Population change in breeding boreal waterbirds in a 25-year perspective : What characterises winners and losers?

Understanding drivers of variation and trends in biodiversity change is a general scientific challenge, but also crucial for conservation and management. Previous research shows that patterns of increase and decrease are not always consistent at different spatial scales, calling for approaches combining the latter. We here explore the idea that functional traits of species may help explaining divergent population trends. Complementing a previous community level study, we here analyse data about breeding waterbirds on 58 wetlands in boreal Fennoscandia, covering gradients in latitude as well as trophic status. We used linear mixed models to address how change in local abundance over 25 years in 25 waterbird species are associated with life history traits, diet, distribution, breeding phenology, and habitat affinity. Mean abundance increased in 10 species from 1990/1991 to 2016, whereas it decreased in 15 species. Local population increases were associated with species that are early breeders and have small clutches, an affinity for luxurious wetlands, an herbivorous diet, and a wide breeding range rather than a southern distribution. Local decreases, by contrast, were associated with species having large clutches and invertivorous diet, as well as being late breeders and less confined to luxurious wetlands. The three species occurring on the highest number of wetlands all decreased in mean abundance. The fact that early breeders have done better than late fits well with previous research about adaptability to climate change, that is, response to earlier springs. We found only limited support for the idea that life history traits are good predictors of wetland level population change. Instead, diet turned out to be a strong candidate for an important driver of population change, as supported by a general decrease of invertivores and a concomitant increase of large herbivores. In a wider perspective, future research needs to address whether population growth of large-bodied aquatic herbivores affects abundance of co-occurring invertivorous species, and if so, if this is due to habitat alteration, or to interference or exploitative competition.Peer reviewe

Pressure observations by the curiosity rover : Initial results

The authors would like to express their gratitude to the MSL and REMS instrument teams in making this wonderful Mars mission come true. Ari-Matti Harri and Hannu Savijarvi are thankful for the Finnish Academy grants 132825 and 131723.Peer reviewedPublisher PD

TIMP-1 Induces an EMT-Like Phenotypic Conversion in MDCK Cells Independent of Its MMP-Inhibitory Domain

Matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) regulate epithelial-mesenchymal transition (EMT) critical for the development of epithelial organs as well as cancer cell invasion. TIMP-1 is frequently overexpressed in several types of human cancers and serves as a prognostic marker. The present study investigates the roles of TIMP-1 on the EMT process and formation of the lumen-like structure in a 3D Matrigel culture of MDCK cells. We show that TIMP-1 overexpression effectively prevents cell polarization and acinar-like structure formation. TIMP-1 induces expression of the developmental EMT transcription factors such as SLUG, TWIST, ZEB1 and ZEB2, leading to downregulation of epithelial marker and upregulation of mesenchymal markers. Importantly, TIMP-1′s ability to induce the EMT-like process is independent of its MMP-inhibitory domain. To our surprise, TIMP-1 induces migratory and invasive properties in MDCK cells. Here, we present a novel finding that TIMP-1 signaling upregulates MT1-MMP and MMP-2 expression, and potentiates MT1-MMP activation of pro-MMP-2, contributing to tumor cell invasion. In spite of the fact that TIMP-1, as opposed to TIMP-2, does not interact with and inhibit MT1-MMP, TIMP-1 may act as a key regulator of MT1-MMP/MMP-2 axis. Collectively, our findings suggest a model in which TIMP-1 functions as a signaling molecule and also as an endogenous inhibitor of MMPs. This concept represents a paradigm shift in the current view of TIMP-1/MT1-MMP interactions and functions during cancer development/progression

Claudins in lung diseases

Tight junctions are the most apically localized part of the epithelial junctional complex. They regulate the permeability and polarity of cell layers and create compartments in cell membranes. Claudins are structural molecules of tight junctions. There are 27 claudins known, and expression of different claudins is responsible for changes in the electrolyte and solute permeability in cells layers. Studies have shown that claudins and tight junctions also protect multicellular organisms from infections and that some infectious agents may use claudins as targets to invade and weaken the host's defense. In neoplastic diseases, claudin expression may be up- or downregulated. Since their expression is associated with specific tumor types or with specific locations of tumors to a certain degree, they can, in a restricted sense, also be used as tumor markers. However, the regulation of claudin expression is complex involving growth factors and integrins, protein kinases, proto-oncogens and transcription factors. In this review, the significance of claudins is discussed in lung disease and development