Glider

I didn't see it, but from the descriptions here, I would say it was a keen bit of observational humour. 'It's funny because it's true'.

Of course it's a ploy for legitimacy. That's the point. If they are called on the lie, they'd either have to put up or shut up.

Definitely maid. Vacuuming is a pain! Everything else I quite like doing myself.

A good point, well made. Nonetheless, I think that a requirement of these "We will write your essay" sites should be to open their databases to anyone who can demonstrate that they are in an authorised, evaluative relationship with the people using the sites. Or, at least open them to to antiplagiarism scanning software from registered academic domains. After all, it would only be helping these sites to ensure that their work was being used for research purposes only and not as course work. It would be helping these sites maintain their stated objectives, and we wouldn't even charge! How could they possibly complain?

Rubbish. Whilst I take your point about mixing entity and function, it is not a particularly strong point in this case. Opioids are not used as antidepressants because they do not have a clinically useful antidepressant effect. If they did then so many methadone patients would not also be on antidepressants (e.g. imipramine). In this case it is you who have mixed your terms. 'Antidepressant' and 'narcotic' (or 'euphoric) refer to different effects. Try prescribing chocolate or coffee to the clinically depressed and see what happens. No opiate drug is sold over the counter. Opiate analgesics are controlled drugs and are available on prescription only. Painkillers are sold over the counter, but there are many kinds of painkillers, only some of which are opiates. At analgesic doses, opioids have no narcotic effect (apart from in those who have an intolerance to opioid drugs) and don't affect mood. The stronger doses (e.g. those used to control cancer pain), there is a clear narcotic effect. However, far from being antidepressant, opiods at this level flatten affect, i.e. they reduce significantly the patient's emotional response to the pain, which, in effect, is the 'suffering' associated with severe pain. This essentially is the primary mechanism of opiate analgesia in controlling severe pain. I don't think frustration is a particularly nasty sentiment, and moreover, it wasn't directed at you. Your original question asked "Antidepressants Vs Opiates: What's the difference?". I think between us, MolotovCocktail, Revenged and I have answered your question quite thoroughly. Geoguy has helpfully pointed out the flaw in your question and continued to do so to revenged in support of his innacurate contention that opioids are antidepressants. Hence Revenge's frustration which was directed at geoguy, not you. So, of all possible outcomes, your getting annoyed at one of the people who was actually answering your question is the least understandable, unless perhaps you are not reading the posts correctly? Similarly, Andean Indians have been chewing cocoa leaves for over 5,000 years for the same reason (as a pick-me-up). Although in high doses kratom leaves act as a sedative, in low doses it's a stimulant, same as cocaine and amphetamines. Although these drugs have a euphoric effect, none of them are used as antidepressants. Stimulants may produce euphoria temporarily (a cocaine high lasts ony 40 minutes), but they are not antidepressants so, no, kratom leaves could not be used as an antidepressant in a clinical setting. As I said, at higher doses it has a sedative effect and is used as an analgesic. Opiods also have a sedative effect at higher doses and also a have a motor supressive effect (e.g. opioids supress respiration). I think the main problem of mixed terms here is between 'stimulant (or euphoric)' and 'antidepressant'. A stimulant drug (cocaine, caffeine, amphetamine, kratom leaves etc.) may put you in a good mood (i.e. produce a temporary euphoria) as their common end effect is to increase levels of dopamine in the brain reward centres (the nucleus accumbens, the ventral tegmental area and the medial forebrain bundle). Opiods have the same common effect (although they also have another mechanism of reinforcement), but that is not an antidepressant effect in the context of this thread. In this thread, the term antidepressant is being (correctly) used as a chemical treatment for depression. The chemical treatment for depression (i.e. antidepressants) works on a different neurological system to stimulants and opioids.

On the most basic level, it's actually tension relief (as is the angry, fist shaking thing). When a person has a near miss with traffic, the body goes immediately into fight/flight mode (acute sympathetic arousal), which is stressful. There's elevated heart rate, respiration, vasovagal responses and large amounts of adrenaline and stuff to deal with. The onset is more or less immediate, but the effects last a little while. As the danger in a near miss passes very quickly, there's no running away or fighting for life to be done, so the person has nothing to do with all that arousal, so the body finds an outlet for it in displacement behaviours. Shouting and fist waving are common displacement behaviours, as is laughing, which is why people do it so often in innapropriate and usually stressful situations (particularly when the stress comes from knowing you must not laugh, ironically).

Ok, new idea. Forget the eccentric weight. I don't think it'd work. I think you need something like a piston and crankshaft design, but in this case, a motor drives the crankshaft which drives a weight up and down (like a piston). I think that would more accurately replicate the forces the rider provides.

I think you'd need a motor spinning an eccentric weight or flywheel (something like the one below, but smaller) to provide the kind of up and down motion the rider does on the full sized thing (like riding a one pedalled bicycle). You'd need to experiment with the RPM to find the optimal cycle rate. The full sized versions seem to cycle at 100/120 per minute (approximately). Standard RC servos would serve for the steering. [edit]Actually, I'm not sure the eccentric weight idea would work. The rider pushes down and rides up, the weight would provide a rotary force (i.e. backwards and forwards too). I'm not an engineer though.[/edit]

Yeah...and it was already shaky.

Revenged is quite right. The reasons why many antidepressants work is far from clear. It's known that SSRI's and MAOIs elevate levels of monoamines, and taking them aleviates depression, but that it's therefore the elevation of monoamines that alleviates depression is only an assumption. There are many studies that have shown lower levels of 5-Ht (or Levels of 5-hydroxyindolacetic (5-HIAA), a 5-Ht metabolite that can be measured from cerebrospinal fluid) in depressed people than non-depressed people, but what is not clear is whether that's a cause or a result of the depression. The relationship is only correlational. To make it worse, there is more than one kind of depression, some of which are completely unaffected by elevating monoamines. It is known however that 5-Ht is also active in the reward centres and is associated with feelings of calm and wellbeing (as opposed to euphoria). There's a similar problem with treatments for schizophrenia. This condition is associated with elevated levels of dopamine. So, they prescribe dopa blockers. These effectively suppress the positive symptoms of schizophrenia (but have no effect on the the negative). However, with long term use of dopa blockers, the body compensates and increases the number of dopamine receptors at the post synaptic membranes so there's as much activity in dopaminergic neurons as there was pre treatment. However, the positive symptoms don't return. And no, opiods are not used as antidepressants. They are analgesics.

Conduction velocities vary between nerve types. The velcoties of big, fast sensory and motor neurons is between 300 and 400 metres per second. In small, non myelinated C fibres, it's only about 0.5 - 2.0 metres per second (C fibres are associated with slow, burning/aching pain like you'd get from YT's chillis).. That's why when you stub your toe, you feel the impact immediately, but you also get that split second when you realise that it's really going to hurt. Then it does.

You could probably download plans. I'm too far from water for it to matter. Althouh, maybe I could scare the ducks on Hampsted ponds?

No it doesn't. An ant is too small and light to accelerate much. Air is quite viscous to an ant, which is why you can blow an ant off a table with a puff of air that would barely ruffle the hairs on your arm. Air resistance would support the ant as it fell. Basically, there is no height an ant could fall from that would kill it.

As a broad division, opiates work on opiate receptors system antidepressants work on serotonergic and dopaminergic systems. Most commonly, depression is associated with reduced levels of the monoamine neurotransmitter serotonin (5-Hydroxytriptamine or 5-Ht). Many antidepressants are designed to elevate levels of serotonin at the synapse. The most common are Specific Serotonin Reuptake Inhibitors (SSRIs) that block the reuptake of 5-Ht by the presynaptic membrane. Others inhibit the ensyme Monoamine Oxidase (MAO) that breaks down 5-Ht (Monoamine Oxydase Inhibitors or MAOIs). These mechanisms serve to increase levels of ambient 5-ht in the synaptic cleft. This will elevate mood in depressed individuals, but not in those who are not depressed. Opiates work on a number of different systems. Opiate receptors have at least five forms: Delta, Kappa , Mu, Sigma and Tau. Delta, Kappa and Tau are found in pathways mediating pain in the brain and spinal cord which makes opioid analgesics the most effective painkiller we have (although nociceptive inhibition is not their main effect). However, opiates also inhibit GABA (Gamma Amino Butyric Acid) receptors in the Ventral Tegmental Area (a part of the brain's reward system). GABA is an inhibitory neurotransmitter, and if you inhibit an inhibitory mechanism, then the systems that mechanism was inhibiting is free to fire at will (like taking your foot of the brake). Inhibition of GABAergic neurons in the VTA allows dopaminergic (DA) neurons to fire more freely and and an elevation of DA in the reward system is ..well...rewarding. It's the basic mechanism that all drugs of abuse share in common.

I agree completely. It's why I found it so funny. When they were actually called on their terms of service clause, they had to cave in to maintain the lie. Given that it is such an obvious lie, I do feel that these companies should be made to open their databases to anti plagiarism software. If their work is genuinely for research purposes only, it'll be cool. If not, they don't really deverve to be in business anyway, it's so obviously unethical. How the hell are they allowed to do that kind of thing anyway?

Not as far as I know. Unethical conduct will get you struck off whatever register you're on that allows you to practice (if you're on one), but it won't get your degree revoked. They see a distinction between whether or not you're qualified to practice and whether or not you should be allowed to practice.

JISC uses a colour doded flag when identical text is detected (green, amber and red depending on the percentage of identical text found), but it's up to the tutor to visually examine the paper. The really helpful thing that JISC does is to hold the student's paper up in one window, and the source of the identical text in another so you can compare them directly and make your own judgements. This is (IMO) a lot better than relying on software to make judgements for you. A real problem is these sites that offer to write essays (for money). They guarantee that the essay will be original and not posted on the internet, ever. These essays are therefore invisible to anti plagiarism software. However, in Uni the other day I was talking to another lecturer who told me that a mutual friend of ours had marked a course work essay he suspected was plagiarised. He approached this online essay writing service and told them his story. They responded that their service guarantees confidentiality, he told them that they also state clearly that their essays are to be used for research purposes only and so if this student had presented it as course work, they had broken the terms of their agreement. The site gave him a temporary login and he was allowed to search their database. He found the essay and the student was busted (yay!). You have to admire his tenacity.

No, I wasn't suggesting that at all, just trying to keep things simple (habit from teaching). You were quite right to point out that higher CNS areas modulate reflex.

Dammit! I've been drunk many times, but never done harm nor foul. I don't think alcohol is the problem here. I think stupid is the problem. Why don't they ban stupid? Stupid is the cause of more crap than alcohol I think, but the combination is lethal.

It's down to convergence. There are 31 pairs of spinal nerves. These spinal nerves contain both afferent (sensory) & efferent (motor) nerves which split into the dorsal & ventral roots (respectively) as they enter/leave the vertebra. Each pair of spinal nerves innervate a limited area of the body called a dermatome (see image: from Kalat, 1992). The equivalent segmentation is also found in the motor system (muscles). These are called myotomes. This pattern of innervation is left over from when we were segmented worms. Anyway, long story short, the afferent nerves converge on their way to the brain. They enter the dorsal horn of the spinal cord and converge on projection neurons. These send information up the spine to the thalamus where they converge further. Occasionally, hyperstimulation of one point in a dermatome can trigger a convergent neurone in such a way that the brain interprets the signal as coming from another area served by the same convergent neurone. A similar phenomenon is responsible for referred pain. In this case, stimulation of deeper nerves can result in sensation apparently from surface nerves in the same dermatome. The brain is unused to recieving sensory information from internal organs (they are innervated, but comparitively poorly). So, when some internal region gets irritated (say, the diaphragm), the brain interprets the signal as having come from an area of skin innervated by the same convergent neuron becuase generally, the source of the signal is more commonly skin and those pathways are more strongly reinforced. In the case of diaphragmatic irritation, the sensation appears to come from the point of the shoulder. Another example is the sharp pain in the left arm and wrist during a heart attack, although nothing happens in those areas to cause the pain, but the brain is unused to recieving sensory information from the heart. Another example is lumbar/hip pain (say, an arthritic hip) can result in pain being located at the front of the knee (and not in the hip).

So Lemmy really doesn't want to live for ever? Damn, I'm gonna miss him.

Teehee.

I think there should be many, many more pubs and bars, at least one on every corner. That way, people wouldn't have to drive to get to them.

We use software for that too (JISC ). It's not infallible, but it's very good. All first-years are required to submit electronic versions of their work and I think that will probably be extended to 2nd and 3rd years. The sad thing is that it's necessary. Plagiarism is on the increase.

Oh, har de har har