530 research outputs found
Towards opportunistic UAV relaying for smart cities
With recent advances in cooperation among mobile computer systems, Unmanned Aerial Vehicles (UAVs) can be expected to be operated in large numbers and become a part of daily life for a variety of use cases. UAVs are already envi- sioned to act as mobile base stations, e.g., for situations with high node densities and strong communication requirements. However, UAVs are typically imagined to be provided specifically for this purpose. In this work, we study the effects of exploiting randomly passing UAVs at an urban intersection for the communication between vehicles on the ground. We show that a UAV, while following its pri- mary mission, can support cooperative driving vehicles in a purely opportunistic fashion by collecting periodic wireless broadcasts from vehicles and propagating all collected information periodically in an aggregated format. Using simulations, we show that such an opportunistic UAV relaying approach can lead to an improvement of approx. 6 percentage points (% points) in terms of perception of other vehicles
Reducing vehicle cold start emissions through carbon pricing: Evidence from Germany
A large proportion of local pollutants originating from the road transport sector
is generated during the so-called cold-start phase of driving, that is, the first
few minutes of driving after a car has stood inactive for several hours. Drawing on
data from the German Mobility Panel (MOP), this paper analyzes the factors that
affect the frequency of cold starts, approximated here by the number of car tours
that a household takes over the course of a week. Based on fixed-effects panel
estimations, we find a negative and statistically significant effect of fuel prices on
the number of tours and, hence, cold starts. Using our estimates to explore the
spatial implications arising from fuel price increases stipulated under Germany’s
Climate Programme 2030, we find substantial impacts on the number of avoided
tours even for modest fuel price increases of 20 cents per liter, particularly in urban
areas. This outcome lends support to using carbon pricing as a means to improve
both global climate and local air quality, pointing to a co-benefit of climate policy
ラット静脈虚血モデ、ルにおけるペナンブラ領域でのセフトリアキソンの神経保護効果
OBJECTIVE: Glutamate transporter-1 (GLT-1) maintains low concentrations of extracellular glutamate by removing glutamate from the extracellular space. It is controversial, however, whether upregulation of GLT-1 is neuroprotective under all ischemic/hypoxic conditions. Recently, a neuroprotective effect of preconditioning with a β-lactam antibiotic ceftriaxone (CTX) that increases expression of GLT-1 has been reported in animal models of focal ischemia. On the other hand, it is said that CTX does not play a neuroprotective role in an in vitro study. Thus, we examined the effect of CTX on ischemic injury in a rat model of two-vein occlusion (2VO). This model mimics venous ischemia during, e.g. tumor surgery, a clinical situation that is best suitable for pretreatment with CTX.
METHODS: CTX (100mg/kg, 200mg/kg per day) or vehicle (0.9% NaCl) was intraperitoneally injected into Wistar rats for 5days before venous ischemia (n=57). Then, animals were prepared for occlusion of two adjacent cortical veins (2VO) by photothrombosis with rose bengal that was followed by KCl-induced cortical spreading depression (CSD). Infarct volume was evaluated with hematoxylin and eosin (H&E) staining 2days after venous occlusion. [(3)H]MK-801, [(3)H]AMPA and [(3)H]Muscimol ligand binding were examined autoradiographically in additional two groups without 2VO (n=5/group). Animals were injected either with NaCl (vehicle) or CTX 200mg/kg for 5days in order to evaluate whether NMDA, AMPA and GABAA ligand binding densities were affected.
RESULTS: CTX pretreatment reduced infarct volume compared to vehicle pretreatment (p<0.05). The effect of CTX pretreatment was attenuated by administration of the GLT-1 inhibitor, dihydrokainate (DHK) 30min before 2VO. CTX had no effect on the number of spontaneous spreading depressions after 2VO. Analysis of quantitative receptor autoradiography showed no statistically significant difference between rats after administration with CTX compared to control rats.
CONCLUSIONS: Pretreatment with CTX has neuroprotective potential without effect on NMDA, AMPA and GABAA receptor density and spontaneous spreading depression. This effect can be abolished by GLT-1 inhibition, indicating that upregulation of GLT-1 is an important mechanism for neuroprotective action in penumbra-like conditions, e.g. if neurosurgeons plan to occlude cerebral veins during tumor surgery.博士(医学)・乙第1320号・平成25年11月27
Sediment release of dissolved organic matter to the oxygen minimum zone off Peru
The eastern tropical South Pacific (ETSP) represents one of the most productive areas in the ocean that is characterized by a pronounced oxygen minimum zone (OMZ). Particulate organic matter (POM) that sinks out of the euphotic zone is supplied to the anoxic sediments and utilized by microbial communities. The degradation of POM is associated with dissolved organic matter (DOM) production and reworking. The release of recalcitrant DOM to the overlying waters may represent an important organic matter escape mechanism from remineralization within sediments but received little attention in OMZ regions so far. Here, we combine measurements of dissolved organic carbon (DOC) and dissolved organic nitrogen (DON) with DOM optical properties in the form of chromophoric (CDOM) and fluorescent (FDOM) DOM from pore waters and near-bottom waters of the ETSP off Peru. We evaluate diffusion–driven fluxes and net in situ fluxes of DOC and DON in order to investigate processes affecting DOM cycling at the sediment–water interface along a transect 12° S. To our knowledge, these are the first data for sediment release of DON and pore water CDOM and FDOM for the ETSP off Peru. Pore-water DOC and DON accumulated with increasing sediment depth, suggesting an imbalance between DOM production and remineralization within sediments. High DON accumulation resulted in very low pore water DOC / DON ratios (> 1) which could be caused by either an "imbalance" in DOC and DON remineralization, or to the presence of an additional nitrogen source. Diffusion driven fluxes of DOC and DON exhibited high spatial variability. They varied from 0.2–0.1 mmol m−2 d−1 to 2.52–1.3 mmol m−2 d−1 and from −0.042–0.02 mmol m−2 d−1 to 3.32–1.7 mmol m−2 d−1, respectively. Generally low net in situ DOC and DON fluxes as well as steepening of spectral slope (S) of CDOM and accumulation of humic-like FDOM at the near-bottom waters over time indicated active microbial DOM utilization at the sediment–water interface, potentially stimulated by nitrate (NO3−) and nitrite (NO2−). The microbial DOC utilization rates, estimated in our study, may be sufficient to support denitrification rates of 0.2–1.4 mmol m−2 d−1, suggesting that sediment release of DOM contributes substantially to nitrogen loss processes in the ETSP off Peru
FTY720 Reduces Post-Ischemic Brain Lymphocyte Influx but Does Not Improve Outcome in Permanent Murine Cerebral Ischemia
BACKGROUND: The contribution of neuroinflammation and specifically brain lymphocyte invasion is increasingly recognised as a substantial pathophysiological mechanism after stroke. FTY720 is a potent treatment for primary neuroinflammatory diseases by inhibiting lymphocyte circulation and brain immigration. Previous studies using transient focal ischemia models showed a protective effect of FTY720 but did only partially characterize the involved pathways. We tested the neuroprotective properties of FTY720 in permanent and transient cortical ischemia and analyzed the underlying neuroimmunological mechanisms. METHODOLOGY/PRINCIPAL FINDINGS: FTY720 treatment resulted in substantial reduction of circulating lymphocytes while blood monocyte counts were significantly increased. The number of histologically and flow cytometrically analyzed brain invading T- and B lymphocytes was significantly reduced in FTY720 treated mice. However, despite testing a variety of treatment protocols, infarct volume and behavioural dysfunction were not reduced 7d after permanent occlusion of the distal middle cerebral artery (MCAO). Additionally, we did not measure a significant reduction in infarct volume at 24 h after 60 min filament-induced MCAO, and did not see differences in brain edema between PBS and FTY720 treatment. Analysis of brain cytokine expression revealed complex effects of FTY720 on postischemic neuroinflammation comprising a substantial reduction of delayed proinflammatory cytokine expression at 3d but an early increase of IL-1β and IFN-γ at 24 h after MCAO. Also, serum cytokine levels of IL-6 and TNF-α were increased in FTY720 treated animals compared to controls. CONCLUSIONS/SIGNIFICANCE: In the present study we were able to detect a reduction of lymphocyte brain invasion by FTY720 but could not achieve a significant reduction of infarct volumes and behavioural dysfunction. This lack of neuroprotection despite effective lymphopenia might be attributed to a divergent impact of FTY720 on cytokine expression and possible activation of innate immune cells after brain ischemia
Influence of eastern boundary circulation variability on hydrography and biogeochemistry off Peru in early 2017
Dissolved oxygen (O2) and nutrient concentrations at the continental margin of the eastern tropical south Pacific exhibit elevated intra-seasonal, seasonal and inter-annual variability. Here, we discuss the impact of intra-seasonal variability of the eastern boundary circulation at 12°S on the hydrography and biogeochemistry. Data from a multi-cruise physical and biogeochemical measurement program conducted between April and June (austral autumn) 2017 are used and compared to earlier cruises.
Upper ocean temperatures were anomalously high and from mid-April onwards the oxycline was displaced downward compared with previous observations in austral summer 2008/09 and 2012/13. We observed the offshore propagation of a newly generated eddy and an associated phase of weak poleward flow. After the reestablishing
of the poleward Peru-Chile Undercurrent (PCUC) the passage of a downwelling coastal trapped wave caused an intensification of poleward velocities exceeding 50 cm/s. Warm temperature anomalies persisted during the intensified PCUC while sea surface temperature anomalies declined after the peak of the 2017 Coastal El Niño event
in March. During the period of PCUC acceleration, nitrate concentrations increased while the phosphate concentrations
were less affected, resulting in a drastically reduced nitrogen deficit. Because the temperature and salinity
properties of the water remained unchanged the pathways of water supply are probably the same. Therefore the reduced nitrogen deficit was likely caused by shorter advection timescales in the intensified flow leaving the water less affected by anaerobic biogeochemistry.
We discuss the occurrence of such events and their implications for the biogeochemical element cycling in the water column and the sediments
IGF1R is a potential new therapeutic target for HGNET-BCOR brain tumor patients
(1) Background: The high-grade neuroepithelial tumor of the central nervous system with BCOR alteration (HGNET-BCOR) is a highly malignant tumor. Preclinical models and molecular targets are urgently required for this cancer. Previous data suggest a potential role of insulin-like growth factor (IGF) signaling in HGNET-BCOR. (2) Methods: The primary HGNET-BCOR cells PhKh1 were characterized by western blot, copy number variation, and methylation analysis and by electron microscopy. The expression of IGF2 and IGF1R was assessed by qRT-PCR. The effect of chemotherapeutics and IGF1R inhibitors on PhKh1 proliferation was tested. The phosphorylation of IGF1R and downstream molecules was assessed by western blot. (3) Results: Phkh1 cells showed a DNA methylation profile compatible with the DNA methylation class “HGNET-BCOR” and morphologic features of cellular cannibalism. IGF2 and IGF1R were highly expressed by three HGNET-BCOR tumor samples and PhKh1 cells. PhKh1 cells were particularly sensitive to vincristine, vinblastine, actinomycin D (IC50 < 10 nM for all drugs), and ceritinib (IC50 = 310 nM). Ceritinib was able to abrogate the proliferation of PhKh1 cells and blocked the phosphorylation of IGF1R and AKT. (4) Conclusion: IGF1R is as an attractive target for the development of new therapy protocols for HGNET-BCOR patients, which may include ceritinib and vinblastine
Decreased hippocampal cell proliferation in mice with experimental antiphospholipid syndrome
The antiphospholipid syndrome (APS) is an autoimmune disease characterized by the presence of antiphospholipid antibodies, which may trigger vascular thrombosis with consecutive infarcts. However, cognitive dysfunctions representing one of the most commonest neuropsychiatric symptoms are frequently present despite the absence of any ischemic brain lesions. Data on the structural and functional basis of the neuropsychiatric symptoms are sparse. To examine the effect of APS on hippocampal neurogenesis and on white matter, we induced experimental APS (eAPS) in adult female Balb/C mice by immunization with β2-glycoprotein 1. To investigate cell proliferation in the dentate gyrus granular cell layer (DG GCL), eAPS and control mice (n = 5, each) were injected with 5-bromo-2′-deoxyuridine (BrdU) once a day for 10 subsequent days. Sixteen weeks after immunization, eAPS resulted in a significant reduction of BrdU-positive cells in the DG GCL compared to control animals. However, double staining with doublecortin and NeuN revealed a largely preserved neurogenesis. Ultrastructural analysis of corpus callosum (CC) axons in eAPS (n = 6) and control mice (n = 7) revealed no significant changes in CC axon diameter or g-ratio. In conclusion, decreased cellular proliferation in the hippocampus of eAPS mice indicates a limited regenerative potential and may represent one neuropathological substrate of cognitive changes in APS while evidence for alterations of white matter integrity is lacking.
Keywords Antiphospholipid syndrome Corpus callosum g-ratio BrdU Neurogenesi
Molecularly defined diffuse leptomeningeal glioneuronal tumor (DLGNT) comprises two subgroups with distinct clinical and genetic features
Diffuse leptomeningeal glioneuronal tumors (DLGNT) represent rare CNS neoplasms which have been included in the 2016 update of the WHO classification. The wide spectrum of histopathological and radiological features can make this enigmatic tumor entity difficult to diagnose. In recent years, large-scale genomic and epigenomic analyses have afforded insight into key genetic alterations occurring in multiple types of brain tumors and provide unbiased, complementary tools to improve diagnostic accuracy. Through genome-wide DNA methylation screening of > 25,000 tumors, we discovered a molecularly distinct class comprising 30 tumors, mostly diagnosed histologically as DLGNTs. Copy-number profiles derived from the methylation arrays revealed unifying characteristics, including loss of chromosomal arm 1p in all cases. Furthermore, this molecular DLGNT class can be subdivided into two subgroups [DLGNT methylation class (MC)-1 and DLGNT methylation class (MC)-2], with all DLGNT-MC-2 additionally displaying a gain of chromosomal arm 1q. Co-deletion of 1p/19q, commonly seen in IDH-mutant oligodendroglioma, was frequently observed in DLGNT, especially in DLGNT-MC-1 cases. Both subgroups also had recurrent genetic alterations leading to an aberrant MAPK/ERK pathway, with KIAA1549:BRAF fusion being the most frequent event. Other alterations included fusions of NTRK1/2/3 and TRIM33:RAF1, adding up to an MAPK/ERK pathway activation identified in 80% of cases. In the DLGNT-MC-1 group, age at diagnosis was significantly lower (median 5 vs 14 years, p < 0.01) and clinical course less aggressive (5-year OS 100, vs 43% in DLGNT-MC-2). Our study proposes an additional molecular layer to the current histopathological classification of DLGNT, of particular use for cases without typical morphological or radiological characteristics, such as diffuse growth and radiologic leptomeningeal dissemination. Recurrent 1p deletion and MAPK/ERK pathway activation represent diagnostic biomarkers and therapeutic targets, respectively—laying the foundation for future clinical trials with, e.g., MEK inhibitors that may improve the clinical outcome of patients with DLGNT
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