~54th Baked Rice with Cheese Crapbox~
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just as i tot.. maybe OM can confirm it... when he comes back from dinner.Originally posted by alfagal:collagen is jus a marketing gimmick. not proven to have effective results...as claimed by FDA...same goes to those products used topically....
while i'm at it... isnt the wad glucosamine also the same?? dunno if i got the right name. the one that is supposedly good for the bones... -
yes.. and you are???Originally posted by Chelzea:U teaching A level students?
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Originally posted by alfagal:
ooo..what is it about?
[b]
met e press
/b] -
yes, these inflammatory cells are alive....neutrophils, lymphocytes, later the neutophils reduce in number and the lymphocytes and macrophages predominate as the surface mucosal cells break down and get phagocytozed..Originally posted by starblue:what you've just said is basically what the websites said. but i wanna know the process of the formation of an ulcer, from the time the cause strikes to the perfect formation of the white disc. but wait, you said the white thing are inflammatory cells. are these cells alive? or are they like pus (with all its dead glory of cells which died in the immune battle)? when the ulcers subside, and the whiteness disappears, is it cos these cells are phagocytosized??
If you take repeated biopsy sample during the formation of the ulcer and look under the microscope, the first thing you will see is dilatation of the capillaries beneath the mucosa. The capillaries become engorged with blood (due to the effect of cytokines like nitrous oxide etc), the neutrophils and lymphocytes move to the sides of the blood stream...what we call margination. Then these white blood cells roll along the endothelium (lining of blood capilaries) slow down and stick to the endothelial cells. This is due to the interaction of molecules on the surface of inflammatory cells and endothelial cells (such as E- selectin on the endothelial cells that have been activated by cytokines eg. TNFalpha) interacting with PSGL1 on the inflammatory cells. Finally, they stop and squeeze through the intercellular spaces between endothelial cells to enter the tissue spaces, along with serum fluid.
The dilation of blood vessels cause the redness in the area that will eventually break down. As the fluid and inflammatory cells exude out, the area becomes swollen and paler in the centre, whilst the periphery which shows the vasodilatation remains red.
The exuded inflammatory cells are attracted there by cytokines such as IL-1 (interleukin-1) and TNF alpha. They degranulate and release the proteolytic enzymes that attack the surface epithelial cells, which break down. As the inflammation proceeeds, lymphocytes (T cells in the main and some studies suggest mainly gamma-delta T cells) come in to the area with macrophages. They begin to mop up and phagocytose the cell debris and dying epithelial cells. The breadown down of surface epithelial cells result in the central defect as the ulcer forms.
sorry very long and boring but you want details right? -
but i have rx good testimonials for glucosamine...Originally posted by starblue:just as i tot.. maybe OM can confirm it... when he comes back from dinner.
while i'm at it... isnt the wad glucosamine also the same?? dunno if i got the right name. the one that is supposedly good for the bones...
it does not reverse e effect of bad joints, but it helps and controls e situation esp for artritis...
its a good supplement for pple who feels ache btw joints, not for bones.. -
took photos..Originally posted by StarPuppy:ooo..what is it about?
prob wld b in e chi papers..sin min i think..but dunno when...
did interview w other gals.. -
whats the great thing u did?Originally posted by alfagal:took photos..
prob wld b in e chi papers..sin min i think..but dunno when...
did interview w other gals..
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hmm.. thought the glucosamine isn't proven stuff yet..
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lol..nothing much..Originally posted by StarPuppy:whats the great thing u did?
jus something bimbo of competing in a pagaent? -
yes, the lactic acid explains the early aches that you get...Originally posted by starblue:i dun quite agree with the lactic acid explanation... i tot the aches triggered by lactic acid build-up is immediate to after the vigorous exercise and is quickly dissipated after you've repaid your oxygen debt? so i dun think that explains the continued and delayed muscle aches we experience after hard exercise.
and if that's the case, then damaged and cytokine-releasing cells are the explanation. in which case, are u saying that muscle aches are a result of damage from exercise? and while we're at cytokines, arent those the buggers which trigger apoptosis?? are our cells dying as we ache, literally?? o.O
If you are referring to the delayed aches the next day, it's the microscopic tears in the muscle fibres...that's why sports medicine people always tell us to stretch and make sure the muscles are warm before vigorous exercise. Muscle contraction is an enzymatic, biochemical process and as you know, enzymes work at an optimal temperature. Also, the contractile properties of muscle is relatewd to the degree of stretch...did you do those experiments measuring the degree contraction in a leg muscle from a frog at different extents of muscle stretch?
Cytokines play a variety of roles..they do trigger apoptosis but they are also very important for inflammation and cancer. Apoptosis can be triggered by various mechanisms and there are two major pathways...intrinsic via bcl2-bax and calicum release or extrinsic by interaction of fas (CD95) and fas-ligand in the TNF receptor pathway.
No t all your cells will die as tyou ache...they are damaged and the cytokines release cause you to ache, telling you there is some injury. But injured cells can recover...not all die... -
okie nightz all..tired le..
*alfagal has jus signed out..* -
good night alfieOriginally posted by alfagal:okie nightz all..tired le..
*alfagal has jus signed out..*
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wow. so that's how it happens. why didnt they teach this in school??Originally posted by oxford mushroom:yes, these inflammatory cells are alive....neutrophils, lymphocytes, later the neutophils reduce in number and the lymphocytes and macrophages predominate as the surface mucosal cells break down and get phagocytozed..
If you take repeated biopsy sample during the formation of the ulcer and look under the microscope, the first thing you will see is dilatation of the capillaries beneath the mucosa. The capillaries become engorged with blood (due to the effect of cytokines like nitrous oxide etc), the neutrophils and lymphocytes move to the sides of the blood stream...what we call margination. Then these white blood cells roll along the endothelium (lining of blood capilaries) slow down and stick to the endothelial cells. This is due to the interaction of molecules on the surface of inflammatory cells and endothelial cells (such as E- selectin on the endothelial cells that have been activated by cytokines eg. TNFalpha) interacting with PSGL1 on the inflammatory cells. Finally, they stop and squeeze through the intercellular spaces between endothelial cells to enter the tissue spaces, along with serum fluid.
The dilation of blood vessels cause the redness in the area that will eventually break down. As the fluid and inflammatory cells exude out, the area becomes swollen and paler in the centre, whilst the periphery which shows the vasodilatation remains red.
The exuded inflammatory cells are attracted there by cytokines such as IL-1 (interleukin-1) and TNF alpha. They degranulate and release the proteolytic enzymes that attack the surface epithelial cells, which break down. As the inflammation proceeeds, lymphocytes (T cells in the main and some studies suggest mainly gamma-delta T cells) come in to the area with macrophages. They begin to mop up and phagocytose the cell debris and dying epithelial cells. The breadown down of surface epithelial cells result in the central defect as the ulcer forms.
sorry very long and boring but you want details right?
so after all these the white thing forms. what happens as it heals??? -
Originally posted by alfagal:took photos..
prob wld b in e chi papers..sin min i think..but dunno when...
did interview w other gals.. 
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melatonin is produced by the pineal gland and regulates the diurnal rhythm in response to light...so people take it to 'reset' their sleep rhythm when travelling and to treat jetlag.Originally posted by starblue:i remember learning about melantonin administered to prevent jetlag. but i still dun exactly understand what time you have to take it (for say, traveling from sg to US) and how it prevents the jetlag by desensitization. alfajie can enlighten me please? -
ah yes... the joints.. slipped my mind for a moment...Originally posted by alfagal:but i have rx good testimonials for glucosamine...
it does not reverse e effect of bad joints, but it helps and controls e situation esp for artritis...
its a good supplement for pple who feels ache btw joints, not for bones..
OM, how is glucosamine suppose to help joints?? does it really work> -
goodnight alfie
sleep well..
i think i'm going to catch some zzzs too..
goodnight everyone -
no wait... the prof says it's used to PREVENT jetlag, not just to treat. something like if you're travelling from sg to us, then u take it dunno how many hours before arrival time (when in the plane) and the brain will be desensitised and not produce any melatonin when u reach. so if you leave sg at night, and expect to arrive at dawn or something liddat. you will have already adjusted your sleep.Originally posted by oxford mushroom:melatonin is produced by the pineal gland and regulates the diurnal rhythm in response to light...so people take it to 'reset' their sleep rhythm when travelling and to treat jetlag.
something lidat. but i might have mixed up the direction of flight and the times... i dunno lah. dun understand a crap. -
The debris and dead inflammatory cells will all be phagocytosed and carried away by macrophages, as long as it is not complicated by superimposed infection...Originally posted by starblue:wow. so that's how it happens. why didnt they teach this in school?? so after all these the white thing forms. what happens as it heals???
btw, very late leow...you better sleep soon -
night bear..sleep wellOriginally posted by the Bear:goodnight alfie
sleep well..
i think i'm going to catch some zzzs too..
goodnight everyone -
night alfajie!! muakz.Originally posted by alfagal:okie nightz all..tired le..
*alfagal has jus signed out..* -
OM, can i ask you...when having a sore throat...any diffrence when drinking cold water and warm water?
i heard cold water is bad for the throat..is it true? -
You take it an hour or so before you sleep. Of course it takes time to reset your cycles and so to be effective, a day or two before your trip you take the pill in Singapore in the day as it is bedtime in your destination, so that when you get there, your cycles reset already.Originally posted by starblue:no wait... the prof says it's used to PREVENT jetlag, not just to treat. something like if you're travelling from sg to us, then u take it dunno how many hours before arrival time (when in the plane) and the brain will be desensitised and not produce any melatonin when u reach. so if you leave sg at night, and expect to arrive at dawn or something liddat. you will have already adjusted your sleep.
something lidat. but i might have mixed up the direction of flight and the times... i dunno lah. dun understand a crap.
Problem is that you may feel sleepy in the day in Singapore as a result...so I usually used it when I am already in the plane or on arrival. Not very nice if doctor falls asleep in the hospital... -
Hmm...no medical reason for that as far as I know...Originally posted by StarPuppy:OM, can i ask you...when having a sore throat...any diffrence when drinking cold water and warm water?
i heard cold water is bad for the throat..is it true? -
nites Bear and AlfaOriginally posted by the Bear:goodnight alfie
sleep well..
i think i'm going to catch some zzzs too..
goodnight everyone