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1.
Ann Emerg Med ; 82(3): e91-e92, 2023 09.
Artigo em Inglês | MEDLINE | ID: mdl-37596028
2.
Comput Biol Med ; 151(Pt B): 106297, 2022 12.
Artigo em Inglês | MEDLINE | ID: mdl-36435054

RESUMO

OBJECTIVES: To calculate the coronary artery calcification score (CACS) obtained from coronary artery computed tomography angiography (CCTA) examination and combine it with the influencing factors of coronary artery calcification (CAC), which is then analyzed by machine learning (ML) to predict the probability of coronary heart disease(CHD). METHODS: All patients who were admitted to the Affiliated Hospital of Traditional Chinese Medicine of Southwest Medical University from January 2019 to March 2022, suspected of CHD, and underwent CCTA inspection were retrospectively selected. The degree of CAC was quantified based on the Agatston score. To compare the correlation between the CACS and clinical-related factors, we collected 31 variables, including hypertension, diabetes, smoking, hyperlipidemia, among others. ML models containing the random forest (RF), radial basis function neural network (RBFNN),support vector machine (SVM),K-Nearest Neighbor algorithm (KNN) and kernel ridge regression (KRR) were used to assess the risk of CHD based on CACS and clinical-related factors. RESULTS: Among the five ML models, RF achieves the best performance about accuracy (ACC) (78.96%), sensitivity (SN) (93.86%), specificity(Spe) (51.13%), and Matthew's correlation coefficient (MCC) (0.5192).It also has the best area under the receiver operator characteristic curve (ROC) (0.8375), which is far superior to the other four ML models. CONCLUSION: Computer ML model analysis confirmed the importance of CACS in predicting the occurrence of CHD, especially the outstanding RF model, making it another advancement of the ML model in the field of medical analysis.


Assuntos
Doença da Artéria Coronariana , Calcificação Vascular , Humanos , Calcificação Vascular/diagnóstico por imagem , Estudos Retrospectivos , Valor Preditivo dos Testes , Fatores de Risco , Doença da Artéria Coronariana/diagnóstico por imagem , Medição de Risco , Aprendizado de Máquina
3.
J Acute Med ; 9(1): 29-33, 2019 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-32995227

RESUMO

Crepitus happened into the soft tissue is indicated subcutaneous emphysema. Subcutaneous emphysema of leg without trauma was likely to diagnose gas gangrene or gas-forming myonecrosis (GFM) at emergency department (ED). On the other hand, abdominal fatal condition with gas from the gut may spread to the leg should be considered a different diagnosis. We report a case of critically ill patient who presented to the ED with initial features suggestive of necrotizing fasciitis with gas gangrene of left leg. Assessment and further intervention revealed subcutaneous emphysema of leg secondary to a perforation of rectum associated with previous anastomosis site for rectal cancer surgery. Subcutaneous emphysema of the leg rarely happened secondary to perforation of the gastrointestinal tract and has often created serious diagnostic problems which may lead to mortality. Consequently, prompt diagnosis and aggressive treatment is imperative. Physicians and surgeons should be aware of this condition that could be fatal but curable by early intervention.

4.
Biomed Res Int ; 2017: 3267325, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28303250

RESUMO

Presynaptic and postsynaptic neurotoxins are proteins which act at the presynaptic and postsynaptic membrane. Correctly predicting presynaptic and postsynaptic neurotoxins will provide important clues for drug-target discovery and drug design. In this study, we developed a theoretical method to discriminate presynaptic neurotoxins from postsynaptic neurotoxins. A strict and objective benchmark dataset was constructed to train and test our proposed model. The dipeptide composition was used to formulate neurotoxin samples. The analysis of variance (ANOVA) was proposed to find out the optimal feature set which can produce the maximum accuracy. In the jackknife cross-validation test, the overall accuracy of 94.9% was achieved. We believe that the proposed model will provide important information to study neurotoxins.


Assuntos
Aminoácidos/química , Neurotoxinas/química , Terminações Pré-Sinápticas/efeitos dos fármacos , Biologia Computacional , Humanos , Modelos Teóricos , Neurotoxinas/uso terapêutico , Terminações Pré-Sinápticas/química
5.
Cardiovasc Res ; 96(3): 524-32, 2012 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-22933322

RESUMO

AIMS: Vascular calcification (VC) is a significant contributor to cardiovascular mortality in patients with chronic kidney disease (CKD) and coronary artery disease (CAD). Osteo/chondrocytic transformation and simultaneous dedifferentiation of smooth muscle cells (SMCs) are important in the pathogenesis of VC. Heat-shock protein 72 (HSP72) is a cardioprotective inducible heat-shock protein that functions as a molecular chaperone. However, its role in the development of accelerated vascular dysfunction and calcification is largely unexplored. METHODS AND RESULTS: We describe for the first time marked reduction in HSP72 expression in arteries from patients with CKD and CAD, compared with healthy controls, in vivo. Induction of HSP72 by heat-shock treatment (HST) significantly prevented the development of calcification of human aortic smooth muscle cells (HA-SMCs), in vitro. These anti-calcific effects were abolished following treatment with both quercetin, an HST inhibitor, and HSP72 siRNA knockdown. Induction of HSP72 suppressed Cbfa-1-dependent osteo/chondrocytic transformation and stabilized SMC contractile phenotype through the myocardin-serum response factor (SRF) pathway. Co-immunoprecipitation studies demonstrated physical association between SRF and HSP72. Furthermore, organ culture of arteries from CKD and CAD patients showed that these arteries retained their ability to induce HSP72 following HST, despite initially reduced expression. CONCLUSION: Our study shows for the first time that intracellular HSP72 may function as a central regulator of molecular pathways involved in the development of VC. We suggest treatment strategies that up-regulate HSP72 as a new approach to inhibit VC.


Assuntos
Doença da Artéria Coronariana/metabolismo , Proteínas de Choque Térmico HSP72/metabolismo , Músculo Liso Vascular/metabolismo , Miócitos de Músculo Liso/metabolismo , Insuficiência Renal Crônica/metabolismo , Calcificação Vascular/prevenção & controle , Adulto , Idoso , Idoso de 80 Anos ou mais , Estudos de Casos e Controles , Células Cultivadas , Subunidade alfa 1 de Fator de Ligação ao Core/metabolismo , Doença da Artéria Coronariana/patologia , Feminino , Proteínas de Choque Térmico HSP72/antagonistas & inibidores , Proteínas de Choque Térmico HSP72/genética , Resposta ao Choque Térmico , Humanos , Masculino , Pessoa de Meia-Idade , Músculo Liso Vascular/efeitos dos fármacos , Músculo Liso Vascular/patologia , Miócitos de Músculo Liso/efeitos dos fármacos , Miócitos de Músculo Liso/patologia , Proteínas Nucleares/metabolismo , Técnicas de Cultura de Órgãos , Fenótipo , Quercetina/farmacologia , Interferência de RNA , RNA Mensageiro/metabolismo , Insuficiência Renal Crônica/patologia , Fator de Resposta Sérica/metabolismo , Transdução de Sinais , Transativadores/metabolismo , Transfecção , Regulação para Cima , Calcificação Vascular/genética , Calcificação Vascular/metabolismo , Calcificação Vascular/patologia , Adulto Jovem
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