Close relationship between diameters at 30cm height and at breast height (DBH) Relações entre diametros a 30 cm de altura e à altura do peito (DAP)

This paper proposes the establishment of a second diameter measuring standard at 30cm shoot extension ('diam30') as input variable for allometric biomass estimation of small and mid-sized plant shoots. This diameter standard is better suited than the diameter at breast height (DBH, i.e. diameter at 1.30m shoot extension) for adequate characterization of plant dimensions in low bushy vegetation or in primary forest undergrowth. The relationships between both diameter standards are established based on a dataset of 8645 tree, liana and palm shoots in secondary and primary forests of central Amazonia (ranging from 1-150mm dbh). Dbh can be predicted from the diam(30) with high precision, the error introduced by diameter transformation is only 2-3% for trees and palms, and 5% for lianas. This is well acceptable for most field study purposes. Relationships deviate slightly from linearity and differ between growth forms. Relationships were markedly similar for different vegetation types (low secondary regrowth vs. primary forests), soils, and selected genera or species. This points to a general validity and applicability of diameter transformations for other field studies. This study provides researchers with a tool for the allometric estimation of biomass in low or structurally heterogeneous vegetation. Rather than applying a uniform diameter standard, the measuring position which best represents the respective plant can be decided on shoot-by-shoot. Plant diameters measured at 30cm height can be transformed to dbh for subsequent allometric biomass estimation. We recommend the use of these diameter transformations only for plants extending well beyond the theoretical minimum shoot length (i.e., >2m height). This study also prepares the ground for the comparability and compatability of future allometric equations specifically developed for small- to mid-sized vegetation components (i.e., bushes, undergrowth) which are based on the diam(30) measuring standard.<br>Este estudo propõe o estabelecimento de um segundo padrão de medição de diâmetro a 30 cm de extensão do tronco ('diam30') para a estimativa alométrica da biomassa de plantas de pequeno até médio porte. Considera-se este padrão de diâmetro mais adequado do que o diâmetro à altura do peito ('DAP', a 1,30m de extensão do tronco) para a caracterização das dimensões de plantas em vegetação baixa ou no sub-bosque da mata primária. O presente trabalho investiga as relações entre os dois padrões de diâmetro, baseado em 8645 troncos de árvores, cipós e palmeiras arbóreas (com diâmetros entre 1 e 150mm DAP) em capoeiras e mata primária da Amazônia Central. Conclui-se que se pode estimar o DAP do diam30 com alta precisão, o erro causado pela transformação dos diâmetros é somente 2-3% para árvores e palmeiras e 5% para os cipós, níveis bem aceitáveis para a maioria dos estudos de campo. As relações entre os diâmetros desviaram levemente da linearidade e são diferentes para os três hábitos de crescimento. No entanto, as equações são bastante similares entre os diferentes tipos de vegetação (capoeira baixa vs. mata primária), solos e gêneros ou espécies, indicando sua aplicabilidade e validade geral para outros estudos de campo. Esse trabalho fornece ao pesquisador de campo uma ferramenta para a estimativa alométrica da biomassa de vegetação baixa ou estruturalmente heterogênea. Em vez de utilizar um único padrão uniforme de diâmetro pode-se escolher livremente e individualmente qual posição de diâmetro melhor representa cada tronco. Os diâmetros a 30 cm de extensão do tronco podem ser transformados para o dap para uma subseqüente estimação alométrica da sua biomassa. Recomenda-se o uso destas transformações de diâmetros somente acima de uma extensão mínima do tronco (>2m de altura). Os resultados do presente trabalho também preparam a base para a comparabilidade e compatibilidade de futuras equações alométricas baseadas no diam(30) para uma melhor estimação da biomassa dos componentes de vegetação baixa e média (arbustos, sub-bosque da mata primária)

Saving and Restoring Mechanisms for Tangible User Interfaces through Tangible Active Objects

Riedenklau E, Hermann T, Ritter H. Saving and Restoring Mechanisms for Tangible User Interfaces through Tangible Active Objects. In: Jacko JA, ed. Human-Computer Interaction. Interaction Techniques and Environments. 14th International Conference, Proceedings, Part II. Lecture Notes in Computer Science. Vol 6762. Heidelberg: Springer; 2011: 110-118.<img src="https://pub.uni-bielefeld.de/download/2696637/2702775" width="200" style="float:right;"> In this paper we present a proof of concept for saving and restoring mechanisms for Tangible User Interfaces (TUIs). We describe our actuated Tangible Active Objects (TAOs) and explain the design which allows equal user access to a dial-based fully tangible actuated menu metaphor. We present a new application extending an existing TUI for interactive sonification of process data with saving and restoring mechanisms and we outline another application proposal for family therapists

Conditional ligands for Asian HLA variants facilitate the definition of CD8+ T-cell responses in acute and chronic viral diseases

10.1002/eji.201243088European Journal of Immunology4341109-1120EJIM

The elevation of circulating fibroblast growth factor 23 without kidney disease does not increase cardiovascular disease risk.

High circulating fibroblast growth factor 23 (FGF23) levels are probably a major risk factor for cardiovascular disease in chronic kidney disease. FGF23 interacts with the receptor FGFR4 in cardiomyocytes inducing left ventricular hypertrophy. Moreover, in the liver FGF23 via FGFR4 increases the risk of inflammation which is also found in chronic kidney disease. In contrast, X-linked hypophosphatemia is characterized by high FGF23 circulating levels due to loss of function mutations of the phosphate-regulating gene with homologies to an endopeptidase on the X chromosome (PHEX), but is not characterized by high cardiovascular morbidity. Here we used a novel murine X-linked hypophosphatemia model, the PhexC733RMhda mouse line, bearing an amino acid substitution (p.Cys733Arg) to test whether high circulating FGF23 in the absence of renal injury would trigger cardiovascular disease. As X-linked hypophosphatemia patient mimics, these mice show high FGF23 levels, hypophosphatemia, normocalcemia, and low/normal vitamin D levels. Moreover, these mice show hyperparathyroidism and low circulating soluble alpha Klotho levels. At the age of 27 weeks we found no left ventricular hypertrophy and no alteration of cardiac function as assessed by echocardiography. These mice also showed no activation of the calcineurin/NFAT pathway in heart and liver and no tissue and systemic signs of inflammation. Importantly, blood pressure, glomerular filtration rate and urea clearance were similar between genotypes. Thus, the presence of high circulating FGF23 levels alone in the absence of renal impairment and normal/high phosphate levels is not sufficient to cause cardiovascular disease

Systemic Jak1 activation provokes hepatic inflammation and imbalanced FGF23 production and cleavage.

Fibroblast growth factor 23 (FGF23) is a main regulator of mineral homeostasis. Low and high circulating FGF23 levels are associated with bone, renal, cardiovascular diseases, and increased mortality. Understanding the factors and signaling pathways affecting FGF23 levels is crucial for the management of these diseases and their complications. Here, we show that activation of the Jak1/Stat3 signaling pathway leads to inflammation in liver and to an increase in hepatic FGF23 synthesis, a key hormone in mineral metabolism. This increased synthesis leads to massive C-terminal FGF23 circulating levels, the inactive C-terminal fragment, and increased intact FGF23 levels, the active form, resulting in imbalanced production and cleavage. Liver inflammation does not lead to activation of the calcineurin-NFAT pathway, and no signs of systemic inflammation could be observed. Despite the increase of active intact FGF23, excessive C-terminal FGF23 levels block the phosphaturic activity of FGF23. Therefore, kidney function and renal αKlotho expression are normal and no activation of the MAPK pathway was detected. In addition, activation of the Jak1/Stat3 signaling pathway leads to high calcitriol levels and low parathyroid hormone production. Thus, JAK1 is a central regulator of mineral homeostasis. Moreover, this study also shows that in order to assess the impact of high FGF23 levels on disease and kidney function, the source and the balance in FGF23 production and cleavage are critical