Association between C-reactive protein-triglyceride glucose index and depressive symptoms in American adults: results from the NHANES 2005 to 2010.

Background: The novel serum C-reactive protein-triglyceride glucose index (CTI) has been identified as an ideal parameter that integrates inflammation and insulin resistance, which are potential mechanisms underlying depressive symptoms. Our research aimed to investigate the association between CTI and depressive symptoms.

Methods: Our cross-sectional investigation utilized data from the National Health and Nutrition Examination Survey conducted between 2005 and 2010.

UCHL3 induces radiation resistance and acquisition of mesenchymal phenotypes by deubiquitinating POLD4 in glioma stem cells.

Background: The high degree of intratumoral genomic heterogeneity is a major obstacle for glioblastoma (GBM) tumors, one of the most lethal human malignancies, and is thought to influence conventional therapeutic outcomes negatively. The proneural-to-mesenchymal transition (PMT) of glioma stem cells (GSCs) confers resistance to radiation therapy in glioblastoma patients. POLD4 is associated with cancer progression, while the mechanisms underlying PMT and tumor radiation resistance have remained elusive.

E2F1-regulated USP5 contributes to the tumorigenic capacity of glioma stem cells through the maintenance of OCT4 stability.

Mesenchymal glioma stem cells (MES GSCs) are a subpopulation of cells in glioblastoma (GBM) that contribute to a worse prognosis owing to their highly aggressive nature and resistance to radiation therapy. Here, OCT4 is characterized as a critical factor in sustaining the stemness phenotype of MES GSC. We find that OCT4 is expressed intensively in MES GSC and is intimately associated with poor prognosis, moreover, OCT4 depletion leads to diminished invasive capacity and impairment of the stem phenotype in MES GSC.

Endoscopic Far-Lateral Supracerebellar Infratentorial Approach for Petroclival Region Meningioma: Surgical Technique and Clinical Experience.

Background: The management of petroclival region meningioma remains the ultimate achievement in neurosurgery, because of the formidable technical challenges involved.

Objective: To describe the technique and feasibility of the purely endoscopic far-lateral supracerebellar infratentorial approach (EF-SCITA) for the treatment of petroclival region meningiomas.

Methods: We reviewed the clinical data of 10 consecutive cases of petroclival region meningiomas treated with the EF-SCITA from August 2018 to August 2020.

Downregulation of Tim-1 inhibits the proliferation, migration and invasion of glioblastoma cells via the miR-133a/TGFBR1 axis and the restriction of Wnt/β-catenin pathway.

Background: Glioblastoma remains one of the most lethal brain cancers. T-cell immunoglobulin and mucin domain 1 (Tim-1) is associated with various immune diseases. The molecular mechanism of Tim-1 in regulating glioblastoma cell proliferation, invasion, and migration is still unknown.

A novel antitumor peptide inhibits proliferation and migration and promotes apoptosis in glioma cells by regulating the MKK6/p38 signaling pathway.

Protein- or peptide-based therapeutics have emerged as an innovative strategy for the treatment of cancer. Our previous research demonstrated that tripartite motif 9 short isoform (TRIM9s) is a tumor suppressor in glioma. In this report, we investigated whether a new peptide derived from TRIM9s, named T9sP, inhibits glioma progression and determined the possible molecular mechanism.

Long non-coding RNA SUMO1P3 promotes tumour progression by regulating cell proliferation and invasion in glioma.

Gliomas account for 50% of primary brain tumours in the central nervous system. Small ubiquitin-like modifier 1 pseudogene 3 (SUMO1P3), a newly identified long non-coding RNA (lncRNA), serves an oncogenic role in various types of cancer. The aim of the present study was to investigate the effect of SUMO1P3 on glioma progression.

Inhibition of Cathepsin S Restores TGF-β-induced Epithelial-to-mesenchymal Transition and Tight Junction Turnover in Glioblastoma Cells.

Invasive growth is one of the most typical features of aggressive types of malignant cancer, including glioblastoma. Lysosomal cysteine protease-cathepsin S (CTSS), has been reported to be involved in invasive growth and distant metastasis of cancer cells. However, the underlying mechanisms remained elusive.

δ-opioid receptor activation protects against Parkinson's disease-related mitochondrial dysfunction by enhancing PINK1/Parkin-dependent mitophagy.

Our previous studies have shown that the δ-opioid receptor (DOR) is an important neuroprotector via the regulation of PTEN-induced kinase 1 (PINK1), a mitochondria-related molecule, under hypoxic and MPP insults. Since mitochondrial dysfunctions are observed in both hypoxia and MPP insults, this study further investigated whether DOR is cytoprotective against these insults by targeting mitochondria. Through comparing DOR-induced responses to hypoxia versus MPP-induced parkinsonian insult in PC12 cells, we found that both hypoxia and MPP caused a collapse of mitochondrial membrane potential and severe mitochondrial dysfunction.

Familial Tuberculum Sellae Meningiomas.

Objectives: The aim of this study was to study and explore the genetic mechanism of familial meningiomas through 3 cases of familial tuberculum sellae meningioma.

Methods: A retrospective analysis of clinical data of 3 cases of familial tuberculum sellae meningioma patients, and the pathological results of types and immunohistochemical results of the 3 patients were compare.

Reults: Three cases of postoperative pathology were meningiomas (mixed type), immunohistochemical examination showed that Vimentin, epithelial membrain antigen , and Ki67 were positive.

p62 acts as an oncogene and is targeted by miR-124-3p in glioma.

Background: Glioma is the most common central nervous system (CNS) tumour. p62, an important autophagy adaptor, plays a crucial role in cancer. However, the role of p62 in the progression of glioma is poorly characterized.

Luteolin suppresses tumor proliferation through inducing apoptosis and autophagy via MAPK activation in glioma.

Purpose: Glioma is a malignant tumor that originates in the brain and spine and is difficult to be completely removed. Though glioma patients receive active treatment, the survival rate is still poor. Therefore, it is urgent to discover a new medicine to treat glioma patients in order to improve the survival rate.

Carnosic acid potentiates the anticancer effect of temozolomide by inducing apoptosis and autophagy in glioma.

Objective: Malignant glioma is a lethal brain tumor with a low survival rate and poor prognosis. New strategies are urgently needed to augment the chemotherapeutic effects of temozolomide (TMZ), the standard drug in glioma treatment. Carnosic acid (CA) has been reported to have anticancer, antioxidant and anti-infectious properties.

miR-454-3p Is an Exosomal Biomarker and Functions as a Tumor Suppressor in Glioma.

Glioma is the most common type of primary malignant brain tumor in adults. Our previous work discovered that plasma miR-454-3p may have some advantages in glioma prognosis, but the clinical significance and the regulatory mechanism of miR-454-3p in glioma have not been systematically investigated, especially regarding the relationship between circulating and tissue miR-454-3p. The expression level of miR-454-3p in glioma serum and tissues was analyzed through quantitative real-time PCR (qRT-PCR).

MicroRNA-29a-3p Downregulation Causes Gab1 Upregulation to Promote Glioma Cell Proliferation.

Background/aims: Glioma causes significant human mortalities annually. Molecularly-targeted therapy is a focus of glioma research.

Methods: Grb2-associated binding 1 (Gab1) expression and microRNA-29a-3p ("miR-29a-3p") expression in human glioma cells and tissues were tested by Western blotting assay and qRT-PCR assay.

δ-Opioid Receptor Activation Attenuates Hypoxia/MPP-Induced Downregulation of PINK1: a Novel Mechanism of Neuroprotection Against Parkinsonian Injury.

There is emerging evidence suggesting that neurotoxic insults and hypoxic/ischemic injury are underlying causes of Parkinson's disease (PD). Since PTEN-induced kinase 1 (PINK1) dysfunction is involved in the molecular genesis of PD and since our recent studies have demonstrated that the δ-opioid receptor (DOR) induced neuroprotection against hypoxic and 1-methyl-4-phenyl-pyridimium (MPP) insults, we sought to explore whether DOR protects neuronal cells from hypoxic and/or MPP injury via the regulation of PINK1-related pathways. Using highly differentiated rat PC12 cells exposed to either severe hypoxia (0.

The long non-coding RNA SNHG14 inhibits cell proliferation and invasion and promotes apoptosis by sponging miR-92a-3p in glioma.

Malignant glioma is one of the most common types of primary brain tumours. Long non-coding RNAs (lncRNAs) have recently emerged as a new class of therapeutic targets for many cancers. In this study, we aimed to explore the functional involvement of small nucleolar RNA host gene 14 (SNHG14) and its potential regulatory mechanism in glioma progression.

Evodiamine activates cellular apoptosis through suppressing PI3K/AKT and activating MAPK in glioma.

Background: Glioblastoma multiforme (GBM) is the most malignant primary tumor of the central nervous system and is associated with a very poor prognosis. No further improvements in outcomes have been reported since radiotherapy-temozolomide therapy was introduced. Therefore, developing new agents to treat GBM is important.

Characteristic MicroRNA Expression Induced by δ-Opioid Receptor Activation in the Rat Liver Under Prolonged Hypoxia.

Background/aims: Hypoxic/ischemic injury to the liver is a frequently encountered clinical problem with limited therapeutic options. Since microRNAs (miRNAs) are involved in hypoxic/ ischemic events, and δ-opioid receptor (DOR) is protective against hypoxic/ischemic injury, we asked if pharmacological activation of DOR can alter hypoxic events by regulating miRNA expression in the liver. As the first step, the present work aimed at testing the effect of DOR activation on hepatic miRNA expression in hypoxia.

Carnosic acid prevents dextran sulfate sodium-induced acute colitis associated with the regulation of the Keap1/Nrf2 pathway.

Crohn's disease and ulcerative colitis are inflammatory bowel diseases (IBDs) with high prevalence in humans. Carnosic acid (CA) has been reported to possess antioxidative properties; however, its role in IBDs has not been determined. In the present study, we found that CA significantly prevented the loss of body weight and shortening of colon length in acute colitis induced by dextran sodium sulfate (DSS).

Intra-Arterial Treatment for Patients with Severe Acute Vertebrobasilar Occlusion: A Single-Center Retrospective Study.

Background: Recently, favorable outcomes from several randomized controlled trials of rapid endovascular treatment for acute ischemic stroke has emerged.

Objective: The aim of this retrospective study is to present our clinical experience in severe acute vertebrobasilar occlusion (AVBO) using intra-arterial treatment (IAT).

Methods: Twenty patients with ischemic stroke in the vertebrobasilar circulation treated by IAT between March 2011 and December 2014 were included.