Título en español.

El 11 de noviembre, cuando el follaje de las demás plantas era amarillo o pardo, se seleccionaron en un campo de New Jersey dos plantas de espárrago, cuyo follaje era de un color verde obscuro, el cual se designó como "verde-persistente". Para estudiar este carácter genético las dos plantas se cruzaron entre sí y luego también se cruzó cada una con otras plantas de color normal. El estudio tuvo como propósito secundario el determinar mediante el uso del espectrofotómetro, el efecto que el gene o genes responsables del color puedan tener sobre el sistema de pigmentación de las plantas de espárrago. También se trató de identificar en plántulas en el invernadero los imitantes de color verde-persistente. El estudio del fenotipo de 17 progenies F1, F2 y del retrocruce1, indicó que el color verde-persistente en el follaje de la planta de espárrago se hereda como un gene recesivo simple. Se observó una gran diferencia cuantitativa de clorofila y carotina entre las plantas de follaje verde-persistente y las de color normal en el mes de octubre, pero no en julio. Aparentemente, los mutantes retienen la clorofila y la carotina hasta más tarde en el otoño que las plantas de color normal. No se observaron diferencias cualitativas entre los pigmentos en ambos tipos de planta durante julio u octubre. Fue fácil diferenciar entre las plantas de espárrago de color verde-persistente (follaje verde) y las de color normal (follaje amarillo) en el invernadero cuando tenían 6 semanas de nacidas.</jats:p

Early-phase (EP) clinical trials (CTs) in the community: Results from the National Cancer Institute (NCI) Community Cancer Centers Program (NCCCP) Early-Phase Working Group (EPWG) Baseline Assessment Study (BAS).

e16561 Background: The NCCCP is a network of 30 community cancer center (CCC) sites that strive to expand cancer research capacity and deliver advanced care in the community. The EPWG was formed to facilitate NCCCP site participation in EP (phase I-II) CTs, thus allowing patients (pts) to be treated within their communities. This study describes the CT infrastructure at NCCCP sites and its association with EP accrual. Methods: A BAS was conducted to obtain data on NCCCP site CT infrastructure, funding, sponsor affiliations, and barriers to EP CTs. To evaluate EP performance, EP accruals during July 2010-June 2011 were obtained. High accruing sites were those with EP accrual above the median EP accrual per 1,000 new analytical cases seen in 2009 or 2010. Results: 27 sites, caring for ~56,000 new cancer pts annually, participated in the study. Median number of accruing EP trials/site was 6 (mean 7.4). Median EP accrual/site was 14 (mean 16). Median EP accrual rate was 7/1,000. Trials with a phase I component were open at 21 sites. Most sites (24) are members of multiple CGs (median 4) and enroll pts via the CTSU (70%). The more common barriers to EP trial implementation were related to infrastructure (59%), cost (52%), and access to trials (41%). When accrual rates to NCCCP CTEP EP trials only were analyzed, we found that between high vs low accruing sites, respectively, higher accrual rates were associated with higher number of CRAs devoted to EP trials (median 3.25 vs 1; P= .05) and lower proportion of funding from industry (median 18% vs 40%; P=.02). We did not, however, find significant associations when EP trials were examined across all sponsors. Conclusions: CCCs are capable of conducting, and actively participating in, EP trials. Infrastructure and collaborations are critical components of success. Our study provides useful information for those planning to begin EP trials in the community setting. [Table: see text] </jats:p

NMDA receptor gene variations as modifiers in Huntington disease: a replication study.

Several candidate modifier genes which, in addition to the pathogenic CAG repeat expansion, influence the age at onset (AO) in Huntington disease (HD) have already been described. The aim of this study was to replicate association of variations in the N-methyl D-aspartate receptor subtype genes GRIN2A and GRIN2B in the “REGISTRY” cohort from the European Huntington Disease Network (EHDN). The analyses did replicate the association reported between the GRIN2A rs2650427 variation and AO in the entire cohort. Yet, when subjects were stratified by AO subtypes, we found nominally significant evidence for an association of the GRIN2A rs1969060 variation and the GRIN2B rs1806201 variation. These findings further implicate the N-methyl D-aspartate receptor subtype genes as loci containing variation associated with AO in HD