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AIMS: Large venous invasion (VI) is prognostically significant in colon cancer. The increased use of elastic stains by pathologists results in higher VI detection rates compared to routine stains alone. This study assesses the prognostic value of VI detected by elastic versus routine stains. METHODS AND RESULTS: Colon cancers resected between 2014 and 2017 underwent pathology slide review for VI. Cases without VI on routine stain were stained by elastic trichrome and re-examined. Demographic, clinical, pathological and outcome data were gathered by retrospective review. Kaplan-Meier curves with log-rank tests were performed for survival categorised by VI status. Cox regression was performed for multivariate analysis. Of 277 cases, 97 (35%) showed VI by routine stain alone, with an additional 58 (21%) discovered by subsequent elastic stains. Thus, elastic trichrome increased VI detection by 60%. However, only VI detected by routine stain showed worse overall survival (P < 0.001). VI detected by elastic stain only was not prognostically different from cases without VI (P = 0.428). For stage 2 cancers, VI was not prognostically significant regardless of method of detection. For stage 3 cases, only VI detected by routine stain was prognostic for overall survival (P = 0.002) with a hazard ratio of 4.04 by multivariate regression (P = 0.028). CONCLUSIONS: VI detectable only by elastic stains do not show prognostic significance for survival in colon cancer. For pathologists with high baseline VI detections rates on routine stain, reflexive use of elastic stain may be of limited value.
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Neoplasias del Colon , Neoplasias Colorrectales , Humanos , Pronóstico , Colorantes , Neoplasias Colorrectales/patología , Estadificación de Neoplasias , Neoplasias del Colon/diagnóstico , Neoplasias del Colon/patología , Invasividad Neoplásica/patología , Estudios RetrospectivosRESUMEN
The detection of clear and encrypted data that are transported through computer networks is of particular importance both for protecting the data and the users to whom they belong and to whom they are intended, as well as the networks through which they are transmitted. The proposed method consists of an algorithm that classifies the data it receives by testing the belongingness of their standard deviation values to established confidence intervals. Following the evaluation of the algorithm, an accuracy of 94.73% was obtained and it appears that the results can be used with certainty in subsequent analyses of the data detection.
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Somatic mutations within noncoding genomic regions that aberrantly activate oncogenes have remained poorly characterized. Here we describe recurrent activating intronic mutations of LMO2, a prominent oncogene in T-cell acute lymphoblastic leukemia (T-ALL). Heterozygous mutations were identified in PF-382 and DU.528 T-ALL cell lines in addition to 3.7% of pediatric (6 of 160) and 5.5% of adult (9 of 163) T-ALL patient samples. The majority of indels harbor putative de novo MYB, ETS1, or RUNX1 consensus binding sites. Analysis of 5'-capped RNA transcripts in mutant cell lines identified the usage of an intermediate promoter site, with consequential monoallelic LMO2 overexpression. CRISPR/Cas9-mediated disruption of the mutant allele in PF-382 cells markedly downregulated LMO2 expression, establishing clear causality between the mutation and oncogene dysregulation. Furthermore, the spectrum of CRISPR/Cas9-derived mutations provides important insights into the interconnected contributions of functional transcription factor binding. Finally, these mutations occur in the same intron as retroviral integration sites in gene therapy-induced T-ALL, suggesting that such events occur at preferential sites in the noncoding genome.
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Proteínas Adaptadoras Transductoras de Señales/genética , Proteínas Adaptadoras Transductoras de Señales/metabolismo , Proteínas con Dominio LIM/genética , Proteínas con Dominio LIM/metabolismo , Mutación , Leucemia-Linfoma Linfoblástico de Células T Precursoras/genética , Leucemia-Linfoma Linfoblástico de Células T Precursoras/metabolismo , Proteínas Proto-Oncogénicas/genética , Proteínas Proto-Oncogénicas/metabolismo , Elementos de Respuesta , Adolescente , Adulto , Niño , Preescolar , Femenino , Regulación Leucémica de la Expresión Génica , Humanos , Células Jurkat , Masculino , Leucemia-Linfoma Linfoblástico de Células T Precursoras/patologíaAsunto(s)
Aminoglicósidos/uso terapéutico , Anticuerpos Monoclonales Humanizados/uso terapéutico , Antineoplásicos Inmunológicos/uso terapéutico , Leucemia Mieloide Aguda/tratamiento farmacológico , Polimorfismo de Nucleótido Simple , Lectina 3 Similar a Ig de Unión al Ácido Siálico/genética , Adulto , Ensayos Clínicos como Asunto , Gemtuzumab , Humanos , Leucemia Mieloide Aguda/genética , Resultado del Tratamiento , Adulto JovenRESUMEN
Hypertrophic cardiomyopathy (HCM) is a common heart disease in cats, characterized by regional or diffuse hypertrophy of the left ventricular walls, with an uncertain etiology and heterogenous natural history. Several types of rhythm disturbances are often associated with the disease. This study conducts a comprehensive review of the current literature, in order to evaluate the diagnostic and prognostic effectiveness of electrocardiography and Holter monitoring in the management of feline hypertrophic cardiomyopathy. The main subjects of discussion will include general information about HCM and its connection to arrhythmias. We will explore the rhythm disturbances documented in the current literature on Holter monitoring, as well as the techniques used for Holter monitoring. Additionally, the review will cover classical electrocardiography (ECG) and its diagnostic utility. Prognostic indicators and anti-arrhythmic therapy will also be discussed in detail. The findings highlight the importance of understanding arrhythmias in feline HCM for accurate diagnosis, risk assessment, and therapeutic intervention. ECG and Holter monitoring may offer valuable insights into managing feline HCM.
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There is currently little research on the effects of reduced left ventricular ejection fraction and altered nutritional status in patients with acute myocardial infarction. We therefore examined the interrelationship between the parameters of left ventricular dysfunction after acute myocardial infarction and changes in the Geriatric Nutrition Risk Index (GNRI) and the Nutrition Status Control Index (CONUT). Based on the evidence, frailty is considered to be an important factor affecting the prognosis of cardiovascular disease, so it is important to detect malnutrition early to prevent adverse cardiovascular events. This study was an observational, prospective study that included a total of 73 subjects who presented at the 3-month AMI follow-up. All subjects were subjected to laboratory tests and the groups were divided as follows: group 1, in which we calculated the CONUT score, (CONUT < 3 points, n = 57) patients with normal nutritional status and patients with moderate to severe nutritional deficiency (CONUT ≥ 3, n = 16). In group 2, the GNRI score was calculated and out of the 73 patients we had: GNRI ≥ 98, n = 50, patients with normal nutritional status, and GNRI < 98, n = 23, patients with altered nutritional status. The results of this study showed that we had significant differences between LVEF values at 3 months post-infarction where, in the CONUT group, patients with altered nutritional status had lower LVEF values (46.63 ± 3.27% versus 42.94 ± 2.54%, p < 0.001) compared to CONUT < 3. Also, in the GNRI group, we had lower LVEF values in patients with impaired nutritional status (46.48 ± 3.35% versus 44.39 ± 3.35%, p = 0.01). It can be seen that LVEF values are improved at 3 months post infarction in both groups, in patients with impaired nutritional status and in patients with good nutritional status. Patients with impaired nutritional status have lower ejection fraction and worse outcomes in both the CONUT and GNRI groups at 3 months post acute myocardial infarction.