Evaluating Long-Term Performance of a Residential Ground-Source Heat Pump System under Climate Change in Cold and Warm Cities of Japan

A residential ground-source heat pump system often requires a long payback time to recover the capital cost. Long-term uncertainty in such a system's performance increases as the climate changes. This study compares 20-years hourly heating/cooling demands of a typical residence in the present (2000-2020) and in the future (2076-2095) for two locations in Japan. This study also calculated soil temperatures as heat sources through 1D heat-transfer simulation based on the A1B climate scenario in the Intergovernmental Panel on Climate Change's Special Report. System performance and simple payback times were compared in one cold and one warm city in Japan (Sapporo and Tokyo, respectively). Soil temperatures at a middle depth of a borehole heat exchanger were predicted to increase in the future by similar to 1 degrees C, with insignificant effects on a borehole heat exchanger. Seasonal performance factors increased in Sapporo because thermal demands would be kept even in the future, but decreased in Tokyo, which has a higher ratio of the energy used in operating the system in cooling mode compared with its small heating demand. The simple payback time was estimated at 16.2 and >20 years in Sapporo and Tokyo, respectively, both in the present and future, with the constant energy prices. If oil and gas prices doubled, the payback time would be halved in Sapporo to 8.4 years but remain around 20 years or more in Tokyo

Video S1. Field observation of<i> Potamostoma shizunaiense</i>, filmed by Hikaru Nagano.

Supplementary video for Hookabe et al. (2024) "Osmotic responses and oceanic dispersal of upper brackish nemertean: ecophysiology from field to in-vitro observation"</p

The Measles Virus V Protein Binding Site to STAT2 Overlaps That of IRF9

Measles virus (MeV) is a highly immunotropic and contagious pathogen that can even diminish preexisting antibodies and remains a major cause of childhood morbidity and mortality worldwide despite the availability of effective vaccines. MeV is one of the most extensively studied viruses with respect to the mechanisms of JAK-STAT antagonism. Of the three proteins translated from the MeV P gene, P and V are essential for inactivation of this pathway. However, the lack of data from direct analyses of the underlying interactions means that the detailed molecular mechanism of antagonism remains unresolved. Here, we prepared recombinant MeV V protein, which is responsible for human JAK-STAT antagonism, and a panel of variants, enabling the biophysical characterization of V protein, including direct V/STAT1 and V/STAT2 interaction assays. Unambiguous direct interactions between the host and viral factors, in the absence of other factors such as Jak1 or Tyk2, were observed, and the dissociation constants were quantified for the first time. Our data indicate that interactions between the C-terminal region of V and STAT2 is 1 order of magnitude stronger than that of the N-terminal region of V and STAT1. We also clarified that these interactions are completely independent of each other. Moreover, results of size exclusion chromatography demonstrated that addition of MeV-V displaces STAT2-core, a rigid region of STAT2 lacking the N- and C-terminal domains, from preformed complexes of STAT2-core/IRF-associated domain (IRF9). These results provide a novel model whereby MeV-V can not only inhibit the STAT2/IRF9 interaction but also disrupt preassembled interferon-stimulated gene factor 3. IMPORTANCE To evade host immunity, many pathogenic viruses inactivate host Janus kinase signal transducer and activator of transcription (STAT) signaling pathways using diverse strategies. Measles virus utilizes P and V proteins to counteract this signaling pathway. Data derived largely from cell-based assays have indicated several amino acid residues of P and V proteins as important. However, biophysical properties of V protein or its direct interaction with STAT molecules using purified proteins have not been studied. We have developed novel molecular tools enabling us to identify a novel molecular mechanism for immune evasion whereby V protein disrupts critical immune complexes, providing a clear strategy by which measles virus can suppress interferon-mediated antiviral gene expression