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Neurophysiological Basis of Visceral Pain
Published in Robert M. Bennett, The Clinical Neurobiology of Fibromyalgia and Myofascial Pain, 2020
Maria Adele Giamberardino, Giannapia Affaitati, Rosanna Lerza, Silvana De Laurentis
In sham-controls, all parameters were not significantly different on the two sides. In stone rats, parameters of the right obliquus externus muscle [i.e., contralateral to the implanted ureter] did not differ significantly from those of sham controls. On the left [ipsilateral] versus right obliquus externus muscle of stone rats, the following significant changes were found: a. decreased I band length/sarcomere length ratio; b. increased muscle cell membrane fluidity; c. increased Ca2+-uptake capacity [correlated linearly to the number of ureteral “crises”]; and d. decreased ryanodine binding. These results suggest the presence, proportional in degree to the activity of the ureteral pain focus, of a state of skeletal muscle contraction in the oblique musculature ipsilateral to the stone, an event which could contribute to the generation of the local hyperalgesia via sensitization of muscle nociceptors. In a parallel study we explored c-Fos expression in the spinal cord of calculosis rats versus sham controls (25). Stone rats were sacrificed two hours after the first ureteral “crisis” and sham controls [no crisis] were suppressed after matching time lapses. All were perfused intracardially; the T9-L3 thoracolumbar spinal cord segment was removed and post-fixed. Frontal frozen sections [40 pm thick] were cut and immunostained for c-Fos-like protein. Four-five sections/level/rat were examined under lightfield microscopy to evaluate Fos-positive cell number.
Genetically Determined Ventricular Arrhythmias
Published in Andrea Natale, Oussama M. Wazni, Kalyanam Shivkumar, Francis E. Marchlinski, Handbook of Cardiac Electrophysiology, 2020
Houman Khakpour, Jason S. Bradfield
Two variants of CPVT have been described based on their genetic mutation and mode of transmission. CPVT1 has a mutation in the ryanodine 2 receptor gene (RyR2) which leads to delayed afterdepolarization (DAD)-induced extrasystolic activity from defective calcium handling. The resulting transmural dispersion of repolarization provides the substrate for the development of re-entrant tachyarrhythmias.13,76 The RyR2 gene shows autosomal dominant inheritance. CPVT2 is defined by a mutation in the calsequestrin (CASQ2) gene and has an autosomal recessive inheritance. Other unidentified genes are also believed to result in CPVT. The ryanodine receptor is located on the sarcoplasmic reticulum and allows the release of calcium into the cell, thus facilitating excitation contraction coupling in the myocardium. Calsequestrin gene mutations interfere with sarcoplasmic calcium storage.13
Upper limb
Published in Aida Lai, Essential Concepts in Anatomy and Pathology for Undergraduate Revision, 2018
Malignant hyperpyrexia Due to defect in muscle ryanodine receptorsCauses: – general anaesthesia (most common)– neurolepticsSigns: – high temperature– widespread rigidity of skeletal muscleManagement: – dantrolene
Impact of intrauterine exposure to the insecticide coragen on the developmental and genetic toxicity in female albino rats
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Amel Ramadan Omar, Ahmed Emam Dakrory, Marwa Mohamed Abdelaal, Heba Bassiony
Despite the potential adverse effects of pesticides on the living organisms including human and the environment, they are still widely used in agriculture due to their benefits to control insects-borne diseases, increase agricultural productivity and control of various pests [1,2]. Pesticides could be taken into the body through oral, inhalation or dermal routes after being ingested in food, drinking water, residential or occupational ways [3]. The biological activity and severity of the pesticides’ toxicity impacts are determined by the type of chemical, the dose, the route and the period of exposure [3]. There are numerous chemical classes of pesticides, which may be insecticide, fungicide or herbicide. Ryanodine is a toxic natural alkaloid isolated from plant Ryania speciose and is best used as insecticide [4]. Chemically synthetic ryanodine compounds such as chlorantraniliprole, flubendiamide, cyantraniliprole, cyclaniliprole and tetraniliprole, are called diamide insecticides that opens muscular calcium channels [5]. Chlorantraniliprole with 18.5% or 20% SC active ingredient in insecticide, has the trade name coragen, that we have investigated in our study. Coragen is being used to fight various types of flies and their larvae [6–8].
Improving genetic diagnostics of skeletal muscle channelopathies
Published in Expert Review of Molecular Diagnostics, 2020
Vinojini Vivekanandam, Roope Männikkö, Emma Matthews, Michael G. Hanna
Mutations in RYR1, ATP1A2, MT-ATP6, and MT-ATP8 have been recently identified in cases of periodic paralysis. Skeletal muscle ryanodine receptor (RYR1) codes for the main sarcoplasmic reticulum-located calcium release channel in muscle and is critical for excitation contraction coupling. RYR1 mutations are known to cause several muscle phenotypes including congenital myopathies, rhabdomyolysis, myalgia, and malignant hyperthermia [77]. A periodic paralysis phenotype caused by RYR1 mutations has been reported in four cases to date [44,78]. Two patients had childhood onset with congenital myopathy and later episodes of periodic paralysis. The other two did not have myopathy but demonstrated later-onset periodic paralysis. Cramps and myalgia were experienced by all patients and typical periodic paralysis triggers such as cold and exercise were described in some.
Targeting pathological leak of ryanodine receptors: preclinical progress and the potential impact on treatments for cardiac arrhythmias and heart failure
Published in Expert Opinion on Therapeutic Targets, 2020
Patrick Connell, Tarah A. Word, Xander H. T. Wehrens
Given the central role of RyR2 dysfunction in the pathogenesis of various cardiac arrhythmia disorders and heart failure, various groups have set out to develop drug compounds that normalize RyR2 channel activity. Here we will focus on several FDA approved drugs that modulate RyR2 activity, as well as small molecules in preclinical development and in clinical trials. A literature search was conducted using the PubMed and MEDLINE databases. The search terms RyR2, arrhythmia, AF, CPVT, HF, and therapy were used and articles from 2010 to 2019 were reviewed. Once identified, a specific search for each compound was conducted in the PubMed and MEDLINE databases as well as a specific search of the clinicaltrials.gov registry. Any previous significant work on each compound was included in this review, even if the work was conducted prior to our specified timeline. If a compound had not been published on within our 10-year timeline it was excluded from this review. We will not discuss the natural alkaloid ryanodine and various toxins but instead refer the reader to previous reviews, as these compounds have provided inspiration for but are not considered viable therapeutic options at this time [1,61].