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Portal frame
This article needs additional citations for verification. (November 2013) |
Portal frame construction is a method of building and designing structures, primarily using steel or steel-reinforced precast concrete although they can also be constructed using laminated timber such as glulam. The connections between the columns and the rafters are designed to be moment-resistant, i.e. they can carry bending forces.[1] "They were first developed in the 1960s, and have now become the most common form of enclosure for spans of 20 to 60 m"[2]
Because of these very strong and rigid joints, some of the bending moment in the rafters is transferred to the columns. This means that the size of the rafters can be reduced or the span can be increased for the same size rafters. This makes portal frames a very efficient construction technique to use for wide span buildings.
Portal frame construction is therefore typically seen in warehouses, barns and other places where large, open spaces are required at low cost and a pitched roof is acceptable.
Generally portal frames are used for single-story buildings but they can be used for low-rise buildings with several floors where they can be economic if the floors do not span right across the building (in these circumstances a skeleton frame, with internal columns, would be a more economic choice). A typical configuration might be where there is office space built against one wall of a warehouse.
Portal frames can be clad with all sorts of material but the most popular solution, for reasons of economy and speed, is some form of lightweight insulated metal cladding with cavity masonry work to the bottom 2m of the wall to provide security and impact resistance. The lightweight cladding would be carried on sheeting rails spanning between the columns of the portal frames.
Portal frames can be defined as two-dimensional rigid frames that have the basic characteristics of a rigid joint between column and beam.
The main objective of this form of design is to reduce bending moment in the beam, which allows the frame to act as one structural unit.
The transfer of stresses from the beam to the column results in rotational movement at the foundation, which can be overcome by the introduction of a pin/hinge joint.
For warehouses and industrial buildings, sloping roof made of purlins and ac sheet roofing between portals is provided. For assembly halls, portals with R.C slab roof cast monolithically is used.
Portal frames are designed for the following loads:
- roof load
- wind load
While designing, care should be taken for proper
- joints
- foundation
- bracing
If the joints at B, C, and D are not rigid, they will "open up" and the frame will be unstable when subjected to loads. This is the pack of cards effect.
- Vertical loading results in A and E pushed outwards. If the foundation cannot resist horizontal push, outward movement will occur and the frame will lose strength.
- Wind subjects the frame to uplift forces. Overturning forces on the sides and ends of the building. Drag forces on the roof and sides.
- These destabilizing forces are resisted essentially by the weight of the building and in this regard, the foundations contribute significantly to this weight. The foundations are regarded as the building's anchors.
- ^ http://www.steelconstruction.info/Portal_frames
- ^ Trebilcock, Peter, and R. M. Lawson. Architectural design in steel. London: Spon Press, 2004. Print. 31.


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Ed Harris
Sarah Palin, John McCain Disparage HBO's Game Change
Originally posted 03/12/2012 11:05AM
Neither appears to have seen it, but Sarah Palin and John McCain both took shots this weekend at Game Change, the HBO movie about their unsuccessful 2008 presidential campaign. The film premiered Saturday night.
Palin, 48, portrayed in the film by Julianne Moore, told Fox News before the premiere that she was "not concerned about an HBO movie based on a false narrative when there are so many other things to be concerned about."
She added: "I believe my family has the right priorities and knows what really matters. For instance, our son called from Afghanistan yesterday and he sounded good, and that's what matters. Being in the good graces of Hollywood's 'Team Obama' isn't top of my list."
Game Change Theatrical Trailer Released
Originally posted 02/22/2012 08:15AM
Moviegoers are getting a peek at Julianne Moore as Sarah Palin in a theatrical trailer for Game Change, HBO's political thriller about the 2008 presidential race.
The movie, which will air on March 10 at 9 p.m., goes behind the scenes of Sen. John McCain's campaign and in particular his decision to pick the relatively unknown Alaska governor as his controversial running mate.
"We need to create a dynamic moment in this campaign," says Woody Harrelson, who plays McCain's adviser Steve Schmidt. "Or we're dead."
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Allie R. Murray
Latest Content
Visiting Teacher Gives Students a Reason To Dance
Dancer Mary Cochran turned to the 20 students warming up on the Rieman Dance Center stage. "Let's add sound!" she
Cast Carries Stylized 'Sisters'
"Whatever happens, you can only be happy when you want to be happy," says Vershinin, played by Thomas H. Price
With A Warm 'Song' In Our Hearts
"Whenever it wants, the past can come kicking the door down. And you never know where it's going to take


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Riverside Park
West 79th Street Boat Basin Cafe
Location: Rotunda at the West 79 Street MarinaPhone: (212) 496-5542
Directions to Riverside Park
Know Before You Go
Riverside Park
The northernmost A-dock at the 79th Street Boat Basin is currently closed to public access for structural enhancements. The dock will be further supported with non-wood pilings and a new wave screen.
Anticipated Completion: Spring 2016
- Baseball Fields
- Basketball Courts
- Bathrooms
- Dog-friendly Areas
- Eateries
- Fitness Equipment
- Handball Courts
- Kayak/Canoe Launch Sites
- Marinas
- Playgrounds
- Roller Hockey
- Running Tracks
- Skate Parks
- Spray Showers
- Tennis Courts
- Wi-Fi Hot Spots
Know when to go:
View upcoming athletic area usage in
Riverside Park


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Turbo Megazord
this wiki
This article is about a/an Megazord in Power Rangers Turbo, the third installment in the Mighty Morphin Power Rangers saga. |
Turbo Megazord | |
Zords: | Red Lightning Turbozord Mountain Blaster Turbozord Desert Thunder Turbozord Dune Star Turbozord Wind Chaser Turbozord |
Season: | Turbo |
First Appearance: | Turbo: A Power Rangers Movie |
Last Appearance: | Chase Into Space Part 1 |
Number of Episode Appearances: | Full list of appearances |
Length: | 30.8 m |
Width: | m |
Height: | 55 m |
Weight: | 7500 t |
Speed: | km/h |
"Initiate Turbo Megazord!"
The Turbo Megazord is the first Megazord of the Turbo Rangers. The five Turbozords combined to form the Turbo Megazord. Zordon claimed that the Turbo Megazord was the most powerful Zord ever created. The Turbo Megazord Saber was its primary weapon and was utilized in the Turbo Megazord Spinout, where the Megazord would "spin-out" while running toward its opponent, slashing it repeatedly and destroying it. The secondary weapon is the Turbo Headlights Blaster, using the lights from Mountain Blaster's chestplate. Another attack by the Turbo Megazord involved using the Artillery Power alongside the Rescue Megazord, in which each Megazord would take one of the weapons provided by Artillatron, and another attack involved the Turbo Megazord slashing the energy beams launched from the Artillery Power with its saber, as a combo attack.
The Turbo Megazord was once stolen by Divatox's brother, General Havoc, and was turned evil, thanks to Divatox and the use of a giant battery pack attached to its waist, powered by the Phantom Ranger's ruby. During this time it was piloted by Crosspatch and Havoc's robotic foot soldiers, however, the Red Ranger was able to locate the Ruby, defeat Crosspatch, fry the battery pack and return the Megazord to the side of good.
"We need Turbo Megazord power, now!"
The Turbozords are the only zords of the original Power Rangers: Turbo except Justin Stewart, and the first zords of the new team of the Power Rangers: Turbo. These are the first and only Zords that were created by the Rangers who pilot them.
The Turbo Zords can shrink to the size of regular cars and are amphibious. They use this to board the Ghost Galleon in "Turbo: A Power Rangers Movie". Adam Park drives Desert Thunder to the shore of Maligore's Island. The rest do the same after Divatox torpedoes the Ghost Galleon. In "Bicycle Built for the Blues" Tommy Oliver calls Red Lighting in it's car form to save Justin Stewart.
Red Lightning Turbozord
Red Lightning Turbozord | |
Pilot: | Red Turbo Ranger |
Length: | 22 m |
Width: | 10.6 m |
Height: | 8.5 m |
Weight: | 900 tons |
Speed: | |
See also: Red Vehicle
Red Lightning is a red race-car zord piloted by Tommy Oliver and later by Theodore Johnson. It forms the head and upper torso of the Turbo Megazord and the Rescue Turbo Megazord.
Mountain Blaster Turbozord
Mountain Blaster Turbozord | |
Pilot: | Blue Turbo Ranger |
Length: | 26.5 m |
Width: | 17.8 m |
Height: | 18.2 m |
Weight: | 2500 tons |
Speed: | 800 km/h |
See also: Blue Vehicle
Mountain Blaster is a blue 4x4 truck zord piloted by Justin Stewart. It forms the lower torso and upper legs of the Turbo Megazord and Rescue Turbo Megazord.
Desert Thunder Turbozord
Desert Thunder Turbozord | |
Pilot: | Green Turbo Ranger |
Length: | 25.8 m |
Width: | 12.8 m |
Height: | 14.8 m |
Weight: | 1500 tons |
Speed: | 840 km/h |
See also: Green Vehicle
Desert Thunder is a green Jeep zord piloted by Adam Park and later by Carlos Vallertes. It forms the right lower leg of the Turbo Megazord.
Dune Star Turbozord
Dune Star Turbozord | |
Pilot: | Yellow Turbo Ranger |
Length: | 25.8 m |
Width: | 12.8 m |
Height: | 14.8 m |
Weight: | 1500 tons |
Speed: | 840 km/h |
See also: Yellow Vehicle
Dune Star is a yellow van zord piloted by Tanya Sloan and later by Ashley Hammond. It forms the left lower leg of the Turbo Megazord.
Wind Chaser Turbozord
Wind Chaser Turbozord | |
Pilot: | Pink Turbo Ranger |
Length: | 23 m |
Width: | 12.8 m |
Height: | 6.9 m |
Weight: | 1100 tons |
Speed: | 889 km/h |
See also: Pink Vehicle
Wind Chaser is a pink sports-car zord piloted by Katherine Hillard and later by Cassie Chan. It forms the arms of the Turbo Megazord.
The Megazord tried to destroy Goldgoyle with the spin-out, but Goldgoyle was unaffected by the drill attack. He then launched a series of energy blasts at the Turbo Megazord, wrecking it completely.
See also
- RV Robo - Super Sentai counterpart in Carranger. See comparison page.


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I'll go for Guard and Reserve. Sounds like a job with the most amount of time to spare…. doing web design… while you "guard and reserve" lol
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lol yeah thats true but I am a student and take web design as a hobby
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Bruins tickets go on sale Sept. 10 |
08.18.10 at 11:25 am ET |
The Bruins announced Wednesday that individual game tickets for the upcoming season will go on sale Friday, Sept. 10, at 11 a.m.
Tickets for the Bruins' home games at TD Garden will be priced from $10-$294 per seat. The cost of the ticket will vary depending on the opponent and date. Both the Tufts Medical Center family section and the Chipotle student section will offer reduced prices at various points of the season.
Tickets can be purchased at the TD Garden box office or at the Bruins official website. Though full season-ticket packages are sold out, 21, 10, and five-game plans are still available for those interested in buying in bulk.
Lehtonen bolts for Sweden |
08.17.10 at 3:35 pm ET |
The Bruins suffered a minor loss Tuesday, but a loss nonetheless when forward Mikko Lehtonen left the states to take a one-year deal in the Swedish Elite League. Though his Bruins career technically isn't over (the Bruins still have his rights), the 23-year-old will play next season with Skelleftea.
In two games with the Bruins over the last two seasons, Lehtonen did not record a point, but he led Providence in goals in each of the campaigns, scoring 28 and 23 goals in 2008-09 and 2009-10, respectively.
Bruins general manager Peter Chiarelli indicated to Fluto Shinzawa of the Boston Globe Tuesday that Lehtonen "felt there was not an opportunity for him in our organization."
Savard 'hurt' by trade rumors |
08.15.10 at 1:21 pm ET |
Bruins center Marc Savard has been popular this offseason. First there was the owners' vote to penalize blindside hits to the head after his scary injury incurred from a Matt Cooke hit in March. Then came the recent news that the veteran's seven-year, $28 million extension inked in December is under investigation by the NHL.
Despite the numerous reasons for the buzz surrounding Savard as he prepares for his fifth season in Boston, nothing compares to the months of speculation as to whether the Bruins would trade the center before he plays the first game of his new contract.
Savard has been quiet throughout everything. In fact, he hadn't spoken at all in the midst of the rumors until recently, when he told the Ottawa Sun that he did indeed hear his name in numerous reports.
Now 33, Savard signed with the Bruins following a 2005-06 season in which the team finished 13th in the Eastern Conference with 74 points. With the Bruins having made it to the second round in each of the last two postseasons, it would seem like the worst time for any player with Stanley Cup aspirations to be shipped out.
'[The rumors] hurt me a little bit just because I went to Boston and I helped to build that team back up,' Savard told the paper. 'I've really tried to work hard with the young guys and being a core player. I was really focused on staying there for the rest of my career. To hear all this stuff this summer bothered me inside more than anything else.'
Though there haven't been concrete reports of specific trade talks regarding Savard, the logic that would lead one to such speculation consists of multiple factors, including the Bruins' salary cap situation and the selection of wunderkind center Tyler Seguin with the second overall pick in June's NHL draft.
In 782 career games, Savard has scored 205 goals and registered 491 assists for 696 points since coming into the league in 1999 with the Flames. Should his contract, which tacks on extra years at lower salaries to decrease his cap hit in an otherwise lucrative deal, be voided, Savard would be free to sign with any team. Speaking with the Sun, however, Savard indicated he's simply staying in the present.
'Right now I'm a Bruin and that's the way it is,' Savard said. '[But] it's been tough.'
Rookie games moved to Boston |
08.13.10 at 1:59 pm ET |
The two preseason rookie games between the Bruins and Islanders scheduled for the two days leading up to training camp have been moved from Shelton, CT to the TD Garden, the team announced Friday. The games will be played on September 15 and 16 before camp opens the following day. Tickets go on sale Thursday, August 19 at 10 a.m. and will cost $5. All proceeds will go the Bruins Foundation.
Quick thoughts on the Savard situation |
08.10.10 at 5:06 pm ET |
It's been a long day for the Bruins, as news hit today that the NHL is indeed investigating center Marc Savard's seven-year, $28.05 million extension. The deal is perceived to be a "retirement contract," as it pays the 33-year-old veteran half its money in the first two years of the deal and the other half over the following five years, which makes for a much more affordable $4.007 million cap hit.
Hours after the news broke, Bruins general manager Peter Chiarelli came out with a statement in which he said that the investigation has been ongoing and that he had met with NHL lawyers as recently as last week. With the Bruins' cap situation up in the air and the team risking the loss of Savard, it might be a little too much to keep track of. Here's what we've learned today, and what it might mean for the Bruins.
– This investigation has been going on for a while, and by a while, we mean since Savard's contract was registered with the league in the first place way back in December. This means two things. First of all, this isn't some new development for the Bruins. Maybe it was the magical cap relief they were expecting all along when they made signings that in total would put them more than $3 million over the salary cap (Savard's cap hit is $4.007 million).
Secondly, it really dents the validity of rumors that the team was working on trades to move Savard out of town this offseason. In addition to there being zero concrete or validated reports of the Bruins and another team discussing a deal for the center, would it really make sense for the Bruins to shop a player knowing full well that the NHL was intent on voiding his deal? That would make the Bruins look awfully bad as a prospective trade partner for any team in the future.
– Savard is not the only one. The only reason the news came about was because Savard's investigation was listed in the footnotes of arbiter Richard Bloch's rejection of Ilya Kovalchuk's appeal. In noting why the NHL was correct in rejecting the winger's 17-year, $102 million contract with the Devils, Bloch also listed Marian Hossa, Chris Pronger and Roberto Luongo as players also being investigated.
– Yes, the Bruins have been looking to save money off the cap (they're right up against it even when factoring in the $3.5 million they will get in relief to begin the season thanks to Marco Sturm's long-term injury status), but there's no way Savard's contract could be viewed as the one that's weighing them down. In fact, the only reason this deal is being investigated is because it is so team-friendly that the NHL is trying to prevent deals like this from being made going forward.
Both Savard and Tim Thomas ($5 million cap hit in each of the next three seasons) have starred in offseason trade rumors, but their values to the team should not be overlooked. If the team does end up losing Savard for nothing, it would seemingly be a huge loss for the Bruins.
Chiarelli: Bruins 'cooperating fully' with league regarding Savard |
08.10.10 at 3:53 pm ET |
The Bruins have released a statement from general manager Peter Chiarelli regarding the league's investigation of the seven-year, $28.05 million contract extension center Marc Savard signed with the team in December. Here's what Chiarelli had to say.
'We are cooperating fully with the League in its investigation of the Marc Savard contract extension. The League informed us upon their registration of the contract on December 1, 2009 that they would be investigating the circumstances surrounding this contract. From that point on, they commenced their investigation and it has been ongoing since then. On August 4th, I met with two League appointed lawyers as part of the investigation. We will continue to cooperate with the League in any future investigative proceedings if necessary and we will have no further comment on the matter at this time.'
Savard will make nearly half of his contract's money in the next two seasons, with the other half being spread out over the following five seasons. As a result, despite making $7 million per year in 2010-11 and 2011-12, he will have a cap hit of just $4.007 as a result of cap numbers in the NHL being determined by total money divided by years. If the deal is ruled as not being in compliance with the CBA, it will be voided and Savard will become an unrestricted free agent.
Savard's deal under investigation |
08.10.10 at 1:45 pm ET |
Bruins fans have wondered all offseason whether center Marc Savard would be back in Boston next season, but this probably isn't what they had in mind. Savard, who signed a seven-year contract extension last season, could have his deal voided by the league as it is currently under investigation.
In rejecting Ilya Kovalchuk's greivance with the league for deeming his 17-year, $102 million deal with the Devils bogus, arbiter Richard Bloch listed in the ruling's footnotes that similar contracts that have already been registered with the league will be under investigation.
These so-called "retirement contracts" that have thrown the league for a loop are made when teams, in an effort to lower a player's cap hit, tack on extra years at minimal dollars. A player's cap number in the NHL is determined by dividing total dollars by the number of years, so even in guaranteeing more money in the early years (such as Savard's $7 million in the first two seasons of the deal, which starts in the upcoming campaign) by adding years at low money, the hit is brought down dramatically (Savard's cap hit will be $4.007).
Here is an excerpt from the ruling, which was leaked by Team 1200 radio in Ottowa:
It is true, as the Association observes, that the NHL has registered contracts with structures similar to the Kovalchuk SPC PA Exh. 8 reflects a list of 11 multi-year agreements, all of which involve players in their mid to late 30's and early 40's. Most of them reflect reasonably substantial 'diveback' (salary reductions that extend over the 'tails' of the Agreement). Of these, four such agreements, with players Chris Pronger, Marc Savard, Roberto Luongo, and Marian Hossa reflect provisions that are relatively more dramatic than the others. Each of these players will be 40 or over at the end of the contract term and each contract includes dramatic divebacks.
[…] The apparent purpose of this evidence is to suggest that the League's concern is late blooming and/or inconsistent. Several responses are in order: First, while the contracts have, in fact, been registered, their structure has not escaped League notice: those SPCs are being investigated currently with at least the possibility of a subsequent withdrawal of the registration.
The Bruins are in a tight spot cap-wise, but in voiding the contract the NHL would let Savard become an unrestricted free agent, which would mean the Bruins would receive nothing for him. His cap hit is very team friendly given his production, and with the 2010-11 season Nathan Horton's first in Boston, one would think the Bruins would like to at least catch a glimpse of what the two could do playing together.
Additionally, it could be interesting to see what would come of Savard being a free agent. He's heard his name in trade rumors all summer and could be willing to test the market if he doesn't feel he'll be a top forward with the Bruins in future years.
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The international financial institutions' relations with Africa: insights from the issue of representation and voice
Thomas, Caroline (2004) The international financial institutions' relations with Africa: insights from the issue of representation and voice. In, Taylor, Ian and Williams, Paul (eds.) Africa in International Politics: External involvement on the continent. Abingdon & New York, Routledge, 174-194.
Full text not available from this repository.
Locating Africa on the global stage, this book examines and compares external involvement in the continent, exploring the foreign policies of major states and international organizations towards Africa. The contributors work within a political economy framework in order to study how these powers have attempted to stimulate democracy, peace and prosperity in the context of neo-liberal hegemony and ask who these attempts have benefited and failed.
Item Type: | Book Section |
ISBNs: | 0415318580 (hardback) 0415358361 (hardback) |
Related URLs: | |
Subjects: | H Social Sciences > HN Social history and conditions. Social problems. Social reform J Political Science > JX International law J Political Science > JC Political theory H Social Sciences > HB Economic Theory |
Divisions: | University Structure - Pre August 2011 > School of Social Sciences > Politics and International Relations |
ePrint ID: | 35168 |
Date Deposited: | 15 May 2006 |
Last Modified: | 27 Mar 2014 18:22 |
URI: | http://eprints.soton.ac.uk/id/eprint/35168 |
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A Practical Approach to the New Lymphoma Classifications
Patrick A. Treseler, M.D., Ph.D.
Division of Surgical Pathology
Department of Pathology
University of California, San Francisco
NOTE: The following monograph is the property of the author and has been provided as a service to the medical community. No part of it may be reproduced without the written consent of the author.
Lymphoma classifications have evolved over the past 20 years from a scheme utilizing purely morphologic assessment (the Working Formulation); to a system that attempted to integrate morphologic, immunophenotypic, and genotypic data (the REAL Classification); and finally to a classification that hopes to integrate all these features into clinically relevant categories of equal use to pathologists and clinicians (the soon-to-be published WHO classification). Despite the proliferation of new names for lymphomas which these various revisions have provided, most of the newer classifications involve entities long recognized by pathologists, with the occasional splitting off (or recombining) of particularly entities based on newly recognized differences in morphology, phenotype, genotype, or behavior. Driving this continual reclassification of lymphoid neoplasms is not only new data concerning the biology of lymphoid neoplasia, but also continuing uncertainty as to what is most important in the accurate classification of lymphomas. Is it morphology, immunophenotype, genotype, clinical behavior, or something else? Obviously, the best system would be one which takes all such factors into account, but when discrepancies arise (as often happens in lymphoma cases), which factor should take precedence? Although modern pathology strives to understand diseases on the basis of genetics and molecular biology, genetic factors in lymphomagenesis are frequently poorly understood, and correlate poorly with clinical outcome in many cases.
A classic example is anaplastic large cell lymphoma (ALCL). Initially, ALCL was described as a neoplasm characterized by large pleomorphic lymphoid cells that expressed the lymphoid activation antigen CD30. When a subset of these tumors was found to contain a characteristic cytogenetic translocation, t(2;5), interest focused on this genetic defect as a possible defining element. It soon became apparent, however, that most such cases (which were generally of T-cell or null-cell phenotype) showed monomorphic rather than pleomorphic cytology (i.e., a "non-anaplastic" form of anaplastic large cell lymphoma) . Only later did it become clear that the t(2;5) abnormality could be found not only in tumors which were not anaplastic, but also in cases that were not CD30-positive, and occasionally in cases not even composed of large cells (the "small cell variant" of ALCL) . Furthermore, CD30-positivity was found to be present not infrequently in many different types of B-cell and T-cell lymphoma that shared little else in common with ALCL. Could a lymphoma be composed of cells which where CD30-positive, anaplastic, and large, and not be ALCL? What about the rare cases that had the t(2;5), but were clearly of B-cell phenotype and genotype? Were these also ALCL, like the more common T/null-cell cases? It all depends on which factor is considered most important morphology, immunophenotype, or genotype. A related issue is whether tumors with different genotypes and behavior always represent different disease entities, or whether these might better be regarded as prognostic features within a given entity in some cases. The new WHO classification will hardly end this continual reconsideration of the relative importance of various factors. It may however provide at least a temporary consensus concerning how specific entities are diagnosed.
B-cell Non-Hodgkin's Lymphomas
B-cell lymphomas are by far the most common non-Hodgkin's lymphomas in the United States. Despite the profusion of B-cell neoplasms recognized in the REAL and WHO classifications, most B-cell lymphomas can be correctly identified by morphologic examination alone if one can recognize a small number of basic lymphoid cell types. (B-cell neoplasms that tend to present with bone marrow and peripheral blood involvement (i.e., leukemias) will not be considered in this discussion, but are well-addressed in both the REAL and proposed WHO Classifications.)
Figure 1 above shows the eight basic lymphoid cell types found in B-cell lymphomas. Under each cell type is the name by which it has been known to many American pathologists, and, in parentheses under that, the name by which it would likely be known to most European pathologists using the Kiel classification. (With increasing usage of terminology of the Kiel classification in the REAL and WHO classifications, these latter terms are becoming more frequent in the U.S. literature.)
The basic initial distinction between the cell types is made on the basis of cell size, with the traditional yardstick being the average size of the nucleus of a phagocytic histiocyte. (Endothelial cell nuclei are about the same size, and are often easier to find.) Lymphoid cells the same size as histiocytic nuclei are considered intermediate in size. Those smaller are small cells, and those larger are large cells. (The confusing use of the term "small non-cleaved cell" for a lymphoid cell of intermediate size dates back to Lukes and Collins, who did not recognize an intermediate size group, and lumped intermediate size cells in the small cell category.)
A glance at Figure 1 will reveal that both small and intermediate size lymphoid cells have relatively scant cytoplasm; abundant cytoplasm is the mark of a large lymphoid cell. Small lymphoid cells all have typical mature lymphoid chromatin as their hallmark; all larger lymphoid cells have either coarsely clumped vesicular chromatin or, in the case of lymphoblasts, much finer nuclear chromatin. Thus it is not even really necessary to compare lymphoid cells to histiocytic or endothelial cell nuclei to judge their size. If the cytoplasm is abundant, the cell is large. If the cytoplasm is scant, mature lymphoid chromatin marks the small cells. Everything else is an intermediate size cell. (This system actually works better than true comparative measurement, since some lymphoblasts and small non-cleaved cells may actually be smaller than histiocytic or endothelial cell nuclei. Thus the adage "Never judge cell size by cell size".) Confusion between small cells and intermediate size cells is possible by morphology alone. (Even Rapaport failed to distinguish lymphoblasts from centrocytes in his initial classification.) However, lymphomas derived from intermediate size cells are very high grade, and almost always display high mitotic and apoptotic rates. Small cell lymphomas usually display relatively low mitotic and apoptotic rates. A final thing to note from Figure 1 is that little separates the morphologic appearance of small non-cleaved cells, centroblasts, and immunoblasts, except the amount of cytoplasm, which can make distinctions between these cells difficult. This is reflected in difficulty in distinguishing between certain lymphomas, as we shall see below.
B-cell lymphomas composed of large cells are large cell lymphomas, according to both the REAL and proposed WHO Classifications, regardless of whether they are composed of centroblasts or immunoblasts. The proposed WHO classification does permit, however, optional subclassification into centroblastic and immunoblastic types, and makes reference to the Kiel classification criteria, which require >90% immunoblasts for the diagnosis of immunoblastic lymphoma. (The subclassification of large cell malignancies will be further discussed in the section on immunophenotypic diagnosis of lymphomas ahead.) B-cell lymphomas composed of a uniform population of small non-cleaved cells are Burkitt's lymphomas. (An entity known as high-grade Burkitt-like B-cell lymphoma exists (as a provisional entity in the REAL, and as a variant of Burkitt's in the WHO) to handle cases that display more pleomorphism or contain more large cells than typical Burkitts lymphoma.) Most B-cell lymphomas with lymphoblastic morphology are lymphoblastic lymphomas, although a "blastic" or "blastoid" variant of mantle cell lymphoma has been described. Markers of early B-cell lineage (TdT, CD34, CD10) are helpful in confirming the diagnosis of lymphoblastic lymphoma. Mantle cell lymphoma, even with "blastic" cytology, will show a mature B-cell phenotype with expression of surface immunoglobulin and other characteristic markers of mantle cell lymphoma (see below).
Such a direct correlation of cell type to tumor type is not seen in the small B-cell lymphomas, several of which may contain a mixture of small lymphoid cell types. Here, however, architectural features and cytology combined will generally give strong clues to the lymphoma type, which can be confirmed by immunophenotyping. Only four types of small B-cell neoplasms typically present as lymphomas (i.e., outside the bone marrow): small lymphocytic lymphoma, follicular lymphoma, mantle cell lymphoma, and marginal zone lymphomas.
Small lymphocytic lymphoma (SLL) is the name given to chronic lymphocytic leukemia (CLL) when it presents outside the bone marrow. SLL displays a characteristic "pseudonodular pattern" at low power due to the presence of proliferation centers containing increased numbers of large lymphoid cells. This feature is highly sensitive and specific for SLL. Outside these proliferation centers, most cells are small round mature lymphocytes, and small cleaved cells (centrocytes) are uncommon.
Follicular lymphomas generally have at least some areas of follicular architecture that can be seen at low power. High power examination will reveal a prominent population of small cleaved cells (or centrocytes), with variable numbers of large non-cleaved cells (or centroblasts). (If a small B-cell lymphoma with numerous centrocytes appears entirely diffuse, one should suspect a mantle cell or marginal zone lymphoma.)
Mantle cell lymphoma (MCL) generally displays a diffuse or vaguely nodular pattern at low power. High power will reveal a population of mature-appearing small lymphoid cells that vary from round to cleaved. The relative lack of admixed large cells is a further clue to the diagnosis.
Like MCL, marginal zone lymphomas (MZLs) are also diffuse lymphomas that generally contain a prominent population of centrocytes. In contrast to the cellular monotony of MCL, however, MZLs are typically quite polymorphous, with frequent admixed plasmacytoid and monocytoid small lymphocytes, large lymphocytes, and histiocytes, producing a picture that may resemble a benign inflammatory infiltrate at high power. MZLs may occur in the lymph nodes ("monocytoid B-cell lymphoma"), extranodal sites ("low grade B-cell lymphomas of MALT type" or "MALToma"), or in the spleen ("splenic marginal zone lymphoma").
Immunophenotyping is quite useful in confirming the diagnosis of small cell B-cell lymphomas. While all are positive for pan-B cell markers (e.g., CD20), only SLL and MCL usually show co-expression of CD5. SLL can be distinguished by its expression of CD23; MCL is generally CD23-negative. MCL is also unique among small cell lymphomas in its expression of cyclin D1, a protein product of the t(11;14) translocation which can be detected immunohistochemically. About 60% of follicular lymphomas express CD10, which is uncommon in other small B-cell lymphomas. MZLs typically show no co-expression of either CD5 or CD10.
With an understanding of lymphoma cytology and architecture, the B-cell lymphomas in the 1994 REAL classification (Table 1) can thus be readily diagnosed in most cases. Immunophenotyping with a pan-B cell marker such as CD20 is recommended in cases of intermediate and large cell lymphoma to exclude non-B-cell tumors, and lymphoblastic lymphoma will require markers to confirm early B-cell phenotype and exclude other blastic neoplasms.
SLL and follicular lymphoma can generally be diagnosed by morphology, but in other cases of suspected small B-cell lymphoma, markers to confirm the diagnosis are suggested as discussed above.
In published reports which describe the proposed new WHO Classification, there are relatively few significant changes in the B-cell lymphomas from the 1994 REAL Classification. Table 2 shows the most recent proposed list of WHO B-cell neoplasms (excluding those that typically present in the bone marrow, and are generally considered leukemias). The only major change is the elimination of high-grade Burkitt-like B-cell lymphoma, however this entity still exists as a morphologic variant of Burkitt's lymphoma. Several significant issues are addressed in the new WHO Classification concerning morphologic and clinical variants and subtypes of particular lymphomas, which will be briefly discussed.
While it lists diffuse large B-cell lymphoma (DLBCL) as single distinct disease entity, the proposed WHO Classification recognizes six morphologic variants (which differ largely in their appearance or phenotype) and three subtypes (which differ in clinical behavior) of DLBCL (Table 3). The recognized six morphologic variants of DLBCL are centroblastic, immunoblastic, T-cell/histiocyte-rich, lymphomatoid granulomatosis type, anaplastic large B-cell, and plasmablastic. Centroblastic lymphoma is the prototypic diffuse large B-cell lymphoma, composed predominantly of large non-cleaved lymphocytes with smaller nucleoli which are frequently multiple and peripheral in the nucleus. Immunoblastic lymphoma, in contrast, is composed mainly of immunoblasts with large, prominent, centrally-located nucleoli. The WHO Committee has called for the development of criteria for distinguishing centroblastic from immunoblastic lymphoma (and cites the Kiel Classification criteria of >90% immunoblasts required for immunoblastic lymphoma). There is some evidence from the Kiel group to suggest that the immunoblastic variant may have a worse prognosis than centroblastic lymphoma. If large numbers of admixed reactive small T-lymphocytes or histiocytes are present, the lesion may be diagnosed as T-cell/histiocyte-rich large B-cell lymphoma. Several reports describe an aggressive clinical course in these patients. The large B-cells in these cases may resemble classical Reed-Sternberg cells or L&H Reed-Sternberg variants, raising the differential diagnosis of classical Hodgkins disease (CHD) or nodular lymphocyte predominance Hodgkins disease (NLPHD). Lack of CD30 and CD15 staining will help exclude classical Hodgkins disease, and lack of nodular architecture and a paucity of background small B-cells argues against NLPHD. Lymphomatoid granulomatosis is a clinically distinctive type of T-cell/histiocyte-rich large B-cell lymphoma that presents in the pulmonary tree. Previously thought to be related to nasal T/NK-cell lymphoma due to the prominent angiocentricity seen frequently in both tumors, recent evidence indicates a large B-cell origin. Diffuse large B-cell lymphomas may express CD30 and/or contain the t(2;5) translocation characteristic of ALCL, and these may be considered the anaplastic large B-cell variant. Most of these cases resemble typical DLBCLs, and do not show morphologic features of ALCL. Whether these cases are related to T-cell ALCL, or differ significantly from other DLBCLs, is controversial. Such tumors often have complex hyperdiploid karyotypes, leading to speculation that the t(2;5) translocation may be a later, secondary event in lymphomagenesis in these cases. Plasmablastic lymphoma is a rare aggressive Epstein-Barr virus (EBV)-positive AIDS-related B-cell malignancy first described by Delecluse et al. in 1997. In these features, and in its morphology, it resembles the high grade primary effusion lymphoma (PEL) also seen in AIDS patients. However, the tumor occurs principally in the oral cavity, and appears to lack the virus KSHV/HHV-8, which is universally present in PEL.
The three subtypes of diffuse large B-cell lymphoma recognized in the proposed WHO Classification are mediastinal (thymic) large B-cell lymphoma, primary effusion lymphoma, and intravascular large B-cell lymphoma. Mediastinal (thymic) large B-cell lymphoma differs from other forms of DLBCL not only in its location, but also in its phenotype and behavior. The tumor is often surface immunoglobulin negative, which is uncommon in DLBCL. CD30 is often positive, raising the differential diagnosis of CHD and ALCL. Clinically, mediastinal large B-cell lymphoma is unusual in that it tends to preferentially involve females in the fourth decade, and relapses are often extranodal, involving sites such as GI tract, liver, ovaries, and kidneys. While early reports suggested a poor prognosis, some recent data suggest that cure rates may be similar to other large cell lymphomas if treatment is appropriate. Primary effusion lymphoma, also known as Primary body-cavity based AIDS-related lymphoma appears to comprise a distinct clinicopathologic disease entity, which differs in many respects from more typical AIDS-related B-cell lymphomas. It generally occurs in late stage AIDS patients with a history of Kaposis sarcoma who present with effusions but no clinically evident mass lesion. Like Kaposis sarcoma, the disease occurs primarily in homosexual males. The disease tends to remain confined to the involved body cavity without further dissemination, but is nonetheless associated with an extremely poor prognosis, in part because the patients are generally debilitated and tolerate chemotherapy poorly. The median survival in reported cases averages two to three months. The tumor has large pleomorphic cells, occasionally multinucleated, with variably prominent, usually multiple nucleoli, and deeply basophilic cytoplasm by Wright-Giemsa stain. This appearance is in contrast to more typical AIDS-related lymphomas that generally appear as more typical large centroblastic, immunoblastic, or Burkitts/Burkitt-like B-cell lymphomas. Immunophenotyping reveals a characteristic "null cell" phenotype, with absence of most pan-B and T-cell markers, including surface and cytoplasmic immunoglobulin, but with uniform expression of CD30 and plasma cell markers such as CD38. B-cell markers that persist on mature plasma cells, such as CD79a, are also frequently expressed. This immunophenotype, which is most suggestive of plasma cell differentiation, contrasts with the mature B-cell phenotype expressed by other AIDS-related lymphomas. Immunoglobulin genes are clonally rearranged by molecular studies, confirming B-cell lineage for these neoplasms. Other significant differences from typical AIDS-related lymphomas are evident on the genetic level, where primary effusion lymphomas are found to be uniformly positive for Epstein-Barr virus (compared with 30-60% for other AIDS lymphomas) and to have consistent germline configuration of the c-myc proto-oncogene (which is rearranged in nearly all other AIDS lymphomas). First described by Walts and coworkers in 1990, primary effusion lymphomas became the focus of considerable attention in 1995, when Cesarman and colleagues found these tumors to contain a newly recognized human herpes virus termed Kaposis sarcoma-associated virus (KSHV) or human herpes virus-8 (HHV-8), which is also found associated with the cells of Kaposis sarcoma and multicentric Castlemans disease. Unlike Kaposis sarcoma, where the virus may only be detectable by PCR (and established KS cell lines may even be virus negative), body cavity-based lymphoma cells contain KSHV/HHV-8 in very high copy numbers. Since co-infection with EBV is seen in virtually every case, there has been speculation that the two viruses may cooperate in neoplastic transformation. Finally, intravascular large B-cell lymphoma, previously known as malignant angioendotheliomatosis, is a rare lymphoma characterized by an unusual tendency to proliferate and remain within vascular spaces. Vessels in virtually any organ may be involved by the disease, and thus the presenting symptoms are commonly non-specific (e.g., FUO, mental status changes, skin rash). This, combined with the absence of a mass lesion, makes diagnosis difficult clinically. The prognosis is extremely poor, although this may be due to long delays in reaching the diagnosis in many cases.
The proposed WHO Classification also takes a stand on the entity known as high grade Burkitt-like B-cell lymphoma, and its relationship to both Burkitt's lymphoma and DLBCL. High-grade Burkitt-like lymphoma had been recognized in the REAL classification as an entity with morphologic features intermediate between Burkitt's lymphoma and DLBCL. Specifically, most cases tended to resemble Burkitts lymphoma, but had either more cellular pleomorphism or more admixed large cells than classical Burkitt's. Lack of CD10 (typically expressed in Burkitt's lymphoma) was felt to favor the diagnosis, but cases could be CD10-positive. In a preliminary 1997 report on the proposed WHO Classification, it was stated that such tumors in non-immunosuppressed adults appeared more closely related to DLBCL than Burkitt's lymphoma. Subsequently, pathologists recommended making high-grade Burkitt-like B-cell lymphoma a subcategory of DLBCL. Pediatric oncologists expressed the concern that in children, cases classified as Burkitt-like behave identically to Burkitt's lymphoma, and would be undertreated if treated like DLBCL. The oncologists argued for the preservation of a category for "tumors that should be treated (like Burkitt's lymphoma), that is, very high-grade tumors." Thus, Burkitt-like lymphoma was retained as a morphologic variant of Burkitt's lymphoma. WHO Committee members expressed the opinion that the gold standard for the diagnosis of Burkitt's lymphoma should be the presence of the t(8;14) translocation (or its light chain variants t(2;8) or t(8;22)) . This translocation results in c-myc gene rearrangement and activation, which in turn causes all cells being perpetually in cycle. In the absence of cytogenetic studies or Southern blot analyses for c-myc rearrangement, a proliferative fraction close to 100% (as measured by Ki-67/MIB1 staining) was felt to be an acceptable surrogate marker. High-grade Burkitt-like lymphoma, as a variant of Burkitt's lymphoma, was further defined as a lymphoma that 1) morphologically resembles Burkitt's lymphoma, but has more pleomorphism or large cells than classical Burkitt's lymphoma; and 2) a proliferation fraction >99%.
The pathologists of the WHO Classification Committee also recommended guidelines for the separation of follicular lymphoma into three grades based on the number of large cells (centroblasts) present. Based on criteria initially developed by Mann and Berard, it was recommended that follicular lymphomas be graded as follows:
Grade 1 (follicular small cleaved): 1-5 centroblasts/high-power field (hpf)
Grade 2 (follicular mixed small and large cell): 6-15 centroblasts/hpf
Grade 3 (follicular large cell): >15 centroblasts/hpf.
Committee members felt that the most important distinction was to separate grade 3 tumors because of higher relapse rates in patients with grade 3 tumors. It was noted to be often difficult for pathologists to discriminate between grade 1 and 2 tumors, but this distinction was felt to be of little clinical significance. As in the REAL Classification, it was suggested that the degree of follicular architecture be reported as follows:
Predominantly follicular: >75% follicular architecture
Follicular and diffuse: 25-75% follicular
Predominantly diffuse: <25% follicular.
Grade 1 follicular lymphomas which appear entirely diffuse should have immunophenotyping performed to confirm follicular origin, and exclude other entities such as mantle cell lymphoma; the term "diffuse follicle center lymphoma, grade 1" can be used for these rare cases to avoid the non sequitur of a "diffuse follicular lymphoma". Areas of diffuse large cell lymphoma should be clearly reported as such, and not as "follicular lymphoma, grade 3, follicular and diffuse", since the presence of any component of DLBCL warrants more aggressive therapy.
The significance of large lymphoid cells in MZLs such as extranodal low grade B-cell lymphomas of MALT type was also addressed by the WHO Committee members. They cite a recent study of patients with low grade MALTomas treated primarily with antibiotics which found that if large cells were increased in number (5-10%, with clusters of <20 cells), patients had a slight but significantly worse prognosis (WHO latest). Cases with confluent clusters or sheets of large cells (defined as >20 cells) were found to behave similar to cases of DLBCL with no low grade component. It was recommended these latter cases be diagnosed as diffuse large cell lymphoma arising in a background of low grade MALToma, and not as high grade MALToma, since the latter term risks confusion with its low grade counterpart. The final WHO Classification will provide criteria for grading, likely along the lines described above.
Post-transplant lymphoproliferative disorders (PTLDs) are recognized by the WHO Committee as unique B-cell proliferations which span the spectrum from benign to malignant, and which require their own classification scheme separate from other B-cell neoplasms. A recent Society for Hematopathology Workshop greatly simplified the classification of these disorders. PTLDs are EBV-induced B-cell proliferations that may arise following either solid organ or bone marrow transplantation. The Workshop report describes three main categories of PTLDs:
"Early lesions" occur primarily in children within three months of transplantation, commonly involving sites such as tonsils or lymph nodes rather than extranodal sites. They do not show architectural effacement of involved tissues, nor destructive tissue infiltration. Most are polyclonal and regress either spontaneously or with minimal reduction in immunosuppression, but they can be fatal in some cases. Polymorphic PTLDs are destructive lesions that efface the architecture of involved tissues, which may be lymph nodes or extranodal sites. Morphologically, they resemble a "diffuse mixed small and large cell lymphoma" such as a marginal zone lymphoma. Most are monoclonal, but clonality does not predict behavior. A variable number will regress with reduction of immunosuppression. Those that persist or progress despite such therapy may require treatment for lymphoma. Monomorphic PTLDs are virtually all monoclonal, and resemble diffuse lymphomas. Indeed, most meet criteria for diffuse large B-cell lymphoma and can be diagnosed as such, but it should be noted that in the clinical setting of the post-transplant state, they are also monomorphic PTLDs. Many monomorphic B-cell cases will show aberrant co-expression of T-cell markers such as CD43 or CD45RO. Rare cases are of T-cell type, and may be considered T-cell lymphomas. Most monomorphic PTLDs are treated initially with reduction of immunosuppression, because occasional cases will respond to such therapy with durable remissions. Others may require standard lymphoma therapy.
Finally, for mantle cell lymphoma, the WHO Committee recognized that certain morphologic variants (such as the mantle zone pattern) have been reported to have a better prognosis in some studies, while cases with a blastic or blastoid morphology (but a mantle cell immunophenotype or genotype) have been reported to have a worse prognosis. The Committee suggests recording such patterns for the purpose of future research, but stratification by morphologic features was not felt to be required for clinical diagnostic purposes at this time since no effective therapy currently exists for any form of mantle cell lymphoma.
T-cell Non-Hodgkin's lymphomas
T-cell non-Hodgkin's lymphomas are much less common and much less well understood than their B-cell counterparts, and morphologic assessment is much less helpful in classification. The T-cell lymphomas recognized by the 1994 REAL Classification are listed in Table 4. While lymphoblastic lymphoma of T-cell type generally displays blastic morphology, the majority of the post-thymic (peripheral) T-cell lymphomas have morphology that can vary from mature appearing small lymphocytes to intermediate size blast-like cells to pleomorphic large cells to combinations of all three. Often, a continuum of atypical cells is seen spanning the size spectrum. Some studies have suggested that, in general, peripheral T-cell lymphomas with significant numbers of large cells may be more aggressive than those composed principally of small cells. However, often the grade is more dependent on tumor type than the cell morphology. For example, hepatosplenic gamma-delta T-cell lymphomas are almost always clinically aggressive, even if composed entirely of small cells. Another general feature of the peripheral T-cell lymphomas is that many are clinicopathologic entities, occurring in specific patient populations and involving particular body sites. Others display characteristic surface markers that aid in diagnosis, or have associations with etiologic viruses that can be detected by clinical tests. This sort of clinical information is frequently of much greater utility in reaching a diagnosis than the tumor cell morphology. For example, nasal T/NK-cell lymphomas typically occur in Asian patients, almost always involve extranodal sites (particularly the nose and palate), and are EBV-positive and clinically aggressive. Intestinal T-cell lymphoma typically involves the jejunum of adults who often have a history of gluten-sensitive enteropathy, and is also clinically aggressive. Overall, peripheral T-cell lymphomas are among the most aggressive of the non-Hodgkins lymphomas. Five year survival is under 30%, placing it in the worst prognostic group in a recent study conducted by the NHL classification project. Details concerning specific types of T-cell non-Hodgkin's lymphomas are provided in several excellent recent reviews.
The WHO Committee suggests in their recent proposed classification scheme that cytologic sub-classification of the peripheral T-cell lymphomas (e.g., as per the Kiel Classification) not be required for clinical diagnostic purposes at this time. They instead stress the importance of clinical correlation and immunophenotyping in the proper diagnosis of these entities, as discussed above. The T-cell lymphomas in the proposed WHO Classification (Table 5) are largely unchanged from the REAL (Table 4). Hepatosplenic gamma-delta T-cell lymphoma and subcutaneous panniculitis-like T-cell lymphomas have moved from provisional to fully accredited disease entities, and ALCL-Hodgkins like has been dropped given lack of evidence that it is a real entity. Angiocentric lymphoma has been changed to extranodal NK/T-cell lymphoma, nasal type, to reflect its lack of angiocentricity in some cases, and its apparent NK-cell origin. Specific conclusions and recommendations regarding anaplastic large cell lymphoma and NK/T-cell lymphomas will be discussed in the section on lymphoma immunophenotyping ahead.
Hodgkin's Disease
In the years since the publication of the REAL Classification, Hodgkin's disease has moved from a tumor of uncertain histogenesis to a neoplasm now felt to be of B-cell origin in the vast majority of cases. Hodgkin's disease is apparently unique among B-cell neoplasms in being derived from germinal center B-cells with non-productive immunoglobulin gene rearrangements, apparently representing failed attempts at B-cell antibody production. Under normal circumstances, such cells undergo apoptosis in the germinal center, and the mechanism by which Reed-Sternberg cells escape cell death remains a mystery. The interested reader is referred to several excellent reviews of this fascinating subject.
Hodgkin's disease was recognized many years ago to consist of two very different entities. Nodular lymphocyte predominance Hodgkin's disease (NLPHD) is a mature B-cell neoplasm that routinely expresses CD45, B-cell antigens, and surface immunoglobulin, and which displays a characteristic nodular architecture and minimally pleomorphic, lobated, "popcorn-like" Reed-Sternberg variants that are generally CD30 and CD15 negative. NLPHD typically follows a very indolent clinical course. Non-lymphocyte predominance forms of Hodgkin's disease (also termed "classical Hodgkin's disease" or CHD) contain highly pleomorphic classical Reed-Sternberg cells, which are generally CD30 and CD15 positive, and are usually CD45 and T-cell/B-cell antigen negative. The 1994 REAL Classification subdivided classical Hodgkin's disease into nodular sclerosis, mixed cellularity, lymphocyte depletion, and lymphocyte-rich classical types (the last category serving largely to distinguish cases of classical Hodgkin's disease with large numbers of background lymphocytes from the very different NLPHD (Table 6).
What's New in the WHO: Hodgkin's Disease
In the proposed WHO Classification, Hodgkin's disease is largely unchanged from the REAL, except for the conversion of the "provisional" category of lymphocyte-rich CHD to a permanent one. Because of the accumulated evidence of B-cell origin, pathologists on the WHO Committee recommended a name change from Hodgkin's disease to Hodgkin's lymphoma. Because of resistance from some committee members concerned about possible confusion with non-Hodgkin's lymphomas, the recommendation was made to permit both terms as acceptable synonyms for the time being. The Committee also recommended that criteria for grading nodular sclerosis Hodgkin's disease (NSHD) be clearly stated in the final document, given that some studies have demonstrated a better prognosis for grade 1 (few RS cells) vs. grade 2 (many RS cells) NSHD. The committee recommended that such grading not be required for clinical purposes in routine diagnosis, but clear criteria may permit better study of the significance of grade in the future.
3. Aisenberg AC: Primary large cell lymphoma of the mediastinum. Semin Oncol 1999 26: 251-8 (1999).
5. Cesarman E; Chang Y; Moore PS et al.: Kaposi's sarcoma-associated herpesvirus-like DNA sequences in AIDS-related body-cavity-based lymphomas [see comments]. N Engl J Med 1995 332: 1186-91 (1995).
10. Delecluse HJ; Anagnostopoulos I; Dallenbach F et al.: Plasmablastic lymphomas of the oral cavity: a new entity associated with the human immunodeficiency virus infection. Blood 1997 89: 1413-20 (1997).
22. Jaffe ES; Harris NL; Chan JKC et al.: Proposed World Health Organization Classification of neoplastic diseases of hematopoietic and lymphoid tissues. Am J Surg Pathol 1997 21: 114-121 (1997).
37. Mann RB; Berard CW: Criteria for the cytologic subclassification of follicular lymphomas: a proposed alternative method. Hematol Oncol 1983 1: 187-92 (1983).
41. Rappaport H: Tumors of the Hematopoietic System (Armed Forces Institute of Pathology, Washington, D.C. 1966).
44. Tindle BH: Malignant lymphomas. Am J Pathol 1984 116: 119-74 (1984).
45. Walts AE; Shintaku IP; Said JW: Diagnosis of malignant lymphoma in effusions from patients with AIDS by gene rearrangement. Am J Clin Pathol 1990 94: 170-5 (1990).


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Will Daniel Craig really make eight James Bond films total?
Five more movies with Daniel Craig.
That's the dream of the producers of the James Bond franchise, anyway, as revealed in a recent Michael Wilson interview with The People, a London-based newspaper. He's apparently very happy with the way "Skyfall" is coming together, and he's ready to start pinning down the star of the series for a truly epic eight total films as James Bond.
That means he'll do as many movies as the character as there were in the entire "Harry Potter" series. As someone who was thrilled by "Casino Royale" and who loves certain things about "Casino Royale Part 1 and a Half," it's exciting to think about what sort of narrative opportunity there is if they're now aware that they've got five movies to play with.
Let me ask something of EON now, though. If they're really going to do this, and Craig agrees, and they gear up for a mad dash through five films, which could take as long as eight to ten years to pull off, then please tell me that there will be some real continuity with real consequences for Bond.
I was not there when "On Her Majesty's Secret Service" was released, but I can only imagine the audience reactions to the end of the movie. I wish I could have had that pop culture moment, and I think it packs a punch even removed from its moment. James Bond finally had something taken away from him, and it made him cold and ambitious in hunting down everyone responsible. It gave him a main villain or organization to chase.
They've already shown that there is real continuity between the two movies Craig has starred in, but they should push it further. I feel like they've already set things in motion, and now they're getting ready to really pay it off.
I'm excited that they're excited. To me, that's what the Bond franchise needs… energy. That's what made "Casino Royale" such a breath of fresh air. It felt like everyone involved was determined to get it right. And by all accounts, Craig is very vocal about what he expects on these films. He's one of the reasons that you've got Sam Mendes onboard directing the new one, and I'm thrilled to see EON stepping up with at least some sort of game plan.
"Skyfall" will arrive in theaters November 9, 2012.


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Special programmes were conducted by various organisations in observance of the International Day of Older Persons here on Monday.
A programme that had been organised in this regard by the Federation of Senior Citizens' Association Kerala was inaugurated by former Supreme Court judge K.T. Thomas. In his inaugural address, Justice Thomas called upon the senior citizens to adapt as much as possible to the gradual changes being witnessed in society. He also said efforts must be made by the section to contribute to society in their own ways.
Delivering the keynote address, Home Minister Thiruvanchoor Radhakrishnan said the government was committed to providing security to the elderly in the State. The Care, Aid and Relief for Elders (CARE) scheme of the Kerala Police has been initiated as part of such efforts. The security net will soon be expanded to be able to provide enhanced protection for senior citizens.
The inmates of the Santhi Bhavan, an old-age home, were felicitated at a function organised by Bipha Ayurveda in association with Kottayam (West) Janamaithri Police. All the 76 inmates of the facility were provided with kits containing traditional attires.


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FOR IMMEDIATE RELEASE Thursday, April 25, 2013
WHAT: An atomic-level snapshot of a respiratory syncytial virus (RSV) protein bound to a human antibody represents a leap toward developing a vaccine for a common—and sometimes very serious—childhood disease. The findings, by scientists from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, define the vulnerable shape of a critical RSV component called the fusion glycoprotein.
The NIAID scientists determined the fusion glycoprotein's shape as it appears before its interaction with human cells. It is this pre-fusion shape that is most vulnerable to neutralizing antibodies. Progress toward an RSV vaccine has been stalled in part because researchers did not previously know about a highly vulnerable site at the tip of the pre-fusion form of the fusion glycoprotein. Now that the structure has been solved and the site of antibody vulnerability revealed, scientists can use the new structural information to design vaccines capable of eliciting potent antibodies aimed at the target on top of the pre-fusion state of the glycoprotein.
Almost everyone is infected with RSV before turning three years of age. Most children recover quickly from such symptoms as sneezing, runny nose and cough, but the virus is a leading cause of hospitalization in children under age one. In the United States each year between 75,000 and 125,000 children in this age group are hospitalized with RSV infection. Globally, RSV infection accounts for nearly 7percent of deaths among children between the age of one month and one year. The only drug available to prevent severe RSV illness is a monoclonal antibody, palivizumab, which binds to the RSV fusion glycoprotein. In their study, the NIAID researchers showed how three antibodies that potently neutralize RSV all bind to the newly revealed site on the fusion glycoprotein of RSV. Thus, in addition to new clues for vaccine developers, the NIAID findings also provide a structural basis for how these antibodies neutralize RSV. This insight could accelerate development of these antibodies into therapies to treat or prevent severe RSV disease in very young infants, who are the most vulnerable to serious illness.
ARTICLE: JS McLellan et al. Structure of RSV fusion glycoprotein trimer bound to a prefusion-specific neutralizing antibody. Science DOI: 10.1126/science.1234914 (2013).
WHO: NIAID Director Anthony S. Fauci, M.D., is available for comment. NIAID researchers Barney S. Graham, M.D., Ph.D, and Peter D. Kwong, Ph.D., NIAID Vaccine Research Center, are also available to comment on their paper.
CONTACT: To schedule interviews, please contact Anne A. Oplinger, (301) 402-1663, email@example.com.
NIAID conducts and supports research—at NIH, throughout the United States, and worldwide—to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID website.
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.
NIH...Turning Discovery Into Health ®
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Last Reviewed April 24, 2013


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MUSE v03
MUSE v03 has been released, get it from the usual place. Changes are: Envelope and arpeggio updates are skipped when NTSC_MODE is enabled. Changed all references from Pornotracker to Musetracker. Added separate SPEED_COMPENSATION and NOTE_FREQ_COMPENSATION flags. Added PAL_MODE and DENDY_MODE flags.
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Pornotracker v1.3
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I've worked a lot on Pornotracker since the v1.2 release, next version may come out pretty soon. Here are some of the changes/additions: FamiTone text export. FamiTone is a relatively lightweight NES music replayer that can be used in games … Continue reading
Pornotracker v1.2
Pornotracker v1.2 has been released. New features: Configuration file OpenGL rendering Fine tune envelope Note cut effect Auto delay effect
Keri Hilson – I Like NES Cover
Spammmmmm, forgot to post this earlier. Here's a new NES cover of a pop song that I made. Be sure to use 720p for the best audio quality. PAL NSF:
Rude Boy NES cover (vocal edition)
Here's a vocal edition of the Rude Boy 8-bit cover that I posted about 6 months ago. You can also grab the MP3 HERE.
Pitch envelope in Pornotracker
Added fine-tune aka pitch envelope to Pornotracker instruments, not yet released. I might add FamiTone support (i.e. text file export) next.
Pornotracker v1.1 BETA
Added Pornotracker v1.1 BETA download link here. Or you can download it directly from here. Quote from README.txt: This is a BETA version! If something doesn't seem to be working right, please let me know! I still have some optimizations … Continue reading


text:
EAGLE open XML format for schematics, PCBs
CadSoft is developing new open, XML-based file formats for the Eagle schematic and PCB editor. This means easier version control, something we gripped about earlier today, and better interoperability among CAD applications.
The CadSoft EAGLE development team is developing a new format for schematic, layout and parts libraries that is XML, this means every object and line will be written out in text description.
This will be a fully documented format and also of course a converter for old CadSoft EAGLE binary-type formats
You won't have to worry about binary file corruption, you will be able to hand-edit or generate schematics and layouts and of course the magic of version-control (such as github) will be easier than ever with real text 'diff's!
Discussion is happening here, thanks Folknology!
Via Adafruit.
This entry was posted in News and tagged Cadsoft Eagle, XML format.Comments
You should include a link to the discussion also:
Al -
To change internal format to xml (or other) not need develop application. Only 2 procedure – Open and Save. So it not a big job.


text:
WHITEHALL -- They sniffed, poked, nibbled and even gobbled.
The first- and second-graders at Whitehall's Shoreline Elementary had varying reactions to the samples of roasted cauliflower handed out in their lunchroom recently.But in the end, a majority announced the vegetable "awesome."
It was a small victory for the food staff at Whitehall District Schools who have been trying to get elementary school students to try, and hopefully like, veggies.
Each week, food service workers are having students at Shoreline, as well as the district's third- through fifth-graders at Ealy Elementary, taste test a different vegetable, such as mashed sweet potatoes, parmesan broccoli or raw green beans.
"We want to expose them to different vegetables and different tastes," said Dan Gorman, food service director for the school district. "We're trying anything to get kids to try vegetables. That's always the challenge."
"Taste It Tuesdays" at Ealy and "Taste it Wednesdays" at Shoreline have become popular with students who compete with each other to see which class can get the most students to at least try the vegetables. Last week, 78 percent of the Ealy students and 70 percent of the Shoreline students tasted the cauliflower and were asked to rate it "yuck," "OK" or "awesome."
Getting them to taste the vegetable is much of the battle, said Laura Neal, a college intern working in the food service department who has been heading up the veggie project.
"A lot of them like it even though they didn't think they'd like it," Neal said.
Nearly 80 percent of the Shoreline taste testers and 70 percent of those at Ealy pronounced the cauliflower awesome, compared with 15 percent and 14 percent, respectively, who decided it was yuck. Fewer still decided it was just OK.
"I didn't think I'd like it," said second-grader Jack Adams, who was among those who decided cauliflower was awesome.
It took a lot of convincing for first-grader Kaitlyn Varela to take a bite of the cauliflower. Cafeteria helper Zach Milliron tried to bribe her with a quarter, but Kaitlyn repeatedly refused, suspiciously eyeing the contents of the sample cup. Finally, the tiny girl relented, took a bite and announced "It tastes good!"
When asked why she was so hesitant, Kaitlyn, clutching the shiny quarter from Milliron, said "because when I licked it didn't taste so good."
Neal said she's puzzled why many children have such a negative attitude about vegetables, especially when infants typically enjoy vegetable baby food.
"I don't know what happens, if they hear vegetables are bad or what," Neal said. "I think a lot of it is the way they're prepared."
She and Gorman said parents need to keep trying different vegetables with their children, and to try different methods of preparation. It helps to get children to try a food if they are included in the preparation of it, Neal said.
Often, Neal said, children prefer raw veggies, especially if they can dip them in a low-fat dressing. Vegetables out of a can can be mushy and not appealing to young ones, she said.
That seemed to be the case with the district's experiment with mashed sweet potatoes, which came out of large cans. Fewer than half the elementary students who tried the potatoes said they were awesome.
According to the U.S. Department of Health and Human Services, only 21 percent of young people eat the recommended five or more servings of fruits and vegetables each day, and nearly half of all vegetable servings are fried potatoes.
Gorman said he is hoping to make eating vegetables a "habit" for children.
"We hope we can grow vegetable-eaters," he said.
But he knows from personal experience that can be tough to do, explaining children are good at "wearing you down" by constantly refusing vegetables. In his own household, he has a rule that his children must at least try the vegetable on their supper plates, but his 12-year-old son still turns his nose up at them.
"He's been eating vegetables for 12 years and he still doesn't like them," Gorman said. "He still makes faces."
That wasn't the case with Shoreline second-grader Leah VanAntwerp, who eagerly gobbled down her sample of cauliflower and then vigorously nodded her head, saying "it's really good."
"My grandma makes it with the same ingredients," Leah said. "It tastes the same."
Each Friday, the vegetable the Whitehall students tried on the previous Wednesday is offered as a choice with their hot lunch. The other vegetable choice is a salad bar.
"The real test is when we serve it on Friday," Gorman said. "Will they take it on their plate?"
E-mail Laura Moore: firstname.lastname@example.com