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4. Inhibition of tracheal smooth muscle contraction and myosin phosphorylation by ryanodine.

Author

Gerthoffer, W T, Murphey, K A, and Khoyi, M A

Abstract

Previous studies have shown that muscarinic activation of airway smooth muscle in low Ca++ solutions increases myosin phosphorylation without increasing tension. Blocking Ca++ influx reduced phosphorylation, but not to basal levels. It was proposed that release of intracellular Ca++ contributed to dissociation of phosphorylation and contraction. To test this hypothesis the effects of ryanodine were studied under similar conditions. Ryanodine (10(-7) to 10(-5) M) antagonized caffeine-induced contraction of canine tracheal smooth muscle. Ryanodine also reduced carbachol-induced contractions and carbachol-induced myosin phosphorylation. The effect of ryanodine on potassium and serotonin-induced contractions was also investigated to test for a nonspecific inhibitory effect. In contrast to the effect on carbachol responses, ryanodine (10(-5) M) potentiated the contractile response to low concentrations of serotonin and potassium, but had no effect on the maximum response to either stimulant. Carbachol (10(-6) M) and ryanodine (10(-5) M) both significantly decreased 45Ca++ content of tracheal muscle. The effect of ryanodine and carbachol together on 45Ca++ content was not greater than either drug alone suggesting that ryanodine reduces the caffeine and carbachol responses by depleting releaseable Ca++ stores. Ryanodine significantly reduced Ca++-induced contraction and myosin phosphorylation in carbachol-stimulated muscle, suggesting that some of the Ca++ responsible for elevated phosphorylation is released from the sarcoplasmic reticulum.

Published
1988

5. Progressive journeying.

Author

Murphey, K. and DeCoker, G.

Subjects
TO Open Minds: Chinese Clues to the Dilemma of Contemporary American Education (Book)
Abstract

Reviews the book `To Open Minds: Chinese Clues to the Dilemma of Contemporary Education,' by Howard Gardner.

Published
1991
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6. Inborn errors of metabolism and pregnancy.

Author

Murphey K, Krishna I, and Li H

Subjects
Humans, Female, Pregnancy, Metabolism, Inborn Errors diagnosis, Metabolism, Inborn Errors metabolism, Metabolism, Inborn Errors therapy, Pregnancy Complications diagnosis, Pregnancy Complications metabolism, Pregnancy Complications therapy
Abstract

As the diagnosis and treatment of patients with inborn errors of metabolism has improved dramatically over the years, more people with these conditions are surviving into child-bearing years. Given the changes in metabolism throughout pregnancy, this time presents a unique challenge in their care. Overall metabolic shifts in pregnancy go from anabolism to catabolism driven by endocrinologic changes, along with changes in rates of gluconeogenesis, glucose consumption, amino acid transport, protein consumption, and lipid breakdown, result in a complicated metabolic picture. Additionally, maternal inborn errors of metabolism can affect a fetus, as in phenylketonuria, and fetal inborn errors of metabolism can affect the mother, as in certain fatty acid oxidation disorders. Data on these conditions is often very limited. A summary of the current literature, risks associated with pregnancy in inborn errors of metabolism, and suggestions for management of these conditions will be presented., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Published
2024
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7. Acute myeloid leukemia and dilated cardiomyopathy in a pediatric patient with D-2-hydroxyglutaric aciduria type I.

Author

Murphey K, George PE, Pencheva B, Porter CC, Wechsler SB, Gambello MJ, and Li H

Subjects
Animals, Child, Humans, Mice, Rare Diseases, Brain Diseases, Metabolic, Inborn complications, Brain Diseases, Metabolic, Inborn diagnosis, Brain Diseases, Metabolic, Inborn genetics, Cardiomyopathies complications, Cardiomyopathy, Dilated complications, Cardiomyopathy, Dilated diagnosis, Cardiomyopathy, Dilated genetics, Leukemia, Myeloid, Acute complications, Leukemia, Myeloid, Acute diagnosis, Leukemia, Myeloid, Acute genetics, Metabolic Diseases, Urogenital Abnormalities
Abstract

D-2-hydroxyglutaric aciduria (D-2-HGA) is a rare neurometabolic disease with two main subtypes, caused by either inactivating variants in D2HGDH (type I) or germline gain of function variants in IDH2 (type II), that result in accumulation of the same toxic metabolite, D-2-hydroxyglutarate. The main clinical features of both are neurologic, including developmental delay, hypotonia, and seizures. Dilated cardiomyopathy is a unique feature thus far only reported in type II. As somatic variants in IDH2 are frequently identified in several different types of cancer, including acute myeloid leukemia (AML), a link between cancer and this metabolic disease has been proposed; however, there is no reported cancer in patients with either type of D-2-HGA. Murine models have demonstrated how D-2-hydroxyglutarate alters metabolism and epigenetics, a potential mechanism by which this metabolite may cause cancer and cardiomyopathy. Here, we report the first case of both AML and dilated cardiomyopathy in a pediatric patient with D-2-HGA type I, who was treated with an anthracycline-free regimen. This report may expand the clinical spectrum of this rare metabolic disease and provide insight on long-term surveillance and care. However, this case is complicated by the presence of a complex chromosomal rearrangement resulting in a 25.5 Mb duplication of 1q41 and a 2.38 Mb deletion of 2q37.3. Thus, the direct causal relationship between D-2-HGA and leukemogenesis or cardiomyopathy warrants further scrutiny., (© 2022 Wiley Periodicals LLC.)

Published
2022
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