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1.
Zhonghua Xin Xue Guan Bing Za Zhi ; 52(6): 690-697, 2024 Jun 24.
Artículo en Chino | MEDLINE | ID: mdl-38880749

RESUMEN

Objective: To evaluate the incidence of arrhythmias and electrocardiographic (ECG) characteristics in cancer patients treated with immune checkpoint inhibitors (ICIs). Methods: This was a cohort study conducted in the Fourth Hospital of Hebei Medical University. Cancer patients initiating ICIs treatments from November 2020 to September 2022 were included in this study. Baseline 12-leads ECG before ICIs initiation and post-treatment ECG were analyzed. An abnormal ECG was defined as the presence of any of the following changes: sinus arrhythmias, atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia, ventricular tachycardia, premature contractions, conduction disorder, and ST-T changes. Results: A total of 87 patients were enrolled, aged 63 (57, 68) years, with 66 (75.9%) males. And 44.8% (39/87) of patients presented with at least one confirmed cardiovascular disease or cardiovascular risk factor at baseline. The incidence of abnormal ECG increased from 31.0% (27/87) at baseline to 65.5% (57/87) after receiving (5.0±2.7) cycles of ICIs treatment (P<0.001). The incidence of sinus arrhythmias was significantly increased after ICIs treatment (23.0% (20/87) vs. 9.2% (8/87), P=0.023), of which only the incidence of sinus tachycardia was significantly increased (11.5% (10/87) vs. 2.3% (2/87), P=0.039). There was also a significantly increased incidence of ST-T changes after ICIs treatment (31.0% (27/87) vs. 17.2% (15/87), P=0.012), which mainly attributed to the T wave changes (29.9% (26/87) vs. 13.8% (12/87), P=0.001). The incidence of premature contractions was also significantly increased after ICIs treatment (9.2% (8/87) vs. 0, P=0.008). Additionally, compared with baseline, the P wave axis was significantly increased after ICIs treatment ((56.94±21.01)° vs. (52.00±22.69)°, P=0.043). After ICIs treatment, the heart rate was significantly increased ((79.07±15.37) beats/min vs. (75.64±13.37) beats/min, P=0.029). Sokolow-Lyon index ((2.21±0.81)mV vs. (2.33±0.75)mV, P=0.138), QTc interval ((431.44±36.04)ms vs. (428.00±30.05)ms, P=0.415) all showed signs of change after treatment, but did not reach the traditional significant level. Conclusions: The incidence of abnormal ECG is significantly increased after ICIs treatment, especially for sinus tachycardia, premature contractions and T wave changes; the P wave axis and heart rate is also significantly increased after treatment. It is important to perform regular ECG monitoring in patients receiving ICIs treatment.


Asunto(s)
Arritmias Cardíacas , Electrocardiografía , Inhibidores de Puntos de Control Inmunológico , Neoplasias , Humanos , Masculino , Persona de Mediana Edad , Femenino , Neoplasias/tratamiento farmacológico , Anciano , Arritmias Cardíacas/inducido químicamente , Arritmias Cardíacas/epidemiología , Inhibidores de Puntos de Control Inmunológico/efectos adversos , Estudios de Cohortes , Incidencia , Factores de Riesgo
3.
Genet Mol Res ; 14(4): 13746-53, 2015 Oct 29.
Artículo en Inglés | MEDLINE | ID: mdl-26535690

RESUMEN

Sepsis is a major cause of morbidity and mortality in critically ill patients. The sepsis syndrome results from a dysregulated inflammatory response to infection that leads to multiple-organ failure, but the underlying mechanisms remain poorly understood. More and more reports show that microRNAs (miRNAs) play an important role in sepsis. In the progression of this syndrome, cells change their behavior in response to cytokines stimulated by sepsis, such as interleukin-10 (IL-10). IL-10 can activate JAK2-STAT3 in the cells to protect them from damage. miR-29a is a potential miRNA directly targeting STAT3. In this study, we investigate the role of miR-29a in targeting STAT3 during sepsis. When cells were treated with IL-10, STAT3 was activated in monocytes, as determined using western blotting. It was verified that STAT3 was a new target gene of miR-29a. miR-29a could inhibit IL-10-induced cytokine release by targeting JAK-STAT3 in monocytes. In conclusion, this study demonstrates for the first time that miR-29a inhibits STAT3 in human monocytes during sepsis.


Asunto(s)
Apoptosis/genética , MicroARNs/genética , Monocitos/metabolismo , Interferencia de ARN , Factor de Transcripción STAT3/genética , Sepsis/genética , Apoptosis/efectos de los fármacos , Secuencia de Bases , Sitios de Unión , Línea Celular , Expresión Génica , Regulación de la Expresión Génica , Genes Reporteros , Humanos , Interleucina-10/sangre , Interleucina-10/genética , Interleucina-10/metabolismo , Interleucina-10/farmacología , MicroARNs/química , Monocitos/efectos de los fármacos , ARN Mensajero/química , ARN Mensajero/genética
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