Encarnacion C.O.,Medical College of Wisconsin |
Loranger A.M.,Medical College of Wisconsin |
Bharatkumar A.G.,Zablocki Va Medical Center |
Almassi G.H.,Medical College of Wisconsin |
Almassi G.H.,Zablocki Va Medical Center
Texas Heart Institute Journal | Year: 2016
Lactobacillus acidophilus rarely causes bacterial endocarditis, because it usually resides in the mucosa of the vagina, gastrointestinal tract, and oropharynx. Moreover, sinus of Valsalva aneurysms are rare cardiac anomalies, either acquired or congenital. We present the case of a middle-aged man whose bacterial endocarditis, caused by Lactobacillus acidophilus, led to an aneurysmal rupture of the sinus of Valsalva into the right ventricular outflow tract. The patient underwent successful surgical repair, despite numerous complications and sequelae. © 2016 by the Texas Heart ® Institute, Houston.
Audi S.H.,Marquette University |
Audi S.H.,Medical College of Wisconsin |
Jacobs E.R.,Medical College of Wisconsin |
Jacobs E.R.,Zablocki Va Medical Center |
And 6 more authors.
Nuclear Medicine and Biology | Year: 2015
Introduction: 99mTc-duramycin, DU, is a SPECT biomarker of tissue injury identifying cell death. The objective of this study is to investigate the potential of DU imaging to quantify capillary endothelial cell death in rat lung injury resulting from hyperoxia exposure as a model of acute lung injury. Methods: Rats were exposed to room air (normoxic) or >98% O2 for 48 or 60hours. DU was injected i.v. in anesthetized rats, scintigraphy images were acquired at steady-state, and lung DU uptake was quantified from the images. Post-mortem, the lungs were removed for histological studies. Sequential lung sections were immunostained for caspase activation and endothelial and epithelial cells. Results: Lung DU uptake increased significantly (p<0.001) by 39% and 146% in 48-hr and 60-hr exposed rats, respectively, compared to normoxic rats. There was strong correlation (r2=0.82, p=0.005) between lung DU uptake and the number of cleaved caspase 3 (CC3) positive cells, and endothelial cells accounted for more than 50% of CC3 positive cells in the hyperoxic lungs. Histology revealed preserved lung morphology through 48hours. By 60hours there was evidence of edema, and modest neutrophilic infiltrate. Conclusions: Rat lung DU uptake in vivo increased after just 48hours of >98% O2 exposure, prior to the onset of any substantial evidence of lung injury. These results suggest that apoptotic endothelial cells are the primary contributors to the enhanced DU lung uptake, and support the utility of DU imaging for detecting early endothelial cell death in vivo. © 2014 Elsevier Inc.