Precisiones a una nueva edición del "Libro de la montería"

Producción CientíficaEn 1874 publicó José Gutiérrez de la Vega el Libro de la Montería del rey Aljonso XI para inaugurar su Biblioteca Venatoria. Ciento nueve años después se vuelve a acometer la labor de editar este magnífico libro de caza medieval, pero con el estudioso en mente y no tan sólo «para ilustración de los cazadores, deleite de los eruditos y gloria de la lengua castellana», como declara Gutiérrez de la Vega en las portadas de su colección. Entre estas dos ediciones modernas, sólo se han escrito algunos artículos, publicado unos pocos fragmentos y una reimpresión de la edición de 1874. Esta nueva edición del profesor Seniff, de la Universidad Estatal de Michigan (HE. UU.), supone un gran avance, pues la que hizo Gutiérrez de la Vega, aunque buena dentro de lo que cabe, no es muy fiable debido a las transgresiones textuales y a que no dijera qué manuscrito era el que seguía, y esto ya lo criticó F. B. Navarro. El profesor Seniff ha basado la suya en el más antiguo y completo códice conservado, el Y-II-19 de la Biblioteca del monasterio de El Escorial

Genetic Variation in Selenoprotein Genes, Lifestyle, and Risk of Colon and Rectal Cancer

BACKGROUND: Associations between selenium and cancer have directed attention to role of selenoproteins in the carcinogenic process. METHODS: We used data from two population-based case-control studies of colon (n = 1555 cases, 1956 controls) and rectal (n = 754 cases, 959 controls) cancer. We evaluated the association between genetic variation in TXNRD1, TXNRD2, TXNRD3, C11orf31 (SelH), SelW, SelN1, SelS, SepX, and SeP15 with colorectal cancer risk. RESULTS: After adjustment for multiple comparisons, several associations were observed. Two SNPs in TXNRD3 were associated with rectal cancer (rs11718498 dominant OR 1.42 95% CI 1.16,1.74 pACT 0.0036 and rs9637365 recessive 0.70 95% CI 0.55,0.90 pACT 0.0208). Four SNPs in SepN1 were associated with rectal cancer (rs11247735 recessive OR 1.30 95% CI 1.04,1.63 pACT 0.0410; rs2072749 GGvsAA OR 0.53 95% CI 0.36,0.80 pACT 0.0159; rs4659382 recessive OR 0.58 95% CI 0.39,0.86 pACT 0.0247; rs718391 dominant OR 0.76 95% CI 0.62,0.94 pACT 0.0300). Interaction between these genes and exposures that could influence these genes showed numerous significant associations after adjustment for multiple comparisons. Two SNPs in TXNRD1 and four SNPs in TXNRD2 interacted with aspirin/NSAID to influence colon cancer; one SNP in TXNRD1, two SNPs in TXNRD2, and one SNP in TXNRD3 interacted with aspirin/NSAIDs to influence rectal cancer. Five SNPs in TXNRD2 and one in SelS, SeP15, and SelW1 interacted with estrogen to modify colon cancer risk; one SNP in SelW1 interacted with estrogen to alter rectal cancer risk. Several SNPs in this candidate pathway influenced survival after diagnosis with colon cancer (SeP15 and SepX1 increased HRR) and rectal cancer (SepX1 increased HRR). CONCLUSIONS: Findings support an association between selenoprotein genes and colon and rectal cancer development and survival after diagnosis. Given the interactions observed, it is likely that the impact of cancer susceptibility from genotype is modified by lifestyle

Long-Term Real-World Effectiveness and Safety of Ustekinumab in Crohn’s Disease Patients: The SUSTAIN Study

Background Large real-world-evidence studies are required to confirm the durability of response, effectiveness, and safety of ustekinumab in Crohn’s disease (CD) patients in real-world clinical practice. Methods A retrospective, multicentre study was conducted in Spain in patients with active CD who had received ≥1 intravenous dose of ustekinumab for ≥6 months. Primary outcome was ustekinumab retention rate; secondary outcomes were to identify predictive factors for drug retention, short-term remission (week 16), loss of response and predictive factors for short-term efficacy and loss of response, and ustekinumab safety. Results A total of 463 patients were included. Mean baseline Harvey-Bradshaw Index was 8.4. A total of 447 (96.5%) patients had received prior biologic therapy, 141 (30.5%) of whom had received ≥3 agents. In addition, 35.2% received concomitant immunosuppressants, and 47.1% had ≥1 abdominal surgery. At week 16, 56% had remission, 70% had response, and 26.1% required dose escalation or intensification; of these, 24.8% did not subsequently reduce dose. After a median follow-up of 15 months, 356 (77%) patients continued treatment. The incidence rate of ustekinumab discontinuation was 18% per patient-year of follow-up. Previous intestinal surgery and concomitant steroid treatment were associated with higher risk of ustekinumab discontinuation, while a maintenance schedule every 12 weeks had a lower risk; neither concomitant immunosuppressants nor the number of previous biologics were associated with ustekinumab discontinuation risk. Fifty adverse events were reported in 39 (8.4%) patients; 4 of them were severe (2 infections, 1 malignancy, and 1 fever). Conclusions Ustekinumab is effective and safe as short- and long-term treatment in a refractory cohort of CD patients in real-world clinical practice

Using Interpretable Machine Learning to Identify Baseline Predictive Factors of Remission and Drug Durability in Crohn’s Disease Patients on Ustekinumab

Ustekinumab has shown efficacy in Crohn's Disease (CD) patients. To identify patient profiles of those who benefit the most from this treatment would help to position this drug in the therapeutic paradigm of CD and generate hypotheses for future trials. The objective of this analysis was to determine whether baseline patient characteristics are predictive of remission and the drug durability of ustekinumab, and whether its positioning with respect to prior use of biologics has a significant effect after correcting for disease severity and phenotype at baseline using interpretable machine learning. Patients' data from SUSTAIN, a retrospective multicenter single-arm cohort study, were used. Disease phenotype, baseline laboratory data, and prior treatment characteristics were documented. Clinical remission was defined as the Harvey Bradshaw Index <= 4 and was tracked longitudinally. Drug durability was defined as the time until a patient discontinued treatment. A total of 439 participants from 60 centers were included and a total of 20 baseline covariates considered. Less exposure to previous biologics had a positive effect on remission, even after controlling for baseline disease severity using a non-linear, additive, multivariable model. Additionally, age, body mass index, and fecal calprotectin at baseline were found to be statistically significant as independent negative risk factors for both remission and drug survival, with further risk factors identified for remission

Ecological distribution conflicts as forces for sustainability : an overview and conceptual framework

Unidad de excelencia María de Maeztu MdM-2015-0552Centre: ICTA Digital object identifier for the 'European Research Council' (http://dx.doi.org/10.13039/501100000781) Digital object identifier for 'Horizon 2020' (http://dx.doi.org/10.13039/501100007601).Can ecological distribution conflicts turn into forces for sustainability? This overview paper addresses in a systematic conceptual manner the question of why, through whom, how, and when conflicts over the use of the environment may take an active role in shaping transitions toward sustainability. It presents a conceptual framework that schematically maps out the linkages between (a) patterns of (unsustainable) social metabolism, (b) the emergence of ecological distribution conflicts, (c) the rise of environmental justice movements, and (d) their potential contributions for sustainability transitions. The ways how these four processes can influence each other are multi-faceted and often not a foretold story. Yet, ecological distribution conflicts can have an important role for sustainability, because they relentlessly bring to light conflicting values over the environment as well as unsustainable resource uses affecting people and the planet. Environmental justice movements, born out of such conflicts, become key actors in politicizing such unsustainable resource uses, but moreover, they take sometimes also radical actions to stop them. By drawing on creative forms of mobilizations and diverse repertoires of action to effectively reduce unsustainabilities, they can turn from 'victims' of environmental injustices into 'warriors' for sustainability. But when will improvements in sustainability be lasting? By looking at the overall dynamics between the four processes, we aim to foster a more systematic understanding of the dynamics and roles of ecological distribution conflicts within sustainability processes