Advanced Search
Display options
Filter resources
Text Availability
Article type
Publication date
Species
Language
Sex
Age
Showing 1 to 12 of 122 entries
Sorted by: Best Match Show Resources per page
Glucose intolerance induced by blockade of central FGF receptors is linked to an acute stress response.

Molecular metabolism

Rojas JM, Matsen ME, Mundinger TO, Morton GJ, Stefanovski D, Bergman RN, Kaiyala KJ, Taborsky GJ, Schwartz MW.
PMID: 26266088
Mol Metab. 2015 Jun 04;4(8):561-8. doi: 10.1016/j.molmet.2015.05.005. eCollection 2015 Aug.

OBJECTIVE: Central administration of ligands for fibroblast growth factor receptors (FGFRs) such as fibroblast growth factor-19 (FGF19) and FGF21 exert glucose-lowering effects in rodent models of obesity and type 2 diabetes (T2D). Conversely, intracerebroventricular (icv) administration of the non-selective...

Cite
Rojas JM, Matsen ME, Mundinger TO, et al. Glucose intolerance induced by blockade of central FGF receptors is linked to an acute stress response. Mol Metab. 2015;4(8):561-8doi: 10.1016/j.molmet.2015.05.005.
Rojas, J. M., Matsen, M. E., Mundinger, T. O., Morton, G. J., Stefanovski, D., Bergman, R. N., Kaiyala, K. J., Taborsky, G. J., & Schwartz, M. W. (2015). Glucose intolerance induced by blockade of central FGF receptors is linked to an acute stress response. Molecular metabolism, 4(8), 561-8. https://doi.org/10.1016/j.molmet.2015.05.005
Rojas, Jennifer M, et al. "Glucose intolerance induced by blockade of central FGF receptors is linked to an acute stress response." Molecular metabolism vol. 4,8 (2015): 561-8. doi: https://doi.org/10.1016/j.molmet.2015.05.005
Rojas JM, Matsen ME, Mundinger TO, Morton GJ, Stefanovski D, Bergman RN, Kaiyala KJ, Taborsky GJ, Schwartz MW. Glucose intolerance induced by blockade of central FGF receptors is linked to an acute stress response. Mol Metab. 2015 Jun 04;4(8):561-8. doi: 10.1016/j.molmet.2015.05.005. eCollection 2015 Aug. PMID: 26266088; PMCID: PMC4529498.
Copy Download .nbib Format: NLM
Niacin plus Simvastatin Reduces Coronary Stenosis Progression Among Patients with Metabolic Syndrome Despite a Modest Increase in Insulin Resistance: A Subgroup Analysis of the HDL-Atherosclerosis Treatment Study (HATS).

Journal of clinical lipidology

Vittone F, Chait A, Morse JS, Fish B, Brown BG, Zhao XQ.
PMID: 18591993
J Clin Lipidol. 2007 Jul;1(3):203-210. doi: 10.1016/j.jacl.2007.05.003.

BACKGROUND: Metabolic syndrome, insulin resistance and diabetes are associated with an increased risk of cardiovascular disease. Niacin is known to increase insulin resistance, and have adverse effects on blood glucose levels, but to have beneficial effects on plasma lipids...

Cite
Vittone F, Chait A, Morse JS, et al. Niacin plus Simvastatin Reduces Coronary Stenosis Progression Among Patients with Metabolic Syndrome Despite a Modest Increase in Insulin Resistance: A Subgroup Analysis of the HDL-Atherosclerosis Treatment Study (HATS). J Clin Lipidol. 2007;1(3):203-210doi: 10.1016/j.jacl.2007.05.003.
Vittone, F., Chait, A., Morse, J. S., Fish, B., Brown, B. G., & Zhao, X. Q. (2007). Niacin plus Simvastatin Reduces Coronary Stenosis Progression Among Patients with Metabolic Syndrome Despite a Modest Increase in Insulin Resistance: A Subgroup Analysis of the HDL-Atherosclerosis Treatment Study (HATS). Journal of clinical lipidology, 1(3), 203-210. https://doi.org/10.1016/j.jacl.2007.05.003
Vittone, Francesca, et al. "Niacin plus Simvastatin Reduces Coronary Stenosis Progression Among Patients with Metabolic Syndrome Despite a Modest Increase in Insulin Resistance: A Subgroup Analysis of the HDL-Atherosclerosis Treatment Study (HATS)." Journal of clinical lipidology vol. 1,3 (2007): 203-210. doi: https://doi.org/10.1016/j.jacl.2007.05.003
Vittone F, Chait A, Morse JS, Fish B, Brown BG, Zhao XQ. Niacin plus Simvastatin Reduces Coronary Stenosis Progression Among Patients with Metabolic Syndrome Despite a Modest Increase in Insulin Resistance: A Subgroup Analysis of the HDL-Atherosclerosis Treatment Study (HATS). J Clin Lipidol. 2007 Jul;1(3):203-210. doi: 10.1016/j.jacl.2007.05.003. PMID: 18591993; PMCID: PMC2157569.
Copy Download .nbib Format: NLM
Should both HDL-C and LDL-C be targets for lipid therapy? A review of current evidence.

Journal of clinical lipidology

Brown BG, Zhao XQ, Cheung MC.
PMID: 21291671
J Clin Lipidol. 2007 Mar;1(1):88-94. doi: 10.1016/j.jacl.2007.02.004. Epub 2007 Feb 15.

The current guidelines for treatment of high-risk of lipid disorders do not specify a therapeutic target level of high-density lipoprotein cholesterol (HDL-C) for prevention of vascular disease in high-risk populations. However, there is a substantial body of evidence from...

Cite
Brown BG, Zhao XQ, Cheung MC. Should both HDL-C and LDL-C be targets for lipid therapy? A review of current evidence. J Clin Lipidol. 2007;1(1):88-94doi: 10.1016/j.jacl.2007.02.004.
Brown, B. G., Zhao, X. Q., & Cheung, M. C. (2007). Should both HDL-C and LDL-C be targets for lipid therapy? A review of current evidence. Journal of clinical lipidology, 1(1), 88-94. https://doi.org/10.1016/j.jacl.2007.02.004
Brown, B Greg, et al. "Should both HDL-C and LDL-C be targets for lipid therapy? A review of current evidence." Journal of clinical lipidology vol. 1,1 (2007): 88-94. doi: https://doi.org/10.1016/j.jacl.2007.02.004
Brown BG, Zhao XQ, Cheung MC. Should both HDL-C and LDL-C be targets for lipid therapy? A review of current evidence. J Clin Lipidol. 2007 Mar;1(1):88-94. doi: 10.1016/j.jacl.2007.02.004. Epub 2007 Feb 15. PMID: 21291671; PMCID: PMC3506118.
Copy Download .nbib Format: NLM
The Evidence for an Obesity Paradox in Type 2 Diabetes Mellitus.

Diabetes & metabolism journal

Han SJ, Boyko EJ.
PMID: 29885111
Diabetes Metab J. 2018 Jun;42(3):179-187. doi: 10.4093/dmj.2018.0055. Epub 2018 May 31.

Although overweight/obesity is a major risk factor for the development of type 2 diabetes mellitus, there is increasing evidence that overweight or obese patients with type 2 diabetes mellitus experience lower mortality compared with patients of normal weight. This...

Cite
Han SJ, Boyko EJ. The Evidence for an Obesity Paradox in Type 2 Diabetes Mellitus. Diabetes Metab J. 2018;42(3):179-187doi: 10.4093/dmj.2018.0055.
Han, S. J., & Boyko, E. J. (2018). The Evidence for an Obesity Paradox in Type 2 Diabetes Mellitus. Diabetes & metabolism journal, 42(3), 179-187. https://doi.org/10.4093/dmj.2018.0055
Han, Seung Jin, and Boyko, Edward J. "The Evidence for an Obesity Paradox in Type 2 Diabetes Mellitus." Diabetes & metabolism journal vol. 42,3 (2018): 179-187. doi: https://doi.org/10.4093/dmj.2018.0055
Han SJ, Boyko EJ. The Evidence for an Obesity Paradox in Type 2 Diabetes Mellitus. Diabetes Metab J. 2018 Jun;42(3):179-187. doi: 10.4093/dmj.2018.0055. Epub 2018 May 31. PMID: 29885111; PMCID: PMC6015958.
Copy Download .nbib Format: NLM
Long-term impact of intensive lifestyle intervention on cognitive function assessed with the National Institutes of Health Toolbox: The Look AHEAD study.

Alzheimer's & dementia (Amsterdam, Netherlands)

Hayden KM, Baker LD, Bray G, Carvajal R, Demos-McDermott K, Hergenroeder AL, Hill JO, Horton E, Jakicic JM, Johnson KC, Neiberg RH, Rapp SR, Wadden TA, Miller ME.
PMID: 29159267
Alzheimers Dement (Amst). 2017 Oct 09;10:41-48. doi: 10.1016/j.dadm.2017.09.002. eCollection 2018.

INTRODUCTION: This study sought to determine whether 10 years of assignment to intensive lifestyle intervention (ILI) relative to diabetes support and education leads to better cognition. We examine intervention effects overall and among clinical subgroups, and report correlations between...

Cite
Hayden KM, Baker LD, Bray G, et al. Long-term impact of intensive lifestyle intervention on cognitive function assessed with the National Institutes of Health Toolbox: The Look AHEAD study. Alzheimers Dement (Amst). 2017;10:41-48doi: 10.1016/j.dadm.2017.09.002.
Hayden, K. M., Baker, L. D., Bray, G., Carvajal, R., Demos-McDermott, K., Hergenroeder, A. L., Hill, J. O., Horton, E., Jakicic, J. M., Johnson, K. C., Neiberg, R. H., Rapp, S. R., Wadden, T. A., & Miller, M. E. (2018). Long-term impact of intensive lifestyle intervention on cognitive function assessed with the National Institutes of Health Toolbox: The Look AHEAD study. Alzheimer's & dementia (Amsterdam, Netherlands), 1041-48. https://doi.org/10.1016/j.dadm.2017.09.002
Hayden, Kathleen M, et al. "Long-term impact of intensive lifestyle intervention on cognitive function assessed with the National Institutes of Health Toolbox: The Look AHEAD study." Alzheimer's & dementia (Amsterdam, Netherlands) vol. 10 (2018): 41-48. doi: https://doi.org/10.1016/j.dadm.2017.09.002
Hayden KM, Baker LD, Bray G, Carvajal R, Demos-McDermott K, Hergenroeder AL, Hill JO, Horton E, Jakicic JM, Johnson KC, Neiberg RH, Rapp SR, Wadden TA, Miller ME. Long-term impact of intensive lifestyle intervention on cognitive function assessed with the National Institutes of Health Toolbox: The Look AHEAD study. Alzheimers Dement (Amst). 2017 Oct 09;10:41-48. doi: 10.1016/j.dadm.2017.09.002. eCollection 2018. PMID: 29159267; PMCID: PMC5675717.
Copy Download .nbib Format: NLM
Loss of Mitochondrial .

Frontiers in molecular neuroscience

Chen B, Hui J, Montgomery KS, Gella A, Bolea I, Sanz E, Palmiter RD, Quintana A.
PMID: 28883788
Front Mol Neurosci. 2017 Aug 24;10:265. doi: 10.3389/fnmol.2017.00265. eCollection 2017.

Inability of mitochondria to generate energy leads to severe and often fatal myoencephalopathies. Among these, Leigh syndrome (LS) is one of the most common childhood mitochondrial diseases; it is characterized by hypotonia, failure to thrive, respiratory insufficiency and progressive...

Cite
Chen B, Hui J, Montgomery KS, et al. Loss of Mitochondrial . Front Mol Neurosci. 2017;10:265doi: 10.3389/fnmol.2017.00265.
Chen, B., Hui, J., Montgomery, K. S., Gella, A., Bolea, I., Sanz, E., Palmiter, R. D., & Quintana, A. (2017). Loss of Mitochondrial . Frontiers in molecular neuroscience, 10265. https://doi.org/10.3389/fnmol.2017.00265
Chen, Byron, et al. "Loss of Mitochondrial ." Frontiers in molecular neuroscience vol. 10 (2017): 265. doi: https://doi.org/10.3389/fnmol.2017.00265
Chen B, Hui J, Montgomery KS, Gella A, Bolea I, Sanz E, Palmiter RD, Quintana A. Loss of Mitochondrial . Front Mol Neurosci. 2017 Aug 24;10:265. doi: 10.3389/fnmol.2017.00265. eCollection 2017. PMID: 28883788; PMCID: PMC5573716.
Copy Download .nbib Format: NLM
A Polygenic Lipodystrophy Genetic Risk Score Characterizes Risk Independent of BMI in the Diabetes Prevention Program.

Journal of the Endocrine Society

Srinivasan S, Jablonski KA, Knowler WC, Dagogo-Jack S, E Kahn S, Boyko EJ, Bray GA, Horton ES, Hivert MF, Goldberg R, Chen L, Mercader J, Harden M, Florez JC.
PMID: 31428720
J Endocr Soc. 2019 Jun 24;3(9):1663-1677. doi: 10.1210/js.2019-00069. eCollection 2019 Sep 01.

CONTEXT: There is substantial heterogeneity in insulin sensitivity, and genetics may suggest possible mechanisms by which common variants influence this trait.OBJECTIVES: We aimed to evaluate an 11-variant polygenic lipodystrophy genetic risk score (GRS) for association with anthropometric, glycemic and...

Cite
Srinivasan S, Jablonski KA, Knowler WC, et al. A Polygenic Lipodystrophy Genetic Risk Score Characterizes Risk Independent of BMI in the Diabetes Prevention Program. J Endocr Soc. 2019;3(9):1663-1677doi: 10.1210/js.2019-00069.
Srinivasan, S., Jablonski, K. A., Knowler, W. C., Dagogo-Jack, S., E Kahn, S., Boyko, E. J., Bray, G. A., Horton, E. S., Hivert, M. F., Goldberg, R., Chen, L., Mercader, J., Harden, M., Florez, J. C. (2019). A Polygenic Lipodystrophy Genetic Risk Score Characterizes Risk Independent of BMI in the Diabetes Prevention Program. Journal of the Endocrine Society, 3(9), 1663-1677. https://doi.org/10.1210/js.2019-00069
Srinivasan, Shylaja, et al. "A Polygenic Lipodystrophy Genetic Risk Score Characterizes Risk Independent of BMI in the Diabetes Prevention Program." Journal of the Endocrine Society vol. 3,9 (2019): 1663-1677. doi: https://doi.org/10.1210/js.2019-00069
Srinivasan S, Jablonski KA, Knowler WC, Dagogo-Jack S, E Kahn S, Boyko EJ, Bray GA, Horton ES, Hivert MF, Goldberg R, Chen L, Mercader J, Harden M, Florez JC. A Polygenic Lipodystrophy Genetic Risk Score Characterizes Risk Independent of BMI in the Diabetes Prevention Program. J Endocr Soc. 2019 Jun 24;3(9):1663-1677. doi: 10.1210/js.2019-00069. eCollection 2019 Sep 01. PMID: 31428720; PMCID: PMC6694040.
Copy Download .nbib Format: NLM
Micro-dystrophin AAV Vectors Made by Transient Transfection and Herpesvirus System Are Equally Potent in Treating mdx Mouse Muscle Disease.

Molecular therapy. Methods & clinical development

Hakim CH, Clément N, Wasala LP, Yang HT, Yue Y, Zhang K, Kodippili K, Adamson-Small L, Pan X, Schneider JS, Yang NN, Chamberlain JS, Byrne BJ, Duan D.
PMID: 32775499
Mol Ther Methods Clin Dev. 2020 Jul 09;18:664-678. doi: 10.1016/j.omtm.2020.07.004. eCollection 2020 Sep 11.

Vector production scale-up is a major barrier in systemic adeno-associated virus (AAV) gene therapy. Many scalable manufacturing methods have been developed. However, the potency of the vectors generated by these methods has rarely been compared with vectors made by...

Cite
Hakim CH, Clément N, Wasala LP, et al. Micro-dystrophin AAV Vectors Made by Transient Transfection and Herpesvirus System Are Equally Potent in Treating mdx Mouse Muscle Disease. Mol Ther Methods Clin Dev. 2020;18:664-678doi: 10.1016/j.omtm.2020.07.004.
Hakim, C. H., Clément, N., Wasala, L. P., Yang, H. T., Yue, Y., Zhang, K., Kodippili, K., Adamson-Small, L., Pan, X., Schneider, J. S., Yang, N. N., Chamberlain, J. S., Byrne, B. J., & Duan, D. (2020). Micro-dystrophin AAV Vectors Made by Transient Transfection and Herpesvirus System Are Equally Potent in Treating mdx Mouse Muscle Disease. Molecular therapy. Methods & clinical development, 18664-678. https://doi.org/10.1016/j.omtm.2020.07.004
Hakim, Chady H, et al. "Micro-dystrophin AAV Vectors Made by Transient Transfection and Herpesvirus System Are Equally Potent in Treating mdx Mouse Muscle Disease." Molecular therapy. Methods & clinical development vol. 18 (2020): 664-678. doi: https://doi.org/10.1016/j.omtm.2020.07.004
Hakim CH, Clément N, Wasala LP, Yang HT, Yue Y, Zhang K, Kodippili K, Adamson-Small L, Pan X, Schneider JS, Yang NN, Chamberlain JS, Byrne BJ, Duan D. Micro-dystrophin AAV Vectors Made by Transient Transfection and Herpesvirus System Are Equally Potent in Treating mdx Mouse Muscle Disease. Mol Ther Methods Clin Dev. 2020 Jul 09;18:664-678. doi: 10.1016/j.omtm.2020.07.004. eCollection 2020 Sep 11. PMID: 32775499; PMCID: PMC7403893.
Copy Download .nbib Format: NLM
Pathology identifies glomerular treatment targets in diabetic nephropathy.

Kidney research and clinical practice

Alpers CE, Hudkins KL.
PMID: 29971205
Kidney Res Clin Pract. 2018 Jun;37(2):106-111. doi: 10.23876/j.krcp.2018.37.2.106. Epub 2018 Jun 30.

The development of the glomerular injury in diabetic nephropathy involves interactions between podocytes, endothelium, and the mesangium. Loss of podocytes is an early and critical step in the development of diabetic nephropathy, and analysis of structural lesions within the...

Cite
Alpers CE, Hudkins KL. Pathology identifies glomerular treatment targets in diabetic nephropathy. Kidney Res Clin Pract. 2018;37(2):106-111doi: 10.23876/j.krcp.2018.37.2.106.
Alpers, C. E., & Hudkins, K. L. (2018). Pathology identifies glomerular treatment targets in diabetic nephropathy. Kidney research and clinical practice, 37(2), 106-111. https://doi.org/10.23876/j.krcp.2018.37.2.106
Alpers, Charles E, and Hudkins, Kelly L. "Pathology identifies glomerular treatment targets in diabetic nephropathy." Kidney research and clinical practice vol. 37,2 (2018): 106-111. doi: https://doi.org/10.23876/j.krcp.2018.37.2.106
Alpers CE, Hudkins KL. Pathology identifies glomerular treatment targets in diabetic nephropathy. Kidney Res Clin Pract. 2018 Jun;37(2):106-111. doi: 10.23876/j.krcp.2018.37.2.106. Epub 2018 Jun 30. PMID: 29971205; PMCID: PMC6027807.
Copy Download .nbib Format: NLM
Leptin receptor neurons in the dorsomedial hypothalamus regulate diurnal patterns of feeding, locomotion, and metabolism.

eLife

Faber CL, Deem JD, Phan BA, Doan TP, Ogimoto K, Mirzadeh Z, Schwartz MW, Morton GJ.
PMID: 33527893
Elife. 2021 Feb 02;10. doi: 10.7554/eLife.63671.

The brain plays an essential role in driving daily rhythms of behavior and metabolism in harmony with environmental light-dark cycles. Within the brain, the dorsomedial hypothalamic nucleus (DMH) has been implicated in the integrative circadian control of feeding and...

Cite
Faber CL, Deem JD, Phan BA, et al. Leptin receptor neurons in the dorsomedial hypothalamus regulate diurnal patterns of feeding, locomotion, and metabolism. Elife. 2021;10doi: 10.7554/eLife.63671.
Faber, C. L., Deem, J. D., Phan, B. A., Doan, T. P., Ogimoto, K., Mirzadeh, Z., Schwartz, M. W., & Morton, G. J. (2021). Leptin receptor neurons in the dorsomedial hypothalamus regulate diurnal patterns of feeding, locomotion, and metabolism. eLife, 10. https://doi.org/10.7554/eLife.63671
Faber, Chelsea L, et al. "Leptin receptor neurons in the dorsomedial hypothalamus regulate diurnal patterns of feeding, locomotion, and metabolism." eLife vol. 10 (2021). doi: https://doi.org/10.7554/eLife.63671
Faber CL, Deem JD, Phan BA, Doan TP, Ogimoto K, Mirzadeh Z, Schwartz MW, Morton GJ. Leptin receptor neurons in the dorsomedial hypothalamus regulate diurnal patterns of feeding, locomotion, and metabolism. Elife. 2021 Feb 02;10. doi: 10.7554/eLife.63671. PMID: 33527893; PMCID: PMC7880681.
Copy Download .nbib Format: NLM
Loss of apoptosis repressor with caspase recruitment domain (ARC) worsens high fat diet-induced hyperglycemia in mice.

The Journal of endocrinology

Templin AT, Schmidt C, Hogan MF, Esser N, Kitsis RN, Hull RL, Zraika S, Kahn SE.
PMID: 34382577
J Endocrinol. 2021 Sep 20;251(2):125-135. doi: 10.1530/JOE-20-0612.

Apoptosis repressor with caspase recruitment domain (ARC) is an endogenous inhibitor of cell death signaling that is expressed in insulin-producing β cells. ARC has been shown to reduce β-cell death in response to diabetogenic stimuli in vitro, but its...

Cite
Templin AT, Schmidt C, Hogan MF, et al. Loss of apoptosis repressor with caspase recruitment domain (ARC) worsens high fat diet-induced hyperglycemia in mice. J Endocrinol. 2021;251(2):125-135doi: 10.1530/JOE-20-0612.
Templin, A. T., Schmidt, C., Hogan, M. F., Esser, N., Kitsis, R. N., Hull, R. L., Zraika, S., & Kahn, S. E. (2021). Loss of apoptosis repressor with caspase recruitment domain (ARC) worsens high fat diet-induced hyperglycemia in mice. The Journal of endocrinology, 251(2), 125-135. https://doi.org/10.1530/JOE-20-0612
Templin, Andrew T, et al. "Loss of apoptosis repressor with caspase recruitment domain (ARC) worsens high fat diet-induced hyperglycemia in mice." The Journal of endocrinology vol. 251,2 (2021): 125-135. doi: https://doi.org/10.1530/JOE-20-0612
Templin AT, Schmidt C, Hogan MF, Esser N, Kitsis RN, Hull RL, Zraika S, Kahn SE. Loss of apoptosis repressor with caspase recruitment domain (ARC) worsens high fat diet-induced hyperglycemia in mice. J Endocrinol. 2021 Sep 20;251(2):125-135. doi: 10.1530/JOE-20-0612. PMID: 34382577; PMCID: PMC8651217.
Copy Download .nbib Format: NLM
Micro-dystrophin gene therapy prevents heart failure in an improved Duchenne muscular dystrophy cardiomyopathy mouse model.

JCI insight

Howard ZM, Dorn LE, Lowe J, Gertzen MD, Ciccone P, Rastogi N, Odom GL, Accornero F, Chamberlain JS, Rafael-Fortney JA.
PMID: 33651713
JCI Insight. 2021 Apr 08;6(7). doi: 10.1172/jci.insight.146511.

Gene replacement for Duchenne muscular dystrophy (DMD) with micro-dystrophins has entered clinical trials, but efficacy in preventing heart failure is unknown. Although most patients with DMD die from heart failure, cardiomyopathy is undetectable until the teens, so efficacy from...

Cite
Howard ZM, Dorn LE, Lowe J, et al. Micro-dystrophin gene therapy prevents heart failure in an improved Duchenne muscular dystrophy cardiomyopathy mouse model. JCI Insight. 2021;6(7)doi: 10.1172/jci.insight.146511.
Howard, Z. M., Dorn, L. E., Lowe, J., Gertzen, M. D., Ciccone, P., Rastogi, N., Odom, G. L., Accornero, F., Chamberlain, J. S., & Rafael-Fortney, J. A. (2021). Micro-dystrophin gene therapy prevents heart failure in an improved Duchenne muscular dystrophy cardiomyopathy mouse model. JCI insight, 6(7), . https://doi.org/10.1172/jci.insight.146511
Howard, Zachary M, et al. "Micro-dystrophin gene therapy prevents heart failure in an improved Duchenne muscular dystrophy cardiomyopathy mouse model." JCI insight vol. 6,7 (2021). doi: https://doi.org/10.1172/jci.insight.146511
Howard ZM, Dorn LE, Lowe J, Gertzen MD, Ciccone P, Rastogi N, Odom GL, Accornero F, Chamberlain JS, Rafael-Fortney JA. Micro-dystrophin gene therapy prevents heart failure in an improved Duchenne muscular dystrophy cardiomyopathy mouse model. JCI Insight. 2021 Apr 08;6(7). doi: 10.1172/jci.insight.146511. PMID: 33651713; PMCID: PMC8119181.
Copy Download .nbib Format: NLM
Showing 1 to 12 of 122 entries