The glucose-dependent insulinotropic polypeptide (GIP) regulates body weight and food intake via CNS-GIPR signaling

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Individual optimization: Mechanisms shaping the optimal reaction norm

In general, optimal reaction norms in heterogeneous populations can be obtained only by iterative numerical procedures (McNamara, 1991; Kawecki and Stearns, 1993). We consider two particular, but biologically plausible and analytically tractable cases of individual optimization to gain insight into the mechanisms which shape the optimal reaction norm of fecundity in relation to an environmental variable or an individual trait. In the first case, we assume that the quality of the environment (e.g. food abundance) or the quality of the individual (e.g. body size) is fixed during its entire life; it may also be a heritable individual trait. In the second case, individual quality is assumed to change randomly such that the probability distribution of quality in the next year is the same for the parent and for her offspring. For these two cases, we obtain analytical expressions for the shape of the optimal reaction norm, which are heuristically interpretable in terms of underlying selective mechanisms. It is shown that better quality may reduce the optimal fecundity. This outcome is particularly likely if better quality increases a fecundity-independent factor of parental survival in a long-lived species with fixed quality. This revised version was published online in July 2006 with corrections to the Cover Date.     

Distribution and Forest Utilization of Saguinus and Other Primates of the Pando Department, Northern Bolivia

We carried out a 4-month census of primates in the Pando Department of northern Bolivia with special emphasis on Saguinus species. Contrary to a previous report by Izawa and Bejarano (1981), there was no evidence for the presence of the two populations of Saguinus mystax that they reported, or that Lagothrix occurs in the Pando. In addition, we found the distribution of Saguinus imperator to be more restricted than they suggested. We confirm the presence of Cebuella south of the Río Tahuamanu (cf. Brown and Rumiz, 1986) and report two new locations for Callimico goeldii. We present data on group sizes, habitat utilization, and locomotor behavior of the primates and compare them with previous studies in the Pando. Differences in body size, diet, foraging techniques, and vertical use of the forest appear to be key factors in both sympatry and in the formation of polyspecific associations.     

Wettability of juvenile plumage as a major cause of mortality threatens endangered Barau's petrel

Seabirds spend most of their life at sea and have to possess a waterproof plumage to be able to sit on water for extended periods. We tracked juvenile Barau's petrels for the first time, when they leave their birth colony and found that half of the transmitters stopped soon after they first landed on the water off Réunion Island. We suspected from observation at sea that birds may have problems with the waterproofness of their plumage. Therefore during the next season we set up a simple protocol to assess waterproofness of the plumage of the birds just before they fledge. This protocol is based on the calculation of a wettability index expressed as the mass of water logged in the plumage after simulating the bird sitting on the sea surface. We found that at least one third of chicks ready to fledge gained more than 4 g of water in 20 s, indicating that plumage was not waterproof. Within a sample of birds having fledged and before reaching the sea surface, a similar proportion of birds had their plumage not waterproof. For the birds tracked, only those with an index indicating a waterproof plumage successfully dispersed after their first touch on the sea surface. We provide evidence of a possible major cause of mortality of juvenile seabirds that has not been described previously in wild seabirds, but could exist in other species. This issue may be a major cause of threat to the endangered Barau's petrel.     

Review of Mathematical Models Describing the Mechanical Motion in a DNA Molecule

Biophysics - Several mechanical models that reproduce the DNA structure were considered. Evolution was described in more detail for the mechanical model proposed for a DNA molecule by Englander,...     

From Metabolomics to Fluxomics: A Computational Procedure to Translate Metabolite Profiles into Metabolic Fluxes

We describe a believed-novel procedure for translating metabolite profiles (metabolome) into the set of metabolic fluxes (fluxome) from which they originated. Methodologically, computational modeling is integrated with an analytical platform comprising linear optimization, continuation and dynamic analyses, and metabolic control. The procedure was tested with metabolite profiles obtained from ex vivo mice Langendorff-heart preparations perfused with glucose. The metabolic profiles were analyzed using a detailed kinetic model of the glucose catabolic pathways including glycolysis, pentose phosphate (PP), glycogenolysis, and polyols to translate the glucose metabolome of the heart into the fluxome. After optimization, the ability of the model to simulate the initial metabolite profile was confirmed, and metabolic fluxes as well as the structure of control and regulation of the glucose catabolic network could be calculated. We show that the step catalyzed by phosphofructokinase together with ATP demand and glycogenolysis exert the highest control on the glycolytic flux. The negative flux control exerted by phosphofructokinase on the PP and polyol pathways revealed that the extent of glycolytic flux directly affects flux redirection through these pathways, i.e., the higher the glycolytic flux the lower the PP and polyols. This believed-novel methodological approach represents a step forward that may help in designing therapeutic strategies targeted to diagnose, prevent, and treat metabolic diseases.     

Loss of tenomodulin expression is a risk factor for age‐related intervertebral disc degeneration

The intervertebral disc (IVD) degeneration is thought to be closely related to ingrowth of new blood vessels. However, the impact of anti‐angiogenic factors in the maintenance of IVD avascularity remains unknown. Tenomodulin (Tnmd) is a tendon/ligament‐specific marker and anti‐angiogenic factor with abundant expression in the IVD. It is still unclear whether Tnmd contributes to the maintenance of IVD homeostasis, acting to inhibit vascular ingrowth into this normally avascular tissue. Herein, we investigated whether IVD degeneration could be induced spontaneously by the absence of Tnmd. Our results showed that Tnmd was expressed in an age‐dependent manner primarily in the outer annulus fibrous (OAF) and it was downregulated at 6 months of age corresponding to the early IVD degeneration stage in mice. Tnmd knockout (Tnmd^?/?) mice exhibited more rapid progression of age‐related IVD degeneration. These signs include smaller collagen fibril diameter, markedly lower compressive stiffness, reduced multiple IVD‐ and tendon/ligament‐related gene expression, induced angiogenesis, and macrophage infiltration in OAF, as well as more hypertrophic‐like chondrocytes in the nucleus pulposus. In addition, Tnmd and chondromodulin I (Chm1, the only homologous gene to Tnmd) double knockout (Tnmd^?/?Chm1^?/?) mice displayed not only accelerated IVD degeneration, but also ectopic bone formation of IVD. Lastly, the absence of Tnmd in OAF‐derived cells promoted p65 and matrix metalloproteinases upregulation, and increased migratory capacity of human umbilical vein endothelial cells. In sum, our data provide clear evidences that Tnmd acts as an angiogenic inhibitor in the IVD homeostasis and protects against age‐related IVD degeneration. Targeting Tnmd may represent a novel therapeutic strategy for attenuating age‐related IVD degeneration.