Effects of foliar fertilization of common bean (Phaseolus vulgaris, L.) during the seed-filling stage

An experiment was carried out with common bean (Phaseolus vulgaris, L.) in a Red Yellow Latossol, sandy phase, in order to study the influence of foliar spraying of the Hanway nutrient solution (NPKS) at grain filling stage on: 1) grain yield; 2) the uptake of fertilizer and soil nitrogen by this crop through the root system and 3) the efficiency of utilization of the nitrogen in the foliar spray solution by the grain. The results of this experiment showed that the foliar application of the Hanway solution with ammonium nitrate at the pod filling period caused severe leaf burn and grain yield was inferior to that of the plants which received a soil application of this fertilizer at the same stage. These facts can be attributed to the presence of ammonium nitrate in the concentration used. The composition of final spray was: 114,28 Kg NH4NO3 + 43,11 Kg potassium poliphosphate + 12,44 Kg potassium sulphate per 500 litres. The uptake of nitrogen fertilizer through the root system and the efficiency of its utilization was greater than that through the leaves.

Can genetic algorithms explain experimental anomalies? An application to common property resources

It is common to find in experimental data persistent oscillations in the aggregate outcomes and high levels of heterogeneity in individual behavior. Furthermore, it is not unusual to find significant deviations from aggregate Nash equilibrium predictions. In this paper, we employ an evolutionary model with boundedly rational agents to explain these findings. We use data from common property resource experiments (Casari and Plott, 2003). Instead of positing individual-specific utility functions, we model decision makers as selfish and identical. Agent interaction is simulated using an individual learning genetic algorithm, where agents have constraints in their working memory, a limited ability to maximize, and experiment with new strategies. We show that the model replicates most of the patterns that can be found in common property resource experiments.

Observations on the morphology of Australorbis nigricans

A morphological study was done on A. nigricans, based on the observation of shell, radula, renal region and genitalia of 50 specimens measuring 18 mm in diameter. The data obtained are to be compared with those recorded in our previous paper (PARAENSE & DESLANDES, 1955) on A. glabratus. The characteristics common to both species will not be mentioned here. The numerals refere to the means and their standard deviations: no special reference being done, they correspond to length measurementes. Shell - 18 mm in diameter, 6.37 ± 0.29 mm in greatest width, 6 whorls. Prevailing colur ferruginous sepia, a minority of olivaceous, ochreous, nigrescent and deeply black specimens being found. Right side variously depressed, umbilicated, 1.5 to 3.5 mm deep from the bottom of the umblicus to the highest level of the last whorl. Left side more depressed than the right one, broadly concave, 1.5 to 3.5 mm deep. Both sides show a varously distinct keel, that looks sharper at the left. Aperture deltoid, varying in outline and width. Body, extended - 60.26 ± 3.62 mm, less pigmented than in glabratus. Renal tube - 30.68 ± 1.69 mm, showing neither ridge nor pigmented line along its ventral surface, this negative character affording a sure means of separation from glabratus. Ovotestis - 14.48 ± 1.93 mm. Ovisperm duct - 13.04 ± 1.60 mm, including the non-unwound seminal vesicle. The latter was 0.97 ± 0,21 mm in greatest width. Carrefour - Resembling that of glabratus. Sperm duct - 21.36 ± 1.53 mm. Prostate - Prostate duct 7.14 ± 0.74 mm, collecting a row of long diverticula numbering 19.6 ± 3.1 and more separate than in glabratus. Last diverticulum generally bifurcate or arborescent, the remaining ones arborescent. Vas deferens - 28.68 ± 1.38. Ratio vas deferens/vergic sac = 6.8±0.8. Verge - 3.08 ± 0.28 mm long, 0.11 ± 0.02 mm wide. Vergic sac - 3.07 ± 0.28 mm long, about 0.20 mm wide. Ratio vergic sac/preputium = 0.84 ± 0.12. Preputium - 3.69 ± 0.47 mm long, 0.85 ± 0.10 mm wide. Albumen gland - Resembling taht of glabratus. Oviduct - 16.26 ± 1.41 mm, swollen at the cephalic end. Uterus - 13.24 ± 1.19 mm. Vagina - 1.70 ± 0.22 mm, swolen at the caudal portion. Spermatheca - 2.78 ± 0.40 mm long, 0.86 ± 0.16 mm wide. Spermathecal duct 1.11 ± 0.20 mm. Radula - 125 to 168 horizontal rows of teeth (mean 153.9 ± 8.4). Radula formula 28-1-28 to 36-1-36 (mean 31.8 ± 1.9). Mode formula 31-1-31. The morphological characteristics of the renal region and shell, and the great body length in the same condition of shell diameter, distinguish A. nigricans from the most related species A. glabratus, giving support to considering it a good species from a txonomic or phenotypic standpoint (morphospecies).

The life history of Hepatozoon leptodactyli (Lesage, 1908) Pessoa, 1970: a parasite of the common laboratory animal: the frog of the genus Leptodactylus

The main object of the present paper is to furnish a brief account to the knowledgement of Protozoa parasitic in common Brazilian frog of the genus Leptodactylus for general students in Zoology and for investigators that use this frog as a laboratory animal. Hepatozoon leptodactyli (Haemogregarina leptodactyli) was found in two species of frogs - Leptodactylus ocellatus and L. pentadactylus - in which develop schizogony whereas sporogony occurs in the leech Haementeria lutzi as was obtainded in experimental conditions. Intracellular forms have been found in peripheral circulation, chiefly in erythrocytes, but we have found them in leukocytes too. Tissue stages were found in frog, liver, lungs, spleen, gut, brain and heart. The occurence of hemogregarine in the Central Nervous System was recorded by Costa & al,(13) and Ball (2). Some cytochemical methods were employed in attempt to differentiate gametocytes from trophozoites in the peripheral blood and to characterize the cystic membrane as well. The speorogonic cycle was developed in only one specie of leech. A brief description of the parasite is given.

Long-term miR-669a therapy alleviates chronic dilated cardiomyopathy in dystrophic mice.

BACKGROUND: Dilated cardiomyopathy (DCM) is a leading cause of chronic morbidity and mortality in muscular dystrophy (MD) patients. Current pharmacological treatments are not yet able to counteract chronic myocardial wastage, thus novel therapies are being intensely explored. MicroRNAs have been implicated as fine regulators of cardiomyopathic progression. Previously, miR-669a downregulation has been linked to the severe DCM progression displayed by Sgcb-null dystrophic mice. However, the impact of long-term overexpression of miR-669a on muscle structure and functionality of the dystrophic heart is yet unknown. METHODS AND RESULTS: Here, we demonstrate that intraventricular delivery of adeno-associated viral (AAV) vectors induces long-term (18 months) miR-669a overexpression and improves survival of Sgcb-null mice. Treated hearts display significant decrease in hypertrophic remodeling, fibrosis, and cardiomyocyte apoptosis. Moreover, miR-669a treatment increases sarcomere organization, reduces ventricular atrial natriuretic peptide (ANP) levels, and ameliorates gene/miRNA profile of DCM markers. Furthermore, long-term miR-669a overexpression significantly reduces adverse remodeling and enhances systolic fractional shortening of the left ventricle in treated dystrophic mice, without significant detrimental consequences on skeletal muscle wastage. CONCLUSIONS: Our findings provide the first evidence of long-term beneficial impact of AAV-mediated miRNA therapy in a transgenic model of severe, chronic MD-associated DCM.

Dilated cardiomyopathy and impaired cardiac hypertrophic response to angiotensin II in mice lacking FGF-2.

FGF-2 has been implicated in the cardiac response to hypertrophic stimuli. Angiotensin II (Ang II) contributes to maintain elevated blood pressure in hypertensive individuals and exerts direct trophic effects on cardiac cells. However, the role of FGF-2 in Ang II-induced cardiac hypertrophy has not been established. Therefore, mice deficient in FGF-2 expression were studied using a model of Ang II-dependent hypertension and cardiac hypertrophy. Echocardiographic measurements show the presence of dilated cardiomyopathy in normotensive mice lacking FGF-2. Moreover, hypertensive mice without FGF-2 developed no compensatory cardiac hypertrophy. In wild-type mice, hypertrophy was associated with a stimulation of the c-Jun N-terminal kinase, the extracellular signal regulated kinase, and the p38 kinase pathways. In contrast, mitogen-activated protein kinase (MAPK) activation was markedly attenuated in FGF-2-deficient mice. In vitro, FGF-2 of fibroblast origin was demonstrated to be essential in the paracrine stimulation of MAPK activation in cardiomyocytes. Indeed, fibroblasts lacking FGF-2 expression have a defective capacity for releasing growth factors to induce hypertrophic responses in cardiomyocytes. Therefore, these results identify the cardiac fibroblast population as a primary integrator of hypertrophic stimuli in the heart, and suggest that FGF-2 is a crucial mediator of cardiac hypertrophy via autocrine/paracrine actions on cardiac cells.

The 16p11.2 locus modulates brain structures common to autism, schizophrenia and obesity

Anatomical structures and mechanisms linking genes to neuropsychiatric disorders are not deciphered. Reciprocal copy number variants at the 16p11.2 BP4-BP5 locus offer a unique opportunity to study the intermediate phenotypes in carriers at high risk for autism spectrum disorder (ASD) or schizophrenia (SZ). We investigated the variation in brain anatomy in 16p11.2 deletion and duplication carriers. Beyond gene dosage effects on global brain metrics, we show that the number of genomic copies negatively correlated to the gray matter volume and white matter tissue properties in cortico-subcortical regions implicated in reward, language and social cognition. Despite the near absence of ASD or SZ diagnoses in our 16p11.2 cohort, the pattern of brain anatomy changes in carriers spatially overlaps with the well-established structural abnormalities in ASD and SZ. Using measures of peripheral mRNA levels, we confirm our genomic copy number findings. This combined molecular, neuroimaging and clinical approach, applied to larger datasets, will help interpret the relative contributions of genes to neuropsychiatric conditions by measuring their effect on local brain anatomy.Molecular Psychiatry advance online publication, 25 November 2014; doi:10.1038/mp.2014.145.

Automatic top-down processing explains common left occipito-temporal responses to visual words and objects.

Previous studies have demonstrated that a region in the left ventral occipito-temporal (LvOT) cortex is highly selective to the visual forms of written words and objects relative to closely matched visual stimuli. Here, we investigated why LvOT activation is not higher for reading than picture naming even though written words and pictures of objects have grossly different visual forms. To compare neuronal responses for words and pictures within the same LvOT area, we used functional magnetic resonance imaging adaptation and instructed participants to name target stimuli that followed briefly presented masked primes that were either presented in the same stimulus type as the target (word-word, picture-picture) or a different stimulus type (picture-word, word-picture). We found that activation throughout posterior and anterior parts of LvOT was reduced when the prime had the same name/response as the target irrespective of whether the prime-target relationship was within or between stimulus type. As posterior LvOT is a visual form processing area, and there was no visual form similarity between different stimulus types, we suggest that our results indicate automatic top-down influences from pictures to words and words to pictures. This novel perspective motivates further investigation of the functional properties of this intriguing region.

Controversies about a common etiology for eating and mood disorders.

Obesity and depression represent a growing health concern worldwide. For many years, basic science and medicine have considered obesity as a metabolic illness, while depression was classified a psychiatric disorder. Despite accumulating evidence suggesting that obesity and depression may share commonalities, the causal link between eating and mood disorders remains to be fully understood. This etiology is highly complex, consisting of multiple environmental and genetic risk factors that interact with each other. In this review, we sought to summarize the preclinical and clinical evidence supporting a common etiology for eating and mood disorders, with a particular emphasis on signaling pathways involved in the maintenance of energy balance and mood stability, among which orexigenic and anorexigenic neuropeptides, metabolic factors, stress responsive hormones, cytokines, and neurotrophic factors.