Unification: An international aerospace information issue

Science and technology projects are becoming more and more international and interdisciplinary. Other parts of the world, notably Europe, are increasingly powerful players in the aerospace business. This change has led to the development of various aerospace information initiatives in other countries. With scarce resources in all areas of government and industry, the NASA STI Program is reviewing its current acquisition and exchange practices and policies to factor in the changing requirements and new opportunities within the international community. Current NASA goals and activities are reviewed with a view toward developing a scenario for establishing an international aerospace data base, maintaining compatibility among national aerospace information systems, eliminating duplication of effort, and sharing resources through international cooperation wherever possible

Unification: An international aerospace information opportunity

Science and technology projects are becoming more and more international and interdisciplinary. Other parts of the world, notably Europe, are increasingly powerful players in the aerospace industry. This change has led to the development of various aerospace information initiatives in other countries. With scarce resources in all areas of government and industry, the NASA STI Program is reviewing its current acquisition and exchange practices and policies to factor in the changing requirements and new opportunities within the international community. Current NASA goals and activities are reviewed with a new view toward developing a scenario for establishing an international aerospace database, maintaining compatibility among national aerospace information systems, eliminating duplication of effort, and sharing resources through international cooperation wherever possible

Access to Japanese aerospace-related scientific and technical information: The NASA Aerospace Database

With Japan's growing R&D strength in aerospace-related fields, it is increasingly important for U.S. researchers to be aware of Japanese advances. However, several factors make it difficult to do so. After reviewing the diffusion of aerospace STI in Japan, four factors which make it difficult for U.S. researchers to gather this information are discussed: language, the human network, information scatter, and document acquisition. NASA activities to alleviate these difficulties are described, beginning with a general overview of the NASA STI Program. The effects of the new National Level Agreement between NASA and NASDA are discussed

Effect of the mycotoxin, ochratoxin A, on hormone-stimulated ion transport in a cultured cell model of the renal principal cell

The mycotoxin ochratoxin A (OTA) is a common contaminant of many foodstuffs and, consequently, is present in a large proportion of tested populations of humans and commercial animals. The predominant effects of OTA are manifested in the kidney where the severity varies from salt wasting to renal carcinoma formation in a concentration-dependent fashion. The MDCK-C7 renal cell culture model responds to various hormones known to regulate electrolyte and fluid balance and was used as a model to study the chronic effects of an acute exposure to low dose OTA. The natriferic hormones aldosterone and insulin-like growth factor 1 (IGF1) both stimulate Na(+) flux in a reabsorptive direction via activation of the epithelial Na(+) channel (ENaC). In contrast, anti-diuretic hormone (ADH) stimulates three separate and temporally distinct ion transport responses, one of which is Na(+) reabsorption. Treatment of MDCK-C7 cells with OTA (100 nM) for 48 h selectively and irreversibly inhibits hormone-stimulated Na(+) reabsorption via ENaC. This effect was retained for 48 cell passages after the removal of the toxin and mimics the OTA-induced salt-wasting that has been documented in clinical studies. These studies indicate that the effect of the toxin is genomic and therefore, likely to be long lasting in exposed animals and humans

Characterization of the ion transport responses to ADH in the MDCK-C7 cell line

The Madin-Darby canine kidney (MDCK) cell line expresses many characteristics of the renal collecting duct. The MDCK-C7 subclone forms a high-resistance, hormone-responsive model of the principal cells, which are found in distal sections of the renal tubule. The electrophysiological technique of short-circuit current measurement was used to examine the response to antidiuretic hormone (ADH) in the MDCK-C7 clone. Three discrete electrogenic ion transport phenomena can be distinguished temporally and by the use of inhibitors and effectors. Initially the cells exhibit anion secretion through the cystic fibrosis transmembrane conductance regulator (CFTR). The presence of CFTR was confirmed by immunoprecipitation followed by Western blotting. The CFTR-mediated anion secretion is transient and is followed, in time, by a verapamil- and Ba(+)-sensitive anion secretion or cation absorption and, finally, by Na+ reabsorption via epithelial Na+ channels (ENaC). In contrast to other studies of MDCK cells, we see no indication that the presence of CFTR functionally inhibits ENaC. The characterization of the various ion transport phenomena substantiates this cell line as a model renal epithelium that can be used to study the hormonal and metabolic regulation of ion transport

Characterization of the ion transport responses to ADH in the MDCK-C7 cell line

The Madin-Darby canine kidney (MDCK) cell line expresses many characteristics of the renal collecting duct. The MDCK-C7 subclone forms a high-resistance, hormone-responsive model of the principal cells, which are found in distal sections of the renal tubule. The electrophysiological technique of short-circuit current measurement was used to examine the response to antidiuretic hormone (ADH) in the MDCK-C7 clone. Three discrete electrogenic ion transport phenomena can be distinguished temporally and by the use of inhibitors and effectors. Initially the cells exhibit anion secretion through the cystic fibrosis transmembrane conductance regulator (CFTR). The presence of CFTR was confirmed by immunoprecipitation followed by Western blotting. The CFTR-mediated anion secretion is transient and is followed, in time, by a verapamil- and Ba(+)-sensitive anion secretion or cation absorption and, finally, by Na+ reabsorption via epithelial Na+ channels (ENaC). In contrast to other studies of MDCK cells, we see no indication that the presence of CFTR functionally inhibits ENaC. The characterization of the various ion transport phenomena substantiates this cell line as a model renal epithelium that can be used to study the hormonal and metabolic regulation of ion transport

Effect of the mycotoxin, ochratoxin A, on hormone-stimulated ion transport in a cultured cell model of the renal principal cell

The mycotoxin ochratoxin A (OTA) is a common contaminant of many foodstuffs and, consequently, is present in a large proportion of tested populations of humans and commercial animals. The predominant effects of OTA are manifested in the kidney where the severity varies from salt wasting to renal carcinoma formation in a concentration-dependent fashion. The MDCK-C7 renal cell culture model responds to various hormones known to regulate electrolyte and fluid balance and was used as a model to study the chronic effects of an acute exposure to low dose OTA. The natriferic hormones aldosterone and insulin-like growth factor 1 (IGF1) both stimulate Na(+) flux in a reabsorptive direction via activation of the epithelial Na(+) channel (ENaC). In contrast, anti-diuretic hormone (ADH) stimulates three separate and temporally distinct ion transport responses, one of which is Na(+) reabsorption. Treatment of MDCK-C7 cells with OTA (100 nM) for 48 h selectively and irreversibly inhibits hormone-stimulated Na(+) reabsorption via ENaC. This effect was retained for 48 cell passages after the removal of the toxin and mimics the OTA-induced salt-wasting that has been documented in clinical studies. These studies indicate that the effect of the toxin is genomic and therefore, likely to be long lasting in exposed animals and humans

A New Missense Mutation in the Leptin Gene Causes Mild Obesity and Hypogonadism without Affecting T Cell Responsiveness

Abstract Objective: Leptin, a protein product of adipocytes, plays a critical role in the regulation of body weight, immune function, pubertal development, and fertility. So far, only three homozygous mutations in the leptin gene in a total of 13 individuals have been found leading to a phenotype of extreme obesity with marked hyperphagia and impaired immune function. Design: Serum leptin was measured by ELISA. The leptin gene (OB) was sequenced in patient DNA. The effect of the identified novel mutation was assessed using HEK293 cells. Results: We describe a 14-yr-old child of nonobese Austrian parents without known consanguinity. She had a body mass index of 31.5 kg/m2 (+2.46 sd score) and undetectable leptin serum levels. Sequencing of the leptin gene revealed a hitherto unknown homozygous transition (TTA to TCA) in exon 3 of the LEP gene resulting in a L72S replacement in the leptin protein. RT-PCR, Western blot, and immunohistochemical analysis indicated that the mutant leptin was expressed in the patient’s adipose tissue but retained within the cell. Using a heterologous cell system, we confirmed this finding and demonstrated that the side chain of Leu72 is crucial for intracellular leptin trafficking. Our patient showed signs of a hypogonadotropic hypogonadism. However, in contrast to the literature, she showed only mild obesity and a normal T cell responsiveness. Conclusions: These findings shed a new light on the clinical consequences of leptin deficiency. Congenital leptin deficiency should be considered possible in pediatric patients with mild obesity even if parents are lean and unrelated.</jats:p