|1.||Thurman, Joshua M: 14 articles (04/2015 - 01/2005)|
|2.||Holers, V Michael: 9 articles (07/2013 - 01/2005)|
|3.||Morgan, B Paul: 4 articles (01/2014 - 03/2009)|
|4.||Chakravarthy, Usha: 4 articles (11/2012 - 02/2009)|
|5.||Kirschfink, Michael: 3 articles (10/2014 - 12/2010)|
|6.||Harris, Claire L: 3 articles (01/2014 - 03/2009)|
|7.||Hughes, Anne E: 3 articles (05/2013 - 02/2009)|
|8.||Atkinson, Carl: 3 articles (11/2012 - 12/2010)|
|9.||Stahl, Gregory L: 3 articles (11/2012 - 03/2010)|
|10.||Tomlinson, Stephen: 3 articles (11/2012 - 12/2010)|
|1.||Demyelinating Diseases (Demyelinating Disease)
07/01/2013 - "These studies demonstrate the therapeutic potential for inhibition of factor B in the chronic phase of demyelinating disease, where treatment options are limited."
11/15/2000 - "In addition, compared with their wild-type littermates, the CNS of both C3(-/-) and factor B(-/-) mice induced for EAE are protected from demyelination. "
07/01/2013 - "Administration of anti-factor B antibody to mice prior to the onset of clinical signs of active EAE had no affect on the onset or acute phase of disease, but significantly attenuated the chronic phase of disease resulting in reduced cellular infiltration, inflammation and demyelination in antibody-treated mice. "
11/01/2012 - "Factor B-deficient or CR2-fH-treated mice were protected in terms of improved neurologic function and reduced cerebral infarct, demyelination, P-selectin expression, neutrophil infiltration, and microthrombi formation. "
12/01/2010 - "Here, we investigated the role of the alternative and terminal complement pathways in SCI. Mice deficient in the alternative pathway protein factor B (fB) were protected from traumatic SCI in terms of reduced tissue damage and demyelination, reduced inflammatory cell infiltrate, and improved functional recovery. "
|2.||Macular Degeneration (Age-Related Maculopathy)
03/17/2009 - "Functional basis of protection against age-related macular degeneration conferred by a common polymorphism in complement factor B."
01/01/2013 - "Complement factor B polymorphism (rs641153) and susceptibility to age-related macular degeneration: evidence from published studies."
03/01/2014 - "Complement factor B polymorphism and the phenotype of early age-related macular degeneration."
01/01/2011 - "Complement factor B polymorphism 32W protects against age-related macular degeneration."
11/01/2012 - "Association between genetic variants in complement factor H (CFH), factor B (CFB), component 2 (C2), and in the ARMS2/HTRA1 region with age-related macular degeneration (AMD) comes mainly from studies of European ancestry and case-control studies of late-stage disease. "
|3.||Middle Cerebral Artery Infarction (Middle Cerebral Artery Syndrome)
|4.||Nephrotic Syndrome (Syndrome, Nephrotic)
08/01/1977 - "Decreased serum factor B concentration associated with decreased opsonization of Escherichia coli in the idiopathic nephrotic syndrome."
08/01/1985 - "T-cell subsets, lymphocyte proliferative response, circulating immune complexes (CIC) and serum C3, C4 and properdin factor B were studied in 22 children suffering from steroid-responsive nephrotic syndrome (SRNS) during the acute, remission and relapse phases. "
07/01/1979 - "Assessment of serum factor B, serum opsonins, granulocyte chemotaxis, and infection in nephrotic syndrome of children."
01/01/1984 - "Complement profiles must be interpreted recognizing that a pattern resembling classical pathway activation can be produced by idiopathic nephrotic syndrome, that hypogammaglobulinemia can reduce Clq levels, and that a primary deficiency of factor H or I or both, will secondarily produce subnormal levels of C3 and factor B. "
06/01/1986 - "The significant reduction in CH50 and Factor B in the more severely affected patients suggests that activation of both classical and alternate pathways occurs in group B meningococcal infection."
06/01/1986 - "During an epidemic of group B meningococcal infection mean values obtained in 96 consecutively affected children showed a reduction in classical pathway function (CH50), normal alternate pathway function (AP50), C4 and factor B levels, and raised C3 levels. "
04/01/2005 - "To evaluate the functional activity of the classical and alternative pathways of the complement system and the levels of C3, C4, and factor B during the first episode of meningococcal infection and during the convalescence period. "
01/01/1983 - "The specific susceptibility to meningococcal infections was connected with half-normal levels of several components of the complement system (C3, C4, C9, factor B, properdin), and reduced antibody responses to group A and group C meningococcal polysaccharides, but not to several other polysaccharide or protein antigens."
|1.||Complement System Proteins (Complement)
|2.||Antigen-Antibody Complex (Immune Complex)
|4.||Complement Factor H (Factor H)
|5.||Complement C3 (C3 Complement)
|6.||Proteins (Proteins, Gene)
|7.||Messenger RNA (mRNA)
|8.||Complement C2 (Complement Component 2)
|9.||Immunoglobulin G (IgG)
|3.||Nutritional Support (Artificial Feeding)
|5.||Transplantation (Transplant Recipients)