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 evidence for convergent evolution around human microsatellites?

A study by Vowles and Amos (2004) identified atypical patterns of base composition around human microsatellites and argued that microsatellites generate mutational biases in their flanking regions. Here, we perform simulations of molecular evolution using a simple model that suggest similar patterns can be produced without any such biases in genome evolution.     

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.     

Is there evidence of optimisation for carbon efficiency in plant proteomes?

Flowering plants, angiosperms, can be divided into two major clades, monocots and dicots, and while differences in amino acid composition in different species from the two clades have been reported, a systematic analysis of amino acid content and distribution remains outstanding. Here, we show that monocot and dicot proteins have developed distinct amino acid content. In Arabidopsis thaliana and poplar, as in the ancestral moss Physcomitrella patens, the average mass per amino acid appears to be independent of protein length, while in the monocots rice, maize and sorghum, shorter proteins tend to be made of lighter amino acids. An examination of the elemental content of these proteomes reveals that the difference between monocot and dicot proteins can be largely attributed to their different carbon signatures. In monocots, the shorter proteins, which comprise the majority of all proteins, are made of amino acids with less carbon, while the nitrogen content is unchanged in both monocots and dicots. We hypothesise that this signature could be the result of carbon use and energy optimisation in fast-growing annual Poaceae (grasses).     

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.     

Is there evidence for automatic imitation in a strategic context?

Over the past decade, a compelling number of studies reported that observing an action makes the imitation of that action more likely. The automatic character of human imitative behaviour was often claimed, but rarely tested. The demonstration of the absence of conscious control has been attempted in a recent report claiming that imitation can occur in the rock-paper-scissors (RPS) game, where strategic players should avoid imitating their opponents. This surprising result could serve as strong evidence that humans imitate each other unconsciously. We find, however, that this conclusion is problematic. In addition to reviewing the original methods, in this work, we also replicated the experiment with double the sample size. Thorough examination of the original analyses and the results of the present replication do not support the original conclusion. In our view, testing the theory of automatic imitation in RPS games is a potentially promising avenue of exploration, yet the interpretation of the data requires further understanding of the subsidiary effects controlling the behaviour of the players.     

Is there evidence for an age-related reduction in metabolic rate?

To determinewhether the age-related reduction in basal metabolic rate (BMR) isexplained by a quantitative and/or qualitative change in thecomponents of lean tissue, we conducted a cross-sectional study ingroups of young (n = 38, 18-35yr) and older (n = 24, 50-77 yr)healthy individuals. BMR was measured by indirect calorimetry. Bodycomposition was obtained by using dual-energy X-ray absorptiometry (DEXA), which permitted four compartments to be quantified [bone mineral mass, fat mass (FM), appendicular lean tissue mass(A_LTM), and nonappendicular leantissue mass (NA_LTM)].Absolute BMR and A_LTM were lower,whereas FM was significantly higher in the older, compared with young,subjects. BMR, adjusted for differences in FM,A_LTM, andNA_LTM, was significantly lower inthe older subjects by 644 kJ/day. In separate regression analyses ofBMR on body compartments, older subjects had significantly lowerregression coefficients for A_LTMand NA_LTM, compared with youngsubjects. Hence, the age-related decline in BMR is partly explained bya reduction in the quantity, as well as the metabolic activity, ofDEXA-derived lean tissue components.

     

Is there really any evidence indicating that animals synthesize glutamate?

In a survey of biochemistry textbooks and reviews, we encountered problems, on the glutamate metabolism in animals. From the perspective of both basic mammalian biochemistry and the world’s major nutritional problems we urge that all textbooks and relevant reviews address the issue of glutamine/glutamate metabolism more clearly and appropriately.     

Is there a gender difference of somatostatin-receptor density in the human brain?

Animal experiments and observations in human brains have convincingly shown that sexual differentiation not only concerns the genitalia but also the brain. This has been investigated also in the light of a possible explanation of a presumed biological aetiology of transsexuality. The volume of the central subdivision of the bed nucleus of the stria terminalis, a brain area that is essential for sexual behaviour, has been reported to be larger in men than in women. Additionally, the number of somatostatin expressing neurons in this region was shown to be higher in men than in women. As neuronal production of somatostatin is involved the idea is striking whether somatostatin-receptor density in the cortex of cerebral hemispheres might be related to gender identity. We investigated in vivo the density of somatostatin-receptors in selected regions of the human brain in both sexes by means of receptor scintigraphy. Basal ganglia tracer uptake of 111-In-Pentreotide was equally low in both genders at 0,80% +/ 0,26 (related to tracer uptake of the whole brain layer). Temporal cortex accumulated at 2,9% +/ 1,1 in men and at 2,3% +/ 0,76 in women. Frontal brain region had an uptake of 3,0% +/ 1,4 in male and of 2,5% +/ 1,3 in female. This shows a tendency in males for relatively augmented uptake indicating higher somatostatin receptor density in temporal and frontal cerebral cortex.     

Is there a role for culture in human behavioral ecology?

Most research in human behavioral ecology has been acultural, which raises the question of how best to incorporate the concept of culture into this approach. A necessary step in this direction is to pare the culture concept down to its ideational elements, excluding behavior and its material products (Durham 1991; Geertz 1973; Keesing 1974). The cultural and reproductive success hypothesis, though empirically successful (Irons 1993), is not a model for all of culture because of widespread discrepancies between behavior and culture to which it does not call attention. Cultural transmission models are also weakened by such discrepancies, but, more importantly, such models are most relevant to phenomena different from those central to human behavioral ecology. A better way to incorporate culture into human behavioral ecology is to see it as the context of human action and as a tool people use in social manipulation. The study of signal systems is a key to an understanding of social manipulation and to the incorporation of culture into human behavioral ecology. Examples of the manipulation of culture for reproductive benefit include Yanomamö kin term manipulation (Chagnon 1988), incest rules (Thornhill 1990, 1991), and the derogation of sexual competitors (Buss and Dedden 1990). The human behavioral ecological study of social manipulation in cultural contexts needs to be expanded. Two phenomena that might shed light on such manipulation are the Rashomon effect and the audience effect.     

Is there a future for therapeutic use of transcranial magnetic stimulation?

Repetitive transcranial magnetic stimulation (rTMS) has in recent years been used to explore therapeutic opportunities in a bewildering variety of conditions. Although there is good evidence that this technique can modify cortical activity, the rationale for its use in many of the conditions investigated so far is not clear. Here we discuss the effects of rTMS in healthy subjects and how it has been used in a number of neurological conditions. We argue that a better understanding of both the effects of rTMS and the pathological processes underlying the conditions for which it is used will reveal whether rTMS really does offer therapeutic potential and, if so, for which conditions.