Matrices of DNA sequences used to generate the phylogeny of Aniba rosiodora and related species (Lauraceae) presented in the manuscript entitled "Chemical and genotypic variations in Aniba species from the Amazonian forest"
This data set includes the raw rare earth element data for all fluorite and calcite samples analyzed by Josh Bergbower for work on his thesis project titled "Trace and Rare Earth Element Chemistry of Fluorite from the Illinois-Kentucky Fluorspar District and its Implications for the Origins of Mineralizing Fluids".
This dataset shows the quantities and findspots of coins minted by the ancient mint(s) at Antioch on the Orontes in northern Syria. The kml files are usable in Google Earth. Coin finds are sorted by material (bronze, silver, antoniniani), type (provincial SC, provincial silver and misc. bronze, civic coins with imperial portrait, civic coins without imperial portrait), and chronology (223 BCE-91 BCE, 90 BCE-31 BCE, 30 BCE-235 CE, 236 CE-283 CE, 284 CE-423 CE).
For the original publication of this data, see the attached appendix.
Additional Figure 1, Additional Figure 2, Additional Table 1, and Additional Table 2 for Norton et al. paper published in BMC Genetics: MC1R diversity in Northern Island Melanesia has not been constrained by strong purifying selection and cannot explain pigmentation phenotype variation in the region
This compressed file contains the GIS files used for the DRAP project in shape file format. There is a Documentation folder with a ReadMe file that contains information about opening the documents as well as notes on their creation and conversion.
There is a file included that will allow opening all of the files in ArcMap (v 10.1 tested) and QGIS (v 2.4 tested) but the data files themselves can be opened in whatever GIS software one chooses that can read ESRI shape file format.
The data stored in this collection were collected during a series of 3 experiments I conducted between 2013 and 2014 to evaluate the effects of population-level extinction within spatial population networks.
For each experiment, I used experimental protozoan population networks (microcosms) that used the common pond species Paramecium caudatum as the focal organism. Each network contained five populations aligned linearly and connected to one another through a migration corridor (see image files).
The experiments were similar in their basic methods. For example, each experiment consisted of three 10-day periods: pre-extinction, extinction, and reestablishment. In addition, each experiment used 8 networks: four treatment networks and four control networks. During the 10-day extinction period, extinction was maintained on the center population of 4 treatment networks. During the reestablishment period, the center population was allowed to reestablish. The 4 control networks had no extinction imposed.
During each experiment I estimated the density of each population within all networks daily as the mean number of paramecia captured in three 0.25 mL samples. The data included in these files shows these density estimates. All calculations used to assess changes in population abundance and dynamics due to extinction were derived from these density estimates.
Additional background for each of the 3 experiments (e.g., how the experiments differed) can be found in the ReadMe file. Detailed methods and results from each of these experiments are documented in Chapters 3, 4, and 5 of my dissertation (see Dissertation file).
Helicobacter pylori (H. pylori) is the major risk factor for the development of gastric cancer. Our laboratory has reported that the Sonic Hedgehog (Shh) signaling pathway is an early response to infection that is fundamental to the initiation of H. pylori-induced gastritis. H. pylori also induces programmed death ligand 1 (PD-L1) expression on gastric epithelial cells, yet the mechanism is unknown. We hypothesize that H. pylori-induced PD-L1 expression within the gastric epithelium is mediated by the Shh signaling pathway during infection. To identify the role of Shh signaling as a mediator of H. pylori-induced PD-L1 expression, human gastric organoids generated from either induced pluripotent stem cells (HGOs) or tissue (huFGOs) were microinjected with bacteria and treated with Hedgehog/Gli inhibitor GANT61. Gastric epithelial monolayers generated from the huFGOs were also infected with H. pylori and treated with GANT61 to study the role of Hedgehog signaling as a mediator of induced PD-1 expression. A patient-derived organoid/autologous immune cell co-culture system infected with H. pylori and treated with PD-1 inhibitor (PD-1Inh) was developed to study the protective mechanism of PD-L1 in response to bacterial infection. H. pylori significantly increased PD-L1 expression in organoid cultures 48 hours post-infection when compared to uninfected controls. The mechanism was cytotoxic associated gene A (CagA) dependent. This response was blocked by pretreatment with GANT61. Anti-PD-L1 treatment of H. pylori infected huFGOs, co-cultured with autologous patient cytotoxic T lymphocytes and dendritic cells, induced organoid death. H. pylori-induced PD-L1 expression is mediated by the Shh signaling pathway within the gastric epithelium. Cells infected with H. pylori that express PD-L1 may be protected from the immune response, creating premalignant lesions progressing to gastric cancer.