The management of outlier grades in positively skewed gold distributions is a contentious issue. Incorporating outliers in standard ordinary kriging (OK) estimation procedures in a way that honours the data without smearing extreme grades into surrounding areas has been problematic. Cutting or capping of outliers to mitigate their influence in estimation techniques is common practice, while methods that manipulate the OK system of equations fail to honour the data. We propose a method of post-processing of kriging weights that provides realistic OK estimates and mitigates smearing without manipulating kriging equations or changing the original grades. The method requires that the data is not clustered, is approximately equally spaced, and is of the same support. Positively skewed data is ordered on attribute grade and nonlinearly transformed to a Gaussian histogram of categorical bins whose frequency is based on their likelihood of occurrence and location in the sample distributions. Factors that restrict kriging weights are calculated by dividing the percentage frequency of data in each bin by the percentage frequency of data in the bin with the highest frequency. Restriction factors applied to the kriging weights in the OK estimation restrict the range of influence in proportion to their probability of occurrence in the distribution. Smear reduction post-processing is easy to implement and addresses issues arising from negative kriging weights while considering the spatial location of samples, the sample grades, and their probability of occurrence. The method mitigates both smoothing and conditional bias .

Stress can be understood as a threat to psychological or physiological integrity of the individual. Stress has previously shown to alter morphology and function of diverse structures of the Central Nervous System related to learning, memory and emotional response, such as hippocampus, amygdala and prefrontal cortex. In the current work we assessed the effect of chronic stress for immobilization on structure of primary visual cortex (area 17) in male adult Sprague-Dawley rats (n=9), of 3 months of age (250-350g.). Stressed rats (n=3) tended to show lower neuronal densities than control rats (n=3) and were significantly lower (p<0.05) than recovered post-stress rats (n=3), which showed the highest neuronal densities observed. Since an inverse correlation between neuronal density and size of neuronal bodies and their respective dendrite branches, these changes might impact processing of visual information.

El estrés puede ser definido como una amenaza a la integridad psicológica o fisiológica de un individuo. Por otro lado, se ha verificado que el estrés tiene efecto sobre la morfología y función de diversas estructuras del Sistema Nervioso Central, relacionadas con el aprendizaje, memoria y respuestas emocionales, tales como el hipocampo, amígdala y corteza prefrontal. Es por lo anterior, que el objetivo del presente trabajo fue realizar un estudio de la anatomía de la corteza visual primaria (área 17), en ratas machos (n=9), de la cepa Sprague-Dawley, de 3 meses de edad (250-350g.), sometidas a estrés crónico por inmovilización. Es así como se observó que el grupo estrés (n=3) presentó una menor densidad neuronal que el grupo control (n=3) y una significativa menor densidad neuronal (p<0,05) que el grupo postestrés (n=3) el cual presentó la más alta densidad neuronal observada. Estableciendo una relación inversa entre densidad neuronal y tamaño de los somas neuronales y sus respectivas conexiones y ramificaciones dendríticas. Lo anterior podría tener incidencia en el procesamiento de la información visual.

Extensive neuronal cell loss is observed in Alzheimer's disease. Laminin immunoreactivity colocalizes with senile plaques, the characteristic extracellular histopathological lesions of Alzheimer brain, which consist of the amyloid ß (Aß) peptide polymerized into amyloid fibrils. These lesions have neurotoxic effects and have been proposed to be a main cause of neurodegeneration. In order to understand the pathological significance of the interaction between laminin and amyloid, we investigated the effect of laminin on amyloid structure and toxicity. We found that laminin interacts with the Aß1-40 peptide, blocking fibril formation and even inducing depolymerization of preformed fibrils. Protofilaments known to be intermediate species of Aß fibril formation were also detected as intermediate species of laminin-induced Aß fibril depolymerization. Moreover, laminin-amyloid interactions inhibited the toxic effects on rat primary hippocampal neurons. As a whole, our results indicate a putative anti-amyloidogenic role of laminin which may be of biological and therapeutic interest for controlling amyloidosis, such as those observed in cerebral angiopathy and Alzheimer's disease.