scholarly journals The Molecular Basis of Self-Association of Antibodies to IgG (Rheumatoid Factors) in Rheumatoid Arthritis

1974 ◽  
Vol 71 (2) ◽  
pp. 517-521 ◽  
Author(s):  
R. M. Pope ◽  
D. C. Teller ◽  
M. Mannik
1997 ◽  
Vol 84 (3) ◽  
pp. 307-317 ◽  
Author(s):  
Richard W. Ermel ◽  
Thomas P. Kenny ◽  
Alice Wong ◽  
Pojen P. Chen ◽  
Wasyl Malyj ◽  
...  

2005 ◽  
Vol 88 (3) ◽  
pp. 157-202 ◽  
Author(s):  
Anthony K. Campbell ◽  
Jonathan P. Waud ◽  
Stephanie B. Matthews

A staggering 4000 million people cannot digest lactose, the sugar in milk, properly. All mammals, apart from white Northern Europeans and few tribes in Africa and Asia, lose most of their lactase, the enzyme that cleaves lactose into galactose and glucose, after weaning. Lactose intolerance causes gut and a range of systemic symptoms, though the threshold to lactose varies considerably between ethnic groups and individuals within a group. The molecular basis of inherited hypolactasia has yet to be identified, though two polymorphisms in the introns of a helicase upstream from the lactase gene correlate closely with hypolactasia, and thus lactose intolerance. The symptoms of lactose intolerance are caused by gases and toxins produced by anaerobic bacteria in the large intestine. Bacterial toxins may play a key role in several other diseases, such as diabetes, rheumatoid arthritis, multiple sclerosis and some cancers. The problem of lactose intolerance has been exacerbated because of the addition of products containing lactose to various foods and drinks without being on the label. Lactose intolerance fits exactly the illness that Charles Darwin suffered from for over 40 years, and yet was never diagnosed. Darwin missed something else – the key to our own evolution – the Rubicon some 300 million years ago that produced lactose and lactase in sufficient amounts to be susceptible to natural selection.


1992 ◽  
Vol 35 (2) ◽  
pp. 149-157 ◽  
Author(s):  
M. ABDERRAZIK ◽  
M. MOYNIER ◽  
R JEFFFRIS ◽  
R. A. K. MAGEED ◽  
B. COMBE ◽  
...  

1988 ◽  
Vol 17 (sup74) ◽  
pp. 41-44 ◽  
Author(s):  
Kimmo Aho ◽  
Tiinamaija Tuomi ◽  
Markku Heliövaara ◽  
Timo Palosuo

1994 ◽  
Vol 37 (6) ◽  
pp. 860-868 ◽  
Author(s):  
Richard W. Ermel ◽  
Thomas P. Kenny ◽  
Alice Wong ◽  
Alan Solomon ◽  
Pojen P. Chen ◽  
...  

2016 ◽  
Vol 2 (3) ◽  
pp. 379-388
Author(s):  
Amoussou Nathalie Gisèle ◽  
Gounongbé Marcelle ◽  
Dougnon Tamègnon Victorien ◽  
Zomalheto Zavier ◽  
Loko Frédéric ◽  
...  

The rheumatoid arthritis (RA) is an auto-immune, rheumatic and chronic inflammatory disease, characterized by joints damage. The early diagnosis of RA allows the initiation of a treatment which offers to the patients more chance of remission and avoids the evolution towards the unrecoverable deformity of joints. The objective of this study is to evaluate the performance of recent tests for the determination of anti -CCP antibodies and FR by ELISA in Benin Republic. This analytical, retrospective (2 years 6 months) and prospective (7 months) study allowed us to collect 36 patients meeting the American College of Rheumatology (ACR) criteria for RA and 24 controls. A comparison was made with the latex agglutination test for rheumatoid factors and a search of rheumatoid factors (RF) on the one hand and anti-cyclic citrullinated peptide. In our study, the specificity of anti-CCP assay (100 %) is higher than that of RF-ELISA (91.7%). The sensitivity of RF-ELISA assay is higher (77.8 %) than that of anti-CCP assay (66.7%). The latex test for rheumatoid factors has a sensitivity of 33.3 %. The positive predictive value (PPV) of anti-CCP assay (100 %) is higher than that of RF-ELISA assay (93.33 %). The positive-likelihood ratio (LR+) of anti-CCP assay is higher than the LR+ of RF-ELISA assay (4.96). The negative-likelihood ratio (LR-) of anti-CCP assay (0.33) is higher than the LR- of RF-ELISA assay (0.24). In conclusion, the anti-CCP assay has the highest specificity and RF-ELISA assay shows the highest sensitivity. In conclusion, the association of the two assays enhances a better diagnosis value for RA.Asian J. Med. Biol. Res. September 2016, 2(3): 379-388


1993 ◽  
Vol 34 (6) ◽  
pp. 259-264 ◽  
Author(s):  
S. C. Bell ◽  
S. D. Carter ◽  
C. May ◽  
D. Bennett

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