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JTRF2020 is the latest TRF solution computed at JPL by assimilating frame input data submitted by the IVS, IGS, ILRS, and IDS for ITRF2020. JTRF2020, determined with a square-root information filter and Dyer-McReynolds s moother algorithm, adopts a time-series based representation: Its daily time series determined from observations of a multi-technique space-geodetic network of 931 stations describe, through their Cartesian coordinates, the deformation of solid Earth as a function of time. Such coordinates are inherently expressed in Earth’s Center of Mass as sensed by SLR and give access to the quasi-instantaneous scale implied by the underlying frame. JTRF2020, like its predecessor JTRF2014, traditionally adopts a scale relying on VLBI and SLR observations only. In this presentation, we will describe the process we adopted to define and construct JTRF2020, and will discuss metrics constructed to assess the frame quality., The 28th IUGG General Assembly (IUGG2023) (Berlin 2023)

Academia, Industry and Government are investigating the reliability to use the real time kinematic (RTK) Global Navigation Satellite System (GNSS) techniques for centimetre level positioning of many existing and emerging applications. These include for instance mobile mapping and airborne laser scanning systems. The classical RTK methodology allows for an operational distance between the reference station and the user, within a range of 10-15 kilometres, due to the effect of correlation of some GNSS errors which tend to increase with distance. The adoption of a network-based RTK (NRTK) allow to extend centimetric level positioning within continuously operating reference station network (CORS) with separation distance up to 70 kilometres. One of the research aim was to evaluate the positional accuracy of the GNSS NRTK for mobile mapping applications. In order to understand the potentiality and the limitations of this methodology a testing procedure was designed using the BO-POS Network, established in 2003 in an area within Emila-Romagna, Marche e Toscana. From an operational point of view, a double antenna system was mounted on board of a vehicle also equipped with three dual frequency receivers capable of NRTK positioning. In order to investigate the GNSS NRTK positional accuracy for mobile mapping system applications a least square-based algorithm was developed to determine a reference trajectory. This paper describes the Bologna CORS network, the testing procedure adopted and details the algorithm based on a constrained least square adjustment of the phase centres’ coordinates of the 2 antennae. The positional accuracy of the NRTK path will be finally assessed by comparing the results of the NRTK trajectory with post processed adjusted one.

We examined the effect of estrogens on mitogen-activated protein kinase (MAPK) in EPN cells, a line of epithelial cells derived from human normal prostate. 17beta-estradiol (E2) caused a rapid and transient activation of MAPK (ERK1/2) within 5 min. This effect was counteracted by the anti-estrogen ICI 182-780 and by MEK inhibitor PD098059. The activation of ERK1/2 through 17beta-estradiol triggered simultaneous association of endogenous androgen receptor, estrogen receptor alpha and Src. In addition, E2 stimulated the proliferation of EPN cells, suggesting that the formation of the ternary complex and the consequent activation of ERKs are implicated in the mechanism regulating proliferation of epithelial prostate cells.

Estrogen treatment of MCF-7 cells grown in serum-free medium induced a modification of the intracellular distribution of p53 protein. Western blot analysis and immunofluorescence staining showed that p53 was localized in the nucleus of untreated cell and that after 48 h of hormone treatment, it was mostly localized in the cytoplasm. This effect was blocked by the antiestrogen ICI182,780. Intracellular redistribution of p53 was correlated to a reduced expression of the WAF1/CIP1 gene product and to the presence of degradation fragments of p53 in the cytosol. Estradiol treatment prevented the growth inhibition induced by oligonucleotide transfection, simulating DNA damage. This observation indicated that the wild-type p53 gene product present in the MCF-7 cell could be inactivated by estradiol through nuclear exclusion to permit the cyclin-dependent phosphorylation events leading to the G1-S transition. In addition, the estradiol-induced inactivation of p53 could be involved in the tumorigenesis of estrogen-dependent neoplasm.

Tumors arise from single cells that develop into large populations sharing a series of genetic alterations. The single phenotypic feature that best characterizes a transformed cell is its ability to proliferate indefinitely when left undisturbed.1 The recognition of specific genes that modulate proliferation, has led to studies on the cell cycle.2 Homeostasis has a great importance in the development of tumors and is regulated by a balance among proliferation, the arrest of growth and programmed death (apoptosis).

The observatory of Medicina (Italy) hosts a co-location between GPS and VLBI, whose eccentricity vector has been re-measured several times once since 2001. As a result, the co-located site is now provided with a series of nearly annual local tie vectors produced by means of terrestrial and GPS-based observations. This work aims at summarising the results of a systematic analysis of the whole set of local ties produced so far and highlighting at the same time their temporal evolution. As such, the application of algebraic tools focussed on deformation detections can benefit the analysis of the local tie temporal variations and at the same time that one of the “geodynamical” stability of the co-located site. Nevertheless, just like in any other problem of deformation detection, such an analysis would ask for a reproducible local datum, according to which the relative displacements among the points have to be referred to. The application of algebraic projection theory to the local tie oriented-networks will be carried out in order to select a “common and fully reproducible” datum onto which the network solutions will be projected and discuss possible displacements within the re-measured networks.

RNA-binding proteins are crucial to the function of coding and non-coding RNAs. The disruption of RNA–protein interactions is involved in many different pathological states. Several computational and experimental strategies have been developed to identify protein binders of selected RNA molecules. Amongst these, ‘in cell’ hybridization methods represent the gold standard in the field because they are designed to reveal the proteins bound to specific RNAs in a cellular context. Here, we compare the technical features of different ‘in cell’ hybridization approaches with a focus on their advantages, limitations, and current and potential future applications.

PRDM12 is a member of the PRDI-BF1 (positive regulatory domain I-binding factor 1) homologous domain (PRDM)-containing protein family, a subfamily of Kruppel-like zinc finger proteins, controlling key processes in the development of cancer. PRDM12 is expressed in a spatio-temporal manner in neuronal systems where it exerts multiple functions. PRDM12 is essential for the neurogenesis initiation and activation of a cascade of downstream pro-neuronal transcription factors in the nociceptive lineage. PRDM12 inactivation, indeed, results in a complete absence of the nociceptive lineage, which is essential for pain perception. Additionally, PRDM12 contributes to the early establishment of anorexigenic neuron identity and the maintenance of high expression levels of pro-opiomelanocortin, which impacts on the program bodyweight homeostasis. PRDMs are commonly involved in cancer, where they act as oncogenes/tumor suppressors in a “Yin and Yang” manner. PRDM12 is not usually expressed in adult normal tissues but its expression is re-activated in several cancer types. However, little information is currently available on PRDM12 expression in cancers and its mechanism of action has not been thoroughly described. In this review, we summarize the recent findings regarding PRDM12 by focusing on four main biological processes: neurogenesis, pain perception, oncogenesis and cell metabolism. Moreover, we wish to highlight the importance of future studies focusing on the PRDM12 signaling pathway(s) and its role in cancer onset and progression.

The PR/SET domain family (PRDM) comprise a family of genes whose protein products share a conserved N-terminal PR [PRDI-BF1 (positive regulatory domain I-binding factor 1) and RIZ1 (retinoblastoma protein-interacting zinc finger gene 1)] homologous domain structurally and functionally similar to the catalytic SET [Su(var)3-9, enhancer-of-zeste and trithorax] domain of histone methyltransferases (HMTs). These genes are involved in epigenetic regulation of gene expression through their intrinsic HMTase activity or via interactions with other chromatin modifying enzymes. In this way they control a broad spectrum of biological processes, including proliferation and differentiation control, cell cycle progression, and maintenance of immune cell homeostasis. In cancer, tumor-specific dysfunctions of PRDM genes alter their expression by genetic and/or epigenetic modifications. A common characteristic of most PRDM genes is to encode for two main molecular variants with or without the PR domain. They are generated by either alternative splicing or alternative use of different promoters and play opposite roles, particularly in cancer where their imbalance can be often observed. In this scenario, PRDM proteins are involved in cancer onset, invasion, and metastasis and their altered expression is related to poor prognosis and clinical outcome. These functions strongly suggest their potential use in cancer management as diagnostic or prognostic tools and as new targets of therapeutic intervention.

Prostate cancer is one of the most commonly diagnosed cancers in men, and androgen deprivation therapy still represents the primary treatment for prostate cancer patients. This approach, however, frequently fails and patients develop castration-resistant prostate cancer, which is almost untreatable. Cancer cells are characterized by a hierarchical organization, and stem/progenitor cells are endowed with tumor-initiating activity. Accumulating evidence indicates that prostate cancer stem cells lack the androgen receptor and are, indeed, resistant to androgen deprivation therapy. In contrast, these cells express classical (α and/or ß) and novel (GPR30) estrogen receptors, which may represent new putative targets in prostate cancer treatment. In the present review, we discuss the still-debated mechanisms, both genomic and non-genomic, by which androgen and estradiol receptors (classical and novel) mediate the hormonal control of prostate cell stemness, transformation, and the continued growth of prostate cancer. Recent preclinical and clinical findings obtained using new androgen receptor antagonists, anti-estrogens, or compounds such as enhancers of androgen receptor degradation and peptides inhibiting non-genomic androgen functions are also presented. These new drugs will likely lead to significant advances in prostate cancer therapy.

PRDM2/RIZ is a member of a superfamily of histone/protein methyltransferases (PRDMs), which are characterized by the conserved N-terminal PR domain, with methyltransferase activity and zinc finger arrays at the C-terminus. Similar to other family members, two main protein types, known as RIZ1 and RIZ2, are produced from the PRDM2 locus differing by the presence or absence of the PR domain. The imbalance in their respective amounts may be an important cause of malignancy, with the PR-positive isoform commonly lost or downregulated and the PR-negative isoform always being present at higher levels in cancer cells. Interestingly, the RIZ1 isoform also represents an important target of estradiol action downstream of the interaction with hormone receptor. Furthermore, the imbalance between the two products could also be a molecular basis for other human diseases. Thus, understanding the molecular mechanisms underlying PRDM2 function could be useful in the pathophysiological context, with a potential to exploit this information in clinical practice. PRDM2/RIZ is a member of a superfamily of histone/protein methyltransferases (PRDMs), which are characterized by the conserved N-terminal PR domain, with methyltransferase activity and zinc finger arrays at the C-terminus. Similar to other family members, two main protein types, known as RIZ1 and RIZ2, are produced from the PRDM2 locus differing by the presence or absence of the PR domain. The imbalance in their respective amounts may be an important cause of malignancy, with the PR-positive isoform commonly lost or downregulated and the PR-negative isoform always being present at higher levels in cancer cells. Interestingly, the RIZ1 isoform also represents an important target of estradiol action downstream of the interaction with hormone receptor. Furthermore, the imbalance between the two products could also be a molecular basis for other human diseases. Thus, understanding the molecular mechanisms underlying PRDM2 function could be useful in the pathophysiological context, with a potential to exploit this information in clinical practice.

The very long baseline interferometry (VLBI) antenna in Medicina (Italy) is a 32-m AZ-EL mount that was surveyed several times, adopting an indirect method, for the purpose of estimating the eccentricity vector between the co-located VLBI and Global Positioning System instruments. In order to fulfill this task, targets were located in different parts of the telescope’s structure. Triangulation and trilateration on the targets highlight a consistent amount of deformation that biases the estimate of the instrument’s reference point up to 1 cm, depending on the targets’ locations. Therefore, whenever the estimation of accurate local ties is needed, it is critical to take into consideration the action of gravity on the structure. Furthermore, deformations induced by gravity on VLBI telescopes may modify the length of the path travelled by the incoming radio signal to a non-negligible extent. As a consequence, differently from what it is usually assumed, the relative distance of the feed horn’s phase centre with respect to the elevation axis may vary, depending on the telescope’s pointing elevation. The Medicina telescope’s signal path variation ΔL increases by a magnitude of approximately 2 cm, as the pointing elevation changes from horizon to zenith; it is described by an elevation-dependent second-order polynomial function computed as, according to Clark and Thomsen (Techical report, 100696, NASA, Greenbelt, 1988), a linear combination of three terms: receiver displacement ΔR, primary reflector’s vertex displacement ΔV and focal length variations ΔF. ΔL was investigated with a combination of terrestrial triangulation and trilateration, laser scanning and a finite element model of the antenna. The antenna gain (or auto-focus curve) ΔG is routinely determined through astronomical observations. A surprisingly accurate reproduction of ΔG can be obtained with a combination of ΔV, ΔF and ΔR.