Fluxes of gaseous elemental mercury on a Mediterranean coastal grassland

Coastal rural areas can be a source of elemental mercury, but the potential influence of their topographic and climatic particularities on gaseous elemental mercury (GEM) fluxes have not been investigated extensively. In this study, gaseous elemental mercury was measured over Mediterranean coastal grassland located in Northern Greece from 2014 to 2015 and GEM fluxes were evaluated utilizing Monin–Obukhov similarity theory. The GEM fluxes ranged from –50.30 to 109.69 ng m−2 h−1 with a mean value equal to 10.50 ± 19.14 ng m−2 h−1. Concerning the peak events, with high positive and low negative GEM fluxes, those were recorded from the morning until the evening. Rain events were a strong contributing factor for enhanced GEM fluxes. The enhanced turbulent mixing under daytime unstable conditions led to greater evasion and positive GEM fluxes, while, during nighttime periods, the GEM evasion is lower, indicating the effect of atmospheric stability on GEM fluxes. The coastal grassland with its specific characteristics influences the GEM fluxes and this area could be characterized as a source of elemental mercury. This study is one of the rare efforts in the research community to estimate GEM fluxes in a coastal natural site based on aerodynamic gradient method

Publisher Correction: Chemotherapy-induced transposable elements activate MDA5 to enhance haematopoietic regeneration.

Funder: RCUK | Medical Research Council (MRC); doi: https://doi.org/10.13039/501100000265Funder: Max-Planck-Gesellschaft (Max Planck Society); doi: https://doi.org/10.13039/50110000418

Requirements Engineering (Τεχνικές επεξεργασίας απαιτήσεων χρηστών: κοινωνικές μέθοδοι)

Εθνικό Μετσόβιο Πολυτεχνείο--Μεταπτυχιακή Εργασία. Διεπιστημονικό-Διατμηματικό Πρόγραμμα Μεταπτυχιακών Σπουδών (Δ.Π.Μ.Σ.) “Μαθηματική Προτυποποίηση σε Σύγχρονες Τεχνολογίες στην Οικονομία

Ταυτοποίηση και Ανάλυση μη χαρτογραφημένων λειτουργικών περιοχών του ανθρώπινου γονιδιώματος

Η χαρτογράφηση του ανθρώπινου γονιδιώματος ολοκληρώθηκε μετά από μία δεκαετή προσπάθεια. Από τότε μέχρι σήμερα η πρόοδος της τεχνολογίας οδήγησε στην δημιουργία νέων μεθόδων αλληλούχησης, οι οποίες είναι ικανές να χαρτογραφήσουν το ανθρώπινο γονιδίωμα σε λιγότερο από μία ώρα. Σήμερα μπορούμε να διαβάσουμε το ανθρώπινο γονιδίωμα πολύ γρήγορα και με μεγάλη ακρίβεια. Ως αποτέλεσμα αυτής της εξέλιξης ο αριθμός των δεδομένων από τεχνολογίες νέας γενιάς αλληλούχησης DNA αυξάνεται εκθετικά από χρόνο σε χρόνο. Συνεχώς έρχονται στο προσκήνιο νέα δεδομένα και νέες ανακαλύψεις από την αξιοποίηση αυτών των δεδομένων. Ακόμα όμως υπάρχουν πολλά αναπάντητα ερωτήματα. Η μετα-ανάλυση τέτοιου είδους δεδομένων οδηγεί στον υπολογισμό ενός συγκεντρωτικού αποτελέσματος με μεγαλύτερη ακρίβεια και εγκυρότητα. Πολλά από τα δεδομένα που χρησιμοποιούνται σήμερα αντιμετωπίζουν ένα μεγάλο πρόβλημα. Η ταυτοποίηση των τμημάτων που χαρτογραφούνται δεν αντιστοιχούν σε κάποιο γνωστό τμήμα από το ανθρώπινο DNA. Πολλά από αυτά τα τμήματα προέρχονται από την ενσωμάτωση ξένων οργανισμών (ιών , βακτηρίων) αλλά και από τον σχηματισμό χιμαιρικών τμημάτων που δημιουργούνται από την συγκόλληση θραυσμάτων χρωματίνης, τα οποία μπορεί να προέρχονται είτε από την δράση ενζύμων, είτε από το σπάσιμο με τη χρήση υπερήχων. Από την μετα-ανάλυση των δεδομένων σε ανθρώπινα κύτταρα παρατηρήθηκε ότι περίπου ένα 5-30% των τμημάτων που παράγονται μέσω της τεχνικής νέας γενιάς αλληλούχησης δεν χαρτογραφούνται στο ανθρώπινο DNA. Στην παρούσα διπλωματική εργασία επιβεβαιώνεται η ύπαρξη μη χαρτογραφημένων τμημάτων στο ανθρώπινο DNA μετά από μετα-ανάλυση δεδομένων που έχουν προκύψει από την τεχνολογία αλληλούχησης του DNA νέας γενιάς, σε διαφορετικούς κυτταρικούς τύπους. Πολλά από αυτά τα τμήματα που ταυτοποιήθηκαν σε περισσότερες από μία κυτταρικές σειρές, είναι μεγέθους άνω των 1000 βάσεων και πιθανόν να σχετίζονται με την ενσωμάτωση ξένων οργανισμών στο ανθρώπινο DNA. Η χρήση δεδομένων από διαφορετικές τεχνικές όπως ChIP, RNA, DHS, FAIRE, για την συλλογή 6 μη χαρτογραφημένων DNA τμημάτων αποδεικνύουν ότι οι αλληλουχίες αυτές αποτελούν λειτουργικά τμήματα του ανθρώπινου γονιδιώματος, τα όποια πρέπει να χαρακτηριστούν και να αναλυθούν περαιτέρω. Η ταυτοποίηση κοινών κωδικών μορίων αλλά και λειτουργικών περιοχών στις 6 καρκινικές κυτταρικές σειρές A549, GM12878, HeLa, HepG2, HUVEC και K562 αλλά και στην εμβρυική κυτταρική σειρά HESC υποδηλώνουν την ύπαρξη κοινών ρυθμιστικών μηχανισμών, οι οποίοι μέχρι σήμερα δεν έχουν ταυτοποιηθεί.Human Genome Project (HPG) was completed after a ten-year effort. Since then, the technological progress has led to new methods of sequencing, which are able to sequence the human genome in less than an hour. Today we can sequence the human genome very quickly and with great accuracy. As a result of this technological bloom, the number of the data, generated from the Next Generation Sequencing technologies increase exponentially. Constantly new information and new discoveries come forward, from the use of these data, but there are still many unanswered questions. The meta-analysis of such data helps the scientists extract a more specific conclusion with greater sensitivity and specificity. Nowadays, analysis of the next generation sequencing has revealed a big issue. Sequencing techniques generated a great amount of data (DNA fragments) that do not correspond to the known reference genome. Many of these sequences may come from the integration of foreign DNA segments (viruses, bacteria), or from the formation of chimeric fragments, that are generated by the joining of random chromatin fragments, which are generated either or ultrasound fragmentation. Meta-analysis of next generation sequencing data in human cells revealed that a 5-30% of the sequenced DNA fragments are not mapped in the human DNA. In this dissertation we confirm the existence of “unmapped” DNA regions in the human genome. Our analysis revealed that most of these regions are more than 1000 bp length. Identification of such a big number of “unmapped” DNA sequences could be a result of the the incorporation of foreign DNA fragments in the human DNA. This result was consisted in all the human cell lines tested in this dissertation. By combining data from various next generation sequencing techniques such as ChIP-sequencing, RNA-sequencing, Faire-sequencing and DNaseI-sequencing we collected a great number of DNA segments that are considered to have a functional role. Identification of common coding molecules and functional domains in the six cancer cell lines, A549, GM12878, HeLa, HepG2, HUVEC, K562 and the fetal 8 cell line (human embryonic stem cell) hESC, indicate the presence of common regulatory mechanisms among those cell types, which have not been documented before. Data generated from our analysis should be further investigated and analyzed with “in vivo” models

The Role of Circular RNAs in DNA Damage Response and Repair

The role of non-coding RNA, and particularly of circular RNA, in the DNA damage response and repair network is underappreciated. Given the vital role of this network in preserving the genomic integrity and consequently cellular homeostasis, the constantly increasing numbers of discovered circular RNAs and the increasing implication of these molecules in the function of this network unravel a new important field that may open new therapeutic opportunities, but also require detailed investigation. Circular RNAs (circRNA) comprise a distinct class of non-coding RNAs that are abundantly expressed in the cell. CircRNAs have the capacity to regulate gene expression by interacting with regulatory proteins and/or other classes of RNAs. While a vast number of circRNAs have been discovered, the majority still remains poorly characterized. Particularly, there is no detailed information on the identity and functional role of circRNAs that are transcribed from genes encoding components of the DNA damage response and repair (DDRR) network. In this article, we not only review the available published information on DDRR-related circRNAs, but also conduct a bioinformatic analysis on data obtained from public repositories to uncover deposited, yet uncharacterized circRNAs derived from components of the DDRR network. Finally, we interrogate for potential targets that are regulated by this class of molecules and look into potential functional implications

Evaluation of senescent cells in intervertebral discs by lipofuscin staining

Intervertebral disc (IVD) degeneration is considered an important contributor of low back pain, a major age related disease. Interestingly, an unprecedented high number of senescent cells has been reported in aged and degenerated IVDs, most probably affecting tissue homeostasis. In previous studies classical markers of cellular senescence have been used, such as SA-beta-gal staining or p16(Ink4a) expression. Aim of the presented study was a reevaluation of the number of senescent IVD cells by using a newly established staining procedure for lipofuscin, based on a Sudan Black-B analogue (GL13), which can be used in fresh, as well as in fixed and embedded tissues. In cultures of senescent rat and human IVD cells both SA-beta-gal and GL13 gave similar percentages of senescent cells. Similarly, in fresh tissues from old rats the ratios of senescent cells were high with both detection procedures. Finally, in formalin-fixed and paraffin-embedded tissues from humans, a significant increased number of GL13-positive cells was found in herniated tissues, as compared to apparently normal ones, while similar numbers of p16(Ink4a)-positive cells were observed. These data confirm the significantly enhanced number of senescent cells in aged and degenerated IVDs, most probably contributing to the degeneration of this tissue

A metabolic interplay coordinated by HLX regulates myeloid differentiation and AML through partly overlapping pathways

The H2.0-like homeobox transcription factor (HLX) regulates hematopoietic differentiation and is overexpressed in Acute Myeloid Leukemia (AML), but the mechanisms underlying these functions remain unclear. We demonstrate here that HLX overexpression leads to a myeloid differentiation block both in zebrafish and human hematopoietic stem and progenitor cells (HSPCs). We show that HLX overexpression leads to downregulation of genes encoding electron transport chain (ETC) components and upregulation of PPARδ gene expression in zebrafish and human HSPCs. HLX overexpression also results in AMPK activation. Pharmacological modulation of PPARδ signaling relieves the HLX-induced myeloid differentiation block and rescues HSPC loss upon HLX knockdown but it has no effect on AML cell lines. In contrast, AMPK inhibition results in reduced viability of AML cell lines, but minimally affects myeloid progenitors. This newly described role of HLX in regulating the metabolic state of hematopoietic cells may have important therapeutic implications.publishe

Angiopoietin-2 Primes Infection-Induced Preterm Delivery

Current knowledge on the participation of angiopoietin-2 (Ang-2) in the inflammatory process and on the importance of bacterial endotoxins (LPS) in the induction of preterm delivery (PTD) led us to investigate the role of Ang-2/LPS interplay in the pathogenesis of PTD. At a first stage, Ang-2 was measured at the end of the first trimester of pregnancy in the serum of 50 women who delivered prematurely; of 88 women well-matched for age and parity who delivered full-term; and of 20 non-pregnant healthy women. Ang-2 was greater in pregnant than in non-pregnant women. The time until delivery was shorter among those with Ang-2 greater than 4 ng/ml (odds ratio for delivery until week 34; p: 0.040). To further investigate the role of Ang-2 for PTD, an experimental model of PTD induced by the intraperitoneal injection of LPS in mice was used. Ang-2 was administered intraperitoneally before LPS on day 14 of pregnancy. When Ang-2 was administered before the LPS diluent, all mice delivered full-term. However, administration of Ang-2 prior LPS accelerated further the time until delivery. Sacrifice experiments showed that the effect of Ang-2 was accompanied by decrease of the penetration of Evans Blue in the embryos and by increase of its penetration in maternal tissues. In parallel, the concentration of tumour necrosis factor-alpha in the maternal circulation, in fetal tissues and in the placentas was significantly decreased. Results indicate that Ang-2 accelerated the phenomena of PTD induced by LPS. This is related with deprivation of fetal perfusion