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All patients with SLE are indicated (closed symbols) as are the SLE patients with thrombocytopenia (double symbol). The family structures of the African American families that were useful for linkage in which at least one patient with SLE had thrombocytopenia.
Systemic lupus erythematosus (SLE) is a clinically and immunologically complex disease, which can affect any organ system.
The disease may be mild, or severe and life threatening.
This variability is reflected in the classification system proposed by the American College of Rheumatology (ACR)1 in which patients with SLE may fulfill any 4 of 11 criteria.
The presence of antinuclear antibodies (ANA) is the most sensitive of these criteria and is present in virtually all patients. The disease tends to occur within families, but without a clear pattern of inheritance (reviewed in Sestak et al2).
Screening lod scores were calculated by using the MLINK subroutine of the ANALYZE package. E 4.0 package, version Beta 3.29 33 The algorithm regresses the identity by descent sharing values against the mean corrected cross product of the sib-pair trait difference. A total of 47 (12.1%) of the 387 patients with SLE had definite thrombocytopenia as defined by the criteria (platelet count, ] without another cause), a frequency that did not vary among racial groups.
Multipoint linkage analysis on concordant and discordant sibling pairs was performed at 2-c M increments for all 22 autosomes by using the new Haseman-Elston regression technique used by SIBPAL2, a subtest of the S. In addition, we performed a multipoint affected-relative pairs (ARPs) analysis by using LODPAL, also a subroutine of the S. Twenty-seven of those with thrombocytopenia were European American; among the African American patients, 15 patients from 14 families had thrombocytopenia, of which 13 pedigrees were useful for linkage.The family structures of the African American families with thrombocytopenic SLE that were useful for linkage are given in Figure 1.The family structures of the African American families that were useful for linkage in which at least one patient with SLE had thrombocytopenia.We incorporated this difference into the models by using one penetrance function for men and another for women. This analysis models covariance of all affected relative pairs as a function of marker allele-sharing identical by descent using the conditional logistic model proposed by Olson34 and Goddard et al.35 There were a total of 387 patients with SLE in the 184 families evaluated.For each marker, allele frequencies were estimated by allele counting using founders. Of these, 116 families and 233 patients with SLE were of European ancestry, whereas 63 families and 133 patients with SLE were of sub-Saharan African ancestry.ANA, anti–double-stranded (ds) DNA, anti-Sm, antiphospholipid immunoglobulin G (Ig G) and Ig M antibodies were extracted from the medical record and performed in the Oklahoma Medical Research Foundation (OMRF) Clinical Immunology Laboratory (anticardiolipin was measured in our laboratory) using the serum specimens obtained for this project by following standard procedures.25 26 Anti-Ro, anti-La, anti-P, and anti-n RNP (nuclear ribonucleoprotein) were also evaluated by using Ouchterlony immunodiffusion27 in each affected subject.Evidence for biologic false-positive test for syphilis and the lupus anticoagulant was extracted from the medical record.Genomic DNA was isolated from peripheral blood mononuclear cells, buccal cell swabs, or lymphoblastoid cell lines by using conventional methods as previously described.22 A total of 307 microsatellite markers were typed from the Version 8 Weber screening set ( Frames.htm).Polymerase chain reactions were performed as previously described.22 Amplified fragments were detected by using 6% polyacrylamide gels electrophoresed on automated Li Cor (Lincoln, NE) Model 4000 DNA sequencers.Gel images were collected by using Base Imag IR software, version 4.0, and alleles were determined by using Gene Imag IR, version 3.52. 4.0 package, version Beta 3.28 29 For all linkage analyses, the pedigrees were analyzed together and as subsets containing only African American or European American pedigrees.Twenty-nine pedigrees were initially genotyped by the Mammalian Genotyping Center in Marshfield, WI ( using a fluorescent-based detection system. Two-point maximum logarithm of odds (lod) scores were calculated by using FASTLINK, version 4.1P, and the ANALYZE package.30-32 Lod scores were generated for each pedigree by using recombination fractions in increments of 0.05 from 0 (complete linkage) to 0.50 (no linkage).