Mathematical decision theory applied to land capability: a case study in the community of madrid.

In land evaluation science, a standard data set is obtained for each land unit to determine the land capability class for various uses, such as different farming systems, forestry, or the conservation or suitability of a specific crop. In this study, we used mathematical decision theory (MDT) methods to address this task. Mathematical decision theory has been used in areas such as management, finance, industrial design, rural development, the environment, and projects for future welfare to study quality and aptness problems using several criteria. We also review MDT applications in soil science and discuss the suitability of MDT methods for dealing simultaneously with a number of problems. The aim of the work was to show how MDT can be used to obtain a valid land quality index and to compare this with a traditional land capability method. Therefore, an additive classification method was applied to obtain a land quality index for 122 land units that were compiled for a case study of the Community of Madrid, Spain, and the results were compared with a previously assigned land capability class using traditional methods based on the minimum requirements for land attributes.

The genetics of mitral valve prolapse.

Mitral valve prolapse (MVP) is a very common clinical condition that refers to a systolic billowing of one or both mitral valve leaflets into the left atrium. Improvements of echocardiographic techniques and new insights in mitral valve anatomy and physiology have rendered the diagnosis of this condition more accurate and reliable. MVP can be sporadic or familial, demonstrating autosomal dominant and X-linked inheritance. Three different loci on chromosomes 16, 11 and 13 have been found to be linked to MVP, but no specific gene has been described. Another locus on chromosome X was found to cosegregate with a rare form of MVP called 'X-linked myxomatous valvular dystrophy'. MVP is more frequent in patients with connective tissue disorders including Marfan syndrome, Ehlers-Danlos and osteogenesis imperfecta. The purpose of this review is to describe previous studies on the genetics and prevalence of MVP. The report warrants the need for further genetically based studies on this common, albeit not fully understood, clinical entity.

Defective epithelial-mesenchymal interactions dictate the organogenesis of tracheoesophageal fistula.

We have previously suggested that the fistula tract in esophageal atresia with tracheoesophageal fistula (EA/TEF) arises from a trifurcation of the embryonic lung bud. Thus, it appears to be a respiratory-derived structure, and expresses the lung-specific transcription factor TTF-1 in its epithelium. The fistula tract does not give rise to lungs like the other branches from the bud. It grows caudally until it fistulizes with the stomach. We hypothesized that epithelial-mesenchymal interactions (EMI) dictate the differential pattern of growth of the respiratory-derived fistula tract in EA/TEF. EA/TEF was induced in rat embryos via prenatal exposure to adriamycin. Microdissection was performed on E13.5 embryos to isolate developing lung bud, fistula tract, or esophagus from adriamycin-treated or control animals, respectively. The mesenchyme and epithelium from each of these foregut structures were separated. The individual epithelia were recombined with each of the various mesenchymes and grown in culture. They were assayed for relative degrees of branching. Isolated lung-bud epithelia (LBE) or fistula epithelium were also cultured in Matrigel with exogenous fibroblast growth factors (FGF) and subsequently assayed for branching. The fistula-tract mesenchyme relatively inhibited branching of lung epithelium. The epithelium of the fistula tract could be induced to branch by non-fistula (lung or esophageal) mesenchyme. The fistula-tract and adriamycin-treated LBE both branched in response to FGF1. In contrast, neither responded to FGF7 or FGF10. EMI are defective in the developing EA/TEF. The inability to respond to FGF7 and FGF10 suggests an epithelial defect involving the receptor FGF2R-IIIb, to which these mesenchymal factors obligately bind. Thus, the mesenchyme around the developing fistula tract may lack an FGF branching morphogen(s), such as FGF1. Hence, this mesenchyme is unable to induce branching of respiratory epithelia and allows the middle branch of the embryonic tracheal trifurcation to grow caudally as an unbranched tube until it fistulizes into the stomach.

Ontogeny of activin B and follistatin in developing embryonic mouse pancreas: implications for lineage selection.

Activin, a member of the transforming growth factor-beta superfamily, has been shown to be a critical regulator in exocrine and endocrine pancreas formation. The purpose of our study was to describe the ontogeny of activin B and its inhibitor, follistatin, in developing pancreas and to elucidate potential mechanisms for exocrine and endocrine lineage selection. Mouse embryonic pancreata were dissected at various ages (day 10 [E10.5] to birth [E18.5]), sectioned, and immunostained for activin B (one of two existing isomers, A and B), follistatin, insulin, and glucagon. In addition, reverse transcriptase-polymerase chain reaction was employed to determine the messenger RNA expression of follistatin in isolated pancreatic epithelia and mesenchyme of various ages. Activin B was first detected at E12.5 in epithelial cells coexpressing glucagon. At E16.5 these coexpressors appeared as clusters in close proximity to early ducts. By E18.5 activin B was localized to forming islets where cells coexpressed glucagon and were arranged in the mantle formation characteristic of mature alpha cells. Follistatin was found to be ubiquitous in pancreatic mesenchyme at early ages by immunohistochemical analysis, disappearing sometime after E12.5. Follistatin reappeared in E18.5 islets and remains expressed in adult islets. Follistatin messenger RNA was first detected in epithelium at E11.5, preceding its protein expression in islets later in gestation. We propose that mesenchyme-derived follistatin inhibits epithelium-derived activin at early embryonic ages allowing for unopposed exocrine differentiation and relative suppression of endocrine differentiation. At later ages the decrease in the amount of mesenchyme relative to epithelium and the subsequent drop in follistatin levels liberates epithelial activin to allow differentiation of endocrine cells to form mature islets by the time of birth.