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1.
Maciej Zacharski Alicja Tomaszek Liliana Kiczak Maciej Ugorski Jacek Bania Urszula Pasławska Ilona Rybinska Ewa Anita Jankowska Adrian Janiszewski Piotr Ponikowski 《Journal of cardiac failure》2021,27(6):682-692
BackgroundSteroid hormones play an important role in heart failure (HF) pathogenesis, and clinical data have revealed disordered steroidogenesis in male patients with HF. However, there is still a lack of studies on steroid hormones and their receptors during HF progression. Therefore, a porcine model of tachycardia-induced cardiomyopathy corresponding to HF was used to assess steroid hormone concentrations in serum and their nuclear receptor levels in heart tissue during the consecutive stages of HF.Methods and ResultsMale pigs underwent right ventricular pacing and developed a clinical picture of mild, moderate, or severe HF. Serum concentrations of dehydroepiandrosterone, testosterone, dihydrotestosterone, estradiol, aldosterone, and cortisol were assessed by enzyme-linked immunosorbent assay. Androgen receptor, estrogen receptor alpha, mineralocorticoid receptor, and glucocorticoid receptor messenger RNA levels in the left ventricle were determined by qPCR.The androgen level decreased in moderate and severe HF animals, while the corticosteroid level increased. The estradiol concentration remained stable. The quantitative real-time polymerase chain reaction revealed the downregulation of androgen receptor in consecutive stages of HF and increased expression of mineralocorticoid receptor messenger RNA under these conditions.ConclusionsIn the HF pig model, deteriorated catabolic/anabolic balance, manifested by upregulation of aldosterone and cortisol and downregulation of androgen signaling on the ligand level, was augmented by changes in steroid hormone receptor expression in the heart tissue. 相似文献
2.
Victoria L. Zhou Frances S. Shofer Nikita G. Desai Ilona S. Lorincz Nikhil K. Mull David H. Adler John C. Greenwood 《The Journal of emergency medicine》2019,56(2):127-134
Background
The resuscitation and critical care unit is a novel emergency department–intensive care unit designed to provide early critical care to emergency department patients for ≤24 h.Objectives
This study sought to identify clinical variables associated with short intensive care unit (ICU) stays in patients with diabetic ketoacidosis (DKA), who commonly require ICU-level care.Methods
We conducted a retrospective, single-center, cross-sectional study of DKA patients ≥18 years of age who presented to an academic, urban hospital emergency department over 16 months. Patient demographics and clinical variables extracted from medical records were compared between prolonged ICU stay patients of ≥24 h versus short ICU stay patients (SSPs) of <24 h. ICU care was defined as treatment in the resuscitation and critical care unit or inpatient ICU.Results
One hundred sixty-eight emergency department visits with a primary diagnosis of DKA were analyzed. There were 53 prolonged ICU stay patients, 58 SSPs, and 57 patients required no ICU time. SSPs had significantly higher initial serum bicarbonate (13.0 vs. 9.0 mEq/L, p = 0.01) and shorter anion gap closure time (9.8 vs. 14.4 hours, p = 0.003). Medication nonadherence was a significantly more frequent precipitant in SSPs (67.2% vs. 47.2%, p = 0.03). Initial anion gap, glucose, beta-hydroxybutyrate, and severity of illness scores were not significantly different between groups. After multivariate logistic regression adjusting for variables significant from univariate analysis, higher initial bicarbonate (p = 0.04) and medication nonadherence (p = 0.03) remained significantly associated with SSPs.Conclusions
Patients with DKA with short ICU stays have higher initial bicarbonate levels and are more likely to have medication nonadherence than patients requiring prolonged critical care. These variables may identify patients with DKA who are best treated in an emergency department–intensive care unit to potentially reduce inpatient ICU use. 相似文献3.
Ronny Redlich Ilona Schneider Nicole Kerkenberg Nils Opel Jonas Bauhaus Verena Enneking Jonathan Repple Elisabeth J. Leehr Dominik Grotegerd Claas Khler Katharina Frster Katharina Dohm Susanne Meinert Tim Hahn Harald Kugel Kathrin Schwarte Christiane Schettler Katharina Domschke Volker Arolt Walter Heindel Bernhard T. Baune Weiqi Zhang Christa Hohoff Udo Dannlowski 《Human brain mapping》2020,41(3):594-604
Epigenetic alterations of the brain‐derived neurotrophic factor (BDNF) gene have been associated with psychiatric disorders in humans and with differences in amygdala BDNF mRNA levels in rodents. This human study aimed to investigate the relationship between the functional BDNF‐Val66Met polymorphism, its surrounding DNA methylation in BDNF exon IX, amygdala reactivity to emotional faces, and personality traits. Healthy controls (HC, n = 189) underwent functional MRI during an emotional face‐matching task. Harm avoidance, novelty seeking and reward dependence were measured using the Tridimensional Personality Questionnaire (TPQ). Individual BDNF methylation profiles were ascertained and associated with several BDNF single nucleotide polymorphisms surrounding the BDNF‐Val66Met, amygdala reactivity, novelty seeking and harm avoidance. Higher BDNF methylation was associated with higher amygdala reactivity (x = 34, y = 0, z = ?26, t(166) = 3.00, TFCE = 42.39, p(FWE) = .045), whereby the BDNF‐Val66Met genotype per se did not show any significant association with brain function. Furthermore, novelty seeking was negatively associated with BDNF methylation (r = ?.19, p = .015) and amygdala reactivity (r = ?.17, p = .028), while harm avoidance showed a trend for a positive association with BDNF methylation (r = .14, p = .066). The study provides first insights into the relationship among BDNF methylation, BDNF genotype, amygdala reactivity and personality traits in humans, highlighting the multidimensional relations among genetics, epigenetics, and neuronal functions. The present study suggests a possible involvement of epigenetic BDNF modifications in psychiatric disorders and related brain functions, whereby high BDNF methylation might reduce BDNF mRNA expression and upregulate amygdala reactivity. 相似文献
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Anne Liljander Mingyan Yu Elizabeth O'Brien Martin Heller Julia F. Nepper Douglas B. Weibel Ilona Gluecks Mario Younan Joachim Frey Laurent Falquet Joerg Jores 《Journal of clinical microbiology》2015,53(9):2810-2815
Contagious caprine pleuropneumonia (CCPP) is a highly contagious disease caused by Mycoplasma capricolum subsp. capripneumoniae that affects goats in Africa and Asia. Current available methods for the diagnosis of Mycoplasma infection, including cultivation, serological assays, and PCR, are time-consuming and require fully equipped stationary laboratories, which make them incompatible with testing in the resource-poor settings that are most relevant to this disease. We report a rapid, specific, and sensitive assay employing isothermal DNA amplification using recombinase polymerase amplification (RPA) for the detection of M. capricolum subsp. capripneumoniae. We developed the assay using a specific target sequence in M. capricolum subsp. capripneumoniae, as found in the genome sequence of the field strain ILRI181 and the type strain F38 and that was further evidenced in 10 field strains from different geographical regions. Detection limits corresponding to 5 × 103 and 5 × 104 cells/ml were obtained using genomic DNA and bacterial culture from M. capricolum subsp. capripneumoniae strain ILRI181, while no amplification was obtained from 71 related Mycoplasma isolates or from the Acholeplasma or the Pasteurella isolates, demonstrating a high degree of specificity. The assay produces a fluorescent signal within 15 to 20 min and worked well using pleural fluid obtained directly from CCPP-positive animals without prior DNA extraction. We demonstrate that the diagnosis of CCPP can be achieved, with a short sample preparation time and a simple read-out device that can be powered by a car battery, in <45 min in a simulated field setting. 相似文献
6.
Ali Mobasheri Csaba Matta Ilona Uzielienè Emma Budd Pablo Martín-Vasallo Eiva Bernotiene 《Joint, bone, spine : revue du rhumatisme》2019,86(1):29-35
Chondrocytes are the main cells in the extracellular matrix (ECM) of articular cartilage and possess a highly differentiated phenotype that is the hallmark of the unique physiological functions of this specialised load-bearing connective tissue. The plasma membrane of articular chondrocytes contains a rich and diverse complement of membrane proteins, known as the membranome, which defines the cell surface phenotype of the cells. The membranome is a key target of pharmacological agents and is important for chondrocyte function. It includes channels, transporters, enzymes, receptors, and anchors for intracellular, cytoskeletal and ECM proteins and other macromolecular complexes. The chondrocyte channelome is a sub-compartment of the membranome and includes a complete set of ion channels and porins expressed in these cells. Many of these are multi-functional proteins with “moonlighting” roles, serving as channels, receptors and signalling components of larger molecular assemblies. The aim of this review is to summarise our current knowledge of the fundamental aspects of the chondrocyte channelome, discuss its relevance to cartilage biology and highlight its possible role in the pathogenesis of osteoarthritis (OA). Excessive and inappropriate mechanical loads, an inflammatory micro-environment, alternative splicing of channel components or accumulation of basic calcium phosphate crystals can result in an altered chondrocyte channelome impairing its function. Alterations in Ca2+ signalling may lead to defective synthesis of ECM macromolecules and aggravated catabolic responses in chondrocytes, which is an important and relatively unexplored aspect of the complex and poorly understood mechanism of OA development. 相似文献
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Vikash S. Oza M.D. Mark D. Mamlouk M.D. Christopher P. Hess M.D. Ph.D. Erin F. Mathes M.D. Ilona J. Frieden M.D. 《Pediatric dermatology》2016,33(2):e88-e92
Kaposiform hemangioendothelioma (KHE) is an infiltrative vascular tumor that classically presents in infancy. Management typically focuses on treating Kasabach–Merritt phenomenon (KMP), a disorder of severe and at times life‐threatening platelet trapping. However, the morbidity of KHE extends beyond KMP. The infiltrative nature of the tumor can lead to long‐term disability and often makes complete surgical resection impossible. We report the case of a 10‐year‐old boy with a KHE of his right distal thigh who was unable to walk without assistance due to fibrotic change and right knee contracture. He had no laboratory evidence of KMP at the time of representation. Rapamycin was started in hopes of reducing the tumor burden. Within 2 months of therapy, fibrotic areas softened, his contracture nearly resolved, and there was marked improvement in his mobility. Rapamycin has been previously reported to be effective in managing cases of KHE complicated by KMP. Our report emphasizes the role for rapamycin in the treatment of KHE in the absence of KMP through the inhibition of vasculogenesis and fibrotic pathways. 相似文献