The Impact of Turfgrass Pest Management System Techniques on Surface and Ground Water Quality

ReportThe impact of various turfgrass pest management strategies (PMS) on water quality has recently become a concern for many golf course superintendents, sports facilities managers and homeowners. With water quality standards becoming increasingly stringent, management practices have had to follow suit. Uses of alternative control strategies have become increasingly important. This includes the use of biological, cultural and preventative control practices to reduce pest pressure, as well as environmental impacts. Turfgrass is, no doubt, a beneficial addition to most ecosystems, yet when mis-managed can cause harm as well. Mis-management of the turfgrass ecosystem can greatly influence the nitrogen, phosphate and pesticide levels in surface and ground water, causing problems for communities that depend on clean water for consumption as well as recreation. Aquatic ecosystems as well can be severely harmed by increased levels of nitrogen and phosphate, which can cause algal bloom, decreased dissolved oxygen levels, and eutrophication, which in turn has an impact on nearly all ecosystems. Pesticides that find their way into surface or ground water pose a problem to exposed species ranging from fish to humans. When managed correctly, turfgrass provides many positive attributes, including increased UV absorption, CO2 remediation, soil stabilization, ground and surface water filtration, and aesthetic benefits. It is our goal to test the impact of three of the most commonly implemented turfgrass pest management systems, (preventative, IPM, and organic systems) on surface and ground water quality and turfgrass performance. The results will hopefully provide answers on how to produce acceptable turfgrass quality while benefiting the environment

Poly[[μ4-bis­(4-pyridyl­carbon­yl)piperazine-κ4 N:N′:O:O′]bis­(thio­cyanato-κN)cobalt(II)]

In the title compound, [Co(NCS)2(C16H16N4O2)]n, the octa­hedrally coordinated CoII ion lies on a crystallographic inversion center, with trans isothio­cyanate ligands. Pyridyl N-donor atoms and formyl O-donor atoms from exotetra­dentate bis­(4-pyridyl­carbon­yl)piperazine (4-bpfp) ligands link the Co(NCS)2 units into a [Co(NCS)2(4-bpfp)]n coordination polymer layer that is oriented parallel to (101). The layers stack along [010] to construct the pseudo-three-dimensional structure

Angiogenesis-dependent and independent phases of intimal hyperplasia.

BACKGROUND: Neointimal vascular smooth muscle cell (VSMC) proliferation is a primary cause of occlusive vascular disease, including atherosclerosis, restenosis after percutaneous interventions, and bypass graft stenosis. Angiogenesis is implicated in the progression of early atheromatous lesions in animal models, but its role in neointimal VSMC proliferation is undefined. Because percutaneous coronary interventions result in induction of periadventitial angiogenesis, we analyzed the role of this process in neointima formation. METHODS AND RESULTS: Local injury to the arterial wall in 2 different animal models induced periadventitial angiogenesis and neointima formation. Application of angiogenesis stimulators vascular endothelial growth factor (VEGF-A165) or a proline/arginine-rich peptide (PR39) to the adventitia of the injured artery induced a marked increase in neointimal thickening beyond that seen with injury alone in both in vivo models. Inhibition of either VEGF (with soluble VEGF receptor 1 [sFlt1]) or fibroblast growth factor (FGF) (with a dominant=negative form of FGF receptor 1 [FGF-R1DN]), respectively, signaling reduced adventitial thickening induced by VEGF and PR39 to the level seen with mechanical arterial injury alone. However, neither inhibitor was effective in preventing neointimal thickening after mechanical injury when administered in the absence of angiogenic growth factor. CONCLUSIONS: Our findings indicate that adventitial angiogenesis stimulates intimal thickening but does not initiate it

Large Faraday Rotation in Optical-Quality Phthalocyanine and Porphyrin Thin Films

The magneto-optical phenomenon known as Faraday rotation involves the rotation of plane-polarized light as it passes through an optical medium in the presence of an external magnetic field oriented parallel to the direction of light propagation. Faraday rotators find applications in optical isolators and magnetic-field imaging technologies. In recent years, organic thin films comprised of polymeric and small-molecule chromophores have demonstrated Verdet constants, which measure the magnitude of rotation at a given magnetic field strength and material thickness, that exceed those found in conventional inorganic crystals. We report herein the thin-film magnetic circular birefringence (MCB) spectra and maximum Verdet constants of several commercially available and newly synthesized phthalocyanine and porphyrin derivatives. Five of these species achieved maximum Verdet constant magnitudes greater than 105 deg T–1 m–1 at wavelengths between 530 and 800 nm. Notably, a newly reported zinc(II) phthalocyanine derivative (ZnPc-OT) reached a Verdet constant of −33 × 104 deg T–1 m–1 at 800 nm, which is among the largest reported for an organic material, especially for an optical-quality thin film. The MCB spectra are consistent with resonance-enhanced Faraday rotation in the region of the Q-band electronic transition common to porphyrin and phthalocyanine derivatives, and the Faraday A-term describes the electronic origin of the magneto-optical activity. Overall, we demonstrate that phthalocyanines and porphyrins are a class of rationally designed magneto-optical materials suitable for applications demanding large Verdet constants and high optical quality

Photoactivatable genetically encoded calcium indicators for targeted neuronal imaging.

Circuit mapping requires knowledge of both structural and functional connectivity between cells. Although optical tools have been made to assess either the morphology and projections of neurons or their activity and functional connections, few probes integrate this information. We have generated a family of photoactivatable genetically encoded Ca(2+) indicators that combines attributes of high-contrast photolabeling with high-sensitivity Ca(2+) detection in a single-color protein sensor. We demonstrated in cultured neurons and in fruit fly and zebrafish larvae how single cells could be selected out of dense populations for visualization of morphology and high signal-to-noise measurements of activity, synaptic transmission and connectivity. Our design strategy is transferrable to other sensors based on circularly permutated GFP (cpGFP)

Effect of Sex and Menstrual Cycle on Skin Sensory Nerve Contribution to Local Heating

International Journal of Exercise Science 12(2): 1265-1279, 2019. The purpose of this study was to determine sex differences in the contribution of sensory nerves to rapid cutaneous thermal hyperemia. Healthy young females (n = 15, tested during both the early follicular (EF) and the mid-luteal (ML) phase of the menstrual cycle) and males (n = 15) had a 4 cm2 area of skin on one forearm and one leg treated with a eutectic mixture of local anesthetic (EMLA). EMLA sites, along with corresponding control sites, were instrumented with laser Doppler flowmetry probes and local skin heaters. Baseline (33 °C), rapid and sustained vasodilation (42 °C), and maximal vasodilation (44 °C) skin blood flow data were obtained and expressed as a percentage of maximal cutaneous vascular conductance (%CVCmax). Contribution of sensory nerve involvement was determined by comparing the EMLA site to its matched control site utilizing the formula [(% CVCmax control - % CVCmax treatment) / % CVCmax control] × 100. The contribution of sensory nerves to rapid cutaneous thermal hyperemia in the forearm was 24 ± 18 %CVCmax in males, 41 ± 17 %CVCmax in ML females (p = 0.02 vs. males), and 35 ± 17 %CVCmax in EF females (p \u3e 0.05 vs. males). In the leg, the contribution of sensory nerves was 16 ± 15 %CVCmax in males, 34 ± 17 %CVCmax for ML females (p = 0.02 vs. males), and 28 ± 21 %CVCmax in EF females (p \u3e 0.05 vs. males). ML females exhibited a greater contribution of sensory nerves to rapid cutaneous thermal hyperemia in the forearm and leg, possibly attributed to elevated reproductive hormones during the ML phase

Perinatal and long term effects of maternal uterine artery adenoviral VEGF-A165 gene therapy in the growth restricted guinea pig fetus

Uterine artery application of adenoviral vascular endothelial growth factor gene therapy (Ad.VEGF-A165) increases uterine blood flow and fetal growth in experimental animals with fetal growth restriction (FGR). Whether Ad.VEGF-A165 reduces lifelong cardiovascular disease risk imposed by FGR remains unknown. Here, pregnant guinea pigs fed 70% normal food intake to induce FGR received Ad.VEGF-A165 (1x1010 viral particles, n=15) or vehicle (n=10), delivered to the external surface of the uterine arteries, in mid-pregnancy. Ad libitum fed controls received vehicle only (n=14). Litter size, gestation length, and perinatal mortality were similar in control, untreated FGR and FGR+Ad.VEGF-A165 animals. Compared to controls, birth weight was lower in male but higher in female pups following maternal nutrient restriction, whilst both male and female FGR+Ad.VEGF-A165 pups were heavier than untreated FGR pups (P<0.05 ANOVA). Postnatal weight gain was 10-20% greater in female FGR+Ad.VEGF-A165 than untreated FGR pups, depending on age, although neither group differed from controls. Maternal nutrient restriction reduced heart weight in adult female offspring, irrespective of Ad.VEGF-A165 treatment, but did not alter ventricular wall thickness. In males, postnatal weight gain and heart morphology were not affected by maternal treatment. Neither systolic, diastolic nor mean arterial pressure, adrenal weight, basal or challenged plasma cortisol were affected by maternal undernutrition or Ad.VEGF-A165 in either sex. Therefore, increased fetal growth conferred by maternal uterine artery Ad.VEGF-A165 is sustained postnatally in FGR female guinea pigs. In this study we did not find evidence for an effect of maternal nutrient restriction or Ad.VEGF-A165 therapy on adult offspring blood pressure

Peri- and postnatal effects of prenatal adenoviral VEGF gene therapy in growth-restricted sheep

Supported by Wellcome Trust project grant 088208 to A.L.D., J.M.W., D.M.P., I.C.Z., and J.F.M. Wellbeing of Women research training fellowship 318 to D.J.C., Scottish Government work package 4.2 to J.M.W., J.S.M., and R.P.A., as well as funding from the National Institute for Health Research University College London Hospitals Biomedical Research Centre A.L.D. and D.M.P., the British Heart Foundation to I.C.Z., and Ark Therapeutics Oy, Kuopio, Finland, which supplied adenovirus vectors free of charge.Peer reviewedPublisher PD