The correction of bias in magnetic resonance images is an important problem in medical image processing. Most previous approaches have used a maximum likelihood method to increase the likelihood of the pixels in a single image by adaptively estimating a correction to the unknown image bias field. The pixel likelihoods are defined either in terms of a pre-existing tissue model, or non-parametrically in terms of the image’s own pixel values. In both cases, the specific location of a pixel in the image is not used to calculate the likelihoods. We suggest a new approach in which we simultaneously eliminate the bias from a set of images of the same anatomy, but from different patients. We use the statistics from the same location across different images, rather than within an image, to eliminate bias fields from all of the images simultaneously. The method builds a multi-resolution non-parametric tissue model conditioned on image location while eliminating the bias fields associated with the original image set. We present experiments on both synthetic and real MR data sets, and present comparisons with other methods.

To compare spatial patterns of gene expression, one must analyze a large number of images as current methods are only able to measure a small number of genes at a time. Bringing images of corresponding tissues into alignment is a critical first step in making a meaningful comparative analysis of these spatial patterns. Significant image noise and variability in the shapes make it hard to pick a canonical shape model. In this paper, we address these problems by combining segmentation and unsupervised shape learning algorithms. We first segment images to acquire structures of interest, then jointly align the shapes of these acquired structures using an unsupervised nonparametric maximum likelihood algorithm along the lines of congealing, while simultaneously learning the underlying shape model and associated transformations. The learned transformations are applied to corresponding images to bring them into alignment in one step. We demonstrate the results for images of various classes of Drosophila imaginal discs and discuss the methodology used for a quantitative analysis of spatial gene expression patterns.

Infective juveniles of the insect-parastic nematode canjump greater than 6 times their height, a striking evolved novelty in some species of this genus. Using high-speed videography, we observed the kinematics of spontaneousjumping behavior. Our analysis places a lower bound on the velocity and acceleration of these worms.

Aquaporins (AQPs) are a family of ubiquitous membrane channels that conduct water and solutes across membranes. This review focuses on AQP0 and AQP4, which in addition to forming water channels also appear to play a role in cell adhesion. We discuss the recently determined structures of the membrane junctions mediated by these two AQPs, the mechanisms that regulate junction formation, and evidence that supports a role for AQP0 and AQP4 in cell adhesion.

Juvenile hormone (JH) is a key hormone in regulation of the insect’s life history, both in maintaining the larval state during molts and in directing reproductive maturation. This short review highlights the recent papers of the past year that lend new insight into the role of this hormone in the larva and the mechanisms whereby it achieves this role.

Tsetse flies are viviparous insects that nurture a single intrauterine progeny per gonotrophic cycle. The developing larva is nourished by the lipid-rich, milk-like secretions from a modified female accessory gland (milk gland). An essential feature of the lactation process involves lipid mobilization for incorporation into the milk. In this study, we examined roles for juvenile hormone (JH) and insulin/IGF-like (IIS) signaling pathways during tsetse pregnancy. In particular, we examined the roles for these pathways in regulating lipid homeostasis during transitions between non-lactating (dry) and lactating periods. The dry period occurs over the course of oogenesis and embryogenesis, while the lactation period spans intrauterine larvigenesis. Genes involved in the JH and IIS pathways were upregulated during dry periods, correlating with lipid accumulation between bouts of lactation. RNAi suppression of Forkhead Box Sub Group O (FOXO) expression impaired lipolysis during tsetse lactation and reduced fecundity. Similar reduction of the JH receptor Methoprene tolerant (Met), but not its paralog germ cell expressed (gce), reduced lipid accumulation during dry periods, indicating functional divergence between Met and gce during tsetse reproduction. Reduced lipid levels following Met knockdown led to impaired fecundity due to inadequate fat reserves at the initiation of milk production. Both the application of the JH analog (JHA) methoprene and injection of insulin into lactating females increased stored lipids by suppressing lipolysis and reduced transcripts of lactation-specific genes, leading to elevated rates of larval abortion. To our knowledge, this study is the first to address the molecular physiology of JH and IIS in a viviparous insect, and specifically to provide a role for JH signaling through Met in the regulation of lipid metabolism during insect lactation.

In starved larvae of the tobacco hornworm moth Manduca sexta, larval and imaginal tissues stop growing, the former because they lack nutrient-dependent signals but the latter because of suppression by juvenile hormone. Without juvenile hormone, imaginal discs form and grow despite severe starvation. This hormone inhibits the intrinsic signaling needed for disc morphogenesis and does so independently of ecdysteroid action. Starvation and juvenile hormone treatments allowed the separation of intrinsic and nutrient-dependent aspects of disc growth and showed that both aspects must occur during the early phases of disc morphogenesis to ensure normal growth leading to typical-sized adults.

The role of juvenile hormone (JH) in regulating the timing and nature of insect molts is well-established. Increasing evidence suggests that JH is also involved in regulating final insect size. Here we elucidate the developmental mechanism through which JH regulates body size in developing Drosophila larvae by genetically ablating the JH-producing organ, the corpora allata (CA). We found that larvae that lack CA pupariated at smaller sizes than control larvae due to a reduced larval growth rate. Neither the timing of the metamorphic molt nor the duration of larval growth was affected by the loss of JH. Further, we show that the effects of JH on growth rate are dependent on the forkhead box O transcription factor (FOXO), which is negatively regulated by the insulin-signaling pathway. Larvae that lacked the CA had elevated levels of FOXO activity, whereas a loss-of-function mutation of FOXO rescued the effects of CA ablation on final body size. Finally, the effect of JH on growth appears to be mediated, at least in part, via ecdysone synthesis in the prothoracic gland. These results indicate a role of JH in regulating growth rate via the ecdysone- and insulin-signaling pathways.

The development of the adult optic lobe (OL) of is directed by a wave of ingrowth of the photoreceptors over a two day period at the outset of metamorphosis which is accompanied by the appearance of the pupal-specific transcription factor Broad-Z3 (Br-Z3) and expression of early drivers in OL neurons. During this time, there are pulses of ecdysteroids that time the metamorphic events. At the outset, the transient appearance of juvenile hormone (JH) prevents precocious development of the OL caused by the ecdysteroid peak that initiates pupariation, but the artificial maintenance of JH after this time misdirects subsequent development. Axon ingrowth, Br-Z3 appearance and the expression of early drivers were unaffected, but aspects of later development such as the dendritic expansion of the lamina monopolar neurons and the expression of late drivers were suppressed. This effect of the exogenous JH mimic (JHM) pyriproxifen is lost by 24 hr after pupariation. Part of this effect of JHM is due to its suppression of the appearance of ecdysone receptor EcR-B1 that occurs after pupation and during early adult development.