TY - JOUR AB - Preterm birth poses a global challenge with a continuously increasing disease burden during the last decades. Advances in understanding the etiopathogenesis did not lead to a reduction of prematurely born infants so far. A balanced development of the host microbiome in early life is key for the maturation of the immune system and many other physiological functions. With the tremendous progress in new diagnostic possibilities, the contribution of microbiota changes to preterm birth and the acute and long-term sequelae of prematurity have come into the research focus. This review summarizes the latest advances in the understanding of microbiomes in the amniotic cavity and the female lower genital tract and how changes in microbiota structures contribute to preterm delivery. The exhibition of these highly vulnerable infants to the hostile environment in the neonatal intensive care unit necessarily entails the rapid colonization with a nonbalanced microbiome in a situation where the organism is still very prone and at an early stage of development. The global research efforts to decipher pathologic changes will pave the way to new pre- and postnatal therapeutic concepts. AU - Staude, B.* AU - Oehmke, F.* AU - Lauer, T.* AU - Behnke, J.* AU - Göpel, W.* AU - Schloter, M. AU - Schulz, H. AU - Krauss-Etschmann, S.* AU - Ehrhardt, H.* C1 - 54609 C2 - 45694 CY - Adam House, 3rd Flr, 1 Fitzroy Sq, London, W1t 5hf, England TI - The microbiome and preterm birth: A change in paradigm with profound implications for pathophysiologic concepts and novel therapeutic strategies. JO - Biomed Res. Int. VL - 2018 PB - Hindawi Ltd PY - 2018 SN - 2314-6133 ER - TY - JOUR AB - In vertebrates, neurotrophic signaling plays an important role in neuronal development, neural circuit formation, and neuronal plasticity, but its evolutionary origin remains obscure. We found and validated nucleotide sequences encoding putative neurotrophic ligands (neurotrophin, NT) and receptors (Trk and p75) in two annelids, Platynereis dumerilii (Errantia) and Capitella teleta (Sedentaria, for which some sequences were found recently by Wilson, 2009). Predicted protein sequences and structures of Platynereis neurotrophic molecules reveal a high degree of conservation with the vertebrate counterparts; some amino acids signatures present in the annelid Trk sequences are absent in the basal chordate amphioxus, reflecting secondary loss in the cephalochordate lineage. In addition, expression analysis of NT, Trk, and p75 during Platynereis development by whole-mount mRNA in situ hybridization supports a role of these molecules in nervous system and circuit development. These annelid data corroborate the hypothesis that the neurotrophic signaling and its involvement in shaping neural networks predate the protostome-deuterostome split and were present in bilaterian ancestors. AU - Lauri, A. AU - Bertucci, P.* AU - Arendt, D.* C1 - 48393 C2 - 41021 CY - New York TI - Neurotrophin, p75, and Trk signaling module in the developing nervous system of the marine annelid Platynereis dumerilii. JO - Biomed Res. Int. VL - 2016 PB - Hindawi Publishing Corp PY - 2016 SN - 2314-6133 ER - TY - JOUR AU - Carvalho, L.A.* AU - Gerdes, J.M. AU - Strell, C.* AU - Wallace, G.R.* AU - Martins, J.O.* C1 - 46641 C2 - 37654 CY - New York TI - Interplay between the endocrine system and immune cells. JO - Biomed Res. Int. VL - 2015 PB - Hindawi Publishing Corporation PY - 2015 SN - 2314-6133 ER - TY - JOUR AB - Despite a number of prospective registries conducted in past years, the current epidemiology of interstitial lung diseases (ILD) is still not well defined, particularly regarding the prevalence and incidence, their management, healthcare utilisation needs, and healthcare-associated costs. To address these issues in Germany, a new prospective ILD registry, “Exploring Clinical and Epidemiological Characteristics of Interstitial Lung Diseases” (EXCITING-ILD), is being conducted by the German Centre for Lung Research in association with ambulatory, inpatient, scientific pulmonology organisations and patient support groups. This multicentre, noninterventional, prospective, and observational ILD registry aims to collect comprehensive and validated data from all healthcare institutions on the incidence, prevalence, characteristics, management, and outcomes regarding all ILD presentations in the real-world setting. Specifically, this registry will collect demographic data, disease-related data such as ILD subtype, treatments, diagnostic procedures (e.g., HRCT, surgical lung biopsy), risk factors (e.g., familial ILD), significant comorbidities, ILD managements, and disease outcomes as well as healthcare resource consumption. The EXCITING-ILD registry will include in-patient and out-patient ILD healthcare facilities in more than 100 sites. In summary, this registry will document comprehensive and current epidemiological data as well as important health economic data for ILDs in Germany. AU - Kreuter, M.* AU - Herth, F.* AU - Wacker, M. AU - Leidl, R. AU - Hellmann, A.* AU - Pfeifer, M.* AU - Behr, J.* AU - Witt, S. AU - Kauschka, D.* AU - Mall, M.* AU - Günther, A.* AU - Markart, P.* C1 - 47100 C2 - 39169 TI - Exploring clinical and epidemiological characteristics of interstitial lung diseases: Rationale, aims, and design of a nationwide prospective registry - the EXCITING-ILD registry. JO - Biomed Res. Int. VL - 2015 PY - 2015 SN - 2314-6133 ER - TY - JOUR AB - The number of RNA-Seq studies has grown in recent years. The design of RNA-Seq studies varies from very simple (e.g., two-condition case-control) to very complicated (e.g., time series involving multiple samples at each time point with separate drug treatments). Most of these publically available RNA-Seq studies are deposited in NCBI databases, but their metadata are scattered throughout four different databases: Sequence Read Archive (SRA), Biosample, Bioprojects, and Gene Expression Omnibus (GEO). Although the NCBI web interface is able to provide all of the metadata information, it often requires significant effort to retrieve study- or project-level information by traversing through multiple hyperlinks and going to another page. Moreover, project- and study-level metadata lack manual or automatic curation by categories, such as disease type, time series, case-control, or replicate type, which are vital to comprehending any RNA-Seq study. Here we describe "MetaRNA-Seq," a new tool for interactively browsing, searching, and annotating RNA-Seq metadata with the capability of semiautomatic curation at the study level. AU - Kumar, P.* AU - Halama, A.* AU - Hayat, S.* AU - Billing, A.M.* AU - Gupta, M.* AU - Yousri, N.A.* AU - Smith, G.M.* AU - Suhre, K. C1 - 46801 C2 - 37846 CY - New York TI - MetaRNA-Seq: An interactive tool to browse and annotate metadata from RNA-Seq studies. JO - Biomed Res. Int. VL - 2015 PB - Hindawi Publishing Corporation PY - 2015 SN - 2314-6133 ER - TY - JOUR AB - Progression of chronic kidney disease (CKD) is characterized by deposition of extracellular matrix. This is an irreversible process that leads to tubulointerstitial fibrosis and finally loss of kidney function. Wnt/beta-catenin pathway was reported to be aberrantly activated in the progressive damage associated with chronic organ failure. Extensive renal ablation is an experimental model widely used to gain insight into the mechanisms responsible for the development of CKD, but it was not evaluated for Wnt/beta-catenin pathway. This study aimed to elucidate if the rat 5/6 renal mass reduction model (RMR) is a good model for the Wnt/beta-catenin activation and possible next modulation. RMR model was evaluated at 12 and 18 weeks after the surgery, when CKD is close to end-stage kidney disease demonstrated by molecular and histological studies. Wnt pathway components were analyzed at mRNA and protein level. Our results demonstrate that Wnt pathway is active by increase of beta-catenin at mRNA level and nuclear translocation in tubular epithelium as well as some target genes. These results validate the RMR model for future modulation of Wnt pathway, starting at shorter time after the surgery. AU - Banon-Maneus, E. AU - Rovira, J.* AU - Ramirez-Bajo, M.J.* AU - Moya-Rull, D.* AU - Hierro-Garcia, N.* AU - Takenaka, S. AU - Diekmann, F.* AU - Eickelberg, O. AU - Königshoff, M. AU - Campistol, J.M.* C1 - 31755 C2 - 34720 CY - New York TI - Wnt pathway activation in long term remnant rat model. JO - Biomed Res. Int. VL - 2014 PB - Hindawi Publishing Corporation PY - 2014 SN - 2314-6133 ER - TY - JOUR AB - Oxidative stress resulting from an increased amount of reactive oxygen species and an imbalance between oxidants and antioxidants plays an important role in the pathogenesis of asthma. The present study tested the hypothesis that genetic susceptibility to allergic and nonallergic variants of asthma is determined by complex interactions between genes encoding antioxidant defense enzymes (ADE). We carried out a comprehensive analysis of the associations between adult asthma and 46 single nucleotide polymorphisms of 34 ADE genes and 12 other candidate genes of asthma in Russian population using set association analysis and multifactor dimensionality reduction approaches. We found for the first time epistatic interactions between ADE genes underlying asthma susceptibility and the genetic heterogeneity between allergic and nonallergic variants of the disease. We identified GSR (glutathione reductase) and PON2 (paraoxonase 2) as novel candidate genes for asthma susceptibility. We observed gender-specific effects of ADE genes on the risk of asthma. The results of the study demonstrate complexity and diversity of interactions between genes involved in oxidative stress underlying susceptibility to allergic and nonallergic asthma. AU - Polonikov, A.V.* AU - Ivanov, V.P.* AU - Bogomazov, A.D.* AU - Freidin, M.B.* AU - Illig, T. AU - Solodilova, M.A.* C1 - 31543 C2 - 34548 CY - New York TI - Antioxidant defense enzyme genes and asthma susceptibility: Gender-specific effects and heterogeneity in gene-gene interactions between pathogenetic variants of the disease. JO - Biomed Res. Int. VL - 2014 PB - Hindawi Publishing Corporation PY - 2014 SN - 2314-6133 ER -