Education Program for Improved Water Quality in Copano Bay Final Report

The Copano Bay watershed covers approximately 1.4 million acres encompassing portions of Karnes, Bee, Goliad, Refugio, San Patricio and Aransas counties. Copano Bay and its main tributaries, the Mission and Aransas rivers, were placed on the Texas Commission on Environmental Quality (TCEQ) 303(d) list in 1998 due to levels of bacteria that exceed water quality standards established to protect oyster waters use. A Total Maximum Daily Load (TMDL) program was initiated in September 2003 to identify and assess sources of these bacteria. The Center for Research in Water Resources at the University of Texas at Austin (UT CRWR) was funded by TCEQ to conduct computer-based modeling to determine the bacterial loading and reductions necessary to attain water quality standards. Subsequently Texas A&M University-Corpus Christi (TAMU-CC) conducted bacterial source tracking (BST) with funding from Texas General Land Office (TGLO) and the Coastal Bend Bays and Estuaries Program (CBBEP) to determine actual sources of bacteria. Due to the findings of the initial efforts of the TMDL and concerns voiced by stakeholders in the watershed, Texas AgriLife Extension Service was awarded a Clean Water Act § 319(h) Nonpoint Source Grant from the Texas State Soil and Water Conservation Board (TSSWCB) and the U.S. Environmental Protection Agency. The overall goal of this project was to improve water quality in Copano Bay and its tributaries by increasing awareness of water quality issues throughout the watershed. This increased awareness was to be accomplished by providing education and demonstrations for land and livestock owners in the watershed on best management practices (BMPs) to decrease or prevent bacteria from entering waterways. Through creation of a project website, 52 educational programs, and nine one-on-one consultations over the span of the project, we have reached 5,408 residents in and around the Copano Bay watershed. Additionally, through this project all data collected for the initial TMDL efforts was re-evaluated and findings were presented in the “Task 2 Report.” Project members developed a curriculum for horse owners, “A Guide to Good Horsekeeping” that addressed BMPs specific to horse operations. Land and livestock owners who had already implemented BMPs or were interested in implementing BMPs were given a participation certificate

Cervicovaginal fluid and semen block the microbicidal activity of hydrogen peroxide produced by vaginal lactobacilli

BACKGROUND: H(2)O(2 )produced by vaginal lactobacilli is believed to protect against infection, and H(2)O(2)-producing lactobacilli inactivate pathogens in vitro in protein-free salt solution. However, cervicovaginal fluid (CVF) and semen have significant H(2)O(2)-blocking activity. METHODS: We measured the H(2)O(2 )concentration of CVF and the H(2)O(2)-blocking activity of CVF and semen using fluorescence and in vitro bacterial-exposure experiments. RESULTS: The mean H(2)O(2 )measured in fully aerobic CVF was 23 ± 5 μM; however, 50 μM H(2)O(2 )in salt solution showed no in vitro inactivation of HSV-2, Neisseria gonorrhoeae, Hemophilus ducreyii, or any of six BV-associated bacteria. CVF reduced 1 mM added H(2)O(2 )to an undetectable level, while semen reduced 10 mM added H(2)O(2 )to undetectable. Moreover, the addition of just 1% CVF supernatant abolished in vitro pathogen-inactivation by H(2)O(2)-producing lactobacilli. CONCLUSIONS: Given the H(2)O(2)-blocking activity of CVF and semen, it is implausible that H(2)O(2)-production by vaginal lactobacilli is a significant mechanism of protection in vivo

An interdisciplinary framework for measuring and supporting adherence in HIV prevention trials of ARV‐based vaginal rings

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138229/1/jia29158.pd

Low pH immobilizes and kills human leukocytes and prevents transmission of cell-associated HIV in a mouse model

BACKGROUND: Both cell-associated and cell-free HIV virions are present in semen and cervical secretions of HIV-infected individuals. Thus, topical microbicides may need to inactivate both cell-associated and cell-free HIV to prevent sexual transmission of HIV/AIDS. To determine if the mild acidity of the healthy vagina and acid buffering microbicides would prevent transmission by HIV-infected leukocytes, we measured the effect of pH on leukocyte motility, viability and intracellular pH and tested the ability of an acidic buffering microbicide (BufferGel(®)) to prevent the transmission of cell-associated HIV in a HuPBL-SCID mouse model. METHODS: Human lymphocyte, monocyte, and macrophage motilities were measured as a function of time and pH using various acidifying agents. Lymphocyte and macrophage motilities were measured using video microscopy. Monocyte motility was measured using video microscopy and chemotactic chambers. Peripheral blood mononuclear cell (PBMC) viability and intracellular pH were determined as a function of time and pH using fluorescent dyes. HuPBL-SCID mice were pretreated with BufferGel, saline, or a control gel and challenged with HIV-1-infected human PBMCs. RESULTS: Progressive motility was completely abolished in all cell types between pH 5.5 and 6.0. Concomitantly, at and below pH 5.5, the intracellular pH of PBMCs dropped precipitously to match the extracellular medium and did not recover. After acidification with hydrochloric acid to pH 4.5 for 60 min, although completely immotile, 58% of PBMCs excluded ethidium homodimer-1 (dead-cell dye). In contrast, when acidified to this pH with BufferGel, a microbicide designed to maintain vaginal acidity in the presence of semen, only 4% excluded dye at 10 min and none excluded dye after 30 min. BufferGel significantly reduced transmission of HIV-1 in HuPBL-SCID mice (1 of 12 infected) compared to saline (12 of 12 infected) and a control gel (5 of 7 infected). CONCLUSION: These results suggest that physiologic or microbicide-induced acid immobilization and killing of infected white blood cells may be effective in preventing sexual transmission of cell-associated HIV

Flood Proofing Low-Income Houses in India: an Application of Climate-Sensitive Probabilistic Benefit-Cost Analysis

Poor communities in high risk areas are disproportionately affected by disasters compared to their wealthy counterparts; yet, there are few analyses to guide public decisions on pro-poor investments in disaster risk reduction. This paper illustrates an application of benefit-cost analysis (BCA) for assessing investments in structural flood proofing of low-income, high-risk houses. The analysis takes account of climate change, which is increasingly viewed as an important consideration for assessing long-term investments. Specifically, the study focuses on the Rohini river basin of India and evaluates options for constructing non-permanent and permanent residential structures on a raised plinth to protect them against flooding. The estimates show a positive benefit-cost ratio for building new houses on a raised plinth, while the ratio is less than one for demolishing existing houses to rebuild on a raised plinth. Climate change is found to significantly affect the BCA results. From a policy perspective, the analysis demonstrates the potential economic returns of raised plinths for ‘building back better’ after disasters, or as a part of good housing design practice

Temperature Dependent Zero-Field Splittings in Graphene

Graphene is a quantum spin Hall insulator with a 45 $\mu$eV wide non-trivial topological gap induced by the intrinsic spin-orbit coupling. Even though this zero-field spin splitting is weak, it makes graphene an attractive candidate for applications in quantum technologies, given the resulting long spin relaxation time. On the other side, the staggered sub-lattice potential, resulting from the coupling of graphene with its boron nitride substrate, compensates intrinsic spin-orbit coupling and decreases the non-trivial topological gap, which may lead to the phase transition into trivial band insulator state. In this work, we present extensive experimental studies of the zero-field splittings in monolayer and bilayer graphene in a temperature range 2K-12K by means of sub-Terahertz photoconductivity-based electron spin resonance technique. Surprisingly, we observe a decrease of the spin splittings with increasing temperature. We discuss the origin of this phenomenon by considering possible physical mechanisms likely to induce a temperature dependence of the spin-orbit coupling. These include the difference in the expansion coefficients between the graphene and the boron nitride substrate or the metal contacts, the electron-phonon interactions, and the presence of a magnetic order at low temperature. Our experimental observation expands knowledge about the non-trivial topological gap in graphene.Comment: Main text with figures (20 pages) and Supplementary Information (14 pages) Accepted in Phys. Rev.

Resolution of hyposmotic stress in isolated mouse ventricular myocytes causes sealing of t‐tubules

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/98789/1/expphysiol.2013.072470.pd

Microbicide excipients can greatly increase susceptibility to genital herpes transmission in the mouse

<p>Abstract</p> <p>Background</p> <p>Several active ingredients proposed as vaginal microbicides have been shown paradoxically to <it>increase </it>susceptibility to infection in mouse genital herpes (HSV-2) vaginal susceptibility models and in clinical trials. In addition, "inactive ingredients" (or excipients) used in topical products to formulate and deliver the active ingredient might also cause epithelial toxicities that increase viral susceptibility. However, excipients have not previously been tested in susceptibility models.</p> <p>Methods</p> <p>Excipients commonly used in topical products were formulated in a non-toxic vehicle (the "HEC universal placebo"), or other formulations as specified. Twelve hours after exposure to the excipient or a control treatment, mice were challenged with a vaginal dose of HSV-2, and three days later were assessed for infection by vaginal lavage culture to assess susceptibility.</p> <p>Results</p> <p>The following excipients markedly increased susceptibility to HSV-2 after a single exposure: 5% glycerol monolaurate (GML) formulated in K-Y^®Warming Jelly, 5% GML as a colloidal suspension in phosphate buffered saline, K-Y Warming Jelly alone, and both of its humectant/solvent ingredients (neat propylene glycol and neat PEG-8). For excipients formulated in the HEC vehicle, 30% glycerin significantly increased susceptibility, and a trend toward increased HSV-2 susceptibility was observed after 10% glycerin, and 0.1% disodium EDTA, but not after 0.0186% disodium EDTA. The following excipients did not increase susceptibility: 10% propylene glycol, 0.18%, methylparaben plus 0.02% propylparaben, and 1% benzyl alcohol.</p> <p>Conclusions</p> <p>As reported with other surfactants, the surfactant/emulsifier GML markedly increased susceptibility to HSV-2. Glycerin at 30% significantly increased susceptibility, and, undiluted propylene glycol and PEG-8 greatly increased susceptibility.</p

In vaginal fluid, bacteria associated with bacterial vaginosis can be suppressed with lactic acid but not hydrogen peroxide

<p>Abstract</p> <p>Background</p> <p>Hydrogen peroxide (H₂O₂) produced by vaginal lactobacilli is generally believed to protect against bacteria associated with bacterial vaginosis (BV), and strains of lactobacilli that can produce H₂O₂are being developed as vaginal probiotics. However, evidence that led to this belief was based in part on non-physiological conditions, antioxidant-free aerobic conditions selected to maximize both production and microbicidal activity of H₂O₂. Here we used conditions more like those <it>in vivo </it>to compare the effects of physiologically plausible concentrations of H₂O₂and lactic acid on a broad range of BV-associated bacteria and vaginal lactobacilli.</p> <p>Methods</p> <p>Anaerobic cultures of seventeen species of BV-associated bacteria and four species of vaginal lactobacilli were exposed to H₂O₂, lactic acid, or acetic acid at pH 7.0 and pH 4.5. After two hours, the remaining viable bacteria were enumerated by growth on agar media plates. The effect of vaginal fluid (VF) on the microbicidal activities of H₂O₂and lactic acid was also measured.</p> <p>Results</p> <p>Physiological concentrations of H₂O₂(< 100 μM) failed to inactivate any of the BV-associated bacteria tested, even in the presence of human myeloperoxidase (MPO) that increases the microbicidal activity of H₂O₂. At 10 mM, H₂O₂inactivated all four species of vaginal lactobacilli but only one of seventeen species of BV-associated bacteria. Moreover, the addition of just 1% vaginal fluid (VF) blocked the microbicidal activity of 1 M H₂O₂. In contrast, lactic acid at physiological concentrations (55-111 mM) and pH (4.5) inactivated all the BV-associated bacteria tested, and had no detectable effect on the vaginal lactobacilli. Also, the addition of 10% VF did not block the microbicidal activity of lactic acid.</p> <p>Conclusions</p> <p>Under optimal, anaerobic growth conditions, physiological concentrations of lactic acid inactivated BV-associated bacteria without affecting vaginal lactobacilli, whereas physiological concentrations of H₂O₂produced no detectable inactivation of either BV-associated bacteria or vaginal lactobacilli. Moreover, at very high concentrations, H₂O₂was more toxic to vaginal lactobacilli than to BV-associated bacteria. On the basis of these <it>in vitro </it>observations, we conclude that lactic acid, not H₂O₂, is likely to suppress BV-associated bacteria <it>in vivo</it>.</p