Conflict-prevention programs in schools aim to shift the view of students, to encourage them that there is something to live for, that life isn?t unfair, and that school is worth their time and attention.
By John Yemma,?Editor / April 1, 2013
Students line up outside their classroom at a Chicago school.
Melanie Stetson Freeman/Staff/File
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Sometime around Day 1 in our lives, we begin wondering what?s fair and what?s unfair. Are Mom and Dad playing favorites with the ice cream? How can that kid cut in line? C?mon, Mr. SUV, let me into the traffic.
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Editor, The Christian Science Monitor
John Yemma is Editor of The Christian Science Monitor, which publishes international news and analysis at?CSMonitor.com, in the?Monitor Weekly?newsmagazine, and in an email-delivered?Daily News Briefing. He can be reached at editor@csmonitor.com.
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We?re constantly weighing fairness, campaigning for it, and judging it. The perception of unfairness may start as mild annoyance, but it can make or break empires. Get it right and you?re Solomon. Get it wrong and you?re Marie Antoinette.
So basic is the desire for fairness and the revulsion at unfairness that scientists are increasingly convinced that it is innate. A 2008 study by researchers at the California Institute of Technology indicates that the drive for fairness is tied to people?s emotion and that, instead of learning to be fair, humans are born that way. Experiments show that people feel worse when they perceive inequity and better when justice is done. Humanity, in effect, is always putting the universe on trial.
In a Monitor cover story, Stacy Teicher Khadaroo examines the problem of fairness in the meting out of school discipline. School is crucial in transferring civilization from one generation to another. It is where young people determine whether social rules are worth supporting, whether society is going to give them a fair shake, whether centuries-old wisdom really is wise ? whether, in short, they should contribute to the culture they were born into or walk away from it.?
A teacher?s interest, an inspiring class, supportive fellow students ? these slowly encourage adolescents to opt in. A clash with authority can derail that process, especially if a perception of unfairness takes hold. This is where the statistics are troubling.
There are significantly higher rates of suspensions and expulsions for African-Americans, Hispanics, and those with disabilities than for white students in American schools. Meanwhile, discipline has shifted in recent years from after-class detention and stern warnings to ?zero tolerance? of bad behavior. The unintended consequence is that rising numbers of young people don?t get the kind of do-overs that were once common in school. They get bounced. They?re on the streets, heading toward the criminal-justice system, and convinced that life is unfair.
As you?ll see in Stacy?s accompanying article, however, that innate human drive to see justice done is actively trying to counteract that problem. Conflict-prevention programs in Oakland, Calif., and elsewhere aim to shift the view of students, to encourage them that there is something to live for, that life isn?t unfair, and that school is worth their time and attention.
Fair treatment gives rise to hope. But for many people ? especially those traumatized by broken homes, violent neighborhoods, or run-ins with the police ? hope can?t simply be switched on. It has to be earned through one-on-one encounters and trust-building in programs such as the ?restorative justice? initiative in Oakland?s public schools.
If we come into this world wired for fairness, evidence of it convinces us that we aren?t mistaken. That, in turn, builds a defense against the inevitable moment that unfairness asserts itself. A kid will cut in line. A driver will be rude. Injustice will occur. But if an enemy forgives, a judge shows mercy, a teacher takes interest, the balance tips back. In a civilization worth supporting, fair outweighs unfair.
JCI early table of contents for April 1, 2013Public release date: 1-Apr-2013 [ | E-mail | Share ]
Contact: Jillian Hurst press_releases@the-jci.org Journal of Clinical Investigation
Promoting muscle regeneration in a mouse model of muscular dystrophy
Duchenne muscular dystrophy (DMD) is a degenerative skeletal muscle disease caused by mutations in the protein dystrophin. Dystrophin functions to protect muscle cells from injury and loss of functional dystrophin results in break down and loss of muscle cells. A cellular signal relay system, known as a MAP kinase cascade, regulates the function of muscle stem cells, serving as a source of the new cells that are required for muscle regeneration. In this issue of the Journal of Clinical Investigation, researchers led by Anton Bennett at Yale University identified the protein MKP-5 as a negative regulator of MAP kinase cascades in muscle stem cells. Loss of MKP-5 in a mouse model of DMD enhanced the development of new muscle cells (myogenesis) and helped prevent muscle degeneration. These results identify MKP-5 as an important suppressor of myogenesis and suggest that therapeutics that inhibit MKP-5 could be useful in the treatment of degenerative muscle diseases.
TITLE: Improved regenerative myogenesis and muscular dystrophy in mice lacking MKP-5
AUTHOR CONTACT: Anton Bennett Yale University School of Medicine, New Haven, CT, USA Phone: 203-737-2441; Fax: 203-737-2738; E-mail: anton.bennett@yale.edu
View this article at: http://www.jci.org/articles/view/64375?key=bbd026972477a9b98a24
Alternative fuel for your brain
Tight control of blood glucose levels is critical to mitigating the long-term complications of diabetes; however, the intensive insulin therapy required for this control is frequently accompanied by recurrent episodes of low blood sugar (hypoglycemia). Hypoglycemic episodes have been implicated in brain damage and cognitive impairment. Though the brain depends predominantly on glucose as an energy source, it can also use alternative fuels, such as lactate, to satisfy its energy requirements. In this issue of the Journal of Clinical Investigation, Raimund Herzog and colleagues at Yale University used magnetic resonance spectroscopy (MRS) to measure the concentrations and enrichment of different energy substrates and their metabolites in a rat model of recurrent hypoglycemia. They found that recurrent hypoglycemia enhances neuronal uptake of lactate which allows the brain to retain normal neural activity during hypoglycemia. These observations suggest that lactate supports neuronal function and indicate that supplementation of alternative fuels could protect the brain during hypoglycemia.
TITLE: Lactate preserves neuronal metabolism and function following antecedent recurrent hypoglycemia
AUTHOR CONTACT: Raimund I. Herzog Yale School of Medicine, New Haven, CT, USA Phone: 203-737-4773; E-mail: raimund.herzog@yale.edu
View this article at: http://www.jci.org/articles/view/65105?key=b71f996b96b91c84d096
ALSO IN THIS ISSUE
TITLE: MicroRNA-26 governs profibrillatory inward-rectifier potassium current changes in atrial fibrillation
AUTHOR CONTACT: Stanley Nattel Montreal Heart Institute, Montreal, PQ, CAN Phone: (514) 376-3330 ext. 3990; Fax: (514) 376-1355; E-mail: stanley.nattel@icm-mhi.org
View this article at: http://www.jci.org/articles/view/62185?key=ef2561a4a7949ec7f659
TITLE: Melanoma adapts to RAF/MEK inhibitors through FOXD3-mediated upregulation of ERBB3
AUTHOR CONTACT: Andrew Aplin Thomas Jefferson University, Philadelphia, PA, USA Phone: 215 503 7296; E-mail: Andrew.Aplin@KimmelCancerCenter.Org
View this article at: http://www.jci.org/articles/view/65780?key=f9536e266df3ab73b9f1
TITLE: SLITRK6 mutations cause myopia and deafness in humans and mice
AUTHOR CONTACT: Mustafa Tekin University of Miami, Miami, FL, USA Phone: 305-243-2381; Fax: 305-243-2703; E-mail: MTekin@med.miami.edu
View this article at: http://www.jci.org/articles/view/65853?key=b2bb9afa9e0cee02bd6b
TITLE: Co-operativity of imprinted genes inactivated by acquired chromosome 20q deletions
AUTHOR CONTACT: Anthony Green University of Cambridge, Cambridge, , GBR Phone: +44-1223-336829; E-mail: arg1000@cam.ac.uk
View this article at: http://www.jci.org/articles/view/66113?key=73dc8fe4bcb928ca86e4
TITLE: The phosphatase CD148 promotes airway hyperresponsiveness through SRC family kinases
AUTHOR CONTACT: Arthur Weiss Dept. Of Medicine, San Francisco, CA, USA Phone: 415/476-8983; Fax: 415-502-5081; E-mail: aweiss@medicine.ucsf.edu
View this article at: http://www.jci.org/articles/view/66397?key=e400e2a8f6ccf1c7863b
AUTHOR CONTACT: Sebastian Joyce Vanderbilt Univ. School of Medicine, Nashville, TN, USA Phone: 615-322-1472; E-mail: Sebastian.Joyce@Vanderbilt.edu
View this article at: http://www.jci.org/articles/view/67388?key=c7801a36d65b917a2097
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JCI early table of contents for April 1, 2013Public release date: 1-Apr-2013 [ | E-mail | Share ]
Contact: Jillian Hurst press_releases@the-jci.org Journal of Clinical Investigation
Promoting muscle regeneration in a mouse model of muscular dystrophy
Duchenne muscular dystrophy (DMD) is a degenerative skeletal muscle disease caused by mutations in the protein dystrophin. Dystrophin functions to protect muscle cells from injury and loss of functional dystrophin results in break down and loss of muscle cells. A cellular signal relay system, known as a MAP kinase cascade, regulates the function of muscle stem cells, serving as a source of the new cells that are required for muscle regeneration. In this issue of the Journal of Clinical Investigation, researchers led by Anton Bennett at Yale University identified the protein MKP-5 as a negative regulator of MAP kinase cascades in muscle stem cells. Loss of MKP-5 in a mouse model of DMD enhanced the development of new muscle cells (myogenesis) and helped prevent muscle degeneration. These results identify MKP-5 as an important suppressor of myogenesis and suggest that therapeutics that inhibit MKP-5 could be useful in the treatment of degenerative muscle diseases.
TITLE: Improved regenerative myogenesis and muscular dystrophy in mice lacking MKP-5
AUTHOR CONTACT: Anton Bennett Yale University School of Medicine, New Haven, CT, USA Phone: 203-737-2441; Fax: 203-737-2738; E-mail: anton.bennett@yale.edu
View this article at: http://www.jci.org/articles/view/64375?key=bbd026972477a9b98a24
Alternative fuel for your brain
Tight control of blood glucose levels is critical to mitigating the long-term complications of diabetes; however, the intensive insulin therapy required for this control is frequently accompanied by recurrent episodes of low blood sugar (hypoglycemia). Hypoglycemic episodes have been implicated in brain damage and cognitive impairment. Though the brain depends predominantly on glucose as an energy source, it can also use alternative fuels, such as lactate, to satisfy its energy requirements. In this issue of the Journal of Clinical Investigation, Raimund Herzog and colleagues at Yale University used magnetic resonance spectroscopy (MRS) to measure the concentrations and enrichment of different energy substrates and their metabolites in a rat model of recurrent hypoglycemia. They found that recurrent hypoglycemia enhances neuronal uptake of lactate which allows the brain to retain normal neural activity during hypoglycemia. These observations suggest that lactate supports neuronal function and indicate that supplementation of alternative fuels could protect the brain during hypoglycemia.
TITLE: Lactate preserves neuronal metabolism and function following antecedent recurrent hypoglycemia
AUTHOR CONTACT: Raimund I. Herzog Yale School of Medicine, New Haven, CT, USA Phone: 203-737-4773; E-mail: raimund.herzog@yale.edu
View this article at: http://www.jci.org/articles/view/65105?key=b71f996b96b91c84d096
ALSO IN THIS ISSUE
TITLE: MicroRNA-26 governs profibrillatory inward-rectifier potassium current changes in atrial fibrillation
AUTHOR CONTACT: Stanley Nattel Montreal Heart Institute, Montreal, PQ, CAN Phone: (514) 376-3330 ext. 3990; Fax: (514) 376-1355; E-mail: stanley.nattel@icm-mhi.org
View this article at: http://www.jci.org/articles/view/62185?key=ef2561a4a7949ec7f659
TITLE: Melanoma adapts to RAF/MEK inhibitors through FOXD3-mediated upregulation of ERBB3
AUTHOR CONTACT: Andrew Aplin Thomas Jefferson University, Philadelphia, PA, USA Phone: 215 503 7296; E-mail: Andrew.Aplin@KimmelCancerCenter.Org
View this article at: http://www.jci.org/articles/view/65780?key=f9536e266df3ab73b9f1
TITLE: SLITRK6 mutations cause myopia and deafness in humans and mice
AUTHOR CONTACT: Mustafa Tekin University of Miami, Miami, FL, USA Phone: 305-243-2381; Fax: 305-243-2703; E-mail: MTekin@med.miami.edu
View this article at: http://www.jci.org/articles/view/65853?key=b2bb9afa9e0cee02bd6b
TITLE: Co-operativity of imprinted genes inactivated by acquired chromosome 20q deletions
AUTHOR CONTACT: Anthony Green University of Cambridge, Cambridge, , GBR Phone: +44-1223-336829; E-mail: arg1000@cam.ac.uk
View this article at: http://www.jci.org/articles/view/66113?key=73dc8fe4bcb928ca86e4
TITLE: The phosphatase CD148 promotes airway hyperresponsiveness through SRC family kinases
AUTHOR CONTACT: Arthur Weiss Dept. Of Medicine, San Francisco, CA, USA Phone: 415/476-8983; Fax: 415-502-5081; E-mail: aweiss@medicine.ucsf.edu
View this article at: http://www.jci.org/articles/view/66397?key=e400e2a8f6ccf1c7863b
AUTHOR CONTACT: Sebastian Joyce Vanderbilt Univ. School of Medicine, Nashville, TN, USA Phone: 615-322-1472; E-mail: Sebastian.Joyce@Vanderbilt.edu
View this article at: http://www.jci.org/articles/view/67388?key=c7801a36d65b917a2097
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Mar. 31, 2013 ? Scientists at the University of Pittsburgh School of Medicine have discovered a new biological pathway of innate immunity that ramps up inflammation and then identified agents that can block it, leading to increased survival and improved lung function in animal models of pneumonia.
They reported their findings today in Nature Immunology.
Pneumonia and other infections sometimes provoke an inflammatory response from the body that is more detrimental than the disease-causing bacteria, said senior author Rama Mallampalli, M.D, professor and vice chair for research, Department of Medicine, and director of the Acute Lung Injury Center of Excellence at Pitt.
"In our ongoing studies of pneumonia, we found infecting bacteria activate a previously unknown protein called Fbxo3 to form a complex that degrades another protein called Fbxl2, which is needed to suppress the inflammatory response," said Dr. Mallampalli, who is also chief of the pulmonary division of the VA Pittsburgh Healthcare System. "The result is an exaggerated inflammatory response that can lead to further damage of the lung tissue, multi-organ failure and shock."
The research team, led by Bill B. Chen, Ph.D., associate professor, Division of Pulmonary, Allergy and Critical Care Medicine, conducted experiments in which mice that lacked the ability to make Fbxo3 were infected with a strain of Pseudomonas bacteria, and found that they had better lung mechanics and longer survival than mice that still made the protein.
Research team members Bryan J. McVerry, M.D., and Yingze Zhang, Ph.D., both of the Acute Lung Injury Center of Excellence, found that blood samples from 16 people who had sepsis, a condition of systemic inflammation, revealed higher levels of Fbxo3 and other inflammatory proteins and lower levels of Fbxl2 than samples from seven patients who did not have sepsis or lung infection.
Based on the structure of Fbxo3, the researchers developed a family of small molecules with the aim of inhibiting its activity. Administration of one of them, called BC-1215, led to reduced inflammatory markers and improved lung mechanics in mouse models of pneumonia and sepsis.
"The key is to find ways to help the body temper its inflammatory response so that it's able to kill the infectious agent without causing injury to healthy tissue," Dr. Mallampalli said.
"The F-box protein Fbxo3, and other related proteins, represent ideal targets for treatment of acute lung injury, because it controls the innate immune response, is upstream of important inflammatory signaling pathways, and is more selective than traditional drugs that regulate protein turnover," noted Mark T. Gladwin, M.D., chief of the Division of Pulmonary, Allergy and Critical Care Medicine, Pitt School of Medicine.
The team is beginning to study the effects of BC-125 on other conditions of systemic inflammation, such as colitis and arthritis.
Co-authors of the paper include Tiffany A. Coon, Jennifer R. Glasser, Jing Zhao, Ph.D., Yutong Zhao, M.D, Ph.D., Chunbin Zou, Ph.D, Bryon Ellis, and Frank C. Sciurba, M.D., all of the Acute Lung Injury Center of Excellence, University of Pittsburgh.
The study was funded by the U.S. Department of Veterans Affairs; National Institutes of Health grants HL096376, HL097376, HL098174, HL116472, HL01916, and P50HL084948; and the American Heart Association.
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The above story is reprinted from materials provided by University of Pittsburgh Schools of the Health Sciences.
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Journal Reference:
Bill B Chen, Tiffany A Coon, Jennifer R Glasser, Bryan J McVerry, Jing Zhao, Yutong Zhao, Chunbin Zou, Bryon Ellis, Frank C Sciurba, Yingze Zhang, Rama K Mallampalli. A combinatorial F box protein directed pathway controls TRAF adaptor stability to regulate inflammation. Nature Immunology, 2013; DOI: 10.1038/ni.2565
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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
The Sales Excellence Manager role is responsible for processes, systems, tools, business planning, management frameworks, initiatives and programs that will optimize sales and provide the discipline for increases in sales force productivity.
The Sales Excellence Manager role drives towards these results by providing: Sales productivity expertise in Relationship Management, Opportunity Management, and Business Management. Process readiness and coaching. Systems and tools requirements. Planning and Business management frameworks such as Rhythm of the Business (ROB), three-year planning, pipeline management and forecasting support, budgeting management, commitments and quotas. Ensuring sales model implementation through segment strategy, customer segmentation and role taxonomy. Development of initiatives for annuities, customer/partner experience, and Cost of Sale (CoS).
The Sales Excellence Manager role affects Microsoft at the EPG sales organization level within a specified region or subsidiary. The Sales Excellence Manager role focuses on processes, systems, tools, organizational issues, financial, and communication processes that affect effective operations within the entire organization. The Sales Excellence teams are considered to be the change leaders, providing business management expertise and driving sales productivity. This team functions as the execution engine in the field, which means they touch all levels of people and groups throughout the business. This role has significant importance in how we drive the vision for successful change management, business strategy, and sales optimization.
The key decisions made by the Sales Excellence Manager role are: Strategic annual and three-year planning decisions Key metrics to drive plan achievement Rhythm of the Business (ROB) frameworks, processes and metrics Budget investments and resource management
The Sales Excellence Manager role also makes recommendations and decisions with worldwide EPG and field Sales Excellence leadership on vision, direction and plans to roll out efforts to increase sales productivity, drive sales optimization efforts and lead Rhythm of the Business (ROB). The Sales Excellence Manager role is a strategic leader to a community that needs guiding principles to implement and execute against fiscal year Sales Priorities. The Sales Excellence Manager role partners with its manager (the EPG Lead) to develop the priorities and set the strategy accordingly.
The Sales Excellence Manager role works with the following internal resources: EPG Lead (the Sales Excellence Manager functions as the COO for the EPG Lead). ATU, STU, PTU, IU Leads (for driving adoption of sales processes, systems and tools discipline). Finance (for all processes and data related to budgeting, Cost of Sales (CoS), and forecasting). Human Resources (for all interactions related to resource requirements, resource planning, and compensation management). M&O (for determining fiscal year Sales Priorities and investment requirements).
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First off, back a few days ago, an anonymous commenter asked
Do you know of any available resources to build freq hopping and encrypted radios available to the public. It might be a good project to get some of your engineers working on, perhaps using this as a foundation: http://greatscottgadgets.com/hackrf/ All you need is a laptop and the Hackrf USB radio, throw on a GUI that makes signal strength and frequency selection easy, encryption and frequency hop loads, and you've got a military grade radio.?
I haven't kept up with this tech - the last time I saw similar things (and it may have been a dead end on the Internet) it was certainly not military grade, and I wasn't even sure it was Belkin grade.? That is, I'm not sure it was as good as commercial WiFi you can buy anywhere pretty cheaply.? I can't say I'm an expert at this, having just looked it over, but this is not a usable radio; it's a digital board that allows you to experiment with software defined radios (SDRs). ? The HackRF page on Ars Electronica says
There are relatively few people in the world with the knowledge and tools required to develop new radio communications hardware, but there are many millions of people who have the ability to program a computer. General purpose computers are widely deployed, and opportunities to learn how to program them are available to a huge number of people.? HackRF gives all of those people the capability to explore the radio spectrum and develop creative new ways to communicate.
The difference is that HackRF doesn't seem to have any receiver sophistication and only a very low power transmitter stage that I can see.? I freely admit I could be wrong, but the block diagram sure doesn't show anything.? One of the paradoxes of SDRs is that they don't eliminate the need for filters; if anything, they become more important due to the aliases they respond to.? He describes it as combining "Licorice, Lemondrop, and Jellybean into a single USB-powered software radio".? Maybe I'm searching in all the wrong places, but a few searches with Bing retrieve nothing on them.? I don't think this is a GUI away from being useful, but hey!, prove me wrong!
SDRs for experimenters are not new at all.? Hams play with SoftRock, (also) a low power CW transceiver (Continuous Wave, the name hams tend to use for Morse code communications) that plugs into a USB port and a sound card.? These guys produce an HF SDR, transmit and receive, that is architecturally very similar to one I recently completed for a commercial design (naturally, I prefer the design trade choices that I made over theirs).? RFSpace has a product line of SDR receivers.?? FlexRadio is a staple in the ham world; their SDRs are considered among the finest radios on the market.?
I recommend getting an amateur radio license because it brings with it the privileges to experiment with new modes and new technologies all on your own.? You can buy an FRS radio to talk to someone, but if you're a ham, you can invent your own mode with an outwardly similar radio, because you're expected to understand the technical requirements.? The technician class license conveys all amateur privileges above 30 MHz, plus it gives holders some privileges in the HF spectrum (high frequency or shortwave - capable of worldwide communication).? The American Radio Relay League is the dedicated organization that is closest to a "universal American ham club", although like the NRA, the ARRL is often criticized by non-member hams (well, not as often as the NRA).? If you want a completely non-official page, this guy seems pretty good. ?
If you want to experiment with modes that require more than audio bandwidth, you need to be above 30 MHz, and you're going to need to experiment with radios (or have someone in your group that knows radio design).? Simply, most amateur gear is either surplus commercial gear or designed from the ground up for the narrowband modes that dominate.? Except for TV - hams have done regular TV at 400 MHz and above and are now doing digital TV.? A few months ago, I met hams who were buying surplus video equipment at WiFi frequencies and above.? They were playing with extending it out to long distances, and had made WiFi connections at 125 miles.? There is a ham band that overlaps the band allocated to WiFi, so the surplus gear is being used for ham purposes all the time.
As I said the other day, the use of ham radio to send encrypted messages, like a PGP-encrypted text file, is illegal, although the Feds have routinely allowed all sorts of things when a disaster happens.? If there is a total failure of civil order, I can't imagine this would be an enforcement priority.? Sort of like this old Far Side cartoon:
I think if you're going to learn how to set up and use communications, a ham license gets you the ability to do it in a licensed and permitted way. You can save the encrypted stuff for when you need it. Simply using UHF or microwaves on a point to point link (no repeaters) will give you almost total anonymity.?
Finally, a couple of people (here and in email) have asked for book titles or other ways to learn about this field.? Most of the books I know of are at least somewhat mathematical.? Electronic Communications by Robert Schrader is a very good book, often used as a junior college text or supplement in ham classes.? Spread Spectrum Systems by Robert C. Dixon is one of the standard books.? Both of these are available in several editions and are often found used or in library sales.? The ARRL Handbook, published every year, has long been considered a very complete summary of modern ham radio theory and practice.? There's a difference between books published for working engineers and those published for school, where the aim is to impress the professors enough to become the textbook.? Because of this, I have a tendency to pick up old textbooks written from the working engineer's perspective.? I've often thought I've learned more from magazines and ham radio publications than my engineering texts, as those books have more insights per square inch than textbooks do.?
In 2009, ?The Hangover? dominated the summer box office on its way to becoming the most profitable ?R? rated comedy ever. But the film, and its sequel, are certainly not without their critics.
Regardless of where you stand, you?ll probably enjoy this hilariously edited movie trailer for the film, which re-imagines The Hangover as a horror movie.
Warning, there are two spots of foul language in the trailer, so don?t this one in front of your kids.
Film student Richard W. Scott edited the footage as part of his college dissertation in order to, in Scott?s words, serve as, ?part of an experimental investigation into the power of post-production techniques on a movie's genre.?
Scott employs several editing techniques that are common in today?s horror films. For examples, the color-coding of the trailer has been saturated into sepia tones, as opposed to the actual film?s bright and welcoming colors. And the music has been replaced with sharp and harsh sound cues which put the viewer on edge.
But the real creativity lies in the way that Scott has pieced the footage together, to make the film appear to be a dark journey into a world where the character of Alan, portrayed by Zach Galifinakis, is actually a murderer on the loose in Las Vegas wreaking havoc upon the lives of his unsuspecting friends and anyone else who stumbles across his path.
As Alan declares at the end of the clip, ?I don?t care what happens. I don?t care if I kill someone.?
And if you want to see more of Scott's work, he has put together another clip for his dissertation, which re-imagines the 2005 film "Batman Begins" as a comedy.
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