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1.
Front Neurol ; 13: 842212, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35432162

RESUMO

Gamma-delta (γδ) T cells are a small subset of T cells that are reported to have a proinflammatory role in the pathophysiology of cerebral ischemia stroke (CIS). Upon activation by interleukin-1 beta (IL-1ß), IL-23 and IL-18, γδ T cells are stimulated to secrete various cytokines, such as IL-17a, IL-21, IL-22, and interferon-gamma (IFN-γ). In addition, they all play a pivotal role in the inflammatory and immune responses in ischemia. Nevertheless, the exact mechanisms responsible for γδ T cell proinflammatory functions remain poorly understood, and more effective therapies targeting at γδ T cells and cytokines they release remain to be explored, particularly in the context of CIS. CIS is the second most common cause of death and the major cause of permanent disability in adults worldwide. In this review, we focus on the neuroinflammatory and immune functions of γδ T cells and related cytokines, intending to understand their roles in CIS, which may be crucial for the development of novel effective clinical applications.

2.
Small ; 18(12): e2105890, 2022 03.
Artigo em Inglês | MEDLINE | ID: mdl-35072345

RESUMO

This work reports a molecular-scale capacitance effect of the double helical nucleic acid duplex structure for the first time. By quantitatively conducting large sample measurements of the electrostatic field effect using a type of high-accuracy graphene transistor biosensor, an unusual charge-transport behavior is observed in which the end-immobilized nucleic acid duplexes can store a part of ionization electrons like molecular capacitors, other than electric conductors. To elucidate this discovery, a cascaded capacitive network model is proposed as a novel equivalent circuit of nucleic acid duplexes, expanding the point-charge approximation model, by which the partial charge-transport observation is reasonably attributed to an electron-redistribution behavior within the capacitive network. Furthermore, it is experimentally confirmed that base-pair mismatches hinder the charge transport in double helical duplexes, and lead to directly identifiable alterations in electrostatic field effects. The bioelectronic principle of mismatch impact is also self-consistently explained by the newly proposed capacitive network model. The mesoscopic nucleic acid capacitance effect may enable a new kind of label-free nucleic acid analysis tool based on electronic transistor devices. The in situ and real-time nucleic acid detections for virus biomarkers, somatic mutations, and genome editing off-target may thus be predictable.


Assuntos
Técnicas Biossensoriais , Grafite , Ácidos Nucleicos , Capacitância Elétrica , Grafite/química , Transistores Eletrônicos
3.
Biosens Bioelectron ; 196: 113688, 2022 Jan 15.
Artigo em Inglês | MEDLINE | ID: mdl-34700264

RESUMO

Detection of multiple analytes simultaneously in small liquid samples with high efficiency and precision is highly important to the fields like water quality monitoring. In this letter, we present a multiplexed nanosensors with position-encoded aptamer functionalized gold nanorods for heavy metal ions detection. The individual gold nanorods respond specifically to two different heavy metal ions (Pb2+ and Hg2+) with a spectral shift in the scattering spectrum. We used a home-built spectral imaging dark-field microscope to measure the response of thousands of single plasmonic nanosensors with relatively high time resolution and precision. To explore the performance and limit of detection (LOD) of our nanosensor and setup, we recorded the concentration-dependent response of our position-encoded nanosensors with a series of mixture solutions that contain different concentrations of Hg2+ and Pb2+ ions. The LOD levels of our system are around 5 nM for Pb2+ ions and 1 nM for Hg2+ ions. Our method and results demostrate the nanomolar sensitivity and the potential to detect more different heavy metal ions.


Assuntos
Técnicas Biossensoriais , Nanopartículas Metálicas , Metais Pesados , Ouro , Íons
4.
Int J Hyperthermia ; 38(1): 1685-1694, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34843653

RESUMO

AIMS: To retrospectively compare the efficacy of transcatheter chemoembolization (TACE) plus percutaneous radiofrequency ablation (PRFA) (hereafter, TACE + PRFA) and laparoscopic radiofrequency ablation (LRFA) in the treatment of inoperable hepatocellular carcinoma (HCC). METHODS: From July 2014 to December 2017, 132 consecutive patients with inoperable HCC were treated with TACE + PRFA (n = 86) or LRFA (n = 46). Overall survival (OS) and recurrence-free survival (RFS) were analyzed using log-rank test and Cox regression analysis. Propensity score matched (PSM) analyses based on patient and tumor characteristics were also conducted. Additionally, we performed exploratory analyses to determine the effectiveness of TACE + PRFA and LRFA in clinically relevant subsets. RESULTS: The baseline characteristics of TACE + PRFA patients displayed relatively inferior liver status and a higher rate of BCLC-B disease. For unmatched patients, median OS (55.0 vs. 42.0 months; p = .019) and RFS (20.0 vs. 11.0 months; p < .001) were significantly longer in TACE + PRFA group than that in the LRFA group. After PSM, 39 matched pairs were identified. The difference in median OS (60.0 vs. 44.0 months; p = .009) and RFS (27.0 vs. 11.0 months; p < .001) between the two groups remained significant. Multivariate analysis in matched patients showed that treatment modality and response to initial treatment were significant predictors of OS and RFS, while recurrence after resection was an independent prognostic factor of OS. The benefits of TACE + PRFA were consistent across all the subgroups examined. The different treatments had shared a similar complication rate. CONCLUSIONS: Compared to LRFA, TACE + PRFA results in improved OS and RFS in patients not amenable to resection.


Assuntos
Carcinoma Hepatocelular , Ablação por Cateter , Quimioembolização Terapêutica , Laparoscopia , Neoplasias Hepáticas , Ablação por Radiofrequência , Carcinoma Hepatocelular/cirurgia , Terapia Combinada , Humanos , Neoplasias Hepáticas/cirurgia , Recidiva Local de Neoplasia/cirurgia , Estudos Retrospectivos , Resultado do Tratamento
5.
Mediators Inflamm ; 2021: 8874854, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33505221

RESUMO

MicroRNAs are small noncoding RNAs which regulate gene expression at the posttranscriptional level. miR-155 is encoded by the miR-155 host gene (miR155HG), also known as the noncoding B cell integration cluster (BIC). MicroRNAs are widely expressed in various hematopoietic cells and are involved in regulating the immune system. In this review, we summarized how miR-155 modulates specific immune cells and the regulatory role of miR-155 in sepsis. miR-155 is expressed by different populations of innate and adaptive immune cells and is involved in the regulation of development, proliferation, and function in these cells. Sepsis is associated with uncontrollable inflammatory responses, accompanied by unacceptably high mortality. Due to the inadequacy of diagnostic markers as well as treatment strategies, treating sepsis can be a huge challenge. So far, a large number of experiments have shown that the expression of miR-155 is increased at an early stage of sepsis and that this increase is positively correlated with disease progression and severity. In addition, by blocking the proinflammatory effects of miR-155, it can effectively improve sepsis-related organ injury, providing novel insights to identify potential biomarkers and therapeutic targets for sepsis. However, since most of the current research is limited to animal experiments, further clinical research is required to determine the function of miR-155 and its mechanism related to sepsis.


Assuntos
MicroRNAs/metabolismo , Sepse/metabolismo , Animais , Apoptose/genética , Apoptose/fisiologia , Humanos , MicroRNAs/genética , Sepse/genética
6.
Microb Pathog ; 148: 104468, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32866582

RESUMO

Sepsis-associated acute lung injury (ALI) is a clinically critical disease that carries a high mortality rate. The pathogenesis of sepsis-associated ALI has not yet been precisely elucidated and there is a lack of effective treatment. As a new endogenous docosahexaenoic acid (DHA)-derived lipid mediators, Maresin1 has a significant dual role of anti-inflammatory and promoting inflammation regression. In this study, we established the sepsis model by the cecal ligation and puncture method (CLP) to explore the effect of Maresin1 on sepsis-induced lung injury. We found that the intervention of Maresin1 could significantly attenuate the sepsis-induced inflammatory responses, characterized by the down-regulation of the level of IL-1ß, IL-6, TNF-α, MPO, etc. Maresin1 could also significantly decrease the number of neutrophils in lung tissue, thus improving the related lung injury indicators. Our experiment clarified that the protective effect of Maresin1 on sepsis-associated lung injury is closely related to its inhibition function of JAK2/STAT3 and MAPK/NF-κB signaling pathways. Our findings provide new research directions and therapeutic targets for sepsis-associated ALI.


Assuntos
Lesão Pulmonar Aguda , Sepse , Humanos , Janus Quinase 2 , Pulmão/metabolismo , Sistema de Sinalização das MAP Quinases , NF-kappa B/metabolismo , Fator de Transcrição STAT3 , Sepse/complicações , Fator de Necrose Tumoral alfa/metabolismo
7.
Biomed Pharmacother ; 130: 110601, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32784049

RESUMO

Endoplasmic reticulum (ER) stress is an evolutionarily conserved adaptive response that contributes to deal with the misfolded or unfolded protein in the lumen of the ER and restore the ER homeostasis. However, excessive and prolonged ER stress can trigger the cell-death signaling pathway which causes cell death, usually in the form of apoptosis. It is generally accepted that inappropriate cellular apoptosis and a series of the subsequent inflammatory response and oxidative stress can cause disturbance of normal physiological functions and organ damage. A lot of evidence shows that the excessive activation of the ER stress contributes to the pathogenesis of many kinds of diseases and inhibiting the inappropriate stress is of great significance for maintaining the normal physiological function. In recent years, Sirtuin1 (SIRT1) has become a research hotspot on ER stress. As a master regulator of ER stress, increasing evidence suggests that SIRT1 plays a positive role in a variety of ER stress-induced organ damage via multiple mechanisms, including inhibiting cellular apoptosis and promoting autophagy. Furthermore, a lot of factors have shown effective regulation of SIRT1, which indicates the feasibility of treating SIRT1 as a target for the treatment of ER stress-related diseases. We summarize and reveal the molecular mechanisms underlying the protective effect of SIRT1 in multiple ER stress-mediated organ damage in this review. We also summed up the possible adjustment mechanism of SIRT1, which provides a theoretical basis for the treatment of ER stress-related diseases.


Assuntos
Estresse do Retículo Endoplasmático/genética , Sirtuína 1/genética , Sirtuína 1/fisiologia , Animais , Apoptose/genética , Morte Celular/genética , Humanos , Transdução de Sinais/genética , Resposta a Proteínas não Dobradas
8.
Mol Immunol ; 126: 40-45, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32750537

RESUMO

Oxidative stress-related injury is a negative state caused by the imbalance between oxidation and antioxidant effects in the internal environment of the body. Oxidative stress has been confirmed to be an important factor in aging and a variety of diseases and the inhibition of inappropriate oxidative stress responses are important for maintaining normal physiological functions. Recently, considerable attention has been focused on specialized pro-resolving mediators(SPMs). SPMs are endogenous mediators derived from polyunsaturated fatty acids, which have multiple protective effects such as anti-inflammation, pro-resolution, and promoting tissue damage repair, etc. Moreover, the role of SPMs on oxidative stress has been extensively researched and provides a possible treatment method. In the current study, we review the positive role of SPMs in oxidative stress-related disease and outline the possible involved mechanism, thus providing the theoretical support for a better understanding of the roles of SPMs in oxidative stress and the theoretical basis for finding targets for the oxidative stress-related diseases.


Assuntos
Anti-Inflamatórios/metabolismo , Ácidos Graxos Insaturados/metabolismo , Inflamação/imunologia , Estresse Oxidativo/imunologia , Animais , Anti-Inflamatórios/imunologia , Modelos Animais de Doenças , Ácidos Graxos Insaturados/imunologia , Humanos , Espécies Reativas de Oxigênio/metabolismo
9.
Immunol Res ; 68(5): 280-288, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32845434

RESUMO

Previous reports have demonstrated that the newly identified lipid mediator protectin DX (PDX) could effectively attenuate multiple organ injuries in sepsis. The aim of our study was to clarify whether PDX could improve acute lung injury (ALI) induced by sepsis and elucidate the relevant potential mechanism. After inducing sepsis by the cecal ligation and puncture approach, mice were treated with a high or low dose of PDX. Pathological changes in the pulmonary tissue were analyzed by hematoxylin-eosin staining, and lung injury score was evaluated. Lung permeability and edema were assessed by lung wet/dry ratio, and protein and cellular load of the bronchoalveolar lavage fluid (BALF). Inflammatory cytokine levels in BALF were measured by ELISA and the expression of PPARγ in the lung tissue was analyzed by immunoblotting. The results suggested that PDX could diminish the inflammatory response in lung tissue after sepsis by upregulating PPARγ and inhibiting the phosphorylation and activation of NF-κB p65. PDX treatment lowered the levels of pro-inflammation cytokines IL-1ß, IL-6, TNF-α, and MCP-1, and the levels of anti-inflammatory cytokine IL-10 was increased in the BALF. It also improved lung permeability and reduced lung injury. Furthermore, the protective effect of PDX on lung tissue could be reversed by GW9662, a specific PPAR-γ antagonist. Taken together, our study indicated that PDX could ameliorate the inflammatory response in ALI by activating the PPARγ/NF-κB pathway in a mouse model of sepsis.


Assuntos
Lesão Pulmonar Aguda/tratamento farmacológico , Anti-Inflamatórios/administração & dosagem , Ácidos Docosa-Hexaenoicos/administração & dosagem , PPAR gama/metabolismo , Sepse/tratamento farmacológico , Lesão Pulmonar Aguda/diagnóstico , Lesão Pulmonar Aguda/imunologia , Lesão Pulmonar Aguda/patologia , Anilidas/administração & dosagem , Animais , Líquido da Lavagem Broncoalveolar/imunologia , Citocinas/análise , Citocinas/metabolismo , Modelos Animais de Doenças , Humanos , Inflamação/diagnóstico , Inflamação/tratamento farmacológico , Inflamação/imunologia , Mediadores da Inflamação/análise , Mediadores da Inflamação/metabolismo , Pulmão/efeitos dos fármacos , Pulmão/imunologia , Pulmão/patologia , Masculino , Camundongos , PPAR gama/antagonistas & inibidores , Sepse/complicações , Sepse/imunologia , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/imunologia , Fator de Transcrição RelA/metabolismo
10.
Life Sci ; 254: 117773, 2020 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-32418896

RESUMO

The disturbance of the immune homeostasis caused by infection is decisive for multiple organ dysfunction caused by sepsis. Both the th17 cell and the regulatory cell(Tregs) are important components of the immune system and play a crucial role in maintaining immune homeostasis. In this study, we explored the effect of Maresin1, an emerging specific pro-inflammatory mediator, on the balance of Th17/Treg in sepsis, and investigated the underlying mechanism. We used the male C57BL/6 mice to establish the model of sepsis-induced lung injury by cecal ligation and puncture to verify the protective effect of Maresin1. Our study showed that Maresin1 could significantly inhibit the excessive inflammatory response and promote the inflammation regression in the process of sepsis-induced acute lung injury, thereby reducing lung damage and improving lung function. These effects were accompanied with the regulation of Maresin1 on the Th17/Treg balance in the early stages of sepsis. We demonstrated that Maresin1 has a certain effect on increasing the number of Treg and decreasing the number of Th17 cells in the early stages of sepsis, which is consistent with its effect on STAT3/RORγt and STAT5/Foxp3 signal pathways. Our study elucidated for the first time the relationship between Maresin1 and Th17/Treg balance in sepsis-induced acute lung injury.


Assuntos
Lesão Pulmonar Aguda/tratamento farmacológico , Lesão Pulmonar Aguda/imunologia , Ácidos Docosa-Hexaenoicos/farmacologia , Linfócitos T Reguladores/efeitos dos fármacos , Células Th17/efeitos dos fármacos , Animais , Citocinas/imunologia , Modelos Animais de Doenças , Fatores de Transcrição Forkhead/imunologia , Inflamação/tratamento farmacológico , Inflamação/imunologia , Inflamação/patologia , Pulmão/metabolismo , Pulmão/patologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Membro 3 do Grupo F da Subfamília 1 de Receptores Nucleares/imunologia , Distribuição Aleatória , Fator de Transcrição STAT3/imunologia , Fator de Transcrição STAT5/imunologia , Sepse/tratamento farmacológico , Sepse/imunologia , Transdução de Sinais/efeitos dos fármacos , Linfócitos T Reguladores/imunologia , Células Th17/imunologia
11.
Int Immunopharmacol ; 84: 106443, 2020 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-32334385

RESUMO

Pulmonary fibrosis (PF) is a chronic progressive interstitial lung disease. The pathogenesis of PF has not been clearly elucidated, and there is no obvious effective treatment to arrest the progression of PF to date. A long-term chronic inflammatory response and inappropriate repair process after lung injury are important causes and pathological processes of PF. As an influential type of the body's immune cells, regulatory T cells (Tregs) play an irreplaceable role in inhibiting the inflammatory response and promoting the repair of lung tissue. However, the exact roles of Tregs in the process of PF have not been clearly established, and the available literature concerning the roles of Tregs in PF are contradictory. First, Tregs can advance the progression of pulmonary fibrosis by secreting platelet-derived growth factor (PDGF), transforming growth factor-ß (TGF-ß) and other related factors, promoting epithelial-mesenchymal transition (EMT) and affecting the Th1 and Th2 balance, etc. Second, Tregs can inhibit PF by promoting the repair of epithelial cell damage, inhibiting the accumulation of fibroblasts, and strongly inhibiting the production and function of other related pro-inflammatory factors and pro-inflammatory cells. Accordingly, in this review, we focus on the multiple roles of Tregs in different models and different pulmonary fibrosis phases, thereby providing theoretical support for a better understanding of the multiple roles of these cells in PF and a theoretical basis for identifying targets for PF therapy.


Assuntos
Células Epiteliais/imunologia , Fibrose Pulmonar/imunologia , Linfócitos T Reguladores/imunologia , Animais , Transição Epitelial-Mesenquimal , Fibroblastos/imunologia , Humanos , Peptídeos e Proteínas de Sinalização Intracelular/imunologia , Fibrose Pulmonar/metabolismo
12.
Med Sci Monit ; 26: e918523, 2020 Jan 29.
Artigo em Inglês | MEDLINE | ID: mdl-31995551

RESUMO

BACKGROUND Intrathecal dexmedetomidine (DEX) can improve the blockade of spinal anesthesia, but there is no clear conclusion on whether it has an effect on the fetus during cesarean section. Our meta-analysis evaluated the safety and efficacy of intrathecal DEX in cesarean delivery. MATERIAL AND METHODS We searched Cochrane, Embase, PubMed, and CBM for eligible studies, and used the Revised Cochrane Risk of Bias Tool (RoB 2.0) to assess the risk of bias of each study. RevMan was used for statistical analyses. We have registered this meta-analysis on PROSPERO (CRD42019120995). RESULTS The meta-analysis included 10 RCTs, but only 5 were prospectively registered. The results of preregistration studies, including the 1- or 5-min Apgar score (mean difference [MD], -0.03; 95% confidence intervals [CI], -0.16 to 0.10; P=0.64 or MD, 0.00; 95% CI, -0.09 to 0.09; P=1), the umbilical arterial oxygen or carbon dioxide partial pressure (MD, 0.90; 95% CI, -4.92 to 6.72; P=0.76 or MD, 1.20; 95% CI, -2.06 to 4.46; P=0.47), and the cord blood pH (MD, -0.01; 95% CI, -0.05 to 0.03; P=0.72), showed that intrathecal DEX had no significant difference in neonatal outcomes compared with placebo. In maternal outcomes, intrathecal DEX significantly prolonged postoperative pain-free period and reduced the incidence of postoperative shivering, which did not increase spinal anesthesia-associated adverse effects. CONCLUSIONS Intrathecal DEX is safe for the fetus during cesarean section and can improve the blockade effects of spinal anesthesia on puerperae.


Assuntos
Raquianestesia , Cesárea , Feto/fisiologia , Índice de Apgar , Dexmedetomidina/efeitos adversos , Dexmedetomidina/farmacologia , Feminino , Feto/efeitos dos fármacos , Humanos , Recém-Nascido , Período Pós-Operatório , Gravidez , Resultado da Gravidez , Viés de Publicação , Risco , Tremor por Sensação de Frio/efeitos dos fármacos , Escala Visual Analógica
13.
Front Pharmacol ; 10: 1323, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31787899

RESUMO

Acute kidney injury (AKI) is one of the most common and serious complications of sepsis in which the inflammatory cascade plays a crucial role. There is now increasing evidence that lipid mediators derived from the omega-3 fatty acid docosahexaenoic acid (DHA) have potent anti-inflammatory effects that promote the timely regression of acute inflammation. In this study, we investigated the protective effects and molecular mechanism of a novel DHA-derived lipid mediator Maresin 1 (MaR1) on AKI in septic mice. The cecal ligation and puncture (CLP) was used to establish a sepsis mice model. As a result, we found that MaR1 significantly increased the 7-day survival rate of septic mice and the anti-inflammatory factor IL-10 while reducing bacterial load and pro-inflammatory cytokines (TNF-α, IL-6, and IL-1ß). In addition, MaR1 dose dependently reduced renal injury scores and serum creatinine and urea nitrogen levels in septic mice while inhibiting renal neutrophil infiltration and myeloperoxidase (MPO) activity. In terms of signaling pathway, we found that MaR1 inhibits the expression of phosphorylated p65, Stat3, JNK, ERK, and p38 and significantly reduces nuclear translocation of p65. In conclusion, our results indicate that MaR1 is able to reduce neutrophil infiltration and inhibit nuclear factor-kappa B/signal transducer and activator of transcriptor 3/mitogen-activated protein kinase (NF-κB/STAT3/MAPK) activity and regulate inflammatory cytokine level to inhibit inflammatory response and thereby weaken sepsis-associated AKI in mice.

14.
Int Immunopharmacol ; 75: 105825, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31437789

RESUMO

Mechanical ventilation (MV) is a major support for patients with severe clinical disease, surgery and anesthesia. However, complications of mechanical ventilation especially ventilator-induced lung injury(VILI) can make the course and prognosis worse. Resolvin D1(RvD1) is a class of endogenous polyunsaturated fatty acid derivative, which has protective effects on various pulmonary inflammatory diseases. However, the mechanism of RvD1 in the process of VILI has not been fully elucidated. Our study found that RvD1 does have a protective effect on VILI including inhibiting inflammatory responses, reducing tissue damage and improving pulmonary function. The protective effect of RvD1 is positively related to its dose. Our research suggested RvD1 plays a role that increases the expression of heme oxygenase­1 (HO-1) and decreases the expression of the high mobility group chromosomal protein B1 (HMGB-1) in VILI. HO-1 can exert the protective effect of organism through multiple mechanisms such as anti-inflammatory, anti-oxidation, anti-apoptosis, etc. HMGB1 is a potent inflammatory response factor in the body, which can aggravate the inflammatory response of the body. Our study demonstrated that RvD1 can ameliorate lung inflammation and reduce pathological changes in lung tissue in a model of lung injury induced by mechanical ventilation. The protective role of RvD1 is closely linked to the increased expression of HO-1 and the decreased expression of HMGB1. Moreover, we found that RvD1 can increase the expression of Nrf2 and inhibit the expression of NF-κB. We found the specific inhibitor of HO-1, ZnPP, can significantly inhibit the protective role of RvD1 in VILI. When HO-1 is inhibited, pathological damage and inflammatory reaction in the lungs are considerably aggravated, and pulmonary function is significantly weakened. In addition, the expression of HMGB1 is drastically increased. This indicates that the HO-1-HMGB1 pathway plays an important role in the protective effect of RvD1 on mechanical ventilation lung injury.


Assuntos
Ácidos Docosa-Hexaenoicos/farmacologia , Proteína HMGB1/imunologia , Heme Oxigenase-1/imunologia , Proteínas de Membrana/imunologia , Substâncias Protetoras/farmacologia , Lesão Pulmonar Induzida por Ventilação Mecânica/imunologia , Animais , Líquido da Lavagem Broncoalveolar/imunologia , Citocinas/imunologia , Ácidos Docosa-Hexaenoicos/uso terapêutico , Pulmão/efeitos dos fármacos , Pulmão/imunologia , Pulmão/patologia , Masculino , Camundongos Endogâmicos C57BL , Substâncias Protetoras/uso terapêutico , Lesão Pulmonar Induzida por Ventilação Mecânica/tratamento farmacológico , Lesão Pulmonar Induzida por Ventilação Mecânica/patologia , Ventiladores Mecânicos/efeitos adversos
15.
BMC Anesthesiol ; 19(1): 138, 2019 08 01.
Artigo em Inglês | MEDLINE | ID: mdl-31370793

RESUMO

BACKGROUND: The comparative efficacy of ancillary drugs on sevoflurane related emergence agitation (EA) in children undergoing ophthalmic surgery remains controversial. METHODS: The databases were retrieved in an orderly manner from the dates of their establishment to October, 2018, including PubMed, The Cochrane Library and Web of Science, to collect randomized controlled trials (RCT) of different anesthetic drugs combined with sevoflurane for ophthalmic surgery. Then a network meta-analysis was conducted using R and Stata 12.0 softwares. RESULTS: The meta-analysis showed that, in reducing sevoflurane related EA, dexmedetomidine, ketamine, propofol, fentanyl, midazolam, sufentanil, remifentanil and clonidine were superior to placebo (P < 0.05). The network meta-analysis showed that the effects of ancillary drugs combine with sevoflurane in reducing risk of EA in children undergoing ophthalmic surgery was superior to placebo: dexmedetomidine (OR = 0.17, 95% CrI 0.12-0.22), ketamine (OR = 0.30, 95% CrI 0.11-0.49), propofol (OR = 0.24, 95% CrI 0.09-0.63), fentanyl (OR = 0.16, 95% CrI 0.08-0.56), midazolam (OR = 0.20, 95% CrI 0.09-0.40), sufentanil (OR = 0.27, 95% CrI 0.14-0.41), remifentanil (OR = 0.18, 95% CrI 0.08-0.54) and clonidine (OR = 0.14, 95% CrI 0.07-0.41). The SUCRA of placebo, dexmedetomidine, ketamine, propofol, fentanyl, midazolam, sufentanil, remifentanil, clonidine were respectively 0.26, 77.93, 27.71, 42.8, 69.43, 52.89, 59.83, 57.62 and 61.53%. CONCLUSIONS: The effects of dexmedetomidine combine with sevoflurane in reducing risk of emergence agitation in children undergoing ophthalmic surgery was superior to other drugs.


Assuntos
Acatisia Induzida por Medicamentos/prevenção & controle , Período de Recuperação da Anestesia , Anestésicos Inalatórios/efeitos adversos , Sevoflurano/efeitos adversos , Analgésicos/uso terapêutico , Teorema de Bayes , Criança , Clonidina/uso terapêutico , Dexmedetomidina/uso terapêutico , Quimioterapia Combinada , Fentanila/uso terapêutico , Humanos , Ketamina/uso terapêutico , Midazolam/uso terapêutico , Metanálise em Rede , Procedimentos Cirúrgicos Oftalmológicos , Propofol/uso terapêutico , Agitação Psicomotora , Remifentanil/uso terapêutico , Sufentanil/uso terapêutico
16.
Biomed Res Int ; 2019: 6254587, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31275979

RESUMO

As one of the basic treatment modalities in the intensive care unit (ICU), mechanical ventilation can cause or aggravate acute lung injury or ventilator-induced lung injury (VILI). Resolvin D1 (RvD1) is an endogenous polyunsaturated fatty acid derivative with strong anti-inflammatory action. In this study, we explored if RvD1 possesses a protective effect on VILI. Mice were ventilated with high tidal volume (40 mL/kg, HVT) for 4 h and were then intraperitoneally administered RvD1 at the beginning of high tidal volume ventilation and given GW9662 (a PPAR-γ antagonist) intraperitoneally 30 min before ventilation. RvD1 attenuated VILI, as evidenced by improved oxygenation and reduced histological injury, compared with HVT -induced lung injury. Similarly, it could ameliorate neutrophil accumulation and production of proinflammatory cytokines in lung tissue. In contrast, the protective effect of RvD1 on lung tissue could be reversed by GW9662. RvD1 mitigated VILI by activating peroxisome proliferator-activated receptor gamma (PPAR-γ) and inhibiting nuclear factor-kappa B (NF-κB) signaling pathways in mice. In conclusion, RvD1 could reduce the inflammatory response in VILI by activating PPAR-γ and inhibiting NF-κB signaling pathways.


Assuntos
Ácidos Docosa-Hexaenoicos/uso terapêutico , NF-kappa B/metabolismo , PPAR gama/metabolismo , Transdução de Sinais , Lesão Pulmonar Induzida por Ventilação Mecânica/tratamento farmacológico , Lesão Pulmonar Induzida por Ventilação Mecânica/metabolismo , Animais , DNA/metabolismo , Proteínas I-kappa B/metabolismo , Inflamação/patologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Infiltração de Neutrófilos , Subunidades Proteicas/metabolismo , Testes de Função Respiratória , Fator de Transcrição RelA/metabolismo , Lesão Pulmonar Induzida por Ventilação Mecânica/patologia , Lesão Pulmonar Induzida por Ventilação Mecânica/fisiopatologia
17.
Nanoscale ; 8(10): 5599-604, 2016 Mar 14.
Artigo em Inglês | MEDLINE | ID: mdl-26890686

RESUMO

An innovative hydrogen sensing concept is demonstrated based on the field emission from multi-walled carbon nanotubes, where the low emission currents rise in proportion to hydrogen partial pressures above 10(-9) Torr. Experimental and first principles studies reveal that the sensing mechanism is attributed to the effective work function reduction from dissociative hydrogen chemisorption. The embedded Ni catalyst would assist both the hydrogen dissociation and work function reduction. This technique is promising to build miniature low cost hydrogen sensors for multiple applications. This work is valuable for studies of nanocarbon-gas reaction mechanisms and the work function properties in adsorption related applications, including field emission, hydrogen storage, energy cells, and gas sensing.

18.
Anal Chem ; 76(2): 499-501, 2004 Jan 15.
Artigo em Inglês | MEDLINE | ID: mdl-14719905

RESUMO

Quantitative detection of a biological affinity reaction, the biotin/avidin recognition, was achieved using our newly developed photoelectrochemical analytical system. The system is based on the operation mechanism of the well-developed dye-sensitized photoelectrochemical solar cells and comprises a ruthenium tris(2,2'-bipyridine) (Ru-bipy) derivative as the photoelectrochemical signal-generating molecule, oxalate as the sacrificial electron donor, and tin oxide nanoparticle as the semiconductor electrode material. To perform the affinity reaction, avidin was immobilized on SnO(2) electrode by passive adsorption. Biotin-linked bovine serum albumin (BSA) was labeled with an NHS-ester derivative of Ru-bipy. After binding of BSA to the surface-immobilized avidin through biotin, photoelectrochemical measurement was carried out in the presence of oxalate. Anodic photocurrent was turned on and off repeatedly by control of incidental light. The action spectrum of the photocurrent resembled the absorption spectrum of Ru-bipy, proving the photocurrent was generated from the metal complex. A linear relationship between photocurrent and BSA concentration was obtained in the range of 1-100 microg/mL. This is the first case of quantitative photoelectrochemical detection of a biological affinity interaction.


Assuntos
Avidina/análise , Biotina/análise , 2,2'-Dipiridil/análogos & derivados , 2,2'-Dipiridil/química , Avidina/química , Avidina/metabolismo , Ligação Competitiva , Técnicas Biossensoriais/métodos , Biotina/química , Biotina/metabolismo , Coloides/química , Eletroquímica , Eletrodos , Luz , Oxalatos/química , Fotoquímica , Ligação Proteica , Rutênio/química , Soroalbumina Bovina/química , Compostos de Estanho/química
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