Fiber Innervation Research Articles

BRUXISM AS A CAUSE OF NEUROPHYSIOLOGICAL ALTERATIONS IN THE TRIGEMINAL COMPLEX

All components of the dentoalveolar structures demonstrate close interconnections, especially in the intricate relationship between the nervous and muscular aspects of the temporomandibular joint (TMJ). The muscular system relies hierarchically on the regulatory mechanisms of the nervous system. Consequently, any disruption in the interaction between these components can lead to pathology affecting the overall function of the TMJ. One of the most prevalent myogenic disorders is bruxism, impacting 6-20% of the global population. However, pronounced signs of this condition are observed in only 3-5% of individuals. Bruxism is a multifactorial disorder, and its exact etiology remains unclear. Currently, a primary factor in bruxism is considered to be a disturbance in the body's adaptive capacity to cope with stress. Psychological stress induces hyperactivity in the masticatory muscles, leading to intense clenching of the dentition. This, in turn, results in an overload of the supporting tooth tissues, pathological abrasion of the dentition, dysfunction of the temporomandibular joint (TMJ), and the emergence of general clinical symptoms such as headaches, orofacial issues, and neurological symptoms. The pathophysiological foundation of bruxism lies in the excessive strain on the masticatory muscles, causing ischemia and inflammation in the muscle fibers. The inflammatory process in these fibers triggers a persistent excitation of afferent nerve fibers of type C, giving rise to a dull, aching pain. As bruxism is a chronic condition, there is a physiological restructuring of nerve fibers. This involves the initial peripheral and subsequent central sensitization of C-type nerve fibers, resulting in an inappropriate response of the body to physiological stimuli. For instance, the nervous system begins to interpret minor stimuli as painful (hyperalgesia). Currently, no treatment methods completely eliminate bruxism. Modern treatment approaches involve the use of intraoral dental appliances, pharmacotherapy (with muscle relaxants such as botulinum toxin type A and drugs from the benzodiazepine group), and psychotherapy courses aims to teach patients sleep hygiene, self-control, and the elimination of detrimental habits, including clenching the dentition as a response to psychological stress.

Magnesium Sulfate and Its Versatility in Anesthesia: A Comprehensive Review.

In the field of general anesthesia, magnesium sulfate (MgSO4) has become a valuable adjunct because it provides a range of benefits that enhance and optimize conventional aesthetic procedures. This review highlights the various intra-anesthetic benefits of MgSO4 while examining its complex function in the treatment using anesthesia. Magnesium inhibits the release of acetylcholine at the motor endplate and blocks calcium channels at presynaptic nerve terminals. This reduces the amplitude of endplate potential and the excitability of muscle fibers, which increases the potency of a neuromuscular blockade by nondepolarizing neuromuscular blockers. This activity may lessen the need for primary muscle relaxants. Moreover, its capacity to potentially reduce the total amount of main aesthetic agents needed emphasizes its function in maximizing anesthesia dosage, ensuring sufficient depth while perhaps potentially reducing adverse effects linked with increased dosages. MgSO4's adaptable qualities present a viable path for improving anesthetic outcomes, possibly improving patient safety and improving surgical results.

Netrin-1 as A neural guidance protein in development and reinnervation of the larynx

Neural guidance proteins participate in motor neuron migration, axonal projection, and muscle fiber innervation during development. One of the guidance proteins that participates in axonal pathfinding is Netrin-1. Despite the well-known role of Netrin-1 in embryogenesis of central nervous tissue, it is still unclear how the expression of this guidance protein contributes to primary innervation of the periphery, as well as reinnervation. This is especially true in the larynx where Netrin-1 is upregulated within the intrinsic laryngeal muscles after nerve injury and where blocking of Netrin-1 alters the pattern of reinnervation of the intrinsic laryngeal muscles. Despite this consistent finding, it is unknown how Netrin-1 expression contributes to guidance of the axons towards the larynx. Improved knowledge of Netrin-1’s role in nerve regeneration and reinnervation post-injury in comparison to its role in primary innervation during embryological development, may provide insights in the search for therapeutics to treat nerve injury. This paper reviews the known functions of Netrin-1 during the formation of the central nervous system and during cranial nerve primary innervation. It also describes the role of Netrin-1 in the formation of the larynx and during recurrent laryngeal reinnervation following nerve injury in the adult.

Metaoptics for aberration correction in microendoscopy.

Compact and minimally invasive scanning fiber endoscopy probes with micron-level resolution have great potential in detailed tissue interrogation and early disease diagnosis, which are key applications of confocal reflectance imaging at visible wavelengths. State-of-the-art imaging probes commonly employ refractive lens triplets or gradient refractive index (GRIN) lenses as the micro-objective. However, off-axis aberration emerges as a critical factor affecting resolution, especially at the extremities of the imaging field. In response to this challenge, we propose what we believe to be a novel design integrating a metasurface with the GRIN micro-objective to address optical aberrations during beam scan. The metasurface acts as a corrector element for optical aberrations in a fiber-scanning endoscope using the same fiber for excitation and collection. Modeling such hybrid refractive-metasurface designs requires the coupling of simulation techniques across macroscale and nanoscale optics, for which we used an Ansys simulation workflow platform. Operating at a wavelength of 644 nm, this metaoptical element serves as a thin and compact aberration correction surface, ensuring uniform resolution across the entire imaging field. Experimental results from our scanning fiber endoscopy system demonstrate a notable enhancement in optical performance both on-axis and off-axis, achieving a resolution of 3 µm at the center of the imaging field. Impressively, the resolution experiences only a modest degradation by a factor of 0.13 at the edge of the field of view compared to the center.

Gene therapy approaches for obesity-induced adipose neuropathy: Device-targeted AAV-mediated neurotrophic factor delivery to adipocytes in subcutaneous adipose

Maintaining functional adipose innervation is critical for metabolic health. We found that subcutaneous white adipose tissue (scWAT) undergoes peripheral neuropathy (PN) with obesity, diabetes, and aging (reduced small fiber innervation, nerve/synaptic/growth-cone/vesicle markers, altered nerve activity). Unlike peripheral nerve injuries, peripheral nerves don’t regenerate with PN, therefore, new therapies are needed for treatment of this condition that affects 20-30 million Americans. Here we validated a gene therapy approach using an adipocyte-tropic adeno-associated virus (AAV; serotype Rec2) to deliver neurotrophic factors (BDNF and nerve growth factor, NGF) directly to scWAT to improve tissue-specific PN as a proof-of-concept approach. AAVRec2-BDNF intra-adipose delivery improved tissue innervation in obese/diabetic mice with PN, but after longer periods of dietary obesity there was reduced AAVRec2-BDNF effectiveness, revealing a key window for therapies. AAVRec2-NGF increased scWAT innervation in obese mice and was more effective than BDNF, likely because Rec2 targeted adipocytes, the tissue's endogenous NGF source. AAVRec2-NGF also worked well even after 25 weeks of dietary obesity, unlike BDNF which likely needs a vector that targets its physiological cellular source in the stromal vascular fraction of the tissue. Given the differing effects of AAVs carrying NGF versus BDNF, a combined therapy may be ideal for obesity/diabetes neuropathy.

NGF Signaling Exacerbates KOA Peripheral Hyperalgesia via the Increased TRPV1-Labeled Synovial Sensory Innervation in KOA Rats.

Knee osteoarthritis (KOA) pain is caused by nociceptors, which are actually sensory nerve fiber endings that can detect stimuli to produce and transmit pain signals, and high levels of NGF in synovial tissue led to peripheral hyperalgesia in KOA. The purpose of this study is to investigate how sensory nerve fibers respond to the NGF/TrKA signal pathway and mediate the peripheral hyperalgesia in KOA rats. Forty SD male rats were randomly divided into 4 groups: normal, KOA, KOA + NGF, and KOA + siRNA TrKA. KOA model rats were induced by anterior cruciate ligament transection (ACLT). Mechanical and cold withdrawal thresholds (MWT and CWT) were measured 4 times in each group. The synovial tissues were harvested on day 28, and the expressions of NGF, TrKA, TRPV1, IL-1β, and PGP9.5 were determined using western blot, qPCR, and immunofluorescence staining. The primary rat fibroblast-like synoviocytes (FLSs) and DRG cells were divided into 4 groups as in vivo. The expressions of NGF, TrKA, TRPV1, and CGRP in vitro were determined using western blot and qPCR. KOA and intra-articular injection with NGF protein increased both mRNA and protein levels, not only TRPV1, PGP 9.5, and IL-1β in the synovial tissue, but also TRPV1, PGP 9.5, and S100 in the DRG tissue, while above changes were partly reversed after siRNA TrKA intervention. Besides, siRNA TrKA could improve peripheral hyperalgesia and decreased the TRPV1 positive nerve fiber innervation in synovial tissue. The results in vitro were consistent with those in vivo. This study showed the activation of the NGF/TrKA signaling pathway in KOA promoted the release of pain mediators, increased the innervation of sensory nerve fibers in the synovium, and worsened peripheral hyperalgesia. It also showed increased TRPV1 positive sensory innervation in KOA was mediated by NGF/TrKA signaling and exacerbated peripheral hyperalgesia.

Real-time damage identification in composite structures based on pseudo excitation (PE) approach and fiber Bragg grating (FBG) sensor arrays

At present, most of the damage detection techniques based on global vibration and local guided wave have obvious limitations, which brings difficulties to the safety assessment of structures. To solve this problem, a damage location identification method based on micro-dynamic balance and inverse finite element is proposed. Firstly, the vibration frequency, measuring point density and damage magnitude were determined by using finite simulation composite plate structure. Secondly, a fiber grating sensor is attached to the surface of the laminate to receive the strain response signal of the structure under steady-state vibration, and the global displacement of the structure is constructed by inverse finite element method. Finally, the inverse finite element listing is introduced into the theoretical framework of the dynamic response of the micro-element, and the structural damage identification experiment based on the measured strain data is realized. The experimental results show that this method can effectively identify the structural damage area and has a special sensitivity to structural damage, and the identification accuracy and efficiency are high.

Evolution and development of extraocular motor neurons, nerves and muscles in vertebrates

The purpose of this review is to analyze the origin of ocular motor neurons, define the pattern of innervation of nerve fibers that project to the extraocular eye muscles (EOMs), describe congenital disorders that alter the development of ocular motor neurons, and provide an overview of vestibular pathway inputs to ocular motor nuclei. Six eye muscles are innervated by axons of three ocular motor neurons, the oculomotor (CNIII), trochlear (CNIV), and abducens (CNVI) neurons. Ocular motor neurons (CNIII) originate in the midbrain and innervate the ipsilateral orbit, except for the superior rectus and the levator palpebrae, which are contralaterally innervated. Trochlear motor neurons (CNIV) originate at the midbrain-hindbrain junction and innervate the contralateral superior oblique muscle. Abducens motor neurons (CNVI) originate variously in the hindbrain of rhombomeres r4–6 that innervate the posterior (or lateral) rectus muscle and innervate the retractor bulbi. Genes allow a distinction between special somatic (CNIII, IV) and somatic (CNVI) ocular motor neurons. Development of ocular motor neurons and their axonal projections to the EOMs may be derailed by various genetic causes, resulting in the congenital cranial dysinnervation disorders. The ocular motor neurons innervate EOMs while the vestibular nuclei connect with the midbrain-brainstem motor neurons.

Functional Characteristics of the Nav1.1 p.Arg1596Cys Mutation Associated with Varying Severity of Epilepsy Phenotypes.

Mutations of the SCN1A gene, which encodes the voltage-dependent Na+ channel's α subunit, are associated with diverse epileptic syndromes ranging in severity, even intra-family, from febrile seizures to epileptic encephalopathy. The underlying cause of this variability is unknown, suggesting the involvement of additional factors. The aim of our study was to describe the properties of mutated channels and investigate genetic causes for clinical syndromes' variability in the family of five SCN1A gene p.Arg1596Cys mutation carriers. The analysis of additional genetic factors influencing SCN1A-associated phenotypes was conducted through exome sequencing (WES). To assess the impact of mutations, we used patch clamp analysis of mutated channels expressed in HEK cells and in vivo neural excitability studies (NESs). In cells expressing the mutant channel, sodium currents were reduced. NESs indicated increased excitability of peripheral motor neurons in mutation carriers. WES showed the absence of non-SCA1 pathogenic variants that could be causative of disease in the family. Variants of uncertain significance in three genes, as potential modifiers of the most severe phenotype, were identified. The p.Arg1596Cys substitution inhibits channel function, affecting steady-state inactivation kinetics. Its clinical manifestations involve not only epileptic symptoms but also increased excitability of peripheral motor fibers. The role of Nav1.1 in excitatory neurons cannot be ruled out as a significant factor of the clinical phenotype.

Periodic paralysis.

Periodic paralysis is a rare, dominantly inherited disorder of skeletal muscle in which episodic attacks of weakness are caused by a transient impairment of fiber excitability. Attacks of weakness are often elicited by characteristic environmental triggers, which were the basis for clinically delineating subtypes of periodic paralysis and are an important distinction for optimal disease management. All forms of familial periodic paralysis are caused by mutations of ion channels, often selectively expressed in skeletal muscle, that destabilize the resting potential. The missense mutations usually alter channel function through gain-of-function changes rather than producing a complete loss-of-function null. The knowledge of which channel gene harbors a variant, whether that variant is expected to (or known to) alter function, and how altered function impairs fiber excitability aides in the interpretation of patient signs and symptoms, the interpretation of gene test results, and how to optimize therapeutic intervention for symptom management and improve quality of life.

Synergistically Acting on Myostatin and Agrin Pathways Increases Neuromuscular Junction Stability and Endurance in Old Mice.

Sarcopenia is the primary cause of impaired motor performance in the elderly. The current prevailing approach to counteract such condition is increasing the muscle mass through inhibition of the myostatin system: however, this strategy only moderately improves muscular strength, not being able to sustain the innervation of the hypertrophic muscle per se, leading to a progressive worsening of motor performances. Thus, we proposed the administration of ActR-Fc-nLG3, a protein that combines the soluble activin receptor, a strong myostatin inhibitor, with the C-terminal agrin nLG3 domain. This compound has the potential of reinforcing neuro-muscular stability to the hypertrophic muscle. We previously demonstrated an enhancement of motor endurance and ACh receptor aggregation in young mice after ActR-Fc-nLG3 administration. Now we extended these observations by demonstrating that also in aged (2 years-old) mice, long-term administration of ActR-Fc-nLG3 increases in a sustained way both motor endurance and muscle strength, compared with ActR-Fc, a myostatin inhibitor, alone. Histological data demonstrate that the administration of this biological improves neuromuscular stability and fiber innervation maintenance, preventing muscle fiber atrophy and inducing only moderate hypertrophy. Moreover, at the postsynaptic site we observe an increased folding in the soleplate, a likely anatomical substrate for improved neurotransmission efficiency in the NMJ, that may lead to enhanced motor endurance. We suggest that ActR-Fc-nLG3 may become a valid option for treating sarcopenia and possibly other disorders of striatal muscles.

Experimental analysis of water-droplet–fiber interaction on a mechanically excited hydrophobic fiber

In this study, the dynamics of a single water droplet on a mechanically excited single fiber are investigated fundamentally. By utilizing state-of-the-art high-speed camera technology, the droplet's motion is captured with exceptional temporal resolution, enabling a detailed analysis of its position, size, and kinetics. We can identify distinct motion patterns of a droplet adhering to the fiber, which can exhibit either a static, a tilting, or swinging motion. The swinging and tilting motion can be overlaid with a higher-frequency deformation in response to the fiber excitation. Additionally, we examine the detachment of the droplet from the fiber as well as for the first time the (periodic) reattachment resulting from the mechanical excitation. The used droplet volumes are smaller, and the excitation shown here is greater than the excitation acceleration previously investigated in single fiber studies. Insights into droplet–fiber interactions can provide a better understanding of the mechanisms occurring in coalescence filters in harsh environments, which cannot be observed in situ with high temporal and spacial resolution in a full-scale filter due to the lack of optical access.

Validation of the Body Scan®, a new device to detect small fiber neuropathy by assessment of the sudomotor function: agreement with the Sudoscan®.

Sudomotor dysfunction is one of the earliest manifestations of small fiber neuropathy (SFN), reflecting the alteration of sympathetic C fiber innervation of the sweat glands. Among other techniques, such innervation can be assessed by measuring electrochemical skin conductance (ESC) in microsiemens (μS). In this study, ESC was measured at the feet to detect distal SFN. For this objective, the performance of a new device, the Body Scan® (Withings, France), intended for home use, was compared with that of a reference device, the Sudoscan® (Impeto Medical, France), which requires a hospital setting. In patients with diabetes with or without neuropathy or non-diabetic patients with lower-limb neuropathy, the diagnostic performance of the Body Scan® measurement was assessed by calculating its sensitivity (Se) and specificity (Sp) to detect at least moderate SFN (Se70 and Sp70), defined by a value of feet ESC ≤ 70 μS and > 50 μS on the Sudoscan® measure, or severe SFN (Se50 and Sp50), defined by a value of feet ESC ≤ 50 μS on the Sudoscan® measure. The agreement between the two devices was assessed with the analysis of Bland-Altman plots, mean absolute error (MAE), and root mean squared error (RMSE) calculations. The repeatability of the measurements was also compared between the two devices. A total of 147 patients (52% men, mean age 59 years old, 76% diabetic) were included in the analysis. The sensitivity and specificity to detect at least moderate or severe SFN were: Se70 = 0.91 ([0.83, 0.96]), Sp70 = 0.97 ([0.88, 0.99]), Se50 = 0.91 ([0.80, 0.98]), and Sp50 = 0.99 ([0.94, 1]), respectively. The bias and 95% limits of agreement were 1.5 [-5.4, 8.4]. The MAE was 2.9 and the RMSE 3.8. The intra-sample variability was 2.0 for the Body Scan® and 2.3 for the Sudoscan®. The ESC measurements provided by the Body Scan® were in almost perfect agreement with those provided by the reference device, the Sudoscan®, which validates the accuracy of the Body Scan® for the detection of SFN. By enabling simple, rapid, and autonomous use by the patient at home, this new technique will facilitate screening and monitoring of SFN in daily practice. ClinicalTrials.gov, identifier NCT05178459.

Modulation of sarcopenia phenotypes by glutathione peroxidase 4 overexpression in mice.

Our laboratory previously showed lipid hydroperoxides and oxylipin levels are elevated in response to loss of skeletal muscle innervation and are associated with muscle pathologies. To elucidate the pathological impact of lipid hydroperoxides, we overexpressed glutathione peroxidase 4 (GPx4), an enzyme that targets reduction of lipid hydroperoxides in membranes, in adult CuZn superoxide dismutase knockout (Sod1KO) mice that show accelerated muscle atrophy associated with loss of innervation. The gastrocnemius muscle from Sod1KO mice shows reduced mitochondrial respiration and elevated oxidative stress (F2 -isoprostanes and hydroperoxides) compared to wild-type (WT) mice. Overexpression of GPx4 improved mitochondrial respiration and reduced hydroperoxide generation in Sod1KO mice, but did not attenuate the muscle loss that occurs in Sod1KO mice. In contrast, contractile force generation is reduced in EDL muscle in Sod1KO mice relative to WT mice, and overexpression of GPx4 restored force generation to WT levels in Sod1KO mice. GPx4 overexpression also prevented loss of muscle contractility at the single fibre level in fast-twitch fibres from Sod1KO mice. Muscle fibres from Sod1KO mice were less sensitive to both depolarization and calcium at the single fibre level and exhibited a reduced activation by S-glutathionylation. GPx4 overexpression in Sod1KO mice rescued the deficits in both membrane excitability and calcium sensitivity of fast-twitch muscle fibres. Overexpression of GPx4 also restored the sarco/endoplasmic reticulum Ca2+ -ATPase activity in Sod1KO gastrocnemius muscles. These data suggest that GPx4 plays an important role in preserving excitation-contraction coupling function and Ca2+ homeostasis, and in maintaining muscle and mitochondrial function in oxidative stress-induced sarcopenia. KEY POINTS: Knockout of CuZn superoxide dismutase (Sod1KO) induces elevated oxidative stress with accelerated muscle atrophy and weakness. Glutathione peroxidase 4 (GPx4) plays a fundamental role in the reduction of lipid hydroperoxides in membranes, and overexpression of GPx4 improves mitochondrial respiration and reduces hydroperoxide generation in Sod1KO mice. Muscle contractile function deficits in Sod1KO mice are alleviated by the overexpression of GPx4. GPx4 overexpression in Sod1KO mice rescues the impaired muscle membrane excitability of fast-twitch muscle fibres and improves their calcium sensitivity. Sarco/endoplasmic reticulum Ca2+ -ATPase activity in Sod1KO muscles is decreased, and it is restored by the overexpression of GPx4. Our results confirm that GPx4 plays an important role in preserving excitation-contraction coupling function and Ca2+ homeostasis, and maintaining muscle and mitochondrial function in oxidative stress-induced sarcopenia.

Linearly polarized high sub-mode excited long-beaked fiber optic transmission and tracking particulate system

Micro/nano optical fibers are playing an increasingly important role in the fields of targeted drug therapy and biological cell analysis. To achieve fast and stable particle delivery, we designed a long beak-shaped fiber probe that not only increases the fiber optical field gradient force but also enhances the evanescent field around the probe. The evanescent field at the side of the fiber is further enhanced by exploiting the symmetrically distributed four-wave flap mode field of the linearly polarized high sub-mode in the weakly guided fiber, thus ensuring stable particle capture in the axial direction while improving the stability of lateral capture. We conducted a series of experiments using a long-beaked micro-nano fiber in LP21 mode to deliver polystyrene particles, and the results show that the probe can deliver particles rapidly at low input power, verifying the superiority of the long-beaked fiber probe. Finally, we built an FPI interference model to monitor the transport position of the particles in real-time. By processing the interference fringes, we plotted the motion profile of the particles, which helps to further manipulate the motion of the particles.

Local monitoring of photosensitizer transient states provides feedback for enhanced efficiency and targeting selectivity in photodynamic therapy

Photodynamic therapy (PDT) fundamentally relies on local generation of PDT precursor states in added photosensitizers (PS), particularly triplet and photo-radical states. Monitoring these states in situ can provide important feedback but is difficult in practice. The states are strongly influenced by local oxygenation, pH and redox conditions, often varying significantly at PDT treatment sites. To overcome this problem, we followed local PDT precursor state populations of PS compounds, via their fluorescence intensity response to systematically varied excitation light modulation. Thereby, we could demonstrate local monitoring of PDT precursor states of methylene blue (MB) and IRdye700DX (IR700), and determined their transitions rates under different oxygenation, pH and redox conditions. By fiber-optics, using one fiber for both excitation and fluorescence detection, the triplet and photo-radical state kinetics of locally applied MB and IR700 could then be monitored in a tissue sample. Finally, potassium iodide and ascorbate were added as possible PDT adjuvants, enhancing intersystem crossing and photoreduction, respectively, and their effects on the PDT precursor states of MB and IR700 could be locally monitored. Taken together, the presented procedure overcomes current methodological limitations and can offer feedback, guiding both excitation and PDT adjuvant application, and thereby more efficient and targeted PDT treatments.

Two-dimensional patterning of mesoscale fibers using acoustophoresis

The performance of functional composites can rely critically on the arrangement of secondary phases; for example, patterned networks of conductive particles can impart anisotropic thermal, electric or ionic conductivity while preserving flexibility in the matrix. We demonstrate the use of standing acoustic waves to generate periodic patterns of short fibers. We extend the range of possible patterns with the first demonstration of both rectangular grids and arrays of octagons interspersed with rectangles. These newly demonstrated patterns are rationalized using theoretical models of acoustic forces and torques on fibers that account for two-dimensional spatial variations arising from applied acoustic fields. The models enable simulations of fiber motion, which are used to (i) map out final fiber positions as a function of initial position and orientation, and (ii) corroborate experiments visualizing fiber motion and final patterns. This approach provides a fast and accurate way to predict emergent fiber patterns as a function of excitation modality and fiber length. The theory and experiments clearly indicate strong coupling between the length of the fibers and the spacing of the acoustic nodes. This coupling is used to estimate reductions in percolation thresholds associated with the ratio of fiber length and acoustic wavelength.

Modeling the excitation of nerve axons under transcutaneous stimulation

Computational models enable a safe and convenient way to study the excitation of nerve fibers under external stimulation. Contemporary models calculate the electric field distribution from transcutaneous stimulation and the resulting neuronal response separately. This study uses finite element methods to develop a multi-scale model that couples electric fields within macroscopic tissue layers and microscopic nerve fibers in a single-stage computational framework. The model included a triaxial myelinated nerve fiber bundle embedded within a volume conductor of tissue layers to represent the median nerve innervating the forearm muscles. The model captured the excitability of nerve fibers under transcutaneous stimulation and their nerve-tissue interactions to a transient external stimulus. The determinants of the strength-duration curve, rheobase, and chronaxie for the proposed model had close correlations with in-vivo experimentation on human participants. Additionally, the excitability indices for the triaxial myelinated nerve fiber implemented using the finite element method agreed well with experimental data from the literature. The validity of the proposed model encourages its use for applications involving transcutaneous stimulation. Capable of capturing field distribution across realistic morphologies, the model can serve as a testbed to improve stimulation protocols and electrode designs with subject-level specificity.

Epileptic Channelopathies and Neuromuscular Disorders in Newborns: A Narrative Review.

Neonates can have ion channel abnormalities known as channelopathies, which can impact any organ system. These abnormalities cause seizures, which can result in developmental delays and lead to early death. For a child's long-term neurodevelopment, early identification as a channelopathy is essential to avoid any brain damage. Therefore, this review aims to focus on early diagnostic criteria. Since it might be difficult for doctors to interpret the presenting symptoms of channelopathies, a thorough diagnostic examination that follows a methodical step-by-step procedure is essential. Skeletal muscle fiber and neuron excitability depend on voltage-gated sodium channels. It is now known that mutations in voltage-gated sodium channel genes can cause a growing variety of fatal or debilitating pediatric neurological diseases. Episodic paralysis, myotonia, newborn hypotonia, respiratory impairment, laryngospasm/stridor, congenital myasthenia, and myopathy are examples of muscle phenotypes. There may be a connection between sodium channel malfunction and abrupt infant death, according to recent findings. Numerous epilepsy syndromes and complex encephalopathies are among the manifestations of different channelopathies that are becoming more widely recognized.

A Real-Time Fluorescence Feedback System for Infrared Laser Sealing of Blood Vessels.

This study explores UV light induced fluorescence from blood vessels for indicating successful infrared laser sealing of vascular tissues. A light emitting diode (LED) with center wavelength of 340 nm and 0.1 mW power was used with a Y-shaped fiber bundle of seven 200-μm-core fibers. The central excitation fiber was connected to the LED, while the detection ring of six fibers was connected to a spectrometer. The fiber bundle was aligned with porcine renal arteries compressed between optical windows. Fluorescence was acquired before and after vessel sealing, with a 1470 nm laser for 5 s at 30 W (sealing, n = 10) or 5 W (control, n = 10). Signal increase in the 470-520 nm spectrum was correlated with vessel burst pressures (BP). Integrated fluorescence increased 71 ± 25% at 30 W vs. 19 ± 14% at 5 W (p < 0.05), corresponding to a successful BP of 639 ± 189 mmHg vs. failed seal BP of 39 ± 41 mmHg (p < 0.05). Real-time measurements showed a gradual increase in fluorescence with the signal reaching a plateau at 3-4 s, indicating that shorter seal times are possible. The increase in fluorescence signal during laser vessel sealing may provide a non-destructive, real-time, optical method for indicating hemostatic seals.