Is there empirical evidence for the cost of begging?

Offspring should demand more food than the optimal amount for the parents to bring (parent–offspring conflict), and models on the evolution of parent–offspring communication suggest that an equilibrium is reached when the costs associated with begging make it unprofitable for the offspring to increase its level of begging. Empirical evidence for this cost, however, is mixed, and the conclusions of most of authors are that begging is inexpensive. In this study, the existing empirical evidence for this cost is reviewed. One cost proposed is the attraction of predators due to begging calls, but empirical support for this cost is low. However, studies performed cannot dismiss such a cost. Another possible cost is the metabolic expenditure, but empirical evidence for this cost is mixed, with some works contending that it is low, while others deem it important. Other possible metabolic costs have not been studied. A loss of inclusive fitness may be an important cost for the evolution of begging, and robust empirical evidence does exist for this cost. Costs associated with brood reduction also are reviewed. In conclusion, there is not enough empirical evidence to test the models on the evolution of begging. Most costs proposed have not yet been studied or the approach used has been insufficient to reject the null hypothesis (i.e., absence of cost).     

Is there sufficient experimental evidence to consider the mitochondrial cytochromebc 1 complex a proton pump? Probably no.

The electron flow through the cytochromebc ₁ complex of the mitochondrial respiratory chain is accompanied by vectorial proton translocation, though the mechanism of the latter phenomenon has not yet been clarified. Several proposed hypotheses are briefly presented and discussed here. Recently, a number of papers have appeared claiming the existence of a proton pump in the enzyme mainly on the basis of the interaction of the complex with N,N-dicyclohexylcarbodiimide. These data are reviewed here with the aim of showing their ability to fit multiple interpretations. This together with some other arguments leads to the conclusion that a proton pump in the mitochondrialbc ₁ complex has not yet been demonstrated.This article is dedicated to the memory of my friend and long-time close collaborator Dr. Robert P. Casey who has passed away after a short, tragic illness at the age of 34.     

Increased expression of PS1 is sufficient to elevate the level and activity of γ-secretase in vivo

Increase in the generation and deposition of amyloid-β (Aβ) plays a central role in the development of Alzheimer's Disease (AD). Elevation of the activity of γ-secretase, a key enzyme required for the generation for Aβ, can thus be a potential risk factor in AD. However, it is not known whether γ-secretase can be upregulated in vivo. While in vitro studies showed that expression of all four components of γ-secretase (Nicastrin, Presenilin, Pen-2 and Aph-1) are required for upregulation of γ-secretase, it remains to be established as to whether this is true in vivo. To investigate whether overexpressing a single component of the γ-secretase complex is sufficient to elevate its level and activity in the brain, we analyzed transgenic mice expressing either wild type or familial AD (fAD) associated mutant PS1. In contrast to cell culture studies, overexpression of either wild type or mutant PS1 is sufficient to increase levels of Nicastrin and Pen-2, and elevate the level of active γ-secretase complex, enzymatic activity of γ-secretase and the deposition of Aβ in brains of mice. Importantly, γ-secretase comprised of mutant PS1 is less active than that of wild type PS1-containing γ-secretase; however, γ-secretase comprised of mutant PS1 cleaves at the Aβ42 site of APP-CTFs more efficiently than at the Aβ40 site, resulting in greater accumulation of Aβ deposits in the brain. Our data suggest that whereas fAD-linked PS1 mutants cause early onset disease, upregulation of PS1/γ-secretase activity may be a risk factor for late onset sporadic AD.     

Is there evidence of fetal-maternal heart rate synchronization?

Background

The prenatal condition offers a unique possibility of examining physiological interaction between individuals. Goal of this work was to look for evidence of coordination between fetal and maternal cardiac systems.

Methods

177 magnetocardiograms were recorded in 62 pregnancies (16^th–42^nd week of gestation). Fetal and maternal RR interval time series were constructed and the phases, i.e. the timing of the R peaks of one time series in relation to each RR interval of the other were determined. The distributions of these phases were examined and synchrograms were constructed for real and surrogate pairs of fetal and maternal data sets. Synchronization epochs were determined for defined n:m coupling ratios.

Results

Differences between real and surrogate data could not be found with respect to number of synchronization epochs found (712 vs. 741), gestational age, subject, recording or n:m combination. There was however a preference for the occurrence of synchronization epochs in specific phases in real data not apparent in the surrogate for some n:m combinations.

Conclusion

The results suggest that occasional coupling between fetal and maternal cardiac systems does occur.

     

Is there evidence of learned helplessness in horses?

Learned helplessness is a psychological condition whereby individuals learn that they have no control over unpleasant or harmful conditions, that their actions are futile, and that they are helpless. In a series of experiments in which dogs were exposed to inescapable shocks, this lack of control subsequently interfered with the ability to learn an avoidance task. There is evidence that both neural adaptations and behavioral despair occur in response to uncontrollable aversive experiences in rodents, although this has yet to be demonstrated in other species such as horses. However, certain traditional methods of horse training and some behavioral modification techniques--it has been suggested--may involve aversive conditions over which the horse has little or no control. When training and management procedures are repeatedly unpleasant for the horse and there is no clear association between behavior and outcome, this is likely to interfere with learning and performance-in addition to compromising welfare. This article reviews published literature and anecdotal evidence to explore the possibility that the phenomenon, learned helplessness, occurs in the horse.     

Cryptic speciation in the Acari: a function of species lifestyles or our ability to separate species?

There are approximately 55,000 described Acari species, accounting for almost half of all known Arachnida species, but total estimated Acari diversity is reckoned to be far greater. One important source of currently hidden Acari diversity is cryptic speciation, which poses challenges to taxonomists documenting biodiversity assessment as well as to researchers in medicine and agriculture. In this review, we revisit the subject of biodiversity in the Acari and investigate what is currently known about cryptic species within this group. Based on a thorough literature search, we show that the probability of occurrence of cryptic species is mainly related to the number of attempts made to detect them. The use of, both, DNA tools and bioassays significantly increased the probability of cryptic species detection. We did not confirm the generally-accepted idea that species lifestyle (i.e. free-living vs. symbiotic) affects the number of cryptic species. To increase detection of cryptic lineages and to understand the processes leading to cryptic speciation in Acari, integrative approaches including multivariate morphometrics, molecular tools, crossing, ecological assays, intensive sampling, and experimental evolution are recommended. We conclude that there is a demonstrable need for future investigations focusing on potentially hidden mite and tick species and addressing evolutionary mechanisms behind cryptic speciation within Acari.     

Is orchid species richness and abundance related to the conservation status of oak forest?

The response of organisms to anthropogenic or natural modification of the environment is one of the most important questions in conservation biology and ecological theory. In spite of the fact that orchids are one of the most studied groups of plants, little information exists regarding their response to habitat alteration. The few existing studies are biased toward European orchid species and no consensus exists with regard to the response of orchids to human and natural disturbance. In this study, we sampled 30 transects (0.1 ha each) of oak forest located in Morelos, Central Mexico, and measured 13 variables related to forest aging and stump abundance, and six variables of orchid species richness and abundance. Neither abundance nor the richness and specific abundance of orchid genus or species were related to timber extraction. The abundance of dead standing trees in the forest, a surrogate variable of forest age, was positively related to abundance of orchids of the genus Malaxis, orchid richness and orchid abundance. This finding suggests that the conservation of all facets of the studied forest orchid community is dependent on natural processes (such as self-thinning) and the maintenance of older areas of the forest, and concurs with previous studies that suggest that natural disturbance is a key process for orchid survival.     

Is there evidence of adaptation to tidal flooding in saplings of baldcypress subjected to different salinity regimes?

Plant populations may adapt to environmental conditions over time by developing genetically based morphological or physiological characteristics. For tidal freshwater forested wetlands, we hypothesized that the conditions under which trees developed led to ecotypic difference in response of progeny to hydroperiod. Specifically, we looked for evidence of ecotypic adaptation for tidal flooding at different salinity regimes using growth and ecophysiological characteristics of two tidal and two non-tidal source collections of baldcypress (Taxodium distichum (L.) L.C. Rich) from the southeastern United States. Saplings were subjected to treatments of hydrology (permanent versus tidal flooding) and salinity (0 versus ～2 g l^?1) for two and a half growing seasons in a greenhouse environment. Saplings from tidal sources maintained 21–41% lower overall growth and biomass accumulation than saplings from non-tidal sources, while saplings from non-tidal sources maintained 14–19% lower overall rates of net photosynthetic assimilation, leaf transpiration, and stomatal conductance than saplings from tidal sources. However, we found no evidence for growth or physiological enhancement of saplings from tidal sources to tide, or of saplings from non-tidal sources to no tide. All saplings growing under permanent flooding exhibited reduced growth and leaf gas exchange regardless of source, with little evidence for consistent salinity effects across hydroperiods. While we reject our original hypothesis, we suggest that adaptations of coastal baldcypress to broad (rather than narrow) environmental conditions may promote ecophysiological and growth enhancements under a range of global-change-induced stressors, perhaps reflecting a natural resilience to environmental change while precluding adaptations for specific flood regimes.     

Is there any scientific evidence for the use of glucosamine in the management of human osteoarthritis?

Glucosamine in its acetylated form is a natural constituent of some glycosaminoglycans (for example, hyaluronic acid and keratan sulfate) in the proteoglycans found in articular cartilage, intervertebral disc and synovial fluid. Glucosamine can be extracted and stabilized by chemical modification and used as a drug or a nutraceutical. It has been approved for the treatment of osteoarthritis (OA) in Europe to promote cartilage and joint health and is sold over the counter as a dietary supplement in the United States. Various formulations of glucosamine have been tested, including glucosamine sulfate and glucosamine hydrochloride. In vitro and in vivo studies have uncovered glucosamine's mechanisms of action on articular tissues (cartilage, synovial membrane and subchondral bone) and justified its efficacy by demonstrating structure-modifying and anti-inflammatory effects at high concentrations. However, results from clinical trials have raised many concerns. Pharmacokinetic studies have shown that glucosamine is easily absorbed, but the current treatment doses (for example, 1,500 mg/day) barely reach the required therapeutic concentration in plasma and tissue. The symptomatic effect size of glucosamine varies greatly depending on the formulation used and the quality of clinical trials. Importantly, the effect size reduces when evidence is accumulated chronologically and evidence for the structure-modifying effects of glucosamine are sparse. Hence, glucosamine was at first recommended by EULAR and OARSI for the management of knee pain and structure improvement in OA patients, but not in the most recent NICE guidelines. Consequently, the published recommendations for the management of OA require revision. Glucosamine is generally safe and although there are concerns about potential allergic and salt-related side effects of some formulations, no major adverse events have been reported so far. This paper examines all the in vitro and in vivo evidence for the mechanism of action of glucosamine as well as reviews the results of clinical trials. The pharmacokinetics, side effects and differences observed with different formulations of glucosamine and combination therapies are also considered. Finally, the importance of study design and criteria of evaluation are highlighted as new compounds represent new interesting options for the management of OA.     

Is meta-analysis the platinum standard of evidence?

An astonishing volume and diversity of evidence is available for many hypotheses in the biomedical and social sciences. Some of this evidence—usually from randomized controlled trials (RCTs)—is amalgamated by meta-analysis. Despite the ongoing debate regarding whether or not RCTs are the ‘gold-standard’ of evidence, it is usually meta-analysis which is considered the best source of evidence: meta-analysis is thought by many to be the platinum standard of evidence. However, I argue that meta-analysis falls far short of that standard. Different meta-analyses of the same evidence can reach contradictory conclusions. Meta-analysis fails to provide objective grounds for intersubjective assessments of hypotheses because numerous decisions must be made when performing a meta-analysis which allow wide latitude for subjective idiosyncrasies to influence its outcome. I end by suggesting that an older tradition of evidence in medicine—the plurality of reasoning strategies appealed to by the epidemiologist Sir Bradford Hill—is a superior strategy for assessing a large volume and diversity of evidence.     

Is the originality of a species measurable?

In this paper, we introduce the concept of 'originality of a species within a set' in order to indicate the average rarity of all the features belonging to this species. Using a phylogenetic tree of 70 species of New World terrestrial Carnivora, we suggest measuring the originality by a probability distribution. This maximizes the expected number of features shared by two species randomly drawn from the set. By using this new index, we take account of branch lengths whereas current indices of originality focus on tree topology. As a supplement to Nee and May's optimizing algorithm, we find that originality must be one of the criteria used in conservation planning.     

Is phylogenetic relatedness to native species important for the establishment of reptiles introduced to California and Florida?

Aim Charles Darwin posited that introduced species with close relatives were less likely to succeed because of fiercer competition resulting from their similarity to residents. There is much debate about the generality of this rule, and recent studies on plant and fish introductions have been inconclusive. Information on phylogenetic relatedness is potentially valuable for explaining invasion outcomes and could form part of screening protocols for minimizing future invasions. We provide the first test of this hypothesis for terrestrial vertebrates using two new molecular phylogenies for native and introduced reptiles for two regions with the best data on introduction histories. Location California and Florida, USA. Methods We performed an ordination of ecological traits to confirm that ecologically similar species are indeed closely related phylogenetically. We then inferred molecular phylogenies for introduced and native reptiles using sequence data for two nuclear and three mitochondrial genes. Using these phylogenies, we computed two distance metrics: the mean phylogenetic distance (MPD) between each introduced species and all native species in each region (which indicates the potential interactions between introduced species and all native species in the community) and the distance of each introduced species to its nearest native relative – NN (indicating the degree of similarity and associated likelihood of competition between each introduced species and its closest evolutionary analogue). These metrics were compared for introduced species that established and those that failed. Results We demonstrate that phylogenetically related species do share similar ecological functions. Furthermore, successfully introduced species are more distantly related to natives (for NN and MPD) than failed species, although variation is high. Main conclusions The evolutionary history of a region has value for explaining and predicting the outcome of human‐driven introductions of reptiles. Phylogenetic metrics are thus useful inputs to multi‐factor risk assessments, which are increasingly required for screening introduced species.     

Is colour polymorphism advantageous to populations and species?

I am writing in response to an article by Bolton, Rollins and Griffith (2015) entitled ‘The danger within: the role of genetic, behavioural and ecological factors in population persistence of colour polymorphic species’ that was recently published as an Opinion under the NEWS AND VIEWS section in Molecular Ecology. Bolton et al. (Molecular Ecology, 2015, 24 , 2907) argue that colour polymorphism may reduce population fitness and increase extinction risk and emphasize that this is contrary to predictions put forward by Forsman et al. (Ecology, 89 , 2008, 34) and Wennersten & Forsman (Biological Reviews 87 , 2012, 756) that the existence of multiple colour morphs with co‐adapted gene complexes and associated trait values may increase the ecological and evolutionary success of polymorphic populations and species. Bolton et al. (Molecular Ecology, 2015, 24 , 2907) further state that there is no clear evidence from studies of ‘true polymorphic species’ that polymorphism promotes population persistence. In response, I (i) challenge their classifications of polymorphisms and revisit the traditional definitions recognizing the dynamic nature of polymorphisms, (ii) review empirical studies that have examined whether and how polymorphism is associated with extinction risk, (iii) discuss the roles of trait correlations between colour pattern and other phenotypic dimensions for population fitness and (iv) highlight that the causes and mechanisms that influence the composition and maintenance of polymorphisms are different from the consequences of the polymorphic condition and how it may impact on aspects of ecological success and long‐term persistence of populations and species.     

Is there an embryopathy associated with first-trimester exposure to angiotensin-converting enzyme inhibitors and angiotensin receptor antagonists? A critical review of the evidence

Drugs that interfere with the renin-angiotensin system, such as angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), are widely used to manage hypertension and heart failure. Adequate functioning of the RAS is essential for normal fetal kidney development. The potential for ACEIs and ARBs to impair fetal and neonatal renal function if taken after the first trimester of pregnancy has been well documented. Although these drugs were not found to be teratogenic in animals, until recently little was known about the teratogenic effects of ACEIs and ARBs in humans when exposure was limited to the first trimester of pregnancy. New evidence from epidemiologic studies indicates that there may be an elevated teratogenic risk when these drugs are taken during the first trimester of pregnancy. However, this elevated risk does not appear to be specific to ACEIs and ARBs, but is instead related to maternal factors and diseases that typically coexist with hypertension in pregnancy, such as diabetes, advanced maternal age, and obesity. Women who become pregnant while being treated with an ACEI or ARB should be advised to avoid exposure to these drugs during the second and third trimesters of pregnancy by switching to a different class of antihypertensive drugs between weeks 8 and 10 after conception. Birth Defects Research (Part A) 94:576-598, 2012. ? 2012 Wiley Periodicals, Inc.     

Is there gold at the top of the beanstalk?

A report on the 3rd International Legume Genetics and Genomics Conference, Brisbane, Australia, 9-13 April 2006.     

Is there evidence of involvement of DNA repair polymorphisms in human cancer?

DNA suffers from a wide range of damage, both from extracellular agents and via endogenous mechanisms. Damage of DNA can lead to cancer and other diseases. Therefore, it is plausible that sequence variants in DNA repair genes are involved in cancer development. A recent systematic review and meta-analysis, based on the "Venice criteria", showed that out of 241 associations investigated, only three resulted to have a strong grade of cumulative evidence. These associations were: two SNPs rs1799793 and rs13181 in the ERCC2 gene and lung cancer (recessive model) and rs1805794 in the NBN gene and bladder cancer (dominant model). An update of this meta-analysis has been performed in the present paper, and we found partially inconsistent results. Inconsistencies in the literature are thus far not easy to explain. In addition, none of the cancer genome-wide association studies (GWAs) published so far showed highly statistically significant associations for any of the common DNA repair gene variants, in such a way as to place DNA repair genes among the top 10-20 hits identified in GWAs. Though this suggests that it is unlikely that DNA repair gene polymorphisms per se play a major role, a clarification of the discrepancies in the literature is needed. Also, gene/environment and gene/lifestyle interactions for the carcinogenic mechanisms involving DNA repair should be investigated more systematically and with less classification error. Finally, the combined effect of multiple SNPs in several genes in one or more relevant DNA repair pathways could have a greater impact on pathological phenotypes than SNPs in single genes, but this has been investigated only occasionally.     

The chemistry of copper binding to PrP: is there sufficient evidence to elucidate a role for copper in protein function?

There has been an enormous body of literature published in the last 10 years concerning copper and PrP (prion protein). Despite this, there is still no generally accepted role for copper in the function of PrP or any real consensus as to how and to what affinity copper associates with the protein. The present review attempts to look at all the evidence for the chemistry, co-ordination and affinity of copper binding to PrP, and then looks at what effect this has on the protein. We then connect this evidence with possible roles for PrP when bound to copper. No clear conclusions can be made from the available data, but it is clear from the present review what aspects of copper association with PrP need to be re-investigated.