A model for the evolution of crèching behaviour in gulls

A crèche is an aggregation of chicks outside nesting territories, within chicks continue to be fed only by their own parents. Several adaptive functions of crèching have been proposed, the most frequent being a reduction in predator pressure. Using an evolutionary stable strategy approach based on the computation of individuals' fecundity, we examined which regime of aerial and terrestrial predation is likely to favour the evolution and stability of the crèching strategy (CS) in gulls. Our results confirm the hypothesis that habitat instability associated with high levels of terrestrial predation favours the evolution and maintenance of crèching behaviour. Moreover, our results suggest that a low aggressiveness against predators may be a pre-adaptation to a CS. In contrast, the high synchronisation often observed in crèching species does not favour the evolution of a crèching behaviour and is thus probably under selection pressures different from those modelled here.     

Age-grading and growth of Wuchereria bancrofti (Filariidea: Onchocercidae) larvae by growth measurements and its use for estimating blood-meal intervals of its Polynesian vector Aedes polynesiensis (Diptera: Culicidae)

Growth in length and width of Wuchereria bancrofti (Filariidea: Onchocercidae) larvae developing in its Polynesian vector Aedes polynesiensis (Diptera: Culicidae) was analysed using a mathematical approach to objectively extract patterns. L1 had a U-shaped growth in length, while widths followed an S-shaped function. L2 had an S-shaped growth in length and width. Growth in length of L3 was also S-shaped, while widths had an asymptotic size following a period of rapid shrinkage. The greatest difference between length and width was in stage 3 where the length was over 75 times greater than the width. The ratio of length to width was approximately 50 for microfilariae and only 10 for the L1 ('sausage') stage. Characteristic mean length (and width) were approximately 280(7) microm for microfilariae, approximately 181 microm for L1 at their smallest, and approximately 1584(22) microm for L3 infective larvae. There was a great increase in length during stage 2 from approximately 322(27) to approximately 982(31) microm. Stage duration decreased with increasing temperature while growth rate increased, giving steeper growth curves. There was no effect of temperature on size, except for L3, which were shorter when mosquitoes were reared at higher temperature. It appears that larval growth is a continuous process from microfilariae to the young L3 stage, and continuously modifies the larval parasite aspect, even within each stage. Thus, information on larval shape may be used as an age indicator and in some cases, may give an estimation on time elapsed since infection of the vector.An important demographic parameter used in most mathematical models describing transmission of parasites by insect vectors is the length of the gonotrophic cycle of the vector, i.e. the time interval between two successive blood-meals. Usual methods for computing such a parameter are based on mark-recapture techniques. However, reliable estimates need substantial capture rates, which are not always possible. This paper presents another approach in which marked mosquitoes are those naturally infected by W. bancrofti. For one mosquito, the time since infection is simply the age of the developing larval parasite. Our method first expresses the age of larval parasite as a fraction of total development time (from microfilariae entering the vector to L3 larvae) using a regression model based on measurements of the parasite's length and width. This fraction of development is then converted to a chronological age since infection, using a back-calculation procedure involving ambient temperatures and growth rates of W. bancrofti larvae in the vector. The method is applied to wild caught Ae. polynesiensis in French Polynesia to compute the length of the gonotrophic cycle. This mosquito species comes to bite approximately 3, 6-7 and 9 days after a first infectious blood-meal. Then the length of the gonotrophic cycle may be of 3-4 days.     

Anorexia nervosa during adolescence and young adulthood: Towards a developmental and integrative approach sensitive to time course

Anorexia nervosa is situated at the junction between two time scales, the time scale of adolescence, in which intense physiological and psychological upheavals are occurring over a relatively short period of time, and the time scale of the potentially chronic evolution of the disease over the course of the patient’s lifespan. This second time scale links the critical period of adolescence with the pre-morbid period, during which a complex state of vulnerability, often unseen and unheard, combines with different risk factors, which may be isolated, associated, dissociated or concomitant, to produce the emergence of anorexia; it ushers also adolescence into the period of adulthood, flagged with the reorganization that occurs in the course of the healing process (in case of recovery), or pervaded by somatic and mental distress (in cases where the condition becomes chronic). Given the lifespan nature of the disease, it is difficult to differentiate premorbid pathogenic factors from changes resulting from the acute or chronic phases of the illness. It is also difficult to establish straightforward correlations between physiological disturbances and their clinical consequences, or conversely to assume that the restoration of physiological parameters means the disappearance of the underlying mental disorder. Taken together, these observations support an approach to anorexia nervosa that is both developmental and integrative, taking into account both the complexity of the pathways involved and the developmental timescales of these pathways. This type of approach can help to adjust therapeutic strategies and thus enhance prognosis, in particular by integrating the temporal parameter into the dynamics of care plans.     

Histone H2AX suppresses translocations in lymphomas of Eμ-c-Myctransgenic mice that contain a germline amplicon of tumor-promoting genes

The DNA damage response (DDR) can restrain the ability of oncogenes to cause genomic instability and drive malignant transformation. The gene encoding the histone H2AX DDR factor maps to 11q23, a region frequently altered in human cancers. Since H2ax functions as a haploinsufficient suppressor of B lineage lymphomas with c-Myc amplification and/or translocation, we determined the impact of H2ax expression on the ability of deregulated c-Myc expression to cause genomic instability and drive transformation of B cells. Neither H2ax deficiency nor haploinsufficiency affected the rate of mortality of Eμ-c-Myc mice from B lineage lymphomas with genomic deletions and amplifications. Yet H2ax functioned in a dosage-dependent manner to prevent unbalanced translocations in Eμ-c-Myc tumors, demonstrating that H2ax functions in a haploinsufficient manner to suppress allelic imbalances and limit molecular heterogeneity within and among Eμ-c-Myc lymphomas. Regardless of H2ax copy number, all Eμ-c-Myc tumors contained identical amplification of chromosome 19 sequences spanning 20 genes. Many of these genes encode proteins with tumor-promoting activities, including Cd274, which encodes the PD-L1 programmed death ligand that induces T cell apoptosis and enables cancer cells to escape immune surveillance. This amplicon was in non-malignant B and T cells and non-lymphoid cells, linked to the Eμ-c-Myc transgene, and associated with overexpression of PD-L1 on non-malignant B cells. Our data demonstrate that, in addition to deregulated c-Myc expression, non-malignant B lineage lymphocytes of Eμ-c-Myc transgenic mice may have constitutive amplification and increased expression of other tumor-promoting genes.     

FAVL impairment of the Fanconi anemia pathway promotes the development of human bladder cancer

Effectiveness of DNA cross-linking drugs in the treatment of bladder cancer suggests that bladder cancer cells may have harbored an insufficient cellular response to DNA cross-link damage, which will sensitize cells to DNA cross-linking agents. Cell sensitivity benefits from deficient DNA damage responses, which, on the other hand, can cause cancer. Many changed cellular signaling pathways are known to be involved in bladder tumorigenesis; however, DNA cross-link damage response pathway [Fanconi anemia (FA) pathway], whose alterations appear to be a plausible cause of the development of bladder cancer, remains an under-investigated area in bladder cancer research. In this study, we found FAVL (variant of FA protein L—FANCL) was elevated substantially in bladder cancer tissues examined. Ectopic expression of FAVL in bladder cancer cells as well as normal human cells confer an impaired FA pathway and hypersensitivity to Mitomycin C, similar to those found in FA cells, indicating that FAVL elevation may possess the same tumor promotion potential as an impaired FA pathway harbored in FA cells. Indeed, a higher level of FAVL expression can promote the growth of bladder cancer cells in vitro and in vivo, which, at least partly, results from FAVL perturbation of FANCL expression, an essential factor for the activation of the FA pathway. Moreover, a higher level of FAVL expression was found to be associated with chromosomal instability and the invasiveness of bladder cancer cells. Collectively, FAVL elevation can increase the tumorigenic potential of bladder cancer cells, including the invasive potential that confers the development of advanced bladder cancer. These results enhance our understanding the pathogenesis of human bladder cancer, holding a promise to develop additional effective tools to fight human bladder cancer.     

A Novel Ex vivo Culture Method for the Embryonic Mouse Heart

Developmental studies in the mouse are hampered by the inaccessibility of the embryo during gestation. Thus, protocols to isolate and culture individual organs of interest are essential to provide a method of both visualizing changes in development and allowing novel treatment strategies. To promote the long-term culture of the embryonic heart at late stages of gestation, we developed a protocol in which the excised heart is cultured in a semi-solid, dilute Matrigel. This substrate provides enough support to maintain the three-dimensional structure but is flexible enough to allow continued contraction. In brief, hearts are excised from the embryo and placed in a mixture of cold Matrigel diluted 1:1 with growth medium. After the diluted Matrigel solidifies, growth medium is added to the culture dish. Hearts excised as late as embryonic day 16.5 were viable for four days post-dissection. Analysis of the coronary plexus shows that this method does not disrupt coronary vascular development. Thus, we present a novel method for long-term culture of embryonic hearts.