muscular dystrophies/nausea

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[Acute gastric dilatation in Duchenne's muscular dystrophy].

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A 15 year old boy with Duchenne muscular dystrophy had severe pain in the lower abdomen and complained of nausea and bilious vomiting. A physical examination and an abdominal X-ray indicated an acute gastric dilation. With a treatment policy of administering nothing orally, a downward-hanging

A case of Becker muscular dystrophy with early manifestation of cardiomyopathy.

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An 18-year-old boy was admitted with chest discomfort, nausea, and dyspnea at rest. At the age of 3 years, he underwent muscle biopsy and dystrophin gene analysis owing to an enlarged calf muscle and elevated serum kinase level (6,378 U/L) without overt weakness; based on the results, Becker

[The effect of clomipramine to nocturnal periodic hypoxemia in Duchenne muscular dystrophy].

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Respiratory insufficiency is a major cause of death in Duchenne muscular dystrophy (DMD). The earliest sign is a hypoventilation which appears in REM sleep. We administered 20 mg of clomipramine hydrochloride before sleep to two DMD patients with periodic nocturnal hypoxemia. The complaints such as

A community-engaged approach to quantifying caregiver preferences for the benefits and risks of emerging therapies for Duchenne muscular dystrophy.

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BACKGROUND There is growing agreement that regulators performing benefit-risk evaluations should take patients' and caregivers' preferences into consideration. The Patient-Focused Drug Development Initiative at the US Food and Drug Administration offers patients and caregivers an enhanced

Caregiver preferences for emerging duchenne muscular dystrophy treatments: a comparison of best-worst scaling and conjoint analysis.

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BACKGROUND Through Patient-Focused Drug Development, the US Food and Drug Administration (FDA) documents the perspective of patients and caregivers and are currently conducting 20 public meetings on a limited number of disease areas. Parent Project Muscular Dystrophy (PPMD), an advocacy organization

Relationship between Eating and Digestive Symptoms and Respiratory Function in Advanced Duchenne Muscular Dystrophy Patients.

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Duchenne muscular dystrophy (DMD) patients can have various issues that affect their quality of life, including eating and digestive conditions.We sought to identify the relationship between respiratory function and various eating and digestion related

Hypoglycemia in patients with congenital muscle disease.

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Only a few small studies have previously reported episodes of hypoglycemia in children with neuromuscular diseases; however, there has been no broader investigation into the occurrence of hypoglycemia in children with congenital muscle disease

[Intracellular recording of myotonia in mdx mouse and the effect of Ca antagonist in myotonia].

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Bulfield and others found X-linked muscular dystrophic (mdx) mouse by screening C57 BL/10 mice. The serum CK and PK are high in mdx mice, and they develop muscle degeneration 10-15 days after birth. The regeneration is vigorous in mdx mice and almost all the muscle fibers are replaced by regenerated

[Lipidic myopathy with severe cardiomyopathy caused by a generalized carnitine deficiency. Favourable course during carnitine hydrochloride treatment].

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The case of a girl who presented with gastrointestinal upsets with nausea, vomiting and occasional hypoglycaemic attacks during childhood is reported. At about 5 years of age generalised muscular weakness with severe amyotrophy, cardiomegaly with a cardiothoracic ratio of 0,63, left ventricular

Targeting Alternative Splicing as a Potential Therapy for Episodic Ataxia Type 2

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Episodic ataxia type 2 (EA2) is an autosomal dominant neurological disorder characterized by paroxysmal attacks of ataxia, vertigo, and nausea that usually last hours to days. It is caused by loss-of-function mutations in CACNA1A, the gene encoding the pore-forming α₁ subunit of

2,4 Dinitrophenol as Medicine.

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In the sanctity of pure drug discovery, objective reasoning can become clouded when pursuing ideas that appear unorthodox, but are spot on physiologically. To put this into historical perspective, it was an unorthodox idea in the 1950's to suggest that warfarin, a rat poison, could be repositioned

An antisense oligonucleotide against SOD1 delivered intrathecally for patients with SOD1 familial amyotrophic lateral sclerosis: a phase 1, randomised, first-in-man study.

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BACKGROUND Mutations in SOD1 cause 13% of familial amyotrophic lateral sclerosis. In the SOD1 Gly93Ala rat model of amyotrophic lateral sclerosis, the antisense oligonucleotide ISIS 333611 delivered to CSF decreased SOD1 mRNA and protein concentrations in spinal cord tissue and prolonged survival.

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