Antithrombotic drug removal with hemoadsorption during off-pump coronary artery bypass grafting.

Background: Patients requiring coronary artery bypass grafting (CABG) are often loaded with antithrombotic drugs (AT) and are at an increased risk for perioperative bleeding complications. Active AT removal by a hemoadsorption cartridge integrated in the cardiopulmonary bypass circuit is increasingly used in this setting to reduce bleeding, and herein we describe the extension of this application in patients on AT undergoing off-pump coronary artery bypass (OPCAB).

Methods: Ten patients (80% male; mean age: 67.

A New Apheresis Device for Antithrombotic Drug Removal during Off-Pump Coronary Artery Bypass Surgery.

: The hemoadsorption device CytoSorb (CytoSorbents Inc., Princeton, NJ, USA) has been shown to efficiently remove ticagrelor from whole blood in vitro. A promising clinical experience was made with the integration of the hemoadsorption cartridge on the cardiopulmonary bypass (CPB) circuit during cardiac surgery to reduce adverse events.

REDUCE - Indication catalogue based ordering of chest radiographs in intensive care units.

Purpose: To advance a transition towards an indication-based chest radiograph (CXR) ordering in intensive care units (ICUs) without compromising patient safety.

Materials And Methods: Single-center prospective cohort study with a retrospective reference group including 857 ICU patients. The routine group (n = 415) received CXRs at the discretion of the ICU physician, the restrictive group (n = 442) if specified by an indication catalogue.

OPA1 functionally interacts with MIC60 but is dispensable for crista junction formation.

Remodeling of crista junctions (CJs) is observed in numerous human disorders and during apoptosis. The functional interplay of OPA1 and MIC60, two key players in this context, is unclear. We show that OPA1 modulates cristae morphology but is dispensable for CJ formation.

Multiscale coupling of transcranial direct current stimulation to neuron electrodynamics: modeling the influence of the transcranial electric field on neuronal depolarization.

Transcranial direct current stimulation (tDCS) continues to demonstrate success as a medical intervention for neurodegenerative diseases, psychological conditions, and traumatic brain injury recovery. One aspect of tDCS still not fully comprehended is the influence of the tDCS electric field on neural functionality. To address this issue, we present a mathematical, multiscale model that couples tDCS administration to neuron electrodynamics.

The C-terminal domain of Fcj1 is required for formation of crista junctions and interacts with the TOB/SAM complex in mitochondria.

Crista junctions (CJs) are tubular invaginations of the inner membrane of mitochondria that connect the inner boundary with the cristae membrane. These architectural elements are critical for mitochondrial function. The yeast inner membrane protein Fcj1, called mitofilin in mammals, was reported to be preferentially located at CJs and crucial for their formation.

Loss of parkin or PINK1 function increases Drp1-dependent mitochondrial fragmentation.

Loss-of-function mutations in the parkin gene (PARK2) and PINK1 gene (PARK6) are associated with autosomal recessive parkinsonism. PINK1 deficiency was recently linked to mitochondrial pathology in human cells and Drosophila melanogaster, which can be rescued by parkin, suggesting that both genes play a role in maintaining mitochondrial integrity. Here we demonstrate that an acute down-regulation of parkin in human SH-SY5Y cells severely affects mitochondrial morphology and function, a phenotype comparable with that induced by PINK1 deficiency.

Formation of cristae and crista junctions in mitochondria depends on antagonism between Fcj1 and Su e/g.

Crista junctions (CJs) are important for mitochondrial organization and function, but the molecular basis of their formation and architecture is obscure. We have identified and characterized a mitochondrial membrane protein in yeast, Fcj1 (formation of CJ protein 1), which is specifically enriched in CJs. Cells lacking Fcj1 lack CJs, exhibit concentric stacks of inner membrane in the mitochondrial matrix, and show increased levels of F(1)F(O)-ATP synthase (F(1)F(O)) supercomplexes.

Distinct roles of the two isoforms of the dynamin-like GTPase Mgm1 in mitochondrial fusion.

The mitochondrial dynamin-like GTPase Mgm1 exists as a long (l-Mgm1) and a short isoform (s-Mgm1). They both are essential for mitochondrial fusion. Here we show that the isoforms interact in a homotypic and heterotypic manner.

Nephroureteral stent on suction for urethrovesical anastomotic leak after robot-assisted laparoscopic radical prostatectomy.

Objectives: Delayed urinary anastomotic leak after transperitoneal robot-assisted radical prostatectomy (RALP) is an uncommon complication. After failure of conventional measures, we successfully managed this problem using a nephroureteral stent placed on intermittent suction.

Methods: A 62-year-old man with clinical stage T1c prostate cancer (Gleason 3 + 3) developed a persistent urinary anastomotic leak after RALP.

Mrpl36 is important for generation of assembly competent proteins during mitochondrial translation.

The complexes of the respiratory chain represent mosaics of nuclear and mitochondrially encoded components. The processes by which synthesis and assembly of the various subunits are coordinated remain largely elusive. During evolution, many proteins of the mitochondrial ribosome acquired additional domains pointing at specific properties or functions of the translation machinery in mitochondria.

Loss-of-function of human PINK1 results in mitochondrial pathology and can be rescued by parkin.

Degeneration of dopaminergic neurons in the substantia nigra is characteristic for Parkinson's disease (PD), the second most common neurodegenerative disorder. Mitochondrial dysfunction is believed to contribute to the etiology of PD. Although most cases are sporadic, recent evidence points to a number of genes involved in familial variants of PD.

Intrarenal pseudoaneurysm presenting with microscopic hematuria and right flank pain.

We report a case of a 19-year-old female who presented with right flank pain and microscopic hematuria. Three years earlier, she sustained a stab wound to the right flank and was managed conservatively. After being diagnosed with an enhancing renal mass using computed tomography (CT) scan, duplex ultrasound and angiography were performed revealing an intrarenal pseudoaneurysm.

Dynamic subcompartmentalization of the mitochondrial inner membrane.

The inner membrane of mitochondria is organized in two morphologically distinct domains, the inner boundary membrane (IBM) and the cristae membrane (CM), which are connected by narrow, tubular cristae junctions. The protein composition of these domains, their dynamics, and their biogenesis and maintenance are poorly understood at the molecular level. We have used quantitative immunoelectron microscopy to determine the distribution of a collection of representative proteins in yeast mitochondria belonging to seven major processes: oxidative phosphorylation, protein translocation, metabolite exchange, mitochondrial morphology, protein translation, iron-sulfur biogenesis, and protein degradation.

Mitochondrial membrane potential is dependent on the oligomeric state of F1F0-ATP synthase supracomplexes.

The F1F0-ATP synthase in mitochondria, in addition to its function in energy transduction, has a structural role in determining cristae morphology. This depends on its ability to form dimeric and higher oligomeric supracomplexes. Here we show that mutants of the dimer-specific subunits e and g, which destabilize dimeric and oligomeric F1F0-ATP synthase supracomplexes, have a decreased mitochondrial membrane potential delta psi.

Mdm31 and Mdm32 are inner membrane proteins required for maintenance of mitochondrial shape and stability of mitochondrial DNA nucleoids in yeast.

The MDM31 and MDM32 genes are required for normal distribution and morphology of mitochondria in the yeast Saccharomyces cerevisiae. They encode two related proteins located in distinct protein complexes in the mitochondrial inner membrane. Cells lacking Mdm31 and Mdm32 harbor giant spherical mitochondria with highly aberrant internal structure.

Effect of N-acetylcysteine on microcirculation of mucosa in rat ileum in a model of intestinal inflammation.

Oxygen radicals are formed by the endothelium and blood cells and have specific functions in various organs systems. On the level of the microcirculation, oxygen radicals take part in the regulation of the leukocyte-endothelial interaction. The involvement of oxygen radicals has previously been found in conditions such as sepsis, ischemia-reperfusion, and inflammation.

Processing of Mgm1 by the rhomboid-type protease Pcp1 is required for maintenance of mitochondrial morphology and of mitochondrial DNA.

The structure of mitochondria is highly dynamic and depends on the balance of fusion and fission processes. Deletion of the mitochondrial dynamin-like protein Mgm1 in yeast leads to extensive fragmentation of mitochondria and loss of mitochondrial DNA. Mgm1 and its human ortholog OPA1, associated with optic atrophy type I in humans, were proposed to be involved in fission or fusion of mitochondria or, alternatively, in remodeling of the mitochondrial inner membrane and cristae formation (Wong, E.

The inner membrane protein Mdm33 controls mitochondrial morphology in yeast.

Mitochondrial distribution and morphology depend on MDM33, a Saccharomyces cerevisiae gene encoding a novel protein of the mitochondrial inner membrane. Cells lacking Mdm33 contain ring-shaped, mostly interconnected mitochondria, which are able to form large hollow spheres. On the ultrastructural level, these aberrant organelles display extremely elongated stretches of outer and inner membranes enclosing a very narrow matrix space.

A lack of SUMO conjugation affects cNLS-dependent nuclear protein import in yeast.

Yeast SUMO (Smt3) and its mammalian ortholog SUMO-1 are ubiquitin-like proteins that can reversibly be conjugated to other proteins. Among the substrates for SUMO modification in vertebrates are RanGAP1 and RanBP2/Nup358, two proteins previously implicated in nucleocytoplasmic transport. Sumoylated RanGAP1 binds to the nuclear pore complex via RanBP2/Nup358, a giant nucleoporin, which was recently reported to act as a SUMO E3 ligase on some nuclear substrates.

ER-golgi traffic is a prerequisite for efficient ER degradation.

Protein quality control is an essential function of the endoplasmic reticulum. Misfolded proteins unable to acquire their native conformation are retained in the endoplasmic reticulum, retro-translocated back into the cytosol, and degraded via the ubiquitin-proteasome system. We show that efficient degradation of soluble malfolded proteins in yeast requires a fully competent early secretory pathway.

Functional expression of human mitochondrial CYP11B2 in fission yeast and identification of a new internal electron transfer protein, etp1.

Mitochondrial cytochrome P450 enzymes play a crucial role in the steroid biosynthesis in human adrenals, catalyzing regio- and stereospecific hydroxylations. In search of a new model system for the study of these enzymes, we expressed the human CYP11B2 (aldosterone synthase, P450(aldo)) in fission yeast Schizosaccharomyces pombe. Analysis of the subcellular localization of the P450 enzyme by Western blot analysis, fluorescence microscopy, and electron microscopy demonstrated that the mitochondrial localization signal of the human protein is functional in S.