Characterizing the effects of turbulence on sediment oxygen and sediment nitrate demand using flow-through reactors

Onondaga Lake has received the municipal effluent and industrial waste from the city of Syracuse for more than a century. Historically, 75 metric tons of mercury were discharged to the lake by chlor-alkali facilities. These legacy deposits of mercury now exist primarily in the lake sediments. Under anoxic conditions, methylmercury is produced in the sediments and can be released to the overlying water. Natural sedimentation processes are continuously burying the mercury deeper into the sediments. Eventually, the mercury will be buried to a depth where it no longer has an impact on the overlying water. In the interim, electron acceptor amendment systems can be installed to retard these chemical releases while the lake naturally recovers. Electron acceptor amendment systems are designed to meet the sediment oxygen demand in the sediment and maintain manageable hypolimnion oxygen concentrations. Historically, designs of these systems have been under designed resulting in failure. This stems from a mischaracterization of the sediment oxygen demand. Turbulence at the sediment water interface has been shown to impact sediment oxygen demand. The turbulence introduced by the electron amendment system can thus increase the sediment oxygen demand, resulting in system failure if turbulence is not factored into the design. Sediment cores were gathered and operated to steady state under several well characterized turbulence conditions. The relationship between sediment oxygen/nitrate demand and turbulence was then quantified and plotted. A maximum demand was exhibited at or above a fluid velocity of 2.0 mm•s-1. Below this velocity, demand decreased rapidly with fluid velocity as zero velocity was approached. Similar relationships were displayed by both oxygen and nitrate cores

Hydrocarbon seepage in the deep seabed links subsurface and seafloor biospheres

© The Author(s), 2020. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Chakraborty, A., Ruff, S. E., Dong, X., Ellefson, E. D., Li, C., Brooks, J. M., McBee, J., Bernard, B. B., & Hubert, C. R. J. Hydrocarbon seepage in the deep seabed links subsurface and seafloor biospheres. Proceedings of the National Academy of Sciences of the United States of America, 117(20), (2020): 11029-11037, doi: 10.1073/pnas.2002289117.Marine cold seeps transmit fluids between the subseafloor and seafloor biospheres through upward migration of hydrocarbons that originate in deep sediment layers. It remains unclear how geofluids influence the composition of the seabed microbiome and if they transport deep subsurface life up to the surface. Here we analyzed 172 marine surficial sediments from the deep-water Eastern Gulf of Mexico to assess whether hydrocarbon fluid migration is a mechanism for upward microbial dispersal. While 132 of these sediments contained migrated liquid hydrocarbons, evidence of continuous advective transport of thermogenic alkane gases was observed in 11 sediments. Gas seeps harbored distinct microbial communities featuring bacteria and archaea that are well-known inhabitants of deep biosphere sediments. Specifically, 25 distinct sequence variants within the uncultivated bacterial phyla Atribacteria and Aminicenantes and the archaeal order Thermoprofundales occurred in significantly greater relative sequence abundance along with well-known seep-colonizing members of the bacterial genus Sulfurovum, in the gas-positive sediments. Metabolic predictions guided by metagenome-assembled genomes suggested these organisms are anaerobic heterotrophs capable of nonrespiratory breakdown of organic matter, likely enabling them to inhabit energy-limited deep subseafloor ecosystems. These results point to petroleum geofluids as a vector for the advection-assisted upward dispersal of deep biosphere microbes from subsurface to surface environments, shaping the microbiome of cold seep sediments and providing a general mechanism for the maintenance of microbial diversity in the deep sea.We wish to thank Jody Sandel as well as the crew of R/V GeoExplorer for collection of piston cores, onboard core processing, sample preservation, and shipment. Cynthia Kwan and Oliver Horanszky are thanked for assistance with amplicon library preparation. We also wish to thank Jayne Rattray, Daniel Gittins, and Marc Strous for valuable discussions and suggestions, and Rhonda Clark for research support. Collaborations with Andy Mort from the Geological Survey of Canada, and Richard Hatton from Geoscience Wales are also gratefully acknowledged. This work was financially supported by a Mitacs Elevate Postdoctoral Fellowship awarded to A.C.; an Alberta Innovates-Technology Futures/Eyes High Postdoctoral Fellowship to S.E.R.; and a Natural Sciences and Engineering Research Council Strategic Project Grant, a Genome Canada Genomics Applications Partnership Program grant, a Canada Foundation for Innovation grant (CFI-JELF 33752) for instrumentation, and Campus Alberta Innovates Program Chair funding to C.R.J.H

Fostering Preservice Teacher Identity in Science through a Student-Selected Project

This article addresses the problem of authentic student engagement in the science classroom by incorporating a semester long research and writing assignment that enables students to investigate scientific topics related to strong personal, career, or health interests

Kinesin-1 Prevents Capture of the Oocyte Meiotic Spindle by the Sperm Aster

SummaryCentrioles are lost during oogenesis and inherited from the sperm at fertilization. In the zygote, the centrioles recruit pericentriolar proteins from the egg to form a mature centrosome that nucleates a sperm aster. The sperm aster then captures the female pronucleus to join the maternal and paternal genomes. Because fertilization occurs before completion of female meiosis, some mechanism must prevent capture of the meiotic spindle by the sperm aster. Here we show that in wild-type Caenorhabditis elegans zygotes, maternal pericentriolar proteins are not recruited to the sperm centrioles until after completion of meiosis. Depletion of kinesin-1 heavy chain or its binding partner resulted in premature centrosome maturation during meiosis and growth of a sperm aster that could capture the oocyte meiotic spindle. Kinesin prevents recruitment of pericentriolar proteins by coating the sperm DNA and centrioles and thus prevents triploidy by a nonmotor mechanism

Environmental chemical exposures and disturbances of heme synthesis.

Porphyrias are relatively uncommon inherited or acquired disorders in which clinical manifestations are attributable to a disturbance of heme synthesis (porphyrin metabolism), usually in association with endogenous or exogenous stressors. Porphyrias are characterized by elevations of heme precursors in blood, urine, and/or stool. A number of chemicals, particularly metals and halogenated hydrocarbons, induce disturbances of heme synthesis in experimental animals. Certain chemicals have also been linked to porphyria or porphyrinuria in humans, generally involving chronic industrial exposures or environmental exposures much higher than those usually encountered. A noteworthy example is the Turkish epidemic of porphyria cutanea tarda produced by accidental ingestion of wheat treated with the fungicide hexachlorobenzene. Measurements of excreted heme precursors have the potential to serve as biological markers for harmful but preclinical effects of certain chemical exposures; this potential warrants further research and applied field studies. It has been hypothesized that several otherwise unexplained chemical-associated illnesses, such as multiple chemical sensitivity syndrome, may represent mild chronic cases of porphyria or other acquired abnormalities in heme synthesis. This review concludes that, although it is reasonable to consider such hypotheses, there is currently no convincing evidence that these illnesses are mediated by a disturbance of heme synthesis; it is premature or unfounded to base clinical management on such explanations unless laboratory data are diagnostic for porphyria. This review discusses the limitations of laboratory measures of heme synthesis, and diagnostic guidelines are provided to assist in evaluating the symptomatic individual suspected of having a porphyria

Under What Conditions Can Recursion Be Learned? Effects of Starting Small in Artificial Grammar Learning of Center-Embedded Structure

It has been suggested that external and/or internal limitations paradoxically may lead to superior learning, that is, the concepts of starting small and less is more (Elman,; Newport,). In this paper, we explore the type of incremental ordering during training that might help learning, and what mechanism explains this facilitation. We report four artificial grammar learning experiments with human participants. In Experiments 1a and 1b we found a beneficial effect of starting small using two types of simple recursive grammars: right-branching and center-embedding, with recursive embedded clauses in fixed positions and fixed length. This effect was replicated in Experiment 2 (N = 100). In Experiment 3 and 4, we used a more complex center-embedded grammar with recursive loops in variable positions, producing strings of variable length. When participants were presented an incremental ordering of training stimuli, as in natural language, they were better able to generalize their knowledge of simple units to more complex units when the training input “grew” according to structural complexity, compared to when it “grew” according to string length. Overall, the results suggest that starting small confers an advantage for learning complex center-embedded structures when the input is organized according to structural complexity

CDK-1 inhibits meiotic spindle shortening and dynein-dependent spindle rotation in C. elegans

Before chromosome expulsion into polar bodies during female meiosis, the APC inhibits CDK-1 to allow dynein-driven spindle rotation

Thyroid control over biomembranes: VI. Lipids in liver mitochondria and microsomes of hypothyroid rats

The lipids of liver mitochondria prepared from normal rats and from rats made hypothyroid by thyroidectomy and injection with131INa contained similar amounts, per mg protein, of total lipids, phospholipids, neutral lipids and lipid phosphorus. Hypothyroidism caused a doubling of the relative amounts of mitochondrial cardiolipins (CL; to 20.5% of the phospholipid P) and an accompanying trend (although statistically not significant) toward decreased amounts of both phosphatidylcholines (PC) and phosphatidylserines (PS), with phosphatidylethanolamines (PE) remaining unchanged. The pattern of elevated 18∶2 fatty acyl content and depleted 20∶4 acyl groups of the mitochondrial phospholipids of hypothyroid preparations was reflected to varying degrees in the resolved phospholipids, with PC showing greater degrees of abnormality than PE, and CL showing none. Hypothyroidism produced the same abnormal pattern of fatty acyl distributions in liver microsomal total lipids as was found in the mitochondria. Hypothyroid rats, when killed 6 hr after injection of [1‐14C] labeled linoleate, showed the following abnormalities: the liver incorporated less label into lipids, and converted 18∶2 not exclusively to 20∶4 (as normals do) but instead incorporated the label mainly into saturated fatty acids. These data, together with the known decrease in β‐oxidation, suggest that hypothyroidism involves possible defective step(s) in the conversion of 18∶2 to 20∶4.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142296/1/lipd0328.pd