Correction to: Noninvasive Intracranial Pressure Assessment in Acute Liver Failure.

The authors note that the number 14 was inadvertently omitted from the formula listed on page 5 of the article. It currently reads.

Noninvasive Intracranial Pressure Assessment in Acute Liver Failure.

Background: Elevated intracranial pressure (ICP) is an important cause of death following acute liver failure (ALF). While invasive ICP monitoring (IICPM) is most accurate, the presence of coagulopathy increases bleeding risk in ALF. Our objective was to evaluate the accuracy of three noninvasive ultrasound-based measures for the detection of concurrent ICP elevation in ALF-optic nerve sheath diameter (ONSD) using optic nerve ultrasound (ONUS); middle cerebral artery pulsatility index (PI) on transcranial Doppler (TCD); and ICP calculated from TCD flow velocities (ICPtcd) using the estimated cerebral perfusion pressure (CPPe) technique.

Protocol based invasive intracranial pressure monitoring in acute liver failure: feasibility, safety and impact on management.

Background: Acute liver failure (ALF) may result in elevated intracranial pressure (ICP). While invasive ICP monitoring (IICPM) may have a role in ALF management, these patients are typically coagulopathic and at risk for intracranial hemorrhage (ICH). Contemporary ICP monitoring techniques and coagulopathy reversal strategies may be associated with a lower risk of hemorrhage.

Guided transfer of critically ill patients: where patients are transferred can be an informed choice.

Purpose Of Review: Given increasingly scarce healthcare resources and highly differentiated hospitals, with growing demand for critical care, interhospital transfer is an essential part of the care of many patients. The purpose of this review is to examine the extent to which hospital quality is considered when transferring critically ill patients, and to examine the potential benefits to patients of a strategy that incorporates objective quality data into referral patterns.

Recent Findings: Interhospital transfer of critically ill patients is now common and safe.

The vitronectin-binding function of PAI-1 exacerbates lung fibrosis in mice.

Plasminogen activator inhibitor-1 (PAI-1) is increased in the lungs of patients with pulmonary fibrosis, and animal studies have shown that experimental manipulations of PAI-1 levels directly influence the extent of scarring that follows lung injury. PAI-1 has 2 known properties that could potentiate fibrosis, namely an antiprotease activity that inhibits the generation of plasmin, and a vitronectin-binding function that interferes with cell adhesion to this extracellular matrix protein. To determine the relative importance of each PAI-1 function in lung fibrogenesis, we administered mutant PAI-1 proteins that possessed either intact antiprotease or vitronectin-binding activity to bleomycin-injured mice genetically deficient in PAI-1.

The application and diagnostic utility of immunocytochemistry on direct smears in the diagnosis of pulmonary adenocarcinoma and squamous cell carcinoma.

The importance of subclassifying pulmonary nonsmall cell carcinoma (NSCLC) in cytologic material is becoming increasingly paramount. Occasionally, cell blocks traditionally used for ancillary studies are sparsely cellular or acellular. Hence, we investigated the diagnostic utility of immunocytochemistry for Napsin-A, TTF-1, and p63 on direct smears of NSCLC.

The antifibrotic effects of plasminogen activation occur via prostaglandin E2 synthesis in humans and mice.

Plasminogen activation to plasmin protects from lung fibrosis, but the mechanism underlying this antifibrotic effect remains unclear. We found that mice lacking plasminogen activation inhibitor-1 (PAI-1), which are protected from bleomycin-induced pulmonary fibrosis, exhibit lung overproduction of the antifibrotic lipid mediator prostaglandin E2 (PGE2). Plasminogen activation upregulated PGE2 synthesis in alveolar epithelial cells, lung fibroblasts, and lung fibrocytes from saline- and bleomycin-treated mice, as well as in normal fetal and adult primary human lung fibroblasts.