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Social communication in the field of autism has been a growing need. One of the defining characteristics of autism is a deficit in communication skills. The master of arts in social communication and autism spectrum disorders is a unique degree that will prepare students to work in professional settings and to interact with individuals with autism such as educators, group home staff, and within other service agencies.
This degree is targeted toward individuals who are interested in working with individuals with disabilities such as ASD. This degree will allow interested students to learn about the role of social communication in the realm of autism spectrum disorders and will prepare them for employment in schools and service agencies.
This program also offers an accelerated option.


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MISSION STATEMENTThe Marketing Committee will provide a forum for members to discuss ways ASC can enhance its long term value proposition by assisting members with selling their products in the marketplace via tradeshows, virtual events, and an online supplier directory COMMITTEE COMPOSITIONThe Marketing Committee should be comprised of energetic, enthusiastic marketing personnel representing both manufacturer and supplier member companies who have an interest in marketing and are aware of new and emerging markets in which the ASC could actively participate. Committee members will be appointed and serve a 2-3 year term.
COMMITTEE CHAIRCommittee Chair assists ASC staff liaison in planning meeting agendas and identifying key prospects/contact names. Estimate total time commitment of less than 6 to 8 hours per year, including time spent at meetings.
MEETINGSCommittee meets face-to-face at ASC Spring and/or Fall Conventions, as well as by conference call in between (estimate 2 to 3 calls per year, one hour long). CONTACTASC Staff Liaison: Malinda Armstrong, Senior Manager, Meetings & Tradeshows, (301) 986-9700 ext. 106 |
4/3/2017 » 4/4/2017
2017 Waterborne Adhesives Short Course
4/3/2017 » 4/4/2017
2017 Caulks and Sealant Short Course

subset: commoncrawl


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Fettercairn single malt, bottled by Langside for the Hepburn's Choice selection. The Fettercairn distillery up in the Highlands distilled this whisky in 2002 and let it mature in a refill hogshead… More info
A single cask 11 year old Glenlivet single malt Scotch whisky, originally released in the Netherlands. It was bottled at a robust 59.5% ABV in October 2014 and named after Bochel Hill, which is said… More info
A classic, meaty Craigellachie that perfectly showcases the distillery character, which is partly down to their use of traditional worm tub condensers. This single cask also exhibits impressive… More info
A fabulous cask strength release from Caol Ila, this was bottled for the 2011 Feis Ile (Islay Festival). We first tried this in the cold and rain at Caol Ila's blustery distillery day. It was just… More info
Distilled in Autumn 2004 and bottled in Autumn 2015, this 11 year old single cask Dailuaine is from the Provenance range and was matured in a refill ex-Sherry cask. More info
8 year old single malt Scotch whisky from Royal Brackla - which received its regal prefix in 1835 from King William IV - bottled by A. D. Rattray. It was distilled by Royal Brackla in November 2006… More info
Distilled at the popular Orkney distillery in June 2006 and disgorged in May 2015, almost nine years later, this is a bottling of four first fill bourbon barrels (4288, 4290, 4292 & 4293). More info
Released as part of the Douglas Laing Provenance range (which received a redesign in early 2016), this is a single cask 11 year old Benrinnes single malt, matured in a refill hogshead from March 2004… More info
Released for the Douglas Laing Provenance range, this Longmorn single malt Scotch whisky matured in a single cask for 11 years, from the summer of 2003 to the spring of 2015. More info
An 11 year old independent bottling of single malt Scotch whisky from "The Beast of Dufftown" - Mortlach! Known for big, flavoursome whiskies, expect some tasty stuff from this Hunter Laing Old Malt… More info
An 11 year old Benrinnes single malt Scotch whisky, matured in a single Sherry butt from 2002 to 2014. It was bottled with an outturn of 761 bottles by Langside for their Hepburn's Choice range. More info
This Edradour single malt Scotch Scotch whisky was matured exclusively in Super Tuscan wine casks from 2006 to 2015. It was then bottled at 46% ABV without chill filtration or additional colourings.… More info
This is an 11 year old Dailuaine single malt Scotch whisky, released as part of the Managers' Choice range. It was distilled by Dailuaine in June 1997 and set aside to age in a single Sherry oak cask… More info
A light, relaxed Craigellachie single malt Scotch whisky, bottled for Douglas Laing's Provenance range. This was distilled in spring 2006 and set aside to mature in a single Sherry butt for eight… More info
The Provenance collection from Douglas Laing celebrates the seasons in which the whisky is distilled. This yummy 11 year old Glen Moray single malt was distilled in Autumn 2001 and bottled in Summer… More info
The Edradour distillery in the Highlands distilled this single malt in April 2006 and left it to mature in Barolo wine casks for 8 years until September 2014. It was bottled as the third batch of… More info
This is an independently bottled Mortlach single malt Scotch whisky, presented as part of Douglas Laing's Provenance range. It was distilled in the autumn of 2006 and bottled in the spring of 2015 -… More info
This is an independent bottling of 8 year old Ben Nevis single malt Scotch whisky, which was matured in a single refill hogshead. It comes to us from Douglas Laing, whom bottled it as part of their… More info
An official bottling of single cask Kilkerran from Glengyle distillery in Campbeltown. Matured in an ex-Calvados cask, it was distilled back in May 2006 and bottled in 2015! More info
This Edradour single malt Scotch whisky spent its 11 year maturation in casks which has previously served as home to yummy Port! It was distilled in June/July 2003 and bottled in April 2015 - 2250… More info
An independently bottled Caol Ila single malt Scotch whisky, matured in 2 bourbon barrels and bottled without chill filtration or additional colouring. It was distilled on the island of Islay in 2006… More info
Independently bottled Jura single malt Scotch whisky, bottled by Langside for their Hepburn's Choice range. This was distilled on the island, where deer outnumber people 30:1, in 2006 and left to… More info
A single cask bottling of Glenrothes single malt Scotch whisky, matured in a single Sherry butt from 2004 to 2015. It was bottled as part of the Hepburn's Choice range by Langside. 341 bottles were… More info
Dalmore filled up a cask of their brilliant single malt Scotch in December 1996, which the Scotch Malt Whisky Society eventually got their hands on and bottled in June 2008. It was bottled at a… More info
The youngest single malt in GlenDronach's 12th batch of single cask releases is this 11 year old whisky matured in a Pedro Ximénez Sherry puncheon from January 2004 to August 2015. It was bottled… More info


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Brighton's Peggy Sue makes music which reflects that of Coco Rosie, Joanna Newsom and Antony And The Johnsons. Think 1920s rhythms, haunting vocals and gently twisting melodies, drawing the listener in slowly but surely.
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One of the best bands at the Festival, Peggy Sue delighted a few hundred music-lovers with their sweetly constructed set in the Tent. Understated & modest they delivered heartfelt lyrics with melodic vocals and (when required) high impact musicianship. Most listeners left as Peggy Sue fans Gary from Weald
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Tripod Floor Lamp, Chrome
Guide price: £90
Last updated on 6th May 2015
Tags: lighting
Tripod Floor Lamp, Chrome
The tripod floor lamp is a must have, with its over-size pleated drum shade and chrome legs it's perfect for that modern look.Dimensions: Height 158cm x Width 46cmComposition: Steel & taffetaRequires: 60W E27 GLSCare Instructions: Wipe clean with a soft dry clothPlease note: this particular item, will need to be delivered by our specialist courier service, which may result in a slight delay in the arrival of your order
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Features : Includes 9 decals on a 19-inch x 27-inch sheet *Easy to apply - just peel and stick! *Applies to any smooth surface *Removable and repositionable with no sticky residue *Decal is made of vinyl
Features : Red, white and blue pinwheel shaped lights *Set of 10 measuring 7 feet long *Indoor use only
Park Madison Lighting Pmd
This halogen desk lamp has a fully adjustable gooseneck column and a euro style rocker switch. The lamp is made with a black finish and a black gooseneck column. It's perfect for any home or office. It is ETL listed and the bulb is included. Features : Halogen desk lamp with fully adjustable gooseneck column; 5-1/4-Inch diameter, 20-1/2-Inch tall *Black finish *Contemporary design *On/Off euro style rocker switch *ETL listed, uses a 20-watt G4 halogen bulb; bulb included; Not CA compliant Color : Black Finish Product dimensions : 20.5x5.25x5.25 inches
Elimistat™ Floor Finish|ELCOM (UK) LTD
Features : Surface resistivity 107 – 109 ohms per square Can be used on vinyl, linoleum, or ceramic tile


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The booth's central theme is responsible cotton sourcing throughout the supply chain, underscored by the Cotton LEADS program, a joint effort of the U.S. and Australian cotton industries.
At the Heimtextil trade show, suppliers, textile manufacturers and retailers can find out more about Cotton LEADS and see for themselves how they can use this program to easily source reliable and responsible raw material.
Cotton LEADS offers companies across the entire cotton supply chain the confidence that their raw material is responsibly produced and identified. As Cotton Council International (CCI) Executive Director Kevin Latner emphasizes, the challenge is to continually optimize responsible cotton production practices.
Cotton LEADS answers the world market's demand for responsibly-produced cotton that is also available in the volumes required. The chief prerequisite for the production of sustainable products is traceability along the supply chain. This begins with the fiber. In the United States and Australia, comprehensive tracking and identification systems for cotton production are in place and are also the basis for tracing every product back to its place of origin.
CCI, the National Cotton Council of America, Cotton Incorporated and Cotton Australia founded Cotton LEADS to promote awareness of the responsible cotton production practices undertaken in the United States and Australia.
These include extremely stringent national production regulations (in the United States cotton is subject to the production regulations for food crops), monitored reporting, promotion of the implementation of best practices, and constant data collation and evaluation – all with a view toward continuous optimization.
Both the United States and Australia are among the leading suppliers of world-class cotton fiber on the international market. Together, the two countries account for approximately 17 percent of global cotton production and close to 40 percent of global cotton exports.
The United States is the foremost cotton exporter on the world market. The current volume of so-called identified or certified cotton fiber available worldwide is in the region of 4 percent – insufficient for the global market.
From now on, Cotton LEADS will offer retailers, brands and manufacturers that operate with large volumes the capability to source responsibly produced fiber.
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I guess we are ready!hahahaha.. we're done for our final pre prod meeting and ocular check of our venue for this Saturday's Toycon event launch and press con in Resorts World Manila.
I forgot already to post my production note because of my busy schedule. I will try my best to docu everything here via my prod note blog.
This is my VLOG channel, pls watch and SUBSCRIBE https://www.youtube.com/user/azraelcoladilla/
This is my VLOG channel, pls watch and SUBSCRIBE https://www.youtube.com/user/azraelcoladilla/
Thursday, May 29, 2014
13th Philippine Toycon 2014 production note 2 --- we're getting ready for the epic launch in @resortsworldmanila
TweetThe blogger
Azrael Coladilla is the blogger and founder of Azrael's Merryland Blog. This blog started as a personal blog in 2003, and then converted the blog into a lifeblog about his interest and reporting about pop culture, lifestyle, entertainment, technology, food, travel, toys, outdoor adventure, internet and social media. Awarded as the 2009 Most Influential Blogger for Luzon, Philippines, awarded by the Philippine Blog Awards. He is the founder of several online communities - Manila Bloggers Network, PBNetwork PH, Oh My Food! community, Cavite Bloggers, Travel and Blog Community, and Philippine ToyCon. He loves to travel, explore, discover, eat new food, document and record his life, meet new people, do photography and collects Transformers toys.


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Well, well, well, now that's interesting! Amazon has just unveiled its new tablet, the Kindle Fire HD! Ta-daa, now, we wonder if it has what it takes to compete with its impressively tough opponent, the Google Nexus 7…
You know, ever since Google introduced the Nexus 7, the Kindle Fire and its $199 price-tag stopped being such a big deal. Of course, that's completely understandable, having in mind that the Nexus 7 is a full-featured tablet with a quad-core processor and all the bells and whistles one would expect from a modern tablet. And it too is available for $199. The original Kindle Fire, on the other hand, is a somewhat more specialized, limited device, tightly integrated with Amazon's content ecosphere. With both devices going for $199, it doesn't take a genius to know that users will prefer to purchase the more powerful tablet, which also comes with the full Google experience and latest Android version.
But the times, they are a-changin'. One day you're on top, the other… not so much. And the original Kindle Fire is still commanding some 20+% of the Android tablet market. That's because Amazon has this giant retail reach, and Google, well, let's just say that Google isn't that's good at retail. But a fact is a fact – the Nexus 7 is the better device when compared to the Kindle Fire. Amazon isn't dumb, though. It knows its strengths and weaknesses. So, what can the new Amazon Kindle Fire HD models do for the company now, will they be what Amazon needs to beat the Nexus 7?
Although Google isn't really well positioned as far as retail goes, it's still in the position of 'the people's champion'. That's why we belive that it will be very hard for Amazon to preserve its significant lead in the market. And although its lead may not remain as big, the Kindle Fire HDs are a good reason to believe that Amazon will at least remain a prominent player.
Amazon has just announced some very cool devices. It will start offering an upgraded version of the original Kindle Fire for $159, and it will later add a 7″ Kindle Fire HD, and an 8.9″ Kindle Fire HD, with the first one offered for $199, and the latter for $299, which isn't really mind-blowing. Finally, there's the 4G LTE version of the 8.9″ model, will which will sport 32GB storage (the other models will have 16GB), and will sell for $499, as much as a 16GB iPad Wi-Fi. Well, the prices may not be as shocking as the $199 price-tag of the original Kindle Fire once was, but they sure beat the competition. Yeah, the Nexus 7 has hardware that's about as good, and a better, more feature-rich software experience, but don't forget that its $199 version only features 8GB of internal storage, and the 16GB is $249. So, in terms of specs, it's relatively safe to say that the Kindle Fire HD is a step ahead of Google's offering, but when it comes to software, well, we're sure that one can have a much better experience with stock Jelly Bean, compared to the Kindle's custom carousel UI. As a mattery of fact, we still don't know exactly what Android version will the software on the Fire HD be based on, but we presume it will be Android 4.0 ICS.
What matters, though, is if that "full Android experience" will be important for the regular consumer. And the answer is probably 'no'. With its enormous retail reach, Amazon will easily put the Kindle Fire HD front and center, offering it to all kinds of customers visiting its ecosystem. The Nexus 7? It'll probably remain more of a geek product. Actually, making geek-products is something that Google can't seem to escape from, and that's a bit sad, because the company has the potential to achieve great things in the hardware business as well. Anyway, these two companies have walked different roads, and have extremely different ways of doing business (although they both happen to sell tablets, among other things). Right now, Amazon seems to prove that it takes a more than just a great product to be successful in the market. It's a lesson that Google will hopefully learn, but it's not yet clear exactly when this is going to happen.


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Observation Drawing
Every day there will be a different still life, person, or animal to draw. We will work on your drawing skills, including shading, figure drawing, charcoal, and realism. Some of your favorite drawings will be turned into paintings!
January 11 – February 8
Click here to register and pay.
Living Artist
We will be exploring artists that are still alive. We will learn about their artwork and create our own based off of theirs! Artists include Gerhard Richter, Jeff Koons, Richard Serra, and Banksy!
February 15 – March 15
Click here to register and pay.
Explore the most interesting element of art—texture! We will create our own textured artworks with a variety of adventurous materials and mixed media.
March 22 – April 26 (no class March 29)


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To identify the needs of senior citizens and assist the Area 12 Agency on Aging in settling direction for future goals. The Board of Supervisors has the authority to assign representatives from Calaveras County and of the Board of Supervisors and it's alternates only.
Meeting Frequency: Meetings are held on the third Monday of each month at various locations throughout the five county region.
Term Limit: 3 year Terms, unlimited number of Terms.
Positions: 10 in total. 10 occupied. No vacancies.
Member At Large
Commission on Aging
BOS Representative
BOS Alternate


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Pre-tax profits, down 4 per cent at the interim stage, finished the year to 31 October 2.3 per cent higher at pounds 31.1m. Trading since then has improved, although the company said its operating plan was still based on continuing recession.
Recession or not, analysts expect a further profits advance this year. Estimates start at pounds 34m pre- tax, giving projected earnings per share of 16.2p, and a price-earnings multiple of 20 against the sector average of 15.
Earnings per share for 1991/92 improved marginally from 15.67p to 15.83p, but the dividend total is rising 8 per cent to 6.14p.
John Conlan, chief executive, said last year's performance was reasonable, against the recessionary backdrop and the wet summer weather, which unsettled trading at the company's resort operations in Blackpool, Great Yarmouth and Eastbourne.
Trading profits from resorts held at pounds 12.3m, with the completion of the first phase of the upgrading of Blackpool Tower helping to counter the weather.
Returns from ten-pin bowling, predominantly based in the South and South-east, were aided by new openings, and rose 5 per cent to pounds 14.1m. 'We had to work harder to maintain previous levels. And while it is not immune to recession, it remains a good long-term business,' Mr Conlan said.
Bowling activities have been extended to the West. Bristol came on stream during the year, and a superbowl at Plymouth opened recently. Southampton will open soon.
Discos, however, lagged behind the other two divisions, not only because of the squeeze on consumer spending but because six of the larger venues were out of action for around 20 weeks at a time for refurbishment.
Earnings from dancing dipped from pounds 13.1m to pounds 12.5m, but the profit margin improved by more than 1 percentage point to 32.7 per cent, on turnover down from pounds 39.1m to pounds 38.2m.
'Wholesaling discounting on admission charges was of less importance, and spend per head held up. There were modest price increases, and the overall margin was at or marginally below where it was in the peak years,' added Mr Conlan.
Investment in all businesses was increased. Capital expenditure, funded entirely from cash flow, rose by pounds 5m to pounds 34m, and a similar amount, the company said, would be spent this year. Net borrowings remained static at pounds 33m, equal to 12 per cent of shareholders' funds.
- More about:
- Blackpool
- Bowling
- Eastbourne
- Economics


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- He runs meetings like a coach. Basically, Im playing with a coordinator on the field. Hes a football God. He sees everything, and he sees the big picture of everything." - Frank Gore on Andrew Luck
- "He is as smart as Peyton, as accurate as Brady, tougher than Ben and as athletic as RG3." - Anonymous Head Coach on Andrew Luck
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I actually respect them a little more since they've both been with their ladies since high school. It'd probably been real easy for them to have dropped them and got way hotter girls but they've stuck with them.
SF Giants, SF 49ers, Sac Kings since birth.
I also respect them for marrying ugly women. I respect that they chose the person to marry while they were children and settled for them. That's why I still use dial-up internet, just because there is better internet available now and I can afford it, doesn't mean I'll switch.. I chose it as a kid and I'll stick with it because they were nice to me.
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Once someone makes the big bucks, how are they going to weed out the gold diggers? I think the young guys are smart for going with someone they trust and who loves them for who they are.
5 years and counting(2 years married).


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Come back to EngSci to celebrate the role that this program played in your formative years of Skule Life!
All Engineering Science and Engineering Physics graduates are invited to the 17th Annual Engineering Science Alumni Dinner. Upper year students will showcase their research and designs during the cocktail reception, followed by a delicious dinner in the beautiful Great Hall at Hart House.
Keynote address
Cyber-Physical Security for Smart Grid and Beyond
Professor Deepa Kundur, Chair, Division of Engineering Science, and Director of the Centre for Power & Information, Edward S. Rogers Sr. Department of Electrical & Computer Engineering
We are delighted to announce this year's keynote speaker is Professor Deepa Kundur, a leading expert on cyber security and complex dynamical networks who will become Chair of the Division of Engineering Science in 2017.
Live musicians, delectable cuisine, the unforgettable ambiance of Great Hall and fascinating, brilliant people to get to know better – who would miss it?!
Alumni and friends of the Division, purchase tickets here.
Not sure if you're on the mailing list? Update your contact information here to make sure you receive an invitation.
This event is a cornerstone of the EngSci experience. Help us share it with students! Ticket and table sponsorhips are available for as little as $75 and allow deserving students to attend this event free of charge.
During the Praxis II Showcase, students in this second year course share their proposed engineering designs for a wide variety of projects in the Toronto area. Community stakeholders, interested members of the public, students, faculty and alumni are invited to interact with students as they share posters, prototypes and presentations. Media inquiries are welcome, please see the event website for contact details.
The university will be closed.
The university will be closed.
EngSci and EngPhys alumni from the honoured years whose graduation year ends in 2 or 7 are invited to the EngSci Luncheon during Spring Reunion 2017. Mix and mingle with EngSci Chair Professor Deepa Kundur and a select group of current students during an informal luncheon.
This event is exclusive to Engineering Physics and Engineering Science graduates and their families, and registration is required. Visit the Spring Reunion website and search "Engineering Science" to RSVP!
Not sure if you're on the mailing list? Update your contact information here to make sure you receive an invitation.
Need help getting in touch with your old classmates? Join EngSci Connect, the online meeting place exclusively for graduates of our program, or contact Christina Heidorn at email@example.com.
We look forward to celebrating with the graduating class of 2017!


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Bacterial lipopolysaccharide (LPS) is known to induce the expression of inducible nitric oxide synthase (iNOS) in the lung and to lead to increased pulmonary nitric oxide (NO) production. The contribution of various pulmonary cells to this phenomenon remains unclear. In this study, we used gadolinium chloride, a blocker of macrophage activation, to assess… (More)
Increased nitric oxide (NO) synthesis by the inducible nitric oxide synthase (iNOS) has been shown to contribute to the development of acute lung injury and delayed hypotension in animals injected with bacterial lipopolysaccharides (LPS). Recent evidence indicates that endothelin-1 (ET-1) is also elevated in septic humans and in animals. To assess the… (More)
The widespread prevalence of diabetes, caused by impaired insulin secretion and insulin resistance, is now a worldwide health problem. Glucagon-like peptide 1 (GLP-1) is a major intestinal hormone that stimulates glucose-induced insulin secretion from β cells. Prolonged activation of the GLP-1 signal has been shown to attenuate diabetes in animals and human… (More)
Sympathetic innervation to the melanophores of a siluroid Parasilurus has been the sole instance of such innervation among lower vertebrates, in which the peripheral transmission to the effector cells is peculiarly cholinergic (Fujii and Miyashita, 1976). In an effort to find a similar case, we studied the nature of transmission of melanophores of a glass… (More)
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Narcolepsy is considered a primary hypersomnia condition. The word narcolepsy comes from two Greek words roughly translated as "seized by numbness." The two primary symptoms in narcolepsy reflect this phrase:
Some, but not all, patients experience other symptoms:
Rapid eye movement (REM) sleep is abnormal in narcolepsy. In fact, narcolepsy is sometimes defined as the loss of boundaries between wakefulness, non-REM sleep, and REM sleep. REM sleep is the active, dreaming phase of sleep.
Excessive Sleepiness. All people with narcolepsy experience excessive sleepiness during the day with episodes of falling asleep rapidly and inappropriately, even when fully involved in an activity. It is sometime described as an irresistible daytime need for naps, which will generally refresh the patient. These events may be characterized by the following behaviors:
Cataplexy. Cataplexy is an abrupt loss of muscle tone or strength that results in an inability to move and always occurs during wakefulness. Symptoms of excessive daytime sleepiness are often present for years before symptoms of cataplexy develop. Around two thirds of patients with narcolepsy have symptoms of cataplexy. Cataplexy occurs in about two-thirds of narcolepsy patients. The following events may be triggers:
Muscle reflexes are completely absent during a cataplectic attack. Cataplectic attacks can be very minimal and appear as passing weakness or affecting only the eyelids and face. They may, on the other hand, be so severe that they weaken the whole body. In the most severe form of cataplexy, attacks can recur repeatedly for hours or days. Abrupt withdrawal from certain drugs used to treat narcolepsy, notably clomipramine, can trigger this uncommon but troublesome occurrence.
Cataplexy may have the following characteristics:
Atonia. Atonia is a sense of paralysis that occurs between wakefulness and sleep, usually upon waking or sometimes at the onset of sleep. The person is conscious but cannot speak, move (cannot even open the eyes), or breathe deeply. Atonia rarely lasts beyond 20 minutes, but when it first occurs, this experience can be terrifying, particularly if the patient also develops hallucinations.
Hypnagogic Hallucinations. Hypnagogic hallucinations are dreams that intrude on wakefulness, which can cause visual, auditory, or touchable sensations. They occur between waking and sleeping, usually at the onset of sleep, and can also occur about 30 seconds after a cataplectic attack.
Such symptoms may also appear in other sleep disorders and are probably related to extreme sleepiness. In general, cataplexy must also be present for a clear diagnosis of narcolepsy. Some experts believe, however, that some patients with narcolepsy may experience hypnagogic hallucinations and daytime sleepiness and not cataplexy.
Microsleep and Automatic Behavior. In some cases, patients have so-called microsleep episodes, in which they behave automatically without conscious awareness. Such automatic behavior may not be recognized as part of a disorder by either patients or the people around them. Some examples include:
Disturbed Sleep. Nighttime sleep is often disturbed in narcolepsy, but it is usually mild to moderate and does not account for the daytime sleepiness experienced by people with narcolepsy.
Periodic Limb Movement Disorder. Many patients with narcolepsy experience periodic limb movement disorder, also called PLMD (formerly known as nocturnal myoclonus). In PLMD, the leg muscles involuntarily contract every 20 - 40 seconds during sleep, occasionally arousing the patient. The patient is usually unaware of the cause of the interruption.
Most people need about 8 hours of sleep each day. Individual adults differ in the amount of sleep they need to feel well rested, however. (Infants may sleep as many as 16 hours a day.)
The daily cycle of life, which includes sleeping and waking, is called a circadian (meaning "about a day") rhythm, commonly referred to as the biologic clock. Hundreds of bodily functions follow biologic clocks, but sleeping and waking comprise the most prominent circadian rhythm. The sleeping and waking cycle is about 24 hours. (If confined to windowless apartments, with no clocks or other time cues, sleeping and waking as their bodies dictate, humans typically live on slightly longer than 24-hour cycles.) It usually takes the following daily patterns:
In addition, daily rhythms intermesh with other factors that may interfere or change individual patterns:
The response to light signals in the brain is an important key factor in sleep:
Sleep consists of two distinct states that alternate in cycles and reflect differing levels of brain nerve cell activity.
Non-Rapid Eye Movement Sleep (Non-REM). Non-REM sleep is also termed quiet sleep. Non-REM is further subdivided into three stages of progression:
With each descending stage, awakening becomes more difficult. It is not known what governs NonREM sleep in the brain. A balance between certain hormones, particularly growth and stress hormones, may be important for deep sleep.
Rapid Eye-Movement Sleep (REM). REM sleep is termed active sleep. Most vivid dreams occur in REM sleep. REM-sleep brain activity is comparable to that in waking, but the muscles are totally relaxed, possibly preventing people from acting out their dreams. In fact, except for vital organs like lungs and heart, the only muscles not relaxed during REM are the eye muscles. REM sleep may be critical for learning and for day-to-day mood regulation. When people are sleep-deprived, their brains must work harder than when they are well rested.
The REM/Non-REM Cycle. The cycle between quiet (non-REM) and active (REM) sleep generally follows this pattern:
Narcolepsy is a neurological sleep disorder. It is not caused by mental illness or psychological problems. It is most likely the end result of a number of genetic abnormalities that affect specific biologic factors in the brain, coupled with an environmental trigger such as a virus.
Researchers are attempting to come up with a unifying theory involving genetic factors, autoimmunity, and deficiencies in hypocretin, a brain peptide that is important in regulating sleep, particularly REM sleep.
Hypocretin. Hypocretin (also called orexin) is a peptide (small protein) that modulates activity in the hypothalamus (the region in the brain associated with sleep, well-being, and appetite). Hypocretin specifically has properties that promote wakefulness and inhibits REM sleep. Hypocretin may also have other actions that affect feeding behavior and increase activity in the autonomic (sympathetic) nervous system and systems that regulate motor control. Deficiencies in this peptide have been observed in most patients with narcolepsy who also have cataplexy.
Recent autopsy studies have shown a reduced amount of hyprocretin mRNA and hypocretin-positive neurons in patients with narcolepsy with cataplexy. Researchers have postulated that some type of immune response may affect these hypocretin cells.
Deficiencies might set off the following chemical responses that may produce sleep attacks:
Narcolepsy has a genetic component and tends to run in families. Experts estimate that around 8 - 10% of people with narcolepsy have a close relative who has the disorder. The risk for narcolepsy among first-degree relatives (parents or sibling) is 1 - 2%.
However, most experts agree that genetics are not the only factor involved in narcolepsy. Narcolepsy most likely involves a combination of genetics and one or more environmental triggers, such as infection, trauma, hormonal changes, immune system problems, or stress. Researchers are looking for specific genetic mutations that may make individuals susceptible to this disorder, and have discovered recently that most affected individuals carry the HLA-DR15 and HLA-DQ6 gene.
It has been theorized that narcolepsy may be an autoimmune disease, in which the immune system may be tricked into perceiving its own proteins to be antigens. (Antigens are foreign substances targeted for attack by immune factors in the body.)
Important autoimmune diseases include multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, and type 1 diabetes. In such diseases, the immune system overproduces potent factors called cytokines, which cause inflammation and injury in the susceptible cells and tissues affected by the disease. Most autoimmune diseases also tend to afflict those with particular genetically determined molecules of the immune system called human leukocyte antigens (HLAs).
Some research suggests that an immune attack in narcolepsy may occur against cells containing the brain peptide hypocretin (orexin), resulting in deficiencies that are now believed to be major components of the narcolepsy process. HLAs, particularly a subgroup known as (HLA)DQB1-0602, have been strongly associated with narcolepsy and low levels of hypocretin. Narcolepsy patients who carry this HLA group tend to have a specific syndrome of symptoms that include cataplexy and periodic limb movement disorder. However, roughly 20% of people without narcolepsy carry these HLA types.
Narcolepsy affects around 1 in 2,000 people. Experts estimate that around 135,000 - 200,000 Americans have narcolepsy, but the number may be higher. Only about 25% of people who have narcolepsy are actually diagnosed with the disorder. Patients are often mistakenly diagnosed with other conditions, such as psychiatric or emotional problems. Many patients wait decades before receiving a proper diagnosis.
Narcolepsy symptoms usually first appear in adolescence or young adulthood. However, narcolepsy can begin at any age. Growing evidence suggests that the disorder may emerge in early childhood in many patients. It can often be misdiagnosed as another disorder, such as ADHD or depression. People who develop it at a young age often have a family history of the disease and a severe condition, suggesting that genetic factors are important in this group.
Narcolepsy is a life-long problem, but it is not progressive. Symptoms may even lessen over time, but they never completely disappear. In older adults, cataplexy may lessen over time, but sleep disturbances at night may worsen.
Perhaps the most serious consequence of narcolepsy is the high risk for accidents. In one survey, almost 75% of patients with narcolepsy reported falling asleep while driving, and 56% reported nearly having accidents. Other common narcolepsy-related accidents include burns from touching hot objects, cuts from sharp objects, and breaking things.
Some studies report that people with narcolepsy have problems with memory, thinking, and attention. Whether these problems are more likely to be due to tiredness and episodes of sleepiness than to brain abnormalities is not clear.
The patient suffers emotional and social difficulties from the uncontrollable sleep episodes and cataplexy. Studies have reported rates of depression in people with narcolepsy ranging from 30 - 57%. (In the general population, the prevalence of depression is 8%.) Studies have shown severe emotional and social dysfunction in all areas, including work, relationships, and leisure activities. Men with narcolepsy frequently suffer from sexual problems. Some experts believe that the psychological and social effects are more serious than those caused by epilepsy (for which narcolepsy can be mistaken).
Obesity. Evidence suggests that people with narcolepsy are at high risk for obesity compared to the general population. This could be a consequence of low activity level, but research also indicates that deficiencies in the brain peptide hypocretin may play a role in both narcolepsy and eating behaviors, which could increase the risk for obesity.
Although narcolepsy is a physical disorder, doctors are still very likely to misdiagnose patients as having psychological problems. For most patients, narcolepsy is not diagnosed for up to 10 - 15 years after their symptoms first began. To determine specific sleep disorders, the doctor will take a medical and family history and should be told of any medications being taken. The symptoms of narcolepsy are sometimes undeniable if the patient reports all of the major symptoms:
Diagnosis based only on symptoms, however, is often problematic for various reasons:
Levels of hypocretin-1 levels in the cerebrospinal fluid (CSF) may prove valuable in diagnosing difficult cases of narcolepsy in the future, since hypocretin is often absent in patients with the condition.
A doctor may administer certain questionnaires on sleeping habits, such as the Stanford Sleepiness Scale or the Epworth Sleepiness Scale.
The Epworth Sleepiness Scale. The Epworth Sleepiness Scale (ESS) uses a simple questionnaire to measure excessive sleepiness and differentiate it from normal daytime sleepiness.
The Epworth Sleepiness Scale |
Situation |
Chance of Dozing 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing |
Sitting and reading |
(Indicate a score of 0 - 3) |
Watching TV |
(Indicate a score of 0 - 3) |
Sitting inactive in a public place (a theater or a meeting) |
(Indicate a score of 0 - 3) |
As a passenger in a car for an hour without a break |
(Indicate a score of 0 - 3) |
Lying down to rest in the afternoon when circumstances permit |
(Indicate a score of 0 - 3) |
Sitting and talking to someone |
(Indicate a score of 0 - 3) |
Sitting quietly after a lunch without alcohol |
(Indicate a score of 0 - 3) |
In a car, while stopped for a few minutes in traffic |
(Indicate a score of 0 - 3) |
Score Results |
1 - 6: Getting enough sleep 4 - 8: Tends to be sleepy but is average 9 - 15: Very sleepy and should seek medical advice Over 16: Dangerously sleepy |
The multiple sleep latency test (MSLT) uses a machine that measures the time it takes to fall asleep lying in a quiet room during the day. The patient takes 4 or 5 scheduled naps 2 hours apart. People with healthy sleep habits fall asleep in about 10 - 20 minutes. In patients with narcolepsy, polysomnography plus MSLT will show a much shorter duration of time (less than 8 minutes) from wakefulness into sleep. At least 2 of the naps are REM-onset (the active sleep phase associated dreaming). The test has limitations, however. There is no clear definition of exactly which abnormal results would indicate narcolepsy. It is most useful for measuring the severity of the problem. The Epworth Sleepiness Scale may be more accurate in differentiating narcolepsy from normal daytime sleepiness.
An overnight sleep study, called polysomnography, can be a valuable means for determining the basic cause of sleepiness. The patient arrives at the sleep center about 2 hours before bedtime without having made any changes in daily habits. The patient will be monitored by a variety of devices while sleeping:
These instruments record activity as the patient passes, or fails to pass, through the various sleep stages.
Ruling out Other Sleep Disorders . Other sleep disorders can share some or all of the symptoms of narcolepsy:
Ruling out Psychologic Disorders. In one study, 40% of patients who actually had narcolepsy had been diagnosed incorrectly with some psychological or psychiatric problem. Certainly, patients with narcolepsy have emotional difficulties because of the condition, and it is often difficult, particularly for a nonspecialist, to detect the physical problem. Even worse, hypnagogic hallucinations may result in diagnoses of schizophrenia or bipolar disorder, which are treated with potent antipsychotic drugs that have severe side effects and are useless for narcolepsy.
Ruling out Epilepsy. Narcolepsy can easily be mistaken for epilepsy, a group of disorders that cause seizures. Case studies have reported a misdiagnosis of epilepsy in patients who were actually experiencing cataplexy and sleep paralysis.
Other Causes of Persistent Fatigue. A number of conditions can cause persistent fatigue and should be ruled, including:
These conditions may also worsen sleep paralysis in narcolepsy. Narcolepsy sleep paralysis usually occurs at the onset of sleep and is chronic.
Neuroimaging techniques may be used in a research setting to confirm sleep physiological theories in humans and to discover new information about the neurobiological aspects of sleep, dreams, and memory. Few neuroimaging studies have focused on patients with sleep disorders such as narcolepsy.
Lifestyle treatment of narcolepsy includes taking three or more scheduled sleep-times/naps throughout the day. Patients should also avoid heavy meals and alcohol, which can interfere with sleep.
People with mild narcolepsy symptoms who do not need medication may be able to maintain alertness with sleep scheduling. The role of scheduled naps for patients who are responding to medications for narcolepsy remains unclear.
Medications for narcolepsy target the major symptoms of sleepiness and cataplexy. Stimulant drugs are used to manage excessive daytime sleepiness while antidepressants and other compounds address cataplectic symptoms. The FDA has approved two drugs specifically for the treatment of narcolepsy. They are now the first-line treatments:
Modafinil . Modafinil (Provigil) is a drug used to treat the excessive sleepiness associated with narcolepsy and other sleep disorders. It has largely replaced methylphenidate (Ritalin) and other stimulants for treatment of narcolepsy sleepiness. Patients who switch to modafinil from stimulants such as methylphenidate have few problems if they gradually taper off the stimulant dose.
Modafinil helps patients with narcolepsy stay awake during the day. While only some experience normal wake times, patients taking modafinil often have up to a 50% improvement in the ability to stay awake, as well as a 25% reduction in the number of involuntary sleep episodes. It has not been proven to be safe in pregnant women and the risks and benefits should be weighed.
Some of modafinil's additional benefits include what it does not do:
Side effects may include:
Drug Warning
In October 2007, the FDA added new safety information to the prescribing label of modafinil (Provigil) and Armodafinil (Nuvigil). The new information warns that:
A newer drug, armodafinil (NuVigil), which is nearly identical to modafinil, is also approved for treatment of narcolepsy-associated excessive sleepiness. In clinical trials comparing it with placebo, armodafinil improved wakefulness, memory, attention, and fatigue in patients with narcolepsy.
Stimulants . Medications that act as stimulants are standard treatments for narcolepsy. They include:
Methylphenidate and dextroamphetamine last for 2 - 5 hours and used to be the standard drugs for excessive daytime sleepiness. These drugs are useful for people who can manage wakefulness with a night's sleep and scheduled naps. They can improve mood, mental acuity, and other aspects of mental functioning. However, the evidence to support their benefit for patients with narcolepsy is not a strong as with modafinil.
Stimulants can have unpleasant side effects, including:
People with heart disease, hyperthyroidism, glaucoma, anxiety disorder, and high blood pressure should avoid stimulants, or take them only with a doctor's supervision.
These drugs become ineffective if used continuously, and patients are advised to take a drug holiday one day a week or to withdraw gradually and resume treatment at a lower dose. Patients should not engage in activities that require being awake (such as driving) during withdrawal.
Sodium oxybate (Xyrem). Sodium oxybate (Xyrem), also referred to as gamma hydroxybutyrate (GHB), helps reduce the frequency of cataplexy attacks and improve daytime sleepiness. It takes about 4 weeks for significant benefits, which reach their peak at about 8 weeks. Food intake can affect it, so patients are advised to take it at a regular time after the evening meal.
The FDA has placed tight restrictions on the use of this drug. Although the drug appears to be effective and safe when used for narcolepsy, it has a history of illegal and "date-rape" use, with street names such as "Grievous Bodily Harm" or "Liquid Ecstasy." (The last term is not the same as "Ecstasy," another street drug with different effects.) In high doses, it can cause dependence over time.Education through the Xyrem Success Program may be valuable to patients and physicians.
Very serious side effects -- including seizures, coma, respiratory arrest, and death -- have been reported in people who abused GHB. Trials of Xyrem, however, have not reported these effects with the doses used in treatment for cataplexy.
Antidepressants . Antidepressant drugs are not approved for treatment of cataplexy, but they are commonly used to manage this condition. Unfortunately, there have been few studies conducted on antidepressant treatment of cataplexy, and there are little data on which type of antidepressant work bests. A 2008 review of antidepressants for narcolepsy noted the lack of good quality evidence to support their use and urged for more clinical trials.
Antidepressants used for cataplexy, hallucinations, sleep paralysis, and management of REM symptoms include:
Tricyclics were the first antidepressants used for cataplexy; they were also one of the first treatments for cataplexy. They can be helpful for some patients but have many unpleasant side effects, including dry mouth, constipation, and weight gain. Tricyclics can also lower blood pressure and cause disturbances in heart rhythm.
SSRIs have fewer side effects than tricyclics but may not work as well for cataplexy control. The most common side effects include nausea, drowsiness or insomnia, headache, weight gain, and sexual dysfunction.
Venlafaxine (Effexor) is a selective serotonin and norepinephrine reuptake inhibitor (SSNRI) that has shown promising results for treatment of cataplexy. Some patients with narcolepsy, and their doctors, report that venlafaxine seems to work best of all the antidepressants.
Monoamine Oxidase Inhibitors (MAOIs). Selegiline (Eldepryl, Movergan), also known as deprenyl, is an MAOI that blocks monoamine oxidase B, an enzyme that degrades dopamine. MAOIs may play a role in narcolepsy, but how much benefit this group of drugs provides is not well proven.
Selegiline has significant side effects:
Dang-Vu TT, Desseilles M, Petit D, Mazza S, Montplaisir J, Maquet P. Neuroimaging in sleep medicine. Sleep Med . 2007;8:349-372.
Dauvilliers Y, Arnulf I, Mignot E. Narcolepsy with cataplexy. Lancet. 2007 Feb 10;369(9560):499-511.
Dodel R, Peter H, Spottke A, et al. Health-related quality of life in patients with narcolepsy. Sleep Med . 2007 Nov;8(7-8):733-41. Epub 2007 May 18.
Durmer, J. Narcolepsy. Instant diagnosis and treatment. In: Ferri FF, ed. Ferri's Clinical Advisor 2009. 1st ed. Philadelphia, Pa: Mosby Elsevier; 2009.
Harsh JR, Hayduk R, Rosenberg R, Wesnes KA, Walsh JK, Arora S, et al. The efficacy and safety of armodafinil as treatment for adults with excessive sleepiness associated with narcolepsy. Curr Med Res Opin . 2006;22(4):761-774.
Luc ME, Gupta A, Birnberg JM, Reddick D, Kohrman MH. Characterization of symptoms of sleep disorders in children with headache. Pediatr Neurol . 2006;34(1):7-12.
Mahowald, M. Disorders of sleep: Specific Sleep Disorders. In: Goldman L, Ausiello D, eds. Cecil Medicine . 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 429.
Morgenthaler TI, Kapur VK, Brown T, Swick TJ, Alessi C, Aurora RN, et al. Practice parameters for the treatment of narcolepsy and other hypersomnias of central origin. Sleep . 2007 Dec 1;30(12):1705-11.
Owens, J. Sleep medicine. In: Kliegman: Nelson Textbook of Pediatrics . 18th ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 18.
Pagel JF. Excessive daytime seepiness. American Family Physician . 2009;79(5).
Thorpy MJ. Cataplexy associated with narcolepsy: epidemiology, pathophysiology and management. CNS Drugs . 2006;20(1):43-50.
Vignatelli L, D'Alessandro R, Candelise L. Antidepressant drugs for narcolepsy. Cochrane Database Syst Rev . 2008;(1):CD003724.
Xyrem International Study Group. Further evidence supporting the use of sodium oxybate for the treatment of cataplexy: a double-blind, placebo-controlled study in 228 patients. Sleep Med. 2005 Sep;6(5):415-421.


text:
RESPLENDENT GROTESQUECodeTech/Extreme Prog Metal4.32 | 12 ratings |
From Progarchives.com, the ultimate progressive rock music website
Special Collaborator Honorary Collaborator |
"Resplendent Grotesque" is the 2nd full-length studio album by Norwegian/English black metal act Code. The
album was released through Tabu Recordings in June 2009. In the years between the band's debut full-length studio
album "Nouveau Gloaming (2005)" and "Resplendent Grotesque", lead vocalist Kvohst and bassist
Viper (aka Vicotnik) busied themselves with the recording of D'dheimsgard's 4th full-length studio
album "Supervillain Outcast (2007)". ...and there are many similarities between the two projects. Most prominently the distinct sounding lead vocals by Kvohst. His aggressive raspy vocals are caustic as ever, but it's his soaring clean vocals and vocal melodies that stand out the most. Another thing the two projects have in common are the elegant use of dissonance in their music. The music on "Resplendent Grotesque" is not quite as progressive nor is it as adventurous as the music on "Supervillain Outcast (2007)" though. The music on "Resplendent Grotesque" is relatively simple in structure even though the band often incorporate the odd progressive section to keep things interesting. It is Kvohst's vocals and strong voice, that makes all the difference here though. He is such a skilled and distinct sounding vocalist. The band are very well playing and the powerful and clear sound production suits the music well. While the tracks are well composed it's only a few that really stand out and about half of the tracks on the album could have been a bit more memorable. They are still great tracks, but I just feel they could have been better. Some of the tracks that stand out are "Smother the Crones", "In the Privacy of Your Own Bones", "The Rattle of Black Teeth" and "Jesus Fever". While "Resplendent Grotesque" isn't a consistently excellent release, it's still a high quality album for fans of the more twisted and slightly progressive part of the black metal spectrum (acts like Void, Ved Buens Ende and especially D'dheimsgard come to mind) and a 3.5 - 4 star (75%) rating is fully deserved.
4/5 |
MEMBERS LOGIN ZONEAs a registered member (register here if not), you can post rating/reviews (& edit later), comments reviews and submit new albums. You are not logged, please complete authentication before continuing (use forum credentials). |


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Factors Contributing To Attention Deficit Hyperactivity Disorder Biology Essay
Published: Last Edited:
This essay has been submitted by a student. This is not an example of the work written by our professional essay writers.
The symptoms of both types of ADHD. At least two areas from either type need to be observed for 6 months in children under the age of seven for diagnosis to be made. If symptoms are seen from both types, the diagnosis of the combined type is made. (Information adapted from Dunn and Kronenberger, 2003)
Attention Deficit Hyperactivity Disorder (ADHD) is a genetically transmitted neurological disorder which affects 5.3% of children and adolescents worldwide (Polanczykv et al, 2007). Although the onset and diagnosis usually occurs in children before the age of seven, it is also diagnosed in adults. Many children with ADHD lose their symptoms as they get older although some do suffer from the disorder as adults. A person with ADHD may be predominantly hyperactive and impulsive (Hyperactive-Impulsive Type), they may be predominantly inattentive (Inattentive Type) or they may suffer from a combination of both (Combined Type) (McFadden et al, 2005). The typical symptoms of each type are shown in Table 1. In 2009, the National Collaborating Centre for mental health defined impulsivity as having premature and thoughtless actions, hyperactivity as a restless and excess movement and inattention as a disorganised style preventing sustained effort. Although from time to time, these actions are probably seen in all children and adults, patients with ADHD will persistently be showing these characteristics and have no control of them.
Inattentive Type
Hyperactive-Impulsive Type
Difficulty concentrating
Easily distracted
Makes careless mistakes
Cannot complete a task
Cannot follow instructions
Has poor organisation
Loses and misplaces things
Cannot sit in a seat
Running instead of walking
Excessive talking
Interrupts conversations
Shouts out answers to questions
Always loud or noisy
Cannot wait
Constantly 'on the go'
Genetic Causes
Although a definite cause of ADHD is yet to be found, it is for certain that there is a genetic link between ADHD as it is passed on through generations in a family. Twin studies have shown that genetic factors make up between 60% to 94% contribution to ADHD (Hudziak et al 2005). These studies, which compared monozygotic and dizygotic twins showed that if one of the monozygotic twin had ADHD, the chances of the co- twin also having ADHD is much greater than with dizygotic twins. This shows that because the twins are likely to be exposed to a similar environment, the cause of ADHD must have genetic relevance. There have several genes identified which may contribute to ADHD and they can be found in a range of chromosome and affect a range of different chemical systems in the body. The most commonly explored genetic defects are in the dopaminergic systems, with dopamine receptors and transporter genes most commonly associated. Also identified are links to the noradrenaline systems, with defects in genes such as the dopamine β hydroxylase gene, the adrenergic receptor genes and the monoamine oxidase A gene, althought there are many others. Some serotonin genes have also been implicated with ADHD (Comings, 2001).
Dopamine is the one of the principle neurotransmitters in the brain and it is important is modulating feelings such as motivation and reward, and is also important in regulation of voluntary movement, sleep, working memory, learning and attention. These functions are often impaired in sufferers of ADHD and are therefore seen as a good target for medical intervention. Many of the drug therapies for ADHD cause the release of dopamine into the brain, such as methylphenidate and amphetamines. These stimulants act by inhibiting the dopamine transporter, which results in an increase in the extracellular concentration of dopamine in the brain (Gozal and Molfese, 2005). The short term of efficiency of these drugs in reducing the hyperactivity and impulsivity of ADHD patients reflects that the lack of or insensitivity to dopamine must play a role in causing ADHD. Studies which explore the genetics of ADHD have consistently revealed that polymorphisms in the DRD4 receptor subtype gene and the dopamine transporter gene are to some extent responsible for ADHD and these will be explored here.
Dopamine Receptor type 4 (DRD4)
There are 5 different subtypes of dopamine receptors. Of these the type 4 receptor and its genotype is of particular interest for looking at causes of ADHD. The DRD4 receptors are found primarily in GABAergic interneurons in the forebrain structures of the cerebral cortex and hippocampus, although not in the striatum. In a healthy person, activation of DRD4 by dopamine prevents the inhibitory affects of GABA, allowing the pyramidal neurons to function. As DRD4 is a G protein coupled receptor, the inhibition mechanism is due to the inhibition of the enzyme adenylyl cyclase, resulting in a decrease in the production of cAMP (Brennan & Arnsten, 2008). The cerebral cortex and the hippocampus are related to advanced cognitive function, suggesting that a defect in this system contributes to the symptoms seen in ADHD (Spruston, 2008)
The gene that codes for this protein is located on chromosome 11p15.5 in humans (Krämer et al., 2009) and is characterised by a polymorphism which has occurred in exon III with a 48 base pair VNTR. There can be between two to seven repeats of the allele creating a varying size of the third intracellular loop of the GPCR which is important in the intracellular signalling role of the receptor (Grady et al., 2005). Although the evidence of this is disputed between scientists, many experiments have suggested that the seven repeat allele is over expressed in children with ADHD. The 7 repeat allele is less common than the two repeat allele and it is also less potent at inhibiting the production of cAMP (Krämer et al., 2009) when activated, leading to a decrease in pyramidal cell firing due to the lack of inhibition of GABA (Brennan and Arnsten, 2008). This need to link to ADHD
Figure 1. DRD4 Receptor subtypes. Each shaded box is a sequence of 16 conserved amino acids encoded by the polymorphic 48 base pairs. The 2 repeat (a), 4 repeat (b) and 7 repeat (c) are shown. The 7 repeat allele has been seen predominantly in people with ADHD. The number of shaded boxes represents the number of repeats. Here polymorphism in the coding region causes a considerable difference in the structure of the receptor. (adapted from Grady et al., 2005)
This allele has also shown geographical difference as it is less commonly observed in South Asian children (0-2%) but very prevalent in native South Americans (78%) (Nikolaidis and Gray, 2010). This may account for the differences in prevalence of ADHD across the world.
The DRD4 7 repeat allele has been shown to impact upon the time course of ADHD as with time, many patients with ADHD gradually begin to see a decrease in the number and severity of their symptoms, whilst others do see their ADHD characteristic persist into adulthood. ADHD patients who do not have the DRD4 7 repeat allele have a greater reduction in their symptoms with time, compared to those who do bear the DRD4 7 repeat allele (Langley, 2008).
Dopamine Transporter (DAT1)
The dopamine transporter is a protein with twelve transmembrane domains (Lin and Uhl, 2003) in the membranes of axons and presynaptic terminals of neurones in the brain which rapidly reuptakes the dopamine released into the synapse, into the presynaptic terminal in order to terminate the dopamine signal (Zhang et al 2009). This process, often known as dopamine clearance, decreases the amount of dopamine available in the extracellular space. The transporter is usually found in the striatum, which is located in the inner part of the forebrain and is divided into putamen and caudate nucleus by white matter. People with ADHD may have higher levels of DAT1 in their striatum, particularly in the caudate region (Shook, 2011) and hence a higher rate of dopamine clearance, leading to a decrease in the amount of dopamine available to carry out its signalling role (Larisch et al, 2006). Inhibiting this transporter, as occurs by taking the drug methylphenidate, allows the accumulation of extracellular dopamine which may help to restore some of the defects caused from ADHD.
The gene coding for the dopamine transporter (DAT1) has been studied greatly for polymorphisms and mutations which may have caused or contributed to the development of ADHD in individuals. The 15 exon gene is located on chromosome 5 (5p15.3) (Grady et al, 2005). The gene has a number of polymorphism in the form of variable number tandem repeats (VNTR) within a 40 base pair untranslated region at the 3' end of the gene (3' UTR), coded for by exon 15 (Bellgrove et al., 2005). Any variation that occur in the 3' UTR will not affect the transcription of the DNA to the mRNA, as the essential sequence for this should remain unchanged, though there will be an impact upon the transport of the mRNA from the nucleus to the cytosol where it will be translated to the polypeptide sequence making up the transporter. There may also be an adverse effect upon the stability and degradation of the mRNA and this will cause a change in the translation of the protein (Lahey et al., 2011).
A mutation within the coding sequence of the DAT1 causing a single change in an amino acid coding for DAT1 can significantly alter the ability of the transporter to locate its site of action in the plasma membrane and transport dopamine effectively (Lin and Uhl, 2003). The lack of dopamine reaching its site of action is likely to results in the behavioural abnormalities characterised by ADHD.
There is no difference in the alleles for the DRD4 or DAT1, between children diagnosed with the Inattentive Type or the Hyperactive-Impulsive Type of ADHD (Grizenko et al., 2010)
Research on the linkage between the dopamine transporter (DAT1) and ADHD have been varied with some investigations providing some evidence to suggest that there is relation, but on the other hand many studies have failed to provide any verification (Hawi et al, 2010).
Environmental Causes of ADHD
The environmental causes of ADHD may be divided into three categories, which relate to the time the causes take place. These are pre-natal (before birth), peri-natal (from the 20th week of gestation to four weeks after birth) and post natal (after birth and into childhood). Pre-natal causes tend to relate to maternal life style which affects the developing foetus, rendering it more susceptible to ADHD. There have been studies which have provided strong correlation between maternal smoking and alcoholism and the incidence of ADHD in their offspring. The mother's diet is an essential contributor as the foetus depends on nutrients from its mother for its development and if a lack of these can results in growth abnormalities.
Peri-natal traumas such as premature birth have the implications of underdeveloped organs and systems in the body, which may not be able to develop fully unless the correct procedures are carried out by medical staff in sufficient time. Often, immature lungs and inefficient breathing by the baby can lead to hypoxia, resulting in brain damage in areas of the brain related to cognitive functions which are impaired in ADHD, as well as other areas of the brain and other organs and tissues in the body. Peri-natal factors can also include any infections caught at this time by the mother such as measles or rubella, or by the child such as meningitis.
There are numerous theories and myths which surround the causes of ADHD after birth, especially as people's life experiences vary dramatically, depending upon where they live and their conditions. Toxins from the environment such as lead, which can be abundant in water and soils, have been proven to cause ADHD due to their roles in disrupting the circulation of dopamine. Polychlorinated biphenyl (PCB) exposure causes a reduction in the dopamine levels in the prefrontal cortex and the striatum. The dopamine transporter is affected, resulting in altered synaptic and cytosolic dopamine clearance (Eubig et al, 2010). PCBs have also been shown to affect thyroid function (Mill and Petronis, 2008).
ADHD and Thyroid Function
Thyroid hormones are essential for the growth and development of the foetus and as a child. Thyroid hormones have various roles with a primary role in metabolism. Deficiencies in thyroid levels have shown to cause underdevelopment of the central nervous system, with defects particularly in attention, motor function and memory.
Mother's who suffered from a mild iodine deficiency during pregnancy are more likely to have children with ADHD (Vermiglio et al., 2004). The iodine deficiency is passed on to foetus, resulting in symptoms similar to that of Generalised Resistance to Thyroid Hormone (GRTH).
Generalised Resistance to Thyroid Hormone (GRTH) is characterised by increased serum levels of (triodthyronine) T3 and T4 (thyroxine) and increased thyrotropin concentrations. The pituitary gland and the peripheral tissues are less responsive to the actions of thyroid hormone. The disease arises from a mutation that occurs in the gene encoding the thyroid receptor β which is found on chromosome 3. The mutation occurs in the hormone binding domain of the receptor; hence T3 has a lower affinity for the receptor. There have been 30 mutations found in exons 9 and 10 and only one of the two alleles needs to be affected by the mutation to give rise to the disease. This is to say, the abnormal gene is autosomal dominant and is inherited if even one parent suffers from the GRTH. (Hauser et al., 1993)
The mutation is thought to cause inhibitory effects of the action of T3 in several ways. The mutant receptor may heterodimerise with wild type receptors, which are formed from the transcription and translation of the unaffected allele, causing the combinatory receptor to become inactivated. Competition may arise between the mutant receptor and the wild type receptor for a necessary cofactor needed for its function (Melmed & Conn, 2005). This results in a dominant negative phenotype which is thought to down-regulate catecholamine function (Hauser et al., 1993). It is possible for some mutated receptors to become functional is the presence of a high concentration of T3. (Melmed & Conn, 2005)
Thyroid hormone has a crucial role in neuronal development. The thyroid receptors become more predominant between 10 to 16 weeks of foetal development, when the neuroblasts are also proliferating. Experiments carried out in rats showed that activation of the thyroid receptor and interactions with the thyroid response element regulates the expression of myelin basic protein. T3 regulates brain cell proliferation in neonatal rats but not adult rats. These experiments indicate that thyroid hormones play a key role in brain development mechanisms such as cell proliferation, axonal routing and regulation of gene expression which are impaired by mutations in the receptor. (Hauser et al., 1993)
An investigation was conducted by Vermiglio et al. (2004) to see if iodine deficiency in women during pregnancy results in children with ADHD. Almost 70% of the children developed ADHD. Some of the mother's became hypothyroxinaemic (they had low circulating levels of free T4 and thyroid hormone) during the pregnancy, of which nearly 65% had offspring with ADHD. T4 provided from the mother's circulation is essential for foetal growth and development until it is able to produce and secrete its own thyroid hormones from the thyroid gland at the 20th week of gestation. Iodine deficiency is fairly common in all parts of the world, including developed countries, and if identified early (before the 24th week of gestation), administration of iodine or thyroid hormones to the mother may be able to reverse any damage caused to foetus, thereby reducing the risk of the offspring developing ADHD.
Nicotine and ADHD
Exposure to nicotine in utero via maternal smoking has been associated with ADHD. Nicotine can easily cross the placenta and the concentration in the foetus can be up to 15% higher than in the mother. Nicotine causes the constriction of uterine arteries, leading to decreased oxygen and nutrient flow to the foetus (Nomura et al., 2010). As a result of this the developing foetus will suffer from intrauterine growth retardation, and hence a small birth weight, which has also been associated as a cause ADHD.
In 2003, Kahn et al. conducted a study to investigate the affect that maternal smoking during pregnancy has on the dopamine transporter genotype of the child, and how this correlates with the symptoms of ADHD. They found that prenatal nicotine exposure modifies how the genetic polymorphism of the DAT1 gene is likely to impact upon hyperactivity, as it has been shown that the 10 repeat polymorphism of DAT1 does not necessarily lead to ADHD and not everyone with ADHD have the polymorphism. Those that are homozygous for the 10 repeat allele of DAT1 were shown to have an increased risk of hyperactivity-impulsivity. The 10 repeat allele consists of 480 base pairs, although some studies have shown that the 440 base pair allele is also associated with ADHD, in particular when relating to nicotine exposure (Neuman et al., 2007).
Nicotinic acetylcholine receptors are abundant, and exposure to nicotine causes an increase in the number of these receptors. They have very high affinity for nicotine in neurons of the striatum and cerebral cortex and stimulation of these receptors results in increased dopamine release from the synapses, which . Nicotine also stimulates the dopamine D2 receptor family (of which DRD4 is a subtype), altering the outgrowth and branching of the developing neurons (Neuman et al., 2007). Although it had been seen that children with ADHD have insufficiently released dopamine, pre-natal increase in dopamine can affect the development of the dopaminergic system. The brain damage caused by this may result in the behavioural characteristics of ADHD.
Studies conducted on this topic have varied with some studies showing evidence that children whose mother's smoked during pregnancy have double the risk of developing ADHD. Some studies have correlated maternal smoking with ADHD-like symptoms such as aggressive and disruptive behaviour and academic achievement problem. On the other hand, many studies have found that there is no significant relationship between maternal smoking and the offspring developing ADHD. There have been several explanations, which include the difficulty of obtaining a large sample size for the investigations. (Ball et al., 2010)
DAT1 and DRD4 genetic variations can modify frontostriatal (which includes the basal ganglia and dorsolateral prefrontal cortex) gray matter volumes (Neuman et al., 2007). Nicotine causes an increase in the number of nicotine receptors, which enhances the amphetamine induced release of dopamine from DAT1 in the prefrontal cortex of rats.
Pesticides and ADHD
A US study by Bouchard et al. (2010), has identified that organophosphate metabolites which are found in pesticides used to grow fruit and vegetable increases the likeliness of developing ADHD. They measured the urinary concentration of dimethyl alkyphosphate (DMAP), a metabolite of the organophosphate pesticide, to indicate the level of pesticide exposure and to compare this with the prevalence of ADHD. The study was conducted on children between the ages of 8 and 15 and children are more vulnerable to the affects of the pesticides as they are still developing. The organophosphates are thought to contribute to ADHD as it inhibits acetylcholinesterase leading to a disruption in the cholinergic signalling pathway. Even at very low doses, the organophosphates can affect neuronal development and neurotransmitter targeting, which has been has been shown to cause cognitive defects and hyperactivity in animals.
In 1942, Conrad Waddington coined the term epigenetics and defined it as "the branch of biology which studies the causal interaction between genes and their products, which bring the phenotype into being" (McVittie, 2006). In other words, genes can be seen as switches, and chemical modulators and environmental factors can control when and whether or not the gene is expressed. DNA methylation and histone modification are common ways in which gene expression is regulated in an epigenetic manner. A study by Mill and Petronis (2008) looked in particularly at methylation at the fifth position of cytosine residues, where they occur adjacent to guanine residues (CpG sites). Methylation occurs in promoters where there is a high concentration of CpG (CpG islands), thus preventing the binding of transcription factors and attracting methyl binding proteins which cause chromatin condensation. This mechanism prevents the transcription of the gene, and consequently the translation and production of the encoded protein.
The genome of the developing embryo/foetus is more susceptible to epigenetic influences than after birth as, DNA is being synthesised more rapidly during embryogenesis so any environmental change that affects the DNA in one cells can be transmitted to a large proportion of dividing cells. On the other hand, any epigenetic changes that affect the genome after birth are not as likely to be widely incorporated into other cells as the rate of DNA synthesis is slower. (Mill and Petronis, 2008) It is for this reason that the maternal environment, conditions, diet and lifestyle are critical in the development of her offspring.
In order for DNA methylation to take place, methyl donors are required. The methylation of the DNA cytosine residues is carried out by S-adenosylmethionine (SAM) using DNA methyltransferases as a catalyst. SAM needs a methyl donor to become activated and these are often obtained from the diet through vitamins B12, B6 and B2 as wells as folate, methionine and choline. Folate and vitamin B12 are often given supplementary to pregnant vitamin as deficiencies in these can have adverse effects on the development of the central nervous systems of the foetus and has been shown to cause behavioural abnormalities. Folate is essential for the expression of DNA methytransferase, without which, methylation cannot take place, leading to the silencing of certain areas of the genome. (Mill and Petronis, 2008)
With polymorphism is genomes, epigenetic mechanisms can work to either alter the response made by a particular protein as a result of the environmental stimulus, or DNA methylation may influence the expression of the polymorphic gene.
Figure 2. Prenatal and postnatal differences in epigenetic mediation. The filled black circles represent points in the DNA that can be targeted by DNA methylation. Epigenetic regions are not sully established in developing embryos, rendering the DNA more susceptible to epigenetic changes. This in turn leads to changes in gene expression, and hence phenotype. Once DNA synthesis has slowed and epigenetic sites have been established, environmental adversities cannot have a substantial effect. Adapted from Mill and Petronis, (2008)
There is a reduction in the volume of the caudate in subjects with ADHD than controls, which included unaffected siblings (Shook et al., 2011- LOOK HERE AGAIN FOR IMAGE).
"ADHD is characterized by a slightly smaller (by 4%) total brain volume (both white and gray matter), abnormalities of the basal ganglia and a 15% decrease in the volume of decrease in volume of a restricted region of the posterior cerebellum." "suggested causes include brain damage, encephalitis, genetics, food allergies, high lead concentrations and various home and school environments" unlikely to be a single cause. Ritalin is a stimulant which allows a person to concentrate on the task at hand and may have a general affect of sedating children" (Kolb and Whishaw, 2003)
Children who are born with lower than average birth weight have a reduced total brain volume if they were born at the normal gestational period. Children who were born prematurely and had a low birth weight had a significantly smaller absolute cortical gray matter volume and smaller overall total brain volume (Heinonen et al., 2010)
Pre-natal Factor
Premature babies are more likely to suffer from ADHD as they are more likely to have suffered from hypoxia and low blood pressure in the womb. Tests conducted in animals have shown that this causes an increase in the number in dopamine receptors in the brain (Khamsi, 2006).
Heinonen et al. (2010) conducted a study comparing the behavioural symptoms of ADHD in children who were born small for their gestational age (SGA) or appropriate for gestational age (AGA). They found that children born SGA suffered three times more ADHD symptoms that children born AGA. SGA infants may have been born prematurely or at full term.
Post-natal factors
In an experiment conducted in adult rats, which were separated from their mother's for 6 hours a day, as a form a childhood stress, it was found that these rats had
There have been numerous studies conducted which explore the connection between the genetic defects associated with ADHD and its symptoms however there results are contrasting in many situations and can be attributed to a number of factors. For instance small sample sizes used of the scarcity of there being homozygotes of the affected allele.
ADHD has been linked to drug abuse and obesity as the intake of excess foods and drugs is related to the feeling of reward. As people with ADHD have dysfunctional dopamine regulation, which is is involved in the feeling of reward, they are more inclined to take up other methods of rewarding themselves, that is causing further damage to their health.


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Inspired by logcolorizer, colorlog, acl, colorgcc, colortail, and others, Generic Colouriser can be used to colourise any files or outputs of commands. It's written in python and configurable via regular expressions.
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Congenital central hypoventilation syndrome ore CCHS is an extremely rare condition. Some consider it to be one of the most horrific condition a human being could ever suffer from. The reason is that each and every time you fall asleep could be your last. The condition refers to a sudden stop of all respiratory functions while a person is deep asleep. More simply put the brain just forgets to tell the lungs to breathe.
Another famous appellation of the congenital central hypoventilation syndrome is Ondine's curse. It's derives from the ancient German folklore. It was when the famous nymph Ondine falls deeply in love in a mere mortal man. When the mortal man cheats on his beloved nymph he gets cursed by the king of the nymphs. The curse makes the mortal having to remember all important bodily functions. But when he falls asleep he forget.


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