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To identify patients with GFPT1-related limb-girdle myasthenia and analyze phenotypic consequences of the mutations.
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A 15-year-old boy is described with myasthenia gravis, hemophilia A, positive HTLV-III serology, antithyroglobulin and antimicrosomal antibodies, and laboratory evidence of altered cell-mediated immunity. Treatment with pyridostigmine produced dramatic clinical improvement. The results of this patient raise the possibility of myasthenia gravis as the sole or presenting clinical manifestation of infection with HTLV-III.
Reported prevalence and incidence are amongst the highest found in similar studies. This may be explained by optimal case identification, higher incidence of drug requiring MG amongst the elderly, and recurrences of previous MG.
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We compared veteran-reported wartime experiences in a population-based sample of 304 Gulf War veterans: 144 cases who met preestablished criteria for GWI and 160 controls. Veteran subgroups and confounding among deployment variables were considered in the analyses.
The effects of a single intramuscular atropine injection (0.03 mg.kg-1) and a chronic oral pyridostigmine treatment (0.4 mg.kg-1, 3 times/day over a period of 7 d) on the thermoregulatory effector responses of unanesthetized patas monkeys were investigated using indirect calorimetry. The effects of atropine treatment on the thermoregulatory effector responses of patas monkeys exposed to 25 degrees and 35 degrees C were qualitatively similar but quantitatively greater at 35 degrees C. At 35 degrees C atropine decreased sweating (Esw) 52%, increased rectal temperature (Tre), mean skin temperature (Tsk), metabolic rate (MR), and whole body conductance (K), and elicited a consistent 11% increase in heart rate (HR). Daily oral pyridostigmine treatment to patas monkeys produced a significant 25-30% drop in serum cholinesterase activity with no chronic effects on thermoregulatory or cardiovascular functions. The acute effects of oral pyridostigmine treatment in this species included transient 12% and 15% decreases in MR and HR, respectively, and a transient 25% increase in Esw. The latter was associated with significant acute reductions in Tre and Tsk which lasted at least 120 min following pyridostigmine administration. It is concluded that the patas monkey is an excellent animal model for studies to evaluate the effects of neuroactive agents on thermoregulatory and other physiological functions which are difficult, if not impossible, to perform on humans.
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The medical records of 6 boys and 18 girls with ocular MG were reviewed retrospectively.
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Follow up evaluations, performed at 1, 3-6, 12, and 24 months, detailed the frequency of ptosis and diplopia and the amount of ocular motor deviation in primary and downward gaze.
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Pyridostigmine bromide is inferior to fludrocortisone in the treatment of OH in PD. This trial provides first objective evidence of the efficacy of 0.2 mg/day fludrocortisone for OH in PD, causing minor peripheral but no central supine hypertension. In addition to peripheral bp, future trials should include central bp measurements, known to correlate more closely with cardiovascular risk.
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Exposure to DEET (N,N-diethyl-meta-toluamide) may have influenced the pattern of symptoms observed in soldiers with GWI (Gulf War Illness; Haley and Kurt, 1997). We examined how the addition of DEET (400mg/kg; 50% topical) to an exposure protocol of permethrin (2.6mg/kg; topical), chlorpyrifos (CP; 120mg/kg), and pyridostigmine bromide (PB;13mg/kg) altered the emergence and pattern of pain signs in an animal model of GWI pain (Nutter et al., 2015). Rats underwent behavioral testing before, during and after a 4week exposure: 1) hindlimb pressure withdrawal threshold; 2) ambulation (movement distance and rate); and 3) resting duration. Additional studies were conducted to assess the influence of acute DEET (10-100μM) on muscle and vascular nociceptor Kv7, KDR, Nav1.8 and Nav1.9. We report that a 50% concentration of DEET enhanced the development and persistence of pain-signs. Rats exposed to all 4 compounds exhibited ambulation deficits that appeared 5-12weeks post-exposure and persisted through weeks 21-24. Rats exposed to only three agents (CP or PB excluded), did not fully develop ambulation deficits. When PB was excluded, rats also developed rest duration pain signs, in addition to ambulation deficits. There was no evidence that physiological doses of DEET acutely modified nociceptor Kv7, KDR, Nav1.8 or Nav1.9 activities. Nevertheless, DEET augmented protocols decreased the conductance of Kv7 expressed in vascular nociceptors harvested from chronically exposed rats. We concluded that DEET enhanced the development and persistence of pain behaviors, but the anticholinesterases CP and PB played a determinant role.
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All basal hormonal values were similar in younger and older women. Insulin growth like factor-I levels were lower in older women. The GH responses to GH-RH alone, pyridostigmine alone, or the combination were lower in the older than in the younger group and were correlated negatively with age. In contrast, either arginine alone or GH-RH plus arginine produced similar GH responses in the two groups.
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A young female whose pyridostigmine treatment had recently been changed presented with myasthenia gravis, acute respiratory failure, and respiratory infection. She was supported with a noninvasive negative pressure cuirass device as an aid to optimizing medical therapies without the confounding factor of pharmacology-induced sedation and analgesia.
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It is widely accepted that chronic administration of corticoids in man inhibits the GH response to all of the stimuli tested so far. To study the action of corticoids administered acutely, several dexamethasone challenge tests were performed, after which GH levels were measured for 7 h. In eight volunteers, administration of 4 mg dexamethasone (Dex), iv, induced a clear-cut GH release compared with saline administration. The secretion followed an unusual pattern; basal GH levels (1.5 +/- 0.1 micrograms/L) started rising 2 h after Dex injection, reaching a peak of 17.5 +/- 4.4 micrograms/L after 3 or 3.5 h. Peak levels were maintained until 5 h post-Dex and decreased thereafter. Similar data were obtained when Dex was administered to five volunteers at the dose of 8 mg, orally, with a 30-min delay of the GH peak (19.6 +/- 7.9 micrograms/L). To study whether there was a cholinergic input responsible for the Dex action, another group of eight volunteers underwent three Dex tests (4 mg, iv) on three occasions, followed 90 min later by the administration of placebo (control), atropine (0.5 mg, iv), or pyridostigmine (120 mg, orally). The Dex-induced GH peak (20.8 +/- 5.2 micrograms/L) was not significantly increased by pyridostigmine (cholinergic agonist) treatment (24.2 +/- 4.0 micrograms/L). The blockade of muscarinic receptors by atropine induced a delay in the Dex-induced secretory peak, which appeared at 5 h. However, the Dex-atropine GH peak (14.9 +/- 4.1 micrograms/L) was not different from the Dex-placebo one. In conclusion, Dex alone is able to induce a clear-cut GH secretion in man. The stimulus followed a peculiar time pattern, with peaks levels attained 3 h after either iv or oral administration.