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1.
Am Surg ; 90(4): 695-702, 2024 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-37853722

RESUMEN

INTRODUCTION: The anterior stove-in chest (ASIC) is a rare form of flail chest involving bilateral rib or sternal fractures resulting in an unstable chest wall that caves into the thoracic cavity. Given ASIC has only been described in a handful of case reports, this study sought to review our institution's experience in the surgical management of ASIC injuries. METHODS: A retrospective review of patients with ASIC was conducted at our level I trauma center from 1//2021 to 3//2023. Information pertaining to patient demographics, fracture pattern, operative management, and outcomes was obtained and compared across patients in the case series. RESULTS: 6 patients met inclusion criteria, all males aged 37-78 years. 5 suffered motor vehicle collisions, and 1 was a pedestrian struck by an automobile. The median injury severity score was 28. All received ORIF within 5 days of admission, most commonly for ongoing respiratory distress. Patients 2 and 4 underwent bilateral ORIF of the ribs and sternum while patients 1, 5, and 6 underwent left-sided repair. Patient 3 required ORIF of left ribs and the sternum to stabilize their injuries. 5 of 6 patients were liberated from the ventilator and survived to discharge. CONCLUSIONS: This study demonstrates successful operative management of 6 patients with ASIC and suggests that early operative intervention with ORIF for affected segments may improve respiratory mechanics, ability to wean from the ventilator, and overall survival. Further research is needed to generate standardized guidelines for the management of this uncommon and complex thoracic injury.


Asunto(s)
Tórax Paradójico , Fracturas Óseas , Traumatismos Torácicos , Pared Torácica , Masculino , Humanos , Tórax Paradójico/etiología , Tórax Paradójico/cirugía , Costillas , Traumatismos Torácicos/cirugía , Esternón
2.
Am Surg ; 88(5): 1014-1015, 2022 May.
Artículo en Inglés | MEDLINE | ID: mdl-34964692

RESUMEN

We describe the management of bullet embolism from a penetrating cardiac injury, including the clinical, radiographic, and operative considerations in this challenging trauma scenario. Bullet embolism represents a rare but complex subset of ballistic penetrating trauma, and highlights the importance of radiographic correlation with intraoperative findings.


Asunto(s)
Embolia/etiología , Lesiones Cardíacas/complicaciones , Arteria Ilíaca , Heridas por Arma de Fuego/complicaciones , Aorta Abdominal , Embolia/diagnóstico por imagen , Embolia/cirugía , Lesiones Cardíacas/diagnóstico por imagen , Lesiones Cardíacas/etiología , Lesiones Cardíacas/cirugía , Humanos , Arteria Ilíaca/diagnóstico por imagen , Heridas por Arma de Fuego/diagnóstico por imagen , Heridas por Arma de Fuego/cirugía
4.
Cardiovasc Res ; 117(1): 201-211, 2021 01 01.
Artículo en Inglés | MEDLINE | ID: mdl-32176281

RESUMEN

AIMS: Telomere attrition in cardiomyocytes is associated with decreased contractility, cellular senescence, and up-regulation of proapoptotic transcription factors. Pim1 is a cardioprotective kinase that antagonizes the aging phenotype of cardiomyocytes and delays cellular senescence by maintaining telomere length, but the mechanism remains unknown. Another pathway responsible for regulating telomere length is the transforming growth factor beta (TGFß) signalling pathway where inhibiting TGFß signalling maintains telomere length. The relationship between Pim1 and TGFß has not been explored. This study delineates the mechanism of telomere length regulation by the interplay between Pim1 and components of TGFß signalling pathways in proliferating A549 cells and post-mitotic cardiomyocytes. METHODS AND RESULTS: Telomere length was maintained by lentiviral-mediated overexpression of PIM1 and inhibition of TGFß signalling in A549 cells. Telomere length maintenance was further demonstrated in isolated cardiomyocytes from mice with cardiac-specific overexpression of PIM1 and by pharmacological inhibition of TGFß signalling. Mechanistically, Pim1 inhibited phosphorylation of Smad2, preventing its translocation into the nucleus and repressing expression of TGFß pathway genes. CONCLUSION: Pim1 maintains telomere lengths in cardiomyocytes by inhibiting phosphorylation of the TGFß pathway downstream effectors Smad2 and Smad3, which prevents repression of telomerase reverse transcriptase. Findings from this study demonstrate a novel mechanism of telomere length maintenance and provide a potential target for preserving cardiac function.


Asunto(s)
Senescencia Celular/efectos de los fármacos , Miocitos Cardíacos/efectos de los fármacos , Proteínas Proto-Oncogénicas c-pim-1/metabolismo , Homeostasis del Telómero/efectos de los fármacos , Factor de Crecimiento Transformador beta1/farmacología , Células A549 , Animales , Humanos , Masculino , Ratones Noqueados , Miocitos Cardíacos/enzimología , Fosforilación , Proteínas Proto-Oncogénicas c-pim-1/genética , Receptores de Factores de Crecimiento Transformadores beta/metabolismo , Transducción de Señal , Proteína Smad2/metabolismo , Proteína smad3/metabolismo , Telomerasa/metabolismo
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