyA-induced injury was associated with dose- and time-depedent increase in prostacyclin (PGI2) and thromboxane A2 (TxA2) release by endothelial cells exposed to 10 and 50 μM CyA. CyA-induced generation of PGI2 and TxA2 was inhibited when the incubations were carried-on in the presence of acetyl salicilic acid (500 μM). These studies indicate that CyA exerts a direct toxic effect on endothelial cells and might help to understand the pathogenesis of CyA-induced vascular damage.
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Broderick, Stephen P., Gráinne Carroll, and Micheal Walsh. "Geometric Enhancements of an Arteriovenous Graft." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206863.

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End Stage Renal Disease (ESRD) is the degeneration of kidney function to remove uremic toxins from the blood. Currently there are over 484,000 sufferers of ESRD in the United States, with this figure predicted to rise to over 800,000 by 2020 [1]. The total cost of care for patients with ESRD was estimated to exceed 1 billion dollars in the United States [2]. A kidney transplant is the ideal solution for ESRD patients; however with the increasing number of ESRD patients the odds of receiving a donor kidney are poor. The alternative is hemodialysis. This process is involves the extraction of blood from the patient to an extracorporal machine. Blood is pumped at a rate of 350 mL/min to ensure effective dialysis. The blood is then returned to the body cleaned. The gold standard for hemodialysis access is the native arteriovenous fistula [3] with the most common type being the Brescia-Cimino fistula at the wrist [4]. In some subgroups the fistula performs poorly. In diabetics and the elderly, specifically over 70s [2] or can’t be constructed because of unsuitable blood vessels [5]. In this case an alternative is the synthetic AV graft. Made of polytetrafluoroethelyne, it has lower patency rates against the fistula [6] [7] mediated by the susceptibility to thrombosis induced by stenosis development and infection [7].The majority of stenosis development is within the venous anastomosis (kanterman1995). The formation of intimal hyperplasia (IH) leading to stenosis formation is caused by smooth cell proliferation and migration as a result of endothelial cells reacting to shear stress receptors. The development of IH has been linked to local hemodynamics and turbulence in the flow, which in turn are heavily influenced by the geometry of the graft.
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Capata, Roberto. "Peristaltic Roller Pump: Parametric Optimization for Hemolysis Control." In ASME 2020 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/imece2020-23371.

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Abstract This work aims to analyze the various types of peristaltic pumps by studying, in particular, the use of the peristaltic roller pump to highlight its critical issues and propose new effective and innovative solutions. One possible application of this device is in hemodialysis, which is a physical therapy substitution of kidney function that allows, in almost all cases, recovery and maintenance of the main biological functions while remaining the uremic condition. As for the extracorporeal one, the equipment used to purify the blood from toxic substances that are no longer normally eliminated by kidney filtration is divided mainly into two types: rotary peristaltic pump and a linear peristaltic pump. Having to work with a very particular fluid such as blood and in direct contact with the patient, they need to be extremely accurate and must ensure a constant and continuous functioning. The rotary peristaltic pump is the most widely used for hemodialysis and having been extensively studied in literature it has since found extensive solutions in the application field. As is well known, peristaltic pump refers to a device that exploits the principle of peristalsis to function, i.e. the transit of a bottleneck on a tube, in this case, the catheter, to push the fluid contained outwards. In particular, a roundabout peristaltic pump consists of a rotating structure consisting of two or more rollers that in turn revolve around their axis. With their displacement, the rollers clog adjacent catheter sections at a time so that after the first roller has passed the tube returns to its initial size creating the vacuum and then sucking the fluid. In this way, the liquid is pushed from the tube towards the patient. The motion of all these components is powered by an electric motor connected directly to the main rotating structure. The pumping of fluids through hoses using the propagation of a peristaltic wave has been the subject of design and scientific studies for more than 4 decades. This is easily justifiable since the phenomenon of peristalsis is known to be an important responsible mechanism of fluid transport in many biological organs. The goal is (starting on studies on the blood, a variable density fluid) to analyze in detail the peristaltic roller pump and propose its parametric optimization, aimed at determining the critical speed, beyond which the machine damages any kind of fluid that needs special treatment (blood, food, special gel, medical ointments and so on).
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