Something else with the DJ Peter Tripp...

Mr. Tripp attracted just as much national attention, though, for his sleepless promotional gimmick a year earlier.

He spent 201 hours and 10 minutes awake, much of it sitting in a glass booth in Times Square, spinning records and bantering into his microphone three hours a day.

When Mr. Tripp began to fall asleep, nurses shook him; doctors joked with him, played games with him and gave him tests to take. After a few days, he began to hallucinate, seeing cobwebs, mice, kittens; looking through drawers for money that wasn't there; insisting that a technician had dropped a hot electrode into his shoe.

His last 66 hours awake were spent under the influence of drugs administered by the doctors and scientists observing him. Asked at the end of his stunt what he wanted the most, Mr. Tripp said, not surprisingly, that he wanted to sleep, which he then did for 13 hours and 13 minutes.

Some guy named Micheal Corke stayed awake from insomnia for six months and then he died...

This happened in 1991...

quote:

The man who went six months without sleep Michael Corke suffered from the rare genetic disease ‘fatal familial insomnia’, thought to affect just 25 families throughout the world. What happens is that if you have the gene, one day you wake up and never sleep again. Sleeping pills don’t help; even being in a coma will not send you to sleep … People with ‘fatal familial insomnia’ suffer serious mental and physical decline until they die and are finally able to rest. From ‘Altered States’, part of the documentary series, The secrets of sleep, prod. and dir. Joseph Bullman of Twenty Twenty Television for Channel 4, England (1998) Owls and larks: Are you a ‘party animal or party pooper?’ Science writer Lisa Melton writes that: If you wake every morning at the crack of dawn, ready to tackle an exam or a marathon, then you’re probably a lark. If you crawl out of bed after battling with the snooze button, on the other hand, you’re probably an owl. But why do morning and evening types naturally wake at different times? Is it your circadian rhythm? One factor may be the cycle length of their circadian rhythm, says Jeanne Duffy of Harvard Medical School in Boston. Duffy has estimated the cycle length in moderate owls and larks by isolating them in an artificial environment, where all time cues have been removed. Measuring their temperature and levels of melatonin and cortisol in their blood, she has found that owls’ cycles are longer than 24 hours. Larks, on the other hand, have cycles that closely follow a 24-hour pattern. Early birds and night-lovers Yet stereotypical early-birds and night-lovers are in the minority, warns Simon Folkard. Only between five and ten per cent of the population falls at either end of the spectrum, most lie in the middle. But extreme types are easy to spot. Look out for the poor lark who nods off at a dinner party or the owl who clumsily gravitates towards the coffee machine in the morning. Lisa Melton is science writer in-residence at the Novartis Foundation. From New Scientist magazine, vol. 166 issue 2241, 3 July 2000. See: www.newscientist.com Sleep laboratories in Australia The University of Adelaide has a sleep laboratory. To find out more of what they do, visit their website at: www.unisa.edu.au/sleep/main/tcsr_home.html

___________________
- rabbit.joker [funny¿rabbit] | www.rabbitjoker.com |www.ddtt.org

Dark Dirty Tech Tribal. | Hands in air (trance) and feet on the floor (house).

quote:

Fatal Familial Insomnia by: Ann M. Akroush Fatal familial insomnia is a genetic disorder. It manifests itself by many symptoms due to the degeneration of a certain part of the brain, the thalamus. The disease also results in the formation of amyloid plaques. This is the build up of a waxy substance made of proteins associated with polysaccharides. The disease is a result of a mutation of a normal protein that is associated with brain tissue. This is the prion protein. In the case of fatal familial insomnia, the mutation occurs 178 amino acids into the normal protein. Were an asparagine should be, an aspartic acid is instead. This disease is an autosomal dominant, which means that both sexes are affected and there are no carriers. If an individual inherits the mutant gene, that individual will at some point suffer the disease. In the case of fatal familial insomnia, the affected area of the brain is the area responsible for sleep, the thalamus. The thalamus is the center which communications from the brain to the body and the body to the brain pass through for proper directions to where a signal should be received. When sleep takes place, it is thought that the thalamus becomes less efficient at this signal transfer function allowing for the vegetative state of sleep to come over an individual. Consequently, the symptoms of fatal familial insomnia are directly related to the malfunction of the responsibilities of the thalamus, namely sleep. Sleep, blood pressure, heart rate, body core temperature and hormone flow are all affected by the interruption of the body's circadian rhythms which is a direct result of the degeneration of the thalamus in this disease. Other symptoms of this disease include the inability to produce tears or feel pain as well as poor reflexes and dementia. The lack of sleep leads to other problems such as hallucinations and coma. This is a clear demonstration of a pleiotropic disease, a disease with many phenotypic expressions. That is, this disease is the result of one mutant gene yielding one mutant protein, yet causes many physical abnormalities such as skin blotches, lack of tears, etc. In the case study of an Italian family where of 288 relatives over 6 generations, 29 are affected by the disorder. The average age of onset of the disease is 49, but this may vary with the individual as with one female who was 61 years of age. Her disease lasted 18 months and followed the following pattern of the disease. There are four stages of the disease before an individual's life ends. The first stage is progressive insomnia, the trade mark of fatal familial insomnia. The first stage develops over approximately four months and includes a collection of psychiatric problems such as panic attacks and bizarre phobias. The second stage includes hallucinations, panic, agitation and sweating and lasts about five months. The third stage lasts about three months and is total insomnia with weight loss. The individual at this point looks much older and may experience incontinence. The fourth stage is around six months long and is recognized as dementia, total insomnia and sudden death after becoming mute. This disease does not show until or past child bearing years when potentially affected individuals may have already had children that may also be potentially affected. Because of this fact, modern biotechnology must be employed for early diagnosis. Techniques such as DNA sequencing or molecular hybridization with a probe which seeks to detect the defective gene may be used for early diagnosis. As for the treatment of this disease, hope may be found in the advancement of something called gene therapy. This treatment involves the insertion of the correct gene into an affected individual altering his/her gene expression making it what it should be for the expression of the correct protein. In order for this to happen, early diagnosis of an individual must be accomplished, possibly by the mentioned biotechniques above. This is so that the defective gene may be repaired before the onset of the disease. In order for this to be possible, the corrective gene must be isolated. Furthermore, the corrective gene must be good for transfer as well as a the proper vector to effectively execute the transfer. Because there is no cure for this illness, gene therapy may be the only answer if it is one day successful. References Guilleminault, C., Lugaresi, E., at el. Fatal Familial Insomnia: inherited prion diseases, sleep, and the thalamus. Raven Press, 1994. pp.15-20. Klug, W.S., Cummings, M.R. Concepts of Genetics. Prentice-Hall, Inc., 1994. pp. 425-427. Medori, R., Tritschler, H-J., at el. "Fatal Familial Insomnia, a Prion Disease with a Mutation at Codon 178 of the Prion Protein Gene" New England Journal of Medicine, 326 (7): 444-449 (1992). Petersen, R.B., Tabaton, M., at el. "Analysis of the prion Protein gene in Thalamic Dementia" Neurology, 42 (10): 1859-1863 (1992).

___________________
- rabbit.joker [funny¿rabbit] | www.rabbitjoker.com |www.ddtt.org

Dark Dirty Tech Tribal. | Hands in air (trance) and feet on the floor (house).

approx. 50hrs. But there have been multiple times of sleeping 1-2 hrs/day (midterm season).

This is one of my natural talents lol 4 days was my top score. Usually do that for festivals or those clubbing marathons that pop-up time 2 time hehe.

___________________
"Be the change you wish to see in the world"

quote:

Originally posted by newr im an ex-insomniac... my longest before i passed out was 159 hours... and its true... you do begin to hallucinate after being awake for 5 days

WOW! I barely beat DigitalMP, but not you you crazy bastard! 107 hours, Tuesday morning to Saturday night/Sunday morning. I could not imagine having gone another 2 days. Holy Shit!

Nrg2Nfinit and i did 60 some odd hours straight on Dexadrin studying for a calc final once, then aftewards did alot more dex and hiked around ottawa..... note to self dont snort dex ever again

wemf last year i belive it was a total of 80+ hours, up at 4 for work friday morning, finished work drove to oakville, then to orange ville, started doing amphetamines, sunday night on the way home started sketching out, couldnt sleep all night, monday was a depressed zombie, went to sleep finaly monday night.... didnt function properly for weeks after that tho. im getting too old for this crap

___________________

quote:

Originally posted by pkcRAISTLIN I have 3 hobbies: gaming, DJing & correcting maladjusted fools on the internet.

quote:

Originally posted by pkcRAISTLIN Yeah, I’d like to know what horrible, scarring incident in your childhood turned you into such an ignorant, intellectual-hating philistine?