Ever have one of those days when at the end of the day you looked back and realized you hadn't accomplished any of the things you wanted to? That was Monday.
So I decided to go with a re-run today. I might have anyway even if Monday hadn't been so hectic. I've been thinking about the Museum of Broken Relationships, subject of one of my first posts here. Rather than write something new on the topic I thought perhaps I would just re-post it – you probably haven't read it before unless you were here at the very beginning.
The broken camera made absolutely no sense to me; or to Vivian for that matter. Why would a non-functioning digital camera be the first thing we would see at the entrance to The Parlementarium, the museum that tells the history of the European Union parliament? And why was there a story about how this camera had been used in someone's relationship? How does this relate to the European parliamentary process? It was confusing, to say the least.
The answer became clear after we had traversed the entire museum (taking a couple of hours, though you could easily do it faster. I like museums, even though the EU one seemed to me to be more propaganda than analysis). The camera, and a couple of other items at the front of the museum turned out to be part of an exhibit, the rest of which was placed just before the exit, a traveling exhibition from the Museum of Broken Relationships, which is located in Zagreb, Croatia.
There must have been a couple of hundred artifacts on display, each sent to the museum by someone lamenting what once was and what might have been, mourning a lost love, or perhaps just a lost lust. The items were each accompanied by a background story sent by the donor, explaining the significance to a once vibrant relationship now in ruins. In addition to the camera there were books, hats, shirts and other items of clothing, jewelry, toys, stuffed animals, travel guide books, camping gear, a collection of aide-memoires sent in to expunge the memories, or at least put them to rest.
Our European vacation was our 30th wedding anniversary gift to each other. Ours is not a broken relationship, though like any human interaction it has its challenges from time to time. It was fascinating to read other people's stories. While relationships break all the time, the concentration here was on romantic attachment. I wondered about that, whether romantic relationships are all that matter? Aren't there other relationships that get broken? How do we deal with those?
I haven't seen any of my high school classmates for more than a decade. Does that make those broken relationships? I got an email a year ago from a classmate who noticed my name when he was listening to the satellite radio channel I program for. I responded but didn't hear back from him. Probably just as well: we had been acquaintances in high school, not close, I'm not sure there was a friendship to rekindle, especially not when separated by half a continent. Does that count as a broken relationship?
A long time ago I attended a seminar on relationships given by a guy named T.V. Thomas. I don't remember much about it, but I do recall him talking about the human capacity for maintaining relationships. He maintained that we have limited capacity for close friendships, that such relationships take time and effort to maintain, which means most of us only have three to five close friends. The next level after that is a bigger one, I can't remember how many people he said we could handle in that stage, perhaps 100, but don't quote me on that. Those on that level are friends, but you probably wouldn't call them to help with a 2 a.m. emergency. Then there are all those other people we call friends. We know their names, but that's about it. I suspect that'[s what most Facebook friends are for most people.
Interpersonal relationships have always interested me which may be why I found the Museum of Broken Relationships so compelling. I read every explanation of the items on display. I couldn't help myself.


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Q: How to reload element attribute inside jQuery droppable() I have an inventory and every time a user deletes an item (drags it to the trash bin) I check if this item is a stack and remove 1 if it is.
The problem is that the stack number stays the same each time the user drops it
$('#trash-wrapper').droppable({

        accept: ".item",
        drop: function(event, e){

            // If the trashed item has a stack that is bigger than 1, do not remove the element but remove 1 from the stack and return the item back
            if(e.draggable.find('.inventory-stack').data('stack-count') > 1){

                var count = e.draggable.find('.inventory-stack').data('stack-count');

                e.draggable.find('.inventory-stack').attr('data-stack-count', (count - 1)).html(count - 1);
                _ajaxFetch("php/ajax/game/conq-delete-item.php", {dby : 'l', id: e.draggable.attr('data-loot-id')});

            }
            // Otherwise destory the element
            else{

                e.draggable.remove();
                _ajaxFetch("php/ajax/game/conq-delete-item.php", {dby : 'i', id: e.draggable.attr('data-item-id')});

            }

        }

    });

The problem is that Count stays always the same. If there is stack of 20, the first drop works, it changes the attribute and html to 19, but all other drops still use the count variable declared first - 20, so it never goes more than 1 below.
I even tried
e.draggable.find('.inventory-stack').attr('data-stack-count', (e.draggable.find('.inventory-stack').data('stack-count') - 1)).html(e.draggable.find('.inventory-stack').data('stack-count') - 1);

Doesnt work as well

A: Ughhhhhh
data('stack-count');

Seems to save this globally and will not be replaced on new call
attr('data-stack-count');

Fixed it :/

redpajama_set_name: RedPajamaStackExchange


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What Can We Learn From the Sudden Closure of the Cedar Lake Ballet?
April 03, 2015 / Mike Scutari
"Don't put all your eggs in one basket." It's a lesson we've been told since childhood, and as recent news out of New York City suggests, one that many arts nonprofits are rediscovering the hard way.
The Cedar Lake Contemporary Ballet formed in 2004 and exists thanks to the funding of a single donor, a Walmart heiress named Nancy Laurie. In a stunning move that echoed recent events down the I-95 corridor, Laurie announced the company will close in June after performances at the Brooklyn Academy of Music.
What can nonprofits learn from this episode?
First, understand that not all deep-pocketed donors are the same. As the Times article implies, there are two distinct mega-donor profiles at play. Mega-Donor Number One cuts huge checks and seems committed to the cause, but comes across as somewhat insular, relying on small cadre of friends, generally uninterested in outside help.
Mega-Donor Number Two also cuts huge checks, but more importantly, some of these checks go toward setting up an endowment. Furthermore, Mega-Donor Number Two, according to Katharine DeShaw, the president of Philanthropology, a philanthropic consulting firm, "invites other people in, and I would argue early in the game."
Soliciting outside help is, of course, a good idea, but it's easier said then done. Some billionaire benefactors think quite highly of themselves—notice we said "some," not "all"—and don't want to be told that they should partner with organizational development experts or expand the revenue base. "My way or the highway," they say, pounding their desk for good measure. (Indeed, a subset of billionaire benefactors are what you'd call "irreverent.")
Needless to say, Donor Number Two is a better choice—if such a choice exists—for nonprofits committed the long haul.
If any good news can be culled from this development, it's that Cedar Lake Ballet saw the writing on the wall. While Ms. Laurie's checkbook accounted for a whopping 75 percent of the troupe's revenue of $5.9 million as of July 2013, it made recent efforts to broaden its donor base. The Times noted that as recently as October, Cedar Lake had advertised for a manager for external affairs whose duties were to have included developing "multiplatform sponsorship proposals for corporate partners, foundations, government, and individuals." Alas, the position was never filled.
But let's be fair. It's hard to fault the folks who run Cedar Lake. For starters, they, more than anyone, were well aware of the risks of reliance on a single funder. It may not have been an optimal model, but it allowed them to bring dance to New York for over a decade and create an esteemed brand. And even if Ms. Laurie, say, decided to reduce her giving to 50 percent of total revenues, could the troupe realistically close the gap from scratch?
As sad as the news is, the closure of the ballet can simply be chalked up to the unfortunate cost of doing business with a single billionaire benefactor.
April 03, 2015 / Mike Scutari/
Mike Scutari
It's Time to Grand Jete Out West ...
What's Behind Mellon's Massive ...
MORE DANCE NEWS
Sparking Something Bigger: A Donor's Big Bet on Dance Education is Starting to Pay Dividends
With a Growing Stream of Grants, This Stalwart Arts Funder Helps Offset Ominous Trends
Charmed and Charitable: The Archetypal Regional Donors Behind a Big Arts Gift
Individual Mandate: How Artist Trust in Washington State Provides Support
"Where is the Next Voice?" A New Gender Equity Initiative in a Storied Arts Niche
The Kids Will Come: More Insights About How Arts Groups Can Engage Millennials
Lifeline: Some Badly Needed Support for Dance-Driven Musicals
A Friend Indeed: What This Foundation's Giving Says About the Future of Arts Philanthropy
Real Change: How This Grantmaker Got Serious About Diversity
Realignment: A Quick Look at Data-Driven Grantmaking Changes to the National Dance Project
In All The Way: Meet the Donor Committed to Dance Education (and the Occasional Big Bet)
A Donor's Vow: To Place a Certified Dance Teacher in Every NYC Public School

redpajama_set_name: RedPajamaCommonCrawl


This article is perfect for all those who are afraid of credit cards. If you are among those people who are not happy about the issues connected with credit cards then you need to be aware of the cash back rewards that you can get from most credit cards today.
There are some people that would view shopping as spending money only. Take note that there is now a really intense competition in the credit card market because of the increasing numbers of players. There are so many credit card companies that would discover innovative ideas in order for them to bring more customers. In order to make both groups happy and satisfied, the credit card companies would consider giving rewards to their companies.
Knowing more about a cash back reward.
The customers can get rewards if they will be spending more on their credit card, these are the cash back assurance provided by the credit card companies. The cash back is usually a fixed amount from the total purchase that was made and will be credited to the credit card of the client. The purchases that will get cash back are those that were made in a single billing cycle.
There are different conditions on how a cash back reward will work on a credit card. You might need to a total balance due that will be more than or equal to a fixed amount. The purchases that you made will dictate how much cash back rewards you will receive. A lot of the credit cards will provide a maximum cash back of up to 5% of your purchase but it can be less for some other purchases like groceries and more. The amount that you will get from the cash back will be credited to your credit card and will reduce your total balance. There might even be some credit cards that will give you more cash back rewards on various conditions.
There are some things that you need to take note every time you will be choosing a cash back credit card. First you need to take a look at the annual fees, application, and processing of the cash back credit card. Next is for you to look for other conditions such as the amount of purchases and the minimum balance that you will need in order for you to get a cash back.
You also need to check if you will be making the kind of purchases that will provide you a maximum cash back reward.
You need to take note that you will not receive a cash back from balance transfers, cash withdrawals, and accumulated balance because of late fees and finance charges. The fraudulent transactions and returned merchandises will also not get any cash back rewards in a lot of cases.


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CNN Founder Ted Turner Has Lewy Body Dementia: Here's What to Know
Written by Shawn Radcliffe on October 9, 2018
Lewy body dementia is one of the most common types of dementia, but many people don't know about it and it is often misdiagnosed.
CNN founder Ted Turner revealed he had the dementia diagnosis earlier this month. Getty Images
Lewy body dementia is one of the most common types of dementia, affecting approximately 1.4 million Americans.
But many people still do not know much about the disease or its symptoms.
Now that might change after CNN founder and media giant Ted Turner recently told "CBS Sunday Morning" about his diagnosis of Lewy body dementia.
While more than a million people have the disease, getting the right diagnosis can be difficult.
Actor Robin Williams was diagnosed with the disease posthumously.
The symptoms of Lewy body dementia overlap with Alzheimer's disease and Parkinson's disease, which makes it difficult to diagnose correctly. Symptoms like hallucinations may also be misdiagnosed as other psychiatric disorders such as schizophrenia.
Complicating diagnosis, Lewy body dementia can occur alongside other brain disorders, including Alzheimer's disease.
What is Lewy body dementia?
The disease gets its name from abnormal deposits in the brain known as Lewy bodies. These are made of a protein called alpha-synuclein which affects chemicals in the brain, causing problems with thinking, behavior, mood, and movement.
Lewy body dementia is an umbrella term for two related diagnoses — dementia with Lewy bodies and Parkinson's disease dementia.
Both are caused by the buildup of Lewy bodies in the brain. These can only be seen after death during an autopsy.
Dr. Irene Litvan, a professor of neurosciences and director of the UC San Diego Health Movement Disorders Center, said there is disagreement among some doctors about whether dementia with Lewy bodies is part of the "spectrum of Parkinson's disease" or if it is a separate disorder.
In dementia with Lewy bodies, people first show signs of a decline in thinking ability.
This can look like Alzheimer's disease, but early on, people are more likely to have trouble with executive functioning than with memory. Executive tasks include abilities such as planning, multitasking, sequencing, and conceptualizing thoughts.
The main features that distinguish dementia with Lewy bodies from other conditions are:
visual hallucinations, not caused by medications or other drugs
fluctuations in alertness, attention, and mental abilities
slowness of movement, difficulty walking, tremor, or stiffness — this is known as parkinsonism
REM sleep behavior disorder, in which people "act out" their dreams by talking, yelling, kicking, and other movements
The fluctuations are "very typical of this disease," said Litvan. "Sometimes a person can act almost normal, but other times they look like they are completely confused."
Robin Williams' family only learned that he had a severe case of the disease after his death by suicide in 2014.
In an editorial published in 2016 in the journal Neurology, Robin Williams' wife Susan Schneider Williams wrote, "I experienced my brilliant husband being lucid with clear reasoning 1 minute and then, 5 minutes later, blank, lost in confusion."
In contrast, Parkinson's disease dementia starts as a movement disorder (parkinsonism), with later dementia and changes in mood and behavior.
"Dementia occurs five [times more] in Parkinson's disease than in the general population," said Litvan, "but it is usually a late event."
However, not everyone with Parkinson's disease develops dementia.
Litvan added that the distinction between when one of these diagnoses ends and the other begins is somewhat "arbitrary."
Who is affected by Lewy body dementia?
According to the nonprofit Lewy Body Dementia Association, Lewy body dementia affects about 1.4 million Americans. It usually begins after age 50, although some younger people can also have this condition.
Symptoms are typically mild early on and then can dramatically worsen over time.
"It's a clear change from what people were before, socially or at work," said Litvan. "They could do many things before, but they cannot anymore."
People may have difficulty managing their bank accounts, taking their medications, planning for their day, or running errands.
In the later stages, the decline in a person's thinking and movement abilities may be so great that they rely entirely on others to care for them.
On average, the disease lasts 5 to 8 years from diagnosis until death, but this can range from 2 to 20 years.
There is currently no cure for Lewy body dementia, but some medications are used to treat the symptoms of the disease.
This includes cholinesterase inhibitors to treat cognitive symptoms, levodopa (a Parkinson's medication) for movement symptoms, and an antipsychotic medication for hallucinations.
Some doctors believe that people with Lewy body dementia respond better to cholinesterase inhibitors than people with Alzheimer's disease do.
"The good thing for dementia with Lewy bodies is that in general, people respond much better to medications for cognition," said Litvan.
Research is ongoing to find better ways to diagnose and treat Lewy body dementia. Some of this work is being done by a consortium of universities funded by the U.S. National Institutes of Health.
Litvan said one of the challenges in finding treatments for Lewy body dementia is the fluctuations in symptoms. If a person taking a new drug improves, is it because the drug is working or are they just having a "good day?"
She said because of that, many researchers are focusing right now on finding better ways to monitor how far along the disease is.
"The main purpose of these studies is to identify biomarkers that would not fluctuate, but instead would show progression of the illness," said Litvan. "That way you could try to treat or give medications to slow the progression."
Healthline News Fact-Checking Standards
The Healthline News team is committed to delivering content that adheres to the highest editorial standards for accuracy, sourcing, and objective analysis. Every news article is thoroughly fact-checked by members of our Integrity Network. Furthermore, we have a zero-tolerance policy regarding any level of plagiarism or malicious intent from our writers and contributors.
All Healthline News articles adhere to the following standards:
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Robin Williams Had Parkinson's Disease, Widow Says
Fear of the progressive disease may have fed the comedian's depression, but Parkinson's can also cause depression and anxiety.
Diet and Parkinson's
Medically reviewed by Natalie Butler, R.D., L.D.
The causes and triggers that activate Parkinson's disease are still being studied. Since Parkinson's is closely connected to a lack of dopamine cells…
Yoga for Parkinson's Disease: 10 Poses to Try, Why It Works, and More
Medically reviewed by Daniel Bubnis, M.S., NASM-CPT, NASE Level II-CSS
You may already know that yoga is a great way to get moving, but could it also help with Parkinson's symptoms? Here's how it works, poses to try, and…
Early Signs of Dementia May Be Noticeable in At-Home Written Test
The test, known as SAGE, is available online and can completed at home or at a doctor's office. It poses a series of identification and thinking tasks.
How Coffee and Tea Can Help Lower the Risk of Stroke, Dementia
Experts say people who drink a moderate amount of coffee or tea on a daily basis receive a number of health benefits from those beverages.
'Use It or Lose It': Why Retiring Early Can Increase Your Risk of Dementia
Experts say it's important to keep your mind active after retirement with classes, travel, hobbies, and engagement with others.
How Tooth Loss Can Be Connected to Cognitive Decline, Dementia
Experts say it's not certain whether tooth loss or cognitive decline comes first, but there does seem to be a connection between the two conditions.
Too Much TV in Your 40s, 50s Can Affect Brain Health: What You Can Do
Experts say excessive TV watching in midlife can affect brain health in later years. They suggest replacing TV viewing with an activity you enjoy.
A Lack of Sleep in Middle Age Can Increase the Risk of Dementia
Experts say the brain needs those final extra hours of sleep to cleanse itself of potential harmful substances


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These transgenic mice overexpress mutant human APP at levels approximately 5-fold higher than endogenous murine APP. As the mouse ages, levels of "human" Aβ40 and Aβ42 increase, with Aβ42 being the more prevalent species (Chishti et al., 2001). These mice develop early plaque formation with thioflavin S-positive amyloid deposits observed at three months and dense-cored plaques with neuritic pathology by five months, becoming more extensive with advanced age. Activated microglia appear concurrently with plaques and GFAP-positive astrocytes follow later, starting about 13-14 weeks (Dudal et al., 2004). Dystrophic neurites are also observed (Dudal et al., 2004; Woodhouse et al., 2009). There is a decrease in the number of cholinergic neurons in the nucleus basalis magnocellularis as measured by ChAT immunoreactivity (Bellucci et al., 2006) and loss of glutamic acid decarboxylase (GAD)-immunoreactive GABAergic neurons (Krantic et al., 2012).
Behaviorally, these mice show a variety of impairments, including early impairment in acquisition and learning reversal in the reference memory version of the Morris water maze, by three months of age (Chishti et al., 2001). Age-associated cognitive deficits are observed in the step-down inhibitory avoidance test (deficits at seven months, but not at two months). No differences from wild-type mice were observed in motility, exploratory activity, or neuromuscular function at seven months as evaluated by the rotarod, hole board, and grip strength tests (Bellucci et al., 2006). In addition, susceptibility to seizure (Del Vecchio et al., 2004) and LTP-related changes (Jolas et al., 2002; Kimura et al., 2012) have been reported.
Survival rates depend on the genetic background. Survival on the (C57) × (C3H/C57) genetic background was the highest, with 50 percent of mice surviving until postnatal day 365 (the upper limit in the analysis. Mice on the (C3H/C57/129SvEv/Tac) × (129SvEv/Tac) and (FVB)×(C3H/C57) had increased mortality with 25 percent and 17 percent respectively reaching 365 days (Chishti et al., 2001).
Aβ42 immunization reduced deposition of cerebral fibrillar Aβ and improved cognitive dysfunction (Janus et al., 2000).
Transgene contains human APP695 with the Swedish mutation (KM670/671NL) and Indiana mutation (V717F) under the control of the hamster prion (PrP) gene promoter. The expression cassette includes about 90 nucleotides of the APP 5'-untranslated region adjacent to the start codon and 269 nucleotides of the 3′-untranslated region.
Available through the Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto (crnd.info@utoronto.ca).
Amyloid deposition progresses with age. Thioflavin S-positive amyloid deposits at 3 months; dense cored plaques and neuritic pathology by 5 months. Plaques appear first in the subiculum, amygdala and frontal cortex, spread to the dentate gyrus, the olfactory bulb, and later thalamus, cerebral vasculature, and striatum, followed by the cerebellum and brain stem (Chishti et al., 2001).
Neurofibrillary tangles are absent (Chishti et al., 2001). Tau is hyperphosphorylated, nitrosylated and aggregated at 7-12 months especially in the neocortex, dentate gyrus, and the CA1 and CA3 areas of the hippocampus (Bellucci et al., 2007).
Variable cell loss by region. No difference in overall cell count, but fewer hippocampal neurons at 6 months (Brautigam et al., 2012).
Microglia activation appears simultaneously with Aβ deposition, with only rare activated microglia at 9-10 weeks, but by 13-14 weeks microglia cluster around Aβ deposits in the cerebral cortex and hippocampus; numerous by 20 weeks. Robust astrogliosis slightly later with clusters of GFAP+ astrocytes emerging around plaques at 13-14 weeks (Dudal et al., 2004).
Reduced synaptophysin immunoreactivity in the vicinity of plaques at 6 months (Adalbert et al., 2009).
In hippocampal slices from 6- to 12-month-old mice basal excitatory synaptic transmission (as assessed by I/O relationships) and LTP at CA1 are reduced in TgCRND8 mice compared with wild-type mice (Kimura et al., 2012).
Early impairment in acquisition and learning reversal in the reference memory version of the Morris water maze, present by 3 months (Chishti et al., 2001).
Dudal S, Krzywkowski P, Paquette J, Morissette C, Lacombe D, Tremblay P, Gervais F. Inflammation occurs early during the Abeta deposition process in TgCRND8 mice. Neurobiol Aging. 2004 Aug;25(7):861-71. PubMed.
Bellucci A, Luccarini I, Scali C, Prosperi C, Giovannini MG, Pepeu G, Casamenti F. Cholinergic dysfunction, neuronal damage and axonal loss in TgCRND8 mice. Neurobiol Dis. 2006 Aug;23(2):260-72. PubMed.
Krantic S, Isorce N, Mechawar N, Davoli MA, Vignault E, Albuquerque M, Chabot JG, Moyse E, Chauvin JP, Aubert I, McLaurin J, Quirion R. Hippocampal GABAergic Neurons are Susceptible to Amyloid-β Toxicity in vitro and are Decreased in Number in the Alzheimer's Disease TgCRND8 Mouse Model. J Alzheimers Dis. 2012 Jan 1;29(2):293-308. PubMed.
Del Vecchio RA, Gold LH, Novick SJ, Wong G, Hyde LA. Increased seizure threshold and severity in young transgenic CRND8 mice. Neurosci Lett. 2004 Sep 2;367(2):164-7. PubMed.
Jolas T, Zhang XS, Zhang Q, Wong G, Del Vecchio R, Gold L, Priestley T. Long-term potentiation is increased in the CA1 area of the hippocampus of APP(swe/ind) CRND8 mice. Neurobiol Dis. 2002 Dec;11(3):394-409. PubMed.
Van Vickle GD, Esh CL, Kalback WM, Patton RL, Luehrs DC, Kokjohn TA, Fifield FG, Fraser PE, Westaway D, McLaurin J, Lopez J, Brune D, Newel AJ, Poston M, Beach TG, Roher AE. TgCRND8 amyloid precursor protein transgenic mice exhibit an altered gamma-secretase processing and an aggressive, additive amyloid pathology subject to immunotherapeutic modulation. Biochemistry. 2007 Sep 11;46(36):10317-27. PubMed.
Wykes R, Kalmbach A, Eliava M, Waters J. Changes in the physiology of CA1 hippocampal pyramidal neurons in preplaque CRND8 mice. Neurobiol Aging. 2011 Jun 13; PubMed.
Hyde LA, Kazdoba TM, Grilli M, Lozza G, Brusa R, Brussa R, Zhang Q, Wong GT, McCool MF, Zhang L, Parker EM, Higgins GA. Age-progressing cognitive impairments and neuropathology in transgenic CRND8 mice. Behav Brain Res. 2005 May 28;160(2):344-55. PubMed.
Ma K, McLaurin J. α-Melanocyte stimulating hormone prevents GABAergic neuronal loss and improves cognitive function in Alzheimer's disease. J Neurosci. 2014 May 14;34(20):6736-45. PubMed.
Durk MR, Han K, Chow EC, Ahrens R, Henderson JT, Fraser PE, Pang KS. 1α,25-Dihydroxyvitamin D3 reduces cerebral amyloid-β accumulation and improves cognition in mouse models of Alzheimer's disease. J Neurosci. 2014 May 21;34(21):7091-101. PubMed.