Transmission Of Electrical Impulses Research Articles

Bibliometric analysis of myelin imaging studies of patients with multiple sclerosis (2000-2022).

Multiple sclerosis (MS) is a condition that can impact the central nervous system (CNS) and cause damage to the myelin, which is responsible for facilitating the normal transmission of electrical impulses along the nerves. We performed a bibliometric analysis of the scientific publications on myelin imaging in MS to reveal the development trends in this field and to evaluate research trends in myelin imaging in MS. The Web of Science Core Collection was searched for articles related to myelin imaging in MS published between January 2000 and December 2022. CiteSpace, VOSviewer, and R language were used to evaluate and visualize contributions by and co-occurrence relationships among countries and institutions, authors, journals, citations, keywords, and so on. A total of 1,639 articles addressed the topic of myelin imaging in MS. The United States had the largest number of annual publications. The University of London was the institution with the highest number of publications (n=118) and citations (n=9,885). The top 3 productive authors were all from the University of British Columbia in Canada. An article published by Mackay et al. in 1994 had the most citations (n=272). Neuroimage [impact factor (IF) =7.40, Journal Citation Reports quartile 1 (Q1)] was the most productive journal in terms of the number of articles relating to myelin imaging in MS (n=149). In recent years, myelin water imaging, synthetic magnetic resonance imaging (SyMRI), inhomogeneous magnetization, positron emission tomography (PET) imaging, and aquaporin-4 (AQP4) have been researched hotspots of myelin imaging in MS. With advancements in the pathophysiological research on myelin changes in MS, myelin imaging is playing an important role in the diagnosis and treatment of MS. In addition, the use of new sequences of myelin imaging to distinguish MS from other inflammatory demyelinating diseases is a future development trend in this field.

RIT1 deficiency alters cerebral lipid metabolism and reduces white matter tract oligodendrocytes and conduction velocities

Oligodendrocytes (OLs) generate lipid-rich myelin membranes that wrap axons to enable efficient transmission of electrical impulses. Using a RIT1 knockout mouse model and in situ high-resolution matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI) coupled with MS-based lipidomic analysis to determine the contribution of RIT1 to lipid homeostasis. Here, we report that RIT1 loss is associated with altered lipid levels in the central nervous system (CNS), including myelin-associated lipids within the corpus callosum (CC). Perturbed lipid metabolism was correlated with reduced numbers of OLs, but increased numbers of GFAP+ glia, in the CC, but not in grey matter. This was accompanied by reduced myelin protein expression and axonal conduction deficits. Behavioral analyses revealed significant changes in voluntary locomotor activity and anxiety-like behavior in RIT1KO mice. Together, these data reveal an unexpected role for RIT1 in the regulation of cerebral lipid metabolism, which coincide with altered white matter tract oligodendrocyte levels, reduced axonal conduction velocity, and behavioral abnormalities in the CNS.

Brain matters: unveiling the distinct contributions of region, age, and sex to glia diversity and CNS function

The myelinated white matter tracts of the central nervous system (CNS) are essential for fast transmission of electrical impulses and are often differentially affected in human neurodegenerative diseases across CNS region, age and sex. We hypothesize that this selective vulnerability is underpinned by physiological variation in white matter glia. Using single nucleus RNA sequencing of human post-mortem white matter samples from the brain, cerebellum and spinal cord and subsequent tissue-based validation we found substantial glial heterogeneity with tissue region: we identified region-specific oligodendrocyte precursor cells (OPCs) that retain developmental origin markers into adulthood, distinguishing them from mouse OPCs. Region-specific OPCs give rise to similar oligodendrocyte populations, however spinal cord oligodendrocytes exhibit markers such as SKAP2 which are associated with increased myelin production and we found a spinal cord selective population particularly equipped for producing long and thick myelin sheaths based on the expression of genes/proteins such as HCN2. Spinal cord microglia exhibit a more activated phenotype compared to brain microglia, suggesting that the spinal cord is a more pro-inflammatory environment, a difference that intensifies with age. Astrocyte gene expression correlates strongly with CNS region, however, astrocytes do not show a more activated state with region or age. Across all glia, sex differences are subtle but the consistent increased expression of protein-folding genes in male donors hints at pathways that may contribute to sex differences in disease susceptibility. These findings are essential to consider for understanding selective CNS pathologies and developing tailored therapeutic strategies.

An iterative approach using Sawi transform for fractional telegraph equation in diversified dimensions

Abstract In the present study, 1D, 2D, and 3D fractional hyperbolic telegraph equations in Caputo sense have been solved using an iterative method using Sawi transform. These equations serve as a model for signal analysis of electrical impulse transmission and propagation. Along with a table of Sawi transform of some popular functions, some helpful results on Sawi transform are provided. To demonstrate the effectiveness of the suggested method, five examples in 1D, one example in 2D, and one example in 3D are solved using the proposed scheme. Error analysis comparing approximate and exact solutions using graphs and tables has been provided. The proposed scheme is robust, effective, and easy to implement and can be implemented on variety of fractional partial differential equations to obtain precise series approximations.

Adaptive autophagy reprogramming in Schwann cells during peripheral demyelination

The myelin sheath is an essential structure for the rapid transmission of electrical impulses through axons, and peripheral myelination is a well-programmed postnatal process of Schwann cells (SCs), the myelin-forming peripheral glia. SCs transdifferentiate into demyelinating SCs (DSCs) to remove the myelin sheath during Wallerian degeneration after axonal injury and demyelinating neuropathies, and macrophages are responsible for the degradation of myelin under both conditions. In this study, the mechanism by which DSCs acquire the ability of myelin exocytosis was investigated. Using serial ultrastructural evaluation, we found that autophagy-related gene 7-dependent formation of a “secretory phagophore (SP)” and tubular phagophore was necessary for exocytosis of large myelin chambers by DSCs. DSCs seemed to utilize myelin membranes for SP formation and employed p62/sequestosome-1 (p62) as an autophagy receptor for myelin excretion. In addition, the acquisition of the myelin exocytosis ability of DSCs was associated with the decrease in canonical autolysosomal flux and was demonstrated by p62 secretion. Finally, this SC demyelination mechanism appeared to also function in inflammatory demyelinating neuropathies. Our findings show a novel autophagy-mediated myelin clearance mechanism by DSCs in response to nerve damage.

Myelination as a modulating factor in memory circuitry

Myelin has been understood for many years as a static component that regulates the speed of electrical impulse transmission. However, multiple works defend a dynamic role dependent on experience. This has allowed the development of a new concept called myelin plasticity that contributes, together with synaptic plasticity, to the long-term changes that occur in neuronal circuits during learning and memory. Therefore, this review will address the latest published data regarding the role of myelination with memory. Evidence from human neuroimaging studies demonstrates that myelination can change due to activity-dependent modulation, such that learning can modify the axon myelination. Alternatively, it has also been shown that interfering with myelination, using transgenic rodent models, significantly impairs memory processes. This has important implications in alterations as severe as Alzheimer's disease, where transcriptional changes and in the phenotype of cells associated with the myelination process begin to be described. The new knowledge supports the concept of myelin plasticity and its implications for memory, which opens a new opportunity for the treatment of deficits that affect this cognitive function.

Distinct Changes in Calpain and Calpastatin during PNS Myelination and Demyelination in Rodent Models.

Myelin forming around axons provides electrical insulation and ensures rapid and efficient transmission of electrical impulses. Disruptions to myelinated nerves often result in nerve conduction failure along with neurological symptoms and long-term disability. In the central nervous system, calpains, a family of calcium dependent cysteine proteases, have been shown to have a role in developmental myelination and in demyelinating diseases. The roles of calpains in myelination and demyelination in the peripheral nervous system remain unclear. Here, we show a transient increase of activated CAPN1, a major calpain isoform, in postnatal rat sciatic nerves when myelin is actively formed. Expression of the endogenous calpain inhibitor, calpastatin, showed a steady decrease throughout the period of peripheral nerve development. In the sciatic nerves of Trembler-J mice characterized by dysmyelination, expression levels of CAPN1 and calpastatin and calpain activity were significantly increased. In lysolecithin-induced acute demyelination in adult rat sciatic nerves, we show an increase of CAPN1 and decrease of calpastatin expression. These changes in the calpain-calpastatin system are distinct from those during central nervous system development or in acute axonal degeneration in peripheral nerves. Our results suggest that the calpain-calpastatin system has putative roles in myelination and demyelinating diseases of peripheral nerves.

Changes in neuromuscular conduction of workers depending on age

The research was conducted to determine the effect of age on potential functional changes occurring through the transmission of nerve impulses in the motor nerves supplying selected muscles of the lower limb. The nerve conduction parameters in the lower limb were measured, as well as the ability to control muscle tension with pressure on the foot pedal. The study included a group of 54 men, differentiated by age. During the research, the speed of nerve conduction, amplitude and latency of the motor response in the tibial and peroneal nerves were measured. During the RAMP-contraction test, the EMG signal was recorded from the tibialis anterior muscles and the gastrocnemius muscles of the medial head. The results of the research showed that with age the ability to control muscle tone decreases, the speed of transmission of electrical impulses decreases, the motor response is delayed and its amplitude is significantly lower than in the case of younger people. The deterioration of neuromuscular conduction observed with age and a reduction in the ability to control the generated value of muscle strength may result in a deterioration of the ability to operate equipment or drive vehicles. From the point of view of prolonging the activity in working life, identifying all factors limiting the functioning of an older employee in the work environment may be the basis for creating guidelines and recommendations helpful in the design of devices and workstations for older employees. Med Pr. 2022;73(5):417-25.

Abstract 11957: Physical Training Augmented With Whole Body Electronic Muscle Stimulation is Superior to Conventional Training Alone in Healthy Subjects, a Pilot Randomized Controlled Trial

Introduction: Physical activity is protective against cardiovascular (CV) disease and mortality, yet more than 25% of adults do not perform any regular exercise. Whole body electronic muscle stimulation (WB-EMS) is a novel FDA-approved device used for physical training that simultaneously stimulates all major muscle groups using percutaneous electrical impulse transmission during exercise. Preliminary studies demonstrated increased muscle mass, reduced fat mass, and improved functional capacity in elderly individuals who trained with WB-EMS. We evaluated the effects of training with WB-EMS on measures of CV health. Methods: Healthy adults were randomized to physical training with versus without WB-EMS for one 20-minute session each week for 16 weeks. Participants wore a specifically designed vest and arm and leg straps connected to the WB-EMS device (Miha Bodytec, Germany). Biphasic electrical stimulation was delivered through the vest and straps (4 sec on, 4 sec off) at a frequency that elicited a score of 5-6 on the Borg perceived exertion scale when each major muscle group was stimulated. Individuals randomized to no WB-EMS wore the same equipment but received no stimulation. Sessions were provided by trainers certified in WB-EMS training and consisted of a fixed protocol of simple exercises such as squats and lunges. Temporal changes in measures of CV health were compared between groups. Results: Forty-one individuals were recruited between 02/2021 and 02/2022 (n=24 WB-EMS, n=17 no WB-EMS; mean age 35.9±11.2 yrs; 61.3% females; median BMI 24.3 (21.8, 28.1) kg/m 2 . After 16 weeks there were significant and favorable differences in the intervention group compared to controls in waist: hip ratio (-1.2 cm vs. 0.9, p=0.05); total cholesterol (-1.1 mg/kg vs. 14.2 mg/kg, p=0.02); anaerobic threshold (68.2% vs. 30.8%, p=0.03); breathing efficiency (VE/VCO2: -10.36 vs -7.38, p=0.01); and peripheral endothelial function, measured with reactive hyperemia peripheral arterial tonometry (-0.009 vs. -0.29, p=0.06). Conclusions: Once weekly training with WB-EMS yielded more favorable changes in CV biomarkers compared to conventional training alone in healthy adults, and thus may offer an effective and time-efficient method of physical training.

QT interval prolongation, torsades de pointes and psychotropic medication

QT interval reflects the duration of action potential of myocardial cells. Its prolongation in electrocardiogram is related to risk of torsades de pointes (TdP), a form of polymorphous ventricular tachycardia, and sudden cardiac death, which is one of the main causes of early mortality in psychiatric patients. The fact that only a proportion of patients with drug-induced QT prolongation manifest TdP or die shows that QT prolongation alone is not the perfect biological predictive marker of arrhythmia manifestation. Yet, it continues to be useful but needs to be combined with other known risk factors. This paper is a narrative review based on search in reference books and in PubMed and ScienceDirect databases using the terms [Torsades de pointes OR QT prolongation] AND [Psychotropic drugs OR antipsychotics OR antidepressants]. Its aim is to present basic knowledge about the pathophysiology of TdP arrhythmia and QT prolongation and their relationship with psychotropic drugs. TdP is a relatively slow-rate tachycardia and, in some cases, may stop abruptly without manifestation of clinical symptoms. The diagnosis is based on electrocardiographic findings, the symptoms are similar to those of any tachyarrhythmia and they are related to heart rate and its effects on arterial pressure and cardiac work. QT interval prolongation and TdP result from structural and functional disorders of ion channels and related proteins which are implicated in the process of ventricular repolarization. Psychotropic drugs are commonly used not only in psychiatric patients but in many patients with somatic disease as well. They can affect transmission of electrical impulses from sinus node to ventricular myocardium in various ways and most of its classes prolong QT interval in therapeutic doses or in cases of intoxication. Thus, their careful administration and monitoring of patients, especially hospitalized ones, are of vital importance. More data is available concerning the effects of antipsychotic and antidepressant medication. Among the first group, first generation, classical antipsychotics, especially the lower potency drugs, are considered to carry greater risk. Caution should be exercised when administering thioridazine, haloperidol, pimozide, sertindole and ziprasidone. Among antidepressants, caution is warranted when administering tricyclic antidepressants, citalopram and escitalopram. Among the other psychotropics, much information is available about methadone.

A Machine Learning Approach for Wear Monitoring of End Mill by Self-Powering Wireless Sensor Nodes.

There are many tool condition monitoring solutions that use a variety of sensors. This paper presents a self-powering wireless sensor node for shank-type rotating tools and a method for real-time end mill wear monitoring. The novelty of the developed and patented sensor node is that the longitudinal oscillations, which directly affect the intensity of the energy harvesting, are significantly intensified due to the helical grooves cut onto the conical surface of the tool holder horn. A wireless transmission of electrical impulses from the capacitor is proposed, where the collected electrical energy is charged and discharged when a defined potential is reached. The frequency of the discharge pulses is directly proportional to the wear level of the tool and, at the same time, to the surface roughness of the workpiece. By employing these measures, we investigate the support vector machine (SVM) approach for wear level prediction.

Ecological Dynamics: An Inspiration for Triggering Epilepsy

Epilepsy is a rigorous transmission of electrical impulses across neurons of the brain and reported more prevalent in lower-income countries. A systematic literature review has been performed to implicate the impact of environmental variables on the occurrence of epilepsy using the following keywords: Epilepsy or environmental risk factors or seizures. More than 500 genes have been reported to involve in epilepsy potentially. Moreover, family history with neurological disorders, sleep apnea, depression, alcohol, stress, diet, gestational period of mother, and social involvement are among the risk factors which can reliably predict onset and severity of the disease. Hence, minimizing these factors along with recommended therapies, counseling, and awareness could be a miracle in the life of epileptic patients and can improve societies.

Avermectin Derivatives, Pharmacokinetics, Therapeutic and Toxic Dosages, Mechanism of Action, and Their Biological Effects.

Avermectins are a group of drugs that occurs naturally as a product of fermenting Streptomyces avermitilis, an actinomycetes, isolated from the soil. Eight different structures, including ivermectin, abamectin, doramectin, eprinomectin, moxidectin, and selamectin, were isolated and divided into four major components (A1a, A2a, B1a and B2a) and four minor components (A1b, A2b, B1b, and B2b). Avermectins are generally used as a pesticide for the treatment of pests and parasitic worms as a result of their anthelmintic and insecticidal properties. Additionally, they possess anticancer, anti-diabetic, antiviral, antifungal, and are used for treatment of several metabolic disorders. Avermectin generally works by preventing the transmission of electrical impulse in the muscle and nerves of invertebrates, by amplifying the glutamate effects on the invertebrates-specific gated chloride channel. Avermectin has unwanted effects or reactions, especially when administered indiscriminately, which include respiratory failure, hypotension, and coma. The current review examines the mechanism of actions, biosynthesis, safety, pharmacokinetics, biological toxicity and activities of avermectins.

SERUM PHOSPHORYLATED NEUROFILAMENT HEAVY CHAIN AS A MARKER OF AXONAL INJURY AND DISEASE SEVERITY IN MULTIPLE SCLEROSIS PATIENTS

Abstract Axonal damage is the main cause of irreversible neurological complication in multiple sclerosis (MS). Neurofilaments (NFs) are intermediate filaments are present in large amount in axons that responsible for the radial growth of axons and the transmission of electrical impulses. Serum phosphorylated neurofilament-heavy (pNf-H) can be used as a marker to evaluate the presence axonal damage. Aim: To evaluate whether serum pNF-H levels are related to disease severity and the disability in MS patients. Subjects and methods: Study included 35 patients and 35 healthy control. All Subjects were evaluated by history taking, general examination, neurological evaluation and disability scoring by the Expanded Disability Status Score (EDSS), Routine Laboratory Investigations, measuring pNF-H levels and neuroradiological assessment using Magnetic resonance image (MRI) to establish MS diagnosis. Results: higher levels of pNF-H in MS patients compared to healthy controls. The highest levels of proteins were in the secondary progressive MS and these levels significantly correlated with disease severity measured by EDSS.

RIP1 kinase inhibitor halts the progression of an immune-induced demyelination disease at the stage of monocyte elevation

Demyelination in the central nervous system (CNS) underlies many human diseases, including multiple sclerosis (MS). We report here the findings of our study of the CNS demyelination process using immune-induced [experimental autoimmune encephalomyelitis (EAE)] and chemical-induced [cuprizone (CPZ)] mouse models of demyelination. We found that necroptosis, a receptor-interacting protein 3 (RIP3) kinase and its substrate mixed lineage kinase domain-like protein (MLKL)-dependent cell death program, played no role in the demyelination process, whereas the MLKL-dependent, RIP3-independent function of MLKL in the demyelination process initially discovered in the peripheral nervous system in response to nerve injury, also functions in demyelination in the CNS in these models. Moreover, a receptor-interacting protein 1 (RIP1) kinase inhibitor, RIPA-56, blocked disease progression in the EAE-induced model but showed no effect in the CPZ-induced model. It does so most likely at a step of monocyte elevation downstream of T cell activation and myelin-specific antibody generation, although upstream of breakdown of the blood-brain barrier. RIP1-kinase dead knock-in mice shared a similar result as mice treated with the RIP1 inhibitor. These results indicate that RIP1 kinase inhibitor is a potential therapeutic agent for immune-mediated demyelination diseases that works by prevention of monocyte elevation, a function previously unknown for RIP1 kinase.

SUCCESSFUL MANAGEMENT OF RADIAL NERVE PARALYSIS IN A 2 YEAR-OLD MONGREL

A 2 year-old mongrel was presented to the Veterinary teaching hospital, University of Ibadan with knuckling of the right forelimb. The client gave history of automobile accident. The animal was clinically evaluated with rectal temperature 38oC, heart rate 80 beats/minutes and respiratory rate of 16 The animal resented the limb being touched. The case was managed therapeutically with Neurobion® which is a combination of vitamins B1,B6 and B12 , Non-steroidal anti-inflammatory drug (NSAID) which was given by oral administration. The right fore-limb was placed in plaster cast (POP) to discourage the use of the limb so as to avoid further use of the limb while cage rest was advised. The type of nerve injury encountered here falls under the classification of neuropraxia. Here, it presents as minor contusions or compression of the peripheral nerve with a temporary interruption in the transmission of electrical impulses that will typically resolve by 3 to 6 weeks. Finally, the use of plaster cast was to discourage active use of the limb and an anti- inflammatory agent helped to quickly restore the use of the limb.

Arritmias

IntroductionCardiac arrhythmias occur in relation to alterations in the generation and/or transmission of electrical impulses, which can lead to bradyarrhythmias, slow rhythms, or tachyarrhythmias, or rapid rhythms. DiagnosisThe diagnosis is based on the symptoms described by the patient as well as on the electrocardiographic documentation of the arrhythmia. For this, both the conventional electrecardiogram and the prolonged registers are fundamental in the evaluation of a patient with suspected arrhythmias. ManagementIt is essential to understand the most probable mechanism by which the arrhythmia is generated, since it will depend on the treatment in the acute phase, either for the administration of drugs or for the evaluation of the need to place a pacemaker transient.

The role of the carrier waveform in vocoded Mandarin speech perception with applications to cochlear implants

Cochlear implants (CI) enable patients to perceive sound by the generation and transmission of electrical impulses. Voice encoded (vocoded) audio is commonly used as a simulator of CI speech. Past studies of vocoded English concluded that coded speech intelligibility is independent of whether a sinusoidal or noise-based carrier is used. Based on this work, recent CI research for tonal languages like Mandarin, have opted for a sinusoidal carrier without considering the impact of the carrier on intelligibility. The importance of spectral cues in Mandarin speech necessitates further analysis of the relationship between the carrier and intelligibility. This study explored intelligibility differences between English and Mandarin vocoded speech. This approach assessed speech recognition of randomly presented phrases to normal hearing English and Mandarin listeners. Available frequency channels and carrier type were varied to compare their effects on Mandarin word and tone identification. Results indicated that audio processed with a sinusoidal carrier led to significantly lower Mandarin intelligibility scores. In comparison, no effect was observed between English and Mandarin intelligibility when a noise-based carrier was used. The data suggest that the nature of the carrier type affects tonal language intelligibility and warrants further research as an experimental consideration in vocoded speech studies.

Bridging Physics and Biology Using Resistance and Axons

When teaching physics, it is often difficult to get biology-oriented students to see the relevance of physics.1 A complaint often heard is that biology students are required to take physics for the Medical College Admission Test (MCAT) as part of a “weeding out” process, but that they don't feel like they need physics for biology. Despite this impression held by students, there have been calls for better physics education for future physicians and life scientists.2,3 Research is being performed to improve physics classes and labs by linking topics in biology and physics.4,5 Described here is a laboratory experiment covering the topics of resistance of materials and circuits/Kirchhoff's laws in a biology context with their direct application to neurons, axons, and electrical impulse transmission within animals. This experiment will also demonstrate the mechanism believed to cause multiple sclerosis. The apparatus was designed with low-cost and readily available materials in mind.

Isoform Selective Voltage-Gated Sodium Channel Modulators and the Therapy of Pain

Voltage-gated sodium channels are large transmembrane protein complexes responsible for the propagation and transmission of electrical impulses through nerve, muscle and endocrine cells and cell systems. Dysregulated expression and/or functional changes of ion channel isoforms are found in many associated pathological conditions. In such cases, modulation of voltage gated sodium channels (Na(V) channels) is a recognised approach in medicinal chemistry. Multiple small-molecule active compounds are used for a plethora of Na(V) channel-linked indications, for example epilepsy and CNS disorders, arrhythmia, stroke and pain states such as congenital analgesia/hyperalgesia and neuropathic pain. As existent Na(V) channel modulators suffer mainly from selectivity issues and thus exert significant side effects, novel and selective Na(V) channel modulators would be beneficial. Consequently, the increased research on voltage-gated sodium channels has led to a large number of novel compounds that exploit classic binding site selectivity with state-dependence or functional selectivity. Such compounds offer selective targeting and new possibilities for studying the physiology of Na(V) channels and pathophysiology of the associated ailment conditions. This review consolidates the recent literature on Na(V) 1.3, 1.7 and 1.8 channel isoform selective and/or state-dependent modulators. In particular, their structure-activity relationship is illustrated, especially in the context of selectivity on a particular isoform, and their applicability in the therapy of neuropathic pain is described.