Frequency of neuroimaging for pediatric minor brain injury is determined by the primary treating medical department

To investigate the use of neuroimaging in children and adolescents with minor brain injury in pediatric and non-pediatric departments.In this observational cohort study data were extracted from a large German statutory health insurance (AOK Plus Dresden ∼3.1 million clients) in a 7-year period (2010-2016). All patients with International Classification of Diseases (ICD) code S06.0 (concussion; minor brain injury; commotio cerebri) aged ≤ 18 years were included. Demographic and clinical data were analyzed by logistic regression analysis for associations with the use of CT and MRI (independent variables: gender, age, length of stay, pediatric vs non-pediatric department, university vs non-university hospital).A total of 14,805 children with minor brain injuries (mean age 6.0 ± 5.6; 45.5% females) were included. Treatment was provided by different medical departments: Pediatrics (N = 8717; 59%), Pediatric Surgery (N = 3582, 24%), General Surgery (N = 2197, 15%), Orthopedic Trauma Surgery (N = 309, 2.1%). Patients admitted to pediatric departments (Pediatrics and Pediatric Surgery) underwent head CT-imaging significantly less frequently (3.8%) compared to patients treated in non-pediatric departments (18.5%; P < .001; General Surgery: 15.6%; Orthopedic Trauma Surgery: 39.2%). Logistic regression confirmed a significantly higher odds ratio (OR) for the use of cranial CT by the non-pediatric departments (OR: 3.2 [95-%-CI: 2.72-3.76]).CT was significantly less frequently used in pediatric departments. Educational efforts and quality improvement initiatives on physicians, especially in non-pediatric departments may be an effective approach to decreasing rates of CT after minor traumatic brain injuries

Prenatal treatment with rosiglitazone attenuates vascular remodeling and pulmonary monocyte influx in experimental congenital diaphragmatic hernia

Publication history: Accepted - 23 October 2018; Published online - 12 November 2018.Introduction Extensive vascular remodeling causing pulmonary hypertension (PH) represents a major cause of mortality in patients with congenital diaphragmatic hernia (CDH). The chemokine monocyte chemoattractant protein-1 (MCP-1) is a biomarker for the severity of PH and its activation is accompanied by pulmonary influx of monocytes and extensive vascular remodeling. MCP-1 activation can be reversed by application of rosiglitazone (thiazolidinedione). We performed this study to evaluate the role of MCP-1 for the pathogenesis of PH in experimental CDH. We hypothesized that vascular remodeling and MCP-1 activation is accompanied by pulmonary influx of fetal monocytes and can be attenuated by prenatal treatment with rosiglitazone. Methods In a first set of experiments pregnant rats were treated with either nitrofen or vehicle on gestational day 9 (D9). Fetal lungs were harvested on D21 and divided into CDH and control. Quantitative real-time polymerase chain reaction, Western blot (WB), and immunohistochemistry (IHC) were used to evaluate MCP-1 expression, activation, and localization. Quantification and localization of pulmonary monocytes/macrophages were carried out by IHC. In a second set of experiments nitrofen-exposed dams were randomly assigned to prenatal treatment with rosiglitazone or placebo on D18+D19. Fetal lungs were harvested on D21, divided into control, CDH+rosiglitazone, and CDH+placebo and evaluated by WB as well as IHC. Results Increased thickness of pulmonary arteries of CDH fetuses was accompanied by increased systemic and perivascular MCP-1 protein expression and significantly higher amounts of pulmonary monocytes/macrophages compared to controls (p<0.01). These effects were reversed by prenatal treatment with rosiglitazone (p<0.01 vs. CDH+P; control). Conclusion Prenatal treatment with rosiglitazone has the potential to attenuate activation of pulmonary MCP-1, pulmonary monocyte influx, and vascular remodeling in experimental CDH. These results provide a basis for future research on prenatal immunomodulation as a novel treatment strategy to decrease secondary effects of PH in CDH.This work was supported by Children’s Medical & Research Foundation, Dublin, Ireland, https://cmrf.org/, Senior Research Fellowship JG, awarded to JG; German Research Foundation and Leipzig University within the program of Open Access Publishing, awarded to JG, https://www.ub.uni-leipzig.de/open-science/publikationsfonds/. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

Формирование покрытий на основе нитрида титана из вакуумного дугового разряда для защиты конструкционных материалов от водородного охрупчивания

Покрытия из нитрида титана применяется в качестве защитных покрытий, благодаря своей износостойкости, твердости и химической стабильности. Все чаще эти покрытия используются как защитный барьер от проникновения водорода и водородного охрупчивания. Циркониевые сплавы представляются себя широкие применения: насосы и трубозапорная арматура, работающая в условиях воздействия агрессивных сред, материалы ядерной энергетики (ТВЭЛ), биомедицинские имплантаты и т. д.Titanium nitride coatings are used as protective coatings due to their wear resistance, hardness and chemical stability. Increasingly, these coatings are used as a protective barrier against hydrogen penetration and hydrogen embrittlement. Zirconium alloys appear to be of widespread use: pumps and pipe fittings operating in aggressive environments, nuclear energy materials (TVEL), biomedical implants, etc

Activation of Regulatory T Cells during Inflammatory Response Is Not an Exclusive Property of Stem Cells

BACKGROUND: Sepsis and systemic-inflammatory-response-syndrome (SIRS) remain major causes for fatalities on intensive care units despite up-to-date therapy. It is well accepted that stem cells have immunomodulatory properties during inflammation and sepsis, including the activation of regulatory T cells and the attenuation of distant organ damage. Evidence from recent work suggests that these properties may not be exclusively attributed to stem cells. This study was designed to evaluate the immunomodulatory potency of cellular treatment during acute inflammation in a model of sublethal endotoxemia and to investigate the hypothesis that immunomodulations by cellular treatment during inflammatory response is not stem cell specific. METHODOLOGY/PRINCIPAL FINDINGS: Endotoxemia was induced via intra-peritoneal injection of lipopolysaccharide (LPS) in wild type mice (C3H/HeN). Mice were treated with either vital or homogenized amniotic fluid stem cells (AFS) and sacrificed for specimen collection 24 h after LPS injection. Endpoints were plasma cytokine levels (BD™ Cytometric Bead Arrays), T cell subpopulations (flow-cytometry) and pulmonary neutrophil influx (immunohistochemistry). To define stem cell specific effects, treatment with either vital or homogenized human-embryonic-kidney-cells (HEK) was investigated in a second subset of experiments. Mice treated with homogenized AFS cells showed significantly increased percentages of regulatory T cells and Interleukin-2 as well as decreased amounts of pulmonary neutrophils compared to saline-treated controls. These results could be reproduced in mice treated with vital HEK cells. No further differences were observed between plasma cytokine levels of endotoxemic mice. CONCLUSIONS/SIGNIFICANCE: The results revealed that both AFS and HEK cells modulate cellular immune response and distant organ damage during sublethal endotoxemia. The observed effects support the hypothesis, that immunomodulations are not exclusive attributes of stem cells

NADPH oxidase-derived H2O2 subverts pathogen signaling by oxidative phosphotyrosine conversion to PB-DOPA

Strengthening the host immune system to fully exploit its potential as antimicrobial defense is vital in countering antibiotic resistance. Chemical compounds released during bidirectional host–pathogen cross-talk, which follows a sensing-response paradigm, can serve as protective mediators. A potent, diffusible messenger is hydrogen peroxide (H(2)O(2)), but its consequences on extracellular pathogens are unknown. Here we show that H(2)O(2), released by the host on pathogen contact, subverts the tyrosine signaling network of a number of bacteria accustomed to low-oxygen environments. This defense mechanism uses heme-containing bacterial enzymes with peroxidase-like activity to facilitate phosphotyrosine (p-Tyr) oxidation. An intrabacterial reaction converts p-Tyr to protein-bound dopa (PB-DOPA) via a tyrosinyl radical intermediate, thereby altering antioxidant defense and inactivating enzymes involved in polysaccharide biosynthesis and metabolism. Disruption of bacterial signaling by DOPA modification reveals an infection containment strategy that weakens bacterial fitness and could be a blueprint for antivirulence approaches