TAX1BP1/A20 inhibited TLR2-NF-κB activation to induce tolerant expression of IL-6 in endothelial cells.

The inflammatory cascadedriven by interleukin-6 (IL-6) plays a crucial role in the initiation and progression of chronic inflammatory conditions such as atherosclerosis. Research has demonstrated that prolonged exposure to inflammatory stimuli leads to the development of "immune tolerance" in specialized immune cells such as monocytes and macrophages, serving as a mechanism to prevent tissue damage and curb the inflammatory cascade. However, our recent investigation revealed that immune tolerance did not effectively regulate the production of IL-6 in human umbilical vein endothelial cells (HUVECs) when stimulated by a Toll-like receptor 2 (TLR2) ligand Pam3CSK4, which is a potent activator of the pro-inflammatory transcription factor NF-κB.

Proteasome activation is critical for cell death induced by inhibitors of polo-like kinase 1 (PLK1) in multiple cancers.

Inhibitors of polo-like kinase (PLK) are currently being evaluated as anticancer drugs. However, the molecular mechanism of PLK inhibitor-induced cell death is not fully understood. In this study, we found that GW843682X and BI2536, two inhibitors of PLK1, significantly induced cell death in multiple type cells.

STAT3 promotes cytoplasmic-nuclear translocation of RNA-binding protein HuR to inhibit IL-1β-induced IL-8 production.

Signal transducer and activator of transcription 3 (STAT3) functions to regulate inflammation and immune response, but its mechanism is not fully understood. We report here that STAT3 inhibitors Stattic and Niclosamide up-regulated IL-1β-induced IL-8 production in C33A, CaSki, and Siha cervical cancer cells. As expected, IL-1β-induced IL-8 production was also up-regulated through the molecular inhibition of STAT3 by use of CRISPR/Cas9 technology.

Relationship between serum uric acid levels and the outcome of STN-DBS in Parkinson's disease.

Background: Uric acid is a natural antioxidant and it has been shown that low levels of uric acid may be a risk factor for the development of Parkinson's disease. We aimed to investigate the relationship between uric acid and improvement of motor symptoms in patients with Parkinson's disease after subthalamic nucleus deep brain stimulation.

Methods: We analyzed the correlation between serum uric acid levels in 64 patients with Parkinson's disease and the rate of improvement of motor symptoms 2 years after subthalamic nucleus deep brain stimulation.

Physiological and transcriptional effects in the male western mosquitofish (Gambusia affinis) following exposure to dexamethasone.

Dexamethasone (DEX) is a synthetic glucocorticoid widely found in a variety of aquatic environments and has potential adverse effects on aquatic organisms. This study was to assess the toxic effects of exposure to different concentrations (0, 5 and 50 μg/L) of DEX for 60 days on adult male mosquitofish (Gambusia affinis). Morphological analyses of skeleton and anal fin, histological effects of testes and livers, and transcriptional expression levels of genes related to reproductive and immune system were determined.

Development and Validation of a Prediction Model for Anxiety Improvement after Deep Brain Stimulation for Parkinson Disease.

Background: Parkinson's disease (PD) represents one of the most frequently seen neurodegenerative disorders, while anxiety accounts for its non-motor symptom (NMS), and it has greatly affected the life quality of PD cases. Bilateral subthalamic nucleus deep brain stimulation (STN-DBS) can effectively treat PD. This study aimed to develop a clinical prediction model for the anxiety improvement rate achieved in PD patients receiving STN-DBS.

Prediction of STN-DBS for Parkinson's disease by uric acid-related brain function connectivity: A machine learning study based on resting state function MRI.

Introduction: Parkinson's disease (PD) is a neurodegenerative disorder characterized by dyskinesia and is closely related to oxidative stress. Uric acid (UA) is a natural antioxidant found in the body. Previous studies have shown that UA has played an important role in the development and development of PD and is an important biomarker.

LCS-1 inhibition of superoxide dismutase 1 induces ROS-dependent death of glioma cells and degradates PARP and BRCA1.

Gliomas are characterized by high morbidity and mortality, and have only slightly increased survival with recent considerable improvements for treatment. An innovative therapeutic strategy had been developed inducing ROS-dependent cell death by targeting antioxidant proteins. In this study, we found that glioma tissues expressed high levels of superoxide dismutase 1 (SOD1).

Nomogram for Predicting Depression Improvement after Deep Brain Stimulation for Parkinson's Disease.

Background: Parkinson's disease is a common neurodegenerative disease, with depression being a common non-motor symptom. Bilateral subthalamic nucleus deep brain stimulation is an effective method for the treatment of Parkinson's disease. Thus, this study aimed to establish a nomogram of the possibility of achieving a better depression improvement rate after subthalamic nucleus deep brain stimulation in patients with Parkinson's disease.

A New Application of Functional Zonal Image Reconstruction in Programming for Parkinson's Disease Treated Using Subthalamic Nucleus-Deep Brain Stimulation.

Objective: Programming plays an important role in the outcome of deep brain stimulation (DBS) for Parkinson's disease (PD). This study introduced a new application for functional zonal image reconstruction in programming.

Methods: Follow-up outcomes were retrospectively compared, including first programming time, number of discomfort episodes during programming, and total number of programming sessions between patients who underwent image-reconstruction-guided programming and those who underwent conventional programming.

Nomogram to Predict Cognitive State Improvement after Deep Brain Stimulation for Parkinson's Disease.

Purpose: Parkinson's disease (PD) is a common neurodegenerative disease, for which cognitive impairment is a non-motor symptom (NMS). Bilateral subthalamic nucleus deep brain stimulation (STN-DBS) is an effective treatment for PD. This study established a nomogram to predict cognitive improvement rate after STN-DBS in PD patients.

Bilateral Globus Pallidus Interna Combined With Subthalamic Nucleus Variable Frequency Deep Brain Stimulation in the Treatment of Young-Onset Parkinson's Disease With Refractory Dyskinesia: A Case Report.

Main motor characteristics in Parkinson's disease (PD) include bradykinesia, rigidity, and tremors. With the development of neuromodulation techniques, it has become possible to use deep brain stimulation (DBS) to control the symptoms of PD. However, since the subthalamic nucleus(STN) and globus pallidus interna (GPi) DBS have their own advantages and disadvantages, it is difficult to control symptoms of the patients.

Proteasome inhibitors decrease paclitaxel‑induced cell death in nasopharyngeal carcinoma with the accumulation of CDK1/cyclin B1.

Southeast Asia is a region with high incidence of nasopharyngeal carcinoma (NPC). Paclitaxel is the mainstay for the treatment of advanced nasopharyngeal cancer. The present study investigated the effect of proteasome inhibitors on the therapeutic effect of paclitaxel and its related mechanism.

A Novel Biological Activity of the STAT3 Inhibitor Stattic in Inhibiting Glutathione Reductase and Suppressing the Tumorigenicity of Human Cervical Cancer Cells via a ROS-Dependent Pathway.

Introduction: Glutathione reductase (GSR) provides reduced glutathione (GSH) to maintain redox homeostasis. Inhibition of GSR disrupts this balance, resulting in cell damage, which benefits cancer therapy. However, the effect of GSR inhibition on the tumorigenicity of human cervical cancer is not fully understood.

miR-543 in human mesenchymal stem cell-derived exosomes promotes cardiac microvascular endothelial cell angiogenesis after myocardial infarction through COL4A1.

To explore the impact and mechanism of human mesenchymal stem cells (hMSCs) on the angiogenesis of cardiac microvascular endothelial cells (CMECs) after ischemia insult. Exosomes derived from hMSCs (hMSCs-Exo) were identified by Western blotting and labeled by PHK-67. CMECs were isolated from rat myocardial tissues.

Pharmacological inhibition of GSK3 promotes TNFα-induced GM-CSF via up-regulation of ERK signaling in nasopharyngeal carcinoma (NPC).

Granulocyte-macrophage colony stimulating factor (GM-CSF) functions to drive nasopharyngeal cancer (NPC) metastasis via recruitment and activation of macrophages. However, the source and the regulation of GM-CSF in tumor microenvironment of NPC are not fully understood. In this study, we found that TNFα induced GM-CSF production in NPC CNE1, CNE2, and 5-8F cells in time- and dose-dependent manners.

Recurrent mutations in ALK-negative anaplastic large cell lymphoma.

Anaplastic large cell lymphomas (ALCLs) represent a relatively common group of T-cell non-Hodgkin lymphomas (T-NHLs) that are unified by similar pathologic features but demonstrate marked genetic heterogeneity. ALCLs are broadly classified as being anaplastic lymphoma kinase (ALK) or ALK, based on the presence or absence of rearrangements. Exome sequencing of 62 T-NHLs identified a previously unreported recurrent mutation in the musculin gene, , exclusively in ALK ALCLs.

IL-1α and IL-1β promote NOD2-induced immune responses by enhancing MAPK signaling.

Both toll-like receptors (TLRs) and nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) induce a tightly regulated inflammatory response at risk of causing tissue damage, depending on the effectiveness of ensuing negative feedback regulatory mechanisms. Cross-regulation between TLRs, NLRs, and cytokine receptors has been observed. However, the cross-regulation between interleukin-1 (IL-1) receptors and NOD2 is not completely understood.

The activation of Toll-like receptor 4 reverses tumor differentiation in human glioma U251 cells via Notch pathway.

Toll-like receptors (TLRs) are closely related to cancer. However, the mechanism for TLR regulation of cancer is not fully understood. Our previous studies demonstrated that toll-like receptor (TLR) 4 functions to maintain the un-differential stem cell phenotypes of human endothelial progenitor cells.

TNFα induces tolerant production of CXC chemokines in colorectal cancer HCT116 cells via A20 inhibition of ERK signaling.

Ubiquitin editing enzyme A20 functions as a tumor suppressor in various cancer. However, the mechanism for A20 regulation of cancer progress is not fully understood. In this study, we found that in human colorectal cancer HCT116 cells, TNFα induced a tolerant production of CXC chemokines, including CXCL1, 2, and 8 in a dose and time dependent manner.

TNF-α-Induced NOD2 and RIP2 Contribute to the Up-Regulation of Cytokines Induced by MDP in Monocytic THP-1 Cells.

Nucleotide-binding oligomerization domain containing 2 (NOD2)-induced signal transduction and cytokine production is regulated by a number of factors. However, the feedback effect of the pro-inflammatory TNF-α on NOD2-induced inflammation is not fully understood. In this study, we found unexpectedly that TNF-α up-regulated NOD2 ligand MDP-induced production of the CXC chemokines, including CXCL1, 2, and 8, and the pro-inflammatory cytokines, including IL-1β, IL-6, and TNF-α, in a dose-dependent manner at both mRNA and protein levels in monocytic THP-1 cells.

Lymphoma classification update: B-cell non-Hodgkin lymphomas.

Lymphomas are classified based on the normal counterpart, or cell of origin, from which they arise. Because lymphocytes have physiologic immune functions that vary both by lineage and by stage of differentiation, the classification of lymphomas arising from these normal lymphoid populations is complex. Recent genomic data have contributed additional complexity.

Lymphoma classification update: T-cell lymphomas, Hodgkin lymphomas, and histiocytic/dendritic cell neoplasms.

Lymphomas are classified based on the normal counterpart, or cell of origin, from which they arise. Because lymphocytes have physiologic immune functions that vary both by lineage and by stage of differentiation, the classification of lymphomas arising from these normal lymphoid populations is complex. Recent genomic data have contributed additional depth to this complexity.

Oleanolic acid ameliorates high glucose-induced endothelial dysfunction via PPARδ activation.

Oleanolic acid (3β-hydroxyolean-12-en-28-oic acid, OA) is a pentacyclic triterpenes widely distributed in food, medicinal plants and nutritional supplements. OA exhibits various pharmacological properties, such as hepatoprotective and anti-tumor effects. In this study, we analyzed the effect of OA on endothelial dysfunction induced by high glucose in human vascular endothelial cells (ECs).