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We investigated the effects of apocynin (APO) on experimental sciatic nerve compression injury in rabbits. We used 21 male rabbits divided randomly into three groups of seven. The control group was subjected to sciatic nerve compression with no further intervention. The APO treated group was subjected to compression injury and 20 mg/kg APO was administered daily for 21 days by intraperitoneal injection beginning the day after the injury. The sham group was treated with APO without injury. The control group exhibited shrinkage of axons, disruption of myelin sheaths and loss of nerve fibers. The damage for the control group was significantly greater than for the sham group. The severity of histopathology was decreased in the APO treated group compared to the control group, as was the oxidative stress index. Our findings suggest that APO treatment may contribute to healing of sciatic nerve damage. [ABSTRACT FROM AUTHOR]

Introduction Functional healing of peripheral nerve injuries is still difficult. In this study, potential healing effects of thymoquinone and dexpanthenol in sciatic nerve compression injury (SCI) were investigated. Method: Twenty-four male Wistar albino rats which were applied compression injury to their sciatic nerves were randomly separated into four groups as following: “control” group contained six rats administered no pharmacological agent; “TMK” group consisted of six rats administered 10 mg/kg intraperitoneal thymoquinone once a day for one week; “DXP” group contained six rats administered 50 mg/kg intraperitoneal dexpanthenol once a day for one week; and “TMK–DXP” group consisted of six rats administered separately 10 mg/kg intraperitoneal thymoquinone and 50 mg/kg intraperitoneal dexpenthanol once a day for one week. Four weeks later from SCI, sciatic nerve function index (SFI) was applied before sacrifice of all rats, and then their crushed sciatic nerves were histopathologically examined, in terms of “Schwann cell count”, “axon and myelin degeneration”, “axon shape/size differences”, “fibrosis”, and “neovascularisation”. Results: “Schwann cell count” (p = 0.011), “axon and myelin degeneration” (p = 0.001), “axon shape/size differences” (p = 0.011), and “fibrosis and neovascularisation” (p = 0.026) scores were different between the control and TMK–DXP groups. SFI scores were different between the control and TMK groups (p = 0.002), between the control and TMK–DXP groups (p

Compression injuries of the murine spinal cord are valuable animal models for the study of spinal cord injury (SCI) and spinal regenerative therapy. The calibrated forceps model of compression injury is a convenient, low cost, and very reproducible animal model for SCI. We used a pair of modified forceps in accordance with the method published by Plemel et al. (2008) to laterally compress the spinal cord to a distance of 0.35 mm. In this video, we will demonstrate a dorsal laminectomy to expose the spinal cord, followed by compression of the spinal cord with the modified forceps. In the video, we will also address issues related to the care of paraplegic laboratory animals. This injury model produces mice that exhibit impairment in sensation, as well as impaired hindlimb locomotor function. Furthermore, this method of injury produces consistent aberrations in the pathology of the SCI, as determined by immunohistochemical methods. After watching this video, viewers should be able to determine the necessary supplies and methods for producing SCI of various severities in the mouse for studies on SCI and/or treatments designed to mitigate impairment after injury.

Functional healing of peripheral nerve injuries is still difficult. In this study, potential healing effects of thymoquinone and dexpanthenol in sciatic nerve compression injury (SCI) were investigated. Method: Twenty-four male Wistar albino rats which were applied compression injury to their sciatic nerves were randomly separated into four groups as following: "control" group contained six rats administered no pharmacological agent; "TMK" group consisted of six rats administered 10 mg/kg intraperitoneal thymoquinone once a day for one week; "DXP" group contained six rats administered 50 mg/kg intraperitoneal dexpanthenol once a day for one week; and "TMK–DXP" group consisted of six rats administered separately 10 mg/kg intraperitoneal thymoquinone and 50 mg/kg intraperitoneal dexpenthanol once a day for one week. Four weeks later from SCI, sciatic nerve function index (SFI) was applied before sacrifice of all rats, and then their crushed sciatic nerves were histopathologically examined, in terms of "Schwann cell count", "axon and myelin degeneration", "axon shape/size differences", "fibrosis", and "neovascularisation". Results: "Schwann cell count" (p = 0.011), "axon and myelin degeneration" (p = 0.001), "axon shape/size differences" (p = 0.011), and "fibrosis and neovascularisation" (p = 0.026) scores were different between the control and TMK–DXP groups. SFI scores were different between the control and TMK groups (p = 0.002), between the control and TMK–DXP groups (p < 0.001), and between the DXP and TMK–DXP groups (p = 0.029). Conclusions: This study results revealed that these pharmacological agents used alone had no histopathological healing effect in rats with SCI, but thymoquinone could improve walking function. However, thymoquinone and dexpanthenol used together had a significant histopathological and functional healing effect. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) leads to morbidity and mortality worldwide. Reperfusion after ischemia adds detrimental injury to cells. Ischemia/reperfusion (I/R) injures cells in a variety of ways including cell membrane disruption. Hence, methods to improve endogenous membrane resealing capacity are crucial. Poloxamer (P) 188, an amphiphilic triblock copolymer, was found to be effective against I/R and mechanical injury in various experimental settings. The aim of this study was to establish an in vitro mouse neuronal TBI model and, further, to investigate if postconditioning with P188 directly interacts with neurons after compression and simulated I/R injury, when administered at the start of reoxygenation. Cellular function was assessed by cell number/viability, mitochondrial viability, membrane damage by lactated dehydrogenase (LDH) release and FM1-43 incorporation as well as apoptosis-activation by Caspase 3. Five hours hypoxia ± compression with 2 h reoxygenation proved to be a suitable model for TBI. Compared to normoxic cells not exposed to compression, cell number and mitochondrial viability decreased, whereas membrane injury by LDH release/FM1-43 dye incorporation and Caspase 3 activity increased in cells exposed to hypoxic conditions with compression followed by reoxygenation. P188 did not protect neurons from simulated I/R and/or compression injury. Future research is indicated.

Abstract: Background: Recurrent laryngeal nerve (RLN) injury during surgery may reveal differences in electromyographic (EMG) changes after sustained compression or traction. Methods: In 20 pigs with the NIM‐FLEX EMG‐endotracheal tube, EMG was recorded at baseline, during sustained RLN compression, or traction until 70% amplitude decrease and during 30 minutes of recovery. Results: Seventy percent amplitude decrease from baseline was reached after 110 ± 98 seconds (compression group) and 2034 ± 2108 seconds (traction group). Traction induced a pronounced latency increase, peaking at 122 ± 8% in contrast to compression with 106 ± 5% (P < .001). The EMG amplitude recovery to ≥50% of baseline failed in 7 nerves after compression and 8 nerves after traction. Conclusion: Compression caused a fast decrease of EMG amplitude with minor effects on latency. In contrast, RLN traction showed early and significant latency increase preceding a delayed amplitude decrease. Recovery rate of the EMG signals were similar in both groups. [ABSTRACT FROM AUTHOR]

Our current understanding on the molecular mechanisms by which sustained compression induces skeletal muscle injury is very limited. This study aimed to test the hypothesis that activation of SIRT1 by the natural antioxidant resveratrol could deactivate apoptotic and catabolic signalling in skeletal muscle exposed to moderate compression. Two cycles of 6-hour constant pressure at 100 mmHg was applied to the tibialis region of right, but not left hindlimbs of Sprague Dawley rats pre-treated with DMSO (vehicle control) or resveratrol with/without sirtinol. Skeletal muscle tissues lying underneath and spatially corresponding to the compressed sites were collected for analyses. Resveratrol prevented the compression-induced manifestations of pathohistological damages including elevations of the number of interstitial nuclei and area of interstitial space and ameliorated oxidative damages measured as 4-hydroxy-2-nonenal (4HNE) and nitrotyrosine in skeletal muscle. In parallel, resveratrol augmented the expression level and activity of SIRT1 and phosphorylation levels of Foxo3a and Akt while suppressed the increases in protein abundances of p53, Bax, MAFbx and ubiquitin, enzymatic activities of caspase 3 and 20S proteasome, and apoptotic DNA fragmentation in the compressed muscle. These favourable myoprotective effects of resveratrol were diminished upon pharmacological blockade of SIRT1 by using sirtinol. These novel data support the hypothesis that the anti-apoptotic and anti-catabolic effects of resveratrol on compression injury in skeletal muscle required the action of SIRT1.

Purpose: To evaluate the degree of acute or progressive lateral compression needed to cause neurologic injury to the spinal cord assessed by electrophysiological monitoring.Methods: In five domestic pigs, the spinal cord was exposed and compressed between T8-T9 roots using a precise compression device. Two sticks placed on both sides of the spinal cord were sequentially brought together (0.5 mm every 2 min), causing progressive spinal cord compression. Acute compression was reproduced by a 2.5-mm displacement of the sticks. Cord-to-cord evoked potentials were obtained with two epidural catheters.Results: Increasing latency and decreasing amplitude of the evoked potentials were observed after a mean progressive displacement of the sticks of 3.2 ± 0.9 mm, disappearing after a mean displacement of 4.6 ± 1.2 mm. The potential returned after compression removal (16.8 ± 3.2 min). The potentials disappeared immediately after an acute compression of 2.5 ± 0.3 mm, without any sign of recovering after 30 min.Conclusions: The experimental model replicates the mechanism of a spinal cord injury caused by medially displaced screws into the spinal canal. The spinal cord had more ability for adaptation to progressive and slow compression than to acute mechanisms. [ABSTRACT FROM AUTHOR]

Compared with swelling hydrogel bioadhesives, the hydrogel in this study avoids undesirable compression injury to the spinal cord and ensures the transmission of nerve signals when being applied in spinal surgery. Adhesive hydrogels, anti-swelling, hemostasis, wound sealing, compression injury Keywords: adhesive hydrogels; anti-swelling; compression injury; hemostasis; wound sealing EN adhesive hydrogels anti-swelling compression injury hemostasis wound sealing 1 1 1 11/14/22 20221110 NES 221110 B Injectable Anti-Swelling Adhesive Hydrogels b In article number 2207741, Xiaoli Zhao, Haobo Pan, and co-workers develop an injectable anti-swelling adhesive hydrogel with rapid adhesion and volume stability in humid internal environment to achieve fast hemostasis and wound healing. [Extracted from the article]

Decreased cell membrane integrity is a primary pathological change observed in traumatic brain injury (TBI) that activates a number of complex intercellular and intracellular pathological events, leading to further neural injury. In this paper, we assessed the effects of urinary trypsin inhibitor (UTI) on astrocyte membrane integrity by determining the percentage of lactate dehydrogenase (LDH) released after sustained compression injury using a hydrostatic pressure model of mechanical-like TBI. Astrocytes isolated from SD rat pups were injured by sustained compression. At a pressure of 0.3 MPa for 5 min, a significant increase in LDH release was observed compared with control samples. Astrocytes displayed extensive structural disruption of mitochondrial cristae reflected in their swelling. Based on our initial results, injured astrocytes were treated with UTI at a final concentration of 500, 1,000, 3,000 or 5,000 U/ml for 24 h. The percentage of LDH released from injured astrocytes was significantly decreased when 1,000 and 3,000 U/ml of UTI were used. In a separate experiment, astrocytes were treated with UTI at a final concentration of 1,000 U/ml immediately, or at 30 min, 2, 6, or 24 h after sustained compression. The percentage of LDH release was significantly reduced ( P < 0.05) when astrocytes were treated with UTI immediately or 30 min later. Together, our results suggest that UTI may have protective effects on astrocytes injured by sustained compression injury. Furthermore, the early administration (<2 h after injury) of UTI may result in a better outcome compared with delayed administration. [ABSTRACT FROM AUTHOR]

Highlights: [•] The first characterization of axonal pathology in a rat static compression spinal injury. [•] Loss of axonal proteins at the lesion epicenter occurs within 1day of injury. [•] At 6weeks, myelination by oligodendrocytes and Schwann cells follows early myelin loss. [•] The injury spreads both rostral and caudal to the epicenter. [Copyright &y& Elsevier]

Severe compression injury in rats was accompanied by metabolic acidosis, cytolytic syndrome, disturbances in liver excretory function and detoxification, and change in biotransformation processes. [ABSTRACT FROM AUTHOR]

Abstract: It is well established that the cochlear nucleus (CN) of developing species is susceptible to loss of synaptic connections from the auditory periphery. Less information is known about how de-afferentation affects the adult auditory system. We investigated the effects of de-afferentation to the adult CN by mechanical compression. This experimental model is quantifiable and highly reproducible. Five weeks after mechanical compression to the axons of the auditory neurons, the total number of neurons in the CN was evaluated using un-biased stereological methods. A region-specific degeneration of neurons in the dorsal cochlear nucleus (DCN) and posteroventral cochlear nucleus (PVCN) by 50% was found. Degeneration of neurons in the anteroventral cochlear nucleus (AVCN) was not found. An imbalance between excitatory and inhibitory synaptic transmission after de-afferentation may have played a crucial role in the development of neuronal cell demise in the CN. The occurrence of a region-specific loss of adult CN neurons illustrates the importance of evaluating all regions of the CN to investigate the effects of de-afferentation. Thus, this experimental model may be promising to obtain not only the basic knowledge on auditory nerve/CN degeneration but also the information relevant to the application of cochlear or auditory brainstem implants. [Copyright &y& Elsevier]

The aim of this study was to investigate the regeneration potential of RLN after the compression of the nerve, without disrupting its continuity, using neuromonitoring. In the first operation, the RLN and nervus vagus of adult Goettingen minipigs were dissected free, and the neuromonitoring parameters (amplitude, threshold and lag time of signal) were measured. Injury of the RLN was induced using a “bulldog” clamp. When the signal was no longer detectable, after the 15 min regeneration phase, the operation was finished. The neuromonitoring studies (see above) were repeated in a second operation 6 months later. (1) After the first operation, acute clamping of the RLN led to a reduction in the amplitude of the neuromonitoring signal; the lag time and the threshold of signal remained. Complete restitution of the signal was observed during the first regeneration phase. Repeated clamping led to complete disappearance of the signal. (2) During the second operation, i.e., after 6 months of regeneration, the neuromonitoring signals of both RLN and nervus vagus were detected in 93% of the GMP. No statistical differences ( p = 0.17) were noticed between the amplitude of the RLN before the nerve injury (first operation) and after nerve regeneration (second operation). A significant increase in the lag time ( p < 0.0005) was shown for both RLN and nervus vagus. The acute compression of RLN can only be detected by observing the amplitude of the neuromonitoring signal. Restitutio ad integrum is possible after a short clamping period but it is important to preserve the RLN continuity. [ABSTRACT FROM AUTHOR]

Abstract: Mature sympathetic neurons in the superior cervical ganglion (SCG) are regulated by target-derived neurotrophins such as nerve growth factor (NGF) and neurotrophin-3 (NT-3). High molecular weight NGF species and mature NT-3 are the predominant NGF and NT-3 protein isoforms in the SCG, yet it is unknown whether the presence of these species is dependent on intact connection with the target tissues. In an attempt to determine the role of peripheral targets in regulating the neurotrophin species found in the SCG, we investigated the NGF and NT-3 protein species present in the SCG following axotomy (transection) or injury of the post-ganglionic axons. Following a 7 day axotomy, the 22–24 kDa NGF species and the mature 14 kDa NT-3 species in the SCG were significantly reduced by 99% and 66% respectively, suggesting that intact connection with the target is necessary for the expression of these protein species. As expected, tyrosine hydroxylase (TH) protein in the SCG was significantly reduced by 80% at 7 days following axotomy. In order to distinguish between the effects of injury and loss of target connectivity, the SCG was examined following compression injury to the post-ganglionic nerves. Following injury, no reduction in the 22–24 kDa NGF or 14 kDa mature NT-3 species was observed in the SCG. TH protein was slightly, yet significantly, decreased in the SCG following injury. The findings of this study suggest that the presence of the 22–24 kDa NGF and mature 14 kDa NT-3 species in the SCG is dependent on connection with peripheral targets and may influence, at least in part, TH protein expression in adult sympathetic neurons. [Copyright &y& Elsevier]

Abstract: Several animal models of auditory neuropathy (AN) have been produced by employing pharmacological agents to damage auditory neurons or hair cells selectively. The specificity of pharmacological lesions is generally assessed by observation of visible structural damage but it is difficult to localize the delivery, which could lead to functional side effects in other anatomical structures. Although genetic analyses of human AN patients have provided important information on the pathophysiology of AN, specific genetic defects have not been fully correlated with functional deficits in the auditory nervous system. To address this problem, we compressed rat auditory nerves to assess neural degeneration for up to 35 weeks. The method produced a good model of auditory neuropathy, including profound deterioration of the auditory brainstem response and preservation of both cochlear microphonics and distortion product otoacoustic emissions. Histological examination revealed that in spite of profound degeneration of the auditory nerve, the hair cells remained intact. The model provides a complementary alternative to those based on pharmacological lesions and genetic analyses of AN patients and should allow analysis of the pathophysiology of auditory neuropathy with less risk of the results being confounded by unknown deficits in other cell types. [Copyright &y& Elsevier]

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Electron microscopy of musculus bulbi rectus superior in the rat reveales increase in the number of. muscle satellite cells during the first 10-12 hours following compression injury so slight as not to cause degeneration of the muscle fibre. These satellite cells are situated close to the muscle nuclei and, in contrast to those in the intact rectus superior, they have a pale nucleus with a conspicuous nucleolus, sparse, pale cytoplasm containing a few small mitochondria, a mainly agranular endoplasmic reticulum and numbers of pinocytotic vesicles along their cell membrane. Later on, between 24 and 48 hours, the cytoplasm increases greatly in amount and extendes in long processess over a considerable length of the muscle fibre. An increase in the number of mitochondria and free ribosomes, the appearance of polysomes and great numbers of Golgi complexes and a decrease in the number of pinocytotic vesicles is noted. On the 4th day, some of the satellite cells have still further extended their cytoplasm beneath the muscle basement membrane, while others are apposed to the muscle fibre only with a minor part of their membrane. On the 9th day, only satellite cells comparable in number and structure with those in intact muscles are found. The possibility is discussed that the increase and subsequent decrease in the number of these satellite cells as well as the changes in their morphology at different periods after the injury reflect morphogenesis of satellite cells originating from the nuclei of the muscle fibre by mitotic division even after a trauma, too slight to cause any visible muscle injury. The observations are interpreted as giving new support to the hypothesis that muscle satellite cells may be of importance in posttraumatic muscle regeneration. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) leads to morbidity and mortality worldwide. Reperfusion after ischemia adds detrimental injury to cells. Ischemia/reperfusion (I/R) injures cells in a variety of ways including cell membrane disruption. Hence, methods to improve endogenous membrane resealing capacity are crucial. Poloxamer (P) 188, an amphiphilic triblock copolymer, was found to be effective against I/R and mechanical injury in various experimental settings. The aim of this study was to establish an in vitro mouse neuronal TBI model and, further, to investigate if postconditioning with P188 directly interacts with neurons after compression and simulated I/R injury, when administered at the start of reoxygenation. Cellular function was assessed by cell number/viability, mitochondrial viability, membrane damage by lactated dehydrogenase (LDH) release and FM1-43 incorporation as well as apoptosis-activation by Caspase 3. Five hours hypoxia ± compression with 2 h reoxygenation proved to be a suitable model for TBI. Compared to normoxic cells not exposed to compression, cell number and mitochondrial viability decreased, whereas membrane injury by LDH release/FM1-43 dye incorporation and Caspase 3 activity increased in cells exposed to hypoxic conditions with compression followed by reoxygenation. P188 did not protect neurons from simulated I/R and/or compression injury. Future research is indicated. [ABSTRACT FROM AUTHOR]

Abstract: Facial nerve paralysis in the pediatric population is rare. We describe a 2-year old child who was found with his head hanging between the railings of his bed. As a result he suffered a compression injury to his facial nerve; the only reported case that did not occur at the time of forceps delivery. The management of this type of injury is discussed, with a review of the literature. We find that this type of extratemporal injury to the facial nerve almost always results in complete recovery. The necessity of the generally accepted treatment of oral corticosteroid treatment is explored. [Copyright &y& Elsevier]

Background: Mechanical compression on the trigeminal root entry zone (TREZ) by microvascular is the main etiology of primary trigeminal neuralgia (TN)., Objectives: To study the pathogenesis of TN, hub genes screening in the TREZ of TN in an animal model was performed., Study Design: A double blind, randomized study was designed in a controlled animal trial., Setting: The research took place in the Laboratory of Clinical Applied Anatomy at the School of Basic Medical Science of Fujian Medical University., Methods: Twelve male rats were randomly divided into a sham operation group and a TN animal model group. TN animal model was induced by chronic compression of trigeminal nerve root (CCT) operation. Gene expression in the TREZ were analyzed by RNA sequencing (RNA-Seq) technique. KEGG analysis, GO analysis, and PPI analysis were performed in the DEGs. Key signaling pathways analyzing by GSEA and the hub genes in the DEGs were also studied. Reverse transcription real-time polymerase chain reaction (RT-qPCR) was used to verify the RNA-Seq results., Results: Transcriptome data showed that 352 genes up-regulated and 59 genes down-regulated in DEGs on post-operation day 21, after CCT operation in the TN group. KEGG analysis revealed that, "neuroactive ligand receptor interaction" and "cytokine cytokine receptor interaction" may be related to the pathogenesis of TN. GO analysis showed "regulation of signing receptor activity", "chemokine activity", and "carbohydrate binging" may be related to TN. The RT-qPCR results were consistent with the test results, indicating that the transcriptome sequencing results were reliable., Limitations: Although the incidence of TN in female rats was higher than in male rats, we only used male SD rats to establish the TN animal model, to avoid the effect of estrogen on experimental results. This study only presents some respects of RNA-Seq technique and, therefore, did not identify the DEGs at the protein level. The relationship between the DEGs at different levels shoud be done in the future., Conclusions: Based on the results of RNA-seq, this study discovered 6 hub genes in the TREZ that are closely related to the TN animal model, which provide a potential breakthrough point to explore the pathogenesis of TN.