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524601 to 524700 most common queries
List represents a sample of symptoms, diseases, and other queries. Updated weekly.
Online Mendelian Inheritance in Man (OMIM), a knowledgebase of human genes and genetic disorders.
Recent segmental duplications in the human genome.
TGFbeta signaling in growth control, cancer, and heritable disorders.
Disease-specific induced pluripotent stem cells.
Predicting deleterious amino acid substitutions.
The TNF and TNF receptor superfamilies: integrating mammalian biology.
Selecting a maximally informative set of single-nucleotide polymorphisms for association analyses using linkage disequilibrium.
Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals.
TGF-beta signal transduction.
PedCheck: a program for identification of genotype incompatibilities in linkage analysis.
Parametric and nonparametric linkage analysis: a unified multipoint approach.
Recombinant human C1-inhibitor for the treatment of acute angioedema attacks in patients with hereditary angioedema.
The procoagulant and proinflammatory plasma contact system.
The humanistic burden of hereditary angioedema: Impact on health-related quality of life, productivity, and depression.
Hereditary angioedema caused by missense mutations in the factor XII gene: clinical features, trigger factors, and therapy.
DETECTION OF HEREDITARY ANGIONEUROTIC EDEMA BY DEMONSTRATION OF A REDUCTION IN THE SECOND COMPONENT OF HUMAN COMPLEMENT.
C1-inhibitor concentrate for individual replacement therapy in patients with severe hereditary angioedema refractory to danazol prophylaxis.
Hereditary angioneurotic edema. I. Case reports and review of the literature.
Hereditary angio-oedema in Denmark: a nationwide survey.
Benefits and risks of danazol in hereditary angioedema: a long-term survey of 118 patients.
Ecallantide for the treatment of acute attacks in hereditary angioedema.
Initial sequencing and analysis of the human genome.
Evidence-based recommendations for the therapeutic management of angioedema owing to hereditary C1 inhibitor deficiency: consensus report of an International Working Group.
Self-administration of intravenous C1-inhibitor therapy for hereditary angioedema and associated quality of life benefits.
Nanofiltered C1 inhibitor concentrate for treatment of hereditary angioedema.
Hereditary angiodema: a current state-of-the-art review, VII: Canadian Hungarian 2007 International Consensus Algorithm for the Diagnosis, Therapy, and Management of Hereditary Angioedema.
Efficacy of human C1 esterase inhibitor concentrate compared with placebo in acute hereditary angioedema attacks.
Efficacy of mycophenolate mofetil in patients with diffuse proliferative lupus nephritis. Hong Kong-Guangzhou Nephrology Study Group.
Association of increased interferon-inducible gene expression with disease activity and lupus nephritis in patients with systemic lupus erythematosus.
The role of B cells in lpr/lpr-induced autoimmunity.
IL-21 has a pathogenic role in a lupus-prone mouse model and its blockade with IL-21R.Fc reduces disease progression.
Icatibant, a new bradykinin-receptor antagonist, in hereditary angioedema.
T cell receptor alpha/beta expressing double-negative (CD4-/CD8-) and CD4+ T helper cells in humans augment the production of pathogenic anti-DNA autoantibodies associated with lupus nephritis.
ACTION OF COMPLEMENT IN HEREDITARY ANGIONEUROTIC EDEMA: THE ROLE OF C'1-ESTERASE.
Treatment of lupus-prone mice with a dual inhibitor of TLR7 and TLR9 leads to reduction of autoantibody production and amelioration of disease symptoms.
HEREDITARY ANGIONEUROTIC EDEMA: TWO GENETIC VARIANTS.
Mycophenolate mofetil or intravenous cyclophosphamide for lupus nephritis.
Netting neutrophils induce endothelial damage, infiltrate tissues, and expose immunostimulatory molecules in systemic lupus erythematosus.
Genetic reconstitution of systemic lupus erythematosus immunopathology with polycongenic murine strains.
Uncoupling of immune complex formation and kidney damage in autoimmune glomerulonephritis.
Polygenic control of susceptibility to murine systemic lupus erythematosus.
Tumour necrosis factor-alpha in murine autoimmune 'lupus' nephritis.
Toll-like receptor 9 controls anti-DNA autoantibody production in murine lupus.
Impairment of neutrophil extracellular trap degradation is associated with lupus nephritis.
Systemic lupus erythematosus.
Copy number polymorphism in Fcgr3 predisposes to glomerulonephritis in rats and humans.
Development of lupus-like autoimmune diseases by disruption of the PD-1 gene encoding an ITIM motif-carrying immunoreceptor.
Tissue-specific host recognition by complement factor H is mediated by differential activities of its glycosaminoglycan-binding regions.
Pre-emptive eculizumab and plasmapheresis for renal transplant in atypical hemolytic uremic syndrome.
A novel hybrid CFH/CFHR3 gene generated by a microhomology-mediated deletion in familial atypical hemolytic uremic syndrome.
A novel C3 mutation causing increased formation of the C3 convertase in familial atypical hemolytic uremic syndrome.
The development of atypical hemolytic uremic syndrome depends on complement C5.
Binding of the human complement regulators CFHR1 and factor H by streptococcal collagen-like protein 1 (Scl1) via their conserved C termini allows control of the complement cascade at multiple levels.
The role of complement in AMD.
Complement factor I in health and disease.
Combined complement gene mutations in atypical hemolytic uremic syndrome influence clinical phenotype.
Disease-associated N-terminal complement factor H mutations perturb cofactor and decay-accelerating activities.
Genetics and outcome of atypical hemolytic uremic syndrome: a nationwide French series comparing children and adults.
Hemoptysis, Hypoglycemia, Periorbital Edema, purulent sputum
aHUS caused by complement dysregulation: new therapies on the horizon.
Recessive mutations in DGKE cause atypical hemolytic-uremic syndrome.
A prevalent C3 mutation in aHUS patients causes a direct C3 convertase gain of function.
Use of eculizumab for atypical haemolytic uraemic syndrome and C3 glomerulopathies.
Alternative complement pathway assessment in patients with atypical HUS.
Genetics and complement in atypical HUS.
STEC-HUS, atypical HUS and TTP are all diseases of complement activation.
Dual interaction of factor H with C3d and glycosaminoglycans in host-nonhost discrimination by complement.
Atypical hemolytic uremic syndrome.
The pathogenic antigen of Heymann nephritis is a membrane glycoprotein of the renal proximal tubule brush border.
Emmanouil S Ganotakis
Nucleosome: a major immunogen for pathogenic autoantibody-inducing T cells of lupus.
Immunocytochemical localization of the Heymann nephritis antigen (GP330) in glomerular epithelial cells of normal Lewis rats.
The role of anti-glomerular basement membrane antibody in the pathogenesis of human glomerulonephritis.
The spectrum of podocytopathies: a unifying view of glomerular diseases.
Suppression of experimental glomerulonephritis by antiserum against transforming growth factor beta 1.
Anti-neutrophil cytoplasmic autoantibodies with specificity for myeloperoxidase in patients with systemic vasculitis and idiopathic necrotizing and crescentic glomerulonephritis.
Homozygous C1q deficiency causes glomerulonephritis associated with multiple apoptotic bodies.
Translational mini-review series on complement factor H: renal diseases associated with complement factor H: novel insights from humans and animals.
Mutation of E2F2 in mice causes enhanced T lymphocyte proliferation, leading to the development of autoimmunity.
Membranoproliferative glomerulonephritis associated with hepatitis C virus infection.
Variations in the complement regulatory genes factor H (CFH) and factor H related 5 (CFHR5) are associated with membranoproliferative glomerulonephritis type II (dense deposit disease).
Factor H family proteins and human diseases.
Involvement of IL-6 in mesangial proliferative glomerulonephritis.
Open Anterior Fontanel, wide wrist joints, low weight
Translational mini-review series on complement factor H: genetics and disease associations of human complement factor H.
Heterozygous and homozygous factor h deficiencies associated with hemolytic uremic syndrome or membranoproliferative glomerulonephritis: report and genetic analysis of 16 cases.
Hepatitis C: a multifaceted disease. Review of extrahepatic manifestations.
The spectrum of complement alternative pathway-mediated diseases.
Spontaneous hemolytic uremic syndrome triggered by complement factor H lacking surface recognition domains.
Loss of TACI causes fatal lymphoproliferation and autoimmunity, establishing TACI as an inhibitory BLyS receptor.
Activation of latent TGF-beta by thrombospondin-1: mechanisms and physiology.
Enterohaemorrhagic Escherichia coli in human medicine.
Characterisation of the Escherichia coli strain associated with an outbreak of haemolytic uraemic syndrome in Germany, 2011: a microbiological study.
Toxin genotypes and plasmid profiles as determinants of systemic sequelae in Escherichia coli O157:H7 infections.
The risk of the hemolytic-uremic syndrome after antibiotic treatment of Escherichia coli O157:H7 infections.
Epidemiology of Escherichia coli O157:H7 outbreaks, United States, 1982-2002.