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1.
IEEE J Transl Eng Health Med ; 7: 2000203, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31497409

RESUMO

OBJECTIVE: To investigate the feasibility of improving the performance of an EEG-based multistate classifier (MSC) previously proposed by our group. RESULTS: Using the random forest (RF) classifiers on the previously reported dataset of patients, but with three improvements to classification logic, the specificity of our alarm algorithm improves from 82.4% to 92.0%, and sensitivity from 87.9% to 95.2%. DISCUSSION: The MSC could be a useful approach for seizure-monitoring both in the clinic and at home. METHODS: Three improvements to the MSC are described. Firstly, an additional check using RF outputs is made prior to alarm to confirm increasing probability of a seizure onset state. Secondly, a post-alarm detection horizon that accounts for the seizure state duration is implemented. Thirdly, the alarm decision window is kept constant.

2.
Cell Death Dis ; 8(3): e2688, 2017 03 23.
Artigo em Inglês | MEDLINE | ID: mdl-28333142

RESUMO

Hydrogen sulfide (H2S), in its gaseous form, plays an important role in tumor carcinogenesis. This study investigated the effects of H2S on the cell biological functions of hepatocellular carcinoma (HCC). HCC cell lines, HepG2 and HLE, were treated with NaHS, a donor of H2S, and rapamycin, a classic autophagy inducer, for different lengths of time. Western blotting, immunofluorescence, transmission electron microscopy (TEM), scratch assay, CCK-8 and flow cytometric analysis were carried out to examine the effects of H2S on HCC autophagy, cell behavior and PI3K/Akt/mTOR signaling. Treatment with NaHS upregulated expression of LC3-II and Atg5, two autophagy-related proteins, in HepG2 and HLE cells. TEM revealed increased numbers of intracellular double-membrane vesicles in those cells treated with NaHS. Like rapamycin, NaHS also significantly inhibited expression of p-PI3K, p-Akt and mTOR proteins in HCC cells. Interestingly, the expression of LC3-II was further increased when the cells were treated with NaHS together with rapamycin. In addition, NaHS inhibited HCC cell migration, proliferation and cell division. These findings show that H2S can induce HCC cell apoptosis. The biological function of the gasotransmitter H2S in HCC cells was enhanced by the addition of rapamycin. Hydrogen sulfide influences multiple biological functions of HCC cells through inhibiting the PI3K/Akt/mTOR signaling pathway.


Assuntos
Autofagia/efeitos dos fármacos , Carcinoma Hepatocelular/tratamento farmacológico , Sulfeto de Hidrogênio/farmacologia , Neoplasias Hepáticas/tratamento farmacológico , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais/efeitos dos fármacos , Serina-Treonina Quinases TOR/metabolismo , Apoptose/efeitos dos fármacos , Carcinoma Hepatocelular/metabolismo , Linhagem Celular Tumoral , Movimento Celular/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Células Hep G2 , Humanos , Neoplasias Hepáticas/metabolismo
3.
J Immunol ; 162(7): 4311-8, 1999 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-10201963

RESUMO

In humans, the Fc receptor for IgG, FcgammaRIIA, is expressed on macrophages and platelets and may play an important role in the pathophysiology of immune-mediated thrombocytopenia. Mice lack the genetic equivalent of human FcgammaRIIA. To better understand the role of FcgammaRIIA in vivo, FcgammaRIIA transgenic mice were generated and characterized. One transgenic mouse line expressed FcgammaRIIA on platelets and macrophages at levels equivalent to human cells, and cross-linking FcgammaRIIA on these platelets induced platelet aggregation. Immune-mediated thrombocytopenia in this transgenic line was studied using i.v. and i.p. administration of anti-mouse platelet Ab. In comparison with matched wild-type littermates that are negative for the FcgammaRIIA transgene, Ab-mediated thrombocytopenia was significantly more severe in the FcgammaRIIA transgenic mice. In contrast, FcR gamma-chain knockout mice that lack functional expression of the Fc receptors FcgammaRI and FcgammaRIII on splenic macrophages did not demonstrate Ab-mediated thrombocytopenia. We generated FcgammaRIIA transgenic x FcR gamma-chain knockout mice to examine the role of FcgammaRIIA in immune clearance in the absence of functional FcgammaRI and FcgammaRIII. In FcgammaRIIA transgenic x FcR gamma-chain knockout mice, severe immune thrombocytopenia mediated by FcgammaRIIA was observed. These results demonstrate that FcgammaRIIA does not require the FcR gamma-chain for expression or function in vivo. Furthermore, taken together, the data suggest that the human Fc receptor FcgammaRIIA plays a significant role in the immune clearance of platelets in vivo.


Assuntos
Antígenos CD/fisiologia , Plaquetas/imunologia , Receptores de IgG/fisiologia , Trombocitopenia/sangue , Trombocitopenia/imunologia , Transgenes/imunologia , Animais , Antígenos CD/sangue , Antígenos CD/genética , Cruzamentos Genéticos , Modelos Animais de Doenças , Feminino , Humanos , Injeções Intraperitoneais , Injeções Intravenosas , Isoanticorpos/administração & dosagem , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Camundongos Transgênicos , Agregação Plaquetária/imunologia , Contagem de Plaquetas , Receptores de IgG/sangue , Receptores de IgG/genética , Trombocitopenia/etiologia
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