A recurrent neural model for proto-object based contour integration and figure-ground segregation

Visual processing of objects makes use of both feedforward and feedback streams of information. However, the nature of feedback signals is largely unknown, as is the identity of the neuronal populations in lower visual areas that receive them. Here, we develop a recurrent neural model to address these questions in the context of contour integration and figure-ground segregation. A key feature of our model is the use of grouping neurons whose activity represents tentative objects (“proto-objects”) based on the integration of local feature information. Grouping neurons receive input from an organized set of local feature neurons, and project modulatory feedback to those same neurons. Additionally, inhibition at both the local feature level and the object representation level biases the interpretation of the visual scene in agreement with principles from Gestalt psychology. Our model explains several sets of neurophysiological results (Zhou et al. Journal of Neuroscience, 20(17), 6594–6611 2000; Qiu et al. Nature Neuroscience, 10(11), 1492–1499 2007; Chen et al. Neuron, 82(3), 682–694 2014), and makes testable predictions about the influence of neuronal feedback and attentional selection on neural responses across different visual areas. Our model also provides a framework for understanding how object-based attention is able to select both objects and the features associated with them.     

Mapping one of the 2 genes controlling lemon ray flower color in sunflower (Helianthus annuus L.)

In an F2 population of 120 plants derived from a cross between 2 breeding lines with yellow ray flowers, we observed 111 plants with yellow-colored and 9 plants with lemon-colored ray flowers. The segregation pattern fits a 15:1 (chi2(15:1) = 0.32, P > 0.5) ratio, suggesting that the lemon ray flower color is conditioned by 2 independent recessive genes that had been contributed individually by each of the parents. We sampled 111 plants from the 3 F(2:3) families displaying a 3 to 1 segregating ratio for genotyping with molecular markers. One of the genes, Yf(1), was mapped onto linkage group 11 of the public sunflower map. A targeted region amplified polymorphism marker (B26P17Trap13-68) had a genetic distance of 1.5 cM to Yf(1), and one simple sequence repeat marker (ORS733) and one expressed sequence tag (EST)-based marker (HT167) previously mapped to linkage group 11 were linked to Yf(1) with distances of 9.9 and 2.3 cM, respectively.     

An off-line filtering ditch–pond system for diffuse pollution control at Wuhan City Zoo

An off-line filtering ditch–pond system was designed and constructed to control the small point and runoff pollution at the Wuhan City Zoo, Hubei Province, China. The quantity and quality of wastewater discharge and runoff from 16 rainfall events were measured to test the effectiveness of the off-line treatment train. The results showed that the water quality was improved and high retention rates for water and pollutants were also achieved by the off-line treatment train. In the outflows, the event mean concentrations (EMCs) of TSS, COD, TN, TDN, TP and TDP were reduced by 75%, 50%, 50%, 57%, 74% and 80% compared to the inflows. In 2005, the annual inflow volume in the catchment was 6783 m³ and the water retention rate was 80.1%. The retention rates in the annual loads of TSS, COD, TN and TP came to 86.4%, 85.5%, 83.9% and 82.9%, respectively. Therefore, the off-line filtering ditch–pond system was shown to be an effective and economical measure to control diffuse pollution. It would be worthwhile to extend the off-line treatment train to regions with limited land resources, especially in urban areas.     

Biosynthesis of the Metalloclusters of Molybdenum Nitrogenase

Summary: Nitrogenase catalyzes a key step in the global nitrogen cycle, the nucleotide-dependent reduction of atmospheric dinitrogen to bioavailable ammonia. There is a substantial amount of interest in elucidating the biosynthetic mechanisms of the FeMoco and the P-cluster of nitrogenase, because these clusters are not only biologically important but also chemically unprecedented. In this review, we summarize the recent advances in this research area, with an emphasis on our work that aims at providing structural and spectroscopic insights into the assembly of these complex metalloclusters.     

Association between variants of EXT2 and type 2 diabetes: a replication and meta-analysis

Recent publications have found an association between variants of exostosin 2 (EXT2) gene and the risk of type 2 diabetes in some population but not in others. In an attempt to address these inconsistencies, we investigated EXT2 variants in two independent cohorts, and conducted a literature-based meta-analysis. Through regression model, we assessed the relationship between the EXT2 single nucleotide polymorphisms (SNPs) (rs3740878, rs11037909 and rs1113132) and the risk of type 2 diabetes in Han Chinese population, including a total of 2,533 cases and 2,643 controls. We combined our data with that from previously published studies and performed a meta-analysis to evaluate the effect size of the gene. Consistent with some studies, we found marginal association for the rs3740878 (OR = 1.07, 95 % CI = 0.99, 1.16, p = 0.09), rs11037909 (OR = 1.07, 95 % CI = 0.99, 1.16, p = 0.08), and rs1113132 (OR = 1.08, 95 % CI = 1.00, 1.17, p = 0.06) in our 2 cohorts. Meta-analysis, comprising 9,224 type 2 diabetes and 10,484 controls, revealed that three SNPs (rs3740878, rs11037909 and rs1113132) in EXT2 were significantly associated with type 2 diabetes (ORs range from 1.06 to 1.07, p = 0.038, p = 0.008 and p = 0.005, respectively). Variation in the EXT2 locus appears to be associated with a small increase in the risk of type 2 diabetes. However, well-designed prospective studies with larger sample size and more ethnic groups are needed to further validate the results.     

Sphingosine Kinase 1 Is Regulated by Peroxisome Proliferator-activated Receptor α in Response to Free Fatty Acids and Is Essential for Skeletal Muscle Interleukin-6 Production and Signaling in Diet-induced Obesity

We previously demonstrated that sphingosine kinase 1 (Sphk1) expression and activity are up-regulated by exogenous palmitate (PAL) in a skeletal muscle model system and in diet-induced obesity in mice; however, potential functions and in vivo relevance of this have not been addressed. Here, we aimed to determine the mechanism by which PAL regulates SphK1 in muscle, and to determine potential roles for its product, sphingosine-1-phosphate (S1P), in muscle biology in the context of obesity. Cloning and analysis of the mouse Sphk1 promoter revealed a peroxisome proliferator-activated receptor (PPAR) α cis-element that mediated activation of a reporter under control of the Sphk1 promoter; direct interaction of PPARα was demonstrated by chromatin immunoprecipitation. PAL treatment induced the proinflammatory cytokine interleukin (IL)-6 in a manner dependent on SphK1, and this was attenuated by inhibition of the sphingosine-1-phosphate receptor 3 (S1PR3)_. Diet-induced obesity in mice demonstrated that IL-6 expression in muscle, but not adipose tissue, increased in obesity, but this was attenuated in Sphk1^−/− mice. Moreover, plasma IL-6 levels were significantly decreased in obese Sphk1^−/− mice relative to obese wild type mice, and muscle, but not adipose tissue IL-6 signaling was activated. These data indicate that PPARα regulates Sphk1 expression in the context of fatty acid oversupply and links PAL to muscle IL-6 production. Moreover, this function of SphK1 in diet-induced obesity suggests a potential role for SphK1 in obesity-associated pathological outcomes.     

GLUT12 functions as a basal and insulin-independent glucose transporter in the heart

Glucose uptake from the bloodstream is the rate-limiting step in whole body glucose utilization, and is regulated by a family of membrane proteins called glucose transporters (GLUTs). Although GLUT4 is the predominant isoform in insulin-sensitive tissues, there is recent evidence that GLUT12 could be a novel second insulin-sensitive GLUT. However, its physiological role in the heart is not elucidated and the regulation of insulin-stimulated myocardial GLUT12 translocation is unknown. In addition, the role of GLUT12 has not been investigated in the diabetic myocardium. Thus, we hypothesized that, as for GLUT4, insulin regulates GLUT12 translocation to the myocardial cell surface, which is impaired during diabetes. Active cell surface GLUT (-4 and -12) content was quantified (before and after insulin stimulation) by a biotinylated photolabeled assay in both intact perfused myocardium and isolated cardiac myocytes of healthy and type 1 diabetic rodents. GLUT localization was confirmed by immunofluorescent confocal microscopy, and total GLUT protein expression was measured by Western blotting. Insulin stimulation increased translocation of GLUT-4, but not -12, in the healthy myocardium. Total GLUT4 content of the heart was decreased during diabetes, while there was no difference in total GLUT12. Active cell surface GLUT12 content was increased in the diabetic myocardium, potentially as a compensatory mechanism for the observed downregulation of GLUT4. Collectively, our data suggest that, in contrast to GLUT4, insulin does not mediate GLUT12 translocation, which may function as a basal GLUT located primarily at the cell surface in the myocardium.