Publications by authors named "Julio E Figueroa"

C8α-γ deficiency was examined in four unrelated African Americans. Two individuals were compound heterozygotes for a previously reported point mutation in exon 9. mRNA from the remaining six alleles contained a 10 nt insertion between nt 992 and 993 corresponding to the junction between exons 6 and 7.

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Purpose: Skin and soft tissue infections (SSTIs) cause about 15 million cases of infection that result in more than 869,000 annual hospitalizations in the United States. Cellulitis accounted for 63% of all patients hospitalized with SSTIs between 2009 and 2011. The primary objective of this study was to evaluate physician adherence rates to evidence-based practice guidelines.

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Background: Unit-specific antibiograms have developed to guide clinicians to appropriate antibiotic choices for subsets of patients. The additional level of a unit- and respiratory-specific antibiogram for surgical and trauma patients defines key differences in susceptibility information for treating hospital-acquired pneumonia.

Methods: This was a three-year, retrospective single-center study.

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We report the first case of disseminated infection with both Actinomyces graevenitzii and Mycobacterium tuberculosis and review the medical literature. Concomitant actinomycosis and tuberculosis is very rare. The potential of the facultatively aerobic, newly described A.

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In this study, we investigated the effect of the extracellular matrix (ECM) secreted by vascular cells on proteoglycan (PG) synthesis by vascular smooth muscle cells in culture. PG synthesis of human aortic smooth muscle cells plated on plastic or the matrices derived from vascular endothelial cells, vascular smooth muscle cells, or THP-1 macrophages was characterized. Smooth muscle cell and macrophage matrices increased both secreted and cellular smooth muscle cells PG production by 2.

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Azaftig is an urinary proteoglycan present in some cancer and AIDS patients experiencing weight loss. Administration of azaftig to mice results in weight loss that is associated with loss of fat depot. So far, very little is known about the mechanism underlying loss of fat depot in mice or weight loss in patients excreting azaftig.

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One mechanism by which Angiotensin II (AII) may promote atherogenesis is through modulation of proteoglycan (PG) metabolism by vascular smooth muscle cells (SMC). To test this hypothesis, we investigated the effect of AII on PG synthesis by human aortic SMC and the ability of the newly synthesized PG to bind low density lipoprotein (LDL). AII stimulated PG synthesis by SMC in a dose- and time-dependent manner.

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