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  1. Article ; Online: Reply.

    Lu, Yingchang / Zheng, Wei

    Gastroenterology

    2019  Volume 157, Issue 3, Page(s) 896–897

    MeSH term(s) Asian Continental Ancestry Group ; Colorectal Neoplasms ; Genome-Wide Association Study ; Humans
    Language English
    Publishing date 2019-07-12
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 80112-4
    ISSN 1528-0012 ; 0016-5085
    ISSN (online) 1528-0012
    ISSN 0016-5085
    DOI 10.1053/j.gastro.2019.07.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Book ; Thesis: Genetics and genomics of cholesterol and polyunsaturated fatty acid metabolism in relation to coronary heart disease risk

    Lu, Yingchang

    2011  

    Author's details Yingchang (Kevin) Lu
    Language English
    Size 216 p. :, ill. (some col.)
    Publisher s.n.
    Publishing place Wageningen
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Thesis (doctoral)--Wageningen University, 2011
    Note Summary in Dutch. ; Vita. ; "Propositions" ([1] leaf) inserted.
    ISBN 9789461730350 ; 9461730357
    Database NAL-Catalogue (AGRICOLA)

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  3. Article ; Online: Low intensity ultrasound enhances cisplatin uptake in vitro by cochlear hair cells.

    Chu, Ya-Cherng / Chan, Yen-Hui / Lim, Jormay / Ho, Chien-Ying / Lin, Pei-Hsuan / Lu, Ying-Chang / Wu, Chen-Chi / Wang, Jaw-Lin

    JASA express letters

    2022  Volume 1, Issue 7, Page(s) 72001

    Abstract: Drug delivery to the inner ear has been challenging due to the blood-labyrinth barrier. Intracochlear drug delivery is an invasive alternative with less pharmacokinetic variables. In this study, the effect of low intensity ultrasound on drug uptake by ... ...

    Abstract Drug delivery to the inner ear has been challenging due to the blood-labyrinth barrier. Intracochlear drug delivery is an invasive alternative with less pharmacokinetic variables. In this study, the effect of low intensity ultrasound on drug uptake by hair cells is investigated. Cochlear explants harvested from newborn mice were cultured in a medium containing cisplatin to emulate drug delivered to the endolymph. The results demonstrated the exposure to ultrasound stimulation effectively enhanced cisplatin uptake by hair cells. The uptake started from the apical side of the hair cells and progressed inward as the exposure time increased.
    MeSH term(s) Animals ; Cisplatin/pharmacology ; Cochlea ; Ear, Inner ; Endolymph ; Hair Cells, Auditory ; Mice
    Chemical Substances Cisplatin (Q20Q21Q62J)
    Language English
    Publishing date 2022-09-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2691-1191
    ISSN (online) 2691-1191
    DOI 10.1121/10.0005641
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Simulation-predicted and -explained inheritance model of pathogenicity confirmed by transgenic mice models.

    Tsai, Cheng-Yu / Lu, Ying-Chang / Chan, Yen-Hui / Radhakrishnan, Navaneethan / Chang, Yuan-Yu / Lin, Shu-Wha / Liu, Tien-Chen / Hsu, Chuan-Jen / Chen, Pei-Lung / Yang, Lee-Wei / Wu, Chen-Chi

    Computational and structural biotechnology journal

    2023  Volume 21, Page(s) 5698–5711

    Abstract: Variants in the gap junction beta-2 ( ...

    Abstract Variants in the gap junction beta-2 (
    Language English
    Publishing date 2023-11-18
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2694435-2
    ISSN 2001-0370
    ISSN 2001-0370
    DOI 10.1016/j.csbj.2023.11.026
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Generation of induced pluripotent stem cells (IBMSi027-A) from a patient with hearing loss carrying WFS1 c.2051C > T (p.Ala684Val) variant.

    Chan, Yen-Hui / Tsai, Cheng-Yu / Ho, Chang-Han / Lu, Ying-Chang / Lin, Pei-Hsuan / Chen, Ta-Ching / Chen, You-Tzung / Huang, Cheng-Yen / Liu, Tien-Chen / Hsu, Chuan-Jen / Wu, Chen-Chi

    Stem cell research

    2023  Volume 69, Page(s) 103068

    Abstract: Pathogenic variants of the WFS1 gene can cause recessive-inherited Wolfram syndrome or dominant-inherited Wolfram-like syndrome with optic atrophy and hearing impairment. Using the Sendai virus delivery system, we generated induced pluripotent stem cells ...

    Abstract Pathogenic variants of the WFS1 gene can cause recessive-inherited Wolfram syndrome or dominant-inherited Wolfram-like syndrome with optic atrophy and hearing impairment. Using the Sendai virus delivery system, we generated induced pluripotent stem cells from the peripheral blood mononuclear cells of a female patient with the WFS1 pathogenic variant c.2051C > T (p.Ala684Val). The resulting induced pluripotent stem cells exhibited a normal karyotype and pluripotency, as confirmed using immunofluorescence staining, and differentiated into three germ layers in vivo. This cellular model provides a useful platform for investigating the pathogenic mechanisms of both blindness and deafness related to WFS1 variants.
    MeSH term(s) Humans ; Female ; Induced Pluripotent Stem Cells/pathology ; Leukocytes, Mononuclear/pathology ; Hearing Loss/genetics ; Wolfram Syndrome/genetics ; Wolfram Syndrome/pathology ; Mutation
    Language English
    Publishing date 2023-03-16
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2393143-7
    ISSN 1876-7753 ; 1873-5061
    ISSN (online) 1876-7753
    ISSN 1873-5061
    DOI 10.1016/j.scr.2023.103068
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Metabolomic profiling of glucose homeostasis in African Americans: the Insulin Resistance Atherosclerosis Family Study (IRAS-FS).

    Okut, Hayrettin / Lu, Yingchang / Palmer, Nicholette D / Chen, Yii-Der Ida / Taylor, Kent D / Norris, Jill M / Lorenzo, Carlos / Rotter, Jerome I / Langefeld, Carl D / Wagenknecht, Lynne E / Bowden, Donald W / Ng, Maggie C Y

    Metabolomics : Official journal of the Metabolomic Society

    2023  Volume 19, Issue 4, Page(s) 35

    Abstract: Introduction: African Americans are at increased risk for type 2 diabetes.: Objectives: This work aimed to examine metabolomic signature of glucose homeostasis in African Americans.: Methods: We used an untargeted liquid chromatography-mass ... ...

    Abstract Introduction: African Americans are at increased risk for type 2 diabetes.
    Objectives: This work aimed to examine metabolomic signature of glucose homeostasis in African Americans.
    Methods: We used an untargeted liquid chromatography-mass spectrometry metabolomic approach to comprehensively profile 727 plasma metabolites among 571 African Americans from the Insulin Resistance Atherosclerosis Family Study (IRAS-FS) and investigate the associations between these metabolites and both the dynamic (S
    Results: We confirmed increased plasma metabolite levels of branched-chain amino acids and their metabolic derivatives, 2-aminoadipate, 2-hydroxybutyrate, glutamate, arginine and its metabolic derivatives, carbohydrate metabolites, and medium- and long-chain fatty acids were associated with insulin resistance, while increased plasma metabolite levels in the glycine, serine and threonine metabolic pathway were associated with insulin sensitivity. We also observed a differential ancestral effect of glutamate on glucose homeostasis with significantly stronger effects observed in African Americans than those previously observed in Mexican Americans.
    Conclusion: We extended the observations that metabolites are useful biomarkers in the identification of prediabetes in individuals at risk of type 2 diabetes in African Americans. We revealed, for the first time, differential ancestral effect of certain metabolites (i.e., glutamate) on glucose homeostasis traits. Our study highlights the need for additional comprehensive metabolomic studies in well-characterized multiethnic cohorts.
    MeSH term(s) Humans ; Atherosclerosis/metabolism ; Black or African American ; Diabetes Mellitus, Type 2/metabolism ; Glucose ; Glutamates ; Homeostasis/physiology ; Insulin Resistance ; Metabolomics
    Chemical Substances Glucose (IY9XDZ35W2) ; Glutamates
    Language English
    Publishing date 2023-04-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2250617-2
    ISSN 1573-3890 ; 1573-3882
    ISSN (online) 1573-3890
    ISSN 1573-3882
    DOI 10.1007/s11306-023-01984-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Thesis ; Online: Genetics and genomics of cholesterol and polyunsaturated fatty acid metabolism in relation to coronary heart disease risk

    Lu Yingchang (Kevin), Y.

    2011  

    Abstract: Background Coronary heart disease (CHD) continues to be a leading cause of morbidity and mortality among adults worldwide. Deregulated lipid metabolism (dyslipidemia) that manifests as hypercholesterolemia, hypertriglyceridemia, low high-density- ... ...

    Abstract Background Coronary heart disease (CHD) continues to be a leading cause of morbidity and mortality among adults worldwide. Deregulated lipid metabolism (dyslipidemia) that manifests as hypercholesterolemia, hypertriglyceridemia, low high-density-lipoprotein (HDL) cholesterol levels or a combination of those, is an established risk factor for CHD among other established risk factors. Linoleic acid (LA, C18:2n-6) and alpha-linolenic acid (ALA, C18:3n-3) are polyunsaturated fatty acids (PUFAs) that cannot be synthesized de novo by human or animal cells, and therefore must be obtained from the diet. From these two PUFAs, two series of long-chain PUFAs are formed; the omega-6 series that are synthesized from LA, and the omega-3 series that are from ALA. Formation of these long-chain PUFAs involves a series of alternate desaturation and elongation processes. These PUFAs, especially, omega-3 PUFAs, have long been observed to reduce CHD risk. In contrast to the consistently observed cardiovascular protective effects of omega-3 PUFAs, accumulating evidence suggests a potential pro-atherogenic effects of omega-6 PUFAs, which is now still under debate. It has been estimated that genetic factors account for 26%-69% of inter-individual variation in CHD risk. These genetic factors are thought to influence CHD risk both directly and through effects on known CHD risk factors such as plasma lipid levels. The heritability of plasma lipid levels (total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides (TG)) is estimated to be about 50% (ranging from 28%-78%). With the success of recent genome-wide association studies (GWAS), many genetic variants underlying intermediate risk factors of CHD (including plasma lipid levels) and CHD itself have been identified. Whether this new genetic information could be used to improve CHD risk prediction is still marginally explored, and for some variants, the underlying mechanisms for their mediated effects on CHD risk are still unknown. The aim of this research is to investigate ...
    Keywords cholesterol ; genetic factors ; heart diseases ; lipid metabolism ; nutrigenomics ; polyenoic fatty acids ; risk assessment ; genetische factoren ; hartziekten ; lipidenmetabolisme ; meervoudig onverzadigde vetzuren ; nutrigenomica ; risicoschatting
    Subject code 610
    Language English
    Publishing country nl
    Document type Thesis ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article: Obesity genomics: assessing the transferability of susceptibility loci across diverse populations.

    Lu, Yingchang / Loos, Ruth Jf

    Genome medicine

    2013  Volume 5, Issue 6, Page(s) 55

    Abstract: The prevalence of obesity has nearly doubled worldwide over the past three decades, but substantial differences exist between nations. Although these differences are partly due to the degree of westernization, genetic factors also contribute. To date, ... ...

    Abstract The prevalence of obesity has nearly doubled worldwide over the past three decades, but substantial differences exist between nations. Although these differences are partly due to the degree of westernization, genetic factors also contribute. To date, little is known about whether the same genes contribute to obesity-susceptibility in populations of different ancestry. We review the transferability of obesity-susceptibility loci (identified by genome-wide association studies) using both single nucleotide polymorphism (SNP) and locus-wide comparisons. SNPs in FTO and near MC4R, obesity-susceptibility loci first identified in Europeans, replicate widely across other ancestries. SNP-to-SNP comparisons suggest that more than half of the 36 body mass index-associated loci are shared across European and East Asian ancestry populations, whereas locus-wide analyses suggest that the transferability might be even more extensive. Furthermore, by taking advantage of differences in haplotype structure, populations of different ancestries can help to narrow down loci, thereby pinpointing causal genes for functional follow-up. Larger-scale genetic association studies in ancestrally diverse populations will be needed for in-depth and locus-wide analyses aimed at determining, with greater confidence, the transferability of loci and allowing fine-mapping. Understanding similarities and differences in genetic susceptibility across populations of diverse ancestries might eventually contribute to a more targeted prevention and customized treatment of obesity.
    Language English
    Publishing date 2013-06-28
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2484394-5
    ISSN 1756-994X
    ISSN 1756-994X
    DOI 10.1186/gm459
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Gene therapy with a synthetic adeno-associated viral vector improves audiovestibular phenotypes in Pjvk-mutant mice.

    Lu, Ying-Chang / Tsai, Yi-Hsiu / Chan, Yen-Huei / Hu, Chin-Ju / Huang, Chun-Ying / Xiao, Ru / Hsu, Chuan-Jen / Vandenberghe, Luk H / Wu, Chen-Chi / Cheng, Yen-Fu

    JCI insight

    2022  Volume 7, Issue 20

    Abstract: Recessive PJVK mutations that cause a deficiency of pejvakin, a protein expressed in both sensory hair cells and first-order neurons of the inner ear, are an important cause of hereditary hearing impairment. Patients with PJVK mutations garner limited ... ...

    Abstract Recessive PJVK mutations that cause a deficiency of pejvakin, a protein expressed in both sensory hair cells and first-order neurons of the inner ear, are an important cause of hereditary hearing impairment. Patients with PJVK mutations garner limited benefits from cochlear implantation; thus, alternative biological therapies may be required to address this clinical difficulty. The synthetic adeno-associated viral vector Anc80L65, with its wide tropism and high transduction efficiency in various inner ear cells, may provide a solution. We delivered the PJVK transgene to the inner ear of Pjvk mutant mice using the synthetic Anc80L65 vector. We observed robust exogenous pejvakin expression in the hair cells and neurons of the cochlea and vestibular organs. Subsequent morphologic and audiologic studies demonstrated significant restoration of spiral ganglion neuron density and hair cells in the cochlea, along with partial recovery of sensorineural hearing impairment. In addition, we observed a recovery of vestibular ganglion neurons and balance function to WT levels. Our study demonstrates the utility of Anc80L65-mediated gene delivery in Pjvk mutant mice and provides insights into the potential of gene therapy for PJVK-related inner ear deficits.
    MeSH term(s) Mice ; Animals ; Genetic Therapy ; Hair Cells, Auditory/metabolism ; Hearing Loss, Sensorineural/genetics ; Hearing Loss, Sensorineural/therapy ; Hearing Loss, Sensorineural/metabolism ; Cochlea/metabolism ; Phenotype ; Proteins/genetics
    Chemical Substances pejvakin protein, mouse ; Proteins
    Language English
    Publishing date 2022-10-24
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.152941
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Generation of induced pluripotent stem cells from a patient with hearing loss carrying OPA1 c.1468T>C (p.Cys490Arg) variant.

    Chan, Yen-Hui / Ho, Chang-Han / Tsai, Cheng-Yu / Lu, Ying-Chang / Lin, Pei-Hsuan / Chen, Ta-Ching / Chen, You-Tzung / Huang, Cheng-Yen / Liu, Tien-Chen / Hsu, Chuan-Jen / Wu, Chen-Chi

    Stem cell research

    2022  Volume 64, Page(s) 102903

    Abstract: Pathogenic variants of OPA1 have been associated with autosomal dominant optic atrophy (DOA), leading to optic, auditory, and other sensorineural neuropathies and myopathies. Using the Sendai virus delivery system, we generated induced pluripotent stem ... ...

    Abstract Pathogenic variants of OPA1 have been associated with autosomal dominant optic atrophy (DOA), leading to optic, auditory, and other sensorineural neuropathies and myopathies. Using the Sendai virus delivery system, we generated induced pluripotent stem cells from the peripheral blood mononuclear cells of a female patient with the OPA1 pathogenic variant c.1468T>C (p.Cys490Arg). The resulting induced pluripotent stem cells exhibited a normal karyotype and pluripotency, as confirmed using immunofluorescence staining, and differentiated into three germ layers in vivo. This cellular model is a useful platform for investigating the pathogenic mechanisms of both blindness and deafness related to OPA1 variants.
    MeSH term(s) Humans ; Female ; Induced Pluripotent Stem Cells/pathology ; Leukocytes, Mononuclear/pathology ; Mutation ; Optic Atrophy, Autosomal Dominant/genetics ; Optic Atrophy, Autosomal Dominant/pathology ; Hearing Loss/genetics ; GTP Phosphohydrolases/genetics
    Chemical Substances OPA1 protein, human (EC 3.6.1.-) ; GTP Phosphohydrolases (EC 3.6.1.-)
    Language English
    Publishing date 2022-08-26
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2393143-7
    ISSN 1876-7753 ; 1873-5061
    ISSN (online) 1876-7753
    ISSN 1873-5061
    DOI 10.1016/j.scr.2022.102903
    Database MEDical Literature Analysis and Retrieval System OnLINE

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