Status of the tiger beetle Cicindela hirticollis Say (Coleoptera: Cicindelidae) in New York City and on Long Island, New York, USA

Coastal species are under considerable threat from recreational activities and climate change. The tiger beetle Cicindela hirticollis Say (Coleoptera: Cicindelidae) was recorded historically from 30 locations along the shores of New York City and Long Island, New York. We conducted surveys for extant populations of this species at 40 sites from 1989 to 2010. Adults of C. hirticollis were found at 13 beaches. Only four sites had 40 or more adults of C. hirticollis active at the time the beach was surveyed. No beetles were detected on the large coastal beaches that were formerly occupied by this species. Many coastal beaches of New York receive heavy human foot and vehicle traffic and are therefore unlikely to provide suitable habitat for C. hirticollis without a shift in beach management that recognizes the potential of some beaches as wilderness systems capable of supporting the full array of beach-dependent species

Facile Protocol for Water-Tolerant “Frustrated Lewis Pair”-Catalyzed Hydrogenation

Despite rapid advances in the field of metal-free, “frustrated Lewis pair” (FLP)-catalyzed hydrogenation, the need for strictly anhydrous reaction conditions has hampered wide-scale uptake of this methodology. Herein, we report that, despite the generally perceived moisture sensitivity of FLPs, 1,4-dioxane solutions of B(C6F5)3 actually show appreciable moisture tolerance and can catalyze hydrogenation of a range of weakly basic substrates without the need for rigorously inert conditions. In particular, reactions can be performed directly in commercially available nonanhydrous solvents without subsequent drying or use of internal desiccants

Status of the tiger beetle \u3ci\u3eCicindela hirticollis\u3c/i\u3e Say (Coleoptera: Cicindelidae) in New York City and on Long Island, New York, USA

Coastal species are under considerable threat from recreational activities and climate change. The tiger beetle Cicindela hirticollis Say (Coleoptera: Cicindelidae) was recorded historically from 30 locations along the shores of New York City and Long Island, New York. We conducted surveys for extant populations of this species at 40 sites from 1989 to 2010. Adults of C. hirticollis were found at 13 beaches. Only four sites had 40 or more adults of C. hirticollis active at the time the beach was surveyed. No beetles were detected on the large coastal beaches that were formerly occupied by this species. Many coastal beaches of New York receive heavy human foot and vehicle traffic and are therefore unlikely to provide suitable habitat for C. hirticollis without a shift in beach management that recognizes the potential of some beaches as wilderness systems capable of supporting the full array of beach-dependent species

Status of the tiger beetle \u3ci\u3eCicindela hirticollis\u3c/i\u3e Say (Coleoptera: Cicindelidae) in New York City and on Long Island, New York, USA

Coastal species are under considerable threat from recreational activities and climate change. The tiger beetle Cicindela hirticollis Say (Coleoptera: Cicindelidae) was recorded historically from 30 locations along the shores of New York City and Long Island, New York. We conducted surveys for extant populations of this species at 40 sites from 1989 to 2010. Adults of C. hirticollis were found at 13 beaches. Only four sites had 40 or more adults of C. hirticollis active at the time the beach was surveyed. No beetles were detected on the large coastal beaches that were formerly occupied by this species. Many coastal beaches of New York receive heavy human foot and vehicle traffic and are therefore unlikely to provide suitable habitat for C. hirticollis without a shift in beach management that recognizes the potential of some beaches as wilderness systems capable of supporting the full array of beach-dependent species

NOTCH1 inhibition in vivo results in mammary tumor regression and reduced mammary tumorsphere-forming activity in vitro

INTRODUCTION: NOTCH activation has been recently implicated in human breast cancers, associated with a poor prognosis, and tumor-initiating cells are hypothesized to mediate resistance to treatment and disease relapse. To address the role of NOTCH1 in mammary gland development, transformation, and mammary tumor-initiating cell activity, we developed a doxycycline-regulated mouse model of NOTCH1-mediated mammary transformation. METHODS: Mammary gland development was analyzed by using whole-mount analysis and by flow cytometry in nulliparous transgenic mice maintained in the presence/absence of doxycycline (or intracellular NOTCH1). Mammary tumors were examined histologically and immunophenotyped by staining with antibodies followed by flow cytometry. Tumors were transplanted into mammary fat pads under limiting dilution conditions, and tumor-initiating cell frequency was calculated. Mammary tumor cells were also plated in vitro in a tumorsphere assay in the presence/absence of doxycycline. RNA was isolated from mammary tumor cell lines cultured in the presence/absence of doxycycline and used for gene-expression profiling with Affymetrix mouse arrays. NOTCH1-regulated genes were identified and validated by using quantitative real-time polymerase chain reaction (PCR). Mammary tumor-bearing mice were treated with doxycycline to suppress NOTCH1 expression, and disease recurrence was monitored. RESULTS: Similar to published studies, we show that constitutive expression of human intracellular NOTCH1 in the developing mouse mammary gland inhibits side branching and promotes luminal cell fate. These mice develop mammary adenocarcinomas that express cytokeratin (CK) 8/18. In vivo limiting-dilution analyses revealed that these mammary tumors exhibit functional heterogeneity and harbor a rare (1/2,978) mammary tumor-initiating cell population. With this dox-regulated NOTCH1 mammary tumor model, we demonstrate that NOTCH1 inhibition results in mammary tumor regression in vivo and prevents disease recurrence in four of six tumors tested. Consistent with the in vivo data, NOTCH1 inhibition reduces mammary tumorsphere activity in vitro. We also identify the embryonic stem cell transcription factor Nanog as a novel NOTCH1-regulated gene in tumorspheres and in mouse and human breast cancer cell lines. CONCLUSIONS: These data indicate that NOTCH1 inhibition results in mammary tumor regression in vivo and interferes with disease recurrence. We demonstrate that NOTCH1-transformed mouse mammary tumors harbor a rare mammary tumor-initiating population and that NOTCH1 contributes to mammary tumor-initiating activity. This work raises the possibility that NOTCH therapeutics may target mammary tumor-initiating cells in certain human breast cancer subtypes

Enhanced monography in a collaboratively evolved hub for systematic biology

No abstract available

Radio frequency reflectometry and charge sensing of a precision placed donor in silicon

We compare charge transitions on a deterministic single P donor in silicon using radio frequency reflectometry measurements with a tunnel coupled reservoir and DC charge sensing using a capacitively coupled single electron transistor (SET). By measuring the conductance through the SET and comparing this with the phase shift of the reflected RF excitation from the reservoir, we can discriminate between charge transfer within the SET channel and tunneling between the donor and reservoir. The RF measurement allows observation of donor electron transitions at every charge degeneracy point in contrast to the SET conductance signal where charge transitions are only observed at triple points. The tunnel coupled reservoir has the advantage of a large effective lever arm (~35%) allowing us to independently extract a neutral donor charging energy ~62 +/- 17meV. These results demonstrate that we can replace three terminal transistors by a single terminal dispersive reservoir, promising for high bandwidth scalable donor control and readout.Comment: 5 pages, 3 figures. Copyright (2015) American Institute of Physics. This article may be downloaded for personal use only. Any other use requires prior permission of the author and the American Institute of Physic

Nrf2 expression modifies influenza A entry and replication in nasal epithelial cells

Influenza infection is a major cause of morbidity and mortality worldwide, especially during pandemics outbreaks. Emerging data indicate that phase II antioxidant enzyme pathways could play a role in virus-associated inflammation and immune clearance. While Nrf2-dependent gene expression is known to modify inflammation, a mechanistic role in viral susceptibility and clearance has yet to be elucidated. Therefore, we utilized differentiated human nasal epithelial cells (NEC) and an enzymatic virus-like particle entry assay, to examine the role Nrf2-dependent gene expression has on viral entry and replication. Herein, lentiviral vectors that express Nrf2-specific short hairpin (sh)-RNA effectively decreased both Nrf2 mRNA and Nrf2 protein expression in transduced human NEC from healthy volunteers. Nrf2 knockdown correlated with a significant increase in influenza virus entry and replication. Conversely, supplementation with the potent Nrf2 activators sulforaphane (SFN) and epigallocatechin gallate (EGCG) significantly decreased viral entry and replication. The suppressive effects of EGCG on viral replication were abolished in cells with knocked down Nrf2 expression, suggesting a causal relationship between EGCG-induced activation of Nrf2 and ability to protect against viral infection. Interestingly, the induction of Nrf2 via nutritional supplements SFN and EGCG, increased antiviral mediators/responses; RIG-I, IFN-β, and MxA at baseline in the absence of infection. Our data indicate that there is an inverse relationship between the levels of Nrf2 expression, and viral entry/replication. We also demonstrate that supplementation with Nrf2-activating antioxidants inhibit viral replication in human NEC, which may prove to be an attractive therapeutic intervention. Taken together, these data indicate potential mechanisms by which Nrf2-dependent gene expression regulates susceptibility to influenza in human epithelial cells