Eelgrass Wasting Disease: an Overview

During the 1930s, ‘wasting disease’ decimated eelgrass, Zostera marina L., meadows along the Atlantic Coast of North America and Europe with over 90% loss. Outbreaks of wasting disease were also documented in the Pacific Northwest and New Zealand. Wasting disease continues to affect eelgrass meadows with variable degrees of loss, though none as catastrophic as the 1930s. Speculations concerning the causative agent of the 1930s wasting disease included microorganisms, oil pollution, drought, or changes in salinity, temperature, or irradiance. In 1987, it was shown using Koch’s postulates that the eelgrass wasting disease is caused by infection with a marine slime-mold-like protist, Labyrinthula zosterae, a host-specific pathogen. Wasting disease infection spreads either through direct contact with an infected growing plant or drifting detached plant parts. The initial symptoms are black-brown areas on the leaves, which, as the infection develops, coalesce to form patches, larger blackened spots and streaks; ultimately, the plant dies. The photosynthetic efficiency of green leaves is reduced by half at the margins of the necrotic region, and above these blackened spots photosynthetic activity is diminished. Microscopic examination of necrotic leaves reveals that the pathogen moves rapidly (175 μm min–1) through tissues, penetrating cell walls. The protist initiates enzymatic degradation of the cell wall and destruction of the cytoplasm, creating the black spots. Labyrinthula activity slows at salinities less than 20 to 25. Elevated temperature and low light were implicated in the 1930s epidemic. Recent studies show that elevated temperature and prolonged low light levels create metabolic stress which increases plant susceptibility to the disease while high phenolic levels in eelgrass reduce susceptibility. The reports of unexplained eelgrass die-off in Californian estuaries, as well as observations of blackened leaf tissue along the west coast, prompt the need for scientific investigation of wasting disease across the region

The feeding habits of wireworms with special reference to Melanotus spp. (Elateridae)

Typescript, etc.Digitized by Kansas State University Librarie

Is Nitrogen a Major Stressor of Eelgrass (Zostera marina) in Puget Sound?

The deep, cold and well-flushed waters of Puget Sound, WA (USA) are experiencing areas of eelgrass (Zostera marina L.) decline. Eelgrass faces anthropogenic stresses ranging from eutrophication and sedimentation to shoreline hardening, ship traffic, and aquaculture, which are currently being evaluated with a weight-of-evidence analysis. Since 2000, the Washington State Department of Natural Resources’ Submerged Vegetation Monitoring Program has assessed status and trends in eelgrass area and depth distribution throughout Puget Sound. Over this same time period, WA Department of Ecology has been monitoring nitrogen in the Sound’s waters; increasing concentrations of nitrate have been measured, linked to anthropogenic sources. The human-derived nitrogen comes on top of the already high background nitrogen level from the Pacific Ocean upwelling. The result is very high phytoplankton productivity, most evident in the more poorly flushed parts of the Sound. In many of these areas, nitrate concentrations have increased 4-10 times over the last 10 years while eelgrass beds have declined, with eelgrass losses seen at the deep edge where light is most limited. Nitrogen loading is by no means the only stressor impacting eelgrass in the Sound. Sediment loading also shades eelgrass and is derived from river input to the Sound and surface runoff that results from watershed deforestation, agriculture, and impervious surfaces, in addition to the fine sediment from glacial melting. There are a variety of additional direct physical impacts to eelgrass, including aquaculture, shoreline hardening, dredging and filling, boating and fishing practices, and overwater structures all contribute to direct physical impacts on eelgrass and each was evaluated in terms of its spatial extent and type of threat. The weight-of-evidence analysis shows that the nitrogen stressor has the broadest spatial extent and most lethal impacts to eelgrass and is the primary stressor of eelgrass in Puget Sound. The Puget Sound Partnership’s goal of a 20% increase in eelgrass area by 2020 cannot be achieved with existing management practices; the stresses on eelgrass must be reduced to create gains in eelgrass area and insure the health of Puget Sound

Status, Trends, and Conservation of Eelgrass in Atlantic Canada and the Northeastern United States: Workshop Report

Eelgrass (Zostera marina L) is the dominant seagrass occurring in eastern Canada and the northeastern United States, where it often forms extensive meadows in coastal and estuarine areas. Eelgrass beds are extremely productive and provide many valuable ecological functions and ecosystem services. They serve as critical feeding and nursery habitat for a wide variety of commercially and recreationally important fish and shellfish and as feeding areas for waterfowl and other waterbirds. Eelgrass detritus is also transported considerable distances to fuel offshore food webs. In addition, eelgrass beds stabilize bottom sediments, dampen wave energy, absorb nutrients from surrounding waters, and retain carbon through burial

The Iowa Homemaker vol.30, no.8

Seniors Say, Harriet LaRue, page 3 Congratulations from the 1921 Staff, page 4 1921-1951, Mrs. Fred Ferguson, Mrs. Frank Kerekes, Mrs. Eloise Hauser, page 5 College Decision, Anne Ekdahl, page 6 Words From a Waiter, Alane Baird, page 7 9 Previews of Home Economics, Barbara Short, page 8 Godey’s Lady’s Book, Patricia Binder, page 11 Here’s An Idea, Carol Dee Legg, page 14 What’s New, Nancy Voss, page 16 Alums in the News, Jane Novak, page 18 Information, Please, Doris Cook, page 20 Trends, Nancy Butler, page 2

Group IV Phospholipase A2α Controls the Formation of Inter-Cisternal Continuities Involved in Intra-Golgi Transport

The enzyme phospholipase A2 (cPLA2α) is involved in the formation of intercisternal tubules that mediate transport of proteins within the Golgi complex

Adding 6 months of androgen deprivation therapy to postoperative radiotherapy for prostate cancer: a comparison of short-course versus no androgen deprivation therapy in the RADICALS-HD randomised controlled trial

Background Previous evidence indicates that adjuvant, short-course androgen deprivation therapy (ADT) improves metastasis-free survival when given with primary radiotherapy for intermediate-risk and high-risk localised prostate cancer. However, the value of ADT with postoperative radiotherapy after radical prostatectomy is unclear. Methods RADICALS-HD was an international randomised controlled trial to test the efficacy of ADT used in combination with postoperative radiotherapy for prostate cancer. Key eligibility criteria were indication for radiotherapy after radical prostatectomy for prostate cancer, prostate-specific antigen less than 5 ng/mL, absence of metastatic disease, and written consent. Participants were randomly assigned (1:1) to radiotherapy alone (no ADT) or radiotherapy with 6 months of ADT (short-course ADT), using monthly subcutaneous gonadotropin-releasing hormone analogue injections, daily oral bicalutamide monotherapy 150 mg, or monthly subcutaneous degarelix. Randomisation was done centrally through minimisation with a random element, stratified by Gleason score, positive margins, radiotherapy timing, planned radiotherapy schedule, and planned type of ADT, in a computerised system. The allocated treatment was not masked. The primary outcome measure was metastasis-free survival, defined as distant metastasis arising from prostate cancer or death from any cause. Standard survival analysis methods were used, accounting for randomisation stratification factors. The trial had 80% power with two-sided α of 5% to detect an absolute increase in 10-year metastasis-free survival from 80% to 86% (hazard ratio [HR] 0·67). Analyses followed the intention-to-treat principle. The trial is registered with the ISRCTN registry, ISRCTN40814031, and ClinicalTrials.gov, NCT00541047. Findings Between Nov 22, 2007, and June 29, 2015, 1480 patients (median age 66 years [IQR 61–69]) were randomly assigned to receive no ADT (n=737) or short-course ADT (n=743) in addition to postoperative radiotherapy at 121 centres in Canada, Denmark, Ireland, and the UK. With a median follow-up of 9·0 years (IQR 7·1–10·1), metastasis-free survival events were reported for 268 participants (142 in the no ADT group and 126 in the short-course ADT group; HR 0·886 [95% CI 0·688–1·140], p=0·35). 10-year metastasis-free survival was 79·2% (95% CI 75·4–82·5) in the no ADT group and 80·4% (76·6–83·6) in the short-course ADT group. Toxicity of grade 3 or higher was reported for 121 (17%) of 737 participants in the no ADT group and 100 (14%) of 743 in the short-course ADT group (p=0·15), with no treatment-related deaths. Interpretation Metastatic disease is uncommon following postoperative bed radiotherapy after radical prostatectomy. Adding 6 months of ADT to this radiotherapy did not improve metastasis-free survival compared with no ADT. These findings do not support the use of short-course ADT with postoperative radiotherapy in this patient population

Duration of androgen deprivation therapy with postoperative radiotherapy for prostate cancer: a comparison of long-course versus short-course androgen deprivation therapy in the RADICALS-HD randomised trial

Background Previous evidence supports androgen deprivation therapy (ADT) with primary radiotherapy as initial treatment for intermediate-risk and high-risk localised prostate cancer. However, the use and optimal duration of ADT with postoperative radiotherapy after radical prostatectomy remains uncertain. Methods RADICALS-HD was a randomised controlled trial of ADT duration within the RADICALS protocol. Here, we report on the comparison of short-course versus long-course ADT. Key eligibility criteria were indication for radiotherapy after previous radical prostatectomy for prostate cancer, prostate-specific antigen less than 5 ng/mL, absence of metastatic disease, and written consent. Participants were randomly assigned (1:1) to add 6 months of ADT (short-course ADT) or 24 months of ADT (long-course ADT) to radiotherapy, using subcutaneous gonadotrophin-releasing hormone analogue (monthly in the short-course ADT group and 3-monthly in the long-course ADT group), daily oral bicalutamide monotherapy 150 mg, or monthly subcutaneous degarelix. Randomisation was done centrally through minimisation with a random element, stratified by Gleason score, positive margins, radiotherapy timing, planned radiotherapy schedule, and planned type of ADT, in a computerised system. The allocated treatment was not masked. The primary outcome measure was metastasis-free survival, defined as metastasis arising from prostate cancer or death from any cause. The comparison had more than 80% power with two-sided α of 5% to detect an absolute increase in 10-year metastasis-free survival from 75% to 81% (hazard ratio [HR] 0·72). Standard time-to-event analyses were used. Analyses followed intention-to-treat principle. The trial is registered with the ISRCTN registry, ISRCTN40814031, and ClinicalTrials.gov , NCT00541047 . Findings Between Jan 30, 2008, and July 7, 2015, 1523 patients (median age 65 years, IQR 60–69) were randomly assigned to receive short-course ADT (n=761) or long-course ADT (n=762) in addition to postoperative radiotherapy at 138 centres in Canada, Denmark, Ireland, and the UK. With a median follow-up of 8·9 years (7·0–10·0), 313 metastasis-free survival events were reported overall (174 in the short-course ADT group and 139 in the long-course ADT group; HR 0·773 [95% CI 0·612–0·975]; p=0·029). 10-year metastasis-free survival was 71·9% (95% CI 67·6–75·7) in the short-course ADT group and 78·1% (74·2–81·5) in the long-course ADT group. Toxicity of grade 3 or higher was reported for 105 (14%) of 753 participants in the short-course ADT group and 142 (19%) of 757 participants in the long-course ADT group (p=0·025), with no treatment-related deaths. Interpretation Compared with adding 6 months of ADT, adding 24 months of ADT improved metastasis-free survival in people receiving postoperative radiotherapy. For individuals who can accept the additional duration of adverse effects, long-course ADT should be offered with postoperative radiotherapy. Funding Cancer Research UK, UK Research and Innovation (formerly Medical Research Council), and Canadian Cancer Society