



S1: (xx) i had more useful, um comments when each of you only did two, so if you would like to just do two very good evaluations today, that's actually more useful to me and to the people giving the talks, than four yes yes yes yes evaluations, okay, so um, if you could do that. um just a reminder there're a couple of people last week who, forgot to give me their detailed outline and, uh references, um Serena and Reshma if if you need, you need to get those to me, by next week at the latest. people talking today if you don't have your detailed outline and references please get them to me next week, i really, i need to have those. um... i think that's it. once we get this going, we should be all set. <P 1:42> it's gotta be you Paul <P :06> this time it's the_ this won't even come on. this is fine but, this was just working five minutes before i came upstairs. <P 1:00> i think, Paul i think you can come up here. let's see if this will, really blow it if you just walk up here but <P :24> sometimes it's really good. [S2: oh really? ] yeah (yeah) 
S2: oh uh (xx) how long is it supposed to be 
S1: (xx) 
S2: oh wow okay i'll pencil you in <LAUGH> (xx)
S1: i'll tell you what all i'm gonna be sitting (xx) back there, [S2: yeah ] if it gets a little (xx) (xx) 
S2: okay yeah except i think it's pretty cool now. 
S3: it's (a bull.) 
<SU-F LAUGH> 
S1: okay 
S2: (well) it works 
S3: hey Paul you the man. you the man. 
S1: (okay whatever you do don't) trip on anything.
S2: don't trip on anything? [S1: because then we're really screwed ] well that would be fun. 
S1: (xx) to go forward. [S2: (xx) ] um actually (xx) [S2: oh okay ] um, to go forward to ba- (to go back you go like that) to (xx) something, you do that. [S2: alright okay ] (xx) [S2: alright ] (xx) okay 
<P :06> 
S2: okay uh i am uh, Paul Land if you don't know me i'm doing my uh, presentation on Mad Cow Disease and other, transmissible spongiform encephalopathies. okay, uh what really is Mad Cow Disease? it's just uh, it's just the easier name for the disease called Bovine Spongiform Encephalopathy which means um, encephalopathy means just a bad thing in your brain, spongiform means your brain will look like a sponge and then bovine happens in cattle. uh it's just one of many diseases that are called um T-S-Es or transmissible spongiform encephalopathies which are just, uh you know your brain is just like a sponge and it's transmitted from species to species sometimes or just from, uh animal to animal. um, many other well known, uh T-S-Es are scrapie in sheep, and uh Creutzfeld-Jakob disease which affects us humans. uh what is a T-S-E um, what happens it it's a uh spongy degeneration of the brain which means your brain will look like a sponge, which means there's gonna be holes in your brain. which is kind of bad because you don't want holes in your brain, so um, this will cause uh, severe then eventual fatal, uh neurological damage which you'll just die, uh it doesn't last too long, um what causes this is something called a prion which is a protein which i will, get into later, uh (xx) means just it's a bad way to die. it's quick it's painful and, you're gonna die no matter what. <LAUGH> okay uh now we get into the history, um of uh, B-S-E and uh Creutzfeld-Jakob disease, um in nineteen eighty-six that's when it was first pretty much found in uh, a nice amount of numbers in uh in the U-K, and the U-K government pretty much, didn't acknowledge it didn't say it was gonna be important, didn't say humans were gonna be affected by it, um until two years later they realized that, the uh, the cows were getting this by eating a uh, protein slush which contained, either sheep like brains and spinal cords which contained the disease the T-S-E scrapie from sheep, then later on contained, it was like cannibalism they contained co- you know cow brains spinal cords, so they were just, they were cannibals giving it from uh cow to cow. um from nineteen eighty-eight to ninety-three uh, the disease increased in cows every year, and then in ninety-two was it was uh, one of the first bad signs because um, cheetahs and pumas uh cats in zoos, started getting the T-S-E in cats because of eating, uh B-S-E food. this was bad cuz (now it) crossed the species barrier twice, went from sheep to cows and now cows to cats. and then what's even worse in ninety-four a a human Victoria Rimmer uh was claimed to have been dying of a new kind of Creutzfeld-Jakob Disease called Variant Creutzfeld-Jakob Disease, and it was thought she got this by eating um, uh cattle that was infected with B-S-E. so now it's affecting humans not just cows, and then, uh because of this, and um, it started infecting more people, the U-K just started slaughtering all their cattle so their cattle numbers decreased, they couldn't send this out across the world, so pretty much that's one of the main reasons that, the B-S-E decreased cuz they would just kill any cow that may have had it so if some cow is, had it at some farm they killed all the cows in that farm. so because of that, here's the graph of um, how it increased at first and now it's, it's there's almost none now. it's a very small amount con- considered, there was over two-thousand some years you know um, over sorry over, forty-thousand some years uh like eight years ago. so now it's vastly decreased. uh, the link between uh B-S-E and Variant Creutzfeld-Jakob Disease this is important because, this means the B-S-E can, convert over to humans and affect us. uh they first realized this because they both happened out of nowhere and certainly increased out of nowhere, in the same place in the same time in the U-K, in the uh, eighties and then nineties. then there're three other features which really, kind of show that these are similar, it's uh just the pathological features in monkeys when they have either disease are similar, they have similar molecular markers, or when they're transmitted in rats both diseases their characteristics of transmission are identical. so the disease shows the same thing. uh okay now for the rest of my speech i'm pretty much gonna talk about how it's gonna affect us with Variant Creutzfeld-Jakob Disease and then what a prion is and, what a prion can do in our body. um, the main difference between the regular Creutzfeld-Jakob Disease and Variant is that Variant is linked to exposure, meaning, you eat a lot of beef or use a lot of bovine product_ i think it's gelatin's a product uh it's involved in some medications look in the ingredients you can see bovine products, in there and then the other, just simple difference is Variant uh you're a little younger, thirty years old instead of sixty-five, or in Variant you live a little longer two years instead of five months, really you're not living long anyways and it's not fun to live with so it doesn't really matter. <LAUGH> and then patients with Variant also have some psychiatric symptoms, because it's affecting their brain, they have plaques in their brain, so they can become uh, they act schizophrenic they act different then they used to act, or they start seeing hallucinations. okay there are three types of Variant which are the same three types of the, other Creutzfeld-Jakob disease they are um, sporadic familial and iatrogenic. sporadic is the kind, that that we pretty much get from eating the beef, they don't know what the cause is but it's pretty much it's just exposure. this is ninety percent of the cases. even though it's a large amount that's still only, one per million humans so it's very low amount. and the other two familial and the iatrogenic are very small, familial's just you get a gene mutation, you can happen to get this disease, or iatrogenic is what, has been coming up more recently about how you might get a blood transvu- transfusion and you could, somehow get the disease so now it's a ban on, i think anyone from the U-K really can't give blood across the world. <SS LAUGH> in case, we don't want to get that okay. uh diagnosis well first of all, the disease can lay dormant in your body for many years like over ten years so, you could have it now you have no idea. so, who knows but when you really start seeing the symptoms, you're just wasting away eventually you can't talk you can't move you can't think, you're just laying down waiting to die. so at the end you're just waiting to die. um, it's also been called Alzheimer's on fast forward because they get_ i'll talk (about it) later these similar plaques in their brains they get the s- the same kind of thing they lose memory they don't they can't do as many functions, but it happens considerably faster like in a few you know weeks and months span. uh okay how do the, T-S-Es go from animal to animal and species to species? uh they really don't know. the cause or of how it goes in their body and moves they don't really know. they think it's exposure like i said before, the cows ate a protein sludge which had scrapie and they ate the protein sludge which had, uh which had B-S-E, and then we ate cattle that had B-S-E so pretty much, you eat enough of it, and if they have the prions in there, there's a chance you can get the disease. okay here's prions this was a pretty hot topic when it was first discovered because many scientists didn't agree with it. um, it was discovered by Stanley Prusiner and he called it a proteinaceous, uh infectious particle which's just a protein that infects things. and he c- it's a naked protein cuz it contains no nucleic acid which are no D-N-A no R-N-A, and this was odd because there'd never been a- a disease in the past which didn't contain, a nucleic acid. because you need nucleic acids to make the disease grow like from cell to cell in your body. so because of this this was of course laughed at first by the science community they didn't agree with him um, of course scientists can be wrong they once thought the Earth was flat and of course, it isn't flat. um so (xx) information was obtained which i'll explain in a second uh, the prion theory was accepted and Prusiner later like like thirteen years later he discovered it he uh, was something like that he, uh won the Nobel Prize in uh medicine. uh here are the two reasons mainly why the prion theory is accepted now. it's because um nucleic acids are either destroyed or ineffective if you use high temperature low temperature, radiation or ultraviolet light. and when they did this to the prions the prions still worked there was no effect on it. and the other reason is, because prions were inactivated by using by using a protein (xx) chemicals. so, pretty much they showed there was a protein that showed there wasn't any nucleic acid. so that, kind of proved that it was only a prion there. but even with this information many scientists still just won't believe it they think we don't have the techniques to find the nucleic acid so they still claim, they call it a virion or virino which is protein with a tiny piece of D-N-A. so even though they can't see it they won't admit that it's not there. so who knows maybe they're right. uh here's a diagram of, pretty much how, the disease transmits from species to species and what happens in our body. the uh the O is the origin which is probably scrapie, and then the cows ate this then it went from cow to cow then it went from the cow to the humans, um then in the lymphocytes the uh, the prions_ i'll explain what they do they do some of their work and then they get_ go back to the brain, by uh the nerves and the spleen and they make holes in the brain. uh okay here's what the prion really does um, the prion protein is really found in all humans we have this protein that's called prion protein or P-R-P-C. uh it's made by chromosome twenty but um that really doesn't matter um, the infectious prion protein is called P-R-P-S-C because S-C's for scrapie, and this is what calls uh Variant Creutzfeld-Jakob disease, um they're i- they're identical besides in their tertiary confirmation. um pretty much how you get the disease is that the infectious prion protein enters our body and then changes the conformation of the normal prion protein. um yeah this picture, it's hard to follow but if you look at the uh, the green which is P-R-P-C that's our normal and the purple is really the infectious and then you can see, all the way over from the purple, like, <SIGHS> over there it's like half green and half purple so it's changing i don't know i could only find (xx) pictures. um, pretty much the difference in their conformation is that normal prion protein is mostly alpha helices, and infectious prion protein is mostly um, or more beta sheets and less alpha helices, and what happens that the infectious prion protein binds the normal prion protein and changes conformation of beta sheets. they don't know how this happens they think, they make, the infectious prion protein makes a deletion in the regular prion protein it's like, some kind of base pair, then because of that the alpha helix is more easily turned into a beta sheet. and they know this stuff's happened because when they're both put in a um, in a test tube the infectious, prion protein does change all the normal prion protein into infectious. uh here's a picture of the two, you see on the left it's_ they estimate it's about forty-five percent_ this is just general pictures this isn't (xx) what it looks like, um it's mostly alpha helices then on the right infectious, there's a lot more beta sheet that's why the uh, blue arrows so, they don't know why the secon- the second kind will make the disease but it, definitely does make the disease. okay what happens in the body um, well the first one up there definitely do- it happened in some of the patients it's the same as in al- Alzheimer's the different protein they're just plaques on the brain which will cau- this happens at the beginning cause you'll lose memory you'll lose function you can't do as many things your your, the way you act changes but then what really kills you what they think happens in lysosomes, the infectious prion protein enters the lysosomes then bursts kills the cells goes to another cell, bursts kills that it keeps killing cells in your brain, which makes holes in your brain, so that is the spongy brain, there's a- the little holes start little black holes at first then as they accumulate they become bigger and bigger holes so eventually your whole just being torn apart, you brain get (sic) torn apart. uh but the good news is is that Variant Creutzfel- Creutzfeld-Jakob disease hasn't really entered the United States. uh there aren't really any official documents that say it has, i looked online a lot of people claim that some family members died of it by eating you know beef but there's no official document saying it's really entered the United States so that's a good thing. (like) Trojan cow. <SS LAUGH> um, and then the other bad thing is really that there they don't have any treatments yet. these are two possible ones they're looking at, one is a drug that would uh attach the center of the alpha helice helices and that'll make it so they can't change the beta sheets. so pretty much, your normal prion proteins can't change to infectious prion proteins. so then you can't, get the dise- the the disease can't spread so that's good. um the other one which they're still testing and, i hope this'll work but you can just totally splice out the prion protein gene, so that we don't produce any prion proteins so those can't even_ so they can't produce them they can't change to infectious prion proteins. of course they don't know if this'll work because the prion protein (can) have another function in our body which we might need. so they're testing it in mice and hopefully the mice act the same as us and, <LAUGH> we don't need it. uh in conclusion um, uh the T-S-Es you know they're they're rare which is i mean they're rare which is good but they're very lethal which is bad. uh B-S-E has decreased substantially there's not that many anymore i mean it's all over the news because, news stations put out Mad Cow then we watch for what's called Mad Cow. but really it's not that prevalent anymore, and then there's been less than a hundred cases total in the past seven years for Variant Creutzfeld-Jakob disease and that's i think about ninety of them, are all in the U-K there's like less than five other places in Europe and, Asia. so it hasn't really spread that much. but if it does spread like AIDS has, that's bad news again we have no treatment so if spreads, a lot of people are gonna die. (so) that's it. yeah? 
S4: you said if you eat enough that you could potentially get it like do you know any kind of amounts that you would have to eat? 
S2: they don't know [S4: oh ] it's just, uh it's not here y- y- you know if you go to the U-K, don't eat beef. it's very_ it's i mean 
S4: well the when i was in Jamaica someone said that they were importing beef from the U-K and i had found that out after i ate a hamburger so 
S2: if you ate one hamburger? [S4: yeah ] i mean that's pretty slim. [S4: oh ] it's a it's a sub- substantial amount cuz it has to go in there survive in your body and then it has to start infecting everything one hamburger i would doubt it. [S4: <LAUGH> okay ] but it could i mean i don't know. <SS LAUGH> yeah 
S5: is this at all related to hoof and mouth disease? 
S2: no and a lot of people are asking that because, i think it's transmitted the same way it goes from cow to cow by eating cows but it's just another disease in cattle that's not a transmissible, spongiform encephalopathy it's you know it's not prions it's just a disease in cows. i think it's spreading like it was with Mad Cow but it's a total different disease. so, yeah. 
S1: i heard something about elk in the West [S2: yeah ] showing symptoms of, a spongiform encephalopathy did you read anything about that? 
S2: yeah i i i read that also yeah it's there's different species that have gotten it b- you know but 
S1: but that's, we we don't have any B-S-E in the U-S either. [S2: no ] so it's um
S2: so far the elk hasn't gone from another species [S1: right ] so i mean, not not every species can transmit to another species you know? sheep did to cows and cows did to us we don't know what el_ you know (i m-) 
S1: and is there has there been any, evidence of, B-S-E or scrapie going to, birds like chicken or, i i know there's been a lot of transmission through to other mammals but i was wondering (xx) 
S2: i don't think i read that no. (xx) 
S1: so chicken's safe? 
S2: yeah i didn't see anything on chicken no... is that good? okay
S1: thanks Paul. 
<P :07> 
S6: (xx)
S1: okay
S6: it's already set up to work so (xx) [S1: um did you have (xx) ] Benji's not here. i asked him to be here but he's not here.
S1: okay well um... we will try to make it work 
S6: yes 
<P :08> 
S1: (xx) [S6: yeah ] we will try to make it work when we get there. [S6: (thanks) ] and to go forward you do that back you do that and point you do that.
S6: oh, (you can) point (in it?) 
S1: point yeah just (xx)
<P :06> 
S6: hi i'm Gary uh i'm doing hypoxia. if you were here last week and listened to (Sladie's) presentation, just disregard everything. you know, pretend you didn't learn anything. <SU-F LAUGH> um i didn't give you a paper outline since nobody looks at it anyways so, <SS LAUGH> this is my outline. we'll talk about what it is, what the causes are different types, um some of the dangers you face when you jump out of planes then we'll talk about um, people who live at high altitudes and how they adapt to hypoxia, and then we'll talk about some cool interesting stuff that hypoxia does in medicine. alright so what is hypoxia? um, cells need oxygen in the, in the electron transfer chain, as you know it's an electron acceptor and uh, they don't, really, function adequately, when the supply's d- uh when the supply's depleted, and this is what essentially is hypoxia um it's the low levels of oxygen in your body. um low levels of oxygen to the brain, produce inappropriate behavior, and then uh if you're exposed to it for a while you're gonna, lose consciousness and then you're gonna die. um, basically, the brain doesn't sense oxygen directly. there're chemoreceptors in your aorta and your carotid artery and they sense the saturation of hemoglobin. so if the s- he- hemoglobin is not saturated, as it wouldn't be if you went to a high altitude, it'd perform a fu- physiological change make you breathe faster, stuff like that. and then... this i- these are the different, kinds of hypoxium. um hypoxic hypoxia is what happens when um, oxygen pressure is reduced. so the hemoglobin leaving the lungs is not saturated_ that's what you think of when you think of hypoxia. um, it can happen if you go into high altitude, also it can happen, um with anything that reduces respiration like drugs some some diseases, um, cause you to breathe less and you're oxygen ni- partial pressure is not what would be if you were breathing normally. um also anything that weakens the respiratory muscles, causes uh hypoxic hypoxia. uh next is anemic hypoxia is what happens is when uh, the hemoglobin of oxygen is reduced uh hemoglobin is reduced. um, uh, what happens is your red blood cells, production is not what it is when you're healthy, and uh your er basically your erythropoiesis is low. and that can happen from stuff like iron deficiency or vitamin deficiency. alright? um stagnant hypoxia is when um you have reduction of the supply of oxygen because your blood supply isn't as good. so if your heart's weak, doesn't pump as much blood, your cells are gonna be hypoxic in the peripheral, portions of your body. also um, cytotoxic hypoxia this is very uh interesting basically y- your cells can't use oxygen, and that can happen, if you have, um stuff that's more <P :04> uh more has b- better affinity for uh hemoglobin than oxygen. so, let's say you're a smoker right anybody here smoke? yes alright. don't smoke it's really bad. um, <SS LAUGH> so basically right now f- um, your oxygen level, in your tissues is what w- would be at three thousand or eight thousand feet. right and you're ap- approximately at sea level alright? anybody here who's a runner? Doctor Zappa i know you're a runner right? so you ever notice that, if your running down the side of a busy road, you can't do as well as yo- were running in the park that's because all the carbon monoxide that's exp- uh from the cars, has a better affinity for hemoglobin and binds to hemoglobin and you can't get the oxygen to you're body. so, run in the park. <SU-F LAUGH> alright um, short term symptoms basically uh, you get dizziness giddiness, tingling sensations euphoria, blurred or tunnel vision, uh your lack of muscle contraction and a slow reaction time. uh you can see how, jumping out of planes with these symptoms wouldn't be exactly uh beneficial. okay uh, we'll move to parachuting. so there's a joke, uh sky divers say that the reason we jump out of planes is because we don't have enough oxygen to the brain. <SU-F LAUGH> it's not because we're crazy or deranged. alright um a hypoxic altitude abo- around thirteen thousand feet is the critical limit where you don't show any physiological symptoms um, the hemoglobin saturation is about eighty-eight percent um, you go above that symptoms begin to occur, different people show symptoms in different ways and that's, that's pretty much the basic idea there's no set, um, set, signs. different_ some people are gonna start breathing faster, i saw a kid just pass out, righ- right abo- right away we weren't even at, twenty-five thousand feet we were about, twelve and he already passed out. so- so people are, affected but differently. uh, so p- like as i said before hypoxia leads to a variety of symptoms uh which not necessarily conducive to parachuting um, slower reaction times decreased muscular contraction stuff like that can lead to um, a jumper misjudge altitude uh mistake equipment your, different rip cords are on different sides of your body, and you can collide with other jumpers since you have tunnel vision um, critical danger is passing out which prevents you for pulling the rip cord, and this will ultimately lead to a collision with the Earth if you don't have any special equipment on you that's gonna deploy the parachute, and since the momentum is conserved, you're gonna die. i've i've heard of people, that bounced off the ground... it's very rare if you if you're gonna_ i mean there're cases where, stewardess fell off a- air- off twenty-five thousand feet ch- all the way to the ground, and survive. uh these things are very rare and they don't happen often. most of the time, if you do bounce, i've heard of a person that did bounce off of the ground survived, two days later he died of a, massive internal injury. so, what you do to prevent this um, <SU-F LAUGH> jumpers use special oxygen masks and uh high-altitude suits, just like high-altitude pilots um, constant training in, in uh pressure chambers make you recognize these symptoms and know that you have hypoxia so you don't freak out. did anybody see Officer and a Gentleman? yes you know how the guy freaks out in the pressure chamber? you don't want that to happen when jumping out of planes <SS LAUGH> you want that to happen in training you don't want that to happen. alright um, also anytime that you're flying about eighteen thousand feet and doing a jump um there're special technicians that fly and they monitor the crew so if the q- the crew is showing symptoms of uh hypoxia, they're gonna say you can't jump you can jump you can't jump and uh, one of the advice they give if_ since pressure, and volume are, uh related, is don't eat baked b- beans and drink Budweiser before you jump, <SU-F LAUGH> it's not good. alright, now we'll then move to people living in high altitudes um, since person remaining at high altitudes for a long time he gradually become accustomed to it_ if anyone lived in Colorado you realize when you first get there, it's really hard to get up the stairs but maybe uh six months to a year later you're alright you know people come visit you and then you start laughing at 'em because they can't get up stairs. um, different populations show different adaptations. these are the symptoms, um you're increased pulmonary ventilation, you have more hemoglobin increased um diffusing capacity in the lungs increased cardiac output and um, your cells are better adapt to utilize the oxygen, however not everybody shows these symptoms in these particular order or, all these symptoms some populations show some some populations show others some populations show all. for example there was a study done on Tibetan and um, Andean high altitude natives, and the Tibetan ones showed pulmonary ventilation and increased hemoglobin in the blood but the Andean only showed uh increased cardiac output so their heart, uh beat a lot, they uh produced a lot more blood with each beat. uh also certain enzyme sys- sys- systems are mor plen- plentiful in animals that live above thirteen thousand feet and they help them utilize oxygen, more effectively. alright let's move into hypoxia and medicine um, hypoxia is linked to many uh major illnesses for example like Alzheimer's a- arthritis some cancers, occur because you have poor oxygen delivery to uh, vital tissues but, mild hypoxia is very beneficial um, it str- it strengthens the pulmonary system, increases strength and endurance and it boosts the immune system. that's why, um athletes train in high altitudes but, it doesn't necessarily show, performance increase for them, but treasmen- treatments like the hypoxia room, have been developed and what it does you sit in this room for a certain amount of time and then you leave, it's an intermittent, uh treatment you just can't sit in there for, all all the time, it only is effective, when you change your uh level of uh hypoxia that you're exposed to. so what it does is improve your oxygen delivery to the brain the joints and the peripheral tissues, through your body's own mechanisms. so you're not taking any kind of foreign substances in. uh the kidney, detects a lower pressure of oxygen then it releases erythropoietin which is a hormone_ which anybody studying for the M-CAT should memorize. <SU-F LAUGH> um, it stimulates the marrow to produce extra blood cells, the increased amount of red blood cells carry more oxygen to the muscles, making them work harder and longer. um, this system, like i said is only effective, if your exposure is intermittent, it's gonna increase oxygen delivery to the brain and peripheral tissues. so, it's like going to the U-S-A Olympic Center but only you're not there you're here. alright like i said, m- it has to be intermittent otherwise this uh some people show no improvement um, significant results have uh, been shown, with a cure of bronchial asthma sixty-three people have been cured and thirty-four, percent cured... that had diseases dependent o- hormone dependent conditions. um chronic pneumonia, shows a lot of progress shows (xx) disease does too. any kind of disorders protein lipid carbohydrate metabolism, people have been exposed to um, intermittent hypoxia show increased, benefit, an- obesity, depression, uh, post-surgical recovery has been showed to be speeded up. <P :04> alright now then we'll talk about cancer. um tumors are hypoxic, because blood vessels supplying them are relatively poorly organized and disoriented compared to normal tissue. uh this leads to inefficient oxygen, supply which is, hypoxia essentially. also as oxygen diffuses from the blood, it's depleted by normal cell metabolism, so cer- certain cells beyond a certain distance don't receive their share of nutrients and become hypoxic. so, who cares? well, most cancers as you know are treated with radiation right? and since hypoxic cells are uh, a lot more, re- uh resistant to radiation treatment it takes abo- about three times more radiation to kill them. so if you're being thrown in the radiation room, you're gonna be exposed to a lot more radiation so that's why hypoxia is very detrimental to, cancer patients. but the presence of hypoxia in tuma- tumors has been linked to uh, a lot of failures in clinical radio therapy so_ to achieve local tumor control. and the degree o- degree of hypoxia in cancer patients, has been demonstrated to predict the uh, efficacy of treatment. well we're almost done so don't fall asleep. <SS LAUGH> oh, in conclusion we've talked about what hypoxia is, what causes hypoxia different types symptoms we talked about parachuting, and we talked about some medicinal applications. <SS LAUGH> you have any questions. oh, and why i chose this topic <P :07> hey Doctor Zappa 
S1: yeah let's see if we can get this to work. okay, so we (xx)
S6: technical difficulties. 
S6: doesn't it always happen, we always have technology problems no matter (xx)
S1: alright now we have to switch this. <P :10> start it playing, [S6: alright ] <P :08> this might work here we go.
S6: alright, here's me suffering from symptoms at ten-thousand feet. [S1: that's you? ] yeah [SU-F: are you kidding? ] no i'm serious. <P :04> that's why i chose this topic. 
<P :05> 
S1: did we see you come down safely? 
S6: yeah i was fine. <SS LAUGH> <P :05> alright any questions? <P :04> thank you. 
S1: which one's yours 
S7: (xx) <P :05> (xx) easy to follow so 
S1: yeah... take a look (xx) it might take a few minutes to make it work (xx) 
S7: alright my name is Brett Boaton and i'm gonna be talking about, uh ventricular septal defect and other congenital heart disorders 
<P :07> 
S1: if it doesn't go [S7: this, ] right away cuz [S7: oh okay, ] it's probably bloated because you had big pictures on it 
S7: got you. (xx) 
S1: did- you pressed the forward arrow right? 
S7: yeah 
<P :12> 
S1: sorry (xx) 
<P :17> 
S1: it's never done this before. 
<P :05> 
S7: (xx) 
S1: oh yeah (xx) 
S1: oh come on.
S7: isn't there like someplace you can like (xx) fix computers for you.
S1: well, it's not even mine (xx)
S1: anybody with particularly good karma, today? <SS LAUGH> here you are just put your hands on it. 
<SU-M LAUGH> <P :08> 
S8: are the wires working this time? i mean c- 
S1: yes, [S8: okay ] this time it's the computer itself. [S8: oh okay ] that 
S8: cuz you need all the wires to get (xx) 
S1: that's blank because this is blank. 
S1: this is just the last time. 
SU-F: what if you turned it off and started all over? 
S1: yeah that's a possibility... except i can't really turn it off i can only restart it because i can't i can't get it run- i can't turn it (on.) 
S1: okay i'm gonna make the executive decision to give it up... [SS: oh ] [SU-F: sweet ] [S5: i'm so happy i went first oh my god ] so John and Brett we now have spaces for you to do next week we have, things have been moved around will that work? [SU-M: yeah ] okay, i will take the machine and throw it against the wall, <SU-F LAUGH> and go fix it. um so we have three more weeks of presentations. next week we will have six presentations and they will all work, so keep them to twelve minutes or less okay? the following week we now have one opening and the last week we have two openings so if anybody still wants (xx) sorry folks. 
<BREAK IN RECORDING ON 3/15, RESUMED 3/22> 
S1: Mad Cow Disease, by some very hot shot public health types it's gonna be at the School of Public Health tomorrow, in their, School of Public Health Auditorium number two, School of Public Health Building Two, Auditorium. i think that's what it is. it starts at eleven thirty and it goes to one forty-five, um if you're interested that's going on tomorrow. um we have, two proctors of the week this week, um first of all the honorable mentions this week are Andy Snarf Jeff Mack and Mosen Meladie but our winners this week are Brett Boatman and Sandi Johan. yay 
S1: any questions comments things you're beginning to worry about in terms of the end of the semester, student problems? i see that the, ceiling is still not fixed. <SS LAUGH> keep your head out of there. 
S6: i s- i saw them working outside of the lounge and i'm like can you guys do something about that and they were like no. and then they left. 
S1: so they were just ignoring you. 
S6: yeah 
S9: oh one morning i came in and they were in there and they said they were gonna come back (xx) minutes later. 
S1: and that was like weeks ago? 
S6: no they were pretty nice to talk to but they just (xx)
S1: i, i know that they do have trouble if there's still ice on the roof for example they can't get to where they need to be but the that's of course why it's leaking. okay. um how are the students doing are they, keeping up or are we still having people coming in on linear days, they doing alright [SU-M: yeah ] anything i should know about?
S10: i think like the last week wasn't that good (xx) (starting) to fall behind 
S1: they're starting to fall behind? [S10: yeah ] in terms the, of what they know for each quiz or in terms of number of quizzes?
S10: no the numbers of quizzes i mean we're up to like um almost ten pretty soon, and uh most people (got like) six or seven (on the last one so) 
S11: or three 
S12: yeah i had three.
<SS LAUGH> 
S1: okay you you you guys can, can be, you can help them, you can say you gotta get on it now. you can say do you want me to call Doctor Zappa and make her yell at you i mean i will do that but, <SS LAUGH> you're the ones who know [SU-M: i'll say that ] who they are. i- o- you can encourage them_ you know how awful it's gonna be if they don't do it. so use your knowledge you can really help them... anything else? has anybody_ here's a question has anybody not sent me their, peer evaluations? it's the last chance, (i'm gonna) start putting them together so i can send them all back to you. okay i'm gonna assume i have 'em all. who is going first today? 
SS: Wolfe 
S1: Wolfe? 
S1: don't turn this. <LAUGH> [S13: okay ] alright 
S13: so i just push (xx) 
S1: it goes like that if you break it then you're dead. [S13: <LAUGH> alright ] <P :05> and, because we are having somebody tape_ (if i) can't hear you_ i'm gonna be sitting right (there) if i can't hear you i'll stand right up [S13: okay ] at the very [S13: alright ] beginning and i'll do that for everybody.
S13: (alright) my name's John uh i'm doing necrotizing fasciitis, uh if you don't know what that means that's alright cuz, it's actually a pretty rare disease and it wasn't until like the nineteen nineties the media got a hold of it, and uh they coined the term, flesh eating disease. [SU-M: ooh ] so maybe you know it by that name. um, what we're gonna talk about is, what it is and we'll talk about the statistics of the disease, and how rare it is and uh, how a person gets it, and the symptoms of when you get it and uh the treatment, when you have it and uh, how it, how it eats at your skin uh the tissue (so) that's like the biochem part, and then how you can lower your risk, (of getting it.) so whoa what is it. <SS LAUGH> um, necrotizing fasciitis. so the necrotizing the name actually comes from necros- the ne- the necrotizing comes from necrosis which is uh, actually comes from the Greek word necros it's uh killing of the, living flesh. and then the fasciitis part is uh, comes from the word fasciae which is the tissue between the skin and the muscle. so, it's the necrotizing fasciitis and then it's also a bacterial disease not a viral disease, and, also it's caused by either, aerobic bac- bacteria or anaerobic bacteria or a combination of both of them. but the most common one is the aerobic bacteria, uh called the group A streptococcus and that's actually the same one that causes strep throat. so, except uh the only difference is, there's forty strands of um group A streptococcus and only two or three of them, can cause the necrotizing fasciitis. it's just differs in uh, the proteins on the bacteria we'll get into that later. um, so what is it? it continues, <LAUGH> uh so it infects into soft tissue and, um, it spreads pretty rapidly and uh, you, okay ye- n- normally it doesn't get into the muscle it just gets th- the um, tissue where the arteries and the fat, and nerves are, but um if it does get into muscle then that's pretty bad it's called necrotizing myositis um, your chances of survival go down, extremely, and it can destroy flesh of a rate of one inch per hour. and that's actually pretty fast like in grade school i don't know that's <GESTURES> i learned that was an inch so, like let's say you got it at night and you woke up with it and that's like, eight hours of your flesh gone i mean that's, that's pretty fast. but you also see symptoms of it too so, um, okay the statistics of it, <SS LAUGH> uh it's a pretty rare disease only three million people get it a year, uh and also, unfortunately it's a very high mortality rate up to seventy-six percent of people die from it. so um in the United States there's a hundred to four hundred and fifty cases of it. um, there's also like okay the death can occur after uh, up to fifteen hours, so if you think of that that's like, so fifteen inches of your flesh can be gone i mean that's, that's pretty serious so, it makes sense it can uh happen that quickly. and also um, fifteen to thirty percent of people have strep A but that's, that's not um that doesn't relate to necrotizing fasciitis strep that's just regular str- like one of the other, strands of strep A like strep throat or something but um yeah so fifteen to thirty percent don't even show any symptoms but you can still get uh necrotizing fasciitis from that strep... so how do you get it? um the disease itself doesn't spread like what i was just saying um you can't_ so once you get the necrotizing once it starts uh, <SS LAUGH> uh, <LAUGH> once it starts spreading in the flesh you can't like go go rub your hand on someone you don't like and, it's not like they're gonna get it. but um, this the group streptococcus and that's, pretty much all i'm gonna be talking about is the group A strep cuz that's all, that it's the most common and also the doctors know, scientists know the most about it. um so, you can spread that um easily and that's how, people can get the strep. and if you have um, a minor cut or opening or bruised skin it can_ the bacteria can enter through there and if you're in the presence of strep someone that has strep, that helps, get it and um, yeah so we already talked about how it's, your basic, serotype, of a strep so, the different M proteins on the bacteria, um cause it to be more virulent than others and, can therefore make it more um, powerful and it's uh, more powerful in how bad it can get. alright so the high risk groups, um if you're diabetic if you're a I-V drug user, if you're alcoholic or if you have the chicken pox. those these people tend to get it more than others although it doesn't really discriminate between age sex or gender um, i guess age and gender are the same_ or sex and gender but um race doesn't really, uh discriminate cuz um, children can get it and, older people can get it. the average age is like forty-three years old and, both women and men get it the same. so symptoms, within twenty-four hours alright um, the area that's infected will probably become sore you c- it'll um, you might get the flu probably little sick, and you'll probably get really thirsty. so it's really hard to tell if you have it, within the first twenty-four hours cuz you sh- basically show symptoms of having the flu. so if you go to the doctor he probably will have no idea, [SU-M: ew ] that it's that. um yeah sorry about the picture but um, so after three to four days, then you have advanced symptoms the area might swe- will probably swell um, i've actually seen it before and, how i've seen it it looked like a big uh, like a big bruise it looked pur- like a purplish bruise, and like red, and it was like swelled up a lot and, so yeah it that's after that was after like four or five day- like, yeah four or five days of it so, then you can you probably know something is going on uh, <LAUGH> it also starts to hurt really bad too, and um, if tha- if you continue to uh, go without any care then your blood pressure will decrease um, toxic shock can go into effect so your you can have kidney failure or liver failure and, unfortunately if it goes that bad you can, probably get unconscious. um here're some pictures, uh with patients that, with necrotizing fasciitis um, this is, probably this is after like a good six days i think of having it, you can see the, progression and, how it kills the, muscle and they turn black obviously and that's like a blister, that's pretty extreme form i haven't seen one that bad. this is actually isn't a symptom at all but that's uh, a person that had, it removed and that's, she had a skin graft and that's what it what it looks like. treatment um, right. i mean, it's kind of obvious that a treatme- you want to get rid of the infected tissue as soon as possible so it doesn't spread and the only way you can do that is since it's, um below the skin you can't really see it that's wh- th- th- that's why it's so misdiagnosed the first couple days cuz, it's under the skin and you can't really see it so, doctors just think it's a rash or something and, um so, within that first couple days it can spread and you really wanna, the sooner you go to the doctor, the sooner y- you uh can get the get it removed, then your the better your chances are. um also you'll probably get antibiotic like penicillin shots and, most people almost all people will have to um, will have like, flesh missing so they're gonna have to get a skin graft and if it gets bad they um probably usually have to amputate. but that's better than dying obviously. <SS LAUGH> alright the biochem of this so, how does this bacteria do this um it has this_ it gets into the cell by has um, hyaluronic activity which, which is outside the cell and, it has the the causes this protein to break it up and sometime (i me-) somehow it can get_ slide through the membrane to get into the cell. and once it's in the cell you can um it escapes the phagocytes cause once usually when you have a um bacterial disease the phagocytes come and eat it up right? but um it kind of like flows low under the radar, because it has this M protein the certain strand_ the like the two, um virulent strands that has the M, the certain M proteins can get by and it also has a hyaluronic capsule, which um, scientists have found if they have those two things, the phagocytes tend to miss it. and um, it can once it's inside it can uh, release the cytosine uh proteases which, um, break u- uh they cause proteins to_ or they cause_ they destroy tissue by breaking up the proteins, um, in the tissue and that can cause you, blocking uh, cell uh clotted or uh blood clotting and, they can that's basically, the r- the cytosine proteases break up, all the proteins within the tissue. so... and also these same proteins that break up the tissue, [SU-M: whoa ] um, i don't know. 
S1: uh hit cancel you'll pull the [S13: alright ] arrow down and cancel. <P :08> (got it) 
S13: alright so scientists believe this same protein causes the immune system not only to, fight the bacteria and try to kill it but also kill the um, the flesh, around it so, that is also another sign of how rapid it can uh spread cuz it's almost like a two on one, action going. you have the bacteria which is killing the flesh and then you also have the immune system which is trying to kill the bacteria and the flesh at the same time. and then what we know of the anaerobic bacteria is that it causes a to- it gives off toxic gas in the tissue and this causes like a cytotoxic um, hypoxia_ what Gary was kind of talking about last week. and, so it kind of st- starves the tissue of oxygen. and that's all i could find on anaerobic bacteria. to lower your risk um like i said, prompt diagnosis the sooner you b- the sooner you find it the better your chances are, and uh, keep your skin intact don't, cut if you get cuts you know band-aids whatever and, good hygiene. so, we talked about what it is bacterial disease, really rare but um really deadly, and you get you get it from a cut and, i- you can it's passed from strep- uh people that have strep A. and symptoms are the swelling of it and flu-like symptoms. and the treatment uh, is to basically remove the tissue, and we talked about how it eats cuz it has that M protein and the hyaluronic capsule which it kinda, get away, from the phagocytes and then to lower your risk, you uh, basically have good hygiene and uh prompt diagnosis... there are my references, any questions? yeah?
S14: okay let's say that you thought you had this but it didn't like, start eating your flesh yet, [S13: uhuh ] you went to the doctor and you just had like a rash or something but you wanted them to test for it, do they take a sample of your rash then? 
S13: um actually that's a good question um, i found that, they take a sample of your blood and they, test a lot of stuff and i heard um, the one test that helps the most cuz it's ki- it's really hard to tell especially at the beginning but M-R-Is i guess, um can test for it in the early stages and help doctors tell if it's, um, necrotizing fasciitis or not. but yeah usually, that's why it's so deadly cuz after you find it it's, you can_ after it's found it's after the symptoms have like progressed to, um, so bad. <SPEAKER WALKS INTO TABLE> ow. <SS LAUGH> any other questions? yeah Doctor Zappa? 
S1: what was the chicken pox connection? 
S13: yeah i i have no idea about that. <LAUGH> um i'm guessing, beca- i don't really know that much about chicken pox actually so, i'm guessing it probably i- lowers the immune system of the child somehow and, um, 
S1: maybe it's cuz they scratch all the time. 
S13: yeah yeah, [SU-M: (open sores) ] that's (that's true) and any other questions? no, alright. [S1: thanks ] yep. 
S7: alright uh, once again, i'm Brett Boaton and i'll be doing ventricular septal defect and other congenital heart disorders. um first off a congenital disorder is just simply a disorder that's present at birth. and uh, congenital abnor- abnormalities account for the majority of, uh of deaths of children under one year of age. um, as you can see from these numbers right here, uh there's about eighteen deaths per one-hundred thousand live births, of children less than one year old, and as you get older the number of deaths decrease. uh congenital heart disorders are often divided into two types there's are those are cyanotic which is uh blue discoloration caused by a relative lack of oxygen, or those are they're non-cyanotic. the most common cyanotic is uh known as the tetralogy of Fallot which i will be discussing later. uh the most common non-cyanotic ones are ventricular septal defect atrial septal defect and patent ductus arteriosus. uh ventricular septal defect is the most common of the, uh congenital heart disorders and is seen three times as often as uh A-S-D and P-D-A... um, the most cases of C-H-D the cause is unknown and difficult to determine, however there seems to be a strong genetic linkage, especially since, parents who have had one child with a, congenital heart disorder tend to have an increased risk of, having another child with a, congenital heart disorder. this increase in risk ranges from about one in one-thousand to about one in twenty. um, also infections in the mother are usually associated with children having abnormal hearts. uh here is a diagram of the heart and before i go into the specifics of uh V-S-D, it's important to review the anatomy and, cycle of the heart. uh se- as you can see here the inferior vena cava and superior vena cava, they dump blood into the right atrium, and pa- the right atrium it goes into the, right ventricle, from the right ventricle it goes through the pulmonary arteries to the lungs where it loads up on oxygen. it returns to the left atrium via the pulmonary veins, from here the blood flows down into the left ventricle, from the left ventricle it flows to the aorta up here, and the aorta it goes to the rest of the organs throughout the body, known as the systemic circuit. um of the forty thousand babies born each year with an abnormal heart, nine thousand of these babies have what is known as a ventricular septal defect. it's commonly referred to as a hole in the heart for it is simply a, hole in the septum that divides the left and right ventricles, uh this ven- this defect may, will vary in size from small to moderate to large. may vary in the location, possibly along the uh septum or near the heart valves, it also will vary in the number with multiple defects possible. um this hole in the septum allows blood to flow, uh back and forth between the left and right ventricle, and uh the amount and direction of flow is usually based on two things, one the size of the defect with larger defects obviously allowing, more blood to pass through, and also the directi- uh the resistance, the sys- if the systemic resistance is higher than the pulmonary resistance, which is the uh usual circumstance in childhood, the blood w- the blood will flow from the left ventricle to the right ventricle. in other words the blood is taking the uh path of least resistance, and also since the pressure in the, uh left ventricle is much higher than the blood uh pressure in the left vent- right ventricle, and as you know fluids always tend to flow from areas of higher pressure to areas of lower pressure. um, this defect will allow the blood to flow from the left ventricle to the right ventricle and from the right ventricle it will then enter the uh pulmonary arteries increasing the workload on the lungs... uh here's a picture, of a V-S-D, here you see the hole up there allowing the oxygen rich blood and the oxygen poor blood to mix, and the blood then, flows from the higher region to the_ higher pressure region to the lower pressure region and down through the pulmonary arteries to the lungs. here is uh another diagram of a normal heart versus a uh V-S-D, um, you can see here the on the right side the mixing of the blood, and the blood will then flow up through the pulmonary arteries into the lungs... uh there're different types of V-S-Ds based on their anatomic location, there are peri-membranous V-S-Ds which are located in the, membranous septum. which is uh, usually located near the heart valves. or you may have a uh muscular V-S-D which is located in the uh, lower portion of the septum. there're also inlet and outlet V-S-Ds which are located near the, uh entrance to the ventricular chamber and the exit, to the ventricular chamber respectively, uh membranous V-S-Ds account for about eighty percent, of uh congenital heart defects and, uh muscu- muscular V-S-Ds account for about ten percent. uh the symptoms of V-S-D usually include uh frequent respiratory infections, uh shortness of breath sweating paleness, you'll have a increased uh heart rate, and increased breathing due to the uh, extra workload on the heart and lungs, and you'll also will have_ typically have an arrhythmia, which is a disruption in the heart's electrical conduction system which controls the contraction of the atrium and the ventricles. uh possible cause of V-S-D, uh they think if the mother has uh rubella during pregnancy it might be transmitted to the fetus. or uh poor pre-natal nutrition, uh the mother drinks alcohol uh possibly diabetes, and if the mother is over forty years old. from these causes it is, easy to see some possible preventions, if the mother does have r- the mother should be vaccinized against rubella before pregnancy, uh avoid alcohol eat healthy and if they have diabetes make sure they control it uh during and before pregnancy. uh there're many ways to test for a V-S-D uh cardiologists will often use a, just a teth- stethoscope to listen for a heart murmur since a heart murmur is often the first clue of a V- a V-S-D. they also might use a electrocardiogram, which measures the directional spread of electrical activity in the heart. uh often they use echocardiograms which uh evaluate the valves and chambers. they do this by placing uh a transducer on the child's ribs, this transducer, picks up the echoes of high frequency sound waves, and transmit them, to electrical impulses which are then sent to an electrocardiogram machine_ echocardiogram machine. um, there're still questions remaining about the heart's anatomy or if these symptoms seem, uh out of proportion to the size of the defect they will often use a uh, a cardiac catheter. and uh (in) this catheter they make a small incision in the groin and they send it up through a blood vessel to the heart. using X-ray images to guide it through, um they also might use cardiac angiography which measures the degree of blocked blood flow in the coronary arteries, they often might use uh oxygen saturation tests. um if a child has a small defect uh fortunately it'll often, often close on it's own spontaneously, however however (if) the defect is, uh fr- rather large, uh medications such as uh digitalis and diuretics are used. uh digitalis improves the strength and efficiency of the heart, and uh controls the rate of the heartbeat. while diuretics will uh remove excess fluid that builds up in the lungs, which will also uh reduce the workload of the heart. um if the hole is still rather large after a couple years surgery is often necessary, and they do the surgery using a heart lung bypass machine, and they emplace a patch over the defect. here on the left you can see a uh, hole in the septum there. and on the right they've put uh, a small patch on it. usually, this one is made out of fabric uh Dakron, often they will use the patient's own tissue uh, their own pericardian tissue. uh and here's another picture of a uh patched up defect, you can see there is no longer any mixing of the blood, between the left and right ventricle. if left untreated uh V-S-D can lead to congestive heart failure in which the uh the blood is no longer able to meet the demands of the body. if the blood becomes backed up into the uh liver and G-I tract people have a, right sir- right sided heart failure. or if the blood becomes backed up into the lungs you'll have a left sided heart failure. uh most importantly a V-S-D can leave to, lead to infective endocarditis. and uh infective endocarditis is an infection of the linings of the valves and chambers of the heart. um, most common one is bacterial endocarditis, which is usually caused by uh streptococcus viridians, uh this will cause uh li- infections in the lining of the blood, and and uh you'll see some growths and these growths may dislodge and send clots to the brain or lungs. uh you also may see arrhythmias and delayed growth from children zero to five years old. um a very closely related defect is atrial septal defect, it pretty much shows the same symptoms as a ventricular septal defect instead of now there is a hole between the, uh left and right atrium, and you'll see an increase in blood flow in the pulmonary arteries, just like a V-S-D, uh here's a picture of an A-S-D, at the top you see there's a hole, which allows the blood to flow from the left atrium to the right atrium, down through the right ventricle and out to the pulmonary arteries. just like in a V-S-D. um a V-S-D may be part of a, larger scheme of malformation known as a tetralogy of Fallot. this occurs when the heart does not develop properly in the mother's womb, uh it is characterized by uh, a narrow region that leads from the uh right ventricle to the pulmonary artery, and since there's this region's very narrow the right ventricle has to work much harder to get the blood past the blockage, which causes the right ventricle to thicken. uh that is the ventricular hypertrophy. you also have a V-S-D and a uh aortic override, and uh... in this picture you see the rather large aortic valve, which causes the, pulmonary valve on the left to be very narrow. and now this high pressure right ventricle region, will cause blood to flow from the right ventricle to the left ventricle, and out so the uh systemic circuit to the left arm and brain, and since this blood (convicts) and then, go out to the rest of the body the baby will often appear blue, uh usually under its fingernails and its lips... um in nineteen_ in the mid-eighties the N-I-H initiated a series of uh research programs for, cardiac development and now there're currently, one hundred laboratories around the world dedicate full time to this, um they use frogs, fish, chickens rats and mice and fruit flies, in uh one particular fruit fly they found a gene that was needed to develop a heart, and embryos without this, uh gene do not develop a heart so they named it the Tinman Gene. of course after the Wizard of Oz character, um, they also discovered more than thirty other proteins that are import- important to heart development, uh such as muscle development valve formation and the electrical conduction system, uh one group in Cincinnati they produced a mouse without a gene... hold on 
<P :06> 
S1: must be something i didn't, load right.
S6: alright um, they found a mouse without a gene for the transforming growth factor beta-two and this uh mouse showed all the symptoms of a tetralogy of Fallot. they also, studied patients in East Finland with hypertrophic cardiomyopathy, uh this is relevant since muscular V-S-Ds, are often seen in patients with uh, hypertrophic cardiomyopathy more often then the general pediatric population, uh they found mutations in exon nineteen of the beta M-A-C gene and in uh, exon five of the alpha-tropo-miacine gene, interes- interestingly enough they found that, patients with uh mutations in the cardiac, beta-miacine (xx) all had V-S-Ds. um although V-S-Ds are typically congenital you can still get later in life, i read about one case in South Carolina where a five-year-old boy was shot in the chest by his brother with a B-B gun. and the, the pellet ripped a hole through his heart and was later found in his apex. uh fortunately surgery removed the apex and patched up the V-S-D. um the outlook for a complete recovery in patients with a small defect is excellent. as i said before they will often just close on their own. um, uh, these patients with small defects can actually participate in any physical activity any sport, um and even for large defects the outcome of surgery is very good, however if uh if left untreated many complications can arise. in conclusion, most causes of congenital heart disease are unknown, and they seem to be uh, genetic. uh ventricular septal defect is the most common of these congenital heart disorders, and is simply just a hole between the left and right ventricles, uh V-S-D may be part of a larger scheme known as a tetralogy of Fallot which is often very serious and, always requires surgery. also genetic research on cardiac development is still in its infancy and, many developments are sure to come. i chose this topic because um, i was actually born with a V-S-D, at about one week old i went into congestive heart failure, i had an arrhythmia, and my heart rate went up to about a hundred and sixty beats per minute, which really mean_ you're supposed to die when that happens but, lucky me i guess. <SS LAUGH> um, and so i figured i'd wanna research it and see what it's all about. and my resources, any questions?
S1: i assume you had surgery. 
S7: uh, actually i didn't have surgery. they only put me on uh, digitalis for uh, about a year. i had to take two drops a day, for a entire year, and, the hole actually closed on its own, fortunately. Gary? 
S6: why East Finland? is there something special about East Finland? 
S7: i don't know. who knows. 
S1: well i jus- i just have_ did you know that the Tinman Gene was discovered here at University of Michigan [S7: no i did not know that. ] in the Biology Department Rolf Bodmer (xx) discovered that. 
<P :04> 
S7: okay.
S1: thank you 
S15: alright (xx) <P :05> um, my topic is Fetal Alcohol Syndrome. today we're gonna look at what it is, how somebody gets it, biochemically we're gonna look a- at the effects of alcohol on the developing fetus, the symptoms, uh the prevention and then you're gonna get, (a brief) summary at the end. uh basically feta- Fetal Alcohol Syndrome is an A-R-B-D it's an alcohol related birth defect and, what happens is alcohol will cross the placenta from the mother to the fetus and it'll, damage the fetus while it's growing. uh it's the leading cause of mental retardation in the West it's past Down's syndrome, but it's also the leading cause of preventative, uh mental retardation. uh it's a disease that is the direct result of maternal drinking, uh it lasts a lifetime has negative, effects both, pre and post-natally, and fetal alcohol syndrome is characterized by three things it's, facial characteristics of the baby, uh growth growth deficiencies both in the womb and while it's living and then the mental, uh retardation that comes with the disease. um how do you get it? basically the only cause of fetal alcohol syndrome is maternal alcohol consumption, um m- i mean i might go into it later_ it says no alcohol consumption during pregnancy is (only way to be safe.) a lot of physicians are trying to find out you know well this much wine at this stage in the pregnancy you know if i drink you know once a month once a week one-point-five ounces eight ounces stuff like that it all comes down to, if you drink alcohol somehow your baby's gonna get affected however, the probability and severity of the disease does increase with the amount of alcohol consumed. so somebody that's a casual drinker versus a mother that's a binge drinker, the severity degrees_ the disease is gonna increase. um, biochemically alcohol's a teratogen and an embryo toxic it affects the, it affects the baby while it's developing in the fetus. uh one one thing that it does is affects feta- fetal blood flow. basically fetal- the fetus's blood flow is regulated by hormones and not, uh its brain, and what happens is ethanol it induces, it reduces the release of nitric oxide. nitric oxide has two roles in in the fetus. first of all it's a, get rid of free oxygen radicals and the second thing it's a vaso- vasodilator, which uh dilates the, blood vessels. um there's two theories, uh about how it does it they're basically related what happens is, is the moth- the mother will drink alcohol it induce oxidative stress and there'll be a bunch of free radicals those'll come they'll ha- affect the fetus so the nitric oxide's gonna be, shunted away from working on the blood vessels to getting rid of the free oxygen radicals. and one theory is that when it does that you can get a lot of platelet aggregation at the placenta wall and not enough blood is gonna be able to, to go through the placenta and you're not gonna get the nutrients or the oxygen diffusion from the mother to the fetus, and the second one is kind of like along the same lines is that you know nitric oxide is getting rid of these free oxygen radicals it's not gonna be able to dilate the vessels you're gonna have vasal constriction, and then you're gonna have chronic fetal hypoxia. uh oxative rad- i mean oxidative radicals are not good for the baby they, it damages the cells they damage D-N-A, uh induces apoptosis in some brain regions which is- which is how it causes mental retardation. uh the frontal lobe, is used for higher learning, cognitive processes, corpus callosum, uh relays message from the right and left brain a mother that drinks a lot of alcohol it affects the fetus's brain and you will actually, like you'll actually lose brain mass in those areas. also you lose dendrite spines in the hippocampus which is used for memory, um we'll talk about the effects of that later on. the symptoms_ i mean you have this thing called Fetal Alcohol Effects and Fetal Alcohol Syndrome. basically what F-A-E is, is the neurological effects it's not the full-blown Fetal Alcohol Syndrome so basically the baby will come out mentally retarded but it won't have the physical, characteristics. um a baby that's born with Fetal Alcohol Syndrome is really irritable, uh like like he said uh heart defects or fifty percent of the time you get congenitive heart failure, uh little muscle tone they're overreactive to stimuli i mean most babies are supposed to sleep up to twenty hours a day i mean right when they're born, and these babies they don't sleep well. and like i said with fetal alcohol effects i mean some, even if they drink a little, little alcohol can affect uh the baby's development uh drinking at at certain times, in the pregnancy. i mean here's a correlation that shows, N-C is no consumption P-E-A is just a little bit, and F-A-S is the total, and you can see that that uh with F-A-S you're gonna have no children above average, you're gonna have a lot of them with deficiency and then no con- no consumption you're gonna have a lot more children with normal I-Q than without. physical disabilities uh and here's a baby with 'em, doing my research i found a lot of pretty sad pictures a lot of 'em with um cleft palates that were that were messed up i mean, with with their eyes and just horrible pictures this is just one of 'em, you can see he has a small head circumference, uh the baby's eyes have this thing called epicanthal fol- folds which, short narrow eyes. the cle- the cleft palate you ca- really can't see here, um the thin upper lip microcephaly's just a small forehead, and the short upturned nose. um, behavioral disabilities basically you get this thing called static encephalopathy, and it's permanent unchanging brain damage. and so what- i mean what's gonna happen is this baby's gonna get older it's gonna have to function in society. so it'll gonna end up going to school and stuff like that and let's just say one day i- it'll like cheat or it'll steal or something so you tell the baby like you know_ w- well let's take an average baby and tell it you know don't cheat and then, then maybe it'll cheat again then you punish it and stuff like that, and the baby will end up learning right? because because the- they'll see that you know if i cheat i'll get punished i'll get grounded stuff like that. b- but babies with Fetal Alcohol Syndrome they don't have the physical brain matter right? so the- they_ in their brain they don't have the the ne- the nerves and the neurons to make these, to make to make these um, consequence i guess like, uh results you know what i mean like they can't learn. and so in school they d- they don't remember rules they're prone to lying stealing and cheating, sexually inappropriate activities a lot of times these children will have, psychological damage because the way they look children will make fun of 'em and stuff like that, they're really hyperactive they get A-D-D they get, i mean it's just it's just really basically hell for these children, as they go on in life. um, treatment prevention, i mean don't drink while you're pregnant, basically that's it. um, i came across one that said you know even after birth they'll say the mother didn't drink and then she drinks while she's breast feeding, uh the alcohol can affect her levels of prolactin and oxytocin which are used for breast milk, um that's not good for the baby either, and i mean you you'd figure that you know somebody who drinks they get liver failure somebody who drinks they can get into car accidents stuff like that and you've got like a you know big adult, weighs you know a hundred fifty two hundred some pounds and you've got a little fetus (that's) this big. and you'd think it'd be logical you know i mean whatever goes into the mother's gonna cross the placenta and affect the baby, but it's only been around since nineteen seventy-three i think that's when they put the facial the growth and the mental deficiencies and linked it to Fetal Alcohol Syndrome. and um, there's a lot of_ like i said earlier there's a lot of studies being done right now, at a bunch of hospitals i mean what they're trying to do is they're trying to find out you know how much alcohol is safe for the mother to drink. um, they're and they're tr- they're fin- they're also finding out that, like there's also neurotransmitter imbalances with children that that um, drink a lot of alcohol_ i don't want to go into all of the studies cuz, it's kind of boring. um there's this picture i came across that says this is a four-year-old girl that has Fetal Alcohol Syndrome. she will need structure and support services for the rest of her life, without early identifei- fication intervention, many children with F-A-S will end up in jail before they're adults. (and it's) estimated that fifty to eighty percent of the persons in the criminal justice system suffer brain damage due to alcohol exposure before they born. uh, i mean fifty to eighty percent that's pretty big and uh to prevent F-A-S don't drink while you're pregnant. um, summary conclusion Fetal Alcohol Syndrome is a alcohol related birth defect, the three major things is the, growth deficiencies the mental retardation and there's the physical effects of the face. it's a teratogen it'll just cross the placenta from the mother, bypassing diffusion to the baby and it'll screw it up while it's developing. it has like i said negative ef- physical and mental effects and i mean you_ the only cause of it is maternal alcohol consumption so the only prevention is don't drink while you're pregnant. references, questions comments or concerns? yeah?
S16: uh, okay did you, do the <LAUGH> do most of these cases come from, like events where the mother consumes like, large quantities of alcohol or does it ever come from cases where you know someone doesn't know they're pregnant in the early stages and they drink, and then (xx) 
S15: alright, yeah like i said i mean i got this one study that said they did at Chapel Hill North Carolina, that says that even one drinking session, of you know five drinks really early on in the pregnancy can cause to can cause mental retardation (and many of the) facial defects. i mean, i mean obviously you know if a women gets pregnant she doesn't know for a little bit and so even you know drinking really er- early on in the pregnancy can affect it. but obviously if the mother binge drinks and stuff like that, there's a heavy_ like the more alcohol she consumes the more alcohol's gonna be in the fetus, the worse it's gonna be. 
S10: (i thought) the uh first trimester is the most important uh one for, restraining your drinking (xx) did you read anything about like drinking after the, se- second (term?) 
S15: i mean i mean yeah uh, not with me i mean obviously, because the baby the fetus is growing more in the first and second trimester, i mean that's when most of the neurological stuff does happen, but still i mean they are they are trying to do research to find out which stage in the pregnancy is the worst but, i mean i didn't come across one thing that said it's okay to drink in the, s- third trimester it's it's okay to drink in the eighth month i mean any alcohol consumed will affect the baby. 
S13: did you find any stuff that said um, it was eas- or it wasn't as bad when they did it through breast feeding? 
S15: no i mean, i mean the breast feeding thing i mean that's not the that's not it_ breast feeding the baby's already done Fetal Alcohol Syndrome's actually alcohol in utero, it's when the baby is developing and that just affects the amount of breast milk, and it can cross from the mother to the baby, through the through milk. (and that's what i understood) 
S1: i know this isn't, what you were looking at but did you read anything about how, alcohol can harm sperm and therefore there is an effect from, paternal drinking. 
S15: um, no honestly. yeah 
S14: um you know how you showed that picture of the little girl behind bars. [S15: yeah ] you said that fifty to eighty percent of people who are, in prisons um, are related to this um [S15: somehow yeah yeah ] F-A-S how how did they determine that? did the like, can you test for it like in a- an adult or do they just try to go back and talk to (xx) 
S15: i think i i th- well the thing th- the thing that really sucks is that uh, like whenever a mother will come in and she's pregnant a physician will be like you know, are you drinking this and that a lot of mothers don't like, they don't, record it you know what i mean and so, i mean the thing is, i mean i don't want to say they're uneducated or whatever but the doctors are like you know do you smoke do you drink the the mothers don't want to admit it cuz they don't want to look like bad mothers so they won't and then, it'll it'll end up being get worse so, but i mean along those li- i don't know how exactly they did it. but th- but i mean the one thing they're trying to do is they're trying to target like residents and interns, to actually like you know really, really you know hammer the, mother especially in the low socioeconomic areas, where they aren't as educated they they wouldn't know, as much... 
S1: thank you again.
S1: yeah, you are it's jus- just the biochem? (xx) 
S17: (xx) stress and cortisol 
S1: you nervous? 
S17: yeah <LAUGH> 
<P :04> 
S1: lemme show you here how to work this [S17: (oh sorry) ] (this alright?) [S17: yeah <LAUGH> ] um, to go forward you have to push this button, (xx) much better, and if that little thing comes on just hit, cancel. [S17: okay <LAUGH> ] and if you're too quiet, i'll stand up at the very (beginning) yeah. 
<P :08> 
S17: hi i'm Anjali Balaff i'm gonna be talking about stress and cortisol today, and um all the negative effects of that. this is a little, uh it's just a brief outline of what i'm talking about first i'll go into a little bit about stress, uh and the different types of it the symptoms, then i'll talk more about cortisol and then i'll debate the two. um, okay. stress is just basically defined as a reaction of the mind and body against change, the change doesn't have to be an unpleasant one it could be a good change a bad change it's just something that your body's not ready to face that creates stress. and it produces bodily or mental tension it's caused by pressure to meet demands or, just things that your body isn't ready to, uh face. there're mainly three types of stress the first is mechanical stress and that's caused by physical, factors like lifting heavy objects exercising too much or not exercising enough. uh mental stress is caused by emotional aspects or social aspects and that's uh, like not getting enough sleep or marriage problems relationship problems uh, work problems things like that. and finally there's chemical stress which is a much broader category but it's mostly a, chemical input uh in your body and environmental factors, so it's caused by pollution or um, fumes from your furniture or carpets things you may not think that could cause stress but they do. those are chemicals uh, oops it's jus- <SU-M LAUGH> okay um, the different symptoms of stress they're not all that easy to recognize but it's important to make notice of them. they're a result of pressure from change and there're three types of symptoms. physical symptoms are uh, symptoms like, uh, they they include difficulty sleeping nausea dizziness, um they can be even more dangerous like s- chest pains or difficulty breathing. emotional symptoms are uh include troubles relaxing fear anxiety, things like that uh and social, symptoms are uneasiness being alone, uh but not accepting invitations not wanting to go out, things like that... um there're many different effects of stress, it lowers the body's ability to adapt to changes in the environment, but i'm mainly going to be talking about is how it causes elevated levels of cortisol in your body and um, how that creates many problems if you have too much cortisol if you stress too much. so now i'm gonna talk about cortisol that's just uh, the structure of it. um cortisol is also known as hydrocortisone, it's uh it's the principal glucocorticoid and glucocorticoids um, uh stimulate gluconeogenesis they increase the breakdown of proteins they help with mobilization of fatty acids, and they're also inhibitors of inflammatory response. um it's secreted by the adrenal cortex, and uh its secretion enables us to adapt to external changes and stress. this is a, picture of an adrenal gland that_ we have two adrenal glands they're located on top of the kidneys. um each one has an inner medulla and an outer cortex and as you can see cortisol is produced and secreted mainly by the outer cor- uh cortex, along with other hormones... and the way cortisol is synthesized as i said it's co- uh synthesized in the outer cortex of the adrenal glands, it's levels are determined by the hypoth- hypothalamic pituitary adrenal cortex axis and i'll be showing you a picture of that so i'll i'll explain that later. it's also affected by the sleep wake cycle which is the, uh cir- circadian rhythm, and it's monitored by neural stress signals. and its secretion is regulated by A-C-T-H which i'll also, show you a diagram. this is these are just the major steps in the synthesis of cortisol and other, major hormones. they all start out with uh cholesterol, and that produces cortisol. this is the hypothalamic pituitary adrenal cortex, axis and what happens is a stress is put on the hypothalamus and that produces, cort- uh corticotrophic releasing hormone, and then uh that goes into the pituitary which releases adrenal corticotrophic hormone which is A-C-T-H. and then that regulates cortisol production and then cortisol has a negative feedback mechanism on both A-C-T-H and C-R-H, um and so in this uh hypothalamic pituitary axis uh, the negative feedback mechanism suppresses A-C-T-H and C-R-H. <P :04> okay um, levels of cortisol are maintained by a cir- cir- i spelled it wrong but it's circadian rhythm. that's just your sleep wake cycle it's established during infancy, it's regulated by uh, neural signals and, the way they do that is they control the negative feedback mechanism of cortisol in the, hypothalamus, it has episodic secretions due to A-C-T-H um and that's, uh cortisol's transformation from a recursor of A-C-T-H that's how it's, regulated. this is a graph, of the different levels of cortisol in your body, um they're lowest when you first sleep but there's a steep incline around eight A-M, it's highest around nine and then it gradually tapers off until, the night again... okay there're many different roles of cortisol it's essential for protein lipid and carbohydrate metabolism, it aids in muscle tissue maintenance and the way it does that is that it promotes amino acid release giving our body more energy, it suppresses inflammatory responses and the way it does that is it down- regulates phospholipase A-two activity, and that promotes formation of precursors of prostaglandins. um it promotes conservation of gluconeo- g- glucose and the way it does that is by stimulating gluconeogenesis by enhancing the activity of enzymes in the liver, and promoting more glycogen breakdown into glucose. um it also_ oh this is (where we get into) gluconeogenesis. it increases mobilization of free fatty acids, and that it activates the release of these fatty acids from adipose tissues by aiding in the synthesis of hormone sensitive (lygase.) um, and it depresses immune reactions. okay uh the mismatch theory is, uh s- scientists were wondering if elevated levels of cortisol are so bad for the body then why does our body produce so much of it when we're stressed so they traced it back to millions of years ago, to early human life in Africa where, um if a human heard a lion's roar or something related to a life threatening situation then their cortisol levels would immediately rise to counter that, to calm their brain down, release more amino acids and give us more energy. so, back then that was necessary it was important it was life saving. but today we don't really experience life threatening situations but we do experience constant stress, but our body cannot dif- differentiate between a life threatening situation and the stress so, every time we do stress over something as little as meeting a deadline our cortisol levels immediately shoot up, and that leads to many different problems and, um this is called a mismat- a mismatch theory by evolutionary biologists, and uh they just say that it creates health problems mainly due to cortisol cortisol is the main culprit here. so these are some of the effects of high levels of cortisol, uh one is overtraining syndrome and that is when you're working out, you do definitely need cortisol in your body but if you work out too much, then more cortisol's p- pumped out and more proteins are broken down you have less energy, and it ends up, i mean, not being good obviously. there's Addison's disease which is actually due to lower levels of cortisol and that's due to um, it's due to, uh destruction of the adrenal cortex. then there's Cushing syndrome and that's due due to adrenal hyperfunction which produces more A-C-T-H, in the pituitary. other effects are hypertension which is high blood pressure osteoporosis glaucoma impairment of immune and reproductive systems. this is just a, picture of all the different effects that you can have you can start out with just depression but lead to, more dangerous things like cardiovascular disease schizophrenia a- uh anorexia, so you know it's not that good to have high levels. um and this was an interesting thing i found there was uh research done in New York, that showed a correlation between post-traumatic stress disorder and lower levels of cortisol, in humans, and they studied it on Holocaust survivors and they found that, people with post-traumatic stress disorder have lower cortisol levels than other people and, they mainly said that um trauma alone doesn't lead to post-traumatic stress disorder it's cortisol, the lower levels of cortisol that leads that lead to it, and they said uh the reason that maybe is because the brain becomes hypersensitive to the effects of cortisol. and this is a graph that they did um the blue is the control group and as you can see the, Holocaust offspring with the lowest levels of cortisol definitely had post-traumatic stress disorder, whether or not their parents had it. and, this is some other research that's being done on a correlation between stress and H-I-V. there're two theories that are being studied the first is that H-I-V forces adrenal glands to secrete lots of cortisol and that uh in turn damages the immune system, the second theory is that one of H-I-V's proteins acts as a glucocorticoid and this also damages the immune system. it's really controversial they're still doing a lot of research on it um, it's still in its middle stages but what they're basically saying is that H-I-V isn't the killer, cortisol is. that that's the main reason why these people are dying. but as i mean obviously that's very controversial so they're still s- doing research on it. so basically you can see high levels of cortisol are not good you shouldn't stress too much so you should learn stress management and prevention. ways you can do that is you can change your diet um, keep well hydrated eat r- uh foods rich in protein and minerals, but the main thing to do is just relax don't let the stress get to you, be able to recognize your stress symptoms and, um act on that. they've also come up with some medications that are used to lower cortisol levels, R-U-four-eighty-six and procaine are two of the drugs that are being used in the H-I-V s- uh studies. R-U-four-eighty-six is actually an abortion pill they're both, seen to reduce the levels of cortisol in H-I-V patients, cort-block is actually um, the world's first natural cortisol compou- cortisol compou- compound and that's used for weight training and it's just, shown to, suppress cortisol production and enables greater amino acid uptake. um these are just some interesting facts i found, forty-two percent of all adults suffer adverse health effects due to stress, stress has been linked to all the leading causes of death including heart disease cancer accidents cirrhosis and suicide, nearly half of all American workers suffer from symptoms of burnout a disabling reaction to stress on the job, um and then, high cortisol levels predict high alcohol consumption in young adults, alcohol withdrawal leads to increased production of cortisol which can be toxic to nerve cells and even lead to damage to the hippocampus. so, um in conclusion we see that stress leads to high levels of cortisol high levels of cortisol lead to a lot of different problems health problems mental problems so you should learn good stress management to counter the negative effects of this um, you change your diet or just relax, and it's just important to recognize all of that. these are the references... any questions? 
S1: did you see anything about, stress and cortisol levels in relationship to um cancer survival? 
S17: yeah um i s- like it was mentioned in a lot of the articles i read but not like it was also mentioned in the H-I-V article but they never really elaborated on it. so i'm not really sure what the correlation is. there is a correlation but i think there's still a lot of research being done on it so they're not really sure yet. 
<P :04> 
S1: thank you again. 
S18: okay, alright [S1: (xx) ] okay <LAUGH> 
S1: (xx) it's gonna be alright now (xx) [S18: okay ] alright, good. 
<P :05> 
S18: um my name's Paveny by the way um and my talk today's gonna be on obesity, um i's actually just gonna start off with this, i found a really funny article while i was looking this up about how, um the cartoon Fat Albert actually, promoted young children to go out and eat more engage in like <SS LAUGH> binge eating and, they think you know like i- i mean the whole article was_ i mean it was written by some like editorial person it was basically that like this cartoon was like a bad influence on young children so i just thought it was kind of funny so (xx) um, okay. um, so the basic question that is, that underlies obesity is whether it's caused by biological, um whether bio- it's biologically caused or whether it's an environmental um condition. um there's been a lot of research a lot of research on the biology of obesity and there's been a significant amount of it on (the) environmental explanations too so we're just gonna go through both of those and, um try to figure out you know which one it's (leading) to... okay so we're gonna start off by, defining obesity. um obesity's basically when your B-M-I which is your body mass index is greater than or equal to thirty. um basically how y- you guys can all figure out your body mass index if you want to it's um, your weight over your height squared, and um, it's so basically it's an epidemic and it's defined as having an excess of body fat. um the people who are most prone to becoming obese are people who are overweight and that's defined as your body mass index as being between twenty-five and thirty, um people in industrialized countries just because there's a lot of money put into um advertising for food um commercials and stuff like that. um and obviously inactive a- lifestyles um, also leads to obesity. alright these are just some interesting facts that we came ac- that i came across, um twenty-five percent of all American adults are obese which is very high compared to other countries as i mentioned before because we live in an industrialized country um fourteen percent of the children between twelve and nineteen are overweight and, obesity um leads to fifty to a hundred percent increase risk in death which is a pretty serious um, number. so why should we care? um, obesity leads to <SU-M LAUGH> a higher risk of heart attacks and this is because um as we all learned fat um clogs up your arteries and, that causes um, heart attacks. um obesity can also lead to diabetes because fat um tissues are found to um, actually inactivate insulin receptors, and that um can lead to type two diabetes. um obesity also slows down your brain function um, this was actually they did a study on rats um, rats that um take in a lot of fat they actually have problems um with memory and learning so um they, the researchers encourage you to um eat high carbohydrate diets instead of fat diets um so i just thought that would be interesting for all you M-CAT people who are studying now. <SU-M LAUGH> okay is it biological? basically what happens is they found a gene called the O-B gene which is e- responsible for the expression um, of a substance called lipton_ leptin. um leptin is, directly respon- uh or is responsible for decreasing weight or decreasing eating which is you know which would decrease your weight. um and it does this by affecting another substance called neuropeptide Y. so basically, people who are obese_ uh leptin's produced by adipose tissues. so you would think people who are obese, they have a lot of fat tissues so_ and fat tissues secrete leptin so why is that people who are obese tend to overeat a lot? and so that was like the main question that the researchers were trying to figure out. the answer to that question is that, in addition to secreting um leptin fat tissues also inactivate insulin receptors as i mentioned before. so this inactivation of insulin receptors triggers the brain to think that there's not a lot of glucose in your blood. so then the brain's like alright, this this person's hungry so we need to start eating more. so the brain releases neuropeptide Y directly into the hypothalamus, which is responsible for eating, for um increased feeding. so what you have is you have a high level of leptin in your body, and a high level of neuropeptide Y in your brain. neuropeptide Y stimulates feeding whereas leptin, is supposed to act on neuropeptide Y to decrease feeding. but since neuropeptide Y is already in the brain, its effects um or leptin's effects doesn't, leptin does not affect neuropeptide Y's activity cuz it's already synthesized and it's already in the brain. okay we just went through that. alright so basically how is this all found out? they um, did a lot of work on mice and rats obviously and they're_ they have O-B O-B mice which um are lacking the O-B gene and these mi- so these mice they don't produce um, a lot of leptin. and they were found to be obese as um, was hypothesized by the researchers. so then they went and they took out the gene that makes neuropeptide Y as well as the gene that makes leptin. and these mice_ so they thought okay since we're taking out both these genes there's not gonna be any leptin, but there's not gonna be any neuropeptide Y to stimulate feeding. so they thought that these mice um, should show decreased um decreased weight like, lower than normal or like about normal. but what actually ended up happening was these mice were, heavier than the normal mice, but they were, lighter than the mice that were lacked in leptin altogether. so this led to the conclusion by researchers that um leptin acts not just on neuropeptide Y but there's also other um hormones and substances in the body that are responsible for feeding. so that's basically where research is heading now is um trying to figure out exactly, what else is responsible for increased feeding. alright, environmental um, the environmental studies that have been done have been on, family life um it's been found that if you're from a cohesive family w- um that has a set like, kind of like a leader of the family and like rules and stuff um you tend to be better eaters just because you're taught at a younger age um, how to be structured and stuff like that. um whereas if there is no like set leader like, person ru- like leading the f- ruling the family um people tend to not develop um structured eating habits. um moods is another one um it's been found that if you're dieting or restricting um your food intake and if you're feeling lonely or depressed or, just socially withdrawn you actually tend to eat more in those situations than people who are not dieting and who feel lonely. um activity um also is another one obviously um it's a big problem especially in the United States as i mentioned earlier just because of technological advancements that we have um, you know we have cars and T-V and so just, um our a- lifestyles are just a lot more passive than people in um more underdeveloped countries. um in inter- an interesting study that was found um, supporting the environmental causes of obesity, um had to do with a group of Indians um called the Pima Indians. um they were actually separated_ they lived in Mexico and they were actually separated some time around the Middle Ages and they're_ um half of the Indians um moved to Arizona where they were forced to like, take on the American way of eating and um, diets and stuff and the other half still lived uh still lived in Mexico. it was found that the Indians that live in Arizona were on average fifty-seven pounds heavier than the Indians that lived in Mexico. and they're also um, thought to be like, the- they're they're also re- referred to being like the most obese people um in the whole, country so i thought that was just an interesting, study that was done. okay treatments for obesity. um these are the biologic- there's two ways to biologically treat obesity. one is called the single mechanism and, that type of treatment_ or th- those drugs they um, are geared towards just dealing with one problem like, i- an example would be to um decrease neuropeptide Y. like the drug would just be interested in doing that. and these types of drugs are only ten percent efficient cuz as i mentioned earlier there's a lot more that goes on with obesity than just, um the O-B gene and neuropeptide Y. and the- i mean ten percent like it'll decrease your body weight by ten percent and that's, in mo- most cases that's good enough to get out of the danger zone for being obese, but people don't stick with these treatments just because they don't see any progress in their body weight so they're just like alright whatever, and they give up on the treatments. um double mechanism um treatments um, target two pathways and an example would be to stimulate, um epinephrine release and serotonin uptake and these types of drugs show a twenty percent um, decrease in body weight and so they're more successful just because people see the effects um sooner. so basically in conclusion um we just went over the quick facts and tried to identify the problem and the prevalence of the problem, um we searched for a cause, is it biological or environmental? um there hasn't been, i mean people's there hasn't been like, a resolution in this argument um, people think that if you practice good eating habits as well as like, maintain um or exercise once in a while like once or twice a week they say is even good enough. um then you can reduce your, risks of becoming obese. and then we just went through the treatments and, that's it those are my references. any questions? 
S1: is Michigan still (number one) fattest state? 
<SU-F LAUGH> 
S18: yeah... <LAUGH> okay, thanks.
S1: thank you everybody um, five piles on the front and if you wanna look at my new computer (you can) 
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