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2.
JMIR Cardio ; 6(1): e35490, 2022 Mar 30.
Artículo en Inglés | MEDLINE | ID: mdl-35353041

RESUMEN

BACKGROUND: Heart transplant selection committee meetings have transitioned from in-person to remote video meetings during the COVID-19 pandemic, but how this impacts committee members and patient outcomes is unknown. OBJECTIVE: The aim of this study is to determine the perceived impact of remote video transplant selection meetings on usability and patient care and to measure patient selection outcomes during the transition period from in-person to virtual meetings. METHODS: A 35-item anonymous survey was developed and distributed electronically to the heart transplant selection committee. We reviewed medical records to compare the outcomes of patients presented at in-person meetings (January-March 2020) to those presented during video meetings (March-June 2020). RESULTS: Among 83 committee members queried, 50 were regular attendees. Of the 50 regular attendees, 24 (48%) were physicians and 26 (52%) were nonphysicians, including nurses, social workers, and coordinators; 46 responses were received, 23 (50%) from physicians and 23 (50%) from nonphysicians, with 41 responses fully completed. Overall, respondents were satisfied with the videoconference format and felt that video meetings did not impact patient care and were an acceptable alternative to in-person meetings. However, 54% (22/41) preferred in-person meetings, with 71% (15/21) of nonphysicians preferring in-person meetings compared to only 35% (7/20) of physicians (P=.02). Of the 46 new patient evaluations presented, there was a statistically nonsignificant trend toward fewer patients initially declined at video meetings compared with in-person meetings (6/24, 25% compared to 10/22, 45%; P=.32). CONCLUSIONS: The transition from in-person to video heart transplant selection committee meetings was well-received and did not appear to affect committee members' perceived ability to deliver patient care. Patient selection outcomes were similar between meeting modalities.

3.
J Am Heart Assoc ; 10(5): e019321, 2021 02.
Artículo en Inglés | MEDLINE | ID: mdl-33619976

RESUMEN

Background Social media is an effective channel for the advancement of women physicians; however, its use by women in cardiology has not been systematically studied. Our study seeks to characterize the current Women in Cardiology Twitter network. Methods and Results Six women-specific cardiology Twitter hashtags were analyzed: #ACCWIC (American College of Cardiology Women in Cardiology), #AHAWIC (American Heart Association Women in Cardiology), #ilooklikeacardiologist, #SCAIWIN (Society for Cardiovascular Angiography and Interventions Women in Innovations), #WomeninCardiology, and #WomeninEP (Women in Electrophysiology). Twitter data from 2016 to 2019 were obtained from Symplur Signals. Quantitative and descriptive content analyses were performed. The Women in Cardiology Twitter network generated 48 236 tweets, 266 180 903 impressions, and 12 485 users. Tweets increased by 706% (from 2083 to 16 780), impressions by 207% (from 26 755 476 to 82 080 472), and users by 440% (from 796 to 4300), including a 471% user increase internationally. The network generated 6530 (13%) original tweets and 43 103 (86%) amplification tweets. Most original and amplification tweets were authored by women (81% and 62%, respectively) and women physicians (76% and 52%, respectively), with an increase in original and amplification tweets authored by academic women physicians (98% and 109%, respectively) and trainees (390% and 249%, respectively) over time. Community building, professional development, and gender advocacy were the most common tweet contents over the study period. Community building was the most common tweet category for #ACCWIC, #AHAWIC, #ilooklikeacardiologist, #SCAIWIN, and #WomeninCardiology, whereas professional development was most common for #WomeninEP. Conclusions The Women in Cardiology Twitter network has grown immensely from 2016 to 2019, with women physicians as the driving contributors. This network has become an important channel for community building, professional development, and gender advocacy discussions in an effort to advance women in cardiology.


Asunto(s)
Cardiología , Médicos Mujeres , Medios de Comunicación Sociales/estadística & datos numéricos , Realidad Virtual , Femenino , Humanos , Estudios Retrospectivos
5.
Cell Death Differ ; 24(4): 615-625, 2017 04.
Artículo en Inglés | MEDLINE | ID: mdl-28060376

RESUMEN

Necroptosis is a form of necrotic cell death that requires the activity of the death domain-containing kinase RIP1 and its family member RIP3. Necroptosis occurs when RIP1 is deubiquitinated to form a complex with RIP3 in cells deficient in the death receptor adapter molecule FADD or caspase-8. Necroptosis may play a role in host defense during viral infection as viruses like vaccinia can induce necroptosis while murine cytomegalovirus encodes a viral inhibitor of necroptosis. To see how general the interplay between viruses and necroptosis is, we surveyed seven different viruses. We found that two of the viruses tested, Sendai virus (SeV) and murine gammaherpesvirus-68 (MHV68), are capable of inducing dramatic necroptosis in the fibrosarcoma L929 cell line. We show that MHV68-induced cell death occurs through the cytosolic STING sensor pathway in a TNF-dependent manner. In contrast, SeV-induced death is mostly independent of TNF. Knockdown of the RNA sensing molecule RIG-I or the RIP1 deubiquitin protein, CYLD, but not STING, rescued cells from SeV-induced necroptosis. Accompanying necroptosis, we also find that wild type but not mutant SeV lacking the viral proteins Y1 and Y2 result in the non-ubiquitinated form of RIP1. Expression of Y1 or Y2 alone can suppress RIP1 ubiquitination but CYLD is dispensable for this process. Instead, we found that Y1 and Y2 can inhibit cIAP1-mediated RIP1 ubiquitination. Interestingly, we also found that SeV infection of B6 RIP3-/- mice results in increased inflammation in the lung and elevated SeV-specific T cells. Collectively, these data identify viruses and pathways that can trigger necroptosis and highlight the dynamic interplay between pathogen-recognition receptors and cell death induction.


Asunto(s)
Proteína 58 DEAD Box/metabolismo , Gammaherpesvirinae/fisiología , Proteínas de la Membrana/metabolismo , Virus Sendai/fisiología , Clorometilcetonas de Aminoácidos/farmacología , Animales , Apoptosis/efectos de los fármacos , Línea Celular , Cisteína Endopeptidasas/química , Cisteína Endopeptidasas/genética , Cisteína Endopeptidasas/metabolismo , Proteína 58 DEAD Box/antagonistas & inhibidores , Proteína 58 DEAD Box/genética , Enzima Desubiquitinante CYLD , Pulmón/metabolismo , Pulmón/patología , Proteínas de la Membrana/antagonistas & inhibidores , Proteínas de la Membrana/genética , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , Necrosis , Interferencia de ARN , ARN Interferente Pequeño/metabolismo , Proteína Serina-Treonina Quinasas de Interacción con Receptores/antagonistas & inhibidores , Proteína Serina-Treonina Quinasas de Interacción con Receptores/genética , Proteína Serina-Treonina Quinasas de Interacción con Receptores/metabolismo , Transducción de Señal/efectos de los fármacos , Factor de Necrosis Tumoral alfa/farmacología , Ubiquitinación/efectos de los fármacos , Proteínas Virales/genética , Proteínas Virales/metabolismo , Activación Viral
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