An ecological 'footprint' of climate change

Recently, there has been increasing evidence of species' range shifts due to changes in climate. Whereas most of these shifts relate ground truth biogeographic data to a general warming trend in regional or global climate data, we here present a reanalysis of both biogeographic and bioclimatic data of equal spatio-temporal resolution, covering a time span of more than 50 years. Our results reveal a coherent and synchronous shift in both species' distribution and climate. They show not only a shift in the northern margin of a species, which is in concert with gradually increasing winter temperatures in the area, they also confirm the simulated species' distribution changes expected from a bioclimatic model under the recent, relatively moderate climate change.     

Palms tracking climate change

Aim  Many species are currently expanding their ranges in response to climate change, but the mechanisms underlying these range expansions are in many cases poorly understood. In this paper we explore potential climatic factors governing the recent establishment of new palm populations far to the north of any other viable palm population in the world.
Location  Southern Switzerland, Europe, Asia and the world.
Methods  We identified ecological threshold values for the target species, Trachycarpus fortunei , based on gridded climate data, altitude and distributional records from the native range and applied them to the introduced range using local field monitoring and measured meteorological data as well as a bioclimatic model.
Results  We identified a strong relationship between minimum winter temperatures, influenced by growing season length and the distribution of the palm in its native range. Recent climate change strongly coincides with the palm's recent spread into southern Switzerland, which is in concert with the expansion of the global range of palms across various continents.
Main conclusions  Our results strongly suggest that the expansion of palms into (semi-)natural forests is driven by changes in winter temperature and growing season length and not by delayed population expansion. This implies that this rapid expansion is likely to continue in the future under a warming climate. Palms in general, and T. fortunei in particular, are significant bioindicators across continents for present-day climate change and reflect a global signal towards warmer conditions.     

Amphipathic sulfonamidobenzamides mimicking small antimicrobial marine natural products; investigation of antibacterial and anti-biofilm activity against antibiotic resistant clinical isolates

There is an urgent need for novel antimicrobial agents to address the threat of bacterial resistance to modern society. We have used a structural motif found in antimicrobial marine hit compounds as a basis for synthesizing a library of antimicrobial sulfonamidobenzamide lead compounds. Potent in vitro antimicrobial activity against clinically relevant bacterial strains was demonstrated for two compounds, G6 and J18, with minimal inhibitory concentrations (MIC) of 4–16?μg/ml against clinical methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant Enterococcus faecium (VRE). The two compounds G6 and J18, together with several other compounds of this library, also caused ≥90% eradication of pre-established biofilm of methicillin-resistant S. epidermidis (MRSE) at 40?μg/ml. Using a luciferase assay, the mechanism of action of G6 was shown to resemble the biocide chlorhexidine by targeting the bacterial cell membrane.     

Shiga toxin regulates its entry in a Syk-dependent manner

Shiga toxin (Stx) is composed of an A-moiety that inhibits protein synthesis after translocation into the cytosol, and a B-moiety that binds to Gb3 at the cell surface and mediates endocytosis of the toxin. After endocytosis, Stx is transported retrogradely to the endoplasmic reticulum, and then the A-fragment enters the cytosol. In this study, we have investigated whether toxin-induced signaling is involved in its entry. Stx was found to activate Syk and induce rapid tyrosine phosphorylation of several proteins, one protein being clathrin heavy chain. Toxin-induced clathrin phosphorylation required Syk activity, and in cells overexpressing Syk, a complex containing clathrin and Syk could be demonstrated. Depletion of Syk by small interfering RNA, expression of a dominant negative Syk mutant (Syk KD), or treatment with the Syk inhibitor piceatannol inhibited not only Stx-induced clathrin phosphorylation but also endocytosis of the toxin. Also, Golgi transport of Stx was inhibited under all these conditions. In conclusion, our data suggest that Stx regulates its entry into target cells.     

Cosegregation of asymmetric features during cell division

Cellular asymmetry plays a major role in the ageing and evolution of multicellular organisms. However, it remains unknown how the cell distinguishes ‘old’ from ‘new’ and whether asymmetry is an attribute of highly specialized cells or a feature inherent in all cells. Here, we investigate the segregation of three asymmetric features: old and new DNA, the spindle pole body (SPB, the centrosome analogue) and the old and new cell ends, using a simple unicellular eukaryote, Schizosaccharomyces pombe. To our knowledge, this is the first study exploring three asymmetric features in the same cells. We show that of the three chromosomes of S. pombe, chromosome I containing the new parental strand, preferentially segregated to the cells inheriting the old cell end. Furthermore, the new SPB also preferentially segregated to the cells inheriting the old end. Our results suggest that the ability to distinguish ‘old’ from ‘new’ and to segregate DNA asymmetrically are inherent features even in simple unicellular eukaryotes.     

Nitric Oxide Exposure of CC531 Rat Colon Carcinoma Cells Induces γ-glutamyltransferase which May Counteract Glutathione Depletion and Cell Death

&#110 -Glutamyltransferase (GGT) has a central role in glutathione homeostasis by initiating the breakdown of extracellular GSH. We investigated in the present study whether nitric oxide exposure of CC531 rat colon carcinoma cells modulates GGT and how the activity of the enzyme affects the level of intracellular GSH. The data show that GGT activity was induced in a dose-related manner by two NO-donors (spermineNONOate and nitrosoglutathione) and that antioxidants partly inhibited the induction. SpermineNONOate lowered intracellular GSH and induced apoptosis. Cultivating the cells in cystine-depleted medium also resulted in a 50% lowering of GSH, but this was avoided when GSH was added to the medium. This effect was mediated by the activity of GGT and shown after inhibiting GGT activity with acivicin and cyst(e)ine transporters with alanine and homocysteic acid. This shows that the cells benefit from GGT in maintaining the intracellular GSH level. Cells with induced GGT activity obtained after NO incubation showed a higher uptake rate of cysteine (2-fold), measured by incubating the cells with 35 S-radiolabeled GSH. The enzyme was also induced by interferon- &#110 and tumor necrosis factor- &#102, but this induction was not connected to activation of the endogenous nitric oxide synthase, as the addition of aminoguanidine, a NO-synthase inhibitor, did not affect the induction. The present study shows that the activity of GGT is upregulated by NO-donors and that the colon carcinoma cells, when cultivated in cystine-depleted medium, benefit from the enzyme in maintaining the intracellular level of GSH. Thus, the enzyme will add to the protective measures of the tumor cells during nitrosative stress.     

Deep sympatric mtDNA divergence in the autumnal moth (Epirrita autumnata)

Deep sympatric intraspecific divergence in mtDNA may reflect cryptic species or formerly distinct lineages in the process of remerging. Preliminary results from DNA barcoding of Scandinavian butterflies and moths showed high intraspecific sequence variation in the autumnal moth, Epirrita autumnata. In this study, specimens from different localities in Norway and some samples from Finland and Scotland, with two congeneric species as outgroups, were sequenced with mitochondrial and nuclear markers to resolve the discrepancy found between mtDNA divergence and present species‐level taxonomy. We found five COI sub‐clades within the E. autumnata complex, most of which were sympatric and with little geographic structure. Nuclear markers (ITS2 and Wingless) showed little variation and gave no indications that E. autumnata comprises more than one species. The samples were screened with primers for Wolbachia outer surface gene (wsp) and 12% of the samples tested positive. Two Wolbachia strains were associated with different mtDNA sub‐clades within E. autumnata, which may indicate indirect selection/selective sweeps on haplotypes. Our results demonstrate that deep mtDNA divergences are not synonymous with cryptic speciation and this has important implications for the use of mtDNA in species delimitation, like in DNA barcoding.     

Surgical Site Infections after Deep Brain Stimulation Surgery: Frequency,Characteristics and Management in a 10-Year Period

Background/Aims

Deep brain stimulation (DBS) implant infection is a feared complication, as it is difficult to manage and leads to increased patient morbidity. We wanted to assess the frequency and possible risk factors of DBS related infections at our centre. In the purpose of evaluating treatment options, we also analyzed treatment, and the clinical and microbiological characteristics of the infections.

Methods

Electronic medical records of all patients undergoing DBS surgery at our centre, from 2001 through 2010, were retrospectively reviewed.

Results

Of the 588 procedures performed 33 (5.6%) led to an infection. Some patients underwent several procedures, thus 32 out of totally 368 patients (8.7%), and 19 out of 285 patients (6.7%) who received primary lead implantation, developed an infection. Most infections (52%) developed within the first month and 79% within three months. In the majority of the infections (79%) hardware removal was performed. Staphylococcus aureus infections were the most frequent (36%), and more likely to have earlier onset, pus formation, a more aggressive development and lead to hardware removal. No risk factors were identified.

Conclusions

Our results indicate that infections with more severe symptoms and growth of staphylococcus aureus should be treated with local hardware removal and antibiotic therapy. In other infections, an initial trial of antibiotic treatment could be considered. New knowledge about the microbiology of DBS related infections may lead to more effective antimicrobial treatment.     

Silencing of renal DNaseI in murine lupus nephritis imposes exposure of large chromatin fragments and activation of Toll like receptors and the Clec4e

Recent studies demonstrate that transformation of mild lupus nephritis into end-stage disease is imposed by silencing of renal DNaseI gene expression in (NZBxNZW)F1 mice. Down-regulation of DNaseI results in reduced chromatin fragmentation, and in deposition of extracellular chromatin-IgG complexes in glomerular basement membranes in individuals that produce IgG anti-chromatin antibodies. The main focus of the present study is to describe the biological consequences of renal DNaseI shut-down and reduced chromatin fragmentation with a particular focus on whether exposed large chromatin fragments activate Toll like receptors and the necrosis-related Clec4e receptor in murine and human lupus nephritis. Furthermore, analyses where performed to determine if matrix metalloproteases are up-regulated as a consequence of chromatin-mediated Toll like receptors/Clec4e stimulation. Mouse and human mRNA expression levels of DNaseI, Toll like receptors 7-9, Clec4e, pro-inflammatory cytokines and MMP2/MMP9 were determined and compared with in situ protein expression profiles and clinical data. We demonstrate that exposure of chromatin significantly up-regulate Toll like receptors and Clec4e in mice, and also but less pronounced in patients with lupus nephritis treated with immunosuppresants. In conclusion, silencing of renal DNaseI gene expression initiates a cascade of inflammatory signals leading to progression of both murine and human lupus nephritis. Principal component analyses biplot of data from murine and human lupus nephrits demonstrate the importance of DNaseI gene shut down for progression of the organ disease.