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1.
Poult Sci ; 103(6): 103663, 2024 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-38603930

RESUMEN

The enclosed multistory poultry housing is a type of poultry enclosure widely used in industrial caged chicken breeding. Accurate identification and detection of the comb and eyes of caged chickens in poultry farms using this type of enclosure can enhance managers' understanding of the health of caged chickens. However, the accuracy of image detection of caged chickens will be affected by the enclosure's entrance, which will reduce the precision. Therefore, this paper proposes a cage-gate removal algorithm based on big data and deep learning Cyclic Consistent Migration Neural Network (CCMNN). The method achieves automatic elimination and restoration of some key information in the image through the CCMNN network. The Structural Similarity Index Measure (SSIM) between the recovered and original images on the test set is 91.14%. Peak signal-to-noise ratio (PSNR) is 25.34dB. To verify the practicability of the proposed method, the performance of the target detection algorithm is analyzed both before and after applying the CCMNN network in detecting the combs and eyes of caged chickens. Different YOLOv8 detection algorithms, including YOLOv8s, YOLOv8n, YOLOv8m, and YOLOv8x, were used to verify the algorithm proposed in this paper. The experimental results demonstrate that compared to images without CCMNN processing, the precision of comb detection of caged chickens is improved by 11, 11.3, 12.8, and 10.2%. Similarly, the precision of eye detection for caged chickens is improved by 2.4, 10.2, 6.8, and 9%. Therefore, more complete outline images of caged chickens can be obtained using this algorithm and the precision in detecting the comb and eyes of caged chickens can be enhanced. These advancements in the algorithm offer valuable insights for future poultry researchers aiming to deploy enhanced detection equipment, thereby contributing to the accurate assessment of poultry production and farm conditions.


Asunto(s)
Algoritmos , Pollos , Vivienda para Animales , Redes Neurales de la Computación , Animales , Pollos/fisiología , Cabeza , Crianza de Animales Domésticos/métodos , Aprendizaje Profundo
2.
Yao Xue Xue Bao ; 39(3): 227-31, 2004 Mar.
Artículo en Zh | MEDLINE | ID: mdl-15171662

RESUMEN

AIM: To study the cellular uptake of chitosan oligosaccharide nanoparticles by A549 cells and evaluate the possibility of chitosan oligosaccharide nanoparticles used as a potential drug carrier. METHODS: Chitosan oligosaccharide (CSO) was obtained by ultrafiltration separation after regulation of the condition of chitosanase degradation. The molecular weight of CSO was determined by gel permeation chromatography (GPC). Chitosan oligosaccharide nanoparticles (CSO-NPs) were prepared by a novel solvent diffusion method in an oil system after the carrier material grafted fluorescein isothiocyanate (FITC) and the particle size distribution and zeta potential were determined by light scattering and electrophoretic mobility. The cytotoxicity and uptake of FITC-labeled CSO-NPs in A549 cells following various incubation periods were studied by the MTT method and fluorescence microscopy, flow cytometric analysis, respectively. RESULTS: The molecular weight (MW) of CSO was 18,678 u and the particles sizes of CSO-NPs were 133.3 nm (number average) and 368.2 nm (volume average), respectively. The IC50 of CSO and CSO-NPs were 944.36 and 643.16 mg x L(-1), respectively, and the result showed low cytotoxicity. Cellular uptake of CSO and CSO-NPs were relative to the concentration and the incubation time. Internalization of CSO-NPs increased 0.49 - 13.9 times more than that of the CSO with the same incubation time. CONCLUSION: CSO and CSO-NPs have low cytotoxicity. CSO-NPs can significantly improved the uptake of CSO-NPs by A549 cells compared to the same molecular weight of CSO.


Asunto(s)
Quitina/análogos & derivados , Quitina/metabolismo , Oligosacáridos/metabolismo , Adenocarcinoma/patología , Quitina/toxicidad , Quitosano , Relación Dosis-Respuesta a Droga , Portadores de Fármacos/metabolismo , Portadores de Fármacos/toxicidad , Células Epiteliales/efectos de los fármacos , Células Epiteliales/metabolismo , Humanos , Neoplasias Pulmonares/patología , Nanotecnología , Oligosacáridos/toxicidad , Tamaño de la Partícula , Factores de Tiempo , Células Tumorales Cultivadas
3.
Toxicol Sci ; 137(2): 404-15, 2014 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-24194395

RESUMEN

Sertraline is generally used for the treatment of depression and is also approved for the treatment of panic, obsessive-compulsive, and posttraumatic stress disorders. Previously, using rat primary hepatocytes and isolated mitochondria, we demonstrated that sertraline caused hepatic cytotoxicity and mitochondrial impairment. In the current study, we investigated and characterized molecular mechanisms of sertraline toxicity in human hepatoma HepG2 cells. Sertraline decreased cell viability and induced apoptosis in a dose- and time-dependent manner. Sertraline activated the intrinsic checkpoint protein caspase-9 and caused the release of cytochrome c from mitochondria to cytosol; this process was Bcl-2 family dependent because antiapoptotic Bcl-2 family proteins were decreased. Pretreatment of the HepG2 cells with caspase-3, caspase-8, and caspase-9 inhibitors partially but significantly reduced the release of lactate dehydrogenase, indicating that sertraline-induced apoptosis is mediated by both intrinsic and extrinsic apoptotic pathways. Moreover, sertraline markedly increased the expression of tumor necrosis factor (TNF) and the phosphorylation of JNK, extracellular signal-regulated kinase (ERK1/2), and p38. In sertraline-treated cells, the induction of apoptosis and cell death was shown to be the result of activation of JNK, but not ERK1/2 or p38 in the mitogen-activated protein kinase (MAPK) pathway. Furthermore, silencing MAP4K4, the upstream kinase of JNK, attenuated both apoptosis and cell death caused by sertraline. Taken together, our findings suggest that sertraline induced apoptosis in HepG2 cells at least partially via activation of the TNF-MAP4K4-JNK cascade signaling pathway.


Asunto(s)
Antidepresivos/toxicidad , Apoptosis/efectos de los fármacos , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Sertralina/toxicidad , Western Blotting , Caspasa 3/metabolismo , Caspasa 7/metabolismo , Caspasa 9/metabolismo , Técnicas de Cultivo de Célula , Silenciador del Gen , Células Hep G2 , Humanos , Péptidos y Proteínas de Señalización Intracelular/antagonistas & inhibidores , Péptidos y Proteínas de Señalización Intracelular/genética , Potencial de la Membrana Mitocondrial/efectos de los fármacos , Proteínas Serina-Treonina Quinasas/antagonistas & inhibidores , Proteínas Serina-Treonina Quinasas/genética , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , Reacción en Cadena en Tiempo Real de la Polimerasa
4.
Toxicol Lett ; 221(1): 64-72, 2013 Jul 31.
Artículo en Inglés | MEDLINE | ID: mdl-23747414

RESUMEN

Goldenseal has been used for the treatment of a wide variety of ailments including gastrointestinal disturbances, urinary tract disorders, and inflammation. The five major alkaloid constituents in goldenseal are berberine, palmatine, hydrastine, hydrastinine, and canadine. When goldenseal was evaluated by the National Toxicology Program (NTP) in the standard 2-year bioassay, goldenseal induced an increase in liver tumors in rats and mice; however, the mechanism of goldenseal-associated liver carcinogenicity remains unknown. In this study, the toxicity of the five goldenseal alkaloid constituents was characterized, and their toxic potencies were compared. As measured by the Comet assay and the expression of γ-H2A.X, berberine, followed by palmatine, appeared to be the most potent DNA damage inducer in human hepatoma HepG2 cells. Berberine and palmatine suppressed the activities of both topoisomerase (Topo) I and II. In berberine-treated cells, DNA damage was shown to be directly associated with the inhibitory effect of Topo II, but not Topo I by silencing gene of Topo I or Topo II. In addition, DNA damage was also observed when cells were treated with commercially available goldenseal extracts and the extent of DNA damage was positively correlated to the berberine content. Our findings suggest that the Topo II inhibitory effect may contribute to berberine- and goldenseal-induced genotoxicity and tumorigenicity.


Asunto(s)
Alcaloides/toxicidad , ADN/efectos de los fármacos , Hepatocitos/efectos de los fármacos , Hydrastis/metabolismo , Mutágenos/toxicidad , Berberina/química , Berberina/metabolismo , Berberina/toxicidad , Alcaloides de Berberina/química , Alcaloides de Berberina/metabolismo , Alcaloides de Berberina/toxicidad , Ensayo Cometa , Daño del ADN , ADN-Topoisomerasas de Tipo I/genética , ADN-Topoisomerasas de Tipo I/metabolismo , ADN-Topoisomerasas de Tipo II/genética , ADN-Topoisomerasas de Tipo II/metabolismo , Regulación Enzimológica de la Expresión Génica/efectos de los fármacos , Silenciador del Gen , Células Hep G2 , Hepatocitos/metabolismo , Histonas/metabolismo , Humanos , Hydrastis/química , Extractos Vegetales/química , Extractos Vegetales/toxicidad , ARN Interferente Pequeño/genética , Relación Estructura-Actividad
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