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1.
Am Surg ; 89(2): 286-292, 2023 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-34060924

RESUMEN

BACKGROUND: Literature demonstrates increased mortality for the severely injured at a Level II vs. Level I center. Our objective is to reevaluate the impact of trauma center verification level on mortality for patients with an Injury Severity Score (ISS) > 15 utilizing more contemporary data. We hypothesize that there would be no mortality discrepancy. STUDY DESIGN: Utilizing the ACS Trauma Quality Program Participant Use File admission year 2017, we identified severely injured (ISS >15) adult (age >15 years) patients treated at an ACS-verified Level I or Level II center. We excluded patients who underwent interfacility transfer. Logistic regression was performed to determine adjusted associations with mortality. RESULTS: There were 63 518 patients included, where 43 680 (68.8%) were treated at a Level I center and 19 838 (31.2%) at a Level II. Male gender (70.1%) and blunt injuries (92.0%) predominated. Level I admissions had a higher mean ISS [23.8 (±8.5) vs. 22.9 (±7.8), <.001], while Level II patients were older [mean age (y) 52.3 (±21.6) vs. 48.6 (±21.0), <.001] with multiple comorbidities (37.7% vs. 34.9%, <.001). Adjusted mortality between Level I and II centers was similar (12.0% vs. 11.8%, .570). CONCLUSIONS: Despite previous findings, mortality outcomes are similar for severely injured patients treated at a Level I vs. Level II center. We theorize that this relates to mandated Level II resourcing as defined by an updated American College of Surgeons verification process.


Asunto(s)
Heridas y Lesiones , Heridas no Penetrantes , Adulto , Humanos , Masculino , Adolescente , Centros Traumatológicos , Puntaje de Gravedad del Traumatismo , Hospitalización , Modelos Logísticos , Mortalidad Hospitalaria , Estudios Retrospectivos , Heridas y Lesiones/terapia
2.
Cureus ; 13(4): e14462, 2021 Apr 13.
Artículo en Inglés | MEDLINE | ID: mdl-33996322

RESUMEN

Background Studies show increased early and overall mortality at level II compared to level I trauma centers in hemodynamically unstable patients. We hypothesize there is no mortality difference between level I and level II centers applying more contemporary data. Study design Utilizing the 2017 Trauma Quality Program Participant Use File (TQP-PUF), we identified adult patients (age >14 years) who presented to an American College of Surgeons (ACS) verified level I or II center with hypotension (systolic blood pressure [SBP] < 90 mmHg). Logistic regression was performed to identify adjusted associations with mortality. Results A total of 7,264 patients met the inclusion criteria, of whom most were males (4,924 [67.8%]) with blunt trauma (5,924 [81.6%]) being predominated. Mean admission SBP was 73.2 (±13.0) mmHg. There were 1,097 (15.1%) deaths. Level I admissions (4,931 (67.9%]) were more likely male (3,389 [68.7%] vs. 1,535 [65.8]; p=0.012), non-white (3,119 [63.3%] vs. 1,664 [71.3%]; p<0.001), a victim of penetrating trauma (933 [18.9%] vs. 385 [16.5%]; p=0.015), and more severely injured (mean Injury Severity Score: 19.3 [±15] vs. 16.7 [±13.7]; p<0.001). Level II admissions (2,333 [32.1%]) were older (46.8 [±18.5] vs. 50.3 [±20.1] years; p<0.001) with more co-morbidities (mean Charlson Comorbidity Index: 1.43 [±2] vs. 1.77 [±2.2]; p<0.001). Adjusted mortality between level I and II admissions was similar (766 [15.5%] vs. 331 [14.2%]; p=0.918). Early hourly mortality also did not differ. Conclusion There is no overall or hourly mortality discrepancy between ACS-verified level I and II centers for patients presenting with hypotension. This potentially relates to the use of more contemporary data gathered after implementation of updated verification requirements.

3.
Am J Surg ; 221(3): 637-641, 2021 03.
Artículo en Inglés | MEDLINE | ID: mdl-33390245

RESUMEN

BACKGROUND: Previous literature demonstrates mortality discrepancies at Level II vs. Level I centers in patients with isolated Traumatic Brain Injury (TBI). Our hypothesis is that the implementation of the 2014 version of the resources manual ("the Orange Book") is associated with an elimination of this outcome disparity. METHODS: Utilizing the Trauma Quality Program Participant Use File for 2017, we compared TBI outcomes at ACS Level I vs. Level II centers. RESULTS: 39,764 records met inclusion criteria where 25,382 (63.8%) were admitted to a Level I center. Level I patients were younger (56.4 vs.59.1 years, p < 0.001) and less likely to have been injured in a single level fall (39.5%vs.45.5%, p < 0.001). The incidence of severe TBI (11.3%vs.10.3%, p < 0.001) was more common. Adjusted mortality at a Level II vs. Level I center were similar [7.8% vs. 8.4%, 0.669]. CONCLUSIONS: Implementation of 2014 version of the ACS resources manual is associated with improved TBI associated mortality in ACS Level II centers relative to their Level I counterparts.


Asunto(s)
Lesiones Traumáticas del Encéfalo/mortalidad , Lesiones Traumáticas del Encéfalo/terapia , Indicadores de Calidad de la Atención de Salud , Centros Traumatológicos , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Lesiones Traumáticas del Encéfalo/diagnóstico , Protocolos Clínicos , Bases de Datos Factuales , Femenino , Humanos , Masculino , Persona de Mediana Edad , Evaluación de Resultado en la Atención de Salud , Estudios Retrospectivos , Adulto Joven
4.
Acad Emerg Med ; 28(3): 292-299, 2021 03.
Artículo en Inglés | MEDLINE | ID: mdl-33010085

RESUMEN

BACKGROUND: Previous literature demonstrates increased mortality for traumatic brain injury (TBI) with transfer to a Level II versus Level I trauma center. Our objective was to determine the effect of the most recent American College of Surgeons-Committee on Trauma (ACS-COT) "Resources for the Optimal Care of the Injured Patient" resources manual ("The Orange Book") on outcomes after severe TBI after interfacility transfer to Level I versus Level II center. METHODS: Utilizing the Trauma Quality Program Participant Use File of the American College of Surgeons admission year 2017, we identified patients with isolated TBI undergoing interfacility transfer to either Level I or Level II trauma center. Logistic regression was performed to determine independent associations with mortality. RESULTS: There were 10,268 (71.6%) transferred to a Level I center and 4,025 (28.4%) were transferred to a Level II center. They were mostly male (61.4%) with a mean ± SD age of 61 ± 20.8 years. Mean Injury Severity Score was 16.3 ± 6.3 and most were injured in a single-level fall (51.5%). Patients transferred to a Level I center were less likely to be White (82.3% vs. 84.7%, 0.002) and more likely to have sustained penetrating trauma (2.7% vs. 1.6%, <0.001). The incidence of severe TBI (Glasgow Coma Scale [GCS] = 3-8) was similar (9.3% vs. 8.3%, 0.068). On logistic regression, severity of TBI predicted death; however, there was no difference in adjusted mortality outcome with admission to a Level II versus a Level I center (0.998 [0.836-1.192], 0.985). CONCLUSIONS: There is no mortality discrepancy in patients with isolated TBI transferred to a Level II versus Level I center despite previous contrary evidence and thus no reason to bypass a Level II in favor of a Level I. This relative improvement potentially relates to the new requirements as defined in the latest version of the ACS-COT's resources manual.


Asunto(s)
Lesiones Traumáticas del Encéfalo , Heridas Penetrantes , Adulto , Anciano , Anciano de 80 o más Años , Lesiones Traumáticas del Encéfalo/terapia , Escala de Coma de Glasgow , Humanos , Puntaje de Gravedad del Traumatismo , Masculino , Persona de Mediana Edad , Estudios Retrospectivos , Centros Traumatológicos
5.
Aging (Albany NY) ; 4(11): 823-42, 2012 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-23235539

RESUMEN

Cellular senescence is associated with global chromatin changes, altered gene expression, and activation of chronic DNA damage signaling. These events ultimately lead to morphological and physiological transformations in primary cells. In this study, we show that chronic DNA damage signals caused by genotoxic stress impact the expression of histones H2A family members and lead to their depletion in the nuclei of senescent human fibroblasts. Our data reinforce the hypothesis that progressive chromatin destabilization may lead to the loss of epigenetic information and impaired cellular function associated with chronic DNA damage upon drug-evoked senescence. We propose that changes in the histone biosynthesis and chromatin assembly may directly contribute to cellular aging. In addition, we also outline the method that allows for quantitative and unbiased measurement of these changes.


Asunto(s)
Senescencia Celular/genética , Daño del ADN/genética , Histonas/genética , Transducción de Señal/genética , Secuencia de Aminoácidos , Antibióticos Antineoplásicos , Bleomicina , Western Blotting , Senescencia Celular/efectos de los fármacos , Cromatina/genética , Cromatina/metabolismo , Ensamble y Desensamble de Cromatina/efectos de los fármacos , Ensamble y Desensamble de Cromatina/genética , Fibroblastos/efectos de los fármacos , Fibroblastos/metabolismo , Histonas/metabolismo , Humanos , Inmunohistoquímica , Espectrometría de Masas/métodos , Datos de Secuencia Molecular , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Transducción de Señal/efectos de los fármacos
6.
Cell Cycle ; 10(17): 3016-30, 2011 Sep 01.
Artículo en Inglés | MEDLINE | ID: mdl-21862875

RESUMEN

Cellular aging is linked to deficiencies in efficient repair of DNA double strand breaks and authentic genome maintenance at the chromatin level. Aging poses a significant threat to adult stem cell function by triggering persistent DNA damage and ultimately cellular senescence. Senescence is often considered to be an irreversible process. Moreover, critical genomic regions engaged in persistent DNA damage accumulation are unknown. Here we report that 65% of naturally occurring repairable DNA damage in self-renewing adult stem cells occurs within transposable elements. Upregulation of Alu retrotransposon transcription upon ex vivo aging causes nuclear cytotoxicity associated with the formation of persistent DNA damage foci and loss of efficient DNA repair in pericentric chromatin. This occurs due to a failure to recruit of condensin I and cohesin complexes. Our results demonstrate that the cytotoxicity of induced Alu repeats is functionally relevant for the human adult stem cell aging. Stable suppression of Alu transcription can reverse the senescent phenotype, reinstating the cells' self-renewing properties and increasing their plasticity by altering so-called "master" pluripotency regulators.


Asunto(s)
Células Madre Adultas/citología , Elementos Alu , Senescencia Celular , Daño del ADN , Activación Transcripcional , Adenosina Trifosfatasas/metabolismo , Tejido Adiposo/citología , Tejido Adiposo/metabolismo , Células Madre Adultas/metabolismo , Proteínas de Ciclo Celular/metabolismo , Núcleo Celular/genética , Núcleo Celular/metabolismo , Proliferación Celular , Centrómero/genética , Centrómero/metabolismo , Cromatina/genética , Cromatina/metabolismo , Proteínas Cromosómicas no Histona/metabolismo , Cromosomas Humanos/metabolismo , Reparación del ADN , Replicación del ADN , Proteínas de Unión al ADN/metabolismo , Técnica del Anticuerpo Fluorescente , Histonas/metabolismo , Humanos , Lentivirus/genética , Lentivirus/metabolismo , Complejos Multiproteicos/metabolismo , Transfección , Cohesinas
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