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As the electron transport layer in quantum dot light-emitting diodes (QLEDs), ZnO suffers from excessive electrons that lead to luminescence quenching of the quantum dots (QDs) and charge-imbalance in QLEDs. Therefore, the interplay between ZnO and QDs requires an in-depth understanding. In this study, DFT and COSMOSL simulations are employed to investigate the effect of sulfur atoms on ZnO. Based on the simulations, thiol ligands (specifically 2-hydroxy-1-ethanethiol) to modify the ZnO nanocrystals are adopted. This modification alleviates the excess electrons without causing any additional issues in the charge injection in QLEDs. This modification strategy proves to be effective in improving the performance of red-emitting QLEDs, achieving an external quantum efficiency of over 23% and a remarkably long lifetime T95 of >12 000 h at 1000 cd m-2. Importantly, the relationship between ZnO layers with different electronic properties and their effect on the adjacent QDs through a single QD measurement is investigated. These findings show that the ZnO surface defects and electronic properties can significantly impact the device performance, highlighting the importance of optimizing the ZnO-QD interface, and showcasing a promising ligand strategy for the development of highly efficient QLEDs.
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Glioblastoma multiforme (GBM) is the most common and aggressive brain tumor with a poor prognosis. The growth of GBM cells depends on the core transcriptional apparatus, thus rendering RNA polymerase (RNA pol) complex as a candidate therapeutic target. The RNA pol II subunit B (POLR2B) gene encodes the second largest subunit of the RNA pol II (RPB2); however, its genomic status and function in GBM remain unclear. Certain GBM data sets in cBioPortal were used for investigating the genomic status and expression of POLR2B in GBM. The function of RPB2 was analyzed following knockdown of POLR2B expression by shRNA in GBM cells. The cell counting kit-8 assay and PI staining were used for cell proliferation and cell cycle analysis. A xenograft mouse model was established to analyze the function of RPB2 in vivo. RNA sequencing was performed to analyze the RPB2-regulated genes. GO and GSEA analyses were applied to investigate the RPB2-regulated gene function and associated pathways. In the present study, the genomic alteration and overexpression of the POLR2B gene was described in glioblastoma. The data indicated that knockdown of POLR2B expression suppressed tumor cell growth of glioblastoma in vitro and in vivo. The analysis further demonstrated the identification of the RPB2-regulated gene sets and highlighted the DNA damage-inducible transcript 4 gene as the downstream target of the POLR2B gene. The present study provides evidence indicating that RPB2 functions as a growth regulator in glioblastoma and could be used as a potential therapeutic target for the treatment of this disease.
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Neoplasias Encefálicas , Glioblastoma , Humanos , Animais , Camundongos , Glioblastoma/patologia , RNA Polimerase II/genética , RNA Polimerase II/metabolismo , Proliferação de Células/genética , Neoplasias Encefálicas/patologia , RNA Interferente Pequeno/genética , Linhagem Celular Tumoral , Regulação Neoplásica da Expressão GênicaRESUMO
Natural flavonoids are the most plentiful form of polyphenols. Given the anti-inflammatory and antioxidant properties of flavonoids, researchers discovered that it might be effective in treating depression and anxiety. The effect of flavonoids on depression and anxiety was investigated by a meta-analysis and systematic review. We searched PubMed, Embase, and Medline databases up to October 15, 2021. We selected 11 studies, among them, 10 studies were chosen to evaluate the depression effects of flavonoids and 7 studies were used to assess anxiety disorder. The meta-analysis showed that flavonoids have an overall significant effect on depression (p = 0.004, Hedge's g = -0.487, 95% CI -0.814 to -0.160) and anxiety (p = 0.006, Hedge's g = -0.741, 95% CI -1.266 to -0.217). Subgroup analysis indicated that the symptoms of depression were significantly improved in the studies when the dose of flavonoids was 50-100mg/day or the treatment duration was ≥8weeks. Anxiety symptoms were improved in the studies with the dose of flavonoids was ≥50mg/day. There was no evidence of publication bias. Our findings suggest that flavonoids might improve symptoms of depression and anxiety. However, a small number of participants and studies were included in this meta-analysis. Therefore, the results should be interpreted with caution.
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Depressão , Flavonoides , Humanos , Depressão/tratamento farmacológico , Flavonoides/uso terapêutico , Transtornos de Ansiedade/terapia , Ansiedade/tratamento farmacológico , PolifenóisRESUMO
Neuroblastoma(NB) is a common childhood solid tumor, and most patients in the high-risk group with MYCN gene amplification have a poor prognosis. Inhibition of bromodomain and extra terminal (BET) proteins has shown considerable promise in the investigation of MYCN-driven malignancies in recent years. MZ1 is a novel BET inhibitor that employs proteolytic-targeting chimera (PROTAC) technology for proteasomal degradation of target proteins and has shown excellent effects in some tumors, but its role in neuroblastoma remains poorly understood. Herein, we observed that MZ1 suppressed MYC-amplified NB cell proliferation and normal cell cycle, while simultaneously boosting cell apoptosis. MZ1 also provides a significant therapeutic impact in vivo. Mechanistically, MZ1 exhibits anti-tumor effect in NB cells by suppressing the expression of N-Myc or C-Myc as well as the MAPK signaling pathway. Overall, our data imply that MZ1 might be exploited as a possible therapeutic method for NB therapy.
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Proteínas de Ciclo Celular , Dipeptídeos , Compostos Heterocíclicos com 3 Anéis , Proteína Proto-Oncogênica N-Myc , Neuroblastoma , Fatores de Transcrição , Proteínas de Ciclo Celular/antagonistas & inibidores , Linhagem Celular Tumoral , Criança , Dipeptídeos/farmacologia , Regulação Neoplásica da Expressão Gênica , Compostos Heterocíclicos com 3 Anéis/farmacologia , Humanos , Proteína Proto-Oncogênica N-Myc/genética , Proteína Proto-Oncogênica N-Myc/metabolismo , Neuroblastoma/metabolismo , Proteínas Nucleares/genética , Proteínas Nucleares/metabolismo , Fatores de Transcrição/antagonistas & inibidores , Fatores de Transcrição/metabolismoRESUMO
BACKGROUND: Acute myeloid leukemia (AML) is a myeloid neoplasm accounts for 7.6% of hematopoietic malignancies. AML is a complex disease, and understanding its pathophysiology is contributing to the improvement in the treatment and prognosis of AML. In this study, we assessed the expression profile and molecular functions of CCAAT enhancer binding protein gamma (CEBPG), a gene implicated in myeloid differentiation and AML progression. METHODS: shRNA mediated gene interference was used to down-regulate the expression of CEBPG in AML cell lines, and knockdown efficiency was detected by RT-qPCR and western blotting. The effect of knockdown on the growth of AML cell lines was evaluated by CCK-8. Western blotting was used to detect PARP cleavage, and flow cytometry were used to determine the effect of knockdown on apoptosis of AML cells. Genes and pathways affected by knockdown of CEBPG were identified by gene expression analysis using RNA-seq. One of the genes affected by knockdown of CEBPG was Eukaryotic translation initiation factor 4E binding protein 1 (EIF4EBP1), a known repressor of translation. Knockdown of EIF4EBP1 was used to assess its potential role in AML progression downstream of CEBPG. RESULTS: We explored the ChIP-Seq data of AML cell lines and non-AML hematopoietic cells, and found CEBPG was activated through its distal enhancer in AML cell lines. Using the public transcriptomic dataset, the Cancer Cell Line Encyclopedia (CCLE) and western blotting, we also found CEBPG was overexpressed in AML. Moreover, we observed that CEBPG promotes AML cell proliferation by activating EIF4EBP1, thus contributing to the progression of AML. These findings indicate that CEBPG could act as a potential therapeutic target for AML patients. CONCLUSION: In summary, we systematically explored the molecular characteristics of CEBPG in AML and identified CEBPG as a potential therapeutic target for AML patients. Our findings provide novel insights into the pathophysiology of AML and indicate a key role for CEBPG in promoting AML progression.
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Depression is a common and serious psychiatric disorder, but current conventional antidepressants have limited efficacy and significant side effects. Thus, better antidepressants are urgently needed. This study aimed to investigate the antidepressant-like effects and potential mechanism of quercetin by evaluating the changes of serum elements in chronic unpredictable mild stress (CUMS) rats. Based on the results of the sucrose preference test (SPT), 96 rats were randomly assigned to six groups: control, different dosages of quercetin (10 and 50 mg/kg·bw, respectively), depressed, and different dosages quercetin plus depressed groups. After 8 weeks of CUMS modeling, rat serum was collected. Fifteen elements in serum were analyzed by inductively coupled plasma mass spectrometry (ICP-MS), and related enzyme indicators, antioxidant indicators, and inflammatory cytokines were detected to further explore the potential mechanism. Besides, the accuracy and precision of the method were evaluated. The results showed that the levels of iron (Fe), copper (Cu), and calcium (Ca) in serum significantly increased (p ≤ 0.001), while the levels of magnesium (Mg), zinc (Zn), selenium (Se), and cobalt (Co) significantly decreased (p ≤ 0.001) in depressed group compared with the control group. The levels of the remaining eight elements did not change significantly. When high-dose quercetin was administered to depressed rats, the levels of the above seven elements significantly restored (p ≤ 0.001). This study suggests that quercetin (50 mg/kg·bw) has a regulatory effect on serum elements in CUMS rats, which may be mediated by reducing oxidative stress, inhibiting inflammation, and regulating a variety of neurotransmitter systems.
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Depressão/tratamento farmacológico , Quercetina/farmacologia , Animais , Antidepressivos , Cálcio/sangue , Cobre/sangue , Depressão/sangue , Depressão/metabolismo , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Ferro/sangue , Masculino , Espectrometria de Massas , Estresse Oxidativo/efeitos dos fármacos , Ratos , Ratos Sprague-DawleyRESUMO
This study aims to explore the protective effects of quercetin against cadmium-induced nephrotoxicity utilizing metabolomics methods. Male Sprague-Dawley rats were randomly assigned to six groups: control, different dosages of quercetin (10 and 50 mg/kg·bw, respectively), CdCl2 (4.89 mg/kg·bw) and different dosages quercetin plus CdCl2 groups. After 12 weeks, the kidneys were collected for metabolomics analysis and histopathology examination. In total, 11 metabolites were confirmed, the intensities of which significantly changed (up-regulated or down-regulated) compared with the control group (p < 0.00067). These metabolites include xanthosine, uric acid (UA), guanidinosuccinic acid (GSA), hypoxanthine (Hyp), 12-hydroxyeicosatetraenoic acid (tetranor 12-HETE), taurocholic acid (TCA), hydroxyphenylacetylglycine (HPAG), deoxyinosine (DI), ATP, formiminoglutamic acid (FIGLU) and arachidonic acid (AA). When high-dose quercetin and cadmium were given to rats concurrently, the intensities of above metabolites significantly restored (p < 0.0033 or p < 0.00067). The results showed quercetin attenuated Cd-induced nephrotoxicity by regulating the metabolism of lipids, amino acids, and purine, inhibiting oxidative stress, and protecting kidney functions.
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Rim/metabolismo , Metabolômica , Substâncias Protetoras/metabolismo , Quercetina/metabolismo , Animais , Cádmio/toxicidade , Relação Dose-Resposta a Droga , Injeções Intraperitoneais , Rim/efeitos dos fármacos , Rim/patologia , Masculino , Estresse Oxidativo/efeitos dos fármacos , Substâncias Protetoras/administração & dosagem , Substâncias Protetoras/farmacologia , Quercetina/administração & dosagem , Quercetina/farmacologia , Ratos , Ratos Sprague-DawleyRESUMO
This study aimed to investigate the protective effect of quercetin against the toxicity induced by chronic exposure to low levels of cadmium in rats by an ultra performance liquid chromatography mass spectrometer. Rats were randomly divided into six groups as follows: control group (C), low dose of quercetin group (Q1: 10 mg/kg·bw), high dose of quercetin group (Q2: 50 mg/kg·bw), cadmium chloride group (D), low dose of quercetin plus cadmium chloride group (DQ1), and high dose of quercetin plus cadmium chloride group (DQ2). Cadmium chloride (CdCl2 ) was administered to rats by drinking water ad libitum in a concentration of 40 mg/L. The final amount of CdCl2 ingested was estimated from the water consumption data to be 4.85, 4.91, and 4.89 mg/kg·bw/day, for D, DQ1, and DQ2 groups, respectively. After a 12-week treatment, the serum samples of rats were collected for metabonomics analysis. Ten potential biomarkers were identified for which intensities were significantly increased or reduced as a result of the treatment. These metabolites included isorhamnetin 4'-O-glucuronide, 3-indolepropionic acid, tetracosahexaenoic acid, lysophosphatidylcholine (LysoPC) (20:5), lysoPC (18:3), lysophosphatidylethanolamine (LysoPE) (20:5/0:0), bicyclo-prostaglandin E2, sulpholithocholylglycine, lithocholyltaurine, and glycocholic acid. Results indicated that quercetin exerted a protective effect against cadmium-induced toxicity by regulating lipid and amino acid metabolism, enhancing the antioxidant defense system and protecting liver and kidney function.
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Antioxidantes/farmacologia , Biomarcadores/sangue , Cloreto de Cádmio/toxicidade , Quercetina/farmacologia , Aminoácidos/efeitos dos fármacos , Aminoácidos/metabolismo , Animais , Biomarcadores/metabolismo , Cromatografia Líquida , Rim/efeitos dos fármacos , Rim/metabolismo , Rim/patologia , Metabolismo dos Lipídeos/efeitos dos fármacos , Fígado/efeitos dos fármacos , Fígado/metabolismo , Fígado/patologia , Masculino , Espectrometria de Massas , Metabolômica , Estresse Oxidativo/efeitos dos fármacos , Ratos , Ratos Sprague-DawleyRESUMO
The current study aimed to investigate the hepatotoxicity of rats administered with chronic low-dose acrylamide (AA) by using metabonomics technology on the basis of ultraperformance liquid chromatography-mass spectrometry (UPLC-MS). A total of 40 male Wistar rats were randomly divided into the following four groups: control, low-dose AA (0.2 mg/kg bw, non-carcinogenic end-point based on the induction of morphological nerve changes in rats), middle-dose AA (1 mg/kg bw), and high-dose AA (5 mg/kg bw). The rats continuously received AA by administering it in drinking water daily for 16 weeks. After the treatment, rat livers were collected for metabonomics analysis and histopathology examination. Principal components analysis (PCA) and partial least-squares discriminant analysis (PLS-DA) were used to investigate the metabonomics profile changes in rat liver tissues and screen the potential biomarkers.Fourteen metabolites were identified with significant changes in intensities (increased or decreased compared with the control group) as a result of treatment (p < 0.05 or p < 0.01). These metabolites included tauro-b-muricholic acid, docosapentaenoic acid, sphingosine 1-phosphate, taurodeoxycholic acid, lysoPE(20:5), cervonyl carnitine, linoleyl carnitine, docosahexaenoic acid, lysoPC(20:4), lysoPE(18:3), PA(20:4), stearidonyl carnitine, alpha-linolenic acid, and lysoPA(18:0).Results showed that chronic exposure to AA at NOAEL (0.2 mg/kg bw) exhibited no toxic effect in rat livers at the metabolic level. AA induced oxidative stress to the liver and disrupted lipid metabolism. The results of liver histopathology examination further supported the metabonomic results.
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Acrilamida/metabolismo , Acrilamida/administração & dosagem , Acrilamida/toxicidade , Animais , Biomarcadores/metabolismo , Relação Dose-Resposta a Droga , Metabolismo dos Lipídeos/efeitos dos fármacos , Fígado/metabolismo , Masculino , Metaboloma/efeitos dos fármacos , Metabolômica , Estresse Oxidativo , Ratos , Ratos Wistar , Testes de Toxicidade CrônicaRESUMO
This study aimed to investigate the nephrotoxicity in rats administered with chronic low-dose cadmium (Cd) by ultra-performance liquid chromatography-mass spectrometry. A total of 40 male Sprague-Dawley rats were randomly assigned to four groups, namely: control; low-dose (0.13 mg/kg·body weight [bw]); middle-dose (0.80 mg/kg·bw); and high-dose (4.89 mg/kg·bw). The rats received CdCl2 daily via drinking water for 24 weeks. Rat kidneys were collected for metabonomics analysis. Principal components analysis and partial least-squares discriminant analysis were used to investigate the metabonomics profile changes in the kidney samples and to screen the potential biomarkers. Ten metabolites were identified in the positive and negative ion modes. Compared with the control group, the intensities of tetranor 12-HETE, uric acid, hypoxanthine, phenylacetylglycine, guanidinosuccinic acid and xanthosine significantly increased (P < 0.01), and those of imidazolelactic acid, lactose 6-phosphate, l-urobilinogen and arachidonic acid significantly decreased (P < 0.01) in the high-dose group. Results showed that exposure to Cd in rats induced oxidative stress to the kidneys and disrupted amino acid metabolism, fatty acid metabolism and energy metabolism.
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Cádmio/toxicidade , Rim/efeitos dos fármacos , Metabolômica , Animais , Cádmio/metabolismo , Cromatografia Líquida de Alta Pressão/métodos , Rim/metabolismo , Rim/patologia , Masculino , Espectrometria de Massas/métodos , Estresse Oxidativo/efeitos dos fármacos , Ratos , Ratos Sprague-DawleyRESUMO
Acute portal vein thrombosis (PVST), a serious complication of liver cirrhosis, is characterized as abdominal pain secondary to intestinal ischemia, and even intestinal necrosis. Anticoagulation is recommended for the treatment of acute PVST, but is often postponed in cirrhotic patients with acute variceal bleeding or those at a high risk of variceal bleeding. Herein, we reported a 63-year-old male with a 14-year history of alcoholic liver cirrhosis who developed progressive abdominal pain related to acute portal vein and superior mesenteric vein thrombosis immediately after endoscopic variceal ligation combined with endoscopic cyanoacrylate glue injection for acute variceal bleeding. Fortunately, acute PVST was successfully recanalized by the use of low molecular weight heparin. Collectively, this case suggests that acute symptomatic PVST can be secondary to endoscopic variceal therapy in liver cirrhosis, and can be safely and successfully treated by anticoagulation.
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PURPOSE: Vital signs are important for predicting clinical outcomes in patients with trauma. However, their accuracy can be affected in older adults because hemodynamic changes are less obvious. This study aimed to examine the usefulness of changes in vital signs during transportation in predicting the need for hemostatic treatments in older patients with trauma. METHODS: This retrospective cohort study was conducted using data from the Japan Trauma Data Bank (2004-2019). Patients aged ≥ 65 years who were hemodynamically stable at the scene were included in this study. The incidence of emergency surgery within 12 h after hospital arrival was compared between patients with delta Shock Index (dSI) > 0.1 and those with dSI ≤ 0.1. Predicting ability was examined after adjusting for patient demographics, comorbidities, vital signs at the scene and on hospital arrival, Injury Severity Score, and abbreviated injury scale in each region. RESULTS: Among the 139,242 patients eligible for the study, 3,701 underwent urgent hemostatic surgery within 12 h. Patients with dSI > 0.1 showed a significantly higher incidence of emergency surgery than those with dSI ≤ 0.1 (871/16,549 [5.3%] vs. 2,830/84,250 [3.4%]; odds ratio (OR), 1.60 [1.48-1.73]; adjusted OR, 1.22 [1.08-1.38]; p = 0.001). The relationship between high dSI and a higher incidence of intervention was observed in patients with hypertension and those with decreased consciousness on arrival. CONCLUSION: High dSI > 0.1 was significantly associated with a higher incidence of urgent hemostatic surgery in older patients.
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Ferimentos não Penetrantes , Humanos , Idoso , Feminino , Masculino , Estudos Retrospectivos , Ferimentos não Penetrantes/cirurgia , Ferimentos não Penetrantes/epidemiologia , Japão/epidemiologia , Idoso de 80 Anos ou mais , Incidência , Escala de Gravidade do Ferimento , Sinais Vitais , Choque/epidemiologiaRESUMO
Budd-Chiari syndrome (BCS) and sinusoidal obstruction syndrome (SOS) are two major vascular disorders of the liver, of which both can cause portal hypertension related complications, but their locations of obstruction are different. BCS refers to the obstruction from the hepatic vein to the junction between the inferior vena cava and right atrium, which is the major etiology of post-sinusoidal portal hypertension; by comparison, SOS is characterized as the obstruction at the level of hepatic sinusoids and terminal venulae, which is a cause of sinusoidal portal hypertension. Both of them can cause hepatic congestion with life-threatening complications, especially acute liver failure and chronic portal hypertension, and share some similar features in terms of imaging and clinical presentations, but they have heterogeneous risk factors, management strategy, and prognosis. Herein, this paper reviews the current evidence and then summarizes the difference between primary BCS and SOS in terms of risk factors, clinical features, diagnosis, and treatment.
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Síndrome de Budd-Chiari , Hepatopatia Veno-Oclusiva , Hipertensão Portal , Complicações na Gravidez , Feminino , Humanos , Síndrome de Budd-Chiari/diagnóstico , Síndrome de Budd-Chiari/etiologia , Síndrome de Budd-Chiari/terapia , Hepatopatia Veno-Oclusiva/complicações , Veias Hepáticas , Hipertensão Portal/complicaçõesRESUMO
Super enhancers (SEs) are genomic regions comprising multiple closely spaced enhancers, typically occupied by a high density of cell-type-specific master transcription factors (TFs) and frequently enriched in key oncogenes in various tumors, including neuroblastoma (NB), one of the most prevalent malignant solid tumors in children originating from the neural crest. Cyclin-dependent kinase 5 regulatory subunit-associated protein 3 (CDK5RAP3) is a newly identified super-enhancer-driven gene regulated by master TFs in NB; however, its function in NB remains unclear. Through an integrated study of publicly available datasets and microarrays, we observed a significantly elevated CDK5RAP3 expression level in NB, associated with poor patient prognosis. Further research demonstrated that CDK5RAP3 promotes the growth of NB cells, both in vitro and in vivo. Mechanistically, defective CDK5RAP3 interfered with the UFMylation system, thereby triggering endoplasmic reticulum (ER) phagy. Additionally, we provide evidence that CDK5RAP3 maintains the stability of MEIS2, a master TF in NB, and in turn, contributes to the high expression of CDK5RAP3. Overall, our findings shed light on the molecular mechanisms by which CDK5RAP3 promotes tumor progression and suggest that its inhibition may represent a novel therapeutic strategy for NB.
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Proteínas de Ciclo Celular , Regulação Neoplásica da Expressão Gênica , Neuroblastoma , Fatores de Transcrição , Animais , Humanos , Camundongos , Proteínas de Ciclo Celular/genética , Proteínas de Ciclo Celular/metabolismo , Linhagem Celular Tumoral , Proliferação de Células , Retículo Endoplasmático/metabolismo , Elementos Facilitadores Genéticos , Peptídeos e Proteínas de Sinalização Intracelular/genética , Peptídeos e Proteínas de Sinalização Intracelular/metabolismo , Camundongos Nus , Proteínas do Tecido Nervoso/genética , Proteínas do Tecido Nervoso/metabolismo , Neuroblastoma/genética , Neuroblastoma/patologia , Neuroblastoma/metabolismo , Prognóstico , Fatores de Transcrição/genética , Fatores de Transcrição/metabolismo , Proteínas Supressoras de Tumor/genética , Proteínas Supressoras de Tumor/metabolismoRESUMO
Background: Tension-type headache (TTH) is one of the most common primary headaches. Several studies have confirmed the efficacy of acupuncture therapies for TTH, but it is uncertain which treatment is most effective. Objective: This study aimed to compare the effectiveness and safety of different acupuncture therapies for TTH using Bayesian Network Meta-analysis to provide new ideas for treating TTH. Methods: Nine databases were searched for randomized controlled trials (RCTs) about different acupuncture therapies for TTH up to December 1, 2022. The outcome indicators analyzed in our study were total effective rate, visual analog scale (VAS), headache frequency, and safety. Pairwise meta-analysis and risk of bias assessment were performed using Review Manager 5.4. Stata 15.0 generated a network evidence plot and detected publication bias. Finally, a Bayesian network meta-analysis of the data was used by RStudio. Results: The screening process resulted in 30 RCTs that met the inclusion criteria, including 2,722 patients. Most studies failed to report details of trials and were therefore assessed as unclear risks. Two studies were considered high risk because they did not report on all pre-specified outcome indicators or had incomplete data on outcome indicators. The NMA results showed that for total effective rate, bloodletting therapy had the most considerable SUCRA value (0.93156136), for VAS, head acupuncture combined with Western medicine ranked first (SUCRA = 0.89523571), and acupuncture combined with herbal medicine was the most effective in improving headache frequency (p > 0.05). Conclusion: Acupuncture can be used as one of the complementary or alternative therapies for TTH; bloodletting therapy better improves the overall symptoms of TTH, head acupuncture combined with Western medicine is more effective in reducing VAS scores, and acupuncture combined with herbal medicine seems to reduce headache frequency, but the difference is not statistically significant. Overall, acupuncture for TTH is effective with mild side effects, but future high-quality studies are still necessary. Systematic review registration: https://www.crd.york.ac.uk/prospero/, PROSPERO [CRD42022368749].
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Depression is the most prevalent psychiatric disease, and its pathogenesis is still unclear. Currently, studies on the pathogenesis of depression are mainly focused on the brain. The liver can modulate brain function via the liver-brain axis, indicating that the liver plays an important role in the development of depression. This study aims to explore the protective effect of quercetin against chronic unpredictable mild stress (CUMS)-induced metabolic changes and the corresponding mechanisms in the rat liver based on untargeted metabolomics technology. In this study, 96 male rats were divided into six groups: control, different doses of quercetin (10 mg per kg bw or 50 mg per kg bw), CUMS, and CUMS + different doses of quercetin. After 8 weeks of CUMS modeling, the liver samples were collected for metabolomics analysis. A total of 17 altered metabolites were identified, including D-glutamic acid, S-adenosylmethionine, lithocholylglycine, L-homocystine, prostaglandin PGE2, leukotriene E4, cholic acid, 5-methyltetrahydrofolic acid, taurochenodeoxycholic acid, S-adenosylhomocysteine, deoxycholic acid, folic acid, L-methionine, leukotriene C5, estriol-17-glucuronide, PE, and PC, indicating that methionine metabolism, bile acid metabolism, and phosphatidylcholine biosynthesis are the major pathways involved in CUMS-induced hepatic metabolic disorders. Hepatic methylation damage may play a role in the pathophysiology of depression, as evidenced by the first discovery of the abnormality of hepatic methionine metabolism. Abnormal changes in hepatic bile acids may provide stronger evidence for depression pathogenesis involving the microbiota-gut-brain axis, suggesting that the liver is involved in depression development and may be a treatment target. The quercetin treatment alleviated the CUMS-induced liver metabolism disorder, suggesting that quercetin may protect against depression by regulating liver metabolism.
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Depressão , Hepatopatias , Ratos , Masculino , Animais , Depressão/metabolismo , Quercetina/farmacologia , Metabolômica , Metaboloma , Metionina/metabolismo , Estresse Psicológico/metabolismo , Modelos Animais de DoençasRESUMO
In quantum dot light-emitting diodes (QLEDs), even seemingly with interfacial exciton quenching between quantum dots (QDs) and the electron transport layer (ETL) limiting the device efficiency, the internal quantum efficiency of such QLEDs approaches 100%. Therefore, it is a puzzle that QLEDs exhibit high performance although they suffer from interfacial exciton quenching. In this work, we solve this puzzle by identifying the cause of the interfacial exciton quenching. By analyzing the optical characteristics of pristine and encapsulated QD-ETL films, the interfacial exciton quenching in the pristine QD-ETL film is attributed to O2-induced charge transfer. We further investigate the charge transfer mechanism and its effect on the performance of QLEDs. Finally, we show the photodegradation of the pristine QD-ETL film under UV irradiation. Our work bridges interfacial exciton quenching and high performance in hybrid QLEDs and highlights the significance of encapsulation in QLEDs.
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BACKGROUND: Depression after myocardial infarction (MI) is associated with poor prognosis. This study aimed to develop and validate a nomogram to predict the risk of depression in patients with MI. METHODS: This retrospective study included 1615 survivors of MI aged >20 years who were selected from the 2005-2018 National Health and Nutrition Examination Survey database. The 899 subjects from the 2005-2012 survey comprised the development group, and the remaining 716 subjects comprised the validation group. Univariate and multivariate analyses identified variables significantly associated with depression. The least absolute shrinkage and selection operator (LASSO) binomial regression model was used to select the best predictive variables. RESULTS: A full predictive model and a simplified model were developed using multivariate analysis and LASSO binomial regression results, respectively, and validated using data from the validation group. The receiver operator characteristic curve and Hosmer-Lemeshow goodness of fit test were used to assess the nomogram's performance. The full nomogram model included 8 items: age, BMI, smoking, drinking, diabetes, exercise, insomnia, and PIR. The area under the curve for the development group was 0.799 and for the validation group was 0.731, indicating that our model has good stability and predictive accuracy. The goodness of fit test showed a good model calibration for both groups. The simplified model includes age, smoking, PIR, and insomnia. The AUC of the simplified model was 0.772 and 0.711 in the development and validation groups, respectively, indicating that the simplified model still possessed good predictive accuracy. CONCLUSION: Our nomogram helped assess the individual probability of depression after MI and can be used as a complement to existing depression screening scales to help physicians make better treatment decisions.
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Cadmium (Cd) is known to cause damage to the liver. In this study, metabolomics technology was used to investigate the effect of quercetin (QE) on Cd-induced hepatotoxicity. A total of 60 male SD rats were randomly divided into the following six groups: control group (C), low and high-dose QE group (Q1: 10 mg/kg·bw, Q2: 50 mg/kg·bw), Cd group (D), low and high-dose QE and Cd combined intervention group (DQ1, DQ2). The rats were given Cd chloride (CdCl2) at a concentration of 40 mg/L through free drinking water. After 12 weeks of treatment, liver samples of rats were collected for metabonlomic analysis. A total of 12 metabolites were identified, the intensities of PC (18:0/14:1(9Z)) and arachidonate acid were decreased in the Cd-treated group (p < 0.01), whereas the intensities of chenodeoxyglycocholic acid, cholic acid, taurochenodesoxycholic acid, glycocholic acid, prostaglandin D2, 15-deoxy-d-12,14-PGJ2, oxidized glutathione, cholesterol, protoporphyrin IX, bilirubin were increased significantly in the Cd-treated group compared with group C (p < 0.01). When rats were given high doses of QE and Cd at the same time, the intensity of the above metabolites was significantly restored in group DQ2. Results suggest that the protective effect of QE on Cd-induced liver injury is associated with antioxidant activity of QE, as well as QE can regulates hepatic bile acid metabolism by affecting FXR and BSEP, and regulates AA metabolism by inhibiting Cd-induced activities of COX-2 and PLA2.
Assuntos
Cádmio , Quercetina , Animais , Antioxidantes/metabolismo , Cádmio/metabolismo , Cádmio/farmacologia , Fígado/metabolismo , Masculino , Metabolômica , Estresse Oxidativo , Quercetina/farmacologia , Quercetina/uso terapêutico , Ratos , Ratos Sprague-DawleyRESUMO
As an effective manufacturing technology, inkjet printing is very suitable for the fabrication of perovskite light-emitting diodes in next-generation displays. However, the unsatisfied efficiency of perovskite light-emitting diode created with the use of inkjet printing impedes its development for future application. Here, we report highly efficient PeLEDs using inkjet printing, with an external quantum efficiency of 7.9%, a current efficiency of 32.0 cd/A, and the highest luminance of 2465 cd/m2; these values are among the highest values for the current efficiency of inkjet-printed PeLED in the literature. The outstanding performance of our device is due to the coffee-ring-free and uniform perovskite nanocrystal layer on the PVK layer, resulting from vacuum post-treatment and using a suitable ink. Moreover, the surface roughness and thickness of the perovskite layer are effectively controlled by adjusting the spacing of printing dots. This study makes an insightful exploration of the use of inkjet printing in PeLED fabrication, which is one of the most promising ways for future industrial production of PeLEDs.