Vegetated coastal ecosystems provide goods and services to billions of people. In the aftermath of a series of recent natural disasters, including the Indian Ocean Tsunami, Hurricane Katrina and Cyclone Nargis, coastal vegetation has been widely promoted for the purpose of reducing the impact of large storm surges and tsunami. In this paper, we review the use of coastal vegetation as a "bioshield" against these extreme events. Our objective is to alter bioshield policy and reduce the long-term negative consequences for biodiversity and human capital. We begin with an overview of the scientific literature, in particular focusing on studies published since the Indian Ocean Tsunami in 2004 and discuss the science of wave attenuation by vegetation. We then explore case studies from the Indian subcontinent and evaluate the detrimental impacts bioshield plantations can have upon native ecosystems, drawing a distinction between coastal restoration and the introduction of exotic species in inappropriate locations. Finally, we place bioshield policies into a political context, and outline a new direction for coastal vegetation policy and research.

Abstract-The present study was designed to determine whether chemokine receptor 2b (CCR2b) contributes to the development of renal injury in salt-sensitive angiotensin II (ANG) hypertension. Rats were infused with ANG and fed a high-salt diet (HS) for 14 days. Rats were divided into 4 groups: HS; HS administered the CCR2b antagonist, RS102895; Ang/HS hypertensive; and Ang/HS hypertensive administered RS102895. CCR2b inhibition slowed the progression of blood pressure elevation during the first week of ANG/HS hypertension; however, it did not alter blood pressure in the HS group. At 2 weeks, arterial pressure was not significantly different between ANG/HS and ANG/HS hypertensive rats administered RS102895. Renal cortical nuclear factor B activity increased in ANG/HS hypertension compared with the HS group (0.11Ϯ0.006 versus 0.08Ϯ0.003 ng of activated nuclear factor B per microgram of protein), and RS102895 treatment lowered nuclear factor B activity in ANG/HS hypertension (0.08Ϯ0.005 ng of activated nuclear factor B per microgram of protein). Renal tumor necrosis factor-␣ and intercellular adhesion molecule-1 expression increased, and Cyp2c23 expression decreased in ANG/HS hypertension compared with the HS group, and CCR2b inhibition reduced tumor necrosis factor-␣ and intercellular adhesion molecule-1 and increased Cyp2c23 expression. Histological immunostaining revealed increased renal monocyte and macrophage infiltration in ANG/HS hypertensive rats with decreased infiltration in rats receiving RS102895 treatment. Albuminuria and cortical collagen staining also increased in ANG/HS hypertensive rats, and RS102895 treatment lowered these effects. Afferent arteriolar autoregulatory responses to increasing renal perfusion pressure were blunted in ANG/HS hypertension, and RS102895 treatment improved this response. These data suggest that CCR2b inhibition protects the kidney in hypertension by reducing inflammation and delaying the progression of hypertension. Key Words: kidney Ⅲ inflammation Ⅲ hypertension Ⅲ angiotensin Ⅲ MCP-1 Ⅲ CCR2b Ⅲ chemokines S tudies suggest that inflammation is involved in the progression of hypertension-induced kidney diseases. 1 Cytokines have been identified as components of this inflammation. Chemokines are a class of cytokines that are involved in the proinflammatory response in both normal and pathological conditions. 1 The main function of chemokines is to promote leukocyte migration to sites of injury, and this is achieved through ligand/receptor binding with receptors expressed on leukocytes. 2 Through chemokine signaling, monocytes infiltrate tissue, differentiate into macrophages, and release additional chemokines perpetuating the inflammatory cycle.Monocyte chemoattractant protein-1 (MCP-1) plays a pivotal role in the development of the inflammatory response. 1 MCP-1 expression increases at injury sites to direct macrophage recruitment. 2 Mechanistically, MCP-1 binds to the inducible C-C chemokine receptor 2 (CCR2) to promote chemotaxis. 3 There are 2 known subtypes of CCR2, CCR2...

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More than half a decade has passed since the December 26th 2004 tsunami hit the Indian coast leaving a trail of ecological, economic and human destruction in its wake. We reviewed the coastal ecological research carried out in India in the light of the tsunami. In addition, we also briefly reviewed the ecological research in other tsunami affected countries in Asia namely Sri Lanka, Indonesia, Thailand and Maldives in order to provide a broader perspective of ecological research after tsunami. A basic search in ISI Web of Knowledge using keywords ''tsunami'' and ''India'' resulted in 127 peer reviewed journal articles, of which 39 articles were pertaining to ecological sciences. In comparison, Sri Lanka, Indonesia, Thailand and Maldives had, respectively, eight, four, 21 and two articles pertaining to ecology. In India, bioshields received the major share of scientific interest (14 out of 39) while only one study (each) was dedicated to corals, seagrasses, seaweeds and meiofauna, pointing to the paucity of research attention dedicated to these critical ecosystems. We noted that very few interdisciplinary studies looked at linkages between pure/applied sciences and the social sciences in India. In addition, there appears to be little correlation between the limited research that was done and its influence on policy in India. This review points to gap areas in ecological research in India and highlights the lessons learnt from research in other tsunami-affected countries. It also provides guidance on the links between science and policy that are required for effective coastal zone management.

This themed issue of papers for Maritime Studies emerges out of a special session of the MARE 2015 conference held in Amsterdam.