Microbial community composition but not diversity changes along succession in arctic sand dunes

The generality of increasing diversity of fungi and bacteria across arctic sand dune succession was tested. Microbial communities were examined by high‐throughput sequencing of 16S rRNA genes (bacteria) and internal transcribed spacer (ITS) regions (fungi). We studied four microbial compartments (inside leaf, inside root, rhizosphere and bulk soil) and characterized microbes associated with a single plant species (Deschampsia flexuosa) across two sand dune successional stages (early and late). Bacterial richness increased across succession in bulk soil and leaf endosphere. In contrast, soil fungal richness remained constant while root endosphere fungal richness increased across succession. There was, however, no significant difference in Shannon diversity indices between early and late successional stage in any compartment. There was a significant difference in the composition of microbial communities between early and late successional stage in all compartments, although the major microbial OTUs were shared between early and late successional stage. Co‐occurrence network analysis revealed successional stage‐specific microbial groups. There were more co‐occurring modules in early successional stage than in late stage. Altogether, these results emphasize that succession strongly affects distribution of microbial species, but not microbial diversity in arctic sand dune ecosystem and that fungi and bacteria may not follow the same successional trajectories.     

Dietary pattern and 20 year mortality in elderly men in Finland,Italy, and The Netherlands: longitudinal cohort study.

OBJECTIVE: To investigate the association of dietary pattern and mortality in international data. DESIGN: Cohort study with 20 years'' follow up of mortality. SETTING: Five cohorts in Finland, the Netherlands, and Italy. SUBJECTS: Population based random sample of 3045 men aged 50-70 years in 1970. MAIN OUTCOME MEASURES: Food intake was estimated using a cross check dietary history. In this dietary survey method, the usual food consumption pattern in the 6-12 months is estimated. A healthy diet indicator was calculated for the dietary pattern, using the World Health Organisation''s guidelines for the prevention of chronic diseases. Vital status was verified after 20 years of follow up, and death rates were calculated. RESULTS: Dietary intake varied greatly in 1970 between the three countries. In Finland and the Netherlands the intake of saturated fatty acids and cholesterol was high and the intake of alcohol was low; in Italy the opposite was observed. In total 1796 men (59%) died during 20 years of follow up. The healthy diet indicator was inversely associated with mortality (P for trend < 0.05). After adjustment for age, smoking, and alcohol consumption, the relative risk in the group with the healthiest diet indicator compared with the group with the least healthy was 0.87 (95% confidence interval 0.77 to 0.98). Estimated relative risks were essentially similar within each country. CONCLUSIONS: Dietary intake of men aged 50-70 is associated with a 20 year, all cause mortality in different cultures. The healthy diet indicator is useful in evaluating the relation of mortality to dietary patterns.     

Energy Use and Greenhouse Gas Emissions of Air‐Source Heat Pump and Innovative Ground‐Source Air Heat Pump in a Cold Climate

This article compares climate impacts of two heat‐pump systems for domestic heating, that is, energy consumption for space heating of a residential building. Using a life cycle approach, the study compared the energy use and greenhouse gas (GHG) emissions of direct electric heating, a conventional air‐source heat pump, and a novel ground‐source air heat pump innovated by a citizen user, to assess whether such user innovation holds benefit. The energy use of the heat pumps was modeled at six temperature intervals based on duration curves of outdoor temperature. Additionally, two heat pump end‐of‐life scenarios were analyzed. Probabilistic uncertainty analysis was applied using a Monte Carlo simulation. The results indicated that, in ideal conditions, that is, assuming perfect air mixing, the conventional air‐source heat pump's emissions were over 40% lower and the ground‐air heat pump's emissions over 70% lower than in the case of direct electric heating. Although proper handling of the refrigerant is important, total leakage from the retirement of the heat‐pump appliance would increase GHG emissions by just 10%. According to the sensitivity analysis, the most influential input parameters are the emission factor related to electricity and the amount of electricity used for heating.     

Calpains promote α2β1 integrin turnover in nonrecycling integrin pathway

Collagen receptor integrins recycle between the plasma membrane and endosomes and facilitate formation and turnover of focal adhesions. In contrast, clustering of α2β1 integrin with antibodies or the human pathogen echovirus 1 (EV1) causes redistribution of α2 integrin to perinuclear multivesicular bodies, α2-MVBs. We show here that the internalized clustered α2 integrin remains in α2-MVBs and is not recycled back to the plasma membrane. Instead, receptor clustering and internalization lead to an accelerated down-regulation of α2β1 integrin compared to the slow turnover of unclustered α2 integrin. EV1 infection or integrin degradation is not associated with proteasomal or autophagosomal processes and shows no significant association with lysosomal pathway. In contrast, degradation is dependent on calpains, such that it is blocked by calpain inhibitors. We show that active calpain is present in α2-MVBs, internalized clustered α2β1 integrin coprecipitates with calpain-1, and calpain enzymes can degrade α2β1 integrin. In conclusion, we identified a novel virus- and clustering-specific pathway that diverts α2β1 integrin from its normal endo/exocytic traffic to a nonrecycling, calpain-dependent degradative endosomal route.     

Relation between mortality and treated blood pressure in elderly patients with hypertension: report of the European Working Party on High Blood Pressure in the Elderly.

OBJECTIVE--To investigate the relation between mortality and treated systolic and diastolic blood pressures. DESIGN--Randomised double blind placebo controlled trial. Mortality in the two treatment groups was examined in thirds of treated systolic and diastolic blood pressures. PATIENTS--339 And 352 patients allocated to placebo and active treatment, respectively. The groups were similar at randomisation in sex ratio (70% women), mean age (71.5 years), blood pressure (182/101 mm Hg), and proportion of patients with cardiovascular complications (35%). MEASUREMENTS AND MAIN RESULTS--In the placebo group total mortality rose with increasing systolic pressure whereas it had a U shaped relation with diastolic pressure, the total lowest mortality being in patients in the middle third of the distribution of diastolic pressure. In the group given active treatment total mortality showed a U shaped relation with systolic pressure and an inverse association with treated diastolic pressure. In both groups cardiovascular and non-cardiovascular mortality followed the same trends as total mortality. The increased mortality in the lowest thirds of pressure was not associated with an increased proportion of patients with cardiovascular complications at randomisation or with a fall in diastolic pressure exceeding the median fall in pressure in each group. In contrast, patients in the lowest thirds of pressure showed greater decreases in body weight and haemoglobin concentration than those in the middle and upper thirds of pressure. CONCLUSIONS--In patients taking active treatment total mortality was increased in the lowest thirds of treated systolic and diastolic blood pressures. This increased mortality is not necessarily explained by an exaggerated reduction in pressure induced by drugs as for diastolic pressure a U shaped relation also existed during treatment with placebo. In addition, patients in the lowest thirds of systolic and diastolic pressures were characterised by decreases in body weight and haemoglobin concentration, and the patients in the lowest thirds of diastolic pressure taking active treatment also by an increased non-cardiovascular mortality, suggesting some deterioration of general health.     

Genotypes with the apolipoprotein ε4 allele are predictors of coronary heart disease mortality in a longitudinal study of elderly Finnish men

Earlier we reported that allelic variation in the gene coding for apolipoprotein (apoE) is a significant predictor of variation in the risk of coronary heart disease (CHD) death in a longitudinal study of elderly Finnish men. Here we address the question: which of the apoE genotypes confers the risk information in these men, and whether such information persists after other CHD risk factors are considered? We followed two cohorts of elderly Finnish men aged 65 to 84 years, one in Eastern (n = 281) and the other in the Southwestern (n = 344) Finland for 5 years during which 26 (9.3%) of the men from the Eastern cohort and 40 (11.6%) of the men in the Southwestern cohort died from CHD. Baseline high density lipoprotein (HDL) cholesterol and (HDL cholesterol)² in the Eastern cohort and age, and total and HDL cholesterol and smoking status in the Southwestern cohort were significant predictors of CHD death (P < 0.05). The apoE genotypes were significant predictors in the Southwestern cohort atP = 0.02 and in the Eastern cohort atP = 0.18. In multivariable models, information about apoE genotypes improved the prediction atP = 0.10 level of statistical significance in both cohorts. When genotypes were considered separately, the ε2/4 combined with the ε4/4 in the Eastern cohort (odds ratio = 7.69, 95% CI = 1.67-35.52) and the ε3/4 in the Southwestern cohort (odds ratio = 2.44, 95% CI = 1.16–5.10) had sigificanctly greater odds of CHD death compared to the common ε3/3 genotype. We conclude that apoE genotypes confer risk information about CHD death in two cohorts of elderly Finnish men in a longitudinal study, and this information persists after adjustment for other CHD risk factors. Because different genotypes were predictors in these two cohorts, we further conclude that the utility of a particular genotype as a predictor of CHD death in other populations may depend on the distribution of risk factor profiles at baseline, geographically defined environmental exposures, the CHD mortality history, and the evolutionary history of background genotypes in the population considered.     

Familial aggregation of body mass index: a population-based family study in eastern Finland.

In this study, we investigated the familial aggregation of body mass index (BMI) in a sample of families with young offspring from eastern Finland. 15-year-olds were examined from 1996 to 1997, and their biological parents were examined from 1993 to 1994. 224 children were invited; 184 families participated, and 144 were included in the analysis with complete data. Significant positive correlations were found for mother-offspring pairs (correlation [r] = 0.31, p < 0.001, n = 140), father-offspring (r = 0.23, p = 0.017, n = 107), mother-daughter (r = 0.26, p = 0.044, n = 63) and mother-son (r = 0.36, p = 0.001, n = 77). Adjustment for confounding variables did not alter these results. There was a higher proportion of children in the highest quartile of BMI when the mother was obese (odds ratio [OR] = 3.0, 95 % CI = 1.4 - 6.7, n = 140) and when one or both parents were obese (OR = 2.8, 95 % CI = 1.0 - 8.0 when one parent was obese; OR = 4.6, 95 % CI = 1.1 - 20.0 when both parents were obese; n = 103). The study confirmed familial BMI aggregation. The consistent obesity relationship between mother and offspring may indicate the key role of the mother in primary obesity prevention.     

Reexpression of HPRT activity following cell fusion with polyethylene glycol

Polyethylene glycol-1000 (PEG-1000) induced fusion of HPRT (E.C. 2.4.2.8) deficient Chinese hamster cells with -galactosidase A (E.C. 2.3.1.22) deficient cells from a patient with Fabry's disease yielded hybrids which contained both human and hamster HPRT, G6PD (E.C. 1.1.1.49), and APRT (E.C. 2.4.2.7) and Chinese hamster -galactosidase B. Thus PEG-1000 mediated somatic cell fusion led to reexpression of Chinese hamster HPRT. It did not restore the expression of human -galactosidase. Since PEG-1000 treatment of HPRT^– Chinese hamster cells in the absence of human cells yielded no HPRT⁺ cells, it is concluded that the element responsible for the restoration of rodent HPRT was contributed by the human cells and not by the agent employed to promote fusion.This work was supported by research grants from the United States Public Health Services GM 17702, from the National Science Foundation BMS 74-21424, and from the National Foundation March of Dimes 1-377.     

Short feeding period of carrot psyllid (Trioza apicalis) females at early growth stages of carrot reduces yield and causes leaf discolouration

Overwintered adult carrot psyllids [Trioza apicalis Förster (Homoptera: Psylloidea: Triozidae)] damage carrot [(Daucus carota ssp. sativum L.) (Apiaceae)] seedlings by phloem feeding on the leaves. The aim of this study was to investigate the carrot root and shoot growth in relation to carrot psyllid density during early growth stages. One, two, or three carrot psyllids were allowed to feed on carrot seedlings for 3 days. Leaf damage was measured at the 8‐leaf stage, and root, leaf fresh weight, and number of true leaves were measured at harvest. Both the age of the carrot seedling at infestation and the psyllid density had a significant effect on leaf damage at the 8‐leaf stage: seedlings damaged at the cotyledon stage exhibited more leaf damage than seedlings damaged at the 1‐leaf stage. A higher psyllid density significantly reduced the carrot root weight at harvest. The significant interaction of psyllid density with seedling age indicates that differently aged carrot seedlings responded differently to feeding: one psyllid feeding for 3 days at the cotyledon stage caused a significant yield loss, whereas three psyllids were needed to cause the same impact at the 1‐leaf stage. Carrot leaf weight at harvest was not reduced by carrot psyllid feeding: leaves recovered from the damage but roots did not. Our results confirm the farmers’ observations that a trap replacement period of 1 week for carrot psyllid monitoring is too long, especially at the cotyledon stage. Severe leaf discolouration on damaged carrots was observed at harvest. The possible reasons for this discolouration, such as toxin excreted in psyllid saliva or plant pathogenic mycoplasma infection, are discussed.     

Apple proteins that interact with DspA/E, a pathogenicity effector of Erwinia amylovora, the fire blight pathogen

The disease-specific (dsp) gene dspA/E of Erwinia amylovora encodes an essential pathogenicity effector of 198 kDa, which is critical to the development of the devastating plant disease fire blight. A yeast two-hybrid assay and in vitro protein pull-down assay demonstrated that DspA/E interacts physically and specifically with four similar putative leucine-rich repeat (LRR) receptor-like serine/threonine kinases (RLK) from apple, an important host of E. amylovora. The genes encoding these four DspA/E-interacting proteins of Malus xdomestica (DIPM1 to 4) are conserved in all genera of hosts of E. amylovora tested. They also are conserved in all cultivars of apple tested that range in susceptibility to fire blight from highly susceptible to highly resistant. The four DIPMs have been characterized, and they are expressed constitutively in host plants. In silico analysis indicated that the DIPMs have similar sequence structure and resemble LRR RLKs from other organisms. Evidence is presented for direct physical interaction between DspA/E and the apple proteins encoded by the four identified clones, which may act as susceptibility factors and be essential to disease development. Knowledge of DIPMs and the interaction with DspA/E thus may facilitate understanding of fire blight development and lead to new approaches to control of disease.