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A deeper understanding of the underlying biological mechanisms of secondary brain injury induced by traumatic brain injury (TBI) will greatly advance the development of effective treatments for patients with TBI. Hypoxia-inducible factor-1 alpha (HIF-1α) is a central regulator of cellular response to hypoxia. In addition, growing evidence shows that HIF-1α plays the important role in TBI-induced changes in biological processes; however, detailed functional mechanisms are not completely known. The aim of the present work was to further explore HIF-1α-mediated events after TBI. To this end, next-generation sequencing, coupled with cellular and molecular analysis, was adopted to interrogate vulnerable events in a rat controlled cortical impact model of TBI. The results demonstrated that TBI induced accumulation of HIF-1α at the peri-injury site at 24 h post-injury, which was associated with neuronal loss. Moreover, gene set enrichment analysis unveiled that neuroinflammation, especially an innate inflammatory response, was significantly evoked by TBI, which could be attenuated by the inhibition of HIF-1α. Furthermore, the inhibition of HIF-1α could mitigate the activation of microglia and astrocytes. Taken together, all these data implied that HIF-1α might contribute to secondary brain injury through regulating neuroinflammation.

BackgroundTwo randomised trials assessing the effectiveness of decompressive craniectomy (DC) following traumatic brain injury (TBI) were published in recent years: DECRA in 2011 and RESCUEicp in 2016. As the results have generated debate amongst clinicians and researchers working in the field of TBI worldwide, it was felt necessary to provide general guidance on the use of DC following TBI and identify areas of ongoing uncertainty via a consensus-based approach.MethodsThe International Consensus Meeting on the Role of Decompressive Craniectomy in the Management of Traumatic Brain Injury took place in Cambridge, UK, on the 28th and 29th September 2017. The meeting was jointly organised by the World Federation of Neurosurgical Societies (WFNS), AO/Global Neuro and the NIHR Global Health Research Group on Neurotrauma. Discussions and voting were organised around six pre-specified themes: (1) primary DC for mass lesions, (2) secondary DC for intracranial hypertension, (3) peri-operative care, (4) surgical technique, (5) cranial reconstruction and (6) DC in low- and middle-income countries.ResultsThe invited participants discussed existing published evidence and proposed consensus statements. Statements required an agreement threshold of more than 70% by blinded voting for approval.ConclusionsIn this manuscript, we present the final consensus-based recommendations. We have also identified areas of uncertainty, where further research is required, including the role of primary DC, the role of hinge craniotomy and the optimal timing and material for skull reconstruction.

The interseismic behavior of faults (whether they are locked or creeping) and their quantitative kinematic constraints are critical for assessing the seismic hazards of faults and their surrounding areas. Currently, the creep of the eastern segment of the Laohushan Fault in the Haiyuan Fault Zone at the northeastern margin of the Tibetan Plateau, as revealed by InSAR observations, lacks confirmation from other observational methods, particularly high-precision GNSS studies. In this study, we utilized nearly seven years of observation data from a dense GNSS continuous monitoring profile (with a minimum station spacing of 2 km) that crosses the eastern segment of the Laohushan Fault. This dataset was integrated with GNSS data from regional continuous stations, such as those from the Crustal Movement Observation Network of China, and multiple campaign measurements to calculate GNSS baseline change time series across the Laohushan Fault and to obtain a high spatial resolution horizontal crustal velocity field for the region. A comprehensive analysis of this primary dataset indicates that the Laohushan Fault is currently experiencing left-lateral creep, characterized by a partially locked shallow segment and a deeper locked segment. The fault creep is predominantly concentrated in the shallow crustal region, within a depth range of 0–5.7 ± 3.4 km, exhibiting a creep rate of 1.5 ± 0.7 mm/yr. Conversely, at depths of 5.7 ± 3.4 km to 16.8 ± 4.2 km, the fault remains locked, with a loading rate of 3.9 ± 1.1 mm/yr. The shallow creep is primarily confined within 3 km on either side of the fault. Over the nearly seven-year observation period, the creep movement within approximately 5 km of the fault's near field has shown no significant time-dependent variation, instead demonstrating a steady-state behavior. This steady-state creep appears unaffected by postseismic effects from historical large earthquakes in the adjacent region, although the deeper (far-field) tectonic deformation of the Laohushan Fault may have been influenced by the postseismic effects of the 1920 Haiyuan M8.5 earthquake. [ABSTRACT FROM AUTHOR]

This article aims to expound the essence of minimally invasive surgery as well as when and how to use it in craniocerebral trauma surgery according to the characteristics of the disease. In neurosurgery, the importance of tissue protection should be from the inside to the outside, i.e. brain→dura→skull→scalp. In this article, I want to share my opinion and our team’s experience in terms of selecting surgical approaches and incision, surgical treatment of the skull, dura handling, intracranial operation and placement of drainage based on the above theory. I hope this will be helpful for trauma surgeons. Key words: Traumatic brain injuries; Large craniectomy; Surgical procedures, minimally invasive

Byline: Zonggang. Hou, Zhen. Wu, Junting. Zhang, Liwei. Zhang, Runfa. Tian, Baiyun. Liu, Zhongcheng. Wang Objective: To evaluate the unique clinical characteristics and management of lateral ventricular subependymomas (LVSs). Patients [...]

Objective: To evaluate the unique clinical characteristics and management of lateral ventricular subependymomas (LVSs). Patients and Methods : The case records of 27 adult consecutive patients with LVS admitted between March 1996 and May 2011 were reviewed. The relevant clinical data (including patient age and sex, neuroimaging studies, surgical records and follow up) were collected through a chart review. Patient neurological status was recorded using the Karnofsky Performance Scale (KPS).Results: The gender distribution was 14:13 and the age from 33 to 66 years (median 45 years) at the time of operation. Headache and dizziness were the most common initial symptoms (17/27). Most of these tumours were located at the foramen of Monro (12/27). Magnetic resonance imaging (MRI) (21/27) showed well circumscribed tumours with cystic changes (21/27). The lesions were hypointense on T1-weighted images (19/21), hyperintense on T2-weighted images (21/21), and contrast enhancement was no or minimal (19/21). Gross total resection was performed in 23 patients. Five patients required a ventriculo-peritoneal shunt because of postoperative hydrocephalus. The follow-up period ranged from 6 to 188 months (mean 55.5 months). No recurrence was observed during the follow up.Conclusion: In this study LVSs had equal gender distribution. Tumours around the foramen of Monro were the candidates for aggressive treatment; surgery was the best curative treatment; postoperative hydrocephalus should be attended to. [ABSTRACT FROM AUTHOR]

Background: Astaxanthin (ATX) is a carotenoid pigment with effective antioxidant, anti-inflammatory, antitumor and immunomodulatory actions. ATX has been proposed to exert neuroprotective effects and attenuate oxidative stress in mice after traumatic brain injury (TBI). The nuclear factor erythroid 2-related factor 2 (Nrf2)-heme oxygenase 1 (HO-1) signaling pathway is stimulated after TBI and activates a compensatory mechanism against TBI. Nevertheless, the effect of ATX on the pathophysiology of TBI in mice is limited. Our present study evaluated the neuroprotection afforded by ATX and the possible role of the Nrf2/HO-1 pathway in experimental TBI., Materials and Methods: Mice were casually separated into 3 groups: the sham, TBI + vehicle, and TBI + ATX (100 mg/kg, intraperitoneally administered) groups. Neurobehaviors of the mice were assessed using the neurological severity scores (NSSs), the forced swimming test (FST) and the rotarod test. Levels of the Nrf2, HO-1, NAD(P)H: quinine oxidoreductase-1 (NQO1), cleaved caspase3 (C-caspase3), and superoxide dismutase1 (SOD1) proteins and levels of the Nrf2 and HO-1 mRNAs were assessed. In addition, Nrf2 nuclear import and apoptosis were measured after TBI., Results: The ATX treatment significantly improved the neurological status, promoted Nrf2 activation, and upregulated the expression of the Nrf2 and HO-1 mRNAs and the levels of the Nrf2, HO-1, and NQO1 proteins after TBI. The level of the SOD1 protein was decreased after TBI and increased after ATX treatment; however, the difference was not significant. ATX markedly reduced the level of the C-caspase3 protein and the number of TUNEL-positive cells, indicating that it exerted an antiapoptotic effect. Immunofluorescence staining confirmed that ATX promoted Nrf2 nuclear import., Conclusions: Based on our study, ATX possibly affords neuroprotection by activating the Nrf2/HO-1 signaling pathway in mice after TBI., Competing Interests: None., (AJTR Copyright © 2021.)

Maintaining lipid membrane integrity is an essential aspect of plant tolerance to high temperature. P 4 -type ATPases are responsible for flipping and stabilizing asymmetric phospholipids in membrane systems, though their functions in stress tolerance are not entirely clear. Aminophospholipid ATPase6 (ALA6) is a member of the P 4 -type ATPase family, which has 12 members in Arabidopsis thaliana . Here, we show that a loss-of-function mutant of ALA6 ( ala6 ) exhibits clear sensitivity to heat stress, including both basal and acquired thermotolerance treatments. Overexpression of ALA6 improves seedling resistance to heat stress, while mutated ALA6 transgenic plants, in which the conserved functional site of the ALA family has a point mutation, are still susceptible to heat stress like ala6 loss-of-function mutant. In addition, ala6 displays higher ion-leakage during heat treatment, suggesting that the lipid flippase activity of ALA6 plays a vital role in heat stress responses. Transcriptome analysis reveals differences in gene expression between ala6 and wild-type plants with or without heat stress. The differentially expressed genes are involved primarily in the physiological processes of stress response, cellular compartment maintenance, macromolecule stability and energy production. Our results suggest that ALA6 is crucial for the stability of membrane when plants suffer from high temperature stress.

JOURNAL/nrgr/04.03/01300535-202509000-00023/figure1/v/2024-11-05T132919Z/r/image-tiff Although microglial polarization and neuroinflammation are crucial cellular responses after traumatic brain injury, the fundamental regulatory and functional mechanisms remain insufficiently understood. As potent anti-inflammatory agents, the use of glucocorticoids in traumatic brain injury is still controversial, and their regulatory effects on microglial polarization are not yet known. In the present study, we sought to determine whether exacerbation of traumatic brain injury caused by high-dose dexamethasone is related to its regulatory effects on microglial polarization and its mechanisms of action. In vitro cultured BV2 cells and primary microglia and a controlled cortical impact mouse model were used to investigate the effects of dexamethasone on microglial polarization. Lipopolysaccharide, dexamethasone, RU486 (a glucocorticoid receptor antagonist), and ruxolitinib (a Janus kinase 1 antagonist) were administered. RNA-sequencing data obtained from a C57BL/6 mouse model of traumatic brain injury were used to identify potential targets of dexamethasone. The Morris water maze, quantitative reverse transcription-polymerase chain reaction, western blotting, immunofluorescence and confocal microscopy analysis, and TUNEL, Nissl, and Golgi staining were performed to investigate our hypothesis. High-throughput sequencing results showed that arginase 1, a marker of M2 microglia, was significantly downregulated in the dexamethasone group compared with the traumatic brain injury group at 3 days post-traumatic brain injury. Thus dexamethasone inhibited M1 and M2 microglia, with a more pronounced inhibitory effect on M2 microglia in vitro and in vivo . Glucocorticoid receptor plays an indispensable role in microglial polarization after dexamethasone treatment following traumatic brain injury. Additionally, glucocorticoid receptor activation increased the number of apoptotic cells and neuronal death, and also decreased the density of dendritic spines. A possible downstream receptor signaling mechanism is the GR/JAK1/STAT3 pathway. Overactivation of glucocorticoid receptor by high-dose dexamethasone reduced the expression of M2 microglia, which plays an anti-inflammatory role. In contrast, inhibiting the activation of glucocorticoid receptor reduced the number of apoptotic glia and neurons and decreased the loss of dendritic spines after traumatic brain injury. Dexamethasone may exert its neurotoxic effects by inhibiting M2 microglia through the GR/JAK1/STAT3 signaling pathway., (Copyright © 2025 Copyright: © 2025 Neural Regeneration Research.)

The inflammatory response plays a significant role in neuronal cell death and functional deficits after Traumatic brain injury (TBI). Importantly, anti-inflammatory agents have neuroprotective effects. To date, however, no studies have investigated the neuroprotective effects of Saikosaponin a (SSa) after TBI. In the present study, rats with controlled cortical impact (CCI) were used to investigate the neuroprotective effects of SSa. The results showed that SSa reduced body weight loss, improved neurological functions andcognition, and reduced brain edema and blood brain barrier permeability after CCI. Moreover, SSa inhibited aquaporin-4 (AQP-4), matrix metalloprotein-9 (MMP-9), mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (c-JNK), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). The reduction in the loss of occludin mediated by SSa may partially account for its neuroprotective effects. Together, our results suggest that SSa appears to counteract the inflammatory response and neurological function deficits after TBI and possibly via an anti-inflammatory response and inhibition of the MAPK signaling pathway.