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text:
Robert C. Solomon (September 14, 1942 – January 2, 2007) was a philosopher and business ethicist, notable author, and "Distinguished Teaching Professor of Business and Philosophy" at the University of Texas at Austin, where he held a named chair and taught for more than 30 years, authoring The Passions: Emotions and the Meaning of Life (1976) and more than 45 other books and editions.  Critical of the narrow focus of Anglo-American analytic philosophy, which he thought denied human nature and abdicated the important questions of life, he instead wrote analytically in response to the continental discourses of phenomenology and existentialism, on sex and love, on business ethics, and on other topics to which he brought an Aristotelian perspective on virtue ethics.  He also wrote A Short History of Philosophy and others with his wife, Professor Kathleen Higgins.

Professor Solomon won many teaching honors, including the Standard Oil Outstanding Teaching Award in 1973; the University of Texas President's Associates Teaching Award (twice); a Fulbright Lecture Award; University Research and National Endowment for the Humanities Grants; and the Chad Oliver Plan II Teaching Award in 1998.

His many works include About Love, Ethics and Excellence, A Better Way to Think about Business, The Joy of Philosophy, Spirituality for the Skeptic, Not Passion's Slave, and In Defense of Sentimentality.

The passions: emotions and the meaning of life
Solomon developed a cognitivist theory of the emotions as moral judgements about reality that inherently manifest a natural, pre-deliberative logic.  As such, they are susceptible to rational appraisal and revision no less than our beliefs and propositions, and furthermore to strategic ethical reasoning.  Emotions should not be suppressed or repressed by efforts at philosophic rationalism, which suffers a withering critique under his analysis, calling it "emasculated" and "absurd".  It is our passions, according to R.Solomon, and not our reason, which are capable of demonstrating to us the meaning and purpose of life.  Every emotion has an purpose or goal, even those that seem stupid or painful.  Although the objects and strategies differ with each emotion, person, and relationship, the natural purpose of each is to maximize human dignity, the good for oneself and for humankind.  Regarding the "air of paradox surrounding an attempt by philosophy to deal with the passions" and the "certain irony that surrounds an attempt by philosophy to deal with the question of the meaning of life", Solomon asks, "is not philosophy, itself, the problem?".   Romeo's conclusion constitutes his premise: "Hang up philosophy!  Unless philosophy can make a Juliet."

He derides modernist and contemporary theories of the mind and psyche influenced by materialism and scientism as having created a "myth of the passions", which he explodes, exposing the vicissitudes of its "hydraulic model".

On sex, love, marriage, and children
Solomon was particularly interested in the idea of "love", arguing against the notion that romantic love is an inherent state of being, maintaining that it is instead a construct of Western culture, popularized and propagated in such a way that it has achieved the status of a universal in the eyes of many. Love for Solomon is not a universal, static quality, but an emotion, subject to the same vicissitudes as other emotions like anger or sadness.

On business ethics
His book Ethics and Excellence renewed in business ethics — philosophers and managers alike — an interest in Aristotelian virtue ethics, which he explained so that it could be applied to management development and leadership training. This caused the misunderstanding with some authors (Crane/Matten, Business Ethics: A European Perspective) that virtue ethics was a modern approach, unaware of the roots in Aristotle.

He also wrote about business ethics in Above the Bottom Line, It's Good Business, Ethics and Excellence, New World of Business and A Better Way to Think about Business. He had designed and provided programs for corporations and organizations around the world and his books have been translated into more than a dozen languages.

On History of Philosophy

Axial Period and Origins of Philosophy

To Anglo-American analytic philosophy
The topic of the emotions was largely being ignored in anglo-american analytic philosophy and social science, and also on the continent in the new scientism and structuralism when The Passions was written in 1976.

To phenomenology and existentialism

Personal life and career

Early life
Solomon was born in Detroit, Michigan, U.S. His father was a lawyer, and his mother an artist. He was born with a hole in his heart and was not expected to live into adulthood. He earned a bachelor's degree in molecular biology from the University of Pennsylvania in 1963 and his master's and doctoral degrees in philosophy and psychology from the University of Michigan in 1965 and 1967 respectively.

Teaching and research

He held visiting appointments at the University of Pennsylvania; the University of Auckland, New Zealand; Mount Holyoke College; Princeton University; the University of California, Los Angeles, and the University of Pittsburgh.  From 1972 until his death, except for two years at the University of California at Riverside in the mid-1980s, he taught at University of Texas at Austin, serving as Quincy Lee Centennial Professor of Philosophy and Business.  He was a member of the University of Texas Academy of Distinguished Teachers, which is devoted to providing leadership in improving the quality and depth of undergraduate instruction. Solomon was also a member of the inaugural class of Academic Advisors at the Business Roundtable Institute for Corporate Ethics.

His interests were in 19th-century German philosophy—especially Georg Wilhelm Friedrich Hegel and Friedrich Nietzsche—and 20th-century continental philosophy—especially Paul Ricoeur, Jean-Paul Sartre and phenomenology, as well as ethics and the philosophy of emotions. Solomon published more than 40 books on philosophy, and was also a published songwriter.  He made a cameo appearance in Richard Linklater's film Waking Life (2001), where he discussed the continuing relevance of existentialism in a postmodern world.

Solomon received numerous teaching awards at the University of Texas at Austin, and was a frequent lecturer in the highly regarded Plan II Honors Program. Solomon was known for his lectures on Søren Kierkegaard, Nietzsche, Sartre and other existentialist philosophers. Solomon described in one lecture a very personal experience he had while a medical student at the University of Michigan. He recounted how he stumbled as if by chance into a crowded lecture hall. He was rather unhappy in his medical studies at the time, and was perhaps seeking something different that day. He got precisely that. The professor, Frithjof Bergmann, was lecturing that day on something that Solomon had not yet been acquainted with. The professor spoke of how Nietzsche's idea of the eternal return asks the fundamental question: "If given the opportunity to live your life over and over again ad infinitum, forced to go through all of the pain and the grief of existence, would you be overcome with despair? Or would you fall to your knees in gratitude?" After this lecture, Solomon quit medical school and began studies in philosophy.

He taught three courses as part of The Great Courses series: Will to Power: The Philosophy of Friedrich Nietzsche, which he taught alongside his wife; No Excuses: Existentialism and the Meaning of Life; and Passions: Philosophy and the Intelligence of Emotions.

Marriage, family, and legacy
He was married to Kathleen Higgins, with whom he co-authored several of his books. She is a professor of philosophy at University of Texas at Austin. Solomon collapsed and died of pulmonary hypertension on January 2, 2007, while changing planes at Zurich airport.

Published works

Above the Bottom Line (Cengage Learning, 1983)
A Better Way to Think About Business: How Personal Integrity Leads to Corporate Success (Oxford, 1999)
A Handbook for Ethics (Cengage Learning, 1993)
A Passion For Justice (Rowman & Littlefield, 1995)
A Passion for Wisdom: A Very Brief History of Philosophy (Oxford, 1990)
Introducing Philosophy: A Text with Integrated Readings (Oxford, 1977)

About Love: Reinventing Romance for Our Times (Simon & Schuster, 1988)
Building Trust: In Business, Politics, Relationships, and Life (Oxford, 2001)
Continental Philosophy Since 1750 (Oxford, 1988)
Dark Feelings, Grim Thoughts: Experience and Reflection in Camus and Sartre (Oxford, 2006)
Entertaining Ideas (Prometheus Books, 1970)
Ethics and Excellence (Oxford, 1992)
Ethics: A Short Introduction (Brown & Benchmark, 1993)
Ethics and Excellence: Cooperation and Integrity in Business (Oxford, 1992)
From Africa to Zen: An Invitation to World Philosophy (Rowman & Littlefield, 2003)
From Hegel to Existentialism (Oxford, 1987)
From Rationalism to Existentialism: The Existentialists and Their Nineteenth-century Backgrounds (Rowman & Littlefield, 2001)
Existentialism (McGraw–Hill, 1974)
"Graduate Study in Continental Philosophy in American Universities," Teaching Philosophy 1:2, 1975

"Teaching Hegel," Teaching Philosophy 2:3/4, 1977
History and Human Nature: A Philosophical Review of European Philosophy and Culture, 1750–1850 (Harcourt Brace Janovich, 1979)
In Defense of Sentimentality (Oxford, 2004)
In the Spirit of Hegel (Oxford, 1983)
Introducing Philosophy for Canadians: A Text with Integrative Readings (Oxford, 2011)
Introducing philosophy: Problems and perspectives (Harcourt Brace Jovanovich, 1977)
Introducing the Existentialists: Imaginary Interviews with Sartre, Heidegger, and Camus (Hackett Publishing Company, 1981)
Introducing the German Idealists: Mock Interviews with Kant, Hegel and Others and a Letter from Schopenhauer (Hackett Publishing Company, 1981)
It's Good Business: Ethics and Free Enterprise for the New Millennium (Rowman & Littlefield, 1997)
Living with Nietzsche (Oxford, 2003)
Love (Hackett Publishing Company, 2006)
Morality and the Good Life: An Introduction to Ethics Through Classical Sources (McGraw-Hill, 1984)
Not Passion's Slave: Emotions and Choice (Oxford, 2003)
On Ethics and Living Well (Thomson Wadsworth, 2005)
Phenomenology and Existentialism (Rowman & Littlefield, 2001)
Philosophy of Religion: A Global Approach (Harcourt Brace College Publishers, 1996)
Reading Nietzsche (Oxford, 1990)
Sexual Paradigms (Rowman & Littlefield, 2002)
Since Socrates: A Concise Source Book of Classic Readings (Cengage Learning, 2004)
Spirituality for the Skeptic: The Thoughtful Love of Life (Oxford, 2002)

The Bully Culture: Enlightenment, Romanticism, and the Transcendental Pretense, 1750–1850(Littlefield Adams, 1992)
The Big Questions: A Short Introduction to Philosophy (Wadsworth Publishing, 2002)
The Joy of Philosophy (Oxford, 1999)
The Little Philosophy Book (Oxford, 2007)
The New World of Business: Ethics and Free Enterprise in the Global 1990s (Rowman & Littlefield Publishers, 1994)
The Philosophy of (Erotic) Love, with Kathleen M. Higgins (University Press of Kansas, 1991)
Thinking about Feeling: Contemporary Philosophers on Emotions (Oxford, 2004)
True to Our Feelings: What Our Emotions Are Really Telling Us (Oxford, 2006)
Up the : Re-Creating Higher Education in America (Addison-Wesley Publishing Company, 1993)
What Is An Emotion?: Classic and Contemporary Readings (Oxford, 2003)
What Nietzsche Really Said (Random House/Schocken, 2000)
Wicked Pleasures: Meditations on the 'Seven' Deadly Sins (Rowman & Littlefield, 2000)
World Philosophy: A Text with Readings (McGraw-Hill, 1995)

See also
American philosophy
List of American philosophers
Radical center (politics)
Antiphilosophy

Bibliography
   See also: Corporate Social Entrepreneurship

References

1942 births
2007 deaths
20th-century American male writers
20th-century American historians
20th-century American philosophers
20th-century essayists
21st-century American male writers
21st-century American historians
21st-century American philosophers
21st-century essayists
American ethicists
American male essayists
American male non-fiction writers
American philosophy academics
Aristotelian philosophers
Continental philosophers
Critical theorists
Epistemologists
Existentialists
Historians of philosophy
Kierkegaard scholars
Metaphysicians
Nietzsche scholars
Ontologists
People from Cheltenham, Pennsylvania
Phenomenologists
Philosophers of culture
Philosophers of economics
Philosophers of education
Philosophers of history
Philosophers of love
Philosophers of mind
Philosophers of psychology
Philosophers of religion
Philosophers of sexuality
Philosophy writers
Sartre scholars
University of Michigan alumni
University of Texas at Austin faculty

redpajama_set_name: RedPajamaWikipedia


text:
Josep Ballester i Roca (Alcira, 1961) es un poeta y filólogo español en lengua catalana.

Ballester es profesor de bachillerato y de literatura contemporánea en la Universidad de Valencia, vicepresidente de la Associació d'Escriptors en Llengua Catalana (Asociación de escritores en lengua catalana) y miembro de la Associació de Joves Escriptors en Llengua Catalana (Asociación de jóvenes escritores en lengua catalana), Associació Internacional de Llengua i Literatura Catalanes (Asociación internacional de lengua y literatura catalanas), North American Catalan Society (Sociedad catalana-norteamericana) y del PEN catalán, sección catalana del PEN club internacional. Ha sido colaborador de las publicaciones El Temps, Reduccions, La Rella, Avui, Levante, Canal 9, Aiguadolç, Revista de Catalunya, L'Illa, Revista de Lletres, Daina, Serra d'Or y El País. En 1996 fue galardonado con el Premi Vicent Andrés Estellés de poesía y en 2008 con el Premi Ciutat d' Alzira de novela.

Obra

Investigación y divulgación

 Temps de Quarantena: cultura i societat a la postguerra, 1992

Narrativa

 L'estrella dansarina., 1989
 La princesa Neus, 1999

Novela

 La mirada de Xahrazad, 2006
 El col·leccionista de fades, 2008 (XX Premio de Novela Ciudad de Alcira)

 Poesía

 Passadís voraç de silenci, 1985
 Foc al celler, 1988
 Oasi, 1989
 Tatuatge, 1989
 Tàlem, 1992
 L'holandès errant, 1994
 La mar, 1997
 Els ulls al cel i l'ànima al mar, 2004
 L'odi, 2005
 Les muses inquietants. Antologia 1982-2006, 2007
  Diversos i dispersos versos conversos i perversos dels universos, 2013

 Ensayo

 Joan Fuster : una aventura lírica.'', 1990

Enlaces externos
 Dialnet: relación de obras didácticas.
 Biografía.

Poetas de Cataluña
Filólogos de España del siglo XX
Filólogos de España del siglo XXI
Escritores de España del siglo XX
Escritores de España del siglo XXI
Escritores en catalán del siglo XX
Escritores en catalán del siglo XXI
Profesores de educación secundaria
Nacidos en Alcira


text:
Cooper Layne
Follow Cooper Layne
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Cooper Layne Quick Links
Film RSS
The Fog (2005) Review
By Keith Breese
It should be an unwritten rule of moviegoing: if it's not reviewed in the papers (or here) by Friday you shouldn't see it. Studios know when they have critical duds on their hands. They know when a film is atrociously acted, exceedingly dull, and entirely contrived. They don't screen those films for critics. They don't want the bad press on opening night. For a good many films, this sort of passive aggressive deception works. People go to see the films and the studios make their money back. My only hope is that you take my advice: If it hasn't been reviewed on Friday, wait a day. Or two. Then look online for the review. Chances are it'll be like this one.
The Fog is a terrible movie. Simply put, it sucks. It should have gone straight to video. No, even that is a better fate. It should have gone directly to the Sci-Fi Channel, the latest repository for "new" terrible films.
Continue reading: The Fog (2005) Review
The Core Review
By Sean O'Connell
The Core is Armageddon inside the Earth. If you've caught the trailer, spotted the revealing poster, or even overheard a total stranger briefly mentioning the plot in mixed company, then you've figured this much already. What's most distressing is that The Core is Armageddon without a heart to dangle from its sleeves. Michael Bay's bombastic endeavor may have choked itself on chest-heaving male bonding and fist-pumping patriotism, but at least it gave a damn. Here, we're going through the motions.
When the core of our planet stops spinning on its axis - a reason is given, though it makes little sense - a motley crew of hastily-trained scientists must accompany two astronauts (Bruce Greenwood, Hilary Swank) to the Earth's center so they can jump-start our globe using nuclear weapons.
Continue reading: The Core Review
Cooper Layne Movies
The Fog (2005) Movie Review
It should be an unwritten rule of moviegoing: if it's not reviewed in the papers...
The Core Movie Review
The Core is Armageddon inside the Earth. If you've caught the trailer, spotted the revealing...
Filmmakers Index: 0 A B C D E F G H I J K L M N O P Q R S T U V W X Y Z

redpajama_set_name: RedPajamaCommonCrawl


text:
Графы д'Альбон () были незначительными французскими сеньорами в Юго-Восточной Франции, их владения располагались в современном регионе Рона-Альпы между рекой Рона и Альпами. Центром владений был замок Альбон в долине Роны между Вьенном и Валансом.

Первым сеньором д'Альбон был Гиг I Старый, сын Гига II, сеньора де Вион. Он последовательно стал графом Уазана, Грезиводана и Бриансона. Его внук, Гиг III, после раздела графства Вьенн получил в 1129 году титул графа д'Альбон и часть графства. Его потомок Гиг IV, получил прозвище Дофин (), поскольку имел на гербе дельфина, его потомки стали использовать новый титул, Дофин Вьеннский (), названный по области вокруг города Вьенн, входившего в их владения. Позже эта область получила название Дофине ().

Титул и все владения, многие из которых входили в состав Священной Римской империи, были проданы королю Франции Филиппу VI в 1349 году при условии, что наследник французской короны всегда должен носить титул дофин и владеть этими землями.

Сеньоры д'Альбон

Дом д'Альбон

 ????—1070: Гиг I Старый (ум. 1070), граф Уазана, Грезиводана и Бриансона, сеньор д'Альбон, сын Гига II, сеньора де Вион, в 1070 году удалился в монастырь Клюни и умер в этом же году.
 1070—1079: Гиг II Толстый (ум. 1079), граф Грезиводана и Бриансона, сеньор д'Альбон, сын предыдущего

Графы д'Альбон

Дом д'Альбон

 1079—1133: Гиг III (ок. 1050—1133), сеньор д'Альбон с 1079, 1-й граф д'Альбон с 1129, сын предыдущего
 1133—1142: Гиг IV Дофин (ок. 1095—1142), граф д'Альбон с 1133, сын предыдущего

Графы д'Альбон и дофины Вьеннские

Дом д'Альбон

 1142—1162: Гиг V (ок. 1120—1162), граф д'Альбон и Гренобля, дофин Вьеннский с 1142
 1162—1228: Беатрис д'Альбон, (1161—1228), дофина Вьеннская, графиня д'Альбон, Гренобля, Уазана и Бриансона с 1162, дочь предыдущего
 1-й муж: с 1164 Альберик Тайлефер Тулузский (ок. 1157—1183), дофин Вьеннский, граф д'Альбон, Гренобля, Уазана и Бриансона с 1164, второй сын Раймунда V, графа Тулузы
 2-й муж: Гуго III (1148—1192), герцог Бургундии с 1162, дофин Вьеннский, граф д'Альбон, Гренобля, Уазана и Бриансона с 1183
 3-й муж: с 1193 Гуго I де Колиньи (1170—1205), сеньор де Бресс, дофин Вьеннский, граф д'Альбон, Гренобля, Уазана и Бриансона с 1193

Старший Бургундский дом

 1228—1237: Андре Гиг VI (1184—1237), дофин Вьеннский, граф д'Альбон, Гренобля, Уазана и Бриансона с 1228, сын Беатрис от 2-го брака с Гуго III Бургундским
 1237—1269: Гиг VII (ок. 1225—1269), дофин Вьеннский, граф д'Альбон, Гренобля, Уазана и Бриансона с 1237, сын предыдущего
 1269—1282: Жан I (1263—1282), дофин Вьеннский, граф д'Альбон, Гренобля, Уазана и Бриансона с 1269, сын предыдущего
 1282—1298: Анна (1255—1298), дофина Вьеннская, графиня д'Альбон, Гренобля, Уазана и Бриансона с 1298, сестра предыдущего
 муж: с 1273 Умберт I (ок. 1240 — 1307), барон де Ла Тур дю Пэн

Дом де Ла Тур дю Пэн

 1282—1298: Умберт I (ок. 1240 — 1307), барон де Ла Тур дю Пэн, дофин Вьеннский, граф д'Альбон, Гренобля, Уазана и Бриансона с 1282
 1282—1298: Жан II (1280—1318), барон де Ла Тур дю Пэн, дофин Вьеннский, граф д'Альбон, Гренобля, Уазана и Бриансона с 1307, сын предыдущего
 1298—1333: Гиг VIII (1309—1333), барон де Ла Тур дю Пэн, дофин Вьеннский, граф д'Альбон, Гренобля, Уазана и Бриансона с 1318, сын предыдущего
 1333—1349: Умберт II (1312—1355), барон де Ла Тур дю Пэн, дофин Вьеннский, граф д'Альбон, Гренобля, Уазана и Бриансона 1333—1349, брат предыдущего

Умберт II в 1349 году продал владения и титул королю Франции Филиппу VI.

См. также
 Дофин
 Дофин Оверни
 Графство Вьенн

Ссылки

Вьенн (дофины)


text:
"""
Factitious CA to test non-uniform buffer interactions.

Experiment classes included.

"""
from xentica import core
from xentica import seeds
from xentica.core import color_effects

from examples.base import RegularCA, RegularExperiment
from examples.base import run_simulation

class ShiftingSands(RegularCA):
    """
    CA for non-uniform buffer interactions test.

    It emits the whole value to a constant direction, then absorbs
    surrounding values by summing them.

    """
    state = core.IntegerProperty(max_val=1)

    def emit(self):
        """Emit the whole value to a constant direction."""
        direction = 0
        for i in range(len(self.buffers)):
            if i == direction:
                self.buffers[i].state = self.main.state
            else:
                self.buffers[i].state = 0

    def absorb(self):
        """Absorb surrounding values by summing them."""
        new_val = core.IntegerVariable()
        for i in range(len(self.buffers)):
            new_val += self.neighbors[i].buffer.state
        self.main.state = new_val

    @color_effects.MovingAverage
    def color(self):
        """Render contrast black & white cells."""
        red = self.main.state * 255
        green = self.main.state * 255
        blue = self.main.state * 255
        return (red, green, blue)

class ShiftingSandsExperiment(RegularExperiment):
    """Vanilla experiment with randomly initialized area."""

    word = "LET IT SHIFT"
    seed = seeds.patterns.BigBang(
        pos=(320, 180),
        size=(100, 100),
        vals={
            "state": seeds.random.RandInt(0, 1),
        }
    )

if __name__ == "__main__":
    run_simulation(ShiftingSands, ShiftingSandsExperiment)

redpajama_set_name: RedPajamaGithub


Henri Foucault shows the full extent of his art in a very personal exhibition, for the first time at Galerie Thierry Bigaignon.
Though the artist will exhibit for the first time at the Galerie Thierry Bigaignon, Henri Foucault's work is already well-established. This show, starting on April 4th, will thus be a great opportunity to discover or rediscover the artist's specific universe - that of a photographer-sculptor or sculptor-photographer - through a selection of new works focussing on the body.
As an inexhaustible source of inspiration, the body has always been for Henri Foucault, as for many sculptors, a subject for study, and more so, an absolute fascination. Henri Foucault does not only photograph bodies, he sculpts them and tries, through a selection of them, to express their multitude. It is the very sculptural dimension of the body, its fundamental aspect, that draws his interest. The challenge is for him to represent it without ever falling into some kind of eroticism, nor into the figurative.
Sculptor at heart, Henri Foucault nevertheless chose photography a long time ago. Unless photography chose him! Over the years, the artist has developed an artistic universe that, through the play of light, enjoys reinventing new forms of perception. "From this confrontation between[...] the slow shaping of a volume and the dazzling nature of the photographic act," Dominique Païni tells us, "emerges the possibility of merging sculpture and photography. Photographing and sculpting, sculpting and photographing, it is this alternation that is accomplished in Henri Foucault's work."
Alix Agret, who wrote the beautiful text accompanying the exhibition, adds that "Henri Foucault's images conjure up the photographic flatness that transforms photography into a medium of three dimensionality. As if, with a mischievous spirit, it was precisely through photography that Foucault wanted to demonstrate after Rodin that one must always "consider a surface as the end of a volume". Especially since Henri Foucault has found in the body the ideal material - without, however, shaping it in the literal sense - to maintain the forms in a vibratory suspense that makes them oscillate between flattening and relief".
Henri Foucault's career already includes a large number of exhibitions, both personal and collective. His works appear in prestigious private and public collections such as those of François Pinault, Marin Karmitz, Walter Zalenski, Manfred Heitin, Boissonnat, the Daniel and Florence Guerlain Foundation, the Fonds national d'Art Contemporain, and the Montreal Museum of Fine Arts, among others.


text:
HISTADRUT
Community & Administration
The Histadrut House, Rishon LeZion
Rothschild St 60
The Rishon LeZion Histadrut complex was built in a few stages, based on a proposed plan of the office for the entire complex, the first-place winner of a competition which likely took place in 1948. Two alternative plans for the complex were submitted to the competition by the office, each proposing a different physical distribution of three buildings: the Histadrut House, the Worker's House (a gymnasium), and a theater and film structure. By 1950, the Worker's House had likely already been built, and at the end of that year the planning of the Histadrut House had begun with its construction completed in 1953. The House was inaugurated with a ceremony of great splendor – criticized by the Histadrut representatives from Maki (Israeli Communist Party). The third building, the theater and film structure, was built only about twelve years later, in 1965. The complex is used even today by the Rishon LeZion Workers' Council and, with the exception of a late-eighties addition to the film theater building façade, its physical and spatial form has been preserved.
לעיון נוסף
Services & Welfare
Industry & Commerce


On Tuesday and Thursdays during the winter T&F athletes meet at 7 p.m. for circuit training in St. Dominic's Sports Hall on the Navan Road and Cross Country runners meet at the Navan Road Parish Centre, behind the Navan Rd. Church at 7p.m. to go for a run.
Always check training times, dates and venues, as they are liable to change due to weather, competitions or venue availability.
Training times and locations will be posted weekly on our homepage.


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ABROAD WRITERS' CONFERENCE > Abroad Writers Conference > Getting to Know Best-Selling Author Jacquelyn Mitchard
Getting to Know Best-Selling Author Jacquelyn Mitchard
abroadwritersconferenceMay 26, 2013Abroad Writers Conference, Lismore Castle, UncategorizedJacquelyn Mitchard
By Joan Brunwasser
I grew up with the story of Our Lady of Angels fire all around me. It was more than an event, it was a sunset on the bright stable way people saw their world. That fire blew that neighborhood up. There was no one who didn't know someone who'd died in OLA. I was struck by how surviving an event could be just as paralyzing as dying in that event — that the survivors were changed forever.
Trial by Fire, The Backstory of Second Nature
me, literally, today by Chris Cohen [photo credit]
My guest today is best-selling author, Jacquelyn Mitchard. Her first novel, The Deep End of the Ocean, written in 1999, was also the first selection of the Oprah Winfrey's Book Club, making for a stellar career kickstart. Welcome to OpEdNews, Jackie.
hardcover book jacket by Jacquelyn Mitchard website
JB: I just finished reading Second Nature, a novel based on the 1958 fire that killed 92 children in their Chicago school. What made you choose this as the backdrop for your book?
JM: That happened when I was a baby, and I grew up with the story of Our Lady of Angels all around me. It was more than an event, it was a sunset on the bright stable way people saw their world. That had been a close-knit, West Side neighborhood, filled with brothers who married sisters and cousins and grew up down the block from each other, who played cards and had dinner together on Sunday nights.
That fire blew that neighborhood up. People didn't just move to the suburbs; they moved to Miami, to California, as far as they could from that school, because there was no one who didn't know someone who'd died in OLA. A friend's older brother died in that fire, and his presence in that house was as real as any of the living children, even those who never knew him. I was struck by how surviving an event could be just as paralyzing as dying in that event — that the survivors were changed forever.
JB: I grew up in Chicago, too, and that fire has haunted us ever since. You chose Sicily Coyne as your central character. At the time of the fire, she's a 13-year old student. Why a girl and why that particular age, Jackie?
JM: Twelve or thirteen is the time in a girl's life when she's at the end of childhood and becoming aware of herself as a woman. It's when her awareness of her body image is at its most self-critical. She's not a little kid. Little kids adapt to injury; their awareness of themselves in a wheelchair or having lost hair to chemotherapy or sustaining a wound, those are real, but, if the kid has a reasonably supportive family, those things are tempered by the resilience of being accepted, at the deep heart's core, for who you are rather than how you look. Sicily had this sense of herself, too.
So in a very real way, she became trapped in a damaged face — that was all anyone could see — and she was screaming, "Hey, look! I'm still me!" The burn itself was a source of both bitterness and toughness, but her sarcasm and bitterness came from being seen, yet unseen. And I'm just very attracted to understanding the psychology of that age of person, which is why the imprint for which I'm the editor -in- chief is a Young Adult imprint. It's the age of being epic, living a week in an hour, a year in a month, a lifetime in a year.
JB: And, boy, has a lot gone on for Sicily. She's a woman/child who had to grow up fast because of that fire and losing both of her parents. Yet, she's also very unsophisticated and sheltered in many ways. It's an odd combination. Can you talk about this?
JM: Like many "sick kids," Sicily has been both coddled and deprived. Life itself has robbed her of so much; and yet she's given everything but what she can't have — the chance to be normal. She has every material advantage and she's protected from the realities of paying bills and jockeying for social position.
People may whisper about her, but there's a kind of holy deference for a kid who's part of a local legend: her prerogatives are in line with her losses. And the aunt who adopted her, Marie, is torn between those two poles, as well — deeply and nearly neurotically protective of Sicily, but also determined to push her into as normal a life as is possible, for Sicily to be "not as good as, but better than." The reason that some readers found Sicily annoying is that she really never grew up: she's stopped, an accomplished adolescent but in her reactions and her emotional landscape, still a middle-school kid.
JB: Interesting. I didn't find Sicily annoying. I found her situation incredibly and painfully poignant. I admit I'd never really thought about what surviving such an experience might be like before.
JM: Many people thought of her as "spoiled" and "shallow." Many other readers found her affecting and real. I think it often depends on what you've been through in life, and maybe what you've been through in books, what you tend to gravitate toward. Sometimes, people just really don't have a big tolerance for real life in fiction, even though they say they want characters who are "real." Like take Kinsey Mulhone, in Sue Grafton's wonderful mysteries. She's tough, thin, single, smart, and she never gets past the age of about 36. She goes down easy, like a cool drink on a hot day, so the story can gallop off everywhere.
when my last child was born, six years ago by Arty Hitchcock [photo credit]
JB: The Cappadora family was featured in your first book, The Deep End of the Ocean and you bring them back in Second Nature. In fact, we see that Beth Cappadora becomes surprisingly close to Sicily. Why does using utilizing the reappearance of characters from one book to another seem like a good idea?
JM: With continuing characters, you have to be careful about flaws because unless it's a very literary novel or the flaws are the point (I'm thinking here of John Irving's A Prayer for Owen Meany), you have to convince readers to embrace a character who has flaws, because there's a belief about how you'd react in the same circumstances and that way is usually very positive or even heroic — and that's exactly how I am too!
You try to think you'd be the best at this. But the psychology in this book is based on real accounts of people who are disfigured, and it affects people in ways that aren't always attractive. It's the same way as dealing with depression in another person. Depressed people are sad, and it's awful that they're sad, but they sometimes behave in ways that are deeply provocative or upsetting to other people. They're not fun to be with.
Personally, I thought Sicily was just what she should be, smart and strong but also naive and bewildered, and really able to put up a good front by talking tough. As for the Cappadoras, it wasn't a marketing decision. So many people, thousands of people, have asked me, what happened to [Beth's son] Vincent? And I knew that Vincent would not have grown up to be a perfect human being, either, not given his temperament.
I thought, what if Sicily — with this new face which actually would be aesthetically very good, given that this book is set about ten or fifteen years in the future, when face transplants won't be so uncommon — were to run toward love and fall for just the most attractive, worst possible guy, in the encyclopedia entry about commitment issues for reasons of his own past?
But it was natural, because she already loved Beth, who had documented this whole process [face transplant] because of Sicily's past, because of the fire and its being the stuff of legend on the West Side of Chicago. Why think up new people to populate a place you already know, if the people who already know are already there, frozen in time, like the game Statue Maker? They were perfectly interesting people.
with son Rob, 1999 by Jill Krementz [photo credit]
JB: Agreed. All that medical information, both about burns and recovery and the whole field of organ transplants, was fascinating. And I found the most compelling images to be Sicily's prosthetic nose, on the one hand, and her inability to eat properly, a routine task we do daily and take completely for granted. Was it hard to find the right balance between giving enough grisly details to make it real without grossing readers out or turning them off?
JM: Readers still found it grisly! I did an insane amount of research on burn injury and musculature and anatomy. For me, the prosthetic nose was one of the tenderest details, the way she had to take care of it because it was, you know, the Cadillac of prosthetic noses. It was just fascinating, like the way a prosthetic nose, for example, attaches (with magnets!).
I majored in Biology, and, I have nine children, thus, you know, nothing grosses me out. I'd have gone on forever. But yes, had to back off on some of the detail. Burn victims go through an incomprehensible hell — so, by comparison, the face transplant, even though it required, well, removing Sicily's existing face, was relatively simple compared with the fifteen surgeries she'd had to try to mend the tissue on her face. In real life, that would have been more like thirty surgeries, each more appalling than the last.
JB: Magnets? Yikes! What a concept. The book is very steeped in firefighter culture and lore. It sounded very authentic to me. How did you accomplish that? Did you get to ride around with them?
JM: Oh, yes I did! I spent two weeks with the gallant ladies and gents at Madison Wisconsin's Southside Station 6, and they taught me with generosity and detail. Firefighters in a number of cities surrounding Chicago also answered my questions. You know, there is no better job on earth than theirs. Indeed, they could get badly hurt; they could die. But who can do what they do, deny instinct for the greater good, as they do?
Despite danger, there is such intense training, minute attention to safety and detail, that tragedies such as what happened to Jamie Coyne are almost unknown. But authentically, if they happen, they happen in those kind of gruesome old buildings where fire can't escape. My pal Eric used to be an English teacher before he became a firefighter, and he told me, "You know, you admire police. They lay it right down every day. But when the police show up, people grumble. When we show up, everybody cheers. Here come the Marines!" They're just so cool. I guess they know it, but can you blame them?
my favorite, my 'Wuthering Heights' picture by James Schnepf [photo credit]
JB: Lucky you! Thank you, Jackie. Let's take a break here.
When we return for the conclusion of our interview, we'll talk about the time she called Buckingham Palace, how she juggles her writing and her family of nine children, and her quirky ambition now that she's no longer afraid of heights. Please join us!
Mitchard's website
Submitters Website: http://www.opednews.com/author/author79.html
Submitters Bio:
Joan Brunwasser is a co-founder of Citizens for Election Reform (CER) which since 2005 existed for the sole purpose of raising the public awareness of the critical need for election reform. Our goal: to restore fair, accurate, transparent, secure elections where votes are cast in private and counted in public. Because the problems with electronic (computerized) voting systems include a lack of transparency and the ability to accurately check and authenticate the vote cast, these systems can alter election results and therefore are simply antithetical to democratic principles and functioning. Since the pivotal 2004 Presidential election, Joan has come to see the connection between a broken election system, a dysfunctional, corporate media and a total lack of campaign finance reform. This has led her to enlarge the parameters of her writing to include interviews with whistle-blowers and articulate others who give a view quite different from that presented by the mainstream media. She also turns the spotlight on activists and ordinary folks who are striving to make a difference, to clean up and improve their corner of the world. By focusing on these intrepid individuals, she gives hope and inspiration to those who might otherwise be turned off and alienated. She also interviews people in the arts in all their variations – authors, journalists, filmmakers, actors, playwrights, and artists. Why? The bottom line: without art and inspiration, we lose one of the best parts of ourselves. And we're all in this together. If Joan can keep even one of her fellow citizens going another day, she considers her job well done. Joan has been Election Integrity Editor for OpEdNews since December, 2005. Her articles also appear at Huffington Post, RepublicMedia.TV and Scoop.co.nz.
Reading Schedule at PRIM'S BOOKSTORE, Kinsale
Revived Kinsale Schedule
Connie May Fowler will be joining us in Kinsale


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(-) Remove Starting Grant (StG) (307) filter Starting Grant (StG) (307)
Displaying 61 - 70 of 307. Show 10 | 20 | 50 | 100 results per page.
Project acronym cureCD
Project Function of long non-coding RNA in Crohn Disease Ulcer Pathogenesis
Researcher (PI) Yael HABERMAN ZIV
Host Institution (HI) MEDICAL RESEARCH INFRASTRUCTURE DEVELOPMENT AND HEALTH SERVICES FUND BY THE SHEBA MEDICAL CENTER
Summary The Inflammatory Bowel Diseases (IBD), Crohn's Disease (CD) and Ulcerative Colitis (UC) are chronic/relapsing disorders that affect over six million individuals worldwide. Mucosal ulcers, the hallmark of CD, are the result of a complex interaction between microbiota, immune cells, and gut epithelia. Healing of mucosal ulcers is associated with better outcomes, but is achieved in less than half of cases. Past attempts to suppress central and conserved nodes of the immune system failed due to opposing off-target deleterious effects on epithelial renewal. Therefore, there is a critical need to identify more tissue specific targets that lead to mucosal healing and to improved outcomes. Using mRNAseq of intestinal biopsies, we identified a widespread dysregulation of long non-coding RNAs (lncRNA) in the ileum of treatment naïve pediatric CD patients. Importently, we identified significant correlations between lncRNA and mucosal ulcers. CD lncRNA, after carful mechanistic exploration, are highly promising targets for potential future intervention as they regulate diverse cellular functions and exhibit a more tissue specific expression in comparison to protein coding genes. The core goal of this proposal is to understand the role of CD lncRNA in ulcer pathogenesis focusing on granulocytes and epithelial functions in the contexts of their interactions with the microbiota. I plan to utilize state of the art informatics, RNAseq and microbiome profiles together with advanced and novel experimental lab model and co-culture systems, patients-derived prospectively collected tissues, and gut microbiota to explore the role of CD lncRNA function in mediating healing of mucosal ulcers. This work carries the potential to guide new novel therapeutic strategies for mucosal healing with minimal off-targets effects. In a broader prospective, this work will expand our relative limited understanding regarding the role of lncRNA in mediating human diseases.
The Inflammatory Bowel Diseases (IBD), Crohn's Disease (CD) and Ulcerative Colitis (UC) are chronic/relapsing disorders that affect over six million individuals worldwide. Mucosal ulcers, the hallmark of CD, are the result of a complex interaction between microbiota, immune cells, and gut epithelia. Healing of mucosal ulcers is associated with better outcomes, but is achieved in less than half of cases. Past attempts to suppress central and conserved nodes of the immune system failed due to opposing off-target deleterious effects on epithelial renewal. Therefore, there is a critical need to identify more tissue specific targets that lead to mucosal healing and to improved outcomes. Using mRNAseq of intestinal biopsies, we identified a widespread dysregulation of long non-coding RNAs (lncRNA) in the ileum of treatment naïve pediatric CD patients. Importently, we identified significant correlations between lncRNA and mucosal ulcers. CD lncRNA, after carful mechanistic exploration, are highly promising targets for potential future intervention as they regulate diverse cellular functions and exhibit a more tissue specific expression in comparison to protein coding genes. The core goal of this proposal is to understand the role of CD lncRNA in ulcer pathogenesis focusing on granulocytes and epithelial functions in the contexts of their interactions with the microbiota. I plan to utilize state of the art informatics, RNAseq and microbiome profiles together with advanced and novel experimental lab model and co-culture systems, patients-derived prospectively collected tissues, and gut microbiota to explore the role of CD lncRNA function in mediating healing of mucosal ulcers. This work carries the potential to guide new novel therapeutic strategies for mucosal healing with minimal off-targets effects. In a broader prospective, this work will expand our relative limited understanding regarding the role of lncRNA in mediating human diseases.
Project acronym Damocles
Project Modelling brain aneurysm to elucidate the role of platelets
Researcher (PI) Yacine BOULAFTALI
Summary In the European Union, 15 million people have an unruptured intracranial aneurysm (IA) that may rupture one day and lead to subarachnoid haemorrhage (SAH). The IA rupture event is ominous and lingers as a clinical quandary. No safe and effective non-invasive therapies have, as of yet, been identified and implemented in clinical practice mainly because of a lack of knowledge of the underlying mechanisms. Increasing evidence points to inflammation as one of the leading factors in the pathogenesis of IA. Intrasaccular clot formation is a common feature of IA occurring unruptured and ruptured IA. In addition to forming clots, activated platelets support leukocyte recruitment. Interestingly, platelets also prevent local hemorrhage in inflammatory situations independently of their ability to form a platelet plug. We hypothesize that the role of platelet may evolve throughout the development of IA: initially playing a protective role of in the maintenance of vascular integrity in response to inflammation and contributing later to intrasaccular thrombus formation. What are the platelet signaling pathways and responses involved and to what extent do they contribute to the disease and the rupture event? To answer these questions, we designed an interdisciplinary proposal, which gathers biophysical, pharmacological, and in-vivo approaches, with the following objectives: I) To investigate platelet functions from patients diagnosed with intracranial aneurysm at the sites of aneurysm sac. II) To delineate platelet mechanisms and responses in a cutting-edge technology of a 3D reconstruction of IA that will take into account the hemodynamic shear stress. III) To test in a preclinical mouse model of IA efficient anti-platelet therapies and define a therapeutic window to intervene on platelet activation. The proposed project will yield new insights in IA disease and in life science, from cell biology to the discovery of potential new targets in cardiovascular medicine.
In the European Union, 15 million people have an unruptured intracranial aneurysm (IA) that may rupture one day and lead to subarachnoid haemorrhage (SAH). The IA rupture event is ominous and lingers as a clinical quandary. No safe and effective non-invasive therapies have, as of yet, been identified and implemented in clinical practice mainly because of a lack of knowledge of the underlying mechanisms. Increasing evidence points to inflammation as one of the leading factors in the pathogenesis of IA. Intrasaccular clot formation is a common feature of IA occurring unruptured and ruptured IA. In addition to forming clots, activated platelets support leukocyte recruitment. Interestingly, platelets also prevent local hemorrhage in inflammatory situations independently of their ability to form a platelet plug. We hypothesize that the role of platelet may evolve throughout the development of IA: initially playing a protective role of in the maintenance of vascular integrity in response to inflammation and contributing later to intrasaccular thrombus formation. What are the platelet signaling pathways and responses involved and to what extent do they contribute to the disease and the rupture event? To answer these questions, we designed an interdisciplinary proposal, which gathers biophysical, pharmacological, and in-vivo approaches, with the following objectives: I) To investigate platelet functions from patients diagnosed with intracranial aneurysm at the sites of aneurysm sac. II) To delineate platelet mechanisms and responses in a cutting-edge technology of a 3D reconstruction of IA that will take into account the hemodynamic shear stress. III) To test in a preclinical mouse model of IA efficient anti-platelet therapies and define a therapeutic window to intervene on platelet activation. The proposed project will yield new insights in IA disease and in life science, from cell biology to the discovery of potential new targets in cardiovascular medicine.
Project acronym Daphne
Project Circuits of Visual Attention
Researcher (PI) Maximilian Jösch
Summary The evolutionary arms race has optimized and shaped the way animals attend to relevant sensory stimuli in an ever-changing environment. This is a complex task, because the vast majority of sensory experiences are not relevant. In humans, attentional disorders are a serious public health concern because of its high prevalence, but its causes are mostly unknown. In this proposal, I will explore the neuronal mechanisms used by the nervous system to attend visual cues to enable appropriate behaviors. We will combine cutting edge imaging techniques, optogenetic interventions, behavioral read outs and targeted connectomics to study the neuronal transformations of the mouse Superior Colliculus (SC), an evolutionary conserved midbrain area known to process sensorimotor transformations and to be involved in the allocation of attention. First, this work will reveal a detailed description of visual representation in the SC, focusing on understanding how defined retinal information-streams, like motion and color, contribute to these properties. Second, we will characterize sensorimotor transformations instructed by the SC. The combination of the previous two objectives will determine mechanisms of visual saliency and sensory driven attention ("bottom-up" attention). Finally, we will explore the neuronal mechanisms of attention by studying the modulatory effect of higher brain areas ("top-down" attention) on sensory transformation and multisensory integration in the SC. Taken together, this proposal aims to understand principles underlying sensorimotor transformation and build a framework to study attention in health and disease.
The evolutionary arms race has optimized and shaped the way animals attend to relevant sensory stimuli in an ever-changing environment. This is a complex task, because the vast majority of sensory experiences are not relevant. In humans, attentional disorders are a serious public health concern because of its high prevalence, but its causes are mostly unknown. In this proposal, I will explore the neuronal mechanisms used by the nervous system to attend visual cues to enable appropriate behaviors. We will combine cutting edge imaging techniques, optogenetic interventions, behavioral read outs and targeted connectomics to study the neuronal transformations of the mouse Superior Colliculus (SC), an evolutionary conserved midbrain area known to process sensorimotor transformations and to be involved in the allocation of attention. First, this work will reveal a detailed description of visual representation in the SC, focusing on understanding how defined retinal information-streams, like motion and color, contribute to these properties. Second, we will characterize sensorimotor transformations instructed by the SC. The combination of the previous two objectives will determine mechanisms of visual saliency and sensory driven attention ("bottom-up" attention). Finally, we will explore the neuronal mechanisms of attention by studying the modulatory effect of higher brain areas ("top-down" attention) on sensory transformation and multisensory integration in the SC. Taken together, this proposal aims to understand principles underlying sensorimotor transformation and build a framework to study attention in health and disease.
Project acronym DecodingInfection
Project Decoding the host-pathogen interspecies crosstalk at a multiparametric single-cell level
Researcher (PI) Roi AVRAHAM
Host Institution (HI) WEIZMANN INSTITUTE OF SCIENCE
Summary Bacterial pathogens remain a significant threat to global health, necessitating a better understanding of host-pathogen biology. While various evidence point to early infection as a key event in the eventual progression to disease, our recent preliminary data show that during this stage, highly adaptable and dynamic host cells and bacteria engage in complex, diverse interactions that contribute to well-documented heterogeneous outcomes of infection. However, current methodologies rely on measurements of bulk populations, thereby overlooking this diversity that can trigger different outcomes. This application focuses on understanding heterogeneity during the first stages of infection in order to reduce the complexity of these interactions into informative readouts of population physiology and predictors of infection outcome. We will apply multiparametric single-cell analysis to obtain an accurate and complete description of infection with the enteric intracellular pathogen Salmonella of macrophages in vitro, and in early stages of mice colonization. We will characterize the molecular details that underlie distinct infection outcomes of individual encounters, to reconstruct the repertoire of host and pathogen strategies that prevail at critical stages of early infection. We propose the following three objectives: (1) Develop methodologies to simultaneously profile host and pathogen transcriptional changes on a single cell level; 2) Characterizing the molecular details that underlie the formation of subpopulations during macrophage infection; and (3) Determine how host and pathogen encounters in vivo result in emergence of specialized subpopulations, recruitment of immune cells and pathogen dissemination. We anticipate that this work will fundamentally shift our paradigms of infectious disease pathogenesis and lay the groundwork for the development of a new generation of therapeutic agents targeting the specific host-pathogen interactions ultimately driving disease.
Bacterial pathogens remain a significant threat to global health, necessitating a better understanding of host-pathogen biology. While various evidence point to early infection as a key event in the eventual progression to disease, our recent preliminary data show that during this stage, highly adaptable and dynamic host cells and bacteria engage in complex, diverse interactions that contribute to well-documented heterogeneous outcomes of infection. However, current methodologies rely on measurements of bulk populations, thereby overlooking this diversity that can trigger different outcomes. This application focuses on understanding heterogeneity during the first stages of infection in order to reduce the complexity of these interactions into informative readouts of population physiology and predictors of infection outcome. We will apply multiparametric single-cell analysis to obtain an accurate and complete description of infection with the enteric intracellular pathogen Salmonella of macrophages in vitro, and in early stages of mice colonization. We will characterize the molecular details that underlie distinct infection outcomes of individual encounters, to reconstruct the repertoire of host and pathogen strategies that prevail at critical stages of early infection. We propose the following three objectives: (1) Develop methodologies to simultaneously profile host and pathogen transcriptional changes on a single cell level; 2) Characterizing the molecular details that underlie the formation of subpopulations during macrophage infection; and (3) Determine how host and pathogen encounters in vivo result in emergence of specialized subpopulations, recruitment of immune cells and pathogen dissemination. We anticipate that this work will fundamentally shift our paradigms of infectious disease pathogenesis and lay the groundwork for the development of a new generation of therapeutic agents targeting the specific host-pathogen interactions ultimately driving disease.
Project acronym deFIBER
Project Dissecting the cellular and molecular dynamics of bone marrow fibrosis for improved diagnostics and treatment
Researcher (PI) Rebekka SCHNEIDER-KRAMANN
Host Institution (HI) ERASMUS UNIVERSITAIR MEDISCH CENTRUM ROTTERDAM
Summary Bone marrow (BM) fibrosis is the continuous replacement of blood forming cells in the bone marrow by scar tissue, ultimately leading to failure of the body to produce blood cells. Primary myelofibrosis (PMF), an incurable blood cancer, is the prototypic example of the step-wise development of BM fibrosis. The specific mechanisms that cause BM fibrosis are not understood, in particular as the cells driving fibrosis have remained obscure. My recent findings demonstrate that Gli1+ cells are fibrosis-driving cells in PMF, that their frequency correlates with fibrosis severity in patients, and that their ablation ameliorates BM fibrosis. These results indicate that Gli1+ cells are the primary effector cells in BM fibrosis and that they represent a highly attractive therapeutic target. This puts me in a unique position to vastly expand our knowledge of the BM fibrosis pathogenesis, improve diagnostics, and discover new therapeutic strategies for this fatal disease. I will do this by: 1) dissecting the molecular and cellular mechanisms of the fibrotic transformation, 2) defining the stepwise disease evolution by genetic fate tracing and analysis of the previously unknown critical effector cells of BM fibrosis , 3) understanding early forms of BM fibrosis for improved diagnostics in patients, all with the ultimate aim to identify novel therapeutic targets to directly block the cellular and molecular changes occuring in BM fibrosis. I will apply state-of-the-art techniques, including genetic fate tracing experiments, conditional genetic knockout mouse models, tissue engineering of the bone marrow niche and in vivo and in vitro CRISPR/Cas9 gene editing, to unravel the complex molecular and cellular interaction between fibrosis-causing cells and the malignant hematopoietic cells. I will translate these findings into patient samples with the aim to improve the early diagnosis of the disease and to ultimately develop novel targeted therapies with curative intentions.
Bone marrow (BM) fibrosis is the continuous replacement of blood forming cells in the bone marrow by scar tissue, ultimately leading to failure of the body to produce blood cells. Primary myelofibrosis (PMF), an incurable blood cancer, is the prototypic example of the step-wise development of BM fibrosis. The specific mechanisms that cause BM fibrosis are not understood, in particular as the cells driving fibrosis have remained obscure. My recent findings demonstrate that Gli1+ cells are fibrosis-driving cells in PMF, that their frequency correlates with fibrosis severity in patients, and that their ablation ameliorates BM fibrosis. These results indicate that Gli1+ cells are the primary effector cells in BM fibrosis and that they represent a highly attractive therapeutic target. This puts me in a unique position to vastly expand our knowledge of the BM fibrosis pathogenesis, improve diagnostics, and discover new therapeutic strategies for this fatal disease. I will do this by: 1) dissecting the molecular and cellular mechanisms of the fibrotic transformation, 2) defining the stepwise disease evolution by genetic fate tracing and analysis of the previously unknown critical effector cells of BM fibrosis , 3) understanding early forms of BM fibrosis for improved diagnostics in patients, all with the ultimate aim to identify novel therapeutic targets to directly block the cellular and molecular changes occuring in BM fibrosis. I will apply state-of-the-art techniques, including genetic fate tracing experiments, conditional genetic knockout mouse models, tissue engineering of the bone marrow niche and in vivo and in vitro CRISPR/Cas9 gene editing, to unravel the complex molecular and cellular interaction between fibrosis-causing cells and the malignant hematopoietic cells. I will translate these findings into patient samples with the aim to improve the early diagnosis of the disease and to ultimately develop novel targeted therapies with curative intentions.
Project acronym DENOVO
Project Detection and interpretation of de novo mutations and structural genomic variations in mental retardation
Researcher (PI) Joris Andre Veltman
Host Institution (HI) STICHTING KATHOLIEKE UNIVERSITEIT
Summary Mental retardation, like most common neurodevelopmental and psychiatric diseases, shows a strong genetic component, but these underlying genetic causes remain largely unknown. For a long time it was hypothesized that these kind of common diseases are mainly caused by common inherited genetic variants with reduced penetrance. In contrast to this common variant-common disease hypothesis, I here hypothesize that a large proportion of this so-called "missing heritability" for conditions such as mental retardation, schizophrenia, and autism lies in de novo genetic variation that is rapidly eliminated from the population because individuals with such diseases have severely compromised fecundity. My previous work using microarrays has already demonstrated de novo genomic copy number variations in mental retardation and in schizophrenia. However, microarrays do not allow us to capture the most common form of de novo mutations, those occurring at the nucleotide level. Technological innovations now for the first time allow us to comprehensively study the entire genome of an individual for genomic variations at all levels. In this project I will explore the de novo mutation hypothesis in whole exome and whole genome sequence data from patients with mental retardation. I will optimize and apply whole genome sequencing strategies using patient-parent trios, both in rare mental retardation syndromes as well as common forms of mental retardation. Guidelines for pathogenicity will be established by computational studies aimed at unraveling genotype-phenotype correlations in these family-based genome sequence type datasets. This project will contribute significantly to resolving the genetic causes of reproductively lethal disorders such as mental retardation, provide critical knowledge on the frequency and consequences of de novo mutations in our genome and help to establish medical genome sequencing as a routine diagnostic approach.
Mental retardation, like most common neurodevelopmental and psychiatric diseases, shows a strong genetic component, but these underlying genetic causes remain largely unknown. For a long time it was hypothesized that these kind of common diseases are mainly caused by common inherited genetic variants with reduced penetrance. In contrast to this common variant-common disease hypothesis, I here hypothesize that a large proportion of this so-called "missing heritability" for conditions such as mental retardation, schizophrenia, and autism lies in de novo genetic variation that is rapidly eliminated from the population because individuals with such diseases have severely compromised fecundity. My previous work using microarrays has already demonstrated de novo genomic copy number variations in mental retardation and in schizophrenia. However, microarrays do not allow us to capture the most common form of de novo mutations, those occurring at the nucleotide level. Technological innovations now for the first time allow us to comprehensively study the entire genome of an individual for genomic variations at all levels. In this project I will explore the de novo mutation hypothesis in whole exome and whole genome sequence data from patients with mental retardation. I will optimize and apply whole genome sequencing strategies using patient-parent trios, both in rare mental retardation syndromes as well as common forms of mental retardation. Guidelines for pathogenicity will be established by computational studies aimed at unraveling genotype-phenotype correlations in these family-based genome sequence type datasets. This project will contribute significantly to resolving the genetic causes of reproductively lethal disorders such as mental retardation, provide critical knowledge on the frequency and consequences of de novo mutations in our genome and help to establish medical genome sequencing as a routine diagnostic approach.
Project acronym DEVSPACE
Project The development of the hippocampal spatial representation system
Researcher (PI) Francesca Cacucci
Host Institution (HI) UNIVERSITY COLLEGE LONDON
Summary This proposal will address how a multimodal cognitive system, the neural representation of space in the hippocampus, emerges during development. There is a long tradition in neuroscience of studying the development of primary sensory systems, but fewer studies have concentrated on the development of brain networks supporting higher-order cognitive representations. Our recent findings (Wills, Cacucci et al. Science, 2010) provide a starting point to fill this gap, charting the emergence of spatial responses of hippocampal formation neurons, using in vivo recording in awake, behaving rats. The hippocampal formation supports neural representations of the environment ('cognitive maps') by means of which an animal can locate itself and navigate to a goal location. It contains three classes of spatially-tuned cells: place cells, which code for location, head direction cells, which code for directional orientation and grid cells, which may code for distance travelled. The key aim of this proposal is to delineate the developmental processes that create this neural representation of space, focusing on the representations of place and direction. We will delineate which sensory information is capable of driving spatial firing, and whether early hippocampal coding is truly spatial in the sense of representing configurations of stimuli and not single cues. How are abstract spatial constructs (place and head direction) built from raw sensory information during development? We will test whether boundary sensitive neurons and angular velocity tuned neurons are the elemental 'building blocks' making up place and directional signals, as suggested by many theoretical models. We will also investigate the role of experience in the construction of spatial representations. Do the network architectures underlying spatial firing emerge through experience-dependent learning mechanisms, or are they the result of self-organizing processes which take place independently of experience?
This proposal will address how a multimodal cognitive system, the neural representation of space in the hippocampus, emerges during development. There is a long tradition in neuroscience of studying the development of primary sensory systems, but fewer studies have concentrated on the development of brain networks supporting higher-order cognitive representations. Our recent findings (Wills, Cacucci et al. Science, 2010) provide a starting point to fill this gap, charting the emergence of spatial responses of hippocampal formation neurons, using in vivo recording in awake, behaving rats. The hippocampal formation supports neural representations of the environment ('cognitive maps') by means of which an animal can locate itself and navigate to a goal location. It contains three classes of spatially-tuned cells: place cells, which code for location, head direction cells, which code for directional orientation and grid cells, which may code for distance travelled. The key aim of this proposal is to delineate the developmental processes that create this neural representation of space, focusing on the representations of place and direction. We will delineate which sensory information is capable of driving spatial firing, and whether early hippocampal coding is truly spatial in the sense of representing configurations of stimuli and not single cues. How are abstract spatial constructs (place and head direction) built from raw sensory information during development? We will test whether boundary sensitive neurons and angular velocity tuned neurons are the elemental 'building blocks' making up place and directional signals, as suggested by many theoretical models. We will also investigate the role of experience in the construction of spatial representations. Do the network architectures underlying spatial firing emerge through experience-dependent learning mechanisms, or are they the result of self-organizing processes which take place independently of experience?
Project acronym DIAMONDCOR
Project A molecular approach to treat diabetes mellitus onset dependent coronaropathy
Researcher (PI) Rabea HINKEL
Host Institution (HI) KLINIKUM RECHTS DER ISAR DER TECHNISCHEN UNIVERSITAT MUNCHEN
Summary In Europe, 59 million patients suffer from diabetes mellitus with health costs of 142 billion Euros per year. As one of the most challenging consequences, diabetes inflicts cardiovascular disease leading to cardiomyopathy and cardiac death. A global, current aim lies in preventing cardiac complications in patients with diabetes mellitus. In pathogenesis of diabetic cardiomyopathy, the role of microvascular processes remains largely elusive; my proposal aims at solving this key question – an impossible mission so far. As attractive therapeutic concept and overall objective, the present proposal aims at exploiting microvascular mechanisms for preventing and treating diabetic cardiomyopathy. I will study a novel, unique transgenic pig model of diabetes mellitus combined with advanced, patient compatible molecular imaging. We pioneered distinct genetic manipulations in pigs, including adeno-associated viral vectors (AAV) for microvessel stabilization as well as AAV-based CrispR/Cas9 transduction for in vivo genome editing. Using this cutting edge technology, I could decipher an important role for microvascular capillary rarefaction in the development of diabetic cardiomyopathy in my previous work. In the present proposal, I aim at determining 1.	novel, microvascular-focused therapeutic targets for diabetic cardiomyopathy 2.	the effect of reduced microvascular damage on myocardial function in diabetes, both in the absence and presence of ischemia. My approach will implement targeting microvessels as new paradigm for treating diabetic cardiomyopathy. I will identify novel therapeutic targets for tailored drug development by industry and academia. My planned work will improve the success rate of clinical trials for the benefit of patients suffering diabetic cardiomyopathy and putatively other cardiac diseases.
In Europe, 59 million patients suffer from diabetes mellitus with health costs of 142 billion Euros per year. As one of the most challenging consequences, diabetes inflicts cardiovascular disease leading to cardiomyopathy and cardiac death. A global, current aim lies in preventing cardiac complications in patients with diabetes mellitus. In pathogenesis of diabetic cardiomyopathy, the role of microvascular processes remains largely elusive; my proposal aims at solving this key question – an impossible mission so far. As attractive therapeutic concept and overall objective, the present proposal aims at exploiting microvascular mechanisms for preventing and treating diabetic cardiomyopathy. I will study a novel, unique transgenic pig model of diabetes mellitus combined with advanced, patient compatible molecular imaging. We pioneered distinct genetic manipulations in pigs, including adeno-associated viral vectors (AAV) for microvessel stabilization as well as AAV-based CrispR/Cas9 transduction for in vivo genome editing. Using this cutting edge technology, I could decipher an important role for microvascular capillary rarefaction in the development of diabetic cardiomyopathy in my previous work. In the present proposal, I aim at determining 1.	novel, microvascular-focused therapeutic targets for diabetic cardiomyopathy 2.	the effect of reduced microvascular damage on myocardial function in diabetes, both in the absence and presence of ischemia. My approach will implement targeting microvessels as new paradigm for treating diabetic cardiomyopathy. I will identify novel therapeutic targets for tailored drug development by industry and academia. My planned work will improve the success rate of clinical trials for the benefit of patients suffering diabetic cardiomyopathy and putatively other cardiac diseases.
Project acronym DIRONAKI
Project Differentiation and role of Natural Killer cell subsets
Researcher (PI) Thierry Walzer
Summary "NK cells are innate lymphocytes that play a role in the early response against intracellular pathogens and against tumors. Several NK cell subsets have been described in peripheral organs that correspond to discrete stages of in vivo maturation. How NK cells differentiate from early precursors and what are the specific functions of each NK cell subset are unresolved issues. Here, we propose a three-aim program to address these questions. First, we want to revisit the partition of the NK cell population that is currently based on surface markers of undefined function by looking at the expression of transcription factors (TF) essential for NK cell development and maturation, such as T-bet and Eomes, using novel TF reporter mice. This strategy should also allow us to identify very early steps of NK cell development (NK cell progenitors) that remain ill defined. Second, we will try and identify molecular mechanisms that induce transition between NK cell maturation stages. For this we will take advantage of a previous gene profiling analysis that pointed at several pathways and TF that were highly regulated during NK cell maturation. The role of these pathways and TF in the differentiation of NK cells will be measured using a novel Cre/lox system allowing NK-specific gene deletion. Detailed analysis of mouse mutants will be used to delineate the role of selected genes and pathways in NK cell differentiation. Third, we will compare patterns of migration, cytokine secretion, in vivo cytotoxicity and global gene expression by individual NK cell subsets during an airway infection by Influenza to get insight on the specific functions of NK cell subsets during immune responses. Altogether, the results of this study should provide developmental, molecular and functional evidences to support the physiological relevance of NK cell subsets. This may improve strategies that aim at manipulating NK cell function for the benefit of patients with cancer or chronic infectious diseases"
"NK cells are innate lymphocytes that play a role in the early response against intracellular pathogens and against tumors. Several NK cell subsets have been described in peripheral organs that correspond to discrete stages of in vivo maturation. How NK cells differentiate from early precursors and what are the specific functions of each NK cell subset are unresolved issues. Here, we propose a three-aim program to address these questions. First, we want to revisit the partition of the NK cell population that is currently based on surface markers of undefined function by looking at the expression of transcription factors (TF) essential for NK cell development and maturation, such as T-bet and Eomes, using novel TF reporter mice. This strategy should also allow us to identify very early steps of NK cell development (NK cell progenitors) that remain ill defined. Second, we will try and identify molecular mechanisms that induce transition between NK cell maturation stages. For this we will take advantage of a previous gene profiling analysis that pointed at several pathways and TF that were highly regulated during NK cell maturation. The role of these pathways and TF in the differentiation of NK cells will be measured using a novel Cre/lox system allowing NK-specific gene deletion. Detailed analysis of mouse mutants will be used to delineate the role of selected genes and pathways in NK cell differentiation. Third, we will compare patterns of migration, cytokine secretion, in vivo cytotoxicity and global gene expression by individual NK cell subsets during an airway infection by Influenza to get insight on the specific functions of NK cell subsets during immune responses. Altogether, the results of this study should provide developmental, molecular and functional evidences to support the physiological relevance of NK cell subsets. This may improve strategies that aim at manipulating NK cell function for the benefit of patients with cancer or chronic infectious diseases"
Project acronym DIVIMAGE
Project Bridging spatial and temporal resolution gaps in the study of cell division
Researcher (PI) Daniel Wolfram Gerlich
Host Institution (HI) INSTITUT FUER MOLEKULARE BIOTECHNOLOGIE GMBH
Summary Cell division underlies the growth and development of all living organisms. Following partitioning of bulk cytoplasmic contents by cleavage furrow ingression, dividing animal cells split by a distinct process termed abscission. Whereas a number of factors required for abscission have been identified in previous studies, it is not known by which mechanism they mediate fission of the intercellular bridge between the nascent sister cells. Here, we will establish correlative workflows of time-lapse imaging, super resolution fluorescence microscopy, electron tomography, and electrophysiological assays to bridge spatial and temporal resolution gaps in the study of abscission. We will further develop computational tools for image-based RNAi screening. With this, we aim to: 1) elucidate how membrane and cytoskeletal dynamics coordinately split the intercellular bridge; 2) uncover the signaling pathways controlling abscission timing. Failure in abscission can lead to aneuploidy and cancer. Elucidating its mechanism and temporal control is therefore of general biological and medical relevance. The computational and correlative imaging methods developed in this project will further provide the research community new possibilities for mechanistic studies in intact cells.
Cell division underlies the growth and development of all living organisms. Following partitioning of bulk cytoplasmic contents by cleavage furrow ingression, dividing animal cells split by a distinct process termed abscission. Whereas a number of factors required for abscission have been identified in previous studies, it is not known by which mechanism they mediate fission of the intercellular bridge between the nascent sister cells. Here, we will establish correlative workflows of time-lapse imaging, super resolution fluorescence microscopy, electron tomography, and electrophysiological assays to bridge spatial and temporal resolution gaps in the study of abscission. We will further develop computational tools for image-based RNAi screening. With this, we aim to: 1) elucidate how membrane and cytoskeletal dynamics coordinately split the intercellular bridge; 2) uncover the signaling pathways controlling abscission timing. Failure in abscission can lead to aneuploidy and cancer. Elucidating its mechanism and temporal control is therefore of general biological and medical relevance. The computational and correlative imaging methods developed in this project will further provide the research community new possibilities for mechanistic studies in intact cells.


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Why is everyone talking about Catholic Social Teaching these days?
Catholic Social Teaching (CST) is a term we appear to hear more frequently since Francis became Pope in March, 2013. Why is this so? It is not that previous popes did not talk or write about it, they did. However, Pope Francis appears to say the phrase in both words and actions.
• the actions of people in answering the call of Matthew 25:31-46: The Parable of the Sheep and the Goats.
CST principles have been part of our tradition since the time of scripture so it is a fluid term as it belongs to a living, dynamic tradition which is constantly being added to by the Church. CST has been expressed by Pope Francis in his encyclical Laudato Si' when he says, "It is my hope that this encyclical letter, which is now added to the body of the Church's social teaching, can help us to acknowledge the appeal, immensity and urgency of the challenge we face." (LS15) He has also demonstrated CST by his actions, such as opening a laundrette for the homeless in the Vatican.
CST is about being relational, with God, others, self and creation. Each of these areas need to be working in harmony for us to be followers of the Gospel call "to repent and believe in the Good News" (Mark 1:15). CST is about hearing the cry of the poor or marginalised and then being "righteous" doing something about the "cry" we have heard. We are, in CST, to be as God is, active in human history; we too are to active in the world in which we live.
CST is a huge part of the history of the Church. It is full of biblical insights, especially in the books of the prophets, who constantly challenged the status quo and in the life and actions of Jesus. The great writers of the Church have also written widely about CST. Gregory of Nyssa in the fourth century wrote of a Christian as one who was with God by following the example of Christ through righteousness. Today CST is also seen not just through the experiences of the Church writers but also in our own understanding of what it means to be a follower of Christ. Each of us must decide how we are going to personally respond to the word of Jesus, "…whenever you did this for one of the least important of these followers of mine, you did it to me!" (Matthew 25:40).
CST rests upon four permanent principles out of which the other principles are derived. Various scholars propound other such principles. But these four permanent principles are: "the dignity of the human person, which is the foundation of all other principles and content of the Church's social doctrine; the common good; subsidiarity and solidarity" (The Compendium of Social Doctrine of the Church, # 160).
We are all made in the image and likeness of God and so are sacred. We all possess an inalienable dignity regardless of gender, race, class, or other human categorisations. As community, we recognise and protect human dignity and this should enable us to ask fundamental questions about the social development of all people. This is the principle from which all others flow. By acknowledging that we are made in the image and likeness of God also means we must recognise that in ourselves and in others, those we encounter personally and those we do not.
This principle helps us to protect human dignity when we recognise God in others and helps us to respect life in all its forms and asks us to acknowledge God as the giver of life. It means we need to speak out when life is threatened in any way — through abortion, euthanasia, the death penalty or simply in the way people can live.
Pope Francis in the apostolic exhortation Evangelii Gaudium (2013), says "we become fully human when we become more than human, when we let God bring us beyond ourselves in order to attain the fullest truth of our being" (EG 8).
• when interest rates go up?
• when wages are low?
• when benefits are cut?
• when parole conditions are so hard people are bound to break them?
The common good is the total of all those conditions of social living, including political, economic and cultural that means humanity can achieve their full potential in all aspects of their lives. The common good is central to the way in which we should live in and as a community. What is the best outcome for humanity in any decision that is being made, rather than what is best for the majority. The common good helps us to see God in the decisions we make. Our rights are only acceptable if they do not disrespect others or block all love from being transformative.
Pope Francis in Laudato Si' says "The climate is a common good, belonging to all and meant for all" (LS 23).
In relation to justice issues we need to ask ourselves the question — where do I stand in relation to what is best for all and not just a specific group?
We belong to one human family and because of this we have mutual obligations that should promote the rights and development of all people throughout the world. Solidarity helps people to stop becoming indifferent and so often isolationist when faced with our responsibilities or overwhelming situations. Solidarity expects us to put away thoughts that relate to gender, race, national boundaries and to see ourselves and others as made in the image and likeness of God. We are individuals but we are always in relation with God, self, others and creation. Solidarity gives us the opportunity to become one with the other and see ourselves in them.
Pope Francis in Laudato Si' says "all of us are linked by unseen bonds and together forms [a] kind of universal family, a sublime communion which fills us with a sacred affectionate and humble respect" (LS 89).
• how do I reflect Christ to others?
• what of Christ do I see in others?
• how do I encounter the other in my words and actions?
Subsidiarity can be a principle that is not well understand. It states that all responsibilities and decisions should be attended to as close as possible to the level of the individuals who will be affected by the decision being made. The local and immediate individuals and or groups who are affected should be promoted and protected, without completely diminishing the responsibilities of government structures that are needed to coordinate and regulate the greater social community.
Pope Francis, when discussing dialogue and transparency regarding decision making about environmental issues says, "the local population should have a special place at the table: they are concerned about their own future and that of their children and can consider goals transcending immediate economic interest" (Laudato Si' 183).
• how does your local community work?
• how involved are you in the decision making that will affect you?
Lyn Smith is the Head of RE/ NCRS Projects Auckland at The Catholic Institute.