instruction:
In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.
question:
Context: Allergic rhinitis (AR) is a complex chronic inflammatory disease of the nasal mucosa, caused by an interaction between genetic and environmental factors. As evidence suggests that some genetic variants may increase susceptibility to both AR and asthma, the objective of this study was to identify asthma susceptibility variants associated with AR in the Chinese population.', 'A cohort of 402 individuals with physician-diagnosed AR and 416 healthy controls were recruited from the Han Chinese population in Beijing. DNA was extracted from the peripheral blood and a total of 12 single-nucleotide polymorphisms (SNPs) shown to be associated with asthma in Japanese subjects were selected for genotyping using the SequenomMassARRAY technology platform.', 'Analysis of frequency differences of allele between the AR patients and control subjects showed that the C allele of rs204993 in the pre-B-cell leukemia homeobox 2 (PBX2) gene from the 6p21.3 locus was significantly associated with AR (p = 0.0006, pcorrected = 0.0340). Genotype analysis further confirmed the difference in distribution of this variant between AR patients and controls in the both the dominant (pT/C+C/C vs T/T = 7.3710(-5) ) and co-dominant (pT/C vs T/T = 1.98 10(-4) , pC/C vs T/T = 0.004) models.\Question: Does variant of PBX2 gene in the 6p21.3 asthma susceptibility locus is associate with allergic rhinitis in Chinese subjects?
answer:
These results suggest that the PBX2 gene in the 6p21.3 asthma susceptibility locus may be associated with increased risk for both AR and asthma in Chinese subjects.

question:
Context: To determine the role of factor V Leiden and prothrombin gene mutation in the pathogenesis of unexplained second and third trimester nonrecurrent fetal loss.', 'One hundred and fourteen women with unexplained nonrecurrent late fetal loss made up the study group, and 106 normal pregnant women with a history of delivery of at least one healthy fetus and no history of late fetal loss made up the control group. The study group was further divided into two subgroups: second (n = 36) and third (n = 78) trimester fetal loss. All women were tested for factor V Leiden and G20210A prothrombin gene mutations.', 'Twenty-one (18.4%) of the women in the study group and seven (6.6%) of the women in the control group were heterozygous carriers of factor V Leiden mutation (OR = 3.19). Eleven (9.6%) of the women in the study group and three (2.8%) of the women in the control group were heterozygous carriers of prothrombin gene mutation (OR = 3.66). In assessing with regard to trimesters, 18 (23%) factor V Leiden and 10 (12.8%) prothrombin gene mutations were present in the group of third trimester fetal loss (OR = 4.24 and OR = 5.04, respectively). Three (8.3%) factor V Leiden and one (2.7%) prothrombin gene mutation were detected in women with second trimester fetal loss (OR = 1.28 and OR = 0.40, respectively).\Question: Is third trimester nonrecurrent fetal loss associated with factor V Leiden and prothrombin gene mutations?
answer:
Factor V Leiden and prothrombin gene mutations were associated with third trimester nonrecurrent fetal loss. These mutations should be screened in women with third trimester but not second trimester unexplained nonrecurrent late fetal loss.

question:
Context: There are many patients that exhibit connective tissue related cardiac malformations but do not have mutations in collagen genes. The Small Leucine Rich Proteoglycans (SLRP) fibromodulin (FMOD) and lumican (LUM) bind collagen and regulate fibril assembly in other biological contexts.', 'FMOD deficient mice and double deficient FMOD; LUM mice exhibited anomalies in regions where cardiac valve tissue interdigitates with adjacent muscle for support. Ectopic connective and/or myocardial tissue(s) was associated with the more severe cardiac valve anomalies in FMOD; LUM deficient mice. At postnatal day 0 (P0) there was an increase in the mesenchymal cell number in the regions where valve cusps anchor in FMOD; LUM deficient mice compared to WT. The cardiac valve anomalies correlated with the highest levels of FMOD expression in the heart and also where myotendinous junctions (MTJ) components biglycan, collagen type I alpha 1, and collagen type VI, are also localized.\Question: Do development of myotendinous-like junctions that anchor cardiac valves requires fibromodulin and lumican?
answer:
The postnatal assembly of the collagen-rich ECM in regions where cardiac valves anchor, that we have designated 'myotendinous-like junctions' (MTLJ) requires the SLRPs FMOD and LUM. Moreover, FMOD and LUM may facilitate mesenchymal cell differentiation in late stages of cardiac valve development. Developmental Dynamics 245:1029-1042, 2016. ©️ 2016 Wiley Periodicals, Inc.