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[New treatment options of myasthenia gravis, new approach to biological agents, reimbursement of new therapies in Hungary].
Ideggyogy Sz
January 2025
Budapesti Jahn Ferenc Dél-pesti Kórház és Rendelőintézet, Neurológiai Osztály, Budapest.
Myasthenia gravis (MG) is an antibody-mediated disorder of the neuromuscular transmission, presenting with fatigable weakness that is either isolated to ocular muscles only or generalised (limb, bulbar and respiratory muscles can be affected). The disorder is estimated to affect around 1700 patients in our country. In some cases symptomatic treatment with acetylcholinesterase inhibitors may be sufficient, but most patients with MG require immunosuppressive drugs at some point for disease control, which is achieved in about 60-70% of patients.
View Article and Find Full Text PDFEmergence of Pathological Slow Waves due to Elevated Neurotransmitter Release.
Annu Int Conf IEEE Eng Med Biol Soc
July 2024
A physiologically based computational framework was used to develop a novel gastric motility network model. Along with the widely assumed electrical gap junction coupling between the pacemaker and muscle cells as well as the second messenger molecules, in this model we also included a rostro-caudal linear decreasing gradient of neural stimulus to the pacemakers along the length of the stomach to mimic enteric neurotransmitter release and an increasing gradient of muscarinic receptor density. We find that aberrant responses of different parts of the stomach (corpus, antrum etc.
View Article and Find Full Text PDFEmbryonic exposure to valproic acid and neonicotinoid deteriorates the hyperpolarizing GABA shift and impairs long-term potentiation of excitatory transmission in the local circuit of intermediate medial mesopallium of chick telencephalon.
Cereb Cortex
February 2025
Faculty of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Kanazawa 1757, 061-0293 Tobetsu, Japan.
Embryonic exposure to valproic acid and imidacloprid (a neonicotinoid insecticide) impairs filial imprinting in hatchlings, and the deteriorating effects of valproic acid are mitigated by post-hatch injection of bumetanide, a blocker of the chloride intruder Na-K-2Cl cotransporter 1. Here, we report that these exposures depolarized the reversal potential of local GABAergic transmission in the neurons of the intermediate medial mesopallium, the pallial region critical for imprinting. Furthermore, exposure increased field excitatory post-synaptic potentials in pre-tetanus recordings and impaired long-term potentiation (LTP) by low-frequency tetanic stimulation.
View Article and Find Full Text PDFDopamine and acetylcholine correlations in the nucleus accumbens depend on behavioral task states.
Curr Biol
March 2025
National Institute on Drug Abuse Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA. Electronic address:
Dopamine release in the nucleus accumbens (NAcc) changes quickly in response to errors in predicting events like reward delivery but also slowly ramps up when animals are moving toward a goal. This ramping has attracted much recent attention, as there is controversy regarding its computational role and whether they are driven by dopamine neuron firing or local circuit mechanisms. If the latter is true, cholinergic transmission would be a prime candidate mechanism, and acetylcholine and dopamine signals should be positively correlated during behavior, particularly during motivated approach.
View Article and Find Full Text PDFComposition and function of AChR chimeric autoantibody receptor T cells for antigen-specific B cell depletion in myasthenia gravis.
Sci Adv
February 2025
Department of Dermatology, University of Pennsylvania, Philadelphia, PA, USA.
In acetylcholine receptor (AChR)-seropositive myasthenia gravis (MG), anti-AChR autoantibodies impair neuromuscular transmission and cause severe muscle weakness. MG therapies broadly suppress immune function, risking infections. We designed a chimeric autoantibody receptor (CAAR) expressing the 210-amino acid extracellular domain of the AChR α subunit (A210) linked to CD137-CD3ζ cytoplasmic domains to direct T cell cytotoxicity against anti-AChRα B cells.
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