Quantitative analysis of methodological and environmental influences on survival of planted mangroves in restoration and afforestation

Mangrove planting has been employed for decades to achieve aims associated with restoration and afforestation. Often, survival of planted mangroves is low. Improving survival might be aided by augmenting the understanding of which planting methods and environmental variables most influence plant survival across a range of contexts. The aim of this study was to provide a global synthesis of the influence of planting methods and background environment on mangrove survival. This was achieved through a global meta-analysis, which compiled published survival rates for the period 1979–2021 and analyzed the influence of decisions about minimum spacing and which life stage to plant, and environmental contexts such as climate, tidal range and coastal setting on the reported survival of planted individuals, classified by species and root morphology. Generalized Additive Mixed Modeling (GAMM) revealed that planting larger mangrove saplings was associated with increased survival for pencil-rooted species such as Avicennia spp. and Sonneratia spp. (17% increase cf. seedlings), while greater plant spacing was associated with higher survival of stilt-rooted species in the family Rhizophoraceae (39% increase when doubling plant spacing from 1.5 to 3.0 m). Tidal range showed a nonlinear positive correlation with survival for pencil-rooted species, and the coastal environmental setting was associated with significant variation in survival for both pencil-and stilt-rooted species. The results suggest that improving decisions about which species to plant in different contexts, and intensive care after planting, is likely to improve the survival of planted mangroves

Melatonin Chimeras Alter Reproductive Development and Photorefractoriness in Siberian Hamsters

Nightly melatonin (MEL) durations > 8 h provoke gonadal regression and decreases in body mass, whereas signals < 7 h stimulate gonadal and somatic growth in male Siberian hamsters. The authors sought to determine the minimum frequency of short MEL signals sufficient to induce the long-day phenotype in several photoperiodic traits. D,L-propranolol (hereafter propranolol) injections shortened MEL signals on the night of treatment without altering MEL on the subsequent night; this permitted interpolation of short MEL signals at variable frequencies against a background of long MEL signals (chimeras). Hamsters kept in short days (10 h light/day, 10L) were injected with propranolol 6 h after dark onset for 28 consecutive weeks beginning at 30 days of age (Week 0) either every other day or once every 3, 6, or 9 days. Control animals were injected with saline or with propranolol during the light phase or were transferred to long days (16L) at Week 0. Hamsters in 16L underwent rapid gonadal development and increases in body mass and displayed summer pelage color, as did hamsters treated with propranolol every other day. Animals treated with propranolol less frequently than every other day uniformly maintained undeveloped gonads and winter-like body weights, but pelage color becameproportionately darker with increased frequency of propranolol treatments. The onset of spontaneous testicular development in 10L was unaffected by propranolol injections. After termination of injections at Week 28, testicular regression was not observed in most 10L animals that previously had undergone spontaneous testicular development; however, 40% of hamsters that had been injected with propranolol every 3rd night did manifest the winter phenotype after Week 28. In an alternating sequence, short MEL signals completely override long signals and induce the summer phenotype. Threshold frequencies differ for MEL stimulation of long-day pelage and gonadal phenotypes. The timing and development of refractoriness to MEL does not depend in any simple manner on the number of long MEL signals or on the accumulation of a reaction product produced by long, and depleted by short, MEL signals.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/67291/2/10.1177_074873098129000345.pd

The Internationalists: How a Radical Plan to Outlaw War Remade the World

Oona A. Hathaway and Scott J. Shapiro. The Internationalists: How a Radical Plan to Outlaw War Remade the World. New York: Simon &amp; Schuster, 2017. ISBN: 9781501109874 (paperback, $20.00)

The Internationalists: How a Radical Plan to Outlaw War Remade the World

Oona A. Hathaway and Scott J. Shapiro. The Internationalists: How a Radical Plan to Outlaw War Remade the World. New York: Simon &amp; Schuster, 2017. ISBN: 9781501109874 (paperback, $20.00)

Using Propagules to Restore Coastal Marine Ecosystems

publishedVersio

Transverse vibration analysis of a prestressed thin circular plate in contact with an acoustic cavity

This paper describes the free transverse vibration analysis of a thin circular plate, subjected to in plane stretching, whilst in interaction with a cylindrical acoustic cavity. An analysis is performed which combines the equations describing the plate and the acoustic cavity to form a matrix equation which, when solved, produces the natural frequencies (latent roots) of the coupled system and associated latent vectors which describe the mode shape coefficients of the plate. After assessing the numerical convergence of the method, results are compared with those from a commercial finite element code (ANSYS). The results analysis is then extended to investigate the effect of stressing upon the free vibration of the coupled system

IL-25 regulates Th17 function in autoimmune inflammation

Interleukin (IL)-25 is a member of the IL-17 family of cytokines. However, unlike the other members of this family, IL-25 promotes T helper (Th) 2 responses. We now show that IL-25 also regulates the development of autoimmune inflammation mediated by IL-17–producing T cells. We have generated IL-25–deficient (il25−/−) mice and found that they are highly susceptible to experimental autoimmune encephalomyelitis (EAE). The accelerated disease in the il25−/− mice is associated with an increase of IL-23 in the periphery and a subsequent increase in the number of inflammatory IL-17–, IFNγ-, and TNF-producing T cells that invade the central nervous system. Neutralization of IL-17 but not IFNγ in il25−/− mice prevented EAE, suggesting that IL-17 is a major disease-promoting factor. IL-25 treatment at several time points during a relapse-remitting model or chronic model of EAE completely suppressed disease. IL-25 treatment induced elevated production of IL-13, which is required for suppression of Th17 responses by direct inhibition of IL-23, IL-1β, and IL-6 expression in activated dendritic cells. Thus, IL-25 and IL-17, being members of the same cytokine family, play opposing roles in the pathogenesis of organ-specific autoimmunity

The Grizzly, April 28, 2005

Commencement 2005 • Students Protest Laptop Buyback • Got Talent? • Kaleidoscope Opens • Diversity Week a Success • Ursinus Dancers Preview Work in the Scope • Students Prove Educational Value in Buffy • How to Have a Great Summer • Let the Art Speak for Itself : Preview of the Annual Art Exhibition • Opinions: Most Controversial; Thoughts of a Rising Senior; Turn from Intolerance • Road to the Playoffs in Sight • Lacrosse Team Denied First Conference Win • Intramural Sports Becoming a Popular Alternativehttps://digitalcommons.ursinus.edu/grizzlynews/1585/thumbnail.jp

IL-23 stimulates epidermal hyperplasia via TNF and IL-20R2–dependent mechanisms with implications for psoriasis pathogenesis

Aberrant cytokine expression has been proposed as an underlying cause of psoriasis, although it is unclear which cytokines play critical roles. Interleukin (IL)-23 is expressed in human psoriasis and may be a master regulator cytokine. Direct intradermal administration of IL-23 in mouse skin, but not IL-12, initiates a tumor necrosis factor–dependent, but IL-17A–independent, cascade of events resulting in erythema, mixed dermal infiltrate, and epidermal hyperplasia associated with parakeratosis. IL-23 induced IL-19 and IL-24 expression in mouse skin, and both genes were also elevated in human psoriasis. IL-23–dependent epidermal hyperplasia was observed in IL-19−/− and IL-24−/− mice, but was inhibited in IL-20R2−/− mice. These data implicate IL-23 in the pathogenesis of psoriasis and support IL-20R2 as a novel therapeutic target