Revenged

Proteins are made up of amino acids but amino acids aren't proteins...

Allergy isa 'type I hypersensitivity'... It occurs because allegens cause inflammation... Allegen binds to IgE antibodies, which then bind to mast cells in tissues or basophils in blood... The mast cells or basophils release of substances that cause inflammation (histamine, prostglandins, leukotrieneces) It is the dilation of blood vessels that causes the redness of the skin... Histamine is a decarboxylated amino acid not a protein...

I think you are missing the point pioneer... All cells within the body have a negative charge - not just neurones... This is because we need to have higher levels of potassium ions inside cells than outside cells... In order to maintin this we need to have a negative charge... That's the basic reason why cells need a negative charge... Also, activation of nerves only changes the potential difference at the membrane of the nerve... The concentration of potassium and sodium within the nerve (not at the membrane) is constant... The activation of the nerve has vertually no effect on the overall concentration and potential difference within nerve cells (apart from at the membrane)... Nerves have there own way of ensuring that the nerves maintain their negative resting potential after a nerve impulse... When a nerve is activated... 1) Sodium channels open increasing permability of Na+ (Na+ enters and membrane of nerve becomes positive) 2) Potassium channels open increasing permability of K+ (K+ enters and membrane of nerve becomes negative) 3) Refractory period (This is where nerve cannot be activated since the membrane has become too negative) Typically, the activation of nerve takes 1 ms and there is a 1 ms refractory period after the nervous impulse... So the brain's neuronal surfaces are not loaded with positive charge... The recovery of a neurone from hyperpolarisation to resting potential is passive and is not due to the action of the sodium/potassium pump...

CT scan for skin cancer??? Thyroid hormone levels aren't routinely tested for in standard blood tests unless there is indication of thyroid malfunction... Numbness isn't indication of hypo- or hyperthyroidism... Rather than regularly overdosing on NSAIDs - which is crazy... If you are in pain then you should get some stronger pain killers (and not rountinely overdose on them!) e.g. gabapentin or something with codeine in (co-codamol)... Lastly, no one is going to be able to diagnose you online... Go and see a real doctor (i.e. someone who knows what they are doing - not a chiropracter) and then they can reassure you...

Orlistat is a pancreatic lipase inhibitor... You are supposed to have a low fat diet if you take this pill - because undigested fats have a lot of bad side effects... Inducing diarrhoea with orlistat or inducing diuresis with laxatives... Pretty lame science really... That's all these 'weight loss' drugs do... In reality it's not much better than bulimia...

I think you are talking about 'floaters'... http://en.wikipedia.org/wiki/Floater Btw, you can see the back of your eye as well... but usually only happens if a lot of light is going into the eye... for example, I saw the image of my retina when I was at the optician and she shown a ophthalmosope to see my retina... this is what the back of the eye looks like: http://webvision.med.utah.edu/imageswv/retina.jpeg you see the image... the yellow circle to the right is the fovea or the "blind spot"... it is where the optic nerve and the arterial blood vessels travel through... the spider like things that radiate from the fovea are retinal arteries that supply the retina with blood... it is these that you can see sometimes...

ok, perhaps you should have explained it a bit more... i was thinking about what he wrote in his post tbh cuz i read this spiderman had voices trying telling him to kill himself because he had an alien inside of him and he believed he had symbiotes parasites inside of him because he read it in a comic... i just thought that telling him that he might have a brain tumour is a good thing... that was all... i apologise if it was i over reacted... as it was, a CT would have shown a tumour, so i think it's safe to assume that he doesn't have one... i'm no psychiologist either... but one thing i know is that anti-depressants don't work in mania... i read the good long story of Mr lithium for 30 years of notes from private psychiatrists treating him... he was put on just about every anti-depressant known to mankind but none of them worked... btw, i also had the impression that you can't have BOTH bi-polar and depression because anti-depressants don't work on bipolar patients... as for what meds to go on for mania... i guess lithium is the best there is... i don't know that much about how bipolar is treated... the guy with lithium was put on anti-epileptics sodium valporate and i think when he came off lithium was also put on carbamazepine... i guess that anti-epileptics also act as mood stablisers?... he was also on the anti-psychotic olanzapine but he wasn't at all psychotic... i didn't understand what that was for... he also had some ECT and a lot of impatient/respite treatment in private psychiatric hospitals...

ok, sorry about that... i thought you were implying that... i don't disagree that there is a causal link between heavy use of cannabis and schizophrenia... so i agree with you (and wikipaedia) on that... btw, you were right about the atypical ones... they work on D2 receptors as well as serotonin receptors... blockade of D2 receptors causes the 'positive symptoms' of schizophrnia to reduce - that's audiological/visual hallucinations - whilst serotonin receptor blockade reduce the 'negative symptoms' of schizophrnia that's lack of speech, emotion etc.... atypical are better than typical neuroleptics that only act on D2 receptors - as these would only target the 'positive symptoms'... this isn't House... i don't know what you hope to achieve by posting such a post - but whatever it is it isn't going to have a positive effect... whoever spiderman is, he has issues... telling him that he may have a brain tumour when there is no evidence to suggest as such is a resipe for disaster... there is no evidence of seizures, no loss of sensory or motor function, no weakness, no loss of proprioception, no hearing loss, no headache, no hemianopia, no paralysis...etc. in fact - nothing to indicate any neurological abnormality whatsoever... he even has had mental problems all his life... he didn't suddenly end up psychotic out the blue one day... never mind that, any type of cancer is exceptionally rare in someone so young... so please don't try to act like House MD... you should not be making diagnosis based on such little knowledge especially if your 'diagnosis' would cause immense worry and has no legimate basis... you aren't a psychiatrist either... lethargy could easy be side effects of medication - you can't say that it is mania considering that anti-psychotics are major tranquillizers!... so please don't try and diagnose when you aren't medically trained to... and even if you were - it would be malpractice to 'diagnose' online... btw, i would disagree that lithium is perfect for mania... it has it's own problems... i have heard of someone having to be put on dialysis and later on dying of kidney failure due to over 20years of using lithium...

1. i don't agree with wikipaedia... perhaps i'm wrong but i was told that 'atypical' neuroleptics are 'atypical' because they don't work on dopamine receptors... for example, clozapine has a high affinity for the serotonin receptors 5-HT2A and 5-HT2C whilst having a low affinity for the dopamine D2 receptor... 2. as i understand it, there is evidence that activity of the D2 mesolimbic pathway when inhibited reduces psychotic symptoms... but this itself is not evidence of high dopamine causing schizophrenia... and certainly there is no evidence that suggests cannabis causes psychosis by increasing dopamine... every drug that is addictive increases dopamine levels in the brain, as does exercise, as does just about anything - none of which you can state cause psychosis...

Not strictly true... 1) Atypical neuroleptics (e.g. clozapine) don't even work on dopamine receptors 2) There's no evidence schizophrenics have high dopamine levels... 3) Neuroleptic anti-psychotic medication works by blocking dopamine receptors - it doesn't decrease dopamine levels... as for phenylethylamine Mr Spiderman... taking it is next to useless... it is almost entirely metabolised by MAO-B before it is enters the central nervous system...

don't go to a chiropracter... seriously... i met someone who had permanent and irreversible damage because of the 'treatment'... he had compression of the lumbar spine and a right-sided siatica (not uncommon)... he decided to go to a chiropracter who 'manipulated his spine'... after the appointment the man couldn't dorsiflex his right foot (i.e. he couldn't move the foot upwards)... he had total foot drop so whenever he walked he would trip over his right foot... the damage was permanent... chiropracters are not medically trained and do not have access to a patient's medical notes, they do not do MRI scans, they do not know what they are doing and they can cause permanent injury... i myself would never trust one... if you don't want to go to a doctor then you should really go to a physiotherapist (they are just as good and are much better at treating musculo-skeletal pain) - but you should never see a chiropracter!

why exactly did you post this in biochemistry?! and for your information there has been a vaccination produced against cervical cancer, which is caused by a HPV...

ok, sorry if i misunderstood you there... i've never heard of mu opioid receptors been called endophin receptors before but they are certainly the same thing... and prostaglandins are inflammatory mediators - they seem to do just about everything if i remember correctly... i did a libary project on opioids last year and that's the reason i know about it... one thing i found particularly interesting is the research into polymorphisms of the mu opioid (endorphin) receptor... i thought it was quite interesting because resent research showed that people with different polymorphisms of the receptor required very different amounts of morphine to get total analgesia from cancer pain... the difference was quite dramatic... such research is important because it gives a physiological explanation behind why some people require more analgesia than others and it is not purely a psychological responce (as was previously assumed)... the eventual implication for practice may mean that may doctors will be able to adapt medication matched to their particular receptor polymorphisms... references... Klepstad P., Rakvåg T.T., Kaasa S., Holthe M., Dale O., Borchgrevink P.C., Baar C., Vikan T., Krokan H.E., Skorpen F., The 118 A > G polymorphism in the human µ-opioid receptor gene may increase morphine requirements in patients with pain caused by malignant disease, Acta Anaesthesiologica Scandinavica, Vol. 48., (2004), pp. 1232.-1239. Rakvag T.T., Klepstad P., Baar C., Kvam T.M., Dale O., Kaasa S., Krokan H.E., Skorpen F., The Val158Met polymorphism of the human catechol-O-methyltransferase (COMT) gene may influence morphine requirements in cancer pain patients., Pain, 1116, 2005, p 73.78.

Some interesting links there Lockhead... Thanks...

that's a little ironic considering with how much sarcasm you answered my post... you have put me off posting... and since you seem to disregard everything i say i'll give you some evidence... http://www.mrw.interscience.wiley.com/cochrane/clsysrev/articles/CD000076/frame.html http://www.mrw.interscience.wiley.com/cochrane/clsysrev/articles/CD003593/frame.html http://www.mrw.interscience.wiley.com/cochrane/cldare/articles/DARE-20020063/frame.html http://www.mrw.interscience.wiley.com/cochrane/cldare/articles/DARE-970633/frame.html http://www.ncbi.nlm.nih.gov/sites/entrez where is there signficant evidence supporting the effectiveness of ECT?... it is controversial... there is a reason it only happens to desperate people who have been admitted to psychiatric inpatients... there certainly isn't like any prove of effectiveness for depression like there is for CBT or anti-depressants... and ECT certainly does have a tainted past for being giving it's use to psychotic and 'mentally retarded' patients who being 'non-competent' cannot consent to medical conditions and so doctors can treat against their will... the film 'one flew over the cuccko's' nest wasn't to inaccurate... ECT occured in that film and lastly the inpatient had a frontal lobe lobotomy, which was a psychiatric treatment which still took place in the eighties despite making people go into a complete vegetative state... lobotomies were certainly done against people's wills... and ECT can still be done without consent and even in some countries without anasthesia - so of course it is barbaric... http://en.wikipedia.org/wiki/Lobotomy it is shocking that they don't even give people anasthetic for the treatment in some places... it has already been banned from quite a few countries already but yet the UK and USA it's still going strong... the psychriatric profession is very slow to admit they are wrong and change their ways (look at the lobotomy stuff - it was still occuring only twenty years ago!)... btw, the idea that there is informed consent in such cases is madness... when people are admitted to a psychiatric hospital they aren't really in a position to say no to a doctor...

Analgesics work by blocking the path pathways... The major pain pathway is the spinothalamic tract... Nerve impulses travel via a sensory nerve to the spinal cord, then to the brain (first the thalamus then to the somatosensory cortex)... Analgesics can work by inhibiting activation of sensory nerves or central nerves via different mechananisms... Analgesics stop pain whereas sedatives put you to sleep or make you calm... Sedatives include benzodiazepines... short acting ones like diazepam (Valium) to reduce anxiety and long-acting ones like temazepam to put you to sleep... both works on GABA A receptors... You also get major tranquillizers for schizophrenics... e.g. chlorprozamine... Barbituates for induction of anasthesia... e.g. thiopentone... The mechanisms of action are complicated... Non-steroidal anti-inflammatories do inhibit the COX enzyme, they stop prostaglandin production but their main effect (as the name suggests) is to prevent inflammation... it's the inflammation that causes the activation of sensory nerve fibres... btw, i'm pretty sure that nerves sense pain without prostaglandins... NSAIDs are one of the least effect analgesic agents... Morphine works on the central nervous system and acts on mu opioid receptors... Opioid receptors are inhibitory receptors that prevent activation of second order neurones within the spinothalamic tract, which is how they cause almost totaly analgesia... Morphine also causes release of endogenous opioids (such as endophins) that have an additive effect... it also causes release of other neurotransmitters e.g. the 'sense of well-being' is disinhibition of GABA neurones causing dopamine release within reward centres of the brain... I would just like to point out that there are quite a lot of drugs that we don't fully know the mechanism for and some we have no idea how they work... This is especially true for drugs that have actions within the central nervous system...

I have now met two people who have had their brain's electrically shocked by psychiatrists at psychiatric hospitals... One of them had it done two years ago and so I think it's still going strong in the UK... They weren't psychotic or anything - they both just had long going depression... They were treated at a private psychiatric hospital (not going to say which one) but both were paying for the treatment and willingly had ECT done on them... I was very shocked by it all... It reminded me of that film 'one fell over the cucco's nest'... It didn't do any good for either of them... I read their medical notes and their history wasn't abnormal except for suicide attempts... but even so suicide attempts aren't uncommon in depressed people - especially those that have had it for over 30 years... It just seems like absolute madness to me that you would electricute the brain of someone with severe depression as a last resort... Anywayz, what i was wondering was... 1) what good is it supposed to do anyway (i did a wikipaedia and it didn't tell me much) and 2) how can such a thing be legal?...

ok, i get it... 'Sleep paralysis is a condition characterized by temporary paralysis of the body shortly after waking up (known as hypnopompic paralysis) or, less often, shortly before falling asleep (known as hypnagogic paralysis). Physiologically, it is closely related to the paralysis that occurs as a natural part of REM (rapid eye movement) sleep, which is known as REM atonia. Sleep paralysis occurs when the brain awakes from a REM state, but the bodily paralysis persists. This leaves the person fully aware, but unable to move. In addition, the state may be accompanied by hypnagogic hallucinations.' http://en.wikipedia.org/wiki/Sleep_paralysis

it is not a disorder... REM normal is normal and you require it to function... if you didn't have any REM sleep you'd have narcolepsy...

REM sleep ('Rapid eye movement' sleep)... all the muscles in the body are paralysed except for the eyes that rapidly move for some reason...

i don't think the hypothesis works as well for smoking... the problem in the hypothesis is that smoking causes upregulation of nicotic acetylcholine receptors (no one really knows why!)... so even though the receptors become desensitised - there are more receptors - so it is harder to become physically tolerant to nicotine compared to other drugs... i think with smoking other factors are more important... i think tolerance is more important with CNS depressants such as benzos, alcohol and heroin... i think with stimulants like ampetamine and nicotine it is the withdrawal symptoms - i.e. cravings - that are more imporant... e.g. it's very common to hear of people that have their first cigarette whilst in bed whereas it's relatively uncomon that people have their a shot of whilsky whilst in bed before they wake up... but as with all things it is much easy to overdo the science... the reason why a lot of people smoke is often because it's part of their routine, they use it to avoid stress, they want an excuse to have a break (e.g. to get away from work!)... i've myself have started drinking coffee and tea about 5 times a day since i've started working because it's a great excuse to have a 10 minute break... this is not addiction... it's just routine... i think it's importnat to remember that people smoke for something to do... and one of the major factors that makes it hard to quit (aside from the addiction to the drug) is changing out of routine... so basically with smoking, i think it's cravings/withdrawal symptoms and psychological factors (increses in stress/boredom/anxiety) that can explain fairly small increases in cigarette use over a lifetime and psychological factors definely explain increase in use during tense situations... i don't think that tolerance is as important when it comes to smoking...

Thanks for the link... it seems the researchers don't know why it happens either... "Although nicotinic receptor upregulation has been demonstrated after chronic nicotine administration as well as cigarette smoking, neither the physiological significance nor the relationship with the desensitization process are known."

yeah, i already know about depolarisation blockade... i know you use succinylcholine as a muslce relaxant prior to intubation because it causes desensitisation of nACh receptors and i did talk about desensitisation of nAChRs because of high nicotine levels in my previous post... i was more confused about why nicotine intake causes upregulation of nAChRs within the central nervous system... any idea why that happens?

of course withdrawal symptoms occur... you obviously haven't tried to quit or perhaps you aren't smoking enough... try and go without smoking for 4 weeks then you'll see what it's like...

you've got it the wrong way around... nicotine is a stimulant - the sort of addiction you are talking about you get with central nervous system depressants such as alcohol and heroin... when people smoke nicotine, it causes release of neurotransmitters and of adrenaline... this is why people like smoking... if you smoke over a long period of time then your body will counteract the artificial neurotransmitter release... it does this with nicotine by decreasing the neurotransmitter release and by causing the receptors to become desensitised to their neurotransmitters... for example, high levels of nicotine will cause nicotinic acetylcholine receptors to become less easily stimulated... the effect of this would mean that more nicotine would need to be taken in order to get the same effect - this is why you develop tolerance to the drug... the withdrawal symptoms in smokers because the body has become adapted to having regular nicotine intake... you get cravings when your body has no nicotine as you have decreased neurotransmitter and decreased adrenaline release... over time physiological dependence becomes addiction (psychological dependence)... one thing that I am a bit confused about is why nicotine causes increased nicotinic acetylcholine receptors in the central nervous system... i'm genuinely unsure why it happens... what i've got off this off wikipaedia is the following (and it's confusing)... "Like other physically addictive drugs, nicotine causes down-regulation of the production of dopamine and other stimulatory neurotransmitters as the brain attempts to compensate for artificial stimulation. In addition, the sensitivity of nicotinic acetylcholine receptors decreases. To compensate for this compensatory mechanism, the brain in turn upregulates the number of receptors, convoluting its regulatory effects with compensatory mechanisms meant to counteract other compensatory mechanisms." so let me get this right... the body counteracts it's compensatory mechanism to high nicotine intake (which is the desensitisation of nicotinic acetylcholine receptors) by increasing nicotinic receptors?... but why does this happen... what is the point in having a compensatory mechanism if you are going to try to counteract it...