text:
Those who defiantly
survive police-state violence tend to develop a wracking, dark humor.
In 1970, our friend and surrealist co-worker Haifa Zangana* was
jailed in Saddam Husseins horrendous Qasir al-Nihaia political
prison as an enemy of the State. In her grim but poetic memoir,
Haifa recalls the taste of blood in her mouth and the sight of blood
on her thighs, the hot tears she shed for friends executed by security
police, and the cool gorgeous springs of water in her ancestral
homeland of Kurdistan that were plugged silent with cement by Husseins
troops. Yet today, she says with a tough, sad chuckle, she finds
herself (objectively at least) on the side of the dictatorship that
tortured her and against the Western governments who vow to "liberate"
We understand Haifas wise and bitter smile. At present, the
people of Iraq are confronted by the prospect of a Bush-league emperors
ambition to depose their CIA-appointed despot through a U.S. invasion
and military occupation, a scheme we are supposed to believe is
motivated by moral indignation and high-minded righteous regard
for democratic principles. Such malevolent hypocrisy would almost
be funny if the implications were not so catastrophic. Since 1968,
Husseins Baathist regimean unrelenting torturocracyhas
been showered with support of all kinds, including massive shipments
of weapons and incalculable U.S. tax dollars. After Kuwait, the
U.S. effectively rehired Hussein to continue butchering anti-State
separatists, feminists, and anti-capitalists in order to "stabilize"
the region for exploitation by globalized capitalism. U.S. National
Security Advisor Condoleeza Rice proclaims that attacking Iraq now
will aid "the march of freedom"; tellingly, Rice is the
first such Advisor with a 136,000-ton Chevron Corporation oil tanker
named after her.
George Bush and Saddam Hussein are not exactly Tweedledee and Tweedledum,
but the similarities between themideologically, morally, and
as figureheads of Statefar outweigh the differences. Indeed,
the Executive Branch of the Bush-Cheney regime and the ruling circle
of the Baath Party are clearly the most tender and intimate
of enemies. We are not surprised to learn that portions of a recent
televised speech by the most ignorant President in U.S. history,
in which he expressed his "feelings" about "Iraqi
culture," were in truth lifted almost verbatim from a 1990
speech by none other than Saddam Hussein, who was then directing
his own invasion of Kuwait. And we would not be surprised to learn
that Saddam Hussein has in turn plagiarized juicy bits of double-talk
from speeches by one or another U.S. President.
Make no mistake: The proposed "regime change" in Baghdad
is solely about replacing a fractious death-squad subcontractor
with a more passively compliant one. A New World Order "police
action" aimed at Iraq would provide U.S. capital with easy
access to twenty- two percent of the worlds available petroleum,
meaning less dependence upon the doddering feudal oil oligarchy
of Saudi Arabia. In our era of turbo-globalized and genocidal capitalism,
the oil extraction industries are one of the hinges on which international
class relations turn. Any bombs that fall on the people of Iraq
in the next few months will also be a dire "message" pointed
at petroleum workers in such places as the Caspian Sea basin, Angola,
Nigeria, Colombia, and Venezuela. It is no accident that the "interim"
government in Afghanistan that replaced the Taliban ruling clique
is led by a former consultant to the Unocal oil company who is protected
round-the-clock from assassination by a contingent of U.S. Green
Carnage apologists, militarist demagogues, war profiteers, and their
fundamentalist Christian cheerleaders charge that those who are
unable or unwilling to fathom the hateful logic of their policies
are plainly guilty of the terrible crime of being "unrealistic."
For our part, as surrealists, we readily affirm that we despise
the so-called "realism" that is based solely on the clumsy
hypocrisy, swaggering boorishness, and ecocidal greed of a few cowardly
billionaires along with their political/ military/ journalistic
yes-men. Quite simply, a "realism" sustained by nothing
more than shamelessly arrogant celebrations of degradation, persecution,
and miserabilist obfuscation deserves only con-tempt, scorn, and
We say: Neither ruling-class war nor imperial peace! The grubby,
counter-revolutionary opportunism of "realistic"realpolitik
is no excuse for industrialized mass murder. When the U.S. governments
stooges of Capital try to blackmail us with the pseudo-choice of
being "either with us or against us," we wholeheartedly
refuse. In this as in all intercapitalist rivalries, we support
neither side. Heeding our imaginations, we pursue an alternative
set of terms. We do our best to ignore the flags and sneer at the
superstitious calls for some war gods blessings, and focus
instead on our solidarity with the working people of Iraq.
With sorrow, but also with anger, Haifa Zangana reminds us that
siding with the oppressed "does not mean we are unaware of
the complexity of the situation."
Unalterably opposed to yet another sleazy capitalist oil war, we
uphold the tried and true values of class war: the self-emancipation
of the workers of the world from wage-slavery. To quote one of the
oldest and soundest watchwords of the workingclass movement:
The real enemy is in "our own" country! And despite
that enemys penchant for euphemistic pseudonyms ("free
enterprise," "globalization," etc.), his true name
is Capitalism.
We say:
No to Bushs war-plans and globalizations death
industry! No to the outlawing of workers movements!
No to "austerity programs" and the "structural
readjustment" dictates of the World Trade Organization, the
International Monetary Fund, and the World Bank! No to misery
and miserabilism in all their forms!
Yes to revolt! Yes to freedom now! Yes to international
workingclass solidarity! Yes to life, imagination, the Earthand
their marvelous possibilities!
* Born in Baghdad
in 1950, Haifa Zangana was active during the 1970s in the Paris-based
Arab Surrealist Movement in Exile, whose journal, Le Désir
libertaire (Anarchist Desire) was banned in all Arab countries.
More recently she has maintained close ties to the Surrealist Movement
in the U.S. Her first book, Through the Vast Halls of Memory,
appeared in 1991 but is now out of print. As writer and collagist
she is represented in Penelope Rosemonts Surrealist Women:
An International Anthology (University of Texas Press, 1998).
Movement in the United States
October 2002


text:
Friday, May 29, 2009
Oval Slip Stich Doily
This is a gift for my friend. A surprise gift :). Hope she'll love it.
I make with wss thread, crochet hook 1,75mm. Technique : Crochet with free style (without pattern).
Click at the image for larger view
Posted by Thata at 5:06 AM No comments: Links to this post
Labels: doilies
Tuesday, May 26, 2009
My third book will be launch soon
Dear all,
Glad finally I could finish 17 designs for my third book. With knitting and crochet this time.
I hope this book could be an inspiration to all "rajuters" in Indonesia..
Bravo merajut !!
Posted by Thata at 3:23 AM 3 comments: Links to this post
Labels: Book
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subset: commoncrawl


text:
The Road To Success
The road to success is always under construction.
I found this quote a long time ago and not sure who it is by, so far 'anonymous'. I find it very inspiring for an entrepreneur like myself so I used it in my book on digital marketing, Pimp My Site.


text:
I received a warning about being close to or exceeding my quota. What should I do?
Whenever you login, by default, the quota of your locker is checked (and any other lockers that are attached to which you have write permission), to verify that you (or the lockers) are safely under quota.
If you are close to your disk quota, you will see a message such as this one during the login process:
95% of the disk quota on /mit/jruser has been used.
If you are over your disk quota, you may see some popup dialog windows with complicated-looking error messages. Unfortunately, these error messages are not useful in and of themselves, but they indicate that some programs are not able to write files that they'd like to because there is no free space.
If you are over quota or close to your quota, you should IMMEDIATELY take action to reduce the amount of space you are using, or you may not be able to save any new files to your account.
N.B. If you receive a quota message about a locker other than your own (for example, a group locker), you should still take action, but it will not affect your ability to log in or any files stored in your own locker.
For more information, see the following answers in this category:


text: Just wondering if anyone has had experience on the new Sony Z 13, and how it compares to the MBA13. I have a 2011 4G 256 13" MBA, and I absolutely love it. The fact that I can carry it in my bag and not know it is there is great. Bootup time is impecable. The downfalls are the battery life since installing Lion, as well as being in business, the use of windows native programs (dont want to waste time with parallel) So then I see an ad for the Sony Z and started looking into it. Find out it is thinner, lighter, and is a powerful machine. Has anyone had any experience with it, and if so, how does it compare to the MBA? Ive read online articles, but looking for actual insight. Thanks!


text:
The front passenger's side wheel started thumping when going uphill. Could it be the wheel bearing?
It could be from the bearing, or from a tire with a bubble or tread separation. I recommend having a mechanic, such as one from YourMechanic, run a diagnostic on the source of the noise in order to identify and quote the repairs needed.
Our certified mechanics come to you ・Backed by 12-month, 12,000-mile guarantee・Fair and transparent pricing


text:
I bought Nokia Lumia 925 Premium category Smart Phone in Oct-2013 online from Tradus.com. After 1 month of use its Audio jack stopped working for no reason. I gave it for repair at Nokia Service centre Hadapsar, Pune. They took one whole month to fix the small issue. Later in year 2014 I faced hanging problem with the phone but I managed to fix the issue with Hard reset 2 times as instructed on Nokia Lumia support website. In
June-2014, I moved to Australia with the phone and put the Australian sim card and it was working fine. However, in April-2015 my phone was hanged again and didn't come up. It was actually dead. Since Its warranty was over even though I sent the phone back to India to my brother to get is repaired. My brother submitted the phone at Akshay care, Shivaji Nagar service centre for repair. After few days they said they have to send this device to Bangalore as they are not able to fix it. They also gave an estimate of 8000/- if repaired at bangalore. I had no option than to wait for another month to hear back from them. After couple of days, they called up and said the Phone is not repairable because of some major issue of its mother board and handed back the device.
I was very much disappointed with the answer and lost all my hopes to get it fixed. Later I decided to escalate the issue with Nokia itself because I could hardly use the phone for 1.5 years. Then I logged a complaint (ref. no. 1305989121) and I have been told that I will receive a call from technical support. Mr. Bxxxxxxh called and confirmed that he can see the repair history of the phone and due to major fault in the device they can not fix it and they closed the complaint. I again escalated the issue to the next level complaint (ref. no. 1306192506) this time we received the call saying the same thing and closed the call. they also mentioned it will take 80% of the cost if they repair it and give no guarantee of it.
I called Microsoft Lumia Customer care in Australia (1300 366 733 toll free) and they said I need to escalate this issue in India only and they cannot find the details here. I strongly doubt on it as IMEI is a globally unique no. and the details can be seen from any part of the world.
Now, I decided to bring this matter to Consumer forum of India to take care of the case. Please help me because, it seem to have a manufacturing defect or poor quality components were used which could not survive for a long time.
Danish Usmani
Email: danish.usmani]@gmail.com
188.8.131.52 / 30/09/2015 / 11:31 am


text:
IT vulnerabilities such as inadequate documentation and poor PC access controls put enterprises at risk of being noncompliant with regulatory mandates and prone to security events -- and most companies have at least a few such deficiencies present in their environments, according to research released Monday.
The IT Policy Compliance Group surveyed 876 corporations and government agencies, and 69 percent said during the first half of this year they had averaged between three and 15 "compliance deficiencies" that had to be corrected. Another 20 percent said their organizations tallied more than 16 deficiencies, with 36 on average. The remaining 11 percent -- the top performers in the survey -- reported an average of only two compliance deficiencies.
The report, entitled "Managing Spending in IT to Improve Compliance Results," noted that 55 percent of these compliance deficiencies led directly to financial losses due to a security event, and 45 percent were of the type that required remediation to pass external audits or other regulatory reviews.
The survey also identified the Top 10 deficiencies. Beginning with No. 1, they are: documentation; PC and laptop access controls; IT configurations and controls; user, application and server access controls; IT audit, logging and reporting; database access controls; IT security policies and standards; information access controls; business continuity controls; and data archive and management controls.
When the IT Policy Compliance Group asked 520 of the 876 organizations how much money their organizations allocate to IT security as a percentage of the IT budget, the group found -- not surprisingly -- that more spending in general leads to fewer compliance deficiency problems.
Firms that spent more than 10 percent of the IT budget on IT security are consistently among those with the lowest levels of compliance deficiencies. The best-performing segment spent an average of 10 percent of the IT budget on security compared with 7.5 percent spent by the 69 percent of companies deemed the "industry norm," and 6.8 percent spent by the bottom 11 percent or "industry laggards."
Among organizations with stronger policy-compliance track records, there's less spending on contract labor and more on automation of procedures and controls through software or scans, the IT Policy Compliance Group reports.
The firms that were more successful in IT policy compliance are "automating the IT audit and monitoring process on a once every two-days basis, sometimes even more," said Jim Hurley, director of the IT Policy Compliance Group. "The firms that were laggards [in this survey] did the same audits on a once-a-year basis."
IT Policy Compliance Group is a research group formed last year to publish studies on achieving IT policy and regulatory goals. It is supported by the Computer Security Institute and the Institute of Internal Auditors, along with firms Protiviti and Symantec.
This year's survey of 876 organizations is based on interviews with IT managers and directors, as well as individuals from legal, finance and internal audit departments who are knowledgeable about regulatory compliance. The majority of surveyed companies are from North America with some Asian and European organizations are included as well.


text:
From OpenWetWare
TO DO: *Make Competent Cells *Electroporate J37015, J37024 (from ligations) after having made competent cells *Miniprep J37024, J37022 and J37025 (to check whether ligations were successful) *Religation of J37018 ? *Freeze 4G (S01656), J37020 (&J37018?) *Testing (T9002, J37016 & J37020) *PCR
Competent Cells
- New competent cells were made - we have a new stock in the -80[[:Category:{{{1}}}|{{{1}}}]] freezer again
Measuring the growth rate of the prey cells
- JohnChattaway 04:50, 30 August 2006 (EDT)
- We need to do this to work out the growth rate of the prey to give us an idea of the amounts of media we need for the chemostat.IGEM:IMPERIAL/2006/The Talk Page
- Cultured fresh cells at 9.30
- At 11.30 will re-culture to OD of 0.1 then test OD every 30mins untill OD 0.9 is reached
Measuring AHL production overnight
- JohnChattaway 04:50, 30 August 2006 (EDT)
- I will repeat tom's experiment with the frozen Prey Cells
Testing T9002, J37016 and J37020
- Took 16mL cultures out of shaker after 2h at 11:20
- OD measurements:
- Dilute down to OD 0.1 into 25mL
- Put 5mL tubes with AHL in shaker at 12:00 - to be taken out at 16:00
- Tubes were taken out at 16:25
- Fluorescence reading of the 3 plates (17:50 - 19: 10)
- Part J37024 glass milk purified and electroporated.
Minipreps of J37025, J37022, J37018
- See File:Miniprep 30-08.pdf for photo of gel
- Comment: The part outlined in the photo as J37020 is actually J37022 !!
LoxP PCR
- With any luck this should be the final attempt
- Ran along side the maxiprepped DNA
- Loaded 10μL of each PCR reaction into the gel (double the amount of the previous attempts)
Freezing Cells
- Froze S01656 and J37020 (the right ones this time - old ones have been thrown out)
- J37024 (from both plates for miniprep)
- T9002/J37016/J37020/J37015/J37015RS/S01656 (for testing)


text:
Browsing Recipes similiar to Braised Mustard Lamb With Celeriac and Braised Onions.
Loin of lamb with a garlic and anchovy crust, with pea and bean salad, garlic and herb potatoes and red wine and onion reduction
lamb, thyme, rosemary, +black pepper, +garlic, +olive oil, +anchovy fillets, +anchovies, +bread crumbs, +parsley, +dijon mustard, +potato, +water, +butter, +red wine, +onions, +chicken broth, +salad greens, +peas, +broad beans, +tomato
Braised Lamb Shanks With Caramelized Vegetables
Here is another lamb shank recipe, I absolutely love lamb shanks, I just don't seem to be able to buy them often here in Switzerland. This one tastes wonderful...
beef broth, cornflour, thyme, lamb, rosemary, +balsamic vinegar, +bay leaf, +garlic, +celery, +olive oil, +red onions, +red wine
Lamb, red wine and rosemary casserole with herby potato stacks and braised red cabbage
lamb, beef broth, rosemary, thyme, +flour, +olive oil, +butter, +tomato puree, +red wine, +garlic, +carrot, +onions, +celery, +salt, +black pepper, +potato, +cabbage, +jelly, +sherry vinegar, +zest, +port wine, +raisins
Braised lamb shanks with sweet potato puree and sauteed baby spinach in red wine sauce
lamb, thyme, rosemary, cream, +black pepper, +olive oil, +onions, +of a, +carrot, +celery, +leek, +bay leaf, +tomato, +flour, +white wine, +sweet potato, +butter, +spinach
Lamb cutlets with a cheddar and chive crust, creamed leeks and bacon and baby potatoes
rosemary, cream, lamb, thyme, +red pepper, +potato, +seeds, +olive oil, +garlic, +black pepper, +leek, +bacon, +white wine, +butter, +chives, +bread crumbs, +cheddar cheese, +sauce, +brown onions, +red onions, +red wine, +chicken broth, +dijon mustard
Double loin of lamb with a lemon and mint stuffing on rustic ratatouille, with olive oil mash and lamb jus
lamb, thyme, rosemary, +olive oil, +onions, +carrot, +celery, +leek, +garlic, +red wine, +chicken broth, +stuffing, +lemon zest, +mint, +black pepper, +butter, +red onions, +eggplant, +yellow bell pepper, +red pepper, +zucchini, +cherry tomato, +basil, +whole milk, +potato
Braised Lamb Shanks With Fresh Rosemary
A wonderful blend of flavors- perfumes the whole house. Perfect for company, since it can be made the day before. Everyone raves about it! I've doubled...
beef broth, rosemary, thyme, lamb, +carrot, +tomato, +red wine, +garlic, +lemon zest, +chicken broth, +olive oil, +onions
Braised Lamb Shanks And Oxtails With Carrots And Orzo Recipe
Planned on making Oxtails for the first time. I had just enough for two but suddenly we had company......so I defrosted some lamb shanks and cooked them...
beef broth, lamb, +burgundy wine, +bay leaves, +beef, +spinach, +celery, +pasta, +carrot, +chicken broth, +black pepper, +garlic, +onions, +parsley, +olive oil, +orzo, +lamb shank, +tomato, +butter
www.grouprecipes.com - Similiar recipes
Braised Lamb Shanks With Mushrooms and Pasta
If you prefer a thicker sauce add in a little flour mixed with cold water to thicken towards the end of cooking time. This is a really great recipe for...
beef broth, thyme, lamb, +mushroom, +tomato, +marjoram, +red pepper flakes, +white wine, +garlic, +olive oil, +onions, +parmesan cheese, +rigatoni pasta, +salt, +worcestershire sauce
Leg of Lamb with Herbs and Mustard
thyme, lamb, rosemary, beef broth, +bay leaves, +garlic, +sea salt, +black pepper, +dijon mustard, +water
find.myrecipes.com - Similiar recipes
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text:
People are now one step closer to being able to refine their own gas from home thanks to the Carbon-Negative System. The Carbon-Negative System is a machine developed by the Blest Corporation that converts plastic into crude petroleum.
The Carbon-Negative System produces one quart of oil for every two pounds of plastic. The system is currently being sold for a whopping $10,000, but prices should dip down if the demand for the system ever increases. I for one would love to be able to make my own generator fuel. Who's with me?
At-Home Oil Refineries
More Stats +/-
Award-Winning Eco Housing
Recycling Bath Systems
Recycled Book Desks
Stylish Recycling Centers
Clothing Recycling Machines
The Carbon-Negative System Converts Plastic into Fuel
- By: Michael HinesFeb 27, 2011
References: blest.co.jp & ecofriend
References: blest.co.jp & ecofriend


text:
Anchor is England's largest not-for-profit provider of housing and care to older people. We provide retirement housing to rent and to buy and care homes across the country.
Our passion at Anchor is giving older people a choice of great places and ways to live. We do this by treating our colleagues and customers as individuals and by building meaningful, long-term relationships based on happiness, openness and respect.


text:
So, we're back in the office, I'm finishing up here on the computer for now and Brian is checking his email.
Sometimes he reads snippets out loud. Sometimes I respond.
He was moving some paper around, while he read from the latest email.
Him: "I wonder if you have a solution..."
Me: The solution that works best for me is one part vinegar, two parts water.
Him: keeps moving paper. Then he starts laughing. He just realized what I said.
Him: "It's really not worth the price of shipping, you can just go down to the grocery store and get what you need...."
Man, we could have so much fun with his emails.
| | Permalink


text:
The holidays are often thought of as family time. How about making it outdoor family fun?
It's a busy time, so sometimes you must be intentional about scheduling family fun.
In the spirit of exercise and resisting the urge to let your family become couch potatoes from watching too many Christmas movies, take some time to enjoy some outdoors family fun.
Last week I wrote an article for Kids Ski & Rain on 13 outdoor ideas for family fun. Check it out, then get outside and have some fun!
Get my free new report: Sportsparents' Guide: 55 time & money-saving tips guaranteed to make your life easier. You'll also get regular sports parenting tips each week and a weekly parenting tip. Sign up here.


text:
Cancers of the earlobe are skin cancers and are largely caused by exposure to ultraviolet light, according to the Skin Cancer Foundation. In contrast, cancers of the middle ear are rare and may be due to chronic infection, according to the Ear Surgery Information Center.
The earlobes are considered a high-risk area for skin cancer, as reported by the Skin Cancer Foundation. The high risk of developing skin cancer on the earlobes is attributed to their location on the body, neglect of the ears by most people when applying sunscreen and to the difficulty of adequately covering the earlobes with sunscreen due to their complex folds and ridges. Tumors are most common on the front and upper part of the earlobe, though the development of skin cancers in the pit of the ear near the opening of the ear canal does occur.
Cancers of the middle ear are usually squamous cell carcinomas, according to the Ear Surgery Information Center. The rarity and location of these tumors means that they are often well-advanced before they are discovered. However, intermittent bleeding and drainage from the ear may be an early sign of cancers of the middle ear. Most patients with middle ear cancers also usually suffer profound hearing loss as a result of the tumor.


text:
The two-day old baby abandoned in a Dublin hostel has been re-united with his mother and is already back home in Germany with his family.
The Irish Sun newspaper has reported that the little boy found in a hostel bedroom in April is living with his mum again.
She had fled to Dublin airport and boarded a flight to Germany before hostel workers found the newborn baby.
Now the child, named Luke by Dublin police officers investigating the case, is back in the German city of Dusseldorf.
The mum, a student at University College Dublin, has been granted full custody of her child after an Irish Family Court ruled she is fit to raise him.
She could still face child neglect charges after police officers sent a file on the case to the Director of Public Prosecutions.
A source told the Irish Sun said: "Police have made their position clear - the best thing for her was to return to Germany to receive the support of her family.
"The child may be an Irish citizen but he should be with his mother.
"She was in a distressed state but has now accepted her responsibilities."
The baby was found at The Glen Guest House in Dublin on April 14 by cleaning lady Zhana Klisuoska almost three hours after his mother had gone to the airport.
Glen receptionist Goran Josifov, 34, praised the mum for being reunited with her son.
He said: "This is what everyone was praying for and we're delighted."


text:
UFPDF: Quick and dirty fix for page numberingPrint
UFPDF is a Unicode/UTF-8 extension for FPDF by Steven Wittens. It is quite outdated right now, but if for some reasons you're stuck with it, you might not like the fact, that one quite important function is broken.
In FPDF you can use AliasNbPages method, to specify a 'total pages' alias - a short string that will be replaced with total number of pages in document when PDF is generated. So if you for example do:
$this->Cell(0,10,'Page '.$this->PageNo().'/{nb}',0,0,'C'); //{nb} is a default AliasNbPages
and your document has 12 pages, {nb} will be replaced with 12 on each page.
Unfortunately in UFPDF this does not work. UFPDF is replacing and adding some UTF-8 enabled methods to core FPDF class, which on its side does most of the generating PDF work. (BTW: you can safely replace fpdf.php that is in UFPDF download, with the newest version from FPDF site without breaking anything) Substituting AliasNbPages for number of pages is also handled by FPDF by means of simple str_replace. That's where it fails:
function _putpages() { $nb=$this->page; if(!empty($this->AliasNbPages)) { //Replace number of pages for($n=1;$n<=$nb;$n++) $this->pages[$n]=str_replace($this->AliasNbPages,$nb,$this->pages[$n]); } ... }
All content generated by UFPDF is already UTF-8/Unicode encoded at this moment, so str_replace just can't find the alias and replace it. I've spend some time trying to find out a nice fix for this using mb_string or other encoding conversion functions, but ultimately I've come up with this:
function _putpages() { $nb=$this->page; if(!empty($this->AliasNbPages)) { //Replace number of pages $nb = (string)$nb; $nbs = ''; for($i = 0;$i < strlen($nb); $i++) { $nbs .= "\0".$nb[$i]; } $alias = $this->AliasNbPages; $aliass = ''; for($i = 0;$i < strlen($alias); $i++) { $aliass .= "\0".$alias[$i]; } for($n=1;$n<=$nb;$n++) $this->pages[$n]=str_replace($aliass,$nbs,$this->pages[$n]); } ... }
What it does is it adds additional \0 character (essentially a byte with value 0) in front of each character in AliasNbPages. It does the same to the number of pages string. Then it just replaces one with the other.
It's ugly as hell, but it works. One limitation is, you should only use characters from ASCII set to define AliasNbPages (default {nb} works well).


text:
by Sarah
Stay Puft Marshmallow Man Costume
Rate this costume:
4 votes
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Stay Puft Marshmallow Man Costume
Similar costumes:
Baby's Ghostbusters Stay Puft Deluxe Costume (18M/2T)
Ghostbusters Child's Inflatable Stay Puft Marshmallow Man Costume
|Costume type:
|Costumes for Babies
This homemade costume for babies entered our 2015 Halloween Costume Contest.
A word from Tara, the 'Stay Puft Marshmallow Man' costume creator:
My aunt made this son for my 8 month-old son. I wanted something cute to go with his chubby cheeks. I think this fit the bill!
Similar costumes:


text:
Treasurer Joe Hockey has said that businesses should survive or die on their own and can't rely on government assistance.
The ABC reports that Mr Hockey delivered a speech to the Lowy Institute in Sydney that considered welfare spending, as well as government assistance to industry. He foreshadowed welfare cuts in the May budget and also said businesses need to "stand on their own feet".
He said that the budget position was unsustainable and there needs to less reliance on welfare by individuals.
He added, "The business sector must shoulder more of the burden."
"It must restore corporate accountability and rely less on government assistance. It must stand on its own feet and it must pay its fair share of tax."
He also flagged the privatisation of government-owned assets to recycle capital into new infrastructure that would spur economic growth.
Already, assistance has become harder for the private sector to get.
The speech follows the Government's rejection of SPC Ardmona's appeal for government assistance. The troubled food processor requested $25m in assistance as part of a restructure plan to keep the company afloat – a figure that was promised by the previous Labor government.
And the Government has confirmed that it will provide no extra assistance to the struggling auto industry. Only Toyota has a possible long term future in Australia and yesterday Ford confirmed that 300 of its workers will start to be sacked from June.


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Action Congress of Nigeria (ACN) senator representing Lagos East, Gbenga Ashafa, has said the death of Prof Chinua Achebe is a big loss to Nigeria and the rest of the world.
In a condolence message to the family of the renowned writer, the senator urged Nigerians to immortalise him by imbibing his virtues.
He said: "Achebe was an embodiment of the great values most Nigerians crave for; he was an exemplary character. Let us celebrate him. The best way to immortalise him is to imbibe his virtues and what he stood for.
"Achebe was a great patriotic Nigerian, an intellectual asset. He denied himself riches most Nigerians would have taken advantage to make for themselves, despite his international fame and influence. He died when he was most needed in fortifying the Nigerian project.
"Achebe could be put in the class of William Shakespeare, former US President John F. Kennedy, among other great men of the world."
Ashafa condoled with the Achebe family and prayed for the repose of the soul of the deceased.
The senator urged Prof Achebe's widow and other members of his family, the people of Anambra State and Nigerians, to take solace in the integrity, dignity and honour which the late writer bequeathed to Nigeria, the African continent and the international community through his literary accomplishments.


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The unfolded protein response (UPR) is a specific cellular process that allows the cell to cope with the overload of unfolded/misfolded proteins in the endoplasmic reticulum (ER). ER stress is commonly associated with degenerative pathologies, but its role in disease progression is still a matter for debate. Here, we found that mutations in the ER‐resident chaperone, neither inactivation nor afterpotential A (NinaA), lead to mild ER stress, protecting photoreceptor neurons from various death stimuli in adult Drosophila. In addition, Drosophila S2 cultured cells, when pre‐exposed to mild ER stress, are protected from H2O2, cycloheximide‐ or ultraviolet‐induced cell death. We show that a specific ER‐mediated signal promotes antioxidant defences and inhibits caspase‐dependent cell death. We propose that an immediate consequence of the UPR not only limits the accumulation of misfolded proteins but also protects tissues from harmful exogenous stresses.
The unfolded protein response (UPR) is an evolutionary conserved adaptive response to perturbations of normal endoplasmic reticulum (ER) physiology. Strikingly, the UPR is implicated in several human pathologies, such as neurodegeneration, diabetes and cancer (Marciniak and Ron, 2006; Lin et al, 2008). The UPR engages several responses, including transcriptional upregulation of ER‐resident chaperones, selective inhibition of translation and activation of ER‐associated degradation (ERAD) (reviewed in Ron and Walter, 2007). Despite a large body of work in this field, little is known about the cellular consequences of the UPR upon physiological levels of ER stress in vivo.
Genetic and cell culture studies have unveiled the core of the UPR pathway, linking the detection of ER stress to the effector responses. In unstressed cells, the ER stress sensor and chaperone, Bip/Hsc3, binds and restricts the molecular components of the UPR. In stressed cells, Bip/Hsc3 is titrated away by unfolded proteins, relieving its inhibition on the UPR. This leads to trans‐autophosphorylation of the PKR‐like ER kinase (Perk) (Harding et al, 1999). Active Perk phosphorylates eIF2α, inhibiting protein synthesis and limiting the flux of misfolded proteins to the ER. In addition, the UPR promotes the phosphorylation of Inositol‐requiring enzyme 1 (Ire1). Activated Ire1 splices an intron from the mRNA of x‐box binding protein‐1 (xbp1), creating a translational frameshift (Yoshida et al, 2001; Calfon et al, 2002). The spliced form of xbp1 acts as a transcriptional activator, resulting in the expression of ER‐stress target genes, including protein chaperones and components of the ERAD pathway (Travers et al, 2000). In parallel, the membrane‐bound protein Atf6 translocates to the golgi, where it is cleaved by SP1 and SP2. The cleaved peptide translocates to the nucleus, where it acts as a transcription factor (Ye et al, 2000).
If UPR activation cannot overcome ER stress, then its target pathways induce the activation of the apoptotic program (reviewed by Szegezdi et al, 2006). Apoptosis is executed by specific caspases and regulated both by pro‐ and anti‐apoptotic Bcl‐2 proteins. However, the UPR has also been shown to induce an antioxidant response, limiting the deleterious effect of prolonged ER stress (Cullinan and Diehl, 2004). How the UPR switches between inducing two such opposite programs is not clear.
Drosophila melanogaster has recently emerged as a useful in vivo model system to study the UPR pathway (Pomar et al, 2003; Hollien and Weissman, 2006; Ryoo and Steller, 2007; Souid et al, 2007). Most UPR components found in yeast and mammalian cells, such as Atf4 (Crc), Perk and eIF2α, have Drosophila homologs (Pomar et al, 2003 and reviewed in Ryoo and Steller, 2007). In the Drosophila model of autosomal dominant retinitis pigmentosa (ADRP), the misfolding rhodopsin‐1 (Rh1) mutation (ninaEG69D, termed rh1G69D for clarity) induces UPR activation by increasing xbp1 splicing and Ire1‐dependent expression of the heat shock cognate protein 3 (Hsc3, the Drosophila Bip homolog; Ryoo et al, 2007). The reduction of xbp1 expression leads to increased retinal degeneration, indicating that xbp1 and its transcriptional targets are required to reduce the accumulation of misfolded Rh1 in the ER. Although the UPR pathway is conserved in Drosophila, the relationship between ER stress and apoptosis remains to be explored.
Searching for genes that protect adult photoreceptor cells (PRCs) against apoptosis, we identified mutations that disrupt the maturation and folding of the Rh1 protein as strong suppressors of neurodegeneration. These mutations lead to the activation of the UPR, which promotes neuroprotection against cellular insults by inducing an antioxidant response while inhibiting caspase activation. These results are not restricted to photoreceptor neurons, as cultured S2 cells become more resistant to cell death stimuli if pre‐treated with ER stress‐inducing chemical agents.
PRCs exposed to ER stress exhibit death resistance
In a dominant modifier screen to identify cell death regulators in differentiated Drosophila PRCs (CSM, HS and BM, unpublished data), we have found that mutations in the Drosophila cyclophilin B homolog ninaA suppress dp53‐induced cell death in PRCs (Figure 1; Table I). NinaA is a membrane‐bound chaperone localized in the ER devoted exclusively to the biogenesis of the light sensing Rh1 protein. It has been shown that the peptidyl‐prolyl cis‐trans isomerase activity of NinaA allows proper Rh1 folding. In addition, NinaA functions as a chaperone, escorting Rh1 through the secretory pathway from the ER to the rhabdomeres (microvillar membrane in which rhodopsins accumulate) of outer PRCs (the rods‐like PRCs of Drosophila) (Colley et al, 1991; Baker et al, 1994). NinaA amorphs lead to the accumulation of misfolded Rh1 protein in the ER, likely resulting in ER stress (Colley et al, 1991).
We analysed the protective effect induced by the loss of ninaA against several apoptotic stimuli. The expression of the pro‐apoptotic gene reaper (rpr) induces cell death by a caspase‐dependent mechanism through the inactivation of the Drosophila inhibitor of apoptosis (Diap1) (Hay et al, 1995; Goyal et al, 2000). The ectopic expression of rpr, under the control of the rh1 promoter, induces a progressive loss of outer PRCs that can be visualized in tangential plastic retina sections of 2‐day‐old flies (Figure 1D). Loss of one genomic copy of the ninaA gene, using the amorphic allele ninaAE110V, protects the outer PRCs from rpr‐induced apoptosis (Figure 1D and E). This anti‐apoptotic effect is dose dependent, as complete loss of ninaA lead to further protection (Figure 1D–F, K; Supplementary Table 1). To determine whether resistance to PRC death observed in ninaA mutants is specific to rpr‐induced cell death, ninaA mutant retinas were submitted to the ectopic expression of Drosophila p53 (dp53) or death caspase‐1 (dcp‐1, a Drosophila homolog of caspase‐3) (Brodsky et al, 2000; Laundrie et al, 2003). Similarly to rpr, retinas mutant for ninaA were resistant to cell death induced by the ectopic expression of dp53 as well as dcp‐1 (Figure 1, G–J, K; Supplementary Table 1). Similar protective effects were also observed with several ninaA alleles, with the strongest effects associated with strong loss‐of‐function alleles (ninaAE110V, ninaAQ137L in Table I and Supplementary Figure 1). These results support the hypothesis that PRCs with reduced levels of ninaA are protected from apoptosis, either downstream or in parallel to caspase activation.
We next tested whether the resistance to PRC death, induced by loss of ninaA, is due to the accumulation of misfolded Rh1 in the ER. If true, reducing the amount of Rh1 in ninaA mutant retinas should reduce resistance to PRC death. Using a rh1 null allele (ninaEI17, here termed rh1I17), we found that double heterozygous mutants for ninaA and rh1 exhibited similar death sensitivity as wild‐type PRCs (Figure 2B–E and G). In addition, PRCs carrying a heterozygous rh1 null mutation in an otherwise wild‐type background were not protected from cell death (Figure 2D). This indicates that it is the accumulation of unfolded Rh1 in the ninaA mutant retina responsible for the death resistance of PRCs and not the loss of Rh1 function. We then tested whether cells exposed to unfolded Rh1 in the ER could phenocopy the protective effect seen in ninaA mutant retinas. There are several dominant rh1 mutations leading to Rh1 misfolding and accumulation in the ER (Colley et al, 1995). PRCs maintain their integrity for up to 45 days under normal light and temperature conditions, but dominant rh1 mutations cause a slow age‐dependent retinal degeneration when exposed to constant light. (Kurada and O'Tousa, 1995, and data not shown). We examined PRC death sensitivity in rh1G69D retina in 2‐day‐old adults submitted to dp53 or rpr expression. As in ninaA mutant retina, PRCs exhibited strong resistance to dp53 (Figure 2F and G) and rpr expression (data not shown).
To circumvent possible issues relating to the ectopic expression of apoptotic genes under the control of the UAS/GAL4 system, we tested whether ninaA mutations could inhibit cell death in another PRC degeneration paradigm. Loss of apc1 triggers ectopic armadillo expression and PRC degeneration (Ahmed et al, 1998). We found that while apc1Q8 adult retina exhibited complete PRC loss (Figure 2H), heterozygous or homozygous ninaA mutations were sufficient to induce a partial rescue of PRCs (Figure 2I and J). Taken together, these results favour a model in which accumulation of unfolded Rh1 in the ER is responsible for the increased resistance to death in PRCs.
Misfolded Rh1 induces an UPR
We next investigated whether the accumulation of misfolded Rh1 in the ER causes UPR activation in Drosophila. During UPR, Ire1 catalyses the unconventional splicing of a small intron from the mRNA of xbp1 (Yoshida et al, 2001). This splicing creates a frameshift in the xbp1 mRNA, creating an active transcription factor. A stress indicator was engineered by fusing Drosophila Xbp1 with GFP. Upon ER stress, the spliced mRNA is translated into a Xbp1:GFP fusion that can be detected by fluorescence or with antibodies against GFP (Ryoo et al, 2007). To detect the UPR in ninaA and rh1 mutants, we first used the Xbp1:GFP sensor as readout for UPR activation. xbp1 splicing was detected by the presence of GFP, revealed using an antibody against GFP in horizontal cryosections (Figure 3; Supplementary Figure 2). Expression of the Xbp1:GFP sensor in a wild‐type background showed a low level of GFP immunoreactivity (Figure 3A), suggesting that PRCs are exposed to basal UPR activation due to the high levels of rhabdomere‐targeted Rh1 proteins that transit through the ER. We observed high levels of Xbp1:GFP in rh1G69D mutant retina (Figure 3C; Ryoo et al, 2007). Strikingly, the loss of one genomic copy of ninaA was sufficient to cause UPR activation, as indicated by the significant increase of GFP immunoreactivity (Figure 3E; Supplementary Figure 2). This is in accordance with the fact that reducing the dose of ninaA by 50% is sufficient to cause the accumulation of misfolded Rh1 in the ER (Baker et al, 1994). Complete inactivation of ninaA exhibited widespread GFP staining (Figure 3G). These results indicate that Ire1‐dependent xbp1 splicing is activated in response to the accumulation of misfolded Rh1 in the ER of ninaA and rh1G69D mutant PRCs.
To further characterize the extent of UPR activation, we evaluated the levels of Hsc3 expression in ninaA and rh1 mutant retinas (Figure 3). Similarly to Xbp1:GFP, rh1G69D mutant retinas show a robust increase of Hsc3 expression as seen in horizontal cryosections and western blots (Figure 3, D, I, J; Ryoo et al, 2007). The loss of ninaA also led to an increase in the levels of Hsc3 (Figure 3F and H). Interestingly, western blot quantification shows that the increase in Hsc3 protein is dependent on the dosage of ninaA gene expression, as flies heterozygous for ninaA exhibit less of an increase when compared with ninaA amorphs (Figure 3I and J). This is supported by the fact that the amount of unfolded Rh1 is dependent on the genomic dosage of ninaA (Baker et al, 1994). For the rest of the study, we will consider that heterozygous ninaA mutants induce moderate ER stress, while homozygous ninaA or rh1G69D mutants trigger strong ER stress. Taken together, the intensity of UPR activation, visualized by xbp1 splicing and Hsc3 expression, depends on the amount of misfolded Rh1 proteins that accumulate in the ER.
Prolonged and moderate ER stress does not lead to neurodegeneration
Accumulation of misfolded proteins and UPR activation protect PRCs from death in young adult retina (Figures 1 and 2). We next asked whether prolonged ER stress and long‐term UPR activation under normal physiological conditions can affect long‐term PRC survival. PRC integrity was determined in aged flies (60 days old) carrying ninaAE110V or rh1G69D mutations, reared under normal temperature (25°C) and light:dark cycle (12:12 h) conditions. In 60‐day‐old adults, we found that both homozygous ninaAE110V and rh1G69D mutant retinas (strong ER stress) display defects in the ommatidia trapezoidal arrangement and occasional PRC loss (Figure 4C and D, and data not shown). These results correspond with an earlier study showing that long‐term PRC degeneration occurs in homozygous ninaA mutant retinas (Rosenbaum et al, 2006). Conversely, heterozygous ninaAE110V retinas (moderate ER stress) remained intact, showing normal morphology (Figure 4B) despite displaying hallmarks of ER stress and UPR activation (Figure 3E and F, and data not shown). This result indicates that a prolonged moderate ER stress does not cause PRC death.
An ER‐mediated signal inhibits caspase activation
Mutations leading to the accumulation of unfolded Rh1 and activation of the UPR can protect PRCs from cell death induced by dp53, rpr or the caspase dcp‐1 (Figures 1, 2 and 3). We first tested whether the UPR activation could lead to a reduction of the rh1‐GAL4/UAS system and a subsequent decrease of the ectopic expression of the apoptotic proteins. To address this question, we compared GFP expression levels (ectopically expressed using GAL4/UAS system), in ninaA, rh1 mutant and wild‐type retinas (Figure 5). Although GFP levels were decreased in homozygous ninaAE110V or rh1G69D mutant retinas (strong ER stress), no reduction of GFP was observed in heterozygous ninaAE110V mutants (moderate ER stress) compared with the β‐tubulin loading control (Figure 5A and B). These results suggest that while attenuation of the rh1‐GAL/UAS system can contribute to cell death inhibition under strong ER stress conditions, it does not play a role in moderate ER stress situations. In addition, we tested whether the UPR could regulate rh1 promoter activity. We measured rh1 promoter activity (using a rh1‐LacZ transgenic line) by quantifying X‐Gal staining of retinal sections and measuring β‐galactosidase activity with an ONPG assay in ninaAE110V and rh1G69D mutants (Supplementary Figure 3). No difference was observed between the different genotypes, indicating that rh1 promoter activity functions normally in PRCs under ER stress. This result corroborates an earlier study showing that rh1 transcription is unaffected in ninaA mutants (Zuker et al, 1988). Although we cannot exclude that subtle translation attenuation can push the balance in favour of anti‐apoptotic genes in ninaAE110V heterozygous retina, it suggests that another ER‐mediated mechanism inhibits cell death.
Next, we examined whether ER stress inhibits caspase activation. If ninaA mutants block primarily caspases sensitive to the baculovirus caspase inhibitor p35, then ninaA mutations should not show an additive effect on PRC protection mediated by p35 expression. We took advantage that p35 only partially suppresses dp53‐induced death (Figure 6 and data not shown). We found that dp53‐induced PRC death was equally inhibited by the expression of p35 or by ninaA mutation. Moreover, p35‐mediated caspase inhibition was not enhanced by ninaA mutations (Figure 6A–E). These results suggest that ninaA mutation blocks primarily p35‐inhibitable caspases in PRCs submitted to dp53‐mediated PRC death.
We then examined the effector caspase activation levels in PRCs submitted to ER stress by measuring PARP cleavage and using a DEVD‐based caspase activity assay. We first assayed cleavage of the genetically encoded caspase probe CD8:PARP:Venus as a read‐out for effector caspase activation (Williams et al, 2006). We found that loss of ninaA strongly suppressed the dp53‐induced cleavage of CD8:PARP:Venus in PRCs as visualized by western blot analysis (Figure 6F and G). Next, we measured effector caspase activity in retina extracts using a caspase activity assay (Caspase Glo®). DEVD cleavage is strongly impaired in heterozygous ninaAE110V mutants compared with wild‐type retinas (Figure 6H), suggesting an inhibition of Drosophila interleukin‐1 converting enzyme (Drice) activity (Fraser et al, 1997). Together with the observation that ninaA mutants inhibit dcp‐1‐induced apoptosis (Figure 1I and J), our results indicate that an ER‐mediated protective signal inhibits the activation of effector caspases.
An antioxidant response is induced upon ER stress
We found that a moderate ER stress protects PRC from apoptosis (Figures 1, 3 and 6). It has been proposed that the UPR contributes to redox homeostasis after ER stress in mouse fibroblasts (Cullinan and Diehl, 2004). We asked whether an antioxidant response is induced in Drosophila PRCs under ER stress. We have observed that the antioxidant genes ferritins (fer) protect PRCs from death induced by ectopic expression of apoptotic genes or by light‐mediated photo‐oxidation (AG, CSM, HS and BM, unpublished). Fer are iron storage proteins found in all animal species, and thought to sequester ferric iron (Fe3+) in a nonreactive form that cannot promote redox reactions (Harrison and Arosio, 1996). We thus evaluated expression of the antioxidant fer in ER‐stressed retinas. The Drosophila multimeric ferritin complex is composed of fer light chain (fer2lch) and fer heavy chain (fer1hch). As a means to assess transcription activation of fer genes, we used an enhancer trap transposable P‐element, carrying β‐galactosidase inserted in fer1hch or fer2lch gene locus. We found increased fer2lch expression in nuclei of PRCs mutant for ninaAE110V or rh1G69D (Figure 7A–D; Supplementary Figure 4A). However, no Fer2lch protein variation was detected by western blots analysis of dissected ninaAE110V or rh1G69D retinas compared with control retinas (data not shown). This could be due to strong fer2lch levels in the optic lobe, masking any increase of levels in the PRCs due to ER stress (Figure 7A–D). In contrast to fer2lch, fer1hch remained constant (data not shown). The increase of fer2lch transcripts suggests that an antioxidant response could contribute to the protective effect in ER‐stressed retina.
The Drosophila eIF4E binding protein (d4E‐BP) is induced in response to oxidative stress (Tettweiler et al, 2005). Although d4E‐BP is not an antioxidant protein per se, it downregulates translation of cap‐dependent mRNA and mediates survival in animals exposed to oxidative stress. Whether ER stress is capable of inducing d4E‐BP expression is not known. We examined d4E‐BP levels in retinas submitted to ER stress. We found that PRCs under ER stress exhibit an increase of d4E‐BP transcriptional activity and protein expression compared with wild‐type conditions (Figure 7E–I; Supplementary Figure 4B). We used the enhancer trap line Pz [d4E‐BP06270] to evaluate d4E‐BP transcriptional activity in ninaA and rh1 mutant retinas. We observed that the rh1G69D mutant exhibited a marked increase in β‐galactosidase activity staining compared with the wild‐type retina (Figure 7H). Increased staining in ninaAE110V and ninaA1 heterozygotes was modest, which is consistent with the fact that ninaA heterozygous mutants exhibit a weaker UPR than in rh1G69D retinas (Figure 3J). We next tested whether the upregulation of d4E‐BP transcriptional activity is associated with an increase of d4E‐BP protein expression in western blots of ninaA or rh1 mutant retinas (Figure 7I). Retinas submitted to ER stress (ninaA1, ninaAE110V and rh1G69D alleles) exhibited an increase of d4E‐BP protein compared with wild type (Figure 7I, and data not shown). This result shows that PRCs under ER stress trigger a stress response marked by the induction of ferritin and d4E‐BP genes.
To evaluate redox status in PRCs submitted to ER stress, we measured oxidative stress levels by immunodetection of carbonyl groups in oxidized proteins (Levine et al, 1994). We found an overall reduction of carbonylated proteins in ER‐stressed mutant retina, which is most evident in homozygous ninaA retina (ninaA1 and ninaAE110V) (Supplementary Figure 5). This suggests that retinas submitted to ER stress exhibit reduced oxidative stress levels.
We then explored whether an ER‐mediated stress response is capable of protecting from reactive oxygen species (ROS)‐induced cell death. We used an in vitro approach in which pharmacologically induced ER stress protects cultured cells from apoptosis. Drosophila S2 cells can activate an UPR when submitted to tunicamycin (Tm, a glycosylation inhibitor) or thapsigargin treatment (Tg, an ER calcium storage inhibitor) (Plongthongkum et al, 2007; Ryoo et al, 2007). When pre‐treated with a sub‐lethal dose of Tm or Tg, S2 cells exhibit oxidative stress resistance to H2O2 (Figure 8A, and data not shown). This result suggests that moderate ER stress can protect cells from oxidative stress. We did not observe an increase in ferritin expression in S2 cells, suggesting that these cells may induce the expression of other antioxidant genes to promote an antioxidant response. In contrast, we found that Tm or Tg treatments induced a dose dependent increase of d4E‐BP proteins (Figure 8B). This result is consistent with the fact that PRCs submitted to ER stress exhibit an increase of d4E‐BP protein expression.
Next, we tested whether moderate ER stress could also protect from other apoptotic stimuli, such as cycloheximide (CHX) and ultraviolet (UV). We found that Tm and Tg also protected S2 cells from apoptosis induced by CHX and UV. As moderate ER stress is capable of inhibiting caspase activation in the fly retina (Figure 6), we tested whether Tm can limit caspase activation induced by CHX in S2 cells. We found that a pre‐treatment with Tm mitigates caspase activation (Figure 8C).
To test whether Tm‐mediated protection requires the UPR, we inactivated xbp1 gene using RNAi. Double‐stranded RNA (dsRNA) against xbp1 was efficient as it totally abrogated xbp1 and strongly reduced hsc3 transcript expression (Figure 8D). Tm‐mediated protection is xbp1‐dependent as dsRNA against xbp1 restored UV‐induced cell death (Figure 8E). This suggests that the UPR mediates the Tm survival response in S2 cells. All together, these results argue that moderate ER stress protects from both ROS‐ and caspase‐dependent cell death in vitro and in vivo.
In pathological conditions such as diabetes and neurodegenerative diseases, a massive accumulation of misfolded proteins in the ER induces a UPR, which in turn triggers apoptosis (Marciniak and Ron, 2006). Here we show that a more moderate activation of the UPR (ninaA and rh1 mutants) can mediate a survival response. The UPR protects PRCs from apoptosis induced by the expression of pro‐apoptotic genes, rpr, dp53 and dcp‐1, as well as the degeneration observed in apc mutants (Figure 1). We found that the ER inhibits caspase activation and triggers an antioxidant response (Figures 6 and 7). In addition, we showed that a pharmacological pre‐treatment with sub‐lethal dose of the ER inducers (Tm or Tg) protects S2 cells from H2O2, CHX or UV exposure (Figure 8, and data not shown). Our results indicate that moderate ER stress mediates a cellular response that inhibits additional external insults and allows the cells to have a survival response to the initial ER stress.
The ER stress‐mediated protective effect can be assimilated as pre‐conditioning or an adaptative stress response, also termed hormesis. Hormesis is a cellular protective signal induced by exposure to a low dose (or mild) stress‐inducing agent that allows the cell to better respond to a second insult (for review Mattson, 2008). Our work is an example of ER‐mediated hormesis (or ER‐hormesis), because low levels of ER stress cause the UPR to protect the cells against cell death, whereas high levels of ER stress cause the UPR to trigger the apoptosis pathway.
What makes ER stress lethal?
The current view is that prolonged intense ER stress promotes apoptosis. UPR‐regulating proteins have been implicated in the activation of death factors that trigger caspase activation (Nakagawa et al, 2000; Hetz et al, 2006; Puthalakath et al, 2007). Here, we have shown that prolonged but mild ER stress can promote a long‐term survival response, allowing the cells to cope with additional oxidative or apoptotic insults. So what is the cellular switch that pushes the cell from survival to death? Our data suggest that both intensity and duration of the ER stress play a part in this decision. We show that a strong ER has short‐term protective effects but leads to PRC degeneration in the long term (homozygous ninaA mutants and rh1G69D, Figures 1, 2 and 4). In contrast, more moderate ER stress is protective in the short term and remains harmless even if it is maintained the entire life of the animal (heterozygous ninaA mutant tested in 60‐day‐old animals, Figure 4).
Using an ADRP rat model, Peter Walter and colleagues have recently brought some insight to a molecular switch that pushes PRCs towards death pathway (Lin et al, 2007). They have shown that rat PRCs carrying the misfolding mutation rh1 (rh1P23H) degenerate at early post‐natal stages. In contrast with ninaA mutant flies, 'low level' ER stress leads to rat PRC demise within a few weeks (Transgenic rat TgP23H3). This may be due to the fact that the transgenic expression of misfolded Rh1 still generates too much ER stress. Nevertheless, the same group has shown that sustained Ire1 does not promote death, whereas sustained Perk mediates cell death (Lin et al, 2007, 2009). Our results support the hypothesis that Ire1 has a protective effect, as inactivation of xbp1 is sufficient to abolish the Tm protective effect in S2 cells (Figure 8E).
Is a moderate activation of the Ire1 pathway mandatory for long‐term Drosophila PRC survival? Upon ER stress, we have shown that Ire1‐mediated xbp1 splicing is induced in PRCs, as demonstrated by the appearance of spliced xbp1 mRNA and Hsc3/Bip protein (Figure 3). A moderate increase of Hsc3 expression is associated with long‐term resistance to cell death in heterozygous ninaA mutants. In contrast, a more robust Hsc3 expression is associated with short‐term protection and long‐term neurodegeneration in homozygous ninaA mutants (Figures 3 and 4). Thus, a moderate activation of the Ire1 pathway is correlated with a long‐term PRC survival.
Although all UPR branches are activated upon ER stress, the immediate response is Perk/eIF2α‐mediated translation attenuation (Wu and Kaufman, 2006). We found that when the ER stress is intense (homozygous ninaA or rh1G69D mutant retinas), the reduction of protein synthesis limits the expression of proteins in PRCs through the UAS/GAL4 system, hence contributing to attenuated PRC death (Figure 5). In contrast, when ER stress is moderate (heterozygous ninaA mutant retina), there is no apparent reduction of protein synthesis and no long‐term deleterious effects. This suggests that Perk/eIF2α is not activated or does not mediate the translation attenuation in heterozygous ninaA mutant retinas. One possible explanation is that limited activation of the Perk/eIF2α pathway favours survival. In support of this hypothesis, attenuation of Perk‐mediated eIF2α phosphorylation by the compound salubrinal protects cells from the deleterious consequences of prolonged ER stress (Boyce et al, 2005). In addition, the genetic reduction of eIF2α protects from oxidative stress (Tan et al, 2001). Thus, low level of Perk/eIF2α pathway activation is correlated with enhanced cell survival.
What are the signals that inhibit PRC death in ER‐stressed retinas?
We found that ER stress mediates caspase inhibition and apoptosis resistance in PRCs (Figure 6). In addition, ER stress induces an antioxidant response as shown by the increase of fer2lch and d4E‐BP expression (Figures 7 and 8B). This antioxidant response is associated with a reduction of basal oxidative stress levels as visualized by the detection of protein oxidation in the retina (Supplementary Figure 5). We propose that the inhibition of basal levels of oxidative stress limits caspase activation and contributes to the protection of PRC submitted to ER stress.
In support of an ER‐mediated antioxidant response, we show S2 cells, pre‐treated with Tm or Tg, are resistant to ROS exposure (H2O2) (Figure 8A, and data not shown). Similarly, it has been shown that UPR activation counteracts ROS accumulation and cell death induced by tumour necrosis factor alpha in mouse embryonic fibroblasts (Xue et al, 2005). Together, these data argue that the UPR can limit ROS accumulation, inhibiting apoptosis in a conserved process.
Activation of the UPR, as well as the increase of d4E‐BP upon ER stress, suggests that selective changes in protein levels regulate cell death. In support of this hypothesis, it was proposed that 4E‐BP favours the translation of proteins through their internal ribosome‐entry site (IRES), contributing to survival (for review Holcik and Sonenberg, 2005). The translation of genes, such as Bip, that contain IRES in their mRNAs can limit the UPR and protect the cell from excessive ER stress.
Although it has been shown that ER stress can induce the IRES‐dependent translation of the human inhibitory of apoptosis protein 2 and reduce cell death (Warnakulasuriyarachchi et al, 2004), we failed to detect an increase of the Drosophila inhibitory of apoptosis protein 1 (DIAP1), measured by western blot or immunofluorescence of Drosophila retinas exposed to ER stress (data not shown). It is possible that other IRES‐dependent proteins contribute to an increased antioxidant response and the inhibition of caspase activation in PRCs. It has been shown that an antioxidant treatment can prevent JNK‐mediated caspase activation in NF‐κB deficient mouse fibroblasts (Kamata et al, 2005). Whether an ER‐mediated signal can inhibit JNK‐induced cell death remains to be demonstrated.
Relevance to pathology
Increasing evidence has linked ER stress and the UPR to pathologies such as neurodegenerative diseases, cancer and diabetes (Marciniak and Ron, 2006). ER stress markers have been observed in degenerating tissues, and it has been proposed that an overloaded ER promotes cell death. Our data tackle a new and important issue, in that moderate ER stress is not only protective against unfolded protein accumulation but also against external apoptotic insults. We also show that moderate and protective ER stress remains harmless in the long term. Whether moderate ER stress in a healthy mammalian brain could protect against or delay the onset of neurodegenerative diseases remains to be demonstrated.
Materials and methods
Fly stocks
The following genotypes were used: Canton S (CS) and cnbr as wild‐type strains. The ninaA1 (ninaAW208@), pzfer1hch0451, pzfer2lch035, pzthorl(2)06270 alleles were obtained from the Bloomington Stock Center. The ninaA alleles ninaAE110V, ninaAQ137L, ninaAR120K, and ninaAG98D were a gift from Charles Zuker (Ondek et al, 1992). The apcQ8 allele was a gift of Yashi Ahmed. The rh1 alleles, ninaEI17 and ninaEG69D (termed rh1I17 and rh1G69D, respectively in the text) were a gift from Joseph O'Tousa (Kurada and O'Tousa, 1995). The rh1‐Gal4 driver, a gift from Jessica Treisman, was used for ectopic expression in the outer PRCs (Mollereau et al, 2000). The uas‐CD8:PARP:venus stock was a gift from Darren Williams (Williams et al, 2006). The following genetic combinations were used to express transgenes in adult outer PRCs: (1) rh1‐Gal4; uas‐rpr, (2) rh1‐Gal4; uas‐dp53, (3) rh1‐Gal4; uas‐dcp‐1, (4) rh1‐Gal4; uas‐xbp1:GFP, (5) rh1‐Gal4; GMR‐p35, (6) rh1‐Gal4; uas‐GFP and (7) rh1‐Gal4; uas‐CD8:PARP:venus. Flies were maintained at 25°C and a 12:12 h light cycle.
Caspase assay
S2 cells were seeded in 96‐well culture plates at 15 × 103 cells per wells. After a 4‐h Tm treatment, cells were submitted to CHX for 5 h and 30 min. Caspase‐Glo® 3/7 reagent (Promega, France) was added (V/V) to wells and incubated for 1 h 30 min. Luminescence was measured by a luminometer (Veritas™ microplate luminometer).
The effect of xbp1 knock down on S2 cells was monitored by RT–PCR. mRNA was extracted from treated S2 cells using RNeasy Mini Kit (Qiagen). cDNA was produced using the Enhanced Avian RT First Strand Synthesis Kit (Sigma). xbp1 mRNA expression was visualized after 22 cycles and melting temperature of 58°C.
A more detailed Material and methods section can be found in Supplementary data.
Supplementary data
Supplementary data are available at The EMBO Journal Online (http://www.embojournal.org).
Supplementary Information
Supplementary Figure 1 [emboj200976-sup-0001.jpg]
Supplementary Figure 2 [emboj200976-sup-0002.jpg]
Supplementary Figure 3 [emboj200976-sup-0003.jpg]
Supplementary Figure 4 [emboj200976-sup-0004.jpg]
Supplementary Figure 5 [emboj200976-sup-0005.jpg]
Supplementary Table 1 [emboj200976-sup-0006.doc]
Supplementary data [emboj200976-sup-0007.doc]
We thank Samara Brown for critical reading of our paper. We also thank Carmen Garrido, Pierre Copin, Damien Lefer and Clémence Richetta for technical help, the ENS imaging platform (PLATIM) and the IFR128 for their technical facilities. We thank Hugo Aguilaniu's group for technical advices on the Oxyblot™. We are grateful to NJ Colley, J O'Tousa, N Sonenberg, G Tettweiler, J Treisman, D Williams, C Zuker and Flybase for fly stocks and reagents. This work was supported by grants from the National Institute of Health to BM (RO1 EY14025), from the Fondation pour la Recherche Médicale (Equipment and Team programs) from the CNRS (ATIP program) to BM. HS is an Investigator of the Howard Hughes Medical Institute. CSM was a student of the Gulbenkian PhD Program in Biomedicine supported by a fellowship from Fundação para a Ciência e a Tecnologia, Portugal. CL, a student at University Claude Bernard in Lyon, is supported by a graduate fellowship of the cluster 11 HNV (Rhone Alpes, France). AG is a student of the Rockefeller University graduate program.
- Copyright © 2009 European Molecular Biology Organization


text:
After my efforts to get the Anastasia Beverly Hills Dip Brow ended on a disappointing note, I thought I'd give other options a try and bought the Sleek Brow Kit in Dark.
|Sleek Brow Kit in Dark
I got my eyebrow kit from Luxola.com along with my friend rekha's order. I paid Rs. 1050/-. The price I paid is slightly on the higher side for a brand like Sleek but considering that it is an all import duty inclusive, it did not bother me much.
I got the shade in dark as against extra dark because I am blessed with quite thick brows and filling them in an extremely dark shade makes them look too stark for my tastes (and I don't want them to get murdered in a wedding feast #GoT)
|Sleek Brow Kit in Dark - Tools
The brow kit comes in a sturdy matte black box with glossy lettering. It looks chic. The kit has two main products i.e., a brow wax and a brow powder. It also has a mini tweezer, flat brush and an angled brush.
The brushes are extremely tiny. Apart from the angled brush, I do not find the rest of the tools handy.
The brow wax is dark brown in color and extremely pigmented. Unless you are looking for fierce brows every day, a small quantity should suffice. The main purpose of the wax is to control the hair, create a structure and a base for the powder to stick in. The powder is slightly lighter than the wax but still not very light so as to seem odd against a dark surface. It is completely matte and covers up all the bald patches perfectly. It looks very natural.
The brow powder+wax combo stays put throughout the day. Even if the rest of my makeup fades, I am left with perfect brows throughout the day. They don't budge at all. They are water resistant as I have at many times forgotten about the product and splashed water on my face but it has never come off. I don't have the habit of scratching my brows or rubbing them so I don't know about their resistance to deliberate smudging. (who would do that to a perfect pair of brows anyway?)
After using this brow kit, I came to understand that filling your brows with a dark eyeshadow is NOT as same as filling your brows with a dedicated brow kit. This is perfect and takes the brow game to a whole new level.
The only con I feel is, the brow wax/powder needs to be used with considerable caution as it is so easy to go overboard with it.
|Sleek Brow Kit in Dark - Closeup
|Sleek Brow Kit in Dark
How I use my brow kit:
I comb my lashes with a spoolie and take a teeny tiny amount of the brow wax in the brush and start outlining from the arch towards the end. I start with the bottom part. I don't outline the inner corners at all. Once the outlining is done, I take a clean angled brush slightly thicker than the one I used before and pull the lines towards the center. The lower line gets pulled upwards towards the middle and the upper line gets pulled downwards so as to cover the bald areas in the middle but without making the efforts look obvious. After that, I use the same brush to brush through my natural shape and ensure that the hair looks groomed. Only after this, I fill in the inner corner part with the same brush without any extra product.
After I am satisfied with the shape and the grooming, I then set it with the powder. I don't use too much powder for this step either. Less is the key. I don't mess up with the natural shape too much.
I have used the product around 10 times and that's the amount of product I used up.
|Sleek Brow Kit in Dark - The Brow wax is on the left
I have used the brow kit to fill my brows in this look. As you can see, i hardly fill the inner corners. I don't like them to look very defined. Brows tend to look unnatural when they get too perfect.
|Eye Brow filled using the Sleek Brow Kit in Dark
Key Highlights of the Product
Sturdy packing.
Lovely combo.
Mirror is very useful.
Brow stays put throughout the day.
Easy to use.
Dark is perfect for medium toned ladies with thick brows.
Did not feel heavy or artificial during wear time.
Imparts a natural look.
Water resistant.
Does not melt
Only a small quantity is required.
Not easily available in India
The tweezer is too tiny and I don't use it at all.
Indian Beauty Maniac's Rating
I have used the INGLOT brow wax some time back and I really liked it. But it was not water resistant and it was quite transparent compared to the sleek's one. I paid Rs. 300 for the refill. If I wanted a setting powder, I should have spent another 300-400. So, when comparing to that, I don't find the sleek one over priced at all.
Highly recommended.
My next purchase would be Anastasia's Dip Brow. Just to try it before I settle down with my HG product.


text:
Do sunglasses really protect your eyes?
Yes, think of them as a sunscreen for the eyes. Protect your eyes from wind, dust and drying, and UV (ultraviolet), visible light, and glare. Many experts believe that lifetime exposure to UV radiation helps cause cataracts and other eye disorders, but there is some controversy over the amount of sunlight hurts, or what percentage of the falls are a result. Blue, of the visible spectrum, it can damage the retina and impair vision. It makes sense to protect your eyes. Sunlight and glare is unpleasant, even painful, and can be dangerous if you drive or play sports. "
This is a cataract, which scares me. When I was little and my eyes, I'm sure I heard optomotrist I have a cataract, when I'm older. I do not know because he said it, or if I'm dreaming of everything, but it's always been down in my mind.
See Also. Bags, Clothes Design, Cosmetic, Eyes, Face, Fashion Show, Flowers, Glasses, Hair, Jewelry,
Lips, Mehndi, Nails, Rio Fashion, Week, Second Hand fashion, Shoes, Wedding, Wedding Dance,


text:
Keep this date!!! Sunday, August 26
Joyce Olton is a Barbadian Soprano trained in Barbados under Doris Provincal and furthering her training in Toronto Canada at the Royal Conservatory of Music. She attributes her melodic voice to hard work and several years of practice on the local Church Circuit. Through this circuit here and abroad Ms Olton has been able to hone her skills and pick up quite a large following on the way.
Ms Olton has performed successfully here before. Notably at Frank B Collymore Hall, Harrison College School Hall and several Churches. Several venues are on her list of performance spaces in Toronto.
Accompanying Ms Olton will be Pianist Ann Lascelles and Andrew Allman. Internationally known saxophonist Rupert Williams who need no introduction, St Leonards Boy Choir who is of similar notoriety and Calvary Steel Orchestra, a Church ensemble known in their own right.
The concert takes place 6pm at Calvary Moravian Church on Roebuck St, Bridgetown.
Tickets are $40 available from CS Pharmacy, ESSO Tiger Mart Paynes Bay, The Church or Paul Doyle at firstname.lastname@example.com or facebook.
If you enjoy Contemporary Sacred mixed with slight Classical and Pop genre music…..this is it!
A Night of Contemporary & Sacred Music featuring A Soloist, A Sax, A Steel Orchestra and A Choir


text:
I can't figure out why google refuses to index anything. This is my attempt to fix that.
Update: No, I'm not doing that after all. This is still going to be the blog. Sorry for the drama.
'Mechanized' is a second profile I've created. I'll mostly be using that profile from now on.


text:
A long time ago... In my parent's house far far away... I used to collect Star Wars CCG cards... My card collection was a fun part of my childhood that was, during some unfortunate purge of my stuff in my teenage years, lost forever.
A few weeks ago, my wife and I rewatched the Star Wars trilogy for the first time in over 10 years. My interest in Star Wars reawakened, I decided to see if I could reassemble my old card collection digitally (the original Star Wars CCG game now having gone out of print.)
After some searching and a little luck with Google I found a website that hosted individual GIF images of each card! But... Downloading the 1000+ card images was a little daunting, even to my nostalgic fervor. And since I needed an exuse to learn more Python on my Raspberry Pi anyway, I decided to tackle automating the downloads using a web crawler / scraper library written in Python called Scrapy.
Scrapy is installed through
pip, Python's package installer. If you do not have
pip installed it can be installed through
sudo apt-get install python-pip
Before installing scrapy, there are a few additional dependencies needed:
sudo apt-get install python-lxml libffi-dev
Once those are installed you can install Scrapy through
sudo pip install Scrapy
Scrapy also needs an additional Python dependency to handle some hostname verifications when using SSL. You may not need it but better to install now while we are here:
sudo pip install service_identity
Finally, for the downloading images (the goal of this little project) we need to ensure that Python has some additional image handling libraries.
sudo pip uninstall pillow
sudo apt-get install libjpeg-dev
sudo pip install -I pillow
NOTE: Scrapy is not to be confused with Scrappy. Scrappy is a Python library for renaming video files... Mind your Ps and Qs! But especially those Ps...
Once installed you should be able to type
scrapy at your terminal and see the usage for Scrapy.
To start a new scrapy project you can use Scrapy's scaffolding:
scrapy startproject <project name>
This will create a default project structure (including files for Items, ItemPipelines, Spiders, and other goodness discussed below.) You can use these as a starting point to right your own!
Scrapy has several key concepts:
Spider- A Spider is a module that encapsulates the logic for how to traverse URLs and how to extract information from a page for processing.
Item- An Item is a container that holds information from a page. Items are created by Spiders and can be processed in different ways depending on the type of Item.
Item Pipeline- An Item Pipeline is a processor that handles an Item and performs some action on it or with it. Item Pipelines can be chained together to form a pipeline... (You see what happened there?)
The project I am undertaking (scraping all the card images from this site) is relatively simple. So I created a single Spider that goes through the page to find image links. Each image link is encapsulated as an Item. There is a single Item Pipeline in my pipeline that handles downloading the image.
Scrapy already provides an "ImagesPipeline" which provides some basic behavior. If an Item has an
image_urls field, all images in that field are downloaded by
ImagesPipeline. The images are saved as a file in a configurable directory with the hash of the image as the filename. Metadata about the image is saved to a
images field on the Item.
While it is good that Scrapy can handle the heavy lifting of downloading the images, their choice of default file names is not very helpful. So I decided to extend their ImagePipeline and give it more helpful behavior.
First of all, I wrote a simple Item module:
import scrapy
class CardImage(scrapy.Item):
page_title = scrapy.Field()
image_urls = scrapy.Field()
images = scrapy.Field()
As you can see, my
CardImage extends Scrapy's
Item. I gave it a
page_title to assist with debugging, and the required
image_urls and
images field for the default behavior of
Next, I wrote a modified version of
ImagesPipeline. (This required digging around in the Scrapy source code... Fortunately the
ImagesPipeline module was written in a well factored way and I was able to override a single method to achieve the desired behavior.)
import string
import scrapy
from scrapy.contrib.pipeline.images import ImagesPipeline
class CardImagePipeline(ImagesPipeline):
def file_path(self, request, response=None, info=None):
return string.split(request.url, '/')[-3] + '/' + string.split(request.url, '/')[-1]
The prior implementation of
file_path just calculated a hash from the image. This one takes the image url, splits it on / and takes the last and third from the last elements (which, because of the structure of the site correspond to the card name and the expansion name respecively.) This creates a nice directory structure where there is one directory for each expansion and the files inside are named correctly for the card they depict.
NOTE: This highlights an interesting observation about writing web scrapers. Here I am leveraging a specific convention the site authors used. While this makes solving this problem much easier, it means this web scraper is not at all generic. There seems to be a trade off between "generic" and "easy" when it comes to web scraping!
In order to configure Scrapy to use your pipelines, you need to edit the
settings.py file and add an entry to define your pipelines:
ITEM_PIPELINES = {'ccg.pipelines.CardImagePipeline': 1}
The value (1 in my case) is a priority that determines the order in which pipelines are executed.
As mentioned above,
ImagesPipeline by default stores images in a configurable directory. That directory is also configured in
settings.py as follows:
IMAGES_STORE = '/home/pi/work/scrapy/images'
Finally we come to the Spider:
import scrapy
import urlparse
from ccg.items import CardImage
class CcgSpider(scrapy.Spider):
name = "ccg"
# allowed_domains = "starwarsccg.org"
start_urls = [
seen_urls = []
def parse(self, response):
title = response.xpath('//head/title/text()').extract()[0]
for sel in response.xpath('//a'):
link = str(sel.xpath('@href').extract()[0])
if (link.endswith('.gif')):
cardImage = CardImage()
cardImage['page_title'] = title
cardImage['image_urls'] = ['http://www.starwarsccg.org/cardlists/' + link]
yield cardImage
if (not link.startswith('V') and link.endswith('Type.html')):
if (not link in self.seen_urls):
yield scrapy.Request(urlparse.urljoin('http://www.starwarsccg.org/cardlists/', link), callback=self.parse)
A lot to process here! Let's start from the top:
name = "ccg"
# allowed_domains = "starwarsccg.org"
start_urls = [
Important metadata for the Spider. The
start_url will (obviously) be automatically processed first. A spider can generate new urls to follow as it processes its initial
start_urls. I commented out the
allowed_domains field, but that can be used to limit Scrapy to only scraping within certain sites if desired. It is applicable but not important here since I already limit the urls the spider processes through other mean.
NOTE: Scrapy gives a strange error (something to the effect of:
ImportError: No module named items) if you name your Spider module the same name as your project. (My project is named
ccg and my Spider is named "ccg" but the module containing the Spider code is called
parse method contains the core logic of the spider. In this case we use xpath to parse out the page title (which is later saved in the item for debugging), and then process every link on the page.
Inspection of the target website shows that each expansion page (such as Premiere) contain
<a> tags for each image (all ending in
.gif) and links to other expansion pages (each starting with "V" and ending in "Type.html" by internal convention). I wrote the spider to specifically exploit this.
Thus you have this code:
for sel in response.xpath('//a'):
link = str(sel.xpath('@href').extract()[0])
if (link.endswith('.gif')):
<process image>
if (not link.startswith('V') and link.endswith('Type.html')):
if (not link in self.seen_urls):
<process expansion page>
The spider can yields an arbitrary number of Items or Requests (which are themselves, then processed by the spider). For this spider we encapsulate each image as an Item:
cardImage = CardImage()
cardImage['page_title'] = title
cardImage['image_urls'] = ['http://www.starwarsccg.org/cardlists/' + link]
yield cardImage
And each expansion page as a request:
yield scrapy.Request(urlparse.urljoin('http://www.starwarsccg.org/cardlists/', link), callback=self.parse)
Note: To prevent infinite loops, I keep track of what expansion pages I have visited in order to prevent revisiting them. Hence the
seen_urls list. For a general purpose web crawler you would need a much more scalable solution to solve this problem.
Note that when returning a Request you can specific a different method in your spider to handle that Request. This allows you to have different logic for different URLs as needed.
That is all there is to this simple web spider!
Thoughts? Questions? Comments? Email me at: [email protected]


text:
Miracle's BoysBook - 2000
From the critics
Community Activity
QuotesAdd a Quote
The fact that all three of the characters are boys allows Jacqueline Woodson to explore how outside expectations of rough and so-called manly behaviour clash with the grief they're feeling. This is particularly noticeable with Charlie, once a stray-animal-saving boy, who now deals with his emotions by treating everyone with hostility and by hanging out with gang members he used to cross the street to avoid. Miracle's Boys takes a look at what some of the consequences of this idealization of violence can be, and it provides an alternative in the end.
What I liked the most about Miracle's Boys was the depth of the characterization. The characters are all so human – they're not perfect, but they're never vilified either, despite the mistakes they make. Indeed, one of the main things Lafayette learns is that his brothers are human, neither monsters nor saints; that despite being older than he is, they too are young boys who are scared and alone.
Ty'ree was all right after Mama died. But I was all wrong. The year before, I'd seen this show about snakes. They showed this one snake slipping out of its old skin and then leaving the old skin on the ground behind him. That's how I felt—like Mama'd been my skin. But I hadn't grown a new skin underneath, like the snake had. I twas just blood and bones spreading all over the place.
Sometimes I stared in the mirror and was surprised to see how little and lost I looked. That was how Ty'ree looked now—like he was waiting for somebody to take his hand and show him the way home.
CommentAdd a Comment
Memories flood my mind along with tears every time I read Jacqueline. I thought about my mom and brothers while reading this piece. Force fed Joseph Smith from birth, we lacked faith in modern mythology. So when we had to prove a truth, trust or secret we would swear to the three Jimi's in lieu of God. Jimi Hendrix, Jim Morrison and Jimmy Page. While it's hard not to focus on the darkness this book reminded me of the good years with mom when we would watch Mystery Science Theater 3000 for days on end on the Betamax and play spades late into the night.
Woodson has written a thoughtful book about grief, family, and hope.
This book is very good, it is so intersting.If you like this book, you rule, if dont, oh well.
AgeAdd Age Suitability
SummaryAdd a Summary
At twenty-one Ty'ree, the eldest of three brothers, is now caring for his younger siblings. Lafayette, twelve, is still grieving and blames himself for not being able to save his mother, who died from an insulin shock two years earlier; and Charlie, fifteen, has just returned from Rahway Home for Boys where he has been imprisoned for the last three years after being convicted of armed robbery.
Ty'ree and Lafayette have built a stable, if quiet, relationship and are comforted by predictable daily routines. Charlie introduces an element of chaos and hostility that neither of his brothers is able to relate to. In response they begin talking to each other in a way they hadn't been able to previously. They fear for Charlie and want to help him overcome his anger and grief. In attempting to help Charlie, they end up working through their grief as well. The story is told almost exclusively through dialogue with little action actually taking place
NoticesAdd Notices
There are no notices for this title yet.
View originally-listed edition


text:
If you are going all out, you might as well make it good! That's my motto- it has to be memorable or else don't even bring it close to your lips darlin'. Goodiva truffles are pricey and quite honestly they have generally sat in a box on a shelf for goodness knows how long. Homemade truffles is where it's at- and for all you divas who love nutella as much as I do, here you go- Chocolate Hazelnut Truffles.
- 3/4 cup confectioners' sugar
- 2 tablespoons baking cocoa
- 4 milk chocolate candy bars (1.55 ounces each)
- 6 tablespoons butter
- 1/4 cup heavy whipping cream
- 24 whole hazelnuts
- 1 cup ground hazelnuts, toasted
Using a melon baller or spoon, shape candy into 1-in. balls; press a hazelnut into each. Reshape balls and roll in ground hazelnuts. Store in an airtight container in the refrigerator.
Makes 2 dozen truffles


text:
Chargers sweep Bonduel
Jacy Zollar, firstname.lastname@example.com
Bonduel fought hard but could not win a set against Wittenberg-Birnamwood in a Central Wisconsin Conference-East match Tuesday in Wittenberg.
The match was tight from the start, with several lead changes, before the Chargers (3-14, 1-0 CWC) emerged with the sweep, 25-18, 25-17, 25-18.
"Historically, Wittenberg's been at the top of the conference," Bonduel head coach Kim Strayer said, "so we knew coming in here that we were going to have to fight."
Fight, they did. Bonduel kept all of the sets close, and the teams played long rallies throughout the match.
"We felt prepared for it. They practice hard, there's no down time," Wittenberg-Birnamwood head coach Becky Rew said. "It's one drill to the next and just constant. If there's a dead ball, I'm throwing in the next one right away so they don't have a chance to break. That makes them trained for the long rallies."
Bonduel finds practicing long rallies challenging with an eight-person team, compared to Witt-Birn's 12.
"It's really hard with our size to run those rallies in practice," Strayer said. "I need to focus on just feeding them one ball after another to try imitating long rallies, because they're so hard to replicate otherwise."
It also helped that a majority of Witt-Birn's starters are seniors, while Bonduel has a relatively young group.
"Our girls are very close because of their experience together," Rew said, "so you can see that it translates to their cohesiveness on the court. They moved where they needed to be and didn't leave any holes, so they're very connected."
Strayer was impressed with the Bears' play, too.
"They did so many things well," Strayer said. "They attacked the ball well, covered the court well against some hard-hitters, didn't miss very many serves, but they have little things they need to clean up to get past teams like Wittenberg."
Bonduel juniors Mckenzie Wollenberg and Grace Petcka each tallied five kills. Petcka also recorded 13 digs, followed by Wollenberg with 12 and sophomore Megan Zeitler with nine.
Bonduel (4-9, 0-1 CWC) will be at home Thursday against Amherst (3-0).
"We're looking forward to it, because it definitely has an effect on the play," Strayer said. "The girls are familiar and used to everything in our gym, so that's where they feel most comfortable. And they can feed off the fans, so that always gives them more energy."


text:
The motivation through which we encourage our people to intensely assimilate knowledge and explore a customized career graph, leads us to adaptive expertise. Our people are conducted in such a manner that the can enforce their own seamless opportunities. The high aspirations and endeavor that they have in them are encouraged to the core. We are a merit based equal opportunity employer with a view of creating supportive, diverse and a friendly workplace. We offer gamut of services, so we are continuously looking for a variety of people that can bring quality and innovation in our services and provide customized solution to our client for their value creation.
Join us for a Career
Corporate Professionals is a group of seasoned and young professionals offering multi-disciplinary legal, financial and business advisory services. We have successfully executed over 3000 assignments of more than 1000 corporates, domestic as well as international, across Industries. Aiming to become a one-stop-shop offering integrated legal and financial solutions, we have distinctively positioned ourselves as SEBI Registered (Category-I) Merchant Banker with Boutique Investment Banking & Transaction Advisory services. Our services include Merger& Acquisitions, Corporate Affairs &Compliances, Capital Market & Stock Exchange, Securities Law & Transaction Advisory; and Valuation&Biz Modelling. At Corporate Professionals, you will find yourself in a challenging environment that recognizes and rewards outstanding performance. To serve our growing clientele, we are looking to recruit individuals for the following positions:


text:
Wow,..amazing story for sure. I am glad you found some solice in your friend`s arms.
Take what you two did, for the healing properties it was meant to give. Now talk to other women, and form some friendships.
This serves two purposes. I think you can have both worlds. Keeping the friendship with your dear friend. Show her patience, the way she has shown you,..(which I think part of you desires) but also being open to other possibilities, and that will probably relax the husband. If he got a kick out of the sex,...that is a great bonus for him.
If you keep your options open, and forge more friendships,..Over time,..things may change, and you might be able to have more with the friend. Or not. Either way, you have been liberated in a way, and can step forward, and enjoy new friendships.
Note for clarity: 'cuckhold' is originally meant to be a derogatory term. Now its more a humiliation/submission thing. Meaning 'forced' to watch, participate, or be humiliated by the wife having sex with others.
Men who enjoy their wives being elsewhere, experience a sexual surge in a alpha-like reclaiming of their spouse. This is a lot different then a cuckhold fetish,...This situation sounds more like the latter of the two.
Last edited by SourGirl; 05-17-2011 at 02:59 PM. Reason: poor typing when I am tired.
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text:
I don't post English translation of Japanese recipes without permissions from the recipe authors. But feel free to contact me about the dishes you're interested in.
Saturday, June 06, 2009
From Our Veggie Garden (2)
Wow! You know what this means? It means that the start of my very first "fried zucchini flowers" project is drawing near. :D Gee. I wonder how many flowers I'm going to get! About two weeks ago, I thinned out the young zucchini plants and left only four of them. Now they are all looking good.
Here straw mulching is popularly used to keep the soil moist and suppress the growth of weeds.
And other vegetables are looking good, too.
I don't know what this is called in English. Dad said it's a vineless variety.
In addition, leaf vegetables like spinach, lettuce, mizuna and daikon are growing like crazy.
Imagine all these vegetables becoming ready to eat one after another and being brought into our kitchen every day... When mom is on a hunger strike..! We already ate so much of the cucumbers and leafy vegetables, but it was just the beginning, I guess.
Please don't blame me for feeling a bit scared than happy.
7 comments:
- K and S said...
these look great!
- June 7, 2009 at 4:08 PM
They look wonderful obachan!
- June 8, 2009 at 1:24 AM
- Ami said...
Your vegetables have grown so quickly! My zucchini seeds are eaten by rabbits before they grow their real leaves.
I am also growing bush beans this year, they are the only thing the rabbits wont eat.
Do you have any tips on growing Japanese eggplant? My eggplants grow so slowly compared to my other vegetables.
- June 8, 2009 at 4:59 AM
Obachan, do you use pesticides on your crops? I ask because I read somewhere that many Japanese fruits and veg look so nice as a result of the use of pesticides.
- June 8, 2009 at 10:33 AM
- obachan said...
Yep, great... and a bit scary...
Wow! Congratulations! :D
Ritsumei is great. I bet you'll have a great time there. Maybe we can meet up in Kyoto someday?
Actually only zucchini is mine and all other veggies are being taken care of by dad.
Re. growing eggplants:
Dad said that he mixed in some oil meal and dried weeds as fertilizer when he prepared the soil before planting. I'm not sure if it was the reason but dad's eggplants seem to be doing fine.
I haven't used any and I don't think my parents use any on their veggies. But dad does use pesticide on the orange trees.
It is true that pesticides are used on many (most?) commercial fruits and vegetables in Japan and they look nice as a result. On the other hand, more people are becoming interested in healthier crops grown without pesticides, and now such crops are available at regular supermarkets, too, though a little expensive.
I guess people around here do not use pesticides on the fruits and veggies that they eat at home, but use some for the crops they sell. Good looks is a big thing, of course. But the bigger reason is that here in this hot and humid climate, disease and insect damage spread and turn severe so fast. It's terribly phisically demanding to fight against them without chemical pesticide, but around here, almost all farmars are old. Thus, they keep using pesticides, and personally I can't blame them.
- June 10, 2009 at 8:05 AM
wowwee! your garden looks good. haha most definately dont blame you for feeling a bit scared. there's only 3 of you at home. I can relate to that. the fruits from my grandad's garden had such a great impact on my mum that she has never ever bought those fruits even after grandad moved and we never got to eet such fruits again. she remembers too well the weekends of picking, cleaning and frantically distributing fruit so as to let them go to waste.
= ) looking back now it sounds a bit funnie = )
- June 11, 2009 at 12:56 AM
- obachan said...
Hi. Sorry I neglected your comment for more than a month! :O
I can imagine how your mom feels. Food related trauma is very deep-seated. ;)
Say hi to your mom from me.
- July 13, 2009 at 11:46 AM