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Dissecting gene-environment contributions to Type 2 diabetes.

Diabetes management (London, England)

Mitchell BD, Hanson RL.
PMID: 24966891
Diabetes Manag (Lond). 2012 Sep;2(5):375-378. doi: 10.2217/dmt.12.47.

No abstract available.

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Mitchell BD, Hanson RL. Dissecting gene-environment contributions to Type 2 diabetes. Diabetes Manag (Lond). 2012;2(5):375-378doi: 10.2217/dmt.12.47.
Mitchell, B. D., & Hanson, R. L. (2012). Dissecting gene-environment contributions to Type 2 diabetes. Diabetes management (London, England), 2(5), 375-378. https://doi.org/10.2217/dmt.12.47
Mitchell, Braxton D, and Hanson, Robert L. "Dissecting gene-environment contributions to Type 2 diabetes." Diabetes management (London, England) vol. 2,5 (2012): 375-378. doi: https://doi.org/10.2217/dmt.12.47
Mitchell BD, Hanson RL. Dissecting gene-environment contributions to Type 2 diabetes. Diabetes Manag (Lond). 2012 Sep;2(5):375-378. doi: 10.2217/dmt.12.47. PMID: 24966891; PMCID: PMC4067140.
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Genetic Counseling for Diabetes Mellitus.

Current genetic medicine reports

Stein SA, Maloney KL, Pollin TI.
PMID: 25045596
Curr Genet Med Rep. 2014 Jun 01;2(2):56-67. doi: 10.1007/s40142-014-0039-5.

Most diabetes is polygenic in etiology, with (type 1 diabetes, T1DM) or without (type 2 diabetes, T2DM) an autoimmune basis. Genetic counseling for diabetes generally focuses on providing empiric risk information based on family history and/or the effects of...

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Stein SA, Maloney KL, Pollin TI. Genetic Counseling for Diabetes Mellitus. Curr Genet Med Rep. 2014;2(2):56-67doi: 10.1007/s40142-014-0039-5.
Stein, S. A., Maloney, K. L., & Pollin, T. I. (2014). Genetic Counseling for Diabetes Mellitus. Current genetic medicine reports, 2(2), 56-67. https://doi.org/10.1007/s40142-014-0039-5
Stein, Stephanie A, et al. "Genetic Counseling for Diabetes Mellitus." Current genetic medicine reports vol. 2,2 (2014): 56-67. doi: https://doi.org/10.1007/s40142-014-0039-5
Stein SA, Maloney KL, Pollin TI. Genetic Counseling for Diabetes Mellitus. Curr Genet Med Rep. 2014 Jun 01;2(2):56-67. doi: 10.1007/s40142-014-0039-5. PMID: 25045596; PMCID: PMC4097380.
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Metabolic dysfunction in obstructive sleep apnea: A critical examination of underlying mechanisms.

Sleep and biological rhythms

Mesarwi OA, Sharma EV, Jun JC, Polotsky VY.
PMID: 26412981
Sleep Biol Rhythms. 2015 Jan;13(1):2-17. doi: 10.1111/sbr.12078.

It has recently become clear that obstructive sleep apnea (OSA) is an independent risk factor for the development of metabolic syndrome, a disorder of defective energy storage and use. Several mechanisms have been proposed to explain this finding, drawing...

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Mesarwi OA, Sharma EV, Jun JC, et al. Metabolic dysfunction in obstructive sleep apnea: A critical examination of underlying mechanisms. Sleep Biol Rhythms. 2015;13(1):2-17doi: 10.1111/sbr.12078.
Mesarwi, O. A., Sharma, E. V., Jun, J. C., & Polotsky, V. Y. (2015). Metabolic dysfunction in obstructive sleep apnea: A critical examination of underlying mechanisms. Sleep and biological rhythms, 13(1), 2-17. https://doi.org/10.1111/sbr.12078
Mesarwi, Omar A, et al. "Metabolic dysfunction in obstructive sleep apnea: A critical examination of underlying mechanisms." Sleep and biological rhythms vol. 13,1 (2015): 2-17. doi: https://doi.org/10.1111/sbr.12078
Mesarwi OA, Sharma EV, Jun JC, Polotsky VY. Metabolic dysfunction in obstructive sleep apnea: A critical examination of underlying mechanisms. Sleep Biol Rhythms. 2015 Jan;13(1):2-17. doi: 10.1111/sbr.12078. PMID: 26412981; PMCID: PMC4583137.
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Testosterone and Abnormal Glucose Metabolism in an Inner-City Cohort.

Journal of men's health

Monroe AK, Dobs AS, Cofrancesco J, Brown TT.
PMID: 24174995
J Mens Health. 2012 Sep;9(3). doi: 10.1016/j.jomh.2012.03.010.

BACKGROUND: Low testosterone (T) has been associated with insulin resistance and diabetes mellitus (DM) among men in population-based studies. These studies included racially diverse men, but did not target for inclusion individuals with opiate use, Hepatitis C Virus (HCV)...

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Monroe AK, Dobs AS, Cofrancesco J, et al. Testosterone and Abnormal Glucose Metabolism in an Inner-City Cohort. J Mens Health. 2012;9(3)doi: 10.1016/j.jomh.2012.03.010.
Monroe, A. K., Dobs, A. S., Cofrancesco, J., & Brown, T. T. (2012). Testosterone and Abnormal Glucose Metabolism in an Inner-City Cohort. Journal of men's health, 9(3), . https://doi.org/10.1016/j.jomh.2012.03.010
Monroe, Anne K, et al. "Testosterone and Abnormal Glucose Metabolism in an Inner-City Cohort." Journal of men's health vol. 9,3 (2012). doi: https://doi.org/10.1016/j.jomh.2012.03.010
Monroe AK, Dobs AS, Cofrancesco J, Brown TT. Testosterone and Abnormal Glucose Metabolism in an Inner-City Cohort. J Mens Health. 2012 Sep;9(3). doi: 10.1016/j.jomh.2012.03.010. PMID: 24174995; PMCID: PMC3809764.
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Does comorbidity affect the benefit of intensive glycemic control in older patients with type 2 diabetes mellitus?.

Nature clinical practice. Endocrinology & metabolism

Saudek CD, Kalyani RR.
PMID: 19092787
Nat Clin Pract Endocrinol Metab. 2009 Feb;5(2):78-9. doi: 10.1038/ncpendmet1041. Epub 2008 Dec 17.

No abstract available.

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Saudek CD, Kalyani RR. Does comorbidity affect the benefit of intensive glycemic control in older patients with type 2 diabetes mellitus?. Nat Clin Pract Endocrinol Metab. 2008;5(2):78-9doi: 10.1038/ncpendmet1041.
Saudek, C. D., & Kalyani, R. R. (2009). Does comorbidity affect the benefit of intensive glycemic control in older patients with type 2 diabetes mellitus?. Nature clinical practice. Endocrinology & metabolism, 5(2), 78-9. https://doi.org/10.1038/ncpendmet1041
Saudek, Christopher D, and Kalyani, Rita R. "Does comorbidity affect the benefit of intensive glycemic control in older patients with type 2 diabetes mellitus?." Nature clinical practice. Endocrinology & metabolism vol. 5,2 (2009): 78-9. doi: https://doi.org/10.1038/ncpendmet1041
Saudek CD, Kalyani RR. Does comorbidity affect the benefit of intensive glycemic control in older patients with type 2 diabetes mellitus?. Nat Clin Pract Endocrinol Metab. 2009 Feb;5(2):78-9. doi: 10.1038/ncpendmet1041. Epub 2008 Dec 17. PMID: 19092787.
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Depression and type 2 diabetes over the lifespan: a meta-analysis.

Diabetes care

Mezuk B, Eaton WW, Albrecht S, Golden SH.
PMID: 19033418
Diabetes Care. 2008 Dec;31(12):2383-90. doi: 10.2337/dc08-0985.

OBJECTIVE: It has been argued that the relationship between depression and diabetes is bi-directional, but this hypothesis has not been explicitly tested. This systematic review examines the bi-directional prospective relationships between depression and type 2 diabetes.RESEARCH DESIGN AND METHODS:...

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Mezuk B, Eaton WW, Albrecht S, et al. Depression and type 2 diabetes over the lifespan: a meta-analysis. Diabetes Care. 2008;31(12):2383-90doi: 10.2337/dc08-0985.
Mezuk, B., Eaton, W. W., Albrecht, S., & Golden, S. H. (2008). Depression and type 2 diabetes over the lifespan: a meta-analysis. Diabetes care, 31(12), 2383-90. https://doi.org/10.2337/dc08-0985
Mezuk, Briana, et al. "Depression and type 2 diabetes over the lifespan: a meta-analysis." Diabetes care vol. 31,12 (2008): 2383-90. doi: https://doi.org/10.2337/dc08-0985
Mezuk B, Eaton WW, Albrecht S, Golden SH. Depression and type 2 diabetes over the lifespan: a meta-analysis. Diabetes Care. 2008 Dec;31(12):2383-90. doi: 10.2337/dc08-0985. PMID: 19033418; PMCID: PMC2584200.
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Improving the diversity climate in academic medicine: faculty perceptions as a catalyst for institutional change.

Academic medicine : journal of the Association of American Medical Colleges

Price EG, Powe NR, Kern DE, Golden SH, Wand GS, Cooper LA.
PMID: 19116484
Acad Med. 2009 Jan;84(1):95-105. doi: 10.1097/ACM.0b013e3181900f29.

PURPOSE: To assess perceptions of underrepresented minority (URM) and majority faculty physicians regarding an institution's diversity climate, and to identify potential improvement strategies.METHOD: The authors conducted a cross-sectional survey of tenure-track physicians at the Johns Hopkins University School of...

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Price EG, Powe NR, Kern DE, et al. Improving the diversity climate in academic medicine: faculty perceptions as a catalyst for institutional change. Acad Med. 2009;84(1):95-105doi: 10.1097/ACM.0b013e3181900f29.
Price, E. G., Powe, N. R., Kern, D. E., Golden, S. H., Wand, G. S., & Cooper, L. A. (2009). Improving the diversity climate in academic medicine: faculty perceptions as a catalyst for institutional change. Academic medicine : journal of the Association of American Medical Colleges, 84(1), 95-105. https://doi.org/10.1097/ACM.0b013e3181900f29
Price, Eboni G, et al. "Improving the diversity climate in academic medicine: faculty perceptions as a catalyst for institutional change." Academic medicine : journal of the Association of American Medical Colleges vol. 84,1 (2009): 95-105. doi: https://doi.org/10.1097/ACM.0b013e3181900f29
Price EG, Powe NR, Kern DE, Golden SH, Wand GS, Cooper LA. Improving the diversity climate in academic medicine: faculty perceptions as a catalyst for institutional change. Acad Med. 2009 Jan;84(1):95-105. doi: 10.1097/ACM.0b013e3181900f29. PMID: 19116484; PMCID: PMC2824594.
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Sirtuins: from metabolic regulation to brain aging.

Frontiers in aging neuroscience

Duan W.
PMID: 23888142
Front Aging Neurosci. 2013 Jul 23;5:36. doi: 10.3389/fnagi.2013.00036. eCollection 2013.

Brain aging is characterized by progressive loss of neurophysiological functions that is often accompanied by age-associated neurodegeneration. Calorie restriction has been linked to extension of lifespan and reduction of the risk of neurodegenerative diseases in experimental model systems. Several...

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Duan W. Sirtuins: from metabolic regulation to brain aging. Front Aging Neurosci. 2013;5:36doi: 10.3389/fnagi.2013.00036.
Duan, W. (2013). Sirtuins: from metabolic regulation to brain aging. Frontiers in aging neuroscience, 536. https://doi.org/10.3389/fnagi.2013.00036
Duan, Wenzhen. "Sirtuins: from metabolic regulation to brain aging." Frontiers in aging neuroscience vol. 5 (2013): 36. doi: https://doi.org/10.3389/fnagi.2013.00036
Duan W. Sirtuins: from metabolic regulation to brain aging. Front Aging Neurosci. 2013 Jul 23;5:36. doi: 10.3389/fnagi.2013.00036. eCollection 2013. PMID: 23888142; PMCID: PMC3719022.
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Diabetes and cancer (2): evaluating the impact of diabetes on mortality in patients with cancer.

Diabetologia

Renehan AG, Yeh HC, Johnson JA, Wild SH, Gale EA, Møller H.
PMID: 22476948
Diabetologia. 2012 Jun;55(6):1619-32. doi: 10.1007/s00125-012-2526-0. Epub 2012 Apr 04.

In this paper we address methodological aspects of aetiological importance in the link between diabetes and mortality in patients with cancer. We identified nine key points on the cancer pathway at which confounding may arise-cancer screening use, stage at...

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Renehan AG, Yeh HC, Johnson JA, et al. Diabetes and cancer (2): evaluating the impact of diabetes on mortality in patients with cancer. Diabetologia. 2012;55(6):1619-32doi: 10.1007/s00125-012-2526-0.
Renehan, A. G., Yeh, H. C., Johnson, J. A., Wild, S. H., Gale, E. A., Møller, H. (2012). Diabetes and cancer (2): evaluating the impact of diabetes on mortality in patients with cancer. Diabetologia, 55(6), 1619-32. https://doi.org/10.1007/s00125-012-2526-0
Renehan, A G, et al. "Diabetes and cancer (2): evaluating the impact of diabetes on mortality in patients with cancer." Diabetologia vol. 55,6 (2012): 1619-32. doi: https://doi.org/10.1007/s00125-012-2526-0
Renehan AG, Yeh HC, Johnson JA, Wild SH, Gale EA, Møller H. Diabetes and cancer (2): evaluating the impact of diabetes on mortality in patients with cancer. Diabetologia. 2012 Jun;55(6):1619-32. doi: 10.1007/s00125-012-2526-0. Epub 2012 Apr 04. PMID: 22476948.
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O-GlcNAc profiling: from proteins to proteomes.

Clinical proteomics

Ma J, Hart GW.
PMID: 24593906
Clin Proteomics. 2014 Mar 05;11(1):8. doi: 10.1186/1559-0275-11-8.

O-linked β-D-N-acetylglucosamine (O-GlcNAc) modification (O-GlcNAcylation) onto serine and threonine residues of proteins is an important post-translational modification (PTM), which is involved in many crucial biological processes including transcription, translation, proteasomal degradation, and signal transduction. Aberrant protein O-GlcNAcylation is directly...

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Ma J, Hart GW. O-GlcNAc profiling: from proteins to proteomes. Clin Proteomics. 2014;11(1):8doi: 10.1186/1559-0275-11-8.
Ma, J., & Hart, G. W. (2014). O-GlcNAc profiling: from proteins to proteomes. Clinical proteomics, 11(1), 8. https://doi.org/10.1186/1559-0275-11-8
Ma, Junfeng, and Hart, Gerald W. "O-GlcNAc profiling: from proteins to proteomes." Clinical proteomics vol. 11,1 (2014): 8. doi: https://doi.org/10.1186/1559-0275-11-8
Ma J, Hart GW. O-GlcNAc profiling: from proteins to proteomes. Clin Proteomics. 2014 Mar 05;11(1):8. doi: 10.1186/1559-0275-11-8. PMID: 24593906; PMCID: PMC4015695.
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Status of autoimmune diabetes 20-year after generation of BDC2.5-TCR transgenic non-obese diabetic mouse.

World journal of diabetes

Ramirez L, Hamad AR.
PMID: 23961318
World J Diabetes. 2013 Aug 15;4(4):88-91. doi: 10.4239/wjd.v4.i4.88.

Type 1 diabetes (T1D) is an autoimmune disease that results from the destruction of insulin-producing β cells by autoreactive T cells, leading to lifelong dependency on insulin therapy and increased risk of long-term cardiovascular complications. Here we take the...

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Ramirez L, Hamad AR. Status of autoimmune diabetes 20-year after generation of BDC2.5-TCR transgenic non-obese diabetic mouse. World J Diabetes. 2013;4(4):88-91doi: 10.4239/wjd.v4.i4.88.
Ramirez, L., & Hamad, A. R. (2013). Status of autoimmune diabetes 20-year after generation of BDC2.5-TCR transgenic non-obese diabetic mouse. World journal of diabetes, 4(4), 88-91. https://doi.org/10.4239/wjd.v4.i4.88
Ramirez, Lourdes, and Hamad, Abdel Rahim A. "Status of autoimmune diabetes 20-year after generation of BDC2.5-TCR transgenic non-obese diabetic mouse." World journal of diabetes vol. 4,4 (2013): 88-91. doi: https://doi.org/10.4239/wjd.v4.i4.88
Ramirez L, Hamad AR. Status of autoimmune diabetes 20-year after generation of BDC2.5-TCR transgenic non-obese diabetic mouse. World J Diabetes. 2013 Aug 15;4(4):88-91. doi: 10.4239/wjd.v4.i4.88. PMID: 23961318; PMCID: PMC3746090.
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BRMS1 Sensitizes Breast Cancer Cells to ATP-Induced Growth Suppression.

BioResearch open access

Zhang Y, Chin-Quee K, Riddle RC, Li Z, Zhou Z, Donahue HJ.
PMID: 23593560
Biores Open Access. 2013 Apr;2(2):77-83. doi: 10.1089/biores.2012.0260.

Purinergic signaling may represent an effective target in cancer therapy because the expression of purinergic receptors is altered in many forms of cancer and extracellular nucleotides modulate cancer cell growth. We examined the effect of extracellular ATP on the...

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Zhang Y, Chin-Quee K, Riddle RC, et al. BRMS1 Sensitizes Breast Cancer Cells to ATP-Induced Growth Suppression. Biores Open Access. 2013;2(2):77-83doi: 10.1089/biores.2012.0260.
Zhang, Y., Chin-Quee, K., Riddle, R. C., Li, Z., Zhou, Z., & Donahue, H. J. (2013). BRMS1 Sensitizes Breast Cancer Cells to ATP-Induced Growth Suppression. BioResearch open access, 2(2), 77-83. https://doi.org/10.1089/biores.2012.0260
Zhang, Yue, et al. "BRMS1 Sensitizes Breast Cancer Cells to ATP-Induced Growth Suppression." BioResearch open access vol. 2,2 (2013): 77-83. doi: https://doi.org/10.1089/biores.2012.0260
Zhang Y, Chin-Quee K, Riddle RC, Li Z, Zhou Z, Donahue HJ. BRMS1 Sensitizes Breast Cancer Cells to ATP-Induced Growth Suppression. Biores Open Access. 2013 Apr;2(2):77-83. doi: 10.1089/biores.2012.0260. PMID: 23593560; PMCID: PMC3620472.
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Showing 1 to 12 of 50 entries