Central venous pressure and ultrasonographic measurement correlation and their associations with intradialytic adverse events in hospitalized patients: A prospective observational study.

PURPOSE: To investigate correlation of central venous pressure (CVP) with ultrasonographic measurement of central veins, along with association between these variables and occurrence of intradialytic adverse events in hospitalized patients. MATERIALS AND METHODS: Patients requiring hemodialysis via dialysis catheter were prospectively enrolled. CVP measurements through catheter, internal jugular vein aspect ratio, subclavian vein collapsibility, inferior vena cava (IVC) maximal diameter, and IVC collapsibility were recorded before and after hemodialysis. Predictive accuracy of ultrasonographic measurements in discriminating high versus low CVP and their association with intradialytic adverse events were evaluated. Area under receiver operating characteristic curves (AUCs) were calculated. RESULTS: Fifty-nine patients were enrolled. Median (interquartile range) pre- and post-dialysis CVPs were 8 (4-13)mmHg and 6 (3-10)mmHg, respectively (P<0.01). In pre-dialysis, IVC collapsibility had the highest AUC (0.79, P<0.01) to predict CVP >8mmHg. In post-dialysis, IVC maximal diameter had the highest AUC (0.86, P<0.01) to predict CVP ≤4mmHg. Fifteen patients (25%) had adverse events. Neither pre-dialytic CVP nor ultrasonographic variables were associated with occurrence of adverse events. CONCLUSIONS: Highest accuracy in predicting low and high CVP was observed with ultrasonographic assessment of IVC diameter and collapsibility. Adverse events were not predicted by pre-dialytic CVP or ultrasonographic measurements.

Fatal Drug-Resistant Invasive Pulmonary Aspergillus fumigatus in a 56-Year-Old Immunosuppressed Man.

Immune status, severity or burden of disease, appropriate dosing of medication, and drug resistance are important considerations when treating immunosuppressed patients.

Associations between resident physicians' publications and clinical performance during residency training.

BACKGROUND: Both research and clinical medicine requires similar attributes of efficiency, diligence and effective teamwork. Furthermore, residents must succeed at scholarship and patient care to be competitive for fellowship training. It is unknown whether research productivity among residents is related to broad measures of clinical achievement. Our goal was to examine associations between the quantity of internal medicine residents' publications and validated measures of their knowledge, skills and multi-source evaluations of performance. METHODS: This was a longitudinal study of 308 residents graduating from Mayo Clinic from 2006 to 2012. We identified peer-reviewed articles in Ovid MEDLINE between July of each resident's match year and the end of their graduation. Outcomes included American Board of Internal Medicine (ABIM) certification examination scores, mini clinical examination (mini-CEX) scores, and validated assessments of clinical performance by resident-peers, faculty and non-physicians. Performance assessments were averaged to form an overall score ranging from 1 to 5. Associations between quantity of resident publications--and ABIM, mini-CEX and performance assessment scores--were determined using multivariate linear regression. RESULTS: The residents published 642 papers, of which 443 (69.0%) were research papers, 198 (30.8%) were case reports, and 380 (59.2%) were first-authored. On adjusted analysis, multi-source clinical performance evaluations were significantly associated (beta; 99% CI; p-value) with the numbers of research articles (0.012; 0.001-0.024; 0.007), and overall publications (0.012; 0.002-0.022; 0.002). CONCLUSIONS: To our knowledge, this is the first study to demonstrate that scholarly productivity based on journal publication is associated with clinical performance during residency training. Our findings suggest that residents who invest substantial efforts in research are not compromised in their abilities to learn medicine and care for patients.

Transcription factor p53 influences microglial activation phenotype.

Several neurodegenerative diseases are influenced by the innate immune response in the central nervous system (CNS). Microglia have proinflammatory and subsequently neurotoxic actions as well as anti-inflammatory functions that promote recovery and repair. Very little is known about the transcriptional control of these specific microglial behaviors. We have previously shown that in HIV-associated neurocognitive disorders (HAND), the transcription factor p53 accumulates in microglia and that microglial p53 expression is required for the in vitro neurotoxicity of the HIV coat glycoprotein gp120. These findings suggested a novel function for p53 in regulating microglial activation. Here, we report that in the absence of p53, microglia demonstrate a blunted response to interferon-γ, failing to increase expression of genes associated with classical macrophage activation or secrete proinflammatory cytokines. Microarray analysis of global gene expression profiles revealed increased expression of genes associated with anti-inflammatory functions, phagocytosis, and tissue repair in p53 knockout (p53(-/-)) microglia compared with those cultured from strain matched p53 expressing (p53(+/+)) mice. We further observed that p53(-/-) microglia demonstrate increased phagocytic activity in vitro and expression of markers for alternative macrophage activation both in vitro and in vivo. In HAND brain tissue, the alternative activation marker CD163 was expressed in a separate subset of microglia than those demonstrating p53 accumulation. These data suggest that p53 influences microglial behavior, supporting the adoption of a proinflammatory phenotype, while p53 deficiency promotes phagocytosis and gene expression associated with alternative activation and anti-inflammatory functions.