Publications by authors named "Zhixia Bai"

Dysfunction in either embryonic or postnatal vascular smooth muscle cells (SMCs) significantly contributes to the progression of various cardiovascular diseases. Therefore, elucidating the molecular mechanisms governing VSMC development and homeostasis is crucial. is the most reliable lineage gene for SMCs and has been utilized to develop tamoxifen-inducible Cre driver lines for achieving SMC-specific gene manipulation by crossing with mice carrying the lox -flanked gene, particularly in adult mice.

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Background: Anesthesia techniques and drug selection may influence tumor recurrence and metastasis. Neutrophil extracellular trapping (NETosis), an immunological process, has been linked to an increased susceptibility to metastasis in individuals with tumors. Furthermore, recurrence may be associated with vascular endothelial growth factor A (VEGF-A), a mediator of angiogenesis.

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Bupivacaine (BPV) can cause severe central nervous system toxicity when absorbed into the blood circulation system. Rapid intravenous administration of lipid emulsion (LE) could be used to treat local anaesthetic toxicity. This study aimed to investigate the mechanism by which the BDNF-TrkB/proBDNF-p75 pathway regulation by LE rescues BPV induced neurotoxicity in hippocampal neurons in rats.

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Objective: To compare the effectiveness and safety of central venous catheter thoracic drainage (CVCTD) with traditional closed thoracic drainage (TCTD) after minimally invasive surgery for esophageal cancer.

Methods: We conducted a retrospective investigation of 103 patients who underwent minimally invasive esophageal cancer surgery at our institution between January 2017 and December 2019. Among them, 44 patients underwent CVCTD, while 59 received TCTD.

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Background: Recent years have seen an increase in gastric cancer incidence. The most effective method of treating gastric cancer is still surgical resection. Over the past few decades, minimally invasive surgery has rapidly developed, reducing post-operative complications and speeding up recovery.

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The gut microbiome has been implicated in the development of cardiovascular disease (CVD) and atherosclerosis (AS), a chronic inflammatory condition. Aspirin may improve the immuno-inflammatory status in AS by regulating microbiota dysbiosis. However, the potential role of aspirin in modulating gut microbiota and microbial-derived metabolites remains less explored.

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Chronic low-grade inflammation is regarded to an important signature of atherosclerosis (AS). Macrophage (Mψ) and related polarization have been demonstrated to play a crucial role in the occurrence and development of AS inflammation. Butyrate, a bioactive molecule produced by the intestinal flora, has been increasingly demonstrated to exhibit a vital role for regulating the inflammation in chronic metabolic diseases.

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Atherosclerosis (AS) is closely associated with abnormally chronic low-grade inflammation and gut dysbiosis. Flaxseed oil (FO) rich in omega-3 polyunsaturated fatty acids (PUFAs), which are mainly composed of alpha-linolenic acid (ALA, 18:3 omega-3), has been demonstrated to exhibit pleiotropic benefits in chronic metabolic diseases. However, the impact of dietary ALA-rich FO on AS and its associated underlying mechanisms remain poorly understood.

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Local anesthetics can cause severe toxicity when absorbed systemically. Rapid intravenous administration of lipid emulsion (LE) is the standard of care for severe local anesthetic systemic toxicity which can cause cardiovascular and central nervous system (CNS) injury. The biological mechanism by which LE alleviates CNS toxicity remains unknown and understudied.

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To investigate whether intrathecal administration of 10% glucose increases functional impairment and histologic damage in rats when mixed with 5% lidocaine. After implanted intrathecal catheter, 32 male Sprague-Dawley rats were randomly assigned to one of four groups: lidocaine group (Group L, n=8) received 5% lidocaine 20 µL, lidocaine with glucose group (Group LG, n=8) received 5% lidocaine with 10% glucose 20 µL, glucose group (Group G, n=8) received 10% glucose 20 µL and normal saline group received normal saline 20 µL (Group NS, n=8). Four days after intrathecal injection, sensory impairments of rats in the four groups were evaluated by using the tail-flick test.

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Some findings have suggested that the rescue of bupivacaine (BPV)-induced cardiotoxicity by lipid emulsion (LE) is associated with inhibition of mitochondrial permeability transition pore (mPTP). However, the mechanism of this rescue action is not clearly known. In this study, the roles of phosphoinositide 3-kinase (PI3K)/Akt and glycogen synthase kinase-3β (GSK-3β) in the molecular mechanism of LE-induced protection and its relationship with mPTP were explored.

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Purpose: The sedative efficacy of propofol anesthesia is enhanced in patients with hepatic cirrhosis. Establish a rat model to investigate the efficacy of propofol.

Methods: 100 healthy Sprague-Dawley rats were divided into three groups and administered Phenobarbital sodium, carbon tetrachloride and ethanol solution for 0 (control), 9 (mild cirrhosis, M1), or 12 (severe cirrhosis, M2) weeks to induce hepatic cirrhosis.

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The aim of the present study was to investigate the mechanism underlying the rescue effect of lipid emulsion on bupivacaine (BPV)‑induced cardiomyocyte toxicity. The inhibitory effects of BPV on H9c2 myoblast cell proliferation were investigated using an MTT assay. The H9c2 myoblast cells were treated with either 1 mM BPV or 1% lipid emulsion (LE) alone, or co‑treated with both of the drugs.

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