Publications by authors named "Guo-biao Liang"

Background: Neuropathic pain (NP) takes a heavy toll on individual life quality, yet gaps in its molecular characterization persist and effective therapy is lacking. This study aimed to provide comprehensive knowledge by combining transcriptomic and proteomic data of molecular correlates of NP in the anterior cingulate cortex (ACC), a cortical hub responsible for affective pain processing.

Methods: The NP model was established by spared nerve injury (SNI) in Sprague-Dawley rats.

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Soluble epoxide hydrolase (sEH) serves as a potential target in inflammation-related diseases. Based on the bioactivity-guided separation, a new sesquiterpenoid inulajaponoid A (1) was isolated from Inula japonica with a sEH inhibitory effect, together with five known compounds, such as 1-O-acetyl-6-O-isobutyrylbritannilactone (2), 6β-hydroxytomentosin (3), 1β,8β-dihydroxyeudesma-4(15),11(13)-dien-12,6α-olide (4), (4S,6S,7S,8R)-1-O-acetyl-6-O-(3-methylvaleryloxy)-britannilactone (5), and 1-acetoxy-6α-(2-methylbutyryl)eriolanolide (6). Among them, compounds 1 and 6 were assigned as mixed and uncompetitive inhibitors, respectively.

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Prostate cancer (PCa) has become one of the most common malignancies in men, and its incidence is increasing year by year in China. When PCa develops into castration-resistant PCa (CRPC), it deteriorates rapidly. So, it is important to find more sensitive molecular markers and effective therapeutic targets for the diagnosis and treatment of the malignancy.

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We assessed the use of common urodynamics (CUD) combined with contrast-enhanced ultrasound (CEUS) to investigate the efficacy and durability of sigmoid cystoplasty alone in patients with low bladder compliance associated with vesicoureteric reflux (VUR). In this study, we recruited 25 patients with low bladder compliance and VUR who underwent bladder augmentation without antireflux surgery at our institutions between June 2017 and June 2021. The bladder condition and VUR grade were assessed preoperatively and postoperatively via CUD combined with CEUS.

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The previous three decades have witnessed a prosperity of contralateral C7 nerve (CC7) transfer in the treatment of upper-extremity paralysis induced by both brachial plexus avulsion injury and central hemiplegia. From the initial subcutaneous route to the pre-spinal route and the newly-established post-spinal route, this surgical operation underwent a series of innovations and refinements, with the aim of shortening the regeneration distance and even achieving direct neurorrhaphy. Apart from surgical efforts for better peripheral nerve regeneration, brain involvement in functional improvements after CC7 transfer also stimulated scientific interest.

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To explore the effects of anxiety and depression on the self-management ability and endogenous creatinine clearance rate of renal transplant patients. Eighty-eight renal transplant recipients who were followed up in the outpatient clinic of the Affiliated Hospital of Zunyi Medical University were selected using convenient sampling. The self-made general data sheet, Self-Rating Anxiety Scale, Self-Rating Depression Scale, and Self-Management Scale for Kidney Transplant Recipients were used.

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Sterile-20-like mitogen-activated protein kinase kinase kinase kinase 4 (MAP4K4) is expressed in endothelial cells and activates inflammatory vascular damage. Endothelial cells are important components of the blood-brain barrier. To investigate whether MAP4K4 plays a role in the pathophysiology of subarachnoid hemorrhage, we evaluated the time-course expression of MAP4K4 after subarachnoid hemorrhage.

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The formation of intracranial aneurysm (IA) is associated with the destruction of various cellular and structural components, which induces pathogenic inflammatory responses that further propagate tissue damage. The regulatory immune system can suppress exacerbated inflammation and offer tissue protection; however, previous studies by others and us have demonstrated that the regulatory T (Treg) cells were functionally impaired in IA patients. Hence, strategies that can improve Treg function in IA patients should be investigated.

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Pathogenic inflammation contributes to aneurysm formation by mediating the destruction of the endothelium and the extracellular matrix and promoting pathogenic proliferation of smooth muscle cells. In mouse models, tolerance-inducing T regulatory (Treg) cells could significantly reduce the incidence and severity of aneurysms. Hence, it should be investigated why in human intracranial aneurysm (IA) patients, Treg cells failed to provide protection against aneurysm formation.

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Patients with intracranial aneurysm (IA) present a dysregulated immune system with lower frequency of regulatory T (Treg) cells. Here, we examined whether galectin 9 (Gal-9), the natural ligand of Tim-3, could promote Treg cells in IA patients. We first discovered that the intracellular and extracellular Gal-9 was primarily expressed by CD4 CD25 T conventional (Tconv) cells, and also by monocytes at lower levels, but rarely by CD4 CD25 Treg cells.

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Objective: To evaluate the clinical value of minimally invasive stereotactic puncture therapy (MISPT) combined with external ventricular drainage (EVD) on secondary intraventricular hemorrhage (SIVH).

Methods: A retrospective analysis of the patients of intraventricular hemorrhage from May 2013 to January 2015 was conducted in our hospital, according to the enrollment criterion; of which 40 patients were treated by MISPT combined with EVD (ME group) and 45 patients by conventional craniotomy combined with EVD (CE group). Related indicators were compared in the two groups of patients with short- and long-term efficacy.

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BACKGROUND Ischemia-reperfusion injury (IRI) is a clinically common pathologic process defined as the inability to improve neuronal function. This study aimed to investigate the pathological mechanism of IRI and to explore effects of hyperbaric oxygenation (HBO) on autophagy and inflammatory response in IRI. MATERIAL AND METHODS Ninety Sprague-Dawley (SD) rats were randomly divided into a Sham group, a kidney transplant group (Trans), and a kidney transplant plus HBO treatment group (Trans+HBO).

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Intracranial aneurysms (IAs) and potential IA rupture are one of the direct causes of permanent brain damage and mortality. Interestingly, the major risk factors of IA development, including hemodynamic stress, hypertension, smoking, and genetic predispositions, are closely associated with a proinflammatory immune status. Therefore, we examined the roles of CD4(+) T cells in IA pathogenesis.

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Chronic allograft nephropathy (CAN) is a major cause of graft loss following kidney transplantation and may result from the interactions of various immune and non-immune factors. The aim of the present study was to establish an in vitro model of glomerular mesangial cell injury in order to examine the gene expression levels of indoleamine 2,3-dioxygenase (IDO), heme oxygenase-1 (HO-1) and interleukin-7 (IL-7) in mesangial cells during the healing process as well as to investigate the effects of various immunosuppressants on the expression of these genes. The HBZY-1 glomerular mesangial cell line was pre-treated in vitro with cytochalasin B for 2 h to induce reversible damage.

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Evidence has shown that inflammation acts as a critical contributor to the pathogenesis of intracranial aneurysm (IA), a potentially devastating clinical problem. T cell immunoglobulin and mucin protein 3 (Tim-3) is a negative regulatory molecule and plays important roles in the inflammation process. In the current study, we investigated the expression of Tim-3 and its correlation with tumor necrosis factor alpha (TNF-α) in IA patients.

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β-elemene, a plant-derived drug extracted from Curcuma wenyujin, has demonstrated marked antiproliferative effects on glioblastoma, while toxicity remains low. However, the underlying molecular mechanisms of the antitumor activity of β-elemene remain to be elucidated. Previously, it was identified that the glia maturation factor β (GMFβ)/mitogen-activated protein kinase kinase (MAPK) 3/6/p38 pathway participates in the antiproliferative activity of β-elemene on glioblastoma.

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Accumulating evidence indicates that glioblastoma stem-like cells (GSCs) are key factors in tumour development, recurrence and chemoresistance. The impairment of stemness and the enhancement of differentiation contributes to the weakening of radiation and chemotherapy resistance of GSCs. We previously found that β-elemene was an effective anti-glioblastoma agent and chemosensitizer.

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The key signaling networks regulating glioma cell proliferation remain poorly defined. The leucine-rich repeat containing G-protein coupled receptor 4 (Lgr4) has been implicated in intestinal, gastric, and epidermal cell functions. We investigated whether Lgr4 functions in glioma cells and found that Lgr4 expression was significantly increased in glioma tissues.

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In this report, we describe an efficient and non-enzymatic method for isolating and culturing endothelial cells (ECs) from the nidus of surgically resected arteriovenous malformation (AVM) specimens. These cultured cells possessed typical phenotypic markers (i.e.

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Intracranial aneurysm (IA) lingers as a potentially devastating clinical problem, in which inflammation acts as a critical contributor to the pathogenesis of this disease. Cytokines play a major role in regulating inflammation. The aim of this study was to gain insight in the inflammatory response in IA by assessing plasma cytokine profiles.

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Aims: The MS-275 is a selective inhibitor of class I histone deacetylases (HDACs), which has been reported as a potential strategy in some central nervous system diseases associated with neurodegeneration and disturbed learning. However, its role in traumatic brain injury is not well defined. In this study, we examined the behavioral-cognitive performance as well as histology outcome in adult rats to evaluate whether postinjury administration of MS-275 (15 and 45 mg/kg) would provide neuroprotection benefits and ameliorate cognitive deficits following fluid percussion injury.

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The study was performed to investigate the effect of combination therapy with melatonin and dexamethasone (DEX) on brain injury in intracerebral hemorrhage (ICH) model in rats. Compared to the control group, combination therapy group with melatonin (10 mg/kg) and DEX (0.025 mg/kg) significantly reduced the degree of (1) brain edema, (2) the permeability of blood brain barrier (measured by Evans blue), (3) Oxidative stress (evaluated by malondialdehyde assay), (4) cytokines expression (tumor necrosis factor-alpha and interleukin-1beta), and (5) apoptosis (measured by Bax and Bcl-2 expression).

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