BACKGROUND Platelet transfusion–refractoriness is a challenging and expensive clinical scenario seen most often in patients with hematologic malignancies. Although the majority of platelet transfusion–refractory cases are due to nonimmune causes, a significant minority are caused by alloimmunization against Class I human leukocyte antigens (HLAs) or human platelet antigens (HPAs). Such platelet transfusion–refractory patients can be effectively managed with appropriate antigen‐negative products. STUDY DESIGN AND METHODS Our institution has developed a diagnostic and management algorithm for the platelet transfusion–refractory patient with an early focus on identifying those cases caused by immune‐mediated factors. Using physical platelet cross‐matches to initially classify platelet transfusion–refractory patients as immune‐mediated or not, cross‐match–compatible inventory is then provided to immune‐mediated patients, whereas subsequent HLA (with or without HPA) testing is performed. RESULTS Our blood donor program performs Class I HLA typing of all repeat platelet donors to facilitate the identification of antigen‐negative platelet units (virtual cross‐matching) as well as the recruitment of HLA‐matched donors. The platelet transfusion–refractoriness algorithm realizes an initial net cost savings once two apheresis platelets are saved from use for each newly identified, immune‐mediated platelet transfusion–refractory patient. CONCLUSION An algorithm utilizing physical platelet cross‐matches, Class I HLA and HPA antibody testing, and upfront Class I HLA typing of platelet donors leads to overall resource savings and improved clinical management for platelet transfusion–refractory patients.
Does emotional intelligence change during medical school gross anatomy course? Correlations with students’ performance and team cohesion
AbstractIntroductionSepsis biomarker research requires an infrastructure to identify septic patients efficiently and to collect and store specimens properly. We developed a novel infrastructure to study biomarkers of sepsis in children.MethodsPatients in pediatric and neonatal intensive care units were enrolled prospectively; enrollment information was stored in a secure, remotely accessible database. Researchers were notified of electronic medical record (EMR) orders for blood cultures (a surrogate for a diagnostic evaluation of suspected sepsis) by a page triggered by the order. Staff confirmed patient enrollment and remotely submitted an EMR order for collection of study specimens simultaneous with the blood culture. Specimens were processed and stored by a mobile clinical research unit.ResultsOver 2 years, 2029 patients were admitted; 138 were enrolled. Staff received pages for 95% of blood cultures collected from enrolled patients. The median time between the blood culture order and collection was 34 minutes (range 9–241). Study specimens were collected simultaneously with 41 blood cultures. The median times between specimen collection and storage for flow cytometry and cytokine analysis were 33 minutes (range 0–82) and 52 minutes (range 28–98), respectively.ConclusionThis novel infrastructure facilitated prompt, proper collection and storage of specimens for sepsis biomarker analysis. Clin Trans Sci 2012; Volume #: 1–5
Genetic deficiency of Smad3 protects the kidneys from atrophy and interstitial fibrosis in 2K1C hypertension
American Journal of Physiology-Renal Physiology | March 1, 2012 | Volume: 302 | Issue: 11 | Pages: F1455-F1464
Although the two-kidney, one-clip (2K1C) model is widely used as a model of human renovascular hypertension, mechanisms leading to the development of fibrosis and atrophy in the cuffed kidney and compensatory hyperplasia in the contralateral kidney have not been defined. Based on the well-established role of the transforming growth factor (TGF)-β signaling pathway in renal fibrosis, we tested the hypothesis that abrogation of TGF-β/Smad3 signaling would prevent fibrosis in the cuffed kidney. Renal artery stenosis (RAS) was established in mice with a targeted disruption of exon 2 of the Smad3 gene (Smad3 KO) and wild-type (WT) controls by placement of a polytetrafluoroethylene cuff on the right renal artery. Serial pulse-wave Doppler ultrasound assessments verified that blood flow through the cuffed renal artery was decreased to a similar extent in Smad3 KO and WT mice. Two weeks after surgery, systolic blood pressure and plasma renin activity were significantly elevated in both the Smad3 KO and WT mice. The cuffed kidney of WT mice developed renal atrophy (50% reduction in weight after 6 wk, P < 0.0001), which was associated with the development of interstitial fibrosis, tubular atrophy, and interstitial inflammation. Remarkably, despite a similar reduction of renal blood flow, the cuffed kidney of the Smad3 KO mice showed minimal atrophy (9% reduction in weight, P = not significant), with no significant histopathological alterations (interstitial fibrosis, tubular atrophy, and interstitial inflammation). We conclude that abrogation of TGF-β/Smad3 signaling confers protection against the development of fibrosis and atrophy in RAS.