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Haplotype B (haplotype + b)

Distribution by Scientific Domains

Medical Sciences	60%
Life Sciences	40%

Selected Abstracts

INCREASED SAMPLING FOR INFERRING PHYLOGEOGRAPHIC PATTERNS IN BOSTRYCHIA RADICANS/B.

JOURNAL OF PHYCOLOGY, Issue 6 2006
MORITZIANA (RHODOMELACEAE, RHODOPHYTA) IN THE EASTERN USA
Zuccarello and West (2003) reported on the phylogenetic diversity of algae identified as Bostrychia radicans (Montagne) Montagne and B. moritziana (Sonder ex Kützing) J. Agardh from around the world. They showed that the species complex consisted of seven distinct lineages, of which two lineages were common on the East Coast of the USA and eastern Gulf of Mexico. The distribution of haplotypes within these lineages on the East Coast of the USA showed a general north,south distribution. One haplotype of lineage 5 (B) was mostly collected in northern areas, while the other common haplotype (C) was more southerly in distribution. Samples in lineage 6 (haplotype D) were not found north of Sapelo Island, Georgia. Increased sampling from the eastern USA over 5 years later has revealed an altered pattern. Haplotype D is distributed in North Carolina and is common in some populations. Haplotype C is rare or absent in many sampled populations. Haplotype B is only observed in the northern sampled sites on both sides of the Florida peninsula. This disjunct distribution agrees with geological scenarios for a strait between the western Gulf of Mexico and southern Georgia in the Miocene/Pliocene, which closed in the late Pliocene. This paper highlights the importance of increased sampling to determine phylogeographic patterns and hypotheses of dispersal scenarios in algae. [source]

A poly(ADP-ribose) polymerase haplotype spanning the promoter region confers susceptibility to rheumatoid arthritis

ARTHRITIS & RHEUMATISM, Issue 3 2003
M. Pascual
Objective To investigate the association of the poly(ADP-ribose) polymerase 1 (PARP-1) gene promoter polymorphism with rheumatoid arthritis (RA) predisposition. Methods An association study with 213 Spanish RA patients and 242 healthy subjects was carried out to investigate the association of all known PARP-1 gene promoter polymorphisms, i.e., a CA microsatellite repeat, a poly(A)n, and 3 single point mutations (C410T, C1362T, and G1672A), with disease susceptibility. Additionally, we analyzed the distribution of PARP-1 polymorphisms in 58 Spanish families with 1 or more affected members. Results Upon complete genotyping of the panel of 455 samples, strong linkage disequilibrium was observed among the 5 PARP-1 polymorphisms. Only 2 PARP-1 haplotypes were detected: haplotype A (410T,[A]10,[CA]10,12,1362C, which includes short PARP-1 CA alleles) and haplotype B (410C,[A]11,[CA]13,20,1362T, always paired with long PARP-1 CA variants). Regarding the G1672A variation, although linkage disequilibrium was detected, it did not seem to be part of the conserved haplotypes described. Haplotype B was statistically overrepresented in the RA patient group compared with the healthy subjects (odds ratio 1.42, 95% confidence interval 1.06,1.91, P = 0.019). In addition, a significant dose effect of PARP-1 haplotype carriage on disease predisposition was observed. Of note, within haplotype B, the PARP-1 CA 97-bp allele was found to be the RA-predisposing marker (odds ratio 2.17, 95% confidence interval 1.27,3.72, P = 0.003, corrected P < 0.05). Conclusion Our results demonstrate the existence of 2 unique PARP-1 haplotypes in the Spanish population and provide the first evidence that PARP-1 haplotypes play a role in susceptibility to RA. [source]

Cholesteryl Ester Transfer Protein (CETP) Genetic Variation and Early Onset of Non-Fatal Myocardial Infarction

ANNALS OF HUMAN GENETICS, Issue 6 2008
V. Meiner
Summary Although Cholesteryl Ester Transfer Protein (CETP) mediates the transfer of cholesteryl esters and triglycerides between lipoprotein particles and thus plays a crucial role in reverse cholesterol transport, the association of variations in the CETP gene with acute myocardial infarction (MI) remains unclear. In this study we examined whether common genetic variation in the CETP gene is related to early-onset non-fatal MI risk in a population-based case-control study from western Washington State. Genotyping for the CETP ,2708 G/A, ,971 A/G, ,629 A/C, Intron-I TaqI G/A and exon-14 A/G (I405V) SNPs was performed in 578 cases with first acute non-fatal MI and in 666 demographically similar controls, free of clinical cardiovascular disease, identified randomly from the community. In-person interviews and non-fasting blood specimens provided data on coronary heart disease risk factors. In men, there was little evidence for an association between single SNPs and MI risk, but in women the age- and race-adjusted OR was found to be significant in 4 out of the 5 CETP single variants. Haplotype analysis revealed two haplotypes associated with MI risk among men. As compared to men homozygous for the most common haplotype D (,2708 G, ,971 G, ,629 C, TaqI G and exon-14 A), the fully-adjusted multiplicative model identified haplotype G (,2708 G, ,971 A, ,629 A, TaqI G and exon-14 G) was associated with a 4.0-6.0-fold increased risk of MI for each additional copy; [95%CI 2.4,14.8] and haplotype B (,2708 G, ,971 G, ,629 A, TaqI A and exon-14 A) showed a significant decreased risk for early onset MI [OR = 0.18; 95%CI 0.04 , 0.75]. An evolutionary-based haplotype analysis indicated that the two haplotypes associated with the MI risk are most evolutionarily divergent from the other haplotypes. Variation at the CETP gene locus is associated with the risk of early-onset non-fatal MI. This association was found to be independent of HDL-C levels. These data and the sex-specific findings require confirmation in other populations. [source]

A poly(ADP-ribose) polymerase haplotype spanning the promoter region confers susceptibility to rheumatoid arthritis

ORIGINAL ARTICLE: Syngeneic Immune-Dependent Abortions in Mice Suggest Paternal Alloantigen-Independent Mechanisms

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 4 2008
Jean A. Kundert
Problem, Recurrent immune-associated miscarriages in humans are thought to result from maternal immune responses to paternal alloantigens. We investigated the role of paternal alloantigens in a mouse model of immune-dependent abortion. Method of study, Sib-crosses of C57Bl/6J (haplotype b/b) mice heterozygous for a targeted hypomorphic allele of the tbp gene (tbp,,/+) resulted in selective mid-gestational abortion of 88% of the tbp,,/,, fetuses. In dams lacking mature lymphocytes (rag1,/,), nearly all tbp,,/,, fetuses survived to birth, indicating abortions were immune-dependent. Allogeneic pregnancies bearing tbp,,/,, fetuses were established by either hybridizing the paternal lineage to BALB/cJ (haplotype d/d) and mating hybrid tbp,,/+ sires to haplotype b/b tbp,,/+ C57Bl/6J dams, or by transfer of haplotype b/b zygotes from tbp,,/+ × tbp,,/+ matings into pseudopregnant wild-type CByD2F1/J dams (haplotype d/d). Results, Neither hemizygous paternal allogeneic loci nor homozygous allogeneic loci, including a haplotype-mismatched major histocompatibility complex (MHC), increased abortion frequencies. Conclusion, Results suggested that mechanisms for maternal tolerance of paternal alloantigens, including mismatched MHC antigens, were intact in these pregnancies, yet maternal immune-dependent paternal antigen-independent abortion of mutants occurred. These data indicate that, in some cases of immune-mediated abortions, the presence of paternal alloantigens can be coincidental and superfluous to the compromising rejection response. [source]