text:
Filip Mlody

Hi there!

Happy you found your way to my blog. I’m not very regular with my posts but when the inspiration strikes me I’m writing about marketing automation, hacking your company’s growth, business books and events.

Marketing Automation and Inbound Marketing Expert in B2B SaaS

Few Facts:

  • Head of Marketing Automation at Xero (ranked as #1 at Forbes’ “Most Innovative Growth Company” in 2014 and 2015)
  • Led the marketing automation effort at Mimecast and Xero
  • Part of the team that received the Marketo 2017 Revvie Globetrotter Award for Most Successful Global Rollout with Xero – while on the position of Marketing Automation Manager in the Global team
  • One of the first hires in the original team that built Dasdak, a Washington, DC based startup with Tracy McGrady (7 time NBA All Star) as an investor and Reggie Love (former personal aide to former US President, Barack Obama) as an adviser
Reggie, Filip, Tmac
Reggie, Filip & T-Mac

Filip Mlody Marketo Certified Expert

I’m writing for people who have 10 minutes to read about marketing and business. Some posts are for advanced players, some for newbies and some just for fun. All are the results of my successes and failures.

For fun I:

  • Read Books
  • Travel
  • Go to the gym
  • Hang out with my close friends
  • Learn ever more about marketing

See my full professional experience on my LinkedIn profile.

Let me know if you think I could help you:

One thought on “Filip Mlody

Leave a Reply

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out /  Change )

Google+ photo

You are commenting using your Google+ account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s


Content-Type: application/http; msgtype=response

WARC-Identified-Payload-Type: text/html

WARC-Type: response

text:
Video Sources 29010 Views

  • Watch From Server 1
  • Watch From Server 2
  • Watch trailer
Devdas (2002)

Devdas (2002)

Jul 12, 2002 India 185 Min.
Your rating: 0
6.5 64 votes
what going on?

Watch Devdas (2002) Full Movie Online, Free Download Devdas (2002) Full Movie, Devdas (2002) Full Movie Download in HD Mp4 Mobile Movie. Devdas is sent away by his father so he can improve himself but upon his return his father still doesn’t welcome him back. Devdas and Paro are in love but Paro is a lower caste and is set to be married to an older widower. Devdas is devastated & leaves home. He becomes an alcoholic womanizer and falls in love with a courtesan. Paro tries to get Devdas away from drinking before he self destructs.

Devdas (2002)
Devdas (2002)
Devdas (2002)
Devdas (2002)
Devdas (2002)
Devdas (2002)
Original title Devdas
IMDb Rating 7.6 29,787 votes
TMDb Rating 7.4 votes

Shah Rukh Khan isDevdas Mukherjee
Devdas Mukherjee
Madhuri Dixit isChandramukhi
Jackie Shroff isChunnilal ("
Chunnilal ("
Smita Jaykar isKaushalya Mukherjee
Kaushalya Mukherjee
Manoj Joshi isDwijdas Mukherjee
Dwijdas Mukherjee
Ananya Khare isKumud Mukherjee
Kumud Mukherjee
Kirron Kher isSumitra Chakraborty
Sumitra Chakraborty

Similar titles

Mr Perfect (2011) Hindi Dubbed
Melancholia (2011)
Iqbal (2005)
Romance Complicated (2016)
Sirf Tum (1999)
Christmas at Holly Lodge (2017)
Bal Ganesh (2007)
The Only Living Boy in New York (2017)
Phir Hera Pheri (2006)
Kill the Messenger (2014) Hindi Dubbed
Theeram (2017)
Yeh Faasley (2011)

warcinfo:
isPartOf: CC-MAIN-2018-39
publisher: Common Crawl
description: Wide crawl of the web for September 2018
operator: Common Crawl Admin (info@commoncrawl.org)
hostname: ip-10-45-127-147.ec2.internal
software: Apache Nutch 1.15 (modified, https://github.com/commoncrawl/nutch/)
robots: checked via crawler-commons 0.11-SNAPSHOT (https://github.com/crawler-commons/crawler-commons)
format: WARC File Format 1.1
conformsTo: http://iipc.github.io/warc-specifications/specifications/warc-format/warc-1.1/


text:
U.S. Markets closed

Anna Faris doesn't seem to care for the 'SNL' impression of her

Anna Faris dropped by Watch What Happens Live with Andy Cohen Thursday night, where she responded to a question about what she thought of Abby Elliott’s impression of her on Saturday Night Live. Faris seemed at a loss for words at first but then did an impression of Elliott doing an impression of her.

“Apparently I have a really breathy voice,” Faris said as Elliott as Faris.

Elliott left SNL in 2012, so it has been quite a while since she did her impression of Faris. But the portrayal always made the actress look less than intelligent, so who can blame Faris if the wound still smarts?

Faris said, “I guess, you know, I don’t know. There’s, I don’t know. There’s a worse impression. But no — I loved it?” “That’s the right answer,” Cohen replied.

Watch What Happens Live with Andy Cohen airs Sundays through Thursdays at 11 p.m. on Bravo.

Watch Ellen confront Kate McKinnon about her SNL impression:

Read more from Yahoo Entertainment:

Tell us what you think! Hit us up on Twitter, Facebook, or Instagram — or leave your comments below. And check out our host, Kylie Mar, on Twitter, Facebook, or Instagram.


text:
U.S. Markets closed

Masters 2018 odds: Tiger Woods remains one of the favorites

As the Masters comes into view, we’re getting our last look at who the oddsmakers like to win a green jacket … and who the oddsmakers believe bettors will like, too. Tiger Woods, back in the field for the first time since 2015, jumped from 100-1 odds just a few months ago right to the top of the list in recent weeks … an indicator not just of Woods’s resurgence, but of bettors’ willingness to throw money Tiger’s way.

Now that we’ve had a bit of time to watch Woods in action, as well as his competition, though, the stakes have shifted just a bit. Woods has fallen behind two recent champions, Rory McIlroy and Bubba Watson, as well as the No. 1 and No. 2 players in the world in Dustin Johnson and Justin Thomas.

Yet Woods, who hasn’t won at Augusta since 2005 and hasn’t won anything anywhere since 2013, still somehow comes in ahead of Jordan Spieth, Rickie Fowler, and Justin Rose, among many, many others. That’s less a testament to Woods’s playing ability than Vegas’s need to hedge itself against astronomical odds on a popular betting figure, but even so: Woods wouldn’t be drawing enough action to move the lines this much if he weren’t playing some respectable golf.

The complete odds as of Monday, via BetDSI and CBS Sports:

• Rory McIlroy: 19-2
• Bubba Watson: 10-1
• Dustin Johnson: 11-1
• Justin Thomas: 11-1
• Tiger Woods: 12-1
• Jordan Spieth: 13-1
• Phil Mickelson: 15-1
• Rickie Fowler: 35-2
• Justin Rose: 25-1
• Alex Noren: 25-1
• Paul Casey: 27-1
• Hideki Matsuyama: 27-1
• Jason Day: 30-1
• Jon Rahm: 30-1
• Sergio Garcia: 31-1
• Tommy Fleetwood: 38-1
• Henrik Stenson: 38-1

Regardless of how Woods finishes out this week, it’s clear he’s still got drawing power. And since we’re not likely to see anything like him ever again, you can see why fans are lining up to throw a few bucks behind his name. If he comes up big, it’ll be one of the finest stories in sports … and one of the most profitable, too.

Justin Thomas (center) is one of the few golfers with better odds at Augusta this week than Tiger Woods. (Reuters)

Jay Busbee is a writer for Yahoo Sports. Contact him at jay.busbee@yahoo.com or find him on Twitter or on Facebook.
More from Yahoo Sports:
Pete Thamel: Can Condoleezza Rice save college basketball?
Twins not happy with Oriole rookie’s bunt
Dramatic finish in NCAA women’s title game
Pat Forde: How Jay Wright transformed Villanova


text:
U.S. Markets closed

Paul Tudor Jones warns the next recession will be 'really frightening'

Legendary global macro trader Paul Tudor Jones is warning that asset prices are too high. Furthermore, he’s concerned about what the next recession might look like. He shared his thoughts on Monday during a conversation with Goldman Sachs CEO Lloyd Blankfein as part of the firm's Talks at GS series.


text:
U.S. Markets closed

Toni Kroos' stoppage-time wonder strike rescues World Cup hopes for Germany

For most of Saturday’s match against Sweden, defending World Cup champion Germany’s hopes of repeating appeared to be hanging by a thread. But a full five minutes into stoppage time, midfielder Tony Kroos stepped up to a free kick deep in Sweden’s end and curled his right footed shot past keeper Robin Olsen, the 2-1 victory vaulting Germany into second place in the Group F behind Mexico.


text:
Boys Varsity Basketball · Boys Varsity Basketball beats Franklin Central 59 – 58

W 59 Fishers High School
58 Franklin Central High School
Away   Home
Away Home
Fishers High School vs Franklin Central High School
59 58
1 13   9
2 13   9
3 8   10
4 14   20
OT1 11   10

The Tigers Varsity Boys Basketball team was in action last night to face the Franklin Central Flashes. In the 1st quarter, the Tigers picked up where they left off from the night before. The Tigers led 13-9 in the quarter. In the 2nd quarter, the Tigers expanded their lead and went into halftime with control of the game. FHS was ahead at the half 26-18. In the 3rd quarter, Franklin Central made their adjustments and fought their way back into the game. Franklin Central cut the Tigers lead to six points. The Tigers were still in control at the end of the 3rd quarter with the lead 34-28. In the 4th quarter, the Flashes continued to battle their way back into the game and tied the score 48-48 at the end of regulation. In overtime, both teams battled back and forth to take control of the game. With the Tigers down two points, FHS Terry Hicks knocked down a late 3-point shot to seal the victory for the Tigers. The Tigers beat Franklin Central with a final score of 59-58. Josiah Matthews led the Tigers in scoring with 14 points. Willie Jackson had 11 points and 4 rebounds. Terry Hicks chipped in with 9 points and 8 rebounds. Alex Szilagyi added 8 points and 3 rebounds. Jeremy Szilagyi had 6 points. The Tigers are now 10-9 on the season and 2-3 in conference play. The Tigers are back in action at home to face conference opponent the Zionsville Eagles on February 16th with a 7:30 pm tip-off.


text:
Skip to main content
Parker Wins Houston Mayoralty

Democrat Annise Parker won yesterday’s run-off election for the Houston mayor’s seat. Here is Bloomberg reporter Darrell Preston’s report early this morning, in its entirety:

Dec. 13 (Bloomberg) — Houston voters chose Annise Parker to replace Bill White as the next mayor of the fourth-largest U.S. city by population.

Parker won by a margin of 53.6 percent to 46.4 percent for Gene Locke, according Harris County election data. Parker, 53, is in her third term as city controller. Locke, 62, is a Houston attorney and former chief of staff for U.S. Representative Mickey Leland.

White isn’t running after serving the limit of three terms. He has been at odds with Parker about the size of the deficit in the city’s budget. Parker said the city faces a $103 million revenue shortage, while White put the potential gap at $25 million after a series of cost reductions.

Parker and Locke were forced into a runoff in November after Parker won 31 percent of the vote and Locke won 25 percent, according to the city secretary’s office. Two other candidates, Peter Brown, a city councilman, and Roy Morales, a retired air force officer, were eliminated in the primary.

Parker served on the city council for six years and worked in the oil and gas industry for 20 years.

Houston’s mayoral candidates don’t run as representatives of any political party.

I make a point of saying the article was reproduced in full because you’ll notice nowhere does it say that Parker is a lesbian. That fact distinguishes her as the gay candidate to win the mayoralty of the largest American city to date. (Openly gay, that is; see: Koch, Edward.) If you are cheered by what her election demonstrates, as I am, you may be further cheered that a major news wire service needn’t mention the fact of her orientation–a testament to the progress we’ve made as a nation on this count.

Now, many other reports during the campaign mentioned or discussed Parker’s sexual orientation. And there were last-ditch efforts by anti-gay groups to cite her orientation as an electoral disqualifier. But still, this is progress. Though we may have to qualify the victory as a result of a run-off between two Democrats, the other of whom is an African American, Houston is not San Francisco.

Parker’s win may also testify to the power of people voting their pocketbooks despite attempts to distract them with divisive, culture-war politics. Because the run-off between Parker and Gene Locke divided Democrats, with white liberals favoring Parker and black Democrats favoring the African American Locke, as the New York Times surmised on the eve of the run-off, the race would therefore be decided by less liberal whites.

“White liberal Democrats are behind Parker, and African-Americans are going to go with Locke” said Marc Campos, a consultant to the Locke campaign. “Moderate Republicans, fiscal conservatives — they’re going to be the ones who decide this.”

One open question is whether conservatives will come out to vote against Ms. Parker because she is a lesbian, strategists said. The dynamics of the race mirror the vote against same-sex marriage last year in California, in which black voters joined with conservatives to approve the ban, some political scientists say.

But Ms. Parker’s sexuality was not an issue in the election, and it is unclear how much impact the anti-gay groups have had.

Richard W. Murray, a political scientist at the University of Houston, said the turnout among blacks, which was low in the general election, might be critical. To offset Ms. Parker’s apparent advantage among white liberals, Professor Murray said, Mr. Locke needs a large turnout by blacks, a majority of whom supported him in November.

“Virtually all the white Democrats are going to Parker, and she’s very competitive among Republicans,” Professor Murray said. “Locke is particularly behind the eight ball unless there is robust black voting.”

But even if black turnout in the run-off was low, had the lion’s of moderate-to-conservative Republican votes gone to Locke, Parker couldn’t have won. Yet she did.

Now, I suppose the dimmer, alternative view is that whites would rather vote for a white lesbian than a straight black man. But I’ll opt for the more comforting conclusion, which is that Houston does not have a problem with being represented by a gay mayor.


text:
Nostradamus: The Last Prophecy Crack

Nostradamus: The Last Prophecy Nostradamus: The Last Prophecy is set in 16th century Provence, in a country ravaged by religious wars and devastated by the plague. It has been three years since Catherine de MГ©dicis' rule as regent came to an end, but she still holds the reins of power, making her the target of repeated attacks from the French nobility. One day in March 1566, when she realises that she has fallen victim to a terrible curse, she turns to her doctor and astrologer, Michel de Nostre-Dame, better known as Nostradamus. Unfortunately, the famous prophet is too old and weak to take on such a mission alone. Refusing to abandon his queen in her hour of need, he sends his daughter Madeleine in his place. However, there is no such thing as women astrologers, let alone women doctors in medieval times. To be accepted as such, the young woman must go in disguise and assume her younger brother's identity, CГ©sar, who is away for some time. Alternating between Madeleine the young woman and Madeleine disguised as CГ©sar, players are plunged into a thriller where political scheming and ancestral prophecies are intertwined. The game begins as an initiatory adventure in the footsteps of her father, the prophet and astrologer, before creating all the suspense of a detective novel: from one murder to another, players make their way through a test-riddled forensic investigation. [Kheops Studio]

Download Nostradamus: The Last Prophecy Crack & Serial

how to download
Platform PC
Our rating
71 / 100
User rating 5.9
Downloads 517
Genres Adventure, General
Encore Software, Inc. , MC2 Entertainment
Developer Kheops Studio


text:
For Excellent Service

Kevin Fleming has worked in the construction business for 29 years. Kevin brings a diverse background after working in several areas of the construction industry, including a small carpentry business and a major development company. Kevin’s business degree helps to provide a clear understanding of the entire project up front. His use of technology keeps the customer continually up-to-date on the progress of their projects.

What Our Customers Are Saying

Read More
Kevin Fleming has been in my employ on several occaasions in the last year as an independent contractor and has proven himself to be a capable resourceful, and reliable business person. Kevin has been required to attack tasks that would challenge any carpenter in the restoration and renovation of my 115 year old home. He has successfully completed jobs that require adapting new construction methods to replace or repair the old and he always ends up with a product which is tastefully done. These jobs are completely executed by Kevin, from contract to receipt. Many of the elements of these jobs have required that he be very innovative in order to integrate the restorations into the existing structures in a harmonious manner. Kevin has proven to be exceptionally reliable and honest in our dealings. His word is as good as a contract, which he always fulfills completely. I have complete confidence in his integrity.
Bill Harmon
I actually found Kevin from Houzz.com. After an unexpected flood that destroyed my basement, Kevin was a welcome breath of sunshine. He was very communicative, helpful, and thorough when he arrived to complete a free estimate for the job. Not only did Kevin answer questions before I could ask them, he understood personal extenuating circumstances such as budget, a baby due in a few weeks. He was able to schedule and complete our job in the exact time frame he detailed. He also went above and beyond to negotiate prices with our insurance adjuster. Sean and Bryan, the two men who worked on our home, were incredibly trustworthy, reliable, and clean. They worked every day tirelessly to complete the job on time. They were polite and willing to answer all of my questions. I cannot speak highly enough of Fleming Construction. They did wonderful, timely work and were a pleasure to work with.
Rebecca Lory

Recent Projects

Providing Excellent Service since 1989 and … still loving what we do!

View Our Work
Helping Customers

Transform or Build Their Home

Kitchen Remodel

Custom Built Home

Ready to Start Your Next Project?

At Fleming Construction Services, we will help you achieve the look of your dreams, from the smallest to the most complex jobs.

Get in Touch


text:
Narrow Way Chronicles: Exclusivity of Inclusion

In a recent tweet I shared:

#Pride, #Presumption, and #Partiality create a culture of self-righteousness and hidden agendas. #churchpolitics”.

I thought it appropriate to elaborate because intent can be misconstrued and I wanted to allow for robust discussion.

Today, the term “inclusivity” does not prompt ideas of church unity. Opponents of the Way continue to do a “bang-up” job in hijacking and perverting the Creator’s intent on certain ideologies that is designed to reflect His glory. The ideology of “Inclusivity” is no different. History teaches that diversity and inclusivity have existed since the beginning of time. The Old and New Testament scriptures clearly show examples of communities that included all races and social-economic backgrounds.  It is only after the coming of the Anointed One, Jesus the Christ, do we see intentionality of this idea of Inclusive Communities. ….so let’s not get it twisted. ;-).

The intention of the tweet; however, was addressing my limited time and experience with the subject with regard to church unity. My sincere hope and prayer is that the Holy Spirit will be active in guiding my hand to write; as well as an active guide to those who are reading these thoughts.

It is written, He who has an ear, let him hear what the Spirit says to the Churches:

This is the message we have heard from him and proclaim to you, that God is light, and in him is no darkness at all. If we say we have fellowship with him while we walk in darkness, we lie and do not practice the truth. But if we walk in the light, as he is in the light, we have fellowship with one another, and the blood of Jesus his Son cleanses us from all sin. If we say we have no sin, we deceive ourselves, and the truth is not in us.  If we confess our sins, he is faithful and just to forgive us our sins and to cleanse us from all unrighteousness. If we say we have not sinned, we make him a liar, and his word is not in us.

Compassion and True Fellowship

The issue: Are our churches TRULY inclusive? With our drive to expose evil, false doctrine and plant churches, have we created a culture of elite communities? Is the mission still about the Gospel or has the mission become about growing a denomination, positioning for political leverage or making your brand known? Do we reflect true Koinonia or is the local church another social construct that is intended have a “positive” effect on the community? If true Koinonia is the intent, what should it look like and how much of our application is modeled biblically?

I have often been engaged in conversations with persons that boastfully share that they are socially connected with”like-minded” Believers. Notice I didn’t say, fellowship; and, that gave me pause to think (Hence the #ChurchPolitics).

What does the idea of being like-minded mean?

Secular society uses this phrase often. Should I assume that this idea takes on a different connotation because I perceive a spin of conservative Christianity or It is safe to assume that being like-minded is a belief or series of beliefs that is shared commonly through a connection of cultural norms to one may be accustomed; and if not accustomed, Idolize?  We’ve seen this in Charismatic circles.

It is elitism; BKA partiality.

If you initiate a Google search the topic, you will find little teaching or exhortation that addresses this, especially in conservative circles. Largely because most of our siblings still have that big plank in their eye.

Partiality is a sin and it greatly displeases Elohim our God. Because it is hidden, it is easy to deny that we have issues. When we choose to “do life” with people that do not foster sanctification, we stifle growth. Not only of ourselves but others that desire true sanctification.  Jerry Bridges exhorts: “It is not the fact that we are united in common goals or purposes that make(s) us a community. Rather, it is the fact that we share a common life in Christ.

Partiality convinces us that God’s choice isn’t good enough, smart enough, pretty or handsome enough, not quiet enough, or charismatic enough. Partiality says this person is not acceptable to my standards. Partiality shows no grace and therefore, shows no love. This is wickedness.

When we opt in for partiality instead of inclusivity we become complacent in our relationships. We are not intentional with the put offs and put-ons, and we do no “one anothering”.  The result is isolation among the saints. This is a dichotomy of true fellowship. Koinonia and sharing the Gospel is what the Father wants and desires for His children. Lastly, partiality is hidden and presumptuous sins. Partiality is heinous and damaging to the Body of Christ.  In Psalm 19:13 the writer prays:

Keep back your servant also from presumptuous sins; let them not have dominion over me! Then I shall be blameless, and innocent of great transgression.

The church is not as inclusive as we like to think we are. Partiality is a real issue, more than we would like to admit. People choose not to bind themselves to a local body because they do not feel loved or safe.  At any rate, Jesus teaches compassion. Though the Savior operated as a prophet, he was remarkably compassionate to sinners. Do we desire or display that same compassion or do we make assumptions about people based on limited information or gossip? Moreover, what are we willing to risk or sacrifice to engage in true Koinonia? If your local body struggles in this area please check out this teaching by Arturo Azurdia of TCP titled “The Antioch Paradigm”.

Why Prison Ministry IS Important

“Remember those who are in prison, as though in prison with them, and those who are mistreated, since you also are in the body”. (Hebrews 13:3 ESV)

As you read these accounts and thoughts of those returning back to our communities, may the Holy Spirit teach and reveal the true character of God….and…may you desire this attribute for yourselves. For judgment is without mercy to one who has shown no mercy. Mercy triumphs over judgment….Selah

 When the Son of Man comes in his glory, and all the angels with him, then he will sit on his glorious throne. Before him will be gathered all the nations, and he will separate people one from another as a shepherd separates the sheep from the goats. And he will place the sheep on his right, but the goats on the left. Then the King will say to those on his right, ‘Come, you who are blessed by my Father, inherit the kingdom prepared for you from the foundation of the world. For I was hungry and you gave me food, I was thirsty and you gave me drink, I was a stranger and you welcomed me, I was naked and you clothed me, I was sick and you visited me, I was in prison and you came to me.’ Then the righteous will answer him, saying, ‘Lord, when did we see you hungry and feed you, or thirsty and give you drink? And when did we see you a stranger and welcome you, or naked and clothe you? And when did we see you sick or in prison and visit you?’ And the King will answer them, ‘Truly, I say to you, as you did it to one of the least of these my brothers, you did it to me.’ (Matthew 25:31-40 ESV)

The first step …

The first step to true repentance is to overcome our natural, understandable resistance to finding ourselves at fault. If you could put your pride aside, what might you be prepared to admit, to apologize for, or to do differently? –Rabbi Debra Orenstein

Yom Kippur, the Day of Atonement, is the holy of holies of Jewish time. It is that rarest of phenomena, a Jewish festival without food. Instead it is a day of fasting and prayer, introspection and self-judgment when, collectively and repeatedly, we confess our sins and pray to be written into God’s Book of Life.


text:
Emotion questionnaires: Questionnaires on Emotional Functioning and Understanding
With respect to the following questionnaires we have either had responsibility for their development and validation or we have taken part in a similar process. The questionnaires described here have all been developed for and tested on children and adolescents from 9 to 15 years. In principle, there is no upper-bound age limit, but questionnaires for mood, non-productive thoughts, somatic complaints, emotion regulation and emotional intelligence already exist for older adolescents and adults.

For more information on the questionnaires, click on the menu on the right. Most of the questionnaires can be used freely; some can be downloaded from this website. If you want to print these questionnaires, make sure you print double-sided. This will produce a booklet.

If you have any questions regarding the questionnaires, please read the Frequently Asked Questions or e-mail This email address is being protected from spambots. You need JavaScript enabled to view it.. If you would like to obtain questionnaires that cannot be downloaded from this website, please email your request to Carolien Rieffe

International validation

Many of these questionnaires have been translated or are being translated into other languages. Farsi: Habib Nasiri , Shiraz University, Iran. Spanish: Lidon Villanueva, University Jaume I, Castello de la Plana, Spain, Italian: Marina Camodeca, University of Chieti, Italy. Urdu: Rabia Khawar GC University Faisalabad, Pakistan.


text:
Comparative Histomorphological Review of Rat and Human Hepatocellular Proliferative Lesions

Comparative Histomorphological Review of Rat and Human Hepatocellular Proliferative Lesions

View as PDF
Bob Thoolen, Fiebo J.W. ten Kate, Paul J. van Diest, David E. Malarkey, Susan A. Elmore, and Robert R. Maronpot
View as PDF

In this comparative review, histomorphological features of common nonneoplastic and neoplastic hepatocyte lesions of rats and humans are examined using H&E-stained slides. The morphological similarities and differences of both neoplastic (hepatocellular carcinoma and hepatocellular adenoma) and presumptive preneoplastic lesions (large and small cell change in humans and foci of cellular alteration in rats) are presented and discussed. There are major similarities in the diagnostic features, growth patterns and behavior of both rat and human hepatocellular proliferative lesions and in the process of hepatocarcinogenesis. Further study of presumptive preneoplastic lesions in humans and rats should help to further define their role in progression to hepatocellular neoplasia in both species.

liver, hepatocellular carcinoma, hepatocellular adenoma, large cell change, small cell change, foci of cellular alteration

Primary hepatocellular carcinoma (HCC) is the fifth most common cancer in the world and the third most frequent cancer-related cause of death with increasing incidence worldwide1,2,3,4. In addition, HCC is the most common primary liver malignancy in the world5,6,7. In the majority of cases, it is associated with hepatitis B or C viral infections, aflatoxicosis, and/or liver cirrhosis8,9,10,11. Other risk factors for developing HCC include alcoholic liver disease, nonalcoholic steatohepatitis, diabetes, and obesity12,13. Most patients with HCC are diagnosed at a late stage; therefore, the prognosis of HCC patients is generally very poor, with a 5-year survival rate of less than 5%7,14.

Experimental rat and mouse hepatocarcinogenesis models have been used for decades to delineate the pathogenesis of hepatic neoplasia. The rodent experimental model is used to identify potential human carcinogenic risk from exposure to drugs, environmental agents, and other xenobiotics. Rat hepatocellular adenomas (HCAs) and carcinomas are commonly used in tumor response and carcinogenicity bioassays and share some common features with human adenomas and carcinomas15.

In rat experimental models, presumptive preneoplastic foci of cellular alteration occur prior to the appearance of hepatocellular adenomas and HCC; however, there is experimental evidence that not all foci of cellular alteration progress to neoplasia and that some may actually regress16,17. Basophilic (BAS), eosinophilic (EOS), and clear cell (CLEAR) foci of cellular alteration in rats are the counterparts of human liver cell dysplasias classified as large cell change and small cell change. The detection of these presumptive preneoplastic lesions in humans may be indicative of progression towards HCC18,19,20,21 although further investigation is warranted. The purpose of this overview is to compare and contrast the morphological features of representative examples of commonly occurring human and rat hepatoproliferative lesions and to report the biology of these lesions.

Paraffin blocks of adult human cases were selected from the archives of the Departments of Pathology, University Medical Center Utrecht (UMCU) and Erasmus Medical Center Rotterdam, The Netherlands. These surgical specimens were reviewed and considered unequivocal examples of human focal nodular hyperplasias (FNHs), HCCs, HCAs, large cell change (LCC) and small cell change (SCC).

Paraffin blocks of rat cases obtained from the National Toxicology Program (NTP) archives were from studies of chemical-induced liver tumors and represent diagnoses peer reviewed by experienced rodent toxicologic pathologists. Rat cases include HCCs, HCAs and basophilic, eosinophilic and clear cell foci of cellular alteration (FCAs). FNH lesions were not identified as they are rare in rats. However, this lesion was included in humans since it is one of the most common human proliferative liver lesions.

Original slides from the human and rat cases were reviewed by a medical liver pathologist and two toxicologic pathologists and selected using published diagnostic criteria8,22,23,24,25,26 to confirm original diagnoses. Once confirmed, additional sections for this study were prepared, and all hematoxylin and eosin (H&E) staining was performed simultaneously at the UMCU after collection of all unstained paraffin slides on coated glass slides (e.g., Superfrost Plus) (see Table 1).

Table 1. H&E-stained Human (UMCU) / Rat (NTP) Liver Lesions

Human cases

1. Focal nodular hyperplasia (FNH)

Liver samples were derived from surgical excision (hemihepatectomy, partial liver resection or biopsy) of female patients (11/12; 92%) and one male patient (1/12; 8%) at the UMCU. The corresponding resection specimens included in the study for comparison, were grossly nodular and ranged in diameter from 2 to 17 cm. Microscopically, they had classical diagnostic features of FNH consisting of nodules composed of plates of hyperplasic hepatocytes that were two-cell layers thick and subdivided by fibrous septa (Fig. 1). Thick-walled arteries were present in the stellate scars and septa, and there were bile ductules typically located between the scars and the liver parenchyma (Fig. 2). Near the fibrous septa there were occasionally small immature cells with oval to fusiform leptochromatic nuclei and scant cytoplasm that resembled rat oval cells. In addition, transitional cells displaying characteristics of both hepatocytes and bile duct cells were also present in some samples. These results suggest the presence of “undifferentiated progenitor cells” within FNH and further suggests that the ductular reaction, at least partly, can be explained by activation of these cells27.

2. Hepatocellular carcinoma (HCC)

For the human samples, 14/16 HCC (88%) were from male patients. The morphological features consisted of a broad trabecular growth pattern of hepatocytes with occasional mixed growth patterns of trabecular/compact (Fig. 3), trabecular/acinar (Fig. 5) and sometimes a mixture of the three growth patterns. Hemorrhage, ischemic necrosis, neovascularization, angiectasis or peliosis hepatis and cystic changes were more commonly observed in these malignant tumors as compared to the other lesions evaluated.

3. Hepatocellular adenoma (HCA)

HCAs from female patients (n=15) had a maximum diameter of 16 cm. Histologically, they matched the common diagnostic criteria (see Table 2) for this benign liver neoplasm and sometimes showed focal to more diffuse steatosis, which can be observed in these tumors (Fig. 7)28,29,30.

Table 2.
Major Diagnostic Criteria for Proliferative Liver Lesions

Human cases (continued)

1. Liver cell dysplasia – large cell change (LCC) and small cell change (SCC) (human)

Large cell change: LCC (synonyms: large liver cell change (LLCC) or large liver cell dysplasia (LLCD)) has been described in detail by Anthony et al.31 and others24,32,33,34,35,36. Morphological features of hepatocytes with large cell change included cellular enlargement, nuclear pleomorphism with hyperchromasia, prominent nucleoli and occasional multinucleation. Enlargement was usually two- to three-fold and both nuclear and cytoplasmic with a normal nucleus to cytoplasmic ratio. Cytoplasmic staining was normal with occasionally more or less glycogen than that present in the surrounding liver parenchyma31. A classical example of such lesions is illustrated in Fig. 9. The selected cases of LCC (n=19) were all from 10 male patients.

Small cell change: SCC (synonyms: small liver cell change (SLCC) or small liver cell dysplasia (SLCD)) was characterized by small hepatocytes with a high nuclear:cytoplasmic (N:C) ratio. Cells were uniform and differed from cells of the surrounding parenchyma in terms of nuclear atypia and cytoplasmic staining. Fat or glycogen content sometimes differed from that in the adjacent liver parenchyma. These collections of cells with small cell change tended to produce more small round distinct foci with irregular margins similar to foci that are more closely associated with the HCCs (Fig. 11) as reported by others37,38,39. The selected SCC cases (n=17) were from 9 patients (7/9, 78% males and 2/9, 22% females). In the cases evaluated, combined areas of LCC and SCC could sometimes be observed within the same slide.

Rat cases

1. Hepatocellular carcinoma (HCC)

The HCCs reviewed, were from dosed males (3/15 HCC, 20%) and females (12/15, 80%). The morphological features were consistent with published HCC criteria26 and exhibited largely trabecular growth patterns, although mixed growth patterns (trabecular/acinar/solid) and occasionally basophilic and eosinophilic areas were present. In one case, the HCC arose within a hepatocellular adenoma and had an infiltrative growth pattern. A trabecular growth pattern with focal steatosis and mitosis is illustrated in Figure 4. As was seen in human HCCs, sometimes areas with acinar growth patterns were observed (Fig. 6). Most lesions evaluated also had hemorrhage, necrosis, pigment deposition (hemosiderin), angiectasis and/or focal fatty change.

2. Hepatocellular adenoma (HCA)

The selected hepatocellular adenomas (n=10) were from animals of both sexes (6/10, 60% females and 4/10, 40% in males). The histological features were compatible with the common diagnostic criteria (see Table 2). Sometimes, these adenomas also contained diffuse fatty change (steatosis) and angiectasis (Fig. 8).

3. Focus of cellular alteration (FCA)

Eosinophilic foci: Eosinophilic foci of cellular alteration consisted of polygonal enlarged hepatocytes with increased acidophilic staining compared with the surrounding normal liver. Clear cells (glycogen storage) were occasionally present. The cytoplasm was distinctly smooth to sometimes granular and pale pink, with a “ground-glass” appearance. Nuclei were enlarged, and nucleoli were prominent and centrally located. A classical example is illustrated in Fig. 10. For the eosinophilic foci evaluated (n=11), 10/11 (91%) were in male rats.

Basophilic foci: Basophilic foci may show some resemblance with small cell change as observed in humans. Different subtypes have been described26. The tigroid subtype consists of a focus of (small) basophilic cells distinct from the surrounding liver parenchyma and arranged in tortuous cords. Cells display large abundant basophilic bodies often arranged in clumps or long bands with a striped (“tigroid”) pattern in the paranuclear or peripheral regions of the cytoplasm (due to increased rough endoplasmic reticulum). In the samples we evaluated, the diffuse subtype was most common and consisted of small, discrete, clearly demarcated, strongly basophilic foci with irregular borders. These foci were randomly distributed within the hepatic lobule. Although different subtypes have been recognized in rodents, a typical example is shown in Fig. 12. Of the basophilic foci evaluated (n=9), 8/9 (89%) were observed in male rats.

Clear cell foci: Clear cell areas of groups of hepatocytes can be observed in HCCs in both human and rodents40,41,42,43. Clear cell foci consisted of normal or enlarged groups of cells with prominent cell membranes and distinct cytoplasmic clear spaces surrounding a densely stained centrally located nucleus. Some eosinophilic or basophilic cells were occasionally present within clear cell foci. A classical example of a clear cell focus is presented in Fig. 13.

The role of clear cell foci in hepatocarcinogenesis is elusive and poorly described, although metabolic changes in carbohydrate metabolism have been associated with HCCs in both humans and rodents41,42,44,45, and therefore these foci, as observed in the rat liver, could play a role in liver tumor formation. The selected clear cell foci (n=9) were only found in the livers of male rats.

Fig. 1. Human liver. Low magnification of FNH. The upper border of the FNH is indicated by arrows with relatively normal hepatic parenchyma at the top of the figure. H&E.
Fig. 2. Human liver. Higher magnification of Fig. 1. The FNH consists of nodules composed of two-cell layers of hepatocytes subdivided by fibrous septa. Proliferative ductules are present in stellate septal scars. H&E.
Fig. 3. Human liver. Hepatocellular carcinoma composed of atypical hepatocytes arranged in a solid or trabecular growth pattern with normal hepatic parenchyma present at the top of the figure. H&E.
Fig. 4. Rat liver. Hepatocellular carcinoma with a trabecular growth pattern at the top and right of the figure. There is angiectasis in the carcinoma on the right. Normal hepatic parenchyma is present on the lower left of the figure. H&E.
Fig. 5. Human liver. High magnification of a hepatocellular carcinoma with a mixed acinar and trabecular growth pattern. H&E.
Fig. 6. Rat liver. High magnification of a hepatocellular carcinoma with a mixed acinar and trabecular growth pattern. H&E.

Fig. 7. Human liver. Hepatocellular adenoma with multifocal steatosis and thick-wall blood vessel (arrow). Prominent fibrosis is present on right edge of the figure. H&E. Fig. 8. Rat liver. Hepatocellular adenoma. The adenoma is sharply demarcated with slight compression of the adjacent normal parenchyma. H&E. Fig. 9. Human liver. A classic example of large cell change. H&E. Fig. 10. Rat liver. Eosinophilic focus of cellular alteration consisting of enlarged hepatocytes with increased acidophilic staining compared to the surrounding hepatic parenchyma. H&E. Fig. 11. Human liver. Small cell change comprised of a focus of small cells with an irregular margin within a cirrhotic liver. H&E. Fig. 12. Rat liver. A basophilic focus of cellular alteration with irregular but discrete margins surrounded by more eosinophilic normal parenchymal hepatocytes. H&E. Fig. 13. Rat liver. Clear cell focus of cellular alteration with an irregular border and comprised of hepatocytes with clear cytoplasm and a centrally located nucleus. H&E.

Fig. 7. Human liver. Hepatocellular adenoma with multifocal steatosis and thick-wall blood vessel (arrow). Prominent fibrosis is present on right edge of the figure. H&E.
Fig. 8. Rat liver. Hepatocellular adenoma. The adenoma is sharply demarcated with slight compression of the adjacent normal parenchyma. H&E.
Fig. 9. Human liver. A classic example of large cell change. H&E.
Fig. 10. Rat liver. Eosinophilic focus of cellular alteration consisting of enlarged hepatocytes with increased acidophilic staining compared to the surrounding hepatic parenchyma. H&E.
Fig. 11. Human liver. Small cell change comprised of a focus of small cells with an irregular margin within a cirrhotic liver. H&E.
Fig. 12. Rat liver. A basophilic focus of cellular alteration with irregular but discrete margins surrounded by more eosinophilic normal parenchymal hepatocytes. H&E.
Fig. 13. Rat liver. Clear cell focus of cellular alteration with an irregular border and comprised of hepatocytes with clear cytoplasm and a centrally located nucleus. H&E.

Discussion and Conclusion

The liver is a major target organ in preclinical toxicity and oncogenicity safety assessment studies with rodents. The significance of hepatic neoplastic findings in animal models has been questioned with regard to their predictive value, as humans appear resistant to many agents that readily produce liver tumors in rodents46. As toxicity to the liver is reported to be the second most frequent cause of drug failure due to adverse effects in clinical trials of potential drugs15,47,48, the early detection and interpretation of proliferative lesions as well as nonproliferative hepatic lesions is of vital importance. One of the safety issues after long-term administration of a xenobiotic is carcinogenicity assessment, and both early and late proliferative liver lesions might be indicative of potential hepatocarcinogenesis or carcinogenesis at other sites in humans1,16,37,49,50,51,52,53,54. The human and rat cases selected for this review were all morphologically consistent with descriptive features in texts and the peer reviewed literature using the most common and contemporary diagnostic criteria for both human and rat hepatic lesions8,22,23,24,26.

We have reviewed FCAs (eosinophilic, basophilic and clear cell foci) and compared them with the human counterparts of LCC and SCC. LCC and SCC in humans and eosinophilic and basophilic FCA in the rat showed common histomorphological characteristics (Figs. 9,10,11,12), which might be indicative of a mutual presumptive role in the process of hepatocarcinogenesis. FNH is the second most common benign lesion of the liver in humans and occurs more often in young females but can occur in both sexes of adults55,56,57,58,59,60. Cases in children have been reported61,62,63. FNH is a benign lesion, and in contrast to HCA, the risk of complications such as hemorrhage and malignant transformation is virtually absent. The more common occurrence of FNH among young women is in line with our results that show that nearly all FNHs selected for this study were obtained from women (91.7%). FNH is a rare lesion in animals64,65. Immunohistochemistry showed characteristic mild and focal cytokeratin 7 staining of hepatocytes, whereas cytokeratin 7 and cytokeratin 19 show a strong staining of bile ductules in the fibrous septa39. The majority of patients with FNH have normal liver test results and alpha-fetoprotein is mostly in the normal range66. Diagnosis of FNH may be difficult in humans if one or more major features are not prominent (central scar, ductular reaction) or if the FNH is steatotic, or has small nodules57. A clear overview of the clinical and morphological features of FNH is presented by Ferrell and Kakar24 for distinction between FNH, hepatocellular adenoma and HCC. Immunohistochemistry has also been extensively investigated and can be supportive for the differential diagnosis10,28,39,67. The current opinion regarding the etiology of this lesion is that it represents a hyperplastic and altered growth of hepatocytes surrounding a pre-existing arterial malformation in response to changes in blood flow in the parenchyma8,23,68. Treatment of symptomatic FNH in humans consists first of embolization and then resection69.

Following hepatic angioma and FNH, HCA is the third most common benign proliferative lesion in humans and is known to occur in 85% of young female patients taking oral contraceptives70,71. There is considerable overlap in morphologic features of well-differentiated hepatocellular lesions, necessitating the use of immunohistochemistry and other techniques for diagnosis39,72,73,74,75. More current diagnostic criteria distinguish four different subtypes of human HCAs based on their histological and molecular characteristics29. The human HCAs examined were all from female patients, in line with the epidemiology and common occurrence of these tumors. HCA histological features observed in the rat were similar to those in humans. The tumors showed focal fatty change/steatosis and increased numbers of mitoses and there was also normal pre-existing liver present at the periphery. In one case, multiple adenomas were observed in a rat that resembled adenomatosis as seen in humans30,70,76,77. A number of human examples showed variable amounts of steatosis as was also observed in the rat HCAs as well, occasionally accompanied by clear cell foci present in the surrounding liver in the rat. In one rat, an HCC with an infiltrative growth pattern arose within an HCA. It is known that HCA may transform into HCC in humans. Some argue that hepatocyte dysplasia probably is an essential intermediate step between HCA and HCC78. HCA is monoclonal in contrast to FNH (polyclonal) and consequently has an inherent risk for progression to HCC78. Moreover, ß-catenin-mutated HCA has an increased risk of undergoing malignant change79. Both the human and rat hepatocellular carcinomas reviewed in this study had malignant growths pattern that are typical for these tumors. Microscopically, the WHO distinguishes trabecular, acinar (pseudoglandular), scirrhous and solid forms8. Special histological subtypes, not included in this review, are the clear cell, fibrolamellar and mixed hepatocholangiocellular variants. Trabecular growth patterns were the most common in both human and rat HCCs (Figs. 3 andand 4) 4) evaluated; sometimes mixtures of trabecular, solid and acinar/pseudoglandular patterns (Figs. 5 andand 6) 6) were also present in our collection. Both human and rat HCCs showed common histopathological characteristics that are typical for these malignant liver lesions. Liver cell dysplasia (LCD) is described in liver transplants containing underlying liver disease. These dysplastic hepatocytes can frequently be observed in the cirrhotic liver19,80,81 and have been proposed to contain precancerous properties31,38,82. The cytological criteria for the diagnosis of LCD include cytoplasmic and nuclear changes, nuclear crowding or pleomorphism together with prominent nucleoli, hyperchromasia and sometimes multinucleation. The cytological features of liver cell dysplasia can strikingly mimic HCC83 suggesting it is a putative preneoplastic lesion that can precede HCC in various species1,10,41,45,84,85,86,87. The precancerous nature of both LCC and SCC with regard to progression to HCC is somewhat controversial, but some claim that either one or both of them have been associated with development of HCC31,35,38,49,82,87,88,89,90.

In rats, FCAs have likewise been designated to play a precursor role in the process of hepatocarcinogenesis as they represent a localized proliferation of hepatocytes that are phenotypically different from the surrounding liver. These FCAs occur spontaneously in aged rats and other rodents and can be induced by chemical treatment. The incidence of spontaneous foci is highest in rats and can reach nearly 100% in F344 rats by the age of 2 years91. After administration of hepatocarcinogens, their incidence, size and/or multiplicity are usually increased, and latency usually decreased25,41,86. These foci have been described in a number of animal models and are considered as precursor lesions of HCC45, but controversy still remains. Some of these foci may have autonomous growth potential and may show enzyme profiles different from the normal hepatocytes (e.g., positive for γ-glutamyl transpeptidase, α-fetoprotein, glutathione S-transferase placental form, and negative for glucose-6-phosphatase and glycogen phosphorylase). However, it has been shown that certain conditions are required for promotion and progression of initiated cells. In addition, different mechanisms of promotion by different chemicals have been demonstrated in the multistep process of carcinogenesis, and it is stated that not all foci become neoplasms91,92,93,94. Some foci of cellular alteration can even regress, and different types of foci have different potentials for developing into neoplasms17,95.

Since controversy with regard to the significance of presumptive preneoplastic liver lesions still exists, comparative research of these proliferative lesions in both rats and humans is needed.

Based on comparison of the histomorphological features of common nonneoplastic and neoplastic hepatocyte lesions of rats and humans, it is apparent that there are major similarities in diagnostic features, growth patterns, and behavior of these lesions in both species. Further study of presumptive preneoplastic lesions should help to further define their role in progression to malignancy and to provide a basis for using liver responses in rodents exposed to xenobiotics in safety assessment studies to predict potential risks to humans. Morphological similarities as illustrated in this review will be a first step to understanding their significance and relevance in human and animal liver tumor formation.

The authors thank the following people for their technical histology and editorial support: Ronald Herbert (NIEHS/NTP Archives), Keith Connely (EPL, Inc.), Emily Singletary (EPL, Inc.), Mary Ellen Sutphin (EPL, Inc.) and Suzy Tirtodikromo (Global Pathology Support). Special thanks to Nikolas Stathonikos (UMCU) for photography support.

The majority of the photomicrographs used in this document were provided courtesy of the Division of Laboratories and Pharmacy, Department of Pathology, University Medical Center Utrecht, and the National Toxicology Program Archives, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.

This research was supported

[in part] by the Division of the National Toxicology Program of the NIH, National Institute of Environmental Health Sciences. This article may be the work product of an employee or group of employees of the National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health (NIH), however, the statements, opinions or conclusions contained therein do not necessarily represent the statements, opinions or conclusions of NIEHS, NIH or the United States government.

1. Aleem E, Nehrbass D, Klimek F, Mayer D, Bannasch P. Upregulation of the insulin receptor and type I insulin-like growth factor receptor are early events in hepatocarcinogenesis. Toxicol Pathol. 39: 524–543 2011.

2. Lee JS, Heo J, Libbrecht L, Chu IS, Kaposi-Novak P, Calvisi DF, Mikaelyan A, Roberts LR, Demetris AJ, Sun Z, Nevens F, Roskams T, Thorgeirsson SS. A novel prognostic subtype of human hepatocellular carcinoma derived from hepatic progenitor cells. Nat Med. 12: 410–416 2006.

3. Frau M, Biasi F, Feo F, Pascale RM. Prognostic markers and putative therapeutic targets for hepatocellular carcinoma. Mol Aspects Med. 31: 179–193 2010.

4. Lu X, Guo H, Molter J, Miao H, Gerber L, Hu Y, Barnes EL, Vogel H, Lee Z, Luo G, Wang B. Alpha-fetoprotein-thymidine kinase-luciferase knockin mice: A novel model for dual modality longitudinal imaging of tumorigenesis in liver. J Hepatol. 55: 96–102 2011.

5. Stefaniuk P, Cianciara J, Wiercinska-Drapalo A. Present and future possibilities for early diagnosis of hepatocellular carcinoma. World J Gastroenterol. 16: 418–424 2010.

6. Lopez JB. Recent developments in the first detection of hepatocellular carcinoma. Clin Biochem Rev. 26: 65–79 2005.

7. Badvie S. Hepatocellular carcinoma. Postgrad Med J. 76: 4–11 2000.

8. Bosman FT, Carneiro F, Hruban RH, Theise N.D. Tumours of the liver and intrahepatic bile ducts. In: WHO Classification of Tumours of the Digestive System, 4. International Agency for Research on Cancer, Lyon. 195-254. 2010

9. Zender L, Villanueva A, Tovar V, Sia D, Chiang DY, Llovet JM. Cancer gene discovery in hepatocellular carcinoma. J Hepatol. 52: 921–929 2010.

10. Borbath I, Leclercq IA, Sempoux C. barca-Quinones J, Desaeger C, and Horsmans Y. Efficacy of lanreotide in preventing the occurrence of chemically induced hepatocellular carcinoma in rats. Chem-Biol Interactions. 183: 238–248 2010.

11. Ascha MS, Hanouneh IA, Lopez R, Tamimi TA, Feldstein AF, Zein NN. The incidence and risk factors of hepatocellular carcinoma in patients with nonalcoholic steatohepatitis. Hepatology (Baltimore, Md). 51: 1972–1978 2010.

12. Sanyal AJ, Yoon SK, Lencioni R. The etiology of hepatocellular carcinoma and consequences for treatment. The oncologist. 15: 14–22 2010.

13. Liu Y, Wu F. Global Burden of Aflatoxin-Induced Hepatocellular Carcinoma: A Risk Assessment. Environ Health Perspect. 118: 818–824 2010.

14. Spangenberg HC, Thimme R, Blum HE. Serum markers of hepatocellular carcinoma. Semin Liver Dis. 26: 385–390 2006.

15. Tsuda H, Futakuchi M, Fukamachi K, Shirai T, Imaida K, Fukushima S, Tatematsu M, Furukawa F, Tamano S, Ito N. A medium-term, rapid rat bioassay model for the detection of carcinogenic potential of chemicals.Toxicol Pathol. 38: 182–187 2010.

16. Bannasch P, Haertel T, Qin S. Significance of Hepatic Preneoplasia in Risk Identification and Early Detection of Neoplasia. Toxicol Pathol. 31: 134–139 2003.

17. Williams GM. The significance of chemically-induced hepatocellular altered foci in rat liver and application to carcinogen detection. Toxicol Pathol. 17: 663–672 1989.

18. Terada T, Nakanuma Y. Multiple occurrence of borderline hepatocellular nodules in human cirrhotic livers: possible multicentric origin of hepatocellular carcinoma. Virchows Arch. 427: 379–383 1995.

19. Cohen C, Berson SD. Liver cell dysplasia in normal, cirrhotic, and hepatocellular carcinoma patients. Cancer. 57: 1535–1538 1986.

20. Cogliati B, Aloia TP, Bosch RV, Alves VA, Hernandez-Blazquez FJ, Dagli ML. Identification of hepatic stem/progenitor cells in canine hepatocellular and cholangiocellular carcinoma. Vet Comp Oncol. 8: 112–121 2010.

21. Park YN. Update on precursor and early lesions of hepatocellular carcinomas. Arch Pathol Lab Med. 135: 704–715 2011.

22. Goodman ZD, Ishak KG, Ferrell LD, Geisinger KR. Heptobiliary system and pancreas. In: Surgical Pathology and Cytopathology, 4th. SG Silverberg, RA DeLellis, WJ Frable, VA Livolsi, and MR Wick (eds). Elsevier, Philadelphia. 1465–1547. 2006

23. Ishak KG, Goodman ZD, Stocker JT. Tumors of the Liver and Intrahepatic Bile Ducts. Third series, Fascicle 31. Armed Forces Institute of Pathology, Washington, D.C. 2001

24. Ferrell L, Kakar S. Tumors of the liver, gallbladder, and biliary tree. In: Diagnostic Histopathology of Tumors, 3rd. CDM Fletcher (ed). Churchill Livingstone, Elsevier, Edinburgh. 417–461. 2007

25. Bannasch P, Zerban H. Tumours of the liver. In: Pathology of tumours in laboratory animals. Tumours of the rat, vol 1, 2nd. Turusov V and Mohr, U (eds) IARC scientific publications. 199–240 1990.

26. Thoolen B, Maronpot R, Harada T, Nyska A, Rousseaux C, Nolte T, Malarkey D, Kaufmann W, Küttler K, Deschl U, Nakae D, Gregson R, Vinlove M, Brix A, Singh B, Belpoggi F, Ward J. Proliferative and Nonproliferative Lesions of the Rat and Mouse Hepatobiliary System. Toxicol Pathol. 38: 5S–81S 2010.

27. Roskams T, De VR, Desmet V. ‘Undifferentiated progenitor cells’ in focal nodular hyperplasia of the liver. Histopathology. 28: 291–299 1996.

28. van Aalten SM, Verheij J, Terkivatan T, Dwarkasing RS, de Man RA, IJzermans JNM. Validation of a liver adenoma classification system in a tertiary referral centre: Implications for clinical practice. J Hepatol. 55: 120–125 2011.

29. Bioulac-Sage P, Rebouissou S, Thomas C, Blanc JF, Saric J, Sa CA, Rullier A, Cubel G, Couchy G, Imbeaud S, Balabaud C, Zucman-Rossi J. Hepatocellular adenoma subtype classification using molecular markers and immunohistochemistry. Hepatology (Baltimore, Md). 46: 740–748 2007.

30. Rebouissou S, Imbeaud S, Jeannot E, Saric J, Balabaud C, Bioulac-Sage P, Zucman-Rossi J. Role of HNF1 inactivation in hepatocellular adenoma lipogenesis. J Hepatol. 44: S44 2006.

31. Anthony PP, Vogel CL, Barker LF. Liver cell dysplasia: a premalignant condition. J Clin Pathol. 26: 217–223 1973.

32. An CST, Petrovic LM, Reyter I, Tolmachoff T, Ferrell LD, Thung SN, Geller SA, Marchevsky AM. The application of image analysis and neural network technology to the study of large-cell liver-cell dysplasia and hepatocellular carcinoma. Hepatology (Baltimore, Md). 26: 1224–1231 1997.

33. Ganne-Carrié N, Chastang C, Chapel F, Munz C, Pateron D, Sibony M, Deny P, Trinchet JC, Callard P, Guettier C, Beaugrand M. Predictive score for the development of hepatocellular carcinoma and additional value of liver large cell dysplasia in Western patients with cirrhosis. Hepatology (Baltimore, Md). 23: 1112–1118 1996.

34. Ikeda H, Sasaki M, Sato Y, Harada K, Zen Y, Mitsui T, Nakanuma Y. Large cell change of hepatocytes in chronic viral hepatitis represents a senescent-related lesion. Hum Pathol. 40: 1774–1782 2009.

35. Le Bail B, Bernard PH, Carles J, Balabaud C, Bioulac-Sage P. Prevalence of liver cell dysplasia and association with HCC in a series of 100 cirrhotic liver explants. J Hepatol. 27: 835–842 1997.

36. Lee RG, Tsamandas AC, Demetris AJ. Large cell change (liver cell dysplasia) and hepatocellular carcinoma in cirrhosis: matched case-control study, pathological analysis, and pathogenetic hypothesis. Hepatology (Baltimore, Md). 26: 1415–1422 1997.

37. Adachi E, Hashimoto H, Tsuneyoshi M. Proliferating cell nuclear antigen in hepatocellular carcinoma and small cell liver dysplasia. Cancer. 72: 2902–2909 1993.

38. Watanabe S, Okita K, Harada T, Kodama T, Numa Y, Takemoto T, Takahashi T. Morphologic studies of the liver cell dysplasia. Cancer. 51: 2197–2205 1983.

39. Ahmad I, Iyer A, Marginean CE, Yeh MM, Ferrell L, Qin L, Bifulco CB, Jain D. Diagnostic use of cytokeratins, CD34, and neuronal cell adhesion molecule staining in focal nodular hyperplasia and hepatic adenoma. Hum Pathol. 40: 726–734 2009.

40. Maronpot RR, Montgomery CA, Jr, Boorman GA, McConnell EE. National toxicology program nomenclature for hepatoproliferative lesions of rats. Toxicol Pathol. 14: 263–273 1986.

41. Bannasch P, Enzmann H, Klimek F, Weber E, Zerban H. Significance of sequential cellular changes inside and outside foci of altered hepatocytes during hepatocarcinogenesis. Toxicol Pathol. 17: 617–628 1989.

42. Bannasch P. Hepatocellular glycogenosis and hepatic neoplasms. Toxicol Pathol. 38: 1000–1002 2010.

43. Enzmann H, Kaliner G, Watta-Gebert B, Löser E. Foci of altered hepatocytes induced in embryonal turkey liver. Carcinogenesis. 13: 943–946 1992.

44. Enzmann H, Zerban H, Löser E, Bannasch P. Glycogen phosphorylase hyperactive foci of altered hepatocytes in aged rats. Virchows Arch B. 62: 3–8 1992.

45. Libbrecht L, Desmet V, Roskams T. Review Article: Preneoplastic lesions in human hepatocarcinogenesis. Liver Int. 25: 16–27 2005.

46. Anthony PP. Liver tumours. Baillière’s Clin Gastroenterol. 2: 501–522 1988.

47. Foster JR. Spontaneous and drug-induced hepatic pathology of the laboratory Beagle dog, the cynomolgus macaque and the marmoset. Toxicol Pathol. 33: 63–74 2005.

48. Lee S, Lee HJ, Kim JH, Lee HS, Jang JJ, Kang GH. Aberrant CpG island hypermethylation along multistep hepatocarcinogenesis. Am J Pathol. 163: 1371–1378 2003.

49. Cheah PL, Looi LM, Nazarina AR, Goh KL, Rosmawati M, Vijeyasingam R. Histopathological landmarks of hepatocellular carcinoma in Malaysians. Malays J Pathol. 25: 37–43 2003.

50. Hoenerhoff MJ, Pandiri AR, Lahousse SA, Hong H-H, Ton T-V, Masinde T, Sills RC, Auerbach SS, Gerrish K, Bushel PR, Shockley KR, Peddada SD. Global gene profiling of spontaneous hepatocellular carcinoma in B6C3F1 Mice: Similarities in the molecular landscape with human liver cancer. Toxicol Pathol. 39: 678–699 2011.

51. Andersen JB, Loi R, Perra A, Factor VM, Ledda-Columbano GM, Columbano A, Thorgeirsson SS. Progenitor-derived hepatocellular carcinoma model in the rat. Hepatology (Baltimore, Md). 51: 1401–1409 2010.

52. Cohen SM. An enhanced 13-week bioassay: An alternative to the 2-year bioassay to screen for human carcinogenesis. Exp Toxicol Pathol. 62: 497–502 2010.

53. Marquardt JU, Thorgeirsson SS. Stem cells in hepatocarcinogenesis: evidence from genomic data. Semin Liver Dis. 30: 26–34 2010.

54. Samson TJ. Role of cancer stem cells in hepatocarcinogenesis. Gen Med. 3: 11 2011

55. Lefkowitch JH. Advances in hepatobiliary pathology: update for 2010. Clin Liver Dis. 14: 747–762 2010.

56. Bellamy COC. Pathology of liver tumours. Surgery (Oxford). 28: 183–188 2010.

57. Bioulac-Sage P, Laumonier H, Rullier A, Cubel G, Laurent C, Zucman-Rossi J, Balabaud C. Over-expression of glutamine synthetase in focal nodular hyperplasia: a novel easy diagnostic tool in surgical pathology. Liver Int. 29: 459–465 2009.

58. Paradis V. Benign liver tumors: an update. Clin Liver Dis. 14: 719–729 2010.

59. Blanc JF, Jeannot E, Laurent C, Sa Cunha A, Rebuissou A, Lepreux S, Le Bail B, Troutte H, Saric J, Balabaud C, Zucman-Rossi J, Bioulac-Sage P. 232 Focal nodular telangiectasia (FNT) of the liver: Pathological and molecular characterization. J Hepatol. 40: 74 2004.

60. Kayhan A, Venu N, Lakadamyali H, Jensen D, Oto A. Multiple progressive focal nodular hyperplasia lesions of liver in a patient with hemosiderosis. World J Radiol. 2: 405–409 2010.

61. Farruggia P, Alaggio R, Cardella F, Tropia S, Trizzino A, Ferrara F, D’Angelo P. Focal nodular hyperplasia of the liver: an unusual association with diabetes mellitus in a child and review of literature. Ital J Pediatr. 36: 41 2010.

62. Sugito K, Uekusa S, Kawashima H, Furuya T, Ohashi K, Inoue M, Ikeda T, Koshinaga T, Tomita R, Mugishima H, Maebayashi T. The clinical course in pediatric solid tumor patients with focal nodular hyperplasia of the liver. Int J Clin Oncol. 16: 482–487 2011.

63. Towbin AJ, Luo GG, Mo JQ, Mo JQ. Focal nodular hyperplasia in children, adolescents, and young adults. Pediatr Radiol. 41: 341–349 2011.

64. Fujishima J, Satake S, Furukawa T, Kurokawa C, Kodama R, Moriyama A, Sasaki Y, Kamimura Y, Maeda H. Focal nodular hyperplasia in the livers of cynomolgus macaques (Macaca fascicularis). J Toxicol Pathol. 24: 125–129 2011.

65. Sumiyoshi M, Sakanaka M, Kimura Y. Chronic intake of a high-cholesterol diet resulted in hepatic steatosis, focal nodular hyperplasia and fibrosis in non-obese mice. Brit J Nutr. 103: 378–385 2010.

66. Mneineh W, Paradis V. High serum level of alpha-fetoprotein in focal nodular hyperplasia of the liver. Pathol Int. 61: 491–494 2011.

67. Zhu ZW, Friess H, Wang L., bou-Shady M, Zimmermann A, Lander AD, Korc M, Kleeff J, and Büchler MW. Enhanced glypican-3 expression differentiates the majority of hepatocellular carcinomas from benign hepatic disorders. Gut. 48: 558–564 2001.

68. Wanless IR, Mawdsley C, Adams R. On the pathogenesis of focal nodular hyperplasia of the liver. Hepatology (Baltimore, Md). 5: 1194–1200 1985.

69. Arts CH. van HR, de Kort GA, and Moll FL. Inferior caval vein thrombosis owing to compression of focal nodular hyperplasia: surgical resection after shrinkage by hepatic artery embolization. Vascular. 18: 53–58 2010.

70. Maillette De Buy Wenniger L, Terpstra V, Beuers U. Focal nodular hyperplasia and hepatic adenoma: Epidemiology and pathology. Dig Surg. 27: 24–31 2010.

71. Bioulac-Sage P, Laumonier H, Laurent C, Zucman-Rossi J, Balabaud C. Hepatocellular adenoma: what is new in 2008. Hepatol Int. 2: 316–321 2008.

72. Di C. I, Pulvirenti E, Toro A, and Priolo GD. Adenoma or atypical hepatic focal nodular hyperplasia: role of preoperative imaging and laparoscopic treatment. Surg Lapar Endos & Percut Techn. 20: e105–e109 2010.

73. Bioulac-Sage P, Balabaud C, Zucman-Rossi J. Focal nodular hyperplasia, hepatocellular adenomas: past, present, future. Gastroenterol Clin Biol. 34: 355–358 2010.

74. Bioulac-Sage P, Cubel G, Balabaud C, Zucman-Rossi J. Revisiting the pathology of resected benign hepatocellular nodules using new immunohistochemical markers. Semin Liver Dis. 31: 91–103 2011.

75. Shafizadeh N, Kakar S. Diagnosis of well-differentiated hepatocellular lesions: role of immunohistochemistry and other ancillary techniques. Adv Anat Pathol. 18: 438–445 2011.

76. Bioulac-Sage P, Balabaud C, Zucman-Rossi J. Subtype classification of hepatocellular adenoma. Dig Surg. 27: 39–45 2010.

77. Reznik Y, Dao T, Coutant R, Chiche L, Jeannot E, Clauin S, Rousselot P, Fabre M, Oberti F, Fatome A, Zucman-Rossi J, Bellanne-Chantelot C. Hepatocyte nuclear factor-1 alpha gene inactivation: cosegregation between liver adenomatosis and diabetes phenotypes in two maturity-onset diabetes of the young (MODY)3 families. Clin Endocrinol Metab. 89: 1476–1480 2004.

78. Farges O, Dokmak S. Malignant transformation of liver adenoma: an analysis of the literature. Dig Surg. 27: 32–38 2010.

79. Zucman-Rossi J, Jeannot E, Nhieu JT, Scoazec JY, Guettier C, Rebouissou S, Bacq Y, Leteurtre E, Paradis V, Michalak S, Wendum D, Chiche L, Fabre M, Mellottee L, Laurent C, Partensky C, Castaing D, Zafrani ES, Laurent-Puig P, Balabaud C, Bioulac-Sage P. Genotype-phenotype correlation in hepatocellular adenoma: new classification and relationship with HCC. Hepatology (Baltimore, Md). 43: 515–524 2006.

80. Kobayashi M, Ikeda K, Hosaka T, Sezaki H, Someya T, Akuta N, Suzuki F, Suzuki Y, Saitoh S, Arase Y, Kumada H. Dysplastic nodules frequently develop into hepatocellular carcinoma in patients with chronic viral hepatitis and cirrhosis. Cancer. 106: 636–647 2006.

81. Lefkowitch JH, Apfelbaum TF. Liver cell dysplasia and hepatocellular carcinoma in non-A, non-B hepatitis. Arch Pathol Lab Med. 111: 170–173 1987.

82. Libbrecht L, Craninx M, Nevens F, Desmet V, Roskams T. Predictive value of liver cell dysplasia for development of hepatocellular carcinoma in patients with non-cirrhotic and cirrhotic chronic viral hepatitis. Histopathology. 39: 66–73 2001.

83. Tao LC. Oral contraceptive-associated liver cell adenoma and hepatocellular carcinoma. Cytomorphology and mechanism of malignant transformation. Cancer. 68: 341–347 1991.

84. Podda M, Roncalli M, Battezzati PM, Borzio M, Bruno S, Servida E, Coggi G. Liver-cell dysplasia and hepatocellular carcinoma. Ital J Gastroenterol. 24: 39–42 1992.

85. Enzmann H, Kuhlem C, Kaliner G, Löser E, Bannasch P. Rapid induction of preneoplastic liver foci in embryonal turkey liver by diethylnitrosamine. Toxicol Pathol. 23: 560–569 1995.

86. Maronpot RR, Pitot HC, Peraino C. Use of rat liver altered focus models for testing chemicals that have completed two-year carcinogenicity studies. Toxicol Pathol. 17: 651–662 1989.

87. Koo JS, Kim H, Park B, Ahn S, Han KH, Chon C, Park C, Park Y. Predictive value of liver cell dysplasia for development of hepatocellular carcinoma in patients with chronic hepatitis B. J Clin Gastroenterol. 42: 738–743 2008.

88. Borzio M, Bruno S, Roncalli M, Mels GC. Liver cell dysplasia is a major risk factor for hepatocellular carcinoma in cirrhosis: a prospective study. Gastroenterology. 108: 812 1995.

89. Park YN, Roncalli M. Large liver cell dysplasia: a controversial entity. J Hepatol. 45: 734–743 2006.

90. Rubin EM, DeRose PB, Cohen C. Comparative image cytometric DNA ploidy of liver cell dysplasia and hepatocellular carcinoma. Mod Pathol. 7: 677–680 1994.

91. Narama I, Imaida K, Iwata H, Nakae D, Nishikawa A, Harada T. A review of nomenclature and diagnostic criteria for proliferative lesions in the liver of rats by a working group of the Japanese Society of Toxicologic Pathology. J Toxicol Pathol. 16: 1–17 2003.

92. Popp JA, Goldsworthy TL. Defining foci of cellular alteration in short-term and medium-term rat liver tumor models. Toxicol Pathol. 17: 561–568 1989.

93. Harada T, Maronpot RR, Morris RW, Stitzel KA, Boorman GA. Morphological and stereological characterization of hepatic foci of cellular alteration in control Fischer 344 rats. Toxicol Pathol. 17: 579–593 1989.

94. Pitot HC, Campbell HA, Maronpot R, Bawa N, Rizvi TA, Xu YH, Sargent L, Dragan Y, Pyron M. Critical parameters in the quantitation of the stages of initiation, promotion, and progression in one model of hepatocarcinogenesis in the rat. Toxicol Pathol. 17: 594–611 1989.

95. Enzmann H, Bannasch P. Non-persisting early foci of altered hepatocytes induced in rats by N-nitrosomorpholine. J Cancer Res Clin Oncol. 114: 30–34 1988.


text:
Volcom Collaborates With Snowboarder Bryan Iguchi On Boot, Shoe

Volcom has teamed up with artist, snowboard legend and veteran Volcom team rider Bryan Iguchi for a winter-ready footwear collection, featuring signature editions of a popular boot and shoe from the brand.

The Bryan Iguchi Outlander boot and Grimm Mid 2 shoe are available now on the brand’s website, Volcom.com, and retail for $165 and $100, respectively. Both the Outlander and the Grimm Mid 2 feature the snowboarder’s Teepee Stone artwork, which was designed specifically for the collection and symbolizes shelter, comfort and protection from the elements.

The Outlander features water resistant nubuck leather on its upper and back woods design surrounding Iguchi’s artwork, with technical details made for both mountain trails and winter sidewalks. The boot also features a durable rubber outsole with extra grip, a molded heel counter and EVA heel strike for long-lasting comfort, tongue gussets, a padded tongue and collar, rubber mud guard, and RCF Technology footbed.

The Volcom Grimm Mid 2.
CREDIT: Courtesy of brand.

“I spend my winters walking around on snow and ice,” Iguchi said in a statement. “From my home to the trailhead these boots have endured the harshest Wyoming Winters. I live in these.”

The Grimm Mid 2 boasts a water resistant nubuck upper, thinly padded tongue and collar, and a Molded Recliner Comfort Foam insole.

“Guch is passionate about product,” said Jason Smith, footwear director for Volcom, in a statement. “He knows what works in the real world and his input is always on point. The fact that he’s also an artist made this collaboration pretty much seamless.”

Want More?

First Look at Volcom Shoes

Analysts Mixed on Volcom Shoe Prospects

More From Our Brands

Access exclusive content


WARC-Identified-Payload-Type: application/xhtml+xml

text:
Batman v Superman: Pop! Vinyl Figures: Superman

  • Sorry
    This item is currently sold out. Please enter your email address into the box below and press 'notify me' for availability updates.
  • From the Batman v Superman: Dawn of Justice movie comes this Superman Pop! Vinyl Figure.

  • More Below…

Product Description

Customer Reviews

There aren't any reviews published for this product yet, why not be the first to write one?

Write your own review.

All reviews


text:
Two-hour delay for FWCS elementary schools on Feb. 6 - January 30, 2008

Record Number: 3787
Displayed from: Jan 30, 2008 , until: Feb 09, 2008

All 34 Fort Wayne Community Schools elementary schools, as well as the elementary grades at Towles Intermediate School, will have a scheduled two-hour delay day Wednesday, Feb. 6. The schedule for buses, classes, lunches and after-school activities will be the same as a two-hour weather delay. Buses will run two hours later for grades K-5, and school will begin at most schools at 10:40 a.m. Students arriving after 10:50 a.m. will be counted as tardy. Breakfast will not be served. At Towles, elementary students will arrive at 10 a.m. and will be tardy if they arrive after 10:10 a.m. The middle school will remain on its normal schedule, and buses will run the routes twice for Towles. Except for Bunche Early Childhood Center, morning pre-k students will attend from 10:50 a.m.-12:35 p.m., arriving at school with grades K-5. Afternoon pre-k students will get on the bus one hour later than normal and attend school from 1:35-3:20 p.m., dismissing at normal time. At Bunche, pre-k students will not attend, and Kindergarten students will begin at 10:10 a.m. The delay provides valuable professional development time for staff. During the two hours staff members work together on ways to improve instruction and academic achievement in their buildings. Future delay days are scheduled for March 7 and May 6.

With nearly 30,000 students, Fort Wayne Community Schools is one of the largest school districts in Indiana. FWCS proudly allows families to choose any of its 50 schools through its successful school-choice program creating diversity in each school, including some with more than 75 languages spoken. FWCS offers seven magnet schools focusing on areas such as science and math, communication, fine arts or Montessori at the elementary and middle school level. In high school, students can choose from the prestigious International Baccalaureate program, Project Lead the Way or New Tech Academy as well as other rigorous academic and specialty training programs.


text:
Blackhawk Middle School Dress Code

Blackhawk Dress Policy

Early adolescents grow at different rates and families have differing views on what is appropriate for students to wear to school. Our dress policy is designed to be conservative in nature to allow students to safely and comfortably concentrate on scholastic achievement.  Student dress and appearance shall not have a negative effect on or be disruptive to the educational process.

Students who are dressed inappropriately will be asked to change or remove the offending article.

A few general reminders

  • Clothing should be appropriate for school and fit appropriately.  Any tears holes, or rips should not expose skin.
  • Hats, caps, sunglasses, jackets/coats and headphones are not to be worn during the school day.
  • All top must have sleeves.
  • Girls’ tops must be appropriate and no cleavage or undergarments should be visible.
  • Tights, leggings, or similar types of clothing must be worn with another top or dress that is below mid-thigh or finger-tip length.
  • Industrial/pet chains or accessories containing spikes are not to be worn.
  • Suggestive or disruptive clothing or accessories will not be permitted.  Items that have obscene gestures or words, sexual suggestions or over-tones, or items that suggest or mention alcoholic beverages, tobacco products, illegal substances, drugs, gang affiliation and/ or violence will not be permitted.
  • Pants must be worn at the waist at all times.  Shorts worn under pants are considered undergarments.
  • Slippers or pajama-type clothing are not permitted.
  • Shorts and skirts should be below mid-thigh or finger-tip length.
  • Students will wear shoes.
  • For additional information regarding dress policies, please refer to the FWCS Student-Parent Handbook or FWCS Code of Conduct.

Students may carry backpacks/book bags/purses to and from school.  These items must fit and be stored in the student’s locker.  Backpacks, book bags and purses are not permitted in the classroom.


text:
Which Peachtree Amp to use with D5 speakers?

I currently run my Peachtree D5 speakers as part of a surround system...but I was considering breaking them off and using them with an integrated amp.....perhaps one from Peachtree....but I can't decide which one. I emailed Peachtree and they suggested either the Nova125 or Nova220 (i.e. either 125 or 220 wpc). However, they sell the D5's on their website with the Nova65 system...and I found an article with Peachtree running the D5's with Decco65 (at the The 2012 Rocky Mountain Audio Fest). Another extensive review ran the Nova (also about 65 wpc) with the D5 and a slew of other much larger speakers and they it fared very well.

I'm somewhat budget conscious...hoping to pick a system up here hopefully. I certainly don't want to overspend. Anyone else have any experience with Peachtree amps and the D5's?


text:
Dear Customers,

please make sure that the email-adresses you used here at our
portal are still accessible for you and usable.

We soon need that email-adresses to grant you access to
Daemon Tools Pro. Without such email you will not be able
to use Daemon Tools Pro.

In case of trouble you can write to:

So please double-check that the adress you used here for
our portal is still valid!

Alot of people use "one-way"-adresses as well as "Antispam"-
adresses. We do not advice you to use such email-adresses
together with DaemonTools-accounts!

with best regards
DT Team


text:
Samsung Galaxy S8/S8+

  • Hey, I'm just wondering if these rings will work with an s8? Not really interested in buying one of them and then finding out I can't even use it, so if any of you have tested it, or know what the s8 supports and what the rings have, then please let me know :)

  • Hi Kossi,
    the S8/S8+ will be able to see any of the NFC rings. You can either register the ring as a 'trusted device' in
    settings\security, or download the NFCRing app and use that to unlock your phone. The NFCRings are nothing to do with Android pay and cannot be used to pay for things. There is an NFCRing payment ring in the pipeline, but it's not been released yet. The payment ring can also be used to unlock you phone.

  • @didgesteve Okay, so I can read and write to it then I assume :) I couldn't really find any specs (I may just be really bad at searching), but it looks like there are two separate NFC chips which I can program separately? How much can they store each? As I said, I may just be bad at looking, but if you could link me to something or just tell me, id really appreciate it :)

  • Hi,
    a quick search listed these specs, there are different storage sizes for the ceramic and titanium.
    Yes, you are right, there are two chips per ring, independant of each other.
    Obviously the app to program these is NFC Ring Control, although it doesn't get many glowing reviews, so maybe NFC TagWriter is the better option.

  • Hey I just wanted to tell you yes it does work with an s8. It just dosent work with iOS. It might take 5-10 minutes to heat up though. But it's sweet spot is in the middle.

  • @ddprincess9
    No surprise it doesn't work with Apple. They would want to sell you an iRing at three times the price, then claim that it's new groundbreaking technology invented by them, like, err, contactless charging...


text:
Jump to content
Sign in to follow this

3 columns in the middle

Recommended Posts

You can create a 3-column table inside the HTML editor for a page and use CSS (added to the Custom Code area) to style it. Here's a tutorial on how to create simple tables: http://www.w3schools.com/html/html_tables.asp To help you get started, the table you'll need must look something like this:

	row 1, cell 1
	row 1, cell 2
	row 1, cell 3

row 1, cell 1 = The Mr. Rooter Plumber section row 1, cell 2 = Clean & Green row 1, cell 3 = Special Offers Does that make sense?

Please read the docs before posting. Please do not private message me unless I ask you to.

Designer | Catrina Dulay

Founder | Catrina and Mouse

Share this post

Link to post
Share on other sites

Create an account or sign in to comment

You need to be a member in order to leave a comment

Create an account

Sign up for a new account in our community. It's easy!

Register a new account

Sign in

Already have an account? Sign in here.

Sign In Now

Sign in to follow this


text:
Python / PyQt / Qt performance

  • Hello,

    I am not sure if my problem related to Python (I am using 2.7) or PyQt or Qt itself

    I am developing log4j log file viewer. My program loads log file and parses each line to build model for QTreeView. In parallel it collects statistics about some field values. This is done using map <field_value, boolean>

    Now, I have 3 test files - test1.log, test2.log, test3.log. test2.log is actually concatenation of test1.log. test3.log is also concatenation of test1.log 3 times. So set of values and thus size of maps must be the same in all 3 cases:

    test1.log - ~ 50 MB and 383377 records
    test2.log - ~ 100 MB and 383377 x 2 records
    test3.log - ~ 150 MB and 383377 x 3 records

    Now the problem:

    test1 and test2 are loaded in 1-2 second and pythonw process takes ~ 35 MB of RAM (which is already strange given that only file content is 50 or even 100 MB, but that isn't my question, although might trigger a clue)

    test3 loads several minutes and pythonw process takes almost 3 GB of RAM

    Does anyone have a clue what could be a reason for such performance hit?

    Thank you!

  • Lifetime Qt Champion

    Without seeing any code it's very difficult to help. We don't know how you load the log files, if you load all three files together etc...

  • Sorry for late reply, I was fully busy with a different project for all this time.

    I will of course show the code but I want first to understand what parts of it is really relevant, otherwise is going to be quite big. So I want to begin with top-level description of the flow:

    Reading text file into lines array: lines = input.readlines() (then lines = [line. rstrip() for line in lines]

    Parsing each line: for line in lines parser.parseLine(line). Method parseLine() returns array of fields, which is saved as member (in C++ terms) of 'record' (instance of class LogRecord). This record is added to array 'self.records'

    Iterating over array of records to create instance of 'TreeItem' class for each record (you may ask why do I need two classes 'LogRecord' and 'TreeItem' - to have kind of "clean" model with records independent of TreeView specific requirements, 'TreeItem' implements method needed only for TreeView representation of the model, such as child/parent relationship)

    I profiled project with eric4 IDE and got interesting results:
    Method 'loadLogFile' of window class that has just two lines:
    took ~21 seconds
    while method 'loadLogFile' of model (flow described above) took only 9 seconds and 'adjustSectionsWidth()' took another ~12 seconds.
    adjustSectionsWidth() just calls 'sizeHintForColumn' of QTreeView 6 times (and then 'resizeSection' of header). So it looks like 'sizeHintForColumn' is quite expensive method (actually, doesn't surprise me), I will try to use some other ways to estimate header section widths.

    Besides that I think 9 seconds for model's 'loadLogFile' on i7 with 8GB RAM is also too much. I am now trying to drill down this method with profiler

    I will really appreciate any suggestions. And what parts of code should I show?

    Thank you!

  • Lifetime Qt Champion

    Do you use a custom model (i think so) ? If so, how do you propagate the fact that your data has arrived ? Once per item ? Once when you loaded all the data ?

    How does adjustSectionsWidth work ? Does it parse all data or only the visible part ?

    In what kind of structure do you keep your data ? What's it's access speed ?

    Hope these questions help

    loadLogFile and adjustSectionsWidth would be interesting to see i think

  • Answers for your questions:

    Yes, custom model as you correctly guessed )))

    Of course once when data arrived. Here is the code of loadLogFile() of 'LogModel' class:
    (currently split into other method calls to collect profile data, I will paste here code of these methods also):

    def loadLogFile(self, fileName):

        self.lines = None

    current code of 'adjustSectionsWidth' of 'RecordsView', which is derived from QTreeView:

    def adjustSectionsWidth(self):
    #TODO: reimplement adjustSectionsWidth

        header = self.header()
        #Tempral hard-coded widths:
        header.resizeSection(1, 112)
        header.resizeSection(2, 67)
        header.resizeSection(3, 121)
        header.resizeSection(4, 227)
        header.resizeSection(5, 42)
        header.resizeSection(6, 303)
        #original code:
        fieldLogicalIndex = 1 #not 0 because we dont't want to touch leftmost "extra" section
        while fieldLogicalIndex < header.count():
            #resize section to fit hint
            hint = self.sizeHintForColumn(fieldLogicalIndex)
            hint += 3 #TODO: margin pixels, find better way to estimate this number
            sectionSize = header.sectionSize(fieldLogicalIndex)
            if sectionSize < hint:
                sectionSize = hint
                header.resizeSection(fieldLogicalIndex,  sectionSize)
            fieldLogicalIndex += 1

    Now, to drill down 'loadLogFile' let's see profile data:

    As you can see most of the time is spent on QTreeView methods 'endResetModel' and 'hasIndex'

    The number of calls ~260000 looks strange to me given that number of records is 383377

    'rowCount' and 'data' of my model also took some time. rowCount() code I grabbed from some QTreeView's model sample on the web (it took > 3 seconds):
    def rowCount(self, parent=QtCore.QModelIndex()):
    if parent.column() > 0:
    return 0

        if not parent.isValid():
            p_Item = self.rootItem
            p_Item = parent.internalPointer()
        count = p_Item.childCount()
        return count

    you can see at screenshot that childCount() took < 1 second

    What direction would you suggest to go now?

    Thank you again!

Log in to reply

Looks like your connection to Qt Forum was lost, please wait while we try to reconnect.


text:
Deployment fails in Qt5.2-rc1, androiddeployqt.exe exited with code 14

    1. make sure you use the .bat script, not the .cmd, e.g. in Options/Android, my ANT location is
      C:\Program Files\Android\adt-bundle-windows-x86_64-20131030\eclipse\plugins\org.apache.ant_1.8.3.v201301120609\bin\ant.bat
      I don't know why there are both but the cmd causes errors leading to code14.

    2. Set JAVA_HOME in Projects/Build and Run/Build Environment, e.g. mine is
      Do not specify the \bin.

    Then it works, so far so good!

Log in to reply

Looks like your connection to Qt Forum was lost, please wait while we try to reconnect.


text:
HAM MASTERS (#PYRRJ2V), we are allergic to lopsided bases. But we have the proper antidote: skills!!!!

We are an organized war clan, but with a laid back attitude. Most members are from US. We welcome international members as long as they can attack on time in wars. If you are also into clan games, we have never missed any tiers!

Here are our criteria:
* TH7s and up only
* TH8s and up must train up war troops and hit one of our bases in Friendly Challenge, before we put you in wars
* TH9s must have balance heroes/xbows:
** if you have xbows level 3, you need heroes 20+/20+
* TH10s must be at least maxed TH9
* TH11s must be at least maxed TH10
* must speak English, must communicate well
* must be regularly warring, opt out only for heroes or spell factory upgrades and necessary/emergency real life situations (school, work, family, etc -- we are quite reasonable). Long term parking/opting out is discouraged.

If you decide to give us a try, please send a join request with a message "Go HAM on Clash".

See you in game and Go HAM on Clash of Clans!


text:
8 Replies Latest reply on May 20, 2013 5:05 PM by patrickpayne

    Photoshop cs6 and Illustrator cs6 both crashing on start up.

      Hello all,

      I have recently started my venture with the Creative Cloud set. After purchasing it, I ran Photoshop first and it started up perfectly. After playng around with it, I decided to restart my computer as I hear you should do right after installing a big program. One I did that though, now everytime I try to open either Photoshop or Illistrator (64 bit or not) the logo comes up in the middle of my screen then stops responding and has to close (See image). I have tried updating my drivers, I have uninstalled and reinstalled Photoshop but that didn't help (hence why the logo on my quick bar on the bottom for Photosohp is missing) and I have tried deleting preferences (by opening and holding Ctrl + Shift + Alt) but none of these things helped.

      All I want to do is use my new programs

      Here is my computer information from the dxdiag:

      Name: NVIDIA GeForce GT 520

      Manufacturer: NVIDIA

      Chip Type: GoForce GT 520

      DAC Type: Integrated RAMDAC

      I am on Windows 7.

      P.S. the 'insert photo' button isn't working, here's an imgur screen shot: http://i.imgur.com/ean6N2T.jpg


text:
2 Replies Latest reply on Sep 20, 2013 12:25 PM by hoobah645

    Quite urgent guide problem

    hoobah645 Level 1

      Hi all,

      I'm trying to create guides which snap to the ruler divisions (which is set to pixels) for a website layout.

      For some reason holding shift has no effect on making the guide snap to the increments (in this case pixels)

      I'm able to place a couple of guides accurately using view/new guide but I'd like to know why it's not working.

      Any ideas?


text:
Waitlist functionality changed?

  • Hi folks,

    I know it’s been asked before about adding a waitlist and it’s not yet there because of priorities etc and that there was a workaround suggested before by @Nuala-McHale and @Philip-Hennessy to:

    Turn on Ticket Approval’ at the bottom of the edit/create event which puts automatically puts tickets to the waiting list until an admin approves their ticket. This is working out for their Dojo as tickets can then be individually approved within the manage ticket event if spaces open up.

    I’ve this turned on, but when event is fully approved, the book ticket button becomes greyed out. So I added one more place in the hope that the button would still be enabled and a waitlist would kick in, but it seems that the button becomes disabled again based on applicants numbers rather than attending numbers.

    I can obviously add many more tickets and just approve our capacity, but having to jump through all the hoops makes me wonder if the priority of waitlists could be increased and get done in the near term?

  • Hey @KramKroc . Waitlist is definitely something we’d like to get done in the next few months. It’s something a decent number of clubs have asked for (although for many different use cases).

    To give you an idea of priorities. The first was to get the basic experience smooth and not blocking people (as the basic feature set we have now is enough for most clubs once designed correctly).

    We’re still on that path, we’re working on a Zen dashboard and a few other smaller tweaks to check in etc. that partially complete those basic “simple flows” that you’ll see in the next few weeks. After those (think October) we still have to decide what we’re doing. We have some large technical debt projects we have to do before the end of the year but in terms of “significant new features” that you might see waitlist is top of the list. So basically by then end of September we should be able to give a clearer idea of if we’ll be able to do it then.

Log in to reply

Looks like your connection to CoderDojo Forum was lost, please wait while we try to reconnect.


text:
1. Lmoy's Avatar
    The browser on my Classic runs smooth and lovely for the most part (far better than my old 9900), but for some reason whenever I type anything there's massive lag on the input and frequently the phone can't keep up with my typing speed, and words get jumbled and mashed together even though I'm typing with perfect precision. This isn't a problem anywhere else but the browser. Is anyone else experiencing this? Any information on how to fix it?
    12-30-14 07:51 AM
  2. VeryBumpy's Avatar
    This is a known issue, happens only on certain web sites and has been discussed in another thread...somewhere in here.
    12-30-14 09:35 AM
  3. Denny_Crane's Avatar
    12-30-14 09:03 PM
  4. sheradon's Avatar
    This is also the case on the Q10 for certain sites.

    Fingers->Q10->CB10->Your Eyes.
    12-31-14 04:00 AM

Similar Threads

  1. World of Tanks stickers in BBM Shop, but...
    By DaFoxGrey in forum General BBM Chat
    Replies: 7
    Last Post: 06-22-16, 01:45 PM
  2. Replies: 2
    Last Post: 01-03-15, 12:01 AM
  3. Any updates or issue you want changed in you passport
    By wassim29 in forum BlackBerry Passport
    Replies: 10
    Last Post: 12-30-14, 04:11 PM
  4. What do the blue lines on your Glympse location mean?
    By CrackBerry Question in forum Ask a Question
    Replies: 2
    Last Post: 12-30-14, 09:21 AM


text:
FORUMS: list search recent posts

Motion Tracking?

COW Forums : Apple Motion

<< PREVIOUS   •   VIEW ALL   •   PRINT   •   NEXT >>
Motion Tracking?
on Jan 9, 2007 at 7:42:04 pm

Hello All,

So I know there is this great feature in After Effects where you can select a pixel from your video, and AE will draw you a line of motion that you can follow (or attach a graphic to). For example, if you had video of a truck with a logo on the truck, you could motion track one pixel from that logo, and then go back an lay over a new logo, and AE would make your new logo follow the same path as the video - even off screen.

Can this, or anything like this, be done in Motion?

Return to posts index

Noah Kadner
Re: Motion Tracking?
on Jan 10, 2007 at 1:29:06 am

It's worth searching for plugins but natively no. This is an AfterFX, Shake thing more than Motion.

Unlock the secrets of the DVX100 and Final Cut Pro!

Return to posts index

<< PREVIOUS   •   VIEW ALL   •   PRINT   •   NEXT >>
© 2018 All Rights Reserved


text:
Battery Popped?

Discussion in 'MacBook Pro' started by thriii, Nov 4, 2010.

  1. thriii macrumors 6502

    Feb 14, 2007
    I have my laptop on a stand and I noticed it was a little bit lopsided.. looked under it and it seems the battery popped.. I know my computer wasnt dropped but it has some strange dents like somethin strange happened.. Just seems like it popped or exploded or somethin.. has anyone seen anythin like this?

    Heres a pic

    I got this macbook pro in 2007 so I might not be covered by the warranty.. if I'm not is there anywhere I can buy this battery for the 17 inch MBP C2D?

    Will I be ok running it off the powercord without the battery?
  2. eng42ine macrumors 68000

    May 2, 2010
    Running into a burning building...
    I think that you can still get the batteries from Apple.. Not 100% on that though.

    I ran a '06 MacBook with a bad battery on just the power cord, didn't have any problems

Share This Page