On the ultraviolet signatures of small scale heating in coronal loops

Studying the statistical properties of solar ultraviolet emission lines could provide information about the nature of small scale coronal heating. We expand on previous work to investigate these properties. We study whether the predicted statistical distribution of ion emission line intensities produced by a specified heating function is affected by the isoelectronic sequence to which the ion belongs, as well as the characteristic temperature at which it was formed. Particular emphasis is placed on the strong resonance lines belonging to the lithium isoelectronic sequence. Predictions for emission lines observed by existing space-based UV spectrometers are given. The effects on the statistics of a line when observed with a wide-band imaging instrument rather than a spectrometer are also investigated. We use a hydrodynamic model to simulate the UV emission of a loop system heated by nanoflares on small, spatially unresolved scales. We select lines emitted at similar temperatures but belonging to different isoelectronic groups: Fe IX and Ne VIII, Fe XII and Mg X, Fe XVII, Fe XIX and Fe XXIV. Our simulations confirm previous results that almost all lines have an intensity distribution that follows a power-law, in a similar way to the heating function. However, only the high temperature lines best preserve the heating function's power law index (Fe XIX being the best ion in the case presented here). The Li isoelectronic lines have different statistical properties with respect to the lines from other sequences, due to the extended high temperature tail of their contribution functions. However, this is not the case for Fe XXIV which may be used as a diagnostic of the coronal heating function. We also show that the power-law index of the heating function is effectively preserved when a line is observed by a wide-band imaging instrument rather than a spectromenter

Zika Virus Tissue and Blood Compartmentalization in Acute Infection of Rhesus Macaques.

Animal models of Zika virus (ZIKV) are needed to better understand tropism and pathogenesis and to test candidate vaccines and therapies to curtail the pandemic. Humans and rhesus macaques possess similar fetal development and placental biology that is not shared between humans and rodents. We inoculated 2 non-pregnant rhesus macaques with a 2015 Brazilian ZIKV strain. Consistent with most human infections, the animals experienced no clinical disease but developed short-lived plasma viremias that cleared as neutralizing antibody developed. In 1 animal, viral RNA (vRNA) could be detected longer in whole blood than in plasma. Despite no major histopathologic changes, many adult tissues contained vRNA 14 days post-infection with highest levels in hemolymphatic tissues. These observations warrant further studies to investigate ZIKV persistence and its potential clinical implications for transmission via blood products or tissue and organ transplants

Intraamniotic Zika virus inoculation of pregnant rhesus macaques produces fetal neurologic disease.

Zika virus (ZIKV) infection of pregnant women can cause fetal microcephaly and other neurologic defects. We describe the development of a non-human primate model to better understand fetal pathogenesis. To reliably induce fetal infection at defined times, four pregnant rhesus macaques are inoculated intravenously and intraamniotically with ZIKV at gestational day (GD) 41, 50, 64, or 90, corresponding to first and second trimester of gestation. The GD41-inoculated animal, experiencing fetal death 7 days later, has high virus levels in fetal and placental tissues, implicating ZIKV as cause of death. The other three fetuses are carried to near term and euthanized; while none display gross microcephaly, all show ZIKV RNA in many tissues, especially in the brain, which exhibits calcifications and reduced neural precursor cells. Given that this model consistently recapitulates neurologic defects of human congenital Zika syndrome, it is highly relevant to unravel determinants of fetal neuropathogenesis and to explore interventions

Intraamniotic Zika virus inoculation of pregnant rhesus macaques produces fetal neurologic disease.

Zika virus (ZIKV) infection of pregnant women can cause fetal microcephaly and other neurologic defects. We describe the development of a non-human primate model to better understand fetal pathogenesis. To reliably induce fetal infection at defined times, four pregnant rhesus macaques are inoculated intravenously and intraamniotically with ZIKV at gestational day (GD) 41, 50, 64, or 90, corresponding to first and second trimester of gestation. The GD41-inoculated animal, experiencing fetal death 7 days later, has high virus levels in fetal and placental tissues, implicating ZIKV as cause of death. The other three fetuses are carried to near term and euthanized; while none display gross microcephaly, all show ZIKV RNA in many tissues, especially in the brain, which exhibits calcifications and reduced neural precursor cells. Given that this model consistently recapitulates neurologic defects of human congenital Zika syndrome, it is highly relevant to unravel determinants of fetal neuropathogenesis and to explore interventions

C–F Bond activation at Ni(0) and simple reactions of square planar Ni(ii) fluoride complexes

The reaction of Ni(COD)2(COD = 1,5-cyclooctadiene) with triethylphosphine and pentafluoropyridine in hexane has been shown previously to yield trans-[NiF(2-C5NF4)(PEt3)2]( 1a) with a preference for reaction at the 2-position of the heteroaromatic. The corresponding reaction with 2,3,5,6-tetrafluoropyridine was shown to yield trans-[NiF(2-C5NF3H)(PEt3)2]( 1b). In this paper, we show that reaction of Ni(COD)2 with triethylphosphine and pentafluoropyridine in THF yields a mixture of 1a and 1b. Competition reactions of Ni(COD)2 with triethylphosphine in the presence of mixtures of heteroaromatics in hexane reveal a kinetic preference of k(pentafluoropyridine) : k(2,3,5,6-tetrafluoropyridine)= 5.4 : 1. Treatment of 1a and 1b with Me3SiN3 affords trans-[Ni(N3)(2-C5NF4)(PEt3)2]( 2a) and trans-[Ni(N3)(2-C5NHF3)(PEt3)2]( 2b), respectively. The complex trans-[Ni(NCO)(2-C5NHF3)(PEt3)2]( 3b) is obtained on reaction of 1b with Me3SiNCO and by photolysis of 2b under CO, while trans-[Ni(1-CCPh)(2-C5NF4)(PEt3)2]( 4a) is obtained by reaction of phenylacetylene with 1a. Addition of KCN, KI and NaOAc to complex 1a affords trans-[Ni(X)(2-C5NF4)(PEt3)2]( 5a X = CN, 6a X = I, 7a X = OAc), respectively. The PEt3 groups of complex 1a are readily replaced by addition of 1,2-bis(dicyclohexylphosphino)ethane (dcpe) to produce [NiF(2-C5F4N)(dcpe)]( 8a). Addition of dcpe to trans-[Ni(OTf)(2-C5F4N)(PEt3)2]( 10a), however, yields the salt [Ni(2-C5F4N)(dcpe)(PEt3)](OTf)( 9a) by substitution of only one PEt3 and displacement of the triflate ligand. The structures of 2b, 4a, 7a and 8a were determined by X-ray crystallography. The influence of different ancillary ligands on the bond lengths and angles of square-planar nickel structures with polyfluoropyridyl ligands is analysed

Zika Virus Tissue and Blood Compartmentalization in Acute Infection of Rhesus Macaques

<div><p>Animal models of Zika virus (ZIKV) are needed to better understand tropism and pathogenesis and to test candidate vaccines and therapies to curtail the pandemic. Humans and rhesus macaques possess similar fetal development and placental biology that is not shared between humans and rodents. We inoculated 2 non-pregnant rhesus macaques with a 2015 Brazilian ZIKV strain. Consistent with most human infections, the animals experienced no clinical disease but developed short-lived plasma viremias that cleared as neutralizing antibody developed. In 1 animal, viral RNA (vRNA) could be detected longer in whole blood than in plasma. Despite no major histopathologic changes, many adult tissues contained vRNA 14 days post-infection with highest levels in hemolymphatic tissues. These observations warrant further studies to investigate ZIKV persistence and its potential clinical implications for transmission via blood products or tissue and organ transplants.</p></div

ZIKV infection of 2 adult macaques.

<p>a) Virus inoculation and sampling timeline. Two West Nile virus-antibody negative non-pregnant female macaques received an intravenous inoculation of 5.0 log₁₀ PFU of a 2015 Brazilian ZIKV strain on day 0. Signs of clinical disease were recorded twice daily. Animals were anesthetized daily from 1 to 8 then on 10, 12 and 14 dpi for blood collection and euthanized for tissue collection 14 dpi. Plasma and whole blood ZIKV RNA and infectious virus levels and kinetics b) for animal 5021 and c) for animal 5242. ZIKV RNA levels in plasma (filled circles) and whole blood (filled squares) are reported in mean log₁₀ RNA copies/ml and were assayed in duplicate. Infectious virus levels in plasma (open circles) were measured as Vero cell plaque forming units/ml. Colored bars under the graph show the period plasma tested ZIKV RNA reactive by the Aptima<b>®</b> assay. NT indicates ‘not tested. Dotted line shows limits of detection for both assays 1.6 log₁₀ RNA copies or PFU per ml. d) Neutralizing and binding antibody kinetics and magnitude. ZIKV 80PRNT endpoint antibody titers are reported. The first plasma dilution tested was 1:20. The box shows the ZIKV IgG ELISA test results on plasma tested at a dilution of 1:50; plus and minus signs indicate positive or no reactivity, respectively. e) Saliva ZIKV RNA levels and kinetics. ZIKV RNA levels in saliva eluted from cotton swabs placed in the cheek of macaques, reported in mean log₁₀ RNA copies/ml or gram, were assayed in triplicate with standard deviations noted. The dotted line shows the limit of detection, 2.3 log₁₀ RNA copies/ml or gram.</p

ZIKV tissue distribution in macaques.

<p>ZIKV RNA was measured by qRT-PCR assay in triplicate with standard deviations noted for <b>a)</b> animal 5021 and <b>b)</b> animal 5242. The limit of detection varied depending on the weight of tissue sampled and volume of MEM needed to homogenize to liquefaction, with a mean of 2.3 (range 1.4–4) log₁₀ RNA copies per gram; non-reactive samples are reported at 2.0. log₁₀ RNA copies per gram. Arrows indicate qRT-PCR negative samples that tested positive by the qualitative Aptima<b>®</b> assay. nc indicates not collected.</p

The immunomodulatory role of the hypothalamus-pituitary-gonad axis: Proximate mechanism for reproduction-immune trade offs?

The present review discusses the communication between the hypothalamic-pituitary-gonad (HPG) axis and the immune system of vertebrates, attempting to situate the HPG-immune interaction into the context of life history trade-offs between reproductive and immune functions. More specifically, (i) we review molecular and cellular interactions between hormones of the HPG axis, and, as far as known, the involved mechanisms on immune functions, (ii) we evaluate whether the HPG-immune crosstalk serves as proximate mechanism mediating reproductive-immune trade-offs, and (iii) we ask whether the nature of the HPG-immune interaction is conserved throughout vertebrate evolution, despite the changes in immune functions, reproductive modes, and life histories. In all vertebrate classes studied so far, HPG hormones have immunomodulatory functions, and indications exist that they contribute to reproduction-immunity resource trade-offs, although the very limited information available for most non-mammalian vertebrates makes it difficult to judge how comparable or different the interactions are. There is good evidence that the HPG-immune crosstalk is part of the proximate mechanisms underlying the reproductive-immune trade-offs of vertebrates, but it is only one factor in a complex network of factors and processes. The fact that the HPG-immune interaction is flexible and can adapt to the functional and physiological requirements of specific life histories. Moreover, the assumption of a relatively fixed pattern of HPG influence on immune functions, with, for example, androgens always leading to immunosuppression and estrogens always being immunoprotective, is probably oversimplified, but the HPG-immune interaction can vary depending on the physiological and envoironmental context. Finally, the HPG-immune interaction is not only driven by resource trade-offs, but additional factors such as, for instance, the evolution of viviparity shape this neuroendocrine-immune relationship