Influences on effective local wildfire mitigation programs

The purpose of this research is to identify key components of community wildfire risk reduction programs and potential influences on the adoption of these program elements. Community wildfire programs have been developed to educate and encourage property owners to adopt “vegetation management” practices such as creating defensible space around structures, landscaping with fire-resistant plants, and removing potential wildfire fuels such as trees and shrubs. The analyses are based on a survey conducted by investigators from Louisiana State University in conjunction with the U.S. Forest Service. This survey was distributed to wildfire mitigation program managers listed on the National Wildfire Programs Database website. A Principal Component Analysis (PCA) was conducted on the data returned from this sixty-nine-item survey. A range of socioeconomic variables was gathered from the 2000 Census Bureau and was used along with a fire history variable created from data extracted from the survey to examine the extent to which the variables are associated with program development. Five factors were identified from the PCA as being indicators of key components of risk-reduction programs. Local programs with these elements are assumed to have a greater capacity for effectively reducing or mitigating wildfire risks to communities within the wildland-urban interface (WUI). The factors are more local regulations and codes, larger numbers of public education, vegetation disposal, risk assessment activities and fewer reported problems with program funding. These factors were regressed with demographic variables selected for each survey respondent’s geographic area. Several different demographic variables were found to be significantly associated with the selected factors. These are population density, property value, wealth, percent of homeownership, percent of population with a college degree, and population change. Formulation and implementation of these desirable program components were found to be associated with slower growing, less densely populated communities, and those with wealthier and better educated residents

Nuclear receptor agonist-driven modification of inflammation and amyloid pathology enhances and sustains cognitive improvements in a mouse model of Alzheimer's disease

BACKGROUND: Alzheimer's disease (AD) is a highly prevalent neurodegenerative disorder characterized by pathological hallmarks of beta-amyloid plaque deposits, tau pathology, inflammation, and cognitive decline. Treatment remains a clinical obstacle due to lack of effective therapeutics. Agonists targeting nuclear receptors, such as bexarotene, reversed cognitive deficits regardless of treatment duration and age in murine models of AD. While bexarotene demonstrated marked efficacy in decreasing plaque levels following short-term treatment, prolonged treatment did not modulate plaque burden. This suggested that plaques might reform in mice treated chronically with bexarotene and that cessation of bexarotene treatment before plaques reform might alter amyloid pathology, inflammation, and cognition in AD mice. METHODS: We utilized one-year-old APP/PS1 mice that were divided into two groups. We treated one group of mice for 2 weeks with bexarotene. The other group of mice was treated for 2 weeks with bexarotene followed by withdrawal of drug treatment for an additional 2 weeks. Cognition was evaluated using the novel-object recognition test either at the end of bexarotene treatment or the end of the withdrawal period. We then analyzed amyloid pathology and microgliosis at the conclusion of the study in both groups. RESULTS: Bexarotene treatment enhanced cognition in APP/PS1 mice similar to previous findings. Strikingly, we observed sustained cognitive improvements in mice in which bexarotene treatment was discontinued for 2 weeks. We observed a sustained reduction in microgliosis and plaque burden following drug withdrawal exclusively in the hippocampus. CONCLUSIONS: Our findings demonstrate that bexarotene selectively modifies aspects of neuroinflammation in a region-specific manner to reverse hippocampal-dependent cognitive deficits in AD mice and may provide insight to inform future studies with nuclear receptor agonists

An Analysis of the Long-Term Salinity Patterns in the Louisiana Coastal Zone

Saltwater intrusion is believed to be one of the greatest threats to Louisiana\u27s fishery and wildlife resources. The Louisiana Department of Wildlife and Fisheries has maintained salinity recording stations throughout the state\u27s coastal marshes since the 1960\u27s. We applied several different analytical approaches to the salinity data from 17 stations to determine whether this data base could be used to detect and quantity long-term salinity trends in coastal Louisiana. We did not detect a large-scale, consistent trend over time in coastal salinities across the state. Problems that hindered the detection of long-term trends included short periods of record and the placement of the recording stations in salt and brackish marsh areas, where we would not expect to find great changes in salinity. For the data to be useful in monitoring salinity trends in coastal marshes, especially with respect to saltwater intrusion, stations should be added in fresh and intermediate marshes. In addition, the relationships our study revealed between short- and long-term data indicate that records covering less than a decade are insufficient to denote long-term salinity changes, barring some major modification of the hydrologic regime

Emerging wetlands from river diversions can sustain high denitrification rates in a Coastal Delta

Author Posting. © American Geophysical Union, 2021. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Journal of Geophysical Research: Biogeosciences 126(5), (2021): e2020JG006217, https://doi.org/10.1029/2020JG006217.It is assumed that to treat excess NO3− high soil organic matter content (%OM) is required to maintain high denitrification rates in natural or restored wetlands. However, this excess also represents a risk by increasing soil decomposition rates triggering peat collapse and wetland fragmentation. Here, we evaluated the role of %OM and temperature interactions controlling denitrification rates in eroding (Barataria Bay-BLC) and emerging (Wax Lake Delta-WLD) deltaic regions in coastal Louisiana using the isotope pairing (IPT) and N2:Ar techniques. We also assessed differences between total (direct denitrification + coupled nitrification-denitrification) and net (total denitrification minus nitrogen fixation) denitrification rates in benthic and wetland habitats with contrasting %OM and bulk density (BD). Sediment (benthic) and soil (wetland) cores were collected during summer, spring, and winter (2015–2016) and incubated at close to in-situ temperatures (30°C, 20°C, and 10°C, respectively). Denitrification rates were linearly correlated with temperature; maximum mean rates ranged from 40.1–124.1 μmol m−2 h−1 in the summer with lower rates (30 μM) and water temperature is >10°C. In coastal Louisiana, substrates under these regimes are represented by emergent supra-tidal flats or land created by sediment diversions under oligohaline conditions (<1 ppt).This study was supported by the NOAA-Sea Grant Program-Louisiana (Grant 2013R/E-24) to Victor H. Rivera-Monroy and Kanchan Maiti. Victor H. Rivera-Monroy was also supported by the Department of the Interior South-Central Climate Adaptation Science Center (Cooperative Agreement #G12AC00002)

Observation on the ultrastructure morphology of HeLa cells treated with ethanol: Statistical analysis.

It is estimated that 5.9% of all human deaths are attributable to alcohol consumption and that the harmful use of ethanol ranks among the top five risk factors for causing disease, disability, and death worldwide. Ethanol is known to disrupt phospholipid packing and promote membrane hemifusion at lipid bilayers. With the exception of mitochondria involved in hormone synthesis, the sterol content of mitochondrial membranes is low. As membranes that are low in cholesterol have increased membrane fluidity and are the most easily disordered by ethanol, we hypothesize that mitochondria are sensitive targets for ethanol damage. HeLa cells were exposed to 50 mM ethanol and the direct effects of ethanol on cellular ultrastructure were examined utilizing transmission electron microscopy. Our ultramicroscopic analysis revealed that cells exposed to ethanol harbor fewer incidence of apoptotic morphology; however, significant alterations to mitochondria and to nuclei occurred. We observed statistical increases in the amount of irregular cells and cells with multiple nuclei, nuclei harboring indentations, and nuclei with multiple nucleolus-like bodies. Indeed, our analysis revealed that mitochondrial damage is the most extensive type of cellular damage. Rupturing of cristae was the most prominent damage followed by mitochondrial swelling. Ethanol exposure also resulted in increased amounts of mitochondrial rupturing, organelles with linked membranes, and mitochondria localizing to indentations of nuclear membranes. We theorize that these alterations could contribute to cellular defects in oxidative phosphorylation and, by extension, the inability to generate regular levels of cellular adenosine triphosphate

Microglia depletion rapidly and reversibly alters amyloid pathology by modification of plaque compaction and morphologies

Alzheimer's disease (AD) is a prominent neurodegenerative disorder characterized by deposition of β-amyloid (Aβ)-containing extracellular plaques, accompanied by a microglial-mediated inflammatory response, that leads to cognitive decline. Microglia perform many disease-modifying functions such as phagocytosis of plaques, plaque compaction, and modulation of inflammation through the secretion of cytokines. Microglia are reliant upon colony-stimulating factor receptor-1 (CSF1R) activation for survival. In AD mouse models, chronic targeted depletion of microglia via CSF1R antagonism attenuates plaque formation in early disease but fails to alter plaque burden in late disease. It is unclear if acute depletion of microglia during the peak period of plaque deposition will alter disease pathogenesis, and if so, whether these effects are reversible upon microglial repopulation. To test this, we administered the CSF1R antagonist PLX5622 to the 5XFAD mouse model of AD at four months of age for approximately one month. In a subset of mice, the drug treatment was discontinued, and the mice were fed a control diet for an additional month. We evaluated plaque burden and composition, microgliosis, inflammatory marker expression, and neuritic dystrophy. In 5XFAD animals, CSF1R blockade for 28 days depleted microglia across brain regions by over 50%, suppressed microgliosis, and reduced plaque burden. In microglial-depleted AD animals, neuritic dystrophy was enhanced, and increased diffuse-like plaques and fewer compact-like plaques were observed. Removal of PLX5622 elicited microglial repopulation and subsequent plaque remodeling, resulting in more compact plaques predominating microglia-repopulated regions. We found that microglia limit diffuse plaques by maintaining compact-like plaque properties, thereby blocking the progression of neuritic dystrophy. Microglial repopulation reverses these effects. Collectively, we show that microglia are neuroprotective through maintenance of plaque compaction and morphologies during peak disease progression

The brain's response to pleasant touch: an EEG investigation of tactile caressing

Somatosensation as a proximal sense can have a strong impact on our attitude toward physical objects and other human beings. However, relatively little is known about how hedonic valence of touch is processed at the cortical level. Here we investigated the electrophysiological correlates of affective tactile sensation during caressing of the right forearm with pleasant and unpleasant textile fabrics. We show dissociation between more physically driven differential brain responses to the different fabrics in early somatosensory cortex - the well-known mu-suppression (10-20 Hz) - and a beta-band response (25-30 Hz) in presumably higher-order somatosensory areas in the right hemisphere that correlated well with the subjective valence of tactile caressing. Importantly, when using single trial classification techniques, beta-power significantly distinguished between pleasant and unpleasant stimulation on a single trial basis with high accuracy. Our results therefore suggest a dissociation of the sensory and affective aspects of touch in the somatosensory system and may provide features that may be used for single trial decoding of affective mental states from simple electroencephalographic measurements

The Trem2 R47H variant confers loss-of-function-like phenotypes in Alzheimer's disease

BACKGROUND: The R47H variant of Triggering Receptor Expressed on Myeloid cells 2 (TREM2) confers greatly increased risk for Alzheimer's disease (AD), reflective of a central role for myeloid cells in neurodegeneration. Understanding how this variant confers AD risk promises to provide important insights into how myeloid cells contribute to AD pathogenesis and progression. METHODS: In order to investigate this mechanism, CRISPR/Cas9 was used to generate a mouse model of AD harboring one copy of the single nucleotide polymorphism (SNP) encoding the R47H variant in murine Trem2. TREM2 expression, myeloid cell responses to amyloid deposition, plaque burden, and neuritic dystrophy were assessed at 4 months of age. RESULTS: AD mice heterozygous for the Trem2 R47H allele exhibited reduced total Trem2 mRNA expression, reduced TREM2 expression around plaques, and reduced association of myeloid cells with plaques. These results were comparable to AD mice lacking one copy of Trem2. AD mice heterozygous for the Trem2 R47H allele also showed reduced myeloid cell responses to amyloid deposition, including a reduction in proliferation and a reduction in CD45 expression around plaques. Expression of the Trem2 R47H variant also reduced dense core plaque number but increased plaque-associated neuritic dystrophy. CONCLUSIONS: These data suggest that the AD-associated TREM2 R47H variant increases risk for AD by conferring a loss of TREM2 function and enhancing neuritic dystrophy around plaques

Rats use memory confidence to guide decisions.

Memory enables access to past experiences to guide future behavior. Humans can determine which memories to trust (high confidence) and which to doubt (low confidence). How memory retrieval, memory confidence, and memory-guided decisions are related, however, is not understood. In particular, how confidence in memories is used in decision making is unknown. We developed a spatial memory task in which rats were incentivized to gamble their time: betting more following a correct choice yielded greater reward. Rat behavior reflected memory confidence, with higher temporal bets following correct choices. We applied machine learning to identify a memory decision variable and built a generative model of memories evolving over time that accurately predicted both choices and confidence reports. Our results reveal in rats an ability thought to exist exclusively in primates and introduce a unified model of memory dynamics, retrieval, choice, and confidence