Interview with Professor Mark Brodin about his book "William P. Homans Jr.: A Life In Court"

Boston lawyer William P. Homans Jr. devoted his fifty-year career to the defense of the poor and downtrodden, the protection of our most basic civil liberties, and the abolition of the death penalty. Descendant of two of Boston's oldest and most prominent families, and combat veteran of both the British and American Navies during World War II, Homans became unlikely guru to the 1960s generation of radical lawyers and antiwar activists. He was on the defense team in the 1968 conspiracy trial of Dr. Benjamin Spock and four other leading opponents of the Vietnam War accused of aiding and abetting resistance to the military draft, and represented Dr. Kenneth Edelin in the 1975 manslaughter prosecution arising out of a lawful abortion performed after Roe v. Wade. The narrative contrasts Bill Homans' storied legal career with a troubled personal life in a balanced but unvarnished manner, testifying to the strength of the human spirit when committed to the pursuit of the common good. About the author: Mark S. Brodin is Professor of Law at Boston College Law School and the author of numerous books and law journal articles in the areas of civil and criminal procedure, evidence, litigation, and employment discrimination. A graduate of Columbia College (1969) and Columbia Law School (1972), he served as law clerk to United States District Judge Joseph L. Tauro and staff attorney with the Lawyers' Committee for Civil Rights in Boston. He has also practiced for brief periods as a public defender in Boston and a prosecutor in Norfolk County.

An update of the mechanisms of resistance to EGFR-tyrosine kinase inhibitors in breast cancer: gefitinib (Iressatrade mark)-induced changes in the expression and nucleo-cytoplasmic trafficking of HER-ligands (Review)

Intrinsic resistance to the epidermal growth factor receptor (EGFR; HER1) tyrosine kinase inhibitor (TKI) gefitinib, and more generally to EGFR TKIs, is a common phenomenon in breast cancer. The availability of molecular criteria for predicting sensitivity to EGFR-TKIs is, therefore, the most relevant issue for their correct use and for planning future research. Though it appears that in non-small-cell lung cancer (NSCLC) response to gefitinib is directly related to the occurrence of specific mutations in the EGFR TK domain, breast cancer patients cannot be selected for treatment with gefitinib on the same basis as such EGFR mutations have been reported neither in primary breast carcinomas nor in several breast cancer cell lines. Alternatively, there is a general agreement on the hypothesis that the occurrence of molecular alterations that activate transduction pathways downstream of EGFR (i.e., MEK1/MEK2 - ERK1/2 MAPK and PI-3'K - AKT growth/survival signaling cascades) significantly affect the response to EGFR TKIs in breast carcinomas. However, there are no studies so far addressing a role of EGF-related ligands as intrinsic breast cancer cell modulators of EGFR TKI efficacy. We recently monitored gene expression profiles and sub-cellular localization of HER-1/-2/-3/-4 related ligands (i.e., EGF, amphiregulin, transforming growth factor-α, ß-cellulin, epiregulin and neuregulins) prior to and after gefitinib treatment in a panel of human breast cancer cell lines. First, gefitinibinduced changes in the endogenous levels of EGF-related ligands correlated with the natural degree of breast cancer cell sensitivity to gefitinib. While breast cancer cells intrinsically resistant to gefitinib (IC50 ≥15 μM) markedly up-regulated (up to 600 times) the expression of genes codifying for HERspecific ligands, a significant down-regulation (up to 106 times) of HER ligand gene transcription was found in breast cancer cells intrinsically sensitive to gefitinib (IC50 ≤1 μM). Second, loss of HER1 function differentially regulated the nuclear trafficking of HER-related ligands. While gefitinib treatment induced an active import and nuclear accumulation of the HER ligand NRG in intrinsically gefitinib-resistant breast cancer cells, an active export and nuclear loss of NRG was observed in intrinsically gefitinib-sensitive breast cancer cells. In summary, through in vitro and pharmacodynamic studies we have learned that, besides mutations in the HER1 gene, oncogenic changes downstream of HER1 are the key players regulating gefitinib efficacy in breast cancer cells. It now appears that pharmacological inhibition of HER1 function also leads to striking changes in both the gene expression and the nucleo-cytoplasmic trafficking of HER-specific ligands, and that this response correlates with the intrinsic degree of breast cancer sensitivity to the EGFR TKI gefitinib. The relevance of this previously unrecognized intracrine feedback to gefitinib warrants further studies as cancer cells could bypass the antiproliferative effects of HER1-targeted therapeutics without a need for the overexpression and/or activation of other HER family members and/or the activation of HER-driven downstream signaling cascades

Question Mark Perception - example test questions

This set of questions on astronomy can be used to show the main question types available. You will need to log in using your University username and password

INFO1010 Mark Scheme for group presentations

Detailed mark scheme for group presentations, can be used to highlight the various aspects of the content and processes associated with a presentation which need to be addressed

Use of video mark schemes to facilitate student generated feedback and reflection

Presentation

Sustaining Success mark scheme

This explains the mark scheme for the portfolio

Technical report specification, 2015 allocations, mark scheme, links

Specification for technical report, allocations (2015) mark scheme. Also contains a links to supporting materials including Harvard referencing. A template for a technical report is found at http://www.edshare.soton.ac.uk/14581

Technical report mark scheme

Mark scheme for technical report. 2015 COMP1205 assignment is at http://www.edshare.soton.ac.uk/14582

Análisis del gen adra2a receptor alfa 2a adrenergico en pacientes con trastorno de hiperactividad y déficit de atención

El trastorno de hiperactividad y déficit de atención (THDA), es definido clínicamente como una alteración en el comportamiento, caracterizada por inatención, hiperactividad e impulsividad. Estos aspectos son clasificados en tres subtipos, que son: Inatento, hiperactivo impulsivo y mixto. Clínicamente se describe un espectro amplio que incluye desordenes académicos, trastornos de aprendizaje, déficit cognitivo, trastornos de conducta, personalidad antisocial, pobres relaciones interpersonales y aumento de la ansiedad, que pueden continuar hasta la adultez. A nivel global se ha estimado una prevalencia entre el 1% y el 22%, con amplias variaciones, dadas por la edad, procedencia y características sociales. En Colombia, se han realizado estudios en Bogotá y Antioquia, que han permitido establecer una prevalencia del 5% y 15%, respectivamente. La causa específica no ha sido totalmente esclarecida, sin embargo se ha calculado una heredabilidad cercana al 80% en algunas poblaciones, demostrando el papel fundamental de la genética en la etiología de la enfermedad. Los factores genéticos involucrados se relacionan con cambios neuroquímicos de los sistemas dopaminérgicos, serotoninérgicos y noradrenérgicos, particularmente en los sistemas frontales subcorticales, corteza cerebral prefrontal, en las regiones ventral, medial, dorsolateral y la porción anterior del cíngulo. Basados en los datos de estudios previos que sugieren una herencia poligénica multifactorial, se han realizado esfuerzos continuos en la búsqueda de genes candidatos, a través de diferentes estrategias. Particularmente los receptores Alfa 2 adrenérgicos, se encuentran en la corteza cerebral, cumpliendo funciones de asociación, memoria y es el sitio de acción de fármacos utilizados comúnmente en el tratamiento de este trastorno, siendo esta la principal evidencia de la asociación de este receptor con el desarrollo del THDA. Hasta la fecha se han descrito más de 80 polimorfismos en el gen (ADRA2A), algunos de los cuales se han asociado con la entidad. Sin embargo, los resultados son controversiales y varían según la metodología diagnóstica empleada y la población estudiada, antecedentes y comorbilidades. Este trabajo pretende establecer si las variaciones en la secuencia codificante del gen ADRA2A, podrían relacionarse con el fenotipo del Trastorno de Hiperactividad y el Déficit de Atención.

Mark.

Va acompañado de un manual del profesor (ISBN 84-86587-84-0)

Investigación social : manual del profesor para acompañar a Mark.

Complementa a la novela Mark con ISBN 84-86587-68-9

Making their mark : 1870 to 1940.

Forma parte de una serie que estudia la historia del hombre negro y de sus logros en la historia mundial. Estudia el nuevo comienzo de la población afroamericana tras la concesión de la libertad pero no de los mismos derechos que a los demás ciudadanos; el colonialismo europeo en África; la Primera Guerra Mundial; el Movimiento Panafricano en las primeras décadas del siglo XX; el Congresos universal de las razas de 1911; así como el llamado renacimiento artístico con la aparición de los escritores negros caribeños y afrocubanos, de las tradiciones musicales negras y el reconocimiento de artistas, actores y deportistas de esta raza.

De historias, estándares, rendiciones de cuentas y el fin del currículum : la vuelta de Barry Franklin a Granada.

Resumen basado en el de la publicación