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2.
Geosci Model Dev ; 15(8): 3281-3313, 2022 Apr 21.
Artigo em Inglês | MEDLINE | ID: mdl-35664957

RESUMO

A new dynamical core, known as the Finite-Volume Cubed-Sphere (FV3) and developed at both NASA and NOAA, is used in NOAA's Global Forecast System (GFS) and in limited-area models for regional weather and air quality applications. NOAA has also upgraded the operational FV3GFS to version 16 (GFSv16), which includes a number of significant developmental advances to the model configuration, data assimilation, and underlying model physics, particularly for atmospheric composition to weather feedback. Concurrent with the GFSv16 upgrade, we couple the GFSv16 with the Community Multiscale Air Quality (CMAQ) model to form an advanced version of the National Air Quality Forecasting Capability (NAQFC) that will continue to protect human and ecosystem health in the US. Here we describe the development of the FV3GFSv16 coupling with a "state-of-the-science" CMAQ model version 5.3.1. The GFS-CMAQ coupling is made possible by the seminal version of the NOAA-EPA Atmosphere-Chemistry Coupler (NACC), which became a major piece of the next operational NAQFC system (i.e., NACC-CMAQ) on 20 July 2021. NACC-CMAQ has a number of scientific advancements that include satellite-based data acquisition technology to improve land cover and soil characteristics and inline wildfire smoke and dust predictions that are vital to predictions of fine particulate matter (PM2.5) concentrations during hazardous events affecting society, ecosystems, and human health. The GFS-driven NACC-CMAQ model has significantly different meteorological and chemical predictions compared to the previous operational NAQFC, where evaluation of NACC-CMAQ shows generally improved near-surface ozone and PM2.5 predictions and diurnal patterns, both of which are extended to a 72 h (3 d) forecast with this system.

3.
Ann Palliat Med ; 10(1): 372-384, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-33545770

RESUMO

BACKGROUND: Traumatic brain injury (TBI) is a major cause of disability worldwide, without definitive and effective intervention. Dexmedetomidine (DEX) has a neuroprotective effect against TBI; however, the detailed mechanism underlying this effect remains unclear. METHODS: Ten male Sprague Dawley rats were used to establish a TBI model. The rats were randomly divided into two groups: the TBI group (TBI, control group) and the DEX treatment group (DEX). The next day, the neurological function of the rats were evaluated by the modified neurological severity score (mNSS). Then, the rats were sacrificed, and RNA sequencing was performed to identify differentially expressed messenger RNAs (mRNAs) and microRNAs (miRNAs) in brain tissue samples. Additionally, we performed a bioinformatics analysis to explore the candidate genes and pathways that might play important roles in DEX-induced neuroprotection. The most significantly differentially expressed miRNAs and possible hub genes were validated by quantitate reverse transcription-polymerase chain reaction (qRT-PCR) using more samples. RESULTS: In the DEX group, 517 mRNAs (352 up-regulated and 165 down-regulated) and 35 miRNAs (18 up-regulated and 17 down-regulated) were differentially expressed compared to the TBI group. Gene Ontology analysis revealed the up-regulated mRNAs to be significantly enriched in microtubule-based movement or processes, microtubule and tubulin binding. Kyoto Encyclopedia of Genes and Genomes analysis showed that these up-regulated mRNAs were significantly enriched in the B-cell receptor signaling pathway as well as the cell cycle pathway. Also, Lyn and Cdk1 were found to be associated with the B-cell receptor signaling and cell cycle pathways, respectively. Furthermore, the down-regulated miRNAs were significantly enriched in cellular components, although no significant Gene Ontology terms or KEGG pathways were found for the down-regulated mRNAs or up-regulated miRNAs. CONCLUSIONS: Differentially expressed mRNAs and miRNAs were identified after the administration of DEX in a TBI rat model. The B-cell receptor signaling pathway and the cell cycle pathway might be involved in the neuroprotective effect of DEX against TBI, Lyn and Cdk1 might be hub genes.


Assuntos
Biologia Computacional , Dexmedetomidina , Animais , Dexmedetomidina/uso terapêutico , Masculino , Neuroproteção , Ratos , Ratos Sprague-Dawley , Análise de Sequência de RNA
4.
Biomed Chromatogr ; 32(6): e4203, 2018 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-29399849

RESUMO

Salvia miltiorrhiza Bge. is a traditional Chinese medicine applied in the treatment of various diseases in clinical practice. In the course of its processing, S. miltiorrhiza Bge. is usually processed by sweating. This study employed 10-component contents determination coupled with high-performance liquid chromatography (HPLC) fingerprint and antioxidant activity to investigate the effect of sweating on S. miltiorrhiza Bge. so as to evaluate the quality of S. miltiorrhiza Bge. The HPLC method was performed using C18 and 0.05% phosphoric acid aqueous solution-acetonitrile with a gradient elution system. It was validated for linearity, precision, repeatability, stability and recovery. Similarity analysis, principal components analysis and antioxidant activity assays were used to compare sweated S. miltiorrhiza Bge. (SSM) and nonsweated S. miltiorrhiza Bge. (NSSM). SSM and NSSM showed good similarities in HPLC fingerprint (>0.9), but principal components analysis could classify the HPLC fingerprint and 10-component quantitation analysis. Meanwhile, the antioxidant activity of SSM was significantly higher than that of NSSM (p < 0.01). The results of this study indicated that sweating could alter the content of chemical constituents in S. miltiorrhiza Bge., and could also improve its antioxidant activity. In addition, the method not only affords a viable strategy for comparing SSM and NSSM and assessing the quality of S. miltiorrhiza Bge., but also provides a reference for other herbal medicine that suffers from sweating.


Assuntos
Antioxidantes , Cromatografia Líquida de Alta Pressão/métodos , Medicamentos de Ervas Chinesas , Salvia miltiorrhiza/química , Antioxidantes/análise , Antioxidantes/química , Antioxidantes/normas , Medicamentos de Ervas Chinesas/análise , Medicamentos de Ervas Chinesas/química , Medicamentos de Ervas Chinesas/normas , Modelos Lineares , Controle de Qualidade , Reprodutibilidade dos Testes
5.
Neurosci Lett ; 666: 104-110, 2018 02 14.
Artigo em Inglês | MEDLINE | ID: mdl-29273400

RESUMO

The anti-neuroinflammatory effect of Astragaloside IV (ASI) has been reported, but its underlying mechanisms are unclear. This study is further to explore the underlying mechanism of ASI on anti-neuroinflammatory effect in LPS induced microglia cells. The result showed ASI significantly reduced the production of inflammatory mediators NO, TNF-α and IL-6 in BV2 and primary microglial cells. Western blot analysis showed ASI did not inhibit the MAPK activation, on the contrary, the results showed ASI can obviously induce the ERK activation. We also examined the NRF2 and HO-1 activation which were reported to exert anti-neuroinflammatory effect and the results presented it could induce the activation of HO-1 downstream NRF2 in BV2 microglial cells. Further study indicated the NRF2/HO-1 activation via ERK pathway activation. After NRF2 siRNA or HO-1 inhibitor treatment, the anti-neuroinflammatory effect of ASI was attenuated obviously compared with the normal group. Taken together, this study demonstrated that the activation of NRF2/HO-1 via ERK signaling pathway is a novel mechanism of ASI which exerted anti-neuroinflammatory activity in microglia cells, it could be an attractive candidate for the regulation of inflammatory responses in the brain.


Assuntos
Heme Oxigenase-1/metabolismo , Lipopolissacarídeos/farmacologia , Proteínas de Membrana/metabolismo , Microglia/efeitos dos fármacos , Fator 2 Relacionado a NF-E2/metabolismo , Saponinas/farmacologia , Triterpenos/farmacologia , Animais , Anti-Inflamatórios/farmacologia , Sobrevivência Celular/efeitos dos fármacos , Inflamação/tratamento farmacológico , Inflamação/metabolismo , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Camundongos , Microglia/metabolismo
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