Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 4 de 4
Filtrar
Más filtros

Bases de datos
Tipo del documento
Intervalo de año de publicación
1.
J Surg Res ; 284: 151-163, 2023 04.
Artículo en Inglés | MEDLINE | ID: mdl-36571870

RESUMEN

INTRODUCTION: Emergency general surgery (EGS) patients often present with anemia, in which preoperative transfusions are performed to mitigate anemia-associated risks. However, transfusions have also been noted to cause worse postoperative outcomes. This study examined how transfusion-associated outcomes vary at different levels of anemia. MATERIALS AND METHODS: The American College of Surgeons National Surgical Quality Improvement Program database from 2005 to 2019 was used to identify patients who had undergone any of 12 major EGS procedures using Current Procedural Terminology codes. Patients were divided into two cohorts based on receipt of preoperative transfusion. Cohorts were subdivided into anemia severity levels and propensity score-matched within each using patient demographic and comorbidity variables. We analyzed 30-day postoperative outcomes, including morbidity, mortality, and return to odds ratio (OR), using univariate Chi-squared tests, Wilcoxon signed-rank tests, and multivariate logistic regression analyses. RESULTS: 595,407 EGS cases were identified. Receiving preoperative transfusion were 44.45% (n = 3058) of severely anemic, 10.94% (n = 9076) of moderately anemic, 1.34% (n = 1370) of mildly anemic, and 0.174% (n = 704) of no anemia patients. Transfusion resulted in an increased overall morbidity in the severe (OR 1.54), moderate (OR 1.50), mild (OR 1.71), and no anemia (OR 1.85) groups. Mortality increased in the moderate (OR 1.27), mild (OR 1.61), and no anemia (OR 1.76) subgroups. In severe anemia, transfusion status and mortality were not significantly associated. CONCLUSIONS: Transfusion is associated with higher morbidity and mortality rates in those with higher hematocrit levels, even after controlling for pre-existing comorbidities. A restrictive transfusion strategy should be considered to avoid risks for those with a hematocrit level more than 24%.


Asunto(s)
Anemia , Humanos , Factores de Riesgo , Resultado del Tratamiento , Estudios Retrospectivos , Anemia/epidemiología , Anemia/terapia , Transfusión Sanguínea , Complicaciones Posoperatorias/epidemiología , Complicaciones Posoperatorias/etiología , Complicaciones Posoperatorias/terapia
2.
J Biol Chem ; 295(20): 6823-6830, 2020 05 15.
Artículo en Inglés | MEDLINE | ID: mdl-32241911

RESUMEN

The structurally homologous Mtf1 and TFB2M proteins serve as transcription initiation factors of mitochondrial RNA polymerases in Saccharomyces cerevisiae and humans, respectively. These transcription factors directly interact with the nontemplate strand of the transcription bubble to drive promoter melting. Given the key roles of Mtf1 and TFB2M in promoter-specific transcription initiation, it can be expected that the DNA binding activity of the mitochondrial transcription factors is regulated to prevent DNA binding at inappropriate times. However, little information is available on how mitochondrial DNA transcription is regulated. While studying C-terminal (C-tail) deletion mutants of Mtf1 and TFB2M, we stumbled upon a finding that suggested that the flexible C-tail region of these factors autoregulates their DNA binding activity. Quantitative DNA binding studies with fluorescence anisotropy-based titrations revealed that Mtf1 with an intact C-tail has no affinity for DNA but deletion of the C-tail greatly increases Mtf1's DNA binding affinity. Similar observations were made with TFB2M, although autoinhibition by the C-tail of TFB2M was not as complete as in Mtf1. Analysis of available TFB2M structures disclosed that the C-tail engages in intramolecular interactions with the DNA binding groove in the free factor, which, we propose, inhibits its DNA binding activity. Further experiments showed that RNA polymerase relieves this autoinhibition by interacting with the C-tail and engaging it in complex formation. In conclusion, our biochemical and structural analyses reveal autoinhibitory and activation mechanisms of mitochondrial transcription factors that regulate their DNA binding activities and aid in specific assembly of transcription initiation complexes.


Asunto(s)
ADN de Hongos/metabolismo , ADN Mitocondrial/metabolismo , Proteínas Mitocondriales/metabolismo , Proteínas de Saccharomyces cerevisiae/metabolismo , Saccharomyces cerevisiae/metabolismo , Factores de Transcripción/metabolismo , Transcripción Genética , ADN de Hongos/genética , ADN Mitocondrial/genética , ARN Polimerasas Dirigidas por ADN/genética , ARN Polimerasas Dirigidas por ADN/metabolismo , Proteínas Mitocondriales/genética , Dominios Proteicos , Saccharomyces cerevisiae/genética , Proteínas de Saccharomyces cerevisiae/genética , Factores de Transcripción/genética
3.
J Family Med Prim Care ; 13(2): 512-516, 2024 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-38605797

RESUMEN

Background: Homemakers are the backbones of families, but in rural India, females suffer from many musculoskeletal problems due to excessive workload in their houses. The objective of the present study is to compare body composition parameters as predictors of low back pain (LBP) in nonworking rural homemakers of North India. Materials and Methods: The study was conducted among 296 homemakers from rural areas of Lucknow district in Uttar Pradesh. Details of LBP and body composition parameters (body mass index, body fat, visceral fat) were taken. Results: The prevalence of LBP among homemakers was found to be 15.54%. BMI was found to be a better predictor of LBP than body fat and visceral fat. The risk of LBP is 7.24 times higher in BMI ≥23 than in women with BMI <23. The risk of LBP is 3.67 times more in visceral fat % ≥10% than in women with visceral fat % <10%. Conclusion: Age, type of family, socioeconomic status income was identified as risk factors in this population. Maintaining an adequate BMI is essential for the prevention of LBP.

4.
J Clin Med ; 11(19)2022 Sep 22.
Artículo en Inglés | MEDLINE | ID: mdl-36233417

RESUMEN

Small blood vessels express specific phenotypical and functional characteristics throughout the body. Alterations in the microcirculation contribute to many correlated physiological and pathological events in related organs. Factors such as comorbidities and genetics contribute to the complexity of this topic. Small vessel disease primarily affects end organs that receive significant cardiac output, such as the brain, kidney, and retina. Despite the differences in location, concurrent changes are seen in the micro-vasculature of the brain, retina, and kidneys under pathological conditions due to their common histological, functional, and embryological characteristics. While the cardiovascular basis of pathology in association with the brain, retina, or kidneys has been well documented, this is a simple review that uniquely considers the relationship between all three organs and highlights the prevalence of coexisting end organ injuries in an attempt to elucidate connections between the brain, retina, and kidneys, which has the potential to transform diagnostic and therapeutic approaches.

SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA