Seasonal Changes in Chemical Composition of Eurasion Watermilfoil (Myriophyllum spicatum L.) and Water Temperature at Two Sites in northern California: implications for Herbivory

We compared seasonal changes in Eurasian watermilfoil (Myriophyllum spicatum L.) characteristics and water temperature for a shallow poind in Davis, CA, and the Truckee River, near Tahoe City, CA. Tissue C and N were 15% lower in plants from the Truckee River than in plants from the Davis pond. Seasonal fluctuations in tissue N were also different. Mean phenolic acid content of Truckee River palnts (162yM g-1) was less than those from the shallow pond (195 yM g-1). Phenolic acid content was positively related to tissue C for Truckee River and Davis pond plants and, tissue C:N ratio for Truckee River plants. Mean monthly water temperature (1990 to 1998) for the Truckee River site was less than 20 C. Water temperatures were warmer in August and September at this site. However, Eurasian watermilfoil collected during these months was characterized by lower levels of tissue N. During a 29-month period beginning January 1994, mean monthly water temperature for the Davis pond exceeded 20 C, only during July to September 1995. Tissue N was generally greater during summer for watermilfoil growing in the pond. These results imply that Eurasian watermilfoil biological control agents may have different developmental rates in these habitats, and thus different impacts on watermilfoil populations

Do tissue carbon and nitrogen limit population growth of weevils introduced to control waterhyacinth at a site in the Sacramento-San Joaquin Delta, California?

Waterhyacinth (Eichhornia crassipes(Mart.) Solms), is a serious problem in the Sacramento Delta. Two weevil species (Neochetina bruchi Hustache and N. eichhorniae Warner) have been introduced as biological control agents. The purpose of this study was to test the hypothesis that nitrogen (N) in the tissue of waterhyacinth was not sufficient to support weevil growth and reproduction. Because it grows better on plants with high N content and because it has a greater impact on the growth of high N plants, N. bruchi may be a more effective biological control agent in the Sacramento Delta

Interactions between American pondweed and monoecious hydrilla grown in mixtures

To assess the potential for monoecious hydrilla ( Hydrilla verticillata (L.f.) Royle) to invade existing aquatic plant communities, monoecious hydrilla was grown in mixtures with American pondweed ( Potamogeton nodosus Poiret). When grown with hydrilla from axillary turions, American pondweed was a stronger competitor. When grown with hydrilla from tubers, American pondweed was equally as strong a competitor as hydrilla

Influence of Dilute Acetic Acid Treatments on Survival of Monoecious Hydrilla Tubers in the Oregon House Canal, California

Hydrilla (Hydrilla verticillata (L.f.)Royle), a serious aquatic weed, reproduces through formation of underground tubers. To date, attacking this life-cycle stage has been problematic. The purpose of this study was to measure the impact of exposure to dilute acetic acid on monoecious hydrilla tubers under field conditions. In this field experiment, treatments were acetic acid concentration (0, 2.5, or 5%) and sediment condition (perforated or not perforated). Each of 60, 1x1 m plots (in the Oregon House Canal) were randomly assigned to one treatment. Two weeks after treatment, we collected three samples from each plot. One was washed over 2 mm wire mesh screens to separate tubers from sediment. Relative electrolyte leakage was measured for one tuber from each plot. Five additional tubers from each plot were placed in a growth chamber and sprouting monitored for four weeks. A second sample from each plot was placed in a plastic tub and placed in an outdoor tank, filled with water. These samples were monitored for tuber sprouting. Relative electrolyte leakage increased significantly for tubers exposed to 2.5% or 5% acetic acid. Effects on tubers in perforated sediment were reduced. Exposure to acetic acid inhibited tuber sprouting by 80 to 100%, in both chamber and outdoor tests. These results confirm findings from earlier laboratory/greenhouse experiments, and suggest that this approach may be useful in the management of hydrilla tuber banks in habitats where the water level can be lowered to expose the sediments

By Altering Ocular Immune Privilege, Bone Marrow–derived Cells Pathogenically Contribute to DBA/2J Pigmentary Glaucoma

Pigment dispersion syndrome causes iris pigment release and often progresses to elevated intraocular pressure and pigmentary glaucoma (PG). Because melanin pigment can have adjuvant like properties and because the Gpnmb gene, which contributes to pigment dispersion in DBA/2J (D2) mice, is expressed in dendritic cells, we tested the hypothesis that ocular immune abnormalities participate in PG phenotypes. Strikingly, we show that D2 eyes exhibit defects of the normally immunosuppressive ocular microenvironment including inability of aqueous humor to inhibit T cell activation, failure to support anterior chamber (AC)-associated immune deviation, and loss of ocular immune privilege. Histologic analysis demonstrates infiltration of inflammatory leukocytes into the AC and their accumulation within the iris, whereas clinical indications of inflammation are typically very mild to undetectable. Importantly, some of these abnormalities precede clinical indications of pigment dispersal, suggesting an early role in disease etiology. Using bone marrow chimeras, we show that lymphohematopoietic cell lineages largely dictate the progression of pigment dispersion, the ability of the eye to support induction of AC-associated immune deviation, and the integrity of the blood/ocular barrier. These results suggest previously unsuspected roles for bone marrow–derived cells and ocular immune privilege in the pathogenesis of PG

Endomucin prevents leukocyte–endothelial cell adhesion and has a critical role under resting and inflammatory conditions

Endomucin is a membrane-bound glycoprotein expressed luminally by endothelial cells that line postcapillary venules, a primary site of leukocyte recruitment during inflammation. Here we show that endomucin abrogation on quiescent endothelial cells enables neutrophils to adhere firmly, via LFA-1-mediated binding to ICAM-1 constitutively expressed by endothelial cells. Moreover, TNF-α stimulation downregulates cell surface expression of endomucin concurrent with increased expression of adhesion molecules. Adenovirus-mediated expression of endomucin under inflammatory conditions prevents neutrophil adhesion in vitro and reduces the infiltration of CD45+ and NIMP-R14+ cells in vivo. These results indicate that endomucin prevents leukocyte contact with adhesion molecules in non-inflamed tissues and that downregulation of endomucin is critical to facilitate adhesion of leukocytes into inflamed tissues

Opposing Roles for Membrane Bound and Soluble Fas Ligand in Glaucoma-Associated Retinal Ganglion Cell Death

Glaucoma, the most frequent optic neuropathy, is a leading cause of blindness worldwide. Death of retinal ganglion cells (RGCs) occurs in all forms of glaucoma and accounts for the loss of vision, however the molecular mechanisms that cause RGC loss remain unclear. The pro-apoptotic molecule, Fas ligand, is a transmembrane protein that can be cleaved from the cell surface by metalloproteinases to release a soluble protein with antagonistic activity. Previous studies documented that constitutive ocular expression of FasL maintained immune privilege and prevented neoangeogenesis. We now show that FasL also plays a major role in retinal neurotoxicity. Importantly, in both TNFα triggered RGC death and a spontaneous model of glaucoma, gene-targeted mice that express only full-length FasL exhibit accelerated RGC death. By contrast, FasL-deficiency, or administration of soluble FasL, protected RGCs from cell death. These data identify membrane-bound FasL as a critical effector molecule and potential therapeutic target in glaucoma

Membrane-bound and soluble Fas ligands have opposite functions in photoreceptor cell death following separation from the retinal pigment epithelium

Fas ligand (FasL) triggers apoptosis of Fas-positive cells, and previous reports described FasL-induced cell death of Fas-positive photoreceptors following a retinal detachment. However, as FasL exists in membrane-bound (mFasL) and soluble (sFasL) forms, and is expressed on resident microglia and infiltrating monocyte/macrophages, the current study examined the relative contribution of mFasL and sFasL to photoreceptor cell death after induction of experimental retinal detachment in wild-type, knockout (FasL−/−), and mFasL-only knock-in (ΔCS) mice. Retinal detachment in FasL−/− mice resulted in a significant reduction of photoreceptor cell death. In contrast, ΔCS mice displayed significantly more apoptotic photoreceptor cell death. Photoreceptor loss in ΔCS mice was inhibited by a subretinal injection of recombinant sFasL. Thus, Fas/FasL-triggered cell death accounts for a significant amount of photoreceptor cell loss following the retinal detachment. The function of FasL was dependent upon the form of FasL expressed: mFasL triggered photoreceptor cell death, whereas sFasL protected the retina, indicating that enzyme-mediated cleavage of FasL determines, in part, the extent of vision loss following the retinal detachment. Moreover, it also indicates that treatment with sFasL could significantly reduce photoreceptor cell loss in patients with retinal detachment