Completion Report: Arkansas State Pesticides in Ground Water Monitoring Project Phase V: Vulnerable areas in Jackson, Monroe, Lawrence and Lonoke Counties

In 1996, sixty-seven water samples were drawn from 65 wells, including 62 new wells and 3 wells sampled previously . One Woodruff County well and two Pulaski County wells were resampled. Thirty-two samples were drawn from 30 wells in Monroe County (well #1 was sampled 3 times during this phase) . Ten wells in Jackson County, 12 wells in Lawrence County and 10 wells in Lonoke were also tested (Figures 1-5) . With the completion of Phase V, the number of wells tested has risen to 231 with a total of 258 samples analyzed . Initially, the wells were tested for 13 pesticides and ni~rate. Two more pesticides, aldicarb and carbofuran were added to the analyte list during Phase V. The analyte list is shown in Table 3 . All results from all the wells are listed in Appendix A. Quality control information for these data follow the results. The Phase V Quality Assurance Report is included in this document as Part II

Completion Report: Arkansas State Pesticides in Ground Water Monitoring Project Phase IV: Eastern Arkansas (Pulaski, Lee and Jackson Counties)

In 1995, fifty-two water samples were drawn from 49 new wells and 2 wells that had been previously sampled during earlier phases. These included twenty samples from 19 wells in eastern Pulaski County, thirteen wells in Lee County, 16 wells in Jackson County, two wells in Lonoke County, one well in Crittenden County and resamples of two wells in Woodruff County. Figure 1 shows the locations of the 3 counties where the majority of the samples were taken and Figures 2-4 show the monitoring locations withing these counties. The wells were tested for nitrate and 13 pesticides listed in Table 3. The data and associated quality control information for all the wells tested are included in Section 2: Phase IV Quality Assurance Report

Nitric oxide flux-dependent bacterial adhesion and viability at fibrinogen-coated surfaces

Nitric oxide (NO) is an endogenous antibacterial agent produced by immune cells in response to pathogens. Herein, the NO fluxes necessary to reduce bacterial adhesion of different bacteria (S. aureus, methicillin-resistant S. aureus, S. epidermidis, E. faecalis, E. coli, and P. aeruginosa) were investigated to ascertain the sensitivity of these bacteria to NO. S-nitrosothiol NO donor-modified xerogels were selected as a model NO-release surface due to their extended NO-release kinetics relative to other NO donor systems. The xerogels were coated with poly(vinyl chloride) (PVC) to achieve consistent surface energy between NO-releasing and control substrates. Fibrinogen was pre-adsorbed to these materials to more accurately mimic conditions encountered in blood and promote bacteria adhesion. Nitric oxide fluxes ranging from 20–50 pmol cm−2 s−1 universally inhibited the bacterial adhesion by >80% for each strain studied. Maximum bacteria killing activity (reduced viability by 85–98%) was observed at the greatest NO payload (1700 nmol cm−2)

SERCA2 Regulates Non-CF and CF Airway Epithelial Cell Response to Ozone

Calcium mobilization can regulate a wide range of essential functions of respiratory epithelium, including ion transport, ciliary beat frequency, and secretion of mucus, all of which are modified in cystic fibrosis (CF). SERCA2, an important controller of calcium signaling, is deficient in CF epithelium. We conducted this study to determine whether SERCA2 deficiency can modulate airway epithelial responses to environmental oxidants such as ozone. This could contribute to the pathogenesis of pulmonary exacerbations, which are important and frequent clinical events in CF. To address this, we used air-liquid interface (ALI) cultures of non-CF and CF cell lines, as well as differentiated cultures of cells derived from non-CF and CF patients. We found that ozone exposure caused enhanced membrane damage, mitochondrial dysfunction and apoptotic cell death in CF airway epithelial cell lines relative to non-CF. Ozone exposure caused increased proinflammatory cytokine production in CF airway epithelial cell lines. Elevated proinflammatory cytokine production also was observed in shRNA-mediated SERCA2 knockdown cells. Overexpression of SERCA2 reversed ozone-induced proinflammatory cytokine production. Ozone-induced proinflammatory cytokine production was NF-κB- dependent. In a stable NF-κB reporter cell line, SERCA2 inhibition and knockdown both upregulated cytomix-induced NF-κB activity, indicating importance of SERCA2 in modulating NF-κB activity. In this system, increased NF-κB activity was also accompanied by increased IL-8 production. Ozone also induced NF-κB activity and IL-8 release, an effect that was greater in SERCA2-silenced NF-κB-reporter cells. SERCA2 overexpression reversed cytomix-induced increased IL-8 release and total nuclear p65 in CFTR-deficient (16HBE-AS) cells. These studies suggest that SERCA2 is an important regulator of the proinflammatory response of airway epithelial cells and could be a potential therapeutic target

Local delivery of nitric oxide: Targeted delivery of therapeutics to bone and connective tissues

Non-invasive treatment of injuries and disorders affecting bones and connective tissue is a significant challenge facing the medical community. A treatment route that has recently been proposed is nitric oxide (NO) therapy. Nitric oxide plays several roles in physiology with many conditions lacking adequate levels of NO. As NO is a radical, localized delivery via NO donors is essential to promoting biological activity. Herein, we review current literature related to therapeutic NO delivery in the treatment of bone, skin and tendon repair

Photoinitiated Nitric Oxide-Releasing Tertiary S -Nitrosothiol-Modified Xerogels

The synthesis of a tertiary thiol-bearing silane precursor (i.e., N-acetyl penicillamine propyltrimethoxysilane or NAPTMS) to enable enhanced NO storage stability at physiological temperature is described. The novel silane was co-condensed with alkoxy- and alkylalkoxysilanes under varied synthetic parameters (e.g., water to silane ratio, catalyst and solvent concentrations, and reaction time) to evaluate systematically the formation of stable xerogel films. The resulting xerogels were subsequently nitrosated to yield tertiary RSNO-modified coatings. Total NO storage ranged from 0.87–1.78 µmol cm−2 depending on the NAPTMS concentration and xerogel coating thickness. Steric hindrance near the nitroso functionality necessitated the use of photolysis to liberate NO. The average NO flux for irradiated xerogels in physiological buffer at 37 °C was ~23 pmol cm−2 s−1 (20% NAPTMS balance TEOS xerogel film cast using 30 µL). The biomedical utility of the photo-initiated NO-releasing films was illustrated by their ability to both reduce Pseudomonas aeruginosa adhesion by ~90% relative to control interfaces and eradicate the adhered bacteria

Western Diet-Fed, Aortic-Banded Ossabaw Swine: A Preclinical Model of Cardio-Metabolic Heart Failure.

The development of new treatments for heart failure lack animal models that encompass the increasingly heterogeneous disease profile of this patient population. This report provides evidence supporting the hypothesis that Western Diet-fed, aortic-banded Ossabaw swine display an integrated physiological, morphological, and genetic phenotype evocative of cardio-metabolic heart failure. This new preclinical animal model displays a distinctive constellation of findings that are conceivably useful to extending the understanding of how pre-existing cardio-metabolic syndrome can contribute to developing HF