hbim in a semantic 3d gis database

Abstract. This work describes the different attempts and the consequent results derived from the integration of an HBIM model into an already structured spatial database (DB) and its 3D visualisation in a GIS project.This study is connected to the European ResCult (Increasing Resilience of Cultural Heritage) project where a DB for multiscale analyses was defined. To test the methodology proposed, the case study of Santa Maria dei Miracoli church in Venice was chosen since it represents a complex architectural heritage piece in a risk zone, it has been subject to a vast restoration intervention in the recent past but a digital documentation and model concerning it was missing.The 3D model of the church was structured in Revit as a HBIM, with the association of different kind of information and data related to the architectural elements by means of 'shared parameters' and 'system families'. This procedure allows to reach an even higher Level of Detail (LOD4), but lead to some issues related to the semantic and software interoperability. To solve these problems the existing DB for the resilience of cultural heritage was extended adding a new entity representing the architectural elements designed in the BIM project.The aim of the test is to understand how the data and attributes inserted in the HBIM are converted and handled when dealing with a GIS DB, stepping from the IFC to the CityGML standard, through the FME software.</p

Reversible switch from hemoglobin A to C in sheep and recovery from anemia following experimental infection with Anaplasma ovis

Anemia causes a change in the type of circulating hemoglobin (Hb) in sheep carrying the βA-globin haplotype, where the Hb A is replaced with Hb C, unlike Hb B. The effect of the substitution of Hb A with Hb C on the recovery from anemia was investigated by comparing the hematological picture of sheep, following experimental infection with Anaplasma ovis. The blood values were obtained from 3 AB and 3 BB Hb sheep after the development of the disease where anemia is a pathognomonic symptom. The expression of the silent gene encoding for Hb C was detected by isoelectric focusing and quantified by high performance liquid chromatography. Both Hb AB genotype and Hb C occurrence were involved in the lower recovery from anemia in the trial

Economic impact of remote monitoring on ordinary follow-up of implantable cardioverter defibrillators as compared with conventional in-hospital visits: a single-center prospective and randomized study

Few data are available on actual follow-up costs of remote monitoring (RM) of implantable defibrillators (ICD). Our study aimed at assessing current direct costs of 1-year ICD follow-up based on RM compared with conventional quarterly in-hospital follow-ups. Methods and results Patients (N=233) with indications for ICD were consecutively recruited and randomized at implant to be followed up for 1 year with standard quarterly inhospital visits or by RM with one in-hospital visit at 12 months, unless additional in-hospital visits were required due to specific patient conditions or RM alarms. Costs were calculated distinguishing between provider and patient costs, excluding RM device and service cost. The frequency of scheduled in-hospital visits was lower in the RM group than in the control arm. Follow-up required 47 min per patient/year in the RM arm versus 86 min in the control arm (p=0.03) for involved physicians, generating cost estimates for the provider of USD 45 and USD 83 per patient/- year, respectively. Costs for nurses were comparable. Overall, the costs associated with RM and standard follow-up were USD 103±27 and 154±21 per patient/year, respectively (p=0.01). RM was cost-saving for the patients: USD 97±121 per patient/year in the RM group versus 287± 160 per patient/year (p=0.0001). Conclusion The time spent by the hospital staff was significantly reduced in the RM group. If the costs for the device and service are not charged to patients or the provider, patients could save about USD 190 per patient/year while the hospital could save USD 51 per patient/year

Somatostatin: A Novel Substrate and a Modulator of Insulin-Degrading Enzyme Activity

Insulin-degrading enzyme (IDE) is an interesting pharmacological target for Alzheimer's disease (AD), since it hydrolyzes beta-amyloid, producing non-neurotoxic fragments. It has also been shown that the somatostatin level reduction is a pathological feature of AD and that it regulates the neprilysin activity toward beta-amyloid. In this work, we report for the first time that IDE is able to hydrolyze somatostatin [k(cat) (s(-1)) = 0.38 (+/-0.05); K-m (M) = 7.5 (+/-0.9) x 10(-6)] at the Phe6-Phe7 amino acid bond. On the other hand, somatostatin modulates IDE activity, enhancing the enzymatic cleavage of a novel fluorogenic beta-amyloid through a decrease of the K-m toward this substrate, which corresponds to the 10-25 amino acid sequence of the A beta(1-40). Circular dichroism spectroscopy and surface plasmon resonance imaging experiments show that somatostatin binding to IDE brings about a concentration-dependent structural change of the secondary and tertiary structure(s) of the enzyme, revealing two possible binding sites. The higher affinity binding site disappears upon inactivation of IDE by ethylenediaminetetra acetic acid, which chelates, the catalytic Zn2+ ion. As a whole, these features suggest that the modulatory effect is due to an allosteric mechanism: somatostatin binding to the active site of one IDE subunit (where somatostatin is cleaved) induces an enhancement of IDE proteolytic activity toward fluorogenic beta-amyloid by another subunit. Therefore, this investigation on IDE-somatostatin interaction contributes to a more exhaustive knowledge about the functional and structural aspects of IDE and its pathophysiological implications in the amyloid deposition and somatostatin homeostasis in the brain. (C) 2008 Elsevier Ltd. All rights reserved

The imaging properties of the Gas Pixel Detector as a focal plane polarimeter

X-rays are particularly suited to probe the physics of extreme objects. However, despite the enormous improvements of X-ray Astronomy in imaging, spectroscopy and timing, polarimetry remains largely unexplored. We propose the photoelectric polarimeter Gas Pixel Detector (GPD) as an instrument candidate to fill the gap of more than thirty years of lack of measurements. The GPD, in the focus of a telescope, will increase the sensitivity of orders of magnitude. Moreover, since it can measure the energy, the position, the arrival time and the polarization angle of every single photon, allows to perform polarimetry of subsets of data singled out from the spectrum, the light curve or the image of source. The GPD has an intrinsic very fine imaging capability and in this work we report on the calibration campaign carried out in 2012 at the PANTER X-ray test facility of the Max-Planck-Institut f\"ur extraterrestrische Physik of Garching (Germany) in which, for the first time, we coupled it to a JET-X optics module with a focal length of 3.5 m and an angular resolution of 18 arcsec at 4.5 keV. This configuration was proposed in 2012 aboard the X-ray Imaging Polarimetry Explorer (XIPE) in response to the ESA call for a small mission. We derived the imaging and polarimetric performance for extended sources like Pulsar Wind Nebulae and Supernova Remnants as case studies for the XIPE configuration, discussing also possible improvements by coupling the detector with advanced optics, having finer angular resolution and larger effective area, to study with more details extended objects.Comment: Accepted for publication in The Astrophysical Journal Supplemen

Probing the interaction interface of the GADD45β/MKK7 and MKK7/DTP3 complexes by chemical cross-linking mass spectrometry

GADD45β is selectively and constitutively expressed in Multiple Myeloma cells, and this expression correlates with an unfavourable clinical outcome. GADD45β physically interacts with the JNK kinase, MKK7, inhibiting its activity to enable the survival of cancer cells. DTP3 is a small peptide inhibitor of the GADD45β/MKK7 complex and is able to restore MKK7/JNK activation, thereby promoting selective cell death of GADD45β-overexpressing cancer cells. Enzymatic MS foot-printing and diazirine-based chemical cross-linking MS (CX-MS) strategies were applied to study the interactions between GADD45β and MKK7 kinase domain (MKK7_KD) and between DTP3 and MKK7_KD. Our data show that the binding between GADD45β and MKK7 largely occurs between GADD45β loop 2 (region 103–117) and the kinase enzymatic pocket. We also show that DTP3 interferes with this GADD45β/MKK7 interaction by contacting the MKK7 peptides, 113–136 and 259–274. Accordingly, an MKK7_KD Δ(101–136) variant lacking Trp135 did not produce a fluorescence quenching effect upon the binding of DTP3. The assessment of the interaction between GADD45β and MKK7 and the elucidation of the recognition surfaces between DTP3 and MKK7 significantly advance the understanding of the mechanism underlying the inhibition of the GADD45β/MKK7 interaction by DTP3 and pave the way to the design of small-molecule DTP3 analogues

RIP1-HAT1-SirT complex identification and targeting in treatment and prevention of cancer

Purpose: Alteration in cell death is a hallmark of cancer. A functional role regulating survival, apoptosis, and necroptosis has been attributed to RIP1/3 complexes.Experimental Design: We have investigated the role of RIP1 and the effects of MC2494 in cell death induction, using different methods as flow cytometry, transcriptome analysis, immunoprecipitation, enzymatic assays, transfections, mutagenesis, and in vivo studies with different mice models.Results: Here, we show that RIP1 is highly expressed in cancer, and we define a novel RIP1/3-SIRT1/2-HAT1/4 complex. Mass spectrometry identified five acetylations in the kinase and death domain of RIP1. The novel characterized pan-SIRT inhibitor, MC2494, increases RIP1 acetylation at two additional sites in the death domain. Mutagenesis of the acetylated lysine decreases RIP1-dependent cell death, suggesting a role for acetylation of the RIP1 complex in cell death modulation. Accordingly, MC2494 displays tumor-selective potential in vitro, in leukemic blasts ex vivo, and in vivo in both xenograft and allograft cancer models. Mechanistically, MC2494 induces bona fide tumor-restricted acetylated RIP1/caspase-8-mediated apoptosis. Excitingly, MC2494 displays tumor-preventive activity by blocking 7,12-dimethylbenz(α)anthracene-induced mammary gland hyperproliferation in vivoConclusions: These preventive features might prove useful in patients who may benefit from a recurrence-preventive approach with low toxicity during follow-up phases and in cases of established cancer predisposition. Thus, targeting the newly identified RIP1 complex may represent an attractive novel paradigm in cancer treatment and prevention

Contact-force monitoring increases accuracy of right ventricular voltage mapping avoiding “false scar” detection in patients with no evidence of structural heart disease

Purpose: Electroanatomical mapping (EAM) could increase cardiac magnetic resonance imaging (CMR) sensitivity in detecting ventricular scar. Possible bias may be scar over-estimation due to inadequate tissue contact. Aim of the study is to evaluate contact-force monitoring influence during EAM, in patients with idiopathic right ventricular arrhythmias. Methods: 20 pts (13 M; 43 ± 12 y) with idiopathic right ventricular outflow tract (RVOT) arrhythmias and no structural abnormalities were submitted to Smarttouch catheter Carto3 EAM. Native maps included points collected without considering contact-force. EAM scar was defined as area ≥1 cm2 including at least 3 adjacent points with signal amplitude (bipolar &lt;0.5 mV, unipolar 3,5 mV), surrounded by low-voltage border zone. EAM were re-evaluated offline, removing points collected with contact force &lt;5 g. Finally, contact force-corrected maps were compared to the native ones. Results: An EAM was created for each patient (345 ± 85 points). After removing poor contact points, a mean of 149 ± 60 points was collected. The percentage of false scar, collected during contact force blinded mapping compared to total volume, was 6.0 ± 5.2% for bipolar scar and 7.1 ± 5.9% for unipolar scar, respectively. No EAM scar was present after poor contact points removal. Right ventricular areas analysis revealed a greater number of points with contact force &lt; 5 g acquired in free wall, where reduced mean bipolar and unipolar voltage were recorded. Conclusions: To date this is the first work conducted on structurally normal hearts in which contact-force significantly increases EAM accuracy, avoiding “false scar” related to non-adequate contact between catheter and tissue