Targeting nucleus pulposus cell death in the treatment of intervertebral disc degeneration.

Background: Intervertebral disc degeneration (IDD) is a progressive age-related disorder characterized by the reduction in the number of nucleus pulposus cells (NPCs) and degradation of extracellular matrix (ECM), thereby leading to chronic pain and disability. The pathogenesis of IDD is multifaceted, and current therapeutic strategies remain limited. The nucleus pulposus (NP), primarily composed of NPCs, proteoglycans, and type II collagen, constitutes essential components for maintaining intervertebral disc (IVD) function and spinal motion.

Therapeutic targets and potential delivery systems of melatonin in osteoarthritis.

Osteoarthritis (OA) is a highly prevalent age-related musculoskeletal disorder that typically results in chronic pain and disability. OA is a multifactorial disease, with increased oxidative stress, dysregulated inflammatory response, and impaired matrix metabolism contributing to its onset and progression. The neurohormone melatonin, primarily synthesized by the pineal gland, has emerged as a promising therapeutic agent for OA due to its potential to alleviate inflammation, oxidative stress, and chondrocyte death with minimal adverse effects.

The research landscape of oxidative stress in osteoarthritis from 1998 to 2021: a systematic bibliometric analysis.

Objective: A substantial body of literature pertaining to oxidative stress in osteoarthritis (OA) has been published over the past few decades. However, a comprehensive systematic analysis in this field is currently lacking. The objective of this study was to perform a bibliometric analysis to visualize the current research hotspots and evolving trends associated with oxidative stress in OA, in order to contribute to a more comprehensive understanding of this field.

Epithelial SIRT6 governs IL-17A pathogenicity and drives allergic airway inflammation and remodeling.

Dysregulation of IL-17A is closely associated with airway inflammation and remodeling in severe asthma. However, the molecular mechanisms by which IL-17A is regulated remain unclear. Here we identify epithelial sirtuin 6 (SIRT6) as an epigenetic regulator that governs IL-17A pathogenicity in severe asthma.

Identification of EGFR as an essential regulator in chondrocytes ferroptosis of osteoarthritis using bioinformatics, , and study.

Objective: The mechanisms of chondrocytes ferroptosis in osteoarthritis (OA) have not yet been fully elucidated. This study aimed to identify key ferroptosis related genes (FRGs) involved in chondrocytes ferroptosis.

Methods: LASSO, SVM-RFE, and receiver operating characteristic curve (ROC) were performed to screen key differentially expressed FRGs (DEFRGs).

The HDAC10 instructs macrophage M2 program via deacetylation of STAT3 and promotes allergic airway inflammation.

Perturbation of macrophage homeostasis is one of the key mechanisms of airway inflammation in asthma. However, the exact mechanisms remain poorly understood. We sought to examine the role of histone deacetylase (HDAC) 10 as an epigenetic regulator that governs macrophage M2 program and promotes airway inflammation in asthma, and to elucidate the underlying mechanisms.

Myeloid-Specific SIRT6 Deletion Protects Against Particulate Matter (PM)-Induced Airway Inflammation.

Purpose: Particulate matter (PM) is a common risk factor for airway inflammation. Alveolar macrophages play a critical role in airway inflammation. Sirtuin 6 (SIRT6) is a class Ill histone deacetylase that exerts an anti-inflammatory effect in airway diseases.

A glycometabolic gene signature associating with immune infiltration and chemosensitivity and predicting the prognosis of patients with osteosarcoma.

Background: Accumulating evidence has suggested that glycometabolism plays an important role in the pathogenesis of tumorigenesis. However, few studies have investigated the prognostic values of glycometabolic genes in patients with osteosarcoma (OS). This study aimed to recognize and establish a glycometabolic gene signature to forecast the prognosis, and provide therapeutic options for patients with OS.

Emerging roles and therapeutic implications of HDAC2 and IL-17A in steroid-resistant asthma.

Steroid resistance represents a major clinical problem in the treatment of severe asthma, and therefore a better understanding of its pathogenesis is warranted. Recent studies indicated that histone deacetylase 2 (HDAC2) and interleukin 17A (IL-17A) play important roles in severe asthma. HDAC2 activity is reduced in patients with severe asthma and smoking-induced asthma, perhaps accounting for the amplified expression of inflammatory genes, which is associated with increased acetylation of glucocorticoid receptors.

HB-EGF-induced IL-8 secretion from airway epithelium leads to lung fibroblast proliferation and migration.

Background: We have reported that heparin-binding epidermal growth factor (HB-EGF) is increased in patients with chronic obstructive pulmonary disease (COPD) and associated with collagen deposition, but the mechanisms remain unclear. In the present study, we aimed to investigated the inflammatory cytokines secreted by bronchial epithelial cells following exposure to HB-EGF that promoted proliferation and migration of human lung fibroblast.

Methods: HB-EGF-induced inflammatory cytokines were assayed in two airway epithelial cells (primary human bronchial epithelial cells [HBECs] and BEAS-2B cells).

Dl-3-n-Butylphthalide Treatment Enhances Hemodynamics and Ameliorates Memory Deficits in Rats with Chronic Cerebral Hypoperfusion.

Our previous study has revealed that chronic cerebral hypoperfusion (CCH) activates a compensatory vascular mechanism attempting to maintain an optimal cerebral blood flow (CBF). However, this compensation fails to prevent neuronal death and cognitive impairment because neurons die prior to the restoration of normal CBF. Therefore, pharmacological invention may be critical to enhance the CBF for reducing neurodegeneration and memory deficit.

Evaluating the morphological changes of intracranial arteries and whole-brain perfusion in undetermined isolated vertigo.

Purpose: To determine the morphological changes of intracranial arteries and whole-brain perfusion in undetermined isolated vertigo (UIV) patients using 320-detector row computed tomography (CT).

Methods: A total of 150 patients who underwent CT angiography (CTA) and CT perfusion (CTP) imaging were divided into UIV group and benign paroxysmal positional vertigo (BPPV) group. Sixty individuals with sex- and age-matched without vertigo and cerebral diseases served as the control.

Bilateral Atherosclerotic Internal Carotid Artery Occlusion with Intact Cerebral Glucose Metabolism: A Case Report.

Background: Mild neurologic deficits concomitant with bilateral internal carotid artery occlusion (BICAO) is very rare and its treatment is still unclear.

Case Report: Herein, we report a case of a 67-year-old man with BICAO. The collateral circulation was rich, the symptoms were mild, and only standard pharmacotherapy was prescribed.

Chronic cerebral hypoperfusion induces vascular plasticity and hemodynamics but also neuronal degeneration and cognitive impairment.

Chronic cerebral hypoperfusion (CCH) induces cognitive impairment, but the compensative mechanism of cerebral blood flow (CBF) is not fully understood. The present study mainly investigated dynamic changes in CBF, angiogenesis, and cellular pathology in the cortex, the striatum, and the cerebellum, and also studied cognitive impairment of rats induced by bilateral common carotid artery occlusion (BCCAO). Magnetic resonance imaging (MRI) techniques, immunochemistry, and Morris water maze were employed to the study.

VASP phosphorylation and genetic polymorphism for clopidogrel resistance in Chinese patients with non-cardioembolic ischemic stroke.

Background: Clopidogrel resistance(CR)is found in non-cardioembolic ischemic stroke (NCIS) patients. However, it is still largely unknown how to identify CR in NCIS patients by laboratory and genetic characteristics.

Methods: A total of 95 patients with acute NCIS were recruited.