Impacts of Atmospheric Nitrogen Deposition and Coastal Nitrogen Fluxes on Chesapeake Bay Hypoxia

Although rivers are the primary source of dissolved inorganic nitrogen (DIN) inputs to the Chesapeake Bay, direct atmospheric DIN deposition and DIN fluxes from the continental shelf can also significantly impact Chesapeake Bay hypoxia. The relative role of these additional sources of DIN has not previously been thoroughly quantified. In this study, the three-dimensional Estuarine-Carbon-Biogeochemistry model embedded in the Regional Ocean Modeling System (ChesROMS-ECB) is used to examine the relative impact of these three DIN sources. Model simulations highlight that DIN inputs from the atmosphere have roughly the same impact on hypoxia as the same gram for gram change in riverine DIN loading. DIN inputs from the shelf have a similar overall impact on hypoxia as those from the atmosphere (~0.2 mg L-1), however the mechanisms driving these impacts are different. While atmospheric DIN impacts dissolved oxygen (DO) primarily via the decomposition of autochthonous organic matter, coastal DIN also impacts DO via the decomposition of allochthonous organic matter entering the Bay from the continental shelf. The impacts of coastal and atmospheric DIN on estuarine hypoxia are greatest in the summer, and occur farther downstream (lower mesohaline) in wet years than in dry years (upper mesohaline). Integrated analyses of the relative contributions of all three DIN sources on summer bottom DO concentrations indicate that impacts of atmospheric deposition are largest in shallow near-shore regions, riverine DIN has dominant impacts in the largest tributaries and the oligohaline Bay, while coastal DIN fluxes are most influential in the polyhaline region. During the winter when estuarine circulation is strong and shelf DIN concentrations are relatively high, coastal DIN impacts bottom DO throughout the Bay

The role of neurotrophin receptors in taste development.

Brain-derived neurotrophic factor (BDNF) and neurotrophin-4 (NT-4) are two neurotrophins that play distinct roles in geniculate (taste) neuron survival, taste innervation and taste bud formation. These two neurotrophins activate the same receptors tyrosine kinase B (TrkB) and a pan-neurotrophin receptor (p75). While the roles of these neurotrophins have been well studied, it remains unclear how much BDNF and NT-4 function through TrkB and p75 to regulate taste development in vivo. In chapter 2, I compared taste development in TrkB-/- mice and Bdnf-/-/Ntf4-/- mice to determine if these deficits were similar. If so, this would indicate that the functions of both BDNF and NT-4 can be accounted for by TrkB signaling. I found that TrkB-/- mice and Bdnf-/-/Ntf4-/- mice lose the same number of geniculate neurons by E13.5, indicating that BDNF and NT-4 primarily function through TrkB to regulate geniculate neuron survival. Surprisingly, the few geniculate neurons remaining in TrkB-/- mice are more successful in innervating the tongue and taste buds than those remaining in Bdnf-/-/Ntf4-/- mice. As a result these remaining neurons in the TrkB-/- mice innervate and support the development of a surprising number of taste buds. In addition, these remaining neurons do not express the TrkB receptor, indicating the either BDNF or NT-4 must function through an additional receptor to influence taste innervation and/or targeting. The p75 receptor can function as either a pro-survival or pro-death factor during peripheral nervous system development. However, the role of p75 in taste development is unknown. In chapter 3, I examined neuron survival, taste bud formation and tasteinnervation in the p75-/- and TrkB-/-/p75-/- mice. I found that at E13.5, the age after BDNF and NT-4 dependence is established, p75-/- mice did not lose geniculate neurons compared to the wild type mice. This finding indicates that p75 does not mediate neurotrophin neuronal survival at or before this age. Hybrid TrkB-/-/p75-/- mice had the same number of geniculate neurons as TrkB-/- mice, suggesting that p75 does not induce neuron death in the absence of Trk-signaling like it does for some other systems. By E14.5, there is a loss of geniculate neurons in p75-/- mice which continues until E18.5. Also at this age, the pattern of chorda tympani nerve innervation was disrupted in the p75-/- mice. Specifically, the nerves avoid innervating the mid-region of the tongue. Due to the loss of innervation, the taste bud number was decreased in the p75-/- mice. It is possible that the neuron loss is due to this disrupted innervation pattern. Interestingly, TrkB-/-/p75-/- mice have more taste buds than p75-/- mice. These additional taste buds are not innervated which suggests that p75 may function as a pro-death factor in the taste bud during development. Taken together, my results suggest that p75 does not mediate the neurotrophin survival function for taste neuron development. Instead, it is important for taste innervation and branching to the tongue middle line and could influence taste cell survival in the absence of innervation and/or neurotrophin signaling

Central engine afterglow of Gamma-ray Bursts

Before 2004, nearly all GRB afterglow data could be understood in the context of the external shocks model. This situation has changed in the past two years, when it became clear that some afterglow components should be attributed to the activity of the central engine; i.e., the {\it central engine afterglow}. We review here the afterglow emission that is directly related to the GRB central engine. Such an interpretation proposed by Katz, Piran & Sari, peculiar in pre-{\it Swift} era, has become generally accepted now.Comment: 4 pages including 1 figure. Presented at the conference "Astrophysics of Compact Objects" (July 1-7, 2007; Huangshan, China

A γ\gamma-ray Quasi-Periodic modulation in the Blazar PKS 0301−-243?

We report a nominally high-confidence $\gamma$-ray quasi-periodic modulation in the blazar PKS 0301$-$243. For this target, we analyze its \emph{Fermi}-LAT Pass 8 data covering from 2008 August to 2017 May. Two techniques, i.e., the maximum likelihood optimization and the exposure-weighted aperture photometry, are used to build the $\gamma$-ray light curves. Then both the Lomb-Scargle Periodogram and the Weighted Wavelet Z-transform are applied to the light curves to search for period signals. A quasi-periodicity with a period of $2.1\pm0.3$ yr appears at the significance level of $\sim5\sigma$, although it should be noted that this putative quasi-period variability is seen in a data set barely four times longer. We speculate that this $\gamma$-ray quasi-periodic modulation might be evidence of a binary supermassive black hole.Comment: 9 pages, 8 figures; Accepted for publication in Ap

Learning large margin multiple granularity features with an improved siamese network for person re-identification

Person re-identification (Re-ID) is a non-overlapping multi-camera retrieval task to match different images of the same person, and it has become a hot research topic in many fields, such as surveillance security, criminal investigation, and video analysis. As one kind of important architecture for person re-identification, Siamese networks usually adopt standard softmax loss function, and they can only obtain the global features of person images, ignoring the local features and the large margin for classification. In this paper, we design a novel symmetric Siamese network model named Siamese Multiple Granularity Network (SMGN), which can jointly learn the large margin multiple granularity features and similarity metrics for person re-identification. Firstly, two branches for global and local feature extraction are designed in the backbone of the proposed SMGN model, and the extracted features are concatenated together as multiple granularity features of person images. Then, to enhance their discriminating ability, the multiple channel weighted fusion (MCWF) loss function is constructed for the SMGN model, which includes the verification loss and identification loss of the training image pair. Extensive comparative experiments on four benchmark datasets (CUHK01, CUHK03, Market-1501 and DukeMTMC-reID) show the effectiveness of our proposed method and its performance outperforms many state-of-the-art methods

Prokineticin 2 Is a Target Gene of Proneural Basic Helix-Loop-Helix Factors for Olfactory Bulb Neurogenesis

Prokineticin 2, a cysteine-rich secreted protein, regulates diverse biological functions including the neurogenesis of olfactory bulb. Here we show that the PK2 gene is a functional target gene of proneural basic helix-loop-helix (bHLH) factors. Neurogenin 1 and MASH1 activate PK2 transcription by binding to E-box motifs on the PK2 promoter with the same set of E-boxes critical for another pair of bHLH factors, CLOCK and BMAL1, in the regulation of circadian clock. Our results establish PK2 as a common functional target gene for different bHLH transcriptional factors in mediating their respective functions

Associated dataset: Impacts of Atmospheric Nitrogen Deposition and Coastal Nitrogen Fluxes on Oxygen Concentrations in Chesapeake Bay

The dataset includes model outputs used in publication Da et al. (2018), which used the Estuarine-Carbon-Biogeochemistry model embedded in the Regional-Ocean-Modeling-System (ChesROMS-ECB) to examine the relative impact of direct atmospheric dissolved inorganic nitrogen (DIN) deposition and DIN from the continental shelf on the Chesapeake Bay dissolved oxygen. Model simulations highlight that DIN from the atmosphere has roughly the same impact on hypoxia as the same gram-for-gram change in riverine DIN loading. DIN concentrations on the continental shelf has a similar overall impact on hypoxia as DIN from the atmosphere