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Citizen science is a term used to describe the engagement of ordinary citizens in scientific tasks like observation, measurement, and computation. A series of technological innovations, such as the Internet, the upgrade of mobile phones from communication devices to networked mobile personal measurement devices, and the introduction of self-assessment applications to use with them, redefined the activity of citizen science, providing amateur scientists not only with tools to share, but to also record and interpret almost any type of data. These innovations generated an explosion in the number of citizen science projects, with technology on the one hand reducing the need for skills or knowledge which, until then, were a basic requirement to be involved in such projects, while, on the other, guaranteeing that the generated data meets a minimum standard of quality. In this paper we argue that for citizens to become true scientists, a position they used to have before the arrival of the professionals, an additional technological innovation is required to turn mobile devices into tools for experimentation.

• A region with demographic growth, faces shrinkage in certain places. • For Flanders, shrinkage manifests itself on the scale of sub-municipalities. • The opportunities of shrinkage in growth differ from shrinking cities and regions. • Including the risk and the potential of shrinkage can benefit a planning for growth. Demographic transitions have an impact on the landscape and urban development. However, when planning for demographic growth, the concept of demographic shrinkage is seldom considered. Consequently, many opportunities for qualitative landscape interventions and urban development remain unnoticed. This article proposes a conceptualization for demographic shrinkage within the context of the growing region of Flanders, Belgium. Demographic statistics, indicators for the risk of shrinkage, and local opinions from the region are cross-referenced with the shrinking cities discourse. Our research shows that Flanders is shrinking in some parts, has a risk of shrinking in many more areas, and should shrink in strategic places from a resilience perspective. Contrary to demographic shrinkage in other parts of Europe and the world, which covers vast territories and results in urban decline, demographic shrinkage in the region of Flanders manifests itself very locally and on a small scale. The research suggests introducing the use of "shrinkage in growth" to implement its specific opportunities and overcome the possible negative effects of shrinkage. The concept of shrinkage in growth implies a systemic understanding of different scales and an integrated spatial practice that goes beyond the strategy of constructing more housing in order to attract more inhabitants. [ABSTRACT FROM AUTHOR]

In the search of genes potentially implicated in the aetiology of affective disorders (AD), SUBSTANCE P (SP) pathway is receiving increased interest. SP receptor antagonists, such as MK-869 and L-759274, have been shown to have antidepressant effect. Results from preclinical and human studies implicate SP and its pathway in the pathophysiology of mood disorders. We investigated a possible association between 20 single nucleotide polymorphisms (SNPS) among four SP-related genes and unipolar and bipolar ad (UPAD and BPAD) in a first sample of 92 UPAD patients and 92 control individuals and in a replication sample of 92 UPAD patients and 92 control individuals. An additional sample of 113 BPAD patients has also been ascertained. Our results showed a significant association between the angiotensin-converting enzyme gene (ACE1) and UPAD in our first sample, but not in the replication sample. No significant evidence of association was found in other SP-related genes. We did not find any association in the BPAD sample. When pooling first and replication UPAD samples, an association was found between ACE1 and a subgroup of patients remaining depressed after an adequate antidepressant treatment. In conclusion, our findings do not support a major contribution of SP-related genes in UPAD and BPAD, but provides some evidence of an ace influence in treatment response to antidepressants.

Several lines of evidence have suggested an implication of brain-derived neurotrophic factor (BDNF) in unipolar affective disorder (UPAD). In the present study, we investigated the role of BDNF gene in UPAD in two independent samples of 92 patients/92 controls and 156 patients/197 controls. Two single nucleotide polymorphisms (SNPs) were investigated. We found no significant differences of BDNF gene SNPs distribution between UPAD patients and controls in both samples. Haplotype analyses were performed on both samples. A statistical difference was found between cases and controls in the first sample but not in the second. These results are not in favour of an implication of BDNF in UPAD but need to be replicated before final conclusion.

This patient-control association study was conducted to investigate a possible association of two single nucleotide polymorphisms (SNPs), g.11757C > G and g.196G > A, in the brain-derived neurotrophic factor (BDNF) with bipolar affective disorder (BPAD). Two hundred seventy-five individuals of Belgian origin (at least two generations of Belgian ancestors) were genotyped (112 BPAD and 163 controls). No significant differences were found in the frequency of genotypes and alleles of g.196G > A (P = 0.37 and 0.94, respectively) and g.11757C > G (P = 0.49 and 0.59, respectively) between controls and BPAD patients. An haplotype analysis revealed no difference between patients and controls (P = 0.44). We failed to replicate previous findings implicating BDNF in the aetiology of BPAD. However, BDNF remains an interesting target for future genetic studies and should be tested in prospective pharmacogenetic therapeutic trials., (Copyright 2004 Wiley-Liss, Inc.)

Increasing amounts of data suggest that affective disorders might be related to dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, one of the stress-response systems. Arginine vasopressin (AVP) influences several symptoms, relevant to affective disorders, notable memory processes, pain sensitivity, synchronization of biological rhythms and the timing and quality of REM sleep. We examined whether genetic variations in the AVP receptor 1b gene (AVPR1b) could be associated with increased susceptibility to affective disorders using a gene-based association analysis of single-nucleotide polymorphisms (SNPs). Five SNPs were identified in AVPR1b and genotyped in two well-diagnosed samples of patients with recurrent major depression and matched controls. In the Swedish sample, we observed significant allele (P=0.02) and genotype (P=0.01) association with SNP AVPR1b-s3, and in the Belgian sample, a borderline significant association with SNP AVPR1b-s5 (P=0.04). In both patient-control samples, the haplotype defined by alleles A-T-C-A-G for the AVPR1b-s SNPs s1-s2-s3-s4-s5 was significantly over-represented in controls compared to patients. Our data support a protective effect of this major haplotype for recurrent major depression.