RESUMO
OBJECTIVE: This study aims to investigate the risk factors of hemorrhagic transformation (HT) after thrombolysis with recombinant tissue plasminogen activator (rt-PA) in patients with acute cerebral infarction (ACI) and establish a logistic regression equation and the risk prediction model. PATIENTS AND METHODS: One hundred and ninety patients with ACI were divided into the HT group (n=20) and non-HT group (n=170) according to whether HT occurred within 24 hours after rt-PA thrombolysis. The clinical data were collected for analyzing the influencing factors, and a logistic regression analysis model was then established. Besides, patients in the HT group were further grouped into symptomatic hemorrhage (n=7) and non-symptomatic hemorrhage (n=13) according to the type of hemorrhage. The clinical diagnostic value of risk factors in symptomatic hemorrhage after thrombolysis in ACI was analyzed using the ROC curve. RESULTS: We found that history of atrial fibrillation, time from onset to thrombolysis, pre-thrombolytic glucose, pre-thrombolytic National Institute of Health Stroke Scale (NIHSS) score, 24-hour post-thrombolytic NIHSS score, and proportion of patients with large cerebral infarction were all the influencing factors of HT risk after rt-PA thrombolysis in patients with ACI (p<0.05). Logistic regression analysis model was established with an accuracy of 88.42% (168/190), a sensitivity of 75.00% (15/20), and a specificity of 90.00% (153/170). The time from onset to thrombolysis, pre-thrombolytic glucose, and 24-hour post-thrombolytic NIHSS score had higher clinical value in predicting the risk of HT after rt-PA thrombolysis, with the AUCs of 0.874, 0.815 and 0.881, respectively. Blood glucose and pre-thrombolytic NIHSS score were independent risk factors related to symptomatic hemorrhage after thrombolysis in ACI (p<0.05). The AUCs for predicting symptomatic hemorrhage alone and in combination were 0.813, 0.835, and 0.907, respectively, with sensitivities of 85.70%, 87.50% and 90.00%, and specificities of 62.50%, 60.00%, and 75.42% respectively. CONCLUSIONS: The establishment of a prediction model based on the risk factors of HT after rt-PA thrombolysis had a good predictive value in patients with ACI. This model was helpful in guiding clinical judgment and improving the safety of intravenous thrombolysis. Early identification of symptomatic bleeding risk factors provided a reference for clinical treatment and prognostic measures of patients with ACI.
Assuntos
Isquemia Encefálica , Acidente Vascular Cerebral , Humanos , Ativador de Plasminogênio Tecidual/efeitos adversos , Terapia Trombolítica/efeitos adversos , Acidente Vascular Cerebral/tratamento farmacológico , Isquemia Encefálica/tratamento farmacológico , Fibrinolíticos/efeitos adversos , Hemorragia/induzido quimicamente , Infarto Cerebral/tratamento farmacológico , Infarto Cerebral/etiologia , Doença Aguda , Fatores de Risco , Glucose , Hemorragia Cerebral/tratamento farmacológico , Resultado do TratamentoRESUMO
An expressed sequence tag (EST) of B cell translocation gene (BTG) 1 (gcbtg1) was obtained from a grass carp Ctenopharyngodon idellus intestinal complementary (c)DNA library and the full-length cDNA sequence was acquired by rapid amplification of cDNA ends (RACE) technology. The predicted Gcbtg1 protein contains the box A and box B motifs which characterized the BTG and transducer of ERBB2 (TOB) family. Multiple alignment analysis reveals that Gcbtg1 shares an overall identity of 65-94% with Gcbtg1s of other vertebrates. Real-time quantitative PCR analysis reveals that the highest expression level of gcbtg1 was detected in liver and the lowest in muscle. Western blotting analysis indicates that the immunological cross-reactivity occurs between C. idella and human Homo sapiens BTG1 protein. A 1008 bp 5'-flanking region sequence was cloned and analysed.
Assuntos
Carpas/genética , Proteínas de Peixes/genética , Sequência de Aminoácidos , Animais , Sequência de Bases , Carpas/metabolismo , Clonagem Molecular , Etiquetas de Sequências Expressas , Proteínas de Peixes/química , Proteínas de Peixes/metabolismo , Humanos , Dados de Sequência Molecular , Proteínas de Neoplasias/química , Filogenia , RNA Mensageiro/metabolismo , Análise de Sequência de DNARESUMO
beta-catenin has emerged as a key regulator of Wnt signaling pathway, which plays an important role in the development and progression of various cancers. Its accumulation in nucleus of the esophagus squamous epithelium might be the crucial step for the carcinogenesis of esophageal squamous cell carcinoma (ESCC). To detect the proteins correlated with beta-catenin function, we used the established cell lines of pGen-3-con (Eca109 cells transfected by control vector) and pGen-3-CTNNB1 (Eca109 cells transfected by beta-catenin siRNA) as cell models for further analysis. Two-dimensional gel electrophoresis technology was performed to separate the proteins of pGen-3-con and pGen-3-CTNNB1 cell lines, respectively. The differential protein spots were analyzed by software analysis, subjected to in-gel digestion, and identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Consequently, 13 differentially expressed proteins between the two cell lines were identified, of which 14-3-3sigma, prohibitin, and nm23-H1 were further verified by western blotting and quantitative real-time reverse transcriptase-polymerase chain reaction. Then, the tissue microarray and immunohistochemical analysis were employed to research their relationship in ESCC and their corresponding normal mucosa tissues. The upregulation of prohibitin or the downregulation of 14-3-3sigma and nm23-H1 proteins was significantly associated with the proliferation, invasion depth, and lymph node metastasis of ESCC. There were statistically significant correlations between the expression of beta-catenin and the three proteins. The results presented here might provide potential protein markers to elucidate the mechanism of beta-catenin-mediated biologic characteristics for ESCC.
Assuntos
Carcinoma de Células Escamosas/patologia , Neoplasias Esofágicas/patologia , Proteoma/análise , beta Catenina/análise , Proteínas 14-3-3/análise , Proteínas 14-3-3/genética , Biomarcadores Tumorais/análise , Biomarcadores Tumorais/genética , Western Blotting , Carcinoma de Células Escamosas/genética , Linhagem Celular Tumoral , Proliferação de Células , Progressão da Doença , Regulação para Baixo , Eletroforese em Gel Bidimensional , Neoplasias Esofágicas/genética , Esôfago/citologia , Exonucleases/análise , Exonucleases/genética , Exorribonucleases , Regulação Neoplásica da Expressão Gênica/genética , Humanos , Metástase Linfática/patologia , Nucleosídeo NM23 Difosfato Quinases/análise , Nucleosídeo NM23 Difosfato Quinases/genética , Invasividade Neoplásica , Proteínas de Neoplasias/análise , Proteínas de Neoplasias/genética , Proibitinas , Análise Serial de Proteínas , Proteínas Repressoras/análise , Proteínas Repressoras/genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Espectrometria de Massas por Ionização e Dessorção a Laser Assistida por Matriz , Transfecção , Regulação para Cima , beta Catenina/genéticaRESUMO
AIM: To study whether anoxia-induced vasoconstriction was related to the release of endothelin (ET). METHODS: Acute anoxia was induced by gassing the organ chamber with 95% N2 + 5% CO2. Changes in tension of porcine basilar arterial ring was recorded. RESULTS: Anoxia-induced increases in tension were 0.21 g +/- 0.08 g and 0.24 g +/- 0.09 g under basal tension and during ET 3 nmol.L-1-induced contractions, respectively. In the rings tension did not further augment following the increase of ET from 100 to 300 nmol.L-1, acute anoxia did cause further increase in tension of 0.16 g +/- 0.10 g (n = 4). Catalase 800 and 2400 kU.L-1 decreased the anoxia-induced contraction, with inhibitory rate of 33% +/- 7% and 47% +/- 9%, respectively. CONCLUSION: Anoxia-induced vasoconstriction was related to release of hydrogen peroxide from endothelial cells.