Dynamic simulation and analysis of a Passive House case study with direct PV system for heating and domestic hot water production

Different heating systems for space heating and domestic hot water (DHW) preparation are investigated with respect to their energy efficiency. In particular, a case study of a multi-storey Passive House (called An-der-Lan) is analysed by means of dynamic simulations. The first part of dynamic simulations focuses on the comparison of the UA and RC models for a simple office located in Rome. This is a case study from the project IEA SHC T56 – System Simulation Models. In particular, attention is put on the influence of the thermal capacity. Assuming the RC model as the reference case, variants of the UA model with different percentages of the thermal capacity are simulated, in order to find out the most similar to the RC model. The same investigation is carried out for the An-der-Lan building. In general, it is not possible to identify the best UA model, because for every considered quantity, the minimum difference between the UA and RC model is got for a different percentage of the thermal mass. The second part of dynamic simulation focuses on the comparison among different systems for heating and DHW preparation. The realized system is direct electric heating for both space heating and DHW preparation. It is denoted as the reference Case1 and it is compared against alternative solutions. Case2 is based on a central air/water heat pump system for both heating and DHW production. A sensitivity analysis study is conducted. Finally, Case3 and Case4 are a mix of the previous two cases. Results show that Case2 is the best in terms of electric energy required from the grid, although it is the system with the highest thermal losses. Furthermore, the PV system only in the south façade is not sufficient to cover the energy required in neither of the cases. Finally, annual, monthly, daily, hourly and 10 minutes balances are compared. Results show the importance of smaller time step in balances between required and produced energy, in order to have more precise results

Waiting time information in the Italian NHS: A citizen perspective

Public involvement in the management and communication of waiting times is known to support initiatives to reduce waiting times, as well as increase fairness and promote transparency and accountability. In order to improve transparency and communication to citizens, Italy recently updated the National Regulatory Plan for Waiting Lists (2019–2021), which calls for the disclosure of waiting time information on healthcare provider webpages. This study analyses waiting time information for outpatient visits and digital services available on the institutional website pages of 144 public healthcare organisations in nine regions and two autonomous provinces of Italy. Web pages were analysed both in terms of the available information/services, using a grid, and in terms of the quality of the text using an advanced readability assessment tool (READ-IT). This information was complemented and validated by regional healthcare key informants during research-specific workshops. Waiting time information disclosure, digital services and text readability varied both within and between the regional healthcare systems and organisations. The types and characteristics of waiting time information and statistics vary considerably with a negative impact on their use for benchmarking and their readability and usability for booking purposes. Overall, communication weaknesses due to low harmonization and clarity of information can undermine efforts in effectively informing and involving the public through online waiting time data disclosure

Weathering of evaporites: natural versus anthropogenic signature on the composition of river waters

Weathering of evaporites strongly influences the chemistry of continental runoff, making surface waters poorly exploitable for civil uses. In south-central Sicily, this phenomenon is worsened by the occurrence of abandoned landfills of old sulphur and salt mines. The industrial evolution of the Bosco-S. Cataldo mining site leaved two landfills from the early exploitation of a sulphur mine followed by that of a kainite deposit. In particular, the weathering of these landfills leads the dissolved salt (TDS) values up to about 200 g l−1 in the Stincone–Salito Stream waters. This process induces the V, Cr and Fe desorption from sediments and particulates in the aqueous phase under reducing conditions. At the same time, the weathering of salt minerals releases Rb and Cs, originally contained in halite. The overall processes lead to the V, Cr, Fe, Rb and Cs enrichment of waters from the Stincone–Salito Stream system accompanied by a sharp growth of As content, up to about 13 µg l−1, caused by As release from Fe-bearing solids due to the high salinity. Therefore, the scenario of the weathering of Bosco-S. Cataldo mine landfills depicts an environment strongly influenced by effects of the growing salinity and euxinic water conditions where the attained TDS, Eh and pH conditions reduce the natural scavenging capability of the interested river system, favouring a growth of residence time of toxic elements in river waters

TPC2 is a novel NAADP-sensitive Ca2+ release channel, operating as a dual sensor of luminal pH and Ca2+

Nicotinic acid adenine dinucleotide phosphate (NAADP) is a molecule capable of initiating the release of intracellular Ca2+ required for many essential cellular processes. Recent evidence links two-pore channels (TPCs) with NAADP-induced release of Ca2+ from lysosome-like acidic organelles; however, there has been no direct demonstration that TPCs can act as NAADP-sensitive Ca2+-release channels. Controversial evidence also proposes ryanodine receptors as the primary target of NAADP. We show that TPC2, the major lysosomal targeted isoform, is a cation channel with selectivity for Ca2+ that will enable it to act as a Ca2+ release channel in the cellular environment. NAADP opens TPC2 channels in a concentration-dependent manner, binding to high affinity activation and low affinity inhibition sites. At the core of this process is the luminal environment of the channel. The sensitivity of TPC2 to NAADP is steeply dependent on the luminal [Ca2+] allowing extremely low levels of NAADP to open the channel. In parallel, luminal pH controls NAADP affinity for TPC2 by switching from reversible activation of TPC2 at low pH to irreversible activation at neutral pH. Further evidence earmarking TPCs as the likely pathway for NAADP-induced intracellular Ca2+ release is obtained from the use of Ned-19, the selective blocker of cellular NAADP-induced Ca2+ release. Ned-19 antagonizes NAADP-activation of TPC2 in a non-competitive manner at 1 μM but potentiates NAADP activation at nanomolar concentrations. This single-channel study provides a long awaited molecular basis for the peculiar mechanistic features of NAADP signaling and a framework for understanding how NAADP can mediate key physiological events.Publisher PDFPeer reviewe

TRIC-B channels display labile gating: evidence from the TRIC-A knockout mouse model.

The online version of this article (doi:10.1007/s00424-013-1251-y) contains supplementary material, which is available to authorized usersPublished online: 7 March 2013. ©The Author(s) 2013. This article is published with open access at Springerlink.com via: doi:10.1007/s00424-013-1251-y)Available under Open AccessSarcoplasmic/endoplasmic reticulum (SR) and nuclear membranes contain two related cation channels named TRIC-A and TRIC-B. In many tissues, both subtypes are co-expressed, making it impossible to distinguish the distinct single-channel properties of each subtype. We therefore incorporated skeletal muscle SR vesicles derived from Tric-a-knockout mice into bilayers in order to characterise the biophysical properties of native TRIC-B without possible misclassification of the channels as TRIC-A, and without potential distortion of functional properties by detergent purification protocols. The native TRIC-B channels were ideally selective for cations. In symmetrical 210 mM K(+), the maximum (full) open channel level (199 pS) was equivalent to that observed when wild-type SR vesicles were incorporated into bilayers. Analysis of TRIC-B gating revealed complex and variable behaviour. Four main sub-conductance levels were observed at approximately 80 % (161 pS), 60 % (123 pS), 46 % (93 pS), and 30 % (60 pS) of the full open state. Seventy-five percent of the channels were voltage sensitive with Po being markedly reduced at negative holding potentials. The frequent, rapid transitions between TRIC-B sub-conductance states prevented development of reliable gating models using conventional single-channel analysis. Instead, we used mean-variance plots to highlight key features of TRIC-B gating in a more accurate and visually useful manner. Our study provides the first biophysical characterisation of native TRIC-B channels and indicates that this channel would be suited to provide counter current in response to Ca(2+) release from the SR. Further experiments are required to distinguish the distinct functional properties of TRIC-A and TRIC-B and understand their individual but complementary physiological roles.British Heart FoundationEngineering and Physical Sciences Research Council (EPSRC)Japan Society for the Promotion of Scienc

Cardiac deficiency of P21-activated kinase 1 promotes atrial arrhythmogenesis in mice following adrenergic challenge

P21-activated kinase 1 (Pak1) signalling plays a vital and overall protective role in the heart. However, the phenotypes of Pak1 deficiency in the cardiac atria have not been well explored. In this study, Pak1 cardiac-conditional knock-out (cKO) mice were studied under baseline and adrenergic challenge conditions. Pak1cKO mice show atrial arrhythmias including atrial fibrillation (AF) in vivo, detected during anaesthetized electrocardiography without evidence of interstitial fibrosis upon Masson's trichrome staining. Optical mapping of left atrial preparations from Pak1 cKO mice revealed a higher incidence of Ca2+ and action potential alternans under isoprenaline challenge and differences in baseline action potential and calcium transient characteristics. Type-2 ryanodine receptor (RyR2) channels from Pak1 cKO hearts had a higher open probability than those from wild-type. Reverse transcription-quantitative polymerase chain reaction and Western blotting indicated that pCamkIIδ and RyR2 are highly phosphorylated at baseline in the atria of Pak1 cKO mice, while the expression of Slc8a2 and Slc8a3 as a Na+–Ca2+ exchanger, controlling the influx of Ca2+ from outside of the cell and efflux of Na+ from the cytoplasm, are augmented. Chromatin immunoprecipitation study showed that pCreb1 interacts with Slc8a2 and Slc8a3. Our study thus demonstrates that deficiency of Pak1 promotes atrial arrhythmogenesis under adrenergic stress, probably through post-translational and transcriptional modifications of key molecules that are critical to Ca2+ homeostasis

Enhanced activity of multiple TRIC-B channels : an endoplasmic reticulum/sarcoplasmic reticulum mechanism to boost counterion currents

The trimeric intracellular cation channels, TRIC-A and TRIC-B, represent two subtypes of sarcoplasmic reticulum (SR) K+-channel but their individual functional roles are unknown. We therefore compared the biophysical properties of SR K+-channels derived from the skeletal muscle of wild-type (WT) or Tric-a knockout (KO) mice. Because TRIC-A is the major TRIC-subtype in skeletal muscle, WT SR will predominantly contain TRIC-A channels, whereas Tric-a KO SR will only contain TRIC-B channels. When lone SR K+-channels were incorporated into bilayers, the open probability (Po) of channels from Tric-a KO mice was markedly lower than that of channels from WT mice; gating was characterized by shorter opening bursts and more frequent brief subconductance openings. However, unlike channels from WT mice, the Po of SR K+-channels from Tric-a KO mice increased as increasing channel numbers were present in the bilayer, driving the channels into long sojourns in the fully open state. When co-incorporated into bilayers, ryanodine receptor channels did not directly affect the gating of SR K+-channels, nor did the presence or absence of SR K+-channels influence ryanodine receptor activity. We suggest that because of high expression levels in striated muscle, TRIC-A produces most of the counterion flux required during excitation-contraction coupling. TRIC-B, in contrast, is sparsely expressed in most cells and, although lone TRIC-B channels exhibit low Po, the high Po levels reached by multiple TRIC-B channels may provide a compensatory mechanism to rapidly restore K+ gradients and charge differences across the SR of tissues containing few TRIC-A channels

Cooperative gating among ion-channel species in junctional sarcoplasmic reticulum

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Dampened activity of ryanodine receptor channels in mutant skeletal muscle lacking TRIC-A

The type A trimeric intracellular cation channel (TRIC-A) is a major component of the nuclear and sarcoplasmic reticulum (SR) membranes of cardiac and skeletal muscle, and is localized closely with ryanodine receptor (RyR) channels in the SR terminal cisternae. The skeletal muscle of Tric-a knockout (KO) mice is characterized by Ca2+ overloaded and swollen SR and by changes in the properties of SR Ca2+ release. We therefore investigated whether RyR1 gating behaviour is modified in the SR from Tric-a KO mice by incorporating native RyR1 into planar phospholipid bilayers under voltage-clamp conditions. We find that RyR1 channels from Tric-a KO mice respond normally to cytosolic Ca2+, ATP, adenine, caffeine and to luminal Ca2+. However, the channels are more sensitive to the inactivating effects of divalent cations, thus, in the presence of Mg2+, ATP is inadequate as an activator. Additionally, channels are not characteristically activated by protein kinase A even though the phosphorylation levels of Ser2844 are similar to controls. The results of the present study suggest that TRIC-A functions as an excitatory modulator of RyR1 channels within the SR terminal cisternae. Importantly, this regulatory action of TRIC-A appears to be independent of (although additive to) any indirect consequences to RyR1 activity that arise as a result of K+ fluxes across the SR via TRIC-A