text:
In Haiti, I have visited possible locations to build the Barefoot Haiti School, which will provide education, nutrition and psychological support to displaced children.
As I watched Hope For Haiti on January 22nd, I was taken by how we, as a people, mobilize every time there is a disaster. I was also taken by the amazing performances that took place all night.
Tom Petty's album Pack Up The Plantation was a somewhat rockin' example of his stage shows. In comparison, that release was nothing more than a handful of crumbs compared to the feast that is The Live Anthology.
Imagine if an alien landed outside the auditorium Monday night and snuck in for a peek at our culture by watching the AMA's. What impression would the alien have of women? And our society in general?
It's irresponsible for Republicans to label two new cancer-screening recommendations as partisan-based and illustrative of the sort of "rationing" they claim reform will bring.
As dead tree media consolidate and contract and close here in the United States, newspapers are booming in the tiny Himalayan Kingdom of Bhutan.
I get it: times are tough and demand is high for irrelevant mindless content. I mean, what else would we talk about if we didn't have Kanye's idiocracy?
Songs by John Mayer: You're either (a) an overgrown frat-boy douche or (b) a horny teenage girl. Songs by Miley Cyrus: You're either (a) a preteen girl or (b) a middle-aged male sex offender.
Watching Tom DeLay disgrace himself and the United States Congress over the years, I distinctly remember thinking, "Sure, he's ethically challenged, but can he dance?"
Spanning seventeen years, a proper Annie Lennox retrospective of her solo material finally arrives -- a mix of grooves, ballads, and two new recordings.
We can't remember Washington ever being so cool. What follows are our most unforgettable moments from the inauguration festivities.
Featuring over twenty musicians from four continents who have never met, "Don't Worry" makes its auspicious debut today, on Martin Luther King Day, and is featured here.


text:
Whether you're traveling for business or pleasure, the La Quinta Inn & Suites Seabrook has all the right ingredients for a comfortable stay.
Pet Policy
Pets stay FREE at La Quinta! Domestic pets, like cats and dogs, are welcome to stay at La Quinta. While rooms are spacious, no more than two (2) domestic pets are allowed per room. Be sure to keep your pets on a leash or in a carrier if they're outside your room. Pets may remain alone in a guestroom so long as the pet is well-behaved. With the exception of authorized service animals, pets are not allowed in the breakfast area, the fitness center and the laundry room or at the pool. If your cat is staying with you, you'll need to provide a litter box.
Features and Amenities
- Free Internet Access
- Free Breakfast
ReservationsBook Online or call 281-326-7300
Address & Contact:
3636 Nasa Rd 1
Seabrook, TX 77586
United States
3636 Nasa Rd 1
Seabrook, TX 77586
United States

subset: commoncrawl


text:
This seedling has pretty colors.� I like the burgandy falls.
Someone either on Iris-Photos or Iris
Talk, probably about a year ago, made a very wise comment that has stuck with
me.� I wish his name had stuck with me
too, but names never do.� If you
recognize the orginator of this, please post it for all of us.� He said, "Your seedlings are not
competing against those of any other hybridizer.� They are competing against their own
parents.� Unless they are superior to
their parents, keep them to improve them if you like, but don't even
think of introducing them."�
I try to use this rule in making my own
selections, and I recommend it.� Study
your seedlings and study their parents.�
If the seedling is not an improvement over the parents, the world
doesn't need it.
Francelle Edwards� Glendale, AZ�
Zone 9
-----Original Message-----
From: firstname.lastname@example.com
[mailto:firstname.lastname@example.com] On
Behalf Of mahlberg s
Sent: Saturday, June 03, 2006 7:38
To: firstname.lastname@example.com
Subject: [iris-photos] HYB: TB:
seedling (Oretta's Shadow x Romantic Evening) #2
Hello everybody.
Here's a second seedling to bloom from nine total seedlings.
Oretta's Shadow is a purple self. Romantic Evening is the nice purple standards
with dark, near black falls and red beards.
I can see a lot of Romantic Evening, minus the red beards.
Let me know what you folks think of this or the other seedling I posted photos
This one will need improvement on the plant structure, the branching and bud
count isn't anything exciting. The flower size itself is a bit smaller than the
last seedling I showed.
The standards on this flower appear bright purple in real life and the falls
are burgundy, as close as I can think of to describe the color. I know the
monitors differ, so I am trying to clarify for those who are looking at this
The plant is around 31.5 inches in height.
If you'd like any other photos or information about either of the seedlings,
please feel free to contact me.
thanks for looking,
steve m zone 4b northeastern minnesota
Yahoo! Messenger with Voice. Make
PC-to-Phone Calls to the US (and 30+ countries) for 2�/min or less.


text:
From Longman Dictionary of Contemporary Englishflagflag1 /flæɡ/ ●●● S2 W2 noun [countable] 1 Da piece of cloth with a coloured pattern or picture on it that represents a country or organization Children waving flags greeted the Russian leader. the flag of Kenya the Spanish flaga flag is flying (=a flag is shown on a pole) Flags were flying at half-mast because of the death of the Premier.2 a coloured piece of cloth used in some sports as a signal or as a sign showing the position of something The flag went down, and the race began. a free kick near the corner flag (=flag on a football pitch)3 → the flag4 → keep the flag flying5 TBa flagstone → fly the flag at fly1(13)
Examples from the Corpusflag• His tongue is hanging out of the side of his mouth like a flag.• Sighing deeply, Democratic pundits and brokers are beginning to rally to the Clinton flag.• Colored flags flapped in a heavy sea wind.• He saw the red flag come down for the final time over Red Square in Moscow.• the state flag of Montana• He could hear the beck-water rushing beneath the flags at his feet.• There was talk before everyone arrived here that she might be asked to carry the flag.• And take it down: Hotel is told it can't fly the flag.• The children waved flags as the President's car drove by.Flags ... flying at half-mast• The flags were flying at half-mast.corner flag• With 17 minutes remaining the right-back Mario Melchiot was fouled by Ian Taylor near the left-hand corner flag.• Then winger Crawford Dobbin ran half the length of the pitch for the final score at the corner flag.• Dyer was almost over for a try but put a foot in touch at the corner flag spoiled the effort.• Harte fired the ball into the bottom corner before heading for the corner flag to celebrate.• Then Goodman scored a soft goal with his head for a free kick near the corner flag.• It was Harlequins who opened the scoring ... Mike Wedderburn taking the scenic route to the corner flag.flagflag2 verb (flagged, flagging) 1 [transitive]SHOW/LET somebody SEE something to make a mark against some information to show that it is important I've flagged the parts I want to comment on.2 [intransitive]TIRED to become tired or weak By the end of the meeting we had begun to flag. → flag somebody/something ↔ down→ See Verb table
Examples from the Corpusflag• By the fifth game, I could see that my opponent was beginning to flag.• Japan's economic growth was beginning to flag.• Jenny taught for four hours straight without flagging.• Even so, recent economic reports suggest growth is flagging.• In 1988, the 10-year budget flagged a shortfall looming about five years out, because of a slowdown in population growth.• Provided that none of the entries were flagged as requiring attention, the system will permit their transfer to the Main Database.• The knack for capturing the voice of each character, a trademark of Bogosian as performer, flags at times here.• The pace and enthusiasm flagged considerably when attention had to switch from abstract or grand designs to the nitty-gritty of practical details.• The point is simply to flag problems that loom ahead.• I've flagged the sections I have questions about.• But the commissioned research does flag up a number of interesting pointers to building a bigger core support.• The signals you put across at the job interview can flag your future ambitions.From Longman Business Dictionaryflagflag1 /flæg/ verb [transitive]COMPUTING to put a special mark against a piece of writing or an email to show that it is importantYou'll see that I have flagged the sections that need clarifying.Send the minutes to everyone at the meeting and flag the email for follow-up.→ See Verb tableflagflag2 noun [countable]COMPUTING a special mark that you put against a piece of writing or an email to show that it is important
More results
- flag somebody/something ↔ down
- Flag Day
- red flag
- white flag
- flag-waving
- checkered flag
- Confederate flag
Pictures of the day
Explore topicsSee all topics
Word of the day water down to make a statement, report etc less forceful by changing it or removing parts that may offend people – used to show disapproval
Verb tableflag
|Simple Form
|I, you, we, they
|he, she, it
|> View More
|I, you, he, she, it, we, they
|Present perfect
|I, you, we, they
|have flagged
|he, she, it
|has flagged
|Past perfect
|I, you, he, she, it, we, they
|had flagged
|I, you, he, she, it, we, they
|will flag
|Future perfect
|I, you, he, she, it, we, they
|will have flagged
|> View Less
|Continuous Form
|am flagging
|he, she, it
|is flagging
|> View More
|you, we, they
|are flagging
|I, he, she, it
|was flagging
|you, we, they
|were flagging
|Present perfect
|I, you, we, they
|have been flagging
|he, she, it
|has been flagging
|Past perfect
|I, you, he, she, it, we, they
|had been flagging
|I, you, he, she, it, we, they
|will be flagging
|Future perfect
|I, you, he, she, it, we, they
|will have been flagging
|> View Less


text:
Browse By:
All Agencies (A-Z) » Department of State, Executive
Department of State, Executive (71 - 80 of 1,439 items) in Custom Date Range
Combating Terrorism: Foreign Terrorist Organization Designation Process and U.S. Agency Enforcement Actions
GAO-15-629: Published: Jun 25, 2015. Publicly Released: Jun 25, 2015.
The Department of State (State) has developed a six-step process for designating foreign terrorist organizations (FTO) that involves other State bureaus and agency partners in the various steps. State's Bureau of Counterterrorism (CT) leads the designation process for State. CT monitors terrorist activity to identify potential targets for designation and also considers recommendations for potentia...
Cybersecurity: Recent Data Breaches Illustrate Need for Strong Controls across Federal Agencies
GAO-15-725T: Published: Jun 24, 2015. Publicly Released: Jun 24, 2015.
GAO has identified a number of challenges federal agencies face in addressing threats to their cybersecurity, including the following:Designing and implementing a risk-based cybersecurity program.Enhancing oversight of contractors providing IT services.Improving security incident response activities.Responding to breaches of personal information.Implementing cybersecurity programs at small agencie...
Nonproliferation: State Needs to Establish a Reporting Process That Would Minimize the Delays That May Affect Sanctions on Trade with Iran, North Korea, and Syria
GAO-15-703T: Published: Jun 17, 2015. Publicly Released: Jun 17, 2015.
�The Department of State (State) is not providing reports to congressional committees in accordance with the 6-month reporting requirements of the 2006 Iran, North Korea, and Syria Nonproliferation Act (INKSNA). Since 2006, it has provided six reports covering a 6-year period (2006 through 2011), instead of 18 reports covering a 9-year period (2006 through 2014), as required by INKSNA. State provi...
Nonproliferation: State Should Minimize Reporting Delays That May Affect Sanctions on Trade with Iran, North Korea, and Syria
GAO-15-519: Published: May 22, 2015. Publicly Released: Jun 17, 2015.
The Department of State (State) is not providing reports to congressional committees in accordance with the 6-month reporting requirements of the 2006 Iran, North Korea, and Syria Nonproliferation Act (INKSNA). Since 2006, it has provided six reports covering a 6-year period (2006 through 2011), instead of 18 reports covering a 9-year period (2006 through 2014), as required by INKSNA. State provid...
State Department: Preliminary Observations on the Bureau of Counterterrorism's Resources, Performance, and Coordination
GAO-15-655T: Published: Jun 2, 2015. Publicly Released: Jun 2, 2015.
GAO's preliminary analysis shows that the Department of State's (State) Bureau of Counterterrorism has had an annual increase in authorized full-time equivalent (FTE) positions since fiscal year 2011 and has recently undertaken efforts to reduce a persistent staffing gap. The number of FTEs for the bureau increased from 66 in fiscal year 2011 to 96 in fiscal year 2015, and over the same period the...
Afghanistan: Embassy Construction Cost and Schedule Have Increased, and Further Facilities Planning Is Needed
GAO-15-410: Published: May 19, 2015. Publicly Released: May 19, 2015.
Cost and schedule have increased for the Kabul embassy construction project, in part due to incomplete cost and risk assessment. Cost for the 2009 and 2010 contracts has increased by about 27 percent, from $625.4 million to $792.9 million, and is likely to increase further. Projected completion has been delayed over 3 years to fall 2017. The Department of State (State) did not follow its cost cont...
North Korea Sanctions: United States Has Increased Flexibility to Impose Sanctions, but United Nations Is Impeded by a Lack of Member State Reports
GAO-15-485: Published: May 13, 2015. Publicly Released: May 13, 2015.
U.S. executive orders (EO) and the Iran, North Korea, and Syria Nonproliferation Act target activities for the imposition of sanctions that include North Korean (Democratic People's Republic of Korea) proliferation of weapons of mass destruction and transferring of luxury goods. The EOs and the act allow the United States to respond by imposing sanctions, such as blocking the assets of persons inv...
Yemen: DOD Should Improve Accuracy of Its Data on Congressional Clearance of Projects as It Reevaluates Counterterrorism Assistance
GAO-15-493: Published: Apr 28, 2015. Publicly Released: Apr 28, 2015.
Since fiscal year 2009, the Department of Defense (DOD) has disbursed almost $256 million of the $401 million allocated to Yemen under the Section 1206 and 1207(n) security assistance programs, while the Department of State (State) has committed $34 million of the $95 million allocated under the Foreign Military Financing (FMF) program. In light of Yemen's currently unstable situation, security as...
State Department Construction: Basis for Building versus Leasing Decisions Was Insufficiently Documented at Three Embassies
GAO-15-472R: Published: Apr 24, 2015. Publicly Released: Apr 24, 2015.
The U.S. Department of State's (State) Bureau of Overseas Building Operations (OBO) officials made decisions during the construction or renovation process in Sarajevo, Bosnia and Herzegovina; Belgrade, Serbia; and Helsinki, Finland to lease facilities off-site versus build on-site, but they did not provide a clear explanation of how those decisions were made in the documents they used to plan and...
Summer Work Travel Program: State Department Has Taken Steps to Strengthen Program Requirements, but Additional Actions Could Further Enhance Oversight
GAO-15-265: Published: Feb 11, 2015. Publicly Released: Mar 13, 2015.
Each year, college and university students from all over the world participate in the Department of State's (State) Summer Work Travel (SWT) program. State records show that in 2014, about 79,000 participants from more than 120 countries worked up to 4 months in jobs such as lifeguard, cashier, and resort worker throughout the United States (see map). Participants are meant to experience U.S. cult...


text:
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"Jason's Deli has a large selection of salad and great Rueben sandwhiches. Their is icecream for desert. If you get a Jason's mug, you are able to bring ..."
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"Perrotti" Pizza Restaurant I give Perrotti" Pizza 5 stars - For the best Pizza and Salad in Town. (The stuff is very friendly) If you love pizza you ..."
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"It was the worst pizza I've ever eaten. Too much tomato sauce, not enough cheese, tasteless crust. The delivery time was excellent; the people we dealt with were ..."


text:
responsive website
This project was successfully completed by BompokCode for $263 USD in 14 days.Get free quotes for a project like this
Project Budget$30 - $250 USD
Completed In14 days
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Project Description
I have a website that I need to build as responsive,
attached are samples of the layouts,
it's a relatively simple site
we do a lot of projects, so i am also looking for someone or company i can work with on long term
all bidders, please send ONLY 3-4 website samples that we can check,
decision will be based on code cleanlinless and the most positive feedback
please, only 4+ rating bid
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text:
Cornish Hens Tarragon
|Frozen cornish hens
|3⁄4 Cup (12 tbs)
|Dry white wine
|3⁄4 Cup (12 tbs)
|2 Tablespoon
|6 Clove (30 gm), cut fine (Use Less, If Desired)
|Garlic salt
|To Taste
|To Taste
|To Taste
Let Cornish hens thaw overnight in refrigerator; save giblets.
Melt butter or margarine; add the wine, one tablespoon of the tarragon and garlic.
Use this sauce to baste frequently.
Stuff each hen with 1/2 t.of tarragon, and sprinkle inside with 1/4 t.salt, 1/8 t.pepper and 1/8 t.garlic salt.
Bake in 450 degree oven 45 minutes to 1 hour (depending upon size) being sure to baste often.
Serve garnished with watercress or parsley if desired.
The giblets can be used to make a dressing, preferably with wild rice and place in a casserole.
Serves 6.
Recipe Summary
Rate It
Nutrition Rank
Nutrition Facts
Serving size
Calories 727 Calories from Fat 506
% Daily Value*
Total Fat 57 g87.3%
Saturated Fat 23.8 g119.2%
Trans Fat 0 g
Cholesterol 301.9 mg100.6%
Sodium 272.2 mg11.3%
Total Carbohydrates 5 g1.7%
Dietary Fiber 0.48 g1.9%
Sugars 0.4 g
Protein 43 g85.4%
Vitamin A 23.4% Vitamin C 8.8%
Calcium 10.2% Iron 20.3%
*Based on a 2000 Calorie diet


text:
It's not unusual for many of us to feel a little down in the winter. Going to work and coming home is often done in darkness, and when coupled with the horrible weather, it can be a miserable experience. For some of us, this will be a case of winter blues, but for others it can be the more serious seasonal affective disorder (SAD).
SAD is a type of depression which occurs specifically during the winter months, usually developing between September and November and continuing until March or even longer. Symptoms are normally at their worst during December, January and February.
Who gets SAD?
Around two million people in the UK are believed to be affected by SAD, with around 12 million affected across Northern Europe1. It is more common in countries that don't have year-round sunshine, like those on the equator would experience. SAD generally develops between the ages of 20 and 30, but it can in fact develop at any age. It is also three times more common in women than it is in men.2
The exact causes of SAD are unclear. Sunlight has an incredible effect on the body, sending nerve messages to the brain from the eyes, which can affect chemicals and hormones in the brain, such as serotonin and melatonin. In turn this can affect our moods, and with less sunlight available, this change in hormone balance can lead to depression. Interestingly, between 13-17% of people who develop SAD have an immediate family member who is also affected. 3
Symptoms of SAD
People affected by SAD may notice that they start to develop symptoms in September, which can gradually get worse as winter goes on. Between September and October, you may feel:
- Lethargic and lacking in energy
- A craving for sweet and starchy foods
- An increased appetite
- Difficulty in waking up each morning.
Between November and December, you may also notice:
- An increase in weight
- Sleeping for longer
- Difficulty in concentrating
- A lower libido
- Feelings of withdrawal from family and friends.
During January and February, you may feel more anxious or irritable than normal, along with other symptoms of depression. Unlike other forms of depression however, the symptoms are likely to disappear quickly once spring arrives. In small numbers of cases, feelings of depression will change into elation or abnormally high moods, known as mania or hypomania.
The difference between SAD and depression
A specific diagnosis of SAD can only be made by looking back at your history, normally a period of at least two years where you have developed depression-like symptoms in the winter without showing any signs during the spring or summer. Some SAD symptoms are also less usual in classic depression, such as craving sweet foods, increased appetite, weight gain and sleepiness.
It is possible to have SAD for several years without you or your doctor realising. As recurring depression is fairly common, it is possible to be treated for it several times over the years before the seasonal pattern is noticed.
Getting treatment for SAD
There are a number of treatments available for SAD, and indeed, for the more milder winter blues. These include:
- Self help: Making plans to make the most out of any natural sunlight in a day is always a good start, while taking a winter holiday is also a good idea if you can afford it. Even if the holiday only involves staying at home, getting out in the daytime will help lift your brain hormones and chemicals. Telling your family how you are feeling will also help, as will making plans for the spring to give you something to look forward to. Regular exercise can also help
- Light therapy: Light therapy involves sitting in front of a special bright light for a while each day, which many people have found helps to improve their moods. While it is difficult to say if there is any more than a placebo effect, doctors are generally positive about this form of treatment. However, it can take time to work properly so stick with it
- Depression treatment: The depression symptoms of SAD can be treated in the same way as those of classic depression, which includes antidepressant medicine, or psychological treatment such as cognitive behavioural therapy. Your doctor will be able to help identify which of these options could be suitable for you.
1. http://www.nhs.uk/conditions/Seasonal-affective-disorder/Pages/Introduction.aspx
2. http://www.rcpsych.ac.uk/healthadvice/problemsdisorders/seasonalaffectivedisorder.aspx
3. http://www.lef.org/Protocols/Emotional-Health/Seasonal-Affective-Disorder/Page-03?p=1


text:
Game Killer APK is a must have app for every rooted android phone. The best thing about smartphones is its capability and flexibility. One can run many revolutionary applications on their android phones and tablets. Today I am about to talk about a very unique and special apk app which will give you more control over your phone. With Game Killer Apk you can handle the games you have installed. Gamekiller apk has got millions of downloads and all the users are satisfied. There is one big issue with apps like game killer apk that these apps does not support all the android versions. The app belongs to the category of trendy games like Geometry Dash Apk and Clash of Clans Mod Apk.
Game Killer apk is not available on your regular Android Play Store. You have to download it from an online app downloads site, which are plenty in number. What might turn off users from using GameKiller apk is that it has a barebones UI which may cause some users to flock to more illustrious counterparts. But the catch is that the bare bones structure is what makes it so easy to hack the games with this application. In fact, if a newbie were to try his or her hands at game hacking, this is the application that we would recommend.
Game Killer APK
- Searches of game worth with right numbers, HEX edit, unload code and save the taken care of list.
- Well the more you go in depth of game killer apk more you come to know about this app and features.
- You can lock the video game value to a repaired number.
- Modification is quite easy with gamekiller apk and specially in difficult apps.
- You can explore more about game killer when you will use it according to your need or in connection with the app or game you want to use it.
Game Killer APK Download and Install
Here I request you to follow some steps so that you can get and install gamekiller apk in your phone without any issue at all. As usual we are sharing the latest and tested version of this applications.
STEP 1 > Download Game Killer Apk from below mentioned link and if you are downloading it in your PC then move it in you phone.
STEP 2 > Now in the file manager of your phone you will find game killer apk file and click on it to begin installation process. But before this step you should close all the running games and apps.
STEP 3 > During installation if your phone requires permission to install application from unknown resources then allow your android device to do so. Its safe and easy.
STEP 4 > After installation restart your phone and if you like game killer apk then share your review and thoughts in the comment section.


text:
Functional interaction between mouse erbB3 and wild-type rat c-neu in transgenic mouse mammary tumor cells
- Aeree Kim†1, 2,
- Bolin Liu†1,
- Dalia Ordonez-Ercan1,
- Kathy M Alvarez1,
- Lynn D Jones1,
- Christine McKimmey1,
- Susan M Edgerton1,
- XiaoHe Yang1 and
- Ann D Thor1Email author
DOI: 10.1186/bcr1281
© Kim et al. licensee BioMed Central Ltd. 2005
Received: 7 December 2004
Accepted: 10 June 2005
Published: 6 July 2005
Co-expression of several receptor tyrosine kinases (RTKs), including erbB2 and erbB3, is frequently identified in breast cancers. A member of the RTK family, the kinase-deficient erbB3 can activate downstream signaling via heterodimer formation with erbB2. We studied the expression of RTK receptors in mammary tumors from the wild-type (wt) rat c-neu transgenic model. We hypothesized that physical and functional interactions between the wt rat neu/ErbB2 transgene and mouse ErbB3-encoded proteins could occur, activating downstream signaling and promoting mammary oncogenesis.
Immunohistochemical and Western blot analyses were performed to study the expression of rat c-neu/ErbB2 and mouse erbB3 in mammary tumors and tumor-derived cell lines from the wt rat c-neu transgenic mice. Co-immunoprecipitation methods were employed to quantitate heterodimerization between the transgene-encoded protein erbB2 and the endogenous mouse erbB3. Tumor cell growth in response to growth factors, such as Heregulin (HRG), epidermal growth factor (EGF), or insulin-like growth factor-1 (IGF-1), was also studied. Post-HRG stimulation, activation of the RTK downstream signaling was determined by Western blot analyses using antibodies against phosphorylated Akt and mitogen-activated protein kinase (MAPK), respectively. Specific inhibitors were then used with cell proliferation assays to study the phosphoinositide-3 kinase (PI-3K)/Akt and MAPK kinase (MEK)/MAPK pathways as possible mechanisms of HRG-induced tumor cell proliferation.
Mammary tumors and tumor-derived cell lines frequently exhibited elevated co-expression of erbB2 and erbB3. The transgene-encoded protein erbB2 formed a stable heterodimer complex with endogenous mouse erbB3. HRG stimulation promoted physical and functional erbB2/erbB3 interactions and tumor cell growth, whereas no response to EGF or IGF-1 was observed. HRG treatment activated both the Akt and MAPK pathways in a dose- and time-dependent manner. Both the PI-3K inhibitor LY 294002 and MEK inhibitor PD 98059 significantly decreased the stimulatory effect of HRG on tumor cell proliferation.
The co-expression of wt rat neu/ErbB2 transgene and mouse ErbB3, with physical and functional interactions between these two species of RTK receptors, was demonstrated. These data strongly suggest a role for erbB3 in c-neu (ErbB2)-associated mammary tumorigenesis, as has been reported in human breast cancers.
The erbB or epidermal growth factor receptor (EGFR) family forms subclass I of the receptor tyrosine kinase (RTK) superfamily. Type I RTKs are expressed by epithelial, mesenchymal and neural tissues to regulate cell proliferation, differentiation and other important biological functions critical to species development [1]. Dysregulated expression of erbB receptors or mutational events thereof have been implicated in diverse types of human cancers [1, 2]. Members of the family include: ErbB1 (also known as EGFR), ErbB2 (also known as Her-2 or neu), ErbB3 (or Her-3) and ErbB4 (or Her-4) [3–7]. erbB2 is an orphan receptor whereas other family members directly bind ligands (like the epidermal growth factor (EGF) and transforming growth factor-α (TGF-α) for EGFR, and HRG for erbB3 and erbB4) to initiate intracellular signaling [8].
ErbB2 may be activated via either ligand-dependent heterodimeric, or ligand-independent homodimeric processes. In the former, erbB2 is the preferred heterodimerization partner for other erbB family receptors with bound ligand [9]. In ligand-independent signaling, erbB2 may be upregulated as a result of gene amplification, promoting homodimerization, or be activated through mutational events. ErbB2 amplification with enhanced protein expression is noted in approximately one-third of invasive human breast cancers [10]. Selected heterodimers may enhance receptor activation and downstream signaling as compared with homodimers [1, 11, 12]. Although erbB3 lacks a functional kinase to initiate cell signaling [13, 14], the erbB2/erbB3 heterodimer complex is believed to be the most biologically active and pro-tumorigenic form of these receptor complexes [15, 16].
The erbB receptors and their respective ligands influence a wide range of cellular processes such as proliferation, maturation, survival, apoptosis and angiogenesis [11, 17–19]. In general, activated RTKs add phosphorylated tyrosine residues to downstream signaling molecules, such as the p85 subunit of phosphatidylinositol 3-kinase (PI-3K), Shc and/or Grb2 of the mitogen-activated protein kinase (MAPK) pathway. However, because of the complexity of RTK ligand-dependent and -independent mechanisms, the downstream signaling effects may be highly diverse and interactive. RTK-induced signaling is also influenced by, and may modulate, other molecular factors and signaling pathways.
The ErbB2 gene-encoded protein is over-expressed in 25 to 30% of invasive breast and ovarian cancers and has been associated with a poor clinical outcome [20–25].
Evidence of a causal relationship in human breast cancer has been derived from numerous prognostic studies and clinical trials. In vivo and in vitro model systems including transgenic mouse models support a relationship between erbB2 alterations and mammary tumorigenesis. Overexpression of erbB3 is also frequently reported in erbB2 altered breast, ovarian and bladder cancers [23, 26, 27]. Human breast cancer cell lines commonly co-overexpress both erbB2 and erbB3, further supporting their role in breast carcinogenesis [2, 11].
To investigate the role of RTKs in mammary tumorigenesis, transgenic mice bearing the wild-type (wt) or mutated, activated rat c-neu (ErbB2) were generated, and have been widely studied [28–31]. Transgenic mice expressing the activated rat c-neu (with deletion mutations) bear mammary tumors with elevated co-expression of the mutant c-neu/ErbB2 and the endogenous mouse ErbB3-encoded protein [32]. Functional and physical interactions between these two cross-species receptors have not been reported, although interactions have been widely speculated. Transgenic mice bearing the wt-rat c-neu, under control of the mouse mammary tumor virus promoter (MMTV-LTR), typically develop unifocal, well-circumscribed, low-grade tumors after a long latency [29]. In addition to transgene expression and, in some cases, mutation, upregulation of EGFR and p53 have been reported in derived tumors [33, 34].
We have used the wt-erbB2 transgenic mouse model to study the effects of exogenous pharmacological or dietary estrogens and anti-estrogens. In particular, we have studied interactions between RTK-associated mammary tumorigenesis and steroid hormones. From the derived mouse tumors, we have established over 150 novel murine cell lines which have proven useful for in vitro studies [35, 36]. Most tumor-derived cell lines express significant mouse ErbB3-encoded protein, in addition to high levels of the rat c-neu/ErbB2 transgene. These are also typically negative for ERα but show ERβ protein expression. A similar pattern of receptor expression has also been detected in the mouse mammary tumors.
The co-expression of erbB3 with erbB2 in both the activated and wt-neu/ErbB2 transgenic model systems suggested a biological role for erbB3 in mammary tumor pathogenesis. We hypothesized that physical and functional interactions between these RTK receptors should occur, despite their cross-species molecular structures. Signaling initiated by activated erbB2/erbB3 heterodimers should provide a more potent oncogenic signal than erbB2 homodimers alone. This would require ligand binding, most likely HRG, to activate erbB3. To test this hypothesis, we studied the responsiveness of tumor-derived cell lines to growth factors, including HRG, EGF and insulin-like growth factor-1 (IGF-1); we evaluated the effects of ligand stimulation and heterodimer formation on downstream signaling activation; and we sought evidence of physical interactions between the wt-rat c-neu/erbB2 and the endogenous mouse erbB3.
Materials and methods
Cells and cell culture
Human breast cancer cell lines SKBR-3 and BT-474 were obtained from the American Type Culture Collection (Rockville, MD, USA) and maintained in DMEM and Ham's F-12 medium (1:1, v/v) (Invitrogen Corp, Grand Island, NY, USA) supplemented with 10% FBS (Invitrogen Corp). These cell lines were cultured in a 37°C humidified atmosphere containing 95% air and 5% CO2 and were split twice a week. These human breast cancer cells were used primarily as controls.
Establishment of novel, mouse mammary tumor cell lines
Mammary tumors were obtained from the transgenic mice by surgical removal immediately following euthanasia, according to our approved IACUC protocol. The histological pattern and tumor diagnoses were confirmed by microscopic analysis. These methods have been previously described in detail [35], although the specific cell lines described in this work have not been previously published. In brief, solid tumor tissue was transferred into a tissue culture dish containing PBS. After removal of mammary fat and connective tissues, tumors were minced into small pieces and treated with 0.25% trypsin-EDTA (Invitrogen Corp) at 37°C for 30 min. Cells were subsequently centrifuged at 1,200 rpm for 5 min. After discarding supernatant, cells were suspended in DMEM/F12 medium supplemented with 10% FBS and 1% antibiotics and antimycotics (Invitrogen Corp). These mammary tumor cells (~1.0 × 106 cells/plate) were seeded in tissue culture dishes and kept in a 37°C humidified atmosphere containing 95% air and 5% CO2. The media was changed twice a week to maintain cells in culture. Each line was passaged approximately 20 times before stability was assumed.
Soft agar cloning assays
Soft agar cloning was performed as described previously [35] with some modification. The bottom agar was prepared with a mixture of 1.6 ml of 1 × DMEM/F12 (complete medium), 3.2 ml of 2 × DMEM/F12 (complete medium), and 3.2 ml of 1.25% Noble agar (Sigma Co, St Louis, MO, USA) and maintained at 42°C. From this, 2 ml was pipetted into each well of six-well cell culture plates and agar was allowed harden in the hood. For each well, top agar was a mixture of 0.2 ml of 1 × DMEM/F12, 0.4 ml of 2 × DMEM/F12, and 0.4 ml of 0.95% Noble agar. Five thousand cells (in 80 μl complete medium) were added into the top agar mixture. After vortexing gently, the cell containing top agar was added in a drop-wise fashion onto the bottom agar containing six-well plates (in triplicate per cell line). After resting for 10 min in the hood, the six-well plates were cultured in a 37°C incubator for 3 weeks. Colony counts were obtained under an inverted microscope, from three wells per cell line counting all colonies >50 μM in diameter.
Doubling time in culture
Measurement of cell growth rate in culture was determined using sulforhodamine B (SRB; Sigma Co) assays as previously described [35]. Two thousand cells were seeded into each well of a six-well plate with complete medium. Cells were fixed with 50% trichloroacetic acid (TCA) at 24 h intervals for 3 days. TCA-fixed cells were then stained with 0.4% SRB for 30 min followed by three washes. Protein-bound dye was dissolved in 10 mM Tris base. Plates were read at 565 nM using a micro-plate reader. Cell-doubling time was calculated based on proliferation curves that resulted from changes in SRB absorbance over time. Data represent the means of at least three independent experiments.
Cell proliferation assay
A CellTiter96™ AQ non-radioactive cell proliferation kit (Promega Corp, Madison, WI, USA) was used to determine the responsiveness of cells to various growth factors. Cells were plated onto 96-well plates, 5,000 cells/well for each cell line. Twenty-four hours later, the culture media were replaced by 0.5% FBS in DMEM/F12 fresh medium or the same medium containing 25 ng/ml HRG (R&D Systems, Inc, Minneapolis, MN, USA), 10 ng/ml EGF (Sigma Chemical Co), or 40 ng/ml IGF-1 (R&D Systems, Inc) for another 72 h incubation with 5% CO2 at 37°C. After reading at 490 nM with the micro-plate reader, the percentages of viable cells were determined by reduction of MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium; inner salt) relative to controls. Data reflect the means of at least three independent experiments.
RT-PCR and DNA sequencing analysis
RT-PCR analyses were performed as previously described [37]. The primers specific for rat neu were synthesized according to the literature [38]. Forward primer AB2913, 5'-CGG AAC CCA CAT CAG GCC-3' and reverse primer AB1310, 5'-TTT CCT GCA GCA GCC TAC GC-3' amplify the region corresponding to nucleotides 1492 to 2117 of rat neu cDNA [38]. The PCR products purified from agarose gel using QIAquick Gel Extraction Kit (Qiagen, Inc, San Valencia, CA, USA) were submitted to the core facility at the Oklahoma Medical Research Foundation for direct sequencing.
Immunohistochemical staining of mammary tumor tissues was performed as previously described [39]. Briefly, after deparaffinization and rehydration, tissue sections were steamed in a 10 mM citrate buffer, pH 6.0, for 30 min. Non-specific reactivity was blocked with 0.3% H2O2 in buffer. For erbB3 immunoassays, CAS Block (Zymed Laboratories, Inc, South San Francisco, CA, USA) and 10% normal horse serum (Vector Laboratories, Inc, Burlingame, CA, USA) were used sequentially. For phospho-Akt immunostaining, we used 1% H2O2 and 5% normal goat serum (Vector Laboratories, Inc) sequentially. Primary antibodies included an anti-erbB2 (reactive with rat c-neu/erbB2 rabbit polyclonal, dilution 1:1000 (Dako, Carpinteria, CA, USA) for 2 h incubation at room temperature), anti-erbB3 (cross-reacts with mouse and human, mouse monoclonal, dilution 1:50 (NeoMarkers, Inc, Fremont, CA, USA), overnight incubation at 4°C), anti-phospho-Akt (rabbit polyclonal, diluted in 5% normal goat serum 1:12.5 (Cell Signaling Technology, Beverly, MA, USA), overnight at 4°C), or anti-phospho-MAPK (E10 monoclonal antibody, diluted in 5% normal goat serum 1:25 (Cell Signaling Technology), overnight at 4°C). After multiple washes with buffer, tissue sections were sequentially incubated for 30 min at room temperature with diluted biotinylated secondary antibody (1:500; Dako) and VECTASTAIN Elite ABC reagent (Vector Laboratories, Inc) diluted in PBS. After reaction with diaminobenzidine (Dako) and counterstaining with hematoxylin, tumors were individually examined. Each slide was evaluated in its entirety for antigen expression, cell type and histopathological diagnoses.
Immunoprecipitation and Western blot analysis
Immunoprecipitation and Western blot assays were performed as previously described [40]. Briefly, cells were lysed in NP-40 lysis buffer (50 mM Tris-HCl, pH 7.4, 150 mM NaCl, 0.5% NP-40, 50 mM NaF, 1 mM Na3VO4, 1 mM phenylmethylsulfonyl fluoride, 25 μg/ml leupeptin, 25 μg/ml aprotinin). The supernatants were cleared by centrifugation. Protein concentrations were measured using the Coomassie plus protein assay reagent (Pierce Chemical Co, Rockford, IL, USA). Total cell lysates containing 200 μg of protein were subjected to immunoprecipitation in the presence of 1 μg anti-erbB2 antibody (mouse monoclonal antibody, Ab-4; Oncogene Science Products, Cambridge, MA, USA) for 2 h at 4°C, followed by incubation with immobilized protein A-agarose (Roche Diagnostics Corp, Indianapolis, IN, USA) at 4°C overnight with rotation. For Western blot analyses, the immunoprecipitates or equal amounts of crude extracts were boiled in Laemmli SDS-sample buffer, resolved by SDS-polyacrylamide gel electrophoresis, transferred to nitrocellulose (Bio-Rad Laboratories, Hercules, CA, USA), and probed with different primary antibodies. After the blots were incubated for another 1 h at room temperature with horseradish peroxidase-labeled secondary antibody (goat anti-rabbit IgG or goat anti-mouse IgG; Perkin Elmer, Boston, MA, USA), the signals were detected using the Enhanced Chemiluminance assay (Amersham Life Science Inc., Arlington Heights, IL, USA) according to the manufacturer's instructions.
Co-expression of erbB2 and erbB3 protein in tumor-derived cell lines and tumors
Anchorage-independent cloning of mammary tumor-derived cell lines
Cell Lines
Colonies in soft agarb
Sequencing analyses of the transgene neuin established mammary tumor-derived cell lines
Mammary tumor cell response to growth factors corresponds with erbB receptor data
HRG activation of PI-3K/Akt and MAPK kinase (MEK)/MAPK signaling promotes mammary tumor cell growth
Physical interaction between wt-rat-c-neu/ErbB2 and endogenous mouse erbB3
We have shown that transgenic mice bearing the wt-rat c-neu gene, under control of the MMTV promoter, develop mammary tumors that overexpress the rat c-neu transgene [45, 46] and the endogenous mouse erbB3 protein, in the vast majority of cases. We have shown a functional interaction between these two important RTK receptors and a role for ligand-induced signaling in vitro and in vivo. While others have reported that transgenic mice bearing activated forms of rat c-neu/erbB2 have co-expression of erbB2 and endogenous erbB3 in mammary tumors [32], direct physical and functional interactions between these two species receptors have not previously been reported.
Deletion mutants of the neu oncogene have been reported in two out of three of the mammary tumors derived from this wt-rat c-neu transgenic model [38]. We did not find the same mutation rate or type in selected tumor-derived cell lines. However, we have identified a potential point mutation in 83923 cells (Fig. 3). This missense mutation is located inside the same extracellular region of neu where the deletion mutations have been reported. This particular mutation changes the amino acid 654 serine (codon AGC) into cysteine (codon TGC). It is different from the active neu mutation G664V reported in the transmembrane domain [47]. The biological significance of the newly discovered S654C mutant neu is not yet known.
Using ligand stimulation with or without specific inhibitors, we have studied RTK-induced signaling in response to HRG and have shown activation of both PI-3K/Akt and the MEK/MAPK signal transduction pathways. A greater role for PI-3K/Akt signaling was suggested in response to HRG treatment (Fig. 7). PI-3K/Akt signaling is known to be regulated by erbB2-mediated tyrosine kinase activity. This pathway plays a crucial role in cell proliferation and survival [18] and has been associated with the pathogenesis of human breast cancers. PI-3K/Akt activation has also been cited as a key pathway that influences chemo-resistance patterns [48, 49]. Akt is frequently upregulated in ErbB2 amplified or overexpressing human breast cancer cells. These similarities between our transgenic model and human breast carcinogenesis suggest that the model and derived tumor cell lines may be a useful resource to study ligand dependent and independent RTK signaling in vivo and in vitro.
As a major ligand for erbB3, HRG is known to bind to erbB3, foster heterodimer complex formation and promote potent downstream signaling [12]. HRG can thus promote mammary tumorigenesis, cell growth, differentiation and phenotypic aggression [50]. Our immunohistochemical studies of tumors for phosphorylated proteins facilitated studies of the cellular location and architectural context of signaling. We noted enhanced phosphorylated Akt and MAPK in a perivascular distribution in mammary tumors, with overexpression of both erbB2 and erbB3 (Fig. 6), suggesting that circulating HRG may enhance the physical and functional erbB2/erbB3 interactions in vivo, similar to what we observe in vitro. This study has focused primarily on erbB3, whereas others have demonstrated upregulation of EGFR in tumors (by immunohistochemistry and Western blot) in the same model system [33]. Low and variable expression of EGFR has also been found in mammary tumors that develop in transgenic mice bearing activated forms of rat c-neu/ErbB2 [32]. Using in vitro analyses of the tumor-derived cell lines, we have found no significant physical or functional interaction between EGFR (erbB1) and erbB2 in the presence of EGF (data not shown). However, by immunohistochemical study, we also detected erbB1 expression at the tumor periphery as reported by DiGiovanna [33]. These data suggest to us that erbB3 plays a more significant role in tumorigenesis than erbB1 in this model system.
These data and this model probably have relevance to human breast cancer biology and treatment strategies. We have reported that only a minority of erbB2-altered invasive human breast cancers have overexpression of erbB1 (EGFR) and activation of erbB2 [51]. Given the complexity of the RTK receptors, various ligands and downstream signaling, it is likely that combinations of these factors including erbB3 contribute to cell signaling, biological behavior and treatment response [52, 53]. To date, the role of erbB3 in human breast carcinogenesis is not well defined, although many investigators have suggested that HRG-associated signaling may be important. In view of these complexities, it is not surprising that erbB2 aberrant breast cancers have shown variable responses to anti-erbB2 therapeutics [52, 53]. It is widely believed that co-expression of other erbB RTK family members may be one mechanism of Herceptin resistance [54]. Ligand-induced heterodimerization between erbB3 and erbB2, the most potent signaling complex amongst the various heterodimers, is one likely mechanism of Herceptin resistance [55]. More detailed investigations using banks of human tumors and clinical trial-associated specimens, to define the incidence of erbB3 abnormalities, functional complex formation and downstream signaling, may provide important new clues regarding these interactions and their role in breast carcinogenesis.
Our results indicate that over-expression of endogenous mouse erbB3 plays an important role in the development and progression of mammary tumors that arise in mice bearing the wt-rat c-neu transgene. The functional and physical interactions between these important cross-species erbB receptors result in activation of both PI-3K/Akt and MEK/MAPK signaling. These data support the concept that ligand-dependent and -independent signaling through erbB2 may promote mammary tumorigenesis in these transgenic mice, similar to what is observed in human breast cancers.
Dulbecco's modified Eagle's medium
epidermal growth factor
EGF receptor
estrogen receptor
fetal bovine serum
insulin-like growth factor-1
- mAb:
monoclonal antibody
mitogen-activated protein kinase
MAPK kinase
mouse mammary tumor virus
phosphate-buffered saline
receptor tyrosine kinase
phosphoinositide 3-kinase
reverse transcription-polymerase chain reaction
sulforhodamine B
trichloroacetic acid
- TGF-α:
transforming growth factor-α.
This work was supported by NIH 1RO1 CA82848 and 1P50 CA89018 to ADT.
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- Knuefermann C, Lu Y, Liu B, Jin W, Liang K, Wu L, Schmidt M, Mills GB, Mendelsohn J, Fan Z: HER2/PI-3K/Akt activation leads to a multidrug resistance in human breast adenocarcinoma cells. Oncogene. 2003, 22: 3205-3212. 10.1038/sj.onc.1206394.View ArticlePubMedGoogle Scholar
- Lupu R, Cardillo M, Cho C, Harris L, Hijazi M, Perez C, Rosenberg K, Yang D, Tang C: The significance of heregulin in breast cancer tumor progression and drug resistance. Breast Cancer Res Treat. 1996, 38: 57-66. 10.1007/BF01803784.View ArticlePubMedGoogle Scholar
- DiGiovanna MP, Stern DF, Edgerton S, Whalen SG, Moore D, Thor AD: Relationship of epidermal growth factor receptor expression to ErbB2-signaling activity and prognosis in breast cancer patients. J Clin Oncol. 2005, 23: 1152-1160. 10.1200/JCO.2005.09.055.View ArticlePubMedGoogle Scholar
- Baselga J, Tripathy D, Mendelsohn J, Baughman S, Benz CC, Dantis L, Sklarin NT, Seidman AD, Hudis CA, Moore J, et al: Phase II study of weekly intravenous recombinant humanized anti-p185HER2 monoclonal antibody in patients with HER2/neu-overexpressing metastatic breast cancer [comment]. J Clin Oncol. 1996, 14: 737-744.PubMedGoogle Scholar
- Cobleigh MA, Vogel CL, Tripathy D, Robert NJ, Scholl S, Fehrenbacher L, Wolter JM, Paton V, Shak S, Lieberman G, Slamon DJ: Multinational study of the efficacy and safety of humanized anti-HER2 monoclonal antibody in women who have HER2-overexpressing metastatic breast cancer that has progressed after chemotherapy for metastatic disease. J Clin Oncol. 1999, 17: 2639-2648.PubMedGoogle Scholar
- Cardoso F, Piccart MJ, Durbecq V, Di Leo A: Resistance to trastuzumab: a necessary evil or a temporary challenge?. Clin Breast Cancer. 2002, 3: 247-257.View ArticlePubMedGoogle Scholar
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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0,) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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1 (800) 279-8461
Principal Bios
Lake Washington Custom in Seattle is a magnificent architectural success!
Leaders in Custom Home Design & Building Services
Welcome to the Leader in Custom Home Designs & Home Building Construction in Seattle
Schenkar Custom Home Construction
continues to be Seattle's most reputable custom home builder. We provide custom home construction, home remodeling and residential remodeling. The design/build model allows our clients access to the finest services available in the custom remodeling contractor market. We are proud to deliver the finest services available for new home construction, home remodeling, and residential remodeling as Seattle's premier custom home builder. The design/build model provides our clients a comprehensive approach to "custom" building and remodeling.
Our most recent project and publication
Modern Home Builder Magazine
, Schenkar Construction strives to integrate creative architectural solutions to a wide variety of projects and client needs. There is a quintessential need to integrate both "Design" and "Build" during the course of any project. Seattle Design/Build provides a necessary skill set to evaluate the costing of the project as it is being designed. The article highlights the important advantages of this model which results in setting clear and definitive expectations for the client from day one. Our experience has demonstrated how successful this approach is. We have a team of architects, designers, and structural engineers that study and evaluate all aspects of the project in order to coordinate all resources simultaneously during the development process.
Schenkar Construction has around 65-70 tradesman preforming everything from excavation, concrete, framing, electrical and plumbing to drywall, roofing, custom cabinets, flooring and tile. The company's primary services include architecture, design, structural engineering, permit facilitation and general contracting. Schenkar Construction can handle a wide array of projects, including new construction, large-scale remodeling, steep slope construction, house lifting, foundation stabilization, bathrooms and kitchens.
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From the Blog:
Seattles most reputable custom home builder
I really commend this builders creative idea about how to highlight his firms flexibility and ability to customize their work to suit a homeowners tastes and preferences.
Schenkar Construction Videos
Here are a couple videos of some of our most recent work. I wanted to personally thank all of my clients and consultants for contributing to our continued progress as a company. Please take a moment.
"Feature News"
"We are proud to be chosen for the feature article in the national publication of Modern Home Builder Magazine."
Magnolia Waterfront Custom
"This waterfront masterpiece on the shores of Puget Sound in the North Magnolia neighborhood of Seattle allows for fantastic opportunities to integrate sunlight and water views."
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Lake Washington Custom
This 3000 SF custom home on the shores of Lake Washington is Seattle is a magnificent architectural success! The mixed genre of exterior siding materials includes: Vietnamese Mahogany, Galvanized aluminum.
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West Seattle Custom
This West Seattle Custom is an outstanding representation of the craftsman period genre. It was designed by our architect to meet all the specifications of our client to achieve their needs of space planning.
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Samammish Custom
This 4500 SF custom on the shores of Beaver Lake is a beautiful example of mixed genre European design. There are (5) bedrooms, (3) bathrooms, all on a (1) acre wooded lot with views of the lake.
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Lakehouse Project
The Lake House was built for one of our clients whose design concept incorporated a variety of mediums including: steel, glass, and concrete in order to create a state of the art fully automated eco-friendly masterpiece.
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Sandpoint Custom
This masterfully designed custom in Sandpoint embodies true mixed genre design. The exterior reflects more Northwest traditional craftsmanship integrated with modern accent materials of steel, aluminum and paneled siding.
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West Seattle Studio
This 1000 SQ. FT custom studio or mother in law is a fantastic example of integrating traditional NW design with ultra high-end materials to create a curb appeal that will speak for itself.
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Bellevue Custom Kitchen
"This Bellevue custom kitchen exemplifies extraordinary finishes. The counter tops are an extremely rare Calcutta white marble hand chosen in Italy. Each slab was hand fabricated and installed to the client's exact specifications."
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Here are a variety of projects that reflect a wide range of genres, designs and styles. We are capable of delivering any type of style from traditional craftsman to NW traditional, to ultra-modern.
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Here are a number of images showing some of our recent house lifting projects. Please take a moment to visit our blog in conjunction with this portfolio and consider the true value of the house lifting process.
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White Project
This historic 1924 craftsman home was slated for demolition. We worked with our clients to raise and move this home nearly 20 city blocks down California ave to place it on a new lot at 2758 46th Ave SW.
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With the news arriving yesterday that "Lost" co-creator and "Star Trek" director J.J. Abrams will take over from George Lucas and direct "Star Wars: Episode VII," the first in a planned platoon of new "Star Wars" features from Disney, it inevitably means speculation about what, exactly, such a decision will mean for the franchise.
This is, after all, a series that has been almost exclusively under the control of a single man since the original debuted back in 1977 (the two sequels from the original trilogy were directed by journeyman filmmakers under the tight authorial control of Lucas, who exerted his influence more extensively with his constant fussing on the "special editions"). So it seemed like a good moment to start to guess what a J.J. Abrams "Star Wars" joint will really look (and feel and sound) like, based on his earlier work and a general sensation of where the franchise is headed – back to a long time ago and a galaxy far, far away….By the way, in case you missed it here's five directions we suggested the series could go back when it was announced in October of last year.
Lots of lens flares and whip pans? Maybe not so fast.
It birthed a million Twitter jokes, and it is true that Abrams has a trademark visual style, but will he bring the same tools from "Star Trek" to "Star Wars"? The original films had a certain "look," it's one that isn't exactly easy to pin down – a combination of psychedelic '70s album art, pulp magazine covers, and various sci-fi conventions. (The shiny robot! The floating barge lair! A city in the clouds!) By the time the prequels rolled around, Lucas had firmly planted himself in the director's chair and any sense of visual distinction had been blasted into the deep recesses of space. Instead, Lucas relied on extensive green screen work with an emphasis on computer-generated environments, characters and creatures. While seemingly cutting edge, it made the actual human actors seem like they were walking through some elaborate videogame. Nothing felt real or emotionally identifiable – the heart got lost in the pixels. Abrams has a style he honed on both his television series (most notably "Alias," still his crowning small screen achievement) and in the three high-profile features he directed ("Mission: Impossible III," "Super 8" and "Star Trek"), and while it feels like a safe assumption that we'll see some whip pans and lens flares, we're not so sure. One of the biggest concerns among certain segments is having the same guy behind "Star Trek" taking over "Star Wars." We're sure Abrams will want to put a new visual stamp on this franchise not only to assuage fans, but to honor where the series has been while also taking it in a new direction in addition to ensuring it stands apart from Captain Kirk and the gang.
Actual environments!
Along similar lines, one of the better aspects of Abrams' "Star Trek" is that no matter how much computer-generated embroidery was on display, a large majority of the movie was created practically. The movie utilized expansive sets that took up whole soundstages along with actual location photography, like the Budweiser bottling plant that doubled as the spaceship's engine room. He even filmed the skydiving sequence by getting Chris Pine to roll around on a mirror in the Paramount parking lot. Sure, there was a shitload of CGI, but most of that work was done for stuff that Abrams and his talented creative crew couldn't physically build, like the giant snow monster that chases Kirk down an icy hill. "Mission: Impossible III" and "Super 8" too, for all their widescreen spectacle, aren't completely bogged down by ones-and-zeroes, either. We can see Abrams returning to actual location work, ditching much of the smothering green-screen aesthetic, and insisting on props and creatures that were actually built and controlled on set. You know, like how Yoda used to be an on-set puppet before he was turned into a pin-balling tree frog with a lightsaber.
Michael Giacchino does John Williams.
Again. It's getting on eight years since John Williams, the composer of all six "Star Wars" movies to date, wrote a score for anyone but Steven Spielberg (2005's "Memoirs Of A Geisha"). Williams will be close to 85 years old when this new film is being finalized and there's a high probability he'll actually be really-for-real retired by that point. But it's possible that Abrams may not even go back to that well at all. Michael Giacchino, Abrams' longtime composer, will certainly do a bang-up job if he's called for the gig. The musical groundwork has already be laid, as the films will undoubtedly utilize the famous themes that are hummed the world over. What Giacchino will do is fill in the gaps, creating music that harkens back to the beloved original score while striking new, thematically appropriate ground. For Abrams' "Super 8," Giacchino created a dew-dipped score that lovingly recalled Williams' most adored work, and Giacchino already has a longstanding history with Disney having worked extensively with Pixar and scored a number of the parent company's films, like last year's decidedly "Star Wars"-y "John Carter." He's already the "Star Wars" musical heir apparent anyway; last year he created new music based on Williams' original compositions for the recently revised Star Tours attraction at Disneyland in California and Disney's Hollywood Studios in Florida.
A lovable rogue or kick-ass female character will take center stage.
One of the things that was sorely missing from the new films was a character that exemplified the devil-may-care spirit embodied by lovable rascal Han Solo (Harrison Ford, who starred in one of Abrams' first-produced screenplays, "Regarding Henry") in the original trilogy. While it's unknown whether or not Solo (or, by extension, Ford) will be returning to the franchise, since Michael Arndt's script remains a mystery box few have opened, it was pretty clear to anyone who isn't George Lucas that this was a huge issue with the prequels, and something that Abrams will be quick to address. This is the kind of character, after all, that Abrams is obviously fascinated by, the most notable example being the conman Sawyer (Josh Holloway) in "Lost." That said, rumors have suggested that Arndt's script has a female lead (Matthew Vaughn was said to be pitching the idea of Chloe Moretz when he was in the running), and thanks to his TV stable of "Felicity," "Alias," "Fringe" and "Lost," among others, Abrams has form in that regard. Some kind of combination of the two seems likely, but don't expect a bland Luke Skywalker type to be the main character.
Lots of monsters.
Monsters are a hallmark of Abrams' oeuvre – everything from the Abrams-conceived "Cloverfield" to "Star Trek" to "Super 8" to "Lost" have had some manner of thing that goes bump in the night. "Star Wars," obviously, will be no different. We are positively giddy at the idea of Abrams populating a Mos Eisley Cantina-type bar with his decidedly whacked-out take on intergalactic creatures. We would be very surprised if his go-to creature designer Neville Page wasn't one of the first people Abrams called after he got the job. As the prequels wore on, their aliens, robots and creatures became blander and more anonymous, failing to stand out from their equally phony backgrounds. If there's one person to make the "Star Wars" monster mash really shimmy, it's Abrams, who will insist on imaginative design work and an emphasis on practical, on-set critters, though we hope that he stays mostly away from the "Cloverfield"/"Super 8" template for the beasties.
Thoughts? What do you think Abrams can bring to the table that will help redefine "Star Wars"? Will he play safely within the parameters of the franchise or will he making some bold changes? Just how much creative leeway will he get and will Lucas really and truly keep his nose out of it? Lots of questions, but we'll find out in about two years. "Star Wars: Episode VII" is scheduled to hit theaters in 2015.


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What little I know about soil and soil structure etc could be said in
almost one word, nothing, but I don't think it is possible to "feed"
soil. Modern societies, in order to keep up with increasing populations,
has gotten into the terrible practice of dumping huge quantities of
chemicals onto and into soils, thinking they are improving the soil.
This just can't be true. The only thng that improves soils is the
addition of organic composts, thus sustainable agriculture. Growing too
many hostas won't harm anything, but dumping huge amounts of things on
the soil in order to grow them bigger will harm things. If you look
around the forrest in the mountains huge numbers of perennial plants
seem to be gowing in harmony with the forrest (trees) even though the
tree roots are so thick and matted you can hardly dig a hole of any
size. Hostas will do the same, I know this from experience, if they can
survive long enough to develop a competitive root system. They will
generally do this if they have adequate moisture to survive.
To sign-off this list, send email to email@example.com with the
message text UNSUBSCRIBE HOSTA-OPEN


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Duck In A Pot
|4 Pound, Defrosted
|Ground black pepper
|To Taste
|1⁄2 Cup (8 tbs)
|Dry white wine
|1⁄2 Cup (8 tbs)
|1 Clove (5 gm), sliced
|Chopped parsley
|1 Tablespoon
|Salt pork
|1⁄4 Pound, diced and rinsed
|1 Teaspoon
|Butter/Olive oil
|3 Tablespoon
|1⁄4 Pound, diced
|Yellow onions
|3 , peeled and chopped
|3 , chopped
|Chicken stock/Bouillon
|1 Cup (16 tbs)
|To Taste
Cut the duck into four pieces and salt and pepper each.
Place in a stainless steel or glass bowl along with half the brandy and half the white wine.
Add the garlic and parsley.
Marinate the duck in this for 2 hours.
In a small saucepan, place the salt pork, diced and rinsed, the remaining wine and brandy, and the thyme.
Add a bit of black pepper if you wish.
Bring to a boil, cover, and simmer on very low heat for 10 minutes.
Drain the marinade from the duck and reserve it.
Pat the duck pieces dry with paper towels and saute them in a frying pan in the butter.
Just lightly brown each piece, turning once.
Place the duck pieces in a 2-quart ovenproof lidded casserole.
Add the pork and sauce, the marinade from the duck, the bacon, and the onions and carrots.
Cover the mixture with chicken stock and place the lid on the pot.
Bake in a 325° oven for 1 1/2 hours, or until the duck is very tender.
Correct the seasoning before serving.
Add a Green Bean and Filbert Salad, Risotto with Vegetables, and a green salad with Burgundy and Herb Dressing.
Rate It
Nutrition Rank
Nutrition Facts
Serving size: Complete recipe
Calories 5834 Calories from Fat 3784
% Daily Value*
Total Fat 421 g647.9%
Saturated Fat 153.8 g768.8%
Trans Fat 0 g
Cholesterol 1682.9 mg561%
Sodium 4078.2 mg169.9%
Total Carbohydrates 61 g20.5%
Dietary Fiber 12.2 g48.6%
Sugars 14.2 g
Protein 341 g682%
Vitamin A 696.1% Vitamin C 225.6%
Calcium 24.1% Iron 441.9%
*Based on a 2000 Calorie diet


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Discover Tea Time at the Clos Belle Juliette!
Stay 4 nights...And pay only 3!
Stay more time at Hotel & Spa La Belle Juliette ! Stay 4 nights...And pay only 3!
Come with your car at La Belle Juliette !
Book your parking space at the same time as booking your room!
Our private car park is available throughout your stay.
Rooms with Garden View
Discover our rooms with a modern and 20th century vintage mix, fresh fabrics, a remixed colour scheme, authentic wooden art studio floors, a great sense of humour and a few surprises.
La Belle Juliette
Jeanne Francoise Julie Adélaide Bernard, otherwise known as Juliette, was above all a celebrity known throughout Europe, famous for her beauty and virtue.
HPRG label
We explain why you should book on our website, and what HPRG means
Privatising the Clos Belle Juliette
Have the colourful, cosy and chic setting of the Clos Belle Juliette all for yourself - we can organise tailor-made private events like meetings, dinner, cocktails.
La Belle Juliette Location
The hotel is located in one of the most beautiful areas of the Left Bank in the centre of Paris, in Saint Germain des Près.
Rooms watching Paris life
Each floor will surprise you with it refreshing colours inspired by different periods in Juliette's life. These rooms look onto a typically Parisian street, rue du Cherche-Midi.
Who is Juliette
Juliette Récamier was famous all over Europe, best known for her beauty, but she was also a resolutely daring, modern woman who loved the avant-garde and generously supported the arts.
Rooms with Garden View
These rooms our in our new wing overlooking the garden. Interior designer Anne Gelbard was inspired by Juliette's daring, modern nature, a woman who loved the avant-garde and generously supported the arts.
Our Bar Le Clos Belle Juliette
Our new bar is open with a chic snacking menu concocted by Flora Mikula and a new selection of wines and cocktails.
A luxurious spa
The elegant setting of La Belle Juliette is ideal for new beauty experiences and moments of relaxation. Experience the different seasons of Paris!


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The UFC 165 main event between Jon Jones and Alexander Gustafsson was nearly stopped prior to the fifth round. UFC president Dana White praised referee
Watch highlights of UFC light heavyweight champion Jon Jones' win over Alexander Gustafsson and the rest of UFC 165 in super slow motion.
UFC president Dana White weighs in on the classic battle between Jon Jones and Alexander Gustafsson at UFC 165 in Toronto, opening the door for
Glover Teixeira isn't interested in waiting around if a rematch between Jon Jones and Alexander Gustafsson takes place. He just wants to fight.
Following Saturday's UFC 165: Jones vs. Gustafsson event at the Air Canada Centre in Toronto, several of the fighters fielded questions from the media.
UFC 165: Jones vs. Gustafsson gate and attendance from the Air Canada Centre in Toronto.
Light heavyweight champ Jon Jones believes in his skills while challenger Alexander Gustafsson is confident he can walk away with the belt around his waist.
Watch the UFC 165: Jones vs. Gustafsson weigh-in video, courtesy of UFC.com.
Full weigh-ins results from Friday's UFC 165: Jones vs. Gustafsson weigh-in event in Toronto.
Take a behind the scenes look at the UFC 165: Jones vs. Gustafsson media day featuring Alexander Gustafsson, Eddie Wineland, Brendan Schaub, Kyle Noke and
Check out the behind the scenes lead-up to Saturday's UFC 165 fight between Jon Jones and Alexander Gustafsson, as well as Renan Barao vs. Eddie
Check out the behind the scenes lead-up to Saturday's UFC 165 fight between Jon Jones and Alexander Gustafsson. Countdown to UFC 165 premiers at 8
UFC light heavyweight champion Jon Jones doesn't agree with the comparison's between himself and Alexander Gustafsson heading into UFC 165 on Sept. 21.
Get all your information about UFC 165: Jones vs. Gustafsson.
Watch Tuesday's UFC 165 public press conference featuring UFC light heavyweight champion Jon Jones, light heavyweight top contender Alexander Gustafsson and UFC Director of Canadian
UFC 165 fight card rumors and start times for Sept. 21, 2013, in Toronto.
UFC on Fuel TV 9 has undergone drastic changes over the past several days with main event Gegard Mousasi now fighting a training partner of
UFC president Dana White went on Fuel TV following UFC on Fox 5 on Saturday night, among other things, he divulged that Dan Henderson's knee
Shogun may be tiring of all the Jon Jones talk and questions about turning down the fight against the champ, but he's kept his focus
UFC on Fox 5 ends the UFC's efforts on Fox with a star-studded fight card, packing three prominent bouts, including a title fight, onto the
With his latest victory Alexander Gustafsson edges up the light heavyweight rankings.
Alexander Gustafsson picked up his fifth win in a row in the UFC with a shutout performance over Thiago Silva to cap off UFC on
Check out the UFC on Fuel TV 2: Gustafsson vs. Silva weigh-in video from Stockholm, Sweden.
UFC on Fuel TV 2: Gustafsson vs. Silva weigh-in results from Stockholm, Sweden.
MMAWeekly Radio is back with a stacked show for Thursday with UFC on Fuel 2 headliner Alexander Gustafsson and a trio of UFC 145 fighters
The UFC on Tuesday announced the main event for its first trip to Sweden, a light heavyweight bout between Alexander Gustafsson and Antonio Rogerio Nogueira.
If you ask UFC 141 fighter Vladimir Matyushenko if he feels he's a top 10 fighter, he won't be shy about saying yes.
In two UFC 133 preliminary bouts on Spike TV, leading up to Saturday night's main card in Philadelphia, we saw a light heavyweight upstart establish
A slugfest, poor judging and an Australian going down highlighted the preliminary fights on ION TV for UFC 127.
A light heavyweight bout has been added to the upcoming UFC 120 card in London, England as striker extraordinare Cyril Diabate returns for his second


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Pancreatitis is inflammation in the pancreas. The pancreas is a long, flat gland that sits tucked behind the stomach in the upper abdomen. The pancreas produces enzymes that help digestion and hormones that help regulate the way your body processes sugar (glucose).
Pancreatitis can occur as acute pancreatitis — meaning it appears suddenly and lasts for days. Or pancreatitis can occur as chronic pancreatitis, which is pancreatitis that occurs over many years.
Mild cases of pancreatitis may go away without treatment, but severe cases can cause life-threatening complications
Pancreatitis care at Mayo Clinic
Any use of this site constitutes your agreement to the Terms and Conditions and Privacy Policy linked below.
Mayo Clinic is a not-for-profit organization and proceeds from Web advertising help support our mission. Mayo Clinic does not endorse any of the third party products and services advertised.
A single copy of these materials may be reprinted for noncommercial personal use only. "Mayo," "Mayo Clinic," "MayoClinic.org," "Mayo Clinic Healthy Living," and the triple-shield Mayo Clinic logo are trademarks of Mayo Foundation for Medical Education and Research.


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This is the December 28, 2012 news archive. View today's Lions rumors and news.
Detroit Lions
Detroit Lions News and Rumors
Jim Schwartz denies tension with Lions G.M. Martin Mayhew
profootballtalk.com Updated Dec 28, 2012
Lions coach Jim Schwartz says he and General Manager Martin Mayhew have a fine relationship, despite a report to the contrary. A day after Don Banks of SI.com reported that tension has developed between Schwartz and Mayhew about the collection of player…Share Tweet
Bears RB Forte (ankle) expects to start vs. LionsCNNSI.com Dec 28, 2012LAKE FOREST, Ill. (AP) -- Chicago Bears running back Matt Forte expects to start Sunday against the Bears despite an ankle injury suffered last week.Share Tweet
NFC North Friday injury reportESPN.com Dec 28, 2012Let's get inside our last Friday injury report of the 2012 season. Sniff, sniff… Chicago Bears: Linebacker Brian Urlacher practiced for the first time since injuring his hamstring Dec. 2, but he was limited and is listed as doubtful for Sunday's game agShare Tweet
ESPN's Lomas Brown Says He Didn't Send All Those Insulting Tweets Sent By Lomas Browndeadspin.com nytimes.com Dec 28, 2012He's just shocked-shocked!-at what happened the other day, at least now that someone's finally noticed it. Brown's response here only prompts additional questions: Does someone else do his tweeting for him? (If so, this person is awfully prolific.) DoShare Tweet
Brandon Marshall won't be rooting for the Packersprofootballtalk.com Dec 28, 2012The Bears can get to the playoffs only if they beat the Lions and if the Packers knock off the Vikings. But that won't make Bears receiver Brandon Marshall buy a share of Packers non-stock stock. "I'm not cheering for anybody but the Bears," MarShare Tweet
Cliff Avril has no regrets about turning down a long-term dealprofootballtalk.com Dec 28, 2012Lions defensive end Cliff Avril says that he has no regrets about turning down any long-term deals offered by the team before he signed his franchise tag tender to play this season for $10.6 million. Avril wanted more than the Lions were offering and ga…Share Tweet
BBAO: Matthew Stafford nears two recordsESPN.com Dec 28, 2012We're Black and Blue All Over: As we noted earlier in the week, the Detroit Lions' Matthew Stafford is 305 yards away from becoming the first quarterback in NFL history to produce back-to-back 5,000-yard seasons. (New Orleans Saints quarterback Drew Bre…Share Tweet
NFL Kickoff OT: Week 17 PredictionsDec 28NFL Kickoff OT breaks down the key matchups for the final week of the regular season.
'Playbook': Chicago Bears vs. Detroit LionsDec 28The "Playbook" guys break down the Chicago Bears defense and discuss why Detroit Lions QB Matthew Stafford leads the league in pass attempts.
'Playbook': Chicago Bears vs. Detroit LionsDec 28The "Playbook" guys break down the Chicago Bears defense and discuss why Detroit Lions QB Matthew Stafford leads the league in pass attempts.
Week 16: GMC Never Say Never Moment of the Week winnerDec 28Which player stepped up in Week 16 to help lead his team to victory? Find out as the 'GMC Never Say Never' winner is revealed.


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House "Open marriage" episode
I know this link is ugly, and if it doesn't work out for you, try Hulu in a couple of days and they should have it posted there.
I watched this episode last night and thought it interesting that open marriage was so central to the show. If you are familiar with House, you know that it is a show about a special diagnostics team at a hospital who get the hard cases that no one else can figure out.
It was pretty amusing-everyone on the medical team was intrigued to say the least about the status of the couple's marriage-in fact they spent most of the show trying to find a cause for the woman's illness that was related to her or her husband having multiple sexual partners. (it wasn't)
There were a couple lines in the script from different characters that gave credit to the honesty of the married couple's situation, but ultimately the consensus was that because the husband didn't have any other partners and the wife did, that he must be feeling guilty about something and that's why he "let" her have sex with other people, which was proved in the end. Also, one of the doctors, a serial cheater, brought up "open marriage" with his wife, and she reluctantly consented, but at the last minute backed out, and the doctor cheated anyway.
Ugh. anyway, I guess it was a good example of the misunderstandings and reactions that are out there. I think it's an indicator that the idea is becoming a bit more mainstream, even though it was pretty skewed. Enjoy, if you still feel like watching it after this glowing review! :)
I pvred it. My wife gets back tonight and has asked I don't watch it. She is curious to see the show as well
to be fair to the show a bit, without seeing it, the show does usually have the focus on the patients life. Diving into the good the bad and the ugly. They ripped into larpers last episode :)
I caught the episode. I was just thrilled to see it being discussed and a lot of the things being discussed were very valid points. I saw the downside to some of the discussions also, and at the end I told my partner that I was so happy that I never had to worry about him going off with someone else, because he could just tell me if that was something he wanted (like the serial cheater doctor did, and his wife agreed, then backed out, and he ended up cheating anyways).
Ariakas - I need to see the larper episode. My partner and I would thoroughly enjoy that episode also :)
Not really larping...but still role playing
I saw the episode. It was done in the usual style for that show I feel. As a whole, I guess it was handled OK. I've certainly seen it handled worse. I wasn't truly offended and that may be saying a lot.
Wasn't very impressed by the show, myself...
** Spoiler Alert **
First, they only discussed sexually open marriage, not romantically, or at least that was my impression. I guess there was the part where the boyfriend tried to bring her flowers when she was in the hospital, to be met with complete rejection by the husband, whom we later find out is only going along with the open marriage thing because he doesn't want to lose his wife. So because of that lack of real honesty and openness, he is rather miserable with the whole situation.
Meanwhile we have one of the other doctors who's been having an affair and brings up the subject of this patient in an open marriage, testing the waters to see whether she would go for it. She already suspected his infidelity, and that all but confirmed it. She agrees to go along with it, putting up the usual restrictions ("Only on Thursdays and you come home by midnight"), only to pull the plug because she can't deal with it.
What also bothered me about the episode was that at the beginning, the doctors says "open marriages never work, it always ends up with one of the spouses being miserable" and then giving us a glimmer that it's possible, only to have the rug pulled out from under us when we learn that the husband does not truly support the idea.
I think this would be such an awesome idea for a Degrassi episode, though! I like to believe THEY would get it right :D
Ok, DO NOT CLICK ON THE LINK!!!!!!!!!!!!!!
I did, and now I have some sort of "security tool" installed on my computer which I did NOT ask for or approve. This is why I normally don't click on links.
Sorry T- yeah Divxden is fucking annoying- I have popup blockers on and other security stuff so it didn't hurt me, but I'm sorry you got burned. As the link poster-warning- this site will try to throw up all kinds of shit on you- proceed with caution or just look it up for yourself-it's out there.
TRy Stagevu.com
It's a clean sight and has tonnes of shows/documentaries and movies. That's where Redpepper and I wacthed "Shortbus" and another very poly movie I can't remember the name of now.
You could also grab them off of torrents, not quite illegal here :)...
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|"Michael Busch (JIRA)" <j...@apache.org>
|[jira] Updated: (LUCENE-908) MANIFEST.MF cleanup (main jar and luci customizations)
|Wed, 06 Jun 2007 19:39:26 GMT
[ https://issues.apache.org/jira/browse/LUCENE-908?page=com.atlassian.jira.plugin.system.issuetabpanels:all-tabpanel ] Michael Busch updated LUCENE-908: --------------------------------- Attachment: lucene-908.patch In addition to Hoss' great patch this one: - changes the MANIFEST file in the demo jar and war in a consistent way - adds a patternset via refid to the metainf type of jarify. This can be used by contrib modules to add additional files to the META-INF dir. I use it to add SNOWBALL-LICENSE.txt to META-INF of the snowball jar. I'm planning to commit this soon. > MANIFEST.MF cleanup (main jar and luci customizations) > ------------------------------------------------------ > > Key: LUCENE-908 > URL: https://issues.apache.org/jira/browse/LUCENE-908 > Project: Lucene - Java > Issue Type: Bug > Components: Build > Reporter: Michael Busch > Assignee: Michael Busch > Priority: Trivial > Fix For: 2.2 > > Attachments: lucene-908.patch, LUCENE-908.patch > > > there are several problems with the MANIFEST.MF file used in the core jar, and some inconsistencies in th luci jar: > Lucli's build.xml has an own "jar" target and does not use the jar target from common-build.xml. The result > is that the MANIFEST.MF file is not consistent and the META-INF dir does not contain LICENSE.TXT and NOTICE.TXT. > Is there a reason why lucli behaves different in this regard? If not I think we should fix this. -- This message is automatically generated by JIRA. - You can reply to this email to add a comment to the issue online. --------------------------------------------------------------------- To unsubscribe, e-mail: email@example.com For additional commands, e-mail: firstname.lastname@example.com
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