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Diaper dermatitis is an ever-present condition among infants. Little is known about the prevalence among infants in the NICU. This article presents an adaptation of the skin safety model (SSM) for the infant in the NICU. The concepts of the model were extracted, defined, and integrated into an adapted SSM model to provide a focus on the infant with diaper dermatitis in the intensive care setting. It is essential to include all factors of the infant's clinical characteristics and hospital experience in the modeling to accurately predict risk of skin vulnerability in this infant population.

Objective Diaper dermatitis (DD) among NICU infants is preventable and under-recognized. The role of clinical characteristics (CC) on DD is also poorly described. This study examined the: 1) prevalence of DD in NICU; 2) relationship of factors including CC and DD; and 3) contribution of DD and CC factors on NICU Length of stay (LOS). Method Retrospective chart review data was collected on all infants admitted to the NICU. Analyses included bivariate and multivariable logistic regression for DD outcome and negative binomial regression model for predicting infants’ NICU LOS. Results DD prevalence in the NICU sample was 34% (n = 180), 70% White, 56% male, 72% infants born at higher gestational age, and 62.2% born vaginally. Logistic regression results showed that Black infants have lower AOR of DD, whereas, NICU LOS (OR 1.02; 95% CI 1.01, 1.03), number of skin injuries (OR 1.22; 95% CI 1.01–1.47), and older gestational age (OR 3.73; 95%CI 0.83–0.95) increased the odds of DD. Significant interaction of gestational age group and days to full feed was identified. Conclusion DD is common among NICU infants and several CC play an integral role as risk and moderating factors for DD. Routine collection of infant skin integrity data is currently lacking in large collaborative databases, which limits better understanding of DD in NICU. Improvements in preventative measures could benefit from continued study of the impact nutrition and LOS have on DD development. Better systems of collecting and analyzing DD data and its impact on NICU LOS are needed.

The eukaryotic initiation factor 4E binding protein (4E-BP) family is involved in translational control of cell proliferation and pro-angiogenic factors. The zebrafish eukaryotic initiation factor 4E binding protein 3 like (eif4ebp3l) is a member of the 4E-BPs and responsible for activity-dependent myofibrillogenesis, but whether it affects cardiomyocyte (CM) proliferation or heart regeneration is unclear. We examined eif4ebp3l during zebrafish vascular development and heart regeneration post cryoinjury in adult zebrafish. Using morpholino injections we induced silencing of eif4ebp3l in zebrafish embryos, which led to increased angiogenesis at 94 h post fertilization (hpf). For investigation of eif4ebp3l in cardiac regeneration, zebrafish hearts were subjected to cryoinjury. Regenerating hearts were analyzed at different time points post-cryoinjury for expression of eif4ebp3l by in situ hybridization and showed strongly decreased eif4ebp3l expression in the injured area. We established a transgenic zebrafish strain, which overexpressed eif4ebp3l under the control of a heat-shock dependent promotor. Overexpression of eif4ebp3l during zebrafish heart regeneration caused only macroscopically a reduced amount of fibrin at the site of injury. Overall, these findings demonstrate that silencing of eif4ebp3l has pro-angiogenic properties in zebrafish vascular development and when eif4ebp3l is overexpressed, fibrin deposition tends to be altered in zebrafish cardiac regeneration after cryoinjury.

Fur das Analkarzinom wurde eine neue S3-Leitlinie erstellt. Das Analkarzinom tritt v. a. bei Patienten mit Immunsuppression, Z. n. Organtransplantation und bei mit humanem Immundefizienzvirus (HIV-)Infizierten auf. In >90 % der Falle besteht ein Plattenepithelkarzinom des Analkanals oder Analrands, meist liegt dem eine Infektion mit dem humanen Papillomavirus zugrunde. Die entsprechende Prakanzerose wird als anale intraepitheliale Dysplasie bezeichnet. Die Diagnostik umfasst klinische Untersuchung, Endoskopie und multiparametrische Magnetresonanztomographie (MRT) sowie Computertomographie (CT) zum Ausschluss von Fernmetastasen. Allen Patienten mit Analkarzinom soll ein HIV-Test angeboten werden. Neben der chirurgischen Exzision stellt die kombinierte Radiochemotherapie den wichtigsten Baustein der Behandlung dar. Die Nachsorge erfolgt nach Schema, eine histologische Responsebeurteilung sollte in der Woche 26 erfolgen.

Current practice of BIM-based collaboration relies on the exchange of entire domain models, which are managed and shared using Common Data Environments. Such platforms are well standardized in terms of states, roles, and participants. However, the coordination of changes by exchanging entire models requires manual identification of any added, modified, or deleted information from one shared version to another. This paper proposes the application of an eventdriven system architecture, which is in widespread use in modern communication systems. Combining the publish-subscribe design pattern, patch-based update mechanisms for BIM models, and the established concept of asynchronous, decentralized collaboration in BIM projects can significantly ease the process of understanding design changes and reduce the overall overhead of information already shared in previous versions among project members.

A severe consequence of adult Zika virus (ZIKV) infection is Guillain-Barré Syndrome (GBS), where autoreactive antibodies attack peripheral and central nervous systems (CNS) resulting in neuro-ocular pathology and fatal complications. During virally induced GBS, autoimmune brain demyelination and macular degeneration correlate with low virus neutralization and elevated antibody-mediated infection among Fcγ-R bearing cells. The use of interferon-deficient mice for ZIKV studies limits elucidation of antibody-dependent enhancement (ADE) and long-term pathology (≥120 days), due to high lethality post-infection. Here we used immunocompetent BALB/c mice, which generate robust humoral immune responses, to investigate long-term impacts of ZIKV infection. A high infectious dose (1x106 FFU per mouse) of ZIKV was administered intravenously. Control animals received a single dose of anti-IFNAR blocking monoclonal antibody and succumbed to lethal neurological pathology within 13 days. Immunocompetent mice exhibited motor impairment such as arthralgia, as well as ocular inflammation resulting in retinal vascular damage, and corneal edema. This pathology persisted 100 days after infection with evidence of chronic inflammation in immune-privileged tissues, demyelination in the hippocampus and motor cortex regions of the brain, and retinal/corneal hyperplasia. Anti-inflammatory transcriptional responses were tissue-specific, likely contributing to differential pathology in these organs. Pathology in immunocompetent animals coincided with weakly neutralizing antibodies and increased ADE among ZIKV strains (PRVABC59, FLR, and MR766) and all Dengue virus (DENV) serotypes. These antibodies were autoreactive to GBS-associated gangliosides. This study highlights the importance of longevity studies in ZIKV infection and confirms the role of anti-ganglioside antibodies in ZIKV-induced neuro-ocular disease.

Sexuell ubertragbare Infektionen (STI) im Anorektalbereich treten bei Risikopopulationen wie Mannern, die Sex mit Mannern haben (MSM), uberproportional haufig auf, finden sich aber durch ein geandertes Sexualverhalten zunehmend auch bei Heterosexuellen. Nach kurzlicher Implementierung der medikamentosen HIV(„human immunodeficiency virus“)-Praexpositionsprophylaxe ist mit einer weiteren Zunahme von STI zu rechnen, da hierbei meist auf Kondome verzichtet wird. Die Ubersicht behandelt Epidemiologie, klinisches Bild, Diagnostik und aktuelle leitliniengerechte Therapie „klassischer“ bakterieller STI, die sich im Anorektalbereich manifestieren. Bakterielle STI im Analbereich zeigen sich meist klinisch unspezifisch oder verlaufen asymptomatisch, sodass sie hier oft nicht erkannt werden. Bei rektaler Lokalisation besteht auch endoskopisch die Verwechslungsgefahr mit entzundlichen Darmerkrankungen oder Tumoren. Die Kenntnis des Symptomspektrums haufiger STI in dieser Lokalisation ist daher wegweisend fur eine zeitnahe Diagnose. Da Koinfektionen mit anderen STI haufig vorkommen, sollte auch nach weiteren Erregern einschlieslich HIV und Hepatitis B/C gefahndet werden.

Dedifferentiated vascular smooth muscle cells (vSMCs) play an essential role in neointima formation, and we now aim to investigate the role of the bone morphogenetic protein (BMP) modulator BMPER (BMP endothelial cell precursor-derived regulator) in neointima formation. To assess BMPER expression in arterial restenosis, we used a mouse carotid ligation model with perivascular cuff placement. Overall BMPER expression after vessel injury was increased; however, expression in the tunica media was decreased compared to untreated control. Consistently, BMPER expression was decreased in proliferative, dedifferentiated vSMC in vitro. C57BL/6_Bmper+/− mice displayed increased neointima formation 21 days after carotid ligation and enhanced expression of Col3A1, MMP2, and MMP9. Silencing of BMPER increased the proliferation and migration capacity of primary vSMCs, as well as reduced contractibility and expression of contractile markers, whereas stimulation with recombinant BMPER protein had the opposite effect. Mechanistically, we showed that BMPER binds insulin-like growth factor-binding protein 4 (IGFBP4), resulting in the modulation of IGF signaling. Furthermore, perivascular application of recombinant BMPER protein prevented neointima formation and ECM deposition in C57BL/6N mice after carotid ligation. Our data demonstrate that BMPER stimulation causes a contractile vSMC phenotype and suggest that BMPER has the potential for a future therapeutic agent in occlusive cardiovascular diseases.

The purpose of this study is to investigate the role of platelet bone morphogenetic proteins (BMP)-4 during vascular inflammation and remodeling in a mouse model of carotid wire injury. Transgenic mice with a platelet-specific deletion of BMP-4 (BMP4Plt−/−) were generated. Intravital microscopy was performed to evaluate leukocyte adhesion to the vessel wall. Expression of adhesion molecules and chemokines were analyzed. Platelet-leukocyte aggregates (PLAs) were evaluated using flow cytometry. For carotid wire injury, BMP4Plt−/− mice were further crossed with LDLr−/− mice (BMP4Plt−/−/LDLr−/−) and fed with a high cholesterol diet for 2-weeks. Carotid wire injury was performed, and re-endothelialization and neointimal formation were evaluated. In comparison to the control mice, stimulation with TNFα resulted in fewer rolling and adherent leukocytes to the vessel wall in the BMP4Plt−/− mice. mRNA and protein expression of P-selectin and adhesion molecules were reduced in the aorta of the BMP4Plt−/− mice. In platelets from the BMP4Plt−/− mice, the expression of P-selectin was reduced, and fewer PLA formations were measured than in the control mice. Loss of platelet BMP-4 further prevented neointima formation after carotid wire injury. Endothelial regeneration after injury was decelerated in the BMP4Plt−/− mice, and confirmed in-vitro, where the deletion of platelet BMP-4 inhibited endothelial cell proliferation and migration. We demonstrate for the first time that platelet BMP-4 is involved during vascular inflammation and remodeling. This is partially mediated by the inhibition of platelet activation, reduced expression of adhesion molecules and inflammatory responses. Our findings identify platelet BMP-4 as a mediator of vascular inflammation in early atherosclerosis and restenosis.

Leukocyte transmigration through the blood vessel wall is a fundamental step of the inflammatory response and requires expression of adhesion molecule PECAM-1. Accumulating evidence implicates that semaphorin (Sema) 3F and its receptor neuropilin (NRP) 2 are central regulators in vascular biology. Herein, we assess the role of Sema3F in leukocyte migration in vitro and in vivo. To determine the impact of Sema3F on leukocyte recruitment in vivo, we used the thioglycollate-induced peritonitis model. After the induction of peritonitis, C57BL/6 mice were intraperitoneally (i.p.) injected daily with recombinant Sema3F or solvent for 3 days. Compared with solvent-treated controls, leukocyte count was increased in the peritoneal lavage of Sema3F-treated mice indicating that Sema3F promotes leukocyte extravasation into the peritoneal cavity. In line with this observation, stimulation of human endothelial cells with Sema3F enhanced the passage of peripheral blood mononuclear cells (PBMCs) through the endothelial monolayer in the transwell migration assays. Conversely, silencing of endothelial Sema3F by siRNA transfection dampened diapedesis of PBMCs through the endothelium in vitro. xMechanistically, Sema3F induced upregulation of adhesion molecule PECAM-1 in endothelial cells and in murine heart tissue shown by immunofluorescence and western blotting. The inhibition of PECAM-1 by blocking antibody HEC7 blunted Sema3F-induced leukocyte migration in transwell assays. SiRNA-based NRP2 knockdown reduced PECAM-1 expression and migration of PBMCs in Sema3F-treated endothelial cells, indicating that PECAM-1 expression and leukocyte migration in response to Sema3F depend on endothelial NRP2. To assess the regulation of Sema3F in human inflammatory disease, we collected serum samples of patients from day 0 to day 7 after survived out-of-hospital cardiac arrest (OHCA, n = 41). First, we demonstrated enhanced migration of PBMCs through endothelial cells exposed to the serum of patients after OHCA in comparison to the serum of patients with stable coronary artery disease or healthy volunteers. Remarkably, serum samples of OHCA patients contained significantly higher Sema3F protein levels compared with CAD patients (CAD, n = 37) and healthy volunteers (n = 11), suggesting a role of Sema3F in the pathophysiology of the inflammatory response after OHCA. Subgroup analysis revealed that elevated serum Sema3F levels after ROSC are associated with decreased survival, myocardial dysfunction, and prolonged vasopressor therapy, clinical findings that determine the outcome of post-resuscitation period after OHCA. The present study provides novel evidence that endothelial Sema3F controls leukocyte recruitment through a NRP2/PECAM-1-dependent mechanism. Sema3F serum concentrations are elevated following successful resuscitation suggesting that Sema3F might be involved in the inflammatory response after survived OHCA. Targeting the Sema3F/NRP2/PECAM-1 pathway could provide a novel approach to abolish overwhelming inflammation after resuscitation.

Participation in bouldering has increased substantially over the past two decades, with indoor (gym) climbing and bouldering identified as the fastest growing sector of the climbing industry. Thus, for many, their experience with bouldering begins in the gym and then progresses to climbing outdoors. This raises questions regarding the extent to which those who initially learn in a gym setting are making a responsible transition to the outdoors by adopting behaviors that protect and preserve ecological and social conditions, thus ensuring the future of outdoor bouldering access. This article reports on bouldering research conducted in Rocky Mountain National Park, USA in the summer of 2015. The authors conducted an on-site visitor survey that examined attitudes, knowledge, and perceptions of Leave No Trace-related bouldering practices, specifically comparing and contrasting indoor and outdoor learners, as well as self-reported ability, across these measures. A total of 227 boulderers completed the survey, the majority of which initially learned to boulder indoors. Indoor learners and those of novice ability reported less knowledge of Leave No Trace and generally held attitudes and perceptions less congruent with Leave No Trace recommendations. The authors recommend continuing and expanding minimum-impact outdoor bouldering programs designed to educate boulderers making the transition from the gym to the crag to support the long-term viability of outdoor bouldering on public and protected lands. Management implications ● It is essential that recreation managers work in collaboration with emerging user-groups, such as boulderers, in developing management strategies that protect resources while maintaining quality recreational opportunities. ● These findings confirm and provide support for continued and expanded efforts for collaborative work among the gym climbing industry, public land agencies, and bouldering interest and advocacy groups in the development and delivery of minimum-impact bouldering information and educational resources ● This study identified significant differences in attitudes toward, and knowledge of, Leave No Trace practices depending on whether one initially learned to boulder indoors in a gym or an outdoor setting

Aldosterone is a key factor in adverse cardiovascular remodeling by acting on the mineralocorticoid receptor (MR) in different cell types. Endothelial MR activation mediates hypertrophy, inflammation and fibrosis. Cardiovascular remodeling is often accompanied by impaired angiogenesis, which is a risk factor for the development of heart failure. In this study, we evaluated the impact of MR in endothelial cells on angiogenesis. Deoxycorticosterone acetate (DOCA)-induced hypertension was associated with capillary rarefaction in the heart of WT mice but not of mice with cell type-specific MR deletion in endothelial cells. Consistently, endothelial MR deletion prevented the inhibitory effect of aldosterone on the capillarization of subcutaneously implanted silicon tubes and on capillary sprouting from aortic ring segments. We examined MR-dependent gene expression in cultured endothelial cells by RNA-seq and identified a cluster of differentially regulated genes related to angiogenesis. We found opposing effects on gene expression when comparing activation of the mineralocorticoid receptor in ECs to treatment with vascular endothelial growth factor (VEGF), a potent activator of angiogenesis. In conclusion, we demonstrate here that activation of endothelial cell MR impaired angiogenic capacity and lead to capillary rarefaction in a mouse model of MR-driven hypertension. MR activation opposed VEGF-induced gene expression leading to the dysregulation of angiogenesis-related gene networks in endothelial cells. Our findings underscore the pivotal role of endothelial cell MR in the pathophysiology of hypertension and related heart disease.

BACKGROUND The NANN Research Summit has been providing a platform for neonatal scholarship and clinical inquiry for 15 years. As the discipline of nursing and nursing research continue to evolve, it is important to gain perspective on current trends and needs for areas of strength and growth. PURPOSE To evaluate participant outcomes of the NANN Research Summit and determine opportunities for improvement. METHODS A 9-question survey was sent to 90 past participants for the Research Summit years 2015-2019. RESULTS Thirty-seven (41%) participants from 2015 to 2019 responded. Of those responding, 75% continued to pursue their presentation topic; 95% felt empowered to continue their research based on their Summit experience; 84% felt more comfortable presenting their research findings after attending; 84% felt confident in publishing research after attending the Summit, with 43% reporting publications. These accomplished results would not have been possible without Mead Johnson's support. In addition, 57% did not publish the work presented and 65% lacked continued mentorship. IMPLICATIONS FOR PRACTICE A redesigned Summit is presented to address the priorities for growth and alignment with continued emphasis on collegiality among neonatal nurse scholars. The redesigned Summit will promote continued clinical inquiry as a result of intentional focus on mentorship and development of scholarship. IMPLICATIONS FOR RESEARCH The data collected from this initial survey will continue to serve as the basis for future data collection. Continued evaluation of strengths and areas for growth including the number of publications and mentorship experience can lead to expansion of research for the Summit facilitators and participants.

Sexually transmitted infections (STIs) in the anorectal region are disproportionally detected in risk populations such as men who have sex with men (MSM). However, due to changes in sexual behaviour they are increasingly diagnosed in heterosexual individuals. Due to the recent implementation of oral HIV pre-exposure prophylaxis together with lack of condom use, a further rise in STIs is expected.This review addresses epidemiology, clinical picture, diagnostic pitfalls and current therapy guidelines of "classical" bacterial STIs involving the anorectum.STI manifestations in the anal region are frequently nonspecific or asymptomatic so that the diagnosis may be missed. In an endoscopic examination of the rectum, they can even mimic inflammatory bowel disease or malignancy. Therefore, knowledge of possible symptoms of bacterial STIs in this area is helpful for early diagnosis. Coinfections with other STIs are common and should prompt a search of other pathogens including HIV and hepatitis B/C.

Supplemental material, sj-pdf-1-std-10.1177_0956462420959169 for High prevalence of recreational and illicit drug use in German people living with HIV with a potential for drug–drug interactions with antiretroviral therapy by B Funke, CD Spinner, S Esser, HJ Stellbrink, A Stoehr, E Wolf, C Koegl, J Bruening and V Witte in International Journal of STD & AIDS

This research paper introduces a numerical model describing the stripping and drying phase during steam pressure filtration treating water insoluble volatile pore liquids. The model is based on mechanical and thermodynamic equations derived from the theory of steam pressure filtration for aqueous pore liquids and from the steam distillation theory. One main input parameter is the pressure profile determining the state variables of the vapour mixture. This work is first to resolve the pressure profile across a filter cake during stripping and drying based on temperature measurements within the filter cake. The developed model describes the stripping kinetics and the temperature profile across the filter cake and furthermore reveals a complete removal of the volatile organic compounds from the filter cake. The findings are evaluated by the experimentally determined stripping and drying kinetics. Additionally, exemplary calculations of the temporally and spatially resolved model are shown in order to promote the process understanding.

Savannas can be defined by the co-dominance of grasses and trees. Interactions between these two life forms are relatively well studied, whereas tree-tree interactions attracted increased attention only recently. However, the influence of woody plant density on tree-tree interactions is rarely considered. We studied tree-tree interactions in a semi-arid and a mesic savanna to test for differences between open and dense woody vegetation in relation to broad-scale environmental conditions. We applied spatial point pattern analysis to gain a better understanding of processes, such as competition, facilitation and disturbances, affecting the spatial distribution of trees. Competition between trees was most pronounced in dense vegetation, whereas facilitation effects were more common in open vegetation. Further, we found that factors shaping the spatial patterns differ with scale. At short tree-to-tree distances, results indicate limited seed dispersal as the most influential factor explaining the spatial distribution of trees. However, with increasing tree-to-tree distances, environmental heterogeneity in the semi-arid savanna and disturbances in the mesic savanna became more important. We conclude that studying tree-tree interactions in savannas should explicitly consider the actual woody plant density, especially when different savanna types are compared.

Es wird uber den Fall einer Patientin mit zuvor nicht bekannter atypischer Cholinesterase berichtet, bei der die Narkoseeinleitung mit Suxamethoniumchlorid und Mivacuriumchlorid zur einer prolongierten Muskelrelaxation fuhrte, so dass eine Testsondenimplantation zur Sakralnervenstimulation aufgrund der fehlenden Reaktion der analen Sphinktermuskulatur nicht erfolgen konnte. Nach Diagnosestellung durch Bestimmung der Dibucainzahl wurde der erneute Eingriff 2 Monate spater in Lokalanasthesie durchgefuhrt und die Testsonde erfolgreich implantiert. Eine Bestimmung der Dibucainzahl praoperativ konnte Patienten mit atypischer Cholinesterase sicher identifizieren und Verlaufe wie in diesem Fall beschrieben verhindern. Wesentlich erscheint aber das Erarbeiten eines Behandlungspfades mit verbindlich vereinbartem anasthesiologischem Management.

The bone morphogenetic protein (BMP) signaling pathway plays a central role during vasculature development. Mutations or dysregulation of the BMP pathway members have been linked to arteriovenous malformations. In the present study, we investigated the effect of the BMP modulators bone morphogenetic protein endothelial precursor-derived regulator (BMPER) and twisted gastrulation protein homolog 1 (TWSG1) on arteriovenous specification during zebrafish development and analyzed downstream Notch signaling pathway in human endothelial cells. Silencing of bmper and twsg1b in zebrafish embryos by morpholinos resulted in a pronounced enhancement of venous ephrinB4a marker expression and concomitant dysregulated arterial ephrinb2a marker expression detected by in situ hybridization. As arteriovenous specification was disturbed, we assessed the impact of BMPER and TWSG1 protein stimulation on the Notch signaling pathway on endothelial cells from different origin. Quantitative real-time PCR (qRT-PCR) and western blot analysis showed increased expression of Notch target gene hairy and enhancer of split, HEY1/2 and EPHRINB2. Consistently, silencing of BMPER in endothelial cells by siRNAs decreased Notch signaling and downstream effectors. BMP receptor antagonist DMH1 abolished BMPER and BMP4 induced Notch signaling pathway activation. In conclusion, we found that in endothelial cells, BMPER and TWSG1 are necessary for regular Notch signaling activity and in zebrafish embryos BMPER and TWSG1 preserve arteriovenous specification to prevent malformations.

Leukocyte recruitment is a fundamental event in the response of the innate immune system to injury. This process is promoted in part by the opening of endothelial cell adherens junctions that allows leukocyte extravasation through gaps between adjacent endothelial cells. VE-cadherin is a key component of endothelial cell adherens junctions and a negative regulator of leukocyte emigration. Accumulating evidence implicates bone morphogenetic protein (BMP) 4 as a critical regulator in vascular biology, but its role in leukocyte extravasation in vitro and in vivo has not been investigated so far. To assess the impact of BMP4 on leukocyte emigration in vivo, we used the thioglycollate-induced peritonitis model. C57BL/6 mice were intraperitoneally (i.p.) injected with recombinant BMP4 in addition to thioglycollate. Compared to solvent-treated controls, we observed higher accumulation of leukocytes in the peritoneal lavage of BMP4-treated mice indicating that BMP4 promotes leukocyte diapedesis into the inflamed peritoneal cavity. Endothelial cell-specific deletion of BMP4 in mice markedly diminished leukocyte diapedesis following thioglycollate administration suggesting that endothelial BMP4 is required for leukocyte recruitment. Consistent with these in vivo results, transwell migration assays with human umbilical vein endothelial cells (HUVECs) in vitro revealed that recombinant BMP4 enhanced leukocyte transmigration through the endothelial monolayer. Conversely, silencing of endothelial BMP4 by siRNA dampened leukocyte diapedesis in vitro. Mechanistic studies showed that loss of BMP4 improved endothelial junction stability by upregulation of VE-cadherin expression in vitro and in vivo. Vice versa, treatment of HUVECs with recombinant BMP4 decreased expression of VE-cadherin and impaired endothelial junction stability shown by Western blotting and immunocytochemistry. Finally, severe endothelial damage in HUVECs in response to serum of patients collected 24 h after survived cardiac arrest was accompanied by increase in leukocyte migration in transwell assays and activation of the BMP pathway most probably by upregulation of endothelial BMP4 RNA and protein expression. Collectively, the present study provides novel evidence that endothelial BMP4 controls leukocyte recruitment through a VE-cadherin-dependent mechanism and that BMP4-induced inflammation might be involved in the pathogenesis of endothelial cell damage following successful resuscitation after cardiac arrest.

The paper takes up the old ideas of describing porous media with several tube and network models. The well-known models received from literature gave a good concept of dewatering equilibria resulting in capillary pressure curves and pore size distributions (PoSD). However, numerical methods and measurement techniques were not sophisticated allowing to evaluate the models appropriately. In this work, a numerical method based on statistics is introduced to validate the network model of FATT from 1956: The porous filter cake structure is implemented as a matrix, which elements represent the pore size correlating with the capillary entrance pressure for each pore. The input for the calculations can be any mathematical approximation of a PoSD, which can be derived from capillary pressure tests or micro computer tomography (µCT) analysis of the filter cake. A procedure based on the concept of FATT is presented to generate dewatering equilibria for different applied pressures. Therefore, the elements of the matrix are checked to be ‘dewatered’ regarding to their size, position, the applied pressure level and the progress of dewatering. The network model known from literature is improved by implementing additional conditions for the description of physical phenomena, such as the formation of residual bridge liquid or hydrodynamic isolated areas. X-ray microscopy, mercury intrusion tests and laboratory desaturation experiments by using semipermeable membranes for capillary pressure tests are used to validate the pore size distribution. The different results are integrated into the matrix model as starting parameters. For the laboratory experiments, the PoSD is calculated from the measured capillary pressure curve, using the distributed tube model and the YOUNG-LAPLACE-equation on an equal basis to the established mercury intrusion analysis. However, with the tomography measurements, it is possible to determine PoSD using different defined geometry elements fitting inside the pore space. The force balance is evaluated at the pore entrance by using the wetting line of the pore throat. The direct measurement of the void geometry allows the calculation of the pressure distribution without the LAPLACIAN assumptions. In this way, the difference between experimental, measured and modelled PoSDs is emphasised to validate the old (and improved) ideas of network models describing porous media.

The endothelium serves as a selective barrier and controls the exchange of nutrients, hormones, and leukocytes between blood and tissues. Molecular mechanisms contributing to the pathogenesis of endothelial barrier dysfunction remain incompletely understood. Accumulating evidence implicates bone morphogenetic protein (BMP)-modulator BMPER as a key regulator in endothelial biology. Herein, we analyze the impact of BMPER in the control of endothelial barrier function. To assess the role of BMPER in vascular barrier function in mice, we measured the leakage of Evans blue dye from blood into interstitial lung tissue. BMPER+/− mice exhibited a significantly higher degree of vascular leak compared with wild-type siblings. In accordance with our in vivo observation, siRNA-based BMPER knockdown in human umbilical endothelial cells increased endothelial permeability measured by FITC-dextran passage in transwell assays. Mechanistically, BMPER knockdown reduced the expression of VE-cadherin, a pivotal component of endothelial adherens junctions. Conversely, recombinant human BMPER protein upregulated VE-cadherin protein levels and improved endothelial barrier function in transwell assays. The effects of BMPER knockdown on VE-cadherin expression and endothelial permeability were induced by enhanced BMP activity. Supporting this notion, activation of BMP4-Smad-Id1 signaling reduced VE-cadherin levels and impaired endothelial barrier function in vitro. In vivo, Evans blue dye accumulation was higher in the lungs of BMP4-treated C57BL/6 mice compared to controls indicating that BMP4 increased vascular permeability. High levels of BMPER antagonized BMP4-Smad5-Id1 signaling and prevented BMP4-induced downregulation of VE-cadherin and endothelial leakage, suggesting that BMPER exerts anti-BMP effects and restores endothelial barrier function. Taken together, this data demonstrates that BMPER-modulated BMP pathway activity regulates VE-cadherin expression and vascular barrier function.

This paper examines impacts of increased visitation leading to human trampling of vegetation and soil along several trails in Rocky Mountain National Park (RMNP) to understand how abiotic factors and level of use can influence trail conditions. RMNP is one of the most visited national parks in the USA with 3.3 million visitors in 2012 across 1075 km2 and 571 km of hiking trails. 95 % of the park is designated wilderness making the balance between preservation and visitor use challenging. This research involves the application of trail condition assessments to 56 km of trails to determine prevailing factors and what, if any, connection between them exist. The study looked at a variety of inventory and impact indicators and standards to determine their importance and to develop a baseline condition of trails. The data can be used for future comparison and evaluation of development trends. We found that trail widening (mean trail width 88.9 cm) and soil loss (cross sectional area 172.7 cm2) are the most visible effects of trail degradation. Further statistical analyses of data identified the role and influence of various factors (e.g. use level and topography). Insights into the influence of these factors can lead to the selection of appropriate management measures to avoid or minimize negative consequences from increased visitation.

The treatment of solvent-loaded solids, e.g. following a solid–liquid extraction presents a challenge in practice becoming even more complicated if solvents used are volatile organic compounds (VOC) which are poorly water soluble and thus bio-incompatible. A complete mechanical separation of the VOC from solids is not possible and following drying processes are usually energy intensive. Steam pressure filtration provides an efficient alternative combining mechanical and thermal treatment of filter cakes by using steam resulting in excellent washing and dewatering behaviour of the filter cake. A subsequent steam stripping offers a further reduction of the VOC load, which was not part of comprehensive investigations yet. The overarching goal of this paper is to expand understanding of steam pressure filtration in combination with water insoluble VOC. Furthermore, it is shown that a complete purification of the solids by steam stripping is possible with only low steam consumption at moderate filter cake heights.