El psicopedagogo y la intervención en ciencias experimentales

[Resumen] Para que el psicopedagogo pueda intervenir en un trabajo colaborativo en equipo con los profesores de ciencias experimentales en las dificultades de aprendizaje curriculares, es necesario que comparta significados con los profesores de área. Esto implica una mejora de la formación inicial del profesorado de ciencias experimentales, especialmente en la educación secundaria, una formación básica del psicopedagogo sobre la intervención en estas materias y el fomento de una cultura de colaboración entre los distintos profesionales en beneficio de los alumnos[Abstract] For educational psychologists to be able to take part in team work together with teachers of the sciences on curricular leaming difficulties, they need to share meanings with the teachers of that area. To this end it is fundamental that the educational psychologist has specific knowledge of intervention in these subjects. Ihis goal must go hand-in-hand with an improvement in the initial teacher education of teachers of experimental sciences, and the promotion of a culture of collaboration between different professionals for the benefit of our pupil

La posición fetal intrauterina afecta al desarrollo de las estructuras feto-placentarias de la coneja

Un total de 129 fetos de conejas multíparas fueron estudiados según su posición intrauterina. Los más próximos al ovario presentaron mejores valores morfométricos que los más alejados a esta posición, asociándose asimismo un mayor peso placentario a un mayor peso fetal. Estas diferencias fueron mantenidas en la valoración de órganos fetales, como el cerebro, hígado y aparato digestivo, mostrándose un mayor desarrollo en los fetos adyacentes al ovario. A su vez se observó una correlación positiva entre el peso placentario y el peso de estos órganos. Las diferencias de peso dentro de la misma camada podrían estar asociadas a un mayor desarrollo placentario y por consiguiente mayor disponibilidad de nutrientes

Using the posterior distribution of deviance to measure evidence of association for rare susceptibility variants

Aitkin recently proposed an integrated Bayesian/likelihood approach that he claims is general and simple. We have applied this method, which does not rely on informative prior probabilities or large-sample results, to investigate the evidence of association between disease and the 16 variants in the KDR gene provided by Genetic Analysis Workshop 17. Based on the likelihood of logistic regression models and considering noninformative uniform prior probabilities on the coefficients of the explanatory variables, we used a random walk Metropolis algorithm to simulate the distributions of deviance and deviance difference. The distribution of probability values and the distribution of the proportions of positive deviance differences showed different locations, but the direction of the shift depended on the genetic factor. For the variant with the highest minor allele frequency and for any rare variant, standard logistic regression showed a higher power than the novel approach. For the two variants with the strongest effects on Q1 under a type I error rate of 1%, the integrated approach showed a higher power than standard logistic regression. The advantages and limitations of the integrated Bayesian/likelihood approach should be investigated using additional regions and considering alternative regression models and collapsing methods

Tumor location and patient characteristics of colon and rectal adenocarcinomas in relation to survival and TNM classes

<p>Abstract</p> <p>Background</p> <p>Old age at diagnosis is associated with poor survival in colorectal cancer (CRC) for unknown reasons. Recent data show that colonoscopy is efficient in preventing left-sided cancers only. We examine the association of Tumor Node Metastasis (TNM) classes with diagnostic age and patient characteristics.</p> <p>Methods</p> <p>The Swedish Family-Cancer Database has data on TNM classes on 6,105 CRC adenocarcinoma patients. Ordinal logistic regression analysis was performed to model tumor characteristics according to age at diagnosis, tumor localization, gender, socioeconomic status, medical region and family history. The results were compared to results from survival analysis.</p> <p>Results</p> <p>The only parameters systematically associated with TNM classes were age and tumor localization. Young age at diagnosis was a risk factor for aggressive CRC, according to stage, N and M with odds ratios (ORs) ranging from 1.80 to 1.93 for diagnosis before age 50 years compared to diagnosis at 80+ years. All tumor characteristics, particularly T, were worse for colon compared to rectal tumors. Right-sided tumors showed worse characteristics for all classifiers but M. The survival analysis on patients diagnosed since 2000 showed a hazard ratio of 0.55 for diagnosis before age 50 years compared to diagnosis at over 80 years and a modestly better prognosis for left-sided compared to right-sided tumors.</p> <p>Conclusions</p> <p>The results showed systematically more aggressive tumors in young compared to old patients. The poorer survival of old patients in colon cancer was not related to the available tumor characteristics. However, these partially agreed with the limited colonoscopic success with right-sided tumors.</p

Familial association of pancreatic cancer with other malignancies in Swedish families

BACKGROUND: The aim of this study was to characterise the familial association of pancreatic cancer with other malignancies. METHODS: Relative risks (RRs) of pancreatic cancer according to family history of cancer were calculated using the updated Swedish Family-Cancer Database, which includes over 11.5 million individuals. Estimates were based on Poisson regression. RRs of tumours for individuals with a parental history of pancreatic cancer were also estimated. RESULTS: The risk of pancreatic cancer was elevated in individuals with a parental history of cancers of the liver (RR 1.41; 95% CI 1.10-1.81), kidney (RR 1.37; 95% CI 1.06-1.76), lung (RR 1.50; 95% CI 1.27-1.79) and larynx (RR 1.98; 95% CI 1.19-3.28). Associations were also found between parental history of pancreatic cancer and cancers of the small intestine, colon, breast, lung, testis and cervix in offspring. There was an increased risk of pancreatic cancer associated with early-onset breast cancer in siblings. CONCLUSION: Pancreatic cancer aggregates in families with several types of cancer. Smoking may contribute to the familial aggregation of pancreatic and lung tumours, and the familial clustering of pancreatic and breast cancer could be partially explained by inherited mutations in the BRCA2 gene. British Journal of Cancer (2009) 101, 1792-1797. doi: 10.1038/sj.bjc.6605363 www.bjcancer.com Published online 13 October 2009 (C) 2009 Cancer Research U

Pancreatic Cancer Susceptibility Loci and Their Role in Survival

Pancreatic cancer has one of the worst mortality rates of all cancers. Little is known about its etiology, particularly regarding inherited risk. The PanScan project, a genome-wide association study, identified several common polymorphisms affecting pancreatic cancer susceptibility. Single nucleotide polymorphisms (SNPs) in ABO, sonic hedgehog (SHH), telomerase reverse transcriptase (TERT), nuclear receptor subfamily 5, group A, member 2 (NR5A2) were found to be associated with pancreatic cancer risk. Moreover the scan identified loci on chromosomes 13q22.1 and 15q14, to which no known genes or other functional elements are mapped. We sought to replicate these observations in two additional, independent populations (from Germany and the UK), and also evaluate the possible impact of these SNPs on patient survival. We genotyped 15 SNPs in 690 cases of pancreatic ductal adenocarcinoma (PDAC) and in 1277 healthy controls. We replicated several associations between SNPs and PDAC risk. Furthermore we found that SNP rs8028529 was weakly associated with a better overall survival (OS) in both populations. We have also found that NR5A2 rs12029406_T allele was associated with a shorter survival in the German population. In conclusion, we found that rs8028529 could be, if these results are replicated, a promising marker for both risk and prognosis for this lethal disease

Association of colorectal adenoma with other malignancies in Swedish families

Using the Swedish Family-Cancer Database covering over 11.5 million individuals, estimated relative risks (RRs) for colorectal adenoma were using Poisson's regression. The RR of colorectal adenoma was found to be increased among first-degree relatives of patients with colorectal cancer (2.72; 95% confidence interval=2.46–3.00) and among the offspring and siblings of patients with endometrial and prostate cancers. We also found an increased risk of colorectal adenoma for the offspring of individuals with stomach cancer and leukaemia, and for siblings of those with pancreatic cancer and multiple myeloma. Our results suggest that colorectal adenoma may share a genetic aetiology with cancer even at extracolorectal sites. Increases of colorectal adenoma in families affected by prostate cancer and acute leukaemia cannot be attributed to known cancer syndromes, although the play of chance cannot be excluded

The ‘Common Disease-Common Variant’ Hypothesis and Familial Risks

The recent large genotyping studies have identified a new repertoire of disease susceptibility loci of unknown function, characterized by high allele frequencies and low relative risks, lending support to the common disease-common variant (CDCV) hypothesis. The variants explain a much larger proportion of the disease etiology, measured by the population attributable fraction, than of the familial risk. We show here that if the identified polymorphisms were markers of rarer functional alleles they would explain a much larger proportion of the familial risk. For example, in a plausible scenario where the marker is 10 times more common than the causative allele, the excess familial risk of the causative allele is over 10 times higher than that of the marker allele. However, the population attributable fractions of the two alleles are equal. The penetrance mode of the causative locus may be very difficult to deduce from the apparent penetrance mode of the marker locus

Modification of second cancer risk after malignant melanoma by parental history of cancer

The Swedish Family-Cancer Database was used to quantify the incidence of second tumours in melanoma patients with a parental history of cancer. Patients with parents affected by melanoma showed a 32.3-fold risk of second primary melanomas, which was greater than a multiplicative interaction