Beaumont Health

About: Beaumont Health is a nonprofit organization based out in Royal Oak, Michigan, United States. It is known for research contribution in the topics: Medicine & Population. The organization has 1483 authors who have published 1448 publications receiving 15407 citations. The organization is also known as: William Beaumont Health System & Beaumont Hospitals.

Normal and variant coronary arterial and venous anatomy on high-resolution CT angiography.

Abstract: OBJECTIVE. This article displays the normal and variant anatomy of the coronary arteries and subjacent cardiac veins using a high-resolution 64-MDCT scanner.CONCLUSION. Knowledge of the anatomy of the coronary arteries and subjacent cardiac veins as displayed with maximum intensity and volume-rendered projections is important for correct image interpretation of coronary CT angiography examinations.

Cardiorespiratory fitness, body mass index and heart failure incidence

Abstract: AimsObesity is associated with increased risk of heart failure (HF). This risk may be modulated by improved cardiorespiratory fitness (CRF) as CRF is associated with favourable health outcomes. Thus, we assessed the interaction between body mass index (BMI), CRF and HF.Methods and resultsCardiorespiratory fitness and BMI were assessed in 20 254 US male veterans (mean age 58.0 11.3 years), who completed a maximal exercise treadmill test between 1987 and 2017. All had no evidence of ischaemia or HF prior to the exercise test. They were classified based on age-stratified quartiles of peak metabolic equivalents (METs) achieved as: least-fit (4.5 +/- 1.3), low-fit (6.7 +/- 1.3), moderate-fit (8.1 +/- 1.1), and high-fit (11.2 +/- 2.4); and according to BMI as normal weight (18.5-24.9 kg/m(2)), overweight (25-29.9 kg/m(2)), and obese ( 30.0 kg/m(2)). During a median follow-up of 13.4 years, there were 2979 HF events (10.8 events/1000 person-years). HF risk was significantly higher in the obese category [hazard ratio (HR) 1.22, 95% confidence interval (CI) 1.10-1.36; P < 0.001], but was no longer significant after further adjustment for METs. When compared to the least-fit, HF risk declined progressively with increased CRF within all BMI categories. The risk was 63% (HR 0.37, 95% CI 0.30-0.47; P < 0.001), 66% (HR 0.37, 95% CI 0.28-0.40; P < 0.001), and 73% (HR 0.27, 95% CI 0.22-0.34; P < 0.001) lower for high-fit individuals within normal weight, overweight and obese categories, respectively.ConclusionsIncreased CRF was associated with progressively lower HF risk regardless of BMI, suggesting that the elevated HF risk associated with obesity may be modulated by improved CRF.

Recent Time Trends and Predictors of Heart Dose From Breast Radiation Therapy in a Large Quality Consortium of Radiation Oncology Practices.

Abstract: Purpose Limited data exist regarding the range of heart doses received in routine practice with radiation therapy (RT) for breast cancer in the United States today and the potential effect of the continual assessment of the cardiac dose on practice patterns. Methods and Materials From 2012 to 2015, 4688 patients with breast cancer treated with whole breast RT at 20 sites participating in a state-wide consortium were enrolled into a registry. The importance of limiting the cardiac dose has been emphasized in the consortium since 2012, and the mean heart dose (MHD) has been reported by each institution since 2014. The effects on the MHD were estimated for both conventional and accelerated fractionation using regression models, with technique (intensity modulated RT [IMRT] vs 3-dimensional conformal RT), deep inspiration breath hold use, patient position (supine vs prone), nodal RT (if delivered), and boost (yes vs no) as covariates. Results For left-sided breast cancer treated with conventional fractionation, the median MHD in 2012 was 2.19 Gy versus 1.65 Gy in 2015 ( P P Conclusions The MHD for left-sided breast cancer decreased during a recent 4-year period, coincident with an increased focus on cardiac sparing in the radiation oncology community in general and a state-wide consortium specifically. These data suggest a positive effect of systematically monitoring the heart dose delivered.

Leukemia Mediated Endothelial Cell Activation Modulates Leukemia Cell Susceptibility to Chemotherapy through a Positive Feedback Loop Mechanism.

Abstract: In acute myeloid leukemia (AML), the chances of achieving disease-free survival are low. Studies have demonstrated a supportive role of endothelial cells (ECs) in normal hematopoiesis. Here we show that similar intercellular relationships exist in leukemia. We demonstrate that leukemia cells themselves initiate these interactions by directly modulating the behavior of resting ECs through the induction of EC activation. In this inflammatory state, activated ECs induce the adhesion of a sub-set of leukemia cells through the cell adhesion molecule E-selectin. These adherent leukemia cells are sequestered in a quiescent state and are unaffected by chemotherapy. The ability of adherent cells to later detach and again become proliferative following exposure to chemotherapy suggests a role of this process in relapse. Interestingly, differing leukemia subtypes modulate this process to varying degrees, which may explain the varied response of AML patients to chemotherapy and relapse rates. Finally, because leukemia cells themselves induce EC activation, we postulate a positive-feedback loop in leukemia that exists to support the growth and relapse of the disease. Together, the data defines a new mechanism describing how ECs and leukemia cells interact during leukemogenesis, which could be used to develop novel treatments for those with AML.

Androgen receptor non-nuclear regulation of prostate cancer cell invasion mediated by Src and matriptase

Abstract: Castration-resistant prostate cancers still depend on nuclear androgen receptor (AR) function despite their lack of dependence on exogenous androgen. Second generation anti-androgen therapies are more efficient at blocking nuclear AR; however resistant tumors still develop. Recent studies indicate Src is highly active in these resistant tumors. By manipulating AR activity in several different prostate cancer cell lines through RNAi, drug treatment, and the use of a nuclear-deficient AR mutant, we demonstrate that androgen acting on cytoplasmic AR rapidly stimulates Src tyrosine kinase via a non-genomic mechanism. Cytoplasmic AR, acting through Src enhances laminin integrin-dependent invasion. Active Matriptase, which cleaves laminin, is elevated within minutes after androgen stimulation, and is subsequently shed into the medium. Matriptase activation and shedding induced by cytoplasmic AR is dependent on Src. Concomitantly, CDCP1/gp140, a Matriptase and Src substrate that controls integrin-based migration, is activated. However, only inhibition of Matriptase, but not CDCP1, suppresses the AR/Src-dependent increase in invasion. Matriptase, present in conditioned medium from AR-stimulated cells, is sufficient to enhance invasion in the absence of androgen. Thus, invasion is stimulated by a rapid but sustained increase in Src activity, mediated non-genomically by cytoplasmic AR, leading to rapid activation and shedding of the laminin protease Matriptase.