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When it comes to the younger, less seasoned end of the International Sisterhood of Adult Performers, there's no dearth of sites on which to find them posing, preening and playing with each others' pink bits. But at Nubiles, you get all that and the security that comes with knowing you're dealing with a multi-decades-deep catalog of fresh-faced porno wannabes, burgeoning stars about to make their big breaks, and some truly scintillating modeling, masturbation, and sex. There's no such thing as a foolproof plan, not even in porn, but if these are the young ladies that give you a rise, Nubiles is as close to a sure thing as it gets. Nubiles is the site for you!
Home to what is arguably the largest collection of digitized pornography ever assembled, Videobox has been ruling the online porn world for years. Touting 720p HD videos from top-tier studios and A-list stars as well as amateur productions shot with everyday homegrown honeys, Videobox aims to cover all pornographic bases and very nearly does so. (Where's the early-morning-in-a-french-bakery scene I'm after, VB? Where?) Videobox, arguably the most comprehensive porno site currently going, is utterly unmissable.
Since 1999, Met Art has been filling the 'net with some of the most seductive, sensual imagery to ever pour out of Europe's vibrant erotica industry. Beautiful European women posing naked, shot by world-class photographers, and delivered in high-res photo and HD video formats, Met Art clearly takes its erotica very seriously. Now part of a network of the same name, Met Art seems to be branching out, extending its brand, but what does that mean for the casual visitor and the devoted member, both? Mr. Pink will reveal all!
For well over a decade, Twistys has been filling porno fans' plates with glamorous adult entertainment that bridges softcore and hardcore for a style that is distinctly Twistys' own. Now boasting 1080p HD videos to better showcase stunning models like Kayla Kayden and Valentina Nappi, Twistys is a network offering exclusive porn from When Girls Play and Twistys Hard for a more comprehensive take on sexual excitement. With Treats galore just waiting to dazzle you with their undeniable erotic charm and charisma, Twistys is a babe-lover's paradise.
For many, hardcore pornography begins and ends with Evil Angel, the company started by John "Buttman" Stagliano back in 1989. Home to porn's most accomplished and compelling directors and performers, not to mention a litany of depraved, debauched acts that'll redden the cheeks of even the most seasoned porn viewer, Evil Angel is sexual deviancy digitized, the hottest and hardest porn currently produced in the USA, Europe, and elsewhere. What are you gonna do, pass up the perfect opportunity to find out just how much of a deviant you really are? Now that would really be a sin.
If you've never been a Brazzers member and been thrilled by your favorite pornstar's HD anal debut or the pairing of two preferred babes for an aggressive lesbian hookup that puts all sapphic porn to shame, now's the time. Heavily discounted and online for over ten years, Brazzers, with new site Moms in Control in tow, is bigger, bolder, and better than ever. Don't even consider not exploring the annals and anals of the internationally notorious Brazzers, "the world's best porn site."
Having photographed nude and sexually occupied women for well over two decades, you could say Denys Defrancesco knows a thing or ten about erotica and pornography. Put his experience to the test by peeling back the curtains closing Defrancesco's extensive DDF Network and examining its worth. Have you found yourself interested in lesbian whipping and caning sessions, oil-aided footjobs, deep-throat fellatio, or the delightful Hungarian goddess known to mortals as Eve Angel? Then it's likely you'll find DDF Network as thrilling as a virtual roll in the hay with Ms. Angel herself and a few of her girlfriends. After all, in a way that's kind of what DDF Network is all about.
If you're hardly a stickler for pornographic realism, Naughty America won't be for you. If, on the other hand, you desire fantastic sexual scenarios ripped from your daydreams, rendered in stunning 1080p HD and 4K Ultra-HD videos, starring women so fucking enticing they seem like a fantasy-made-flesh, on such sites as My Sister's Hot Friend, Wives on Vacation, Naughty Office, and Diary of a Nanny, the 40-plus-sites of Naughty America should keep you very much entertained and eager for more of this network's unique sexual thrills!
Copyright © 2016 - Mr. Pink's Porn Reviews - MrPinks.com. All rights reserved.


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expert advice MORE
Toilet Training Setbacks
Q: My son is nearly three and has been potty training for about six weeks now. He does well with peeing in the potty, better away from home than at home. He frequently will pee in his pants during time-out and also has trouble pooping in the potty. I am starting to lose patience with the wet pants and I'm trying not to punish him. Could it have something to do with our new five-month-old twins?
A: Overall, it sounds like you are right on target! Although it is best to avoid "traumatic" (in his eyes) events when beginning to toilet train, this obviously is not always possible. The addition of new siblings can initially be difficult to handle for a young preschooler, as he no longer has your totally undivided attention. Continue to praise him for success when he cooperates with practice sessions or has a favorable attempt at going in the potty. Have him regularly sit on the potty after each meal. Learning to use the toilet is like learning to walk -- everyone will do it at some point, but when that is varies from child to child. Many children are trained between 18 and 36 months, although some accomplish it earlier and others do it later.
Bowel training generally takes longer than bladder training. Be sure your son is learning to urinate in the potty while sitting down. Although boys can be trained to urinate standing up, this should only be attempted after bowel control is established. Standing up to urinate may cause them to forget to have BMs sitting down. When your son goes in his diaper, take him to the potty and empty the diaper there with neutral words of encouragement. Although you should never keep children in dirty diapers as punishment because it creates a confusing message of what is truly desired, you also do not need to drop everything as soon as he comes asking to be changed. Tell him you will first finish whatever you are doing and then change it. These times are not meant to be pleasurable or fun, but you should also try not to sound disapproving.
Most importantly, if frustration is setting in for you or him, it may be best to take a break from training for a while. Do not expect perfection -- three steps forward, one step back, is the norm. An important aspect of training is a relaxed, casual attitude with a sense of humor. Avoid pressure, coercion (being too forceful), or punishment at all costs. For your son to succeed, the timing must be right.
Hank Bernstein Children's Hospital
More on: Expert Advice
Henry Bernstein, M.D., is currently the associate chief of the Division of General Pediatrics and director of Primary Care at Children's Hospital, Boston. He also has an academic appointment at Harvard Medical School.

subset: commoncrawl


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TORONTO - Trista Renee Chaney and Matthew James Adams were united in marriage on Sept. 10 at St. Aloysius Catholic Church in East Liverpool. The Rev. William M. Bill Lies, C.S.C., of the University of Notre Dame officiated.
The bride is the daughter of Jim and Betsy Chaney of Toronto. The groom is the son of Marty and Patti Adams of Salineville.
The bride was escorted by her father and given in marriage by her parents. The bride wore a white gown with a crossover strapless draped tunic bodice and chapel train. She carried a bouquet of white oriental lilies and blue and white dendrobium orchids, with peacock feathers scattered throughout.
Article Photos
Mrl and Mrs. Matthew Adams
Sisters of the bride Erika Gainer of Kent and Emily Chaney of Daytonserved as matron and maid of honor, respectively. Bridesmaids were Dipali Adams of Cincinnati, sister-in-law of the bride; Sheila Downs of Cleveland; and Julie Cameron of Halifax, Nova Scotia, Canada.
Ava Gainer, niece of the bride, served as flower girl.
Brother of the groom Joshua Adams of Cincinnati served as best man. Groomsmen were Thomas Gainer of Kent, brother-in-law of the bride; Jason Smith of Akron; Charles Gough and Joseph Campbell of Chicago; Douglas Farmer of Honolulu, Hawaii; and Jason Shontz of San Francisco.
Mason Gainer and Parker Adams, nephews of the groom, served as ring bearers.
A reception followed at the Pittsburgh Airport Hyatt.
The couple spent their honeymoon in Nanuya Island, Fiji and Maui and Kuai, Hawaii.
The bride is employed as a staff attorney at the Immigration Reform Law Institute in Washington, D.C.
The groom is employed as an accountant for PricewaterhouseCoopers in the D.C. metro office. The couple reside in Washington, D.C.


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Are Wifi-enabled Blu-ray players worth it?
I use a similar Blu-ray player to the Samsung being sold today on http://sellout.woot.com/sale/22968, a wifi-capable, but not built in device which I picked up for about $40 earlier in the year. What with the fully wifi-enabled models being so expensive, little else quality-wise separating the top-tier from the lower-level wifi-capable devices, and other cheap devices like the Roku box or a wifi dongle making it easy to connect for cheap, why not just settle for the lower-level model? Am I missing something or are these "top-tier" models just a scam?
8 Answers answer
Scam, no. Not everyone wants separate devices, so a BR player that can stream is a nice feature. Likewise, not everyone has convenient cabling options, or wants to bother with external devices, so paying extra for wi-fi built-in is a nice feature too.
If you need such features, pay for them in the higher models. If not, then no worries.
Short answer, yes. And if you can, pick up a refurb ps3; it's worth the extra dinero.
@okham: A PS3 is not necessarily the answer for streaming video or music, although your point is well taken. The PS3 and Xbox are both limited in what they offer for streaming. A Roku or even many Blu-Ray players offer more streaming options for both audio and video. If you only want to stream Netflix or a few other major services, PS3 is fine and a preferred choice in my opinion.
Mine has Wifi, does Netflix, Hulu and Pandora and I'm very happy with it. I'm not sure why I'd get any media device without wifi these day.
@kmeltzer: your what has wifi? i am trying to get a wifi blu ray player that can get hulu,vudu,etc
@scubarob56: The question was about Blue Ray players, and so was my answer.
@wnyx585am: I've been pretty happy with the media capabilities of the ps3. But I guess in the areas it's lacking (Hulu,amazon, iTunes,ect.), I just connect my laptop to the tv, so maybe I don't notice the shortcomings. Never mind the added bonus of blowing stuff up or beating in a zombie's head. :D
I have a Wii for gaming and don't watch Blu-ray videos very often. The wife uses Wii Fit and I almost never use the Wii.
Consequently, for me a cheap Blu-ray player makes a lot more sense than a PS3.
I have a Magnavox BR with WiFi which replaced an older Panasonic BR player that didn't. Since the TV isn't near any of my network wiring, I connected it to my net using a pair of wireless routers set up as a wireless bridge. Upgrading to the Mag allowed me to get rid of that extra hardware. So, for me it's very much worth it.
If you watch a lot of video, use Netflix (I don't), etc. get the PS3. That's when the extra cost is quite justified. For me, not so much.


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Jackson Lab an example of wise spending
It was hailed as a great step forward for Connecticut's biotechnology industry. Passed in October 2011, S.B. 1401 established the Connecticut Bioscience Collaboration Program. The focal point was the Jackson Laboratory for Genomic Medicine, specifically its relocation to Connecticut from Maine and the subsequent construction of a research facility. The building will be at the University of Connecticut Health Center campus in Farmington. Jackson Laboratory's business objective is to develop person- alized medicine through genomics, with treatments tailored for individual patients based on their genetic makeup.


text: Dogs in a curled up pose can prove to be quite difficult for many artists to draw. That's why I made this tutorial; to be able to draw something fairly hard in a fairly easy way. Also, because this is Microsoft Paint I'm working with, it should look a bit better on paper. Have fun!!!


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Workflow TV - WF4 Collection Activities Example
- Posted: Mar 11, 2011 at 12:00AM
- 5,013 views
- 3 comments
Loading user information from Channel 9
Something went wrong getting user information from Channel 9
Loading user information from MSDN
Something went wrong getting user information from MSDN
Loading Visual Studio Achievements
Something went wrong getting the Visual Studio Achievements
Right click "Save as…"
I'm committed to building better samples. In this episode I'm going to show you a new sample for WF4 Collection Activities and some of the new things we are doing to make better samples for you.
Ron Jacobs
Twitter: @ronljacobs
Oops, something didn't work.
I would think that if I have to make a choice between the depth of documentation and the pace at which you are releasing new material, I would give my preference to keep up with the pace of releasing new material. If that doesn't impact the release of new material, then this is very very valuable.
Very Helpfull! Keep up the good work.
Ron, these subjects and videos are definitely worth it. Thanks for your participation, we really enjoy your methodology of video presentation.
Comments have been closed since this content was published more than 30 days ago, but if you'd like to continue the conversation, please create a new thread in our Forums, or Contact Us and let us know.


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Tying corporate tax rates to CEO/Worker pay ratios
Since the English translation of Thomas Piketty's book, Capital in the Twenty-First Century, became a best-seller, the national conversation about economic inequality has returned to its proper focus: ratios.
In a country as broad and regionally diverse as ours, emphasizing absolute income metrics has less relevance than zeroing in on relative ones, such as the CEO-to-median-worker pay ratio. (This blog has talked about it multiple times in the past year or so.) Absolute income metrics, such as a $100,000 salary, become nearly meaningless when one contrasts cost-of-living indexes in, say, New York and South Bend.
Reading the commentary around Piketty's book last week, and especially conservative analyses from open-minded free-marketers (e.g., Pascal Emmanuel-Gobry), I wondered if anyone had yet proposed tying corporate tax rates to CEO/Worker pay ratio.
That is to say, the tax rate would not be based in any way on an absolute number, such as a corporation's profits, but rather based on how the corporation distributes those profits within its corporation.
A large, profitable company with a somewhat compressed compensation scale would thus have a lower tax rate than a less profitable company with a large CEO/Worker pay ratio.
This would incentivize distributive justice on a smaller scale (of the corporation), in order to reduce the need for redistributive justice on a large scale (of the federal government).
In terms of Catholic social teaching, it would emphasize subsidiarity in alleviating the problems of economic inequality. Such a change would increase the flow of capital between citizens and reduce the role of the federal government.
If we have to do something about the historic levels of inequality in our country, isn't this one of the least worst things we could try?
It turns out that California is considering trying it on the state level. Here's Paul Hodgson at Reuters:
Two state senators want to make sure that companies based in California pay a price for granting super-sized salaries to their CEOs. Businesses that reward their top officials with outlandish bonuses and salaries would be forced to pay a special tax.
The ratio between the pay for a company's CEO and the median pay of all other employees — known as the CEO/worker pay ratio — has been getting a lot of political attention lately. The most contentious component of the Dodd-Frank financial reform bill has been the CEO/worker pay ratio disclosure requirement — not Say on Pay (the right of shareholders to vote on executive pay), or financial oversight agencies, or creating the Consumer Financial Protection Bureau or even initiating the Volcker rule. More letters have been written by more corporations, shareholders, lawyers and consultants to the Securities and Exchange Commission than ever before, both supporting the disclosure and fighting against it. [...]
The legislation proposed by California state senators Mark DeSaulnier and Loni Hancock seeks to put teeth in the disclosure requirement. If the compensation of a company's CEO exceeds 100 times the median wage of the workforce, the company's state corporation tax rate goes up incrementally to a maximum of 13 percent if the ratio is greater than 400 times. If it's lower than 100 times, the corporation's tax rate goes down.
The bill passed California's Senate Governance and Finance Committee last week. But it will need a two-thirds majority in the senate to be signed into law.
Some further details about the bill can be found here.
Is this the kind of effort that could unite different parties? Could Paul Ryan and Nancy Pelosi negotiate such a bill at the federal level?
Indeed, it would make more sense as a federal law, to prevent companies from relocating in order to avoid the new metric. In addition, perhaps requiring two ratios in the law would eliminate possible manipulation of the median figure: the rate could be tied to both the lowest earner and the median earner. Finally, the concept would need a spoonful of sugar (or two!) to help its medicine go down for libertarian-leaning conservatives. One possibility would be to make the lowest ratio completely tax free. That is, if a corporation's ratio is below X-to-1, its corporate tax rate is zero.
If this were to become a federal idea, it could include non-profit corporations in the mix too. Some of the compensation packages at non-profits have raised eyebrows in recent years. But under a federal ratio-driven policy, the government could say that if a non-profit's ratio exceeds a certain number, it is no longer tax-exempt.
Of course, libertarian-leaning conservatives are not going to like a progressive corporate taxation proposal based on ratios. But they don't like progressive taxation at all. The question is, will the Paul Ryans of the world like this more or less than the current state of affairs?
About the Author
Michael Peppard is associate professor of theology at Fordham University, author of The World's Oldest Church and The Son of God in the Roman World, and on Twitter @MichaelPeppard.
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"the national conversation about economic inequality has returned to its proper focus: ratios." Sez who?
I'd rather be paid $100,000 than $50,000 no matter what the CEO/median ratio is. As Robert Solow recently remarked, "you eat your wage, not your share of national income."
And another thing - despite its presumed good intentioms the California scheme would penalize companies disproportionately hiring low income workers.
I'm glad to see that Patrick Molloy has been reading Robert Solow. But the sentence he quotes comes from a review of Piketty's book in which Solow, a Nobel Prize–winning economist, affirms that income and wealth ratios are indeed something that a democratic country has to concern itself with—that is, if it wants to remain democratic. As Solow writes, "If the ownership of wealth in fact becomes even more concentrated during the rest of the twenty-first century, the outlook is pretty bleak unless you have a taste for oligarchy." Here's a link to Solow's review, which appeared in the New Republic.
Pascal Emmanuel-Gobry is quick on the response! Writing on the Forbes blog here:
CEO Salary excesses are one thing ..another is the fact that most CEOs have unlimited expence accounts that take care of their every day spending. We plebs spend for meals out, townhouses entertainment,[sports, theater etc] travel, [air and car], gas, subscriptions, tips, gifts to family and friends..and whatever.CEOs charge it to the corp.
See GM CEO Jack Welsh's divorce filings and then try to figure what he spent his huge salary on., his ex wife listed how all his/hers daily expences were charged to his GM expense account. All his meals at the GM townhose were charged to GM by the 4 star restaurant on the ground floor of the condo complex.. I bet he used the GM account to give the door man the annual Christmas bonus too.
It's an interesting idea. I agree with Emmanuel-Gobry that it is questionable that CEOs would just take a pay cut and like it (and I think it's still less likely that firms would respond by raising their workers' wages). As Emmanuel-Gobry points out, CEOs would find non-wage ways of being compensated, a treasure hunt at which they are already experts.
I saw in a recent interview with Piketty that he believes there is some sort of overall negative correlation between CEO pay and worker pay. Perhaps at the macro-macro levels that Piketty looks at there is some evidence of that, but I'm skeptical that's it's a rule that almost always obtains, or that there is some compelling reason that things must work that way, such that a highly paid CEO will have low-wage workers and vice-versa. I expect we can find many instances of firms that exemplify each of the different possible permutiations/combinations: high-CEO/low-worker; low-CEO/high worker; high-CEO/high worker; low-CEO/low-worker. My view is that CEOs of major companies are in a completely different labor market than the average joes and worker bees, and what prevails in the one labor market has little or no impact on what happens in the others.
There is this, too: a couple of times in the past when we've discussed high executive compensation here at dotCom, we've talked about how outrageous it is that the CEOs at firms like JC Penney and Home Depot made gazillions in compensation while their companies were doing poorly and laying off workers. It seems to me that Michael's proposed CEO/worker ratio tax could be ineffective from that perspective. After all, the entity being incentivized/disincentivized by Michael's proposed tax is not the CEO but the firm. It's not difficult to imagine that there will be some CEOs who frankly don't care whether the firm pays higher taxes (perhaps even resulting in layoffs), as long as it does not effect the CEO's personal compensation.
Emmanuel-Gobry's reply points to a variation on Michael's idea that might have some merit: rather than attempt to tie worker compensation to CEO compensation, base both the CEO's and the workers' compensation, at least in part, on profitability and customer satisfaction. If the firm is growing and customers are happy, the workers whose work made those good things possible can share in the rewards. And if the firm is not doing well, everybody suffers at least a bit. This is not a radical idea. Many firms pay their workers this way already. But perhaps there are fiscal-policy levers that can make this idea more widespread.
Whatever the merit of the particulars of this proposal it has the great merit of recognizing that a fair wage is fair *relative to other wages* paid by the company. It's not just the character of the work that has to be taken into account.
And while the Congress is inventing this new law it should be careful to outlaw "golden parachute" severance payments in cases where an executive has run a company into the ground or been fired.
I do have one theoretical problem with this: some executives are far more valuable than others, and in effect putting a cap on their earnings would not be fair. But it seems to me that problem might be worked out somehow..
That just seems like a recipe for rounds of increasing the complexity of corporate structure and compensation followed by increasing the complexity of the law to close loopholes.
I'd prefer to keep it simple. If you are worried about the disparity between CEOs and the median worker, raise taxes on high earners and redistribute the money. If you are concerned about the increasing share going to capital, raise capital gains taxes and eliminate sources of rents. If you are concerned about dynasties accumulating wealth, raise the estate tax.
Indeed, [taxing excessive CEO-to-median-worker ratio wages] would make more sense as a federal law, to prevent companies from relocating in order to avoid the new metric.
Thinking of relocations as being constrained by such flimsy barriers as oceans and national borders is so last century. Here is John McCarron on what seems to be a growing trend: inversion, aka moving headquarters overseas as a tax avoidance scheme.
It has always been known that there is a vast inequity even in the US. Ditto that it has always been known that this happens because of Middle Class agreement. This happened because the Middle Class felt reasonably compensated. That reasonable compensation may be the reason why the Middle Class will not tolerate this now.
And there is the glaring fact that no one had the courage to jail the big bankers who were the principal culprits for the Great Recession. http://www.nytimes.com/2014/05/04/magazine/only-one-top-banker-jail-fina...
Ryan --
I agree that taxing the over-paid executives would be good idea, certainly better than capping their earnings someow. It seems to me that most competitive business people are motivated not so much by the desire fo be able o buy a lot of stuff but by the competitive urge to beat their opponents, and their earnings become their way of keeping score. and the highest-paid execs are the winners. Let them have their glory -- they might even deserve some of it, and a few might deserve a lot of it. But tax them and see to it that their poorly paid employees get theirs.
Given my druthers, I'd go with Ryan Rowekamp's "keep it simple" and tax them. That's what we used to do, by the way.
But, given our political-economic divisions, the CEO-to-median ratio is something worth looking into. The devil will be in the details, though. For an obvious example, when Bill Gates was a CEO his contributions went well beyond management, since he practically invented the company. Of course the kind of company he invented made a lot of median-salary workers rich, too, when it went public.
For less obvious examples, back when I used to follow corporate governance, there were dozens of examples of a $10 million executive running a company into the ground and being succeeded by a $10 million executive who turned it around and saved it. I'd say the second guy was worth a premium over the standard for a well-performing CEO in a well-performing company.
BTW, The best-compensated yacht-owner and CEO in the USA these days runs a company that is getting the blame for screwing up Oregon's heath insurance computer program to a fare-thee-well.
A big change in the inequity reality came when mutual fund managers and hedge fund managers took over American finance. A famous story occurred in the 90s when a mutual fund manager approached Arthur Ryan head of Chase. The manager told Ryan that he had to do something to raise the stock value of Chase. Ryan promptly laid of thousands of employees as a way to reduce cost, thereby elevating the stock price.
Shareholders should not have the preeminent position they have now. This system favors those who have capital against those who have not. Thus acquisitions occur, the employees are cut, the stock goes up and the company is sold again. Many times it leads to the detriment of the company and employees.
A world in which only shareholders have rights is the problem. A reasonable return on investment is fine. But the returns are beyond reasonable disenfranching the majority of the population.
@ed gleason -- Welsh (sic) was CEO of General Electric, not General Motors.
@bill mazella -- Chase was the dog of NY bank stocks, underachieving in almost all measures of performance.
@michael peppard -- Pikkety's book is full of logical errors and risible economic thinking. Most glaringly, as pointed out in the financial press, he has made a wild and baseless assumption on "the return of capital" from the time of Moses into the distant future. As I said, risible and not to be taken seriously.
I think the idea is compelling. However, I think that it would need to be married to another absolute metric, so that it only kicks in if the average income of the company were under a certain level. So, a company can have a high ratio as long as everyone is paid well. Essentially, the tax penalty would only apply to companies that both pay their CEOs exorbidently and their workers poorly.
So, a company can have a high ratio as long as everyone is paid well.
I've argued in the past that this is consonant with a preferential option for the poor. On the other hand, in another recent thread, an article was referenced in the comments that described some of the social and moral dangers of inequality, even considered apart from the problem of poverty. For example, inequality puts the social fabric at risk as the ultra-wealthy tend to wrap themselves in enclaves. Inequality is not nothing.
Essentially, the tax penalty would only apply to companies that both pay their CEOs exorbidently and their workers poorly.
Boards of directors are supposed to (at least, morally and ethically they are supposed to) provide appropriate governance, such that the firm's performance, the executives' compensation and the workers' compensation are all aligned. If boards were functional, the ratio might happen as it is supposed to. I don't believe for a moment that legislation could be written to take into account all the possible factors that lead to "fair" or "unfair" executive compensation. I believe we need to do a deeper dive on the governance of corporations in order to find workable remedies. New laws or regulations might well be part of the solution, but they might work by placing some constraints or limits on what boards can pay their executives, perhaps by making it contingent on profitability and employment. For example, there may be times when workers must be laid off or worker wages frozen, but executives should also take a compensation hit when that happens.
"@bill mazella -- Chase was the dog of NY bank stocks, underachieving in almost all measures of performance."
Right, John Walton. Now Chase is doing very well since it has raped the country out of billions while paying nominal fines. Making hundreds of billions while being fined only a few billion and avoiding jail. Any criminal will take that tradeoff any day.


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Tell us: What do you think of 80's Haircuts?
We already knew about ankle boots and skinny jeans, but now it looks like the 80's are coming back for hairstyles, too. Or do VMA nominee Pink (left) and singer Kelis just have the same hairdresser? They are definitely both channeling a tougher, punkier look these days that suits their risk-taking styles. Just as long as no one starts looking like Flock of Seagulls. . . Tell us: Is this a look that you think is coming back into style? Would you ever wear it?
Photo: Debbie VanStory/iPhoto; Jerome Ware/ZUMA


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Hi,All: I am seeing a result in which the following sequence, in the context of the genus-g surface Sg, is described as being exact:
1-->Tg-->$M^{(2)}g$-->$Sp^{(2)}(2g,\mathbb Z)$-->1
Where : i)Tg is the Torelli group ( subgroup of Mg--mapping-class group on Sg) which induces the identity map in homology $H_1(Sg,\mathbb Z)$;
ii) $M^{(2)}g$ is the subgroup of Mg that induces the identity in $H_1(Sg,\mathbb Z_2)$
iii)$Sp^{(2)}(2g,\mathbb Z)$ is the subgroup of $Sp(2g,\mathbb Z)$ that acts trivially on
$H_1(Sg,\mathbb Z_2)$, i.e., if f(c)=c', then c~c' (homologous). Equivalently,
it is also the kernel of the mod2-reduction map (map that takes a $\mathbb Z$-chain into
a $\mathbb Z_2$-chain coefficient-by-coefficient.
$Sp(2g,\mathbb Z)$ is the subgroup of Aut$H_1(Sg,\mathbb Z)$ that preserves the intersection
form in $H_1(Sg,\mathbb Z)$
And the only non-trivial map $\Phi: M^{(2)}g$-->$Sp^{(2)}(2g,\mathbb Z)$ is the induced
map on $H_1(Sg,\mathbb Z)$ (other maps are inclusions/projections) by $M^{(2)}g$.
Now, I get the first part: by the naturality of the mod2-reduction from $H_1(Sg,\mathbb Z)$
to $H_1(Sg,\mathbb Z_2)$ , maps that induce the identity in $H_1(Sg,\mathbb Z)$ also induce
the identity in $H_1(Sg,\mathbb Z_2)$, so that Tg is contained in $M^{(2)}g$, but I cannot
see why the kernel of the induced map is precisely Tg.
Any Ideas?


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There's a line in "Gunsmoke" that goes, "Well look there, Marshal Dillon, there comes a covered wagon." Like many others, Larry Osborn was drawn to Dodge City because of the popular TV and radio series. But unlike many others, Osborn decided to make the journey the old fashioned way. Osborn and friend Josh Johnson rode their 1930's covered wagon, driven by two Percheron draft horses, from Asbury, Mo. to the Boot Hill museum, arriving Friday afternoon. They started on Oct. 5 and rode 370 miles, mostly on Hwy 160, averaging between 12 and 26 miles per day. "It was kind of a bucket list thing," Osborn said. "I'm 66 years old and there's a lot of people I met that said, 'I wish I'd have tried that.'" Osborn's wagon was built in Springfiled, Mo. The two Percherons, six-year-old Tessa and 12-year-old Maggie, both belong to him. He has made one similar trip, traveling from Liberal, Mo. to Cato, Kan. with five other carriages. But this is the first time he's made the trip with just one companion, and the first time he's gone this far. "I'm proud of them," Johnson's mother Sherri said. "This is a big accomplishment for them to travel this far." "You definitely see things that none of these vehicles will ever see," added Andrea Ritcheson, who helped bring supplies during the trip. For the first leg of the journey Ritcheson would drive back and forth to the wagon, bringing food and water. She then joined them for the last portion of the trip. Although the wagon held up for the duration of the trip, the journey wasn't without it's share of difficulties. With the exception of nights when strangers would take them in, Osborn and Johnson slept on the side of the road. Every four days they would stop to grease up the wagon wheels. Tessa wore out a pair of shoes 235 miles into the trip, forcing them to stop to put on a new pair in Hartford, Kan. According to Johnson, the most difficult part of the trip was finding water for the horses, since their GPS could only provide them with limited information. The passing of nearby cars also proved dangerous. When asked what was the best part of the trip, Johnson said, "I'm speechless." A number of people approached Osborn and Johnson on the trip, whether to offer a helping hand or just take a picture. "I've had so many people help and just open their doors," Osborn said. "It's an incredible experience. You forget the greatness of people until you get out there like this."
Location, ST | website.com


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There was a question at SO living for a long time (around 2 years) avialable, with a great amount of views. I can see it why it was closed as "argumentative" a few months ago, but I don't see the point in deleting it.
The FAQ said that a post should be "extremely off topic" (it wasn't, it was programming realted),"of very low quality" (it was argumentative but not low quality) and "not useful as signpoints" (it was viewed by a lot of people, and was one of the few posts in the internet about JD-GUI) to be deleted.
So why?


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18 Mar 2011 2:22 PM #1
Deselect ListItem on Tap?
Sorry, it's me again. It's been a long day today and I'm tired so perhaps I missed it, but I can't get the items in a List to deselect when showing an ActionSheet.
Essentially, I want the list to display an ActionSheet when the user taps an item. I've got all of this working without problem, but for I can't figure out to remove the selected class once the ActionSheet has been displayed. Here's a screenshot of the situation at the moment:
As you can see, the item is still selected underneath the overlay. Any idea how I can prevent it from remaining selected?
19 Mar 2011 3:32 AM #2
You could call the deselect method of the Ext.List class when you show the action sheet passing in the output of the getSelectedRecords method?Want to build better Sencha apps? Check out my free email course Best Practices for Improving your Sencha Apps
Learn Ext JS 6 with my new ebook - Ext JS 6: Getting Started. Get a Sample Chapter now!
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19 Mar 2011 5:11 AM #3
Thanks Stoot, this is the solution I have at the moment, but just wondered if there was a parameter built into the List constructor?
20 Mar 2011 7:54 AM #4
Back again, and still not able to solve the problem here - sorry to be such a pain.
Here's the function I have bound to the itemTap event:
itemTap: function(list, index) { // Deselect the selected record: var currentRecord = list.getStore().getAt(index); currentRecord.forename = currentRecord.get('forename'); currentRecord.surname = currentRecord.get('surname'); currentRecord.phoneNumber = currentRecord.get('phoneNumber'); currentRecord.shortFullName = currentRecord.forename + ' ' + currentRecord.surname[0]; list.getStore().deselect(index, true); callButton.setText('Call ' + currentRecord.shortFullName + ' (' + currentRecord.phoneNumber + ')'); unfriendButton.setText('Remove ' + currentRecord.shortFullName + ' as friend'); friendActionSheet.show(); }Code:
Object [object Object] has no method 'deselect'
20 Mar 2011 7:58 AM #5
I think the deselect method is a method of the List rather than the store.Want to build better Sencha apps? Check out my free email course Best Practices for Improving your Sencha Apps
Learn Ext JS 6 with my new ebook - Ext JS 6: Getting Started. Get a Sample Chapter now!
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20 Mar 2011 8:01 AM #6
Thanks for the quick reply, that seems to have prevented the error from occurring, but no deselect occurs. Am I using the method correctly?
list.deselect(list.getStore().getAt(index), true);
20 Mar 2011 11:06 AM #7
It seems that calling list.refresh() removes the highlighting, but also prevents the item from appearing in the 'x-view-selected' completely, which I don't think is good for HCI (there's no feedback to the user as to which list item was tapped.
I noticed that if I remove the showing of the ActionSheet, the list item remains selected unless I tap another item, in which case the latter is given the blue 'selected' class. Surely there must be away to deselect the current list item in Sencha, since the built-in methods of the ListView seem to achieve it? Any help?
20 Mar 2011 5:28 PM #8
This is how i do it on my lists:
listeners: { itemtap: function(dv, ix, item, e) { // Delay the selection clear // so they get a nice blue flash for HCI's sake setTimeout(function(){dv.deselect(ix);},500); } }
21 Mar 2011 2:02 AM #9
Hi Chris,
That was fantastic and did the job precisely. Thanks for your help!
Best regards,
8 Oct 2012 9:50 PM #10
In Sencha Touch 2, we can add a config while creating a list as disableSelection: true
Ext.define('App.view.NewsList',{ extend: 'Ext.List', xtype: NEWS_LIST, config: { store: NEWS_FEED, //deselectOnContainerClick: true,// not working in Sencha Touch 2 disableSelection: true, // since Sencha Touch 2 itemTpl: '{heading}' } });
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10 Tips for Filling Out The FAFSA
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text:
The paper by Walsh et al. is an important addition to the...
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The paper by Walsh et al. is an important addition to the expanding literature on copy number variations in the human genome and their potential role in causing neuropsychiatric disorders. It is clear that copy number variations are important aspects of human genetic variation and that deletions and duplications in diverse genes throughout the genome are likely to affect the function of these genes and possibly the development and function of the human brain. So-called private variations, such as those described in this paper, i.e., changes in the genome found in only a single individual, as all of these variations are, are difficult to establish as pathogenic factors, because it is hard to know how much they contribute to the complex problem of human behavioral variation in a single individual. If the change is private, i.e., only in one case and not enriched in cases as a group, as are common genetic polymorphisms such as SNPs, how much they account for case status is very difficult to prove.
An assumption implicit in this paper is that these private variations may be major factors in the case status of the individuals who have them. The data of this paper suggest, however, this is actually not the case, at least for the childhood onset cases. Here's why: mentioned in the paper is a statement that only two of the CNVs in the childhood cases are de novo, i.e., spontaneous and not inherited (and one of these is on the Y chromosome, making its functional implications obscure). If most of the CNVs are inherited, they can't be causing illness per se as major effect players because they are coming from well parents.
Also, if you add up all CNVs in transmitted and non-transmitted chromosomes of the parents, it's something like 31 gene-based CNVs in 154 parents (i.e., 20 percent of the parents have a gene-based deletion or duplication in the very illness-related pathways that are highlighted in the cases), which is at least as high a frequency as in the adult-onset schizophrenia sample in this study…and three times the frequency as found in the adult controls. This is not to say that such variants might not represent susceptibility genetic factors, or show variable penetrance between individuals, like other polymorphisms, and contribute to the complex genetic risk architecture, like other genetic variations that have been more consistently associated with schizophrenia. However, the CNV literature has tended to seek a more major effect connotation to the findings.
As new technologies are applied to understanding the...
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As new technologies are applied to understanding the etiology and pathophysiology of schizophrenia, considering the clinical features of the cases studied and the implications of the findings is of value. The conclusion of the Walsh et al. paper, "these results suggest that schizophrenia can be caused by rare mutations…." is worth considering carefully.
What evidence is needed to link an observation in the laboratory or clinic to cause? Recent recommendations for the content of papers in epidemiology (von Elm et al., 2008) remind us of the suggestions of A.V. Hill (Hill, 1965). To discern the implications of a finding, or association, for causality, Hill suggests assessment of the following:
1. Strength of the association: this is not the observed p-value, but a measure of the magnitude of the association. In the Walsh et al. study, the primary outcome measure, structural variants duplicating or deleting genes was observed in 15 percent of cases, and 5 percent of controls. But what is the association with? The diagnostic entity of schizophrenia, or some risk factor for the illness? Of interest, and noted in the Supporting Online Material, these variants were present in 7/15 (47 percent) of the cases with presumed IQ <80, but only 15/135 (11 percent) of the cases with IQ >80. Are the structural variants more strongly associated with mental retardation (within schizophrenia 47 percent vs. 11 percent) than with diagnosis (11 percent vs. 5 percent of controls, assuming normal IQ)? This is of particular interest in the context of the speculation in the paper concerning the importance of genes putatively involved with brain development in the etiology of schizophrenia.
2. Consistency of results in the literature across studies and research groups: there are now several papers examining copy number variation in schizophrenia, including a report from our group (Wilson et al., 2006). The authors of the present paper state that each variant observed was unique, and so consistency of the specific findings could be argued to be irrelevant, if the model is of novel mutations (more on models below). Undoubtedly, future meta-analyses and accumulating databases help determine if there is anything consistent in the findings, other than a higher frequency of any abnormalities in cases rather than controls.
3. Specificity of the findings to the illness in question: this was not addressed experimentally in the paper. However, the findings of more abnormalities in the putative low IQ cases, and the similarity of the findings to reports in autism and mental retardation, suggest that this criterion for supporting causality is unlikely to be met.
4. Temporality: the abnormalities should precede the illness. If DNA from terminally differentiated neurons harbors the same variants as DNA from constantly renewed populations of lymphocytes, then clearly this condition is met. While it seems highly likely that this is the case, it is worthwhile considering the possibility that DNA structure may vary between tissue types, or between cell populations. Even within human brain there is some evidence for chromosomal heterogeneity (Rehen et al., 2005).
5. Biological gradient: presence of a "dose-response" curve strengthens the likelihood of a causal relationship. This condition is not met within cases: only 1/115 appeared to have more than one variant. However, in the presumably more severe childhood onset form of schizophrenia, four individuals carried multiple variants, and the observation of a higher prevalence of variants overall. Still, the question of what the observations of CNV are associated with is relevant, since one of the inclusion/exclusion criteria for COS allowed IQ 65-80, and it is uncertain how many of these cases had some degree of intellectual deficit.
6. Plausibility: biological likelihood—quite difficult to satisfy as a criterion, in the context of the limits of knowledge concerning the mechanisms of illness of schizophrenia.
7. Coherence of the observation with known facts about the illness: the genetic basis of schizophrenia is quite well studied, and there is no dearth of theories concerning genetic architecture. However, a coherent model remains lacking. As examples, the suggestion is made that the observations concerning inherited CNVs in the COS cases are linked with a severe family history in this type of illness. This appears inconsistent with a high penetrance model for CNVs as suggested in the opening of the paper (presuming the parents in COS families are unaffected, as would seem likely). Elsewhere, CNVs are proposed by the authors to be related to de novo events, and an interaction with an environmental modifier, folate (and exposure to famine), is posited (McClellan et al., 2006). A model of the effects of CNVs, which generates falsifiable hypotheses is needed.
8. Experiment: the ability to intervene clinically to modify the effects of CNVs disrupting genes seems many years away.
9. Analogy: the novelty of the CNV findings is both intriguing, but limiting in understanding the likelihood of causal relationships.
The intersection of clinical realities and novel laboratory technologies will fuel the need for better translational research in schizophrenia for many, many more years.
von Elm E, Altman DG, Egger M, Pocock SJ, Gøtzsche PC, Vandenbroucke JP. Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) statement: guidelines for reporting observational studies. J Clin Epidemiol. 2008 Apr 1;61(4):344-349. Abstract
HILL AB. THE ENVIRONMENT AND DISEASE: ASSOCIATION OR CAUSATION? Proc R Soc Med. 1965 May 1;58():295-300. Abstract
Wilson GM, Flibotte S, Chopra V, Melnyk BL, Honer WG, Holt RA. DNA copy-number analysis in bipolar disorder and schizophrenia reveals aberrations in genes involved in glutamate signaling. Hum Mol Genet. 2006 Mar 1;15(5):743-9. Abstract
Rehen SK, Yung YC, McCreight MP, Kaushal D, Yang AH, Almeida BSV, Kingsbury MA, Cabral KMS, McConnell MJ, Anliker B, Fontanoz M, Chun J: Constitutional aneuploidy in the normal human brain. J Neurosci 2005; 25:2176-2180. Abstract
McClellan JM, ESusser E, King M-C: Maternal famine, de novo mutations, and schizophrenia. JAMA 2006; 296:582-584. Abstract
The new study by Walsh et al. (2008), as well as recent...
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The new study by Walsh et al. (2008), as well as recent data from other groups working in schizophrenia, autism, and mental retardation, make a strong case for including copy number variants as an important source of risk for neurodevelopmental phenotypes. These findings raise several intriguing new questions for future research, including: the degree of causality/penetrance that can be attributed to individual CNVs; diagnostic specificity; and recency of their origins. While these questions are difficult to address in the context of private mutations, one potential source of additional information is the examination of common, recurrent CNVs, which have not yet been systematically studied as potential risk factors for schizophrenia.
Still, the association of rare CNVs with schizophrenia provides additional evidence that genetic transmission patterns may be a complex hybrid of common, low-penetrant alleles and rare, highly penetrant variants. In diseases ranging from Parkinson's to colon cancer, the literature demonstrates that rare penetrant loci are frequently embedded within an otherwise complex disease. Perhaps the most well-known example involves mutations in amyloid precursor protein and the presenilins in Alzheimer's disease (AD). Although extremely rare, accounting for <1 percent of all cases of AD, identification of these autosomal dominant subtypes greatly enhanced understanding of pathophysiology. Similarly, a study of consanguineous families in Iran has very recently identified a rare autosomal recessive form of mental retardation (MR) caused by glutamate receptor (GRIK2) mutations, thereby opening new avenues of research (Motazacker et al., 2007). In schizophrenia, we have recently employed a novel, case-control approach to homozygosity mapping (Lencz et al., 2007), resulting in several candidate loci that may harbor highly penetrant recessive variants. Taken together, these results suggest that a diversity of methodological approaches will be needed to parse genetic heterogeneity in schizophrenia.
Motazacker MM, Rost BR, Hucho T, Garshasbi M, Kahrizi K, Ullmann R, Abedini SS, Nieh SE, Amini SH, Goswami C, Tzschach A, Jensen LR, Schmitz D, Ropers HH, Najmabadi H, Kuss AW. (2007) A defect in the ionotropic glutamate receptor 6 gene (GRIK2) is associated with autosomal recessive mental retardation. Am J Hum Genet. 81(4):792-8. Abstract
Lencz T, Lambert C, DeRosse P, Burdick KE, Morgan TV, Kane JM, Kucherlapati R,Malhotra AK (2007). Runs of homozygosity reveal highly penetrant recessive loci in schizophrenia. Proc Natl Acad Sci U S A. 104(50):19942-7. Abstract
In my mind, the study of CNVs in autism (and likely soon...
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In my mind, the study of CNVs in autism (and likely soon in schizophrenia/bipolar disorder, which are a little behind) is likely to put biological meat on the bones of illness etiology and finally lay to rest the annoyingly persistent taunts that genetics hasn't delivered on its promises for psychiatric illness.
I don't think it's necessary at the moment to wring our hands at any inconsistencies between the Walsh et al. and previous studies of CNV in schizophrenia (e.g., Kirov et al., 2008). There are a number of factors which I think are going to influence the frequency, type, and identity of CNVs found in any given study.
1. CNVs are going to be found at the rare/penetrant/familial end of the disease allele spectrum—in direct contrast to the common risk variants which are the targets of recent GWAS studies. In the short term, we are likely to see a large number of different CNVs identified. The nature of this spectrum, however, is that there will be more common pathological CNVs which should be replicated sooner—NRXN1, APBA2 (Kirov et al., 2008), CNTNAP2 (Friedman et al., 2008)—and may be among some of these "low hanging fruit." For the rarer CNVs, proving a pathological role is going to be a real headache. Large studies or meta-analyses are never going to yield significant p-values for rare CNVs which, nevertheless, may be the chief causes of illness for those few individuals who carry them. Showing clear segregation with illness in families is likely to be the only means to judge their role. However, we must not expect a pure cause-and-effect role for all CNVs: even in the Scottish t(1;11) family disrupting the DISC1 gene, there are several instances of healthy carriers.
2. Sample selection is also likely to be critical. In the Kirov paper, samples were chosen to represent sporadic and family history-positive cases equally. In the Walsh paper, samples were taken either from hospital patients (the majority) or a cohort of childhood onset schizophrenia. Detailed evidence for family history on a case-by-case basis was not given but appeared far stronger in the childhood onset cases. CNVs appeared to be more prevalent, and as expected, more familial, in the latter cohort. A greater frequency was also observed in the Kirov study familial subset.
3. Inclusion criteria are likely to be important—particularly in the more sporadic cases without family history. This is because CNVs found in this group may be commoner and less penetrant—they will be more frequent in cases than in controls but not exclusively found in cases. Any strategy, such as that used in the Kirov paper, which discounts a CNV based on its presence—even singly—in the control group is likely to bias against this class.
4. Technical issues. Certainly, the coverage/sensitivity of the method of choice for the "event discovery" stage is going to influence the minimum size of CNV detectable. However, a more detailed coverage often comes with a greater false-positive rate. Technique choice may also have more general issues. In both of the papers, the primary detection method is based on hybridization of case and pooled control genomes prior to detection on a chip. Thus, a more continuously distributed output may result—and the extra round of hybridization might bias against certain sequences. More direct primary approaches such as Illumina arrays or a second-hand analysis of SNP genotyping arrays may provide a more discrete copy number output, but these, too, can suffer from interpretational issues.
The other major implication of these and other CNV studies is the observation that certain genes "ignore" traditional disease boundaries. For example, NRXN1 CNVs have now been identified in autism and schizophrenia, and CNTNAP2 translocations/CNVs have been described in autism, Gilles de la Tourette syndrome, and schizophrenia/epilepsy. This mirrors the observation of common haplotypes altering risk across the schizophrenia-bipolar divide in numerous association studies. It might be the case that these more promiscuous genes are likely to be involved in more fundamental CNS processes or developmental stages—with the precise phenotypic outcome being defined by other variants or environment. The presence of mental retardation comorbid with psychiatric diagnoses in a number of CNV studies suggests that this might be the case. I look forward to the Venn diagrams of the future which show us the shared neuropsychiatric and disease-specific genes/gene alleles. It will also be interesting to see if the large deletions/duplications involving numerous genes give rise to more severe, familial, and diagnostically more defined syndromes or, alternatively, a more diffuse phenotype. Certainly, it has not been easy to dissect out individual gene contributions to phenotype in VCFS or the minimal region in Down syndrome.
Friedman JI, Vrijenhoek T, Markx S, Janssen IM, van der Vliet WA, Faas BH, Knoers NV, Cahn W, Kahn RS, Edelmann L, Davis KL, Silverman JM, Brunner HG, van Kessel AG, Wijmenga C, Ophoff RA, Veltman JA. CNTNAP2 gene dosage variation is associated with schizophrenia and epilepsy. Mol Psychiatry. 2008 Mar 1;13(3):261-6. Abstract
We agree with the comments of Weinberger, Lencz and...
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We agree with the comments of Weinberger, Lencz and Malhotra, and Pickard, and the question raised by Honer about the extent to which the association may be more to mental retardation than schizophrenia. These new studies of copy number variation represent important advances, but need to be interpreted carefully.
We are now getting two different kinds of data on schizophrenia, which can be seen as two opposite poles. The first is from association studies with common variants, in which large numbers of people are required to see significance, and the strengths of the associations are quite modest. These kinds of vulnerability factors would presumably contribute a very modest increase in risk, and many taken together would cause the disease. By contrast, the "private" mutations, as identified by the Sebat study, could potentially be completely causative, but because they are present in only single individuals or very small numbers of individuals, it is difficult to be certain of causality. Furthermore, since some of them in the early-onset schizophrenia patients were present in unaffected parents, one might have to assume the contribution of a common variant vulnerability (from the other parent) as well.
If a substantial number of the private structural mutations are causal, then one might expect to have seen multiple small Mendelian families segregating a structural variant. The situation would then be reminiscent of the autosomal dominant spinocerebellar ataxis, in which mutations (currently about 30 identified loci) in multiple different genes result in similar clinical syndromes. The existence of many small Mendelian families would be less likely if either 1) structural variants that cause schizophrenia nearly always abolish fertility, or 2) some of the SVs detected by Walsh et al. are risk factors, but are usually not sufficient to cause disease. The latter seems more likely.
We think these two poles highlight the continued importance of segregation studies, as have been used for the DISC1 translocation. In order to validate these very rare "private" copy number variations, we believe that it would be important to look for sequence variations in the same genes in large numbers of schizophrenia and control subjects, and ideally to do so in family studies.
One very exciting result of the new copy number studies is the implication of whole pathways rather than just single genes. This highlights the importance of a better understanding of pathogenesis. The study of candidate pathways should help facilitate better pathogenic understanding, which should result in better biomarkers and potentially improve classification and treatment. In genetic studies, development of pathway analysis will be fruitful. Convergent evidence can come from studies of pathogenesis in cell and animal models, but this will need to be interpreted with caution, as it is possible to make a plausible story for so many different pathways (Ross et al., 2006). The genetic evidence will remain critical.
Ross CA, Margolis RL, Reading SA, Pletnikov M, Coyle JT. Neurobiology of schizophrenia. Neuron. 2006 Oct 5;52(1):139-53. Abstract
The idea that a proportion of schizophrenia is associated...
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The idea that a proportion of schizophrenia is associated with rare chromosomal abnormalities has been around for some time, but it has been difficult to be sure whether such events are pathogenic given that most are rare. Two instances where a pathogenic role seems likely are first, the balanced ch1:11 translocation that breaks DISC1, where pathogenesis seems likely due to co-segregation with disease in a large family, and second, deletion of chromosome 22q11, which is sufficiently common for rates of psychosis to be compared with that in the general population. This association came to light because of the recognizable physical phenotype associated with deletion of 22q11, and the field has been waiting for the availability of genome-wide detection methods that would allow the identification of other sub-microscopic chromosomal abnormalities that might be involved, but whose presence is not predicted by non-psychiatric syndromal features. This technology is now upon us in the form of various microarray-based methods, and we can expect a slew of studies addressing this hypothesis in the coming months.
Structural chromosomal abnormalities can take a variety of forms, in particular, deletions, duplication, inversions, and translocations. Generally speaking, these can disrupt gene function by, in the case of deletions, insertions and unbalanced translocations, altering the copy number of individual genes. These are sometimes called copy number variations (CNVs). Structural chromosomal abnormalities can also disrupt a gene sequence, and such disruptions include premature truncation, internal deletion, gene fusion, or disruption of regulatory or promoter elements.
It is, however, worth pointing out that structural chromosomal variation in the genome is common—it has been estimated that any two individuals on average differ in copy number by a total of around 6 Mb, and that the frequency of individual duplications or deletions can range from common through rare to unique, much in the same way as other DNA variation. Also similar to other DNA variation, many structural variants, indeed almost certainly most, may have no phenotypic effects (and this includes those that span genes), while others may be disastrous for fetal viability. Walsh and colleagues have focused upon rare structural variants, and by rare they mean events that might be specific to single cases or families. For this reason, they specifically targeted CNVs that had not previously been described in the published literature or in the Database of Genomic Variants. The reasonable assumption was made that this would enrich for CNVs that are highly penetrant for the disorder. Indeed, Walsh et al. favor the hypothesis that genetic susceptibility to schizophrenia is conferred not by relatively common disease alleles but by a large number of individually rare alleles of high penetrance, including structural variants. As we have argued elsewhere (Craddock et al., 2007), it seems entirely plausible that schizophrenia reflects a spectrum of alleles of varying effect sizes including common alleles of small effect and rare alleles of larger effect, but data from genetic epidemiology do not support the hypothesis that the majority of the disorder reflects rare alleles of large effect.
Walsh et al. found that individuals with schizophrenia were >threefold more likely than controls to harbor rare CNVs that impacted on genes, but in contrast, found no significant difference in the proportions of cases and controls carrying rare mutations that did not impact upon genes. They also found a similar excess of rare structural variants that deleted or duplicated one or more genes in an independent series of cases and controls, using a cohort with childhood onset schizophrenia (COS).
The results of the Walsh study are important, and clearly suggest a role for structural variation in the etiology of schizophrenia. There are, however, a number of caveats and issues to consider. First, it would be unwise on the basis of that study to speculate on the likely contribution of rare variants to schizophrenia as a whole. It is likely correct that, due to selection pressures, highly penetrant alleles for disorders (like schizophrenia) that impair reproductive fitness are more likely to be of low frequency than they are to be common, but this does not imply that the converse is true. That is, one cannot assume that the penetrance of low frequency alleles is more likely to be high than low. Thus, and as pointed out by Walsh et al., it is not possible to know which or how many of the unique events observed in their study are individually pathogenic. Whether individual loci contribute to pathogenesis (and their penetrances) is, as we have seen, hard to establish. Estimating penetrance by association will require accurate measurement of frequencies in case and control populations, which for rare alleles, will have to be very large. Alternatively, more biased estimates of penetrance can be estimated from the degree of co-segregation with disease in highly multiplex pedigrees, but these are themselves fairly rare in schizophrenia, and pedigrees segregating any given rare CNV obviously even more so.
As Weinberger notes, the case for high penetrance (at the level of being sufficient to cause the disorder) is also undermined by their data from COS, where the majority of variants were inherited from unaffected parents. This accords well with the observation that 22q11DS, whilst conferring a high risk of schizophrenia, is still only associated with psychosis in ~30 percent of cases. It also accords well with the relative rarity of pedigrees segregating schizophrenia in a clearly Mendelian fashion, though the association of CNVs with severe illness of early onset might be expected to reduce the probability of transmission.
Third, there are questions about the generality of the findings. Cases in the case control series were ascertained in a way that enriched for severity and chronicity. Perhaps more importantly, the CNVs were greatly overrepresented in people with low IQ. Thus, one-third of all the potentially pathogenic CNVs in the case control series were seen in the tenth of the sample with IQ less than 80. The association between structural variants and low IQ is well known, as is the association between low IQ and psychotic symptoms, and it seems plausible to assume that forms of schizophrenia accompanied by mental retardation (MR) are likely to be enriched for this type of pathogenesis. The question that arises is whether the CNVs in such cases act simply by influencing IQ, which in turn has a non-specific effect on increasing risk of schizophrenia, or whether there are specific CNVs for MR plus schizophrenia, and some which may indeed increase risk of schizophrenia independent of IQ. In the case of 22q11 deletion, risk of schizophrenia does not seem to be dependent on risk of MR, but more work is needed to establish that this applies more generally.
Another reason to caution about the generality of the effect is that Walsh et al. found that cases with onset of psychotic symptoms at age 18 or younger were particularly enriched for CNVs, being greater than fourfold more likely than controls to harbor such variants. There did remain an excess of CNVs in cases with adult onset, supporting a more general contribution, although it should be noted that even in this group with severe disorder, this excess was not statistically significant (Fisher's exact test, p = 0.17, 2-tailed, our calculation). The issue of age of onset clearly impacts upon assessing the overall contribution CNVs may make upon psychosis, since onset before 18, while not rare, is also not typical. A particular contribution of CNVs to early onset also appears supported by the second series studied, which had COS. However, this is a particularly unusual form of schizophrenia which is already known to have high rates of chromosomal abnormalities. Future studies of more typical samples will doubtless bear upon these issues.
Even allowing for the fact that many more CNVs may be detected as resolution of the methodology improves, the above considerations suggest it is premature to conclude a substantial proportion of cases of schizophrenia can be attributed to rare, highly penetrant CNVs. Nevertheless, even if it turns out that only a small fraction of the disorder is attributable to CNVs, as seen for other rare contributors to the disorder (e.g., DISC1 translocation), such uncommon events offer enormous opportunities for advancing our knowledge of schizophrenia pathogenesis.
Craddock N, O'Donovan MC, Owen MJ. Phenotypic and genetic complexity of psychosis. Invited commentary on ... Schizophrenia: a common disease caused by multiple rare alleles.Br J Psychiatry. 2007 90:200-3. Abstract
Walsh et al. claim that rare and severe chromosomal...
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Walsh et al. claim that rare and severe chromosomal structural variants (SVs) (i.e., not described in the literature or in the specialized databases as of November 2007) are highly penetrant events each explaining a few, if not singular, cases of schizophrenia.
However, their definition of rareness is questionable. Indeed, it is unclear why SVs that are rare (<1 percent) but previously described should be omitted from their analysis. In addition, contrary to their own definition of rareness, the authors included in the COS sample several SVs that have been previously mentioned in the literature (e.g. "115 kb deletion on chromosome 2p16.3 disrupting NRXN1"). Furthermore, some of these SVs (entire Y chromosome duplication) are certainly not rare (by the authors' definition), nor highly penetrant with regard to psychosis (Price et al., 1967). Finally, as their definition of rareness depends on a specific date, the results of this study will change over time.
As to the assessment of severity, it can equally be concluded from table 2 and using their statistical approach that "patients with schizophrenia are significantly more likely to harbor rare structural variants (6/150) that do not disrupt any gene compared to controls(2/268) (p = 0.03)", thus contradicting their claim. In fact, had they used criteria in the literature (Lee et al., 2007; (Brewer et al., 1999) (i.e., deletion SVs are more likely than duplications to be pathogenic) and appropriate statistical contrasts, deletions are significantly (p = 0.02) less frequent in patients (5/23) than in controls (9/13) who have SVs. In addition, the assumption of high penetrance is questionable given the high level (13 percent) of non-transmitted SVs in parents of COS patients. Is the rate of psychosis proportionately high in the parents? From the data presented, we know that only 2/27 SVs in COS patients are de novo and that "some" SVs are transmitted. Adding this undetermined number of transmitted SVs to the reported non-transmitted SVs will lead to an even larger proportion of parents carrying SVs. Disclosing the inheritance status of SVs in COS patients along with information on diagnoses in parents from this "rigorously characterised cohort," represents a major criterion for assessing the risk associated with these SVs.
Consequently, it appears that the argument of rareness is rather idiosyncratic and contains inconsistencies, and the one of severity is very open to interpretation. Most importantly, it should be emphasized that amalgamated gene effects at the population level do not allow one to conclude that any single SV actually contributes to schizophrenia in an individual. Thus it is unclear how this study of grouped events differs from the thousands of controversial and underpowered association studies of single genes.
Price WH, Whatmore PB. Behaviour Disorders and Pattern of Crime among XYY males Identified at a Maximum Security Hospital. Brit Med J 1967;1:533-6.
Lee C, Iafrate AJ, Brothman AR. Copy number variations and clinical cytogenetic diagnosis of constitutional disorders. Nat Genet 2007 July;39(7 Suppl):S48-S54.
Brewer C, Holloway S, Zawalnyski P, Schinzel A, FitzPatrick D. A chromosomal duplication map of malformations: regions of suspected haplo- and triplolethality--and tolerance of segmental aneuploidy--in humans. Am J Hum Genet 1999 June;64(6):1702-8.
RELATED NEWSCopy Number Variations in Schizophrenia: Rare But Powerful?


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Finding Expert Care
Last Modified: January 7, 2013
Are their specialists that can see patients or take a look at previous scans? My mom was told there isn't any because it was so rare so they continue with CT scans and urine analysis every 3 months.
Katie Fanslau, RN, MSN, Nurse in Nuclear Medicine at Penn Medicine responds.
At Penn, our radiologists review outside films and images all the time. There are also other imaging studies done to evaluate neuroendocrine cancers such as MIBG scans, Octreotide scans, MRIs, etc.
As for physicians who are experts in Neuroendocrine tumors, there are many in the U.S. and abroad. They may not be in your immediate area, but when you have a rare disease, it is worth traveling to get expert input into your care. The Carcinoid Foundation maintains a list of experts around the world.
This question and answer was part of the OncoLink Brown Bag Chat Series. View the entire transcript from the Focus on Neuroendocrine Tumors Webchat.


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Soccer referee clinic scheduled
STEUBENVILLE - The Jefferson County Soccer Officials Association will offer a 25-hour course at Eastern Gateway Community College to license adults as high school soccer officials. Applicants must be 18 years of age and be a high school graduate or have a GED. Current Grade 8 USSF soccer officials need only take 10 of the 25 hours.
The course begins Saturday, will be held on three Saturdays and includes an exam and five hours field training. The course is regulated by the Ohio High School Athletic Association. The season begins Aug. 17 and the licensee will be able to referee games immediately.
To register or for information call instructor Bill Ferroni at (740) 317-1054 or recruiter Tom Bright at (740) 457-9537. The course and license cost is $80.
Big Red parents meeting to be held
STEUBENVILLE - A Steubenville Big Red football/cheerleader parents meeting will be held at 7:30 p.m. today at the side door of Harding School. Freshman parents are invited to come and learn about the coming games and projects.
Youth football clinic to be held
WHEELING - The Ohio Valley Athletic Conference will host its ninth-annual free youth football clinic in conjunction with the Rudy Mumley OVAC All-Star Charity Football Classic. The clinic will take place July 28 at the Wheeling Island Stadium.
Registration will take place from noon to 12:45 p.m. The clinic will be held from 1 p.m. to 2:30 p.m. and will be directed by OVAC football coaches, including members of coach Chris Daugherty's Wheeling Park High School football staff. The instructors will teach the basic fundamentals of football with a focus on building self-esteem.
The clinic is free and open to boys and girls ages 6-13.
Parents or legal guardians are required to have insurance and be present the day of the clinic to sign a waiver form.
For information, visit www.OVAC.org call (304) 639-1238 or send an e-mail to firstname.lastname@example.com.


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Whole-Grain, High-Fiber Breakfast Recipes for Weight Loss (Slide 1)
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Recipe: Buttermilk Oatcakes with Raspberry Compote
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Buttermilk Oatcakes with Ra…
These high-fiber oatcakes are made with 100% whole grains and no butter. A quick raspberry compote i…View slide
Healthy Pancakes
EatingWell reader Kathy Moseler of Barrington Hills, Illinois, contributed this convenient recipe to…View slide
Savory Breakfast Muffins
If you're tired of sweet breakfast muffins or just looking for a savory breakfast, try these--you'll…View slide
Oatmeal-Rhubarb Porridge
Perk up your morning oatmeal with the addition of tangy rhubarb. Using milk for this oatmeal gives i…View slide
Lemon-Cranberry Muffins
These lemony cranberry-studded muffins crunch lightly with cornmeal and are topped with a kiss of su…View slide
Pear-Hazelnut Quick Bread
Toasted hazelnuts and ripe pears add a sophisticated note to a homey quick bread.…View slide
Crunchy Granola Wedges
This recipe was inspired by chef Lars Kronmark's granola wedges from the Culinary Institute of Ame…View slide
Banana-Blueberry Muffins
The slight acidity of buttermilk tenderizes and moistens baked goods while allowing you to cut way b…View slide
Maple Nut & Pear Scones
Delicate pears, pecans and maple flavor make these scones really special. Our makeover of this tende…View slide
Wheat Berry Pudding
Here, wheat berries are cooked with maple-sweetened, spiced milk to make a homey pudding. Try it for…View slide
Almond-Honey Power Bar
Great for breakfast on the go! Golden roasted nuts, seeds and oats are enveloped by flavorful almond…View slide
Banana-Bran Muffins
By the end of the week, any bananas left in the fruit bowl are past their prime—just right for the…View slide
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The History of Typography
Category: Animation / Motion Graphics, Design / Typography, Designers/Studios,
Posted by: TheaAn incredibly detailed stop-motion animation from designer Ben Barrett-Forrest covering the history of typography. 291 paper letters. 2,454 photographs. 140 hours of work. Phwoar! ...
Posted: May 13th 2013
No. of comments: 1
Posted: May 13th 2013
No. of comments: 1


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There was a recent XSS exploit on Facebook that posted a vulgar message and got users to click on a link to spread the payload. What vulnerability was exploited, and what can other sites do to avoid a similar attack?
Here is a good overall reference http://cwe.mitre.org/data/definitions/79.html
per www.infosecisland.com:
So the issue is related to neutralizing data input into web pages.
Of course, we now live in the internet era, so, there's a video for that!
It is almost 10 minutes long, complete with all the details you would like, reviewing the exploit code and its functionality.


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This is Jakarta's largest and most popular recreation park, more popularly known as "Ancol Dreamland". The Ancol Dreamland has an extensive range of attractions that include a Seaworld, a water park with artificial waves, an lagoon for fishing and boating, exciting rides such as the Torpedo and the Hysteria, an art center, a convention hall and hotels.
In the Ancol complex are also a marina, the Dunia Fantasi (Fantasy World), a drive-in theatre. The 'Pasar Seni' or art market has a varied collection of Indonesian handicraft, paintings and souvenirs on sale. An open-air theatre features live performances by local artists.
Watch the video about Jakarta:
Within Ancol Jakarta BayCity area, you will find several hotels such as Raddin Hotel, Wisata Hotel, Mercure Hotel and Putri Duyung Cottages with various prices and facilities.
• Equip yourself with sun protection and bathing suit
• Donot forget to bring an extra clothes
• Many souvenirs are sold with fixed prices. But, there are ample possibilities to try out your bargaining skills at Pasar Seni or Art Market
Ancol Bay can be reached by bus, taxis, or rented cars. If you're coming from Bogor, there's a train available, but only on Sundays.
You can move around inside Ancol Bay area by using a car, take a walk or ride a shuttle car which are provided in the complex.


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Donna's Pregnant
Last Modified: November 1, 2001
Copyright © 1999, Douglas R. Murray
I was suddenly sad this morning when Donna appeared in the doorway. Her bright red top covered an 8-month pregnancy. I hadn't seen her in two months, but how could I have missed this condition the last time? She appeared radiant, as they say, and was the perfect vision of a healthy happy mother-to-be. So why was I sad?
Donna has been part of my oncology team for the last year. She weighed me in each visit, took my blood pressure and carried a warm smile in my transition from the waiting room to the exam room. She was there when I was told this lymphoma was stage 4 and that it was, most likely, here to stay.
The strongest memory of Donna was her role during a bone marrow biopsy. A good-sized needle is inserted into the large pelvic bone and marrow is extracted while you lie face down. It is an uncomfortable procedure, and for me it was especially frightening because I remembered my Mom having one 10 years earlier.
The doctor began injecting a local anesthetic and at the same time Donna gently placed her hands on my back. I no longer felt alone, or afraid. As the procedure progressed she gave me a back rub and felt like my emotional ally. When it was over I looked at her with tears in my eyes and asked, "Do you know how important that was for me?" She tried briefly to explain that it was something they usually do, but I persisted, "That was very powerful, it really helped me, thank you."
I don't know if Donna ever understood what I meant. My medical treatment had been very mechanical and sterile, while at the same time frightening. But for a few minutes, the caring touch of another person became the most powerful drug available.
So why was I sad when I saw Donna pregnant? I think it may have been the juxtaposition in our lives and current situation. Donna was creating life in an oncology unit where all of us were fighting to keep ours. She and I were both looking forward to raising a child to adulthood, but chemotherapy and, hopefully, a long remission were in front of me first. I wish I could rejoin her world where the prospect of death is remote and bringing forth life is the essence.
Editor's Note: See also Douglas R. Murray'sSurvivor Story "Lessons from Lymphoma."


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Please vote for the remix you prefer the most.
In two weeks we (well my 4 year old) will randomly select 3 of the voters to receive any plugin of ours for free.
You can discuss the contest here or listen to the 198! other entries here.
And for all competitors : DE GUSTIBUS ET COLORIBUS NON DISPUTANDUM (EST)!!!!!


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Gold and Silver
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Shelter From the Storms


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Check out her latest release!
Valkyrie's Vow, Book 1
Ellora's Cave Publishing
For a thousand years, Mist has shepherded battle-slain warriors to their choice of Valhalla or Asgard. It's the task she was charged with upon her own death, the mission she chose when becoming Valkyrie. Never before has she fallen for one of those warriors. But then, never has she felt emotions like those evoked by Kurt Stone.
As an undercover cop, Kurt expected a shortened life. He didn't expect an afterlife spent jumping from realm to realm, screwing a tattooed hottie who makes his blood boil. He should be choosing his next destination, but he'd rather spend eternity indulging in Mist's delectable body.
The vicious betrayal that led to her death has made Mist reluctant to trust, let alone love. If Kurt can help her face ancient demons, they both might find their idea of Heaven…together.
Read and Excerpt HERE.
Ali: Is there an author that makes you go all "fangirl?"
Mari: Yeah. Stephen King would probably do that. But within the romance genre, I would say it's a little different. I've met so many of the greats at conferences and have spent time chatting with them that I don't get quite the flutters I used to. I did go fan girl on Mary Janice Davidson in a big way at the Romantic Times convention a few years ago. It was really embarrassing since I was dressed as a vampire killer at the time in leather pants and a skull corset. I'm sure I scared the crap out of her.
Ali: If you could co-write with another author who would it be and why?
Mari: This dream I've gotten to live out. I've co-written a western steampunk series with the amazing Samantha Kane. Our rock star agent, Eric Ruben, is currently trying to find the series a place to live. I look forward to the first book coming out and writing more with Sam. She's been my crit partner and best friend for years, so working with her was an absolute blast.
Ali: What are you looking forward to most about AADNola?
Mari: Ummm. It's New Orleans! The food...the parties....The Quarter. I love the city. I've spent a good deal of time there over the years. And the AAD con is one of the best. I really get to meet a lot of readers. Plenty of quality time with them and my favorite authors. Stella puts together some interesting panels and parties too.
Ali: The world is under attack and you are forced to run for your life. You only have room for one book in your survival kit, what book do you take?
Mari: There are 7 bookcases in my house right now and you want me to pick just one !?! *faints* No way. I get eaten taking too long to decide. Zombies win.
Ali: Who are your favorite literary characters? (Yours or someone else's)
Mari: Wow. You're asking hard ones here. So many…However, I was mesmerized by the Grimm stories as a child. Not the cleaned up Disney versions either. Nope. Dad gave me the classic tales of hard lessons learned and personal accountability. Ashella, that eventually became Cinderella, was my fav. In the original version, once the prince figures out the stepsister's and Stepmom's deceit, they're cursed to blindness for life. I know… not very romantic, but I pull many different elements into every story. I do write paranormal romance after all. Deserved comeuppance (*shivers*) gets me every time!
Ali: Are there any of your secondary characters you would like to give more life to?
Mari: All of them. Secondary characters are one of my strengths. But most are not hero and heroine worthy. I have a weird gremlin in Birthright who I HAD to give a little romance to in the course of the book because I loved him so much.
Ali: If you friends were asked to describe you in one word what would it be?
Mari: My mom describes me as loud. She's not talking volume either.
*Favorite color: Green
*Favorite food: Steak
*Boots or heels: Both, why choose?
*eReader or Print: And again....Both!
*Beer, Liquor or Wine: Wine, Red
*Favorite place to get it on besides the bedroom: Outside.
*Favorite TV Show: Big Bang Theory
*Favorite Book series (besides your own): The Tower series by King and JR Ward's Brotherhood books
Mari is giving one lucky winner their choice of one ebook from her backlist!! Thank you Mari!!
Don't forget your comment enters you not only in the daily prize but the Grand Prize Drawings for One Kindle Fire & One AAD Nola Registration to one winner AND One Loaded Kindle to another winner!!
Don't forget your EMAIL! :)
Tomorrow Simply Ali welcomes Author Erin Kellison! You do not want to miss it!!


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Peter Rotatori Jr.
Distinguished career as a lawyer
Peter Rotatori Jr.
Peter was born on Aug. 29, 1935, in Naugatuck, a son of the late Pietro and Carmella Rotatori. He was raised in Naugatuck, the son of Italian immigrant parents who came through Ellis Island in New York City, N.Y. He was a graduate of Naugatuck High School, Fairfield University and Fordham Law School, where he was secretary of his class and was a member of the Moot Court Board. He was a veteran of the Armed Forces, having served in the Army National Guard and United States Army Reserve.
Peter had a distinguished career as a lawyer for more than 50 years. He began his career as a law clerk in the Waterbury Superior Court, then served as a special public defender at the Waterbury Superior Court, and also served as general counsel to the Connecticut State Development Commission in 1969. Then, after founding his own private practice in Naugatuck, he was appointed corporation counsel where he served for more than a decade. He also was a member and an executive director of the Connecticut Association of Municipal Attorneys, and the executive director and general counsel of the Painting & Decorating Contractors of America. He was past vice chairman of the Democratic Town Committee, delegate to the 1976 Democratic National Convention, and served on the board of directors for the American Red Cross in Naugatuck. He was the former vice president and member of the board of directors for the Knights of Columbus in Naugatuck, and was also member of the Board of Finance and Charter Revision Commission for the Borough. Later, a resident of Goshen, he was elected justice of the peace and was a parishioner of St. Thomas of Villanova in Goshen.
Besides his wife, Michelle, of 50 years, he is survived by a daughter, Carla Barbieri; two sons, Mark P. Rotatori Esq. and Peter Rotatori III Esq.; a sister, Marie Swiencicki; and two brothers, Richard Rotatori and Anthony Rotatori. He will also be missed by four grandchildren, J.P. Rotatori, Thomas Rotatori and Kellen Rotatori of River Forest, Ill., and Grace Elizabeth Rotatori of Southbury.
The funeral will be held 10 a.m. Friday, Aug. 2, 2013, at St. Francis of Assisi Church, 318 Church St., Naugatuck. Everyone is asked to meet directly at the church. Burial will be in St. James Cemetery. Friends may call at the Buckmiller Brothers Funeral Home, 82 Fairview Ave., Naugatuck, on Thursday evening from 5 to 8 p.m.
In lieu of flowers, please send donations to Fairfield University or Fordham Law school. For Fairfield, to give online, select the Fairfield Fund as a designation and type in "In memory of Peter Rotatori Jr. '57" in the Memorial/Honorary Gift text box. Or, mail checks to Fairfield University, Bellarmine Hall, 1073 North Benson Road, Fairfield, CT 06824. For Fordham Law School, donate online at //law.fordham.edu/giving, or checks can be mailed to Fordham Law School, Development Office RM 125, 140 West 62nd St., New York, NY 10023.
To place online condolences, please log on to: www.buckmillerbrothers.com.
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I'm writing application using quickly Pygtk and glade.
this application should have database connection (such as MySQL) for reading and writing data from the local or outsourcing machine \ server.
However, in my machine there is MySQL installed, but when releasing the app it sould be installed on another ubuntu machine, which may not have mysql and moreover not the same database with the required database name and structure....
So my questions are:
Is it a good choice using mysql as database
1.2 If not what is?
Is it posible to embeding mysql or other database program during the installation from ubuntu software center?
2.2 If it's posible: hwo(any tutorial?)
Where to store secure data outside the mysql (or whatever) for conecting the database every time a user launch the application


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Why is the first chapter break in B'reishit where it is, and not a few verses later at the beginning of the second creation telling (where we place the aliya break)?
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Many chumashim at the end of each of the five books list the number of pesukim and the number of parshas and the number of chapters in each book. For example, at the end of the book of Bereishis it says that there are 1534 pesukim, twelve parshas and fifty chapters.
But note also that it says וסדריו מ"ג - and the number of sedarim is 43. These sedarim are the original, Jewish divisions of the Tanach handed down to us by the Baalei Hamesorah, and if you look in the Koren Tanach you will see these marked in the wider, outside margin (to give them more prominence). And the second sedra starts at Bereishis 2:4, which is the logical place as was pointed out in the question.
What follows is a summary of the historical background of this topic from the sefer מודע לבינה here, some of which has already been mentioned in previous answers and comments, but he adds more details and brings sources:
R. Eliyahu HaLevi in his introduction to his sefer הבחור writes that the division into chapters is not part of our tradition from the Baalei Hamesorah (the Masters of the Tradition), but are the invention of the person who first translated the Tanach into Latin (according to the Koren Tanach this was an English priest in the 13th century) and saw the need to divide up the books, and so divided them up according to his own logic. Later, in the year 5198 (1458) when R. Yitzchok Nasan came to write his sefer מאיר נתיב which is known as the Concordance, he was forced to use this division since it was already in widespread use in his day, and also because he did not have at that time an alternative division - that of the Baalei Hamesorah.
Later still, when printing presses became available and Sifrei Kodesh started to be printed, they also used this chapter division, and R. Yaakov ben Chaim in his introduction to the first edition of the Mikros Gedolos in the year 5286 (1546) apologized for this, saying that since he made extensive use of the Concordance in his editing of the Mikros Gedolos, he had to use the same divisions as that sefer had used. But he added that if he would have had available the division of the Baalei Hamesorah he would have preferred to use that. And afterwards, when he had nearly finished the preparations for printing, he finally found the division of the Baalei Hamesorah, and he decided to add it to the printing so that it would not become lost forever.
(In addition, the books of Shmuel, Melachim and Divrei Hayamim (Samuel, Kings and Chronicles are not divided into two according our tradition - this was also done by the Christians according to the Koren Tanach) _
As l' said, the chapter divisions are indeed of Christian origin. This article says that the originator of this division separated Shabbos from the other weekdays for reasons having to do with Christian theology, but doesn't specify how. I seem to recall reading a suggestion that the idea behind it was to downplay our Shabbos in favor of their Sunday.
According to Wikipedia, the Chapters were divided by Christians, based on their understanding of the bible. Although we use their system, we only use it for reference. Regarding understanding, we have our own division, comprised of setumot, petuchot, aliyot (to some extent), and parshiyot. The breakup of chapters in no way represents Jewish understanding.
Perhaps, the reason is to distinguish the holiness of Shabbat from the rest of the week, which, in comparison, is more mundane. Shabbat, being holy, is level two; and the rest of the week, being mundane, is only on level one.