Publications by authors named "YaLong Gao"

Background: Gliomas constitute a category of malignant tumors originating from brain tissue, representing the majority of intracranial malignancies. Previous research has demonstrated the pivotal role of CLEC7A in the progression of various cancers, yet its specific implications within gliomas remain elusive. The primary objective of this study was to investigate the prognostic significance and immune therapeutic potential of CLEC7A in gliomas through the integration of bioinformatics and clinical pathological analyses.

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Intestinal injury caused by traumatic brain injury (TBI) seriously affects patient prognosis; however, the underlying mechanisms are unknown. Recent studies have demonstrated that ferritinophagy-mediated ferroptosis is involved in several intestinal disorders. However, uncertainty persists regarding the role of ferritinophagy-mediated ferroptosis in the intestinal damage caused by TBI.

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Previous studies have proved that cardiac dysfunction and myocardial damage can be found in TBI patients, but the underlying mechanisms of myocardial damage induced by TBI can't be illustrated. We want to investigate the function of ferroptosis in myocardial damage after TBI and determine if inhibiting iron overload might lessen myocardial injury after TBI due to the involvement of iron overload in the process of ferroptosis and inflammation. We detect the expression of ferroptosis-related proteins in cardiac tissue at different time points after TBI, indicating that TBI can cause ferroptosis in the heart in vivo.

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The role of extracellular vesicles (EV) in various diseases is gaining increased attention, particularly due to their potent procoagulant activity. However, there is an urgent need for a bedside test to assess the procoagulant activity of EV in clinical settings. This study proposes the use of thrombin activation time of EV-rich plasma as a measure of EV's procoagulant activity.

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Article Synopsis
  • Traumatic brain injury (TBI) can cause damage not only to the brain but also to systemic organs, increasing the risk of death and disability.
  • Brain-derived extracellular vesicles (BDEVs), released from the injured brain, were found to induce harm to organs like the heart, lungs, liver, and kidneys by causing cell damage and dysfunction.
  • The study suggests that targeting and removing BDEVs from circulation may alleviate this secondary multi-organ damage caused by TBI.
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Article Synopsis
  • - The study focuses on microparticles (MPs) and their role in increasing blood clotting (hypercoagulability), leading to thrombosis, and introduces a new assay called the MPs-Activated Clotting Time (MPs-ACT) to measure this effect.
  • - The MPs-ACT assay was developed by analyzing the viscoelastic changes in MPs-rich plasma and correlating these changes with the concentration of MPs using techniques like flow cytometry and identifying clotting products.
  • - The findings suggest that MPs-ACT is reliable and sensitive for detecting hypercoagulable conditions, such as those seen in patients with pre-eclampsia, hip fractures, and lung tumors, indicating its potential use in diagnosing disorders related
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Traumatic brain injury often causes poor outcomes and has few established treatments. Neuroinflammation and ferroptosis hinder therapeutic progress in this domain. Annexin A5 (A5) has anticoagulant, anti-apoptotic and anti-inflammatory bioactivities.

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Brain induced extracellular vesicle (BDEV) elevates after traumatic brain injury (TBI) and contributes to secondary brain injury. However, the role of BDEV in TBI remains unclear. In this study, we determined the mechanisms of BDEV in brain injury and explored whether neuroprotective drug BKca channel opener NS1619 may attenuate BDEV-induced brain injury.

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Background And Purpose: Neuroinflammation has been shown to play a critical role in secondary craniocerebral injury, leading to poor outcomes for TBI patients. Abrocitinib, a Janus kinase1 (JAK1) selective inhibitor approved to treat atopic dermatitis (AD) by the Food and Drug Administration (FDA), possesses a novel anti-inflammatory effect. In this study, we investigated whether abrocitinib could ameliorate neuroinflammation and exert a neuroprotective effect in traumatic brain injury (TBI) models.

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Cerebral vasospasm is a frequently encountered clinical problem, especially in patients with traumatic brain injury and subarachnoid hemorrhage. Continued cerebral vasospasm can cause cerebral ischemia, even infarction and delayed ischemic neurologic deficits. It significantly affects the course of the disease and the outcome of the patient.

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Annexin A5 (ANXA5) exhibited potent antithrombotic, antiapoptotic, and anti-inflammatory properties in a previous study. The role of ANXA5 in traumatic brain injury (TBI)-induced intestinal injury is not fully known. Recombinant human ANXA5 (50 µg/kg) or vehicle (PBS) was administered to mice via the tail vein 30 min after TBI.

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Article Synopsis
  • Artificial enzymes are gaining attention in medicine and biotechnology due to their stability, simple production, and cost efficiency, but their effectiveness is limited by slow electron transfer rates.
  • The new oligomeric nanozyme (O-NZ) achieves incredibly fast electron transfer, resulting in significantly enhanced catalytic activity that matches natural enzymes in performance.
  • O-NZ has shown promising results in improving survival rates and cognitive recovery in mice after acute brain trauma by reducing harmful compounds and inflammation in the body.
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Natural enzymes are efficient and versatile biocatalysts but suffer in their environmental tolerance and catalytic stability. As artificial enzymes, nanozymes can improve the catalytic stability, but it is still a challenge to achieve high catalytic activity. Here, we employed atomic engineering to build the artificial enzyme named AuAg clusterzyme that hosts an ultrahigh catalytic activity as well as strong physiological stability via atom manipulation.

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Traumatic brain injury (TBI) is a sudden injury to the brain, accompanied by the production of large amounts of reactive oxygen and nitrogen species (RONS) and acute neuroinflammation responses. Although traditional pharmacotherapy can effectively decrease the immune response of neuron cells via scavenging free radicals, it always involves in short reaction time as well as rigorous clinical trial. Therefore, a noninvasive topical treatment method that effectively eliminates free radicals still needs further investigation.

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Traumatic brain injury frequently leads to serious mortality and physical disability, yet effective treatments remains insufficient. TBI always leads to a series of secondary brain injuries including neuronal apoptosis, continuous inflammation, endoplasmic reticulum stress, and disruption of the blood-brain barrier. Sartans that block angiotensin II type 1 receptors are strongly neuroprotective, neurorestorative and anti-inflammatory.

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Free radical-induced oxidative damage and nitrosative stress have been identified as key factors in neuroinflammation responses after traumatic brain injury (TBI), with which reactive oxygen and nitrogen species (RONS), especially nitrogen signaling molecules, are strongly associated. Here, we prepared ultrasmall carbon dot (CD) by using a simple and facile method. In vitro assessment experiments show that the antioxidative CD exhibits an ultrahigh target-scavenging effect for nitrogen signaling molecules, especially the highly reactive ˙NO and ONOO-.

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Objective: Mitochondrial dysfunction plays an essential role in secondary brain injury following traumatic brain injury (TBI). Interestingly, accumulating evidence has shown that therapeutic benefits of mitochondrial transplantation exist. Therefore, we hypothesized that the injection of exogenous mitochondria would contribute to the mitigation of cellular energy metabolism disorders and neurologic functions after TBI.

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Background And Purpose: Previous studies have identified many risk factors related to the recurrence of chronic subdural hematomas (CSDHs). Among these factors, there may be deviations in measuring the midline shift, preoperative hematoma volume (PreHV), postoperative hematoma residual volume, and postoperative pneumocephalus in bilateral CSDHs. The aims of this study were to eliminate the impact of complicated situations on parameter measurement and to identify actual predictors for CSDH recurrence, and finally, to develop a grading system to predict unilateral CSDH (uCSDH) recurrence.

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To investigate whether methylene blue (MB) treatment can reverse neuronal mitochondrial dysfunction caused by oxygen glucose deprivation/reoxygenation (OGD) injury and then investigate whether MB treatment can reduce neuronal apoptosis and improve blood-brain barrier (BBB) integrity in traumatic brain injury (TBI) animals. Reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and adenosine triphosphate (ATP) were used to evaluate mitochondrial function. The terminal deoxynucleotidyl transferase-dUTP nick end labeling (TUNEL) assay was used to assess neuronal apoptosis .

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Neurotrauma is one of the most serious traumatic injuries, which can induce an excess amount of reactive oxygen and nitrogen species (RONS) around the wound, triggering a series of biochemical responses and neuroinflammation. Traditional antioxidant-based bandages can effectively decrease infection preventing oxidative stress, but its effectiveness is limited to a short period of time due to the rapid loss of electron-donating ability. Herein, we developed a nanozyme-based bandage using single-atom Pt/CeO with a persistent catalytic activity for noninvasive treatment of neurotrauma.

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BACKGROUND Research on microparticles is rapidly evolving and has extended to the field of many diseases. It is unclear whether microparticles can be stored frozen. In this study, our goal was to verify whether cryopreservation had an effect on the properties of the microparticles.

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We performed a meta-analysis to systematically assess the efficacy and safety of intravenous tranexamic acid in revision total hip arthroplasty. Potential academic articles were identified from Cochrane Library, Medline, PubMed, EMBASE, ScienceDirect and other databases. The time range we retrieved from was that from the inception of electronic databases to February 2019.

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Reactive oxygen and nitrogen species (RONS), especially reactive nitrogen species (RNS) are intermediate products during incidence of nervous system diseases, showing continuous damage for traumatic brain injury (TBI). Here, we developed a carbogenic nanozyme, which shows an antioxidant activity 12 times higher than ascorbic acid (AA) and behaves as multienzyme mimetics. Importantly, the nanozyme exhibits an ultrahigh scavenging efficiency (∼16 times higher than AA) toward highly active RNS, such as NO and ONOO as well as traditional reactive oxygen species (ROS) including O, HO, and OH.

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Background: Most patients with bilateral chronic subdural hematomas (bCSDH) undergo initial bilateral evacuation. Risk factors associated with the recurrence of bCSDH after initial bilateral evacuation have not been published to date. In this study, we aimed to identify risk factors related to recurrence of bCSDH after initial bilateral evacuation, and to develop a prognostic grading system for clinical reference.

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Objective: The purpose of this study was to conduct a meta-analysis to identify the risk factors for formation of venous thromboembolism (VTE) in patients after spine surgery.

Methods: This study retrieved potential academic articles on the related factors for VTE formation in patients after spine surgery from MEDLINE, PubMed, EMBASE, and the Cochrane Library. The reference articles for the identified studies were carefully reviewed to ensure that all available documents were represented in the study.

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