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Neurotransmitters and Receptors, Ion Channels, G Proteins and Second Messengers
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
There are two types of acetylcholine receptors: nicotinic and muscarinic (Table 3.1). In peripheral nerves, nicotinic receptors are present at the neuromuscular junction and in autonomic ganglia. Muscarinic receptors are present at parasympathetic postganglionic nerve endings (Figure 3.3).
Double Vision and New Onset Strabismus in an Adult
Published in Amy-lee Shirodkar, Gwyn Samuel Williams, Bushra Thajudeen, Practical Emergency Ophthalmology Handbook, 2019
Other specific tests include: Variable signs and symptoms of fatigue: Bloods to include serum autoantibodies (anti-acetylcholine receptor and anti-MUSK) for myasthenia gravis. The ice pack test: measure deviation or ptosis before and after applying an ice pack to the eyes for 2 minutes. However, in practice it is almost impossible to find ice in a regular eye clinic.Proptosis, lid lag: Consider thyroid function, thyroid peroxidase and imaging for thyroid eye disease.Imaging: MRI gives better soft tissue definition but CTs may be easier and faster to organise. Imaging will help identify bleeds, stroke, space occupying lesions, abnormal muscle size and vascular anomalies such as an aneurysm or carotid cavernous fistula.
Immunopathology
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
The cardinal symptom of myasthenia gravis is generalized muscle weakness, the result of autoantibody binding to acetylcholine receptors on skeletal muscle. Not only does antibody binding prevent the normal action of the agonist, acetylcholine, but it also causes removal of receptors from the cell membrane. Serum antibodies from myasthenics reproduce the symptoms of muscle weakness when injected into rats.
Prospects for CAR T cell immunotherapy in autoimmune diseases: clues from Lupus
Published in Expert Opinion on Biological Therapy, 2022
Marko Radic, Indira Neeli, Tony Marion
Certain autoimmune diseases result from the effects of a single autoantibody specificity. Pemphigus is an autoimmune skin blistering disorder, in which autoantibodies play a central role. Most patients with pemphigus exhibit autoantibodies to desmoglein, a cadherin-like adhesion molecule that connects keratinocytes to each other and gives elasticity and cohesion to the epidermis [71]. Ellebrecht et al. [72] constructed CARs with extracellular domains derived from desmoglein to serve as ‘bait’ for anti-desmoglein B cells (Figure 3B). Upon binding to anti-desmoglein B cells, the redesigned chimeric autoantibody receptor (CAAR) triggers the specific killing of the autoreactive B cells. The success of this approach in animals provided preclinical data used in an application to the FDA for the initiation of clinical trials [73]. A similar approach has been developed for myasthenia gravis (MG), a progressive and debilitating disease with autoimmune disruption of acetylcholine receptor function at the neuromuscular junctions. A subset of patients with MG make autoantibodies to muscle signaling kinase (MuSK) and CAAR T cells using a portion of MuSK as the extracellular bait for autoreactive B cells are in early development (Oh S, 2020). Yet to be tested in the context of autoimmunity, a CAR T cell incorporating domains from a scavenging protein (Figure 3C) could offer an alternative approach to deplete excessive circulating IC, as shown by engineering in a phagocytic cell population [74].
Indacaterol/glycopyrronium/mometasone fixed dose combination for uncontrolled asthma
Published in Expert Review of Respiratory Medicine, 2022
Corrado Pelaia, Claudia Crimi, Nunzio Crimi, Luisa Ricciardi, Nicola Scichilone, Giuseppe Valenti, Ornella Bonavita, Stefano Andaloro, Paolo Morini, Andrea Rizzi, Girolamo Pelaia
Anticholinergic bronchodilators antagonize the parasympathetic system by acting on the acetylcholine receptors expressed on airway smooth muscles and lung parasympathetic nerves. There are two groups of acetylcholine receptors: nicotinic- and muscarinic- and the muscarinic subtypes M1, M2 and M3 are primarily involved in the regulation of bronchoconstriction. All muscarinic receptor subtypes are widely expressed in different tissues (smooth muscles, brain, heart and the sinoatrial node, gastrointestinal tract, pupils, blood vessels and the parasympathetic nervous system). Muscarinic M2 receptors in the heart regulate heart beating by reducing the activation of the sinus node, while the M3 subtypes are responsible of contraction of the muscles of gastrointestinal tract, or blood vessel vasodilation [32,33]. Specifically referring to airway tract activity, M1 receptors are widely distributed in all parasympathetic ganglia and they act by regulating cholinergic transmission. M2 receptors are found in the pre-junctional membranes of the neuromuscular junctions of airway smooth muscles and reduce acetylcholine transmission through a negative feedback. M3 receptors are mainly expressed in smooth muscle cells in the lungs, regulating muscle contraction, while within the submucosal glands of the lung, M3 receptors regulate mucus secretion. Thus, it is preferable that antimuscarinic bronchodilators present higher affinity for M1 and M3 receptors, and lower affinity for M2 receptors [34].
Isolating the Superficial Peroneal Nerve Motor Branch to the Peroneus Longus Muscle with Concentric Stimulation during Diagnostic Motor Nerve Biopsy
Published in The Neurodiagnostic Journal, 2022
Ashley Rosenberg, Rachel Pruitt, Sami Saba, Justin W. Silverstein, Randy S. D’Amico
Admission neurological exam was consistent with hypoxic hypercapnic encephalopathy, as well as a distal predominant polyneuropathy likely related to his history of diabetes mellitus and/or alcohol use. Electrodiagnostic studies demonstrated bilateral phrenic nerve impairment and diffusely decreased motor potentials, suggestive of either a motor neuropathy, myopathy, or, least likely, motor neuron disease. Acetylcholine receptor binding, blocking, and modulating antibodies were negative. At this point, neurosurgery was consulted for a possible muscle/nerve biopsy. A lumbar puncture was performed to evaluate for possible inflammatory neuropathy, which was negative, and a normal creatine kinase level and a lack of spontaneous activity on electromyography argued against inflammatory myopathy. Due to bilateral phrenic nerve impairment, the decision was made to pursue a muscle and motor nerve biopsy for further evaluation. Peroneal nerve decompression at the fibular head with biopsy of the motor branch to the peroneus longus muscle and biopsy of the peroneus longus muscle were performed.