Site of graviperception in roots: a re-examination

Two lines of evidence have been cited to support the assertion that the root cap is the sole site of graviperception in the root. The first evidence is based on surgical removal of the cap, which abolishes the response to gravity. This is sufficient to conclude that the cap is involved in gravitropism, but not to conclude that the cap is the site of graviperception. The second is based on the results of centrifugation experiments, in which different parts of the plant are subjected to different centrifugal forces. The data from such experiments have been cited to support the conclusion that the perception of gravity is limited to the rootcap. However, these data actually support the conclusion that gravity is perceived throughout the root tip, and not only in the root cap. We believe that the data support the conclusion that the root cap is involved in root gravitropism, but that there is inadequate evidence to conclude that the cap is the sole site of graviperception.     

Rationality, biology and optimality*

A historical theory of rational norms claims that, if we are supposed to think rationally, this is because it is biologically normal for us to do so. The historical theorist is committed to the view that we are supposed to think rationally only if, in the past, adult humans sometimes thought rationally. I consider whether there is any plausible model of rational norms that can be adopted by the historical theorist that is compatible with the claim that adult human beings are subject to rational norms, given certain plausible empirical assumptions about our history and capabilities. I suggest that there is one such model: this model centres on the idea that a procedure is rational if it has been endorsed (or at least not rejected) by mechanisms that have the function to ensure that the subject learns to reason in a way that approaches a certain kind of optimality. This revised version was published online in July 2006 with corrections to the Cover Date.     

Modelling Thrombin Generation in Human Ovarian Follicular Fluid

A mathematical model is constructed to study thrombin production in human ovarian follicular fluid. The model results show that the amount of thrombin that can be produced in ovarian follicular fluid is much lower than that in blood plasma, failing to reach the level required for fibrin formation, and thereby supporting the hypothesis that in follicular fluid thrombin functions to initiate cellular activities via intracellular signalling receptors. It is also concluded that the absence of the amplification pathway to thrombin production in follicular fluid is a major factor in restricting the amount of thrombin that can be produced. Titration of the initial concentrations of the various reactants in the model lead to predictions for the amount of tissue factor and phospholipid that is required to maintain thrombin production in the follicle, as well as to the conclusion that tissue factor pathway inhibitor has little effect on the time that thrombin generation is sustained. Numerical experiments to determine the effect of factor V, which is at a much reduced level in follicular fluid compared to plasma, and thrombomodulin, illustrate the importance for further experimental work to determine values for several parameters that have yet to be reported in the literature.     

CONSPIRATORIAL WHISPERS AND CONSPICUOUS DISPLAYS: GAMES OF SIGNAL DETECTION

Recent models of signaling have assumed that the expenditure required to ensure detection of a display is negligible and have concentrated instead on the costs that may be necessary to maintain honesty. Such models predict that individuals who share the same interests are likely to communicate using “conspiratorial whispers,” signals that are cheap and inconspicuous. Here, I present a game-theoretical model of signal detection (in a noisy environment, in the presence of potential eavesdroppers), which demonstrates that the idea of conspiratorial whispers is far too simplistic. It is true that in “cooperative” signaling systems (where signalers attempt to elicit responses that are beneficial for receivers), signal cost is not required to maintain honesty. However, some level of expenditure is still needed to ensure that a signal is reliably detected. Moreover, there exists a conflict of interest between signalers and receivers over the division of this expenditure. To predict the stable level of display in such cases, one needs to know how this conflict of interest will be resolved. The model reveals that the outcome may range from a whisper to a conspicuous and costly (though still conspiratorial) display. The more closely related the receiver is to the signaler, the greater the level of signal exaggeration that is expected—the opposite prediction to that of honest signaling models.     

Cancer Development and Progression: A Non-Adaptive Process Driven by Genetic Drift

The current mainstream in cancer research favours the idea that malignant tumour initiation is the result of a genetic mutation. Tumour development and progression is then explained as a sort of micro-evolutionary process, whereby an initial genetic alteration leads to abnormal proliferation of a single cell that leads to a population of clonally derived cells. It is widely claimed that tumour progression is driven by natural selection, based on the assumption that the initial tumour cells acquire some properties that endow such cells with a selective advantage over the normal cells from which the tumour cells are derived. The standard view assumes that the transformed bodily cell somehow acquires "responsiveness" to natural selection independently of the whole organism to which the cell belongs. Yet, it is never explained where such an acquired capacity to respond to natural selection by the individual bodily cell comes from. This situation poses many difficult questions that so far have been left unanswered. For example, there is no explanation why some cells belonging to an organised whole and as such having no independent capacity for survival, apparently become 'independent' entities, able to respond to selective pressures in an autonomous fashion and then to be evaluated by natural selection. Hereunder it is argued that such a qualitative change cannot be the consequence of specific genetic mutations. Moreover, it is shown that natural selection is unlikely to be acting within the organism during tumour development and progression and that tumour evolution is a random, non-adaptive process, driven by no fundamental biological principle. Thus, mutations in the so-called oncogenes and tumour suppressor genes observed in epithelial cancers (that constitute more than 90% of all cancers) are not the result of selection for better cellular growth or survival under restrictive conditions. Instead, here it is suggested that they are the consequence of genetic drift acting upon gene functions that become non-relevant, either for the individual or the species fitness, once the organism is past its reproductive prime and as such, they also become superfluous for cell survival in the short term. It is proposed that the origin of cancer is epigenetic and it is a consequence of the need for a continued turnover of the individuals that constitute a species.     

THE ROLE OF GLUCOCORTICOID HORMONES IN THE CONTROL OF EPIDERMAL MITOSIS

It has previously been established that the epidermal chalone inhibits epidermal mitotic activity more powerfully in the presence of adrenalin, although adrenalin itself is not a mitotic inhibitor. It is now shown that in low concentrations hydrocortisone has little if any antimitotic activity, that when it is present together with chalone and adrenalin it does not markedly increase their antimitotic activity, but that it does act to prolong the mitotic depression which they induce. It is known that, without hydrocortisone, adrenalin rapidly escapes from epidermal cells so that the chalone action is weakened. It appears that the role of hydrocortisone may be to reduce the rate of adrenalin loss and thus to prolong the chalone-adrenalin activity. It is also shown that the rate of loss of adrenalin from epidermal cells is inhibited, though to a much lesser extent, in the presence of excess chalone.     

CHEAP LISTENING? – REFLECTIONS ON THE CONCEPT OF WRONGFUL DISABILITY1

This paper investigates the concept of wrongful disability. That concept suggests that parents are morally obligated to prevent the genetic transmission of certain conditions and so, if they do not, any resulting disability is 'wrongful'. In their book From Chance to Choice, Buchanan, Brock, Daniels and Wikler defend the concept of wrongful disability using the principle of avoidability via substitution. That principle is scrutinised here. It is argued that the idea of avoidability via substitution is both conceptually problematic and rather insensitive. Instead, it is suggested that the question of whether or not bringing a particular disability about is wrongful does not simply hinge on whether or not substitution takes place. Rather, it involves an evaluation of parental aspirations and responsibilities. It is argued that the desire need not be responsible for creating challenges for others that lie outside what is perceived to be an acceptable range provides a justification for termination of pregnancy on the grounds of projected disability that neither commits one to wrongful life claim, nor requires that one substitute a non-disabled child instead. The ramifications of such an approach are explored. The paper concludes by suggesting that the question of what is considered to be an acceptable range of human capability is an increasingly important one. It is argued that, when addressing that question, we should be acutely aware of the social context that may go some way to define what we consider to be an acceptable range.     

Interaction of thyrotropin (TSH) and gonadotropins in the function of genital organs I. Investigations in the frog

Earlier data indicate that TSH, which has a structure similar to that of gonadotropins, is able to evoke ejaculation in the frog (Galli-Mainini reaction). The present experiments provide evidence that TSH, in a dose that by itself is ineffective, is able to potentiate the effect of HCG. This action of TSH is more pronounced if the drug is administered prior to HCG; it is less evident upon simultaneous administration. Since FSH + LH has similar effects the experiments provide further evidence for the concept that TSH acts like gonadotropin in this system.     

The role of variant surface antigens on malaria-infected red blood cells.

It has been proposed that the primary role of variant antigens appearing on the surface of red blood cells infected with malaria parasites is to mediate cytoadherence, and that the antigenic variation they display is an adaptation to avoid immune attack. Here, Allan Saul proposes that their role is the opposite: that their primary purpose is to generate an immune response, which regulates their growth and thereby establishes a chronic infection, and that the role of cytoadherence is to ensure that parasites failing to express this flag to the immune system are destroyed by the spleen.     

The interpretation of habitat preference metrics under use�Cavailability designs

Models of habitat preference are widely used to quantify animal–habitat relationships, to describe and predict differential space use by animals, and to identify habitat that is important to an animal (i.e. that is assumed to influence fitness). Quantifying habitat preference involves the statistical comparison of samples of habitat use and availability. Preference is therefore contingent upon both of these samples. The inferences that can be made from use versus availability designs are influenced by subjectivity in defining what is available to the animal, the problem of quantifying the accessibility of available resources and the framework in which preference is modelled. Here, we describe these issues, document the conditional nature of preference and establish the limits of inferences that can be drawn from these analyses. We argue that preference is not interpretable as reflecting the intrinsic behavioural motivations of the animal, that estimates of preference are not directly comparable among different samples of availability and that preference is not necessarily correlated with the value of habitat to the animal. We also suggest that preference is context-dependent and that functional responses in preference resulting from changing availability are expected. We conclude by describing advances in analytical methods that begin to resolve these issues.     

Patterning the vertebrate head: murine Hox 2 genes mark distinct subpopulations of premigratory and migrating cranial neural crest.

The structures of the face in vertebrates are largely derived from neural crest. There is some evidence to suggest that the form of the facial pattern is determined by the crest, and that it is specified before migration as to the structures that is is able to form. The neural crest is able to control the form of surrounding, non-neural crest tissues by an instructive interaction. Some of this cranial crest is derived from a region of the hindbrain that expresses Hox 2 homeobox genes in an overlapping and segment-restricted pattern. We have found that neurogenic and mesenchymal neural crest expresses Hox 2 genes from its point of origin beside the neural plate, during migration and after migration has ceased and that rhombomeres 3 and 5 do not have any expressing neural crest beside them. Each branchial arch expresses a different combination or code of Hox genes in a segment-restricted way. The surface ectoderm over the arches initially does not express Hox genes, and later adopts an expression pattern that reflects that of neural crest that has come to underlie it. We suggest that initially the neural plate and neural crest are spatially specified, while the surface ectoderm is unpatterned. Subsequently some positional information could be transferred to the surface ectoderm as a result of an interaction with the neural crest. Given that the role of the homologous genes in insects is position specification, and that neural crest is imprinted before migration, we suggest that Hox 2 genes are providing part of this positional information to the neural crest and hence are involved in patterning the structures of the branchial arches.     

Codon bias and gene expression.

The frequencies with which individual synonymous codons are used to code their cognate amino acids is quite variable from genome to genome and within genomes, from gene to gene. One particularly well documented codon bias is that associated with highly expressed genes in bacteria as well as in yeast; this is the so-called major codon bias. Here, it is suggested that the major codon bias is not an arrangement for regulating individual gene expression. Instead, the data suggest that this codon bias, which is correlated with a corresponding bias of tRNA abundance, is a global arrangement for optimizing the growth efficiency of cells. On the practical side, it is suggested that heterologous gene expression is not as sensitive to codon bias as previously thought, but that it is quite sensitive to other characteristics of the heterologous gene.     

Diminishing returns: the influence of experience and environment on time-memory extinction in honey bee foragers

Classical experiments demonstrated that honey bee foragers trained to collect food at virtually any time of day will return to that food source on subsequent days with a remarkable degree of temporal accuracy. This versatile time-memory, based on an endogenous circadian clock, presumably enables foragers to schedule their reconnaissance flights to best take advantage of the daily rhythms of nectar and pollen availability in different species of flowers. It is commonly believed that the time-memory rapidly extinguishes if not reinforced daily, thus enabling foragers to switch quickly from relatively poor sources to more productive ones. On the other hand, it is also commonly thought that extinction of the time-memory is slow enough to permit foragers to ‘remember’ the food source over a day or two of bad weather. What exactly is the time-course of time-memory extinction? In a series of field experiments, we determined that the level of food-anticipatory activity (FAA) directed at a food source is not rapidly extinguished and, furthermore, the time-course of extinction is dependent upon the amount of experience accumulated by the forager at that source. We also found that FAA is prolonged in response to inclement weather, indicating that time-memory extinction is not a simple decay function but is responsive to environmental changes. These results provide insights into the adaptability of FAA under natural conditions.     

John Harris' argument for a duty to research

John Harris suggests that partcipation in or support research, particularly medical research, is a moral duty. One kind of defence of this position rests on an appeal to the past, and produces two arguments. The first of these arguments is that it is unfair to accept the benefits of research without contributing something back in the form of support for, or participation in, research. A second argument is that we have a social duty to maintain those practices and institutions that sustain us, such as those which contribute to medical knowledge. This argument is related to the first, but it does not rely so heavily on fairness. Another kind of defence of the duty to research rests on an appeal to the future benefits of research: research is an effective way to discharge a duty to rescue others from serious illness or death, therefore we have a duty to research. I suggest that all three of Harris' lines fail to provide a compelling duty to research and spell out why. Moreover, not only do the lines of argument fail in their own terms: in combination, they turn out to be antagonistic to the very position that Harris wants to defend. While it is not my intention here to deny that there might be a duty to research, I claim that Harris' argument for the existence of such a duty is not the best way to establish it.     

The amplification of environmental noise in population models: causes and consequences

Environmental variability is a ubiquitous feature of every organism's habitat. However, the interaction between density dependence and those density-independent factors that are manifested as environmental noise is poorly understood. We are interested in the conditions under which noise interacts with the density dependence to cause amplification of that noise when filtered by the system. For a broad family of structured population models, we show that amplification occurs near the threshold from stable to unstable dynamics by deriving an analytic formula for the amplification under weak noise. We confirm that the effect of noise is to sustain oscillations that would otherwise decay, and we show that it is the amplitude and not the phase that is affected. This is a feature noted in several recent studies. We study this phenomenon in detail for the lurchin and LPA models of population dynamics. We find that the degree of amplification is sensitive to both the noise input and life-history stage through which it acts, that the results hold for surprisingly high levels of noise, and that stochastic chaos (as measured by local Lyapunov exponents) is a concomitant feature of amplification. Further, it is shown that the temporal autocorrelation, or "color," of the noise has a major impact on the system response. We discuss the conditions under which color increases population variance and hence the risk of extinction, and we show that periodicity is sharpened when the color of the noise and dynamics coincide. Otherwise, there is interference, which shows how difficult it is in practice to separate the effects of nonlinearity and noise in short time series. The sensitivity of the population dynamics to noise when close to a bifurcation has wide-ranging consequences for the evolution and ecology of population dynamics.     

Adaptive amplification

Modern techniques are revealing that repetition of segments of the genome, called amplification or gene amplification, is very common. Amplification is found in all domains of life, and occurs under conditions where enhanced expression of the amplified genes is advantageous. Amplification extends the range of gene expression beyond that which is achieved by control systems. It also is reversible because it is unstable, breaking down by homologous recombination. Amplification is believed to be the driving force in the clustering of related functions, in that it allows them to be amplified together. Amplification provides the extra copies of genes that allow evolution of functions to occur while retaining the original function. Amplification can be induced in response to cellular stressors. In many cases, it has been shown that the genomic regions that are amplified include those genes that are appropriate to upregulate for a specific stressor. There is some evidence that amplification occurs as part of a broad, general stress response, suggesting that organisms have the capacity to induce structural changes in the genome. This then allows adaptation to the stressful conditions. The mechanisms by which amplification arises are now being studied at the molecular level, but much is still unknown about the mechanisms in all organisms. Recent advances in our understanding of amplification in bacteria suggests new interpretations of events leading to human copy number variation, as well as evolution in general.     

From single biobanks to international networks: developing e-governance

The future holds the possibility to link and network biobanks, existing biorepositories and reference databases for research purposes in ways that have not been possible before. There is the potential to develop 'research portals' that will enable researchers to access these research resources that are located around the globe with the click of a mouse. In this paper, I will argue that our current governance system for research is unable to provide all of the oversight and accountability mechanisms that are required for this new way of doing research that is based upon flows of data across international borders. For example, our current governance framework for research is nationally based, with a complex system of laws, policies and practice that can be unique to a jurisdiction. It is also evident that many of the nationally based governance bodies in this field do not have the legal powers or expertise to adjudicate on the complex issues, such as privacy and disclosure risks that are raised by cross-border data sharing. In addition, the conceptual underpinning of this research governance structure is based on the "one researcher, one project, one jurisdiction" model. In the conclusion of this paper, I lay out some preliminary ideas as to how this system has to change to accommodate research that is based on networks. I suggest that a move to digital governance mechanisms might be a start to making research governance systems more appropriate for the 21st century.     

The norm for perceived husband superiority: a cause of human assortative marriage

I have suggested that human assortative marriage for a number of variables is partially caused by behavior in accordance with two norms. Epstein and Guttman (1987) have suggested that there is no empirical evidence for these norms. In this note evidence is reviewed for the norm of perceived husband-superiority. Others have shown that the evidence for this norm is strong in regard to height, and it is shown here that the evidence is strong also in regard to age. Evidence for the norm seems suggestive in regard to IQ, education, and social class, and nonexistent in regard to physical attractiveness. With respect to height, it seems that the magnitude of the correlation between spouses is associated with the size of the breeding population to which they belong. Thus, it seems likely that the hypothesized norms are learned rather than genetically coded.