A bankable method for the field testingor a CPV plant

The bankability of CPV projects is an important issue to pave the way toward a swift and sustained growth in this technology. The bankability of a PV plant is generally addressed through the modeling of its energy yield under a b aseline loss scenario, followed by an on-site measurement campaign aimed at verifying its energetic behavior. The main difference between PV and CPV resides in the proper CPV modules, in particular in the inclusion of optical lements and III-V multijunction cells that are much more sensitive to spectral variations than xSi cells, while the rest of the system behaves in a way that possesses many common points with xSi technology. The modeling of the DC power output of a CPV system thus requires several impo rtant second order parameters to be considered, mainly related to optics, spectral direct solar radiation, wind speed, tracker accuracy and heat dissipation of cells.

Estudio de las dinámicas de pérdida de peso corporal en los programas de ejercicio físico y nutrición = Study of the dynamics of body weight loss in exercise and nutritional programs

Introducción. La obesidad puede definirse como una enfermedad metabólica crónica de origen multifactorial, lo que provoca trastornos o problemas físicos y psicológicos a la persona, con patologías asociadas que limitan la esperanza de vida y deterioran la calidad de la misma, siendo determinante para sus áreas sociales y laborales. Este trastorno metabólico crónico se caracteriza por una acumulación excesiva de energía en el cuerpo en forma de grasa, lo que lleva a un aumento de peso con respecto al valor esperado por sexo, edad y altura. La gestión y el tratamiento de la obesidad tienen objetivos más amplios que la pérdida de peso e incluyen la reducción del riesgo y la mejora de la salud. Estos pueden ser alcanzados por la pérdida modesta de peso (es decir, 10.5% del peso corporal inicial), la mejora del contenido nutricional de la dieta y un modesto incremento en la actividad física y condición física. La dieta es uno de los métodos más populares para perder peso corporal. El ejercicio es otra alternativa para perder peso corporal. El aumento de ejercicio provoca un desequilibrio cuando se mantiene la ingesta calórica. También tiene ventajas, como la mejora del tono muscular, la capacidad cardiovascular, fuerza y flexibilidad, aumenta el metabolismo basal y mejora el sistema inmunológico. Objetivos. El objetivo de esta tesis es contribuir en un estudio de intervención para aclarar la evolución del peso corporal durante una intervención de dieta y ejercicio. Para ello, se evaluaron los efectos de la edad, sexo, índice de masa corporal inicial y el tipo de tratamiento en las tendencias de pérdida de peso. Otro objetivo de la tesis era crear un modelo de regresión lineal múltiple capaz de predecir la pérdida de peso corporal después del periodo de intervención. Y, por último, determinar el efecto sobre la composición corporal (peso corporal, índice de masa corporal, la masa grasa, y la masa libre de grasa) de las diferentes intervenciones basadas en ejercicios (fuerza, resistencia, resistencia combinada con fuerza, y las recomendaciones de actividad física (grupo control)) en combinación con dieta de adultos con sobrepeso y obesidad, después de la intervención, así como los cambios de la composición corporal 3 años más tarde. Diseño de la investigación. Los datos empleados en el análisis de esta tesis son parte del proyecto “Programas de Nutrición y Actividad Física para el tratamiento de la obesidad” (PRONAF). El proyecto PRONAF es un estudio clínico sobre programas de nutrición y actividad física para el sobrepeso y la obesidad, desarrollado en España durante varios años de intervención. Fue diseñado, en parte, para comparar diferentes tipos de intervención, con el objetivo de evaluar su impacto en las dinámicas de pérdida de peso, en personas con sobrepeso y obesidad. Como diseño experimental, el estudio se basó en una restricción calórica, a la que, en algunos casos, se le añadió un protocolo de entrenamiento (fuerza, resistencia, o combinado, en igualdad de volumen e intensidad). Las principales variables para la investigación que comprende esta tesis fueron: el peso corporal y la composición corporal (masa grasa y masa libre de grasa). Conclusiones. En esta tesis, para los programas de pérdida de peso en personas con sobrepeso y obesidad con un 25-30% de la restricción calórica, el peso corporal se redujo significativamente en ambos sexos, sin tener en cuenta la edad y el tipo de tratamiento seguido. Según los resultados del estudio, la pérdida de peso realizada por un individuo (hombre o mujer) durante los seis meses puede ser representada por cualquiera de las cinco funciones (lineal, potencial, exponencial, logarítmica y cuadrática) en ambos sexos, siendo la cuadrática la que tiende a representarlo mejor. Además, se puede concluir que la pérdida de peso corporal se ve afectada por el índice de masa corporal inicial y el sexo, siendo mayor para las personas obesas que para las de sobrepeso, que muestran diferencias entre sexos sólo en la condición de sobrepeso. Además, es posible calcular el peso corporal final de cualquier participante involucrado en una intervención utilizando la metodología del proyecto PRONAF sólo conociendo sus variables iniciales de composición corporal. Además, los cuatro tipos de tratamientos tuvieron resultados similares en cambios en la composición corporal al final del período de intervención, con la única excepción de la masa libre de grasa, siendo los grupos de entrenamiento los que la mantuvieron durante la restricción calórica. Por otro lado, sólo el grupo combinado logra mantener la reducción de la masa grasa (%) 3 años después del final de la intervención. ABSTRACT Introduction. Obesity can be defined as a chronic metabolic disease from a multifactorial origin, which leads to physical and psychological impacts to the person, with associated pathologies that limit the life expectancy and deteriorate the quality of it, being determinant for the social and labor areas of the person. This chronic metabolic disorder is characterized by an excessive accumulation of energy in the body as fat, leading to increased weight relative to the value expected by sex, age and height. The management and treatment of obesity have wider objectives than weight loss alone and include risk reduction and health improvement. These may be achieved by modest weight loss (i.e. 5–10% of initial body weight), improved nutritional content of the diet and modest increases in physical activity and fitness. Weight loss through diet is one of the most popular approaches to lose body weight. Exercise is another alternative to lose body weight. The increase of exercise causes an imbalance when the caloric intake is maintained. It also has advantages such as improved muscle tone, cardiovascular fitness, strength and flexibility, increases the basal metabolism and improves immune system. Objectives. The aim of this thesis is to contribute with an interventional study to clarify the evolution of the body weight during a diet and exercise intervention. For this, the effects of age, sex, initial body mass index and type of treatment on weight loss tendencies were evaluated. Another objective of the thesis was to create a multiple linear regression model able to predict the body weight loss after the intervention period. And, finally, to determine the effect upon body composition (body weight, body mass index, fat mass, and fat-free mass of different exercise-based interventions (strength, endurance, combined endurance and strength, and physical activity recommendations group (control group)) combined with diet in overweight and obese adults, after intervention as well as body composition changes 3 years later. Research Design. The data used in the analysis of this thesis are part of the project "Programs of Nutrition and Physical Activity for the treatment of obesity" (PRONAF). The PRONAF project is a clinical trial program about nutrition and physical activity for overweight and obesity, developed in Spain for several years of intervention. It was designed, in part, to compare different types of intervention, in order to assess their impact on the dynamics of weight loss in overweight and obese people. As experimental design, the study was based on caloric restriction, which, in some cases, added a training protocol (strength, endurance, or combined in equal volume and intensity). The main research variables comprising this thesis were: body weight and body composition outcomes (fat mass and fat-free mass). Conclusions. In this thesis, for weight loss programs in overweight and obese people with 25-30% of caloric restriction, the body weight was significantly decreased in both sexes, regardless the age and type of followed treatment. According to the results of the study, the weight loss performed by an individual (male or female) during six months can be represented by any of the five functions (linear, power law, exponential, logarithmic and quadratic) in both sexes, being the quadratic one which tends to represent it better. In addition, it can be concluded that the body weight loss is affected by the initial body mass index and sex condition, being greater for the obese people than for the overweight one, showing differences between sexes only in the overweight condition. Moreover, it is possible to calculate the final body weight of any participant engaged in an intervention using the PRONAF Project methodology only knowing their initial body composition variables. Furthermore, the four types of treatments had similar results on body composition changes at the end of the intervention period, with the only exception of fat-free mass, being the training groups the ones that maintained it during the caloric restriction. On the other hand, only the combined group achieved to maintain the fat mass (%) reduced 3 years after the end of the intervention.

A bankable method of assessing the performance of a CPV plant

Concentrating Photovoltaics (CPV) is an alternative to flat-plate module photovoltaic (PV) technology. The bankability of CPV projects is an important issue to pave the way toward a swift and sustained growth in this technology. The bankability of a PV plant is generally addressed through the modeling of its energy yield under a baseline loss scenario, followed by an on-site measurement campaign aimed at verifying its energy performance. This paper proposes a procedure for assessing the performance of a CPV project, articulated around four main successive steps: Solar Resource Assessment, Yield Assessment, Certificate of Provisional Acceptance, and Certificate of Final Acceptance. This methodology allows the long-term energy production of a CPV project to be estimated with an associated uncertainty of ≈5%. To our knowledge, no such method has been proposed to the CPV industry yet, and this critical situation has hindered or made impossible the completion of several important CPV projects undertaken in the world. The main motive for this proposed method is to bring a practical solution to this urgent problem. This procedure can be operated under a wide range of climatic conditions, and makes it possible to assess the bankability of a CPV plant whose design uses any of the technologies currently available on the market. The method is also compliant with both international standards and local regulations. In consequence, its applicability is both general and international.

Loss of the circadian clock-associated protein 1 in Arabidopsis results in altered clock-regulated gene expression

Little is known about plant circadian oscillators, in spite of how important they are to sessile plants, which require accurate timekeepers that enable the plants to respond to their environment. Previously, we identified a circadian clock-associated (CCA1) gene that encodes an Myb-related protein that is associated with phytochrome control and circadian regulation in plants. To understand the role CCA1 plays in phytochrome and circadian regulation, we have isolated an Arabidopsis line with a T DNA insertion that results in the loss of CCA1 RNA, of CCA1 protein, and of an Lhcb-promoter binding activity. This mutation affects the circadian expression of all four clock-controlled genes that we examined. The results show that, despite their similarity, CCA1 and LHY are only partially redundant. The lack of CCA1 also affects the phytochrome regulation of gene expression, suggesting that CCA1 has an additional role in a signal transduction pathway from light, possibly acting at the point of integration between phytochrome and the clock. Our results indicate that CCA1 is an important clock-associated protein involved in circadian regulation of gene expression.

Disease sequence from mutant rhodopsin allele to rod and cone photoreceptor degeneration in man

Mutations in the gene encoding rhodopsin, the visual pigment in rod photoreceptors, lead to retinal degeneration in species from Drosophila to man. The pathogenic sequence from rod cell-specific mutation to degeneration of rods and cones remains unclear. To understand the disease process in man, we studied heterozygotes with 18 different rhodopsin gene mutations by using noninvasive tests of rod and cone function and retinal histopathology. Two classes of disease expression were found, and there was allele-specificity. Class A mutants lead to severely abnormal rod function across the retina early in life; topography of residual cone function parallels cone cell density. Class B mutants are compatible with normal rods in adult life in some retinal regions or throughout the retina, and there is a slow stereotypical disease sequence. Disease manifests as a loss of rod photoreceptor outer segments, not singly but in microscopic patches that coalesce into larger irregular areas of degeneration. Cone outer segment function remains normal until >75% of rod outer segments are lost. The topography of cone loss coincides with that of rod loss. Most class B mutants show an inferior-nasal to superior-temporal retinal gradient of disease vulnerability associated with visual cycle abnormalities. Class A mutant alleles behave as if cytotoxic; class B mutants can be relatively innocuous and epigenetic factors may play a major role in the retinal degeneration.

Selective loss of dopaminergic nigro-striatal neurons in brains of Atm-deficient mice

Ataxia-telangiectasia (AT) is a human disease caused by mutations in the ATM gene. The neural phenotype of AT includes progressive cerebellar neurodegeneration, which results in ataxia and eventual motor dysfunction. Surprisingly, mice in which the Atm gene has been inactivated lack distinct behavioral ataxia or pronounced cerebellar degeneration, the hallmarks of the human disease. To determine whether lack of the Atm protein can nonetheless lead to structural abnormalities in the brain, we compared brains from male Atm-deficient mice with male, age-matched controls. Atm-deficient mice exhibited severe degeneration of tyrosine hydroxylase-positive, dopaminergic nigro-striatal neurons, and their terminals in the striatum. This cell loss was accompanied by a large reduction in immunoreactivity for the dopamine transporter in the striatum. A reduction in dopaminergic neurons also was evident in the ventral tegmental area. This effect was selective in that the noradrenergic nucleus locus coeruleus was normal in these mice. Behaviorally, Atm-deficient mice expressed locomotor abnormalities manifested as stride-length asymmetry, which could be corrected by peripheral application of the dopaminergic precursor l-dopa. In addition, these mice were hypersensitive to the dopamine releasing drug d-amphetamine. These results indicate that ATM deficiency can severely affect dopaminergic neurons in the central nervous system and suggest possible strategies for treating this aspect of the disease.

Inactivation of the mitogen-activated protein kinase Mps1 from the rice blast fungus prevents penetration of host cells but allows activation of plant defense responses

The rice blast fungus, Magnaporthe grisea, generates enormous turgor pressure within a specialized cell called the appressorium to breach the surface of host plant cells. Here, we show that a mitogen-activated protein kinase, Mps1, is essential for appressorium penetration. Mps1 is 85% similar to yeast Slt2 mitogen-activated protein kinase and can rescue the thermosensitive growth of slt2 null mutants. The mps1–1Δ mutants of M. grisea have some phenotypes in common with slt2 mutants of yeast, including sensitivity to cell-wall-digesting enzymes, but display additional phenotypes, including reduced sporulation and fertility. Interestingly, mps1–1Δ mutants are completely nonpathogenic because of the inability of appressoria to penetrate plant cell surfaces, suggesting that penetration requires remodeling of the appressorium wall through an Mps1-dependent signaling pathway. Although mps1–1Δ mutants are unable to cause disease, they are able to trigger early plant-cell defense responses, including the accumulation of autofluorescent compounds and the rearrangement of the actin cytoskeleton. We conclude that MPS1 is essential for pathogen penetration; however, penetration is not required for induction of some plant defense responses.

Human ATP-binding cassette transporter 1 (ABC1): Genomic organization and identification of the genetic defect in the original Tangier disease kindred

Tangier disease is characterized by low serum high density lipoproteins and a biochemical defect in the cellular efflux of lipids to high density lipoproteins. ABC1, a member of the ATP-binding cassette family, recently has been identified as the defective gene in Tangier disease. We report here the organization of the human ABC1 gene and the identification of a mutation in the ABC1 gene from the original Tangier disease kindred. The organization of the human ABC1 gene is similar to that of the mouse ABC1 gene and other related ABC genes. The ABC1 gene contains 49 exons that range in size from 33 to 249 bp and is over 70 kb in length. Sequence analysis of the ABC1 gene revealed that the proband for Tangier disease was homozygous for a deletion of nucleotides 3283 and 3284 (TC) in exon 22. The deletion results in a frameshift mutation and a premature stop codon starting at nucleotide 3375. The product is predicted to encode a nonfunctional protein of 1,084 aa, which is approximately half the size of the full-length ABC1 protein. The loss of a Mnl1 restriction site, which results from the deletion, was used to establish the genotype of the rest of the kindred. In summary, we report on the genomic organization of the human ABC1 gene and identify a frameshift mutation in the ABC1 gene of the index case of Tangier disease. These results will be useful in the future characterization of the structure and function of the ABC1 gene and the analysis of additional ABC1 mutations in patients with Tangier disease.

Precursor B cells for autoantibody production in genomically Fas-intact autoimmune disease are not subject to Fas-mediated immune elimination

The Fas/Fas ligand (FasL) system participates in regulation of the immune system through the apoptotic process. However, the extent to which abnormalities in this system are involved in the loss of self-tolerance and development of autoimmune disease not associated with Fas/FasL mutations remains unknown. The present study addresses this issue in Fas/FasL-intact, systemic lupus erythematosus (SLE)-prone (NZB × NZW) (NZB/W) F1 mice. While splenic B cells from 2-month-old mice before overt SLE expressed Fas poorly, in vitro stimulation with an agonistic anti-CD40 mAb up-regulated their Fas expression, thus revealing the existence of two populations: one was Fashigh and highly susceptible to anti-Fas mAb-induced apoptosis, and the other was Faslow and apoptosis-resistant. The Faslow cells were included in the CD5+ B cell subpopulation and contained most of the cells that produced IgM anti-DNA antibodies. The isotype of anti-DNA antibodies switches from IgM to IgG in NZB/W F1 mice at ages beginning at about 6 months. These IgG anti-DNA antibodies were produced almost exclusively by a subpopulation of splenic B cells that spontaneously expressed low levels of Fas in vivo and were apoptosis-resistant. The findings indicate that precursor B cells for autoantibody production and presumably autoantibody-secreting cells in these mice are relatively resistant to Fas-mediated apoptosis, a finding supporting the concept that abnormalities of Fas-mediated apoptotic process are involved in the development of autoreactive B cells in Fas/FasL-intact autoimmune disease.

Compromised disease resistance in saponin-deficient plants

Saponins are glycosylated plant secondary metabolites found in many major food crops [Price, K. R., Johnson, I. T. & Fenwick, G. R. (1987) CRC Crit. Rev. Food Sci. Nutr. 26, 27–133]. Because many saponins have potent antifungal properties and are present in healthy plants in high concentrations, these molecules may act as preformed chemical barriers to fungal attack. The isolation of plant mutants defective in saponin biosynthesis represents a powerful strategy for evaluating the importance of these compounds in plant defense. The oat root saponin avenacin A-1 fluoresces under ultraviolet illumination [Crombie, L., Crombie, W. M. L. & Whiting, D. A. (1986) J. Chem. Soc. Perkins 1, 1917–1922], a property that is extremely rare among saponins. Here we have exploited this fluorescence to isolate saponin-deficient (sad) mutants of a diploid oat species, Avena strigosa. These sad mutants are compromised in their resistance to a variety of fungal pathogens, and a number of lines of evidence suggest that this compromised disease resistance is a direct consequence of saponin deficiency. Because saponins are widespread throughout the plant kingdom, this group of secondary metabolites may have general significance as antimicrobial phytoprotectants.

Plasminogen deficiency accelerates vessel wall disease in mice predisposed to atherosclerosis

A critical link between hemostatic factors and atherosclerosis has been inferred from a variety of indirect observations, including the expression of procoagulant and fibrinolytic factors within atherosclerotic vessels, the presence of fibrin in intimal lesions, and the cellular infiltration of mural thrombi leading to their incorporation into developing plaques. To directly examine the role of the key fibrinolytic factor, plasminogen, in atherogenesis, plasminogen-deficient mice were crossed to hypercholesterolemic, apolipoprotein E-deficient mice predisposed to atherosclerosis. We report that the loss of plasminogen greatly accelerates the formation of intimal lesions in apolipoprotein E-deficient animals, whereas plasminogen deficiency alone does not cause appreciable atherosclerosis. These studies provide direct evidence that circulating hemostatic factors strongly influence vessel wall disease in the context of a disorder in lipid metabolism.

Cell type-specific loss of atp6 RNA editing in cytoplasmic male sterile Sorghum bicolor

RNA editing and cytoplasmic male sterility are two important phenomena in higher plant mitochondria. To determine whether correlations might exist between the two, RNA editing in different tissues of Sorghum bicolor was compared employing reverse transcription–PCR and subsequent sequence analysis. In etiolated shoots, RNA editing of transcripts of plant mitochondrial atp6, atp9, nad3, nad4, and rps12 genes was identical among fertile or cytoplasmic male sterile plants. We then established a protocol for mitochondrial RNA isolation from plant anthers and pollen to include in these studies. Whereas RNA editing of atp9, nad3, nad4, and rps12 transcripts in anthers was similar to etiolated shoots, mitochondrial atp6 RNA editing was strongly reduced in anthers of the A3Tx398 male sterile line of S. bicolor. atp6 transcripts of wheat and selected plastid transcripts in S. bicolor showed normal RNA editing, indicating that loss of atp6 RNA editing is specific for cytoplasmic male sterility S. bicolor mitochondria. Restoration of fertility in F1 and F2 lines correlated with an increase in RNA editing of atp6 transcripts. Our data suggest that loss of atp6 RNA editing contributes to or causes cytoplasmic male sterility in S. bicolor. Further analysis of the mechanism of cell type-specific loss of atp6 RNA editing activity may advance our understanding of the mechanism of RNA editing.

Expression of the Bs2 pepper gene confers resistance to bacterial spot disease in tomato

The Bs2 resistance gene of pepper specifically recognizes and confers resistance to strains of Xanthomonas campestris pv. vesicatoria that contain the corresponding bacterial avirulence gene, avrBs2. The involvement of avrBs2 in pathogen fitness and its prevalence in many X. campestris pathovars suggests that the Bs2 gene may be durable in the field and provide resistance when introduced into other plant species. Employing a positional cloning strategy, the Bs2 locus was isolated and the gene was identified by coexpression with avrBs2 in an Agrobacterium-mediated transient assay. A single candidate gene, predicted to encode motifs characteristic of the nucleotide binding site–leucine-rich repeat class of resistance genes, was identified. This gene specifically controlled the hypersensitive response when transiently expressed in susceptible pepper and tomato lines and in a nonhost species, Nicotiana benthamiana, and was designated as Bs2. Functional expression of Bs2 in stable transgenic tomatoes supports its use as a source of resistance in other Solanaceous plant species.

Marked decrease of neuropeptide Y Y2 receptor binding sites in the hippocampus in murine prion disease

Using autoradiographic binding methodology with monoiodinated peptide YY together with the agonists neuropeptide Y (NPY) and NPY (13–36), as well as in situ hybridization with oligonucleotide probes complementary to the NPY Y2 receptor (Y2-R) mRNA, we have studied whether or not intracerebral prion inoculation affects Y2-Rs in male CD-1 mice. Monoiodinated peptide YY binding, mainly representing Y2-Rs, was down-regulated by 85% in the CA1 strata oriens and radiatum and by 50–65% in the CA3 stratum oriens 110–140 days postinoculation. In the CA3 stratum radiatum, where the mossy fibers from the dentate granule cells project, there was a significant decrease in PYY binding at 110–120 days. Y2-R mRNA, moderately expressed both in the CA1 and CA3 pyramidal cell layers and the granule cell layer in the dentate gyrus, showed a slight, but not significant, decrease in CA3 neurons 130 days postinoculation. The results indicate that the accumulation of the scrapie prion protein in the CA1–3 region strongly inhibits NPY binding at the Y2-Rs, which, however, is only marginally due to reduced Y2-R mRNA expression. The loss of the ability of NPY to bind to inhibitory Y2-Rs may cause dysfunction of hippocampal circuits and may contribute to the clinical symptoms in mouse scrapie.

Disruption of the telomerase catalytic subunit gene from Arabidopsis inactivates telomerase and leads to a slow loss of telomeric DNA

Telomerase is an essential enzyme that maintains telomeres on eukaryotic chromosomes. In mammals, telomerase is required for the lifelong proliferative capacity of normal regenerative and reproductive tissues and for sustained growth in a dedifferentiated state. Although the importance of telomeres was first elucidated in plants 60 years ago, little is known about the role of telomeres and telomerase in plant growth and development. Here we report the cloning and characterization of the Arabidopsis telomerase reverse transcriptase (TERT) gene, AtTERT. AtTERT is predicted to encode a highly basic protein of 131 kDa that harbors the reverse transcriptase and telomerase-specific motifs common to all known TERT proteins. AtTERT mRNA is 10–20 times more abundant in callus, which has high levels of telomerase activity, versus leaves, which contain no detectable telomerase. Plants homozygous for a transfer DNA insertion into the AtTERT gene lack telomerase activity, confirming the identity and function of this gene. Because telomeres in wild-type Arabidopsis are short, the discovery that telomerase-null plants are viable for at least two generations was unexpected. In the absence of telomerase, telomeres decline by approximately 500 bp per generation, a rate 10 times slower than seen in telomerase-deficient mice. This gradual loss of telomeric DNA may reflect a reduced rate of nucleotide depletion per round of DNA replication, or the requirement for fewer cell divisions per organismal generation. Nevertheless, progressive telomere shortening in the mutants, however slow, ultimately should be lethal.