Publications
Department of Medicine faculty members published more than 3,600 peer-reviewed articles in 2024.
2017
2017
BACKGROUND
Incomplete immune reconstitution may occur despite successful antiretroviral therapy (ART). Gut-associated lymphoid tissue (GALT) fibrosis may contribute via local CD4 T lymphocyte depletion, intestinal barrier disruption, microbial translocation, and immune activation.
METHODS
In a cross-sectional analysis, we measured circulating fibrosis biomarker levels on cryopreserved plasma from adult HIV-infected (HIV+) SCOPE study participants on suppressive ART who also had fibrosis quantification on recto-sigmoid biopsies. Relationships among biomarker levels, clinical and demographic variables, GALT lymphoid aggregate (LA) collagen deposition, and LA CD4 T lymphocyte density were analyzed using simple regression. Biomarker levels were also compared to levels in HIV+ viremic SCOPE participants and a convenience sample of HIV-uninfected (HIV-) samples.
RESULTS
HIV+ aviremic participants (n = 39) were 92% male and 41% non-white, with median age 48 years, CD4 T lymphocyte count 277 cells/mm, and 17 years since HIV diagnosis. Most biomarkers were lower in HIV- (n = 36) vs HIV+ aviremic individuals, although CXCL4 levels were higher. HIV+ viremic individuals (N = 18) had higher median TGF-β, CIC-C1Q, and TIMP-1 ( < 0.05) and lower LOXL2 levels ( = 0.08) than HIV+ aviremic individuals. Only higher LOXL2 levels correlated with more GALT collagen deposition (R = 0.44, = 0.008) and lower LA CD4 T lymphocyte density (R = -0.32, = 0.05) among aviremic individuals.
CONCLUSIONS
Circulating LOXL2 levels may be a noninvasive measure of intestinal fibrosis and GALT CD4 T lymphocyte depletion in treated HIV infection. LOXL2 crosslinks elastin and collagen, and elevated LOXL2 levels occur in pathologic states, making LOXL2 inhibition a potential interventional target for intestinal fibrosis and its sequelae.
View on PubMed2017
2017
INTRODUCTION
Open reduction and internal fixation has long been accepted as optimal treatment for displaced olecranon fractures based on poor results seen with conservative management. With the presence of comminution, tension-band wiring constructs are contraindicated due to tendency to compress through fragments, thereby shortening the articular segment. Therefore, plate fixation is typically employed. Our hypothesis was that in a comminuted fracture model, 2.7 mm reconstruction plating without locking screws will perform equally to 3.5 mm locked plating in terms of fracture displacement and rotation (shear).
MATERIALS AND METHODS
A three-part comminuted olecranon fracture pattern was created in nine matched pairs of cadaveric specimen using an oscillating saw in standardized, reproducible fashion. Each matched pair was then randomized to receive either 2.7 mm reconstruction plating or 3.5 mm proximal ulna locked plating. Random allocation software was used to assign the 2.7 mm plate construct to either the right or left side of each pair with the contralateral receiving the 3.5 mm plate construct. Specimens were cyclically loaded simulating passive range of motion exercises commonly performed during rehabilitation. Displacement and rotation in relation to the long axis of the ulna were measured through motion capture. Fragment gapping and rotation was quantified following 100 cycles at 10 N and again following 100 cycles at 500 N.
RESULTS
No significant differences were detected between the 2.7 and 3.5 mm plates in fracture rotation or gapping following loads at 10 N (0.5° and 0.7°; 0.6 and 1.2 mm; respectively; p > 0.05) or 500 N (2.3° and 1.6°; 3.8 and 3.1 mm; respectively; p > 0.05) loading. Fragment rotation and gapping were positively correlated within each plate construct (R > 0.445; p < 0.05).
CONCLUSIONS
2.7 mm plating is an alternative to 3.5 mm locked plating with decreased plate prominence without significantly sacrificing displacement and rotational control. This is beneficial in fracture patterns where the traditional dorsal plating does not offer optimal screw trajectory.
View on PubMed2017
2017
2017