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Search Results: 1 - 10 of 493622 matches for " Daniel A Nelson "
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Phenotypic plasticity and morphological integration in a marine modular invertebrate
Juan A Sánchez, Catalina Aguilar, Daniel Dorado, Nelson Manrique
BMC Evolutionary Biology , 2007, DOI: 10.1186/1471-2148-7-122
Abstract: To characterize the genotype/environment relationship and phenotypic plasticity in P. bipinnata, two microsatellite loci, mitochondrial (MSH1) and nuclear (ITS) DNA sequences, and (ITS2) DGGE banding patterns were initially compared among the populations present in the coral reefs of Belize (Carrie Bow Cay), Panama (Bocas del Toro), Colombia (Cartagena) and the Bahamas (San Salvador). Despite the large and discrete differentiation of morphotypes, there was no concordant genetic variation (DGGE banding patterns) in the ITS2 genotypes from Belize, Panama and Colombia. ITS1–5.8S-ITS2 phylogenetic analysis afforded evidence for considering the species P. kallos (Bielschowsky) as the shallow-most morphotype of P. bipinnata from exposed environments. The population from Carrie Bow Cay, Belize (1–45 m) was examined to determine the phenotypic integration of modular features such as branch thickness, polyp aperture, inter-polyp distance, internode length and branch length. Third-order partial correlation coefficients suggested significant integration between polypar and colonial traits. Some features did not change at all despite 10-fold differences in other integrated features. More importantly, some colonial features showed dependence on modular features.Consequently, module integration in gorgonian corals can be shifted, switched or canalized along lineages. Modular marine organisms such as corals are variations on a single theme: their modules can couple or decouple, allowing them to adapt to all marine benthic environments.Important questions in the study of evolution are whether the characteristics of organisms are mutually independent or behave and evolve as integrated systems or modules, and whether the integration of modules can be shifted, switched or canalized along lineages [1]. In modular colonial organisms, which form by the reiteration of identical units, the emergent forms are usually complex networks [2,3]. Colony form in these invertebrates is a consequenc
Gammarus-Microbial Interactions: A Review
Daniel Nelson
International Journal of Zoology , 2011, DOI: 10.1155/2011/295026
Abstract: Gammarus spp. are typically classified as shredders under the functional feeding group classification. In the wild and in the laboratory, Gammarus spp. will often shred leaves, breaking them down into finer organic matter fractions. However, leaf litter is a poor quality food source (i.e., high C?:?N and C?:?P ratios) and very little leaf material is assimilated by shredders. In freshwater habitats leaf litter is colonized rapidly (within ~1-2 weeks) by aquatic fungi and bacteria, making the leaves more palatable and nutritious to consumers. Several studies have shown that Gammarus spp. show preference for conditioned leaves over nonconditioned leaves and certain fungal species to others. Furthermore, Gammarus spp. show increased survival and growth rates when fed conditioned leaves compared to non-conditioned leaves. Thus, Gammarus spp. appear to rely on the microbial biofilm associated with leaf detritus as a source of carbon and/or essential nutrients. Also, Gammarus spp. can have both positive and negative effects on the microbial communities on which they fed, making them an important component of the microbial loop in aquatic ecosystems. 1. Introduction The diets of amphipods in the genus Gammarus are variable [1]. For example, Gammarus spp. can serve as detritivores [2, 3], herbivores [4, 5], predators [6, 7], and even cannibals [2, 8, 9] in aquatic ecosystems. However, under the functional feeding group classification [10–12], Gammarus spp. are typically classified as shredders/facultative shredder collectors [1]. In the wild and in the laboratory, Gammarus spp. often function as shredders consuming leaves and other coarse particulate organic matter (CPOM), breaking it down into smaller fractions or fine particulate organic matter (FPOM). Microbes, such as bacteria and fungi, are often associated with particulate organic matter such as leaves and decaying wood [13, 14]. Leaf detritus, in particular, is an important carbon source for the microbial loop in aquatic ecosystems [13]. Leaf matter serves as a substrate for bacterial and fungal growth, while at the same time supplying the microbial community with carbon in the form of leached dissolved organic carbon (DOC) [13]. Along with physical abrasion and soluble organic matter leaching, microbial decomposition and invertebrate feeding interact to regulate leaf litter breakdown rate in aquatic ecosystems [15]. Detritus-associated bacteria and fungi are responsible for detrital decomposition and its increase in palatability and nutritional quality to consumers [11, 16, 17]. Invertebrate consumers
BST2/Tetherin Enhances Entry of Human Cytomegalovirus
Kasinath Viswanathan,M. Shane Smith,Daniel Malouli,Mandana Mansouri,Jay A. Nelson,Klaus Früh
PLOS Pathogens , 2011, DOI: 10.1371/journal.ppat.1002332
Abstract: Interferon-induced BST2/Tetherin prevents budding of vpu-deficient HIV-1 by tethering mature viral particles to the plasma membrane. BST2 also inhibits release of other enveloped viruses including Ebola virus and Kaposi's sarcoma associated herpesvirus (KSHV), indicating that BST2 is a broadly acting antiviral host protein. Unexpectedly however, recovery of human cytomegalovirus (HCMV) from supernatants of BST2-expressing human fibroblasts was increased rather than decreased. Furthermore, BST2 seemed to enhance viral entry into cells since more virion proteins were released into BST2-expressing cells and subsequent viral gene expression was elevated. A significant increase in viral entry was also observed upon induction of endogenous BST2 during differentiation of the pro-monocytic cell line THP-1. Moreover, treatment of primary human monocytes with siRNA to BST2 reduced HCMV infection, suggesting that BST2 facilitates entry of HCMV into cells expressing high levels of BST2 either constitutively or in response to exogenous stimuli. Since BST2 is present in HCMV particles we propose that HCMV entry is enhanced via a reverse-tethering mechanism with BST2 in the viral envelope interacting with BST2 in the target cell membrane. Our data suggest that HCMV not only counteracts the well-established function of BST2 as inhibitor of viral egress but also employs this anti-viral protein to gain entry into BST2-expressing hematopoietic cells, a process that might play a role in hematogenous dissemination of HCMV.
Exacerbated metastatic disease in a mouse mammary tumor model following latent gammaherpesvirus infection
Vinita S Chauhan, Daniel A Nelson, Lopamudra Das Roy, Pinku Mukherjee, Kenneth L Bost
Infectious Agents and Cancer , 2012, DOI: 10.1186/1750-9378-7-11
Abstract: Mice latently infected with HV-68 had a similar primary tumor burden, but much greater metastatic disease, when compared to mock treated mice given the transplantable tumor, 4?T1. This was true for lung lesions, as well as secondary tumor masses. Increased expression of pan-cytokeratin and VEGF-A in tumors from HV-68 infected mice was consistent with increased metastatic disease in these animals. Surprisingly, no viral particles could be cultured from tumor tissues, and the presence of viral DNA or RNA transcripts could not be detected in primary or secondary tumor tissues.Latent HV-68 infection had no significant effect on the size of primary 4?T1 mammary tumors, but exacerbated the number of metastatic lung lesions and secondary tumors when compared to mock treated mice. Increased expression of the tumor marker, pan-cytokeratin, and VEGF-A in tumors of mice harboring latent virus was consistent with an exacerbated metastatic disease. Mechanisms responsible for this exacerbation are indirect, since no virus could be detected in cancerous tissues.
Cyclophilin nomenclature problems, or, 'a visit from the sequence police'
Daniel W Nebert, Nickolas A Sophos, Vasilis Vasiliou, David R Nelson
Human Genomics , 2004, DOI: 10.1186/1479-7364-1-5-381
Murine gammaherpesvirus-68 expands, but does not activate, CD11b+ gr-1+ splenocytes in vivo
Daniel A Nelson, Vinita S Chauhan, Melanie D Tolbert, Kenneth L Bost
Journal of Inflammation , 2012, DOI: 10.1186/1476-9255-9-14
Abstract: Mice were infected with HV-68, with viral latency being established in these animals. At varying times post-infection, cells were isolated for detection of viral genomes, phenotyping of myeloid cell populations, and ex vivo analysis of suppressor activity of myeloid cells.CD11b?+?Gr-1+ myeloid cells accumulated in the spleens, but not the bone marrow, of HV-68 infected mice. These cells were predominantly Gr-1+ Ly-6?G+, and could be found to contain viral genomes. Increased levels of serum S100A8/A9 produced during viral infection were consistent with the expansion of these CD11b?+?Gr-1+ myeloid cells. Despite their expansion, these cells exhibited no increased arginase 1 or iNOS activity, and did not have the ability to suppress anti-CD3 antibody activated T lymphocyte responses.We concluded that HV-68 infection was capable of expanding a population of myeloid cells which were phenotypically similar to MDSC. However these cells were not sufficiently activated during the establishment of viral latency to actively suppress T cell responses.
Características del castigo físico infantil administrado por padres de tres colegios de Santiago Features of physical maltreatment given by parents to school children in metropolitan Santiago, Chile
Nelson A Vargas C,Daniel López S,Paulina Pérez R,Pamela Zú?iga C
Revista chilena de pediatría , 1993,
An expanded myeloid derived suppressor cell population does not play a role in gammaherpesvirus-exacerbated breast cancer metastases
Nelson Daniel A,Chauhan Vinita S,Tolbert Melanie D,Bost Kenneth L
Infectious Agents and Cancer , 2012, DOI: 10.1186/1750-9378-7-22
Abstract: Background Mice latently infected with murine gammaherpesvirus 68 (HV-68) and transplanted with 4 T1 breast cancer cells developed exacerbated metastatic lesions when compared to controls. The mechanisms responsible for this viral-exacerbated disease were not clear. The ability of HV-68 infection to induce S100A8 and S100A9 production and to expand a population of CD11b+Gr-1+ cells suggested that increased numbers, or activity, of viral-expanded myeloid derived suppressor cells (MDSCs) might contribute to HV-68-associated metastatic breast cancer in this model. We questioned whether mock or HV-68 infected mice with significant breast cancer might have differences in the number and/or activity of MDSCs. Methods Myeloid-derived macrophages and dendritic cells were isolated from normal mice and cultured in vitro with HV-68 to assess S100A8 and S100A9 mRNA and protein expression. In vivo studies were performed using groups of mice that were mock treated or infected with HV-68. After viral latency was established, 4 T1 breast cancer cells were transplanted in mice. When primary breast tumors were present mice were euthanized and cells isolated for phenotyping of myeloid cell populations using FACS, and for ex vivo analysis of suppressor activity. Serum from these animals was also collected to quantify S100A8 and S100A9 levels. Results In vitro studies demonstrated that direct exposure of myeloid cells to HV-68 did not induce increased expression of S100A8 or S100A9 mRNAs or secreted protein. HV-68 infected mice with metastatic breast cancer disease had no increases in S100A8/A9 levels and no significant increases in the numbers or activation of CD11b+Gr-1+MDSCs when compared to mock treated mice with breast cancer. Conclusions Together these studies are consistent with the notion that expanded myeloid derived suppressor cells do not play a role in gammaherpesvirus-exacerbated breast cancer metastases. The mechanisms responsible for HV-68 induced exacerbation of metastatic breast cancer remain unclear.
Divergence of Acoustic Signals in a Widely Distributed Frog: Relevance of Inter-Male Interactions
Nelson A. Velásquez, Daniel Opazo, Javier Díaz, Mario Penna
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0087732
Abstract: Divergence of acoustic signals in a geographic scale results from diverse evolutionary forces acting in parallel and affecting directly inter-male vocal interactions among disjunct populations. Pleurodema thaul is a frog having an extensive latitudinal distribution in Chile along which males' advertisement calls exhibit an important variation. Using the playback paradigm we studied the evoked vocal responses of males of three populations of P. thaul in Chile, from northern, central and southern distribution. In each population, males were stimulated with standard synthetic calls having the acoustic structure of local and foreign populations. Males of both northern and central populations displayed strong vocal responses when were confronted with the synthetic call of their own populations, giving weaker responses to the call of the southern population. The southern population gave stronger responses to calls of the northern population than to the local call. Furthermore, males in all populations were stimulated with synthetic calls for which the dominant frequency, pulse rate and modulation depth were varied parametrically. Individuals from the northern and central populations gave lower responses to a synthetic call devoid of amplitude modulation relative to stimuli containing modulation depths between 30–100%, whereas the southern population responded similarly to all stimuli in this series. Geographic variation in the evoked vocal responses of males of P. thaul underlines the importance of inter-male interactions in driving the divergence of the acoustic traits and contributes evidence for a role of intra-sexual selection in the evolution of the sound communication system of this anuran.
Human Cytomegalovirus miR-UL112-3p Targets TLR2 and Modulates the TLR2/IRAK1/NFκB Signaling Pathway
Igor Landais?,Chantel Pelton?,Daniel Streblow?,Victor DeFilippis?,Shannon McWeeney?,Jay A. Nelson
PLOS Pathogens , 2015, DOI: 10.1371/journal.ppat.1004881
Abstract: Human Cytomegalovirus (HCMV) encodes multiple microRNAs (miRNAs) whose functions are just beginning to be uncovered. Using in silico approaches, we identified the Toll-Like Receptor (TLR) innate immunity pathway as a possible target of HCMV miRNAs. Luciferase reporter assay screens further identified TLR2 as a target of HCMV miR-UL112-3p. TLR2 plays a major role in innate immune response by detecting both bacterial and viral ligands, including HCMV envelope proteins gB and gH. TLR2 activates a variety of signal transduction routes including the NFκB pathway. Furthermore, TLR2 plays an important role in controlling CMV infection both in humans and in mice. Immunoblot analysis of cells transfected with a miR-UL112-3p mimic revealed that endogenous TLR2 is down-regulated by miR-UL112-3p with similar efficiency as a TLR2-targeting siRNA (siTLR2). We next found that TLR2 protein level decreases at late times during HCMV infection and correlates with miR-UL112-3p accumulation in fibroblasts and monocytic THP1 cells. Confirming direct miR-UL112-3p targeting, down-regulation of endogenous TLR2 was not observed in cells infected with HCMV mutants deficient in miR-UL112-3p expression, but transfection of miR-UL112-3p in these cells restored TLR2 down-regulation. Using a NFκB reporter cell line, we found that miR-UL112-3p transfection significantly inhibited NFκB-dependent luciferase activity with similar efficiency as siTLR2. Consistent with this observation, miR-UL112-3p transfection significantly reduced the expression of multiple cytokines (IL-1β, IL-6 and IL-8) upon stimulation with a TLR2 agonist. Finally, miR-UL112-3p transfection significantly inhibited the TLR2-induced post-translational activation of IRAK1, a kinase located in the upstream section of the TLR2/NFκB signaling axis. To our knowledge, this is the first identified mechanism of TLR2 modulation by HCMV and is the first report of functional targeting of TLR2 by a viral miRNA. These results provide a novel mechanism through which a HCMV miRNA regulates the innate immune response by down-regulating TLR-2 expression.
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