Publications by authors named "Alexander W Bray"

Background: Elevated serum carcinoembryonic antigen (CEA) is used to identify "treatment emergent" forms of castration-resistant prostate cancer (CRPC) such as aggressive variant prostate cancer (AVPC). However, its individual utility as a prognostic marker and the genetic alterations associated with its expression have not been extensively studied in CRPC.

Methods: This study retrospectively analyzed clinical outcomes and circulating tumor DNA profiles in 163 patients with CRPC and elevated or normal serum CEA.

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Phlebotomus papatasi sand flies inject their hosts with a myriad of pharmacologically active salivary proteins to assist with blood feeding and to modulate host defenses. In addition, salivary proteins can influence cutaneous leishmaniasis disease outcome, highlighting the potential of the salivary components to be used as a vaccine. Variability of vaccine targets in natural populations influences antigen choice for vaccine development.

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We demonstrate a clear similarity between attoclock offset angles and Rutherford scattering angles taking the Keldysh tunneling width as the impact parameter and the vector potential of the driving pulse as the asymptotic velocity. This simple model is tested against the solution of the time-dependent Schrödinger equation using hydrogenic and screened (Yukawa) potentials of equal binding energy. We observe a smooth transition from a hydrogenic to "hard-zero" intensity dependence of the offset angle with variation of the Yukawa screening parameter.

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Article Synopsis
  • Phlebotomus papatasi sand flies are significant vectors for Leishmania major and phlebovirus and this study looks at genetic differences between populations in Egypt and Jordan, considering their distinct habitats.
  • Researchers sequenced a part of the mtDNA cytochrome b gene from 116 female sand flies and found 13 haplotypes, with Jordanian populations displaying more private haplotypes than those in Egypt.
  • The results indicate strong genetic differentiation between the sand fly populations of Egypt and Jordan, suggesting environmental factors play a role in this variation rather than mere geographical distance.
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Purpose Of Review: Cardiovascular disease (CVD) is responsible for more morbidity and mortality worldwide than any other ailment. Strategies for reducing CVD prevalence must involve identification of individuals at high risk for these diseases, and the prevention of its initial development. Such preventive efforts are currently limited by an incomplete understanding of the genetic determinants of CVD risk.

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We study the time delay in the primary photoemission channel near the opening of an additional channel and compare it with the Wigner time delay in elastic scattering of the photoelectron near the corresponding inelastic threshold. The photoemission time delay near threshold is significantly enhanced, to a measurable 40 as, in comparison to the corresponding elastic scattering delay. The enhancement is due to the different lowest order of interelectron interaction coupling the primary and additional photoemission channels.

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Background: We hypothesized that endothelial cells having distinct mitochondrial genetic backgrounds would show variation in mitochondrial function and oxidative stress markers concordant with known differential cardiovascular disease susceptibilities. To test this hypothesis, mitochondrial bioenergetics were determined in endothelial cells from healthy individuals with African versus European maternal ancestries.

Methods And Results: Bioenergetics and mitochondrial DNA (mtDNA) damage were assessed in single-donor human umbilical vein endothelial cells belonging to mtDNA haplogroups H and L, representing West Eurasian and African maternal ancestries, respectively.

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Current paradigms of carcinogenic risk suggest that genetic, hormonal, and environmental factors influence an individual's predilection for developing metastatic breast cancer. Investigations of tumor latency and metastasis in mice have illustrated differences between inbred strains, but the possibility that mitochondrial genetic inheritance may contribute to such differences in vivo has not been directly tested. In this study, we tested this hypothesis in mitochondrial-nuclear exchange mice we generated, where cohorts shared identical nuclear backgrounds but different mtDNA genomes on the background of the PyMT transgenic mouse model of spontaneous mammary carcinoma.

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Cardiovascular disease (CVD) is the leading cause of death worldwide and it exhibits a greatly increasing incidence proportional to aging. Atherosclerosis is a chronic condition of arterial hardening resulting in restriction of oxygen delivery and blood flow to the heart. Relationships between mitochondrial DNA damage, oxidant production, and early atherogenesis have been recently established and it is likely that aspects of atherosclerotic risk are metabolic in nature.

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