A multicenter prospective analysis of pediatric trauma activation criteria routinely used in addition to the six criteria of the American College of Surgeons.

Background: The American College of Surgeons has defined six minimum activation criteria (ACS-6) for the highest level of trauma activations at trauma centers. The verification criteria also allow for the inclusion of additional criteria at the institution's discretion. The purpose of this prospective multicenter study was to evaluate the ACS-6 as well as commonly used activation criteria to evaluate overtriage and undertriage rates for pediatric trauma team activation.

The effect of comorbidity on the prognosis of acute lung injury and acute respiratory distress syndrome.

Objective: We conducted a retrospective study assessing the relationship between comorbidity, using the Charlson Comorbidity Index (CCI), and the prognoses of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) patients.

Methods: We analyzed the data of 47 patients with ALI and ARDS who were admitted to our center between April 2004 and July 2009. The patients were classified into 2 groups (survival and non-survival) 3 months after diagnosis, and demographic and clinical characteristics were analyzed.

Testing retina fate commitment in Xenopus by blastomere deletion, transplantation, and explant culture.

The lineages of individual cells of the Xenopus cleavage-stage embryo have been fate-mapped to reveal the subset of blastomeres that are the major and minor precursors of the retina. Using this retina fate map, one can test the commitment of each of these cells to various retinal cell fates by manipulating the environment in which they develop. This chapter presents the techniques for identifying specific retina blastomere precursor cells, deleting them to test whether they are required for producing specific kinds of retinal cells, transplanting them to novel embryonic locations in host embryos to test whether they are committed to produce specific kinds of retinal cells, and growing them in explant culture to determine if their ability to produce specific kinds of retinal cells is autonomous.

Targeted microinjection of synthetic mRNAs to alter retina gene expression in Xenopus embryos.

The individual cells of the Xenopus cleavage-stage embryo have been fate mapped, revealing which of these cells contribute to the retina. Using this retina fate map, one can specifically modulate levels of gene expression in retina lineages to determine the function of proteins in various aspects of early retinal development, such as formation of the eye fields and determination of specific cell fates. This chapter presents the techniques for identifying specific retina blastomere precursor cells, and injecting them with lineage tracers, mRNAs encoding wild-type and mutant constructs or morpholino antisense oligonucleotides to alter gene expression.

Dysferlinopathy presenting as rhabdomyolysis and acute renal failure.

Dysferlinopathies are a heterogeneous group of autosomal recessive muscle disorders resulting from defects or deficiencies in dysferlin. Reported phenotypes range from isolated hyperCKemia to muscular dystrophy. We present a 15-year-old male adolescent who was diagnosed with a dysferlinopathy after presenting with acute renal failure secondary to rhabdomyolysis.

Specific domains of FoxD4/5 activate and repress neural transcription factor genes to control the progression of immature neural ectoderm to differentiating neural plate.

FoxD4/5, a forkhead transcription factor, plays a critical role in establishing and maintaining the embryonic neural ectoderm. It both up-regulates genes that maintain a proliferative, immature neural ectoderm and down-regulates genes that promote the transition to a differentiating neural plate. We constructed deletion and mutant versions of FoxD4/5 to determine which domains are functionally responsible for these opposite activities, which regulate the critical developmental transition of neural precursors to neural progenitors to differentiating neural plate cells.

Using 32-cell stage Xenopus embryos to probe PCP signaling.

Use of loss-of function (via antisense Morpholino oligonucleotides (MOs)) or over-expression of proteins in epithelial cells during early embryogenesis of Xenopus embryos, can be a powerful tool to understand how signaling molecules can affect developmental events. The techniques described here are useful for examining the roles of proteins in cell-cell adhesion, and planar cell polarity (PCP) signaling in cell movement. We describe how to target specific regions within the embryos by injecting an RNA encoding a tracer molecule along with RNA encoding your protein of interest or an antisense MO to knock-down a particular protein within a specific blastomere of the embryo.

Secondary erythromelalgia successfully treated with intravenous immunoglobulin.

Erythromelalgia is a rare condition characterized by episodic painful erythema and warmth often affecting, but not limited to, the distal extremities. This condition is notoriously difficult to treat. We report a young female patient with seronegative polyarthritis who presented with a 6-year history of recurrent bouts of painful erythema and swelling often triggered by minor trauma.

Investigating conservation of the albaflavenone biosynthetic pathway and CYP170 bifunctionality in streptomycetes.

Albaflavenone, a tricyclic sesquiterpene antibiotic, is biosynthesized in Streptomyces coelicolor A3(2) by enzymes encoded in a two-gene operon. Initially, sesquiterpene cyclase catalyzes the cyclization of farnesyl diphosphate to the terpenoid epi-isozizaene, which is oxidized to the final albaflavenone by cytochrome P450 (CYP)170A1. Additionally, this CYP is a bifunctional enzyme, being able to also generate farnesene isomers from farnesyl diphosphate, owing to a terpene synthase active site moonlighting on the CYP molecule.

Yes-associated protein 65 (YAP) expands neural progenitors and regulates Pax3 expression in the neural plate border zone.

Yes-associated protein 65 (YAP) contains multiple protein-protein interaction domains and functions as both a transcriptional co-activator and as a scaffolding protein. Mouse embryos lacking YAP did not survive past embryonic day 8.5 and showed signs of defective yolk sac vasculogenesis, chorioallantoic fusion, and anterior-posterior (A-P) axis elongation.

Aging disaster: mortality, vulnerability, and long-term recovery among Katrina survivors.

Data from this multiyear qualitative study of the effects of Hurricane Katrina and flooding in New Orleans suggest differences in how the elderly cope with disaster. At the time of the disaster, the elderly of New Orleans were at greater risk than other groups, and more elderly died than any other group during the storm and in the first year after. Those who did survive beyond the first year report coping with the long-term disaster aftermath better than the generation below them, experiencing heightened stresses, and feeling as if they are "aging" faster than they should.

Developmental expression patterns of candidate cofactors for vertebrate six family transcription factors.

Six family transcription factors play important roles in craniofacial development. Their transcriptional activity can be modified by cofactor proteins. Two Six genes and one cofactor gene (Eya1) are involved in the human Branchio-otic (BO) and Branchio-otic-renal (BOR) syndromes.

Microarray identification of novel downstream targets of FoxD4L1/D5, a critical component of the neural ectodermal transcriptional network.

FoxD4L1/D5 is a forkhead transcription factor that functions as both a transcriptional activator and repressor. FoxD4L1/D5 acts upstream of several other neural transcription factors to maintain neural fate, regulate neural plate patterning, and delay the expression of neural differentiation factors. To identify a more complete list of downstream genes that participate in these earliest steps of neural ectodermal development, we carried out a microarray analysis comparing gene expression in control animal cap ectodermal explants (ACs), which will form epidermis, to that in FoxD4L1/D5-expressing ACs.

The future of health care relies on motivated people.

I read with interest Rose-Marie Gilbert's experience of negative comments when mentioning community nursing as a career choice (letters September 8).

Development of a rapid emergency hemorrhage panel.

Background: Evaluation of hemostasis in bleeding patients requires both accuracy and speed.

Study Design And Methods: As an alternative to point-of-care testing, we developed an emergency hemorrhage panel (EHP: prothrombin time [PT], fibrinogen, platelet count, hematocrit) for use in making transfusion decisions on bleeding patients with a goal of less than 20-minute turnaround time (TAT) when performed in the clinical laboratory on automated instruments. Because point-of-care samples are not checked for clotting or hemolysis, we evaluated their effect on automated testing.

Functional genomics and cancer drug target discovery.

The recent development of technologies for whole-genome sequencing, copy number analysis and expression profiling enables the generation of comprehensive descriptions of cancer genomes. However, although the structural analysis and expression profiling of tumors and cancer cell lines can allow the identification of candidate molecules that are altered in the malignant state, functional analyses are necessary to confirm such genes as oncogenes or tumor suppressors. Moreover, recent research suggests that tumor cells also depend on synthetic lethal targets, which are not mutated or amplified in cancer genomes; functional genomics screening can facilitate the discovery of such targets.

Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1.

The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. A complementary strategy for targeting KRAS is to identify gene products that, when inhibited, result in cell death only in the presence of an oncogenic allele.

Neural induction and factors that stabilize a neural fate.

The neural ectoderm of vertebrates forms when the bone morphogenetic protein (BMP) signaling pathway is suppressed. Herein, we review the molecules that directly antagonize extracellular BMP and the signaling pathways that further contribute to reduce BMP activity in the neural ectoderm. Downstream of neural induction, a large number of "neural fate stabilizing" (NFS) transcription factors are expressed in the presumptive neural ectoderm, developing neural tube and ultimately in neural stem cells.

Notch signaling downstream of foxD5 promotes neural ectodermal transcription factors that inhibit neural differentiation.

We investigated the role of the Notch signaling pathway in regulating several transcription factors that stabilize a neural fate and expand the neural plate. Increased Notch signaling in a neural lineage via a constitutively activated form (NICD) up-regulated geminin and zic2 in a cell-autonomous manner, and expanded the neural plate domains of sox11, sox2, and sox3. Loss- and gain-of-function assays show that foxD5 acts upstream of notch1 gene expression.

foxD5 plays a critical upstream role in regulating neural ectodermal fate and the onset of neural differentiation.

foxD5 is expressed in the nascent neural ectoderm concomitant with several other neural-fate specifying transcription factors. We used loss-of-function and gain-of-function approaches to analyze the functional position of foxD5 amongst these other factors. Loss of FoxD5 reduces the expression of sox2, sox11, soxD, zic1, zic3 and Xiro1-3 at the onset of gastrulation, and of geminin, sox3 and zic2, which are maternally expressed, by late gastrulation.

A hyperthermal energy ion beamline for probing hot electron chemistry at surfaces.

An ultrahigh vacuum ion beamline and chamber have been assembled to produce hyperthermal (<400 eV) energy ions for studying hot electron chemistry at surfaces. The specific design requirements for this modified instrument were chosen to enable the exposure of a metal-oxide-semiconductor (MOS) device to monoenergtic, well-collimated beams of alkali ions while monitoring both the scattered beam flux and the device characteristics. Our goal is to explore the role that hot electrons injected toward the MOS device surface play in the neutralization of scattered ions.