RESUMEN
It is generally accepted that near infrared reflectance spectroscopy (NIRS) can be used to identify variety authenticity of bare maize seeds. In practical, maize seeds are covered with seed coating agents. Therefore it's of huge significance to investigate the feasibility of identifying coated maize seeds by NIRS. This study employed NIRS to quickly determine the variety of coated maize seeds. Influence of seed coating agent on NIR spectra was discussed. The NIR spectra of coated maize seeds were obtained using an innovative method to avoid the impact of the seed coating agent. Coated seeds were cut open, and the sections were scanned by the spectrometer, so as to acquire the information of the seed itself. Then, support vector machine (SVM), soft independent modeling of class analogy (SIMCA), and biomimetic pattern recognition (BPR) was employed to establish the identification model for four maize varieties, and yield 93%, 95.8%, 98% average correct rate respectively. BPR model showed better performance than SVM and SIMCA models. The robustness of identification model was tested by seeds harvested from four regions and model showed good performance.
Asunto(s)
Semillas , Zea mays/clasificación , Estudios de Factibilidad , Modelos Teóricos , Programas Informáticos , Espectroscopía Infrarroja Corta , Máquina de Vectores de SoporteRESUMEN
Myeloperoxidase (MPO) is an endogenous oxidant enzyme and can generate reactive oxygen species. The MPO G463A polymorphism influences MPO transcription levels and has been proposed to be associated with risk of lung cancer. To assess the effect of MPO G463A polymorphism on lung cancer risk in Asians, a pooled analysis of published case-control studies was performed. PubMed, Embase, China Biomedical Literature, and Wanfang Medicine databases were searched for eligible studies. The strength of the association between MPO G463A polymorphism and lung cancer risk was measured by odds ratio (OR) with 95 % confidence interval (95% CI). Finally, eight studies with a total of 1,679 lung cancer cases and 1,876 non-cancer controls were included. Overall, MPO G463A polymorphism was associated with decreased risk of lung cancer risk in Asians under two genetic models (OR AA vs. GG = 0.58, 95% CI 0.36-0.96, P = 0.033; OR AA vs. GG+AG = 0.60, 95% CI 0.37-0.98, P = 0.040). There was no obvious risk of publication bias in this meta-analysis. In conclusion, the pooled analysis suggests that MPO G463A polymorphism is associated with decreased risk of lung cancer risk in Asians.
Asunto(s)
Neoplasias Pulmonares/genética , Peroxidasa/genética , Polimorfismo de Nucleótido Simple , Pueblo Asiatico , Estudios de Casos y Controles , Estudios de Asociación Genética , Predisposición Genética a la Enfermedad , Humanos , Neoplasias Pulmonares/enzimología , Oportunidad RelativaRESUMEN
Epithelial-mesenchymal transition (EMT) is an essential step for cancer metastasis. MicroRNAs (miRNAs) are small non-coding RNAs that regulate target-mRNAs post-transcriptionally. The expression and function of miRNAs in EMT of HT-29 colonic cells remain elusive. This study looks at expression of miRNAs in EMT and explores the effects of miRNAs on EMT in HT-29 cell line. HT-29 was treated with TGF ß to establish an EMT model, in which a collection of miRNAs was dynamically regulated by real-time PCR (qPCR) analysis. Among them, miR-21 and miR-27 were significantly upregulated, while miR-22, miR-26, miR-30, miR-181, miR-200b, miR-200c and miR-214 were markedly downregulated. MiRNA-inhibitors were used to knockdown miRNAs in HT-29 and EMT markers were determined by qPCR to monitor the effects of miRNAs on EMT process. Results showed that miR-22 could not alter the expression of EMT markers, while knockdown of miR-200b could significantly increase that of epithelial markers, N-cadherin, Vimentin, α-Sma and Twist1 and decrease that of mesenchymal marker, E-cadherin. Bioinformatic analysis and Western blot showed that ZEB1 was directly suppressed by miR-200b. In conclusion, miRNAs are dynamically regulated in TGF ß-induced EMT of HT-29 and miR-200b was essential for EMT by suppressing the expression of ZEB1 in HT-29.
Asunto(s)
MicroARNs/metabolismo , Regiones no Traducidas 3' , Actinas/genética , Actinas/metabolismo , Cadherinas/genética , Cadherinas/metabolismo , Biología Computacional , Regulación hacia Abajo/efectos de los fármacos , Transición Epitelial-Mesenquimal , Células HT29 , Proteínas de Homeodominio/genética , Proteínas de Homeodominio/metabolismo , Humanos , MicroARNs/antagonistas & inhibidores , Proteínas Nucleares/genética , Proteínas Nucleares/metabolismo , Factores de Transcripción/genética , Factores de Transcripción/metabolismo , Factor de Crecimiento Transformador beta/farmacología , Proteína 1 Relacionada con Twist/genética , Proteína 1 Relacionada con Twist/metabolismo , Regulación hacia Arriba/efectos de los fármacos , Vimentina/genética , Vimentina/metabolismo , Homeobox 1 de Unión a la E-Box con Dedos de ZincRESUMEN
Acute lung injury is characterized by an increase of inflammatory reaction and severe lung edema. Even if there have been great advances in the identification of genes and signaling pathways involved in acute lung injury, the fundamental mechanisms of initiation and propagation of acute lung injury have not been understood completely. A growing amount of evidence indicates that microRNAs (miRNAs) are involved in various human diseases. However, the expression profile and function of miRNAs in acute lung injury have not been investigated. Here, using real-time polymerase chain reaction analysis, we show that a collection of miRNAs is dynamically regulated in lipopolysaccharide (LPS)-induced mouse acute lung injury. Among them, miR-199a and miR-16 are the most significantly down-regulated miRNAs. To study the role of miR-199a and miR-16 in acute lung injury, an over-expression of miR-199a or miR-16 assay was performed in LPS-treated A549 cells, and then the expression of inflammatory factors was analyzed. Over-expression of miR-199a could not alter the expression level of interleukin (IL)-6 and tumor necrosis factor-alpha (TNFα), while up-regulation of miR-16 could significantly down-regulate IL-6 and TNFα expression level. Using bioinformatic analysis, we show that a 3' untranslational region (UTR) of IL-6 and TNFα contains the binding sites of miR-16. Accordingly, over-expression of miR-16 could significantly suppress the luciferase activity of reporter fusion with the binding sites of TNFα in its 3'UTR region, suggesting that miR-16 played its role in LPS-induced lung inflammation by a direct manner. In this study, we show for the first time that miRNAs are dynamically regulated and play an important function in LPS-induced lung injury.
Asunto(s)
Lesión Pulmonar Aguda/fisiopatología , MicroARNs/fisiología , Lesión Pulmonar Aguda/inducido químicamente , Lesión Pulmonar Aguda/metabolismo , Animales , Células Cultivadas , Modelos Animales de Enfermedad , Regulación hacia Abajo/fisiología , Humanos , Interleucina-6/biosíntesis , Lipopolisacáridos , Ratones , MicroARNs/biosíntesis , Transfección/métodos , Factor de Necrosis Tumoral alfa/biosíntesis , Regulación hacia Arriba/fisiologíaRESUMEN
The asymmetric unit of the title compound, (C(13)H(11)Cl(2)N(2))(2)[Ni(C(4)N(2)S(2))(2)], contains one-half of a centrosymmetric [Ni(mnt)(2)] anion (where mnt is maleonitrile-dithiol-ate or 1,2-dicyano-1,2-ethyl-enedithiol-ate) and an (E)-1-(3,4-dichloro-benzyl-ideneamino)-4-methyl-pyridinium cation. In the anion, the coordination around the Ni atom is a distorted square. In the cation, the aromatic rings are oriented at a dihedral angle of 7.81â (3)°. In the crystal structure, inter-molecular C-Hâ¯N hydrogen bonds link the cations and anions. π-π Contacts between the nickel dithiol-ene and pyridine rings and between the benzene and pyridine rings, [centroid-centroid distances = 3.682â (3) and 3.643â (3)â Å, respectively] may further stabilize the structure.
RESUMEN
The asymmetric unit of the title compound, (C(6)H(9)N(2))(2)[Ni(C(4)N(2)S(2))(2)], contains one half of an [Ni(mnt)(2)](2-) anion (mnt is maleonitrile-dithiol-ate or 1,2-dicyano-ethene-1,2-dithiol-ate) and one 1-amino-4-methyl-pyridinium cation. The Ni(II) atom is located on an inversion centre. In the crystal structure, inter-molecular N-Hâ¯N hydrogen bonds link the mol-ecules.
RESUMEN
This report presents the extracorporeal membrane oxygenation (ECMO)-assisted surgical as a treatment of benign double tracheoesophageal fistula. The patient was a 43-year-old woman who presented the airway obstruction for 3 weeks after the esophagus metal stent implantation for the tracheoesophageal fistula 1 year ago. The airway obstruction was due to the expansion and piercing of the metal stent through the upper part of the esophagus into the tracheal cavity. In view of the failure of endotracheal intubation, we finally used ECMO-assisted surgery to remove the stent. And at the same time, cervical esophagostomy externa, exclusion of the thoracic tracheoesophageal fistulas and gastrostomy were performed.