@misc{yao_chung_lin_tsai_chang_yeh_tsai_liao_hua_lai_et al._2019, title={Genetic loci determining total immunoglobulin E levels from birth through adulthood}, volume={74}, ISSN={["1398-9995"]}, DOI={10.1111/all.13654}, abstractNote={ferentiation of the cutaneous microbiota in psoriasis. Microbiome. 2013;1:31. 6. Chng KR, Tay AS, Li C, et al. Whole metagenome profiling reveals skin microbiome‐dependent susceptibility to atopic dermatitis flare. Nat Microbiol. 2016;1:16106. 7. St Laurent G 3rd, Seilheimer B, Tackett M, et al. Deep sequencing transcriptome analysis of murine wound healing: effects of a multicomponent, Multitarget Natural Product Therapy‐Tr14. Front Mol Biosci. 2017;4:57. 8. Caley MP, Martins VL, O'Toole EA. Metalloproteinases and wound healing. Adv Wound Care (New Rochelle). 2015;4:225‐234. 9. Hoffmann AR, Patterson AP, Diesel A, et al. The skin microbiome in healthy and allergic dogs. PLoS One. 2014;9:e83197.}, number={3}, journal={ALLERGY}, author={Yao, Tsung-Chieh and Chung, Ren-Hua and Lin, Chung-Yen and Tsai, Pei-Chien and Chang, Wei-Chiao and Yeh, Kuo-Wei and Tsai, Ming-Han and Liao, Sui-Ling and Hua, Man-Chin and Lai, Shen-Hao and et al.}, year={2019}, month={Mar}, pages={621–625} }
 @article{zhang_martin_chung_li_morris_2008, title={X-LRT: A likelihood approach to estimate genetic risks and test association with X-linked markers using a case-parents design}, volume={32}, ISSN={["0741-0395"]}, DOI={10.1002/gepi.20311}, abstractNote={Abstract}, number={4}, journal={GENETIC EPIDEMIOLOGY}, author={Zhang, Li and Martin, Eden R. and Chung, Ren-Hua and Li, Yi-Ju and Morris, Richard W.}, year={2008}, month={May}, pages={370–380} }
 @article{chung_hauser_martin_2007, title={Interpretation of simultaneous linkage and family-based association tests in genome screens}, volume={31}, ISSN={["1098-2272"]}, DOI={10.1002/gepi.20196}, abstractNote={Abstract}, number={2}, journal={GENETIC EPIDEMIOLOGY}, author={Chung, Ren-Hua and Hauser, Elizabeth R. and Martin, Eden R.}, year={2007}, month={Feb}, pages={134–142} }
 @article{chung_morris_zhang_li_martin_2007, title={X-APL: An improved family-based test of association in the presence of linkage for the X chromosome}, volume={80}, ISSN={["0002-9297"]}, DOI={10.1086/510630}, abstractNote={Family-based association methods have been developed primarily for autosomal markers. The X-linked sibling transmission/disequilibrium test (XS-TDT) and the reconstruction-combined TDT for X-chromosome markers (XRC-TDT) are the first association-based methods for testing markers on the X chromosome in family data sets. These are valid tests of association in family triads or discordant sib pairs but are not theoretically valid in multiplex families when linkage is present. Recently, XPDT and XMCPDT, modified versions of the pedigree disequilibrium test (PDT), were proposed. Like the PDT, XPDT compares genotype transmissions from parents to affected offspring or genotypes of discordant siblings; however, the XPDT can have low power if there are many missing parental genotypes. XMCPDT uses a Monte Carlo sampling approach to infer missing parental genotypes on the basis of true or estimated population allele frequencies. Although the XMCPDT was shown to be more powerful than the XPDT, variability in the statistic due to the use of an estimate of allele frequency is not properly accounted for. Here, we present a novel family-based test of association, X-APL, a modification of the test for association in the presence of linkage (APL) test. Like the APL, X-APL can use singleton or multiplex families and properly infers missing parental genotypes in linkage regions by considering identity-by-descent parameters for affected siblings. Sampling variability of parameter estimates is accounted for through a bootstrap procedure. X-APL can test individual marker loci or X-chromosome haplotypes. To allow for different penetrances in males and females, separate sex-specific tests are provided. Using simulated data, we demonstrated validity and showed that the X-APL is more powerful than alternative tests. To show its utility and to discuss interpretation in real-data analysis, we also applied the X-APL to candidate-gene data in a sample of families with Parkinson disease.}, number={1}, journal={AMERICAN JOURNAL OF HUMAN GENETICS}, author={Chung, Ren-Hua and Morris, Richard W. and Zhang, Li and Li, Yi-Ju and Martin, Eden R.}, year={2007}, month={Jan}, pages={59–68} }
 @article{chung_hauser_martin_2006, title={The APL test: Extension to general nuclear families and haplotypes and examination of its robustness}, volume={61}, ISSN={["1423-0062"]}, DOI={10.1159/000094774}, abstractNote={<i>Objective:</i> The Association in the Presence of Linkage test (APL) is a powerful statistical method that allows for missing parental genotypes in nuclear families. However, in its original form, the statistic does not easily extend to mixed nuclear family structures nor to multiple-marker haplotypes. Furthermore, the robustness of APL in practice has not been examined. Here we present a generalization of the APL model and examination of its robustness under a variety of non-standard scenarios. <i>Methods:</i> The generalization is made possible by incorporating a bootstrap variance estimator instead of the original robust variance estimator. This allows for use of more than two affected siblings. Haplotype analysis was accomplished by combining estimation of haplotype phase into the EM algorithm. Computer simulation was used to examine robustness of the APL to departures from test assumptions. <i>Results:</i> The extended APL tests both single-marker and multiple-marker haplotypes and shows more power than other association methods. Simulation results showed that the single-marker APL test is robust to the departure from HWE. For the haplotype test, violation of the HWE assumption can inflate type I error. We also evaluated general guidelines for the validity of APL with rare alleles and rare haplotypes. Software for the APL test is available from http://www.chg.duke.edu/research/apl.html.}, number={4}, journal={HUMAN HEREDITY}, author={Chung, Ren-Hua and Hauser, Elizabeth R. and Martin, Eden R.}, year={2006}, pages={189–199} }
 @article{martin_bronson_li_wall_chung_schmechel_small_xu_bartlett_schnetz-boutaud_et al._2005, title={Interaction between the alpha-T catenin gene (VR22) and APOE in Alzheimer's disease}, volume={42}, ISSN={["0022-2593"]}, DOI={10.1136/jmg.2004.029553}, abstractNote={Background: APOE is the only gene that has been consistently replicated as a risk factor for late onset Alzheimer’s disease. Several recent studies have identified linkage to chromosome 10 for both risk and age of onset, suggesting that this region harbours genes that influence the development of the disease. A recent study reported association between single nucleotide polymorphisms (SNPs) in the VR22 gene (CTNNA3) on chromosome 10 and plasma levels of Aβ42, an endophenotype related to Alzheimer’s disease. Objective: To assess whether polymorphisms in the VR22 gene are associated with Alzheimer’s disease in a large sample of Alzheimer’s disease families and an independent set of unrelated cases and controls. Results: Several SNPs showed association in either the family based or case–control analyses (p<0.05). The most consistent findings were with SNP6, for which there was significant evidence of association in both the families and the unrelated cases and controls. Furthermore, there was evidence of significant interaction between APOE-4 and two of the VR22 SNPs, with the strongest evidence of association being concentrated in individuals carrying APOE-4. Conclusions: This study suggests that VR22 or a nearby gene influences susceptibility to Alzheimer’s disease, and the effect is dependent on APOE status.}, number={10}, journal={JOURNAL OF MEDICAL GENETICS}, author={Martin, ER and Bronson, PG and Li, YJ and Wall, N and Chung, RH and Schmechel, DE and Small, G and Xu, PT and Bartlett, J and Schnetz-Boutaud, N and et al.}, year={2005}, month={Oct}, pages={787–792} }