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• This review evaluated the add-on effects of Xiaojin capsule on Hashimoto's thyroiditis. • Xiaojin capsule was effective in lowing thyroid antibody levels. • No serious adverse events were observed from Xiaojin capsule. • Xiaojin capsule shows potential clinical use in Hashimoto's thyroiditis. Hashimoto's thyroiditis (HT) is a common autoimmune disease of the thyroid gland and the main cause of hypothyroidism. Currently, Chinese medicine is widely used in clinical treatment, and Chinese patent medicine is more convenient for application. We conducted a meta-analysis of previously published literature to evaluate the efficacy and safety of Xiaojin capsule combined with levothyroxine (LT4) or selenium yeast in the treatment of HT, which also provided evidence-based medical evidence for traditional Chinese medicine in HT treatment. We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) to evaluate the effect of Xiaojin capsule on HT. The study was funded by National Natural Science Foundation of China (No. 81973855), and registered on PROSPERO (CRD42023412656). We searched PubMed, Embase, Web of Science, Cochrane Library, Chinese Scientific Journal Database (VIP), WanFang Database, China National Knowledge Information Database (CNKI), and SinoMed from inception to August 15, 2023. Two independent authors reviewed and coded the identified literature. Data analysis was performed using RevMan 5.3 software. We synthesized the results as standardized mean differences (SMD), mean difference (MD) 95 % confidence interval (CI) or relative risk (RR) 95 % CI. The Cochrane Systematic Risk of Bias Assessment Tool was used to assess the quality of the included studies. Thirteen RCTs with 1414 participants were included. The meta-analysis showed that compared with LT4 or selenium yeast alone, oral Xiaojin capsule combined with LT4 significantly reduced serum antibody levels against thyroid peroxidase (TPOAb) (SMD= −3.4, 95 % CI: −4.52 to −2.27, P<0.00001), oral Xiaojin capsule combined with selenium yeast reduced serum TPOAb (MD= −39.13, 95 % CI: −49.97 to −28.3, P<0.00001); oral Xiaojin capsule combined with LT4 significantly reduced serum antibody levels against thyroglobulin (TGAb) (SMD= −3.06, 95 % CI: −4.12 to −1.99, P<0.00001); increased clinical efficiency rate (RR=1.16, 95 % CI: 1.10 to 1.21, P<0.00001) and serum free thyroxine (FT4; SMD=1.18, 95 % CI: 0.47 to 1.88, P <0.00001) levels, and reduced thyroid volume (SMD =−0.59, 95 % CI: −0.87 to −0.32, P<0.0001). The effect on serum free triiodothyronine levels in two groups was not significant, and Xiaojin capsules did not increase the incidence of adverse events. Xiaojin capsule combined with LT4 for treating HT significantly reduced serum TPOAb and TGAb levels, increased serum FT4 levels, and improved goiter. However, the strength of the evidence needs to be improved because of the poor quality of the included studies, and further validation by multiple high-quality randomized controlled trials with comprehensive outcome reporting is needed in the future. [ABSTRACT FROM AUTHOR]

The outbreak of a new coronavirus (severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]) in China in December 2019 has brought serious challenges to disease prevention and public health. Patients with severe coronavirus disease 2019 (COVID-19) who undergo cardiovascular surgery necessitate extremely high demands from anesthesia personnel, and face high risks of mortality and morbidity. Based on the current understanding of COVID-19 and the clinical characteristics of cardiovascular surgical patients, the authors provide anesthesia management guidelines for cardiovascular surgery along with the prevention and control of COVID-19. [ABSTRACT FROM AUTHOR]

The complex progression of type-2 diabetes (T2DM) may result in increased susceptibility to myocardial ischemia-reperfusion (IR) injury. IR injuries in multiple organs involves ferroptosis. Recently, the clock gene Rev-erbα has aroused considerable interest as a novel therapeutic target for metabolic and ischemic heart diseases. Herein, we investigated the roles of Rev-erbα and ferroptosis in myocardial IR injury during T2DM and its potential mechanisms. A T2DM model, myocardial IR and a tissue-specific Rev-erbα−/− mouse in vivo were established, and a high-fat high glucose environment with hypoxia-reoxygenation (HFHG/HR) in H9c2 were also performed. After myocardial IR, glycolipid profiles, creatine kinase-MB, AI, and the expression of Rev-erbα and ferroptosis-related proteins were increased in diabetic rats with impaired cardiac function compared to non-diabetic rats, regardless of the time at which IR was induced. The ferroptosis inhibitor ferrostatin-1 decreased AI in diabetic rats given IR and LPO levels in cells treated with HFHG/HR, as well as the expression of Rev-erbα and ACSL4. The ferroptosis inducer erastin increased AI and LPO levels and ACSL4 expression. Treatment with the circadian regulator nobiletin and genetically targeting Rev-erbα via siRNA or CRISPR/Cas9 technology both protected against severe myocardial injury and decreased Rev-erbα and ACSL4 expression, compared to the respective controls. Taken together, these data suggest that ferroptosis is involved in the susceptibility to myocardial IR injury during T2DM, and that targeting Rev-erbα could alleviate myocardial IR injury by inhibiting ferroptosis. [Display omitted] • The T2DM in rats have a higher susceptibility to myocardial IR, relating to the clock gene Rev-erbα and ferroptosis. • ACSL4 participates in diabetic myocardial IR injury, also characterized by rhythmic expression across the circadian cycle. • Pharmacological or genetic targeting of Rev-erbα attenuated myocardial IR injury during T2DM by inhibiting ferroptosis. [ABSTRACT FROM AUTHOR]

Neuroinflammation is a major driver of postoperative cognitive dysfunction (POCD). The cyclic GMP-AMP synthase-stimulator of interferon gene (cGAS–STING) signaling is a prominent alarming device for aberrant double-stranded DNA (dsDNA) that has emerged as a key mediator of neuroinflammation in cognitive-related diseases. However, the role of the cGAS–STING pathway in the pathogenesis of POCD remains unclear. A POCD model was developed in male C57BL/6J mice by laparotomy under isoflurane (Iso) anesthesia. The cGAS inhibitor RU.521 and caspase-3 agonist Raptinal were delivered by intraperitoneal administration. BV2 cells were exposed to Iso and lipopolysaccharide (LPS) in the absence or presence of RU.521, and then cocultured with HT22 cells in the absence or presence of Raptinal. Cognitive function was assessed using the Morris water maze test and novel object recognition test. Immunofluorescence assays were used to observe the colocalization of dsDNA and cGAS. The downstream proteins and pro-inflammatory cytokines were detected using the Western blot and enzyme-linked immunosorbent assay (ELISA). Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was used to assess the degree of cell death in the hippocampus following anesthesia/surgery treatment. Isoflurane/laparotomy and Iso + LPS significantly augmented the levels of cGAS in the hippocampus and BV2 cells, accompanied by mislocalized dsDNA accumulation in the cytoplasm. RU.521 alleviated cognitive impairment, diminished the levels of 2′3′-cGAMP, cGAS, STING, phosphorylated NF-κB p65 and NF-κB-pertinent pro-inflammatory cytokines (TNFα and IL-6), and repressed pyroptosis-associated elements containing cleaved caspase-3, N-GSDME, IL-1β and IL-18. These phenotypes could be rescued by Raptinal in vivo and in vitro. These findings suggest that pharmacological inhibition of cGAS mitigates neuroinflammatory burden of POCD by dampening caspase-3/GSDME-dependent pyroptosis, providing a potential therapeutic strategy for POCD. • The cGAS-STING pathway was up-regulated in the hippocampus of POCD mice. • The cGAS inhibitor RU.521 ameliorated POCD. • Inhibition of cGAS mitigated neuronal caspase-3/GSDME-mediated pyroptosis. [ABSTRACT FROM AUTHOR]

[Display omitted] Ovarian tumor domain-containing protease 1 (OTUD1) is a critical negative regulator that promotes innate immune homeostasis and is extensively involved in the pathogenesis of sepsis. In this study, we performed a powerful integration of multiomics analysis and an experimental mechanistic investigation to elucidate the immunoregulatory role of OTUD1 in sepsis at the clinical, animal and cellular levels. Our study revealed the upregulation of OTUD1 expression and the related distinctive alterations observed via multiomics profiling in clinical and experimental sepsis. Importantly, in vivo and in vitro , OTUD1 was shown to negatively regulate inflammatory responses and play a protective role in sepsis-induced pathological lung injury by mechanistically inhibiting the activation of the transforming growth factor-beta-activated kinase 1 (TAK1)-mediated mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-κB) signaling pathways in the present study. Subsequently, we probed the molecular mechanisms underlying OTUD1′s regulation of NF-κB and MAPK pathways by pinpointing the target proteins that OTUD1 can deubiquitinate. Drawing upon prior research conducted in our laboratory, it has been demonstrated that tumor necrosis factor-α-induced protein 8-like 2 (TIPE2) performs a protective function in septic lung injury and septic encephalopathy by suppressing the NF-κB and MAPK pathways. Hence, we hypothesized that TIPE2 might be a target protein of OTUD1. Additional experiments, including Co-IP, immunofluorescence co-localization, and Western blotting, revealed that OTUD1 indeed has the ability to deubiquitinate TIPE2. In summary, OTUD1 holds potential as an immunoregulatory and inflammatory checkpoint agent, and could serve as a promising therapeutic target for sepsis-induced lung injury. [ABSTRACT FROM AUTHOR]

Diabetes is a widespread disease that threatens the life and health of human beings, and diabetic cardiomyopathy (DCM) is one of the major complications of diabetic patients. The pathological mechanisms of DCM are complex, including inflammation, endoplasmic reticulum stress, and oxidative stress that have been reported previously. Although recent studies suggested that ferroptosis is also involved in the progression of DCM, the exact mechanism remains unclear. Rev-erbα cardiac conditional knockout mice were generated and type 2 diabetes were induced by high fat diet (HFD) and intraperitoneal injection of streptozotocin (STZ) in in vivo experiments. In parallel, our in vitro experiments entailed the introduction of elevated levels of glucose (HG) and palmitic acid (PA) to induce glycolipid toxicity in H9c2 cardiomyocytes. Further deterioration of cardiac function was detected by echocardiography after the clock gene rev-erbα was knocked out. This was accompanied by significant elevations in markers of inflammation, myocardial fibrosis, and oxidative stress. In addition, iron content, transmission electron microscopy (TEM), and RT-PCR assays confirmed significantly increased levels of ferroptosis in rev-erbα-deficient DCM. Intriguingly, Co-Immunoprecipitation (Co-IP) data uncovered an interaction between rev-erbα and nuclear factor E2-related factor 2 (NRF2) in diabetic myocardial tissues. It is worth highlighting that ferroptosis within cardiomyocytes witnessed significant mitigation upon the administration of sulforaphane (SFN), an NRF2 agonist, to HG + PA-incubated H9c2 cells. Our study demonstrates for the first time that knockdown of the clock gene rev-erbα exacerbates myocardial injury and ferroptosis in type 2 diabetic mice, which can be reversed by activating NRF2. • Our study is the first study to identify rev-erbα as a potentially promising molecular target for the treatment of DCM. • The deletion of rev-erbα can have deleterious effects by exacerbating myocardial inflammation, oxidative stress, cardiac dysfunction, and ferroptosis. • And we found that rev-erbα could regulate ferroptosis by regulating the antioxidant factor NRF2. [ABSTRACT FROM AUTHOR]

• COVID-19 spread rapidly around the world. • Assessed the abnormal coagulation parameters in infected patients. • Coagulopathy could be considered as a risk factor for disease severity and mortality of COVID-19. • Help clinicians to identify the incidence of poor outcomes in COVID-19 patients. To determine whether abnormal coagulation parameters are associated with disease severity and poor prognosis in patients with 2019 Corona Virus Disease (COVID-19). A systematic literature search was conducted using the databases PubMed, Embase, and Web of sciences until April 25, 2020. We included a total of 15 studies with 2277 patients. Platelet count (PLT), prothrombin time (PT), activated partial thromboplastin time (APTT), D-dimer (D-D), and fibrinogen (FIB) were collected and analyzed. The statistical results were expressed as the effect measured by mean difference (MD) with the related 95% confidence interval (CI). The PLT level of severe cases was lower than that of mild cases, while the levels of PT, D-D, and FIB were higher than those of mild cases (P < 0.05). The level of APTT had no statistical difference between two groups (P > 0.05). PT of ICU patients was significantly longer (P < 0.05) than that of non-ICU patients. In non-survivors, PT and D-D were higher, yet PLT was lower than that of survivors (P < 0.05). There was no significant difference in APTT between survivors and non-survivors (P > 0.05). The funnel plot and Egger's regression test demonstrated that there was no publication bias. Our data support the notion that coagulopathy could be considered as a risk factor for disease severity and mortality of COVID-19, which may help clinicians to identify the incidence of poor outcomes in COVID-19 patients. [ABSTRACT FROM AUTHOR]

[Display omitted] Sepsis-associated encephalopathy (SAE) is an acute brain dysfunction induced by systemic inflammation caused by sepsis and is one of the most common types of encephalopathy in intensive care units. Deteriorative neuroinflammation is closely related to the development of brain injury, which often transforms into common pathological manifestations in patients with severe sepsis. Therefore, taking necessary preventive and protective measures for potential brain injury and promptly reducing neuroinflammatory injury is necessary to improve the long-term prognoses of patients. Tumor necrosis factor-α-induced protein 8-like 2 (TIPE2) can play a significant protective role in septic lung injury, but studies on its expression and role in neurological diseases are rare. In the present study, we found that TIPE2 can expressed in microglia and ameliorate brain injury caused by SAE by suppressing neuroinflammation. The RhoA/ROCK2 pathway is the central coordinator of tissue injury response, and the activation of RhoA participates in the lipopolysaccharide-induced activation of the nuclear factor kappa B (NF-κB) signaling pathway. The activation of RhoA and phosphorylation of NF-κB was enhanced after TIPE2 deficiency. Importantly, TIPE2 negatively regulates inflammatory responses in vivo and in vitro and plays a protective role in SAE by inhibiting the activation of RhoA/ROCK2–NF-κB signaling pathways. The ultimate aim of our proposed project is to provide a theoretical basis for the development of a novel strategy for the early prevention and therapy of SAE. [ABSTRACT FROM AUTHOR]

Highlights • Sleep deprivation impairs memory and prolongs recovery after sevoflurane inhalation. • Sleep deprivation induces hippocampal clock gene expression abnormalities. • Sleep deprivation raises hippocampal inflammatory levels via astrocytic activation. • Sleep deprivation harms hippocampal neuron morphology after sevoflurane inhalation. Abstract Sleep disturbance can result in memory impairment, and both sleep and hippocampal memory formation are maintained by circadian clock genes. Although preoperative sleep deprivation is known to be an independent risk factor for postoperative cognitive dysfunction (POCD) after inhalation anesthesia, the circadian mechanisms involved are currently unclear. To examine this issue, we constructed models of rapid eye movement sleep deprivation (RSD) and POCD after sevoflurane inhalation, to evaluate the circadian mechanisms underlying preoperative sleep deprivation-induced POCD after sevoflurane inhalation. Morris water maze probe test performance revealed that RSD aggravated the hippocampal-dependent memory impairment induced by sevoflurane anesthesia, and the recovery period of memory impairment was prolonged for more than a week by sleep deprivation. Western blot analysis revealed that sleep deprivation inhibited hippocampal Bmal1 and Egr1 expression for more than 7 days after sevoflurane inhalation. Importantly, hippocampal Per2 expression levels were first decreased by sevoflurane inhalation then increased from the third day by sleep deprivation. Sleep deprivation enhanced the expression of hippocampal inflammatory factors IL-1β and IL-6 after sevoflurane inhalation. In addition, sevoflurane inhalation activated the plasma expression of S100β and IL-6, particularly after sleep deprivation. Sleep deprivation aggravated pathogenic impairment of pyramidal neurons and activated astrocytes in CA1 after sevoflurane inhalation. These results suggest that preoperative RSD aggravates hippocampal memory impairment by enhancing neuroinflammatory injuries after sevoflurane inhalation, which is related to hippocampal clock gene abnormalities. [ABSTRACT FROM AUTHOR]

Myocardial ischemia-reperfusion injury is a common condition in cardiovascular diseases, and the mechanism of its occurrence involves multiple complex metabolic pathways and signaling pathways. Among these pathways, glucose metabolism and lipid metabolism play important roles in regulating myocardial energy metabolism. Therefore, this article focuses on the roles of glucose metabolism and lipid metabolism in myocardial ischemia-reperfusion injury, including glycolysis, glucose uptake and transport, glycogen metabolism and the pentose phosphate pathway; and triglyceride metabolism, fatty acid uptake and transport, phospholipid metabolism, lipoprotein metabolism, and cholesterol metabolism. Finally, due to the different alterations and development of glucose metabolism and lipid metabolism in myocardial ischemia-reperfusion, there are also complex interregulatory relationships between them. In the future, modulating the equilibrium between glucose metabolism and lipid metabolism in cardiomyocytes and ameliorating aberrations in myocardial energy metabolism represent highly promising novel strategies for addressing myocardial ischemia-reperfusion injury. Therefore, a comprehensive exploration of glycolipid metabolism can offer novel theoretical and clinical insights into the prevention and treatment of myocardial ischemia-reperfusion injury. [Display omitted] • An overview of myocardial metabolism and mechanisms of myocardial metabolism in myocardial ischemia-reperfusion injury. • Mechanisms and recent studies of glucose metabolism and lipid metabolism in myocardial ischemia-reperfusion injury. • Interactions and mechanisms between glucose metabolism and lipid metabolism in myocardial ischemia-reperfusion injury. • Targeting glucolipid metabolism is an effective strategy for the treatment of myocardial ischemia-reperfusion injury. [ABSTRACT FROM AUTHOR]

Critical components of the Qinghai-Tibet Plateau natural-gas hydrate (NGH) petroleum system has been examined in this study. The results demonstrate that the Kaixinling-Wuli permafrost region contains viable prospects for gas hydrate exploration within favorable temperature and pressure stability conditions. In the study area, the average annual temperature of ground surface is −4.2 °C, the thickness of permafrost ranges from 40 to 150 m (average 84 m), and the geothermal gradient beneath the permafrost is between 1.54 °C/100 m and 2.67 °C/100 m (average 2.03 °C/100 m). The thickness of the methane-gas hydrate stability zone (GHSZ) is approximately 240–450 m. The Upper Permian Nayixiong Formation is dominated by braided delta and shallow shelf facies under mostly reducing conditions. The potential swamp deposited source rocks have a high total organic carbon (TOC) content that features a mixture of kerogen types II or III and an average vitrinite reflectance (R o ) of 2.04%. Overall, the thick sedimentary column in this region, its abundance of organic matter and its high thermal maturity suggest that the Nayixiong Formation source rocks have a high gas-generation potential. An effective fault-fracture-pore system also provides migration channels for deeper gas and also act as a reservoir for vein-type gas hydrate occurrences. The Kaixinling-Wuli area, when compared to other regions in the Qinghai-Tibet Plateau, exhibits greater gas hydrate petroleum system exploration potential as a result of the favorable temperature/pressure stability conditions and effective gas and gas-hydrate migration-storage system. [ABSTRACT FROM AUTHOR]

Dexmedetomidine has been introduced in emergence coughing, agitation, and shivering prevention. This study aimed to investigate the optimal dose of dexmedetomidine for emergence cough prophylaxis. In this randomized, double-blinded, and prospective trial, 356 patients scheduled for an endovascular interventional procedure were randomly assigned to 0.3 (D 0.3), 0.4 (D 0.4), 0.5 (D 0.5), and 0.6 (D 0.6) μg·kg−1·h−1 dexmedetomidine rate, or saline control (C), from anesthesia induction until the end of surgery. The primary outcomes measured were cough grade and frequency. Additionally, groups were compared according to mean arterial pressure (MAP), heart rate, agitation, shivering, postoperative nausea and vomiting (PONV), extubation time, sedation scores, and postoperative first night sleep quality (secondary outcomes). A total of 351 patients were included in the analysis. The respective incidences of D 0.3, D 0.4, and D 0.5 versus C group were: 78.6%, 68.6%, 53.4% and 42.9% vs 89.7% for cough (p = 0.002, p < 0.001, and p < 0.001 between group D 0.4, D 0.5 and D 0.6 vs C, respectively); 30%, 27.1%, 20.5%, 15.7% vs 44.1% for agitation (p = 0.04, p = 0.003, and p < 0.001 between group D 0.4, D 0.5 and D 0.6 vs C, respectively); 8.6%, 7.1%, 6.8%, 5.7% vs 22.1% for shivering (p = 0.027, p = 0.013, p = 0.01, and p = 0.01 between D 0.3, D 0.4, D 0.5 and D 0.6 vs C, respectively); and 52.9%, 57.1%, 42.5%, 44.3% vs 61.8% for poor sleep quality (p = 0.02 and p = 0.04 between group D 0.5 and D 0.6 vs C, respectively). D 0.4, D 0.5 and D 0.6 showed lower MAP during extubation, compared with the C group. Also, D 0.5 and D 0.6 presented a slight delay in extubation (3.1 and 3.3 min longer than C; p = 0.002 and p < 0.001, respectively). Meanwhile, the frequency of atropine, vasopressor administration, PONV and dizziness were similar to the control. Both 0.5 and 0.6 μg·kg−1·h−1 dexmedetomidine infusion rates effectively mitigated emergence coughing with prolonged extubation time, besides sleep disturbance. D 0.4, D 0.5, and D 0.6 reduced agitation and sustained hemodynamic stability. Finally, the four doses applied were effective in shivering attenuation. [Display omitted] [ABSTRACT FROM AUTHOR]

Chronic stress is associated with impairment of synapse plasticity in hippocampus and cognitive dysfunction in rodent and human. Notably, corticosterone (CORT) is believed to take responsibility for dendritic atrophy and reduction of spine number induced by chronic stress in hippocampus. But little is known about the molecular mechanisms underlying CORT induced abnormal synapse plasticity and cognitive dysfunction. Drebrin is an F-actin binding protein that modulates memory formation and maintenance by controlling the genesis and morphology of dendritic spines. In addition, miRNAs have been reported to participate in the negative regulation of protein-coding genes. In this study, five miRNAs capable of targeting Drebrin were selected by searching miRNA databases. One of these miRNAs, miR-19b-3p, was found to be upregulated in the hippocampal neurons of mice with chronic restraint stress (CRS). Luciferase reporter assay and Fluorescence in situ hybridization (FISH) were employed to identify the interaction between miR-19b-3p and Drebrin. In addition, silencing miR-19b-3p expression in vivo using an antagomir or in vitro using an inhibitor increased Drebrin expression, ameliorated the abnormal dendritic structure and upregulated the spine density in hippocampal CA1 pyramidal neurons of CRS mice and primary hippocampal neurons cultured under CORT stimulation, respectively. Electrophysiological analysis revealed that inhibition of miR-19b-3p rescued the limited synaptic transmission and synaptic plasticity in hippocampal neurons. Moreover, blocking miR-19b-3p drastically protected against cognitive deficits in CRS mice. These in vivo and in vitro findings indicate that the upregulation of miR-19b-3p exacerbates CRS-induced abnormal synaptic plasticity and cognitive impairment by targeting Drebrin. • CRS stimulation was able to up-regulate miR-19b-3p and down-regulate Drebrin in hippocampal neurons. • CORT mediated miR-19b-3p/Drebrin axis under CRS stimulation. • Inhibition of miR-19b-3p rescued abnormal synaptic plasticity and cognitive deficits by targeting Drebrin in CRS mice. [ABSTRACT FROM AUTHOR]

• The IgA and IgE levels increased significantly, while C3 level decreased in non-survivors. • Decreased complement C3 level was correlated with increased odds of death. • Low level of C3 may be an alert to the attending that patients may be of additional management. • Inhibition of the complement pathway might be an effective therapeutic to COVID-19 patients. To describe the humoral immune feature of patients with coronavirus disease 2019 (COVID-19). The levels of total immunoglobulins (IgG, IgM, IgA, and IgE), complement (C3, C4) results were retrospectively analyzed in COVID-19 patients. Univariable and multivariable logistic regression were performed to explore the risk factors associated with the in-hospital death. A total of 236 patients were enrolled in this study, of which 169 were transferred to another institution or discharged (survival group) and 67 died in hospital (non-survival group). Compared with survivors, the levels of IgA and IgE in non-survivors increased significantly, and level of complement C3 decreased. Non-survivors also showed higher incidence of chest tightness, breath shortness and dyspnoea; higher levels of inflammatory indicators, leukocytes and neutrophils; and low levels of lymphocyte subsets. Multivariable regression showed increasing odds of in-hospital death associated with older age (HR: 1.099; 95%CI: 1.057–1.143; p < 0.0001), d-dimer greater (HR: 1.294; 95%CI: 1.138–1.473; p < 0.0001) and decreased complement C3 level (HR: 0.073; 95%CI: 0.007–0.722; p = 0.025) on admission. Finally, in survival COVID-19 patients whose humoral immunity was re-examined, C3 levels tended to increase, while in non-survivors it decreased. Low level of complement C3 may be an alert to the admitted COVID-19 patients with additional management. Inhibition of the complement pathway might be an effective therapeutic to COVID-19 patients. [ABSTRACT FROM AUTHOR]

• Performing intubation for COVID-19 patients have a risk of contracting the disease, ranging from 1.56%-4.37%. • The symptoms from intubation acquired COVID-19 are generally mild to moderate. • Preventable intubation acquired infection should be a top priority to protect those involved in intubations. [ABSTRACT FROM AUTHOR]