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Background: There are limited data available on the survival and early complications of preterm infants with less than 500 g birthweight. To estimate the outcomes for these infants, it is important for caregivers to be aware of perinatal factors that may affect survival.Objectives: We assessed the mortality and certain early complications of preterm infants born with less than 500 g in Hungary between 2006 and 2015.Methods: We reviewed data of 486 infants from the database of the Hungarian Central Statistical Office and in parallel of 407 infants from the "NICU database." The study period was divided into two epochs: 2006-2010 and 2011-2015.Results: The survival was 27.1% in the first epoch and 39.1% in the second epoch, and the incidence of early complications was slightly higher in the second epoch. In the surviving group (first and second epoch combined), gestational age (25.1 vs 23.7 weeks), birthweight (458 vs 447 g) antenatal steroid treatment (66.3% vs 52.3%), surfactant therapy (95.1% vs 84.3%), median Apgar scores (6 vs 3 and 8 vs 5 at 1 and 5 minutes, respectively) and proportion of caesarean delivery (89.3% versus 68.5%) were higher than in the non-surviving group (first and second epoch combined). The proportion of multiple births was lower in the surviving group (15.7% vs 33.4%).Conclusions: Survival of infants with less than 500 g improved between 2006-2010 and 2011-2015 in Hungary. The slightly higher occurrence of early complications might be associated with improving survival. [ABSTRACT FROM AUTHOR]

Recent evidence implicates the myocardin‐related transcription factors (MRTFs) as key mediators of the phenotypic plasticity leading to the conversion of various cell types into myofibroblasts. This review highlights the function of MRTFs during development, fibrosis and cancer, and the role of MRTFs during epithelial–mesenchymal transitions (EMTs) underlying these processes. EMT is a sequentially orchestrated process where cells undergo a rearrangement of their cell contacts and activate a fibrogenic and myogenic expression program. MRTFs interact with and regulate the major signaling pathways and the expression of key markers and transcription factors involved in EMT. These functions indicate a central role for MRTFs in controlling the process of EMT. Developmental Dynamics 247:396–404, 2018. © 2017 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

This article develops a method for recovering a one‐dimensional rough surface profile from scattered wave field, using a single receiver and repeated measurements when the surface is moving with respect to source and receiver. This extends a previously introduced marching method utilizing low grazing angles, and addresses the key issue of the requirement for many simultaneous receivers. The algorithm recovers the surface height below the receiver point step‐by‐step as the surface is moved, using the parabolic wave integral equations. Numerical examples of reconstructed surfaces demonstrate that the method is robust in both Dirichlet and Neumann boundary conditions, and with respect to different roughness characteristics and measurement noise. [ABSTRACT FROM AUTHOR]

Purpose: The rapid switching of the gradient fields induces eddy currents in neighboring metallic structures, causing undesirable effects. Numerical computations are thus required to understand eddy‐currents effects for designing/implementing mitigation (involving passive shielding) and compensating techniques (using pre‐emphasis). Previously, the network‐analysis (NA) method was introduced to compute z‐gradient eddy currents, although limited to a circularly symmetric and unconnected coil. Multi‐layer integral method (MIM) method was recently introduced, modifying the circuit equation involving stream functions. We tailor MIM (TMIM) for a more general eddy‐currents analysis in thin structures. Z‐gradient eddy currents are analyzed and then compared using three methods (NA, TMIM, and Ansys). The analysis helps to evaluate the efficiency of passive shielding and to compensate eddy currents. Methods: NA and TMIM computational frameworks for harmonic and transient eddy‐currents analysis were implemented and cross‐validated against Ansys Maxwell. A pre‐emphasis pulse was modeled for compensating eddy currents. Results: Eddy‐currents analysis of an unconnected z‐gradient coil in both the passive shield and cryostat were computed, and results were comparable to the least computationally efficient Ansys simulations. Although NA computations are fast, TMIM is implemented with reasonable efficiency and applied to circularly unsymmetric geometries. TMIM computations were further validated against Ansys using a connected z‐gradient. Our computations allowed the effective evaluation of the performance of three various passive‐shielding configurations, non‐capped, capped, and slitted (for the first time), and an effective pre‐emphasis compensation model was computed. Conclusion: Three eddy‐currents analysis methods were studied and compared. Computationally efficient TMIM allows both harmonic and transient eddy‐currents analysis involving different/complex gradient configurations/situations as well as involved shielding structures. Eddy‐currents pre‐emphasis compensation was demonstrated. [ABSTRACT FROM AUTHOR]

Aim: The aim is to provide an overview of recent research on genetic factors that influence preterm birth in the context of neonatal phenotypic assessment. Methods: This is a nonsystematic review of the recent scientific literature. Results: Maternal and fetal genetic diversity and rare genome variants are linked with crucial immune response sites. In addition, more frequent in preterm neonates, de novo variants may lead to attention deficits, hyperactivity, autism spectrum disorders, and infertility of both sexes later in life. Environmental factors may also greatly burden fetal, and consequently, neonatal development and neurodevelopment through a failure in the fetal epigenome reprogramming process and even influence the initiation of spontaneous preterm pregnancy termination. Minimally invasive analysis of the transcription factors associated with preterm birth helps elucidate labor mechanisms and predict its timing. We also provide valuable summaries of genomic and transcriptomic factors that contribute to preterm birth. Conclusions: Investigation of the human genome, epigenome, and transcriptome helps to identify molecular mechanisms linked with preterm delivery and premature newborn clinical appearance in early and late neonatal life and even predict developmental outcomes. Further studies are needed to fully understand the implications of genetic changes in preterm births. These data could be used to develop targeted interventions aimed at selecting the most effective individual treatment and rehabilitation plan. [ABSTRACT FROM AUTHOR]

Preterm birth and enteral feeding are two main factors leading to necrotizing enterocolitis (NEC). The metabolomics of preterm infants before and after feeding can provide a basis for the prediction of NEC. Using the method of cross‐sectional study, the mode was established with the serum samples of 19 premature infants at birth and after feeding as the control group. The serum was analyzed using GC–MS. Chemometric analysis includes principal component analysis, partial least squares‐discriminant analysis, and orthogonal partial least squares‐discriminant analysis. Spectral separation of serum metabolites occurred in premature infants before and after feeding. The levels of xylose, d‐talose, phosphoglycolic acid, maleimide, l‐gulonolactone, maleic acid, β‐hydroxypyruvate, itaconic acid, and pantothenic acid in the serum of premature infants after feeding were significant in both multidimensional and single‐dimensional modes (variable importance in projection >2, P < 0.01). There was a moderate correlation between total bilirubin and l‐gulonolactone and β‐hydroxypyruvate (0.8 > r > 0.5). Maleimide, maleic acid, and itaconic acid have diagnostic value (area under the curve >0.9). The results indicated that serum metabolism of preterm infants changes significantly after feeding. Some metabolites have potential value in predicting NEC. [ABSTRACT FROM AUTHOR]

Aim: To describe survival and neonatal morbidities in infants born before 24 weeks of gestation during a 12‐year period. Methods: Data were retrieved from national registries and validated in medical files of infants born before 24 weeks of gestation 2007–2018 in Sweden. Temporal changes were evaluated. Results: In 2007–2018, 282 live births were recorded at 22 weeks and 460 at 23 weeks of gestation. Survival to discharge from hospital of infants born alive at 22 and 23 weeks increased from 20% to 38% (p = 0.006) and from 45% to 67% (p < 0.001) respectively. Caesarean section increased from 12% to 22% (p = 0.038) for infants born at 22 weeks. Neonatal morbidity rates in infants alive at 40 weeks of postmenstrual age (n = 399) were unchanged except for an increase in necrotising enterocolitis from 0 to 33% (p = 0.017) in infants born at 22 weeks of gestation. Bronchopulmonary dysplasia was more common in boys than girls, 90% versus 82% (p = 0.044). The number of infants surviving to 40 weeks doubled over time. Conclusion: Increased survival of infants born before 24 weeks of gestation resulted in increasing numbers of very immature infants with severe neonatal morbidities likely to have a negative impact on long‐term outcome. [ABSTRACT FROM AUTHOR]

Breast cancer (BC)‐related mortality primarily results from metastatic colonization of disseminated cells. Actin polymerization plays an important role in driving post‐extravasation metastatic outgrowth of tumor cells. This study examines the role of myocardin‐related transcription factor (MRTF)/serum‐response (SRF), a transcription system well known for regulation of cytoskeletal genes, in metastatic colonization of BC cells. We demonstrated that co‐depletion of MRTF isoforms (MRTF‐A and MRTF‐B) dramatically impairs single‐cell outgrowth ability of BC cells as well as retards growth progression of pre‐established BC cell colonies in three‐dimensional (3D) cultures. Conversely, overexpression of MRTF‐A promotes initiation and progression of tumor‐cell outgrowth in vitro, primary tumor formation, and metastatic outgrowth of seeded BC cells in vivo, and these changes can be dramatically blocked by molecular disruption of MRTF‐A's interaction with SRF. Correlated with the outgrowth phenotypes, we further demonstrate MRTF's ability to augment the intrinsic cellular ability to polymerize actin and formation of F‐actin‐based protrusive structures requiring SRF's interaction. Pharmacological proof‐of‐concept studies show that small molecules capable of interfering with MRTF/SRF signaling robustly suppresses single‐cell outgrowth and progression of pre‐established outgrowth of BC cells in vitro as well as experimental metastatic burden of BC cells in vivo. Based on these data, we conclude that MRTF activity potentiates metastatic colonization of BC cells and therefore, targeting MRTF may be a promising strategy to diminish metastatic burden in BC. [ABSTRACT FROM AUTHOR]

Oncological diseases have become the second leading cause of death from noncommunicable diseases worldwide and a major threat to human health. With the continuous progress in cancer research, the mechanical cues from the tumor microenvironment environment (TME) have been found to play an irreplaceable role in the progression of many cancers. As the main extracellular mechanical signal carrier, extracellular matrix (ECM) stiffness may influence cancer progression through biomechanical transduction to modify downstream gene expression, promote epithelial‐mesenchymal transition (EMT), and regulate the stemness of cancer cells. EMT is an important mechanism that induces cancer cell metastasis and is closely influenced by ECM stiffness, either independently or in conjunction with other molecules. In this review, the unique role of ECM stiffness in EMT in different kinds of cancers is first summarized. By continually examining the significance of ECM stiffness in cancer progression, a biomimetic culture system based on 3D manufacturing and novel material technologies is developed to mimic ECM stiffness. The authors then look back on the novel development of the ECM stiffness biomimetic culture systems and finally provide new insights into ECM stiffness in cancer progression which can broaden the fields' horizons with a view toward developing new cancer diagnosis methods and therapies. [ABSTRACT FROM AUTHOR]

Fused deposition modeling (FDM), one among the most commonly used additive manufacturing (AM), techniques has been widely used in recent years to produce customized parts with intricate geometries, especially from thermoplastics. This method was limited in its ability to produce parts for industrial applications due to inferior properties and the poor quality of fabricated parts. Hence, researchers are being driven to discover novel materials that are viable for FDM in order to keep up with enormous demand for functional products. In the recent years, it is widely recognized that the emphasis was placed on the bio‐based polymer composite matrices rather than conventional thermoplastics due to its vital advantages that aid in the replacement of synthetic and perilous materials. On this context, this review focuses on the recent advancements in FDM printing with biomaterials. Specifically, attempts have been made to investigate and provide nutshell of 3D printing of current bio‐based nanocomposites which consist of either bio‐derived filler or polymer matrices in order to make 3D printing sustainable. The effect of fillers on the filaments and FDM based products, evolution of novel characteristics of bio nanocomposites, the printability of the developed composites and their development in leading applications were also investigated and summarized. [ABSTRACT FROM AUTHOR]

Research on fluxgate magnetic sensors (FMS) has been in progress for past decades and has become popular for high precision results, external magnetic field detection, and simple design structure. The basic fluxgate magnetic sensor structure consists of an excitation coil, and pickup coils twist around the soft magnetic material. Although sensor size is simple, researchers, and engineers have been looking for decades to take advantage and integrate these devices into the tiny circuitry. This review will discuss the classic and new‐related fluxgate sensor design structures. Moreover, this review presents the main existing of the conventional/ micro/PCB (Printed circuit board) devices, materials and elements used for the fabrication, analytical models, and simulation tools. Future challenges in the fluxgate sensor fabrication are analyzed critically, and alternative approaches for better design are presented. The review emphasizes the benefits of fluxgate sensors in terms of translation. The particular segment includes a comparison of micro technology design against printed circuit board design. Improvements in fluxgate sensor noise, sensitivity concerning design parameters are reviewed and summarized chronologically. Compared with the previous studies published several decades ago, it will help beginners learn the step‐by‐step fabrication stages of fluxgate sensors for advanced applications and also complete overview about fabrication advancements of fluxgate sensors. [ABSTRACT FROM AUTHOR]

Exosomes are nanometer-sized small EVs coated with bilayer structure, which are released by prokaryotic and eukaryotic cells. Exosomes are rich in a variety of biologically active substances, such as proteins, nucleotides, and lipids. Exosomes are widely present in various body fluids and cell culture supernatants, and it mediates the physiological and pathological processes of the body through the shuttle of these active ingredients to target cells. In recent years, studies have shown that exosomes from a variety of cell sources can play a beneficial role in acute and chronic kidney disease. In particular, exosomes derived from mesenchymal stem cells have significant curative effects on the prevention and treatment of kidney disease in preclinical trials. Besides, some encapsulated substances are demonstrated to exert beneficial effects on various diseases, so they have attracted much attention. In addition, exosomes have extensive sources, stable biological activity, and good biocompatibility and are easy to store and transport; these advantages endow exosomes with superior diagnostic value. With the rapid development of liquid biopsy technology related to exosomes, the application of exosomes in the rapid diagnosis of kidney disease has become more prominent. In this review, the latest development of exosomes, including the biosynthesis process, the isolation and identification methods of exosomes are systematically summarized. The utilization of exosomes in diagnosis and their positive effects in the repair of kidney dysfunction are discussed, along with the specific mechanisms. This review is expected to be helpful for relevant studies and to provide insight into future applications in clinical practice. [ABSTRACT FROM AUTHOR]

Fibrotic diseases are still a serious concern for public health, due to their high prevalence, complex etiology and lack of successful treatments. Fibrosis consists of excessive accumulation of extracellular matrix components. As a result, the structure and function of tissues are impaired, thus potentially leading to organ failure and death in several chronic diseases. Myofibroblasts represent the principal cellular mediators of fibrosis, due to their extracellular matrix producing activity, and originate from different types of precursor cells, such as mesenchymal cells, epithelial cells and fibroblasts. Profibrotic activation of myofibroblasts can be triggered by a variety of mechanisms, including the transforming growth factor‐β signalling pathway, which is a major factor driving fibrosis. Interestingly, preclinical and clinical studies showed that fibrotic degeneration can stop and even reverse by using specific antifibrotic treatments. Increasing scientific evidence is being accumulated about the role of sirtuins in modulating the molecular pathways responsible for the onset and development of fibrotic diseases. Sirtuins are NAD+‐dependent protein deacetylases that play a crucial role in several molecular pathways within the cells, many of which at the crossroad between health and disease. In this context, we will report the current knowledge supporting the role of sirtuins in the balance between healthy and diseased myofibroblast activity. In particular, we will address the signalling pathways and the molecular targets that trigger the differentiation and profibrotic activation of myofibroblasts and can be modulated by sirtuins. [ABSTRACT FROM AUTHOR]

There is a growing controversy about the role of the epithelial to mesenchymal transition (EMT) in the fibrosis associated with chronic disease. Recent studies suggest that it is not the EMT transcriptional program but differentiation of progenitor cells, response to chronic inflammation, or some combination of both which cause the appearance of fibroblasts and the production of the extracellular matrix. To address this issue, we study the EMT process in the zebrafish keratocytes which migrate from primary explants of epithelial tissue as these cells are both terminally differentiated and able to divide. To firmly place this EMT process in the context of other systems, we first demonstrate that the zebrafish keratocyte EMT process involves nuclear accumulation of twist and snail/slug transcription factors as part of a TGFβR‐mediated EMT process. As assessed by the expression and localization of EMT transcription factors, the zebrafish keratocyte EMT process is reversed by the addition of Rho‐activated kinase (ROCK) in combination with TGFβR inhibitors. The complete cycle of EMT to MET observed in this system links these in vitro results more closely to the process of wound healing in vivo. However, the absence of observable activation of EMT transcription factors when keratocytes are cultured on compliant substrata in a TGFβ1‐containing medium suggests that ROCK signaling, initiated by tension within the sheet, is an essential contributor to the EMT process. Most importantly, the requirement for ROCK activation by culturing on noncompliant substrata suggests that EMT in these terminally differentiated cells would not occur in vivo. [ABSTRACT FROM AUTHOR]

This work investigates the radiation resistance of a structural material based on modified titanium hydride and a Portland cement in a flux of neutron and γ-radiation. An assessment of the geometric and physicomechanical properties is given, along with the surface structure of irradiated cement composites, and the phase composition of the main hydrosilicates of the hydrated cement matrix during its γ-irradiation. It is shown that the use of a shot of titanium hydride increases the radiation resistance of radiation shielding based on a cement matrix, in comparison with the unmodified shot. A composite based on a modified shot of titanium hydride retains its basic properties after γ-irradiation, at an absorbed dose of up to 10 MGy. At an absorbed dose of 2 MGy in the Portland cement matrix of a composite based on a modified shot of titanium hydride, the formation of suolunite hydrosilicates occurs. It was established using X-ray fluorescence that, in the titanium hydride, a redistribution of the electron density occurs at an absorbed dose of γ radiation of 5 MGy, caused by structural phase changes due to the ongoing dehydrogenation processes. [ABSTRACT FROM AUTHOR]

The tumor microenvironment (TME) consists of various components including cancer cells, tumor vessels, cancer‐associated fibroblasts (CAFs), and inflammatory cells. These components interact with each other via various cytokines, which often induce tumor progression. Thus, a greater understanding of TME networks is crucial for the development of novel cancer therapies. Many cancer types express high levels of TGF‐β, which induces endothelial‐to‐mesenchymal transition (EndMT), leading to formation of CAFs. Although we previously reported that CAFs derived from EndMT promoted tumor formation, the molecular mechanisms underlying these interactions remain to be elucidated. Furthermore, tumor‐infiltrating inflammatory cells secrete various cytokines, including TNF‐α. However, the role of TNF‐α in TGF‐β‐induced EndMT has not been fully elucidated. Therefore, this study examined the effect of TNF‐α on TGF‐β‐induced EndMT in human endothelial cells (ECs). Various types of human ECs underwent EndMT in response to TGF‐β and TNF‐α, which was accompanied by increased and decreased expression of mesenchymal cell and EC markers, respectively. In addition, treatment of ECs with TGF‐β and TNF‐α exhibited sustained activation of Smad2/3 signals, which was presumably induced by elevated expression of TGF‐β type I receptor, TGF‐β2, activin A, and integrin αv, suggesting that TNF‐α enhanced TGF‐β‐induced EndMT by augmenting TGF‐β family signals. Furthermore, oral squamous cell carcinoma‐derived cells underwent epithelial‐to‐mesenchymal transition (EMT) in response to humoral factors produced by TGF‐β and TNF‐α‐cultured ECs. This EndMT‐driven EMT was blocked by inhibiting the action of TGF‐βs. Collectively, our findings suggest that TNF‐α enhances TGF‐β‐dependent EndMT, which contributes to tumor progression. [ABSTRACT FROM AUTHOR]

Calcineurin inhibitors (CNI) are the pillars of immunosuppression in transplantation. However, they display a potent nephrotoxicity whose mechanisms remained widely unsolved. We used an untargeted quantitative proteomic approach (iTRAQ technology) to highlight new targets of CNI in renal proximal tubular cells (RPTCs). CNI‐treated RPTCs proteome displayed an over‐representation of actin‐binding proteins with a CNI‐specific expression profile. Cyclosporine A (CsA) induced F‐actin remodeling and depolymerization, decreased F‐actin‐stabilizing, polymerization‐promoting cofilin (CFL) oligomers, and inhibited the G‐actin‐regulated serum response factor (SRF) pathway. Inhibition of CFL canonical phosphorylation pathway reproduced CsA effects; however, S3‐R, an analogue of the phosphorylation site of CFL prevented the effects of CsA which suggests that CsA acted independently from the canonical CFL regulation. CFL is known to be regulated by the Na+/K+‐ATPase. Molecular docking calculations identified two inhibiting sites of CsA on Na+/K+‐ATPase and a 23% decrease in Na+/K+‐ATPase activity of RPTCs was observed with CsA. Ouabain, a specific inhibitor of Na+/K+‐ATPase also reproduced CsA effects on actin organization and SRF activity. Altogether, these results described a new original pathway explaining CsA nephrotoxicity. [ABSTRACT FROM AUTHOR]

Renal tubulointerstitial fibrosis is the final common pathway in end-stage renal disease and is characterized by aberrant accumulation of extracellular matrix (ECM) components secreted by myofibroblasts. Tubular type 2 EMT, induced by TGF-β, plays an important role in renal fibrosis, by participating directly or indirectly in myofibroblasts generation. TGF-β1-induced apoptosis and fibrosis in experimental chronic murine kidney diseases are concomitantly associated with an intrarenal decreased expression of the IL-15 survival factor. Since IL-15 counteracts TGF-β1 effects in different cell models, we analyzed whether (1) human chronic inflammatory nephropathies evolving towards fibrosis could be also characterized by a weak intrarenal IL-15 expression and (2) IL-15 could inhibit epithelial-mesenchymal transition (EMT) and excess matrix deposition in human renal proximal tubular epithelial cells (RPTEC). Our data show that different human chronic kidney diseases are characterized by a strong decreased expression of intrarenal IL-15, which is particularly relevant in diabetic nephropathy, in which type 2 tubular EMT plays an important role in fibrosis. Moreover, primary epithelial tubular cultures deprived of growth supplements rapidly produce active TGF-β1 inducing a "spontaneous" EMT process characterized by the loss of membrane-bound IL-15 (mbIL-15) expression. Both "spontaneous" EMT and recombinant human (rh) TGF-β1-induced EMT models can be inhibited by treating RPTEC and HK2 cells with rhIL-15. Through a long-lasting phospho-c-jun activation, IL-15 inhibits rhTGF-β1-induced Snail1 expression, the master inducer of EMT, and blocks TGF-β1-induced tubular EMT and downstream collagen synthesis. In conclusion, our data suggest that intrarenal IL-15 could be a natural inhibitor of TGF-β in human kidney able to guarantee epithelial homeostasis and to prevent EMT process. Thus, both in vivo and in vitro an unbalance in intrarenal IL-15 and TGF-β1 levels could render RPTEC cells more prone to undergo EMT process. Exogenous IL-15 treatment could be beneficial in some human nephropathies such as diabetic nephropathy. [ABSTRACT FROM AUTHOR]

Breast cancer and melanoma are among the most frequent cancer types leading to brain metastases. Despite the unquestionable clinical significance, important aspects of the development of secondary tumours of the central nervous system are largely uncharacterized, including extravasation of metastatic cells through the blood‐brain barrier. By using transmission electron microscopy, here we followed interactions of cancer cells and brain endothelial cells during the adhesion, intercalation/incorporation and transendothelial migration steps. We observed that brain endothelial cells were actively involved in the initial phases of the extravasation by extending filopodia‐like membrane protrusions towards the tumour cells. Melanoma cells tended to intercalate between endothelial cells and to transmigrate by utilizing the paracellular route. On the other hand, breast cancer cells were frequently incorporated into the endothelium and were able to migrate through the transcellular way from the apical to the basolateral side of brain endothelial cells. When co‐culturing melanoma cells with cerebral endothelial cells, we observed N‐cadherin enrichment at melanoma‐melanoma and melanoma‐endothelial cell borders. However, for breast cancer cells N‐cadherin proved to be dispensable for the transendothelial migration both in vitro and in vivo. Our results indicate that breast cancer cells are more effective in the transcellular type of migration than melanoma cells. [ABSTRACT FROM AUTHOR]

Background: Magnetic field therapy is a popular approach to pain therapy, but scientific evidence on treatment effects or even effects on sensory and pain perception in healthy controls is scarce.Methods: In the present randomized, placebo-controlled study, we investigated the influence of static magnetic field exposure on sensory (touch) and pain (pinprick, pressure and heat) perception. Eighteen healthy volunteers (age: 23 ± 2 years, nine women) underwent three 10-min static magnetic field exposures using field strengths of 0 T (placebo), 1.5 T and 3 T within clinical MR scanners in randomized order on three separate days. Participants were blinded to magnetic field strength. Experimental sensory and pain testing was performed immediately before and after each magnetic field exposure.Results: There was no significant effect of field strength on the assessed experimental sensory and pain testing parameters (mechanical detection threshold, pinprick threshold, pressure pain threshold, heat pain threshold and suprathreshold heat pain rating).Conclusion: We found no evidence that a 10-min 1.5 T or 3 T static magnetic field exposure affects experimental sensory or pain perception in young healthy volunteers.Significance: We used clinical MR scanners to investigate the effect of magnetic fields on pain perception. Using a rigorous, straightforward, placebo-controlled design, no effect of static magnetic fields on human experimental pain perception was detected. This provides a base for a more systematic investigation of magnetic field effects on pain. [ABSTRACT FROM AUTHOR]

Background: Myostatin (MSTN), a member of the transforming growth factor‐β (TGF‐β) superfamily, has been implicated in the negative regulation of skeletal myogenesis. However, the molecular mechanism through which MSTN regulates early embryonic myogenesis is not well understood. Results: We demonstrate that MSTN regulates early embryonic myogenesis by promoting the epithelial‐to‐mesenchymal transition (EMT) of the dermomyotome during somitogenesis in chicks. We show that the MSTN gene is first expressed at the center of the dermomyotome. As somitogenesis progresses, its expression extends dorsally and ventrally along the plane of the dermomyotome. By combining in situ hybridization and immunofluorescence assays, we demonstrate that the expression pattern of MSTN is spatiotemporally well correlated with EMT of the dermomyotome. Our gain‐ and loss‐of‐function experiments further reveal that MSTN can induce EMT of the chick dermomyotome. We also show that MSTN induces EMT of a nonsmall cell lung carcinoma cell line (A549) and Madin‐Darby canine kidney cells in vitro. Conclusions: Our experimental data suggest that MSTN regulates myogenesis by promoting EMT during somitogenesis. These findings provide novel insights into the functions of MSTN during early embryonic myogenesis. Developmental Dynamics 247:1241–1252, 2018. © 2018 Wiley Periodicals, Inc. Key Findings: MSTN; EMT; chick embryo [ABSTRACT FROM AUTHOR]

The process named endothelial‐to‐mesenchymal transition (EndMT) was observed for the first time during the development of the chicken embryo several decades ago. Of interest, accumulating evidence suggests that EndMT plays a critical role in the onset and progression of multiple postnatal cardiovascular diseases. EndMT is controlled by a set of developmental signaling pathways, very similar to the process of epithelial‐to‐mesenchymal transition, which determine the activity of several EndMT transcriptional effectors. Once activated, these EndMT effectors regulate the expression of endothelial‐ and mesenchymal‐specific genes, in part by interacting with specific motifs in promoter regions, eventually leading to the down‐regulation of endothelial‐specific features and acquisition of a fibroblast‐like phenotype. Important technical advances in lineage tracing methods combined with experimental mouse models demonstrated the pathophysiological importance of EndMT for human diseases. In this review, we discuss the major signal transduction pathways involved in the activation and regulation of the EndMT program. Furthermore, we will review the latest discoveries on EndMT, focusing on cardiovascular diseases, and in particular on its role in vascular calcification, pulmonary arterial hypertension, and organ fibrosis. Developmental Dynamics 247:492–508, 2018. © 2017 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Members of the myocardin family bind to the transcription factor serum response factor (SRF) and act as coactivators controlling genes of relevance for myogenic differentiation and motile function. Binding of SRF to DNA is mediated by genetic elements called CArG boxes, found often but not exclusively in muscle and growth controlling genes. Studies aimed at defining the full spectrum of these CArG elements in the genome (i.e. the CArGome) have in recent years, unveiled unexpected roles of the myocardin family proteins in lipid and glucose homeostasis. This coactivator family includes the protein myocardin (MYOCD), the myocardin-related transcription factors A and B (MRTF-A/MKL1 and MRTF-B/MKL2) and MASTR (MAMSTR). Here we discuss growing evidence that SRF-driven transcription is controlled by extracellular glucose through activation of the Rho-kinase pathway and actin polymerization. We also describe data showing that adipogenesis is influenced by MLK activity through actions upstream of peroxisome proliferator-activated receptor γ with consequences for whole body fat mass and insulin sensitivity. The recently demonstrated involvement of myocardin coactivators in the biogenesis of caveolae, Ω-shaped membrane invaginations of importance for lipid and glucose metabolism, is finally discussed. These novel roles of myocardin proteins may open the way for new unexplored strategies to combat metabolic diseases such as diabetes, which, at the current incidence, is expected to reach 333 million people worldwide by 2025. This review highlights newly discovered roles of myocardin-related transcription factors in lipid and glucose metabolism as well as novel insights into their well-established role as mediators of stretch-dependent effects in smooth muscle. As co-factors for serum response factor (SRF), MKLs regulates transcription of genes involved in the contractile function of smooth muscle cells. In addition to mechanical stimuli, this regulation has now been found to be promoted by extracellular glucose levels in smooth muscle. Recent reports also suggest that MKLs can regulate a subset of genes involved in the formation of lipid-rich invaginations in the cell membrane called caveolae. Finally, a potential role of MKLs in non-muscle cells has been discovered as they negatively influence adipocyte differentiation. [ABSTRACT FROM AUTHOR]

A new efficient method was developed to detect biotin in Antarctic krill by Vis-absorbance detection. DMF was used after chloroform pretreatment to extract biotin and two chromogenic methods were developed. The development system consisted of dichloromethane/dimethylcarbinol/methanol/glacial acetic acid (3:3:2:0.015, v/v/v/v). Samples were separated on precoated silica gel GF254 high-performance TLC plates. Densitometric analysis of biotin was carried out in the absorbance mode at 400 and 530 nm. The biotin content was determined to be 1.0948 ± 0.0097 and 1.1212 ± 0.0155 mg/g in Antarctic krill with the two chromogenic methods, which had no significant difference. [ABSTRACT FROM AUTHOR]

The article presents abstracts on several medical studies including relationship between ageing and dementia, effect of Ginkgo biloba extract on elderly people's cognitive function and olfactory impairment in Alzheimer's disease or Parkinson's disease.

An author index for the "European Journal of Neurology," for the 2012 issue is presented.

No absract. [ABSTRACT FROM AUTHOR]

No absract. [ABSTRACT FROM AUTHOR]

Background/purpose: Magnetic therapy has been popular for ages, but its therapeutic abilities remain to be demonstrated. We aimed to develop a homogeneous, stable dispersion of magnetic nanoparticles in a skin-care preparation, as a tool to analyze the biological and physiological effects of superficial magnetism in skin. Methods: SrFe12O19 nanoparticles were generated by ultrasound, dispersed in glycerol, stabilized in Dermud™ cream and permanently magnetized. The magnetic cream was applied on the epidermis of human skin organ cultures. The effects on UV-induced cell toxicity, apoptosis and inflammatory cytokine expression were analyzed. A clinical test was performed to check skin moisturization. Results: Nanomagnets were found to be homogenously and stably dispersed. After magnetization, the preparation generated a magnetic field of 1–2 G. Upon cream application, no cytotoxicity and no impairment of cellular vitality were found after 24 and 48 h, respectively. The anti-apoptotic and anti-inflammatory properties of Dermud™ were not modified, but its long-term effect on moisturization in vivo was slightly increased. Conclusion: Nanomagnetic Dermud™ cream can be used as a tool to analyze the biological effects of nanomagnets dispersed on the skin surface at the cellular and molecular levels, thus allowing to explore the possible therapeutic uses of superficial magnetism for skin care. [ABSTRACT FROM AUTHOR]

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In order to keep subscribers up-to-date with the latest developments in their field, John Wiley &Sons are providing a current awareness service in each issue of the journal. The bibliography contains newly published material in the field of phytochemical analysis. Each bibliography is divided into 13 sections: 1 Books, Reviews &Symposia; 2 General; 3 Nucleic Acids; 4 Amino Acids, Proteins &Enzymes; 5 Carbohydrates; 6 Lipids; 7 Secondary Products; 8 Growth Regulators; 9 Industrially-Important Products; 10 Toxins/Allergens; 11 Pigments; 12 Vitamins; 13 Others. Within each section, articles are listed in alphabetical order with respect to author. If, in the preceding period, no publications are located relevant to any one of these headings, that section will be omitted. [ABSTRACT FROM AUTHOR]