Lionsgate Exec Details Expanding Role Of The Hunger Games Adventures Facebook Game
Director Gary Ross' film adaptation of Suzanne Collins' bestselling The Hunger Games novel has already broken Hollywood box office records in its opening weekend ($152.5 million). Now Lionsgate is about to unleash an even deeper experience based on both the novel and the film with The Hunger Games Adventures Facebook game.
As part of the Hollywood studio's "fan first" marketing approach, only fans of the film (through fan Websites) have been able to play the free to play social game over the past few weeks. On March 30, the beta for the Facebook game opens up to the general public. Once Facebook's 800 million users have access to this mainstream focused game, this franchise could break even more records.
David Hayes, vice president of digital marketing at Lionsgate, said Collins has worked closely with game developer Funtactix on this brand new extension of the universe she's created. While the books flesh out the world in vivid detail and the movies take another slant on the material, the game goes beyond both of those experiences and delivers new quests, new characters and allows fans to create new avatars and explore all of the districts from the universe.
"This game is an opportunity for fans to experience this world beyond the books and the movie," said Hayes. "The game plays an important role in allowing us to bridge the time period between the DVD and Blu ray releases and the theatrical release of Catching Fire."
Fans of the books and movie have long been speculating which States line up with the districts in the fiction. Panem is a post Apocalyptic North America. And the official launch of the full Facebook game in the near future (not the beta launch) will reveal the official locations of each district on a North American map.
"There are so many amazing opportunities and plans for this game," said Hayes. "A great example of how we can amplify the marketing through this game is the official map. This is something that fans have wanted to see for a year and a half. There are hundreds of fan maps that have been created, but there's only one official map from Suzanne and this game will reveal that over time."
Lionsgate has been connecting the film world with the game world already. A teaser trailer for the film debuted this week in the game. And March 30 marks the unveiling of an exclusive clip from the movie. Earlier this week, players were able to unlock an exclusive track, "Rue's Song," performed by Sting. Hayes said these types of exclusives aren't hidden and are easily available for players to enjoy. More of these types of in game rewards will be released on a regular basis.
In addition, the developer will release new quests and content on a weekly basis. And when the official game releases, additional Districts will be available for exploration. The current beta features District 12, home of Katniss Everdeen (played by Jennifer Lawrence in the film). Players will work closely with Katniss, who appears as a stylized 2 version of Lawrence from the film. Other central characters from the film will also play roles in the Facebook game, including Gale Hawthorne (played by Liam Hemsworth in the film) and Peeta Mellark (played by Josh Hutcherson in the movie).
"What people will begin to see is an almost surreal ability for The Hunger Games Adventures to mirror the next film or next phase of the marketing campaign," said Hayes. "This game is 100 percent not about letting people fight in The Hunger Games arena. It takes people beyond that and it's really a testament to how rich this universe is. It's a huge, sprawling social game experience."
Fans of the film will also have another free game option on iOS devices. The Hunger Games: Girl on Fire for iPhone and iPad was developed by acclaimed mobile game developers Adam Saltsman, Mark Johns and Paul Veer. Hayes said this game's Bernie Parent Authentic Jersey narrative is a prologue to the book and has Katniss running through the forest trying to avoid deadly Tracker Jackers sent by the Capital.
Lionsgate is hitting two for two with its game offerings. The mobile game offers a cool retro sidescrolling action experience through District 12 that's simple and Erik Karlsson Jersey fun to play. This contrasts nicely with the 2 adventure game experience of the Facebook game, which offers MMO light gaming and the ability to interact with other fans.
Rather than trying to rush a console game out the door with the first film (three more movies are in the works), Lionsgate has focused on a Facebook game that will allow for continual updates and a mobile game that anyone can access maybe www.officialhockeyauthentic.com/womens-youth-bernie-parent-authentic-jersey-c-1_350_352.html even while waiting in line to catch the movie again.
I've been covering the video game space for 20 years for outlets like The Washington Post, Reuters, CNET, AOL, Wired Magazine, Yahoo!, Entertainment Weekly, NBC, Variety, Maxim, EGM, and ESPN. I www.officialhockeyauthentic.com/womens-youth-erik-karlsson-authentic-jersey-c-1_340_349.html also cover games for outlets like The Hollywood Reporter, IGN, Geek Monthly, CNN, DigitalTrends and PrimaGames.
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Frontotemporal dementia produces selective brain atrophy involving the frontal www.officialhockeyauthentic.com/womens-youth-chris-kreider-authentic-jersey-c-1_283_706.html and temporal lobes, requiring brain magnetic resonance imaging for accurate diagnosis
Clinically, these diseases present chiefly as progressive aphasia or as disintegration of personality and behaviour that may be misdiagnosed as a psychiatric disorder
Treatment remains supportive, but patients and families need extensive counselling, future planning, and involvement of social and mental health services
Frontotemporal dementia (FTD) is a clinically and pathologically heterogeneous group of non Alzheimer dementias characterised collectively by relatively selective, progressive atrophy involving the frontal or temporal lobes, or both.1 2 3 4 Cases of FTD have been described since the late 19th century, initially most comprehensively by Arnold Pick, who lent his name to the historical designation of the entire FTD spectrum as Pick's disease. Only in the past three decades, however, has the clinical and pathological complexity of these diseases and their unique status as examples of selective brain degeneration been fully appreciated. FTD is substantially less common than Alzheimer's disease, with estimates of population prevalence ranging from four to 15 per 100000 before age 65 years in European and US epidemiological studies.1 However, this disease group is of disproportionate importance as a cause of young onset dementia and all the attendant socioeconomic and human costs that entails. Although onset is typically in the sixth decade of life, it may begin as early as the third or as late as the ninth decade, and the prevalence of FTD in older age groups has almost certainly been underestimated.
Here we provide a general overview of FTD, emphasising clinical aspects and highlighting recent progress and prospects. Figure 1 provides a schematic overview of FTD showing major clinical and neuroanatomical syndromes Brad Richards Kids Jersey and diseases, and the relations between them.
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Fig 1 Molecular pathologies and phenotypic correlations in frontotemporal dementia. The schematic shows major genes causing frontotemporal dementia, histopathological substrates, and clinical phenotypes. Neuroanatomical profiles are shown as coronal magnetic resonance imaging sections (left hemisphere displayed on the right) abutting the corresponding pathological substrates, with regions of predominant regional atrophy demarcated by white rectangles. Genetic bases for pathological substrates and phenotypic associations of tissue pathologies are shown as intersecting (for example, mutations in the progranulin gene (GRN) are associated with TDP 43 type A (TDP A) pathology, which may be associated with clinical syndromes of behavioural variant frontotemporal dementia (bvFTD), progressive non fluent aphasia (PNFA), corticobasal syndrome (CBS), and frontotemporal dementia with motor neurone disease (FTD MND)). Group functional neuroimaging studies have demonstrated involvement of intrinsic, large scale brain networks in FTD syndromes: a medial paralimbic network (including anterior cingulate, orbital frontal, and frontoinsular cortices) in bvFTD32; an anterior temporal and inferior frontal network in semantic dementia32 33; and dorsally directed dominant hemisphere language networks in PNFA.32 33 However, the network correlates of particular molecular pathologies are less well established.34 This scheme arranges diseases according to whether they produce damage that is relatively more restricted to anterior (toward left of figure) areas or extends posteriorly (toward right of figure) within each cerebral hemisphere; whether damage within a hemisphere is more focally restricted to the temporal lobes (toward bottom of figure) or more distributed (toward top of figure); and according to the degree of asymmetry of involvement between the two hemispheres (more asymmetrical diseases shown more centrally)21 34
Sources and selection criteria
We examined recent literature on frontotemporal dementia, targeting full text English language studies published since 1990. We selected articles on the basis of our personal knowledge and searches of the Medline database using the terms "frontotemporal dementia," "frontotemporal lobar degeneration," "progressive nonfluent aphasia," "semantic dementia," and "logopenic aphasia," and each of these terms www.officialhockeyauthentic.com/womens-youth-brad-richards-authentic-jersey-c-1_283_304.html in conjunction with "diagnosis," "treatment," and "therapy." The final selection of references was based on our judgment of relevance, completeness, and compatibility with recent clinical, pathological, and genetic criteria.
What Chris Kreider Kids Jersey are the different syndromes of frontotemporal dementia?
There are three main clinical syndromes of FTD, defined on the basis of leading features at presentation. About half of cases present with behavioural change (behavioural variant frontotemporal dementia), and the remainder present with language decline (primary progressive aphasia) characterised either by impaired speech production (progressive non fluent aphasia) or by impaired word comprehension and semantic memory (that is, memory for meaning) (semantic dementia). There is variable overlap clinically between the syndromes and atypical parkinsonism and motor neurone disease. New consensus diagnostic criteria for FTD5 and the progressive aphasias6 have recently been formulated, but they are likely to be refined as more specific information about disease pathophysiology arises and neuroimaging and other techniques that can capture pathophysiological changes become available.
Methods for bedside assessment of behavioural variant frontotemporal dementia and the progressive aphasias are presented in the table and figure 2, respectively. It is particularly important for the non specialist to have a workable framework for suspecting FTD, as diagnosis, particularly early in the course of the disease, is often challenging. In contrast to Alzheimer's disease (the most common cause of dementia in later life), FTD often presents in middle life, and memory and navigational skills and other aspects of general intellect are often well maintained initially. Behavioural or personality changes may at first suggest a primary psychiatric disorder, particularly if accompanied by psychotic features: clues that such features are harbingers of FTD may include a lack of any prior psychiatric history and emergence of certain specific symptoms such as changes in eating behaviour or social faux pas. Isolated language disturbances may also be misattributed to psychological factors: early features of primary progressive aphasia may include stumbling over longer words, emergence (or re emergence) of a stutter, grammatical slips or problems using more specialised vocabulary associated with a profession or hobby (for example, a keen gardener may lose the names for flowers). Brain imaging (ideally with magnetic resonance imaging) is mandatory in all suspected cases of FTD to rule out mimic conditions such as brain tumours and to demonstrate signature atrophy patterns that may confirm the diagnosis or identify a non degenerative "phenocopy."7
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This syndrome is characterised by progressive decline in interpersonal and executive skills, with altered emotional responsivity and emergence of a variety of abnormal behaviours including apathy, disinhibition, obsessions, rituals, and stereotypies (see table 1).5 Behavioural variant FTD can develop indolently, and early detection may depend on subtle changes of social circumstances (such as switching jobs or partners), idiosyncratic lapses of taste or social awareness, reduced libido, altered dietary or musical preferences, or more childlike amusements. The relevant history has to be actively sought by speaking with the caregiver alone; forgetfulness may be volunteered as the presenting complaint, even though careful questioning often suggests that the patient's memory for everyday events is well maintained. To probe for a history of subtle behavioural change, we find it useful to ask the caregiver if the patient has said or done anything in public that has embarrassed other parties; if they seem less warm or affectionate (especially toward grandchildren or pets); if their food preferences have altered or narrowed or their table manners have declined; if they seem more concerned with timekeeping or tend to watch the clock; if there has been a change in their sense of humour; or if they have developed new hobbies or interests, especially with a religious or spiritual bent, and if these are pursued obsessively.
During the consultation, patients' spontaneous behaviours and interactions with others are often more revealing than formal neuropsychological testing: they may be impulsive or distractible, inert or impassive, disinhibited (picking up items unbidden from the examiner's desk) or socially unaware (fixing the examiner with a baleful stare). Cognitive assessment may reveal deficits of executive functions requiring formulation of a strategy, response inhibition, or abstraction: widely used bedside executive tests include verbal fluency (list as many words as possible in one minute, according to a nominated criterion such as starting letter or semantic category), cognitive estimates (make an educated guess about some arbitrary property or quantity, for example, the number of lions in Belgium), and proverb interpretation (summarise the abstract meaning behind a familiar saying). Memory and posterior cortical functions are often relatively spared, and indeed performance on standard psychometric tests is sometimes remarkably preserved. There is often a paucity of associated neurological signs, though primitive reflexes (forced grasping or rooting) may emerge later in the course, and behavioural variant FTD may be associated with extrapyramidal or motor neurone signs as part of an overlap syndrome.
Magnetic resonance imaging (MRI) findings in behavioural variant FTD are variable: there is often frontal and anterior temporal lobe atrophy (fig 1), which tends to be asymmetric between hemispheres and to spare more posterior cortical areas, but the degree and extent of atrophy vary widely among individuals. Altered white matter signal may be prominent, usually in close proximity to areas of cortical atrophy, where it may reflect gliosis. Involvement of orbitofrontal cortex is an early harbinger of FTD8 but can be difficult to detect reliably, and brain atrophy may be detected only on serial studies. Typically, semantic dementia initially affects the highly elaborate brain knowledge system that mediates vocabulary that is, knowledge of the meaning of words.10 Asking the meaning of familiar words, encountered, for example, in a menu ("What is asparagus?"), is pathognomonic of semantic dementia. Patients commonly present with fluent (or even garrulous) but empty, circumlocutory speech with early prominent difficulty retrieving names, use of less precise terms, and impaired comprehension of word meanings, accounting for the "semantic variant of progressive aphasia" in the current classification (see fig 2).6 Early in the course of the disease, the semantic deficit may be well compensated and may emerge only on testing more specialised knowledge previously at the patient's command. A more pervasive semantic impairment also affecting visual information (impaired recognition of familiar faces (prosopagnosia) or of visual objects (visual agnosia)) and other non verbal domains such as odours and flavours generally develops later in the disease course, as do behavioural disturbances broadly similar to those in behavioural variant FTD.10 The general neurological examination is usually normal.
shows a highly consistent and characteristic neuroanatomical (MRI) profile with selective, asymmetric anteroinferior temporal lobe cortical atrophy and hypometabolism (fig 1),11 the gyral glia at the temporal poles often persisting only as a residual "knife blade" skeleton. Several more or less distinct neurolinguistic syndromes are subsumed under the general category of progressive non fluent aphasia.13 In some patients, speech sound (phonemic) or articulatory (phonetic, speech apraxic) errors are the dominant feature; whereas in others the syndrome is dominated by expressive agrammatism with terse telegraphic phrases (see fig 2). These features commonly coexist as the disease evolves. Apraxia of other orofacial movements or swallowing often accompanies speech apraxia and is tested by asking the patient to yawn or cough, which they are unable to do to command, although they can as a reflex. Impaired sentence comprehension can generally be demonstrated on neuropsychological assessment, and literacy skills become affected in most cases. may herald the onset of a neurological overlap syndrome with atypical parkinsonism or less commonly motor neurone features.
Brain atrophy and hypometabolism in progressive non fluent aphasia often affects perisylvian cortices in the dominant hemisphere mediating speech production (fig 1).14 However, the profile of atrophy varies widely in extent and severity between patients.
A third clinical syndrome of progressive aphasia, logopenic (Greek "few words") aphasia, presents with hesitant but grammatically correct speech marred by word finding pauses, anomia, and impaired phonological working memory manifesting as disproportionate difficulty repeating spoken phrases versus single words (fig 2). Most cases will have underlying Alzheimer pathology,6 and more widespread cognitive deficits similar to those accompanying other Alzheimer phenotypes emerge later in the disease course. The progressive supranuclear palsy syndrome is characterised by impairment of vertical gaze, early postural instability with falls, and frontal behavioural changes with marked cognitive slowing (fronto subcortical).15 16 Features of corticobasal syndrome include asymmetric apraxia accompanied by rigidity and myoclonus and classically non volitional or "alien" actions of the affected limb.15 The phenotype may include prominent behavioural or language deficits.16
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Check withholdings. If you received a large tax refund this year or were surprised by the amount you owed, take a look at the deductions on your W4 form. Getting back a large sum from the government may seem like a windfall. But it is really an indication that too much is being withheld from your paycheck. In essence, you have allowed the government to hold on to your money interestfree. Your goal should be to break cheap oakleys 2014 even with the Internal Revenue Service (IRS). To ensure that happens, use the IRS Withholding Calculator and adjust your federal income tax withholding allowances accordingly.
Track charitable donations. Several online programs fake oakley sunglasses can help track donations throughout the year. Check out Its Deductible from Intuit (Turbo Tax), or download the iDonatedIt app for noncash charitable donations. You also can check the identify and tax status of any charitable organization at CharityCheck101.
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IRS Publication 526 has more information about charitable contributions.
Combine Large Medical Expenses. Effective for the 2013 tax year, medical expenses that exceed 10 percent of adjusted gross income are taxdeductible. This includes the medical expenses of everyone listed on your tax return. Maximize the amount of expenses by grouping large medical expenses as much as possible. Medical deductions that are often overlooked include uninsured medical expenses (orthodontics, eyeglasses and hearing aids), travel expenses for medical treatments, alcohol or drug abuse rehabilitation, laser vision corrective surgery, and the cost michael kors outlet store of longterm care insurance. Certain weight loss or smoking cessation programs also can be included. In addition, you can deduct expenses for healthrelated changes to your home, such as adding a wheelchair ramp, installing a chair lift, or purchasing a device that enables a deaf or blind person to make or receive phone calls. Free online services like CakeHealth and Simplee can make it easier to track medical expenses. IRS Publication 502 has more information about taxdeductible medical expenses.
Devise a tax organization system. Designate a place such as a filing cabinet, file box or expandable organizer to store important tax documents throughout the year. Create designated spots for receipts and files for income, medical expenses, charitable donations, investments, business deductions, mortgage statements, student loans, childcare expenses and anything else that applies to your personal tax scenario. IRS publication 552 provides additional information about the documents you cheap oakley sunglasses outlet need to keep and how long you should keep them.
The key to a stressfree tax experience is to get in the habit of dealing with and filing tax documents and receipts on a regular basis. When tax time rolls around next year, knowing that all of your documents are easily accessible will help make tax preparation faster and less stressful. He also is coCEO of Freedom Financial Network, LLC providing comprehensive consumer credit advocacy and debt relief services. Housser holds a Master of Business Administration degree from Stanford University and Bachelor of Arts degree from Dartmouth College.
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