Serpina3c Deficiency Promotes Obesity-related Hypertriglyceridemia and Inflammation through Activation of the Hif1α-glycolysis Axis in Adipose Tissue.

Adipose tissue dysfunction leads to abnormal lipid metabolism and high inflammation levels. This research aims to explore the role of Serpina3c, which is highly expressed in adipocytes, in obesity-related hypertriglyceridemia and metaflammation. Serpina3c global knockout (KO) mice, adipocyte-specific Serpina3c overexpressing mice, Serpina3c knockdown (KD) mice, and hypoxia-inducible factor 1 alpha (Hif1α) KD mice were fed a high-fat diet (HFD) for 16 weeks to generate obesity-related hypertriglyceridemia mice models.

Magnetic nitrogen-doped activated carbon improved biohydrogen production.

Low biological hydrogen (bioH) production due to non-optimal metabolic pathways occurs frequently. In this work, magnetic nitrogen-doped activated carbon (MNAC) was prepared and added into the inoculated sludge with glucose as substrate to enhance hydrogen (H) yield by mesophilic dark fermentation (DF). The highest H yield appeared in 400 mg/L AC (252.

Overexpression of S100A1 in Osteosarcoma Inhibits Tumor Proliferation and Progression.

Background: Osteosarcoma is the most common primary malignant tumor of bone. Abnormal expression of S100A1 protein is closely related to the occurrence and development of malignant tumors. However, S100A1 in osteosarcoma has not been studied.

Hyperadhesive von Willebrand Factor Promotes Extracellular Vesicle-Induced Angiogenesis: Implication for LVAD-Induced Bleeding.

Bleeding associated with left ventricular assist device (LVAD) implantation has been attributed to the loss of large von Willebrand factor (VWF) multimers to excessive cleavage by ADAMTS-13, but this mechanism is not fully supported by the current evidence. We analyzed VWF reactivity in longitudinal samples from LVAD patients and studied normal VWF and platelets exposed to high shear stress to show that VWF became hyperadhesive in LVAD patients to induce platelet microvesiculation. Platelet microvesicles activated endothelial cells, induced vascular permeability, and promoted angiogenesis in a VWF-dependent manner.

Anticoagulation targeting membrane-bound anionic phospholipids improves outcomes of traumatic brain injury in mice.

Severe traumatic brain injury (TBI) often causes an acute systemic hypercoagulable state that rapidly develops into consumptive coagulopathy. We have recently demonstrated that TBI-induced coagulopathy (TBI-IC) is initiated and disseminated by brain-derived extracellular vesicles (BDEVs) and propagated by extracellular vesicles (EVs) from endothelial cells and platelets. Here, we present results from a study designed to test the hypothesis that anticoagulation targeting anionic phospholipid-expressing EVs prevents TBI-IC and improves the outcomes of mice subjected to severe TBI.

Conformation-dependent blockage of activated VWF improves outcomes of traumatic brain injury in mice.

Traumatic brain injury-induced coagulopathy (TBI-IC) causes life-threatening secondary intracranial bleeding. Its pathogenesis differs mechanistically from that of coagulopathy arising from extracranial injuries and hemorrhagic shock, but it remains poorly understood. We report results of a study designed to test the hypothesis that von Willebrand factor (VWF) released during acute TBI is intrinsically hyperadhesive because its platelet-binding A1-domain is exposed and contributes to TBI-induced vascular leakage and consumptive coagulopathy.

Comparison of Calcium Oxide and Calcium Peroxide Pretreatments of Wheat Straw for Improving Biohydrogen Production.

Wheat straw was pretreated with either CaO or CaO to improve biohydrogen production. Both CaO and CaO pretreatments improved the biodegradability of the wheat straw. CaO pretreatment raised the H yield by between 48.

Dexmedetomidine attenuates endoplasmic reticulum stress-induced apoptosis and improves neuronal function after traumatic brain injury in mice.

Traumatic brain injury (TBI) is one of the leading causes of mortality and disability worldwide. Emerging studies have shown that endoplasmic reticulum (ER) stress plays an important role in the pathophysiology of TBI. Dexmedetomidine (Dex), a highly selective α2-adrenoreceptor agonist, has been shown to attenuate ER stress.

Elevated microRNA‑145‑5p increases matrix metalloproteinase‑9 by activating the nuclear factor‑κB pathway in rheumatoid arthritis.

The present study explored whether miR‑145‑5p can aggravate the development and progression of rheumatoid arthritis (RA) by regulating the expression of matrix metalloproteinases (MMPs). ELISAs, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), and western blotting were used to examine the expression levels of MMP‑1, MMP‑3, MMP‑9, and MMP‑13 in fibroblast‑like synoviocytes (FLS) from patients with RA. Levels of MMP‑1, MMP‑3, MMP‑9, and MMP‑13 were assessed in the right hind ankles of a murine collagen‑induced arthritis (CIA) model by RT‑qPCR and immunohistochemical (IHC) analysis.

Meta-Analysis of Prognosis of Different Treatments for Symptomatic Moyamoya Disease.

Objective: The purpose of this study was to evaluate the efficacy of surgical revascularization versus conservative treatment and different surgical modalities, in order to provide evidence for the patient with moyamoya disease (MMD) to choose the appropriate treatment.

Methods: We comprehensively searched PubMed, Embase, Web of Science, and the Cochrane Library for articles published regarding MMD treatment. If the I value, which evaluated the heterogeneity, was <50%, a fixed-effect model was used; if not, a random effect model was applied.

Semaphorin 3A Contributes to Secondary Blood-Brain Barrier Damage After Traumatic Brain Injury.

Semaphorin 3A (SEMA3A) is a member of the Semaphorins family, a class of membrane-associated protein that participates in the construction of nerve networks. SEMA3A has been reported to affect vascular permeability previously, but its influence in traumatic brain injury (TBI) is still unknown. To investigate the effects of SEMA3A, we used a mouse TBI model with a controlled cortical impact (CCI) device and a blood-brain barrier (BBB) injury model with oxygen-glucose deprivation (OGD).

Thiosquaramide-catalysed asymmetric double Michael addition of 2-(3H)-furanones to nitroolefines.

New chiral thiosquaramides and their applications in catalytic asymmetric double addition of 5-methyl-2(3H)-furanones to nitroolefins were described. Enantiomerically enriched 2,4,4-trisubstituted butenolides bearing a quaternary stereogenic center could be smoothly constructed with high diastereoselectivities (up to >99 : 1 dr) and excellent enantioselectivities (up to 95% ee) under mild conditions.

Atorvastatin Protects Against Cerebral Aneurysmal Degenerative Pathology by Promoting Endothelial Progenitor Cells (EPC) Mobilization and Attenuating Vascular Deterioration in a Rat Model.

BACKGROUND Endothelial injury is the early pathological change of cerebral aneurysm (CA) formation. In addition to its lipid-lowering activity, atorvastatin (ATR) also reportedly promotes vascular repair via mobilizing endothelial progenitor cells (EPC). Here, we investigated the influence of ATR on vascular worsening after CA induction in rats.

Cognitive impairment after traumatic brain injury is associated with reduced long-term depression of excitatory postsynaptic potential in the rat hippocampal dentate gyrus.

Traumatic brain injury can cause loss of neuronal tissue, remote symptomatic epilepsy, and cognitive deficits. However, the mechanisms underlying the effects of traumatic brain injury are not yet clear. Hippocampal excitability is strongly correlated with cognitive dysfunction and remote symptomatic epilepsy.

miR-145-5p Increases Osteoclast Numbers In Vitro and Aggravates Bone Erosion in Collagen-Induced Arthritis by Targeting Osteoprotegerin.

BACKGROUND Osteoprotegerin (OPG) inhibits bone resorption and binds with strong affinity to receptor activator of NF κB ligand (RANKL), thereby preventing RANKL from binding to its receptor RANK. Osteoclasts have documented effects on bone erosion of rheumatoid arthritis (RA). The aim of this study was to examine the role of miR-145-5p in the regulation of RA osteoclast differentiation and bone erosion.

Highly enantioselective Michael addition of pyrazolin-5-ones to nitroolefins catalyzed by cinchona alkaloid derived 4-methylbenzoylthioureas.

Cinchona alkaloid-derived 4-methyl/nitro benzoylthioureas were synthesized, which smoothly catalyzed the asymmetric Michael addition of pyrazolin-5-ones to nitroolefins. The results showed that electronic effects of substituents in the benzene ring of benzoylthioureas have subtle influences on their catalytic abilities and electron donating methyl group is favored than electron withdrawing nitro group. Preliminary Hartree-Fock calculations revealed that in the catalytic cycle, hydrogen bond energies of the complex formed with 4-methylbenzoylthioureas are about 0.

Selective NLRP3 inflammasome inhibitor reduces neuroinflammation and improves long-term neurological outcomes in a murine model of traumatic brain injury.

The nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) inflammasome-mediated inflammatory response has emerged as a prominent contributor to the pathophysiological processes of traumatic brain injury (TBI). Recently, a potent, selective, small-molecule NLRP3 inflammasome inhibitor, MCC950, was described. Here, we investigated the effect of MCC950 on inflammatory brain injury and long-term neurological outcomes in a mouse model of TBI.

Brain-derived microparticles activate microglia/macrophages and induce neuroinflammation.

Microparticles are cell fragments derived from damaged cells that are able to present an antigen from the parent cells to other cells to activate intracellular signaling pathways. Microparticles are closely related to the inflammatory response. Brain-derived microparticles (BDMPs) play an important role in brain injury.

Increased miR-21-3p in Injured Brain Microvascular Endothelial Cells after Traumatic Brain Injury Aggravates Blood-Brain Barrier Damage by Promoting Cellular Apoptosis and Inflammation through Targeting MAT2B.

Our recent articles have reported that increased miR-21-5p in brain after traumatic brain injury (TBI) could improve the neurological outcome through alleviating blood-brain barrier (BBB) damage. miR-21-3p is another mature miRNA derived from pre-miR-21 after Dicer Procession other than miR-21-5p. Its roles in various diseases, such as tumors and myocardial disease, aroused great interest for research in recent years.

Administration of Tauroursodeoxycholic Acid Attenuates Early Brain Injury via Akt Pathway Activation.

Traumatic brain injury (TBI) is one of the leading causes of trauma-induced mortality and disability, and emerging studies have shown that endoplasmic reticulum (ER) stress plays an important role in the pathophysiology of TBI. Tauroursodeoxycholic acid (TUDCA), a hydrophilic bile acid, has been reported to act as an ER stress inhibitor and chemical chaperone and to have the potential to attenuate apoptosis and inflammation. To study the effects of TUDCA on brain injury, we subjected mice to TBI with a controlled cortical impact (CCI) device.

Highly enantioselective Michael addition of cyclohexanone to nitroolefins catalyzed by pyrrolidine-based bifunctional benzoylthiourea in water.

Organocatalysis and aqueous reactions are identified as the focus of the greening of chemistry. Combining these two strategies effectively remains an interesting challenge in organic synthesis. Herein, we used pyrrolidine-based benzoylthiourea 1c to catalyze the asymmetric Michael addition of cyclohexanone to various nitroolefins in water to afford the corresponding compounds in moderate to good yields, and with excellent diastereoselectivities (up to >99:1 dr) and enantioselectivities (up to 99% ee).