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1.
Hum Exp Toxicol ; : 9603271211058884, 2021 Nov 18.
Artigo em Inglês | MEDLINE | ID: mdl-34792426

RESUMO

Allergic rhinitis (AR) is a common allergic inflammatory and chronic reactive disease caused by allergen-induced immunoglobulin E (IgE). Tanshinone IIA (Tan IIA) is one of the active ingredients in Salvia miltiorrhiza Bunge (Danshen) and plays a vital role in inhibiting inflammation. Thus, we hypothesized that Tan IIA has anti-allergic effects and studied the function of Tan IIA in mast cells and an AR animal model. We induced RBL-2H3 cell sensitization with monoclonal anti-2,4,6-dinitrophenyl-immunoglobulin (Ig) E/human serum albumin (DNP-IgE/HSA) and constructed an ovalbumin (OVA)-induced AR model in mice. The role of Tan IIA in AR progression was studied using the MTT assay, ELISA, western blot, toluidine blue staining, HE staining, and Alcian blue and safranin O (A&S) staining. Tan IIA treatment significantly increased IgE/HSA-induced cell viability. However, Tan IIA treatment markedly downregulated the expression levels of ß-hexosaminidase, histamine, tumor necrosis factor (TNF-α), interleukin 1ß (IL-1ß), IL-4, and IL-5 in IgE/HSA-induced cells. Furthermore, Tan IIA improved typical symptoms in the OVA-induced AR model mice by inhibiting the phospholipase Cγ1 (PLCγ1)/protein kinase C (PKC)/IP3R pathway. Additionally, Tan IIA effectively improved the degranulation of RBL-2H3 cells and OVA-induced AR in mice. Together, these results suggest that Tan IIA may be a potential drug for the treatment of AR in the future.

2.
Nat Commun ; 12(1): 6589, 2021 11 15.
Artigo em Inglês | MEDLINE | ID: mdl-34782621

RESUMO

ASH1L, a histone methyltransferase, is identified as a top-ranking risk factor for autism spectrum disorder (ASD), however, little is known about the biological mechanisms underlying the link of ASH1L haploinsufficiency to ASD. Here we show that ASH1L expression and H3K4me3 level are significantly decreased in the prefrontal cortex (PFC) of postmortem tissues from ASD patients. Knockdown of Ash1L in PFC of juvenile mice induces the downregulation of risk genes associated with ASD, intellectual disability (ID) and epilepsy. These downregulated genes are enriched in excitatory and inhibitory synaptic function and have decreased H3K4me3 occupancy at their promoters. Furthermore, Ash1L deficiency in PFC causes the diminished GABAergic inhibition, enhanced glutamatergic transmission, and elevated PFC pyramidal neuronal excitability, which is associated with severe seizures and early mortality. Chemogenetic inhibition of PFC pyramidal neuronal activity, combined with the administration of GABA enhancer diazepam, rescues PFC synaptic imbalance and seizures, but not autistic social deficits or anxiety-like behaviors. These results have revealed the critical role of ASH1L in regulating synaptic gene expression and seizures, which provides insights into treatment strategies for ASH1L-associated brain diseases.

3.
J Hepatol ; 2021 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-34736969

RESUMO

BACKGROUND & AIMS: Drug-induced liver injury (DILI) is a leading cause of acute liver failure, and treatment of DILI remains a challenge. MG53 is a muscle-derived tissue-repair protein that circulates in the bloodstream whose physiological role in protection against DILI has not been examined. METHODS: Recombinant MG53 protein (rhMG53) was administered exogenously, using mice with deletion of MG53 or RIPK3. Live cell imaging, histological, biochemical, and molecular studies were used to investigate the mechanisms that underlie the extracellular and intracellular action of rhMG53 in hepatoprotection. RESULTS: Systemic administration of rhMG53 protein, in mice, can prophylactically and therapeutically treat DILI induced through exposure to acetaminophen tetracycline, concanavalin A, carbon tetrachloride, or thioacetamide. Circulating MG53 protects hepatocytes from injury through direct interaction with MLKL at the plasma membrane. Extracellular MG53 can enter hepatocytes and act as an E3-ligase to mitigate RIPK3-mediated MLKL phosphorylation and membrane translocation. CONCLUSIONS: Our data show that the membrane-delimited signaling and cytosolic dual action of MG53 effectively preserves hepatocyte integrity during DILI. rhMG53 may be a potential treatment option for patients with DILI. LAY SUMMARY: Interventions to treat drug-induced liver injury and halt its progression into liver failure are of great value to the medical society. The present study reveals that muscle-liver cross talk, with MG53 as a messenger, serves an important role in liver-cell protection.

4.
Antioxidants (Basel) ; 10(10)2021 Sep 25.
Artigo em Inglês | MEDLINE | ID: mdl-34679657

RESUMO

Respiratory failure from progressive respiratory muscle weakness is the most common cause of death in amyotrophic lateral sclerosis (ALS). Defects in neuromuscular junctions (NMJs) and progressive NMJ loss occur at early stages, thus stabilizing and preserving NMJs represents a potential therapeutic strategy to slow ALS disease progression. Here we demonstrate that NMJ damage is repaired by MG53, an intrinsic muscle protein involved in plasma membrane repair. Compromised diaphragm muscle membrane repair and NMJ integrity are early pathological events in ALS. Diaphragm muscles from ALS mouse models show increased susceptibility to injury and intracellular MG53 aggregation, which is also a hallmark of human muscle samples from ALS patients. We show that systemic administration of recombinant human MG53 protein in ALS mice protects against injury to diaphragm muscle, preserves NMJ integrity, and slows ALS disease progression. As MG53 is present in circulation in rodents and humans under physiological conditions, our findings provide proof-of-concept data supporting MG53 as a potentially safe and effective therapy to mitigate ALS progression.

6.
Mol Cancer ; 20(1): 118, 2021 09 14.
Artigo em Inglês | MEDLINE | ID: mdl-34521423

RESUMO

BACKGROUND: Cancer cells develop resistance to chemotherapeutic intervention by excessive formation of stress granules (SGs), which are modulated by an oncogenic protein G3BP2. Selective control of G3BP2/SG signaling is a potential means to treat non-small cell lung cancer (NSCLC). METHODS: Co-immunoprecipitation was conducted to identify the interaction of MG53 and G3BP2. Immunohistochemistry and live cell imaging were performed to visualize the subcellular expression or co-localization. We used shRNA to knock-down the expression MG53 or G3BP2 to test the cell migration and colony formation. The expression level of MG53 and G3BP2 in human NSCLC tissues was tested by western blot analysis. The ATO-induced oxidative stress model was used to examine the effect of rhMG53 on SG formation. Moue NSCLC allograft experiments were performed on wild type and transgenic mice with either knockout of MG53, or overexpression of MG53. Human NSCLC xenograft model in mice was used to evaluate the effect of MG53 overexpression on tumorigenesis. RESULTS: We show that MG53, a member of the TRIM protein family (TRIM72), modulates G3BP2 activity to control lung cancer progression. Loss of MG53 results in the progressive development of lung cancer in mg53-/- mice. Transgenic mice with sustained elevation of MG53 in the bloodstream demonstrate reduced tumor growth following allograft transplantation of mouse NSCLC cells. Biochemical assay reveals physical interaction between G3BP2 and MG53 through the TRIM domain of MG53. Knockdown of MG53 enhances proliferation and migration of NSCLC cells, whereas reduced tumorigenicity is seen in NSCLC cells with knockdown of G3BP2 expression. The recombinant human MG53 (rhMG53) protein can enter the NSCLC cells to induce nuclear translation of G3BP2 and block arsenic trioxide-induced SG formation. The anti-proliferative effect of rhMG53 on NSCLC cells was abolished with knockout of G3BP2. rhMG53 can enhance sensitivity of NSCLC cells to undergo cell death upon treatment with cisplatin. Tailored induction of MG53 expression in NSCLC cells suppresses lung cancer growth via reduced SG formation in a xenograft model. CONCLUSION: Overall, these findings support the notion that MG53 functions as a tumor suppressor by targeting G3BP2/SG activity in NSCLCs.

7.
Cell Discov ; 7(1): 81, 2021 Sep 07.
Artigo em Inglês | MEDLINE | ID: mdl-34489415

RESUMO

Human blastocysts are comprised of the first three cell lineages of the embryo: trophectoderm, epiblast and primitive endoderm, all of which are essential for early development and organ formation. However, due to ethical concerns and restricted access to human blastocysts, a comprehensive understanding of early human embryogenesis is still lacking. To bridge this knowledge gap, a reliable model system that recapitulates early stages of human embryogenesis is needed. Here we developed a three-dimensional (3D), two-step induction protocol for generating blastocyst-like structures (EPS-blastoids) from human extended pluripotent stem (EPS) cells. Morphological and single-cell transcriptomic analyses revealed that EPS-blastoids contain key cell lineages and are transcriptionally similar to human blastocysts. Furthermore, EPS-blastoids are similar with human embryos that were cultured for 8 or 10 days in vitro, in terms of embryonic structures, cell lineages and transcriptomic profiles. In conclusion, we developed a scalable system to mimic human blastocyst development, which can potentially facilitate the study of early implantation failure that induced by developmental defects at early stage.

8.
Aging Cell ; 20(10): e13456, 2021 10.
Artigo em Inglês | MEDLINE | ID: mdl-34547169

RESUMO

Epigenetic abnormality is implicated in neurodegenerative diseases associated with cognitive deficits, such as Alzheimer's disease (AD). A common feature of AD is the accumulation of neurofibrillary tangles composed of hyperphosphorylated tau. Transgenic mice expressing mutant P301S human tau protein develop AD-like progressive tau pathology and cognitive impairment. Here, we show that the euchromatic histone-lysine N-methyltransferase 2 (EHMT2) is significantly elevated in the prefrontal cortex (PFC) of P301S Tau mice (5-7 months old), leading to the increased repressive histone mark, H3K9me2, which is reversed by treatment with the selective EHMT inhibitor UNC0642. Behavioral assays show that UNC0642 treatment induces the robust rescue of spatial and recognition memory deficits in P301S Tau mice. Concomitantly, the diminished PFC neuronal excitability and glutamatergic synaptic transmission in P301S Tau mice are also normalized by UNC0642 treatment. In addition, EHMT inhibition dramatically attenuates the hyperphosphorylated tau level in PFC of P301S Tau mice. Transcriptomic analysis reveals that UNC0642 treatment of P301S Tau mice has normalized a number of dysregulated genes in PFC, which are enriched in cytoskeleton and extracellular matrix organization, ion channels and transporters, receptor signaling, and stress responses. Together, these data suggest that targeting histone methylation enzymes to adjust gene expression could be used to treat cognitive and synaptic deficits in neurodegenerative diseases linked to tauopathies.

9.
Commun Biol ; 4(1): 1067, 2021 09 13.
Artigo em Inglês | MEDLINE | ID: mdl-34518628

RESUMO

Cell embedment into a solid support matrix is considered essential for the culture of intestinal epithelial organoids and tumoroids, but this technique presents challenges that impede scalable culture expansion, experimental manipulation, high-throughput screening and diagnostic applications. We have developed a low-viscosity matrix (LVM) suspension culture method that enables efficient establishment and propagation of organoids and tumoroids from the human large intestine. Organoids and tumoroids cultured in LVM suspension recapitulate the morphological development observed in solid matrices, with tumoroids reflecting the histological features and genetic heterogeneity of primary colorectal cancers. We demonstrate the utility of LVM suspension culture for organoid and tumoroid bioreactor applications and biobanking, as well as tumoroid high-throughput drug sensitivity testing. These methods provide opportunities for the study and use of patient-derived organoids and tumoroids from the large intestine.

10.
Bioengineered ; 12(1): 5870-5882, 2021 12.
Artigo em Inglês | MEDLINE | ID: mdl-34477474

RESUMO

Although osteosarcoma (OS) is the most common malignant tumor among juvenile bone tumors, its treatment plan and clinical outcome have not improved significantly in recent decades. Tetrandrine (TET), a Chinese medicine that is usually used in the therapy of silicosis, hypertension and arthritis, has been confirmed by many studies to possess potent antitumour growth properties, but there are different limitations when describing specific mechanisms. Here, we found that TET can obviously prevent the proliferation, migration and invasion of both 143B and MG63 cells and promote their apoptosis in vitro. Our results for luciferase reporter and Western blotting assays show that TET may exert its antitumour activity by regulating multiplex signaling pathways, including the MAPK/Erk, PTEN/Akt, Juk and Wnt signaling pathways. Furthermore, the regulatory effect of TET on OS cells and related signaling pathways was verified again in vivo. Our findings suggest that the anticancer function of TET on human OS may be mediated by its targeting of multiple signaling pathways and that TET may be used as a single drug or in combination with other drugs during the treatment of OS.

11.
J Obstet Gynaecol ; : 1-6, 2021 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-34590963

RESUMO

Whether paternal epigenetic changes resulting from nutrition might be inherited by their offspring remains unknown. This study evaluated the relationship between preconception paternal body weight and their offspring's birth weight in 1,810 Chinese mother-father-baby trios. Information on paternal and maternal preconception body weight and height was collected via a self-reported questionnaire. Birth weight was collected from medical records. Paternal preconception body weight was associated with offspring's birth weight (p trend = .02) after multivariate adjustment. Each standard deviation increment of paternal body mass index was associated with an additional 29.6 g increase of birth weight (95% confident interval: 5.7 g, 53.5 g). The association was more pronounced in male neonates, and neonates with overweight mothers, and with mothers who gained excessive gestational weight, compared to their counterparts (all p interaction < .05). Sensitivity analyses showed similar pattern to that of the main analysis. Paternal preconception body weight was associated with birth weight of their offspring.Impact statementWhat is already known on this subject? More efforts have previously been put on the maternal contribution to birth weight, however, it is uncertain whether paternal pre-conceptional body weight, an indicator for epigenetic information, might be inherited by their offspring.What do the results of this study add? In the current study that included 1,810 Chinese mother-father-baby trios, a small but significant association was observed between paternal preconception body weight and offspring's birth weight (p trend =.02).What are the implications of these findings for clinical practice and/or further research? Paternal epigenetic information of nutrition could be inherited by their offspring.

12.
BMC Cardiovasc Disord ; 21(1): 469, 2021 09 28.
Artigo em Inglês | MEDLINE | ID: mdl-34583633

RESUMO

OBJECTIVE: We aimed to evaluate the association between the shift of metabolic status and future risk of carotid artery plaque (CAP) in community-based Chinese adults. METHODS: The current study included 9836 Chinese adults (4085 males and 5751 females, mean age 35.8 years) with metabolically healthy status at baseline (2013). Metabolically healthy status was defined as no self-reported history of metabolic diseases and cancer, and normal blood pressure, fasting blood glucose, glycated hemoglobin A1c level, and lipid profiles. Metabolically unhealthy status was defined if any of the following metabolic abnormalities were confirmed twice during follow up: high blood pressure, impaired glucose regulation, high triglycerides, high total cholesterol, high low-density lipoprotein cholesterols, or low high-density lipoprotein cholesterols. The transition was confirmed if participants' metabolic status shifted from baseline healthy to unhealthy status during follow up (2014-2018). RESULTS: We have identified 133 incident cases of CAP during follow up. Compared to those who remained metabolically healthy, the transition to high blood pressure, high total cholesterol, and high low-density lipoprotein cholesterols, were associated with high risk of developing carotid artery plaque (Hazards ratios (HRs) ranged from 1.69 to 2.34; p < 0.05 for all). The transition to impaired glucose regulation, high total triglycerides, and low high-density lipoprotein cholesterols, were associated with high risk of carotid artery plaque only in participants with metabolically healthy overweight at baseline (HR ranged from 1.95 to 4.62; p < 0.05 for all). CONCLUSION: The transition from baseline metabolically healthy status to unhealth status was associated with high risk of incident CAP.

13.
Dalton Trans ; 50(35): 12137-12146, 2021 Sep 14.
Artigo em Inglês | MEDLINE | ID: mdl-34396381

RESUMO

In this article, we synthesized a series of new warm-white emitting persistent luminescent phosphors by co-doping Zn2+ into Pr3+ activated BaLu2Al2Ga2SiO12, and systematically investigated the effect of Zn2+ co-doping on both their photoluminescence and persistent luminescence properties. Following the removal of UV excitation, the phosphor emits warm-white persistent luminescence consisting of greenish-blue and red emissions originating from 3P0 and 1D2 multiplet electron transitions at the 4f level of Pr3+. The luminescence properties of the Ba1-xZnxLu2Al2Ga2SiO12:Pr3+ phosphors can be modified by changing the content of Ba/Zn in the host, which affects the non-radiative energy flow between 5d1-3P0-1D2 levels and resultantly enhances the intensity of the 4f → 4f transition. Compared with the undoped sample, Zn2+ co-doping can significantly enhance the persistent luminescence intensity of the phosphors in the range of 400-800 nm and reduce the intensity in the UV region. Meanwhile, Zn2+ co-doping can also change the intensity ratio between the greenish-blue and red emissions, and the persistent luminescence color can be tuned from red to warm-white with the increase of Zn2+ concentration. Besides, the Zn2+ ions entering the crystal lattice also enhance the persistent luminescence performance by modifying the defect levels in the phosphor. For the optimized phosphor, bright warm-white persistent luminescence can be observed by the naked eye in the dark after the removal of the excitation source for 4 h. Based on the experimental results, a feasible mechanism was also proposed to reveal the persistent luminescence generation process for the BaLu2Al2Ga2SiO12:Pr3+,Zn2+ phosphor.

14.
JCI Insight ; 6(17)2021 Sep 08.
Artigo em Inglês | MEDLINE | ID: mdl-34292883

RESUMO

Aging is associated with chronic oxidative stress and inflammation that affect tissue repair and regeneration capacity. MG53 is a TRIM family protein that facilitates repair of cell membrane injury in a redox-dependent manner. Here, we demonstrate that the expression of MG53 was reduced in failing human hearts and aged mouse hearts, concomitant with elevated NF-κB activation. We evaluated the safety and efficacy of longitudinal, systemic administration of recombinant human MG53 (rhMG53) protein in aged mice. Echocardiography and pressure-volume loop measurements revealed beneficial effects of rhMG53 treatment in improving heart function of aged mice. Biochemical and histological studies demonstrated that the cardioprotective effects of rhMG53 are linked to suppression of NF-κB-mediated inflammation, reducing apoptotic cell death and oxidative stress in the aged heart. Repetitive administration of rhMG53 in aged mice did not have adverse effects on major vital organ functions. These findings support the therapeutic value of rhMG53 in treating age-related decline in cardiac function.

15.
FEBS Open Bio ; 2021 Jun 06.
Artigo em Inglês | MEDLINE | ID: mdl-34092045

RESUMO

Allergic rhinitis (AR) is a long-term noncommunicable inflammatory disease of the nasal mucosa mediated by immunoglobulin E and is mainly caused by exposure of genetically susceptible individuals to environmental allergens. Mast cells contribute to the pathogenesis of allergic and nonallergic inflammatory diseases. Salvinorin A has been previously shown to inhibit leukotriene production and mast cell degranulation to suppress airway hyperresponsiveness caused by sensitization; thus, we hypothesized that salvinorin A has an anti-AR effect. We tested this hypothesis using monoclonal anti-2,4,6-dinitrophenyl immunoglobulin E/human serum albumin-induced rat basophilic leukemia cells (RBL-2H3 cells) and ovalbumin (OVA)-induced AR in mice as in vivo and in vitro AR models, respectively. The expression levels of histamine, ß-hexosaminidase, interleukin-4 and tumor necrosis factor-α were decreased by salvinorin A in vitro. Granule release and F-actin organization were also suppressed by salvinorin A. Furthermore, salvinorin A inhibited OVA-induced features of AR in mice, including nasal rubbing and sneezing, as well as increased OVA-specific immunoglobulin E, histamine, tumor necrosis factor-α and interleukin-4 levels. In addition, salvinorin A decreased the phosphorylation of phosphoinositide 3-kinase/Akt in vitro and in vivo. Our work suggests that salvinorin A suppresses AR caused by sensitization by inhibiting the inflammatory responses of mast cells; thus, salvinorin A may have potential for treatment of AR.

17.
Diagn Interv Radiol ; 27(3): 315-322, 2021 May.
Artigo em Inglês | MEDLINE | ID: mdl-34003119

RESUMO

PURPOSE: We aimed to compare the diagnostic performance and interobserver variability in breast tumor classification with or without the aid of an innovative dual-mode artificial intelligence (AI) architecture, which can automatically integrate information from ultrasonography (US) and shear-wave elastography (SWE). METHODS: Diagnostic performance assessment was performed with a test subset, containing 599 images (from September 2018 to February 2019) from 91 patients including 64 benign and 27 malignant breast tumors. Six radiologists (three inexperienced, three experienced) were assigned to read images independently (independent diagnosis) and then make a secondary diagnosis with the knowledge of AI results. Sensitivity, specificity, accuracy, receiver-operator characteristics (ROC) curve analysis and Cohen's κ statistics were calculated. RESULTS: In the inexperienced radiologists' group, the average area under the ROC curve (AUC) for diagnostic performance increased from 0.722 to 0.765 (p = 0.050) with secondary diagnosis using US-mode and from 0.794 to 0.834 (p = 0.019) with secondary diagnosis using dual-mode compared with independent diagnosis. In the experienced radiologists' group, the average AUC for diagnostic performance was significantly higher with AI system using the US-mode (0.812 vs. 0.833, p = 0.039), but not for dual-mode (0.858 vs. 0.866, p = 0.458). Using the US-mode, interobserver agreement among all radiologists improved from fair to moderate (p = 0.003). Using the dual-mode, substantial agreement was seen among the experienced radiologists (0.65 to 0.74, p = 0.017) and all radiologists (0.62 to 0.73, p = 0.001). CONCLUSION: AI assistance provides a more pronounced improvement in diagnostic performance for the inexperienced radiologists; meanwhile, the experienced radiologists benefit more from AI in reducing interobserver variability.


Assuntos
Neoplasias da Mama , Técnicas de Imagem por Elasticidade , Inteligência Artificial , Neoplasias da Mama/diagnóstico por imagem , Feminino , Humanos , Radiologistas , Estudos Retrospectivos , Sensibilidade e Especificidade , Ultrassom , Ultrassonografia Mamária
18.
Curr Opin Pharmacol ; 59: 26-32, 2021 08.
Artigo em Inglês | MEDLINE | ID: mdl-34052525

RESUMO

Through stress and injury to tissues, the cell membrane is damaged and can lead to cell death and a cascade of inflammatory events. Soluble factors that mitigate and repair membrane injury are important to normal homeostasis and are a potential therapeutic intervention for regenerative medicine. A myokine is a type of naturally occurring factors that come from muscle and have impact on remote organs. MG53, a tripartite motif-containing family protein, is such a myokine which has protective effects on lungs, kidneys, liver, heart, eye, and brain. Three mechanisms of action for the beneficial regenerative medicine potential of MG53 have been identified and consist of 1) repair of acute injury to the cellular membrane, 2) anti-inflammatory effects associated with chronic injuries, and 3) rejuvenation of stem cells for tissue regeneration. As such, MG53 has the potential to be a novel and effective regeneration medicine therapeutic.


Assuntos
Músculo Esquelético , Cicatrização , Membrana Celular , Homeostase , Proteínas com Motivo Tripartido
19.
Virulence ; 12(1): 1199-1208, 2021 12.
Artigo em Inglês | MEDLINE | ID: mdl-33870852

RESUMO

Background: COVID-19 has rapidly become a major health emergency worldwide. The characteristic, outcome, and risk factor of COVID-19 in patients with decompensated cirrhosis remain unclear.Methods: Medical records were collected from 23 Chinese hospitals. Patients with decompensated cirrhosis and age- and sex-matched non-liver disease patients were enrolled with 1:4 ratio using stratified sampling.Results: There were more comorbidities with higher Chalson Complication Index (p < 0.001), higher proportion of patients having gastrointestinal bleeding, jaundice, ascites, and diarrhea among those patients (p < 0.05) and in decompensated cirrhosis patients. Mortality (p < 0.05) and the proportion of severe ill (p < 0.001) were significantly high among those patients. Patients in severe ill subgroup had higher mortality (p < 0.001), MELD, and CRUB65 score but lower lymphocytes count. Besides, this subgroup had larger proportion of patients with abnormal (PT), activated partial thromboplatin time (APTT), D-Dimer, alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBL) and Creatinine (Cr) (p < 0.05). Multivariate logistic regression for severity shown that MELD and CRUB65 score reached significance. Higher Child-Pugh and CRUB65 scores were found among non-survival cases and multivariate logistic regression further inferred risk factors for adverse outcome. Receiver Operating Characteristic (ROC) curves also provided remarkable demonstrations for the predictive ability of Child-Pugh and CRUB65 scores.Conclusions: COVID-19 patients with cirrhosis had larger proportion of more severely disease and higher mortality. MELD and CRUB65 score at hospital admission may predict COVID-19 severity while Child-Pugh and CRUB65 score were highly associated with non-survival among those patients.


Assuntos
COVID-19/mortalidade , Cirrose Hepática/complicações , SARS-CoV-2 , Índice de Gravidade de Doença , Adulto , Idoso , COVID-19/etiologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Fatores de Risco
20.
Dalton Trans ; 50(16): 5666-5675, 2021 Apr 28.
Artigo em Inglês | MEDLINE | ID: mdl-33908955

RESUMO

A series of novel non-gallate near-infrared long-persistent phosphorescence Mg2-xZnxSnO4:Cr3+ phosphors were synthesized, and their structure and luminescence properties were investigated systematically. Under 448 nm blue light excitation, all the phosphors exhibit a broad emission band centered at 730 nm and a shoulder peak at 708 nm, which are attributed to the 4T2(4F) → 4A2 and 2E → 4A2 transitions of Cr3+, respectively. The excitation spectra of the samples clearly show the characteristic excitation of Cr3+ in the octahedral crystal field, with three obvious peaks at 324, 448 and 620 nm respectively. The phosphor with a composition of Mg1.4Zn0.6SnO4:0.03Cr3+ shows the strongest photoluminescence intensity which is 2.87 times and 3.09 times that of Mg2SnO4:0.03Cr3+ and Zn2SnO4:0.03Cr3+, respectively. Besides, all the samples show intense near-infrared long-persistent phosphorescence. For the optimized sample Mg1.4Zn0.6SnO4:0.005Cr3+, its phosphorescence can still be observed with a night vision instrument 18 h after removing the 365 nm UV light source. Finally, a feasible phosphorescence mechanism of the Mg1.4Zn0.6SnO4:Cr3+ phosphor was proposed and discussed. This study may provide a new method for developing novel near-infrared long-persistent phosphorescence phosphors through crystal structure modification.

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