'SSW to NNE'– North Atlantic Oscillation affects the progress of seasons across Europe

Three European plant phenological network datasets were analysed for latitudinal and longitudinal gradients of nine phenological ‘seasons’ spanning the entire year. The networks were: (1) the historical first European Phenological Network (1882–1941) by Hoffmann & Ihne, (2) the network of the International Phenological Gardens in Europe (1959–1998), founded by Schnelle & Volkert in 1957 and based on cloned plants, and (3) a dataset (1951–1998) that was recently collated during the EU Fifth Framework project POSITIVE, which included network data of seven Central and Eastern European countries. Our study is most likely the first, for over a century, to analyse average onset and year‐to‐year variability of the progress of seasons across a continent. For early, mid, and late spring seasons we found a marked progress of the seasonal onset from SW to NE throughout Europe, more precisely from WSW to ENE in early spring, then from SW to NE and finally from SSW to NNE in late spring, as exhibited by the relationship between latitudinal and longitudinal gradients. The movement of summer was more south to north directed, as the longitudinal gradient (west–east component) strongly declined or was even of opposite sign. Autumn, as shown by leaf colouring dates, arrived from NE to SW. Possible reasons for the differences among the three datasets are discussed. The annual variability of latitudinal and longitudinal gradients of the seasons across Europe was closely related to the North Atlantic Oscillation (NAO) index; in years with high NAO in both winter and spring, the west–east component of progress was more pronounced; in summer and autumn, the pattern of the seasons may be more uniform.     

The Role and Metabolism of Sulfatide in the Nervous System

3-O-sulfogalactosylceramide or sulfatide is a major component of the myelin sheath in the central and peripheral nervous system. The examination of mice deficient in the sulfatide-synthesizing enzyme, cerebroside sulfotransferase, provided new insight into the role of sulfatide in the differentiation of myelinating cells, formation of the paranodal junction, and myelin maintenance. Although in general regarded as a marker for oligodendrocytes and Schwann cells, sulfatide is also present in astrocytes and neurons. The relatively low amount of sulfatide in neurons can dramatically increase in the absence of the sulfatide-degrading enzyme, arylsulfatase A, as in metachromatic leukodystrophy. Recent advance in the understanding of this disease comes from studies on new transgenic mouse models. Significant changes in sulfatide levels have also been observed more recently in Alzheimer's disease and other diseases, suggesting that sulfatide might be involved in the pathogenesis of these diseases as well. This review summarizes recent studies on the physiological and pathophysiological role of sulfatide using transgenic mice deficient in its synthesis or degradation.     

Is amino acid racemization a useful tool for screening for ancient DNA in bone?

Many rare and valuable ancient specimens now carry the scars of ancient DNA research, as questions of population genetics and phylogeography require larger sample sets. This fuels the demand for reliable techniques to screen for DNA preservation prior to destructive sampling. Only one such technique has been widely adopted: the extent of aspartic acid racemization (AAR). The kinetics of AAR are believed to be similar to the rate of DNA depurination and therefore a good measure of the likelihood of DNA survival. Moreover, AAR analysis is only minimally destructive. We report the first comprehensive test of AAR using 91 bone and teeth samples from temperate and high-latitude sites that were analysed for DNA. While the AAR range of all specimens was low (0.02–0.17), no correlation was found between the extent of AAR and DNA amplification success. Additional heating experiments and surveys of the literature indicated that d/l Asx is low in bones until almost all the collagen is lost. This is because aspartic acid is retained in the bone within the constrained environment of the collagen triple helix, where it cannot racemize for steric reasons. Only if the helix denatures to soluble gelatin can Asx racemize readily, but this soluble gelatine is readily lost in most burial environments. We conclude that Asx d/l is not a useful screening technique for ancient DNA from bone.     

T-lymphocyte responses to intestinally absorbed antigens can contribute to adipose tissue inflammation and glucose intolerance during high fat feeding

Background

Obesity is associated with inflammation of visceral adipose tissues, which increases the risk for insulin resistance. Animal models suggest that T-lymphocyte infiltration is an important early step, although it is unclear why these cells are attracted. We have recently demonstrated that dietary triglycerides, major components of high fat diets, promote intestinal absorption of a protein antigen (ovalbumin, “OVA”). The antigen was partly transported on chylomicrons, which are prominently cleared in adipose tissues. We hypothesized that intestinally absorbed gut antigens may cause T-lymphocyte associated inflammation in adipose tissue.

Methodology/Principal Findings

Triglyceride absorption promoted intestinal absorption of OVA into adipose tissue, in a chylomicron-dependent manner. Absorption tended to be higher in mesenteric than subcutaneous adipose tissue, and was lowest in gonadal tissue. OVA immunoreactivity was detected in stromal vascular cells, including endothelial cells. In OVA-sensitized mice, OVA feeding caused marked accumulation of CD3+ and osteopontin+ cells in mesenteric adipose tissue. The accumulating T-lymphocytes were mainly CD4+. As expected, high-fat (60% kCal) diets promoted mesenteric adipose tissue inflammation compared to low-fat diets (10% Kcal), as reflected by increased expression of osteopontin and interferon-gamma. Immune responses to dietary OVA further increased diet-induced osteopontin and interferon-gamma expression in mesenteric adipose. Inflammatory gene expression in subcutaneous tissue did not respond significantly to OVA or dietary fat content. Lastly, whereas OVA responses did not significantly affect bodyweight or adiposity, they significantly impaired glucose tolerance.

Conclusions/Significance

Our results suggest that loss or lack of immunological tolerance to intestinally absorbed T-lymphocyte antigens can contribute to mesenteric adipose tissue inflammation and defective glucose metabolism during high-fat dieting.     

The NLRP3 inflammasome contributes to brain injury in pneumococcal meningitis and is activated through ATP-dependent lysosomal cathepsin B release

Streptococcus pneumoniae meningitis causes brain damage through inflammation-related pathways whose identity and mechanisms of action are yet unclear. We previously identified caspase-1, which activates precursor IL-1 type cytokines, as a central mediator of inflammation in pneumococcal meningitis. In this study, we demonstrate that lack of the inflammasome components ASC or NLRP3 that are centrally involved in caspase-1 activation decreases scores of clinical and histological disease severity as well as brain inflammation in murine pneumococcal meningitis. Using specific inhibitors (anakinra and rIL-18-binding protein), we further show that ASC- and NLRP3-dependent pathologic alterations are solely related to secretion of both IL-1β and IL-18. Moreover, using differentiated human THP-1 cells, we demonstrate that the pneumococcal pore-forming toxin pneumolysin is a key inducer of IL-1β expression and inflammasome activation upon pneumococcal challenge. The latter depends on the release of ATP, lysosomal destabilization (but not disruption), and cathepsin B activation. The in vivo importance of this pathway is supported by our observation that the lack of pneumolysin and cathepsin B inhibition is associated with a better clinical course and less brain inflammation in murine pneumococcal meningitis. Collectively, our study indicates a central role of the NLRP3 inflammasome in the pathology of pneumococcal meningitis. Thus, interference with inflammasome activation might be a promising target for adjunctive therapy of this disease.     

Eggshell pigmentation has no evident effects on offspring viability in common kestrels

Infectious diseases and parasitism are major environmental forces decreasing fitness, and thus individual strategies aimed at preventing pathogen infections, either in an individual or their offspring, should be favoured by natural selection. The mineral fraction and some organic compounds in the shells of bird eggs are considered physical and chemical barriers against pathogen penetration to the embryo. However, eggshell pigment deposition has only recently been considered as a mechanism to resist pathogen penetration into the egg. By wiping the eggshell surface, the amount of pigment and some cuticle proteins were experimentally manipulated for the first time in nature. The effects on egg hatchability and offspring viability measured as nestling condition, immunocompetence and probability of recruitment were investigated in the common kestrel Falco tinnunculus. Protoporphyrin IX and biliverdin IXα to a lesser extent were the only identified pigments. The concentration of protoporphyrin IX and cuticle proteins were significantly reduced in the wiped with respect to the control treatment. Our study shows no evidence of a detrimental effect of the reduction of eggshell pigments on egg hatchability, mortality of the chicks during the nesting period, nestling body condition, nestling local immune response to PHA antigen or probability of recruitment. Further research will be necessary to elucidate the direct role of protoporphyrins and other pigments in egg bacterial infection.     

Genetics of Lipid-Storage Management in Caenorhabditis elegans Embryos

Lipids play a pivotal role in embryogenesis as structural components of cellular membranes, as a source of energy, and as signaling molecules. On the basis of a collection of temperature-sensitive embryonic lethal mutants, a systematic database search, and a subsequent microscopic analysis of >300 interference RNA (RNAi)–treated/mutant worms, we identified a couple of evolutionary conserved genes associated with lipid storage in Caenorhabditis elegans embryos. The genes include cpl-1 (cathepsin L–like cysteine protease), ccz-1 (guanine nucleotide exchange factor subunit), and asm-3 (acid sphingomyelinase), which is closely related to the human Niemann-Pick disease–causing gene SMPD1. The respective mutant embryos accumulate enlarged droplets of neutral lipids (cpl-1) and yolk-containing lipid droplets (ccz-1) or have larger genuine lipid droplets (asm-3). The asm-3 mutant embryos additionally showed an enhanced resistance against C band ultraviolet (UV-C) light. Herein we propose that cpl-1, ccz-1, and asm-3 are genes required for the processing of lipid-containing droplets in C. elegans embryos. Owing to the high levels of conservation, the identified genes are also useful in studies of embryonic lipid storage in other organisms.