The use of a multiple criteria decision analysis to evaluate the effectiveness of landscape and habitat enhancement mechanisms: an example from the South Downs

A range of funding schemes and policy instruments exist to effect enhancement of the landscapes and habitats of the UK. While a number of assessments of these mechanisms have been conducted, little research has been undertaken to compare both quantitatively and qualitatively their relative effectiveness across a range of criteria. It is argued that few tools are available for such a multi-faceted evaluation of effectiveness. A form of Multiple Criteria Decision Analysis (MCDA) is justified and utilized as a framework in which to evaluate the effectiveness of nine mechanisms in relation to the protection of existing areas of chalk grassland and the creation of new areas in the South Downs of England. These include established schemes, such as the Countryside Stewardship and Environmentally Sensitive Area Schemes, along with other less common mechanisms, for example, land purchase and tender schemes. The steps involved in applying an MCDA to evaluate such mechanisms are identified and the process is described. Quantitative results from the comparison of the effectiveness of different mechanisms are presented, although the broader aim of the paper is that of demonstrating the performance of MCDA as a tool for measuring the effectiveness of mechanisms aimed at landscape and habitat enhancement.

Towards a resolution of ‘the paradox of the plankton’: a brief overview of the proposed mechanisms

In plankton ecology, it is a fundamental question as to how a large number of competing phytoplankton species coexist in marine ecosystems under a seemingly-limited variety of resources. This ever-green question was first proposed by Hutchinson [Hutchinson, G.E., 1961. The paradox of the plankton. Am. Nat. 95, 137–145] as ‘the paradox of the plankton’. Starting from Hutchinson [Hutchinson, G.E., 1961. The paradox of the plankton. Am. Nat. 95, 137–145], over more than four decades several investigators have put forward varieties of mechanisms for the extreme diversity of phytoplankton species. In this article, within the boundary of our knowledge, we review the literature of the proposed solutions and give a brief overview of the mechanisms proposed so far. The proposed mechanisms that we discuss mainly include spatial and temporal heterogeneity in physical and biological environment, externally imposed or self-generated spatial segregation, horizontal mesoscale turbulence of ocean characterized by coherent vortices, oscillation and chaos generated by several internal and external causes, stable coexistence and compensatory dynamics under fluctuating temperature in resource competition, and finally the role of toxin-producing phytoplankton in maintaining the coexistence and biodiversity of the overall plankton population that we have proposed recently. We find that, although the different mechanisms proposed so far is potentially applicable to specific ecosystems, a universally accepted theory for explaining plankton diversity in natural waters is still an unachieved goal.

Mechanisms for consideration for intervention in the development of organophosphorus-induced delayed neuropathy

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Losing identity: structural diversity of transposable elements belonging to different classes in the genome of Anopheles gambiae

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Clinical and histomorphometric characteristics of three different families with hereditary gingival fibromatosis

Objective. To examine the histomorphologic and histomorphometric features of tissue from 3 unrelated families with hereditary gingival fibromatosis (HGF).Study design. Twelve affected individuals from 3 HGF families and 3 control subjects were evaluated. Gingival samples were fixed in formalin and embedded in paraffin for hematoxylin and eosin stain to count the number of fibroblast and inflammatory cells. Sirius red staining was performed to quantitate the amount of collagen present.Results. Histomorphologic analysis of HGF showed extension of epithelial rete ridges into the underlying lamina propria and the presence of collagen bundles in the connective tissue. Analysis of the mean area fraction of collagen showed that there were significant increases in the collagen fraction for all HGF types compared with control subjects (P < .05). There were significant increases in the number of fibroblasts for HGFa and HGFb compared with control subjects (P < .05). The number of fibroblasts for HGFc were similar to that for control subjects.Conclusions. The collagen fraction was significantly greater in all HGF types compared with controls. The number of fibroblasts was significantly increased in 2 of the 3 HGF types compared with controls. These data indicate that different mechanisms may be responsible for tissue enlargement in different forms of HGF.

Mechanisms underlying the hypotensive and vasodilator effects of Ru(terpy)(bdq)NO](3+), a nitric oxide donor, differ between normotensive and spontaneously hypertensive rats

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Neutrophil extracellular traps identification in tegumentary lesions of patients with paracoccidioidomycosis and different patterns of NETs generation in vitro

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Reconnection studies under different types of turbulence driving

We study a model of fast magnetic reconnection in the presence of weak turbulence proposed by Lazarian and Vishniac (1999) using three-dimensional direct numerical simulations. The model has been already successfully tested in Kowal et al. (2009) confirming the dependencies of the reconnection speed V-rec on the turbulence injection power P-inj and the injection scale l(inj) expressed by a constraint V-rec similar to P(inj)(1/2)l(inj)(3/4)and no observed dependency on Ohmic resistivity. In Kowal et al. (2009), in order to drive turbulence, we injected velocity fluctuations in Fourier space with frequencies concentrated around k(inj) = 1/l(inj), as described in Alvelius (1999). In this paper, we extend our previous studies by comparing fast magnetic reconnection under different mechanisms of turbulence injection by introducing a new way of turbulence driving. The new method injects velocity or magnetic eddies with a specified amplitude and scale in random locations directly in real space. We provide exact relations between the eddy parameters and turbulent power and injection scale. We performed simulations with new forcing in order to study turbulent power and injection scale dependencies. The results show no discrepancy between models with two different methods of turbulence driving exposing the same scalings in both cases. This is in agreement with the Lazarian and Vishniac (1999) predictions. In addition, we performed a series of models with varying viscosity nu. Although Lazarian and Vishniac (1999) do not provide any prediction for this dependence, we report a weak relation between the reconnection speed with viscosity, V-rec similar to nu(-1/4).

Mechanisms of ring chromosome formation, ring instability and clinical consequences

Background The breakpoints and mechanisms of ring chromosome formation were studied and mapped in 14 patients. Methods Several techniques were performed such as genome-wide array, MLPA (Multiplex Ligation-Dependent Probe Amplification) and FISH (Fluorescent in situ Hybridization). Results The ring chromosomes of patients I to XIV were determined to be, respectively: r(3)(p26.1q29), r(4)(p16.3q35.2), r(10)(p15.3q26.2), r(10)(p15.3q26.13), r(13)(p13q31.1), r(13)(p13q34), r(14)(p13q32.33), r(15)(p13q26.2), r(18)(p11.32q22.2), r(18)(p11.32q21.33), r(18)(p11.21q23), r(22)(p13q13.33), r(22)(p13q13.2), and r(22)(p13q13.2). These rings were found to have been formed by different mechanisms, such as: breaks in both chromosome arms followed by end-to-end reunion (patients IV, VIII, IX, XI, XIII and XIV); a break in one chromosome arm followed by fusion with the subtelomeric region of the other (patients I and II); a break in one chromosome arm followed by fusion with the opposite telomeric region (patients III and X); fusion of two subtelomeric regions (patient VII); and telomere-telomere fusion (patient XII). Thus, the r(14) and one r(22) can be considered complete rings, since there was no loss of relevant genetic material. Two patients (V and VI) with r(13) showed duplication along with terminal deletion of 13q, one of them proved to be inverted, a mechanism known as inv-dup-del. Ring instability was detected by ring loss and secondary aberrations in all but three patients, who presented stable ring chromosomes (II, XIII and XIV). Conclusions We concluded that the clinical phenotype of patients with ring chromosomes may be related with different factors, including gene haploinsufficiency, gene duplications and ring instability. Epigenetic factors due to the circular architecture of ring chromosomes must also be considered, since even complete ring chromosomes can result in phenotypic alterations, as observed in our patients with complete r(14) and r(22).

Translocation and cellular entering mechanisms of nanoparticles in the respiratory tract

Anthropogenic nano-sized particles (NSP), ie, particles with a diameter of less than 100 nm, are generated with or without purpose as chemically and physically well-defined materials or as a consequence of combustion processes respectively. Inhalation of NSP occurs on a regular basis due to air pollution and is associated with an increase in respiratory and cardiovascular morbidity and mortality. Manufactured NSP may intentionally be inhaled as pharmaceuticals or unintentionally during production at the workplace. Hence the interactions of NSP with the respiratory tract are currently under intensive investigation. Due to special physicochemical features of NSP, its biological behaviour may differ from that of larger sized particles. Here we review two important themes of current research into the effects of NSP on the lungs: 1) The potential of NSP to cross the blood-air barrier of the lungs, thus gaining access to the circulation and extrapulmonary organs. It is currently accepted that a small fraction of inhaled NSP may translocate to the circulation. The significance of this translocation requires further research. 2) The entering mechanisms of NSP into different cell types. There is evidence that NSP are taken up by cells via well-known pathways of endocytosis but also via different mechanisms not well understood so far. Knowledge of the quantitative relationship between the different entering mechanisms and cellular responses is not yet available but is urgently needed in order to understand the effects of intentionally or unintentionally inhaled NSP on the respiratory tract.

The Salmonella pathogenicity island (SPI)-2 and SPI-1 type III secretion systems allow Salmonella serovar typhimurium to trigger colitis via MyD88-dependent and MyD88-independent mechanisms.

Salmonella typhimurium can colonize the gut, invade intestinal tissues, and cause enterocolitis. In vitro studies suggest different mechanisms leading to mucosal inflammation, including 1) direct modulation of proinflammatory signaling by bacterial type III effector proteins and 2) disruption or penetration of the intestinal epithelium so that penetrating bacteria or bacterial products can trigger innate immunity (i.e., TLR signaling). We studied these mechanisms in vivo using streptomycin-pretreated wild-type and knockout mice including MyD88(-/-) animals lacking an adaptor molecule required for signaling via most TLRs. The Salmonella SPI-1 and the SPI-2 type III secretion systems (TTSS) contributed to inflammation. Mutants that retain only a functional SPI-1 (M556; sseD::aphT) or a SPI-2 TTSS (SB161; DeltainvG) caused attenuated colitis, which reflected distinct aspects of the colitis caused by wild-type S. typhimurium: M556 caused diffuse cecal inflammation that did not require MyD88 signaling. In contrast, SB161 induced focal mucosal inflammation requiring MyD88. M556 but not SB161 was found in intestinal epithelial cells. In the lamina propria, M556 and SB161 appeared to reside in different leukocyte cell populations as indicated by differential CD11c staining. Only the SPI-2-dependent inflammatory pathway required aroA-dependent intracellular growth. Thus, S. typhimurium can use two independent mechanisms to elicit colitis in vivo: SPI-1-dependent and MyD88-independent signaling to epithelial cells and SPI-2-dependent intracellular proliferation in the lamina propria triggering MyD88-dependent innate immune responses.

Examination of synthetic retinoid -induced apoptosis in cutaneous squamous cell carcinomas: Mechanisms and implications for chemoprevention and chemotherapy with retinoids

Non-melanoma skin cancers, including basal cell carcinoma and squamous cell carcinoma (SCC), are the most common neoplasms in the United States with a lifetime risk nearly equal to all other types of cancer combined. Retinoids are naturally occurring and synthetic analogues of vitamin A that bind to nuclear retinoid receptors and modulate gene expression as a means of regulating cell proliferation and differentiation. Retinoids have been employed for many years in the treatment of various cutaneous lesions and for cancer chemoprevention and therapy. The primary drawback limiting the use of retinoids is their toxicity, which is also associated with receptor-gene interactions. In this study, the effects of the synthetic retinoids N-(4-hydroxyphenyl)retinamide (4HPR) and 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid (CD437) were examined in cutaneous keratinocytes. Four human cutaneous SCC cell lines were examined along with normal human epidermal keratinocyte (NHEK) cells from two donors. Sensitivity to 4HPR or CD437 alone or in combination with other agents was determined via growth inhibition, cell cycle distributions, or apoptosis induction. Both synthetic retinoids were able to promote apoptosis in SCC cells more effectively than the natural retinoid all-trans retinoic acid. Apoptosis could not be inhibited by nuclear retinoic acid receptor antagonists. In NHEK cells, 4HPR induced apoptosis while CD437 promoted G1 arrest. 4HPR acted as a prooxidant by generating reactive oxygen species (ROS) in SCC and NHEK cells. 4HPR-induced apoptosis in SCC cells could be inhibited or potentiated by manipulating cellular defenses against oxidative stress, indicating an essential role for ROS in 4HPR-induced apoptosis. CD437 promoted apoptosis in SCC cells in S and G2/M phases of the cell cycle within two hours of treatment, and this rapid induction could not be blocked with cycloheximide. This study shows: (1) 4HPR- and CD437-induced apoptosis do not directly involve a traditional retinoid pathway; (2) 4HPR can act as a prooxidant as a means of promoting apoptosis; (3) CD437 induces apoptosis in SCC cells independent of protein synthesis and is potentially less toxic to NHEK cells; and (4) 4HPR and CD437 operate under different mechanisms with respect to apoptosis induction and this may potentially enhance their therapeutic index in vivo. ^

Assessment of irrigators’ preferences for different water supply risk management tools: option contract and insurance.

Irrigators face the risk of not having enough water to meet their crops’ demand. There are different mechanisms to cope with this risk, including water markets (option contracts) or insurance. A farmer will purchase them when the expected utility change derived from the tool is positive. This paper presents a theoretical assessment of the farmer’s expected utility under two different option contracts, a drought insurance and a combination of an option contract and the insurance. We analyze the conditions that determine farmer’s reference for one instrument or the other and perform a numerical application that is relevant for a Spanish region.

tRNAs and Proteins Are Imported into Mitochondria of Trypanosoma brucei by Two Distinct Mechanisms

Import of tRNA into the mitochondrial matrix of Trypanosoma brucei was reconstituted in vitro. Efficient import required the hydrolysis of externally added ATP and was shown to be a carrier-mediated process depending on proteinaceous receptors on the surface of mitochondria. A partly synthetic tRNATyr as well as a physiological tRNALys were imported along the same pathway. Contrary to import of all matrix-localized proteins, tRNA import does not require a membrane potential. Furthermore, addition of an excess of import-competent tRNA had no effect on import of a mitochondrial matrix protein. In summary, these results show that tRNAs and proteins in T. brucei are imported by fundamentally different mechanisms.

Minimal and optimal mechanisms for GroE-mediated protein folding

We have analyzed the effects of different components of the GroE chaperonin system on protein folding by using a nonpermissive substrate (i.e., one that has very low spontaneous refolding yield) for which rate data can be acquired. In the absence of GroES and nucleotides, the rate of GroEL-mediated refolding of heat- and DTT-denatured mitochondrial malate dehydrogenase was extremely low, but some three times higher than the spontaneous rate. This GroEL-mediated rate was increased 17-fold by saturating concentrations of ATP, 11-fold by ADP and GroES, and 465-fold by ATP and GroES. Optimal refolding activity was observed when the dissociation of GroES from the chaperonin complex was dramatically reduced. Although GroEL minichaperones were able to bind denatured mitochondrial malate dehydrogenase, they were ineffective in enhancing the refolding rate. The spectrum of mechanisms for GroE-mediated protein folding depends on the nature of the substrate. The minimal mechanism for permissive substrates (i.e., having significant yields of spontaneous refolding), requires only binding to the apical domain of GroEL. Slow folding rates of nonpermissive substrates are limited by the transitions between high- and low-affinity states of GroEL alone. The optimal mechanism, which requires holoGroEL, physiological amounts of GroES, and ATP hydrolysis, is necessary for the chaperonin-mediated folding of nonpermissive substrates at physiologically relevant rates under conditions in which retention of bound GroES prevents the premature release of aggregation-prone folding intermediates from the chaperonin complex. The different mechanisms are described in terms of the structural features of mini- and holo-chaperones.