The role of ecotourism in conservation: panacea or Pandora’s box?

Does ecotourism contribute towards conservation of threatened species and habitats or is it just a marketing ploy of the tourism industry? Using 251 case studies on ecotourism from the literature, I looked at the distribution of case studies over continents, habitats and flagship species types and what factors influenced whether an ecotourism regime was perceived as ecologically sustainable by authors. Over 50% of ecotourism case studies were reported from Africa and Central America. The overall distribution of ecotourism case studies did not reflect vertebrate endemism, nor overall tourism distribution in terms of tourist numbers and receipts. There were significant differences between continents and habitats with regard to the proportion of sustainable case studies: ecotourism is perceived to be less sustainable in South America and Asia, and in island and mountain habitats. The type of flagship species also influenced whether ecotourism was classified as sustainable or not: ecotourism with no flagship species was rarely classified as sustainable while charismatic bird and mammal species were associated with a higher probability of sustainability. In a multivariate analysis, flagship species type and local community involvement were important predictors of sustainability in ecotourism. Detailed a priori planning, local involvement and control measures were perceived by authors of case studies to increase the success of ecotourism in conservation. They also perceived that ecotourism can only be an effective conservation tool under certain conditions. If these are met, the evidence indicates that ecotourism can make a contribution to conservation.     

The α7β1 integrin in muscle development and disease

The alpha7beta1 integrin is a laminin receptor on the surface of skeletal myoblasts and myofibers. Alternative forms of both the alpha7 and beta1 chains are expressed in a developmentally regulated fashion during myogenesis. These different alpha7beta1 isoforms localize at specific sites on myofibers and appear to have distinct functions in skeletal muscle. These functions include the migration and proliferation of developing myoblasts, the formation and integrity of neuromuscular and myotendinous junctions, and the "gluing" together of muscle fibers that is essential to the generation of contractile force. The alpha7beta1 integrin appears to be both directly and indirectly causally related to several muscle diseases. Enhanced expression of alpha7beta1-mediated linkage of the extracellular matrix is seen in Duchenne muscular dystrophy and may compensate for the absence of the dystrophin-mediated linkage. Downregulation of expression of the integrin may contribute to the development of pathology in congenital laminin deficiencies. Mutations in the alpha7 integrin gene underlie additional congenital muscle diseases. The functional roles of this integrin in the formation and stability of the neuromuscular and myotendinous junctions and its localization between fibers suggest that altered expression or function of this integrin may have widespread involvement in other myopathies. The localization of the alpha7 gene at human chromosome 12q13 is a useful clue for focusing such studies.     

Epigenetics in disease: Leader or follower?

Epigenetic silencing is a pervasive mode of gene regulation in multicellular eukaryotes: stable differentiation of somatic cell types requires the maintenance of subsets of genes in an active or silent state. The variety of molecules involved, and the requirement for active maintenance of epigenetic states, creates the potential for errors on a large scale. When epigenetic errors - or epimutations - activate or inactivate a critical gene, they may cause disease. An epimutation that occurs in the germline or early embryo can affect all, or most, of the soma and phenocopy genetic disease. But the stochastic and reversible nature of epigenetic phenomena predicts that epimutations are likely to be mosaic and inherited in a nonmendelian manner; epigenetic diseases will thus rarely behave in the comfortably predictable manner of genetic diseases but will display variable expressivity and complex patterns of inheritance. Much phenotypic variation and common disease might be explained by epigenetic variation and aberration. The known examples of true epigenetic disease are at present limited, but this may reflect only the difficulty in distinguishing causal epigenetic aberrations from those that are merely consequences of disease, a challenge further extended by the impact of environmental agents on epigenetic mechanisms. The rapidly developing molecular characterization of epigenomes, and the new ability to survey epigenetic marks on whole genomes, may answer many questions about the causal role of epigenetics in disease; these answers have the potential to transform our understanding of human disease.     

Antiviral TRIMs: friend or foe in autoimmune and autoinflammatory disease?

The concept that viral sensing systems, via their ability to drive pro-inflammatory cytokine and interferon production, contribute to the development of autoimmune and autoinflammatory disease is supported by a wide range of clinical and experimental observations. Recently, the tripartite motif-containing proteins (TRIMs) have emerged as having key roles in antiviral immunity - either as viral restriction factors or as regulators of pathways downstream of viral RNA and DNA sensors, and the inflammasome. Given their involvement in these pathways, we propose that TRIM proteins contribute to the development and pathology of autoimmune and autoinflammatory conditions, thus making them potential novel targets for therapeutic manipulation.     

Vitamin C: poison,prophylactic or panacea?

Ascorbate is an essential enzyme cofactor but is often also regarded as an important antioxidant in vivo, protecting against cancer by scavenging DNA-damaging reactive oxygen species. Recent studies suggest that ascorbate sometimes increases DNA damage in humans. Although there is no evidence that any of these effects are deleterious to humans, we might need to change our thinking about the mechanisms of the antioxidant action of ascorbate in vivo.     

Friend or foe? Targeting microglia in Alzheimer’s disease

Inflammation is believed to be a component of a number of degenerative brain diseases including Alzheimer’s disease. A recent article by Fu and colleagues (2016) demonstrated that the cytokine IL-33 can modulate microglia in an animal model of AD to become better scavengers of beta-amyloid and less pro-inflammatory. The findings have potential therapeutic implications for a number of brain conditions.     

Spotlight surveys for white-tailed deer: Monitoring panacea or exercise in futility?

Many monitoring programs for white-tailed deer (Odocoileus virginianus) on both private and public lands across the United States have long relied on the use of road-based spotlight surveys for monitoring population size and trends. Research has suggested spotlight surveys are ineffective and that road-based surveys for deer are biased because of highly variable detection rates. To evaluate variability in detection rates relative to the assumption that repeated surveys along roads will provide reliable trend data for use in calculating deer density estimates, we collected 5 years of thermal-imager and spotlight survey data using a multiple-observer, closed-capture approach. Using a Huggin's closed capture model, data bootstrapping, and variance components analyses, our results suggest that density estimates for white-tailed deer generated from data collected during road-based spotlight surveys are likely not reflective of the standing deer population. Detection probabilities during individual spotlight surveys ranged from 0.00 to 0.80 (median = 0.45) across all surveys, and differed by observer, survey, management unit, and survey transect replicate. Mean spotlight detection probability (0.41) and process standard deviation (0.12) estimates indicated considerable variability across surveys, observers, transects, and years, which precludes the generation of a correction factor or use of spotlight data to evaluate long-term trends at any scale. Although recommended by many state, federal, and non-governmental agencies, our results suggest that the benefit of spotlight survey data for monitoring deer populations is limited and likely represents a waste of resources with no appreciable management information gained. © 2012 The Wildlife Society.     

ABA and sugar interactions regulating development: cross-talk or voices in a crowd?

Plant growth and development are controlled by the concerted action of many signaling pathways that integrate information from environmental signals with that from developmental and metabolic cues. Physiological studies have demonstrated that abscisic acid and sugars have both similar and antagonistic effects on diverse processes, including seed development, germination, and seedling growth. Recent genetic studies have identified several loci that are involved in both sugar and hormonal responses. It is rarely clear whether these apparent linkages reflect direct or indirect interactions between sugar and hormone signaling pathways, but the identification of gene products that are encoded at these loci is allowing these possibilities to be tested.     

Birth weight and cognitive development in adolescence: causal relationship or social selection?

Using data from the National Longitudinal Survey of Adolescent Health (Add Health), I investigate the relationship between birth weight and cognitive development among adolescents aged 12-17. Initial OLS regression models reveal a significant, positive relationship between low birth weight and verbal ability. Controlling for demographic, socioeconomic, and other adolescent characteristics modifies, but does not eliminate, this relationship. Additional models that stratify the sample by parental education illustrate the greater importance of other family and adolescent characteristics for cognitive development in adolescence, and a diminished role of birth weight. In the final section of the paper, fixed effects models of non-twin full siblings indicate no significant association between birth weight and verbal ability, suggesting that traditional cross-sectional models overstate the influence of birth weight for cognitive development in adolescence.     

Who put the "A" in Atg12: autophagy or apoptosis?

Much deliberation surrounds how the two homeostatic pathways, autophagy and apoptosis, converge; in the December 9 issue of Molecular Cell, Rubinstein et al. (2011) identify a proapoptotic role for the autophagic protein Atg12, based on a BH3-like domain, which enables binding and inhibition of antiapoptotic Bcl-2 family proteins.     

Oxidative DNA damage in cancer patients: a cause or a consequence of the disease development?

A wide variety of oxidative DNA lesions are present in living cells. One of the best known lesions of this type is 8-oxoguanine (8-oxoGua) which has been shown to have mutagenic properties. An influence of antioxidative vitamins and labile iron pool on the background level of 8-oxoGua in cellular DNA is discussed and oxidative damage to free nucleotide pool as a possible source of 8-oxo-2'-deoxyguanosine in DNA and urine is described. An involvement of 8-oxoGua in the origin and/or progression of cancer is reviewed. It is concluded that a severe oxidative stress manifested as a high level of 8-oxoGua in cellular DNA as well as in urine of cancer patients is a consequence of development of many types of cancer. Although at present it is impossible to answer directly the question concerning involvement of oxidative DNA damage in cancer etiology it is likely that oxidative DNA base modifications may serve as a source of mutations that initiate carcinogenesis (i.e. they may be causal factors responsible for the process).     

Folic acid - vitamin and panacea or genetic time bomb?

We live in a health-conscious age - many of us supplement our diet with essential micronutrients through the discretionary use of multivitamin pills or judicious selection of foods that have a health benefit beyond that conferred by the nutrient content alone - the so-called 'functional foods'. Indeed, the citizens of some nations have little choice, with a mandatory fortification policy in place for certain vitamins. But do we ever stop to consider the consequences of an increased exposure to micronutrients? We examine this issue in relation to the B-group vitamin folic acid, and ask whether supplementation with this vitamin could introduce a strong genetic selection pressure - one that has the side effect of increasing the prevalence of some of the most significant, human life-threatening diseases. Are we affecting our genetics - is this a case of human evolution in progress by altering our diet?     

Smoking and nicotine in inflammatory bowel disease: good or bad for cytokines?

Smoking has either a beneficial or harmful effect on the course and recurrence of ulcerative colitis and Crohn''s disease respectively. Transdermal application of nicotine had similar effects in ulcerative colitis and therefore was considered to be an effective basic drug which could be further developed in the search for new compounds in the treatment of acute exacerbations of corticosteroid resistant ulcerative colitis. In this communication the short-term use of nicotine in ulcerative colitis is reviewed.     

Heat shock proteins in health and disease: therapeutic targets or therapeutic agents?

For many years, heat shock or stress proteins have been regarded as intracellular molecules that have a range of housekeeping and cytoprotective functions, only being released into the extracellular environment in pathological situations such as necrotic cell death. However, evidence is now accumulating to indicate that, under certain circumstances, these proteins can be released from cells in the absence of cellular necrosis, and that extracellular heat shock proteins have a range of immunoregulatory activities. The capacity of heat shock proteins to induce pro-inflammatory responses, together with the phylogenetic similarity between prokaryotic and eukaryotic heat shock proteins, has led to the proposition that these proteins provide a link between infection and autoimmune disease. Indeed, both elevated levels of antibodies to heat shock proteins and an enhanced immune reactivity to heat shock proteins have been noted in a variety of pathogenic disease states. However, further evaluation of heat shock protein reactivity in autoimmune disease and after transplantation has shown that, rather than promoting disease, reactivity to self-heat shock proteins can downregulate the disease process. It might be that self-reactivity to heat shock proteins is a physiological response that regulates the development and progression of pro-inflammatory immunity to these ubiquitously expressed molecules. The evolving evidence that heat shock proteins are present in the extracellular environment, that reactivity to heat shock proteins does not necessarily reflect adverse, pro-inflammatory responses and that the promotion of reactivity to self-heat shock proteins can downregulate pathogenic processes all suggest a potential role for heat shock proteins as therapeutic agents, rather than as therapeutic targets.     

Airway imaging in disease: Gimmick or useful tool?

Airway remodeling is an important pathophysiological mechanism in a variety of chronic airway diseases. Historically investigators have had to use invasive techniques such as histological examination of excised tissue to study airway wall structure. The last several years has seen a proliferation of relatively noninvasive techniques to assess the airway branching pattern, wall thickness, and more recently, airway wall tissue components. These methods include computed tomography, magnetic resonance imaging, and optical coherence tomography. These new imaging technologies have become popular because to understand the physiology of lung disease it is important we understand the underlying anatomy. However, these new approaches are not standardized or available in all centers so a review of their validity and clinical utility is appropriate. This review documents how investigators are working hard to correct for inconsistencies between techniques so that they become more accepted and utilized in clinical settings. These new imaging techniques are very likely to play a frontline role in the study of lung disease and will, hopefully, allow clinicians and investigators to better understand disease pathogenesis and to design and assess new therapeutic interventions.     

Autophagy defects in Lafora disease: cause or consequence?

Lafora disease (LD) is an inherited and fatal form of neurodegenerative disorder characterized by the presence of an abnormal form of glycogen inclusions, called Lafora bodies, in neurons and other tissues. While Lafora bodies have been thought to underlie the neuropathology in LD, the specific process by which these inclusions might affect the neuronal functions was not very well understood. Here we review one of our recent studies on the LD animal model, wherein we have shown that the Lafora bodies might contribute to the impairment in the endosomal-lysosomal and autophagy pathways.     

Prion: disease or relief?

The self-perpetuating amyloid isoform, or prion, of the yeast translation termination factor eRF3 modulates programmed translational frameshifting that controls a regulatory circuit determining the polyamine levels in a yeast cell. But it is still unclear whether this effect is adaptive or pathological.