Publications
398 results found
Sun Q, Kamath P, Sun Y, et al., 2024, Dexmedetomidine attenuates lipopolysaccharide-induced renal cell fibrotic phenotypic changes by inhibiting necroinflammation via activating α2-adrenoceptor: A combined randomised animal and in vitro study., Biomedicine and Pharmacotherapy, Vol: 174, Pages: 116462-116462, ISSN: 0753-3322
BACKGROUND: Acute kidney injury (AKI) was reported to be one of the initiators of chronic kidney disease (CKD) development. Necroinflammation may contribute to the progression from AKI to CKD. Dexmedetomidine (Dex), a highly selective α2-adrenoreceptor (AR) agonist, has cytoprotective and "anti-" inflammation effects. This study was designed to investigate the anti-fibrotic properties of Dex in sepsis models. METHODS: C57BL/6 mice were randomly treated with an i.p. injection of lipopolysaccharides (LPS) (10 mg/kg) alone, LPS with Dex (25 μg/kg), or LPS, Dex and Atipamezole (Atip, an α2-adrenoreceptor antagonist) (500 μg/kg) (n=5/group). Human proximal tubular epithelial cells (HK2) were also cultured and then exposed to LPS (1 μg/ml) alone, LPS and Dex (1 μM), transforming growth factor-beta 1 (TGF-β1) (5 ng/ml) alone, TGF-β1 and Dex, with or without Atip (100 μM) in culture media. Epithelial-mesenchymal transition (EMT), cell necrosis, necroptosis and pyroptosis, and c-Jun N-terminal kinase (JNK) phosphorylation were then determined. RESULTS: Dex treatment significantly alleviated LPS-induced AKI, myofibroblast activation, NLRP3 inflammasome activation, and necroptosis in mice. Atip counteracted its protective effects. Dex attenuated LPS or TGF-β1 induced EMT and also prevented necrosis, necroptosis, and pyroptosis in response to LPS stimulation in the HK2 cells. The anti-EMT effects of Dex were associated with JNK phosphorylation. CONCLUSIONS: Dex reduced EMT following LPS stimulation whilst simultaneously inhibiting pyroptosis and necroptosis via α2-AR activation in the renal tubular cells. The "anti-fibrotic" and cytoprotective properties and its clinical use of Dex need to be further studied.
Gong C, Jin Y, Wang X, et al., 2024, Lack of S1PR2 in Macrophage Ameliorates Sepsis-associated Lung Injury through Inducing IL-33-mediated Type 2 Immunity., Am J Respir Cell Mol Biol, Vol: 70, Pages: 215-225
The function of type 2 immunity and mechanisms underlying the initiation of type 2 immunity after sepsis-induced lung injury remain unclear. Sphingosine-1-phosphate receptor 2 (S1PR2) has been demonstrated to modulate type 2 immunity in the context of asthma and pulmonary fibrosis. Thus, this study aims to investigate the role of type 2 immunity and whether and how S1PR2 regulates type 2 immunity in sepsis. Peripheral type 2 immune responses in patients with sepsis and healthy control subjects were assessed. The impact of S1PR2 on type 2 immunity in patients with sepsis and in a murine model of sepsis was further investigated. The type 2 innate immune responses were significantly increased in the circulation of patients 24 hours after sepsis, which was positively related to clinical complications and negatively correlated with S1PR2 mRNA expression. Animal studies showed that genetic deletion or pharmacological inhibition of S1PR2 induced type 2 innate immunity accumulation in the post-septic lungs. Mechanistically, S1PR2 deficiency promoted macrophage-derived interleukin (IL)-33 increase and the associated type 2 response in the lung. Furthermore, S1PR2-regulated IL-33 from macrophages mitigated lung injury after sepsis in mice. In conclusion, a lack of S1PR2 modulates the type 2 immune response by upregulating IL-33 release from macrophages and alleviates sepsis-induced lung injury. Targeting S1PR2 may have potential therapeutic value for sepsis treatment.
Liu W, Jia M, Zhang K, et al., 2024, Increased A1 astrocyte activation-driven hippocampal neural network abnormality mediates delirium-like behavior in aged mice undergoing cardiac surgery., Aging Cell, Vol: 23
Delirium is the most common neurological complication after cardiac surgery with adverse impacts on surgical outcomes. Advanced age is an independent risk factor for delirium occurrence but its underlying mechanisms are not fully understood. Although increased A1 astrocytes and abnormal hippocampal networks are involved in neurodegenerative diseases, whether A1 astrocytes and hippocampal network changes are involved in the delirium-like behavior of aged mice remains unknown. In the present study, a mice model of myocardial ischemia-reperfusion mimicking cardiac surgery and various assessments were used to investigate the different susceptibility of the occurrence of delirium-like behavior between young and aged mice and the underlying mechanisms. The results showed that surgery significantly increased hippocampal A1 astrocyte activation in aged compared to young mice. The high neuroinflammatory state induced by surgery resulted in glutamate accumulation in the extrasynaptic space, which subsequently decreased the excitability of pyramidal neurons and increased the PV interneurons inhibition through enhancing N-methyl-D-aspartate receptors' tonic currents in the hippocampus. These further induced the abnormal activities of the hippocampal neural networks and consequently contributed to delirium-like behavior in aged mice. Notably, the intraperitoneal administration of exendin-4, a glucagon-like peptide-1 receptor agonist, downregulated A1 astrocyte activation and alleviated delirium-like behavior in aged mice, while IL-1α, TNF-α, and C1q in combination administered intracerebroventricularly upregulated A1 astrocyte activation and induced delirium-like behavior in young mice. Therefore, our study suggested that cardiac surgery increased A1 astrocyte activation which subsequently impaired the hippocampal neural networks and triggered delirium development.
Jiang C, Gonzalez-Anton S, Li X, et al., 2024, General anaesthetics reduce acute lymphoblastic leukaemia malignancies in vitro and in vivo via CXCR4 and osteopontin mediated mechanisms, F1000Research, Vol: 11, Pages: 1491-1491
<ns3:p>Background Acute lymphoblastic leukaemia (ALL) is a common type of cancer in children. General anaesthetics are often used on patients undergoing painful procedures during ALL treatments but their effects on ALL malignancy remain unknown. Herein, we aim to study the effect of propofol and sevoflurane on the migration, homing and chemoresistance of ALL cells. Methods NALM-6 and Reh cells were treated with propofol (5 and 10 μg/ml) or sevoflurane (3.6%) <ns3:italic>in vitro</ns3:italic> for six hours. Then, cells were harvested for adhesion assay and migration assay <ns3:italic>in vitro</ns3:italic>. In <ns3:italic>in vivo</ns3:italic> experiments, GFP-NALM-6 cells were pre-treated with propofol (10 μg/ml) or sevoflurane (3.6%) for six hours. Then, cells were injected intravenously to C57BL/6 female mice followed by intravital microscopy. For chemoresistance study, cells were treated with rising concentrations of Ara-c (0.05-50 nM) plus 10μg/ml of propofol or Ara-C plus 3.6% of sevoflurane for 4 hours, followed by the assessment of cell viability via CCK-8 assay and detection of autophagy via flow cytometry. Results Both anaesthetics reduced <ns3:italic>in vivo</ns3:italic> migration and <ns3:italic>in vivo</ns3:italic> homing as exemplified by 1) the reduction in the number of cells entering the bone marrow and 2) the disturbance in homing location in relation to endosteal surface. Our results indicated that general anaesthetics reduced the surface CXCR4 expression and the adhesion of leukaemia cells to thrombin cleaved osteopontin (OPN) was reduced. Those changes might result in the alterations in migration and homing. In addition, both anaesthetics sensitised ALL cells to Ara-c possibly through CXCR4 mediated mechanisms. Propofol but not sevoflurane enhanced chemo-related cell death via inducing cytotoxic autophagy. Conclusion Together, our data suggest that both propofol and sevoflur
Zhu J, Chen C, Liu X, et al., 2024, Cerebellar Purkinje cell firing promotes conscious recovery from anesthesia state through coordinating neuronal communications with motor cortex., Theranostics, Vol: 14, Pages: 480-495
Background: The neurobiological basis of gaining consciousness from unconscious state induced by anesthetics remains unknown. This study was designed to investigate the involvement of the cerebello-thalamus-motor cortical loop mediating consciousness transitions from the loss of consciousness (LOC) induced by an inhalational anesthetic sevoflurane in mice. Methods: The neural tracing and fMRI together with opto-chemogenetic manipulation were used to investigate the potential link among cerebello-thalamus-motor cortical brain regions. The fiber photometry of calcium and neurotransmitters, including glutamate (Glu), γ-aminobutyric acid (GABA) and norepinephrine (NE), were monitored from the motor cortex (M1) and the 5th lobule of the cerebellar vermis (5Cb) during unconsciousness induced by sevoflurane and gaining consciousness after sevoflurane exposure. Cerebellar Purkinje cells were optogenetically manipulated to investigate their influence on consciousness transitions during and after sevoflurane exposure. Results: Activation of 5Cb Purkinje cells increased the Ca2+ flux in the M1 CaMKIIα+ neurons, but this increment was significantly reduced by inactivation of posterior and parafascicular thalamic nucleus. The 5Cb and M1 exhibited concerted calcium flux, and glutamate and GABA release during transitions from wakefulness, loss of consciousness, burst suppression to conscious recovery. Ca2+ flux and Glu release in the M1, but not in the 5Cb, showed a strong synchronization with the EEG burst suppression, particularly, in the gamma-band range. In contrast, the Glu, GABA and NE release and Ca2+ oscillations were coherent with the EEG gamma band activity only in the 5Cb during the pre-recovery of consciousness period. The optogenetic activation of Purkinje cells during burst suppression significantly facilitated emergence from anesthesia while the optogenetic inhibition prolonged the time to gaining consciousness. Conclusions: Our data indicate that cerebe
Murphy O, Forget P, Ma D, et al., 2023, Tumour excisional surgery, anaesthetic-analgesic techniques, and oncologic outcomes: a narrative review., Br J Anaesth, Vol: 131, Pages: 989-1001
Cancer is a growing global burden; there were an estimated 18 million new cancer diagnoses worldwide in 2020. Excisional surgery remains one of the main treatments for solid organ tumours in cancer patients and is potentially curative. Cancer- and surgery-induced inflammatory processes can facilitate residual tumour cell survival, growth, and subsequent recurrence. However, it has been hypothesised that anaesthetic and analgesic techniques during surgery might influence the risk of cancer recurrence. This narrative review aims to provide an updated summary of recent observational studies and new randomised controlled clinical trials on whether certain specific anaesthetic and analgesic techniques or perioperative interventions during tumour resection surgery of curative intent materially affect long-term oncologic outcomes.
Wu L, Zhao H, Zhang M, et al., 2023, Regulated cell death and inflammasome activation in gut injury following traumatic surgery in vitro and in vivo: implication for postoperative death due to multiorgan dysfunction, Cell Death Discovery, Vol: 9, ISSN: 2058-7716
Postoperative multi-organ dysfunction (MOD) is associated with significant mortality and morbidity. Necroptosis has been implicated in different types of solid organ injury; however, the mechanisms linking necroptosis to inflammation require further elucidation. The present study examines the involvement of necroptosis and NLR family pyrin domain containing 3 (NLRP3) inflammasome in small intestine injury following traumatic surgery. Kidney transplantation in rats and renal ischaemia-reperfusion (I/R) in mice were used as traumatic and laparotomic surgery models to study necroptosis and inflammasome activation in the small intestinal post-surgery; additional groups also received receptor-interacting protein kinase 1 (RIPK1) inhibitor necrostatin-1s (Nec-1s). To investigate whether necroptosis regulates inflammasome activity in vitro, necroptosis was induced in human colonic epithelial cancer cells (Caco-2) by a combination of tumour necrosis factor-alpha (TNFα), SMAC mimetic LCL-161 and pan-caspase inhibitor Q-VD-Oph (together, TLQ), and necroptosis was blocked by Nec-1s or mixed lineage kinase-domain like (MLKL) inhibitor necrosulfonamide (NSA). Renal transplantation and renal ischaemia-reperfusion (I/R) upregulated the expression of necroptosis mediators (RIPK1; RIPK3; phosphorylated-MLKL) and inflammasome components (P2X purinoceptor subfamily 7, P2X7R; NLRP3; caspase-1) in the small intestines at 24 h, and Nec-1s suppressed the expression of inflammasome components. TLQ treatment induced NLRP3 inflammasome, promoted cleavage of caspase-1 and interleukin-1 beta (IL-1β), and stimulated extracellular ATP release from Caco-2 cells, and MLKL inhibitor NSA prevented TLQ-induced inflammasome activity and ATP release from Caco-2 cells. Our work suggested that necroptosis and inflammasome interactively promote remote postoperative small intestinal injury, at least in part, through ATP purinergic signalling. Necroptosis-inflammasome axis may be considere
Wu X, Gao Y, Shi C, et al., 2023, Complement C1q drives microglia-dependent synaptic loss and cognitive impairments in a mouse model of lipopolysaccharide-induced neuroinflammation., Neuropharmacology, Vol: 237
Activated microglia and subsequent release of pro-inflammatory cytokines result in neuroinflammatory status which further damage neurological function including cognitive impairments in various neurological conditions. However, the underlying molecular mechanisms during these pathological processing remain unknown. In the current study, mice received intraperitoneal administrations of LPS (0.5 mg/kg, daily, Escherichia coli O55:B5) for seven consecutive days and their different cohorts were used for behavioral assessment with open field, Y maze, and novel object recognition test or for electrophysiology recordings of mEPSC, LFP or LTP in in vivo or ex vivo preparation. The hippocampus from some cohorts were harvested for immunostaining or Western blotting of c1q, Iba-1, CD68, PSD95 and dendritic spine density or for transcriptome and proteomics analysis. Repeated LPS injections induced an up-regulation of complement system protein c1q and distinct microglial phenotype with an enrichment of the complement-phagosome pathway. Microglial synaptic engulfment and profound synaptic loss were found. These pathological changes were accompanied with the significantly decreased excitatory synaptic transmission, disturbed theta oscillations, impaired hippocampal long-term potentiation, and cognitive impairments. Notably, neutralization of c1q signaling robustly prevented these changes. Collectively, our data provide evidence that activated microglia and complement cascade c1q signaling in the hippocampus may account for synaptic loss and cognitive impairments in a mouse model of neuroinflammation induced by repeated LPS injections. Our work implicates that complement system may be a therapeutic target for developing therapies to prevent or treat cognitive disorders related to neuroinflammation or other disease conditions including neurodegenerative disease per se.
Zhang Y, Su Y, Wang Z, et al., 2023, TAK1 Reduces Surgery-induced Overactivation of RIPK1 to Relieve Neuroinflammation and Cognitive Dysfunction in Aged Rats, NEUROCHEMICAL RESEARCH, Vol: 48, Pages: 3073-3083, ISSN: 0364-3190
Zhang X, Sun B, Pac-Soo C, et al., 2023, A case report: A patient rescued by VA-ECMO after cardiac arrest triggered by trigeminocardiac reflex after nasal surgery, MEDICINE, Vol: 102, ISSN: 0025-7974
Duan W, Zhou C-M, Yang J-J, et al., 2023, A long duration of intraoperative hypotension is associated with postoperative delirium occurrence following thoracic and orthopedic surgery in elderly, JOURNAL OF CLINICAL ANESTHESIA, Vol: 88, ISSN: 0952-8180
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Zhai Q, Zhang Y, Ye M, et al., 2023, Reducing complement activation during sleep deprivation yields cognitive improvement by dexmedetomidine, BRITISH JOURNAL OF ANAESTHESIA, Vol: 131, Pages: 542-555, ISSN: 0007-0912
Zhu J, Chen C, Wu J, et al., 2023, Effects of propofol and sevoflurane on social and anxiety-related behaviours in sleep-deprived rats, BRITISH JOURNAL OF ANAESTHESIA, Vol: 131, Pages: 531-541, ISSN: 0007-0912
Huang J, Gao X, Wang M, et al., 2023, Prophylactic Administration with Methylene Blue Improves Hemodynamic Stabilization During Obstructive Jaundice-Related Diseases' Operation: a Blinded Randomized Controlled Trial, JOURNAL OF GASTROINTESTINAL SURGERY, Vol: 27, Pages: 1837-1845, ISSN: 1091-255X
Cao S-J, Zhang Y, Zhang Y-X, et al., 2023, Long-term survival in older patients given propofol or sevoflurane anaesthesia for major cancer surgery: follow-up of a multicentre randomised trial., Br J Anaesth, Vol: 131, Pages: 266-275
BACKGROUND: Experimental evidence indicates that i.v. anaesthesia might reduce cancer recurrence compared with volatile anaesthesia, but clinical information is observational only. We therefore tested the primary hypothesis that propofol-based anaesthesia improves survival over 3 or more years after potentially curative major cancer surgery. METHODS: This was a long-term follow-up of a multicentre randomised trial in 14 tertiary hospitals in China. We enrolled 1228 patients aged 65-90 yr who were scheduled for major cancer surgery. They were randomised to either propofol-based i.v. anaesthesia or to sevoflurane-based inhalational anaesthesia. The primary endpoint was overall survival after surgery. Secondary endpoints included recurrence-free and event-free survival. RESULTS: Amongst subjects randomised, 1195 (mean age 72 yr; 773 [65%] male) were included in the modified intention-to-treat analysis. At the end of follow-up (median 43 months), there were 188 deaths amongst 598 patients (31%) assigned to propofol-based anaesthesia compared with 175 deaths amongst 597 patients (29%) assigned to sevoflurane-based anaesthesia; adjusted hazard ratio 1.02; 95% confidence interval (CI): 0.83-1.26; P=0.834. Recurrence-free survival was 223/598 (37%) in patients given propofol anaesthesia vs 206/597 (35%) given sevoflurane anaesthesia; adjusted hazard ratio 1.07; 95% CI: 0.89-1.30; P=0.465. Event-free survival was 294/598 (49%) in patients given propofol anaesthesia vs 274/597 (46%) given sevoflurane anaesthesia; adjusted hazard ratio 1.09; 95% CI 0.93 to 1.29; P=0.298. CONCLUSIONS: Long-term survival after major cancer surgery was similar with i.v. and volatile anaesthesia. Propofol-based iv. anaesthesia should not be used for cancer surgery with the expectation that it will improve overall or cancer-specific survival. CLINICAL TRIAL REGISTRATIONS: ChiCTR-IPR-15006209; NCT02660411.
Iwasaki M, Zhao H, Hu C, et al., 2023, The differential cancer growth associated with anaesthetics in a cancer xenograft model of mice: mechanisms and implications of postoperative cancer recurrence, CELL BIOLOGY AND TOXICOLOGY, Vol: 39, Pages: 1561-1575, ISSN: 0742-2091
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Hu C, Wang B, Liu Z, et al., 2023, Sevoflurane but not propofol enhances ovarian cancer cell biology through regulating cellular metabolic and signaling mechanisms, Cell Biology and Toxicology: an international journal devoted to research at the cellular level, Vol: 39, Pages: 1395-1411, ISSN: 0742-2091
Perioperative risk factors, including the choice of anesthetics, may influence ovarian cancer recurrence after surgery. Inhalational anesthetic sevoflurane and intravenous agent propofol might affect cancer cell metabolism and signaling, which, in turn, may influence the malignancy of ovarian cancer cells. The different effects between sevoflurane and propofol on ovarian cancer cell biology and underlying mechanisms were studied. Cultured ovarian cancer cells were exposed to 2.5% sevoflurane, 4 μg/mL propofol, or sham condition as the control for 2 h followed by 24-h recovery. Glucose transporter 1 (GLUT1), mitochondrial pyruvate carrier 1 (MPC1), glutamate dehydrogenase 1 (GLUD1), pigment epithelium-derived factor (PEDF), p-Erk1/2, and hypoxia-inducible factor 1-alpha (HIF-1α) expressions were determined with immunostaining and/or Western blot. Cultured media were collected for 1H-NMR spectroscopy-based metabolomics analysis. Principal component analysis (PCA) and orthogonal projections to latent structures discriminant analysis (OPLS-DA) were used to analyze metabolomics data. Sevoflurane increased the GLUT1, MPC1, GLUD1, p-Erk1/2, and HIF-1α expressions but decreased the PEDF expression relative to the controls. In contrast to sevoflurane, propofol decreased GLUT1, MPC1, GLUD1, p-Erk1/2, and HIF-1α but increased PEDF expression. Sevoflurane increased metabolite isopropanol and decreased glucose and glutamine energy substrates in the media, but the opposite changes were found after propofol treatment. Our data indicated that, unlike the pro-tumor property of sevoflurane, propofol negatively modulated PEDF/Erk/HIF-1α cellular signaling pathway and inhibited ovarian cancer metabolic efficiency and survival, and hence decreased malignancy. The translational value of this work warrants further study.
Cao S-J, Zhang Y, Zhang Y-X, et al., 2023, Delirium in older patients given propofol or sevoflurane anaesthesia for major cancer surgery: a multicentre randomised trial., Br J Anaesth, Vol: 131, Pages: 253-265
BACKGROUND: Delirium is a common and disturbing postoperative complication that might be ameliorated by propofol-based anaesthesia. We therefore tested the primary hypothesis that there is less delirium after propofol-based than after sevoflurane-based anaesthesia within 7 days of major cancer surgery. METHODS: This multicentre randomised trial was conducted in 14 tertiary care hospitals in China. Patients aged 65-90 yr undergoing major cancer surgery were randomised to either propofol-based anaesthesia or to sevoflurane-based anaesthesia. The primary endpoint was the incidence of delirium within 7 postoperative days. RESULTS: A total of 1228 subjects were enrolled and randomised, with 1195 subjects included in the modified intention-to-treat analysis (mean age 71 yr; 422 [35%] women); one subject died before delirium assessment. Delirium occurred in 8.4% (50/597) of subjects given propofol-based anaesthesia vs 12.4% (74/597) of subjects given sevoflurane-based anaesthesia (relative risk 0.68 [95% confidence interval {CI}: 0.48-0.95]; P=0.023; adjusted relative risk 0.59 [95% CI: 0.39-0.90]; P=0.014). Delirium reduction mainly occurred on the first day after surgery, with a prevalence of 5.4% (32/597) with propofol anaesthesia vs 10.7% (64/597) with sevoflurane anaesthesia (relative risk 0.50 [95% CI: 0.33-0.75]; P=0.001). Secondary endpoints, including ICU admission, postoperative duration of hospitalisation, major complications within 30 days, cognitive function at 30 days and 3 yr, and safety outcomes, did not differ significantly between groups. CONCLUSIONS: Delirium was a third less common after propofol than sevoflurane anaesthesia in older patients having major cancer surgery. Clinicians might therefore reasonably select propofol-based anaesthesia in patients at high risk of postoperative delirium. CLINICAL TRIAL REGISTRATION: Chinese Clinical Trial Registry (ChiCTR-IPR-15006209) and ClinicalTrials.gov (NCT02662257).
West R, Soo CP, Murphy J, et al., 2023, A protocol for a pilot study to assess the feasibility of a randomised clinical trial of perioperative intravenous lidocaine on colorectal cancer outcome after surgery (FLICOR trial)., BJA Open, Vol: 6
BACKGROUND: Cancer recurrence after curative cancer surgery significantly impacts patients and healthcare services. Before surgery, a small number of clinically undetectable circulating tumour cells are often present. The surgical stress response promotes the distribution and proliferation of circulating tumour cells leading to cancer recurrence and metastasis. Preclinical evidence suggests that lidocaine may exert 'anti-cancer' effects and alleviate pro-metastatic environments. The Feasibility Study of Lidocaine Infusion During Bowel Cancer Surgery for Cancer Outcome (FLICOR) will assess the feasibility of conducting a clinical trial on perioperative intravenous lidocaine infusion for postoperative colorectal cancer outcomes. METHODS: The study is a double-blinded, randomised, controlled pilot study for a full trial comparing intravenous lidocaine administration at 1.5 mg kg-1 bolus followed by 1.5 mg kg-1 h-1 infusion for 24 h with placebo in patients undergoing minimally invasive (laparoscopy or robotic) colorectal cancer surgery. The feasibility of data collection instruments will be measured, including those for future economic evaluation and clinical and patient-reported outcomes. For the exploratory outcomes, blood samples will be collected before and after surgery on days 0, 1, and 3. Recruitment is planned for two NHS Trusts over 6 months with a 12-month follow-up. Patients and clinicians will be asked for their feedback on the study process. DISSEMINATION PLAN: Study data will be disseminated to trial participants, the public, and academic communities. The work will be presented at national and international conferences to stimulate interest and enthusiasm for centres to participate in the future definitive trial. This research will also be published in peer-reviewed open-access journals. CLINICAL TRIAL REGISTRATION: ISRCTN29594895 (ISRCTN), NCT05250791 (ClinicalTrials.gov). PROTOCOL VERSION NUMBER AND DATE: 3.0, February 8, 2023.
Xia M, Ma W, Zuo M, et al., 2023, Expert consensus on difficult airway assessment, HEPATOBILIARY SURGERY AND NUTRITION, ISSN: 2304-3881
Wang L, Zhang N, Liu J, et al., 2023, Macrophagic Sclerostin Loop2-ApoER2 Interaction Required by Sclerostin for Suppressing Inflammatory Responses, Publisher: W B SAUNDERS CO-ELSEVIER INC, Pages: S6-S6, ISSN: 0026-0495
Jiang H, Li D, Wang L, et al., 2023, Sclerostin loop3-LRP4 Interaction Required by Sclerostin for Lipid and Glucose Metabolism Impairment in Adipocyte, Publisher: W B SAUNDERS CO-ELSEVIER INC, Pages: S8-S9, ISSN: 0026-0495
Li D, Jiang H, Wang L, et al., 2023, Sclerostin Loop3 Participates in Whole-body Lipid and Glucose Metabolism Impairment Effects of Sclerostin, Publisher: W B SAUNDERS CO-ELSEVIER INC, Pages: S12-S12, ISSN: 0026-0495
Chang E, Wang Y, Zhu R, et al., 2023, General anesthetic action profile on the human prefrontal cortex cells through comprehensive single-cell RNA-seq analysis, iScience, Vol: 26, Pages: 1-19, ISSN: 2589-0042
The cellular and molecular actions of general anesthetics to induce anesthesia state and also cellular signaling changes for subsequent potential "long term" effects remain largely elusive. General anesthetics were reported to act on voltage-gated ion channels and ligand-gated ion channels. Here we used single-cell RNA-sequencing complemented with whole-cell patch clamp and calcium transient techniques to examine the gene transcriptome and ion channels profiling of sevoflurane and propofol, both commonly used clinically, on the human fetal prefrontal cortex (PFC) mixed cell cultures. Both propofol and sevoflurane at clinically relevant dose/concentration promoted "microgliosis" but only sevoflurane decreased microglia transcriptional similarity. Propofol and sevoflurane each extensively but transiently (<2 h) altered transcriptome profiling across microglia, excitatory neurons, interneurons, astrocytes and oligodendrocyte progenitor cells. Utilizing scRNA-seq as a robust and high-through put tool, our work may provide a comprehensive blueprint for future mechanistic studies of general anesthetics in clinically relevant settings.
Mok V, Nixon J, Hu J, et al., 2023, The impact of perioperative acute kidney injury/failure on short and long surgical outcomes, Anesthesiology and Perioperative Science, Vol: 1
<jats:title>Abstract</jats:title><jats:p>The development of acute kidney injury after surgery is associated with significant mortality and morbidity and with worse short and long-term outcomes. Patients who develop acute kidney injury are at an increased risk of developing long-term renal dysfunction, which leads to lower quality of life and greater financial burden on the healthcare system. Although there are various systems to classify the severity of acute kidney injury, most systems only measure components that deteriorate after significant renal damage, such as urine output and serum creatinine. Surgical trauma and stress trigger acute kidney injury development, in addition to multiple co-morbidities, cardiovascular disease, and postoperative factors. The pathophysiology of acute kidney injury is complex, and this is reflected in the heterogenous population that is affected. Treatment is largely supportive and focuses on ensuring adequate renal perfusion, correcting electrolyte abnormalities and avoiding further renal injury. Current research focuses on novel biomarkers that detect decreased renal function earlier and that the deteriorating renal function can be treated before long-lasting damage occurs. This review discusses the epidemiology, aetiology, risk factors, and short and long-term surgical outcomes of acute kidney injury. Treatment, prevention, and recent developments in future research are also discussed.</jats:p> <jats:p><jats:bold>Graphical Abstract</jats:bold></jats:p>
Saito J, Zao H, Wu L, et al., 2023, "Anti-cancer" effect of ketamine in comparison with MK801 on neuroglioma and lung cancer cells., Eur J Pharmacol, Vol: 945
Ketamine, a N-methyl-D-aspartate (NMDA) receptor antagonist, is commonly used to induce anaesthesia during cancer surgery and relieve neuropathic and cancer pain. This study was conducted to assess whether ketamine has any inhibiting effects on neuroglioma (H4) and lung cancer cells (A549) in vitro. The cultured H4 and A549 cells were treated with ketamine and MK801 (0.1, 1, 10, 100, or 1000 μM) for 24 h. The expressions of glutamate receptors on both types of cancer cells were assessed with qRT-PCR. In addition, cell proliferation and migration were assessed with cell counting Kit-8 and wound healing assays. Cyclin D1, matrix metalloproteinase 9 (MMP9), phosphorylation of extracellular signal-regulated kinase (pERK), and cleaved-caspase-3 expression together with reactive oxygen species (ROS) were also assessed with Western blot, immunostaining, and/or flowcytometry. NMDA and α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors were expressed on both H4 and A549 cells. Ketamine inhibited cancer cell proliferation and migration in a dose-dependent manner by suppressing the cell cycle and inducing apoptosis. Ketamine decreased cyclin D1, pERK, and MMP9 expression. In addition, ketamine increased ROS and cleaved caspase-3 expression and induced apoptosis. The anti-cancer effect of ketamine was more pronounced in A549 cells when compared with H4 cells. MK801 showed similar effects to those of ketamine. Ketamine suppressed cell proliferation and migration in both neuroglioma and lung cancer cells, likely through the antagonization of NMDA receptors.
Li X, Chang E, Cui J, et al., 2023, Bv8 mediates myeloid cell migration and enhances malignancy of colorectal cancer, Frontiers in Immunology, Vol: 14, Pages: 1-13, ISSN: 1664-3224
Colorectal cancer (CRC) is the third most predominant malignancy in the world. Although the importance of immune system in cancer development has been well established, the underlying mechanisms remain to be investigated further. Here we studied a novel protein prokineticin 2 (Prok2, also known as Bv8) as a key pro-tumoral factor in CRC progression in in vitro and ex vivo settings. Human colorectal tumor tissues, myeloid cell lines (U937 cells and HL60 cells) and colorectal cancer cell line (Caco-2 cells) were used for various studies. Myeloid cell infiltration (especially neutrophils) and Bv8 accumulation were detected in human colorectal tumor tissue with immunostaining. The chemotactic effects of Bv8 on myeloid cells were presented in the transwell assay and chemotaxis assy. Cultured CRC cells treated with myeloid cells or Bv8 produced reactive oxygen species (ROS) and vascular endothelial growth factor (VEGF). Furthermore, ROS and VEGF acted as pro-angiogenesis buffer in myeloid cell-infiltrated CRC microenvironment. Moreover, myeloid cells or Bv8 enhanced energy consumption of glycolysis ATP and mitochondria ATP of CRC cells. Interestingly, myeloid cells increased CRC cell viability, but CRC cells decreased the viability of myeloid cells. ERK signalling pathway in CRC cells was activated in the presence of Bv8 or co-cultured myeloid cells. In conclusion, our data indicated the vital roles of Bv8 in myeloid cell infiltration and CRC development, suggesting that Bv8 may be a potential therapeutic target for colorectal cancer-related immunotherapy.
Zhao J, Le Z, Chu L, et al., 2023, Risk factors and outcomes of intraoperative hypothermia in neonatal and infant patients undergoing general anesthesia and surgery, FRONTIERS IN PEDIATRICS, Vol: 11, ISSN: 2296-2360
Rampes S, Ma D, 2023, The potential impact of COVID-19 disease caused multi-organ injuries on patients' surgical outcomes, Anesthesiology and Perioperative Science, Vol: 1
<jats:title>Abstract</jats:title><jats:sec> <jats:title>Purpose</jats:title> <jats:p>To provide an expert commentary on the impact of prior COVID-19 infection on patient’s surgical outcomes and postoperative recovery. To highlight the need for greater focus on peri-operative care of patients who have recovered from COVID-19.</jats:p> </jats:sec><jats:sec> <jats:title>Methods</jats:title> <jats:p>A narrative review of the literature was conducted by searching Pubmed and EMBASE for relevant articles using keywords such as “COVID-19”, “Coronavirus”, “surgery” and “peri-operative infection”.</jats:p> </jats:sec><jats:sec> <jats:title>Results</jats:title> <jats:p>Post-COVID-19 condition also known as long COVID has an estimated incidence of between 3.0 to 11.7%. COVID-19 has been shown to cause a series of short and long-term sequelae including cardiopulmonary complications, renal impairment, chronic fatigue and muscular deconditioning. Peri-operative infection with COVID-19 is associated with increased peri-operative mortality. Elective surgery patients who developed COVID-19 were 26 times more likely to die whilst in hospital compared to controls without COVID-19 infection, and for emergency surgery patients with COVID-19 infection were six times more likely to die. A large international prospective cohort study identified that patients who had surgery delayed over 7 weeks from the date of COVID-19 infection had no increased 30-day postoperative mortality, except those with ongoing symptoms.</jats:p> </jats:sec><jats:sec> <jats:title>Conclusions</jats:title> <jats:p>COVID-19 infection and its complications have be
Li P, Wang Y, Li H, et al., 2023, Prediction of postoperative infection in elderly using deep learning-based analysis: an observational cohort study, AGING CLINICAL AND EXPERIMENTAL RESEARCH, Vol: 35, Pages: 639-647, ISSN: 1594-0667
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