8 results on '"Margaret Haberman"'
Search Results
2. Cardioprotective effect of nicorandil on isoproterenol induced cardiomyopathy in the Mdx mouse model
- Author
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Rachel T. Sullivan, Ngoc T. Lam, Margaret Haberman, Margaret J. Beatka, Muhammad Z. Afzal, Michael W. Lawlor, and Jennifer L. Strande
- Subjects
Duchenne muscular dystrophy ,DMD ,Cardiomyopathy ,Nicorandil ,Diseases of the circulatory (Cardiovascular) system ,RC666-701 - Abstract
Abstract Background Duchenne muscular dystrophy (DMD) associated cardiomyopathy is a major cause of morbidity and mortality. In an in vitro DMD cardiomyocyte model, nicorandil reversed stress-induced cell injury through multiple pathways implicated in DMD. We aimed to test the efficacy of nicorandil on the progression of cardiomyopathy in mdx mice following a 10-day treatment protocol. Methods A subset of mdx mice was subjected to low-dose isoproterenol injections over 5 days to induce a cardiac phenotype and treated with vehicle or nicorandil for 10 days. Baseline and day 10 echocardiograms were obtained to assess cardiac function. At 10 days, cardiac tissue was harvested for further analysis, which included histologic analysis and assessment of oxidative stress. Paired student’s t test was used for in group comparison, and ANOVA was used for multiple group comparisons. Results Compared to vehicle treated mice, isoproterenol decreased ejection fraction and fractional shortening on echocardiogram. Nicorandil prevented isoproterenol induced cardiac dysfunction. Isoproterenol increased cardiac fibrosis, which nicorandil prevented. Isoproterenol increased gene expression of NADPH oxidase, which decreased to baseline with nicorandil treatment. Superoxide dismutase 2 protein expression increased in those treated with nicorandil, and xanthine oxidase activity decreased in mice treated with nicorandil during isoproterenol stress compared to all other groups. Conclusions In conclusion, nicorandil is cardioprotective in mdx mice and warrants continued investigation as a therapy for DMD associated cardiomyopathy.
- Published
- 2021
- Full Text
- View/download PDF
3. A Long-Term Study Evaluating the Effects of Nicorandil Treatment on Duchenne Muscular Dystrophy-Associated Cardiomyopathy in Mice
- Author
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Melanie Gartz PhD, MS, MHS, Margaret Haberman BS, Mariah J. Prom BS, Margaret J. Beatka BS, Jennifer L. Strande MD, PhD, and Michael W. Lawlor MD, PhD
- Subjects
Diseases of the circulatory (Cardiovascular) system ,RC666-701 ,Therapeutics. Pharmacology ,RM1-950 - Abstract
Background: Duchenne muscular dystrophy (DMD) is a neuromuscular disease caused by dystrophin gene mutations affecting striated muscle. Due to advances in skeletal muscle treatment, cardiomyopathy has emerged as a leading cause of death. Previously, nicorandil, a drug with antioxidant and nitrate-like properties, ameliorated cardiac damage and improved cardiac function in young, injured mdx mice. Nicorandil mitigated damage by stimulating antioxidant activity and limiting pro-oxidant expression. Here, we examined whether nicorandil was similarly cardioprotective in aged mdx mice. Methods and Results: Nicorandil (6 mg/kg) was given over 15 months. Echocardiography of mdx mice showed some functional defects at 12 months compared to wild-type (WT) mice, but not at 15 months. Disease manifestation was evident in mdx mice via treadmill assays and survival, but not open field and grip strength assays. Cardiac levels of SOD2 and NOX4 were decreased in mdx vs. WT. Nicorandil increased survival in mdx but did not alter cardiac function, fibrosis, diaphragm function or muscle fatigue. Conclusions: In contrast to our prior work in young, injured mdx mice, nicorandil did not exert cardioprotective effects in 15 month aged mdx mice. Discordant findings may be explained by the lack of cardiac disease manifestation in aged mdx mice compared to WT, whereas significant cardiac dysfunction was previously seen with the sub-acute injury in young mice. Therefore, we are not able to conclude any cardioprotective effects with long-term nicorandil treatment in aging mdx mice.
- Published
- 2022
- Full Text
- View/download PDF
4. ACTA1 H40Y mutant iPSC-derived skeletal myocytes display mitochondrial defects in an in vitro model of nemaline myopathy
- Author
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Melanie Gartz, Margaret Haberman, Jessica Sutton, Rebecca A. Slick, Shawn M. Luttrell, David L. Mack, and Michael W. Lawlor
- Subjects
Cell Biology - Published
- 2023
- Full Text
- View/download PDF
5. Influence of microRNAs and exosomes in muscle health and diseases
- Author
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Melanie Gartz, Margaret Haberman, Jennifer L. Strande, Ngoc Thien Lam, and Leah Thomas
- Subjects
0301 basic medicine ,Physiology ,Muscles ,Cardiac muscle ,Skeletal muscle ,Cell Biology ,Biology ,Exosomes ,Biochemistry ,Article ,Microvesicles ,Cell biology ,MicroRNAs ,03 medical and health sciences ,Circulating MicroRNA ,Crosstalk (biology) ,030104 developmental biology ,0302 clinical medicine ,medicine.anatomical_structure ,Gene expression ,microRNA ,medicine ,Humans ,Myocyte ,030217 neurology & neurosurgery - Abstract
MicroRNAs are short, (18–22 nt) non-coding RNAs involved in important cellular processes due to their ability to regulate gene expression at the post-transcriptional level. Exosomes are small (50–200 nm) extracellular vesicles, naturally secreted from a variety of living cells and are believed to mediate cell-cell communication through multiple mechanisms, including uptake in destination cells. Circulating microRNAs and exosome-derived microRNAs can have key roles in regulating muscle cell development and differentiation. Several microRNAs are highly expressed in muscle and their regulation is important for myocyte homeostasis. Changes in muscle associated microRNA expression are associated with muscular diseases including muscular dystrophies, inflammatory myopathies, and congenital myopathies. In this review, we aim to highlight the biology of microRNAs and exosomes as well as their roles in muscle health and diseases. We also discuss the potential crosstalk between skeletal and cardiac muscle through exosomes and their contents. skeletal and cardiac muscle through exosomes and their contents.
- Published
- 2019
- Full Text
- View/download PDF
6. Cardioprotective effect of nicorandil on isoproterenol induced cardiomyopathy in the Mdx mouse model
- Author
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Margaret Haberman, Michael W. Lawlor, Jennifer L. Strande, Ngoc Thien Lam, Rachel T. Sullivan, Muhammad Afzal, and Margaret Beatka
- Subjects
Cardiac function curve ,Duchenne muscular dystrophy ,Xanthine Oxidase ,mdx mouse ,Cardiac fibrosis ,Cardiomyopathy ,030204 cardiovascular system & hematology ,Pharmacology ,medicine.disease_cause ,Ventricular Function, Left ,03 medical and health sciences ,0302 clinical medicine ,DMD ,medicine ,Animals ,Diseases of the circulatory (Cardiovascular) system ,Myocytes, Cardiac ,Nicorandil ,NADPH oxidase ,biology ,Superoxide Dismutase ,business.industry ,Research ,Isoproterenol ,NADPH Oxidases ,Stroke Volume ,medicine.disease ,Fibrosis ,Muscular Dystrophy, Duchenne ,Disease Models, Animal ,RC666-701 ,Mice, Inbred mdx ,biology.protein ,cardiovascular system ,Female ,Cardiomyopathies ,Reactive Oxygen Species ,Cardiology and Cardiovascular Medicine ,business ,030217 neurology & neurosurgery ,Oxidative stress ,medicine.drug - Abstract
Background Duchenne muscular dystrophy (DMD) associated cardiomyopathy is a major cause of morbidity and mortality. In an in vitro DMD cardiomyocyte model, nicorandil reversed stress-induced cell injury through multiple pathways implicated in DMD. We aimed to test the efficacy of nicorandil on the progression of cardiomyopathy in mdx mice following a 10-day treatment protocol. Methods A subset of mdx mice was subjected to low-dose isoproterenol injections over 5 days to induce a cardiac phenotype and treated with vehicle or nicorandil for 10 days. Baseline and day 10 echocardiograms were obtained to assess cardiac function. At 10 days, cardiac tissue was harvested for further analysis, which included histologic analysis and assessment of oxidative stress. Paired student’s t test was used for in group comparison, and ANOVA was used for multiple group comparisons. Results Compared to vehicle treated mice, isoproterenol decreased ejection fraction and fractional shortening on echocardiogram. Nicorandil prevented isoproterenol induced cardiac dysfunction. Isoproterenol increased cardiac fibrosis, which nicorandil prevented. Isoproterenol increased gene expression of NADPH oxidase, which decreased to baseline with nicorandil treatment. Superoxide dismutase 2 protein expression increased in those treated with nicorandil, and xanthine oxidase activity decreased in mice treated with nicorandil during isoproterenol stress compared to all other groups. Conclusions In conclusion, nicorandil is cardioprotective in mdx mice and warrants continued investigation as a therapy for DMD associated cardiomyopathy.
- Published
- 2021
7. In February
- Author
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Margaret Haberman
- Subjects
Fuel Technology ,Process Chemistry and Technology ,Economic Geology - Published
- 2021
- Full Text
- View/download PDF
8. Clinical potential of psilocybin as a treatment for mental health conditions
- Author
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Margaret Haberman and Jeremy Daniel
- Subjects
Hallucinogen ,medicine.medical_specialty ,media_common.quotation_subject ,Alcohol use disorder ,Disease ,Psilocybin ,03 medical and health sciences ,0302 clinical medicine ,medicine ,Pharmacology (medical) ,General Pharmacology, Toxicology and Pharmaceutics ,Psychiatry ,Depression (differential diagnoses) ,media_common ,Therapeutic Uses for Illicit Substances ,Addiction ,medicine.disease ,Mental health ,030227 psychiatry ,Neuropsychology and Physiological Psychology ,Anxiety ,Neurology (clinical) ,medicine.symptom ,Psychology ,030217 neurology & neurosurgery ,medicine.drug ,Clinical psychology - Abstract
Psilocybin, a classic hallucinogen, is a chemical produced by more than 100 species of mushrooms worldwide. It has high affinity for several serotonin receptors, including 5-HT1A, 5-HT2A, and 5-HT2C, located in numerous areas of the brain, including the cerebral cortex and thalamus. With legislation introduced in 1992, more work is being done to further understand the implications of psilocybin use in a number of disease states. Certain mental health disease states and symptoms have been studied, including depressed mood, anxiety disorders, obsessive-compulsive disorder, alcohol use disorder, and tobacco use disorder. This article provides an in-depth review of the study design and results of psilocybin in each of these conditions and discusses the clinical potential for use.
- Published
- 2018
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