Results 71 to 80 of about 343,841 (303)

Bloqueo del complemento: promesas terapéuticas y retos pendientes en la práctica clínica

Nefrología
Resumen: La comprensión del complemento en las glomerulopatías ha avanzado notablemente, mostrando que este sistema, más allá de la inmunidad innata, es un mediador clave del daño renal en un amplio espectro de nefropatías, desde las mediadas por ...
Gema Fernández-Juárez, Javier Azores-Moreno, Lina León-Machado, Irene Vázquez-Raso, María Soriano-Guillén, Ana Mendoza, María Maldonado, Begoña Rivas Becerra, Cristina Vega Cabrera, Amir Shabaka   +9 more
doaj   +1 more source

Blockade of Alternative Complement Pathway in Dense Deposit Disease

Case Reports in Nephrology, 2014
A patient aged 17 with dense deposit disease associated with complement activation, circulating C3 Nef, and Factor H mutation presented with nephrotic syndrome and hypertension.
Aurore Berthe-Aucejo, Mathieu Sacquépée, Marc Fila, Michel Peuchmaur, Emilia Perrier-Cornet, Véronique Frémeaux-Bacchi, Georges Deschênes   +6 more
doaj   +1 more source

Small-molecule factor D inhibitors selectively block the alternative pathway of complement in paroxysmal nocturnal hemoglobinuria and atypical hemolytic uremic syndrome

Haematologica, 2017
Paroxysmal nocturnal hemoglobinuria and atypical hemolytic uremic syndrome are diseases of excess activation of the alternative pathway of complement that are treated with eculizumab, a humanized monoclonal antibody against the terminal complement ...
Xuan Yuan, Eleni Gavriilaki, Jane A. Thanassi, Guangwei Yang, Andrea C. Baines, Steven D. Podos, Yongqing Huang, Mingjun Huang, Robert A. Brodsky   +8 more
doaj   +1 more source

Linking neurogenesis, oligodendrogenesis, and myelination defects to neurodevelopmental disruption in primary mitochondrial disorders

FEBS Letters, EarlyView.
Mitochondrial remodeling shapes neural and glial lineage progression by matching metabolic supply with demand. Elevated OXPHOS supports differentiation and myelin formation, while myelin compaction lowers mitochondrial dependence, revealing mitochondria as key drivers of developmental energy adaptation.
Sahitya Ranjan Biswas, Porter L. Tomsick, Alicia M. Pickrell, Paul D. Morton   +3 more
wiley   +1 more source

Complement-Amplifying Conditions in Atypical Hemolytic Uremic Syndrome: A Canadian Case Series

Canadian Journal of Kidney Health and Disease, 2022
Rationale: Thrombotic microangiopathies (TMAs) are systemic disorders that often affect the kidneys and encompass a heterogeneous group of conditions, including atypical hemolytic uremic syndrome (aHUS).
Christopher J. Patriquin, Katerina Pavenski, Jocelyn Garland, Louis-Philippe Girard, Paul Isenring   +4 more
doaj   +1 more source

Complement depletion during haemofiltration with polyacrilonitrile membranes [PDF]

, 2017
Background Polyacrylonitrile (PAN, AN69®) dialysis membranes have been shown to improve the outcome of critically ill patients. Factor D is an essential enzyme of the alternative pathway of complement and is increased during renal failure.
Chevrolet, Jean-Claude, Favre, Hervé, Gasche, Yvan, Pascual, Manuel, Schifferli, Jürg A., Suter, Peter. M.   +5 more
core  

Anti-factor B autoantibody in dense deposit disease [PDF]

, 2010
Dense deposit disease (DDD), also known as membranoproliferative glomerulonephritis type II, is a rare kidney disorder that is associated with dysregulation of the alternative pathway of complement.
Józsi, Mihály, Papp, Krisztián, Prechl, József, Strobel, S., Zimmering, M.   +4 more
core   +1 more source

An isoform of 14‐3‐3 protein regulates transbilayer lipid movement at the plasma membrane

FEBS Letters, EarlyView.
Loss of 14‐3‐3ζ in CHO cells confers resistance to exogenous phosphatidylserine (PS) and impairs endocytosis‐independent inward flip‐flop of fluorescent PS at the plasma membrane. RNAi‐mediated knockdown reproduces this defect, while no additive effect is seen in ATP11C‐deficient cells.
Akiko Yamaji‐Hasegawa, Akira Hattori, Masafumi Tsujimoto, Toshihide Kobayashi   +3 more
wiley   +1 more source

Classical and alternative complement pathway activation by pneumococci [PDF]

Infection and Immunity, 1977
Sixty-two strains of Streptococcus pneumoniae were studied for their abilities to consume selected components of classical and alternative complement pathways in human sera. The classical pathway was blocked by chelating calcium with ethyleneglycol-bios (beta-aminoethyl ether)-N,N-tetraacetic acid and by removing C4. The alternative pathway was blocked
C G, Stephens, R C, Williams, W P, Reed
openaire   +2 more sources

The role of complement in Streptococcus pneumoniae-associated haemolytic uraemic syndrome [PDF]

, 2013
Background. Atypical forms of haemolytic uraemic syndrome (aHUS) include HUS caused by defects in the regulation of alternative complement pathway and HUS linked to neuraminidase- producing pathogens, such as Streptococcus pneumoniae. Increasing data
Szilágyi, Ágnes
core