Effect of small dose esketamine on perioperative neurocognitive disorder and postoperative depressive symptoms in elderly patients undergoing major elective noncardiac surgery for malignant tumors: A randomized clinical trial.

Background: Perioperative neurocognitive disorder and postoperative depressive symptoms are significant complications after surgery. Studies have indicated that esketamine possesses neuroprotective and antidepressant qualities.

Methods: This trial included 209 patients aged 60 to 86 years undergoing tumor resection who received esketamine (Group E) or not (Group C) during and after surgery.

Effects of dexmedetomidine on early postoperative cognitive function and postoperative inflammatory response: a systematic review and network meta-analysis.

Background: Dexmedetomidine (DEX) has demonstrated potential as an effective agent for enhancing early postoperative cognitive function. However, there is ongoing debate regarding its optimal dosage and impact on early postoperative inflammatory response. This study aimed to assess and prioritize the effects of varying doses of DEX on early postoperative cognitive function and inflammatory response, in order to identify the most effective intervention dosage.

Transforming growth factor-β1 attenuates inflammation and lung injury with regulating immune function in ventilator-induced lung injury mice.

Ventilator-induced lung injury (VILI) is a lung injury induced or aggravated by mechanical ventilation. Transforming growth factor (TGF)-β1 is a cytokine that mediates immune function, enabling inflammatory attenuation and tissue repair. Here, we hypothesized that it plays an important role in the attenuation of VILI and inflammation.

Inhibition of PD-1 Alters the SHP1/2-PI3K/Akt Axis to Decrease M1 Polarization of Alveolar Macrophages in Lung Ischemia-Reperfusion Injury.

Polarization of alveolar macrophages (AMs) into the M1 phenotype contributes to inflammatory responses and tissue damage that occur during lung ischemia-reperfusion injury (LIRI). Programmed cell death factor-1 (PD-1) regulates polarization of macrophages, but its role in LIRI is unknown. We examined the role of PD-1 in AM polarization in models of LIRI in vivo and in vitro.

Downregulation of SIRT3 Aggravates Lung Ischemia Reperfusion Injury by Increasing Mitochondrial Fission and Oxidative Stress through HIF-1-Dependent Mechanisms.

Lung ischemia-reperfusion injury (LIRI) is a severe multifaceted pathological condition that can lead to poor patient outcome where oxidative stress and the resulting inflammatory response can trigger and exacerbate tissue damage in LIRI patients. Sirtuin3 (SIRT3), a member of the sirtuin family, protects against oxidative stress-related diseases. However, it remains unclear if and how SIRT3 alleviates lung injury induced by ischemia/reperfusion (I/R).

Propofol produces neurotoxicity by inducing mitochondrial apoptosis.

Propofol is a fast and short-acting intravenous anesthetic widely used in clinical anesthesia and intensive care unit sedation. However, its use can cause abnormal effects on the central nervous system. Thus, the purpose of this study was to investigate the mechanism of propofol on primary hippocampal neuron injury.

microRNA-130b-3p delivery by mesenchymal stem cells-derived exosomes confers protection on acute lung injury.

Objective: Researchers have investigated miR-130b-3p in lung disease pathology, such as lung fibrosis. The present study was performed to elucidate the miR-130b-3p-involved mechanism in acute lung injury (ALI) through delivery by mesenchymal stem cells-derived exosomes (MSCs-Exo).

Methods: ALI mouse models were induced via intratracheal administration of lipopolysaccharide (LPS) and treated with MSCs-Exo.

Neutrophil-Derived IL-17 Promotes Ventilator-Induced Lung Injury p38 MAPK/MCP-1 Pathway Activation.

Ventilator-induced lung injury (VILI) is one of the most common complications of mechanical ventilation and can severely affect health. VILI appears to involve excessive inflammatory responses, but its pathogenesis has not yet been clarified. Since interleukin-17 (IL-17) plays a critical role in the immune system and the development of infectious and inflammatory diseases, we investigated here whether it plays a role in VILI.

Silencing ROCK1 ameliorates ventilator-induced lung injury in mice by inhibiting macrophages' NLRP3 signaling.

Rho kinase, including two subtypes, ROCK1 and ROCK2, controls a variety of biological processes helping coordinate the tissues response to stress and injury. Some authors believe that alveolar macrophages (AMs) play a key role in the early phase of ventilator-induced lung injury (VILI), which is closely related to the activation of NLRP3 inflammasome and NF-κB signaling. However, there is currently little known about the relationship between ROCK signaling and NLRP3 inflammasome.

Increased plasmin-mediated proteolysis of L1CAM in a mouse model of idiopathic normal pressure hydrocephalus.

Idiopathic normal pressure hydrocephalus (iNPH) is a common neurological disorder that is characterized by enlarged cerebral ventricles, gait difficulty, incontinence, and dementia. iNPH usually develops after the sixth decade of life in previously asymptomatic individuals. We recently reported that loss-of-function deletions in lead to the development of iNPH in a subgroup of patients, but how this occurs is poorly understood.

Morphine may act via DDX49 to inhibit hepatocellular carcinoma cell growth.

Pain in hepatocellular carcinoma (HCC) is a frequent cause of low quality of life, and morphine is routinely used as a first-line opiate analgesic in HCC. Morphine may exert not only analgesic effects but also anti-cancer effects via unknown mechanisms. Here we show that morphine can inhibit HCC cell proliferation.

Deletions in CWH43 cause idiopathic normal pressure hydrocephalus.

Idiopathic normal pressure hydrocephalus (iNPH) is a neurological disorder that occurs in about 1% of individuals over age 60 and is characterized by enlarged cerebral ventricles, gait difficulty, incontinence, and cognitive decline. The cause and pathophysiology of iNPH are largely unknown. We performed whole exome sequencing of DNA obtained from 53 unrelated iNPH patients.

Mitophagy-Mediated mtDNA Release Aggravates Stretching-Induced Inflammation and Lung Epithelial Cell Injury via the TLR9/MyD88/NF-κB Pathway.

Background: In animal models of ventilation-induced lung injury, mitophagy triggers mitochondria damage and the release of mitochondrial (mt) DNA, which activates inflammation. However, the mechanism of this process is unclear.

Methods: A model of cyclic stretching (CS)-induced lung epithelial cell injury was established.

Clinical impact of type 2 diabetes mellitus on outcomes after one-lung ventilation during thoracic surgery: a retrospective cohort study.

Background: The preoperative presence of diabetes mellitus (DM) has been recently demonstrated to be a risk factor for adverse events after thoracic surgery. However, the specific effects of presence of DM preoperatively on thoracic surgery is not known. This study aimed to investigate the association between preoperative DM and clinical outcomes and the short-term survival rates after thoracic surgery.

Preconditioning with rHMGB1 ameliorates lung ischemia-reperfusion injury by inhibiting alveolar macrophage pyroptosis via the Keap1/Nrf2/HO-1 signaling pathway.

Background: Lung ischemia-reperfusion injury (LIRI) is a complex pathophysiological process that can lead to poor patient outcomes. Inflammasome-dependent macrophage pyroptosis contributes to organ damage caused by ischemia/reperfusion injury. Oxidative stress and antioxidant enzymes also play an important role in LIRI.

[Dexamethasone on alleviating lung ischemia/reperfusion injury in rats by regulating PI3K/AKT pathway].

Objective: To investigate the protective effect and mechanism of dexamethasone in lung ischemia/reperfusion injury (LIRI) rats.

Methods: (1) Part one experiment: 24 Sprague-Dawley (SD) rats were divided into four groups according to the random number method (n = 6): standard ventilation group (N group), normal saline group (NS group), LIRI group, and dexamethasone+LIRI group (DEX group). The rat model of LIRI was established by clamping the left pulmonary hilum for 1 hour and reperfusing it for 2 hours.

Impact of Sevoflurane Versus Propofol Anesthesia on Post-Operative Cognitive Dysfunction in Elderly Cancer Patients: A Double-Blinded Randomized Controlled Trial.

BACKGROUND Research on the clinical outcomes of surgical patients anaesthetized with sevoflurane and the association of sevoflurane with post-operative cognitive dysfunction (POCD) is scarce. We evaluated whether sevoflurane-based anesthesia increased the incidence of POCD and worsened prognosis compared to propofol-based anesthesia in elderly cancer patients. MATERIAL AND METHODS This single-center, prospective, double-blind randomized controlled trial included 234 patients aged 65 to 86 years undergoing tumor resection who received sevoflurane-based (Group S) or propofol-based (Group P) anesthesia during surgery.

Endoplasmic reticulum stress is involved in ventilator-induced lung injury in mice via the IRE1α-TRAF2-NF-κB pathway.

Inflammation plays a criticalrole in the development of ventilator-induced lung injury (VILI). Endoplasmic reticulum (ER) stress is associated with a variety of diseases through the modulation of inflammatory responses. However, little is known about how ER stress is implicated in VILI.

Ly-6C inflammatory-monocyte recruitment is regulated by p38 MAPK/MCP-1 activation and promotes ventilator-induced lung injury.

Lymphocyte antigen 6Chigh (Ly-6C) inflammatory monocytes, as novel mononuclear cells in the innate immune system, participate in infectious diseases. In this study, we investigated the potential role of these monocytes in ventilator-induced lung injury (VILI) and the possible mechanism involved in their migration to lung tissue. Our results showed that mechanical ventilation with high tidal volume (HTV) increased the accumulation of Ly-6C inflammatory monocytes in lung tissues and that blocking C‑C chemokine receptor 2 (CCR2) could significantly reduce Ly-6C inflammatory-monocyte migration and attenuate the degree of inflammation of lung tissues.

Non-intubated anesthesia in patients undergoing video-assisted thoracoscopic surgery: A systematic review and meta-analysis.

Introduction: Non-intubated anesthesia (NIA) has been proposed for video-assisted thoracoscopic surgery (VATS), although how the benefit-to-risk of NIA compares to that of intubated general anesthesia (IGA) for certain types of patients remains unclear. Therefore, the aim of the present meta-analysis was to understand whether NIA or IGA may be more beneficial for patients undergoing VATS.

Methods: A systematic search of Cochrane Library, Pubmed and Embase databases from 1968 to April 2019 was performed using predefined criteria.

[Role and mechanism of Ly6C monocyte in ventilator-induced lung injury in mice].

Objective: To investigate the role and mechanism of Ly6C monocyte in mice with ventilator-induced lung injury (VILI).

Methods: Forty-eight healthy male SPF C57BL/6 mice were divided into spontaneous breathing group (n = 8), normal tidal volume (VT) group (VT was 8 mL/kg, n = 8), and high VT group (VT was 20 mL/kg, n = 32). The mice in the high VT group were subdivided into 1, 2, 3 and 4 hours subgroups, with 8 mice in each subgroup.

Celecoxib Inhibits Hepatocellular Carcinoma Cell Growth and Migration by Targeting PNO1.

BACKGROUND Celecoxib has shown anti-tumor activities against several types of cancer. Although the majority of research focuses on its mechanism via cyclooxygenase-2 (COX-2) enzyme inhibition, we identified a distinct mechanism behind celecoxib anti-cancer abilities. MATERIAL AND METHODS We treated hepatocellular carcinoma (HCC) Huh-7 cells and tumor xenograft mice models with celecoxib to test its effects on the tumor.

RhoA inhibitor suppresses the production of microvesicles and rescues high ventilation induced lung injury.

Microvesicles (MVs) have been extensively identified in various biological fluids including bronchoalveolar lavage fluid (BALF), peripheral blood and ascitic fluids. Our previous study showed that MVs are responsible for acute lung injury, but the exact mechanism underlying MVs formation remains poorly understood. In the present study, we investigate the potential role of RhoA/Rock signaling in MVs generation and the biological activity of MVs in ventilator-induced lung injury (VILI).