Monday, 25 September 2006

evolution - Origin of human intelligence and thought

Evolutionary theory is a little over my head, but there are some obvious problems with your question.




We don't descend from any Chimpanzee or Orangutan because, if we did,
they would also have the cognitive thinking ability that we have.




  1. We aren't closely related to orangutans, period.


  2. The chimpanzee is considered our closest living relative, but that doesn't mean it's a direct ancestor.


  3. Why would an ancestor have to have the same cognitive thinking ability we have? Isn't cognition something that evolves?


  4. I'm going way out on a limb, but who really knows what kind of cognitive abilities apes have? They probably aren't equal to ours, but still...



I am arguing that a high protein diet allowed the first humans to have
the possibility to develop a higher memory, intelligence and other
mental procedures.




Gorillas are herbivores, and they rank among the most intelligent species. Come to think of it, a lot of people are vegetarians.




But after all, what would be the real origin of the intelligence?




I'm going out on a limb a bit, but I think many scientists associate the evolution of intelligence in humans with a combination of physical traits - particularly binocular vision, bipedalism and our opposable thumb. Walking upright freed our ancestors' hands so they could manipulate objects, stimulating the brain. Note that octopuses - which can similarly manipulate objects with their tentacles - are considered among the most intelligent invertebrates.




If animals do have intelligence too, why isn't theirs as advanced as
us.




Mammals have more complex brains than birds, herptiles and other groups; that gives us a head start.



We're also unique in being completely bipedal AND having opposable thumbs. Which isn't to say only animals with these features can be intelligent; whales may rival us in intelligence. But we obviously have some very unique physical traits.



The human brain is also relatively large and complex - though some might argue that that's a result of our physical characteristics.

biochemistry - Pharmacologically, can tricyclic antidepressants have a side-effect profile similar to neuroleptics?

Torticollis can occur for several reasons, one of which is a side effect of certain drugs. Rather than highlight one specific drug it is perhaps better to talk about the mechanism of action by which this occurs.



Torticollis in a drug induced form is classed as an extrapyramidial side effect. Classically results from some medications which have anti-dopaminergic effects. The neurotransmitter dopamine is important for the regulation of movement. Different medications have different degrees of anti-dopaminergic effect. To complicate things further there are several different types of dopamine receptors and different drugs have different effects depending on their action on these receptors.



Classically drugs that have been associated with extrapyramidial side effects are some of the antipsychotics but there are case reports of this with trycyclics http://www.ncbi.nlm.nih.gov/pmc/articles/PMC489096/ however this appears to be a very rare, see http://www.sciencedirect.com/science/article/pii/S0924977X97004057.



The paradoxical treatment of torticollis might be dependent on the cause of the condition. Tricyclic anti-depressants have anti-cholinergic effects, i.e. they block the effects of the neurotransmitter acetylcholine. This neurotransmitter works in opposition to dopamine in the basal ganglia (part of the brain responsible for movement control) as such might be used when the dystonia is as a result of doperminergic disregulation.



If you are at all concerned that you may be suffering side effects of any medication, then I highly recommend that you go and discuss this matter with your doctor. The above is a simplified explanation of some of the reasons why these side effects may occur. It is not intended as information for the purposes of self diagnosis and treatment.

Saturday, 23 September 2006

pharmacology - How does paracetamol interfere with immune system?

First question: Yes. The immune system releases pyrogenic cytokines such as IL-1. Bacteria aren't typically used to 37C, they prefer working at under that temperature to function in the environment. Our body however can take a few degrees here or there however this severely compromises the bacterial enzyme activity. The same is true for other pathogen enzymes. The body also increases copper concentrations in the blood for similar reasons. Problem is of course if the body goes into overdrive and raises our temperature too much, this compromises our own ability to fight the infection so in that case antipyretics like paracetamol can reduce fever.



Second question. It isn't a side effect, however paracetamol works by blocking things like IL-1 that raise temperature. How IL-1 raises your temperature is quite interesting, it tells the hypothalamus (our thermostat) that it should be set higher. So we feel cold (so we try to keep ourselves warm) and the body thinks it's cold (so it increases the temperature by burning glucose mainly)

evolution - What does "fit" mean in "survival of the fittest"?

'Survival of the fittest' has never really made sense, because it confuses the scientific (evo. biological) and colloquial definitions of the word - which some of the previous posters have also done.



Biological fitness simply refers to an individuals genetic contribution to the following generation. That is, a 'fitter' individual, in an evolutionary sense, is one whose genetic material is proportionally overrepresented in the next generation.



The mechanism by which an individual achieves this may include out-surviving competitors, but it's certainly not the only way to increase fitness. Two individuals may live for the same length of time, but one may successfully court more females, or out-compete the other for food resources, for example. So when we refer to a 'fitter' individual (or individuals), we're saying nothing about why they are so. It's not a comment on their 'fitness' in the human sense of the word (bigger, stronger, longer-living), it simply refers to how well they pass on their genetic material.



So you can see why the phrase is nonsense. If we're being precise, then 'survival of the fittest' translates to 'survival of the individual who is better able to pass on their genetic material to the next generation' - which is meaningless because it tangles up these different concepts.

Thursday, 21 September 2006

evolution - Why are some fungi poisonous?

The same reason some plants are poisonous: to stop animals from eating them.



The visible part of the fungus is called, rather misleadingly, the fruiting body. It exists to produce and spread spores and thus produce the next fungal generation. Getting eaten, rather obviously, inhibits its ability to do this. Being poisonous discourages animals from eating the fruiting body and thus permits it to complete its life cycle.

physiology - Which is the tissue damaging agent in krokodil (street desomorphine)

Note: Don't click on the links, or even search for information, if you don't have a strong stomach



From what I've read, it's not necessarily 100% known, most likely because it's not easy to study (small, reclusive users who die quickly of a complex concoction) but the line everyone has quoted is:




"They extract [the drug] and even though they believe that most of the oil and gasoline is gone, there is still remnants of it. You can imagine just injecting a little bit of it into your veins can cause a lot of damage… it eats you from the inside out".




That's from Dr. Frank LoVecchio in Phoenix, Arizona, who saw two cases within a week. It's not hugely scientific, but it's not wrong. Krokodil is never pure and highly toxic chemicals are thus injected into the veins. If you want specifics, then gasoline, hydrochloric acid, phosphorous scraped off matchboxes, paint thinner, iodine, and cleaning oils. Injecting any one of those should be enough to kill a repeated user. Those substances rupture blood vessels, and the subsequent leakage creates gangrenous wounds like you see in the pictures.

Monday, 18 September 2006

biochemistry - Simple diffusion of lipid-soluble molecules through phospholipid bilayer -- does anything get "stuck" in transit?

I think, given Alan's answer the question you might be asking is something like
'do compounds become concentrated in the lipid bilayer', as opposed to achieving high concentration inside the cell after diffusing through the membrane as he describes.



This could certainly happen (if that's what you're thinking), but usually won't for I think two reasons.



The first is that any molecule that would not soluble in the interior of the cell is going to have a correspondingly small not going to be found in the blood or lymph, tissue, ocean or other milieu the cell is living in, which will be mostly water.



You might well ask whether there are cases where the compounds in question might be available in low concentrations around the cell and over time accumulate in the lipid bilayer. This slow concentration model probably happens, but there is a compensating mechanism - the lipid bilayer is taken into vescicles and degraded, to be replaced by newly synthesized such that membrane components renew themselves. This process includes the cell engulfing by endocytosis and specifically turning over membrane proteins.



The turnover rate for most cells is on the order of days, some of the best numbers for this are behind a paywall, but a reference to synaptic membrane turnover shows some components turn over varying between 6 and 24 days. Different components such as cholesterol, phosphatidylcholine and phosphatidylethanolamine have differing rates of turnover.



So between these two effects, the concentration of 'permeant molecules' would be low for most cases.