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751. Genetic Susceptibility to Vitiligo: GWAS Approaches for Identifying Vitiligo Susceptibility Genes and Loci

Title Tesim:
Genetic Susceptibility to Vitiligo: GWAS Approaches for Identifying Vitiligo Susceptibility Genes and Loci
Creator:
Zhang, Xuejun, Sun, Liangdan, Yin, Xianyong, Zhu, Caihong, Dou, Jinfa, Tang, Xianfa, Shen, Changbing, Cui, Yong, Sheng, Yujun, Zhou, Fusheng, Gao, Jing, Zheng, Xiaodong, and Ko, Randy
Date of publication:
2016
Abstract Tesim:
Vitiligo is an autoimmune disease with a strong genetic component, characterized by areas of depigmented skin resulting from loss of epidermal melanocytes. Genetic factors are known to play key roles in vitiligo through discoveries in association studies and family studies. Previously, vitiligo susceptibility genes were mainly revealed through linkage analysis and candidate gene studies. Recently, our understanding of the genetic basis of vitiligo has been rapidly advancing through genome-wide association study (GWAS). More than 40 robust susceptible loci have been identified and confirmed to be associated with vitiligo by using GWAS. Most of these associated genes participate in important pathways involved in the pathogenesis of vitiligo. Many susceptible loci with unknown functions in the pathogenesis of vitiligo have also been identified, indicating that additional molecular mechanisms may contribute to the risk of developing vitiligo. In this review, we summarize the key loci that are of genome-wide significance, which have been shown to influence vitiligo risk. These genetic loci may help build the foundation for genetic diagnosis and personalize treatment for patients with vitiligo in the future. However, substantial additional studies, including gene-targeted and functional studies, are required to confirm the causality of the genetic variants and their biological relevance in the development of vitiligo.
Resource type:
Article
Affiliation Label Tesim:
University of North Carolina at Chapel Hill
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/e2/82/bb/5c/e282bb5c-ecfc-4dd2-8603-2a46b5cc8e4b
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/t33v-2g16
Identifier:
Onescience id: d8dfa3b57d8a5fc8d67cc0711ba25da0b02698c6, PMID: 26870082, Publisher DOI: https://doi.org/10.3389/fgene.2016.00003, and PMCID: PMC4740779
ISSN:
1664-8021
Journal Title:
Frontiers in Genetics
Journal Volume:
7
Keyword:
loci, Genetic Susceptibility, Genes, QH426-470, Genetics, Review, genetic susceptibility, genes, Vitiligo, and GWASs
Language Label:
English
ORCID:
Other Affiliation:
Department of Dermatology; The Second Affiliated Hospital; Anhui Medical University, Institute and Department of Dermatology; The First Affiliated Hospital; Anhui Medical University, Department of Dermatology; China-Japan Friendship Hospital, and Department of Biochemistry; University of New Mexico
Person:
Zhang, Xuejun, Sun, Liangdan, Yin, Xianyong, Zhu, Caihong, Dou, Jinfa, Tang, Xianfa, Shen, Changbing, Cui, Yong, Sheng, Yujun, Zhou, Fusheng, Gao, Jing, Zheng, Xiaodong, and Ko, Randy
Rights Statement Label:
In Copyright
Source:
d217qt98k

752. Admixture Mapping of African–American Women in the AMBER Consortium Identifies New Loci for Breast Cancer and Estrogen-Receptor Subtypes

Title Tesim:
Admixture Mapping of African–American Women in the AMBER Consortium Identifies New Loci for Breast Cancer and Estrogen-Receptor Subtypes
Creator:
Bensen, Jeannette T., Yao, Song, Bandera, Elisa V., Hu, Jennifer J., Haiman, Christopher A., John, Esther M., Ambrosone, Christine B., Haddad, Stephen, Sucheston-Campbell, Lara, Deming, Sandra L., Ziegler, Regina G., Ruiz-Narváez, Edward A., Lunetta, Kathryn L., Olshan, Andrew F., Bernstein, Leslie, and Palmer, Julie R.
Date of publication:
2016
Abstract Tesim:
Recent genetic admixture coupled with striking differences in incidence of estrogen receptor (ER) breast cancer subtypes, as well as severity, between women of African and European ancestry, provides an excellent rationale for performing admixture mapping in African American women with breast cancer risk. We performed the largest breast cancer admixture mapping study with in African American women to identify novel genomic regions associated with the disease. We conducted a genome-wide admixture scan using 2,624 autosomal ancestry informative markers (AIMs) in 3,629 breast cancer cases (including 1,968 ER-positive, 1093 ER-negative, and 601 triple-negative) and 4,658 controls from the African American Breast Cancer Epidemiology and Risk (AMBER) Consortium, a collaborative study of four large geographically different epidemiological studies of breast cancer in African American women. We used an independent case-control study to test for SNP association in regions with genome-wide significant admixture signals. We found two novel genome-wide significant regions of excess African ancestry, 4p16.1 and 17q25.1, associated with ER-positive breast cancer. Two regions known to harbor breast cancer variants, 10q26 and 11q13, were also identified with excess of African ancestry. Fine-mapping of the identified genome-wide significant regions suggests the presence of significant genetic associations with ER-positive breast cancer in 4p16.1 and 11q13. In summary, we identified three novel genomic regions associated with breast cancer risk by ER status, suggesting that additional previously unidentified variants may contribute to the racial differences in breast cancer risk in the African American population.
Resource type:
Article
Affiliation Label Tesim:
Department of Epidemiology
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/e2/82/bb/5c/e282bb5c-ecfc-4dd2-8603-2a46b5cc8e4b
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/stmr-k483
Identifier:
Onescience id: 17b262a5adbaff80272111d36d3d66ea3d5e6660, PMID: 27708667, PMCID: PMC5030764, and Publisher DOI: https://doi.org/10.3389/fgene.2016.00170
ISSN:
1664-8021
Journal Title:
Frontiers in Genetics
Journal Volume:
7
Keyword:
Incidence, Risk, Receptors, Estrogen, Amber, Breast Neoplasms, Homo sapiens, Genome, Epidemiologic Studies, and Case-Control Studies
Language Label:
English
ORCID:
Other Affiliation:
Department of Cancer Prevention and Control; Roswell Park Cancer Institute, Rutgers Cancer Institute of New Jersey, Sylvester Comprehensive Cancer Center and Department of Public Health Sciences; University of Miami Miller School of Medicine, Department of Preventive Medicine; Keck School of Medicine; University of Southern California/Norris Comprehensive Cancer Center, Cancer Prevention Institute of California, Slone Epidemiology Center; Boston University, College of Pharmacy; The Ohio State University, College of Veterinary Medicine; The Ohio State University, Vanderbilt Epidemiology Center; Vanderbilt University and the Vanderbilt-Ingram Cancer Center, Epidemiology and Biostatistics Program; Division of Cancer Epidemiology and Genetics; National Cancer Institute, Department of Biostatistics; Boston University School of Public Health, and Division of Cancer Etiology; Department of Population Science; Beckman Research Institute
Person:
Bensen, Jeannette T., Yao, Song, Bandera, Elisa V., Hu, Jennifer J., Haiman, Christopher A., John, Esther M., Ambrosone, Christine B., Haddad, Stephen, Sucheston-Campbell, Lara, Deming, Sandra L., Ziegler, Regina G., Ruiz-Narváez, Edward A., Lunetta, Kathryn L., Olshan, Andrew F., Bernstein, Leslie, and Palmer, Julie R.
Rights Statement Label:
In Copyright
Source:
3197xr82r

753. Exercise Regulation of Marrow Adipose Tissue

Title Tesim:
Exercise Regulation of Marrow Adipose Tissue
Creator:
Styner, Maya and Pagnotti, Gabriel M.
Date of publication:
2016
Abstract Tesim:
Despite association with low bone density and skeletal fractures, marrow adipose tissue (MAT) remains poorly understood. The marrow adipocyte originates from the mesenchymal stem cell (MSC) pool that also gives rise to osteoblasts, chondrocytes, and myocytes, among other cell types. To date, the presence of MAT has been attributed to preferential biasing of MSC into the adipocyte rather than osteoblast lineage, thus negatively impacting bone formation. Here, we focus on understanding the physiology of MAT in the setting of exercise, dietary interventions, and pharmacologic agents that alter fat metabolism. The beneficial effect of exercise on musculoskeletal strength is known: exercise induces bone formation, encourages growth of skeletally supportive tissues, inhibits bone resorption, and alters skeletal architecture through direct and indirect effects on a multiplicity of cells involved in skeletal adaptation. MAT is less well studied due to the lack of reproducible quantification techniques. In recent work, osmium-based 3D quantification shows a robust response of MAT to both dietary and exercise intervention in that MAT is elevated in response to high-fat diet and can be suppressed following daily exercise. Exercise-induced bone formation correlates with suppression of MAT, such that exercise effects might be due to either calorie expenditure from this depot or from mechanical biasing of MSC lineage away from fat and toward bone, or a combination thereof. Following treatment with the anti-diabetes drug rosiglitazone – a PPARγ-agonist known to increase MAT and fracture risk – mice demonstrate a fivefold higher femur MAT volume compared to the controls. In addition to preventing MAT accumulation in control mice, exercise intervention significantly lowers MAT accumulation in rosiglitazone-treated mice. Importantly, exercise induction of trabecular bone volume is unhindered by rosiglitazone. Thus, despite rosiglitazone augmentation of MAT, exercise significantly suppresses MAT volume and induces bone formation. That exercise can both suppress MAT volume and increase bone quantity, notwithstanding the skeletal harm induced by rosiglitazone, underscores exercise as a powerful regulator of bone remodeling, encouraging marrow stem cells toward the osteogenic lineage to fulfill an adaptive need for bone formation. Thus, exercise represents an effective strategy to mitigate the deleterious effects of overeating and iatrogenic etiologies on bone and fat.
Resource type:
Article
Affiliation Label Tesim:
Department of Medicine
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/e2/82/bb/5c/e282bb5c-ecfc-4dd2-8603-2a46b5cc8e4b
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/ay1d-hx18
Identifier:
Publisher DOI: https://doi.org/10.3389/fendo.2016.00094, PMID: 27471493, PMCID: PMC4943947, and Onescience id: 2716b4f2a993439dedbaebe7b23b201f0e1f4e54
ISSN:
1664-2392
Journal Title:
Frontiers in Endocrinology
Journal Volume:
7
Keyword:
Lipid, PPARγ, high fat diet, marrow adipose tissue (MAT), Bone micro-architecture, Exercise, quantitative image analysis, bone quality, and rosiglitazone
Language Label:
English
ORCID:
Other Affiliation:
Department of Biomedical Engineering; Stony Brook University
Person:
Styner, Maya and Pagnotti, Gabriel M.
Rights Statement Label:
In Copyright
Source:
x920g241t

754. Structural and Functional Characterization of the FadR Regulatory Protein from Vibrio alginolyticus

Title Tesim:
Structural and Functional Characterization of the FadR Regulatory Protein from Vibrio alginolyticus
Creator:
Lin, Jingxia, Zhu, Jun, Gao, Rongsui, Xia, Xiaoyun, Lin, Yuan, Hassan, Bachar, Li, Defeng, Feng, Youjun, Wang, Shihua, Wang, Hui, and Bi, Lijun
Date of publication:
2017
Abstract Tesim:
The structure of Vibrio cholerae FadR (VcFadR) complexed with the ligand oleoyl-CoA suggests an additional ligand-binding site. However, the fatty acid metabolism and its regulation is poorly addressed in Vibrio alginolyticus, a species closely-related to V. cholerae. Here, we show crystal structures of V. alginolyticus FadR (ValFadR) alone and its complex with the palmitoyl-CoA, a long-chain fatty acyl ligand different from the oleoyl-CoA occupied by VcFadR. Structural comparison indicates that both VcFadR and ValFadR consistently have an additional ligand-binding site (called site 2), which leads to more dramatic conformational-change of DNA-binding domain than that of the E. coli FadR (EcFadR). Isothermal titration calorimetry (ITC) analyses defines that the ligand-binding pattern of ValFadR (2:1) is distinct from that of EcFadR (1:1). Together with surface plasmon resonance (SPR), electrophoresis mobility shift assay (EMSA) demonstrates that ValFadR binds fabA, an important gene of unsaturated fatty acid (UFA) synthesis. The removal of fadR from V. cholerae attenuates fabA transcription and results in the unbalance of UFA/SFA incorporated into membrane phospholipids. Genetic complementation of the mutant version of fadR (Δ42, 136-177) lacking site 2 cannot restore the defective phenotypes of ΔfadR while the wild-type fadR gene and addition of exogenous oleate can restore them. Mice experiments reveals that VcFadR and its site 2 have roles in bacterial colonizing. Together, the results might represent an additional example that illustrates the Vibrio FadR-mediated lipid regulation and its role in pathogenesis.
Resource type:
Article
Affiliation Label Tesim:
Department of Biochemistry and Biophysics
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/e2/82/bb/5c/e282bb5c-ecfc-4dd2-8603-2a46b5cc8e4b
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/sx0m-0y82
Identifier:
PMID: 29312893, Publisher DOI: https://doi.org/10.3389/fcimb.2017.00513, PMCID: PMC5733061, and Onescience id: a9e97b0757a720592329d9ae9d98c747f8abc06f
ISSN:
2235-2988
Journal Title:
Frontiers in Cellular and Infection Microbiology
Journal Volume:
7
Keyword:
virulence, ligand, Vibrio alginolyticus, FadR, and fatty acid sensing
Language Label:
English
ORCID:
Other Affiliation:
Department of Medical Microbiology and Parasitology; Zhejiang University School of Medicine, Department of Microbiology; Perelman School of Medicine; University of Pennsylvania, Department of Microbiology; Nanjing Agricultural University, School of Life Sciences; Fujian Agriculture and Forestry University, and Institute of Biophysics; Chinese Academy of Sciences
Person:
Lin, Jingxia, Zhu, Jun, Gao, Rongsui, Xia, Xiaoyun, Lin, Yuan, Hassan, Bachar, Li, Defeng, Feng, Youjun, Wang, Shihua, Wang, Hui, and Bi, Lijun
Rights Statement Label:
In Copyright
Source:
0g354k960

755. Persistent Decreases in Adult Subventricular and Hippocampal Neurogenesis Following Adolescent Intermittent Ethanol Exposure

Title Tesim:
Persistent Decreases in Adult Subventricular and Hippocampal Neurogenesis Following Adolescent Intermittent Ethanol Exposure
Creator:
Liu, Wen and Crews, Fulton T.
Date of publication:
2017
Abstract Tesim:
Neurogenesis in hippocampal dentate gyrus (DG) and subventricular zone (SVZ) matures during adolescence to adult levels. Binge drinking is prevalent in adolescent humans, and could alter brain neurogenesis and maturation in a manner that persists into adulthood. To determine the impact of adolescent binge drinking on adult neurogenesis, Wistar rats received adolescent intermittent ethanol (AIE) exposure (5.0 g/kg/day, i.g., 2 days on/2 days off from postnatal day, P25–P54) and sacrificed on P57 or P95. Neural progenitor cell proliferation, differentiation, survival and maturation using immunohistochemistry was determined in the DG and SVZ. We found that AIE exposure decreased neurogenesis in both brain regions in adulthood (P95). In the DG at P57, AIE exposure resulted in a significant reduction of SOX2+, Tbr2+, Prox1+ and parvalbumin (PV)+IR expression, and at P95 decreased DCX+ and PV+IR expression. AIE exposure also reduced the expression of two cell proliferation markers (Ki67+ and BrdU+IR with 300 mg/kg, 2 h) at P95. The immune signaling molecule β-2 microglobulin+ and the cell death marker activated caspase-3+IR were significantly increased in the DG by AIE exposure. In the SVZ, AIE exposure decreased SOX2+, Mash1+, DCX+ and Dlx2+IR expression at P95, but not at P57. Thus, in adulthood both brain regions have reduced neurogenesis following AIE exposure. To assess progenitor cell survival and maturation, rats were treated with BrdU (150 mg/kg/day, 14 days) to label proliferating cells and were sacrificed weeks later on P95. In the hippocampus DG, AIE exposure increased survival BrdU+ cells which differentiated into Iba1+ microglia. In contrast, SVZ had decreased BrdU+ cells similar to decreased DCX+ neurogenesis. These data indicate that AIE exposure causes a lasting decrease in both adult hippocampal DG and forebrain SVZ neurogenesis with brain regional differences in the AIE response that persist into adulthood.
Resource type:
Article
Affiliation Label Tesim:
School of Medicine
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/e2/82/bb/5c/e282bb5c-ecfc-4dd2-8603-2a46b5cc8e4b
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/zvyx-xv63
Identifier:
PMID: 28855864, Publisher DOI: https://doi.org/10.3389/fnbeh.2017.00151, Onescience id: 21a362c51723aa92a30dcab57e4a2a356552ffe6, and PMCID: PMC5557743
ISSN:
1662-5153
Journal Title:
Frontiers in Behavioral Neuroscience
Journal Volume:
11
Keyword:
Adolescent Intermittent Ethanol, adolescent intermittent ethanol, Subventricular zone, rat, neurogenesis, Neurogenesis, subventricular zone, and hippocampal dentate gyrus
Language Label:
English
ORCID:
Person:
Liu, Wen and Crews, Fulton T.
Rights Statement Label:
In Copyright
Source:
f4752n703

756. Nucleus Accumbens MC4-R Stimulation Reduces Food and Ethanol Intake in Adult Rats Regardless of Binge-Like Ethanol Exposure during Adolescence

Title Tesim:
Nucleus Accumbens MC4-R Stimulation Reduces Food and Ethanol Intake in Adult Rats Regardless of Binge-Like Ethanol Exposure during Adolescence
Creator:
Cubero, Inmaculada, Carvajal, Francisca, Thiele, Todd E., Alcaraz-Iborra, Manuel, Navarro, Montserrat, and Lerma-Cabrera, José M.
Date of publication:
2017
Abstract Tesim:
The melanocortin (MC) system regulates feeding and ethanol consumption. Recent evidence shows that melanocortin 4 receptor (MC4-R) stimulation within the nucleus accumbens (NAc) elicits anorectic responses and reduces ethanol consumption and ethanol palatability in adult rats. Ethanol exposure during adolescence causes long-lasting changes in neural pathways critically involved in neurobehavioral responses to ethanol. In this regard, binge-like ethanol exposure during adolescence reduces basal alpha-melanocyte-stimulating hormone (α-MSH) and alters the levels of agouti-related peptide (AgRP) in hypothalamic and limbic areas. Given the protective role of MC against excessive ethanol consumption, disturbances in the MC system induced by binge-like ethanol exposure during adolescence might contribute to excessive ethanol consumption during adulthood. In the present study, we evaluated whether binge-like ethanol exposure during adolescence leads to elevated ethanol intake and/or eating disturbance during adulthood. Toward that aim, Sprague-Dawley rats were treated with ethanol (3 g/kg i.p.; BEP group) or saline (SP group) for 14 days (PND 25 to PND 38). On PND73, all the groups were given access to 20% ethanol on an intermittent schedule. Our results showed that adult rats given intermittent access (IAE) to 20% ethanol achieved high spontaneous ethanol intake that was not significantly enhanced by binge-like ethanol pretreatment during adolescence. However, BEP group exhibited an increase in food intake without a parallel increase in body weight (BW) relative to SP group suggesting caloric efficiency disturbance. Additionally, we evaluated whether binge-like ethanol exposure during adolescence alters the expected reduction in feeding and ethanol consumption following NAc shell administration of a selective MC4-R agonist in adult rats showing high rates of ethanol consumption. For that, animals in each pretreatment condition (SP and BEP) were divided into three subgroups and given bilateral NAc infusions of the selective MC4-R agonist cyclo(NH-CH2-CH2-CO-His-D-Phe-Arg-Trp-Glu)-NH2 (0, 0.75 or 1.5 μg). Results revealed that MC4-R stimulation within the NAc reduced feeding and ethanol intake in high ethanol-drinking adult rats, regardless of previous binge-like ethanol exposure during adolescence, which adds new evidence regarding the dual ability of MC compounds to control excessive ethanol and food intake.
Resource type:
Article
Affiliation Label Tesim:
Department of Psychology and Neuroscience
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/e2/82/bb/5c/e282bb5c-ecfc-4dd2-8603-2a46b5cc8e4b
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/cekt-m923
Identifier:
PMCID: PMC5594710, Onescience id: 9588ffade33cd5675e5c9f2a71d6bb0abb0ab8f2, PMID: 28936166, and Publisher DOI: https://doi.org/10.3389/fnbeh.2017.00167
ISSN:
1662-5153
Journal Title:
Frontiers in Behavioral Neuroscience
Journal Volume:
11
Keyword:
melanocortin, nucleus accumbens, intermittent-access ethanol paradigm, nucleus accumbens., adolescence, binge-like ethanol exposure, and MC4-R
Language Label:
English
ORCID:
Other Affiliation:
Institute of Biomedical Sciences; Universidad Autonoma de Chile, Department of Psychology; University of Almeria, and Department of Psychology; University of Oviedo
Person:
Cubero, Inmaculada, Carvajal, Francisca, Thiele, Todd E., Alcaraz-Iborra, Manuel, Navarro, Montserrat, and Lerma-Cabrera, José M.
Rights Statement Label:
In Copyright
Source:
wp988q99p

757. Chronic Nicotine Exposure Initiated in Adolescence and Unpaired to Behavioral Context Fails to Enhance Sweetened Ethanol Seeking

Title Tesim:
Chronic Nicotine Exposure Initiated in Adolescence and Unpaired to Behavioral Context Fails to Enhance Sweetened Ethanol Seeking
Creator:
Robinson, Donita L., Wangler, Lynde M., Czarnecki, Kyle S., and Madayag, Aric C.
Date of publication:
2017
Abstract Tesim:
Nicotine use in adolescence is pervasive in the United States and, according to the Gateway Hypothesis, may lead to progression towards other addictive substances. Given the prevalence of nicotine and ethanol comorbidity, it is difficult to ascertain if nicotine is a gateway drug for ethanol. Our study investigated the relationship between adolescent exposure to nicotine and whether this exposure alters subsequent alcohol seeking behavior. We hypothesized that rats exposed to nicotine beginning in adolescence would exhibit greater alcohol seeking behavior than non-exposed siblings. To test our hypothesis, beginning at P28, female rats were initially exposed to once daily nicotine (0.4 mg/kg, SC) or saline for 5 days. Following these five initial injections, animals were trained to nose-poke for sucrose reinforcement (10%, w/v), gradually increasing to sweetened ethanol (10% sucrose; 10% ethanol, w/v) on an FR5 reinforcement schedule. Nicotine injections were administered after the behavioral sessions to minimize acute effects of nicotine on operant self-administration. We measured the effects of nicotine exposure on the following aspects of ethanol seeking: self-administration, naltrexone (NTX)-induced decreases, habit-directed behavior, motivation, extinction and reinstatement. Nicotine exposure did not alter self-administration or the effectiveness of NTX to reduce alcohol seeking. Nicotine exposure blocked habit-directed ethanol seeking. Finally, nicotine did not alter extinction learning or cue-induced reinstatement to sweetened ethanol seeking. Our findings suggest that nicotine exposure outside the behavioral context does not escalate ethanol seeking. Further, the Gateway Hypothesis likely applies to scenarios in which nicotine is either self-administered or physiologically active during the behavioral session.
Resource type:
Article
Affiliation Label Tesim:
School of Medicine
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/e2/82/bb/5c/e282bb5c-ecfc-4dd2-8603-2a46b5cc8e4b
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/nb4t-9x26
Identifier:
Publisher DOI: https://doi.org/10.3389/fnbeh.2017.00153, PMCID: PMC5562684, PMID: 28860980, and Onescience id: 97844f865758d1fe9dbef764d842f99e32eeab3d
ISSN:
1662-5153
Journal Title:
Frontiers in Behavioral Neuroscience
Journal Volume:
11
Keyword:
tobacco, Addiction, Tobacco, alcohol use disorder, addiction, juvenile, cigarette smoking, adolescent, Original Research, and Neuroscience
Language Label:
English
ORCID:
Other Affiliation:
Department of Psychiatry and Department of Pharmacology
Person:
Robinson, Donita L., Wangler, Lynde M., Czarnecki, Kyle S., and Madayag, Aric C.
Rights Statement Label:
In Copyright
Source:
jw827h61g

758. Multi-Modal Homing in Sea Turtles: Modeling Dual Use of Geomagnetic and Chemical Cues in Island-Finding

Title Tesim:
Multi-Modal Homing in Sea Turtles: Modeling Dual Use of Geomagnetic and Chemical Cues in Island-Finding
Creator:
Lohmann, Kenneth J., Ernst, David A., Kurth, Jessica A., Putman, Nathan F., Lohmann, Catherine M. F., and Endres, Courtney S.
Date of publication:
2016
Abstract Tesim:
Sea turtles are capable of navigating across large expanses of ocean to arrive at remote islands for nesting, but how they do so has remained enigmatic. An interesting example involves green turtles (Chelonia mydas) that nest on Ascension Island, a tiny land mass located approximately 2000 km from the turtles’ foraging grounds along the coast of Brazil. Sensory cues that turtles are known to detect, and which might hypothetically be used to help locate Ascension Island, include the geomagnetic field, airborne odorants, and waterborne odorants. One possibility is that turtles use magnetic cues to arrive in the vicinity of the island, then use chemical cues to pinpoint its location. As a first step toward investigating this hypothesis, we used oceanic, atmospheric, and geomagnetic models to assess whether magnetic and chemical cues might plausibly be used by turtles to locate Ascension Island. Results suggest that waterborne and airborne odorants alone are insufficient to guide turtles from Brazil to Ascension, but might permit localization of the island once turtles arrive in its vicinity. By contrast, magnetic cues might lead turtles into the vicinity of the island, but would not typically permit its localization because the field shifts gradually over time. Simulations reveal, however, that the sequential use of magnetic and chemical cues can potentially provide a robust navigational strategy for locating Ascension Island. Specifically, one strategy that appears viable is following a magnetic isoline into the vicinity of Ascension Island until an odor plume emanating from the island is encountered, after which turtles might either: (1) initiate a search strategy; or (2) follow the plume to its island source. These findings are consistent with the hypothesis that sea turtles, and perhaps other marine animals, use a multi-modal navigational strategy for locating remote islands.
Resource type:
Article
Affiliation Label Tesim:
Department of Biology
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/e2/82/bb/5c/e282bb5c-ecfc-4dd2-8603-2a46b5cc8e4b
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/txpj-gs79
Identifier:
Onescience id: 9c29bb6d2181a3f92272cf38b754137b25142a69, PMCID: PMC4761866, PMID: 26941625, and Publisher DOI: https://doi.org/10.3389/fnbeh.2016.00019
ISSN:
1662-5153
Journal Title:
Frontiers in Behavioral Neuroscience
Journal Volume:
10
Keyword:
olfaction, navigation, homing, sea turtles, and magnetism
Language Label:
English
ORCID:
Other Affiliation:
Cooperative Institute for Marine and Atmospheric Studies; Rosenstiel School for Marine and Atmospheric Science; University of Miami
Person:
Lohmann, Kenneth J., Ernst, David A., Kurth, Jessica A., Putman, Nathan F., Lohmann, Catherine M. F., and Endres, Courtney S.
Rights Statement Label:
In Copyright
Source:
dj52w983d

759. Abnormal Changes of Brain Cortical Anatomy and the Association with Plasma MicroRNA107 Level in Amnestic Mild Cognitive Impairment

Title Tesim:
Abnormal Changes of Brain Cortical Anatomy and the Association with Plasma MicroRNA107 Level in Amnestic Mild Cognitive Impairment
Creator:
Jin, Yan, Jiang, Weixiong, Shen, Dinggang, Xiao, Shifu, Shi, Feng, and Wang, Tao
Date of publication:
2016
Abstract Tesim:
MicroRNA107 (Mir107) has been thought to relate to the brain structure phenotype of Alzheimer’s disease. In this study, we evaluated the cortical anatomy in amnestic mild cognitive impairment (aMCI) and the relation between cortical anatomy and plasma levels of Mir107 and beta-site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1). Twenty aMCI (20 aMCI) and 24 cognitively normal control (NC) subjects were recruited, and T1-weighted MR images were acquired. Cortical anatomical measurements, including cortical thickness (CT), surface area (SA), and local gyrification index (LGI), were assessed. Quantitative RT-PCR was used to examine plasma expression of Mir107, BACE1 mRNA. Thinner cortex was found in aMCI in areas associated with episodic memory and language, but with thicker cortex in other areas. SA decreased in aMCI in the areas associated with working memory and emotion. LGI showed a significant reduction in aMCI in the areas involved in language function. Changes in Mir107 and BACE1 messenger RNA plasma expression were correlated with changes in CT and SA. We found alterations in key left brain regions associated with memory, language, and emotion in aMCI that were significantly correlated with plasma expression of Mir107 and BACE1 mRNA. This combination study of brain anatomical alterations and gene information may shed lights on our understanding of the pathology of AD.
Resource type:
Article
Affiliation Label Tesim:
Department of Radiology
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/e2/82/bb/5c/e282bb5c-ecfc-4dd2-8603-2a46b5cc8e4b
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/2anf-8097
Identifier:
Publisher DOI: https://doi.org/10.3389/fnagi.2016.00112, PMCID: PMC4870937, PMID: 27242521, and Onescience id: 1bcd12196adf6e4133c6d142a0c970df81730628
ISSN:
1663-4365
Journal Title:
Frontiers in Aging Neuroscience
Journal Volume:
8
Keyword:
genetics, amnestic mild cognitive impairment, surface-based morphometry, biological markers, and Alzheimer’s disease
Language Label:
English
ORCID:
Other Affiliation:
Department of Brain and Cognitive Engineering; Korea University, Department of Geriatric Psychiatry; Shanghai Mental Health Center; Shanghai Jiao Tong University School of Medicine, and Alzheimer's Disease and Related Disorders Center; Shanghai Jiao Tong University
Person:
Jin, Yan, Jiang, Weixiong, Shen, Dinggang, Xiao, Shifu, Shi, Feng, and Wang, Tao
Rights Statement Label:
In Copyright
Source:
0g354k95q

760. The role of EGFR in influenza pathogenicity: Multiple network-based approaches to identify a key regulator of non-lethal infections

Title Tesim:
The role of EGFR in influenza pathogenicity: Multiple network-based approaches to identify a key regulator of non-lethal infections
Creator:
Stratton, Kelly G., Le, Mai Q., Gralinski, Lisa E., Heller, Natalie C., Kawaoka, Yoshihiro, Sims, Amy C., Waters, Katrina, Eisfeld, Amie J., McDermott, Jason E., Baric, Ralph S., Bramer, Lisa M., Wen, Ji, and Mitchell, Hugh D.
Date of publication:
2019
Abstract Tesim:
Despite high sequence similarity between pandemic and seasonal influenza viruses, there is extreme variation in host pathogenicity from one viral strain to the next. Identifying the underlying mechanisms of variability in pathogenicity is a critical task for understanding influenza virus infection and effective management of highly pathogenic influenza virus disease. We applied a network-based modeling approach to identify critical functions related to influenza virus pathogenicity using large transcriptomic and proteomic datasets from mice infected with six influenza virus strains or mutants. Our analysis revealed two pathogenicity-related gene expression clusters; these results were corroborated by matching proteomics data. We also identified parallel downstream processes that were altered during influenza pathogenesis. We found that network bottlenecks (nodes that bridge different network regions) were highly enriched in pathogenicity-related genes, while network hubs (highly connected network nodes) were significantly depleted in these genes. We confirmed that this trend persisted in a distinct virus: Severe Acute Respiratory Syndrome Coronavirus (SARS). The role of epidermal growth factor receptor (EGFR) in influenza pathogenesis, one of the bottleneck regulators with corroborating signals across transcript and protein expression data, was tested and validated in additional mouse infection experiments. We demonstrate that EGFR is important during influenza infection, but the role it plays changes for lethal versus non-lethal infections. Our results show that by using association networks, bottleneck genes that lack hub characteristics can be used to predict a gene’s involvement in influenza virus pathogenicity. We also demonstrate the utility of employing multiple network approaches for analyzing host response data from viral infections.
Resource type:
Article
Admin Note:
deposited with permission of Ralph Baric
Affiliation Label Tesim:
Department of Microbiology and Immunology
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/1736-x458
Identifier:
https://doi.org/10.3389/fcell.2019.00200
ISSN:
2296-634X
Journal Title:
Frontiers in Cell and Developmental Biology
Journal Volume:
7
Keyword:
systems biology, SARS-CoV, data integration, network topology, and influenza
Language Label:
English
License Label:
Attribution 3.0 United States
ORCID:
Other Affiliation:
Pacific Northwest National Laboratory, National Institute of Hygiene and Epidemiology, , and University of Wisconsin-Madison
Person:
Stratton, Kelly G., Le, Mai Q., Gralinski, Lisa E., Heller, Natalie C., Kawaoka, Yoshihiro, Sims, Amy C., Waters, Katrina, Eisfeld, Amie J., McDermott, Jason E., Baric, Ralph S., Bramer, Lisa M., Wen, Ji, and Mitchell, Hugh D.
Rights Statement Label:
In Copyright
Source:
sb397d70d