Trophic ecology of the invasive argentine ant: spatio-temporal variation in resource assimilation and isotopic enrichment

Studies of food webs often employ stable isotopic approaches to infer trophic position and interaction strength without consideration of spatio-temporal variation in resource assimilation by constituent species. Using results from laboratory diet manipulations and monthly sampling of field populations, we illustrate how nitrogen isotopes may be used to quantify spatio-temporal variation in resource assimilation in ants. First, we determined nitrogen enrichment using a controlled laboratory experiment with the invasive Argentine ant (Linepithema humile). After 12 weeks, worker δ15N values from colonies fed an animal-based diet had δ15N values that were 5.51% greater compared to colonies fed a plant-based diet. The shift in δ15N values in response to the experimental diet occurred within 10 weeks. We next reared Argentine ant colonies with or without access to honeydew-producing aphids and found that after 8 weeks workers from colonies without access to aphids had δ15N values that were 6.31% larger compared to colonies with access to honeydew. Second, we sampled field populations over a 1-year period to quantify spatio-temporal variability in isotopic ratios of L. humile and those of a common native ant (Solenopsis xyloni). Samples from free-living colonies revealed that fluctuations in δ15N were 1.6–2.4‰ for L. humile and 1.8–2.9‰ for S. xyloni. Variation was also detected among L. humile castes: time averaged means of δ15N varied from 1.2 to 2.5‰ depending on the site, with δ15N values for queens ≥ workers > brood. The estimated trophic positions of L. humile and S. xyloni were similar within a site; however, trophic position for each species differed significantly at larger spatial scales. While stable isotopes are clearly useful for examining the trophic ecology of arthropod communities, our results suggest that caution is warranted when making ecological interpretations when stable isotope collections come from single time periods or life stages

Model checking system software with CMC

Complex systems have errors that involve mishandled cor-ner cases in intricate sequences of events. Conventional test-ing techniques usually miss these errors. In recent years, formal verification techniques such as [5] have gained pop-ularity in checking a property in all possible behaviors of a system. However, such techniques involve generating an ab-stract model of the system. Such an abstraction process is unreliable, difficult and miss a lot of implementation errors. CMC is a framework for model checking a broad class of software written in the C programming language. CMC runs the software implementation directly without deriving an ab-stract model of the code. We used CMC to model check an existing implementation of AODV (Ad Hoc On Demand Dis-tance Vector) routing protocol and found a total of bugs in two implementations [7],[6] of the protocol. One of them is a bug in the actual specification of the AODV protocol [3]. We also used CMC on the IP Fragmentation module in the Linux TCP/IPv4 stack and verified its correctness for up to fragments per packet.

SCUBA-2 Ultra Deep Imaging EAO Survey (STUDIES). II. Structural Properties and Near-infrared Morphologies of Faint Submillimeter Galaxies

We present structural parameters and morphological properties of faint 450 μm selected submillimeter galaxies (SMGs) from the JCMT Large Program, STUDIES, in the COSMOS-CANDELS region. Their properties are compared to an 850 μm selected and a matched star-forming samples. We investigate stellar structures of 169 faint 450 μm sources (S 450 = 2.8–29.6 mJy; S/N > 4) at z 2 mJy) and more extended than the star-forming galaxies in the same redshift range. For the stellar mass and SFR-matched sample at z sime 1 and z sime 2, the size differences are marginal between faint SMGs and the matched galaxies. Moreover, faint SMGs have similar Sérsic indices and projected axis ratios as star-forming galaxies with the same stellar mass and SFR. Both SMGs and the matched galaxies show high fractions (~70%) of disturbed features at z sime 2, and the fractions depend on the SFRs. These suggest that their star formation activity is related to galaxy merging and the stellar structures of SMGs are similar to those of star-forming galaxies. We show that the depths of submillimeter surveys are approaching the lower luminosity end of star-forming galaxies, allowing us to detect galaxies on the main sequence

Differential baseline and response profile to IFN-γ gene transduction of IL-6/IL-6 receptor-α secretion discriminate primary tumors versus bone marrow metastases of nasopharyngeal carcinomas in culture

<p>Abstract</p> <p>Background</p> <p>Understanding of immunobiology of bone marrow metastases (designated BM-NPC) <it>versus </it>primary tumors (P-NPC) of the nasopharynx is far from complete. The aim of this study was to determine if there would be differences between cultured P-NPCs and BM-NPCs with respect to (i) constitutive IL-6 and the IL-6 receptor gp80 subunit (IL-6Rα) levels in the spent media of nontransduced cells, and (ii) IL-6 and IL-6Rα levels in the spent media of cells transduced with a retroviral vector containing the <it>IFN-γ </it>gene.</p> <p>Methods</p> <p>A panel of NPC cell lines were transduced with the <it>IFN-γ </it>gene through a retroviral vector. Four clonal sublines were isolated <it>via </it>limiting dilution methods. Cytofluorometric analysis was performed for the detection of cell surface antigens of HLA class I, HLA class II and ICAM-1. ELISA was used to assay for IFN-γ, IL-6 and IL-6Rα in the spent media of cultured cell lines.</p> <p>Results</p> <p>Our results showed that in day 3 culture supernatants, low levels of soluble IL-6 were detected in 5/5 cultured tumors derived from P-NPCs, while much higher constitutive levels of IL-6 were detected in 3/3 metastasis-derived NPC cell lines including one originated from ascites; the difference was significant (<it>p </it>= 0.025). An inverse relationship was found between IL-6Rα and IL-6 in their release levels in cultured P-NPCs and metastasis-derived NPCs. In <it>IFN-γ</it>-transduced-P-NPCs, IL-6 production increased and yet IL-6Rα decreased substantially, as compared to nontransduced counterparts. At variance with P-NPC cells, the respective ongoing IL-6 and IL-6Rα release patterns of BM-NPC cells were not impeded as much following <it>IFN-γ </it>transduction. These observations were confirmed by extended kinetic studies with representative NPC cell lines and clonal sublines. The latter observation with the clonal sublines also indicates that selection for high IL-6 or low IL-6Rα producing subpopulations did not occur as a result of <it>IFN-γ</it>-transduction process. P-NPCs, which secreted constitutively only marginal levels of IFN-γ (8.4 ~ 10.5 pg/ml), could be enhanced to produce higher levels of IFN-γ (6.8- to 10.3-fold increase) after <it>IFN-γ </it>transduction. Unlike P-NPCs, BM-NPCs spontaneously released IFN-γ at moderate levels (83.8 ~ 100.7 pg/ml), which were enhanced by 1.3- to 2.2-fold in the spent media of their <it>IFN-γ</it>-transduced counterparts.</p> <p>Conclusion</p> <p>Our results showed that cultured P-NPCs and BM-NPCs could be distinguished from one another on the basis of their differential baseline secretion pattern of IFN-γ, IL-6 and IL-6Rα, and their differential response profiles to <it>IFN-γ </it>gene transfer of the production of these three soluble molecules. These results suggest that the IL-6 and IFN-γ pathways in a background of genetic instability be involved in the acquisition of metastatic behaviour in BM-NPCs.</p

Simultaneous siRNA Targeting of Src and Downstream Signaling Molecules Inhibit Tumor Formation and Metastasis of a Human Model Breast Cancer Cell Line

Src and signaling molecules downstream of Src, including signal transducer and activator of transcription 3 (Stat3) and cMyc, have been implicated in the development, maintenance and/or progression of several types of human cancers, including breast cancer. Here we report the ability of siRNA-mediated Src knock-down alone, and simultaneous knock-down of Src and Stat3 and/or cMyc to inhibit the neoplastic phenotype of a highly metastatic human model breast cancer cell line, MDA-MB-435S, a widely used model for breast cancer research.Src and its downstream signaling partners were specifically targeted and knocked-down using siRNA. Changes in the growth properties of the cultured cancer cells/tumors were documented using assays that included anchorage-dependent and -independent (in soft agar) cell growth, apoptosis, and both primary and metastatic tumor growth in the mouse tumor model. siRNA-mediated Src knock-down alone, and simultaneous knock-down of Src and Stat3 and/or cMyc inhibited the neoplastic phenotype of a highly metastatic human model breast cancer cell line, MDA-MB-435S. This knock-down resulted in reduced growth in monolayer and soft agar cultures, and a reduced ability to form primary tumors in NOD/SCID mice. In addition, direct intra-tumoral injection of siRNAs targeting these signaling molecules resulted in a substantial inhibition of tumor metastases as well as of primary tumor growth. Simultaneous knock-down of Src and Stat3, and/or Myc exhibited the greatest effects resulting in substantial inhibition of primary tumor growth and metastasis.These findings demonstrate the effectiveness of simultaneous targeting of Src and the downstream signaling partners Stat3 and/or cMyc to inhibit the growth and oncogenic properties of a human cancer cell line. This knowledge may be very useful in the development of future therapeutic approaches involving targeting of specific genes products involved in tumor growth and metastasis

The Human Gonadotropin Releasing Hormone Type I Receptor Is a Functional Intracellular GPCR Expressed on the Nuclear Membrane

The mammalian type I gonadotropin releasing hormone receptor (GnRH-R) is a structurally unique G protein-coupled receptor (GPCR) that lacks cytoplasmic tail sequences and displays inefficient plasma membrane expression (PME). Compared to its murine counterparts, the primate type I receptor is inefficiently folded and retained in the endoplasmic reticulum (ER) leading to a further reduction in PME. The decrease in PME and concomitant increase in intracellular localization of the mammalian GnRH-RI led us to characterize the spatial distribution of the human and mouse GnRH receptors in two human cell lines, HEK 293 and HTR-8/SVneo. In both human cell lines we found the receptors were expressed in the cytoplasm and were associated with the ER and nuclear membrane. A molecular analysis of the receptor protein sequence led us to identify a putative monopartite nuclear localization sequence (NLS) in the first intracellular loop of GnRH-RI. Surprisingly, however, neither the deletion of the NLS nor the addition of the Xenopus GnRH-R cytoplasmic tail sequences to the human receptor altered its spatial distribution. Finally, we demonstrate that GnRH treatment of nuclei isolated from HEK 293 cells expressing exogenous GnRH-RI triggers a significant increase in the acetylation and phosphorylation of histone H3, thereby revealing that the nuclear-localized receptor is functional. Based on our findings, we conclude that the mammalian GnRH-RI is an intracellular GPCR that is expressed on the nuclear membrane. This major and novel discovery causes us to reassess the signaling potential of this physiologically and clinically important receptor