Publications by authors named "Christian Junker"

Introduction: Clinical ultrasound training is essential to any emergency medicine (EM) clinician's skill set. We aim to understand the current training patterns of clinical ultrasound training within Advanced Practice Provider (APP) residencies.

Methods: In a survey sent electronically to 17 active EM APP residencies, data were obtained from 21 responses to questions about structure of ultrasound faculty, quality assessment, feedback, and competency evaluation.

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Background Pediatric residencies expanding their point-of-care ultrasound (POCUS) education face barriers, including a lack of established curriculum and qualified educators. Prior studies report partnerships between pediatrics and pediatric emergency medicine (PEM); however, many non-PEM emergency medicine (EM) physicians with POCUS fellowship training also have experience with pediatric POCUS and represent an alternate educational partner. Objectives To improve pediatric residents' POCUS skills through collaborative education with EM and evaluate perceptions of the teaching format and instructors.

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Background: Helping Babies Breathe (HBB) is an American Academy of Pediatrics neonatal resuscitation program designed to reduce neonatal mortality in low resource settings. The 2017 neonatal mortality rate in Haiti was 28 per 1000 live births and an estimated 85 % of Haitian women deliver at home. Given this, the Community Health Initiative implemented an adapted HBB (aHBB) in Haiti to evaluate neonatal mortality.

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Staphyloccocus aureus is a major human pathogen and a common cause for superficial and deep seated wound infections. The pathogen is equipped with a large arsenal of virulence factors, which facilitate attachment to various eukaryotic cell structures and modulate the host immune response. One of these factors is the extracellular adherence protein Eap, a member of the "secretable expanded repertoire adhesive molecules" (SERAM) protein family that possesses adhesive and immune modulatory properties.

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Cell polarization enables restriction of signalling into microdomains. Polarization of lymphocytes following formation of a mature immunological synapse (IS) is essential for calcium-dependent T-cell activation. Here, we analyse calcium microdomains at the IS with total internal reflection fluorescence microscopy.

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Lytic granule (LG)-mediated apoptosis is the main mechanism by which CTL kill virus-infected and tumorigenic target cells. CTL form a tight junction with the target cells, which is called the immunological synapse (IS). To avoid unwanted killing of neighboring cells, exocytosis of lytic granules (LG) is tightly controlled and restricted to the IS.

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EMBO J 30 7, 1238–1250 (2011); published online February 15 2011 Proper positioning of mitochondria is critical for cellular function. Mitochondria localization close to synapses regulates signalling at neuronal and immune synapses (ISs). Vice versa, synapses influence activity, motility and the fusion/fission balance of close-by mitochondria.

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SNARE proteins are essential fusion mediators for many intracellular trafficking events. Here, we investigate the role of Syntaxin7 (Stx7) in the release of lytic granules from cytotoxic T lymphocytes (CTLs). We show that Stx7 is expressed in CTLs and is preferentially localized to the region of lytic granule release, the immunological synapse (IS).

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Cell polarization is a key feature of T-cell function. The immunological synapse (IS) between T cells and antigen-presenting cells is a beautiful example of how polarization of cells is used to guide cell function. Receptors, signal transducers, the cytoskeleton, and organelles are enriched at or depleted from the IS after its formation, and in many cases these re-localizations have already been linked with certain T-cell functions.

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Sustained Ca(2+) influx through plasma membrane Ca(2+) released-activated Ca(2+) (CRAC) channels is essential for T cell activation. Since inflowing Ca(2+) inactivates CRAC channels, T cell activation is only possible if Ca(2+)-dependent inactivation is prevented. We have previously reported that sustained Ca(2+) influx through CRAC channels requires both mitochondrial Ca(2+) uptake and mitochondrial translocation towards the plasma membrane in order to prevent Ca(2+)-dependent channel inactivation.

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