Extracellular vesicles loaded with ApoB-100 protein affect the occurrence of coronary heart disease in patients after injury of spinal cord.

Spinal cord injury (SCI) patients have an increased susceptibility to coronary heart disease (CHD) due to dysregulated lipid deposition. We conducted a comprehensive investigation to gain insights into the specific roles of Apolipoprotein B-100 (APOB-100) in the development of CHD in patients suffering from SCI. First, we established an SCI rat model through semitransection.

PKM2 functions as a histidine kinase to phosphorylate PGAM1 and increase glycolysis shunts in cancer.

Phosphoglycerate mutase 1 (PGAM1) is a key node enzyme that diverts the metabolic reactions from glycolysis into its shunts to support macromolecule biosynthesis for rapid and sustainable cell proliferation. It is prevalent that PGAM1 activity is upregulated in various tumors; however, the underlying mechanism remains unclear. Here, we unveil that pyruvate kinase M2 (PKM2) moonlights as a histidine kinase in a phosphoenolpyruvate (PEP)-dependent manner to catalyze PGAM1 H11 phosphorylation, that is essential for PGAM1 activity.

ACOD1, rather than itaconate, facilitates p62-mediated activation of Nrf2 in microglia post spinal cord contusion.

Background: Spinal cord injury (SCI)-induced neuroinflammation and oxidative stress (OS) are crucial events causing neurological dysfunction. Aconitate decarboxylase 1 (ACOD1) and its metabolite itaconate (Ita) inhibit inflammation and OS by promoting alkylation of Keap1 to induce Nrf2 expression; however, it is unclear whether there is another pathway regulating their effects in inflammation-activated microglia after SCI.

Methods: Adult male C57BL/6 ACOD1 mice and their wild-type (WT) littermates were subjected to a moderate thoracic spinal cord contusion.

The decreased interface tension increased the transmembrane transport of soy hull polysaccharide-derived SCFAs in the Caco-2 cells.

Polysaccharides impact intestinal fermentation and regulate interfacial properties which affect absorption and transportation. Short-chain fatty acids (SCFAs), the main metabolites of soy hull polysaccharide lysate, are readily absorbed by the body and perform various physiological functions. We analysed the interfacial properties and transport of soy hull polysaccharide-derived SCFAs in the Caco-2 cell model to clarify the transmembrane transport mechanism.

Caffeic acid phenethyl ester inhibits neuro-inflammation and oxidative stress following spinal cord injury by mitigating mitochondrial dysfunction via the SIRT1/PGC1α/DRP1 signaling pathway.

Background: The treatment of spinal cord injury (SCI) has always been a significant research focus of clinical neuroscience, with inhibition of microglia-mediated neuro-inflammation as well as oxidative stress key to successful SCI patient treatment. Caffeic acid phenethyl ester (CAPE), a compound extracted from propolis, has both anti-inflammatory and anti-oxidative effects, but its SCI therapeutic effects have rarely been reported.

Methods: We constructed a mouse spinal cord contusion model and administered CAPE intraperitoneally for 7 consecutive days after injury, and methylprednisolone (MP) was used as a positive control.

Review on active components and mechanism of natural product polysaccharides against gastric carcinoma.

One of the malignant tumors with a high occurrence rate worldwide is gastric carcinoma, which is an epithelial malignant tumor emerging from the stomach. Natural product polysaccharides are a kind of natural macromolecular polymers, which have the functions of regulating immunity, anti-oxidation, anti-fatigue, hypoglycemia, etc. Natural polysaccharides have remarkable effectiveness in preventing the onset, according to studies, and development of gastric cancer at both cellular and animal levels.

Camk2a suppresses denervated muscle atrophy by maintaining the Ca2+ homeostasis in muscle cells.

Denervated muscle atrophy is a severe neurological complication that significantly impacts patients' quality of life. Currently, there is a lack of effective treatment methods. This study aims to investigate the molecular mechanisms associated with denervated muscle atrophy and explore potential therapeutic targets.

A Disintegrin and Metalloproteinase-8 Protects Against Erastin-Induced Neuronal Ferroptosis via Activating Nrf2/HO-1/FTH1 Signaling Pathway.

Ferroptosis is a type of iron-dependent programmed cell death caused by the imbalance between oxidants and antioxidants. A disintegrin and metalloproteinase-8 (ADAM8) is a metalloproteinase that mediates cell adhesion, cell migration, and proteolytic activity. However, the molecular mechanism of ADAM8 regulating ferroptosis after neural disorder is unclear, especially in the neuron.

Na/K enhanced the stability of the air/water interface of soy hull polysaccharide and intestinal mucus.

The stable energy barrier of mucin and soy hull polysaccharide (SHP) is established at the air/water interface in the intestinal fluid and is conducive to the absorption and transportation of nutrients. This study aimed to investigate the effect of different concentrations (0.5 % and 1.

Deficiency of CD93 exacerbates inflammation-induced activation and migration of BV2 microglia by regulating the TAK1/NF-κB pathway.

The role of CD93 in inflammatory response has been reported in multiple previous studies. However, the underlying mechanism of CD93 in microglial activation and migration during neuroinflammation post spinal cord injury (SCI) remains elusive. In the current study, we performed western blot, qRT-PCR, immunofluorescence analyses Transwell assay, and ELISA to determine the expression change and in-depth molecular mechanism of CD93 in microglia post inflammatory initiation.

Cannabinoid receptor-2 attenuates neuroinflammation by promoting autophagy-mediated degradation of the NLRP3 inflammasome post spinal cord injury.

Background: Neuroinflammation following spinal cord injury (SCI) results in prolonged neurological damage and locomotor dysfunction. Polarization of microglia is vital to regulation of neuroinflammation, although the underlying mechanisms have not yet been elucidated. Endocannabinoid receptor subtype 2 (CB2R) is reported to ameliorate neurodegeneration immunomodulation activities.

C-reactive protein and its ratio are useful indicators to exclude anastomotic leakage requiring intervention after laparoscopic rectal surgery.

The goal of this study was to determine whether C-reactive protein (CRP) levels and its ratios can be used as indicators to exclude postoperative anastomotic leak (AL) requiring intervention in patients undergoing elective laparoscopic total mesorectal excision (TME) without a diverting ileostomy for middle or low rectal cancer. We measured CRP values on postoperative days (POD) 1, 2, and 4 and CRP ratios between two PODs in 1278 consecutive patients undergoing rectal surgery. The incidence of AL requiring intervention was 5.

Forsythoside B attenuates neuro-inflammation and neuronal apoptosis by inhibition of NF-κB and p38-MAPK signaling pathways through activating Nrf2 post spinal cord injury.

Background: Spinal cord injury (SCI) is a ruinous neurological pathology that results in locomotor and sensory impairment. Neuro-inflammation and secondary neuronal apoptosis contribute to SCI, with anti-inflammatory therapies the focus of many SCI studies. Forsythoside B (FTS•B), a phenylethanoid glycoside extracted from the leaves of Lamiophlomis rotata Kudo, has been shown previously to have anti-inflammatory properties.

EGF promotes PKM2 O-GlcNAcylation by stimulating O-GlcNAc transferase phosphorylation at Y976 and their subsequent association.

Epidermal growth factor (EGF) is one of the most well-characterized growth factors and plays a crucial role in cell proliferation and differentiation. Its receptor EGFR has been extensively explored as a therapeutic target against multiple types of cancers, such as lung cancer and glioblastoma. Recent studies have established a connection between deregulated EGF signaling and metabolic reprogramming, especially rewiring in aerobic glycolysis, which is also known as the Warburg effect and recognized as a hallmark in cancer.

Growth Differentiation Factor 15 Regulates Oxidative Stress-Dependent Ferroptosis Post Spinal Cord Injury by Stabilizing the p62-Keap1-Nrf2 Signaling Pathway.

Background: Spinal cord injury (SCI) is a severe traumatic disorder of the central nervous system (CNS) that causes irreversible damage to the nervous tissue. The consequent hemorrhage contributed by trauma induces neuronal ferroptosis post SCI, which is an important death mode to mediate neuronal loss. Growth differentiation factor 15 (GDF15) is a cytokine that regulates cell proliferation, differentiation, and death.

A glutathione-responsive sulfur dioxide polymer prodrug selectively induces ferroptosis in gastric cancer therapy.

Nanoparticle-induced ferroptosis has been proven to be an appealing strategy in cancer treatment. Previously, we reported the synthesis of an amphiphilic polymer prodrug of SO, mPEG-PLG(DNs), which could self-assemble to formulate nanoparticles (NP-DNs) and trigger cancer cell death by GSH consumption and SO release. In the current study, the potential mechanism of NP-DNs-induced cell death was further investigated.

FANCC deficiency mediates microglial pyroptosis and secondary neuronal apoptosis in spinal cord contusion.

Background: Traumatic spinal cord injury (SCI)-induced neuroinflammation results in secondary neurological destruction and functional disorder. Previous findings showed that microglial pyroptosis plays a crucial role in neuroinflammation. Thus, it is necessary to conduct a comprehensive investigation of the mechanisms associated with post-SCI microglial pyroptosis.

Activation of glucagon-like peptide-1 receptor in microglia attenuates neuroinflammation-induced glial scarring via rescuing Arf and Rho GAP adapter protein 3 expressions after nerve injury.

The neuroinflammation is necessary for glial group initiation and clearance of damaged cell debris after nerve injury. However, the proinflammatory polarization of excessive microglia amplifies secondary injury via enhancing cross-talk with astrocytes and exacerbating neurological destruction after spinal cord injury (SCI). The glucagon-like peptide-1 receptor (GLP-1R) agonist has been previously shown to have a neuroprotective effect in neurodegeneration, whereas its potency in microglial inflammation after SCI is still unknown.

LncRNA-COX2 inhibits Fibroblast Activation and Epidural Fibrosis by Targeting EGR1.

Epidural fibrosis is one of the contributors to failed back surgery syndrome (FBSS) with a high incidence of about 80,000 cases per year. The fibrosis spreads from the operative region to the dura mater or the nerve root and results in functional incapacity and pain after laminectomy. Our previous study showed that down-regulation of lncRNA-COX2 is involved in the epidural scar formation.

Silencing TAK1 reduces MAPKs-MMP2/9 expression to reduce inflammation-driven neurohistological disruption post spinal cord injury.

Microglia activation post traumatic spinal cord injury (SCI) provokes accumulation of inflammatory metabolites, leading to increasing neurological disruption. Our previous studies demonstrated that blocking MAPKs pathway mitigated microglia inflammatory activation and prevented cords from neuroinflammation-induced secondary injury. Transforming growth factor-β-activated kinase 1 (TAK1) is an upstream gate regulating activation of MAPKs signaling.

Oncometabolic surgery: Emergence and legitimacy for investigation.

Studies on morbid obesity have shown remarkable improvement of diabetes in patients who have undergone bariatric operations. It was subsequently shown that these operations induce diabetes remission independent of the resultant weight loss; as a result, surgeons began to investigate whether operations for gastric cancer (GC) could have the same beneficial effect on diabetes as bariatric operations. It was then shown in multiple reports that followed that certain operations for GC were able to improve or even cure type 2 diabetes mellitus (T2DM) in GC patients.

Practicality and short-term outcomes of intracorporeal gastroduodenostomy in totally laparoscopic distal gastrectomy for gastric cancer: A single-centre retrospective study.

Objective: Totally laparoscopic distal gastrectomy (TLDG) with intracorporeal anastomosis is feasible because of improved approaches to laparoscopic surgery and the availability of a variety of surgical instruments. This study was designed to evaluate the practicality, safety and short-term operative outcomes of intracorporeal gastroduodenostomy in TLDG for gastric cancer.

Materials And Methods: Medical records of patients with primary distal gastric cancer undergoing Billroth I (B-I) (n = 37) or B-II anastomosis (n = 41) in TLDG from February 2010 to November 2015 were retrospectively analysed.

Laparoscopic Radical Gastrectomy for Resectable Advanced Gastric Cancer Within Enhanced Recovery Programs: A Prospective Randomized Controlled Trial.

Background: Enhanced recovery programs have become an important focus of perioperative management. A few studies have demonstrated the efficacy of an enhanced recovery after surgery (ERAS, which includes optimized pain control, restricted I.V.

MicroRNA-145 regulates platelet-derived growth factor-induced human aortic vascular smooth muscle cell proliferation and migration by targeting CD40.

The objective of this study is to investigate the expression of microRNA (miR)-145 in human aortic vascular smooth muscle cells (VSMCs) and the effect of miR-145 in the biological behavior and expression of CD40 in VSMCs. Cells were treated with either miR-145 or miR-145 inhibitor. Cell proliferation was analyzed by a colony formation assay and a methyl thiazolyl tetrazolium assay.