One of the biggest challenges facing us today is what to do with our growing mountains of rubbish. Recycling has found a solid niche in our households, but how can we help shrink the landfills that number more than 150,000 in Europe? According to

A conference entitled 'Challenges of multilingualism in Europe - core findings of the Languages in a Network of European Excellence (Linee) Network of Excellence' will be held on 23 September 2010 in Brussels, Belgium. Linee is an

The 13th International Conference of the European Association of Southeast Asian Archaeologists, entitled 'Crossing borders in southeast Asian archaeology', will be held from 27 September to 1 October 2010 in Berlin, Germany. The

The IMI Partnering Platform (set up by the German National Contact Point Life Sciences with support from the German Federal Ministry of Education and Research) has been updated with regard to the indicative 3rd Call topics, which have been published by IMI JU.

The launch of the 3rd IMI Call 2010 is announced for the last trimester of 2010. The Platform allows potential IMI applicants to identify suitable cooperation partners for the upcoming Call of the Innovative Medicines Initiative.

The IMI Partnering Platform does not only facilitate the quick and targeted search for possible partners but also displays European-wide cooperation offers specific to IMI. Networking via the Platform is open to all IMI applicants on the European level. For the 2nd IMI Call 2009, more than 500 profiles from 38 different countries were published.

The Platform is available under http://www.imi-partnering.eu/.

Today, all FP7 2011 calls have been published:

You can find the FP7 Work Programme Cooperation Health 2011 at

http://cordis.europa.eu/fp7/dc/index.cfm?fuseaction=UserSite.FP7CallsPage#Health

New: Two Calls for Proposals have been published under the Health theme:
o FP7-HEALTH-2010-single-stage , indicative budget: EUR 160.5 million, deadline: 10 November 2010 , http://cordis.europa.eu/fp7/dc/index.cfm?fuseaction=UserSite.CooperationDetailsCallPage&call_id=323

o FP7-HEALTH-2011-two-stage , indicative budget : EUR 498 million, deadline: 13 October 2010 (for stage 1 proposals) , http://cordis.europa.eu/fp7/dc/index.cfmfuseaction=UserSite.cooperationDetailsCallPage&call_id=324

Additional information:
- explanatory note on the proposed high impact research (PDF) [ftp://ftp.cordis.europa.eu/pub/fp7/health/docs/explanatory1june2010_en.pdf
- explanatory note on the proposed clinical trial topics (PDF) [ftp://ftp.cordis.europa.eu/pub/fp7/health/docs/explanatory27may2010_en.pdf

In oder to get an orientation in FP7, the SME Techweb offers a kind of orientation est for SMEs:

Which sort of SME are you?

Detailed information is available under http://ec.europa.eu/research/sme-techweb/index_en.cfm

 

EU-funded scientists have discovered that a mutated protein inherent in Huntington's disease (HD) performs an unforeseen role in neurogenesis. The finding could lead to a better understanding of HD, an inherited neurodegenerative disorder that is characterised by severe psychiatric, cognitive and motor defects, and neuronal death in the brain. The work was supported by CEPODRO ('Cell polarization in Drosophila'), a project that received EUR 1.159 million under the European Research Councils Starting Grant scheme. Findings from the study are published in the journal Neuron.

The next generation of mobile phones will be able to do more than ever before both safely and efficiently. An EU-funded team has created a software platform that enables the use of multi-core technology on mobile embedded computing devices by way of virtualisation techniques. The dual multi-core and virtualisation solution developed by the EMUCO ('Embedded multi-core processing for mobile communication systems') team allows for both higher processing capacity and low power consumption, with the added value of security and flexibility. The project received almost EUR 3 million in support under the 'Information and communication technologies' (ICT) Theme of the EU's Seventh Framework Programme (FP7).

EU-funded scientists have discovered that temperatures greater than 16°C can cause skeletal deformities in young salmon. The finding is part of the FINE FISH ('Reduction of malformations in farmed fish species') project, which received EUR 3.02 million under the SME (small and medium-sized enterprise) cross cutting activity of the Sixth Framework Programme (FP6). Results of the study were recently published in BMC (BioMed Central) Physiology.

Background: Studies have shown that insomnia is a common sleep disorder among patients with end-stage renal disease (ESRD). This study aimed to assess the prevalence of insomnia in Saudi patients with ESRD who are on maintenance dialysis. Methods: This was an observational cross-sectional study carried out over a period of five months in two hemodialysis centers in Saudi Arabia. To assess the prevalence of insomnia, we used the ICSD-2 definition. We also examined the association between insomnia and other sleep disorders, the underlying causes of renal failure, dialysis duration, dialysis shift, and other demographic data. Results: Out of 227 enrolled patients, insomnia was reported by 60.8%. The mean patient age was 55.7 ± 17.2 years; 53.7% were male and 46.3% were female. Insomnia was significantly associated with female gender, afternoon hemodialysis, Restless Legs Syndrome, high risk for obstructive Sleep Apnea Syndrome and excessive daytime sleepiness (P-values: 0.05, 0.01, < 0.0001, < 0.0001, and < 0.0001, respectively). No significant association was found between insomnia and other variables, including BMI, smoking habits, underlying etiology of renal failure, dialysis duration, association with hemoglobin, ferritin, and phosphorus or dialysis adequacy as measured by the Kt/V index. Conclusion: Insomnia is common in dialysis patients and was significantly associated with other sleep disorders. Greater attention needs to be given to the care of dialysis patients with regard to the diagnosis and management of insomnia and associated sleep disorders.

Background: Immunosenescence is a process that affects all cell compartments of the immune system and the contribution of the immune system to healthy aging and longevity is still an open question. Lymphocyte subpopulations present different patterns of circadian variation and in the elderly alteration of circadian rhythmicity has been evidenced. The aim of our study was to analyze the dynamics of variation of specific cytotoxic lymphocyte subsets in old aged subjects. Methods: Lymphocyte subpopulation analyses were performed and cortisol serum levels were measured on blood samples collected every four hours for 24 hours from fifteen healthy male young-middle aged subjects (age range 36-55 years) and fifteen healthy male old aged subjects (age range 67-79 years). Results: In healthy young-middle aged subjects CD20 were higher and at 06:00 h CD8+ dim correlated positively with CD16+ and positively with TCR+ cells, CD16 correlated positively with TCR+ cells At 18:00 h CD8+ dim correlated positively with CD16+ and positively with TCR+ cells, CD16+ correlated positively with TCR+ cells and a clear circadian rhythm was validated for the time-qualified changes of CD3+, CD4+, CD20+, CD25+ and HLA-DR+ cells with acrophase during the night and for the time-qualified changes of CD8+, CD8+ bright, CD8+ dim, CD16+ and TCR+ cells with acrophase during the day. In old aged subjects CD25, DR+ T cells and cortisol serum levels were higher, but there was no statistically significant correlation among lymphocyte subpopulations and a clear circadian rhythm was evidenced for time-qualified changes of CD3+ and CD25+ cells with acrophase during the night and for the time-qualified changes of CD8+ cells and cortisol with acrophase during the day. Conclusion: Our study has evidenced aging-related changes of correlation and circadian rhythmicity of variation of cytotoxic lymphocyte subpopulations that might play a role in the alteration of immune system function in the elderly.

Background: Most mammals are seasonal breeders whose gonads grow to anticipate reproduction in the spring and summer. As day length increases, secretion increases for two gonadotropins, luteinizing hormone (LH) and follicle stimulating hormone (FSH). This response is largely controlled by light. Light effects on gonadotropins are mediated through effects on the suprachiasmatic nucleus and responses of the circadian system. There is some evidence that seasonal breeding in humans is regulated by similar mechanisms, and that light stimulates LH secretion, but primate responses seem complex. Methods: To gain further information on effects of bright light on LH and FSH secretion in humans, we analyzed urine samples collected in three experiments conducted for other goals. First, volunteers ages 18-30 years and 60-75 commenced an ultra-short 90-min sleep-wake cycle, during which they were exposed to 3000 lux light for 3 hours at balanced times of day, repeated for 3 days. Urine samples were assayed to explore any LH phase response curve. Second, depressed participants 60-79 years of age were treated with bright light or dim placebo light for 28 days, with measurements of urinary LH and FSH before and after treatment. Third, women of ages 20-45 years with premenstrual dysphoric disorder (PMDD) were treated to one 3-hour exposure of morning light, measuring LH and FSH in urine before and after the treatments. Results: Two of the three studies showed significant increases in LH after light treatment, and FSH also tended to increase, but there were no significant contrasts with parallel placebo treatments and no significant time-of-day treatment effects. Conclusions: These results gave some support for the hypothesis that bright light may augment LH secretion. Longer-duration studies may be needed to clarify the effects of light on human LH and FSH.

Background: Glioblastoma is one of the deadliest forms of cancer, in part because of its highly invasive nature. The tumor suppressor PTEN is frequently mutated in glioblastoma and is known to contribute to the invasive phenotype. However the downstream events that promote invasion are not fully understood. PTEN loss leads to activation of the atypical protein kinase C, PKCiota. We have previously shown that PKCiota is required for glioblastoma cell invasion, primarily by enhancing cell motility. Here we have used time-lapse videomicroscopy to more precisely define the role of PKCiota in glioblastoma. Results: Glioblastoma cells in which PKCiota was either depleted by shRNA or inhibited pharmacologically were unable to coordinate the formation of a single leading edge lamellipod. Instead, some cells generated multiple small, short-lived protrusions while others generated a diffuse leading edge that formed around the entire circumference of the cell. Confocal microscopy showed that this behavior was associated with altered behavior of the cytoskeletal protein Lgl, which is known to be inactivated by PKCiota phosphorylation. Lgl in control cells localized to the lamellipod leading edge and did not associate with its binding partner non-muscle myosin II, consistent with it being in an inactive state. In PKCiota-depleted cells, Lgl was concentrated at multiple sites at the periphery of the cell and remained in association with non-muscle myosin II. Videomicroscopy also identified a novel role for PKCiota in the cell cycle. Cells in which PKCiota was either depleted by shRNA or inhibited pharmacologically entered mitosis normally, but showed marked delays in completing mitosis. Conclusions: PKCiota promotes glioblastoma motility by coordinating the formation of a single leading edge lamellipod and has a role in remodeling the cytoskeleton at the lamellipod leading edge, promoting the dissociation of Lgl from non-muscle myosin II. In addition PKCiota is required for the transition of glioblastoma cells through mitosis. PKCiota therefore has a role in both glioblastoma invasion and proliferation, two key aspects in the malignant nature of this disease.

The small RNA molecules of about 19-22 nucleotides in length, aptly called microRNAs, perform the task of gene regulation in the cell. Interestingly, till the early nineties very little was known about them but eventually, the microRNAs have become forefront in the area of research. The huge number of microRNAs plus each one of them targeting a vast number of related as well as unrelated genes makes them very interesting molecules to study. To add to the mystery of miRNAs is the fact that the same miRNA can have antagonizing role in two different cell types i.e. in one cell type; the miRNA promotes proliferation whereas in another cell type the same miRNA inhibits proliferation. Another remarkable aspect of the microRNAs is that many of them exist in clusters. In humans alone, out of 721 microRNAs known, 247 of them occur in 64 clusters at an inter-miRNA distance of less than 5000bp. The reason for this clustering of miRNAs is not fully understood but since the miRNA clusters are evolutionary conserved, their significance cannot be ruled out. The objective of this review is to summarize the recent progress on the functional characterization of miR-23a~27a~24-2 cluster in humans in relation to various health and diseased conditions and to highlight the cooperative effects of the miRNAs of this cluster.

Background: Disorganized angiogenesis is associated with several pathologies, including cancer. The identification of new genes that control tumor neovascularization can provide novel insights for future anti-cancer therapies. Sprouty1 (SPRY1), an inhibitor of the MAPK pathway, might be one of these new genes. We identified SPRY1 by comparing the transcriptomes of untreated endothelial cells with those of endothelial cells treated by the angiostatic agent 16K prolactin (16K hPRL). In the present study, we aimed to explore the potential function of SPRY1 in angiogenesis. Results: We confirmed 16K hPRL induced up-regulation of SPRY1 in primary endothelial cells. In addition, we demonstrated the positive SPRY1 regulation in a chimeric mouse model of human colon carcinoma in which 16K hPRL treatment was shown to delay tumor growth. Expression profiling by qRT-PCR with species-specific primers revealed that induction of SPRY1 expression by 16K hPRL occurs only in the (murine) endothelial compartment and not in the (human) tumor compartment. The regulation of SPRY1 expression was NF-kappaB dependent. Partial SPRY1 knockdown by RNA interference protected endothelial cells from apoptosis as well as increased endothelial cell proliferation, migration, capillary network formation, and adhesion to extracellular matrix proteins. SPRY1 knockdown was also shown to affect the expression of cyclinD1 and p21 both involved in cell-cycle regulation. These findings are discussed in relation to the role of SPRY1 as an inhibitor of ERK/MAPK signaling and to a possible explanation of its effect on cell proliferation. Conclusions: Taken together, these results suggest that SPRY1 is an endogenous angiogenesis inhibitor.

Background: Ultrasound elasticity imaging provides biomechanical and elastic properties of vascular tissue, with the potential to distinguish between tissue motion and tissue strain. To validate the ability of ultrasound elasticity imaging to predict structurally defined physical changes in tissue, strain measurement patterns during angioplasty in four bovine carotid artery pathology samples were compared to the measured physical characteristics of the tissue specimens. Methods: Using computational image-processing techniques, the circumferences of each bovine artery specimen were obtained from ultrasound and pathologic data. Results: Ultrasound-strain-based and pathology-based arterial circumference measurements were correlated with an R^2 value of 0.94 (p = 0.03). The experimental elasticity imaging results confirmed the onset of deformation of an angioplasty procedure by indicating a consistent inflection point where vessel fibers were fully unfolded and vessel wall strain initiated. Conclusion: These results validate the ability of ultrasound elasticity imaging to measure localized mechanical changes in vascular tissue.

Background: One of the goals of computational immunology is to facilitate the study of infectious diseases. Dynamic modeling is a powerful tool to integrate empirical data from independent sources, make novel predictions, and to foresee the gaps in the current knowledge. Dynamic models constructed to study the interactions between pathogens and hosts' immune responses have revealed key regulatory processes in the infection.Optimum complexity and dynamic modelingWe discuss the usability of various deterministic dynamic modeling approaches to study the progression of infectious diseases. The complexity of these models is dependent on the number of components and the temporal resolution in the model. We comment on the specific use of simple and complex models in the study of the progression of infectious diseases. Conclusions: Models of sub-systems or simplified immune response can be used to hypothesize phenomena of host-pathogen interactions and to estimate rates and parameters. Nevertheless, to study the pathogenesis of an infection we need to develop models describing the dynamics of the immune components involved in the progression of the disease. Incorporation of the large number and variety of immune processes involved in pathogenesis requires tradeoffs in modeling.

Background: Serotonin is a neurotransmitter that has been linked to a wide variety of behaviors including feeding and body-weight regulation, social hierarchies, aggression and suicidality, obsessive compulsive disorder, alcoholism, anxiety, and affective disorders. Full understanding of serotonergic systems in the central nervous system involves genomics, neurochemistry, electrophysiology, and behavior. Though associations have been found between functions at these different levels, in most cases the causal mechanisms are unknown. The scientific issues are daunting but important for human health because of the use of selective serotonin reuptake inhibitors and other pharmacological agents to treat disorders in the serotonergic signaling system. Methods: We construct a mathematical model of serotonin synthesis, release, and reuptake in a single serotonergic neuron terminal. The model includes the effects of autoreceptors, the transport of tryptophan into the terminal, and the metabolism of serotonin, as well as the dependence of release on the firing rate. The model is based on real physiology determined experimentally and is compared to experimental data. Results: We compare the variations in serotonin and dopamine synthesis due to meals and find that dopamine synthesis is insensitive to the availability of tyrosine but serotonin synthesis is sensitive to the availability of tryptophan. We conduct in silico experiments on the clearance of extracellular serotonin, normally and in the presence of fluoxetine, and compare to experimental data. We study the effects of various polymorphisms in the genes for the serotonin transporter and for tryptophan hydroxylase on synthesis, release, and reuptake. We find that, because of the homeostatic feedback mechanisms of the autoreceptors, the polymorphisms have smaller effects than one expects. We compute the expected steady concentrations of serotonin transporter knockout mice and compare to experimental data. Finally, we study how the properties of the the serotonin transporter and the autoreceptors give rise to the time courses of extracellular serotonin in various projection regions after a dose of fluoxetine. Conclusions: Serotonergic systems must respond robustly to important biological signals, while at the same time maintaining homeostasis in the face of normal biological fluctuations in inputs, expression levels, and firing rates. This is accomplished through the cooperative effect of many different homeostatic mechanisms including special properties of the serotonin transporters and the serotonin autoreceptors. Many difficult questions remain in order to fully understand how serotonin biochemistry affects serotonin electrophysiology and vice versa, and how both are changed in the presence of selective serotonin reuptake inhibitors. Mathematical models are useful tools for investigating some of these questions.