Sustained corneal nerve loss predicts the development of diabetic neuropathy in type 2 diabetes.

Introduction: This study was undertaken to investigate whether sustained rather than a single measure of corneal nerve loss was associated with the onset of diabetic peripheral neuropathy (DPN) and the progression of neuropathic symptoms and deficits in individuals with type 2 diabetes (T2D). Methods: Participants underwent clinical, metabolic testing and assessment of neuropathic symptoms, vibration perception threshold (VPT), sudomotor function, and corneal confocal microscopy (CCM) at baseline, 1, 2, and 4-7 years. Sustained corneal nerve loss was defined as abnormal corneal nerve fiber density (CNFD, <24 fibers/mm2), corneal nerve branch density (CNBD, <21 branches/mm2), and corneal nerve fiber length (CNFL, <16 mm/mm2) persisting for ≥50% of the study duration. Results: A total of 107 participants with a mean duration of T2D of 13.3 ± 7.3 years, aged 54.8 ± 8.5 years, underwent baseline and follow-up assessments over a median duration of 4 years, ranging from 1 to 7 years. The DPN prevalence at baseline was 18/107 (16.8%), and of the 89 participants without DPN at baseline, 13 (14.6%) developed DPN during follow-up. Approximately half of the cohort had sustained corneal nerve damage, and corneal nerve measures were significantly lower in this group than those without sustained damage (p < 0.0001). Sustained corneal nerve damage was associated with the development of DPN (p < 0.0001), a progressive loss of vibration perception (p ≤ 0.05), an increased incidence of burning pain, numbness, or a combination of both (p = 0.01-0.001), and a borderline association with progressive sudomotor dysfunction (p = 0.07). Sustained abnormal CNFL effectively distinguished between participants who developed DPN and those who did not (AUC: 76.3, 95% CI: 65.9-86.8%, p < 0.0001), while baseline and other sustained measures did not predict DPN onset. Conclusion: Sustained abnormal CCM is associated with more severe corneal nerve damage, DPN development, and the progression of neuropathic symptoms and deficits. Regular CCM monitoring may enable the identification of those at greater risk of developing and worsening DPN who may benefit from more aggressive risk factor reduction.

Injectable Hydrogel Loaded with CDs and FTY720 Combined with Neural Stem Cells for the Treatment of Spinal Cord Injury.

Purpose: Spinal cord injury (SCI) is an incurable and disabling event that is accompanied by complex inflammation-related pathological processes, such as the production of excessive reactive oxygen species (ROS) by infiltrating inflammatory immune cells and their release into the extracellular microenvironment, resulting in extensive apoptosis of endogenous neural stem cells. In this study, we noticed the neuroregeneration-promoting effect as well as the ability of the innovative treatment method of FTY720-CDs@GelMA paired with NSCs to increase motor function recovery in a rat spinal cord injury model. Methods: Carbon dots (CDs) and fingolimod (FTY720) were added to a hydrogel created by chemical cross-linking GelMA (FTY720-CDs@GelMA). The basic properties of FTY720-CDs@GelMA hydrogels were investigated using TEM, SEM, XPS, and FTIR. The swelling and degradation rates of FTY720-CDs@GelMA hydrogels were measured, and each group's ability to scavenge reactive oxygen species was investigated. The in vitro biocompatibility of FTY720-CDs@GelMA hydrogels was assessed using neural stem cells. The regeneration of the spinal cord and recovery of motor function in rats were studied following co-treatment of spinal cord injury using FTY720-CDs@GelMA hydrogel in combination with NSCs, utilising rats with spinal cord injuries as a model. Histological and immunofluorescence labelling were used to determine the regeneration of axons and neurons. The recovery of motor function in rats was assessed using the BBB score. Results: The hydrogel boosted neurogenesis and axonal regeneration by eliminating excess ROS and restoring the regenerative environment. The hydrogel efficiently contained brain stem cells and demonstrated strong neuroprotective effects in vivo by lowering endogenous ROS generation and mitigating ROS-mediated oxidative stress. In a follow-up investigation, we discovered that FTY720-CDs@GelMA hydrogel could dramatically boost NSC proliferation while also promoting neuronal regeneration and synaptic formation, hence lowering cavity area. Conclusion: Our findings suggest that the innovative treatment of FTY720-CDs@GelMA paired with NSCs can effectively improve functional recovery in SCI patients, making it a promising therapeutic alternative for SCI.

A comparative study of urinary levels of multiple metals and neurotransmitter correlations between GDM and T2DM populations.

OBJECTIVE: The pathogenesis of GDM and T2DM are closely related to various metals in vivo, and changes in the concentration of these metal exposures can lead to neuropathy through the DNA damage pathway caused by the accumulation of ROS. METHOD: Urine samples were analyzed for heavy metals and trace elements by ICP-MS, neurotransmitter metabolites by HPLC, 8-OH-dG by HPLC-MS and metabolomics by UPLC-MS. RESULT: Cd and Hg were risk factors for T2DM. There was a positive correlation between 8-OH-dG and neurotransmitter metabolites in both two populations. For GDM, the metabolite with the largest down-regulation effect was desloratadine and the largest up-regulation effect was D-glycine. That tyrosine and carbon metabolites were upregulated in the GDM population and downregulated in the T2DM population. CONCLUSION: The BMI, urinary Cd and Hg endo-exposure levels correlated with elevated blood glucose, and the latter may cause changes in the DNA damage marker 8-OH-dG in both study populations and trigger common responses to neurological alterations changes in the neurotransmitter. Tyrosine, carbonin metabolites, alanine, aspartate, and glutamate were signature metabolites that were altered in both study populations. These indicators and markers have clinical implications for monitoring and prevention of neurological injury in patients with GDM and T2DM.

A prospective case series to evaluate subcostal nerve injury with high-resolution ultrasound in posterior retroperitoneoscopic adrenalectomy.

BACKGROUND: Posterior retroperitoneoscopic adrenalectomy has several advantages over transabdominal laparoscopic adrenalectomy regarding operating time, blood loss, postoperative pain, and recovery. However, postoperatively several patients report chronic pain or hypoesthesia. We hypothesized that these symptoms may be the result of damage to the subcostal nerve, because it passes the surgical area. METHODS: A prospective single-center case series was performed in adult patients without preoperative pain or numbness of the abdominal wall who underwent unilateral posterior retroperitoneoscopic adrenalectomy. Patients received pre- and postoperative questionnaires and a high-resolution ultrasound scan of the subcostal nerve and abdominal wall muscles was performed before and directly after surgery. Clinical evaluation at 6 weeks was performed with repeat questionnaires, physical examination, and high-resolution ultrasound. Long-term recovery was evaluated with questionnaires, and photographs from the patients were examined for abdominal wall asymmetry. RESULTS: A total of 25 patients were included in the study. There were no surgical complications. Preoperative visualization of the subcostal nerve was possible in all patients. At 6 weeks, ultrasound showed nerve damage in 15 patients, with no significant association between nerve damage and postsurgical pain. However, there was a significant association between nerve damage and hypoesthesia (p = 0.01), sensory (p < 0.001), and motor (p < 0.001) dysfunction on physical examination. After a median follow-up of 18 months, 5 patients still experienced either numbness or muscle weakness, and one patient experienced chronic postsurgical pain. CONCLUSION: In this exporatory case series the incidence of postoperative damage to the subcostal nerve, both clinically and radiologically, was 60% after posterior retroperitoneoscopic adrenalectomy. There was no association with pain, and the spontaneous recovery rate was high.

Assessment of focused ultrasound stimulation to induce peripheral nerve activity and potential damage in vivo.

Introduction: Peripheral neuroprostheses are aimed to restore loss of sensory and motor functions by interfacing axons in the peripheral nerves. Most common interfaces in neuroprostheses are electrodes that establish electrical connection with peripheral axons. However, some challenges arise related to long-term functionality, durability, and body response. Recently, focused ultrasound stimulation (FUS) has emerged as a non-invasive approach to modulate the nervous system. However, it is controversial whether FUS can induce axon depolarization. Methods: We have assessed FUS applied in vivo to the rat peripheral nerve, with two objectives: first, to test whether FUS activates peripheral nerves under different stimulation conditions, and second, to evaluate if FUS inflicts damage to the nerve. FUS was delivered with three ultrasound transducers (Sonic Concept H115, H107, and H102) covering the largest set of parameters examined for FUS of peripheral nerves so far. Results: We did not obtain reliable evoked action potentials in either nerves or muscles, under any FUS condition applied, neither over the skin nor directly to the nerve exposed. Additional experiments ex vivo and in vivo on mice, confirmed this conclusion. When FUS stimulation was applied directly to the exposed sciatic nerve, neuromuscular function decreased significantly, and recovered one week later, except for FUS at 0.25 MHz. Histologically, degenerating nerve fibers were observed, with a tendency to be higher with the lower FUS frequency. Discussion: Past reports on the ability of ultrasound to stimulate the peripheral nerve are controversial. After testing a wide range of FUS conditions, we conclude that it is not a reliable and safe method for stimulating the peripheral nerve. Special consideration should be taken, especially when low-frequency FUS is applied, as it may lead to nerve damage.

The role of ferroptosis in central nervous system damage diseases.

Ferroptosis is a form of cell death, i.e., programmed cell death characterized by lipid peroxidation and iron dependence, which has unique morphological and biochemical properties. This unique mode of cell death is driven by iron-dependent phospholipid peroxidation and regulated by multiple cell metabolic pathways, including redox homeostasis, iron metabolism, mitochondrial activity, and the metabolism of amino acids, lipids, and sugars. Many organ injuries and degenerative pathologies are caused by ferroptosis. Ferroptosis is closely related to central nervous system injury diseases and is currently an important topic of research globally. This research examined the relationships between ferroptosis and the occurrence and treatment of central nervous system injury diseases. Additionally, ferroptosis was assessed from the aspect of theory proposal, mechanism of action, and related signaling pathways per recent research. This review provides a relevant theoretical basis for further research on this theory, the prospect of its development, and the prevention and treatment of such diseases.

Protective effect of sterubin against neurochemical and behavioral impairments in rotenone-induced Parkinson's disease

This study was conducted to evaluate how sterubin affects rotenone-induced Parkinson's disease (PD) in rats. A total of 24 rats were distributed into 4 equal groups: normal saline control and rotenone control were administered saline or rotenone (ROT), respectively, orally; sterubin 10 received ROT + sterubin 10 mg/kg po; and sterubin alone was administered to the test group (10 mg/kg). Rats of the normal saline and sterubin alone groups received sunflower oil injection (sc) daily, 1 h after receiving the treatments cited above, while rats of the other groups received rotenone injection (0.5 mg/kg, sc). The treatment was continued over the course of 28 days daily. On the 29th day, catalepsy and akinesia were assessed. The rats were then euthanized, and the brain was extracted for estimation of endogenous antioxidants (MDA: malondialdehyde, GSH: reduced glutathione, CAT: catalase, SOD: superoxide dismutase), nitrative (nitrite) stress markers, neuroinflammatory cytokines, and neurotransmitter levels and their metabolites (3,4-dihydroxyphenylacetic acid (DOPAC), dopamine (DA), norepinephrine (NE), serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), and homovanillic acid (HVA)). Akinesia and catatonia caused by ROT reduced the levels of endogenous antioxidants (GSH, CAT, and SOD), elevated the MDA level, and altered the levels of nitrites, neurotransmitters, and their metabolites. Sterubin restored the neurobehavioral deficits, oxidative stress, and metabolites of altered neurotransmitters caused by ROT. Results demonstrated the anti-Parkinson's activities of sterubin in ROT-treated rats.

A Novel Multi-compartment Rotating Bioreactor for Improving ADSC--Spheroid Formation and its Application in Neurogenic Erectile Dysfunction.

OBJECTIVE: The aim of this study was to construct a multicompartment synchronous rotating bioreactor (MCSRB) for batch-production of homogenized adipose-derived stem cell (ADSC) microspheres and treat neurogenic erectile dysfunction (ED). METHODS: Firstly, an MCSRB was constructed using a centrifugal device and hinged trays. Secondly, influence factors (density, rotational speed) on the formation of ADSC-spheroids were explored. Finally, a neurogenic ED model was established to verify the effectiveness and safety of ADSC-spheroids for ED treatment. RESULTS: An MCSRB promoted ADSCs to gather microspheres, most of which were 90-130 µm in diameter. Supernatant from three-dimensional culture led to a significant increase in cytokine expression in ADSCs and migration rate in human umbilical vein endothelial cells (HUVECs) compared to control groups. The erectile function and pathological changes of the penis were improved in the ADSC-spheroids treatment group compared to the traditional ADSCs treatment group (p < 0.01). CONCLUSION: Efficient, batch, controlled and homogenized production of ADSC stem cell microspheres, and effective improvement of erectile dysfunction in neurogenic rats can be achieved using the MCSRB device.

Heat stroke-induced cerebral cortex nerve injury by mitochondrial dysfunction: A comprehensive multi-omics profiling analysis.

In recent years, global warming has led to frequent instances of extremely high temperatures during summer, arousing significant concern about the adverse effects of high temperature. Among these, heat stroke is the most serious, which has detrimental effects on the all organs of human body, especially on brain. However, the comprehensive pathogenesis leading to brain damage remains unclear. In this study, we constructed a mouse model of heat stroke and conducted multi-omics profiling to identify relevant pathogenesis induced by heat stroke. The mice were placed in a constant temperature chamber at 42 °C with a humidity of 50 %, and the criteria for success in modeling were that the rectal temperature reached 42 °C and that the mice were trembling. Then the mice were immediately taken out for further experiments. Firstly, we conducted cFos protein localization and identified the cerebral cortex, especially the anterior cingulate cortex as the region exhibiting the most pronounced damage. Secondly, we performed metabolomics, transcriptomics, and proteomics analysis on cerebral cortex. This multi-omics investigation unveiled noteworthy alterations in proteins and metabolites within pathways associated with neurotransmitter systems, heatstroke-induced mitochondrial dysfunction, encompassing histidine and pentose phosphate metabolic pathways, as well as oxidative stress. In addition, the cerebral cortex exhibited pronounced Reactive Oxygen Species (ROS) production, alongside significant downregulation of the mitochondrial outer membrane protein Tomm40 and mitochondrial permeability transition pore, implicating cerebral cortex mitochondrial dysfunction as the primary instigator of neural impairment. This study marks a significant milestone as the first to employ multi-omics analysis in exploring the molecular mechanisms underlying heat stroke-induced damage in cerebral cortex neurons. It comprehensively identifies all potentially impacted pathways by heat stroke, laying a solid foundation for ensuing research endeavors. Consequently, this study introduces a fresh angle to clinical approaches in heatstroke prevention and treatment, as well as establishes an innovative groundwork for shaping future-forward environmental policies.

Investigation of the efficacy of two different laser types in the treatment of lower lip paresthesia after sagittal split ramus osteotomy.

Orthognathic surgery involves invasive and major surgical procedures commonly used to correct maxillofacial deformities. Bilateral sagittal split ramus osteotomy (BSSO) is often used to treat dentofacial anomalies related to the mandible, but it can result in various complications, the most common of which is inferior alveolar nerve damage. Nerve damage-induced paresthesia of the lower lip significantly affects patient comfort. Medical treatments such as steroids and vitamin B, low-level laser therapy (LLLT), and platelet-rich fibrin (PRF) can be used as supportive therapies for nerve regeneration after damage. This study aimed to investigate the effectiveness of two different types of lasers in treating lower lip paresthesia after BSSO. This clinical trial was a controlled, single-center, prospective, single-blind, randomized study. Thirty patients were included in the study and randomly assigned to three groups: Group I (laser GRR, n = 10) received transcutaneous and transmucosal GRR laser treatment, Group II (Epic10 laser, n = 10) received transmucosal and transcutaneous Epic10 laser treatment, and Group III (vitamin B, n = 10) received B-complex vitamin tablets orally once a day. Two-point and brush tests were performed six times at specific intervals, and a visual analog scale was used to evaluate pain and sensitivity. Both vitamin B and laser therapies accelerated nerve regeneration. The contribution of the laser groups to the healing rate was better than that of the vitamin B group. Although there was no statistically significant difference between the two laser groups, clinical observations indicated better results in the GRR laser group.

Molecular Investigation and Preliminary Validation of Candidate Genes Associated with Neurological Damage in Heat Stroke.

Heat stroke (HS) is a severe medical condition characterized by a systemic inflammatory response that may precipitate multi-organ dysfunction, with a particular predilection for inducing profound central nervous system impairments. We aim to employ bioinformatics techniques for the retrieval and analysis of genes associated with heat stroke-induced neurological damage. We performed a comprehensive analysis of the GSE64778 dataset from the Sequence Read Archive, resulting in the identification of 1178 significantly differentially expressed genes (DEGs). We retrieved 2914 genes associated with heat stroke from the GeneCards database and 2377 genes associated with heat stroke from the Comparative Toxicogenomics Database (CTD). The intersection of the top 300 DEGs in the GSE64778 dataset intersected with the search results of GeneCards and CTD, yielding 25 final candidates for DEGs associated with heat stroke. Gene Ontology functional annotation results indicated that the target genes were mainly involved in apoptosis, stress response, and negative regulation of cellular processes and function in processes such as protein dimerization and protein binding. The Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis revealed a predominant enrichment of candidate target genes within the PI3K-AKT signaling pathway. Subsequent protein-protein interaction network analysis highlighted HSP90aa1 as a central gene, indicating its pivotal role by possessing the highest number of edges among the genes enriched in the PI3K-AKT signaling pathway. Quantitative reverse transcription-polymerase chain reaction analysis performed on blood samples from patients validated the expression of Hsp90aa1 in individuals exhibiting early neurological damage in HS, consistent with the findings from the mRNA bioinformatics analysis. Additionally, the bioinformatics analysis of the upstream microRNAs (miRNAs) regulating HSP90aa1 and the target miRNAs associated with candidate long non-coding RNAs (lncRNAs) identified three lncRNAs, eight miRNAs, and one mRNA in the regulatory network. The DIANA Tools database and algorithms were employed for pathway enrichment and correlation analysis, revealing a significant association between LOC102547734 and MIR-206-3p, with the latter being identified as a target binding site Moreover, the analysis unveiled a correlation between MIR-206-3p and HSP90aa1, implicating the latter as a potential target binding site within the regulatory network.

TRPV: An emerging target in glaucoma and optic nerve damage.

Transient receptor potential vanilloid (TRPV) channels are members of the TRP channel superfamily, which are ion channels that sense mechanical and osmotic stimuli and participate in Ca2+ signalling across the cell membrane. TRPV channels play important roles in maintaining the normal functions of an organism, and defects or abnormalities in TRPV channel function cause a range of diseases, including cardiovascular, neurological and urological disorders. Glaucoma is a group of chronic progressive optic nerve diseases with pathological changes that can occur in the tissues of the anterior and posterior segments of the eye, including the ciliary body, trabecular meshwork, Schlemm's canal, and retina. TRPV channels are expressed in these tissues and play various roles in glaucoma. In this article, we review various aspects of the pathogenesis of glaucoma, the structure and function of TRPV channels, the relationship between TRPV channels and systemic diseases, and the relationship between TRPV channels and ocular diseases, especially glaucoma, and we suggest future research directions. This information will help to further our understanding of TRPV channels and provide new ideas and targets for the treatment of glaucoma and optic nerve damage.

Latarjet procedure for shoulder instability: Implications in the innervation of the subscapularis muscle. / Técnica de Latarjet para la inestabilidad anterior de hombro: implicaciones en la inervación del músculo subescapular.

INTRODUCTION: Our aim was to describe whether Latarjet's technique affects subscapularis muscle innervation. MATERIALS AND METHODS: We studied 12 embalmed shoulders. Subscapularis muscle innervation pattern was registered. Dimensions of the subscapularis at the glenohumeral joint line and the nerves entry point were measured. Horizontal distances from the nerves to the glenohumeral joint line as well as vertical ones to the split were measured before and after Latarjet procedure. A safe zone for the split was designed to avoid damage to subscapularis innervation. RESULTS: Subscapularis muscle is innervated by three principal branches: upper, middle, and inferior subscapularis nerves. No statistical differences were found between innervation distances before and after Latarjet procedure. To perform subscapularis split along the muscle safe zone, two thirds' proportions throughout all the split must be maintained. CONCLUSIONS: Subscapularis muscle has a triple innervation and was not altered after Latarjet procedure. Therefore, Latarjet technique seems to respect subscapularis muscle innervation if its split is placed through the subscapularis muscle safe zone.

[Translated article] Latarjet procedure for shoulder instability: Implications in the innervation of the subscapularis muscle.

INTRODUCTION: Our aim was to describe whether Latarjet's technique affects subscapularis muscle innervation. MATERIALS AND METHODS: We studied 12 embalmed shoulders. Subscapularis muscle innervation pattern was registered. Dimensions of the subscapularis at the glenohumeral joint line and the nerves entry point were measured. Horizontal distances from the nerves to the glenohumeral joint line as well as vertical ones to the split were measured before and after Latarjet procedure. A safe zone for the split was designed to avoid damage to subscapularis innervation. RESULTS: Subscapularis muscle is innervated by three principal branches: upper, middle, and inferior subscapularis nerves. No statistical differences were found between innervation distances before and after Latarjet procedure. To perform subscapularis split along the muscle safe zone, two thirds' proportions throughout all the split must be maintained. CONCLUSIONS: Subscapularis muscle has a triple innervation and was not altered after Latarjet procedure. Therefore, Latarjet technique seems to respect subscapularis muscle innervation if its split is placed through the subscapularis muscle safe zone.

Contralateral Astrocyte Response to Acute Optic Nerve Damage Is Mitigated by PANX1 Channel Activity.

Glial reactivity is considered a hallmark of damage-induced innate immune responses in the central nervous system. In the visual system, unilateral optic nerve damage elicits dramatic glial reactivity in the retina directly affected by the lesion and a similar, albeit more modest, effect in the contralateral eye. Evaluation of astrocyte changes in a mouse model of optic nerve crush indicates that astrocyte reactivity, as a function of retinal coverage and cellular hypertrophy, occurs within both the experimental and contralateral retinas, although the hypertrophic response of the astrocytes in the contralateral eyes is delayed for at least 24 h. Evaluation of astrocytic reactivity as a function of Gfap expression indicates a similar, muted but significant, response in contralateral eyes. This constrained glial response is completely negated by conditional knock out of Panx1 in both astrocytes and Müller cells. Further studies are required to identify if this is an autocrine or a paracrine suppression of astroglial reactivity.

Does mandibular osteotomy affect the infraorbital nerve? a prospective study.

OBJECTIVES: The aim of this study was to evaluate the sensory function of the infraorbital nerve after orthognathic surgery (OS). MATERIALS AND METHODS: Patients who underwent Le Fort I osteotomy with or without BSSO for dentofacial deformity treatment were studied. Two groups were created according to whether BSSO was performed. Class A tests were performed to determine the degree of peripheral nerve damage. The Class B test was performed if decreased sensation was detected in at least one of these tests. A Class C test was performed if abnormal sensation was detected. RESULTS: Twenty-eight patients (n=56) who underwent OS were included in this prospective study. Of the patients, 57.1% were female, 42.9% were male, and the mean age was 24.6 (±3.8). Seven patients were in group 1 (n=14), and 21 patients were in group 2 (n=42). In both groups, there were statistically significant differences between T1 and T2 (p<0.001), and the mean NSD score at T2 was higher than that at T1. The mean NSD score in the single jaw group was higher than that in the double jaw group at all time points. CONCLUSIONS: Bimaxillary surgeries had a negative effect on the somatosensory changes that developed in the early period. The upper lip's somatosensorial recovery was faster than IOR and single jaw recovery was faster than double jaw. CLINICAL RELEVANCE: Maxillofacial surgeons performing orthognathic surgery should be aware that in double jaw operations, changes in the somatosensory function of the ION are more severe.

The effect of individual drilling sleeves on the precision of coronectomy tooth sections. An in vitro 3D-printed jaw model experiment.

OBJECTIVES: The aim of this in vitro study was to evaluate the effect of a 3D-printed drill sleeve (DS) on the precision and duration of coronectomy sections. MATERIALS AND METHODS: Thirty-six trainees and oral surgeons performed 72 coronectomy cuts in a 3D-printed, entirely symmetric mandible model. Coronectomy was performed freehand (FH) on one side and with a DS on the other side. The occurrence of "too superficial" (≥ 4 mm unprepared lingual tooth tissue) and "too deep" (drilling ≥ 1 mm deeper as tooth contour) cuts and sectioning times were registered. RESULTS: In 7 cases, the sections were "too deep" with FH, while none with DS (OR: 18.56; 95%CI: 1.02-338.5; p = 0.048). The deviation between virtually planned and real cut depths was significantly greater in the FH group (1.91 ± 1.62 mm) than in DS group (1.21 ± 0.72 mm) (p < 0.001). A total of 18 "too superficial" buccolingual sections occurred with FH, while 8 cases with DS (OR: 3.50; 95%CI: 1.26-9.72; p = 0.016). Suboptimal sections did not correlate with experience (p = 0.983; p = 0.697). Shortest, suboptimal drillings were most frequently seen distolingually (OR: 6.76; 95% CI: 1.57-29.07; p = 0.01). In the inexperienced group, sectioning time was significantly longer with FH (158.95 ± 125.61 s vs. 106.92 ± 100.79 s; p = 0.038). CONCLUSIONS: The DS effectively reduced tooth sectioning times by less experienced colleagues. Independently from the level of experience, the use of DS obviated the need for any preparation outside the lingual tooth contour and significantly decreased the occurrence of "too superficial" cuts, leaving thinner unprepared residual tooth tissue lingually. CLINICAL RELEVANCE: Coronectomy sections may result in lingual hard and soft tissue injury with the possibility of damaging the lingual nerve. The precision of the buccolingual depth-control can be improved, while surgical time can be reduced when applying a drilling sleeve.

[A comparative study of detection methods for assessing superior and inferior vestibular nerve damages in patients with vestibular neuritis].

Objective:This study aims to compare the examination results of the vestibular evoked myogenic potential（VEMP） and video head impulse testing（vHIT） in patients with vestibular neuritis（VN）, thus exploring the methods to distinguish superior and inferior vestibular nerve damages in VN patients, and their feasibility. Methods:A total of 25 patients with unilateral VN treated in the Otology Department of the First Hospital of Qinhuangdao from May 2018 to July 2021 were recruited. They were respectively tested for ocular VEMP（oVEMP）, cervical VEMP（cVEMP） and vHIT, and the examination results were analyzed. Results:Examination results of oVEMP showed that 96%（24/25） patients had one-ear abnormalities with the amplitude decline or no waveform introduced, and 4%（1/25） patient had no waveform introduced of both ears. The overall abnormal rate examined by oVEMP was 100%（26/26）. Examination results of cVEMP showed that 36%（9/25） patients had one-ear abnormalities with the amplitude decline or no waveform introduced, and 4%（1/25） patients had no waveform introduced of both ears. The overall abnormal rate examined by cVEMP was 40%（10/25）, and 60%（15/25） patients had normal waveforms of both ears. Examination results of vHIT showed that 100%（25/25） patients had semicircular canal gain decline of one side, 92%（23/25） had anterior Semicircular canal decline of one side, and 36%（9/25） had posterior semicircular canal decline of one side. VEMP and vHIT results were compared. Examination results of VEMP showed that 60%（15/25） VN patients had superior vestibular nerve damage, and 40%（10/25） had both superior and inferior vestibular nerve damages. Examination results of vHIT showed that 64%（16/25） VN patients had superior vestibular nerve damage, and 36%（9/25） had both superior and inferior vestibular nerve damages. There was no significant difference in the ratio of VN patients with superior and inferior vestibular nerve damages examined by VEMP or vHIT（χ²=0.085, P>0.05）. The matching ratio of VEMP and vHIT results was 80%（20/25）, and the non-matching ratio was 20%（5/25）. Conclusion:Consistent results obtained from both VEMP and vHIT can preliminarily identify the type of vestibular nerve damage. If their results are not consistent, it is recommended not to identify the scope of the vestibular nerve damage.

Optimizing Noninvasive Vagus Nerve Stimulation for Systemic Lupus Erythematosus: Protocol for a Multicenter Randomized Controlled Trial.

BACKGROUND: Systemic lupus erythematosus is a chronic, multisystem, inflammatory disease of autoimmune etiology occurring predominantly in women. A major hurdle to the diagnosis, treatment, and therapeutic advancement of this disease is its heterogeneous nature, which presents as a wide range of symptoms such as fatigue, fever, musculoskeletal involvement, neuropsychiatric disorders, and cardiovascular involvement with varying severity. The current therapeutic approach to this disease includes the administration of immunomodulatory drugs that may produce unfavorable secondary effects. OBJECTIVE: This study explores the known relationship between the autonomic nervous system and inflammatory pathways to improve patient outcomes by treating autonomic nervous system dysregulation in patients via noninvasive vagus nerve stimulation. In this study, data including biomarkers, physiological signals, patient outcomes, and patient quality of life are being collected and analyzed. After completion of the clinical trial, a computer model will be developed to identify the biomarkers and physiological signals related to lupus activity in order to understand how they change with different noninvasive vagus nerve stimulation frequency parameters. Finally, we propose building a decision support system with integrated noninvasive wearable technologies for continuous cardiovascular and peripheral physiological sensing for adaptive, patient-specific optimization of the noninvasive vagus nerve stimulation frequency parameters in real time. METHODS: The protocol was designed to evaluate the efficacy and safety of transauricular vagus nerve stimulation in patients with systemic lupus erythematosus. This multicenter, national, randomized, double-blind, parallel-group, placebo-controlled study will recruit a minimum of 18 patients diagnosed with this disease. Evaluation and treatment of patients will be conducted in an outpatient clinic and will include 12 visits. Visit 1 consists of a screening session. Subsequent visits up to visit 6 involve mixing treatment and evaluation sessions. Finally, the remaining visits correspond with early and late posttreatment follow-ups. RESULTS: On November 2022, data collection was initiated. Of the 10 participants scheduled for their initial appointment, 8 met the inclusion criteria, and 6 successfully completed the entire protocol. Patient enrollment and data collection are currently underway and are expected to be completed in December 2023. CONCLUSIONS: The results of this study will advance patient-tailored vagus nerve stimulation therapies, providing an adjunctive treatment solution for systemic lupus erythematosus that will foster adoption of technology and, thus, expand the population with systemic lupus erythematosus who can benefit from improved autonomic dysregulation, translating into reduced costs and better quality of life. TRIAL REGISTRATION: ClinicalTrials.gov NCT05704153; https://clinicaltrials.gov/study/NCT05704153. INTERNATIONAL REGISTERED REPORT IDENTIFIER (IRRID): DERR1-10.2196/48387.

The Effect of Adipose-Derived Mesenchymal Stem Cells on Peripheral Nerve Damage in a Rodent Model.

Peripheral nerve damage is a significant clinical problem with limited therapeutic options. Adipose-derived mesenchymal stem cells (ADSCs) have emerged as a promising therapeutic approach due to their regenerative potential. However, the underlying mechanisms by which ADSCs promote peripheral nerve regeneration remain unclear. In this study, we investigated the role of syndecan-1 and heat shock protein 70 (HSP-70) in mediating the regenerative effects of ADSCs on peripheral nerves. ADSCs were characterized and isolated from the adipose tissue of rats. In vitro experiments were conducted to evaluate the ability of ADSCs to secrete syndecan-1 and HSP-70 in response to stress conditions. To evaluate the therapeutic potential of ADSCs, rats with sciatic nerve injuries were treated with ADSCs and assessed for functional recovery, nerve regeneration, and changes in syndecan-1 and HSP-70 levels. Regeneration was evaluated with Electromyography (EMG) histology. The results showed that ADSCs could secrete syndecan-1 and HSP-70 in response to stress conditions. Furthermore, ADSC treatment significantly improved functional recovery and nerve regeneration and increased syndecan-1 and HSP-70 levels in the injured nerve. On the other hand, ADSCs make improvements histologically through the influence of Nerve growth factor (NGF), Malondialdehyde (MDA), and EMG.