“Ghosts of the past”: flightless saproxylic weevils (Coleoptera: Curculionidae) are relict species in ancient woodlands

Historic maps show that the Central European landscape was influenced by exploitive human land-use during the middle ages and in the following centuries. A mixture of ancient woodlands, which survived the period of woodland destruction, and recent woodlands, which were established after 1800, cover about 10% of the study area in NW Germany today. Weevils (Coleoptera: Curculionidae) of the subfamily Cryptorhynchinae with the genera Acalles, Kyklioacalles, Ruteria and of the subfamily Molytinae, tribe Acicnemidini with the genus Trachodes are all flightless and possibly influenced by landscape history. The aims of this investigation are (1) to examine the spatial distribution of flightless saproxylic weevils in ancient and recent woodlands in NW Germany and (2) to test the frequency of possible relict species in relation to historical and current woodland size. Based on a field study in 29 deciduous woodlands and species records in collections and literature, six flightless saproxylic weevils were found to be associated with ancient woodlands in NW Germany. None of these were recorded in any of the 14 recent woodlands studied. The frequency of these relict species is correlated with historical, but not with current, woodland size. Distribution maps for Lower Saxony and data on the phenology of the relict species are presented. These weevils are relict species of ancient woodland, because they were unable to colonise isolated woods that were established after 1800. All of them are dependent on dead or dying wood for larval development. The results show that ancient broadleaved woodlands with long-lasting habitat continuity are of high conservation value for invertebrate species such as saproxylic weevils.     

Closed loop control of human body temperature: results from a one-dimensional model

A one-dimensional model of human thermoregulation is used to solve a variety of basic problems in determining an adequate structure of the controller for metabolic heat production, skin blood flow and sweat production. Assuming one integrated central and one integrated peripheral afferent signal the controller parameters are evaluated by analysis of the control performance. Based on a validation by experimental results this allows the determination of a first optimized set of values for controller gains and weight of skin temperature feedback. Furthermove we analyse the effect of inhomogeneous distribution of heat production and blood flow, the influence of body fat content, of controller gains, of weight of skin temperature feedback and of depth of peripheral receptors on the dynamic performance. Increase of peripheral blood flow in particular evokes essentially both an increase of energy requirement in the cold and a quicker system response. Differing rates of increase of metabolic heat production are the consequence of differing body fat content. The weight of skin temperature feedback can be limited to 5...20%, because values outside this range evoke dynamic responses incompatible with the experiments. The actual value can only be determined if there is a correct assumption for the depth of the skin receptors. The use of measured superficial skin temperatures brings about an underestimation of the peripheral afferent signal. Of the controller gains it is primarily the gain of the metabolic controller which affects the dynamic response of the system. The experimental fact of a delayed onset of sweat production after a transition from cold to heat is the consequence of a high gain of the vasomotor system.     

Temperature profiles with respect to inhomogeneity and geometry of the human body

Temperature profiles within the human body are highly dependent on the geometry and inhomogeneity of the body. Physical parameters such as density and heat conductivity of the various tissues and variables such as blood flow and metabolic heat production of different organs are spatially distributed and thereby influence the temperature profiles within the human body. Actual physiological knowledge allows one to take into account up to 54 different spatially distributed values for each parameter. An adequate representation of the anatomy of the body requires a spatial three-dimensional grid of at least 0.5-1.0 cm. This is achieved by photogrammetric treatment of three-dimensional anatomic models of the human body. As a first essential result, the simulation system has produced a realistic picture of the topography of temperatures under neutral conditions. Compatibility of reality and simulation was achieved solely on the basis of physical considerations and physiological data base. Therefore the simulation is suited to the extrapolation of temperature profiles that cannot be obtained experimentally.     

Social complexity in bees is not sufficient to explain lack of reversions to solitary living over long time scales

Background  

The major lineages of eusocial insects, the ants, termites, stingless bees, honeybees and vespid wasps, all have ancient origins (≥ 65 mya) with no reversions to solitary behaviour. This has prompted the notion of a 'point of no return' whereby the evolutionary elaboration and integration of behavioural, genetic and morphological traits over a very long period of time leads to a situation where reversion to solitary living is no longer an evolutionary option.     

Mechanisms of high-glucose/insulin-mediated desensitization of acute insulin-stimulated glucose transport and Akt activation

High-glucose/low-dose insulin-mediated insulin resistance of glucose transport was studied in 3T3-L1 adipocytes. In this model, proximal insulin signaling, including insulin receptor substrate (IRS)-1-bound phosphatidylinositol 3-kinase (PI 3-kinase) activation, is preserved, but insulin-stimulated protein kinase B (Akt) activation is markedly impaired. To assess a difference in acute insulin-stimulated production of phosphatidylinositol 3,4,5-trisphosphate [PtdIns(3,4,5)P3], cells were labeled with [32P]orthophosphate, and glycerophosphoinositides were quantified by HPLC. Although basal PtdIns(3,4,5)P3 was similar, insulin stimulated its production 33.6% more in controls (P < 0.03) than in insulin-resistant cells. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) protein, a lipid phosphatase that dephosphorylates PtdIns(3,4,5)P3 in the 3-position, was significantly and specifically increased in insulin-resistant cells. Treatment with rapamycin [a specific inhibitor of mammalian target of rapamycin complex 1 (mTORC1)] inhibited the increased PTEN expression and partially restored insulin-stimulated glucose transport and Akt activation to insulin-resistant cells. Acute insulin markedly stimulated Ser(636/639) phosphorylation of IRS-1; this was rapamycin inhibited but was significantly decreased in cells that had been preexposed to insulin, whereas total IRS-1 was unaffected. These findings were essentially paralleled by changes in the activation of p70 S6 kinase and S6-ribosomal protein. Overexpression of uncoupling protein-1 or manganese superoxide dismutase did not prevent the development of insulin-resistant glucose transport and impaired Akt activation in high-glucose/low-insulin-pretreated cells. The insulin resistance associated with glucotoxicity in our model reflects in part decreased availability of PtdIns(3,4,5)P3, which correlates with increased PTEN protein expression. Chronic activation of mTORC1 plays a role in stimulating PTEN expression and possibly in activation or induction of a phosphoprotein phosphatase. No evidence was found for a role for increased mitochondrial superoxide production in this model.