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There is increasing interest in mitigating the loss of kelp forests through restoration, but this has received scant attention relative to other coastal habitats. We evaluate current knowledge centered on key restoration principles to provide guidelines for best practice in kelp restoration. The cause and scale of degradation is fundamental in determining if kelp can be restored and the methods required to promote reestablishment. Removal of stressors may be adequate to achieve restoration goals where degradation is not too widespread or acute. Extensive losses of kelp forests will often require active reseeding of areas because of the low dispersal ability of many kelp species. Restoration efforts have generally taken a trial-and-error approach at experimental scales to develop techniques for establishing individuals. Furthermore, studies that inform cost–benefit analysis and the appropriate spatial scales for restoration of sustainable kelp forests are urgently needed for prioritizing and scaling up restoration efforts globally. [ABSTRACT FROM AUTHOR]

Background and Aims Coastal protection from erosion and flooding is a significant ecosystem service provided by vegetated marine systems. Kelp beds are a dominant habitat-forming species on temperate reefs worldwide. While they are valued as hotspots of biodiversity, there is a paucity of information that supports their use in nature-based coastal defence. This includes the effectiveness of kelp beds in attenuating waves approaching the shore and how this influences sediment transport. Methods Wave loggers were deployed at paired kelp bed and control (urchin barren) treatments at four sites in Port Phillip Bay, Australia. The significant wave height offshore (exposed side) to onshore (sheltered side) of the treatment were compared to determine wave attenuation. Key Results At three sites, the wave attenuation of kelp beds was significantly less than that of the control. This result was consistent across the environmental conditions recorded in this study. At the fourth site, on average there was no significant difference in wave transmission between kelp and control. However, wave attenuation at kelp beds was 10 % greater than the control during periods of northerly winds. We highlight the importance of disentangling the effects of the reef substratum and kelp when evaluating the efficacy of kelp at providing coastal protection. Conclusions We have highlighted a significant gap in the research on ecosystem services provided by kelp beds. A greater understanding is needed on which kelp species are able to provide coastal protection, and under what conditions. Such future research is essential for providing managers and policy makers with actionable information on sustainable and cost-effective solutions for coastal defence when faced with a changing climate. [ABSTRACT FROM AUTHOR]

The ∼50 km long Rosario segment of the Cretaceous Alisitos oceanic arc terrane provides undeformed three-dimensional exposures of the upper 7 km of an oceanic extensional arc, where crustal generation processes are recorded in both the volcanic and underlying plutonic rocks. These exceptional exposures allow for the study of the physical and chemical links between the rock units and help constrain the differentiation processes active during the growth and evolution of arc crust. This study focuses on the southern third of the Rosario segment, previously referred to as the southern volcano-bounded basin, and its plutonic underpinnings. Upper crustal rocks in the Rosario segment consist of a 3–5 km thick volcanic–volcaniclastic section with hypabyssal intrusions. Plutons intrude these units at various levels along-strike, but at each intrusive contact the transition is complete over a distance of <150 m, where stoped volcanic blocks are present. There is striking compositional overlap in whole-rock and mineral chemistry between the plutonic and volcanic units, suggesting a comagmatic source. Whole-rock geochemistry shows coherent trends in major and trace elements in mafic to intermediate compositions, but less coherent trends above 63 wt % SiO2. Units are predominantly low-K with flat rare earth element patterns, and show large ion lithophile element enrichment and high field strength element depletion. Initial Nd and Pb isotope ratios overlap for all units and imply no cratonic continental involvement. This agrees with low Sr/Y ratios of all rock types, indicative of thin, immature oceanic arc crust. Modeling results show that closed-system fractional crystallization drove crustal differentiation from mafic to intermediate compositions, but open-system processes likely occurred to produce some of the felsic compositions. Differentiation occurred in a two-step fractionation process. Step 1, from basaltic andesite to andesite, fractionated an anhydrous gabbroic cumulate (∼40% crystallization). Step 2, from andesite to rhyolite, fractionated a hydrous amphibole cumulate (∼65% crystallization, total), which is similar to what fluid dynamical models suggest for production of rhyolite (between 50–70% crystallization). Our results can be used as a reference model for differentiation processes relating to the growth of the middle and upper crust within active extensional arc systems. The Rosario segment plutonic rocks may be analogous to the low-velocity zone (V p = 6·0–6·5 km s–1) imaged within the extensional Izu–Bonin arc. The chemistry of the plutonic and volcanic rocks is most similar to those of volcanic rocks in the Izu–Bonin active rift. [ABSTRACT FROM AUTHOR]

Objectives: The potential for synergy between colistin and fusidic acid in the treatment of MDR Acinetobacter baumannii has recently been shown. The aim of this study was to perform an extensive in vitro characterization of this effect using pharmacokinetic-pharmacodynamic modelling (PKPD) of time-kill experiments in order to estimate clinical efficacy.Methods: For six clinical strains, 312 individual time-kill experiments were performed including 113 unique pathogen-antimicrobial combinations. A wide range of concentrations (0.25-8192 mg/L for colistin and 1-8192 mg/L for fusidic acid) were explored, alone and in combination. PKPD modelling sought to quantify synergistic effects.Results: A PKPD model confirmed synergy in that colistin EC50 was found to decrease by 83% in the presence of fusidic acid, and fusidic acid maximum increase in killing rate (Emax) also increased 58% in the presence of colistin. Simulations indicated, however, that at clinically achievable free concentrations, the combination may be bacteriostatic in colistin-susceptible strains, but growth inhibition probability was <20% in a colistin-resistant strain.Conclusions: Fusidic acid may be a useful agent to add to colistin in a multidrug combination for MDR Acinetobacter baumannii. [ABSTRACT FROM AUTHOR]

Induction of ornithine decarboxylase (ODC), a key enzyme in polyamine biosynthesis, in ODC transgenic skin stimulates epidermal proliferation but not hyperplasia, activates underlying stromal cells and promotes skin tumorigenesis following a single subthreshold dose of a carcinogen. Because chronic wounds are a well-recognized risk factor for skin cancer, we investigated the response to a tissue remodeling event in normal skin that is abraded to remove only the epidermal layer in K6/ODC transgenic (follicular ODC expression) and in inducible ODCER transgenic mice (suprabasal ODC expression). When regenerative epidermal hyperplasia was resolved in normal littermates following abrasion, ODC transgenic mice exhibited progressive epidermal hyperplasia with formation of benign tumor growths and maintained an increased epidermal proliferation index and activation of translation-associated proteins at abrasion sites. The epidermal hyperplasia and tumor-like growth was accompanied by activation of underlying stromal cells and prolonged infiltration of inflammatory cells. Treatment with the anti-inflammatory agent dexamethasone did not reduce the high proliferative index in the regenerated epidermis but dramatically reduced the epidermal hyperplasia and prevented the wound-induced tumor growths in abraded ODCER skin. Treatment with α-difluoromethylornithine, a specific inhibitor of ODC activity, normalized the wound response in transgenic mice and decreased wound-induced inflammation if administered from the time of abrasion but not if initiated 4 days following abrasion. These results suggest a role for polyamines in prolonging wound-associated inflammation in addition to stimulating proliferation both of which are sufficient to sustain epidermal hyperplasia and benign tumor growth even in the absence of genetic damage. [ABSTRACT FROM AUTHOR]

Several converging lines of evidence suggest that keratinocyte stem cells including those clonogenic in vitro, are the target cells in skin carcinogenesis. However, the mechanism of their involvement in carcinogenesis continues to be unknown. Recently, we have demonstrated that the number of keratinocyte clonogenic stem cells from mice is a genetically defined and quantitative complex trait. In this study, we analyzed the size of the colonies in BALB/c, C57BL/6, and their (BALB/c×C57BL/6)F1 hybrid mice. We found that the size of the colonies is also genetically regulated and that there are at least two types of clonogenic keratinocytes that form either small or large colonies. Small and large colony numbers were significantly different in BALB/c and C57BL/6 mice. We performed a genome-wide scan of small and large colony number in the two backcrosses [BALB/c× (BALB/c×C57BL/6)F1]; [C57BL/6× (BALB/c×C57BL/6) F1]; and [(BALB/c×C57BL/6)F1× (BALB/c×C57BL/6)F1] intercross mice. We report here that the loci on chromosomes 4 and 9 play a role in the regulation of large and small colony number respectively. We conclude that mouse epidermis has two major types of stem cells generating small and large colonies, and regulated by different genes. Our results suggest that the loci, including one major and several minor loci linked to the subpopulation of keratinocytes forming small colonies were related, if not identical to, the loci linked to susceptibility or resistance to skin tumor promotion and skin tumor development. [ABSTRACT FROM PUBLISHER]

Transgenic Tg.AC (v-Ha-ras ) mice develop skin tumors in response to specific carcinogens and tumor promoters. The Tg.AC mouse carries the coding sequence of v-Ha ras, linked to a ζ-globin promoter and an SV40 polyadenylation signal sequence. The transgene confers on these mice the property of genetically initiated skin. This study examines the age-dependent sensitivity of the incidence of skin papillomas in Tg.AC mice exposed to topically applied 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment, full thickness skin wounding or UV radiation. Skin tumor incidence and multiplicity were strongly age-dependent, increasing with increasing age of the animal when first treated at 5, 10, 21 or 32 weeks of age. Furthermore, the temporal induction of transgene expression in keratinocytes isolated from TPA-treated mouse skin was also influenced by the age of the mice. Transgene expression was seen as early as 14 days after the start of TPA treatment in mice that were 10–32 weeks of age, but was not detected in similarly treated 5-week old mice. When isolated keratinocytes were fractionated by density gradient centrifugation the highest transgene expression was found in the denser basal keratinocytes. Transgene expression could be detected in the denser keratinocyte fraction as early as 9 days from start of TPA treatment in 32-week old mice. Using flow cytometry, a positive correlation was observed between expression of the v-Ha-ras transgene and enriched expression of the cell surface protein β1-integrin, a putative marker of epidermal stem cells. This result suggests that, in the Tg.AC mouse, an age-dependent sensitivity to tumor promotion and the correlated induction of transgene expression are related to changes in cellular development in the follicular compartment of the skin. [ABSTRACT FROM PUBLISHER]