Optimal Management of a Multispecies Shorebird Flyway under Sea-Level Rise

Every year, millions of migratory shorebirds fly through the East Asian-Australasian Flyway between their arctic breeding grounds and Australasia. This flyway includes numerous coastal wetlands in Asia and the Pacific that are used as stopover sites where birds rest and feed. Loss of a few important stopover sites through sea-level rise (SLR) could cause sudden population declines. We formulated and solved mathematically the problem of how to identify the most important stopover sites to minimize losses of bird populations across flyways by conserving land that facilitates upshore shifts of tidal flats in response to SLR. To guide conservation investment that minimizes losses of migratory bird populations during migration, we developed a spatially explicit flyway model coupled with a maximum flow algorithm. Migratory routes of 10 shorebird taxa were modeled in a graph theoretic framework by representing clusters of important wetlands as nodes and the number of birds flying between 2 nodes as edges. We also evaluated several resource allocation algorithms that required only partial information on flyway connectivity (node strategy, based on the impacts of SLR at nodes; habitat strategy, based on habitat change at sites; population strategy, based on population change at sites; and random investment). The resource allocation algorithms based on flyway information performed on average 15% better than simpler allocations based on patterns of habitat loss or local bird counts. The Yellow Sea region stood out as the most important priority for effective conservation of migratory shorebirds, but investment in this area alone will not ensure the persistence of species across the flyway. The spatial distribution of conservation investments differed enormously according to the severity of SLR and whether information about flyway connectivity was used to guide the prioritizations. With the rapid ongoing loss of coastal wetlands globally, our method provides insight into efficient conservation planning for migratory species

Recent advances in deuterium permeation induced transmutation experiments using nano-structured Pd/CaO/Pd multilayer thin film

Permeation induced transmutation reactions, which we originally found in the nanostructured Pd multilayer film composed of Pd and CaO thin film and Pd substrate, have been observed in our laboratory and other research institutes. Recently, Toyota R&D centre reported almost complete replication experiments on the transmutation of Cs into Pr at ICCF-17. We observed transmutation reactions of Cs into Pr, Ba into Sm, W into Pt up to now. Especially, transmutation of Cs into Pr has been confirmed by "in-situ" measurements using x-ray fluorescence spectrometry (XRF) at SPring-8 in Japan. Experimental data that indicates the presence of transmutation have been accumulated and the underlying mechanism for inducing low energy transmutation reactions is gradually becoming clear, although systematic experimental study is still insufficient. The permeation induced transmutation technology would be expected as an innovative nuclear transmutation method for radioactive waste and a new energy source if we would be able to increase the amount of transmutation products. We have been trying to increase the amount of transmutation products these years for the practical application. The following factors are assumed to be important for inducing deuterium permeation transmutation. 1) Local Deuteron Density 2) Electronic Structure Based on this assumption, we applied an electrochemical method to increase the local deuteron density near the surface of the nano-structured Pd multilayer film. We also tried to increase the transmutation products by changing surface electronic state. These recent experimental methods gave us increased transmutation products, gamma-ray emissions, and new implications on Deuterium Permeation Induced Transmutation

Measurement of the electron transmission rate of the gating foil for the TPC of the ILC experiment

We have developed a gating foil for the time projection chamber envisaged as a central tracker for the international linear collider experiment. It has a structure similar to the Gas Electron Multiplier (GEM) with a higher optical aperture ratio and functions as an ion gate without gas amplification. The transmission rate for electrons was measured in a counting mode for a wide range of the voltages applied across the foil using an $^{55}$Fe source and a laser in the absence of a magnetic field. The blocking power of the foil against positive ions was estimated from the electron transmissions.Comment: 25 pages containing 14 figures and 1 tabl

Enhanced Hyperthermia Induced by MDMA in Parkin Knockout Mice

MDMA (3,4-methylenedioxymethamphetamine) is reportedly severely toxic to both dopamine (DA) and serotonin neurons. MDMA significantly reduces the number of DA neurons in the substantia nigra, but not in the nucleus accumbens, indicating that MDMA causes selective destruction of DA neurons in the nigrostriatal pathway, sparing the mesolimbic pathway. Parkinson’s disease (PD) is a neurodegenerative disorder of multifactorial origin. The pathological hallmark of PD is the degeneration of DA neurons in the nigrostriatal pathway. Mutations in the parkin gene are frequently observed in autosomal recessive parkinsonism in humans. Parkin is hypothesized to protect against neurotoxic insult, and we attempted to clarify the role of parkin in MDMA-induced hyperthermia, one of the causal factors of neuronal damage, using parkin knockout mice. Body temperature was measured rectally before and 15, 30, 45, and 60 min after intraperitoneal injection of MDMA (30 mg/kg) at an ambient temperature of 22 ± 2°C. Significantly enhanced hyper-thermia after MDMA injection was observed in heterozygous and homozygous parkin knockout mice compared with wildtype mice, suggesting that parkin plays a protective role in MDMA neurotoxicity

Effects of MDMA on Extracellular Dopamine and Serotonin Levels in Mice Lacking Dopamine and/or Serotonin Transporters

3,4-Methylendioxymethamphetamine (MDMA) has both stimulatory and hallucinogenic properties which make its psychoactive effects unique and different from those of typical psychostimulant and hallucinogenic agents. The present study investigated the effects of MDMA on extracellular dopamine (DAex) and serotonin (5-HTex) levels in the striatum and prefrontal cortex (PFC) using in vivo microdialysis techniques in mice lacking DA transporters (DAT) and/or 5-HT transporters (SERT). subcutaneous injection of MDMA (3, 10 mg/kg) significantly increased striatal DAex in wild-type mice, SERT knockout mice, and DAT knockout mice, but not in DAT/SERT double-knockout mice. The MDMA-induced increase in striatal DAex in SERT knockout mice was significantly less than in wildtype mice. In the PFC, MDMA dose-dependently increased DAex levels in wildtype, DAT knockout, SERT knockout and DAT/SERT double-knockout mice to a similar extent. In contrast, MDMA markedly increased 5-HTex in wildtype and DAT knockout mice and slightly increased 5-HTex in SERT-KO and DAT/SERT double-knockout mice. The results confirm that MDMA acts at both DAT and SERT and increases DAex and 5-HTex

Interhemispheric Interactions between the Human Primary Somatosensory Cortices

In the somatosensory domain it is still unclear at which processing stage information reaches the opposite hemispheres. Due to dense transcallosal connections, the secondary somatosensory cortex (S2) has been proposed to be the key candidate for interhemispheric information transfer. However, recent animal studies showed that the primary somatosensory cortex (S1) might as well account for interhemispheric information transfer. Using paired median nerve somatosensory evoked potential recordings in humans we tested the hypothesis that interhemispheric inhibitory interactions in the somatosensory system occur already in an early cortical processing stage such as S1. Conditioning right S1 by electrical median nerve (MN) stimulation of the left MN (CS) resulted in a significant reduction of the N20 response in the target (left) S1 relative to a test stimulus (TS) to the right MN alone when the interstimulus interval between CS and TS was between 20 and 25 ms. No such changes were observed for later cortical components such as the N20/P25, N30, P40 and N60 amplitude. Additionally, the subcortically generated P14 response in left S1 was also not affected. These results document the existence of interhemispheric inhibitory interactions between S1 in human subjects in the critical time interval of 20–25 ms after median nerve stimulation