Finding the first generation of galaxies in the early Universe is the greatest step forward towards understanding galaxy formation and evolution. For a strategic survey of such galaxies and the ...interpretation of the obtained data, this paper presents an ultraviolet-to-optical spectral model of galaxies with a great care of the nebular emission. In particular, we present a machine-readable table of intensities of 119 nebular emission lines from Lyα to the rest-frame 1
m as a function of metallicity from zero to the solar one. Based on the spectral model, we present criteria of equivalent widths of Lyα, He iiλ1640, Hα, Hβ and O iiiλ5007 to select extremely metal-poor and metal-free galaxies although these criteria have uncertainty caused by the Lyman continuum escape fraction and the star formation duration. We also present criteria of broad-band colours which will be useful to select candidates for spectroscopic follow-up from drop-out galaxies. We propose the line intensity ratio of O iiiλ5007 to Hβ < 0.1 as the most robust criterion for <1/1000 of the solar metallicity. This ratio of a galaxy with a few M⊙ yr−1 at z∼ 8 is detectable by spectroscopy with the James Webb Space Telescope within a reasonable exposure time.
Summary
A platelet activation receptor, C‐type lectin‐like receptor 2 (CLEC‐2), has been identified as a receptor for a platelet‐activating snake venom, rhodocytin. CLEC‐2 protein is highly expressed ...in platelets/megakaryocytes, and at lower levels in liver Kupffer cells. Recently, podoplanin has been revealed as an endogenous ligand for CLEC‐2. Podoplanin is expressed in certain types of tumor cells, fibroblastic reticular cells (FRCs) in lymph nodes, kidney podocytes, and lymphatic endothelial cells, but not in vascular endothelial cells. CLEC‐2 in platelets cannot have access to podoplanin under normal conditions, but they interact with each other under pathologic conditions or during developmental stages, and play various pathophysiologic roles. CLEC‐2 facilitates hematogenous metastasis of podoplanin‐expressing tumors. During development, the interaction between CLEC‐2 and podoplanin in lymphatic endothelial cells or neuroepithelial cells facilitates blood–lymphatic vessel separation and cerebrovascular patterning and integrity, respectively. In adulthood, platelet CLEC‐2 binding to FRCs is crucial for maintenance of the integrity of high endothelial venules in lymph nodes. Podoplanin‐expressing FRC‐like cells have recently been identified in the bone marrow, and facilitate megakaryocyte proliferation and proplatelet formation by binding to megakaryocyte CLEC‐2. Podoplanin is inducibly expressed in liver monocytes and keratinocytes during Salmonella infection and wound healing, and regulates thrombus formation in the liver and controlled wound healing, respectively. By binding to unknown ligands, platelet CLEC‐2 regulates the maintenance of vascular integrity during inflammation, thrombus stability under flow, and maintenance of quiescence of hematopoietic stem cells. Podoplanin is expressed in various cells, and additional roles of the CLEC‐2–podoplanin interaction will be revealed in the future.
Full text
Available for:
FZAB, GEOZS, GIS, IJS, IMTLJ, IZUM, KILJ, KISLJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBJE, SBMB, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Context. Measuring how the physical properties of galaxies change across cosmic times is essential to understand galaxy formation and evolution. With the advent of numerous ground-based and ...space-borne instruments launched over the past few decades we now have exquisite multi-wavelength observations of galaxies from the far-ultraviolet (FUV) to the radio domain. To tap into this mine of data and obtain new insight into the formation and evolution of galaxies, it is essential that we are able to extract information from their spectral energy distribution (SED). Aims. We present a completely new implementation of Code Investigating GALaxy Emission (CIGALE). Written in python, its main aims are to easily and efficiently model the FUV to radio spectrum of galaxies and estimate their physical properties such as star formation rate, attenuation, dust luminosity, stellar mass, and many other physical quantities. Methods. To compute the spectral models, CIGALE builds composite stellar populations from simple stellar populations combined with highly flexible star formation histories, calculates the emission from gas ionised by massive stars, and attenuates both the stars and the ionised gas with a highly flexible attenuation curve. Based on an energy balance principle, the absorbed energy is then re-emitted by the dust in the mid- and far-infrared domains while thermal and non-thermal components are also included, extending the spectrum far into the radio range. A large grid of models is then fitted to the data and the physical properties are estimated through the analysis of the likelihood distribution. Results. CIGALE is a versatile and easy-to-use tool that makes full use of the architecture of multi-core computers, building grids of millions of models and analysing samples of thousands of galaxies, both at high speed. Beyond fitting the SEDs of galaxies and parameter estimations, it can also be used as a model-generation tool or serve as a library to build new applications.
Full text
Available for:
FMFMET, NUK, UL, UM, UPUK
Over the past decade, a number of excellent reviews on hyperbranched polymers and dendrimers have been published covering the topics from details to highlights and perspectives. The purpose of the ...present article is to review the synthesis, properties, and functionality of dendrimers, hyperbranched polymer, and star polymers with emphasis on functional aspects.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Essentials
The role of C‐type lectin‐like receptor‐2 (CLEC‐2) in cancer progression is unclear.
CLEC‐2‐depleted mouse model is generated by using a rat anti‐mouse CLEC‐2 monoclonal antibody.
CLEC‐2 ...depletion inhibits hematogenous tumor metastasis of podoplanin‐expressing B16F10 cells.
CLEC‐2 depletion prolongs cancer survival by suppressing thrombosis and inflammation.
Summary
Background
C‐type lectin‐like receptor 2 (CLEC‐2) is a platelet activation receptor of sialoglycoprotein podoplanin, which is expressed on the surface of certain types of tumor cells. CLEC‐2–podoplanin interactions facilitate hematogenous tumor metastasis. However, direct evidence of the role of CLEC‐2 in hematogenous metastasis and cancer progression is lacking.
Objective and methods
We generated immunological CLEC‐2‐depleted mice by using anti‐mouse CLEC‐2 monoclonal antibody 2A2B10 and investigated whether CLEC‐2 promoted hematogenous tumor metastasis and tumor growth and exacerbated the prognosis of mice bearing podoplanin‐expressing B16F10 melanoma cells.
Results
Our results showed that hematogenous metastasis was significantly inhibited in CLEC‐2‐depleted mice. B16F10 cells co‐cultured with wild‐type platelets, but not with CLEC‐2‐deficient platelets, showed increased proliferation. However, B16F10 cell proliferation was not inhibited in CLEC‐2‐depleted mice. Histological analysis showed that thrombus formation in tumor vessels was significantly inhibited and functional vessel density was significantly increased in CLEC‐2‐depleted mice. These data suggest that CLEC‐2 deficiency may inhibit thrombus formation in tumor vessels and increase the density of functional vessels, thus improving oxygen and nutrient supply to tumors, indirectly promoting tumor proliferation. Furthermore, the overall survival of CLEC‐2‐depleted mice was significantly prolonged, which may be due to the suppression of thrombus formation in the lungs and subsequent inhibition of systemic inflammation and cachexia.
Conclusions
These data provide a rationale for the targeted inhibition of CLEC‐2 as a new strategy for preventing hematogenous tumor metastasis and for inhibiting cancer‐related thromboembolism.
Full text
Available for:
FZAB, GEOZS, GIS, IJS, IMTLJ, IZUM, KILJ, KISLJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBJE, SBMB, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
We present an updated version of the so-called Madau model for attenuation of the radiation from distant objects by intergalactic neutral hydrogen. First, we derive the distribution function of ...intergalactic absorbers from the latest observational statistics of the Lyα forest, Lyman-limit systems and damped Lyα systems. The distribution function reproduces the observed redshift evolution of the Lyα depression and the mean-free path of the Lyman continuum excellently and simultaneously. We then derive a set of analytic functions describing the mean intergalactic attenuation curve for objects at z > 0.5. The new model predicts less (or more) Lyα attenuation for z ≃ 3–5 (z > 6) sources through the usual broad-band filters relative to the original Madau model. This may cause a systematic difference in the photometric redshift estimates, which is, however, still small: about 0.05. Finally, we find a more than 0.5 mag overestimation of Lyman-continuum attenuation in the original Madau model at z > 3, which causes a significant overcorrection against direct observations of the Lyman continuum of galaxies.
It has been proposed that supermassive black holes (SMBHs) are originated from direct-collapse black holes (DCBHs) that are formed at z ≳ 10 in the primordial gas in the case where H2 cooling is ...suppressed by strong external radiation. In this work, we study the critical specific intensity J
crit required for DCBH formation for various radiation spectral shapes by a series of one-zone calculations of a collapsing primordial-gas cloud. We calculate the critical specific intensity at the Lyman–Werner (LW) bands
$J_{\rm LW,21}^{\rm crit}$
(in units of 10−21 erg s−1 Hz−1 sr−1 cm−2) for realistic spectra of metal-poor galaxies. We find that J
crit is not sensitive to the age or metallicity for the constant star formation galaxies with
$J_{\rm LW,21}^{\rm crit}=1300-1400$
, while J
crit decreases as galaxies become older or more metal-enriched for the instantaneous starburst galaxies. However, for the young (the age < 100 Myr) and/or extremely metal poor (Z < 5 × 10−4 Z⊙) instantaneous starburst galaxies, such dependence is not strong and
$J_{\rm LW,21}^{\rm crit}= 1000-1400$
. We also find that J
crit is solely determined by the ratio between the H− and H2 photodissociation rate coefficients,
$k_{\rm H^-,pd}/k_{\rm H_2,pd}$
, with which we develop a formula to estimate J
crit for a given spectrum. The higher value of J
crit for the realistic spectra than those expected in the literature significantly reduces the estimated DCBH number density n
DCBH. By extrapolating the result of Dijkstra, Ferrara & Mesinger, we obtain n
DCBH ∼ 10−10 cMpc−3 at z = 10, which is roughly consistent with the observed number density of high-redshift SMBHs n
SMBH ∼ 10−9 cMpc−3 at z ∼ 6, considering large uncertainties in the estimation.
Purinergic systems in microglia Inoue, K
Cellular and molecular life sciences : CMLS,
10/2008, Volume:
65, Issue:
19
Journal Article
Peer reviewed
Accumulating findings indicate that nucleotides play an important role in microglia through P2 purinoceptors. P2 purinoceptors are divided into two families, ionotropic receptors (P2X) and ...metabotropic receptors (P2Y). P2X receptors (7 types; P2X₁ - P2X₇) contain intrinsic pores that open by binding with ATP. P2Y receptors (8 types; P2Y₁, ₂, ₄, ₆, ₁₁, ₁₂, ₁₃ and ₁₄) are activated by nucleotides and couple to intracellular second-messenger systems through heteromeric G-proteins. Nucleotides are released or leaked from non-excitable cells as well as neurons in physiological and pathophysiological conditions. Microglia express many types of P2 purinoceptors and are known as resident macrophages in the CNS. ATP and other nucleotides work as 'warning molecules' especially through activating microglia in pathophysiological conditions. Microglia play a key role in neuropathic pain, chemotaxis and phagocytosis through nucleotide-evoked activation of P2X₄, P2Y₁₂ and P2Y₆ receptors, respectively. These findings indicate that extracellular nucleotides are important players in the central stage of microglial function.
Full text
Available for:
EMUNI, FZAB, GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UL, UM, UPUK, VKSCE, ZAGLJ
C‐type lectin‐like receptor 2 (CLEC‐2) has been identified as a receptor for the platelet activating snake venom rhodocytin. CLEC‐2 elicits powerful platelet activation signals in conjunction with ...Src, Syk kinases, and phospholipase Cγ2, similar to the collagen receptor glycoprotein (GP) VI/FcRγ‐chain complex. In contrast to GPVI/FcRγ, which initiates platelet activation through the tandem YxxL motif immunoreceptor tyrosine‐based activation motif (ITAM), CLEC‐2 signals via the single YxxL motif hemi‐ITAM. The endogenous ligand of CLEC‐2 has been identified as podoplanin, which is expressed on the surface of tumour cells and facilitates tumour metastasis by inducing platelet activation. Studies of CLEC‐2‐deficient mice have revealed several physiological roles of CLEC‐2. Podoplanin is also expressed in lymphatic endothelial cells as well as several other cells, including type I alveolar cells and kidney podocytes, but is absent from vascular endothelial cells. In the developmental stages, when the primary lymph sac is derived from the cardinal vein, podoplanin activates platelets in lymphatic endothelial cells by binding to CLEC‐2, which facilitates blood/lymphatic vessel separation. Moreover, CLEC‐2 is involved in thrombus stabilisation under flow conditions in part through homophilic interactions. However, the absence of CLEC‐2 does not significantly increase bleeding tendency. CLEC‐2 may be a good target protein for novel anti‐platelet drugs or anti‐metastatic drugs having therapeutic and preventive effects on arterial thrombosis and cancer, the primary causes of mortality in developed countries. In this article, we review the mechanisms of signal transduction, structure, expression, and function of CLEC‐2.
Full text
Available for:
FZAB, GEOZS, GIS, IJS, IMTLJ, IZUM, KILJ, KISLJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBJE, SBMB, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Abstract
We present an analysis to disentangle the connection between physical quantities that characterize the conditions of ionized H ii regions – metallicity (Z), ionization parameter (U), and ...electron density (ne) – and the global stellar mass (M*) and specific star formation rate (sSFR = SFR/M*) of the host galaxies. We construct composite spectra of galaxies at 0.027 ≤ z ≤ 0.25 from Sloan Digital Sky Survey, separating the sample into bins of M* and sSFR, and estimate the nebular conditions from the emission-line flux ratios. Specially, metallicity is estimated from the direct method based on the faint auroral lines O iiiλ4363 and O iiλλ7320,7330. The derived metallicities cover a range of 12 + log O/H ∼ 7.6–8.9. It is found that the three nebular parameters, Z, U, and ne, are tightly correlated with the location in the M*–sSFR plane. With simple physically motivated ansätze, we derive scaling relations between these physical quantities by performing multiregression analysis. In particular, we find that U is primarily controlled by sSFR, as U∝sSFR0.43, but also depends significantly on both Z and ne. The derived partial dependence of U∝Z−0.36 is weaker than the apparent correlation (U∝Z−1.52). The partial dependence of U on ne is found to be $U \propto n_\mathrm{e}^{-0.29}$. The scaling relations we derived are in agreement with predictions from theoretical models and observations of each aspect of the link between these quantities. Our results provide a useful set of equations to predict the nebular conditions and emission-line fluxes of galaxies in semi-analytic models.