Analysis of Spanish vocational radiographers' education through clinical training and perceptions of core subject teachers: A survey.

INTRODUCTION: This work presents a prospective analysis of the key aspects involved in the Spanish radiographer's perception of the weaknesses of the current educational curriculum in terms of teaching staff's qualifications and composition in the clinical training and core subjects. The goal is to show clinical training and professional's perception of the teaching quality and to characterise the weakness detected within the context of the European radiographer's academic system. METHODS: The perception of the quality of the training received by the professionals was collected through an anonymous survey. A total of 758 valid responses were received, and were analysed to three hypotheses: the variability of the teachers' qualifications in the core subjects, the variability in terms of internships time carried out by the students, and assessment about teaching quality of the teachers. RESULTS: The results prove there is a huge variability and little academic affinity of the teachers' degrees with the core subjects. On the other hand, the results shows there is a scarcity of clinical training hours in Spain, especially compared to European standards. It was demonstrated that teachers with a specific radiographer degree obtained the best scores. CONCLUSION: It is mandatory to adjust the criteria for selecting clinical imaging teachers to improve the teaching quality in Spain and increase the clinical training period of the Spanish radiographers to match their European counterparts. IMPLICATION FOR PRACTICE: Improving the training of Spanish radiographers will contribute to standardising the training quality of the whole European profession.

Glycolytic enzyme activities are decreased during acute rejection in transplanted rat hearts.

Metabolic alterations have been characterized in various heart diseases. However, no data are available concerning metabolic changes during acute rejection episodes. Heterotopic heart transplantations in rats were done using Lewis rats as donors and recipients as a control group. The rejection group included Brown-Norway rat donors to Lewis rat recipients. Nonoperated hearts were also studied. Enzyme activities were determined for phosphofructokinase, pyruvate kinase, and lactate dehydrogenase. There were no alterations in the control group compared to nonoperated hearts. However, the rejection cohort of hearts showed decreased glycolytic enzymes. Although lactate dehydrogenase maintained similar levels compared to the control group, phosphofructokinase showed only 50% activity, and pyruvate kinase showed less than 10% of the activity compared with controls. These results suggested that metabolic alterations in rejected hearts differ from other cardiomyopathies.

Cellular functions of TC10, a Rho family GTPase: regulation of morphology, signal transduction and cell growth.

The small Ras-related GTPase, TC10, has been classified on the basis of sequence homology to be a member of the Rho family. This family, which includes the Rho, Rac and CDC42 subfamilies, has been shown to regulate a variety of apparently diverse cellular processes such as actin cytoskeletal organization, mitogen-activated protein kinase (MAPK) cascades, cell cycle progression and transformation. In order to begin a study of TC10 biological function, we expressed wild type and various mutant forms of this protein in mammalian cells and investigated both the intracellular localization of the expressed proteins and their abilities to stimulate known Rho family-associated processes. Wild type TC10 was located predominantly in the cell membrane (apparently in the same regions as actin filaments), GTPase defective (75L) and GTP-binding defective (31N) mutants were located predominantly in cytoplasmic perinuclear regions, and a deletion mutant lacking the carboxyl terminal residues required for post-translational prenylation was located predominantly in the nucleus. The GTPase defective (constitutively active) TC10 mutant: (1) stimulated the formation of long filopodia; (2) activated c-Jun amino terminal kinase (JNK); (3) activated serum response factor (SRF)-dependent transcription; (4) activated NF-kappaB-dependent transcription; and (5) synergized with an activated Raf-kinase (Raf-CAAX) to transform NIH3T3 cells. In addition, wild type TC10 function is required for full H-Ras transforming potential. We demonstrate that an intact effector domain and carboxyl terminal prenylation signal are required for proper TC10 function and that TC10 signals to at least two separable downstream target pathways. In addition, TC10 interacted with the actin-binding and filament-forming protein, profilin, in both a two-hybrid cDNA library screen, and an in vitro binding assay. Taken together, these data support a classification of TC10 as a member of the Rho family, and in particular, suggest that TC10 functions to regulate cellular signaling to the actin cytoskeleton and processes associated with cell growth.

[Evolution of mortality amongst the youth of Navarra: 1985-1995]. / Evolución de la mortalidad en los jóvenes de Navarra: 1985-1995.

Recent publications show that mortality rates amongst young people and adolescents in some industrialised countries have increased in recent years. The addition of new diseases such as AIDS, which principally affect the young population, to those inevitable deaths brought about through causes such as traffic accidents has increased interest in this public health problem. The number of deaths and the adjusted global mortality rates amongst men and women of 15-34 years did not increase in Navarra in the 1985-1995 period. These are situated around 70 per 100,000. Changes have taken place in the pattern of causes, similar to those observed in other industrialised areas, with an increase of deaths through overdose and AIDS, and a decline in mortality due to traffic accidents in recent years. Traffic accidents were the first cause of death amongst youths until 1993. From this year onwards deaths from AIDS became the first cause amongst women, while amongst men the number of deaths from AIDS is equal to those caused by traffic accidents.

A T42A Ran mutation: differential interactions with effectors and regulators, and defect in nuclear protein import.

Ran, the small, predominantly nuclear GTPase, has been implicated in the regulation of a variety of cellular processes including cell cycle progression, nuclear-cytoplasmic trafficking of RNA and protein, nuclear structure, and DNA synthesis. It is not known whether Ran functions directly in each process or whether many of its roles may be secondary to a direct role in only one, for example, nuclear protein import. To identify biochemical links between Ran and its functional target(s), we have generated and examined the properties of a putative Ran effector mutation, T42A-Ran. T42A-Ran binds guanine nucleotides as well as wild-type Ran and responds as well as wild-type Ran to GTP or GDP exchange stimulated by the Ran-specific guanine nucleotide exchange factor, RCC1. T42A-Ran.GDP also retains the ability to bind p10/NTF2, a component of the nuclear import pathway. In contrast to wild-type Ran, T42A-Ran.GTP binds very weakly or not detectably to three proposed Ran effectors, Ran-binding protein 1 (RanBP1), Ran-binding protein 2 (RanBP2, a nucleoporin), and karyopherin beta (a component of the nuclear protein import pathway), and is not stimulated to hydrolyze bound GTP by Ran GTPase-activating protein, RanGAP1. Also in contrast to wild-type Ran, T42A-Ran does not stimulate nuclear protein import in a digitonin permeabilized cell assay and also inhibits wild-type Ran function in this system. However, the T42A mutation does not block the docking of karyophilic substrates at the nuclear pore. These properties of T42A-Ran are consistent with its classification as an effector mutant and define the exposed region of Ran containing the mutation as a probable effector loop.

2,3-Bisphosphoglycerate-independent phosphoglycerate mutase is conserved among different phylogenic kingdoms.

We have previously demonstrated that maize (Zea mays) 2,3-bisphosphoglycerate-independent phosphoglycerate mutase (PGAM-i) is not related to 2,3-bisphosphoglycerate-dependent phosphoglycerate mutase. With the aid of specific anti-maize PGAM-i antibodies, we demonstrate here the presence of a closely related PGAM-i in other plants. We also describe the isolation and sequencing of a cDNA-encoding almond (Prunus amygdalus) PGAM-i that further demonstrates this relationship among plant PGAM-i. A search of the major databases for related sequences allowed us to identify some novel PGAM-i from different sources: plants (Arabidopsis thaliana, Oryza sativa and Antithamniom sp.), monera (Escherichia coli, Bacillus subtilis and Bacillus megaterium) and animals (Caenorhabditis elegans). All of these amino acid sequences share a high degree of homology with plant PGAM-i. These observations suggest that the PGAM-i from several biological kingdoms constitute a family of protein different from other proteins with related enzymatic function and arose from a common ancestral gene that has diverged throughout its evolution.

Isolation and characterization of cofactor-independent phosphoglycerate mutase gene from maize.

The isolation and characterization of cofactor-independent phosphoglycerate mutase gene from maize (Zea mays) is here reported. This gene sequence constitutes the first described from this enzyme. The gene spans 5.4 kilo base pairs and has nine exons in the translated region. Canonical TATA and CCAAT and Sp1-like boxes are present upstream of the gene. Comparison with cofactor-dependent phosphoglycerate mutase genes revealed no similarity between both groups of enzymes.