Publications by authors named "Zhang Bingxi"

Background: β-glucosidase is an important biomass-degrading enzyme and plays a vital role in generating renewable biofuels through enzymatic saccharification. In this study, we analyzed the transcriptome of Trichoderma harzianum HTASA derived from Hainan mangrove and identified a new gene encoding β-glucosidase Bgl3HB. And the biochemically characterization of β-glucosidase activity was performed.

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The zoonotic enterohaemorrhagic Escherichia coli (EHEC) O157:H7 can disrupt intestinal epithelial barrier function and in turn leading to serious intestinal and systemic disease. PR39 could effectively inhibit the growth of Gram-negative bacteria, but there is little knowledge of its effects on intestinal barrier function and the microbiota in E. coli-challenged mice.

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Lactoferricin (Lfcin) B, derived from lactoferrin in whey, has attracted considerable attention because of its multiple biological functions. Zoonotic enterohemorrhagic Escherichia coli (EHEC) O157:H7 has adverse effects on intestinal epithelial barrier function, leading to serious intestinal disease. In this study, the EHEC O157:H7-induced intestinal dysfunction model was developed to investigate the effects of Lfcin B on EHEC O157:H7-induced epithelial barrier disruption and microbiota dysbiosis.

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Serine alleviates inflammatory responses and is beneficial for gut health; however, whether it exerts any effects on ulcerative colitis or regulates intestinal microbiota remains unknown. We investigated the effects of serine supplementation on colonic morphology, inflammation, and microbiota composition in dextran sulfate sodium (DSS)-induced colitis model in mice. Acute colitis was induced through the oral intake of 3.

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cAMP response‑element binding protein (CREB) functions in hippocampal synaptic plasticity and memory formation. However, it remains unknown whether intravenous anesthetics modulate CREB. The present study aimed to examine the effects of intravenous anesthetics on CREB phosphorylation in the mouse hippocampus.

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Cathelicidins are the largest family of antimicrobial peptides. C-BF, which is short for Cathelicidin-Bungarus Fasciatus, was isolated from snake venom. C-BF was found to be the most potential substitutes for antibiotics.

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Background: Extracellular signal-regulated kinase 1/2 (ERK1/2) has been implicated in learning and memory; however, whether intravenous anesthetics modulate ERK1/2 remains unknown. The aim of this study was to examine the effect of several intravenous anesthetics on the phosphorylation of ERK1/2 in the hippocampus of adult mice.

Methods: Western blotting was used to examine cellular levels of phosphorylated and unphosphorylated ERK1/2 in mouse hippocampus slices, which were incubated with or without anesthetics including propofol, etomidate, ketamine and midazolam, a protein kinase C (PKC) activator or inhibitor, or phospholipase C (PLC) activator or inhibitor.

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During the perinatal period, the pharmacokinetics and pharmacodynamics of drugs may be altered. Data about the neurotoxicity of intrathecal local anesthetics in the peripartum period are lacking. So we hypothesized that the neurotoxicity of intrathecal lidocaine during perinatal period may be changed.

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Large epiglottic cysts can block the glottis, leading to serious consequences. This condition presents a challenge in terms of airway management for anesthesiologists during induction of anesthesia. We report the use of a Shikani™ Seeing Optical Stylet combined with a Macintosh laryngoscope to aid tracheal intubation in seven patients with large epiglottic cysts.

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Propofol and ketamine may provide certain degree of neuroprotection, but the underlying mechanism remains unclear to date. The cAMP response element-binding protein (CREB) was proposed that its phosphorylation at Ser133 (P-CREB) constituted a convergence point involved in neuroprotection. The purpose of this study was to determine whether different dosages of propofol and ketamine could provide neuroprotection against permanent middle cerebral artery occlusion (MCAO)-induced ischemic injuries and the involvement of P-CREB.

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Objective: To develop a novel chronic intermittent hypoxia chamber for rat models.

Design: The intermittent hypoxia chamber included two animal cabins (28 × 20 × 15 cm) and a hypoxia chamber (80 × 80 × 60 cm) between them, as well as the actuating device. Pure nitrogen was fed into the hypoxia chamber continuously in order to keep the low O(2) concentration.

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Background: Adenosine monophosphate-activated protein kinase (AMPK) orchestrates the regulation of energy-generating and -consuming pathways, and protects the heart against ischemic injury and apoptosis. Recent progress shed light on various factors, including adiponectin, MIF, H11K, and metformin in the activation of AMPK. It is uncertain whether the activation of AMPK is contributed to cardioprotection of opioids.

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The chronic intrathecal catheterization of the subarachnoid space in the rat is a very useful model in the research of neuroscience, anesthesiology, neurotoxicity, and etc. To avoid high postoperative mortality and neurological impairment, the catheterization from the lumbar interspace has been widely used in recent years. But one of the most discouraging disadvantages is that the external portion of the chronic indwelling catheters is easily damaged by rats.

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Ca/calmodulin-dependent protein kinase II (CaMKII) activation through autophosphorylation at threonine 286 was involved in the modulation of neuronal excitability and neurotransmission. Both propofol and ketamine may affect the intracellular Ca levels through N-methyl-D-aspartate receptors or voltage-dependent Ca channels, but they have different mechanisms in general anesthesia. The purpose of this study was to investigate the effects of propofol and ketamine on CaMKII total protein and phosphorylation (p-CaMKII) levels in the brain of rats.

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Background: In this study, we evaluated the predicted blood and effect-site C(50) for propofol and remifentanil target-controlled infusion and the Bispectral Index (BIS) values at loss of consciousness (LOC) and response to a standard noxious painful stimulus in Chinese patients. We hypothesized that these values would be different from previously published data on Caucasians.

Methods: Five medical centers enrolled 405 ASA physical status I and II unpremedicated Chinese patients (97 men, 308 women) aged 18-65 yr.

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We previously reported that novel protein kinase C (nPKC) epsilon and N-methyl-d-aspartic acid (NMDA) receptors participated in morphine preconditioning (MP)-induced neuroprotection. In this study, we used Western blot analysis, 2,3,5-triphenyltetrazolium chloride (TTC) staining and lactate dehydrogenase (LDH) leakage assay to determine the involvement of conventional PKC isoforms (cPKC) in MP-induced neuroprotection against oxygen-glucose deprivation (OGD). Hippocampus slices (400-microm thickness) from healthy male BALB/c mice exposed to OGD for 5-45 min to mimic mild, moderate and severe ischemia in the presence of MP pretreatment.

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Background: Postconditioning is a novel strategy of attaining cardioprotection. Previous studies have suggested morphine mimics the effects of ischemic preconditioning. Whether it is also capable of producing postconditioning or not is still unclear.

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Morphine pretreatment induces ischemic tolerance in neurons, but it remains uncertain whether novel protein kinase C epsilon isoform (nPKCepsilon) and N-methyl-D-aspartate (NMDA) receptors are involved in this neuroprotection. The present study examined this issue. Hippocampal slices from adult BALB/C mice were incubated with morphine at 0.

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