text:
L'Hippodrome du Deffends se situe à Sault dans le Vaucluse.

Historique
L'hippodrome de Sault a été créé et construit par Charles Magnan également maire de Sault de 1904 à 1912.

Courses
Il n'est organisé qu'une réunion par an. Il s'agit de courses de trot, essentiellement attelé.

Il y a généralement 7 courses de trotteurs

Caractéristiques
Piste en herbe, corde à droite, de 850 mètres. Les distances les plus utilisées sont de  mètres et de  mètres. Sa caractéristique principale est d'être situé à  d'altitude, ce qui en fait le plus haut de France, autour d'un champ de lavande, au milieu des bois.

Budget

Avenir

Autres activités de l'hippodrome
 Fête de la lavande du pays de Sault.

Notes et références

Voir aussi

Articles connexes
 Liste des hippodromes
 Dolmen dit l'Autel du Loup

Liens externes
 Fédération hippique du sud-est

Deffends
Équipement sportif en Vaucluse
Sault (Vaucluse)


text:
BOOK REVIEW: 'Why Meadow Died'
How government, not guns, enabled the Parkland school shooting
Nikolas Cruz
Meadow Died
Andrew Pollack
'Why Meadow Died' (book jacket) more >
By Corey A. DeAngelis - - Friday, September 13, 2019
A sick person killed 17 people at Marjory Stoneman Douglas High School in Parkland last year. Conventional wisdom is that enacting various gun control laws, including banning assault weapons, is the solution to school shootings.
But as Andrew Pollack, the father of one of the Parkland victims, and Max Eden, an education policy expert, explain in their new book "Why Meadow Died: The People and Policies that Created the Parkland Shooter and Endanger America's Students," the story is far more complicated than that.
As the book's title suggests, government policy bears significant blame for the Parkland tragedy.
The shooter, Nikolas Cruz, showed serious signs of violent and erratic behavior for years. He mutilated animals, brought bullets to school, made death threats and attempted suicide. And everyone — local and federal law enforcement, school staff, teachers, students and his family — knew it.
Police officers were called to his house 45 times before the tragedy. His mother's friend called the sheriff's office, telling them "this might be Columbine in the making" — but they never called her back. Multiple students reported Cruz to school leaders. And the school security staff even had a meeting where they agreed that if anyone would become a school shooter, it would be Cruz.
If everyone knew something was wrong, how did he slip through the cracks?
As Mr. Pollack and Mr. Eden write, "Every institution around Cruz, especially the school system, failed."
On their own, each government failure was arguably a rational response to the incentives created by well-intentioned but flawed government policies. For example, Broward school district's PROMISE program had a well-meaning goal: Lower petty arrests in schools to prevent students from getting criminal records that would hurt them in life.
School officials knew Cruz got into a fight at school, vandalized school property and made death threats, yet he was never arrested.
District policy also required schools to send students to the juvenile justice system if they skipped the PROMISE program. Cruz was referred to the PROMISE program, but he did not attend nor was he sent to the juvenile justice system. If Cruz had earned a criminal record for any of these acts, local police and the FBI might have taken reports of his subsequent death threats more seriously. And if Cruz had felonies on his record, he would not have been able to legally purchase a gun.
But that's just the tip of the iceberg.
Guidance from the federal government also had an honorable goal of preventing discriminatory discipline and reducing the number of suspensions and expulsions. A federal Dear Colleague Letter pressured schools to avoid disproportionately punishing students from different groups, including minority students and those with disabilities.
However, for "emotional and behavioral disabilities," the guidance essentially pressured schools "to discipline students who behave badly at the same rate as students who behave well, which creates predictably perverse incentives and consequences," Mr. Pollack and Mr. Eden write.
Similarly, the federal Individuals with Disabilities Education Act's pressure to place students in the "least restrictive environment" might have inadvertently contributed to the school's principal at Cruz's alternative school deciding to put Cruz back into the regular high school, where support staff knew he didn't belong. Likewise, the Youth Emergency Services group evaluated Cruz three times but decided he didn't need to be institutionalized.
Then on the day of the shooting, there were several publicized government failures. A school security officer saw Cruz enter the campus with a rifle bag and heard shots, but never called Code Red because he claimed he didn't want to "get the cops out there for nothing." Eight Broward sheriff's deputies heard shots but none of them went in the building to face the shooter, perhaps because the policy had recently changed from saying deputies "shall" enter a building to address a shooter to saying that they "may."
Law enforcement failed. In other instances, well-intentioned school and government employees were just doing their jobs but the government's top-down incentives and lack of accountability increased the chances of this tragedy. It is possible that Cruz would have killed 17 people, including Mr. Pollack's daughter, Meadow, even without these failures and perverse incentives in place. But it would be irresponsible not to consider that even the most well-intentioned government policies often come with unintended and, in this case, fatal consequences.
• Corey A. DeAngelis is the director of school choice at Reason Foundation and an adjunct scholar at Cato Institute. You can reach him on Twitter at @DeAngelisCorey and via email at Corey.DeAngelis@Reason.org.
WHY MEADOW DIED: THE PEOPLE AND POLICIES THAT CREATED THE PARKLAND SHOOTER AND ENDANGER AMERICA'S STUDENTS
By Andrew Pollack and Max Eden
Post Hill Press, $27, 336 pages

redpajama_set_name: RedPajamaCommonCrawl


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text:
Arsenal Line-ups
The Arsenal History Advent Calendar – Day 14
by Mark Andrews
Exhausted Arsenal lose to the Champions Elect
Woolwich Arsenal versus Newcastle United: Saturday December 31st 1904
by Mark Andrews and Andy Kelly
The cartoon has a worried Nurse, Miss Manor Field, asking the doctor whether the defeat is serious for Redshirt. The avuncular Doctor's response is a reference to Woolwich Arsenal's unbelievably tough Christmas schedule with Woolwich Arsenal having been promoted to the First Division for the first time, playing four games in five days during the Christmas period, three of them away.
They started at home against Sheffield United winning 1-0 on Christmas Eve in front of a festive 20,000 Woolwichers. The team was graciously given Christmas Day, a Sunday, off by the Football League, but were back on the train to the Midlands for Boxing Day.
The game on the 26 December was against Aston Villa in front of 40,000. Unfortunately, the result was a reverse for Woolwich Arsenal as they lost 1-3. We have to assume they stayed at a hotel in Birmingham rather than go back to South London for the next day they made their way to Nottingham to play Forest on 27 December.
Here they won 3-0 watched by a crowd of 16,000 and, from Nottingham, the next day travelling took them to Sheffield for the return against Sheffield United. An unseasonally large reverse of 0-4 was seen by 30,000 on 28 December.
The team returned to Plumstead for a well earned rest, but was soon in action again three days later at home on New Years Eve playing Newcastle in front of the second largest crowd of the whole season.
Newcastle ran out easy winners with two second half goals in front of 30,000 festive fans who were in good voice, insulting the Newcastle players freely especially Appleyard who, after some foul play on Percy Sands, received a verbal torrent from the Spion Kop. He responded in a manner well known to Gooners fans in the 70s with a Charlie George style V sign.
Newcastle were crowned champions at the end of the season, and should really have had a toast to the Plumstead fog during their victory celebrations.
Don't forget to subscribe to the blog (top right). You know it makes sense.
Woolwich Arsenal: The club that changed football – Arsenal's early years
The Crowd at Woolwich Arsenal – crowd behaviour at the early matches
Posted in: Games, Phil Kelso, Woolwich Arsenal
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Yossef Bodansky is director of research for the International Strategic Studies Association, where he is also a senior editor for their Defense and Foreign Affairs publications. He is director of the Congressional Task Force on Terrorism and Unconventional Warfare for the U.S. House of Representatives. In addition, Bodansky has served as a consultant on terrorism for the U.S. government and other organizations.
Target America: Terrorism in the U.S. (1993, Shapelsky Publishers Inc.).
Crisis in Korea (1994, Shapelsky Publishers Inc.).
Terror: The Inside Story of The Terrorist Conspiracy in America (1994, Shapelsky Publishers Inc.).
Offensive in the Balkans: The Potential for a Wider War as a Result of Foreign Intervention in Bosnia-Herzegovina (1995, International Media Corp./ISSA).
Some Call It Peace: Waiting for War In the Balkans (1996, International Media Corp./ISSA).
Osama Bin Laden: The Man Who Declared War on America (1999, 2001, Random House).
Islamic Anti-Semitism as a Political Instrument (1999, 2000, ACPR Publications and Tammuz Publishers).
The High Cost of Peace: How Washington's Middle East Policy Left America Vulnerable to Terrorism (2002, Random House).
The Secret History of the Iraq War (2004, Harper).
Chechen Jihad: Al Qaeda's Training Ground and the Next Wave of Terror (2007, Harper).
Tehran, Baghdad and Damascus: The New Axis Pact--August 1992 at the Conference for Middle East Peace.
Iran's European Springboard?--with Vaughn S. Forrest, September 1992 at the Serbian Unity Congress.
Islamic Terrorism in the United States--1993? at the National Security Caucus Foundation.
The Precedent Is Set-August 1993 at the Centre for Peace in the Balkans.
Islam Versus Christianity and Its Eastern Salient: Israel--with Vaugn S. Forrest, 1994? at the Conference for Middle East Peace.
The Truth About Gorazde--with Vaughn S. Forrest, May 1994 at the Serbian Unity Congress.
North Korea's Preparations for War; DPRK Intel., Special Forces Change--May 1994 in Defense & Foreign Affairs Strategic Policy of International Strategic Studies Association.
Pakistan Supports Terrorist Rebels in Kashmir--with Vaughn S. Forrest, June 1994 at the Federation of American Scientists.
The North Korean Nuclear Arsenal is Deployed, Despite Face-Saving Agreements with the US--July 1994 in Defense & Foreign Affairs Strategic Policy of International Strategic Studies Association.
Pyongyang and the U.S. Nuclear Gambit--August 1994 at the Conference for Middle East Peace.
Beijing's Surge for the Strait of Malacca--1995 at Freeman Center for Strategic Studies.
Pakistan, Kashmir and the Trans-Asian Axis: Pakistan's Kashmir Strategy and Islamabad's Road Warriors--1995 at Freeman Center for Strategic Studies.
Pakistan's Nuclear Brinkmanship--1995 at Freeman Center for Strategic Studies.
Jerusalem in Context--July 1995 at the Conference for Middle East Peace.
Peres and the New Middle East--December 1995 at Freeman Center for Strategic Studies.
Syria's Strategic Posture--February 1996 at Freeman Center for Strategic Studies.
Negotiating With Terrorists London-Style--March 1996 at Freeman Center for Strategic Studies.
Like the Wings of a Bird: The Myths and Realities in the PLO-HAMAS Relationship--April 1996 at Freeman Center for Strategic Studies.
Approaching the New Cycle of Arab-Israeli Fighting--with Vaughn S. Forrest, December 1996 at Freeman Center for Strategic Studies.
Arafat's, "Peace Process"--1997, at the Ariel Center for Policy Research.
The Peace Process Syrian Style--February 1997 at Freeman Center for Strategic Studies.
Arafat: Between Jihad and Survivalism--May 1997 at Freeman Center for Strategic Studies.
Dejavu All Over Again--July 1997 at Freeman Center for Strategic Studies.
Escalation in the North--July 1997 at Freeman Center for Strategic Studies.
Syria Embarks on a Massive Purchase of Weapons--July 1997 at Freeman Center for Strategic Studies.
Mubarak's Wedge--September 1997 at Freeman Center for Strategic Studies.
The Balkans Conflict: Turning Point in Brcko--November 1997? at the Centre for Peace in the Balkans.
Chechnya: The Mujahedin Factor--January 1998 at Freeman Center for Strategic Studies.
Islamic Anti-Semitism as a Political Instrument--January 1998 at Freeman Center for Strategic Studies.
The Iraqi WMD Challenge--Myths and Reality--February 1998 from the Task Force on Terrorism and Unconentional Warfare, on the Christian Action for Israel web site.
The Price of Washington's Bosnia Policy--February 1998 at Freeman Center for Strategic Studies.
Reflections on the 'Peace Process'--February 1998 at Freeman Center for Strategic Studies.
Terrorism and the Balkans: Italy Becomes Iran's New Base for Terrorist Operations--February 1998 at the Centre for Peace in the Balkans.
Expediting the Return of Salah Al-Din--June 1998 at Freeman Center for Strategic Studies.
Pakistan's Islamic Bomb--July 1998 at Freeman Center for Strategic Studies.
Italy Becomes Iran's New Base For Terrorist Operations--October? 1998 in Defense & Foreign Affairs Strategic Policy of International Strategic Studies Association.
The New Crisis On The Korean Peninsula Is Worst in 50 Years--January 1999 in Defense & Foreign Affairs Strategic Policy of International Strategic Studies Association.
Osama Bin Laden and the Latest Phase in the US War on Terrorism--November 2002 at International Strategic Studies Association.
Iraq War Planning and Strategy Show Detailed Preparations for a Geographically Wide and Multi-Layered Conflict--November 2002 at International Strategic Studies Association.
Iraq's Leadership Moves Discreetly to Conflict Locations--December 2002 at International Strategic Studies Association.
Tehran Maneuvers for a Wider War with Israel to Ensure that the US-Led War on Iraq Does Not Leave Iran Isolated and Surrounded--December 2002 at International Strategic Studies Association.
Osama Bin Laden and the New Crusade War: Bin Laden's New, Secret Message to the Islamist Leadership--February 2003 at International Strategic Studies Association.
Iran's Iraqi Gambit: Tehran Decides to Move Specifically Against the US--February 2003 at International Strategic Studies Association.
Saddam's Further Preparations for War: Forces in Position; Commanders Named Early Start Options Open--February 2003 at International Strategic Studies Association.
Saddam Delivers Islamist Message to Prepare for His Possible Disappearances During Conflict--March 2003 at International Strategic Studies Association.
Two Wars, One Battlefield: The New Jihad is Called in the Iraq War--March 2003 at International Strategic Studies Association.
Yossef Bodansky--at the Freeman Center for Strategic Studies.
Articles by Yossef Bodansky--at Kashmiri Pandits web site.
Writings of Yossef Bodansky--at the Conference for Middle East Peace.
International Strategic Studies Association--where Bodansky is director of research.
© 2002-2003, 2008 by Wm. Robert Johnston.
Last modified 8 June 2008.


Speed filing and retrieval time by using color to categorize different types of folders. Single-ply is the economical choice for files that are seldom accessed. File folders are made of 11 point stock. They also feature undercut front panel and rounded top corners. 1/3-cut tabs are 1/2" high. Folders are scored for 3/4" expansion.


Once again our end of term party and picnic was a great success! The picnic was very well attended by parents and we think everyone had a good time?
We were overwhelmed by the gifts, cards and kind words we received and would like to say a very BIG THANK YOU! to our lovely families.
We wish our leavers the very best of luck in their new schools and look forward to welcoming our present children back in September in addition to our new families!


text:
WNBA Player Won't Return To Russia After Brittney Griner Arrest Despite Making Entire Salary In One Month Overseas
by Mark Harris December 9, 2022, 11:30 am updated December 9, 2022, 1:15 pm
Like many other WNBA players, Angel McCoughtry has played professionally in Russia during the WNBA offseason in the past. She recently explained she won't go that route again following Brittney Griner's arrest despite saying she made her entire WNBA salary in one month playing in Russia.
"It's tough on us because Russia was one of the places where we made the most money," McCoughtry told TMZ. "I was making my WNBA salary in one month in Russia. My whole salary. I think girls are going to go elsewhere and play, probably."
The overwhelming majority of WNBA players earn less than $230,000 per season. Only 11 players in the league will earn over $200,000 in 2022.
Russia can pay four times what the WNBA pays its players, which is why Angel McCoughtry, Griner, and a large number of other players take their talents to Russia.
BRITTNEY GRINER'S FRIEND SELLS OUT, WILL PLAY IN RUSSIA THIS SEASON PROVING HER LOVE FOR CAPITALISM
Russia traded Brittney Griner back to the United States after she was arrested in a Moscow airport in February.
Griner was arrested on drug charges in February after authorities said she had cannabis oil inside her luggage, which is an illegal substance in Russia. She pleaded guilty to the drug charges in July and was sentenced to nine years in a Russian prison.
STEPH CURRY THANKS BRITTNEY GRINER FOR HER 'SACRIFICE' AFTER HER RELEASE FROM RUSSIAN PRISON
The 31-year-old was released on Thursday via a prisoner swap in return for notorious arms dealer Viktor Bout, who is better known as 'The Merchant of Death.'
McCoughtry believes that Griner will make her return to the WNBA hardwood during the 2023 season, which begins in May.
I think by that time she'll have herself together to be ready to play – because everyone's going to want to watch her play," McCoughtry said. "It's going to be amazing."
Angel McCoughtryBrittney GrinerRussiaWNBA


text:
Home / Anna Elias And The Forlorn Hope / ANNA ELIAS AND THE FORLORN HOPE - VALLEYS IN THE FLATLANDS
Anna Elias and the Forlorn Hope – Valleys in the Flatlands
For a debut album, Anna Elias has gathered together some of the finest talents on the UK folk scene to help produce this 14 track disc; but one listen through and it's obvious that this is an album that has been crafted and considered over time, and it's presented here with real confidence.
Built around the beautiful vocals of Anna Elias the whole album slots very comfortably into the UK contemporary folk scene, alongside the likes of Karine Polwart, Megson and Emily Smith, with a sound that feels modern, but with enough links to the tradition for the listener to know where the roots of the album lay.
The beautifully elegant vocals are backed up by subtle arrangements of acoustic guitars, cello, bass, melodeon, percussion and some exceptional backing vocals – all this is added by a group of musicians that include Saul Rose, Karine Polwart and Will Pound.
The lyrics and the melodies share equal billing as songs of landscapes and towns are delivered in tunes that feel timeless and familiar on the very first listen – this is an album of real charm and instant appeal, and the songs 'Plough Song' and 'Where We Stand' are real highlights in amongst an album of strong material.
Anna Elias and the Forlorn Hope will be a new name to most, but this is an accomplished and high quality collection that really stands out from the crowd.
ANNA ELIAS AND THE FORLORN HOPE - VALLEYS IN THE FLATLANDS
CD (Cat No: 13689)


text:
Q: The controller must return a response (Object(Symfony\Component\Form\Form) given) We are using the below bundles with Symfony2 to create a RESTful API.
new FOS\RestBundle\FOSRestBundle(),
new JMS\SerializerBundle\JMSSerializerBundle(),
new Nelmio\ApiDocBundle\NelmioApiDocBundle(),

We get the below error after running php composer.phar update
[2014-12-05 10:39:41] security.INFO: Populated SecurityContext with an anonymous Token [] []
[2014-12-05 10:39:41] request.CRITICAL: Uncaught PHP Exception LogicException: "The controller must return a response (Object(Symfony\Component\Form\Form) given)." at /var/www/html/symfony2/app/bootstrap.php.cache line 3020 {"exception":"[object] (LogicException: The controller must return a response (Object(Symfony\\Component\\Form\\Form) given). at /var/www/html/symfony2/app/bootstrap.php.cache:3020)"} []
[2014-12-05 10:39:41] security.DEBUG: Write SecurityContext in the session [] []

We installed Symfony2 on our server using the below steps
//install symfony
php composer.phar create-project symfony/framework-standard-edition symfony2/

//move composer into symfony folder
cp composer.phar symfony2/composer.phar
rm composer.phar
cd symfony2

//symfony dependencies
php composer.phar require doctrine/doctrine-fixtures-bundle
php composer.phar require "friendsofsymfony/rest-bundle" "@dev"
php composer.phar require "jms/serializer-bundle" "@dev"
php composer.phar require "nelmio/api-doc-bundle" "@dev"

The API requests return a 500 server error.
I have traced the error to the below point by am unsure why it is not working.
@Annotations\View(
     templateVar = "form"
)

the ClassResourceInterface class is responsible for the above.
This may be related to this question but the solutions posted here do not work:
FOSRestBundle: The controller must return a response (Array()) given
Something is wrong with this class:
Nelmio\ApiDocBundle\Annotation\ApiDoc

Has anyone had issues with this as well?
Thank you

A: You should set FOS REST config in file /app/config/config.yml
For example:
#/app/config/config.yml
fos_rest:
param_fetcher_listener: true
body_listener: true
format_listener: false
routing_loader:
   default_format: json
view:
    view_response_listener: 'force'
    formats:
        xml: true
        json : true
    default_engine: none
    templating_formats:
        html: true
access_denied_listener:
    json: true
allowed_methods_listener: true

A: Try to self-update your composer file before starting any new project to avoid issues.
composer self-update

or if composer is installed in your www directory:
php composer.phar self-update

then you can create a new symfony project with all the bundles you need:
composer create-project symfony/framework-standard-edition symfony2/
cd symfony2
composer require doctrine/doctrine-fixtures-bundle
composer require friendsofsymfony/rest-bundle
composer require jms/serializer-bundle
composer require nelmio/api-doc-bundle

Sometimes at this point I need to give read/write permissions to some directories such as "app/cache" or  "app/bootstrap.php.cache" because my terminal uses my user but apache uses a _www user.
Then you have to register your new bundles in app/AppKernel.php
new Doctrine\Bundle\FixturesBundle\DoctrineFixturesBundle(),
new FOS\RestBundle\FOSRestBundle(),
new JMS\SerializerBundle\JMSSerializerBundle(),
new Nelmio\ApiDocBundle\NelmioApiDocBundle(),

Then your Bundle NelmioApiDocBundle needs to register its own routing and config:
# app/config/routing.yml
NelmioApiDocBundle:
    resource: "@NelmioApiDocBundle/Resources/config/routing.yml"
    prefix:   /api/doc

# app/config/config.yml
nelmio_api_doc: ~

Everything have to work at this point as I already did that.

redpajama_set_name: RedPajamaStackExchange


text:
Q: Nonlinear matrix differential equation I am working with the following differential equation:
$$\dot{x_i} = \sum_j A_{ij} x_j + x_i \sum_j B_{ij}x_j$$
which is essentially in matrix notation:
$$\dot{\mathbf{x}} = A\mathbf{x} + \mathrm{diag}(\mathbf{x)}B\mathbf{x}$$
with $x\in \mathbb{R}^n$ and $A,B\in \mathbb{R}^{n\times n}$ and
$B^T=-B$ and A normal.
I wondered if you had any idea how to approach the nonlinear part?
I found the paper (1) which gives some hints for approximations, but essentially it is of no help. Maybe you know how to deal with it?
(1) Elliot W.Montroll: On coupled Rate Equations with Quadratic Nonlinearities


Mantle cell lymphoma (MCL) is a relatively uncommon yet distinct type of malignant lymphoma whose clinical and pathological characterization has been limited by the small numbers of cases published to date. We studied 80 cases of MCL seen at a single institution over 7 years to determine both clinical and pathological prognostic factors. The patients in this study were predominantly male (70%) and older (mean age, 63 years) and presented with advanced-stage disease (88%). Extranodal involvement was common. Median overall survival (OS) was 43 months. Except for performance status, prognosis was not significantly influenced by clinical prognostic factors. Histologically, MCL architecture was classified as diffuse (78%), nodular (16%), or mantle zone (6%); the OS among these groups was identical. Increased mitotic activity (<20 mitotic figures per 10 high power fields), blastic transformation, and peripheral blood involvement at diagnosis also predicted for a worse outcome, but bone marrow involvement did not. The presence or absence of a translocation t(11; 14) by cytogenetic analysis or a bcl-1 rearrangement by Southern analysis did not significantly predict outcome. In summary, this study of 80 cases of MCL highlights its distinctive clinicopathologic features and shows that increased mitotic activity, blastic morphology, and peripheral blood involvement at diagnosis are prognostically important factors.
Morphologically, MCL can be recognized as a distinct type of ML by its monotonous, diffuse, and/or nodular proliferation of small- to medium-sized cells with slightly irregular nuclei, inconspicuous nucleoli, and absence of both large transformed (noncleaved) cells and proliferation centers. Immunophenotypically, MCL coexpresses pan-B–cell antigens and CD5, a pan-T–cell antigen. A recurring cytogenetic abnormality, t(11; 14), occurs in MCL, resulting in rearrangement of the bcl-1 gene locus and overexpression of the cyclin D1 (CCND1/PRAD1) gene.3 This genetic event is thought to have an important role in the pathogenesis of MCL, because overexpression of cyclin D1 protein is thought to lead to deregulation of the normal cell cycle, particularly at the G1- S-phase transition. Despite refinements in the diagnostic criteria, clinical classification of MCL into existing schemes has been problematic. In the past, most cases of MCL were classified in the Working Formulation as diffuse small cleaved-cell lymphoma, with a minority classified as small lymphocytic, follicular small cleaved-cell, or lymphoblastic lymphoma. These difficulties in classification, as well as the lack of large numbers of cases of MCL for study, have hindered the understanding of its clinical behavior.
Clinically, MCL is considered by most investigators as an ML of intermediate grade, with a median overall survival (OS) of 2 to 5 years.4-12 Some studies suggest that specific morphological subsets of MCL, particularly those with a mantle zone (MZ) pattern, behave in a more indolent manner.13-16 Others have suggested that blastic cell morphology,4-6 13 14 peripheral blood (PB) involvement,8 14 15 17 18 and increased mitotic activity8 11 14 connote a poor prognosis, although the numbers of cases in each study were small. The objective of this study was to examine these and other relevant clinicopathologic variables in a population-based cohort of patients with MCL, diagnosed and treated at the British Columbia Cancer Agency (BCCA). Its aim was not to uncover novel diagnostic features of MCL, but to illustrate the clinical and pathological findings of MCL in British Columbia and to provide further insight into the factors that may have prognostic significance in this disease.
Eighty cases diagnosed as MCL between 1988 and 1995 were obtained from the pathology files of the BCCA, the main cancer referral center for the province of British Columbia, which has a population of approximately 3.6 million people. All cases were reviewed by two pathologists to ensure that each case had an adequate tissue biopsy specimen procured before the initiation of treatment and that the biopsy material met the accepted morphological criteria for MCL.1 2 19 Examination of the biopsy material was undertaken without knowledge of any individual patient's outcome. Cases in which treatment was initiated based solely on bone marrow (BM) and/or PB findings were excluded (n = 29) . Detailed clinical information including stage, treatment, and follow-up was available for each of these 80 cases.
Tissue biopsy specimens were fixed in buffered formalin or B5 fixative, routinely processed, sectioned at 3 μm, and stained with hematoxylin and eosin. BM biopsy specimens were fixed in B5, decalcified with 10% nitric acid, processed, and sectioned in the usual manner. BM and PB smears were stained with a Wright-Giemsa stain. Immunoperoxidase staining was performed according to well-established protocols.
For immunophenotyping, cell suspensions of tissue and mononuclear cell suspensions of PB and BM specimens were prepared according to well-established methods. A direct antibody-labeling technique was employed using mouse monoclonal antibodies CD2, CD3, CD4, CD5, CD7, CD8, CD10, CD11c, CD14, CD19, CD20, CD23, and CD45 (Becton Dickinson, San Jose, CA); goat polyclonal anti-κ and anti-λ (Tago Inc, Burlingame, CA); and FMC-7 (Silenus Laboratories) labeled with either phycoerythrin or fluorescein isothiocyanate. Specimens were analyzed on the Coulter Epics Profile II flow cytometer (Coulter, Hialeah, FL).
Cytogenetic analyses were performed according to established protocols. Southern analysis (SA) to detect bcl-1 gene rearrangements was performed in a manner similar to previously described methods.20 In summary, high molecular weight DNA was extracted from fresh or frozen material, digested with EcoRI, BamHI, and HindIII restriction endonucleases, electrophoresed on 0.7% agarose gels, and transferred onto nylon filters. A 2.1-kb Sst I fragment representing the major translocation cluster on chromosome 11q13 was used as the probe (courtesy of Dr A. Bakhshi, Bethesda, MD).
MCL comprised approximately 4% of ML cases observed at the BCCA during the 7-year study period. The clinical characteristics of the 80 patients are summarized in Table 1. The median age at presentation was 65 years, with a mean age of 63 years (range, 39 to 86 years). The majority of patients were male, with a male-to-female ratio of 2.3:1. Most patients (88%) presented with advanced-stage disease (IIB bulky, III, or IV). Bulk disease was defined as lymph node masses greater than 10 cm. Extranodal involvement at presentation occurred in 76% of cases; the most common sites were BM (63%), PB (34%), gastrointestinal tract (10%), Waldeyer's ring (10%), and liver (8%). In 25% of cases, extranodal localization of disease was the primary presentation. Multiple lymphomatous polyposis, defined as two or more sites of gastrointestinal mucosal involvement, was found in 5 patients either at presentation or during the course of their disease. Coincident breast cancer was present in 2 patients. The median follow-up period for the entire group was 39 months (range, 1 to 101 months).
OS for the whole group of 80 patients is graphically shown in Fig 1, with a median OS of 43 months. Comparisons of OS between clinically relevant patient subsets were performed. Survival was significantly influenced by performance status (PS), in that those patients with PS of greater than 1 (n = 12) had a significantly shorter OS than did those with PS of ≤1 (n = 45; OS, 14 v 45 months; P < .01). Age (≤60 v >60 years), stage (limited versus advanced), serum lactate dehydrogenase (LDH; normal versus elevated), and number of extranodal sites of involvement (≤1 v >1 site) did not significantly predict for patient outcome, but each of these clinical variables did show a trend toward shorter survival in the presence of the respective adverse factor. A calculated International Prognostic Index (IPI) score,24 available for 44 patients, did not significantly predict for patient outcome. Survival differences between clinically relevant treatment groups was limited by small numbers; however, in the group of patients under the age of 60, the BP-VACOP/IRRT group (n = 16) did not have significantly different survival from that of the remainder (n = 13).
OS of all 80 patients with MCL. (MED SURV, median OS in months).
Lymph node biopsy specimens were obtained from 60 patients at presentation, whereas biopsy specimens were obtained from extranodal sites in the remaining 20. All biopsy material fulfilled the diagnostic criteria for MCL.1 19 At low power, lymph nodes were completely effaced by small- to medium-sized lymphocytes in a diffuse and/or nodular pattern. Extranodal tissue, depending on the site, showed either sheets or nodules of small/medium-sized lymphocytes replacing normal structures or invading stromal tissue. No proliferation centers were observed in any case. Occasional compressed germinal centers lacking a normal MZ (naked germinal centers) were observed in a minority of cases with diffuse architecture and were not taken as evidence of a true MZ pattern. At low power, a characteristic mottled pattern was observed, imparted by scattered, large epithelioid histiocytes with pale eosinophilic cytoplasm and no tingible bodies (Fig 2A). In 1 case, the histiocytic component was florid, forming nodules and small sheets. Tingible body macrophages were observed in only a minority of cases; in the 6 cases in which they were numerous (at least one in every high power field [hpf ]), there was evidence of increased cellular proliferation, in particular, increased numbers of mitoses and lymphoblast-like cells. Perivascular hyaline sclerosis was also a feature common to the majority of involved lymph nodes.
Composite photograph showing the three low-power architectural patterns observed in MCL and their prognostic significance: (A) Diffuse pattern; (B) nodular pattern; and (C) MZ pattern. (D) OS of 80 patients based on the predominant architectural pattern observed at diagnosis. No significant differences in OS were shown.
Cytologically, MCL nuclei were round to ovoid, slightly irregular with inconspicuous nucleoli and slightly clumped chromatin (Fig 3A). Cytoplasm was scant. Larger cells with medium-sized nuclei, fine chromatin, inconspicuous nucleoli, and scant cytoplasm were present in most cases to varying degrees. These cells resembled lymphoblasts rather than large noncleaved cells, prolymphocytes, or paraimmunoblasts. In some cases, lymphoblast-like cells were present in significantly increased numbers (Figs 3B and C), implying cytologic transformation (discussed below). Mitoses were easily found in the majority of cases, the prognostic significance of which is discussed below.
Composite photograph showing the cytologic features of MCL. (A) Typical cytology of MCL characterized by cells with small, slightly irregular nuclei, inconspicuous nucleoli, and minimal cytoplasm. Note the frequent epithelioid histiocytes (arrows). (B) MCL with prominent features of transformation, but not clearly blastic. Increased numbers of larger cells with fine chromatin and inconspicuous nucleoli are shown (arrows). (C) Blastic MCL. Note the cytologic resemblance to lymphoblastic lymphoma. (D) OS of 80 patients with MCL based on the presence of blastic features. The 5 cases designated as blastic MCL were associated with a significantly shorter survival when compared with that of all others (n = 75) including those with features of transformation as shown in (B).
Patterns of pretreatment biopsy architecture, mitotic activity, and features of cytologic transformation were analyzed to determine their prognostic significance in terms of overall patient survival. The criteria used for defining these histological parameters are discussed below, and the results of survival analysis are shown in Figs 2D, 3D, and 4 and are summarized in Table 2.
OS of 80 patients with MCL bases on MS (mitoses/10 random hpf ). An MS of greater than 20 was associated with a significantly shorter survival.
Architecture.The architecture of both nodal and extranodal tissue was classified as diffuse, nodular, or MZ according to the predominant pattern observed with the low power (2×) objective and shown in Fig 2. Cases with clear, well-defined nodularity and lacking a significant MZ pattern (n = 13) were classified as "nodular," similar to those of other investigators.6 Cases with diffuse architecture lacked any nodularity, although scattered, compressed germinal centers were occasionally observed. When a mixture of patterns was encountered, architecture was arbitrarily assigned based on which pattern occupied greater than 50% of the cross-sectional area of all sections available for review. In 5 cases, architecture was difficult to assign for two main reasons, biopsy size and extranodal origin. The 5 biopsy specimens, obtained from colonic, conjunctival, gastric, hepatic, or pleural sites, morphologically fit the criteria of MCL and had ancillary studies providing confirmation. Because none of these 5 biopsy specimens showed any evidence of nodularity, all were arbitrarily assigned to the diffuse category.
Between these architectural subtypes, no statistically significant differences in OS were observed (Fig 2D), nor were any significant differences in OS observed after exclusion of the 20 extranodal cases. Also, no survival differences were observed when the nodular and MZ cases were combined and compared with the cases with a diffuse architecture.
Mitotic activity.A mitotic score (MS) was calculated for each case by counting mitotic figures in 10 hpf (40× objective, 10× ocular) selected at random within a representative tissue section. In virtually all 80 cases, it was found that mitoses were uniformly distributed. This was confirmed by counting mitoses in an additional 10 or 20 hpf in approximately 30% of cases, with special attention to those with low mitotic activity (MS ≤ 5). Overall, the mean MS was 16, with a median of 10 and a range of 0 to 87. In 22 cases the MS was low (≤5), and, of note, 14 of these represented biopsy specimens from extranodal sites. Fewer cases were present at the other extreme, with only 8 cases having an MS greater than 40. On average, the mean MS was higher in cases with diffuse histology (MS = 18) than in those with nodular (MS = 11) and MZ (MS = 7) patterns. A statistically significant difference in OS was observed between those cases with an MS ≤20 and MS greater than 20 (Fig 4). The analysis was repeated with other MS cutoff levels (5, 10, and 15), but 20 was found to be the most discriminant (data not shown). When the 20 extranodal cases were excluded from the analysis, the results were the same.
Blastic features.Virtually all 80 cases had at least a few cells with larger nuclei, finer chromatin, and inconspicuous nucleoli; however, in the majority of cases, these cells were present in small numbers. When present in increased numbers, these lymphoblast-like cells were almost always accompanied by an increase in mitotic activity and, occasionally, the presence of tingible body macrophages (Fig 3B). These cases were designated as having prominent features of cytologic transformation. In a minority (n = 5), the blastic cells were so numerous that the histology was nearly indistinguishable from that of lymphoblastic lymphoma; these cases were designated blastic MCL (Fig 3C). The mean MS in the blastic MCL cases was 57.
The OS was significantly shorter for those cases with blastic morphology (Fig 3D). No statistically significant differences in survival were observed between the 16 cases that were transformed to some degree but not truly blastic and the remaining 59 cases that showed no evidence of transformation.
PB films were available for review in 69 cases. The results are summarized in Table 3. The typical PB appearance of circulating MCL was a polymorphous mixture of small, medium, and large lymphocytes, a pattern also described by others.17 The predominant cell type in most cases had a slightly irregular nucleus with fine chromatin, a small nucleolus, and a thin rim of gray-blue cytoplasm. Cells with a small cleaved or chronic lymphocytic leukemia (CLL)-like morphology were often present, as were immature cells with L1 and L2 lymphoblast-like morphology (Fig 5A). In 1 case, the blastic population predominated, creating the initial impression of acute lymphoblastic leukemia. Although absolute lymphocyte counts were not recorded, a significant proportion of cases with PB involvement did not have an elevated lymphocyte count by peripheral smear assessment. Leukemic involvement at diagnosis was defined as the presence of any detectable circulating MCL cells observed on the PB smear at the time of staging and was confirmed by flow cytometry in all cases in which the number of circulating MCL cells was low.
(A) PB involvement in MCL is characterized by a polymorphous cell population including larger cells with immature nuclei and prominent nucleoli. (B) OS of 80 cases of MCL based on PB involvement at diagnosis. Those cases positive for PB involvement (n = 27) were associated with a significantly shorter survival when compared with those in which PB was not involved or not assessed (n = 53).
OS was compared between those patients that presented with PB involvement and the remainder of the patients in which PB involvement was either not present or unknown. Survival was significantly shorter in those who were leukemic at presentation (Fig 5B).
Staging BM trephine biopsies were performed in 75 patients. In 47, there was clear histological evidence of involvement by MCL, the patterns of which are summarized in Table 4. In 3 cases, the core biopsy specimen was histologically nondiagnostic; however, in each of these 3, flow cytometric immunophenotyping showed a clonal B-cell population with CD5 coexpression. In 2 cases, the core biopsy specimen was suspicious but not diagnostic for involvement by MCL, and, in 23, no evidence of MCL was observed. Biopsies were not performed in 5 cases for various reasons including advanced comorbid neurological disease (n = 2), the presence of circulating lymphoma cells (n = 1), and undefined (n = 2).
In all histologically positive BM biopsy specimens, the lymphomatous infiltration was found predominantly in an interstitial or intertrabecular location, arranged in either nodular aggregates or diffuse infiltrates, or a combination of both. A few cases showed a prominent paratrabecular pattern reminiscent of small cleaved-cell lymphoma. In all cases, the cellular morphology was virtually identical to that of MCL observed in lymph nodes, lacking large transformed cells and proliferation centers. In 1 case, the cytomorphology was indistinguishable from acute lymphoblastic leukemia. Prognostic significance was determined by comparing those cases (n = 50) that were positive for involvement with the remainder of cases (n = 30), in which BM involvement was not evident (n = 25) or was unknown (n = 5). No significant difference in survival was found (data not shown). Outcome was also assessed based on the degree of staging BM involvement, estimated on the core biopsy specimen as less than or greater than 50% (Table 4). Those with heavy involvement by MCL (n = 12) tended to have a shorter OS than did those with partial involvement (n = 35), although the results were of borderline significance (median OS, 26 v 45 months; P = .06; data not shown).
Thirty-seven patients underwent additional biopsies during the course of their illness. The material examined included BM (n = 9), extranodal tissue (n = 9), lymph node (n = 5), spleen (n = 4), fine-needle aspirate of an involved site (n = 7), and PB (n = 3). A median period of 22 months (range, 1 to 70 months) separated the procurement of these specimens from the time of the diagnostic biopsy. In 29 of these cases (78%), the cytology and/or architecture were unchanged from the time of diagnosis (median interval from original biopsy, 15 months; range, 1 to 67 months). In the remaining 8 (22%), increased numbers of larger, lymphoblast-like cells were observed, indicating cytologic transformation (median interval from original biopsy, 34 months; range, 14 to 70 months). Of these 8, the 5 open lymph node biopsy specimens showed more mitotic activity and blastic cells than were observed in the original biopsy specimens, but none were frankly blastic. In another 2 cases, increased numbers of blastic cells were present in the PB. In the eighth case, transformation was diagnosed on a lymph node fine-needle aspirate. Large noncleaved cells were not observed in any of this material. Nodal architecture remained diffuse in 4 cases, nodular in 1 case, and changed from nodular to diffuse in 1 case. All 8 patients in which cytologic change was found died within 12 months (median, 9 months), whereas only 16 of 29 patients without cytologic change have died (median follow-up period for all 29 patients, 8 months; range, 0 to 67 months). No significant difference in OS between the two groups was found.
Immunophenotyping by flow cytometry was performed in 49 cases (19 from lymph node tissue, 26 from BM or PB, and 4 from extranodal or unspecified sites). In 5 cases, the results were not diagnostic of lymphoma. Results of the 44 positive cases are shown in Table 5. The characteristic immunophenotype of the MCL cases analyzed was CD19+, CD20+, CD5+, and FMC-7+ and CD10− and CD23−, with a slight preponderance of λ surface Ig (SIg) positivity. SIg brightness was documented in only one quarter of the cases, and, in all of these, SIg was moderate to bright. Three cases showed an aberrant immunophenotype. One coexpressed both CD5 and CD10, and another lacked CD5 expression, while the third weakly coexpressed CD23. All 3 had other data to substantiate the diagnosis of MCL. CD11c expression, although not shown in Table 5, was consistently negative in all cases analyzed.
Cytogenetic analysis was performed in 31 cases. Results are summarized in Table 6. The translocation t(11; 14) (q13; q32), characteristic of MCL, was the most frequently occurring abnormality in this group. The next most common groups of abnormalities involved chromosomes 9 and 17. Monosomy 9 was observed in 2 cases; whereas, in 3 cases, structural abnormalities of 9q were found, ie, an inversion, a deletion, and a balanced translocation with 14q32. In 2 cases, 17p11 was disrupted because of balanced translocations with chromosomes 3 and 15, respectively; whereas, in another 2 cases, monosomy 17 was found. The cases with abnormal clones not obviously including t(11; 14) may have had complex or cryptic alterations involving the bcl-1 and Ig heavy-chain loci. No significant differences were found between the 14 cases with t(11; 14) and the 4 cases in which analysis was successful but failed to show a t(11; 14). Similarly, no differences in survival could be shown between the groups of patients with chromosome 9 and 17 abnormalities and the remainder of MCL cases. However, the number of cases was too small to make a meaningful statistical comparison.
SA for bcl-1 gene rearrangement was performed in 20 cases. Table 7 summarizes these results and compares them with the cytogenetic results. No significant differences in survival could be shown between the 11 cases with and 9 cases without SA evidence of bcl-1 rearrangement.
The pathology of MCL is well defined, but the criteria for and clinical relevance of histological subclassification remain controversial. Some regard MCL with an MZ architecture as "low grade," whereas others find that survival in these cases is similar to that of cases with a diffuse growth pattern.2 In addition, some studies have suggested that factors such as mitotic activity and increased numbers of blast-like cells signal a worse outcome. Resolution of these issues has been slow because of the small numbers of cases available for study and the lack of consensus diagnostic criteria. This analysis of 80 cases of MCL, the largest series to date, was undertaken with the intent to help resolve some of these questions.
In this study, all 80 cases had clinical features and survival characteristics fully compatible with those described for MCL, as summarized in Table 1 and shown in Fig 1. Of the IPI clinical prognostic variables,24 prognosis was significantly influenced by PS but was not significantly influenced by age, stage, LDH level, and extranodal involvement, although a trend toward a worse outcome was observed for the latter four factors. The IPI score also did not significantly predict for patient outcome. Although the numbers of patients, particularly those with limited-stage disease, may not have been large enough to permit detection of a survival difference using the IPI prognostic variables, it is more likely that simply having the diagnosis of MCL, with its inherently poor outcome, supersedes any prediction of behavior based on clinical factors. Definitive statements of effectiveness of certain treatment protocols were not possible in this study because no treatment group did well. Even the more intense BP-VACOP/IRRT regimen did not produce a survival advantage despite being administered only to patients under the age of 60.
All 80 cases met the accepted histological criteria for MCL.1 Particularly useful features distinguishing MCL from other diffuse small-cell ML include the monotonous lymphoid infiltrate, absence of growth centers, scattered epithelioid histiocytes, perivascular hyaline sclerosis, and virtual absence of large transformed cells. Although mitotic figures were conspicuous in most cases, it is important to note that, in 22 cases, the MS was low (≤5). Also, it is apparent from examination of sequential biopsy specimens that the pattern of transformation of MCL can be best described as a progressive increase in cells with slightly larger nuclei and finer chromatin, but a lack of nucleoli in tissue sections. This cytologic transformation is often accompanied by an increase in mitotic rate.
The prognostic significance of three histological features, architecture, mitotic activity, and relative number of lymphoblast-like cells is summarized above; however, several points need to be addressed. First, this study failed to show any significant differences in OS between the MZ, nodular, and diffuse subtypes. These results are similar to the findings of Norton et al6 but contrast those of Duggan et al,14 who found MCL with an MZ architecture to be indolent. Although the appearance of an MZ pattern is well described in the literature, the criteria for a true MZ pattern are undefined and are subject to interobserver variability. When compared with other MCL series, the proportion of MZ cases observed here (6%) is similar to that observed by Norton et al6 (6%) and Pittaluga et al15 (11%) but is significantly lower than that reported by Lardelli et al5 (55%) and Weisenburger et al25 (30%), two studies in which there were demonstrable differences in survival between MZ and other architectural subtypes. The reasons for this are unclear but are likely to be caused by differences in criteria for defining an MZ pattern, rather than true geographic differences in frequency. Because the criteria for defining an MZ pattern in this study may have been more strict than those in other series, we also pooled the nodular and MZ cases together and compared them with the diffuse cases. However, once again, no difference in OS was found.
A diagnosis of blastic MCL, defined in this study and by others5 as MCL with the appearance of lymphoblastic lymphoma, assigns the patient a very unfavorable prognosis. This histological pattern should be relatively reproducible; however, it is unclear what number of blastic cells is needed to make the diagnosis. The fact that others refer to similar cases as "blastoid,"6 "large-cell,"26 or "anaplastic"27 variants attests to the current lack of standardized diagnostic criteria. Attempts have been made by others to count large cells manually14 28 or by image analysis26; however, the cytomorphology of MCL cell is a spectrum, making it a difficult task when applied in a routine clinical setting, excepting those cases with florid blastic change as described herein. More objective methods of assessing the proliferation rate, including mitotic counts and Ki67 nuclear antigenic expression, have also been applied to MCL and appear to be closely linked with blastic morphology, as would be expected. It has been shown by the results of this study and by those of others, that increased mitotic activity predicts for a worse outcome, although the exact number of mitoses at which prognosis was found to be different varies from study to study (10 of 10 hpf,14 20 of 30 hpf,8 and 20 of 10 hpf11 ). Although not evident from examination of the results of these studies, this variability may be the result of differences in patient populations, but is more likely to be caused by the inherent interobserver variability of counting mitotic figures. Regardless, the data indicate that prognosis is closely linked to the mitotic count in MCL, which is similar to that observed in other lymphomas of aggressive histology,29 and mitotic activity and blastic morphology are unlikely to be independent variables, although this postulate can only be tested with multivariate analysis.
Cytologic evidence of blastic change in sequential biopsy specimens was found in 8 patients (11% of the total nonblastic cases), all 8 of whom died within 12 months. However, the OS of these patients was no different from those without transformation and may reflect a lead-time bias: the patients with transformation were serially biopsied later in their course (median, 34 months from original biopsy) than were those without transformation (median, 15 months). Unfortunately, the exact incidence of blastic change in this patient population is not known because autopsy follow-up results were unavailable, but the results of Norton et al6 suggest that it occurs at a higher frequency (28%) than is currently recognized.
The high incidence of PB and BM involvement by MCL at diagnosis observed in 34% and 63% of cases, respectively, is in keeping with that found by others.6 11 15 PB involvement at diagnosis predicted for a shortened survival in our study; however, interestingly, the presence or absence of BM involvement did not. Although heavy BM infiltration was associated with a trend toward shorter survival, no correlation of this feature with PB involvement could be shown. The predictive power of PB involvement may be the result of a bias toward increased numbers of cases with MS of greater than 20 in the leukemic group versus that in the nonleukemic group (41% v 17%; P = .03); in contrast, cases with MS of greater than 20 were evenly distributed throughout both positive and negative BM cases (data not shown). Multivariate analysis would be necessary to confirm PB involvement as an independent variable; however, these data imply that, in some cases, leukemic involvement may reflect increased biological aggressiveness rather than only overall tumor burden.
No morphologic or clinical differences could be attributed to the presence or absence of the t(11; 14)(q13; q32) or bcl-1 gene rearrangement. Addtionally, no outcome or histological differences were observed for those cases with chromosome 9 or 17 abnormalities, but the number of affected cases was too small to allow for a meaningful statistical comparison. Most reports have identified t(11; 14) and bcl-1 gene rearrangements as highly specific for MCL32-34; however, these abnormalities have also been rarely described in SLL and plasma cell dyscrasias. In a recent report in which the presence of a t(11; 14) or bcl-1 rearrangement was associated with ML with morphologic findings atypical for MCL, the clinical course of these patients was similar to that of MCL.35 Similarly, we have recently observed a case of ML with a t(11; 14) and a bcl-1 rearrangement that had classical proliferation centers in which the clinical course was more akin to MCL than to SLL. We were unable to show a survival difference in this study for cases with or without a t(11; 14) or a bcl-1 rearrangement. It is unlikely that the presence of these cytogenetic and/or molecular genetic findings will be prognostically important, because the recent development of sophisticated fluorescence in situ hybridization techniques has shown that virtually all cases of MCL possess these abnormalities.36 37 We did not stain these cases for cyclin D1 protein, but virtually all cases of MCL overexpress this protein,3 38-42 making it a useful diagnostic reagent but an unlikely prognostic marker. Perhaps, the interaction of cyclin D1 with other cellular proteins (retinoblastoma gene, p16, p21, ubiquitin, and so on) contributes to lymphoma development, and measurement of one or more of these proteins may prove to be independent prognostic factors in MCL.
In summary, this study confirms the aggressive nature of MCL and provides evidence that MS, blastic morphology, and leukemic involvement at diagnosis predict for poor outcome. Standard clinical indicators of prognosis such as age, stage, number of extranodal sites, or presence of B symptoms had little discernable impact because the overall prognosis was so poor. Such factors are unlikely to be predictive until more effective treatments become available. We have also shown that, although architecture does not have prognostic importance, there is a need to develop standardized histological criteria for both "MZ" and "blastic" morphologies. Resolution of these problems together with large collaborative studies are crucial to provide further insight into the effective treatment and possible cure of this disease.
The authors thank Drs S. O'Reilly, P. Hoskins, and T. Shenkier for their help in providing clinical data for this study; Drs C. Coppin and A. Coldman for their assistance with statistical analysis; and Ms C. Wong for her help with data collection.
Address reprint requests to Randy D. Gascoyne, MD, Department of Pathology, British Columbia Cancer Agency, 600 W 10th Ave, Vancouver, British Columbia, V5Z 4E6, Canada.
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. Rearrangement of CCND1(BCL1/PRAD1 ) 3′ untranslated region in mantle-cell lymphomas and t(11q13)-associated leukemias. Blood 1994;83:3689.
. Cyclin D1 expression in non-Hodgkin's lymphomas. Detection by immunohistochemistry. Am J Clin Pathol 1995;103:756.
. Cyclin D1 protein analysis in the diagnosis of mantle cell lymphoma. Blood 1995;86:2715.
. Clinicopathologic study of PRAD1/ cyclin D1 overexpressing lymphoma with special reference to mantle cell lymphoma. Am J Surg Pathol 1996;20:1110.
Argatoff, L. H., Connors, J. M., Klasa, R. J., Horsman, D. E., & Gascoyne, R. D. (1997). Mantle Cell Lymphoma: A Clinicopathologic Study of 80 Cases. Blood, 89(6), 2067-2078. Accessed April 24, 2019. Retrieved from http://www.bloodjournal.org/content/89/6/2067.


text:
Barthélémy Toguo — Strange Fruit — Lelong & Co Gallery — Exhibition — Slash Paris
Barthélémy Toguo — Strange Fruit
Barthélémy Toguo, vue de l'exposition © Galerie Lelong & Co.
Barthélémy Toguo
Past: October 12 → November 25, 2017
Six months after his nomination for the Marcel Duchamp prize and his installation entitled Vaincre le virus, Barthélémy Toguo is presenting a series of works produced over the summer. The title of the exhibition, Strange Fruit is, of course, an evocation of the famous song by Billie Holiday:
Southern trees bear strange fruit Blood on the leaves and blood on the root Black bodies swinging in the southern breeze Strange fruit hanging from poplar trees
As the song unfolds, the Strange Fruit is revealed to be people hanging from tree branches, the bodies of blacks lynched in the segregationist states of the southern United States. Now, in the early years of the 21st Century, Barthélémy Toguo is using his rich and perceptive universe to denounce the rise in racist violence around the world. Bronze crows, perched on branches from whence his drawings hang, and dogs with sharp teeth await the visitor. At the heart of the installation, a bust of Ida B. Wells (1862-1931) will serve as a reminder of the difficult struggle against segregation and lynching led by this Afro-American journalist, little known in Europe, and whose book, Southern Horrors, was only translated into French and published in Geneva in 2016.
© Galerie Lelong & Co.
Lelong & Co Gallery Gallery Details
08 Paris 8 Zoom in 08 Paris 8 Zoom out
13, rue de Téhéran – Second espace au 38, avenue Matignon
T. 01 45 63 13 19 — F. 01 42 89 34 33
www.galerie-lelong.com
Miromesnil
Tuesday – Friday, 10:30 AM – 6 PM
Saturday, 2 PM – 6:30 PM
Venue schedule
David Hockney — Ma Normandie Ends in about 1 month
Simone Fattal — au bord du Barada Ends in about 1 month
Barthélémy Toguo Cameroonian artist born in 1967 in Cameroon.


text:
The GCDb
About the GCDB
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From The Grindhouse Cinema Database
Revision as of 11:33, 24 June 2019 by Pete (talk | contribs)
Press Kit • @ SWDB • @ IMDB
Ivan Rassimov (May 7, 1938 – March 14, 2003) was an Italian film actor (of Croatian descent) who appeared in many horror and exploitation films. Rassimov was known for his unique screen presence and menacing persona which led him to often play villains and heavies. Some of his notable films include: Planet of The Vampires (1965), Don't Wait Django...Shoot! (1968), The Strange Vice of Mrs Wardh (1971), Man From Deep River (1972) and Eaten Alive (1980).
Pages in category "Ivan Rassimov"
Atlantis Interceptors
Beyond The Door II
Colt 38 Special Squad
Doomed To Die
The Eerie Midnight Horror Show
Emanuelle Around The World
Emanuelle In Bangkok
Emanuelle in the Country
Mafia Junction
Man From Deep River
The Odd Squad
Overrun!
Planet of The Vampires
The Seven Red Berets
Spasmo
The Strange Vice of Mrs Wardh
The Tough Ones
A White Dress for Marialé
Retrieved from "https://www.grindhousedatabase.com/index.php?title=Category:Ivan_Rassimov&oldid=153421"
© 2007-2019 THE GRINDHOUSE CINEMA DATABASE. Read about Copyright [DMCA/UrhR] on the GCDb.


The timeline was extremely tight. Mother Nature was not helping and neither was the traffic. But, perseverance paid off for the Copperas Cove Five Hills royalty which captured not one but two first place awards in Christmas parades on Saturday.
Having just wrapped up the Krist Kindl Charity Pageant, the titleholders rushed to the Copperas Cove Christmas Parade, scurrying to get the city float looking a lot like Christmas in less than an hour before the judges came to view the entry.
With winds gusting up to 30 miles per hour, the royalty struggled to get their float uncovered and hold onto the three layers that protect the tourism equipment. With the help of Fort Hood soldiers also in the parade, the group added the final touches just as the judges arrived to score the entry. Ultimately, the City of Copperas Cove float, complete with a lighted Christmas tree, giant light-up ornaments, and the royalty all dressed in formal wear in holiday colors, captured the First Place Float Award.
When the parade ended, the titleholders rushed to pack up the float, heading to Lampasas for its lighted Christmas parade. The float rolled into Lampasas at 4:50 p.m. with judging beginning at 5:30 p.m. Parade officials agreed to judge the entry last.
With the parade theme of Barnyard Christmas, the float was completely transformed with bales of hay, wagon wheels, a giant lighted cowboy boot, and lighted fencing around the top of the float. The titleholders had also transformed from formal wear to western wear complete with boots, belts and cowboy hats.
After receiving third place in the parade last year, the royalty hoped to do at least as well this year. The float did indeed capture first place honors which included a $300 cash prize.
The royalty represent the City in both the Gatesville and Killeen parades on Saturday, wrapping up more than a half dozen parades this holiday season.


Growing up in a literary household I felt obligated to follow in my parent's footsteps. I began reading to myself as soon as I learned how to properly turn a page. Despite the paper cuts and the sometimes confusing words I fell in love with it. Would lose myself in stories about heroic mice fighting to save their abbey from the evil ferrets plotting to take it over. While knew that these books lacked the depth of meaning that my parents were used to, it felt good to share my thoughts on what was currently reading at the dinner table.
My love for reading only grew as I progressed into middle school. Signed up for a club called Battle of the Books and dove into the competitive side of reading. We would be tested on both our comprehension and memorization of the books that were assigned to us. I would use reading as an escape. I found myself living vicariously through the protagonists of the many novels that read; loving what they loved, fighting against the same evils they fought against, and feeling the same loss that they felt. Somewhere around eighth grade I decided to focus more on my social life and redefine my image.
This meant dropping all activities that didn't fit into y new vision I had for myself. Unfortunately, this included reading. Replaced my love for books with a love of sports and social recognition, choosing to demean and humiliate those who reminded me of my past self. I would neglect the required readings in class and rely on spark notes to get me through school. This pattern persisted throughout high school and into my freshman year of college. My drop in reading inversely paralleled a rise in my anxiety and depression. Would find myself hyper focusing on how everyone else perceived me.
This caused me to isolate and avoid all social interaction. Because I was terrified of the very thing that had learned to thrive on I started to give up on myself. I did not know what to do with myself most days and started losing who was. It was not until my friend gave me her copy of George OR Martin's Game of Thrones that was able to break away from this vicious cycle. Once again I was engrossed in a mythical world that had nothing to do with my own. Was able to relate to people again and slowly broke out of my shell. Since then I have been able to use reading as a tool to manage my anxiety.
Being able to roger about the stress that everyday life presents me with has been the most effective coping mechanism for me so far. Because of this I find that I am partial to fantasy novels because they least resemble the world around me. I tell you this not to gain your sympathy or even understanding but to illustrate the profound impact that reading can have on a person. Books have shaped my life and I doubt that I would be the same person that am today if didn't have the love for novels that I do. Reading has helped me in so many ways and the only way that can think of to repay the favor is to continue to nurture my love for it.


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https://www.sfgate.com/world/article/Philippines-leader-calls-for-calm-over-sinking-14006523.php
Philippines leader calls for calm over sinking
Published 1:19 pm PDT, Monday, June 17, 2019
MANILA — The Philippine president on Monday called the sinking of a Filipino fishing boat that was hit by a Chinese vessel in the disputed South China Sea "a little maritime accident" and urged calm amid an outcry. Twenty-two crewmen aboard the sunken boat were rescued by a Vietnamese fishing boat.
President Rodrigo Duterte said the June 9 incident at Reed Bank should not be blown out of proportion and should be investigated, and that China's side should be heard.
Duterte's reaction contrasted with that of some of his own officials, including the defense chief, who strongly condemned the Chinese vessel for sailing away as the fishing boat sank at night. The Department of Foreign Affairs filed a diplomatic protest against China.
Duterte came under fire from nationalists and opposition politicians for his silence days after the incident was made public by Defense Secretary Delfin Lorenzana. One opposition senator called on the president to downgrade diplomatic ties with China, which has been criticized for aggressive actions in the disputed waters.
"It's just a collision of ships. Do not make it worse," Duterte said in his first public remarks about the incident, adding he would not reach any conclusion or take any action until an investigation is complete.
Normally known for his temper and spontaneous outbursts, Duterte this time underscored the importance of handling the incident by the rule of law. He said politicians who urged him to deploy the navy in response to the incident were "stupid."
China has acknowledged its fishing vessel hit a Filipino boat in the vicinity of Reed Bank but denied the collision was intentional.


Debunking store bought HS 3 going bad after a short time.
This actually began last Summer...so to speak... alumilite.freeforums.net/thread/475/25-scale-dry-sump-mold in late August,I had said "Full disclosure.....except for aprox. 10g for the 2nd half of the Lego box mold which was the last of the HS-2 that I had purchased direct from Alumilite, the rest is HS-3 purchased from a local Hobby Lobby.....I plan on doing a post dispelling any negative consequences about purchasing from a big box store vs. purchasing from Alumilite direct where HS-3 is concerned ...stay tuned."
Printed off the 40% discount coupon before heading out...saved $12.00 I purposely pulled the box from the back of the rack...there where only 2, looks like that is/was all they would have on the floor at any given time. I pulled the back one thinking that if the front one had been sold, an associate would have simply restocked the shelf by placing a box of HS 3 in the open part up front verses rotating stock.
1) Left the lids off for extended periods of time....introducing air and perhaps moisture during the Summer to the product.
2) Variances in temperatures....even though I have kept it in the hobby room, there has been temperature changes from Summer, to Fall to Winter...exposer to direct Sunlight, storage in a dark,cool area, back to direct sunlight for weeks, back to a dark, cool area for weeks more.
I am going to assume that everyone who has purchased the HS 3 has read the back side of the box where the directions are located and noticed where it states "Best if used within 6 months of purchase" ...so technically I still have aprox. 2 months to go where its "best" performance will/would occur. I have been kicking around the idea of making another purchase of HS-3 , doing the same things described above (lids off, variances in room temperatures) as well as an extreme temperature fluctuation from Winter to Summer by storing it in my non heated, non air conditioned garage ( below freezing to near triple digits in the Summer) and doing a pour 9 months to a year after purchase just to see what will happen.
As previously mentioned, I'll be using the deliberately abused HS 3 that I purchased back in August of 2018 for this pour.
This is also going to W.I.P utilizing a multiple small piece gang mold. In this case , these are 1/25th scale dry sump oil system parts and pieces. I figure small pieces with fine detail will really put the HS 3 to the test.
Dug out the LEGOs and built a mold box. The box is aprox. 1/4" larger than the area comprised of the pieces to be molded.
A LEGO is just over a 1/4" tall. I use this as a gauge for pouring and modeling clay thickness....knowing the height of the block lets me know aprox. how thick the pour is or the depth of the modeling clay for a multi part mold.
Using the X-Acto knife handle , I rolled the modeling clay out till it was aprox. 1/4" thick using the LEGO block as my gauge. I then pressed the assembled LEGO blocks down onto the modeling clay , leaving an impression in the clay.
Using a knife, trim away the excess modeling clay....everything from the inner portion of the blocks imprint outward is excess. Once that is done, the clay block should fit inside the assembled LEGO block portion.
I've placed the parts into the modeling clay as this is going to be a 2 part mold. The oil sump "pan" has been filled with modeling clay so that not as much RTV silicone will used on something that's not going to be visible when the engine is assembled.
I chunked up some of my no longer used molds for filler....like I have stated several times in the past,Silicone bonds to itself quite well.
Mixed up the HS 3 ...I am going to make a some suggestions to Alumilite.
On the HS 3 instructions, there are a couple of areas that I see that could stand a change.
My suggestion Brushing the silicone rubber on the item(s) to be molded will reduce the chances of air bubbles being trapped between the item(s) being molded and the silicone rubber.
. Always shake the catalyst bottle before using.
My suggestion Always shake the catalyst bottle for approximately 1 minute before using.
Back to the project....since the work time is aprox. 45 minutes, I took the time to carefully brush on the silicone rubber to the pieces before the pour. I have found , in the past, that this greatly reduces the chances of air bubbles being trapped on the piece that I am making a mold of and since RTV silicone bonds to itself quite well, no issues.
Poured into the left side allowing the silicone to flow over the pieces. The rising air bubbles don't worry me much since I brushed silicone on the pieces prior to the pour. The corner blocks that stick out will be the alignment lugs for the 2 part mold.
I poured this around 2 O'clock this afternoon, it's now 5:15 p.m The mold is curing quite well at this writing...I see absolutely no reason why I wont be able to pour the second part tomorrow after work.
The fallowing day aprox. 6:15 a.m I checked the mold. It was firm enough to pour the 2nd part. Had I had enough time that day, I am positive that I could have been pouring resin that evening....that's 2 separate pours of at least 6-7 month old HS-3 that had NOT been stored properly(variations in room temperatures, lids left off for extended periods of time) fully cured and ready to pour resin aprox. 24 hours after the first RTV Silicone was poured for the first part of a 2 part mold.
Second pour of this 2 part mold. Alignment lugs in all four corners. Used petroleum jelly for rubber to rubber mold release. I used my finger for the larger spaces and a small, cheap paint brush, like you would used on a model kit, to brush the petroleum jelly near the pieces to be cast or to remove excess petroleum jelly that got on the pieces by accident. Resealed the LEGO mold box to the window pane to prevent seepage with modeling clay.
I am going to cut the vents and pour gates after the second part is cured.
I poured the 2nd part early yesterday afternoon.....by 10 p.m the RTV Silicone had cured enough that if I had wanted to, I could have poured resin.
Took a sharpie pen and marked where I want to cut the pour gates and vents. I tried to capture all of the detail with a picture, but it just doesn't come thru. The HS-3 was able to pick up all of the fine detail on the parts....the cooling fins on the sump pan, the cooling fin details on the oil cooler, the cogs on the pump drive belt and the fittings on the oil tank.
I did everything that I could think of to deliberately make the HS-3 not to perform as advertised.....I didn't go to extremes, but rather did things that plausibly could happen after initial purchase but before actual use. I fallowed the instructions that come with the HS-3.....even though they are through, they do lack the actual time durations that I have come to discover make the difference between a good Silicone pour verses a pour that has issues. Hopefully the next version of the instructions will include the reference to the time durations needed for a successful pour.
The detail that the RTV Silicone was able to pick up was outstanding . I attribute this to brushing the Silicone on the pieces to be molded prior to the pours verses just pouring....this is something else that should be included in the instructions as I had no evidence of air bubbles being trapped against the pieces to be molded while there was many air bubbles/pockets that where present moments after the pour was completed.
There still could be issues encountered if mixing by volume, particularly if its a smaller mold and either the Silicone or Catalyst amount is off due to not being mixed correctly where as I used a Gram scale to help insure a proper mix ratio. More attention and caution is needed when mixing by volume , where as by weight is more accurate in my honest opinion.
If the instructions are fallowed accordingly and the advise that has been given in this forum used, there is no reason why any HS-3 that is purchased from a retail store would have any issues as in a bad batch....not saying that it could never happen, but I am lead to believe that it was the user and not so much the product that was at fault in past complaints leveled against Alumilite.


First Solo Tour and Furniture Research!
On Tuesday I gave my first solo A World Made Small tour! The tour was centered around an exhibit showcasing the museum's dollhouse collection, as well as other miniature play sets from colonial times through the 20th century. I think the tour went fairly well–the only issue was that I went a little too quickly. Next time, I plan on slowing down my information and adding a sentence or two about each of the pieces that I discuss. I also tag-teamed the Dog's Life tour yesterday with my co-supervisor, Christina, and I think that one went well too! We had a lot of fun splitting up the different objects since she is also new to that tour and the information that it presents about dogs and other pets during colonial times. Did you know that Colonial Williamsburg had a law preventing homeowners from having more than two dogs, neither one of which could be female? Well, now you do.
This afternoon my schedule was pretty open, so I was able to walk over to Bruton heights and did some hands-on research in the file room regarding a potential new tour/family guide idea: Hidden Compartments in Colonial Furniture! I thought of the idea on Tuesday during one of our programs, and both Trish and Christina are supportive of my researching a variety of pieces in the collection that all had some sort of secret drawers/compartments. I want to present information about how the compartments worked, what types of furniture had these compartments, as well as what kinds of valuables were stored in them. So far, I've learned a decent amount, including that colonial Americans were obsessed with secret drawers and even had different keys/locks for every regular drawer, and I'm sure that the information will just keep coming. I am also now capable of turning on the moveable drawers in the file room. A true accomplishment in the eyes of many.


text:
Biografia

Nato a Mount Vernon, New York, Kagan ha conseguito il B.A. dalla Harvard University nel 1967. Ha continuato a frequentare il neo-costituito Graduate Institute of Film & Television della New York University ed era in prima classe al Conservatorio AFI.

Carriera cinematografica e televisiva

I crediti cinematografici di Kagan includono il successo al botteghino Heroes (1977), The Big Fix (1978), una commedia thriller politica con Richard Dreyfuss; Gli eletti (1981), dal libro omonimo di Chaim Potok; Il viaggio di Natty Gann (1985); la commedia underground Ragazze, il mostro è innamorato (1989); il film cult della scherma By The Sword (1991); e il film Golda's Balcony (2006), tratto dall'omonima commedia.

È stato anche un prolifico regista televisivo, iniziando già nel 1972 all'età di 26 anni, dirigendo "The Most Crucial Game", episodio della seconda stagione de Colombo. Nel 1996, Kagan ha vinto un Primetime Emmy Award per la miglior regia di una serie drammatica per l'episodio "Leave of Absence" di Chicago Hope. Altri crediti includono il film televisivo Katherine: The Making of an American Revolutionary, che ha anche scritto, e Conspiracy: The Trial of the Chicago 8 per il quale ha vinto il CableACE Award per il miglior speciale drammatico. Kagan ha anche diretto Roswell: The UFO Conspiracy che ha ottenuto una nomination ai Golden Globe.

Altri film per la televisione includono The Ballad of Lucy Whipple, Courage con Sophia Loren, Scott Joplin, Descending Angel per HBO e per Showtime Color of Justice, Bobbie's Girl, e Crown Heights, sui disordini del 1991 che hanno vinto il Premio Humanitas nel 2004. Questo film ha anche ricevuto un NAACP Image Award e la nomination alla Directors Guild come miglior film per famiglie. Kagan ha anche diretto un episodio del film Taken di Steven Spielberg, vincitore di un Emmy. Ha lavorato a diverse altre serie televisive tra cui The West Wing, The Guardian, Resurrection Blvd., Picket Fences, Boomtown.

Kagan ha prodotto e diretto la serie in dieci parti The ACLU Freedom Files, nel 2006 e nel 2007 che ha ricevuto numerosi premi ed è stata trasmessa su Link TV, Court TV e PBS. Kagan ha recentemente realizzato una serie di brevi documentari e film di advocacy per le ONG, tra cui The Doe Fund, che lavora con i senzatetto e gli ex carcerati, e The Democracy School, un movimento che sviluppa la governance locale, e Bioneers, che promuove i risultati nella giustizia ambientale e sociale.

Altre attività

Kagan è professore di ruolo presso la University of Southern California, dove tiene corsi di laurea in regia.

È stato direttore artistico del Sundance Institute di Robert Redford ed è membro del consiglio nazionale della Directors Guild of America e presidente del comitato per i progetti speciali che fornisce programmi culturali ed educativi per i 14.000 membri. Nel 2004 è stato insignito del Robert Aldrich Award per "servizio straordinario all'associazione".

Nella sua veste di membro della Directors Guild of America, Kagan modera anche la tavola rotonda annuale del gruppo con i cinque candidati di quell'anno per la miglior regia – lungometraggio.

Kagan è anche l'autore del libro Directors Close Up (2006).

Vita privata
Kagan vive a Venice, in California, con la sua compagna Anneke Campbell, scrittrice. Sua figlia Eve si è laureata alla Harvard Ed School ed è ora attrice, scrittrice e insegnante di yoga.

Filmografia

Regista

Cinema

 The Love Song of Charles Farberman (1972)
 Scott Joplin (1977)
 Heroes (1977)
 Moses Wine detective (The Big Fix) (1978)
 Gli eletti (The Chosen) (1981)
 La stangata II (The Sting II) (1983)
 Il viaggio di Natty Gann (The Journey of Natty Gann) (1985)
 Ragazze, il mostro è innamorato (Big Man on Campus) (1989)
 Sfida d'onore (By the Sword) (1991)
 Golda's Balcony (2007)
 Shot (2017)

Televisione

 Un vero sceriffo (Nichols) – serie TV, episodio 1x23 (1972)
 I nuovi medici (The Bold Ones: The New Doctors) – serie TV, episodio 4x07 (1972)
 Colombo (Columbo) – serie TV, episodio 2x03 (1972)
 ABC Afterschool Specials – serie TV, episodio 2x02 (1973)
 Unwed Father – film TV (1974)
 Il monastero della morte (Judge Dee and the Monastery Murders) – film TV (1974)
 Katherine – film TV (1975)
 Scott Joplin – film TV (1977)
 Nel regno delle fiabe (Faerie Tale Theatre) – serie TV, episodio 2x03 (1983)
 Madre coraggio (Courage) – film TV (1986)
 Conspiracy: The Trial of the Chicago 8 – documentario TV (1987)
 Discesa pericolosa (Descending Angel) – film TV (1990)
 La signora del West (Dr. Quinn, Medicine Woman) – serie TV, 1 episodio (1993)
 Roswell – film TV (1994)
 La famiglia Brock (Picket Fences) – serie TV, episodi 1x03-1x15-4x06 (1992-1995)
 Chicago Hope – serie TV, episodi 1x02-2x08 (1994-1995)
 Color of Justice – film TV (1997)
 The Hired Heart – film TV (1997)
 Ally McBeal – serie TV, episodio 1x16 (1998)
 Resurrection Blvd. – serie TV, episodi 1x04-1x08-1x16 (2000)
 The Ballad of Lucy Whipple – film TV (2001)
 In tribunale con Lynn (Family Law) – serie TV, episodio 2x15 (2001)
 West Wing - Tutti gli uomini del Presidente (The West Wing) – serie TV, episodi 2x06-3x18 (2000-2002)
 Bobbie's Girl – film TV (2002)
 Boomtown – serie TV, episodio 1x08 (2002)
 Taken – miniserie TV, episodio 1x07 (2002)
 The Guardian – serie TV, episodio 1x08-1x12-2x19 (2001-2003)
 Karen Sisco – serie TV, episodio 1x02 (2003)
 The Handler – serie TV, episodio 1x07-1x09 (2003)
 Crown Heights – film TV (2004)
 Blind Justice – serie TV, episodio 1x05 (2005)

Premi e riconoscimenti
Primetime Emmy Awards
1996 - Migliore regia di una serie drammatica - Chicago Hope, episodio Leave of Absence

Note

Collegamenti esterni

Ebrei statunitensi
Primetime Emmy alla miglior regia per una serie drammatica
Professori della University of Southern California
Registi cinematografici statunitensi
Registi televisivi statunitensi
Studenti dell'Università di Harvard
Studenti dell'Università di New York

redpajama_set_name: RedPajamaWikipedia


Logan Green (co-founder and CEO, Lyft), Dan Amman (President, General Motors), and John Zimmer (co-founder and President, Lyft).
Uber might finally have some competition. Today, General Motors and Lyft announced that they are partnering to develop a network of self-driving cars.
As part of the announcement, San Francisco-based ridesharing company Lyft announced a $1 billion series F funding round, led by $500 million from Detroit-based General Motors, valuing the Uber competitor at $5.5 billion.
"We see the future of personal mobility as connected, seamless and autonomous," says GM President Dan Ammann, in a written statement.
The news comes on the heels of rumors that Google and Ford will be announcing a partnership to create a fleet of autonomous vehicles.
Also part of the partnership, Lyft and General Motors will work together to develop a network of hubs around the U.S. where people can rent cars, according to the joint statement. The goal is to make it possible for drivers to share rides without having to own a car.
"Together we will build a better future by redefining traditional car ownership," says John Zimmer, president and co-founder of Lyft.
Indeed, self-driving cars are expected to be increasingly common over the next decade. By 2025, there will be upwards of 20 million autonomous vehicles on the road, according to a recent report from Juniper Research. Currently, Google has a a few dozen self-driving cars roaming the streets of Mountain View, Calif., and Austin, Texas.


text:
'Howard The Duck' remake is horse feathers, James Gunn says
The rumor that the "Guardians of the Galaxy" director will re-create the cult classic for Marvel isn't all it's quacked up to be.
June 29, 2017 8:03 AM PDT
Howard the Duck had a cameo in the "Guardians of the Galaxy" end credits.
Video screenshot by Bonnie Burton/CNET
Hollywood seems to be clamoring to remake, reboot or reimagine every single '80s movie, except for the one movie everyone loves to hate: "Howard the Duck."
The 1986 Lucasfilm-produced comedy starred Chip Zien, Lea Thompson, Jeffrey Jones and Tim Robbins and told the story of an alien duck who gets transported to Earth, where he falls in love with a woman who plays in a band called Cherry Bomb. And that's the best part of the movie.
While the film bombed at the box office, it did eventually earn an avid fanbase, which includes "Guardians of the Galaxy" director James Gunn, who collects all the Howard the Duck comics the movie is based on and is very vocal about his love for the character.
Gunn also gave Howard a cameo in the end credits of "Guardians of the Galaxy."
However, just because Gunn has a soft spot for Marvel's foul-mouthed feathered comic book character doesn't mean he's making a feature-length film about the duck.
Gunn posted a tweet Wednesday that settled all "Howard the Duck" movie rumors once and for all.
"There is NO Howard the Duck movie at the present time. There are a lot of comic characters I love but I'm not making films of them all."
This can't come as a complete surprise for fans, especially since actor Seth Green -- who lent his voice to Howard's cameo in "Guardians" -- told fans in 2015 that "nobody's thinking about a Howard the Duck movie. It's not going to happen."
So "Howard the Duck" fans will have to keep waiting for a new take on their feathered friend.
All the songs from Big Little Lies season 2 so far: Sufjan Stevens, Portishead, Donna Summers and Patti Smith are among the artists underscoring the Monterey Five.
Our biggest Stranger Things season 3 WTF questions: Hawkins is full of loose ends, but there are even more mysteries lurking far further from the city limits.
TV and Movies Marvel
Discuss: 'Howard The Duck' remake is horse feathers, James Gunn says


text:
Sierra Leone's top Ebola doctor dies from virus
(Reuters) – Sierra Leone's top doctor fighting an outbreak of Ebola has died from the virus, the country's chief medical officer, Brima Kargbo, said on Tuesday.
Sheik Umar Khan, who was credited with treating more than 100 patients, was infected with Ebola this month and had been moved to a treatment ward run by medical charity Medecins Sans Frontieres in the far north of the country.
(Reporting by Umaru Fofana and Adam Bailes; Writing by David Lewis)
For more, please click here
Ebola, Ebola doctor dies from virus, Sierra Leone