Opioid-free anesthesia with esketamine-dexmedetomidine versus opioid-based anesthesia with propofol-remifentanil in shoulder arthroscopy: a randomized controlled trial.

BACKGROUND: OFA (Opioid-free anesthesia) has the potential to reduce the occurrence of opioid-related adverse events and enhance postoperative recovery. Our research aimed to investigate whether OFA, combining esketamine and dexmedetomidine, could serve as an alternative protocol to traditional OBA (opioid-based anesthesia) in shoulder arthroscopy, particularly in terms of reducing PONV (postoperative nausea and vomiting). METHODS: A total of 60 patients treated with shoulder arthroscopy from September 2021 to September 2022 were recruited. Patients were randomly assigned to the OBA group (n = 30) and OFA group (n = 30), receiving propofol-remifentanil TIVA (total intravenous anesthesia) and esketamine-dexmedetomidine intravenous anesthesia, respectively. Both groups received ultrasound-guided ISBPB(interscalene brachial plexus block)for postoperative analgesia. RESULTS: The incidence of PONV on the first postoperative day in the ward (13.3% vs. 40%, P < 0.05) was significantly lower in the OFA group than in the OBA group. Moreover, the severity of PONV was less severe in the OFA group than in the OBA group in PACU (post-anesthesia care unit) (0 [0, 0] vs. 0 [0, 3], P<0.05 ) and in the ward 24 h postoperatively ( 0 [0, 0] vs. 0 [0, 2.25], P<0.05). Additionally, the OFA group experienced a significantly shorter length of stay in the PACU compared to the OBA group (39.4 ± 6.76 min vs. 48.7 ± 7.90 min, P < 0.001). CONCLUSIONS: Compared to the OBA with propofol-remifentanil, the OFA with esketamine- dexmedetomidine proved to be feasible for shoulder arthroscopy, resulting in a reduced incidence of PONV and a shorter duration of stay in the PACU. TRIAL REGISTRATION: The Chinese Clinical Trial Registry (No: ChiCTR2100047355), 12/06/2021.

Protective effect of Limosilactobacillus reuteri-fermented yogurt on mouse intestinal barrier injury induced by enterotoxigenic Escherichia coli.

BACKGROUND: Enterotoxigenic Escherichia coli (ETEC) is a pathogen that causes traveler's diarrhea, for which an effective vaccine is lacking. Previous studies showed that Limosilactobacillus reuteri could inhibit E. coli, effectively increase the expression of its tight junction protein, and reduce the adhesion of ETEC to the intestinal epithelial Caco-2 cell line. In this study, three kinds of yogurt with different starter cultures were first prepared: Lm. reuteri yogurt (fermented by Lm. reuteri alone), traditional yogurt (fermented by Streptococcus thermophilus and Lactobacillus delbrueckii subsp. bulgaricus at a ratio of 1:1) and mixed yogurt (fermented by Lm. reuteri, S. thermophilus and L. delbrueckii subsp. bulgaricus at a ratio of 1:1:1). The physiological properties, oxidative stress, intestinal barrier function, tight junction protein, pathological conditions and intestinal microbiota composition were investigated. RESULTS: The data showed that Lm. reuteri-fermented yogurt pregavage could effectively alleviate the intestinal barrier impairment caused by ETEC in mice. It alleviated intestinal villus shortening and inflammatory cell infiltration, decreased plasma diamine oxidase concentration and increased claudin-1 and occludin expression in the jejunum of ETEC-infected mice. In addition, Lm. reuteri-fermented yogurt significantly reduced the ETEC load in fecal samples, reversed the increase in Pseudomonadota abundance and decreased Bacteroidota abundance caused by ETEC infection. Furthermore, the composition of the intestinal microbiota could maintain a stable state similar to that in healthy mice. CONCLUSION: These findings indicate that Lm. reuteri-fermented yogurt could alleviate intestinal barrier damage, inhibit ETEC growth and maintain the stability of the intestinal microbiota during ETEC infection. © 2023 Society of Chemical Industry.

Effect of ethanolamine utilization on the pathogenicity and metabolic profile of enterotoxigenic Escherichia coli.

Bacterial pathogenicity is greatly affected by nutrient recognition and utilization in the host microenvironment. The characterization of enteral nutrients that promote intestinal pathogen virulence is helpful for developing new adjuvant therapies and inhibiting host damage. Ethanolamine (EA), as a major component of intestinal epithelial cells and bacterial membranes, is abundant in the intestine. Here, we provide the first demonstration that the critical human and porcine pathogen enterotoxigenic Escherichia coli (ETEC) can utilize EA as a nitrogen source, which affects its virulence phenotype. We found that compared with that in M9 medium (containing NH4Cl), EA inhibited ETEC growth to a certain extent; however, the relative expression levels of virulence-related genes, such as ltA (3.0-fold), fimH (2.9-fold), CfaD (2.6-fold), gspD (3.6-fold), and qesE (1.3-fold), increased significantly with 15 mM EA as a nitrogen source (P < 0.05), and the adhesion efficiency of ETEC to Caco-2 cells increased approximately 4.2-fold. In Caco-2 cells, the relative cell viability decreased from 74.8 to 63.4%, and the transepithelial electrical resistance (TEER) cells decreased to 74.8% with intestinal EA (4 mM). In addition, the relative expression levels of proinflammatory factors, such as TNF-α (3.2-fold), INF-γ (2.9-fold), and IL-1ß (1.98-fold), in ETEC-infected Caco-2 cells were significantly upregulated (P < 0.05) under EA exposure; however, the above virulence changes were not found in ΔeutR and ΔeutB ETEC. A gas chromatography-mass spectrometry (GC-MS)-based untargeted metabolomics approach was then employed to reveal EA-induced metabolic reprogramming related to ETEC virulence. The data showed that most metabolites related to carbohydrate, aspartate and glutamate metabolism, shikimic acid metabolism, and serine metabolism in ETEC exhibited a decreasing trend with increases in the EA concentration from 0 to 15 mM, but the branched-chain amino acid (BCAA) levels in ETEC increased in a dose-dependent manner under EA exposure. Our data suggest that the intestinal EA concentration can significantly affect the virulence phenotype, metabolic profile, and pathogenicity of ETEC. KEY POINTS: • ETEC growth and virulence gene expression could be regulated by ethanolamine. • The intestinal concentration of EA promoted the damaging effect of ETEC on the host epithelial barrier. • The promoting effect of EA on ETEC toxicity may be related to BCAA metabolism.

Endobronchial Lipoma: A Rare Cause of Bronchial Stenosis or Obstruction.

Endobronchial lipoma (EL) is a rare benign tumor characterized by tracheobronchial smooth-surfaced mass, often resulting in bronchial obstruction without standard guidelines for management. This study seeks to clarify the clinical features and interventions of EL, aiming to improve its diagnosis and outcomes. A retrospective review was conducted on 28516 outpatients treated between January 2015 and December 2019 at the Department of Respiratory and Critical Care Medicine of the Second Affiliated Hospital of Air Force Medical University to collect patients diagnosed with EL. Their clinical, bronchoscopic, chest imaging, and histopathological features along with management were analyzed. Among the patients reviewed, nine were histopathologically diagnosed with EL, comprising seven males and two females. All EL patients exhibited noticeable symptoms, including cough (in eight patients), dyspnea (in six patients), fever (in three patients), expectoration (in two patients), chest pain (in two patients), hemoptysis (in one patient), and fatigue (in one patient). Chest CT abnormalities included endobronchial mass (in four patients), inflammatory exudation (in three patients), atelectasis (in three patients), and infiltration or consolidation (in two patients). In three patients, imaging showed fat density, directly leading to the diagnosis of EL. The EL lesions were distributed with six in the right lung and three in the left lung, all located within the first three subdivisions of the tracheobronchial tree. Treatment approaches varied, with one patient undergoing combined bronchoscopic resection and surgery. The remaining patients received bronchoscopic intervention such as electrosurgical snare resection, argon plasma coagulation (APC), cryotherapy, and holmium laser. Histopathological analysis confirmed the EL diagnosis. Finally, the mass removal restored bronchus patency. Taken together, EL symptoms lack specificity, necessitating reliance on histopathology for EL accurate diagnosis. Bronchoscopic interventions emerge as the preferred option for EL management, surpassing surgical approaches.

Seawater inhalation induces acute lung injury via ROS generation and the endoplasmic reticulum stress pathway.

Seawater (SW) inhalation can induce acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). In the present study, SW induced apoptosis of rat alveolar epithelial cells and histopathological alterations to lung tissue. Furthermore, SW administration increased generation of reactive oxygen species (ROS), whereas pretreatment with the ROS scavenger, N­acetyl­L­cysteine (NAC), significantly decreased ROS generation, apoptosis and histopathological alterations. In addition, SW exposure upregulated the expression levels of glucose­regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP), which are critical proteins in the endoplasmic reticulum (ER) stress response, thus indicating that SW may activate ER stress. Conversely, blocking ER stress with 4­phenylbutyric acid (4­PBA) significantly improved SW­induced apoptosis and histopathological alterations, whereas an ER stress inducer, thapsigargin, had the opposite effect. Furthermore, blocking ROS with NAC inhibited SW­induced ER stress, as evidenced by the downregulation of GRP78, phosphorylated (p)­protein kinase R­like ER kinase (PERK), p­inositol­requiring kinase 1α (IRE1α), p­50 activating transcription factor 6α and CHOP. In addition, blocking ER stress with 4­PBA decreased ROS generation. In conclusion, the present study indicated that ROS and ER stress pathways, which are involved in alveolar epithelial cell apoptosis, are important in the pathogenesis of SW­induced ALI.