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Showing 1 to 12 of 85 entries
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Behavioral Weight Loss Treatment in Antipsychotic Treated Youth.

Scandinavian journal of child and adolescent psychiatry and psychology

Nicol GE, Kolko RP, Mills M, Gunnarsdottir T, Yingling MD, Schweiger JA, Lenze EJ, Newcomer JW, Wilfley D.
PMID: 27347489
Scand J Child Adolesc Psychiatr Psychol. 2016 May;4(2):96-104. doi: 10.21307/sjcapp-2016-014.

BACKGROUND: Antipsychotic-treated youth have increased risk for the development of obesity and type 2 diabetes. Behavioral weight loss treatments show promise in reducing obesity and diabetes risk in antipsychotic treated adults, but have received no study in antipsychotic treated...

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Nicol GE, Kolko RP, Mills M, et al. Behavioral Weight Loss Treatment in Antipsychotic Treated Youth. Scand J Child Adolesc Psychiatr Psychol. 2016;4(2):96-104doi: 10.21307/sjcapp-2016-014.
Nicol, G. E., Kolko, R. P., Mills, M., Gunnarsdottir, T., Yingling, M. D., Schweiger, J. A., Lenze, E. J., Newcomer, J. W., & Wilfley, D. (2016). Behavioral Weight Loss Treatment in Antipsychotic Treated Youth. Scandinavian journal of child and adolescent psychiatry and psychology, 4(2), 96-104. https://doi.org/10.21307/sjcapp-2016-014
Nicol, Ginger E, et al. "Behavioral Weight Loss Treatment in Antipsychotic Treated Youth." Scandinavian journal of child and adolescent psychiatry and psychology vol. 4,2 (2016): 96-104. doi: https://doi.org/10.21307/sjcapp-2016-014
Nicol GE, Kolko RP, Mills M, Gunnarsdottir T, Yingling MD, Schweiger JA, Lenze EJ, Newcomer JW, Wilfley D. Behavioral Weight Loss Treatment in Antipsychotic Treated Youth. Scand J Child Adolesc Psychiatr Psychol. 2016 May;4(2):96-104. doi: 10.21307/sjcapp-2016-014. PMID: 27347489; PMCID: PMC4916921.
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Elastin Insufficiency Predisposes Mice to Impaired Glucose Metabolism.

Journal of molecular and genetic medicine : an international journal of biomedical research

DeMarsilis AJ, Walji TA, Maedeker JA, Stoka KV, Kozel BA, Mecham RP, Wagenseil JE, Craft CS.
PMID: 26167199
J Mol Genet Med. 2014 Oct;8(3). doi: 10.4172/1747-0862.1000129.

Williams-Beuren syndrome is the consequence of a large contiguous-gene deletion on the seventh human chromosome that includes the elastin gene. Elastin is an extracellular matrix protein responsible for the cardiovascular abnormalities associated with Williams's syndrome, including hypertension and aortic...

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DeMarsilis AJ, Walji TA, Maedeker JA, et al. Elastin Insufficiency Predisposes Mice to Impaired Glucose Metabolism. J Mol Genet Med. 2014;8(3)doi: 10.4172/1747-0862.1000129.
DeMarsilis, A. J., Walji, T. A., Maedeker, J. A., Stoka, K. V., Kozel, B. A., Mecham, R. P., Wagenseil, J. E., & Craft, C. S. (2014). Elastin Insufficiency Predisposes Mice to Impaired Glucose Metabolism. Journal of molecular and genetic medicine : an international journal of biomedical research, 8(3), . https://doi.org/10.4172/1747-0862.1000129
DeMarsilis, Antea J, et al. "Elastin Insufficiency Predisposes Mice to Impaired Glucose Metabolism." Journal of molecular and genetic medicine : an international journal of biomedical research vol. 8,3 (2014). doi: https://doi.org/10.4172/1747-0862.1000129
DeMarsilis AJ, Walji TA, Maedeker JA, Stoka KV, Kozel BA, Mecham RP, Wagenseil JE, Craft CS. Elastin Insufficiency Predisposes Mice to Impaired Glucose Metabolism. J Mol Genet Med. 2014 Oct;8(3). doi: 10.4172/1747-0862.1000129. PMID: 26167199; PMCID: PMC4497575.
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Genetic association analysis of coronary heart disease by profiling gene-environment interaction based on latent components in longitudinal endophenotypes.

BMC proceedings

Gu CC, Yang WW, Kraja AT, de Las Fuentes L, Dávila-Román VG.
PMID: 20018082
BMC Proc. 2009 Dec 15;3:S86. doi: 10.1186/1753-6561-3-s7-s86.

Studies of complex diseases collect panels of disease-related traits, also known as secondary phenotypes or endophenotypes. They reflect intermediate responses to environment exposures, and as such, are likely to contain hidden information of gene-environment (G x E) interactions. The...

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Gu CC, Yang WW, Kraja AT, et al. Genetic association analysis of coronary heart disease by profiling gene-environment interaction based on latent components in longitudinal endophenotypes. BMC Proc. 2009;3:S86doi: 10.1186/1753-6561-3-s7-s86.
Gu, C. C., Yang, W. W., Kraja, A. T., de Las Fuentes, L., & Dávila-Román, V. G. (2009). Genetic association analysis of coronary heart disease by profiling gene-environment interaction based on latent components in longitudinal endophenotypes. BMC proceedings, 3S86. https://doi.org/10.1186/1753-6561-3-s7-s86
Gu, C Charles, et al. "Genetic association analysis of coronary heart disease by profiling gene-environment interaction based on latent components in longitudinal endophenotypes." BMC proceedings vol. 3 (2009): S86. doi: https://doi.org/10.1186/1753-6561-3-s7-s86
Gu CC, Yang WW, Kraja AT, de Las Fuentes L, Dávila-Román VG. Genetic association analysis of coronary heart disease by profiling gene-environment interaction based on latent components in longitudinal endophenotypes. BMC Proc. 2009 Dec 15;3:S86. doi: 10.1186/1753-6561-3-s7-s86. PMID: 20018082; PMCID: PMC2795989.
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Dissemination of effective physical activity interventions: are we applying the evidence?.

Health education research

Ballew P, Brownson RC, Haire-Joshu D, Heath GW, Kreuter MW.
PMID: 20156839
Health Educ Res. 2010 Apr;25(2):185-98. doi: 10.1093/her/cyq003. Epub 2010 Feb 15.

BACKGROUND: Given sparse knowledge on dissemination, this study sought to explore key benefits, barriers and contextual factors that are perceived to be important to the adoption and implementation of the 'Community Guide's' evidence-based physical activity recommendations.DESIGN: We conducted case...

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Ballew P, Brownson RC, Haire-Joshu D, et al. Dissemination of effective physical activity interventions: are we applying the evidence?. Health Educ Res. 2010;25(2):185-98doi: 10.1093/her/cyq003.
Ballew, P., Brownson, R. C., Haire-Joshu, D., Heath, G. W., & Kreuter, M. W. (2010). Dissemination of effective physical activity interventions: are we applying the evidence?. Health education research, 25(2), 185-98. https://doi.org/10.1093/her/cyq003
Ballew, Paula, et al. "Dissemination of effective physical activity interventions: are we applying the evidence?." Health education research vol. 25,2 (2010): 185-98. doi: https://doi.org/10.1093/her/cyq003
Ballew P, Brownson RC, Haire-Joshu D, Heath GW, Kreuter MW. Dissemination of effective physical activity interventions: are we applying the evidence?. Health Educ Res. 2010 Apr;25(2):185-98. doi: 10.1093/her/cyq003. Epub 2010 Feb 15. PMID: 20156839; PMCID: PMC3276220.
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The Whole Genome Expression Analysis using Two Microarray Technologies to Identify Gene Networks That Mediate the Myocardial Phenotype of CD36 Deficiency.

Bioinformation

Sabaouni I, Moussa A, Vannier B, Semlali O, Pietka TA, Abumrad NA, Ibrahimi A.
PMID: 24250110
Bioinformation. 2013 Oct 16;9(17):849-52. doi: 10.6026/97320630009849. eCollection 2013.

We have previously shown that CD36 is a membrane protein that facilitates long chain fatty acid (FA) transport by muscle tissues. We also documented the significant impact of muscle CD36 expression on heart function, skeletal muscle insulin sensitivity as...

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Sabaouni I, Moussa A, Vannier B, et al. The Whole Genome Expression Analysis using Two Microarray Technologies to Identify Gene Networks That Mediate the Myocardial Phenotype of CD36 Deficiency. Bioinformation. 2013;9(17):849-52doi: 10.6026/97320630009849.
Sabaouni, I., Moussa, A., Vannier, B., Semlali, O., Pietka, T. A., Abumrad, N. A., & Ibrahimi, A. (2013). The Whole Genome Expression Analysis using Two Microarray Technologies to Identify Gene Networks That Mediate the Myocardial Phenotype of CD36 Deficiency. Bioinformation, 9(17), 849-52. https://doi.org/10.6026/97320630009849
Sabaouni, Imane, et al. "The Whole Genome Expression Analysis using Two Microarray Technologies to Identify Gene Networks That Mediate the Myocardial Phenotype of CD36 Deficiency." Bioinformation vol. 9,17 (2013): 849-52. doi: https://doi.org/10.6026/97320630009849
Sabaouni I, Moussa A, Vannier B, Semlali O, Pietka TA, Abumrad NA, Ibrahimi A. The Whole Genome Expression Analysis using Two Microarray Technologies to Identify Gene Networks That Mediate the Myocardial Phenotype of CD36 Deficiency. Bioinformation. 2013 Oct 16;9(17):849-52. doi: 10.6026/97320630009849. eCollection 2013. PMID: 24250110; PMCID: PMC3819569.
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PGC-1β and ChREBP partner to cooperatively regulate hepatic lipogenesis in a glucose concentration-dependent manner.

Molecular metabolism

Chambers KT, Chen Z, Lai L, Leone TC, Towle HC, Kralli A, Crawford PA, Finck BN.
PMID: 24049734
Mol Metab. 2013 May 09;2(3):194-204. doi: 10.1016/j.molmet.2013.05.001. eCollection 2013.

Peroxisome proliferator-activated receptorγ coactivators (PGC-1α and PGC-1β) play important roles in the transcriptional regulation of intermediary metabolism. To evaluate the effects of overexpressing PGC-1α or PGC-1β at physiologic levels in liver, we generated transgenic mice with inducible overexpression of...

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Chambers KT, Chen Z, Lai L, et al. PGC-1β and ChREBP partner to cooperatively regulate hepatic lipogenesis in a glucose concentration-dependent manner. Mol Metab. 2013;2(3):194-204doi: 10.1016/j.molmet.2013.05.001.
Chambers, K. T., Chen, Z., Lai, L., Leone, T. C., Towle, H. C., Kralli, A., Crawford, P. A., & Finck, B. N. (2013). PGC-1β and ChREBP partner to cooperatively regulate hepatic lipogenesis in a glucose concentration-dependent manner. Molecular metabolism, 2(3), 194-204. https://doi.org/10.1016/j.molmet.2013.05.001
Chambers, Kari T, et al. "PGC-1β and ChREBP partner to cooperatively regulate hepatic lipogenesis in a glucose concentration-dependent manner." Molecular metabolism vol. 2,3 (2013): 194-204. doi: https://doi.org/10.1016/j.molmet.2013.05.001
Chambers KT, Chen Z, Lai L, Leone TC, Towle HC, Kralli A, Crawford PA, Finck BN. PGC-1β and ChREBP partner to cooperatively regulate hepatic lipogenesis in a glucose concentration-dependent manner. Mol Metab. 2013 May 09;2(3):194-204. doi: 10.1016/j.molmet.2013.05.001. eCollection 2013. PMID: 24049734; PMCID: PMC3773825.
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Relationship between Changes in Plasma Adiponectin Concentration and Insulin Sensitivity after Niacin Therapy.

Cardiorenal medicine

Fraterrigo G, Fabbrini E, Mittendorfer B, O'Rahilly S, Scherer PE, Patterson BW, Klein S.
PMID: 22969777
Cardiorenal Med. 2012 Aug;2(3):211-217. doi: 10.1159/000340037. Epub 2012 Jul 18.

BACKGROUND: Niaspan® (extended-release niacin) is a nicotinic acid formulation used to treat dyslipidemia in obese subjects. Niaspan binds to the GPR109A receptor in adipose tissue and stimulates adiponectin secretion, which should improve insulin sensitivity. However, Niaspan therapy often causes...

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Fraterrigo G, Fabbrini E, Mittendorfer B, et al. Relationship between Changes in Plasma Adiponectin Concentration and Insulin Sensitivity after Niacin Therapy. Cardiorenal Med. 2012;2(3):211-217doi: 10.1159/000340037.
Fraterrigo, G., Fabbrini, E., Mittendorfer, B., O'Rahilly, S., Scherer, P. E., Patterson, B. W., & Klein, S. (2012). Relationship between Changes in Plasma Adiponectin Concentration and Insulin Sensitivity after Niacin Therapy. Cardiorenal medicine, 2(3), 211-217. https://doi.org/10.1159/000340037
Fraterrigo, Gemma, et al. "Relationship between Changes in Plasma Adiponectin Concentration and Insulin Sensitivity after Niacin Therapy." Cardiorenal medicine vol. 2,3 (2012): 211-217. doi: https://doi.org/10.1159/000340037
Fraterrigo G, Fabbrini E, Mittendorfer B, O'Rahilly S, Scherer PE, Patterson BW, Klein S. Relationship between Changes in Plasma Adiponectin Concentration and Insulin Sensitivity after Niacin Therapy. Cardiorenal Med. 2012 Aug;2(3):211-217. doi: 10.1159/000340037. Epub 2012 Jul 18. PMID: 22969777; PMCID: PMC3433009.
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Similar effects on cognitive performance during high- and low-carbohydrate obesity treatment.

Nutrition & diabetes

Makris A, Darcey VL, Rosenbaum DL, Komaroff E, Vander Veur SS, Collins BN, Klein S, Wyatt HR, Foster GD.
PMID: 24061557
Nutr Diabetes. 2013 Sep 23;3:e89. doi: 10.1038/nutd.2013.29.

OBJECTIVE: Low-carbohydrate (L-CHO) diets are often used for weight loss but their effects on cognitive function are not well understood. The present study compared the effects of a L-CHO and high-carbohydrate (H-CHO) weight-loss diet on cognitive function adults.DESIGN: PARTICIPANTS...

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Makris A, Darcey VL, Rosenbaum DL, et al. Similar effects on cognitive performance during high- and low-carbohydrate obesity treatment. Nutr Diabetes. 2013;3:e89doi: 10.1038/nutd.2013.29.
Makris, A., Darcey, V. L., Rosenbaum, D. L., Komaroff, E., Vander Veur, S. S., Collins, B. N., Klein, S., Wyatt, H. R., & Foster, G. D. (2013). Similar effects on cognitive performance during high- and low-carbohydrate obesity treatment. Nutrition & diabetes, 3e89. https://doi.org/10.1038/nutd.2013.29
Makris, A, et al. "Similar effects on cognitive performance during high- and low-carbohydrate obesity treatment." Nutrition & diabetes vol. 3 (2013): e89. doi: https://doi.org/10.1038/nutd.2013.29
Makris A, Darcey VL, Rosenbaum DL, Komaroff E, Vander Veur SS, Collins BN, Klein S, Wyatt HR, Foster GD. Similar effects on cognitive performance during high- and low-carbohydrate obesity treatment. Nutr Diabetes. 2013 Sep 23;3:e89. doi: 10.1038/nutd.2013.29. PMID: 24061557; PMCID: PMC3789132.
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Dietary iron interacts with genetic background to influence glucose homeostasis.

Nutrition & metabolism

Miranda MA, St Pierre CL, Macias-Velasco JF, Nguyen HA, Schmidt H, Agnello LT, Wayhart JP, Lawson HA.
PMID: 30820238
Nutr Metab (Lond). 2019 Feb 18;16:13. doi: 10.1186/s12986-019-0339-6. eCollection 2019.

BACKGROUND: Iron is a critical component of metabolic homeostasis, but consumption of dietary iron has increased dramatically in the last 30 years, corresponding with the rise of metabolic disease. While the link between iron metabolism and metabolic health is...

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Miranda MA, St Pierre CL, Macias-Velasco JF, et al. Dietary iron interacts with genetic background to influence glucose homeostasis. Nutr Metab (Lond). 2019;16:13doi: 10.1186/s12986-019-0339-6.
Miranda, M. A., St Pierre, C. L., Macias-Velasco, J. F., Nguyen, H. A., Schmidt, H., Agnello, L. T., Wayhart, J. P., & Lawson, H. A. (2019). Dietary iron interacts with genetic background to influence glucose homeostasis. Nutrition & metabolism, 1613. https://doi.org/10.1186/s12986-019-0339-6
Miranda, Mario A, et al. "Dietary iron interacts with genetic background to influence glucose homeostasis." Nutrition & metabolism vol. 16 (2019): 13. doi: https://doi.org/10.1186/s12986-019-0339-6
Miranda MA, St Pierre CL, Macias-Velasco JF, Nguyen HA, Schmidt H, Agnello LT, Wayhart JP, Lawson HA. Dietary iron interacts with genetic background to influence glucose homeostasis. Nutr Metab (Lond). 2019 Feb 18;16:13. doi: 10.1186/s12986-019-0339-6. eCollection 2019. PMID: 30820238; PMCID: PMC6380031.
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Expression and function of ATP-dependent potassium channels in zebrafish islet β-cells.

Royal Society open science

Emfinger CH, Welscher A, Yan Z, Wang Y, Conway H, Moss JB, Moss LG, Remedi MS, Nichols CG.
PMID: 28386438
R Soc Open Sci. 2017 Feb 08;4(2):160808. doi: 10.1098/rsos.160808. eCollection 2017 Feb.

ATP-sensitive potassium channels (K

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Emfinger CH, Welscher A, Yan Z, et al. Expression and function of ATP-dependent potassium channels in zebrafish islet β-cells. R Soc Open Sci. 2017;4(2):160808doi: 10.1098/rsos.160808.
Emfinger, C. H., Welscher, A., Yan, Z., Wang, Y., Conway, H., Moss, J. B., Moss, L. G., Remedi, M. S., & Nichols, C. G. (2017). Expression and function of ATP-dependent potassium channels in zebrafish islet β-cells. Royal Society open science, 4(2), 160808. https://doi.org/10.1098/rsos.160808
Emfinger, Christopher H, et al. "Expression and function of ATP-dependent potassium channels in zebrafish islet β-cells." Royal Society open science vol. 4,2 (2017): 160808. doi: https://doi.org/10.1098/rsos.160808
Emfinger CH, Welscher A, Yan Z, Wang Y, Conway H, Moss JB, Moss LG, Remedi MS, Nichols CG. Expression and function of ATP-dependent potassium channels in zebrafish islet β-cells. R Soc Open Sci. 2017 Feb 08;4(2):160808. doi: 10.1098/rsos.160808. eCollection 2017 Feb. PMID: 28386438; PMCID: PMC5367309.
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Lipid metabolism of phenol-tolerant .

Biotechnology for biofuels

Henson WR, Hsu FF, Dantas G, Moon TS, Foston M.
PMID: 30607174
Biotechnol Biofuels. 2018 Dec 28;11:339. doi: 10.1186/s13068-018-1337-z. eCollection 2018.

BACKGROUND: Lignin is a recalcitrant aromatic polymer that is a potential feedstock for renewable fuel and chemical production. RESULTS: We hypothesize that the composition of lipids plays an important role in phenol tolerance. To test this hypothesis, we applied...

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Henson WR, Hsu FF, Dantas G, et al. Lipid metabolism of phenol-tolerant . Biotechnol Biofuels. 2018;11:339doi: 10.1186/s13068-018-1337-z.
Henson, W. R., Hsu, F. F., Dantas, G., Moon, T. S., & Foston, M. (2018). Lipid metabolism of phenol-tolerant . Biotechnology for biofuels, 11339. https://doi.org/10.1186/s13068-018-1337-z
Henson, William R, et al. "Lipid metabolism of phenol-tolerant ." Biotechnology for biofuels vol. 11 (2018): 339. doi: https://doi.org/10.1186/s13068-018-1337-z
Henson WR, Hsu FF, Dantas G, Moon TS, Foston M. Lipid metabolism of phenol-tolerant . Biotechnol Biofuels. 2018 Dec 28;11:339. doi: 10.1186/s13068-018-1337-z. eCollection 2018. PMID: 30607174; PMCID: PMC6309088.
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Ablation of VLA4 in multiple myeloma cells redirects tumor spread and prolongs survival.

Scientific reports

Hathi D, Chanswangphuwana C, Cho N, Fontana F, Maji D, Ritchey J, O'Neal J, Ghai A, Duncan K, Akers WJ, Fiala M, Vij R, DiPersio JF, Rettig M, Shokeen M.
PMID: 34996933
Sci Rep. 2022 Jan 07;12(1):30. doi: 10.1038/s41598-021-03748-0.

Multiple myeloma (MM) is a cancer of bone marrow (BM) plasma cells, which is increasingly treatable but still incurable. In 90% of MM patients, severe osteolysis results from pathological interactions between MM cells and the bone microenvironment. Delineating specific...

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Hathi D, Chanswangphuwana C, Cho N, et al. Ablation of VLA4 in multiple myeloma cells redirects tumor spread and prolongs survival. Sci Rep. 2022;12(1):30doi: 10.1038/s41598-021-03748-0.
Hathi, D., Chanswangphuwana, C., Cho, N., Fontana, F., Maji, D., Ritchey, J., O'Neal, J., Ghai, A., Duncan, K., Akers, W. J., Fiala, M., Vij, R., DiPersio, J. F., Rettig, M., & Shokeen, M. (2022). Ablation of VLA4 in multiple myeloma cells redirects tumor spread and prolongs survival. Scientific reports, 12(1), 30. https://doi.org/10.1038/s41598-021-03748-0
Hathi, Deep, et al. "Ablation of VLA4 in multiple myeloma cells redirects tumor spread and prolongs survival." Scientific reports vol. 12,1 (2022): 30. doi: https://doi.org/10.1038/s41598-021-03748-0
Hathi D, Chanswangphuwana C, Cho N, Fontana F, Maji D, Ritchey J, O'Neal J, Ghai A, Duncan K, Akers WJ, Fiala M, Vij R, DiPersio JF, Rettig M, Shokeen M. Ablation of VLA4 in multiple myeloma cells redirects tumor spread and prolongs survival. Sci Rep. 2022 Jan 07;12(1):30. doi: 10.1038/s41598-021-03748-0. PMID: 34996933; PMCID: PMC8741970.
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Showing 1 to 12 of 85 entries