Low-frequency signals produced by Northeast Atlantic killer whales (Orcinus orca)

Killer whale acoustic behavior has been extensively investigated, however most studies have focused on pulsed calls and whistles. This study reports the production of low-frequency signals by killer whales at frequencies below 300 Hz. Recordings of killer whales were made in Iceland and Norway when whales were observed feeding on herring, and no other cetacean species were nearby. Low-frequency sounds were identified in Iceland and ranged in duration between 0.14 and 2.77 seconds and in frequency between 50 and 270 Hz, well below the previously reported lower limit for killer whale tonal sounds of 500 Hz. LFS appeared to be produced close in time to tail slaps, indicative of feeding attempts, suggesting that these sounds may be related to a feeding context. However, their precise function is unknown and they could be the by-product of a non-vocal behavior, rather than a vocal signal deliberately produced by the whales. Although killer whales in Norway exhibit similar feeding behavior, this sound was not detected in recordings from Norway. This study suggests that, like other delphinids, killer whales also produce low-frequency sounds but further studies will be required to understand whether similar sounds exist in other killer whale populations

Lift Energy Storage Technology: A solution for decentralized urban energy storage

The world is undergoing a rapid energy transformation dominated by growing capacities of renewable energy sources, such as wind and solar power. The intrinsic variable nature of such renewable energy sources calls for affordable energy storage solutions. This paper proposes using lifts and empty apartments in tall buildings to store energy. Lift Energy Storage Technology (LEST) is a gravitational-based storage solution. Energy is stored by lifting wet sand containers or other high-density materials, transported remotely in and out of the lift with autonomous trailer devices. The system requires empty spaces on the top and bottom of the building. An existing lift can be used to transport the containers from the lower apartments to the upper apartments to store energy and from the upper apartments to the lower apartments to generate electricity. The installed storage capacity cost is estimated at 21 to 128 USD/kWh, depending on the height of the building. LEST is particularly interesting for providing decentralized ancillary and energy storage services with daily to weekly energy storage cycles. The global potential for the technology is focused on large cities with high-rise buildings and is estimated to be around 30 to 300 GWh

Underground Gravity Energy Storage: A Solution for Long-Term Energy Storage

Low-carbon energy transitions taking place worldwide are primarily driven by the integration of renewable energy sources such as wind and solar power. These variable renewable energy (VRE) sources require energy storage options to match energy demand reliably at different time scales. This article suggests using a gravitational-based energy storage method by making use of decommissioned underground mines as storage reservoirs, using a vertical shaft and electric motor/generators for lifting and dumping large volumes of sand. The proposed technology, called Underground Gravity Energy Storage (UGES), can discharge electricity by lowering large volumes of sand into an underground mine through the mine shaft. When there is excess electrical energy in the grid, UGES can store electricity by elevating sand from the mine and depositing it in upper storage sites on top of the mine. Unlike battery energy storage, the energy storage medium of UGES is sand, which means the self-discharge rate of the system is zero, enabling ultra-long energy storage times. Furthermore, the use of sand as storage media alleviates any risk for contaminating underground water resources as opposed to an underground pumped hydro storage alternative. UGES offers weekly to pluriannual energy storage cycles with energy storage investment costs of about 1 to 10 USD/kWh. The technology is estimated to have a global energy storage potential of 7 to 70 TWh and can support sustainable development, mainly by providing seasonal energy storage services

Microparticles from apoptotic platelets promote resident macrophage differentiation

Platelets shed microparticles not only upon activation, but also upon ageing by an apoptosis-like process (apoptosis-induced platelet microparticles, PMap). While the activation-induced microparticles have widely been studied, not much is known about the (patho)physiological consequences of PMap formation. Flow cytometry and scanning electron microscopy demonstrated that PMap display activated integrins and interact to form microparticle aggregates. PMap were chemotactic for monocytic cells, bound to these cells, an furthermore stimulated cell adhesion and spreading on a fibronectin surface. After prolonged incubation, PMap promoted cell differentiation, but inhibited proliferation. Monocyte membrane receptor analysis revealed increased expression levels of CD11b (integrin αMβ2), CD14 and CD31 (platelet endothelial cell adhesion molecule-1), and the chemokine receptors CCR5 and CXCR4, but not of CCR2. This indicated that PMap polarized the cells into resident M2 monocytes. Cells treated with PMap actively consumed oxidized low-density lipoprotein (oxLDL), and released matrix metalloproteinases and hydrogen peroxide. Further confirmation for the differentiation towards resident professional phagocytes came from the finding that PMap stimulated the expression of the (ox)LDL receptors, CD36 and CD68, and the production of proinflammatory and immunomodulating cytokines by monocytes. In conclusion, interaction of PMap with monocytic cells has an immunomodulating potential. The apoptotic microparticles polarize the cells into a resident M2 subset, and induce differentiation to resident professional phagocytes

An association between anti-platelet drug use and reduced cancer prevalence in diabetic patients: results from the Vermont Diabetes Information System Study

<p>Abstract</p> <p>Background</p> <p>Diabetes is associated with an increased risk of several malignancies. Both diabetic patients and patients with cancer have an increase in platelet reactivity and platelet activation has recently emerged as a potential mediator of cancer progression. Drug therapies, such as aspirin, that reduce platelet reactivity reduce both cardiovascular and cancer risk.</p> <p>Methods</p> <p>We performed a cross-sectional analysis to assess the association between history of cancer and current anti-platelet drug use in a primary care population of adults with diabetes enrolled in the Vermont Diabetes Information System.</p> <p>Results</p> <p>Self-reported characteristics, medical history, and a complete medication list were recorded on 1007 diabetic adults. Fifty percent of diabetic patients used an anti-platelet drug. In unadjusted analysis, no association was seen between anti-platelet drug use and cancer history (OR = 0.93; <it>P </it>= .70). Platelet inhibitor use was associated with a decreased patient-reported history of malignancy in a multivariate logistic regression adjusted for age, sex, body mass index, comorbidity, and number of medications (OR = 0.66; CI 0.44-0.99; <it>P </it>= .045). Similar odds of association were seen in both males and females, and for aspirin and non-aspirin platelet inhibitor therapy.</p> <p>Conclusions</p> <p>Our data suggest an association between anti-platelet drug use and reduced cancer prevalence in patients with diabetes. Given the potentially large implications of our observations in the diabetic population, further studies are required to determine if this association is causal.</p

Hydropower and seasonal pumped hydropower storage in the Indus basin:pros and cons

The Indus basin has a large hydropower untapped potential for electricity generation and to regulate the Indus river flow, which could reduce flooding events and provide water supply during drought periods. In this paper, a computational module is developed to localize potential sites for hydropower generation and seasonal pumped hydropower storage (SPHS). The levelized costs for hydropower generation in the basin with conventional dams are as low as 12 USD/MWh, the cost of energy storage is 1 USD/MWh. In case of SPHS plants, the cost of energy storage is 2 USD/MWh. It can be concluded that the conventional hydropower potential is, for the moment, less expensive than SPHS, but its potential in the Indus basin is limited to 26 GW with hydropower costs below 50 USD/MWh and its reservoirs have a short lifetime due to the high sedimentation rates of the basin. SPHS would be an interesting alternative to complement the hydropower potential adding long-term water and energy storage with fewer sediments, social and environmental impacts. Given that the region has the highest potential and lowest costs for SPHS in the world, it could become a major player on seasonal and pluri-annual energy storage in Asia and globally

Enhanced Platelet Activation Mediates the Accelerated Angiogenic Switch in Mice Lacking Histidine-Rich Glycoprotein

BACKGROUND: The heparin-binding plasma protein histidine-rich glycoprotein (HRG; alternatively, HRGP/HPRG) can suppress tumor angiogenesis and growth in vitro and in vivo. Mice lacking the HRG gene are viable and fertile, but have an enhanced coagulation resulting in decreased bleeding times. In addition, the angiogenic switch is significantly enhanced in HRG-deficient mice. METHODOLOGY/PRINCIPAL FINDINGS: To address whether HRG deficiency affects tumor development, we have crossed HRG knockout mice with the RIP1-Tag2 mouse, a well established orthotopic model of multistage carcinogenesis. RIP1-Tag2 HRG(-/-) mice display significantly larger tumor volume compared to their RIP1-Tag2 HRG(+/+) littermates, supporting a role for HRG as an endogenous regulator of tumor growth. In the present study we also demonstrate that platelet activation is increased in mice lacking HRG. To address whether this elevated platelet activation contributes to the increased pathological angiogenesis in HRG-deficient mice, they were rendered thrombocytopenic before the onset of the angiogenic switch by injection of the anti-platelet antibody GP1bα. Interestingly, this treatment suppressed the increase in angiogenic neoplasias seen in HRG knockout mice. However, if GP1bα treatment was initiated at a later stage, after the onset of the angiogenic switch, no suppression of tumor growth was detected in HRG-deficient mice. CONCLUSIONS: Our data show that increased platelet activation mediates the accelerated angiogenic switch in HRG-deficient mice. Moreover, we conclude that platelets play a crucial role in the early stages of tumor development but are of less significance for tumor growth once angiogenesis has been initiated

Physiologic and molecular consequences of endothelial Bmpr2 mutation

<p>Abstract</p> <p>Background</p> <p>Pulmonary arterial hypertension (PAH) is thought to be driven by dysfunction of pulmonary vascular microendothelial cells (PMVEC). Most hereditary PAH is associated with BMPR2 mutations. However, the physiologic and molecular consequences of expression of BMPR2 mutations in PMVEC are unknown.</p> <p>Methods</p> <p>In vivo experiments were performed on adult mice with conditional endothelial-specific expression of the truncation mutation Bmpr2^delx4+, with age-matched transactivator-only mice as controls. Phenotype was assessed by RVSP, counts of muscularized vessels and proliferating cells, and staining for thromboses, inflammatory cells, and apoptotic cells. The effects of BMPR2 knockdown in PMVEC by siRNA on rates of apoptosis were assessed. Affymetrix expression arrays were performed on PMVEC isolated and cultured from triple transgenic mice carrying the immortomouse gene, a transactivator, and either control, Bmpr2^delx4+or Bmpr2^R899Xmutation.</p> <p>Results</p> <p>Transgenic mice showed increased RVSP and corresponding muscularization of small vessels, with histologic alterations including thrombosis, increased inflammatory cells, increased proliferating cells, and a moderate increase in apoptotic cells. Expression arrays showed alterations in specific pathways consistent with the histologic changes. Bmpr2^delx4+and Bmpr2^R899Xmutations resulted in very similar alterations in proliferation, apoptosis, metabolism, and adhesion; Bmpr2^delx4+cells showed upregulation of platelet adhesion genes and cytokines not seen in Bmpr2^R899XPMVEC. Bmpr2 mutation in PMVEC does not cause a loss of differentiation markers as was seen with Bmpr2 mutation in smooth muscle cells.</p> <p>Conclusions</p> <p>Bmpr2 mutation in PMVEC <it>in vivo </it>may drive PAH through multiple, potentially independent, downstream mechanisms, including proliferation, apoptosis, inflammation, and thrombosis.</p