Willow bud and shoot foraging by ptarmigan in relation to snow level in NW Finnish Lapland

Willow buds and twigs compose the main part of the willow ptarmigan’s (Lagopus lagopus) diet during winter. This study evaluated how position of willow ramets in relation to snow level affects the browsing of willow ptarmigan in NW Finland. Ramet position in relation to snow level affected the browsing intensity of willow ptarmigan: 5% of shoots were cut and more than 8% of buds were eaten by willow ptarmigan when ramet was staked at the maximum snow level, whereas ramets bent down were unbrowsed and browsing of ramets staked upright was negligible. Browsing significantly decreased the number of vegetative buds and catkins. The results show that snow level and ramet characteristics are important determinants of willow ptarmigan foraging.     

Comparison of sialylated N‐glycopeptide levels in serum of pancreatic cancer patients,acute pancreatitis patients,and healthy controls

Serum protein glycosylation is known to be affected by pathological conditions, including cancer and inflammatory diseases. Pancreatic cancer patients would benefit from early diagnosis, as the disease is often detected in an advanced stage and has poor prognosis. Searching for changes in serum protein site‐specific glycosylation could reveal novel glycoprotein biomarkers. We used Sambucus nigra lectin affinity chromatography to enrich α‐2,6 sialylated tryptic N‐glycopeptides from albumin‐depleted sera of pancreatic cancer patients, acute pancreatitis patients, and healthy individuals, and compared their relative abundance using ultra performance LC‐MS. Relative quantitation was done using the spectrum processing software MZmine. Identification was performed on the web‐based tool GlycopeptideID, developed for in silico analysis of intact N‐glycopeptides. Seventeen high‐abundance serum proteins, mainly acute‐phase proteins, and immunoglobulins, with total 27 N‐glycosylation sites, and 62 glycoforms, were identified. Pancreatitis patient sera contained 38, and pancreatic cancer patients sera contained 13 glycoform changes with statistical significance (p < 0.05). In pancreatitis, up to tenfold changes were found in some glycoforms, and in pancreatic cancer, threefold. Analysis showed that the changes often concerned one or two, but not all, N‐glycosylation sites in a specific glycoprotein. In conclusion, the analysis shows that pancreatic cancer, and acute pancreatitis are associated with changes in concentrations of intact sialylated N‐glycopeptides derived from acute‐phase proteins, and immunoglobulins, and that changes are site specific.     

Leptin receptor Arg109 homozygotes display decreased total mortality as well as lower incidence of cardiovascular disease and related death

Two leptin receptor single nucleotide polymorphisms, Lys109Arg and Gln223Arg, have been shown to associate with several risk factors for cardiovascular disease. In addition, we have previously shown that Arg109 and Arg223 homozygotes displayed lower intima-media thickness in our well-defined OPERA (Oulu Project Elucidating Risk of Atherosclerosis) study. This current research investigated the impact of these LEPR polymorphisms on cardiovascular events and related death as well as to total mortality in the 19-year follow-up of OPERA. Subjects were randomly selected, middle-aged drug-treated hypertensives and their age- and sex-matched control subjects recruited to the OPERA study between 1990 and 1993. Mortality and hospital events of 1045 subjects were followed up until 2009. A total of 151 coronary heart disease (CHD) and 211 cardiovascular disease (CVD) events or deaths including 58 CHD and 69 CVD deaths occurred. Furthermore, during this follow-up, a total of 165 subjects died. Logistic regression analysis was performed to assess the impact of Lys109Arg and Gln223Arg on the events and death. Further modeling was performed with Cox regression for Lys109Arg. The logistic regression analysis revealed a significant protective impact of Arg109Arg genotype on CHD (OR 0.433; CI 95% 0.217–0.863) and CVD (OR 0.540; CI 95% 0.309–0.942) events or death as well as on total mortality (OR 0.390; CI 95% 0.196–0.775) when adjusted with age, sex and study group. Even after further adjustment with BMI, smoking status, systolic blood pressure and low-density lipoprotein cholesterol, the protective effect of Arg109Arg on CHD events or death and total mortality still remained statistically significant (OR 0.463; CI 95% 0.230–0.931 and OR 0.442; CI 95% 0.218–0.896, respectively). Arg109Arg was also shown to confer protection against CHD mortality (HR 0.224; CI95% 0.055–0.919) and overall mortality (HR 0.413; CI95% 0.218–0.783) also in Cox regression analysis. In conclusion, the Arg109Arg genotype of LEPR seems to be protective from cardiovascular events and death and this phenomenon seems to be independent of the traditional risk factors for atherosclerosis.     

Chronic Total Occlusions in Sweden – A Report from the Swedish Coronary Angiography and Angioplasty Registry (SCAAR)

Introduction

Evidence for the current guidelines for the treatment of patients with chronic total occlusions (CTO) in coronary arteries is limited. In this study we identified all CTO patients registered in the Swedish Coronary Angiography and Angioplasty Registry (SCAAR) and studied the prevalence, patient characteristics and treatment decisions for CTO in Sweden.

Methods and Results

Between January 2005 and January 2012, 276,931 procedures (coronary angiography or percutaneous coronary intervention) were performed in 215,836 patients registered in SCAAR. We identified all patients who had 100% luminal diameter stenosis known or assumed to be ≥3 months old. After exclusion of patients with previous coronary artery bypass graft (CABG) surgery or coronary occlusions due to acute coronary syndrome, we identified 16,818 CTO patients. A CTO was present in 10.9% of all coronary angiographies and in 16.0% of patients with coronary artery disease. The majority of CTO patients were treated conservatively and PCI of CTO accounted for only 5.8% of all PCI procedures. CTO patients with diabetes and multivessel disease were more likely to be referred to CABG.

Conclusion

CTO is a common finding in Swedish patients undergoing coronary angiography but the number of CTO procedures in Sweden is low. Patients with CTO are a high-risk subgroup of patients with coronary artery disease. SCAAR has the largest register of CTO patients and therefore may be valuable for studies of clinical importance of CTO and optimal treatment for CTO patients.     

Apelin Increases Cardiac Contractility via Protein Kinase Cε- and Extracellular Signal-Regulated Kinase-Dependent Mechanisms

Background

Apelin, the endogenous ligand for the G protein-coupled apelin receptor, is an important regulator of the cardiovascular homoeostasis. We previously demonstrated that apelin is one of the most potent endogenous stimulators of cardiac contractility; however, its underlying signaling mechanisms remain largely elusive. In this study we characterized the contribution of protein kinase C (PKC), extracellular signal-regulated kinase 1/2 (ERK1/2) and myosin light chain kinase (MLCK) to the positive inotropic effect of apelin.

Methods and Results

In isolated perfused rat hearts, apelin increased contractility in association with activation of prosurvival kinases PKC and ERK1/2. Apelin induced a transient increase in the translocation of PKCε, but not PKCα, from the cytosol to the particulate fraction, and a sustained increase in the phosphorylation of ERK1/2 in the left ventricle. Suppression of ERK1/2 activation diminished the apelin-induced increase in contractility. Although pharmacological inhibition of PKC attenuated the inotropic response to apelin, it had no effect on ERK1/2 phosphorylation. Moreover, the apelin-induced positive inotropic effect was significantly decreased by inhibition of MLCK, a kinase that increases myofilament Ca²⁺ sensitivity.

Conclusions

Apelin increases cardiac contractility through parallel and independent activation of PKCε and ERK1/2 signaling in the adult rat heart. Additionally MLCK activation represents a downstream mechanism in apelin signaling. Our data suggest that, in addition to their role in cytoprotection, modest activation of PKCε and ERK1/2 signaling improve contractile function, therefore these pathways represent attractive possible targets in the treatment of heart failure.     

Diversity and Community Structure of Primary Wood-Inhabiting Bacteria in Boreal Forest

DNA-based pyrosequencing analysis of the V1- V3 16S rRNA gene region was used to identify bacteria community and shift during early stages of wood colonization in boreal forest soils. The dataset comprised 142,447 sequences and was affiliated to 11 bacteria phyla, 25 classes and 233 genera. The dominant groups across all samples were Proteobacteria, followed by Bacteroidetes, Acidobacteria, Actinobacteria, Amatimonadetes, Planctomycetes and TM7 group. The community structure of the primary wood-inhabiting bacteria differed between types of forest soils and the composition of bacteria remained stable over prolonged incubation time. The results suggest that variations in soil bacterial community composition have an influence on the wood-inhabiting bacterial structure.     

Structure and dynamics of dioxygen bound to cobalt and iron heme

In this study we use ab initio molecular dynamics simulations to analyze the structure and dynamics of the oxygen ligand in models of the oxymyoglobin active site and its cobalt-substituted analog. Our calculations are performed for iron-porphyrin and cobalt-porphyrin complexes with imidazole and oxygen as axial ligands, and we investigate the effect of the distal histidine in the structure and dynamics of the metal-oxygen unit (MeO(2), Me = Fe, Co). We find that the interaction between the distal histidine and the oxygen ligand is stronger for the cobalt complex than for the iron one, consistent with the superoxide ion character of the bound O(2). The dynamics of the O(2) ligand can be described as oscillations of the O-O axis projection on the porphyrin plane within a porphyrin quadrant combined with frequent jumps from one quadrant to another. However, the ligand motion is significantly faster for CoO(2) compared to FeO(2). As a result, the iron complex shows localized ligand sites, whereas for cobalt several configurations are possible. This gives support to the highly dynamic motion of the oxygen ligand found in several experiments on cobalt oxymyoglobin and model complexes and underlines the higher mobility of the CoO(2) fragment compared to FeO(2).     

Increased sensitivity of homozygous Sod2 mutant mice to oxygen toxicity.

Induction or overexpression of pulmonary manganese superoxide dismutase (MnSOD) has been shown to protect against oxygen (O2) toxicity. Genetic inactivation of MnSOD (Sod2) results in multiple organ failure and early neonatal death. However, lungs or O2-tolerance of Sod2 knockout mice have not been investigated. We evaluated survival, lung histopathology, and other pulmonary antioxidants (glutathione cycle) of homozygous (-/-) and heterozygous (+/-) Sod2 mutant mice compared with wild-type controls (Sod2+/+) following 48 h exposure to either room air or to O2. The ability of antioxidant N-acetylcysteine to compensate for the loss of MnSOD was explored. Mortality of Sod2-/- mice increased from 0% in room air to 18 and 83% in 50 and 80% O2, respectively. N-acetylcysteine did not alter mortality of Sod2-/- mice. Histopathological analysis revealed abnormalities in saccules of Sod2-/- mice exposed either to room air or to 50% O2 suggestive of delayed postnatal lung development. In 50% O2, activities of glutamate-cysteine ligase (GCL) (previously known as gamma-glutamylcysteine synthetase, gamma-GCS) and glutathione peroxidase increased in Sod2-/- (35 and 70%, respectively) and Sod2+/- (12 and 70%, respectively) mice, but glutathione levels remained unaltered. We conclude that MnSOD is required for normal O2 tolerance and that in the absence of MnSOD there is a compensatory increase in pulmonary glutathione-dependent antioxidant defense in hyperoxia.     

Critical temperatures for xylogenesis in conifers of cold climates

Aim To identify temperatures at which cell division and differentiation are active in order to verify the existence of a common critical temperature determining growth in conifers of cold climates. Location Ten European and Canadian sites at different latitudes and altitudes. Methods The periods of cambial activity and cell differentiation were assessed on a weekly time‐scale on histological sections of cambium and wood tissue collected over 2 to 5 years per site from 1998 to 2005 from the stems of seven conifer species. All data were compared with daily air temperatures recorded from weather stations located close to the sites. Logistic regressions were used to calculate the probability of xylogenesis and of cambium being active at a given temperature. Results Xylogenesis lasted from May to October, with a growing period varying from 3 to 5 months depending on location and elevation. Despite the wide geographical range of the monitored sites, temperatures for onset and ending of xylogenesis converged towards narrow ranges with average values around 4–5, 8–9 and 13–14 °C for daily minimum, mean and maximum temperature, respectively. On the contrary, cell division in the cambium stopped in July?August, when temperatures were still high. Main conclusions Wood formation in conifers occurred when specific critical temperatures were reached. Although the timing and duration of xylogenesis varied among species, sites and years, the estimated temperatures were stable for all trees studied. These results provide biologically based evidence that temperature is a critical factor limiting production and differentiation of xylem cells in cold climates. Although daily temperatures below 4?5 °C are still favourable for photosynthesis, thermal conditions below these values could inhibit the allocation of assimilated carbon to structural investment, i.e. xylem growth.