Dexmedetomidine Alleviates Brain Ischemia/Reperfusion Injury by Regulating Metastasis-associated Lung Adenocarcinoma Transcript 1/MicroRNA-140-5p/ Nuclear Factor Erythroid-derived 2-like 2 Axis.

Background: Dexmedetomidine (Dex) is widely used in perioperative anesthesia, and recent studies have reported that it protects organs from ischemia/reperfusion (I/R) injury.

Objectives: This study was performed to investigate the role of Dex in alleviating cerebral I/R injury and its regulatory effects on metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)/microRNA-140-5p (miR-140-5p)/nuclear factor erythroid-derived 2-like 2 (Nrf2) axis.

Methods: In vivo rat middle cerebral artery occlusion (MCAO) model and oxygen-glucose deprivation/re-oxygenation (OGD/R)-induced neuronal injury model were constructed.

Thymic stromal lymphopoietin suppresses markers of neuroinflammation and the JAK2/STAT5 pathway in activated microglia.

Thymic stromal lymphopoietin (TSLP) is highly expressed in the central nervous system in response to inflammation, but its exact function remains unclear. In this study, we used a model of LPS-stimulated microglia to investigate the direct impact of TSLP on microglial activation and the underlying mechanism. We measured oxidative stress, expression of microglial activation markers, and inflammatory indexes.

As an inhibitor of norepinephrine release, dexmedetomidine provides no improvement on stroke-associated pneumonia in mice.

Dexmedetomidine (DEX) is commonly employed as a sedative agent to attenuate sympathetic tone and reduce norepinephrine (NE) levels. In the context of stroke-associated pneumonia (SAP), which is believed to arise from heightened sympathetic nervous system activity and elevated NE release, the precise influence of DEX remains uncertain. In this study, we generated an SAP model using middle cerebral artery occlusion (MCAO) and examined NE levels, immunological statuses in the brain and periphery, pneumonia symptoms, and extent of infarction.

The Role of Macrophages and Alveolar Epithelial Cells in the Development of ARDS.

Acute lung injury (ALI) usually causes acute respiratory distress syndrome (ARDS), or even death in critical ill patients. Immune cell infiltration in inflamed lungs is an important hallmark of ARDS. Macrophages are a type of immune cell that participate in the entire pathogenic trajectory of ARDS and most prominently via their interactions with lung alveolar epithelial cells (AECs).

Development of an immune-related prognostic biomarker for triple-negative breast cancer.

Oncology studies employing digital dissection methodologies have provided some insight on the biological features of tumor microenvironment of Triple-negative breast cancer (TNBC), but molecular diagnostics rarely have therapeutic impact. We aimed to identify a novel prognostic biomarker to investigate immune characteristics of TNBC using transcriptomic features. We extracted whole transcriptome from breast cancer tissue of 30 TNBC patients and then used bioinformatics approaches to characterize the different immune cell contents in tumor tissue and para-cancerous tissue.

Clenbuterol, a Selective β2-Adrenergic Receptor Agonist, Inhibits or Limits Post-Stroke Pneumonia, but Increases Infarct Volume in MCAO Mice.

Background: Large ischemic stroke provokes an inflammatory response, promoting the release of norepinephrine (NE) by intensifying the sympathetic nervous system. This augmented sympathetic outflow was deemed to act on β2-adrenergic receptors (β2-ARs) expressed by immune cells, rendering organisms to post-stroke infections, like pneumonia. To clarify this issue, we introduced selective β2-ARs agonist clenbuterol (CLEN) to stroke mice to investigate how β2-adrenergic signaling augmentation after stroke affects immune response and post-stroke outcomes, including central and peripheral.

Effects of Remifentanil and Sufentanil Anesthesia on Cardiac Function and Serological Parameters in Congenital Heart Surgery.

In this study, we have investigated feasibility of remifentanil and sufentanil anesthesia in children with congenital heart disease surgery and its effects on cardiac function and serological parameters. For this purpose, a retrospective study was conducted on 120 children with congenital heart disease who underwent repair of ventricular septum or atrial septum in our hospital, specifically from January 2016 to January 2018, and 60 patients in each group were randomly divided into the control and treatment groups, respectively. The control group was anesthetized with sufentanil, and the treatment group was anesthetized with remifentanil.

Vascular endothelial growth factor increased the permeability of respiratory barrier in acute respiratory distress syndrome model in mice.

Background: Acute respiratory distress syndrome is associated with a mortality of 45%. The authors investigated the possible mechanisms and effect of vascular endothelial growth factor on alveolar epithelial barrier permeability in acute respiratory distress syndrome mice model.

Methods: Eighty Male BALB/c mice were randomly assigned to four group: PBS group, LPS group, sFlt group, or LPS + sFlt group.

Nuclear Spin Attenuates the Anesthetic Potency of Xenon Isotopes in Mice: Implications for the Mechanisms of Anesthesia and Consciousness.

What We Already Know About This Topic: WHAT THIS ARTICLE TELLS US THAT IS NEW: BACKGROUND:: Xenon is an elemental anesthetic with nine stable isotopes. Nuclear spin is a quantum property which may differ among isotopes. Xenon 131 (Xe) has nuclear spin of 3/2, xenon 129 (Xe) a nuclear spin of 1/2, and the other seven isotopes have no nuclear spin.

Erlotinib Protects LPS-Induced Acute Lung Injury in Mice by Inhibiting EGFR/TLR4 Signaling Pathway.

Epidermal growth factor receptor (EGFR) has been reported to initiate the inflammatory response, but its activation in lipopolysaccharide (LPS)-induced murine model of acute lung injury (ALI) remains unclear. In this study, we investigated the role of EGFR in the LPS-induced murine model of ALI and explored whether its inhibitor erlotinib could affect the progression of lung injury. We first detected the phosphorylated EGFR (p-EGFR)/EGFR ratio at different time points after LPS stimulation, and then different concentrations of erlotinib were used to treat mice at 1 h before LPS stimulation and collected samples at the time point of the highest p-EGFR/EGFR ratio.

Classically Activated Macrophages Protect against Lipopolysaccharide-induced Acute Lung Injury by Expressing Amphiregulin in Mice.

Background: Alveolar macrophages (AMs) activated into M1 phenotype are involved in the development of lipopolysaccharide-induced acute lung injury (ALI). However, whether AMs express amphiregulin and what roles amphiregulin plays in lipopolysaccharide-induced ALI remain poorly understood.

Methods: Acute lung injury was induced by intratracheal instillation of lipopolysaccharide in male C57BL/6 mice.

Amphiregulin may be a new biomarker of classically activated macrophages.

Amphiregulin (Areg) participates in tissue repair and inflammation regulation. As important effector cells in inflammation, macrophages can be polarized to classically (M1) or alternatively (M2) activated phenotype with diverse functions in immunity. However, the relationship between Areg expression and macrophage activation is poorly understood.

Ketamine promotes inflammation through increasing TLR4 expression in RAW264.7 cells.

Ketamine (KTM), a N-methyl-D-aspartate (NMDA) receptor antagonist, was found to has an anti-inflammatory effect, but some patients suffered from exacerbated pro-inflammatory reactions after anesthesia with KTM. The present study was aimed to examine the underlying mechanism of pro-inflammatory effects of KTM. In this study, RAW264.

Volatile anesthetics inhibit the activity of calmodulin by interacting with its hydrophobic site.

Background: Volatile anesthetics (VAs) may affect varied and complex physiology processes by manipulating Ca(2+)-calmodulin (CaM). However, the detailed mechanism about the action of VAs on CaM has not been elucidated. This study was undertaken to examine the effects of VAs on the conformational change, hydrophobic site, and downstream signaling pathway of CaM, to explore the possible mechanism of anesthetic action of VAs.

Anesthetic action of volatile anesthetics by using Paramecium as a model.

Although empirically well understood in their clinical administration, volatile anesthetics are not yet well comprehended in their mechanism studies. A major conundrum emerging from these studies is that there is no validated model to assess the presumed candidate sites of the anesthetics. We undertook this study to test the hypothesis that the single-celled Paramecium could be anesthetized and served as a model organism in the study of anesthetics.

Adenovirus-delivered angiopoietin 1 accelerates the resolution of inflammation of acute endotoxic lung injury in mice.

Background: The immune system plays a key role in protecting the organism from infection. Timely resolution of the inflammatory response to infection plays a vital role in returning homeostasis and maintaining normal organ function. Angiopoietin1 prevents endothelial activation, part of the inflammatory response to a pathogen, and has an anti-inflammatory effect in acute lung injury.

Preventive effect of gastrodin on cognitive decline after cardiac surgery with cardiopulmonary bypass: a double-blind, randomized controlled study.

Cognitive decline is a common complication after cardiac surgery with cardiopulmonary bypass (CPB), but as such no pharmacological therapy has been shown to be efficacious in preventing the decline. However, gastrodin has been shown to have multi-pharmacological effects on neurological functions. We undertook this study to test the hypothesis that gastrodin would potentially prevent CPB-associated neurocognitive decline.