Volatiles in glasses from the HSDP2 drill core

H2O, CO2, S, Cl, and F concentrations are reported for 556 glasses from the submarine section of the 1999 phase of HSDP drilling in Hilo, Hawaii, providing a high-resolution record of magmatic volatiles over ~200 kyr of a Hawaiian volcano's lifetime. Glasses range from undegassed to having lost significant volatiles at near-atmospheric pressure. Nearly all hyaloclastite glasses are degassed, compatible with formation from subaerial lavas that fragmented on entering the ocean and were transported by gravity flows down the volcano flank. Most pillows are undegassed, indicating submarine eruption. The shallowest pillows and most massive lavas are degassed, suggesting formation by subaerial flows that penetrated the shoreline and flowed some distance under water. Some pillow rim glasses have H2O and S contents indicating degassing but elevated CO2 contents that correlate with depth in the core; these tend to be more fractionated and could have formed by mixing of degassed, fractionated magmas with undegassed magmas during magma chamber overturn or by resorption of rising CO2-rich bubbles by degassed magmas. Intrusive glasses are undegassed and have CO2 contents similar to adjacent pillows, indicating intrusion shallow in the volcanic edifice. Cl correlates weakly with H2O and S, suggesting loss during low-pressure degassing, although most samples appear contaminated by seawater-derived components. F behaves as an involatile incompatible element. Fractionation trends were modeled using MELTS. Degassed glasses require fractionation at pH2O ≈ 5–10 bars. Undegassed low-SiO2 glasses require fractionation at pH2O ≈ 50 bars. Undegassed and partially degassed high-SiO2 glasses can be modeled by coupled crystallization and degassing. Eruption depths of undegassed pillows can be calculated from their volatile contents assuming vapor saturation. The amount of subsidence can be determined from the difference between this depth and the sample's depth in the core. Assuming subsidence at 2.5 mm/y, the amount of subsidence suggests ages of ~500 ka for samples from the lower 750 m of the core, consistent with radiometric ages. H2O contents of undegassed low-SiO2 HSDP2 glasses are systematically higher than those of high-SiO2 glasses, and their H2O/K2O and H2O/Ce ratios are higher than typical tholeiitic pillow rim glasses from Hawaiian volcanoes

Exosomes Mediate Zika Virus Transmission Through SMPD3 Neutral Sphingomyelinase in Cortical Neurons

The harmful effects of ZIKA virus (ZIKV) infection are reflected by severe neurological manifestations such as microcephaly in neonates and other complications associated with Guillain-Barre syndrome in adults. The transmission dynamics of ZIKV in or between neurons, or within the developing brains of the foetuses are not fully understood. Using primary cultures of murine cortical neurons, we show that ZIKV uses exosomes as mediators of viral transmission between neurons. Cryo-electron microscopy showed heterogeneous population of neuronal exosomes with a size range of 30-200 nm. Increased production of exosomes from neuronal cells was noted upon ZIKV infection. Neuronal exosomes contained both ZIKV viral RNA and protein(s) that were highly infectious to naive cells. RNaseA and neutralizing antibodies treatment studies suggest the presence of viral RNA/proteins inside exosomes. Exosomes derived from time- and dose-dependent incubations showed increasing viral loads suggesting higher packaging and delivery of ZIKV RNA and proteins. Furthermore, we noted that ZIKV induced both activity and gene expression of neutral Sphingomyelinase (nSMase)-2/SMPD3, an important molecule that regulates production and release of exosomes. Silencing of SMPD3 in neurons resulted in reduced viral burden and transmission through exosomes. Treatment with SMPD3 specific inhibitor GW4869, significantly reduced ZIKV loads in both cortical neurons and in exosomes derived from these neuronal cells. Taken together, our results suggest that ZIKV modulates SMPD3 activity in cortical neurons for its infection and transmission through exosomes perhaps leading to severe neuronal death that may result in neurological manifestations such as microcephaly in the developing embryonic brains

The character of Vermont : twentieth-anniversary reflections

Occasional paper (University of Vermont. Center for Research on Vermont) ; no. 19. pt. 1. The character of Vermont : then and now / Michael Sherman and Jennie Versteeg -- pt. 2. Vermont research and the center for research on Vermont / Samuel B. Hand, Paul Gillies

Evaluating the Potential Efficacy of Invasive Lionfish (Pterois volitans) Removals

The lionfish, Pterois volitans (Linnaeus) and Pterois miles (Bennett), invasion of the Western Atlantic Ocean, Caribbean Sea and Gulf of Mexico has the potential to alter aquatic communities and represents a legitimate ecological concern. Several local removal programs have been initiated to control this invasion, but it is not known whether removal efforts can substantially reduce lionfish numbers to ameliorate these concerns. We used an age-structured population model to evaluate the potential efficacy of lionfish removal programs and identified critical data gaps for future studies. We used high and low estimates for uncertain parameters including: length at 50% vulnerability to harvest (Lvul), instantaneous natural mortality (M), and the Goodyear compensation ratio (CR). The model predicted an annual exploitation rate between 35 and 65% would be required to cause recruitment overfishing on lionfish populations for our baseline parameter estimates for M and CR (0.5 and 15). Lionfish quickly recovered from high removal rates, reaching 90% of unfished biomass six years after a 50-year simulated removal program. Quantifying lionfish natural mortality and the size-selective vulnerability to harvest are the most important knowledge gaps for future research. We suggest complete eradication of lionfish through fishing is unlikely, and substantial reduction of adult abundance will require a long-term commitment and may be feasible only in small, localized areas where annual exploitation can be intense over multiple consecutive years

Discovery of Exosomes From Tick Saliva and Salivary Glands Reveals Therapeutic Roles for CXCL12 and IL-8 in Wound Healing at the Tick-Human Skin Interface

Ticks secrete various anti-coagulatory, anti-vasoconstrictory, anti-inflammatory, and anti-platelet aggregation factors in their saliva at the bite site during feeding to evade host immunological surveillance and responses. For the first time, we report successful isolation of exosomes (small membrane-bound extracellular signaling vesicles) from saliva and salivary glands of partially fed or unfed ixodid ticks. Our data showed a novel role of these in vivo exosomes in the inhibition of wound healing via downregulation of C-X-C motif chemokine ligand 12 (CXCL12) and upregulation of interleukin-8 (IL-8). Cryo-electron microscopy (cryo-EM) analysis revealed that tick saliva and salivary glands are composed of heterogeneous populations of in vivo exosomes with sizes ranging from 30 to 200 nm. Enriched amounts of tick CD63 ortholog protein and heat shock protein 70 (HSP70) were evident in these exosomes. Treatment of human skin keratinocytes (HaCaT cells) with exosomes derived from tick saliva/salivary glands or ISE6 cells dramatically delayed cell migration, wound healing, and repair process. Wound healing is a highly dynamic process with several individualized processes including secretion of cytokines. Cytokine array profiling followed by immunoblotting and quantitative-PCR analysis revealed that HaCaT cells treated with exosomes derived from tick saliva/salivary glands or ISE6 cells showed enhanced IL-8 levels and reduced CXCL12 loads. Inhibition of IL-8 or CXCL12 further delayed exosome-mediated cell migration, wound healing, and repair process, suggesting a skin barrier protection role for these chemokines at the tick bite site. In contrast, exogenous treatment of CXCL12 protein completely restored this delay and enhanced the repair process. Taken together, our study provides novel insights on how tick salivary exosomes secreted in saliva can delay wound healing at the bite site to facilitate successful blood feeding

Discovery of Exosomes From Tick Saliva and Salivary Glands Reveals Therapeutic Roles for CXCL12 and IL-8 in Wound Healing at the Tick–Human Skin Interface

© Copyright © 2020 Zhou, Tahir, Wang, Woodson, Sherman, Karim, Neelakanta and Sultana.Ticks secrete various anti-coagulatory, anti-vasoconstrictory, anti-inflammatory, and anti-platelet aggregation factors in their saliva at the bite site during feeding to evade host immunological surveillance and responses. For the first time, we report successful isolation of exosomes (small membrane-bound extracellular signaling vesicles) from saliva and salivary glands of partially fed or unfed ixodid ticks. Our data showed a novel role of these in vivo exosomes in the inhibition of wound healing via downregulation of C-X-C motif chemokine ligand 12 (CXCL12) and upregulation of interleukin-8 (IL-8). Cryo-electron microscopy (cryo-EM) analysis revealed that tick saliva and salivary glands are composed of heterogeneous populations of in vivo exosomes with sizes ranging from 30 to 200 nm. Enriched amounts of tick CD63 ortholog protein and heat shock protein 70 (HSP70) were evident in these exosomes. Treatment of human skin keratinocytes (HaCaT cells) with exosomes derived from tick saliva/salivary glands or ISE6 cells dramatically delayed cell migration, wound healing, and repair process. Wound healing is a highly dynamic process with several individualized processes including secretion of cytokines. Cytokine array profiling followed by immunoblotting and quantitative-PCR analysis revealed that HaCaT cells treated with exosomes derived from tick saliva/salivary glands or ISE6 cells showed enhanced IL-8 levels and reduced CXCL12 loads. Inhibition of IL-8 or CXCL12 further delayed exosome-mediated cell migration, wound healing, and repair process, suggesting a skin barrier protection role for these chemokines at the tick bite site. In contrast, exogenous treatment of CXCL12 protein completely restored this delay and enhanced the repair process. Taken together, our study provides novel insights on how tick salivary exosomes secreted in saliva can delay wound healing at the bite site to facilitate successful blood feeding

Arthropod EVs Mediate Dengue Virus Transmission Through Interaction With a Tetraspanin Domain Containing Glycoprotein Tsp29Fb

Dengue virus (DENV) is a mosquito-borne flavivirus that causes dengue fever in humans, worldwide. Using in vitro cell lines derived from Aedes albopictus and Aedes aegypti, the primary vectors of DENV, we report that DENV2/DENV3-infected cells secrete extracellular vesicles (EVs), including exosomes, containing infectious viral RNA and proteins. A full-length DENV2 genome, detected in arthropod EVs, was infectious to naïve mosquito and mammalian cells, including human-skin keratinocytes and blood endothelial cells. Cryo-electron microscopy showed mosquito EVs with a size range from 30 to 250 nm. Treatments with RNase A, Triton X-100, and 4G2 antibody-bead binding assays showed that infectious DENV2-RNA and proteins are contained inside EVs. Viral plaque formation and dilution assays also showed securely contained infectious viral RNA and proteins in EVs are transmitted to human cells. Up-regulated HSP70 upon DENV2 infection showed no role in viral replication and transmission through EVs. In addition, qRT-PCR and immunoblotting results revealed that DENV2 up-regulates expression of a mosquito tetraspanin-domain–containing glycoprotein, designated as Tsp29Fb, in A. aegypti mosquitoes, cells, and EVs. RNAi-mediated silencing and antibody blocking of Tsp29Fb resulted in reduced DENV2 loads in both mosquito cells and EVs. Immunoprecipitation showed Tsp29Fb to directly interact with DENV2 E-protein. Furthermore, treatment with GW4869 (exosome-release inhibitor) affected viral burden, direct interaction of Tsp29Fb with E-protein and EV-mediated transmission of viral RNA and proteins to naïve human cells. In summary, we report a very important finding on EV-mediated transmission of DENV2 from arthropod to mammalian cells through interactions with an arthropod EVs-enriched marker Tsp29Fb