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What percentage of fish are herbivorous vs. carnivorous?
It appears that the majority of fish we eat are carnivorous, such as salmon and tuna. This got me wondering how common herbivores and carnivores are among fish species. I couldn't find an answer to this question through a cursory search of the internet.

I don't have an answer to this but there are a number of elements I think can be helpful for you in finding an answer.
First, a helpful word for searching here if you didn't know or hadn't thought of it is "trophic", as in "trophic level", as in "how high this organism is in the food chain".
Making searches related to fish and trophic levels I didn't find a single result for all fish; there are plenty of papers and graphs about the trophic distribution of fish but it's usually within a specific context or ecosystem. For example this graph gotten from Google Images, from a paper that looks at reef fish in Hawaii:

You can see in that graph, and plenty of other papers confirmed, that "herbivore/carnivore" may not always the most relevant distinction in terms of what a fish eats; unlike on land, where the base of the food chain is plants which are pretty big and visible and so are most of the organisms that eat them, in the ocean the base of the food chain is phytoplankton, which is eaten by zooplankton, both of which are what most of the fish we consider "at the bottom" of the fish food chain eat, so by that standard almost all fish are carnivores. But it doesn't seem to be how the word is used by everyone in the field; the graph in question being an example, distinguishing "Benthic carnivores" from "Planktivores" (Plankton-eaters) and "Piscivores" (fish eaters; presumably the "carnivores" eat non-fish animals).
See also this graph looking at reef fishes at various sites in the Caribbean:

Or this graph looking at the trophic structure in a stream

both of which similarly distinguish things more finely than "herbivore/carnivore".
And this, that I got from a search for "fish trophic histogram", ties the concepts to trophic levels (but on a local scale only again, this time the Mediterranean):

Otherwise the FishBase database seems to contain trophic pyramids but they need to be seen per ecosystem and there are a lot of available ecosystems, and given the shape of most pyramids they might include more than just fish.
As an aside, this paper might give a good explanation for why most of the fish we eat are carnivorous:
Trophic level scales positively with body size in fishes

I was indeed thinking pescivores/invertivores vs. herbivore/planktivore/detritivore. Very good information +1


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How long does it take for a hard clam (Mercenaria mercenaria) to reach sexual maturity?
How long does it take for a wild hard clam (Mercenaria mercenaria) to reach an age where they are reproductive? How does fecundity depend on age and size? I've looked at several hard clam life cycles and none of them have this information. They tend to agree that hard clams are long lived and take multiple years to reach a size suitable for harvest. While I am more interested in wild hard clam, please do also share information on farmed hard clam if you have it?

According to Ebersole 1987, Mercenaria mercenaria reaches sexual maturity at two years of age although some individuals can reach maturity at 1 year of age under certain growing conditions.  The mean size of individuals reaching sexual maturity is 33 mm with males somewhat smaller than females.
Ebersole cited a few studies that estimated fecundity of M. mercenaria. The results were highly variable. Individuals of about 60 mm in size released between 2 million and 6 million eggs.  Other estimates were as high as 25 million eggs.  Ebersole also cited a paper by Bricelj and Malouf (1980) where they found a general association of increasing fecundity with increasing clam size.  I don't have access to that paper but a book called The Great South Bay edited by Schubel et al. 1991 discussed the results of Bricelj and Malouf. Scroll to page 45 of the Google Books preview.  They show the mean fecundity and size as follows:
Seed (<48mm): 1.6 million eggs / individual
Little Necks (48-70mm): 2.9 million
Cherrystones (70-79mm): 5.9 million
Chowders (>79mm): 6.3 million
However, the figure on page 45 of Schubel et al., and taken from the Bricelj and Malout (1980) paper, shows a lot of variability in fecundity at different size classes.  Hopefully, the citations in the Ebersole paper will point you to other useful studies. If you don't have ready access to the book, your local library may be able to get it for you on loan.
Literature Cited
Bricelj, V.M. and R.E. Malout. 1980. Aspects of reproduction of hard clams (Mercenaria mercenaria) in Great South Bay, New York. Proceedings of the National Shellfish Association 70: 216-229.
Ebersole, 1987. Species profiles: Life histories and environmental requirements of coastal fishes and invertebrates (South Atlantic). Hard clams. US Fish and Wildlife Service Biological Report 82 (11.75).
Schubel, J.R. et al. (editors) 1991. The Great South Bay.  State University of New York Press, Albany, New York, USA.

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How effective is spraying disinfectant on streets?
I always wondered how effective spaying disinfectant onto outdoor ground is.

Source: Wikimedia
I understand that viruses and bacteria will sink down to the ground. I further understand that pedestrians may transport it across the area via their shoes, which shall be prevented.

Is the outdoor concentration of virus/bacteria particles really that high, that it helps to approach them with disinfectant?
Wouldn't it dilute too quickly?
Will the disinfectant droplets effectively touch the particles to inactivate them?

To me this looks more like this done to show "something" is done.

SE Biology is a question and answer site — not a discussion site or a site for floating ideas. It is concerned with the mechanisms of biological processes, not medical or social aspects of biology. For one of these reasons I think  that your question on the coronavirus outbreak is off-topic here. Question of a medical nature might be on-topic at SE Medical Sciences. Otherwise you are advised to consult more appropriate reputable sources for such information, some of which are listed here.

Thanks for your advice, I'll look into that. Though, of course, the SARS-CoV-2 outbreak pushed me to write this today, I wondered about this in the past too. And I don't want to discuss, I seek answers, so I thought my Q's nicely fit the Q&A scheme.

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Electrocardiogram: Difference between Atrial Fibrillation and Atrial Flutter
I have been working on analyzing Electrocardiogram data.
I have read several documents related to conditions of the Atria during fibrillation and flutter, the most lucid being that atria quiver with rapid rate.
This manifests as multiple P-waves (some documentation refers to them as "F-waves" and regards P-waves as absent) in the Electrocardiogram.
However in this condition, we get a completed QRS-complex in the Electrocardiogram.
Now, coming to my question, in both scenarios i.e. Atrial Flutter and Atrial Fibrillation, i get multiple P-waves(or F-waves) with completed QRS.
So how do i differentiate between the two conditions ??

A-Flutter will have discernible waves that can be counted, usually. The R-R interval will be regular or maybe slightly irregular if there's a variable conduction block in the AV Node. A-Fib will ALWAYS be completely irregular without discernible pattern.
You can also modify the position of your limb leads. There is an EKG placement called the S5-Lead that basically makes it where the QRS disappears because it's electrical impulse is perpendicular to the monitoring leads. The Atria however, become super-visible on the EKG.
To do S5:
Place the RA electrode on the patient's manubrium.
Place the LA electrode on the 5th intercostal space, right sternal border.
Place the LL electrode on the right lower costal margin.
Then set the EKG to view Lead I

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What is the relationship between W, X, Y and P, M retinal ganglion cells?
In Guyton and Hall Textbook of Medical Physiology (12e) the retinal ganglion cells (RGCs) are classified into W, X, and Y types. However, in Gray's Anatomy (40th ed.), RGS are subdivided into midget and parasol cells. What is the relationship between the W-X-Y versus midget-parasol classifications?
Summary of the WXY classification as in Medical Physiology:
About 40% ganglion cells are W cells. They are the smallest (<10 μm), and the slowest (8 m/s) to transmit signals, but they have the broadest receptive field. They receive signals from rods and detect directional movement.
About 55% are X cells. They have medium size (10~15 μm) and transmission speed (14 m/s). Their fields are small. They transmit color vision.
About 5% are Y cells. They are the largest (<35 μm) and the fastest (35 m/s) to transmit signals. They have broad fields. They respond to rapid changes in the vision.

Short answer
X = P = midget = β
Y = M = parasol = α
W = γ

Background
First off, P and M cells are not equal to parasol and midget cells; on the contrary - P cells are midgets and M cells are considered to be parasols.
X, Y and W cells are used to denote different retinal ganglion cells in cats, as proposed by experiments Enroth-Gubel & Robson (1966). As you already indicate, these cells have different physiological response properties. X and Y cells have the standard center-surround distribution of their receptive field, X cells having linear additive response properties in center and surround and Y cells nonlinear properties. X cells therefore have predictive responses such that responses can be predicted to be maximal (e.g. light shining on the ON center and no light stimulation on the OFF surround). Y cells tend to respond in more complex ways. W cells do not have a center-surround structure (Bruce et al, 1996).
Based on morphology, retinal ganglion cells in the cat have been labelled α, β and γ cells, which are thought to correspond to the physiological classes of Y, X and W cells, respectively (Boycott & H. Wässle, 1974).
The P and M division was introduced by De Monasterio & Gouras (1975) based on monkey experiments. P and M refer to the parvocellular and magnocellular connections retinal ganglion cells in monkeys make in the LGN of the brain. Both types of cells have a center-surround receptive field structure like X and Y cells in the  cat. P cells show color opponency and respond to specific wavelengths of light, and are involved in color vision. P cells respond to a range of wavelengths and respond most vigorous when different light intensities illuminate the center and surround (Bruce et al, 1996).
P cells are considered to be mostly midget ganglion cells, and equivalent to β cells of cat. M cells, on the other hand are considered to be mostly parasol cells and resembling α cells (Kolb, 2001).
References
- Boycott & H. Wässle, J Physiol (1974); 240(2): 397–419
- Bruce et al, Visual Perception (1996); 3rd ed. Psychology Press
- De Monasterio & Gouras, J Physiol (1975); 251(1): 167–95
- Enroth-Gubel & Robson, J Physiol (1966); 187(3): 517–52
- Kolb H. Webvision (2001). Salt Lake City (UT): University of Utah Health Sciences Center

According to Comparative Vertebrate Neuroanatomy, the XYW classfication is used for cat retina. They roughly correspond to the M, P, K cells in primates, respectively.


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What are dreams, biologically?
Falling asleep or states of subconsciousness does not stop the mind from making its own fictional images. These seem like sensations just like those received from human eyes. But, how do we define these visual sensations biologically?

Short answer
In terms of visual function, the low-tier primary visual cortex and high-tier frontal cortex are inactivated. The activity of the intermediate ventral stream and limbic regions are increased, apparently uncoupling low- and high-level vision processing from the system.
Background
The sleep stage where visualizations (dreaming) occur is called the rapid-eye movement (REM) sleep.
Brain imaging studies have shown pronounced effects of REM sleep on the functioning of the visual system.
In the awake state, the primary visual cortex (V1, or striate cortex) is activated, which is mainly concerned with low-level visual processing such as contrast perception. This cortical region in turn projects to higher-level (extrastriate) regions for more complex processing of visual information.
During REM sleep, however, a selective activation of extrastriate visual cortices is observed. Particularly the ventral processing stream is activated, which is associated with perception and recognition in the awake state (Deubel et al., 1998). Also the limbic and paralimbic regions are active (the emotional brain centers).
Interestingly, activity in the primary visual cortex (V1) is attenuated, as well as the frontal association areas of the brain. V1 is the primary, most 'primitive' visual cortex, while the frontal association areas are the highest-tier cortex that integrates complex perceptual information across perceptual modalities (Braun et al., 1998).
Overall, this pattern suggests a model of REM sleep where visual association cortices and their paralimbic projections may operate as a closed system dissociated from the regions at either end of the visual hierarchy that mediate interactions with the external world (Braun et al., 1998).
References
- Braun et al., Science (1998); 279: 91-5
- Deubel et al., Vis Cognition (1998); 5(1/2), 81–107

I need to learn some patience from you. Quite an informative answer for a broad question +1 :)


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Does our heart stop when we sneeze?
Is it fact or myth that our heart stops beating for moments when we sneeze? If it is fact, what drives the heart to start beating again?

Both your linked fact from the University of Arkansas

When you sneeze, the intrathoracic pressure in your body momentarily increases. This will decrease the blood flow back to the heart. The heart compensates for this by changing its regular heart beat momentarily to adjust. However, the electrical activity of the heart does not stop during the sneeze.

...as well as your 'myth' from webMD

For instance, it's not true that your heart stops when you sneeze. When your chest contracts because of a sneeze, your blood flow is momentarily constricted as well. As a result, the rhythm of your heart may change, but it definitely doesn't stop.

...come to the same conclusion, namely the heart does not stop during a sneeze.

Isn't the length of a sneeze less than the time between resting heartbeats, at least for most healthy people?  So it seems odd to say that the heart would stop.


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Can men also become only bald on their legs?
Often hair loss that primarily affects the top and front of the scalp will happen to men (and female) during aging. Male pattern hair loss is believed to be due to a combination of genetics and the male hormone dihydrotestosterone.
Men with androgenic alopecia typically have higher 5-alpha-reductase, lower total testosterone, higher unbound/free testosterone, and higher free androgens, including DHT.
The question is whether this kind of balding is only present in the hair of the scalp or can this proces also happen on the legs (or other parts of the body)?

Hair loss is known as alopecia, and is often associated with hair loss on the head. This type of hair loss is most noticeable, but hair loss can occur in nearly any part of the body, including the legs (source: Healthline). As an anecdote - my father in law (65+) has lost all his hair on his legs. This hair loss is referred to as anterolateral leg alopecia
About 35 percent of older men have this condition. The exact causes of anterolateral leg alopecia are unknown, but there may be a genetic component.
Age related hair loss in men is referred to as male pattern baldness, or androgenic alopecia. This type is related to hormones and certain genes.

For those who are interested, here is the current best genomic predictor of male-pattern baldness. Currently, about 15-20% of the variance in liability can be predicted directly from DNA (will increase when better data comes).

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What are most common natural causes of death?
What are most frequently occurring natural causes of death?

Without defining 'natural death' this question is opinion-based. I vote to close until clarified.

@Christiaan moreover, I see no point or purpose behind this question. This is not strictly in the realm of the biology that we consider here. This is more of a census report.

@WYSIWYG, agreed, and perhaps even more a definition question than anything else.

Beside the other comments, this also differes between countries, which makes the question a bit unclear and also very broad. And I assume you are talking about human causes of death?

The WHO has data from 2002 where they have classified and counted causes of death. I have treated the following as natural causes:

Cardiovascular disease (29.34%)
Infectious & Parasitic disease (23.04%)
Cancers (12.49%)
Respiratory disease (6.49%)
Perinatal conditions (4.32%)
Digestive disease (3.45%)
Neuropsychiatric disorders (1.95%)
Diabetes (1.73%)
Genitourinary disease (1.49%)
Maternal conditions (<1%)
Congenital abnormalities (<1%)
Nutritional deficiencies (<1%)
Endocrine disorders (<1%)
Neoplasms (<1%)
Musculoskeletal disease (<1%)
Skin disease (<1%)

I treated the following as non-natural causes:

Intentional injuries
Non-intentional injuries

The sum of the groups explains 96.7% of deaths. I think the remaining 3.3% would be other or undetermined causes, and rounding errors in the data. The natural causes accounted for 87.9%, and non-natural causes were 9.1%. The most common causes were cardiovascular diseases, infectious/parasitic diseases, and cancers.
It is difficult to assess how natural the cause of deaths are. For example, many cancers, cardiovascular, and respiratory diseases are more common in obese people and smokers (often self-inflicted damage), nutritional deficiencies are often caused by failing welfare and social systems.
Additionally, among the recorded causes of death in England and Wales in 2011, of the total 484,367 deaths recorded, 17,590* deaths were from extrinsic sources (accidents, homicides etc.). This is around 3.6% of deaths. In this data, the most common causes were cancers (29.6%), circulatory diseases 28.8%, and respiratory diseases (14.0%).
According to the CDC, in 2013 there were 2,596,993 deaths in the US, and 92.5% were of natural causes. Of those, the principle causes were heart disease (24%) and cancer (23%). There's a good table at the bottom of this site.
Rates of natural and non-natural causes of death will likely vary greatly by country given different health risks (e.g. malaria in Africa vs Europe), health care services, extrinsic risks (e.g. traffic accidents in Sweden vs India).
$*$ The table in the article features a potential mistake, it seems the columns are incorrectly labelled

I wonder if suicide due to depression should be considered natural.

I'd say depression is a natural disease, the whole division in to natural and non-natural causes is weird, too difficult to determine in many cases.

What is a natural death? All the lung cancers due to smoking? Cardiovascular disease due to overweight? The question, imo, is primarily what the definition of a 'natural' death is, more so than what the various examples are from a medical or pathological standpoint.

The question is, among deaths by natural causes, what are the most common? There is a general consensus, at least, as to what constitutes natural causes.

And which is...?


text:
Do nematodes have organ-level organisation?
Some introductory biology books state that nematodes have a pseudocoelom. So, they have a false body cavity. So, does it also mean that they have organ level body organisation?

In Fig.1 is shown the body plan of a round worm:

Fig. 1. Nematode. source: University of Illinois
You ask whether there is an organization in terms of organs; an organ is:

A group of tissues that perform a specific function or group of functions;

A tissue is:

An aggregate of cells in an organism that have similar structure and function;

As you can see in Fig. 1, there are clearly organs present, including a mouth, pharynx, reproductive organs, among others. They fulfill different tasks and contain various tissues, each dedicated to specific functions. Hence, they fulfill the definitional requirement of being organs.

Adding to Christiaan's answer, I quote Caenorhabditis elegans' anatomy to substantiate that nematode have proper organ development.


text:
Why do typical acetylcholinesterase inhibitors (like carbamates) have a greater parasympathetic effect than a sympathetic effect?
I understand that the post-ganglionic neurones of the sympathetic system are adrenergic, but surely these neurones will be excited to the same extent as the parasympathetic post-ganglionic neurones (due to the ganglionic synapses being cholinergic), and thus target organs/tissues will be receiving equal and opposite sympathetic/parasympathetic stimulation, or rather equal and opposite activation of the muscarinic/adrenergic receptors. (Sub-question: Why does caffeine, a perhaps atypical acetylcholinesterase inhibitor have a greater sympathetic effect than parasympathetic effect?).

We were taught that ganglionic receptors have very high thresholds. So we need a very high concentration of the drug to produce the sympathetic effects. We even solved a hypothetical problem in class, where a patient presented with a pinpoint pupil (typical insecticide poisoning) and increased secretions but an increased heart rate (usually they present with bradycardia). We would still treat the patient with atropine since the combo of pinpoint pupil and increased secretions would be exclusively explained by insecticide poisoning (either organophosphate or carbamate). The increased heart rate could be explained by ganglionic action leading to sympathetic activation of the heart.
But as said this was only a hypothetical case and patients of organophosphate or carbamate poisoning always present with bradycardia. To elicit ganglionic responses the person has to consume a dose way higher which would certainly lead to sudden death.
Hope that helps :)

I guess why ganglionic receptors have high thresholds would be the actual answer to your question. Ya, but this is what I have!

Thanks! Yeah that helps a lot, should put me on the right track for some further research - I'll have a further look about the ganglionic thresholds & the caffeine.


text:
How much energy does a neuron use for information processing as opposed to just surviving?
That is, as part of a neural network in a brain.

There are many, many different types of neurons. Some of them show very high spontaneous firing rates, while others are pretty silent. I think @Mustang's is great, but this question needs clarification.

Mainly interested from a theoretical computer science POV

http://quantum-mind.co.uk/anaesthetics-and-brain-energy/
About 80% of the brain’s energy consumption is devoted to neuronal firing with only 20% involved in maintenance activity.
The energy for firing is mainly supplied by glia and astrocytes, the maintenance of the neuron itself is done mainly by the cellular machinery in the neuron.

The text literally says "neural signalling", which is a lot broader than APs only. Without other references you may want to edit the wording. +1 nonetheless, nice way to tackle such a broad question.


text:
I know how to solve these equations, but I'm not sure what t' represents?
I am investigating the Wilson Cowan neuron population model, and I can follow most of it, but I'm not sure what is meant by t' in the equation for proportion of neurons in the refractory period. The equation of interest is below.

As a side note. The mathematical expression you drew is not an equation (there is no equal sign).

I figured it out, t' is just a dummy variable used to represent time over the refractory period since the integral is from t-r to t.


text:
How to calculate the percentage of heterozygous cells based on a gene map
I've encountered the following question and am quite stumped by it.
A female with genotype AABBCC has been hybridized with a male that has the genotype aabbcc. The first generation (F1) has been hybridized again (backcross) with offsprings that have the genotype aabbcc. Given the following genetic map, what would be the percentage of F2 offsprings that are heterozygous to all three genes:
A------- 20 MU ------- B -- 10 MU --- C
How should I approach the following question, the brute force approach is too difficult, I keep getting things wrong.

if this is homework please tag it as such and we would appreciate to see some previous attempts at tackling the question. We are not here to do your homework :)

actually, this is a question from an exam I am preparing for. the exam is tomorrow :)

What happens when you draw out all the possible offspring genotypes and calculate the percentage chance?

I get horribly confused and after several attempts can't seem to come to the correct answer, is there no technique to do it without writing down all possible outcomes?

+1 thanks for the edits. I'm not a geneticist, so I hope someone else here may help you further! Good luck tomorrow :)

Units of genetic distance
It took me a little while to understand what MU means. I have never seen MU but rather m.u. for map unit, or cM for centiMorgane.
Solving the problem
This problem got me thinking a little bit. My logic is the following:
Probability of being heterozygous at the first locus
You cross two individuals (we'll call them individual 1 and 2)that are both heterozygote at each locus A, B and C (not to be confused with the alleles A and a, B and b and C and c). We'll start with locus A. The probability of being heterozygous at locus A is the probability that individual 2 gives another allele than individual 1. This occurs with probability 0.5. If the three loci were perfectly independent, then the probability of being heterozygous for a given offspring at all 3 loci would just be $0.5^3 = 0.125$... but that would be too easy so let's keep going with the second locus.
Probability of being heterozygote at the two first loci
So let's assume our offspring of interest, got two different alleles for the locus A. The probability to receive two different alleles at the locus B is the probability that either no individual recombine between A and B or both individuals recombine between A and B. It is therefore: $0.2^2 + 0.8^2$. Put together this probability with the probability that the first locus was heterozygote it gives $0.5 \cdot (0.2^2 + 0.8^2)$.
Probability of being heterozygous for all 3 loci
Finally, we can just keep going with he next locus. Let's assume that the offspring have received two different alleles for both loci A and B. The probability to receive different alleles at locus C is the probability that either both parents recombine (between B and C) or none recombine. This occurs with probability $0.1^2 + 0.9^2$.
Put the whole thing together, the probability of a given offspring to be heterozygote (or the frequency of heterozygotes offsprings if you prefer) is $0.5 \cdot (0.2^2 + 0.8^2) \cdot (0.1^2 + 0.9^2) = 0.2788$
Note that calculating the probability that exactly 2 loci are heterozygous would have been a bit trickier.
Good luck for your exam tomorrow!


text:
Can someone identify this stinging plant?
I have no idea where this plant came from, or what it is. What I do know is its leaves are covered in little hairs, there's little thorns growing all over it, and just by rubbing its leaf it burns you and leaves a red mark as well as blisters. It stung my mother and I would like to know what it is so I can find a remedy.

larger image:
http://i1094.photobucket.com/albums/i449/cupcaketurtle1/20150714_225505_zpskr24gklq.jpg

It would help if you could add in what country you mother was stung by this plant.

The littles hairs are called trichomes :) I had bad experience when visiting a tropical bushy area. If you don't mind, could you please share where (roughly the region and city) your mother came into to contact with this plant?

I think it is a common stinging nettle, Urtica dioica. It is a native to Europe, Asia, northern Africa, and western North America and is the best-known member of the nettle genus Urtica. As commented by others, your geographical location would be helpful to obtain a more accurate identification.
Like other stinging nettles, it is unpleasant to the touch, but harmless. Just be patient. The redness and burning/itching will disappear. If the pain gets serious or other complaints arise, go to your GP.

Stinging nettle. Source: Health Direct.

It's a nettle (genus Urtica).
The one on your photo really looks like the one I'm used to see in France:
Urtica dioica.
I read in herbal lore books that the sting of the nettle could be appeased by rubbing it with Plantago leafs. But that might just be placebo effect.
See also this section of the wikipedia page.

Common folklore where I live is to sooth the irritation by rubbing the affected area with the leaves of Dock (Rumex obtusifolius) - which often grow near nettles. As a child I recall it being effective (though some of that was probably psychological reassurance).


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Have webs woven by LSD-intoxicated spiders ever been studied for their efficiency in fly catching?
I ask, because I have a different interpretation of the experiments performed on web-weaving spiders. The famous Robert Pirsig maintains that LSD is somehow helpful to web-weaving spiders, because it makes their web more straight. Pirsig seems to imply, as I remember, that the spider is somehow more attentive to its web while on LSD.
However, I maintain that it isn't the case and that it is actually the reverse.  The spider is much less attentive, for it needs chaos in its web to catch the fly!

Could you add a reference or link to his work?

Why do you think a chaotic web would be more effective?

I thought the titled question itself was related to Pirsig's claim, however upon further thought they are not related, and thus an answer to the titled question wouldn't disprove Pirsig's interpretation of the experiment.
However the quote does exist and is on p. 36 of Lila:  Inquiry into morals!

It also depends on how you measure efficiency. Of course the spider must expend fewer calories than it takes in from prey, but there is an implicit movement cost as well, in terms of N spiders caught moving around by, say, birds. There's also variety in species - some orb-weavers repair their webs, others construct new ones regularly. Clearly, we need to give more spiders more LSD.

In my flawed thought experiment I was thinking the fly could somehow sense the web, however, that is not the case in most circumstances.

Short answer
A low dose of LSD has been shown to lead to larger, more regular webs. This obsessive perfection of the web comes with an increased effort and likely an increased required building time. Whether LSD-affected webs are more effective or not has not been assessed as far as I am aware. Personally I think that, if anything, larger webs are more efficient for their purpose, regardless of their enhanced regularity.
Background
I traced down the experiments with d-lysergic acid dietheylamide (LSD-25) and web-building spiders to the experiments of [Peter Witt]*1 performed in the 1950's and 60's.
The original article of Witt (1951), dealing with the effects of LSD on the web building behavior of spiders (Zygiellax nohta) is not accessible to me. He reiterates on the data in a review (Witt, 1971). In this review he discusses the effect of a low dose of LSD on web building (Fig. 1).

Fig. 1. Web of an untreated spider (Araneus diadematus) (left) and a web of a spider (Zygiellax nohta) treated with a low dose of LSD-25. Source: Witt, 1971
Witt concludes that low dosages of LSD increase the regularity of the webs. Spiders which had received less than 0.05 pg LSD-25 built larger webs, with fewer oversized angles and significantly more regular central angles. The spiral was unusually regularly spaced. He did not investigate the effectiveness of these webs (Witt, 1971). However, I reckon that because of the larger size they may be more effective.
Witt notes that the normal web is far from a perfect geometric structure and that one can think of a web as a compromise between regularity, which serves to cover a wide area with a trap of a certain mesh size, and a quick construction. For example, Araneus diadematus makes a new web every morning before sunrise. It requires quite some labor producing and the webs are, arguably, structures of precision and beauty (Fig. 1). The webs take between 20 and 30 minutes to build. (Witt, 1971).
The balance between regularity and quick construction of the web is what may be distorted after relatively low doses of LSD (Witt, 1971). The spider seems to put too much and almost compulsory effort in making the perfect web, and likely without too much benefit in efficiency (The Guardian, 1971). But again, the author has not addressed this hypothesis directly.
Note that higher dosages of LSD (>0.05 pg) result in smaller and more irregular webs. The Guardian (1971) reproduced some figures on this (Fig. 2), showing an example of a grossly distorted and inefficient web.

Fig. 2. Web before and after a high dose of LSD. Source: The Guardian (1971)
References
- Witt, Experientia (1951); 7(8): 310-1
- Witt, Behav Sci (1971); 16(1): 98-113
Note
*Robert Pirsig is an American writer and philosopher who has not devoted his time to spiders as far as I know.

Although he didn't perform the experiment, his interpretation of it appears on p 40 of "Lila:  An Inquiry into Morals".

I might also add, he is a trained biochemist, and a living, breathing guy.


text:
Has anyone modelled calcium oscillations using Matlab software?
I have been trying to model calcium oscillations using MatLab, but I cannot obtain the oscillation.
I created a function where I put all the equations and used ode15s to call the function.  I have listed the equations and the code.
Can anyone tell me why I am not obtaining the oscillations?
These are the equations along with the codes:

r(:,3) = ( (((.029*0.13*1.049 + .21.*.5.*.144).*initi(:,1)) ./  (.144.*1.049.*(.5+ .13)) ) .*( 1- initi(:,3)) ) - (( (.21 *.5 + .029 *.9434) ./ (.5 +.9434) ).*initi(:,3));

The values of the upper case Ks are obtained as follows:

and the value of p is 0.5

a(:,1) = power (( (.5 .* initi(:,1) .*(1 - initi(:,3))) ./ ((.5 + .13 ).*(initi(:,1) + .0823)) ),3); % p_o

Jserca is directly substituted in the equation shown below

r(:,1) = (( 1.11.*  a(:,1) + .02 ) .* (  initi(:,2) - initi(:,1) ) ) -( .9 .*  power(initi(:,1),2)) ./ ( power(.1,2) + power(initi(:,1),2) );

 r(:,2) = - r(:,1) .*5.5; % Ce

The constants are shown here:

And this is the desired result:

But I obtain this!

And this is my code:

function[t, initi, r,a]= deyoung()
clear all;
clc;
close all;

%--------------------------------------------------------------------------
% Initial conditions
%--------------------------------------------------------------------------
initi(:,1) = 0;  %  C
initi(:,2) = .9; %  y
initi(:,3) = .5; %  Ce

%--------------------------------------------------------------------------
% ODEs
%--------------------------------------------------------------------------
icon=initi;

tspan=[0 100];

options = odeset('RelTol', 1e-08, 'AbsTol', 1e-08);

[t,initi] = ode15s(@(t,initi) oper(t,initi),tspan,icon, options );

[r,a] = oper(t,initi);

figure();
plot(t,initi(:,1),t,initi(:,3));

end

function [r,a]=oper(t,initi)

    initiSize = size(initi);

    initiColumnCount = initiSize(2);

    if ( initiColumnCount == 1)
        initi = initi';
        a = zeros(1,1);
    else
        initiRowCount = initiSize(1);
        a = zeros(initiRowCount, 1);
        r = zeros(initiRowCount, initiColumnCount);
    end

    % y
    r(:,3) = ( (((.029*0.13*1.049 + .21.*.5.*.144).*initi(:,1)) ./  (.144.*1.049.*(.5+ .13)) ) .*( 1- initi(:,3)) ) - (( (.21 *.5 + .029 *.9434) ./ (.5 +.9434) ).*initi(:,3));

    %Po
    a(:,1) = power (( (.5 .* initi(:,1) .*(1 - initi(:,3))) ./ ((.5 + .13 ).*(initi(:,1) + .0823)) ),3); % p_o

    %C
    r(:,1) = (( 1.11.*  a(:,1) + .02 ) .* (  initi(:,2) - initi(:,1) ) ) - ( .9 .*  power(initi(:,1),2)) ./ ( power(.1,2) + power(initi(:,1),2) );

    %Ce
    r(:,2) = - r(:,1) .*5.5; % Ce

    r = r';

end

Welcome to Biology.SE. The problem is either specific to programming (there's a bug in your code) or to biology (you did not understand the process you want to simulate). I don't actually know the concept of calcium oscillation but no one can correctly answer your question for the moment. You should add your code, describe it, describe the output and explain why the output is different from what you expected. I vote to close for the moment and will retract my close vote when the question will be improved.

@Remi.b Is that okay now?

Yep, that seems to be answerable now. Good improvement +1.

A general programming tip: define your parameters beforehand instead of directly hardcoding their values in the function. I did not go through your code but it seems that you have incorrectly typed the value of a parameter. As it stands, this question is off topic.

I'm closing this question as off-topic because it is about coding and not really about the computational model of the biological system.

@WYSIWYG Can you please tell me which parameter has been coded incorrectly?

@nashynash It is difficult for me to look through. I just guessed that might be the case. You can try defining the parameters in the beginning of the code and then use them in the equations. Difficult to troubleshoot otherwise. Something like a=1; r(1)=somefunction(a);

@WYSIWYG - your not voting anymore..

@WYSIWYG I think you should have at least checked the  code and the equations before you make such a comment.

@AliceD That is the default line that comes if I select the custom close. Anyways this is clearly off-topic.

@WYSIWYG - oh really? Sorry then! It's an interesting post given my post at meta. I think this one is indeed across the line. Happy I could help on the brink of closure anyhow.

@nashynash This is not the right site for code-checking and troubleshooting. You should do that in stackoverflow. And I commented based on my empirical understanding of systems and codes like these. Oscillations can disappear if some parameters change (Read about Hopf bifurcation). As I said, try to improve your coding style and you may find where you could have gone wrong. And it is better to write 0.5 instead of .5. General stuff.

@WYSIWYG Yes I know that it is more to do with the coding. But just wanted to try if someone from biochemistry would be familiar with Matlab and help me know where I am going wrong. But I will take you tip as well.
Ps: I have tried in stackoverflow, but since most of them are unaware of the mechanism behind calcium oscillations, they cannot fully grasp the idea.

@nashynash You are using the equations from a published study, right. So they should work: therefore I assume that the problem must be with the code. In stackoverflow, you need not explain calcium oscillation because your question is not really about if the model works (it works because it is already done by the people who published it. Your program is not replicating it). But before asking in SO try editing your code and examine if you have mistyped any parameter. Do the basic bug checks. You can try this site too: http://scicomp.stackexchange.com

Okay @WYSIWYG. And thanks for pointing out that page. Didn't know such page existed.

I wish to share an open-source modelling study on Ca2+ oscillations in astrocytes which contains a detailed description of the underlying math and even better, it has supplementary Matlab code published alongside (Zeng et al., 2009). This may be of help to check your formulae and script.
Unfortunately I do not feel inclined to start troubleshooting and bug-fixing your formulae and Matlab code, because, as mentioned in the comments, the issue can be anywhere in the chain of events.
Reference
Zeng et al., Biophys J (2009); 97(9): 2429–37

@nashynash - good luck. I'm sorry to see this question closed after all the efforts you put into it. Perhaps you can try another SE and hope for better luck there.


text:
What happens to IP3 molecules after release from IP3 receptors?
IP3 molecules bind to IP3 receptors and open up the calcium channels on the endoplasmic reticulum. I am wondering what happens to IP3 molecules after they have been released from the IP3 receptor? Do they remain as IP3 molecules, or do they break down? Do they have any purpose after they have been released, and perhaps after been broken down?

All biomolecules are eventually broken down. This process is called turnover. Since inositol is a signalling molecule it is necessary to remove in order to terminate the signal, despite adaptive mechanism in the ER calcium channels.
IP3 is generally dephosphorylated by a family of phosphatase enzymes called inositol polyphosphate phosphatases. After dephosphorylation, the inositol can be recycled into the membrane by phosphatidyl-inositol synthase.
Reference:
The IUPHAR/BPS Guide to PHARMACOLOGY 1

1 I'm citing this website instead of a research article because apart from citing the original research articles, it also has other informative links about the enzymes and the substrate molecules. It is also from a very reliable source.

thank you so much @wysiwyg By the way, how do we know the lifetime of such signalling molecules.

@nashynash There are different assays by which it can be found out. One way is to label the metabolite using an isotope (like ¹³C) and track the loss of radioisotope in the sample using mass spectrometry or NMR. In this case the "lifetime" depends on the phosphorylated state of inositol - so the phosphorous has to be labelled instead of carbon.


text:
Does suffocation pain involve nociceptors?
I never suffocated myself so not entirely sure, but when you suffocate, it's painful, right? But of course different kind of pain than being injured or sick. What I'm wondering is, if the "painful" (or suffering) experience of suffocation involves the standard pain pathway mediated by nociceptors? Or is it some other kind of pain pathway due to a lack of oxygen? I don't mean psychological pain.

I've heard it more commonly described as a sensation of panic rather than of pain, resulting from a rising [CO2] as detected by carotid chemoreceptors

It looks like this question is based on an unfounded assumption that asphyxia should be painful. Hold your breath for as long as you can. Does it hurt?...  I vote to close this question as opinion based as it is likely to generate wild guesses for answers as to whether nociception is involved yes or no. Quite frankly it is impossible to investigate this issue thoroughly due to experimental and ethical difficulties :)

@RoryM and probably also J receptors in the lung itself.

This is more of a hypothesis

I am not sure if suffocation per se would cause pain. Asphyxia, as RoryM indicated in their comments, can lead to anxiety and panic but not really pain. However, forceful breathing may lead to muscular fatigue which may result in pain. Pain induced by muscle fatigue is called myalgia. Myalgia is possibly triggered by low pH generated by lactic acid, via ASIC3 (Acid Sensing Ion Channel) receptor. Carbon dioxide has no role in this process either directly or as a synergist.

Reference:
Alan R. Light, Charles J. Vierck, and Kathleen C. Light. (2010) Translation from Mouse Sensory Neurons to Fibromyalgia and Chronic Fatigue Syndromes. Boca Raton, FL: CRC Press; Chapter 11 (Myalgia and Fatigue)

I think connecting myalgia and asphyxia is kind of far-reached. https://en.wikipedia.org/wiki/Myalgia

@AliceD this is farthest I can go :) I'll add a disclaimer

With a disclaimer you have my vote :) And a tiny edit ;) +1

Being no expert on pain, I will share some thoughts on the issue.
According to the following site(http://www.helpforpain.com/arch2000dec.htm), there are two types of pain: nociceptive and neuropathic pain. Neuropathic pain involves the central and peripheral nervous system, a possibility I would discount due to no apparent link to suffocation.
Thus, it is likely that, if "traditional pain" is felt, nociceptors are involved. A possible pathway is the decrease in oxygen, possibly detected by certain nociceptors which respond to lead to pain. However, I have not suffocated either, not met anyone suffocating so this is only a possibility.

Kudos for the attempt to answer this difficult question. However, it seems to be a wild guess and a reference is really needed here.

Good point. the problem is that I could not find any :(. If anything, I just wanted to add some food for thought; I'll keep looking though!

Yes, thank you :) Does anyone know how I can get more answers? Can I ask this question as another new question?

This is a reasonable stab at things, but has a number of inaccuracies (as does the website linked as a reference). I wouldn't call the pain of suffocation "traditional pain", as it is not usually described in such a way, but one thing that is correct here is the likely receptor is a particular type of nociceptor -- the "J-receptor".


text:
Are there human cells, apart from red blood cells and platelets, without a nucleus?
I know that blood platelets and erythrocytes do not have a nucleus. Are there more cells in the human body without a nucleus, such as pancreas, cartilage, or lung cells?

My lecturer told me that only red blood cells and platelets lack nucleus in humans

Short answer
As far as I know, red blood cells and blood platelets are the only human cells in our body without a nucleus.
Background
Erythrocytes and thrombocytes are the only human cells without a nucleus, as far as I know. However, if you count the gut as being part of the human body (in essence it is a continuation of the skin and as such it can be considered to be on our outside), then we are loaded with cells lacking a nucleus, namely all the bacteria that live in our intestines such as E. coli. Bacteria, being prokaryotes, lack a nucleus. In fact, there are ten times more bacteria than human cells in our gut (Wenner, 2007).
Reference
Wenner, Sci Am 2007

There are a couple of them more if I am not wrong.

Wanted to give a one line answer some day!!
Lens fiber cells and keratinocytes.

That's two lines :) +1 nonetheless, interesting finds!

What do lens fiber cells and keratinocytes do? Thanks for the help, but I just wanted to know of all the common known cells, like cells of organs.

@Ace lens fiber cells differentiate to form the lens of your eye and keratinocytes form skin and hair.

@WYSIWYG Wonderful findings.

Most keratinocyte types have a nucleus. A small subtraction of keratinocytes, namely corneocytes , https://en.wikipedia.org/wiki/Corneocyte , lack a nucleus.


text:
Difference between morphogens and evocators in development?
I am specifically interested in this within the context of 1950's developmental biology (I presume the meaning and scope of usage of the terms has changed since then), as I am reading Alan Turing's paper on 'The chemical basis of Morphogenesis'. Turing first mentions evocators in the context of 'evocators of Waddington'. I have read some articles by Waddinton to try to see what he meant by 'evocator', but have not gained clarification from the articles available online. Turing cites Waddington's "Organisers and Genes", which is not available on the web and I do not have access to.
A more recent article here states

The first element is the inducer (or evocator) defined as the signal emanating from a piece of tissue, such that when the tissue is transplanted to an ectopic position it elicits changes in the behavior of neighboring cells.13 Today, we understand that most of these inducers are secreted proteins and include morphogens belonging to the Wnt, Hedgehog (Hh), TGFβ, EGF, and FGF families.

Which seems to imply that most evocators are morphogens, although from the definition of evocator given I would say that this is exactly what a morphogen is!
Any insights would be much appreciated!

"Since the evocator Waddington and Needham discovered was ether soluble, it was considered to be a sterol, a class of molecules that includes many hormones related to later development" (https://embryo.asu.edu/pages/chemical-induction).
It seems like the termed is outdated, hopefully, you find this information useful.


text:
Action potential frequency presynaptic neuron comared with in post-synaptic neuron/ muscle cells
I am a physicist interested in knowing how the action potential frequency in a presynaptic neuron compares with that in
a) a post-synaptic neuron and
b) membrane depolarisation of muslce cells, and
c) how the membrane depolarisation of muscle cells quantititavely relates to muscle contraction.
From the reading I have done so far, it seems that the theory of c) is standard, and goes by the name is 'excitation-contraction coupling'. I would think that the actual relationship between the frequency of muscle cell membrane depolarisation and degree of muscle contraction- however it is quantitifed- would differ for muscle type, depletion of Ca2+ stores from the sarcoplasmic reticulum, etc. In any case, some theory is covered here for instance, although I haven't seen much mathematical modelling and quanitative comparison here.
In any case, I am then still wondering regarding a) and b). I would think that there isn't a straightforward answer; the sequence of events is action potential -> neurotransmitter release into synaptic cleft -> neurotransmitter binding -> membrane depolarisation -> hopefully an action potential.
I already see some potential sources of non-linear behaviour in the final step, and the neurotransmitter binding ->depolarisation step would prbably also be dependent on the recptor kinetics. Since we are talking on the behaviour on a temporal scale, we would have to consider the degredation rate of the neurotransmitter within the synaptic cleft, and no doubt several pathologies arise because of some dysfunction in changes in neurotransmitter degredation/re-uptake rate... Come to think of it now actually, I think differences in the extent of binding (say due to differences in the number of receptors on post-synaptic neuron membrane) are the basis- or at least one factor- in neuroplasticity. So of course they would differ. But still the question remains as to what extent. I am not sure whether for some circuits, say those in the motor system, there is little deviation between responses in people.
To give some context to my question, I am interested in technologies which actively stimulate, or disrupt stimulation, of neurons in a controlled manner, so as to achieve a desired output effect. There are several technologies and lab techniques being developed with this in mind- optogenetics on the single-neuron level, DBS and epidural stimulation for stimulating large groups of neurons for some non-specific duration of time. I would think that these techniques could be much more powerful and potent, if we knew the temporal relationship between consecutive neural firing rates on stimulation.

To be blunt, if you are interested in technologies to do what you say, you need way more information than an answer to this question, although this question is already extremely broad. I'd suggest starting with a course or textbook in neuroscience. As is, you are drifting into this territory: https://xkcd.com/793/

For example, the statement "hopefully an action potential" is a completely wrong way to think about it. Action potentials aren't an achievement that the nervous system has as a goal, they carry information. Not firing an action potential is also informative, and not nearly every input should cause an output.

@BryanKrause Hi. I am aware of this; i presume my sloppy and half-hearted phrase 'hopefully an action potential', in the context of my being a physicist, gives the impression that I have absolutely no idea about neueoscience principles. I think your comment was a bit sharp. And, if context is of any importance, I am a physicist in training- still an undergraduate- so I think my knowledge of neuroscience considering my present educational status isn't half bad. Plus, when I said 'interested in [these] technologies', I meant that literally. Not that I am trying to revolutionaluse these

Technologies now. I have read quite a bit on the fojndatiknal principles of neuroscience, but am yet to find a reference and quantitative comparison of rate of action potential firing from experiment. And besides, even if my background on this site seems pathetic, at least I am trying to find out. No point sitting like a lemon. And btw I have consulted Bear,Paradiso et al and Connors, White et al.

I only mean to suggest you should start with the biology rather than trying to figure it out from the physics. That approach might make sense if this stuff wasn't already studied, but it has been, and if you want to understand the technologies you will need to be practiced in understanding the biology. The reason that cartoon exists is because this approach is for whatever reason really common with people with a physics background, and it can be very frustrating for the biologists in the room.


text:
Why only heterogeneous SNVs for validation using genotyping arrays?
I am trying to validate the variants I found using whole genome sequencing . The standard practice, I have seen in the two publications below were to check for the number of heterozygous SNPs called by the SNP array.
1) Performance comparison of whole-genome sequencing platforms

To further assess the accuracy of the variant calling, ... Of the 260,112 heterozygous calls detected with the Omni array, 99.5% were present in the entire SNV data set, 99.34% were concordant calls and only 0.16% were platform-specific SNVs. This demonstrates that both platforms are sensitive to known SNVs and that few known single-nucleotide polymorphisms (SNPs) are detected by only one platform.

2) Optimised filtering reduces the error rate in detecting genomic variants by short-read sequencing

To confirm that shared SNVs are indeed true variants, we used Illumina single-nucleotide polymorphism (SNP) arrays and selected all SNPs heterozygous on the SNP array.

My question is - why are only heterozygous SNPs chosen for validation when using Illumina Omni arrays?

The purpose of validating is to find genuine SNPs and not those caused by sequencing or amplification errors. It is extremely unlikely you will have a false homozygous SNP as a result of error. Just think about it. The same error, at the same base, occuring 80%+ of the time? Its not going to happen unless you have low coverage, and these SNPs should be thrown out anyway. You may have some cases where a genuine heterozygous SNP is called as a homozygous SNP. But that isnt much of a problem. It is still a genuine SNP. It would only be a problem if you were only interested in homozygous SNPs, in which case you will just need to validate everything biochemically, which you will need to do anyways.

i think the chance of a sequencing platform calling something A/A when the microarray calls it B/B is virtually nil. Just doesn't happen.


text:
What Biology topics are linked to the Nitrogen Cycle?
What other educational topics are linked to the Nitrogen Cycle? I am a Science teacher, and I need to organise my lessons. Thanks!

As phrased this is currently very broad.  You say "other" but don't say what you've already considered.  What work have you done so far?

@justin other topics may be symbiosis , root nodule formation,chemical "talks" between rhizobium and legumes. Examples of symbiosis like mycorhhizae can also be given.

The nitrogen cycle is a highly biological process. Nitrogen gas is ~75% of the earth's atmosphere and N2 is the most chemically stable form of Nitrogen for conditions in the Earth's crust.
Nitrogen is one of the four most essential and universal elements to terrestrial life (Carbon Hydrogen and Oxygen being the others).  Nitrogen fixation, the name given to the various processes which make chemically reactive forms of Nitrogen available to living things. Ammonia (NH3 / NH4+) and Nitrites / Nitrates (NO2-, NO3-) are chemically unstable compared to N2 and the conventional biosynthetic processes in the cell can use any of these forms to make proteins, nucleic acids and other biologically active molecules necessary for life.
Ammonia and similar compounds like Urea come from the biological byproducts of  living cells - waste.  These are readily recycled in the soil by plants and microorganisms and I imagine some animals and insects.  Nitrogen is a limiting resource for living things and most biomes are pretty efficient at recycling reduced nitrogen from primary (NH3) secondary (NHR2), tertiary (NR3) and quaternary amines (NR4).
But the biosphere has a great demand for bio-useful nitrogen and in most places on earth in deep water and soil microorganisms can break down N2 directly into nitrates/nitrites. This happens deep underwater or underground because the enzymes which perform this activity are delicate and ruined by O2.  This process is entirely performed by anaerobic microorganisms. In recent decades, the ecological importance of subterranean microbial communities has become better appreciated for the complex structure and ecological roles it plays.
An interesting side note to this is that up to the early 20th century, the growth of life and human civilization was really limited by the intense labor required to grow food.  While hydrogen oxygen and carbon are essentially free - obtained from water, atmospheric oxygen and CO2 by plants, Nitrogen was the limiting factor in many cases to growing more crops or animals for food.
The Haber process, which converts nitrogen and hydrogen gas under high temperature and pressure into ammonia over a catalyst was such an important discovery - it allowed the industrial preparation of effective fertilizers and was instrumental in creation of the green revolution.


text:
Is evolution true as Darwin said?
I was telling the theory of evolution to my friends. But they asked me for the proof. They said, we are not seeing any such transition species at present. Neither we have such evidence for evolution. What should I do? I saw many proofs like archaeoptaryx, but now it has been proved that it is fully functional bird and others are also not supporting the theory of evolution given by Darwin!

You may want to look at the excellent series of links reported here: http://skeptics.stackexchange.com/questions/2057/demonstrable-and-repeatable-examples-of-evolution

There is no proving something outside mathematics, there is however the scientific process in which we determine the way reality likely is, in many cases to near certainty. You will not necessarily become convinced by one post here. You will have to learn trust in the scientific community, or learn about enough evidence for evolution yourself to convince you its a sound theory. Two points: there is no alternative to evolution that explains the data, or makes predictions as well as the theory of evolution, and the failing of one point of evidence is not necessarily evidence the theory is wrong.

It may be true that you're seeking scientific evidence but your friends are looking for the black and white answer. If they are, you can preface repeating some of the excellent responses below with a bit of what a scientific theory is. When someone asks me for proof of something I usually can't give them that, I can only give them evidence.

@ktamlyn Ok, seems logical. Mind the word 'seems'. See, even the atomic model that you studied in high school was based on certain observations. But they were all rejected when a more sound model comes up. For instance, Bohr's atomic model was rejected by Schrodinger, which itself was rejected because of just one fault in it, and the world got Quantization model. And even there were some faults in it and therefore, 2nd quantization model comes up and so on. And that is the whole story. The scientific world is always changing! You can't say illogically that Darwin is right.

You have to have prove if something is right. And just having some evidences doesn't make something true! As I mentioned earlier, even there were evidences that supported Bohr's model, but its no more acceptable.

As far as faith is concerned, I have in everything logical and scientific. But now on things given by scientists which have no solid basis! If I believe it today, can you take the responsibility that in this changing scientific world, this theory will remain unchanged? You will say yes only if you are not in depth with the science. I am also a science student. But its not bad to accept its limitations, which makes it changing.

@Smith, I am unsure I understand your response completely. You state "You have to have prove if something is right". No we don't, we "demonstrate that something is very very likely true". Black and white terms like "throwing out" an old model, when there is only "one fault in it" is a false characterization of what happens in science. What happens is augmentation, and modification. This false perspective on science is what leads to a sense we should throw out the entire theory of evolution because one detail is not understood. Minds that think this way cannot practice science.

I should add that augmentation and modification is generally common, not the rule. The examples you provided in my opinion are modification and augmentation.

I saw an excellent public science talk a few weeks ago. The speaker presented 5 questions which, if you answer yes to, you can only come to the conclusion that evolution exists. Firstly though we should define evolution: Evolution is the change in the inherited characteristics of biological populations over successive generations.
It was one of the best arguments I've seen put forward so I'll try to recreate it here. Put this to them and see what they say - and just in case they say no to any, I've put answers in for you ;) There is no hard evidence for the first four points because they are so damn obvious that if people say no, even after a logic based argument, then all they will ever say is no, they shouldn't need a scientific paper.
1) Do individuals reproduce?
The answer to this is undeniably yes, you were the result of reproduction. Reproduction exists.
2) Is there variation among individuals?
Yes, again this is undeniable. Do we all look and act the same? No. Are some people taller than others? Yes. Some more physically fit than others? Yes. Is everyone's hair or eye color the same? No. See, undeniable. Variation exists.
3) Do some individuals die before they get to reproduce?
Obviously yes. Children unfortunately die (of natural causes) which means they do no get to reproduce. Just go look in a cemetery or open the obituaries page of you newspaper and you'll likely find some one who died before they could have reproduced. Some people also never reproduce, because of life choices or fertility problems. Variance in reproductive success exists.
4) Do offspring resemble parents?
The answer to this is also yes, when two humans reproduce they (normally) produce something that resembles a human. And when that human reaches maturity they will likely look a more like their parents than a random stranger. Personally I was looking at old family photos recently and I honestly though I had found a picture of me marrying my mother, that's how similar my dad and I look. Heritability of variance exists.
5) Does heritable variation lead to differences in reproductive success?
If you've answered yes to all of the above then you really should be answering yes to this one too. As a hypothetical illustrative scenario, imagine two male deer. One has big antlers and one has small antlers. The size of antlers is largely genetically determined. The male with big antlers is seen as more attractive by a female. She chooses to mate with him. She gives birth to his offspring (n=2, 1 male 1 female) who inherit his genes for large antlers. This repeats with several females in the population (n=10). The smaller male has fewer mating events (n=2) and therefore sires fewer males in the next generation. The next generation contains more males with large antlers (n=10) than small antlers (n=2). This is evolution, the change in the inherited characteristics of biological populations over successive generations.
Another example is humans. We know some men have low sperm counts leading to low probability of successful mating. Further, we know that male infertility can be genetically caused for example by Y-linked genetic defects. Therefore we can expect that males with low sperm counts, caused by Y-linked defects, will have fewer offspring than a healthy male (given equal opportunity to mate) and because all males inherit their fathers Y chromosome they too will have low sperm counts. They will be represented at a lower level in the population's next generation. Again, this is evolution.
Speciation:
It then doesn't take much to jump from this to speciation. It involves the introduction of isolating mechanisms. These can be things like geography (allopatric speciation), or sympatric mechanisms like morphology, behavior, or any trait which prevents one group of individuals mating with another.
I'll illustrate first, and take the more difficult type - sympatric speciation. Again imagine our deer population. This time there is variance in sperm morphology, and female reproductive tracts. Males can produce two different types of sperm, one (male type S) is a slow moving but more resistant to the hostile female reproductive tract (because it is resistant to all types of antibody the females can produce), the other is faster (male type F) but less resistant (because it is resistant to only some of antibody the females can produce). Female reproductive tracts vary in the number of different antibodies they produce, one produces "all" that can be produced (female type R) and the other only a subset of the full array (female type W).
What will happen is that type S males will be more successful when mating with type R females because their sperm survive (whereas type F males have no sperm fertilizing the egg). However, type F males will be more successful in sperm competition than type S when mating to type W females. Repeated over many generations, these incompatibilities will cause distinct mating groups which do not overlap, i.e. species.
In reality it is much simpler to demonstrate this with allopatric speciation. Here two groups of one species become isolated by a geographical feature, like a river. Over time these populations evolve differently (because genetic mutation is random and selection might differ on opposite sides of the river). When they get the opportunity to mate after X generations, they can't because they have evolved genetic incompatibilities (offspring fail to survive, eggs can't bee fertilized).
One of the absolute classic examples is an experiment using fruit flies by Diane Dodd.   In her experiment she reared a population in two groups, one on starch based food, and one on maltose based food. After many generations (35 I think) the two groups showed mating preference, which is a reproductive isolating barrier, within their groups (mating pairs were more often formed from within treatments). Here is the paper.

Picture from http://evolution.berkeley.edu/

but still it doesn't prove evolution. When I say evolution, I mean formation of completely different species. In biology, two species are considered different if they can't produce a young one without mating. You are just proving that variations are inherited. I agree. But you didn't explain how this variation can lead to two different species. And this is exactly why I asked this question because I am facing a lot of similar questions.

@Smith That's speciation, not evoltuion. I'll add something in shortly, but you should be able to see how this extends to speciation.

Ok. But we have read that this evolution lead to speciation. And that what I want to know, how?

@Smith does this explain it for you?

@Smith. Speciation isn't so cut and dry as being able to mate. Reproductive isolation can exist in many forms. What about two animals that are able to reproduce and have viable offspring, but their reproductive organs have incompatible morphology so fertilization never naturally occurs? This would be a physical barrier to reproduction. Diane Dodd's fly experiment is similar, except that the animals have behavioural barriers.
You accept that variation can happen. What makes you not accept that variation can lead to speciation? What kind of forces would prevent it?

Going from variation to speciation is not that easy as you told. Why? Because different species have different morphology and anatomy. Variations only result in slight change of them. You can't expect a complete different species with variation. For an instance, human from monkey. But if humans evolved from monkeys, why we no more see any of the intermediate species? Even in the example of bee above, you will still get two closely related species. If you have any doubt, you can check with a DNA engineer, who can shower more light on it on the basis of more scientific DNA study.

@Smith Speciation isn't black and white, it is a gradual process.  To say we don't see intermediates between humans and apes is kind of wrong, some apes are closer to humans than others, humans 10000 years ago were more ape like than current humans and in 10000 years humans will be even less ape like, we are still diverging. Evolution and speciation do not stop, speciation is when we diverge enough to be considered separate species, but we will continue to evolve away from apes

@GriffinEvo I think you need to check the fossil records again in more depth which are contradictory to what you said! The human fossils found that are thousands to millions of years old, resemble the same shape. Caution: Dont depend on textbooks you are given. I faced a lot of criticism because of that. Search on internet the records. You would love to see this.

@smith As some one with a degree and a masters in evolution and two years in to a phd on evolution, I think I'm in a good enough position to judge what material to trust for myself but thanks for the great advice. Clearly you don't want to have your question answered by anything other than the answer you want. If you want an argument about the evidence of evolution go to a forum, this place is for questions and answers.

I also happen to work in one of the best departments in the world for the study of human evolution, I'd rather go to them for lessons on human evolution, not some guy on a website and a YouTube video. Science is peer reviewed, YouTube isn't, evidence that goes against the norm is welcomed by the scientific community, but the guy in the video is presenting weak subjective evidence against strong objective evidence.

@smith http://www.nhm.ac.uk/nature-online/evolution/what-is-the-evidence/morphology/hominid-skulls/

@GriffinEvo I know these, I am not a non-evolutionist. But there are evidences of human fossils millions of years old. Thats what I have to say.

@smith that says nothing, yes there are human fossils, but what is that supposedly telling us which goes against what Darwin or the theory if evolution says?

@GriffinEvo and thats why I am sure that Darwin was wrong. Have you read his book The origin of Species? Highly unscientific, although logical. He is assuming a hell lot of things on his own. ID is better option.

@smith so quote me what he said, why your evidence goes against what Darwin or (more importantly) the theory of evolution say, and how does it better suit ID?

The best proof of evolution is not in the fossil record, but perhaps in the living things you see around us right now.
For instance the rise of antibiotic resistant bacteria is the direct result of selection. The environment for the bacteria changed - we introduced antibiotics.  The vast majority of the bacteria die, but eventually the survivors are resistant- just in the space of a few years.
Adaptation and even speciation is occurring around us and can be observed directly.
A case that all of has seen, and was one of the most important to Darwin's argument in the Origin of Species is how we breed domestic animals.  By selecting animals with characteristics they find desirable, all sorts of animals are created by the use of selection - breeding the animals you want and then not breeding animals with characteristics that are not desirable.  Cats, dogs, horses, sheep - using selection any animal you want can be modified nearly to the point you can't recognize it.  This is a multibillion dollar industry when you think of all the livestock and pet breeders in the world.
The most famous scientific experiment along this lines is Dmitry Belyaev's domesticated fox experiment where over 40 years the foxes who were the friendliest to humans and bred them together.  As a control experiment the most hostile foxes were also bred together.  The result is an animal which is as friendly as a golden retriever, even though no fox had ever before been taken as a pet.
There are dozens of other stories.  Selection for breeding plants is another such success story.  Though it takes more work and time, Selection is as reliable as electronics as a technology.
Making someone believe something that they don't want to is much harder though.

ok. May be you are right. But still, this may be valid for asexual reproduction. What about sexual reproduction case. Is there an example in that too?

added another case above

Despite evolution is generally macroscopically appreciable after a long time, there are some examples observable right now.

A classic example is the evolution of the peppered moth (Biston betularia) in the last two hundred years. Originally the predominant color was white, which camouflaged them against light-coloured trees such as Betula plants, while dark-colored moths were rare. During the Industrial Revolution in England the pollution blackened many trees, causing most of the light-coloured moths to die off from predators. The black-coloured ones (called carbonaria) flourished because of their ability to hide on the darkened trees.
The best example about whole species evolving is the ring species. Here is a good definition from wikipedia:

In biology, a ring species is a connected series of neighbouring populations, each of which can interbreed with closely sited related populations, but for which there exist at least two "end" populations in the series, which are too distantly related to interbreed, though there is a potential gene flow between each "linked" species. Such non-breeding, though genetically connected, "end" populations may co-exist in the same region thus closing a "ring".
Ring species provide important evidence of evolution in that they illustrate what happens over time as populations genetically diverge, and are special because they represent in living populations what normally happens over time between long deceased ancestor populations and living populations, in which the intermediates have become extinct. Richard Dawkins observes that ring species "are only showing us in the spatial dimension something that must always happen in the time dimension."

You can continue the reading at the related wikipedia article.

peppered moth just adapted to this change and their body colour changed. But are both different species?

No, they are not. It's an example of current evolution. You can look at the "ring species" example for the speciation (read the wikipedia article!).

I added a larger quotation from wikipedia, now is self-explanatory.

The ring species is an excellent example of evolution of species.  The two endpoint populations are essentially different species, and you can find the gradations between them in the ring around the globe.  Remove the intermediate populations and all you have are two (related) species.

@mgkrebbs - Great comment about ring species.  Here's a nice explanation: http://www.pbs.org/wgbh/evolution/library/05/2/l_052_05.html

But lets become somewhat practical. If you read from that wiki page only, it says only four species are found to follow this concept of ring species. So, again, if this is the right concept, atleast majority of species are supposed to follow it. And thus, this idea still is just a concept and not a law, which is universally applicable. Any comments?

Ring species is a special case in which the intermediates haven't become extinct. The general trend is the contrary. The theory of evolution will be forever a theory: you can't pretend to see the evolution of every single specie in the planet. However, like Stephen Jay Gould said, it is "confirmed to such a degree that it would be perverse to withhold provisional assent." Sure the ring species concept alone can't prove evolution.

so, in the end it comes to faith only! We have to just accept. Then what is the problem in Intelligent Design? Even you have to put faith there! But that is more scientific than saying that everything we see around evolved by chance. I have never seen any discovery taking place by chance. A scientist may be working on something and not getting results. But he may get that by chance. But to believe that anything just came up by change is illogical and unscientific! In ID, atleast they tell its a design by a designer which is more logical than saying chemicals combine on their own and life came!

You have several misconceptions about the theory of evolution, however you wouldn't have written certain things. I can't explain you all because I'm italian and not a good english speaker and because you will need a long answer. Moreover, your question was about present transition species. I suggest you to read a popular-scientific book about evolution. You can ask a new question for suggestions about it!

Of course you dont see a transition species at present! A transitions species is what existed between two other species. When it "becomes" the new species, the transition species no longer exists. Transition species only exist in the past. Its also important to remember that species are a spectrum. When we divide things up into discreet species it makes it seem all neat and tidy but really it is not because of the large amount of variation that exists within a species. When the variation becomes so great that certain members of the species may not be able to interbreed, we break it into two species.
I also do not see why you need to visually see evolution to believe it exists. The strongest evidence can be found in DNA or protein sequences. Look at any conserved protein and see the similarities. I will give you a link that shows the difference between the mouse and human version of a protein called p53. p53 is studied a lot because it is thought to have a role in cancer. Im not even sure if p53 is considered a "highly conserved" gene, but look at how similar it is!
ps53 protein alignment*
How many generations difference do you think there is between a mouse and human? [remeber humans did not evolve from mice, they just had a common ancestor, so what I mean is how many generations have elapsed since the last common ancestor]? It is estimated that mice / humans disverged some 70 million years ago. Lets say a generation (age difference between parent and child) is ~30 years in humans (it is much much much much less in mice but lets forget about that) that means there were some ~2 million generations, and thats being conservative. This website claims there are 74 de novo[new] mutations in humans each generation. Technically this is not all mutations but again we are being conservative. So that is about a 150 million mutation difference between humans and the ancestor that became both humans and mice
My question to you is this: Look again at the similarities between human and mouse p53. You see how there are some differences? Dont you think it is entirely possible that the differences can be accounted for after having 150,000,000 chance mutations?**
Now imagine this happening to every gene, not just p53. That is evolution
*Not sure how long this link will be valid but you can see the sequences at these links and do the alignment yourself here
http://www.ncbi.nlm.nih.gov/protein/200203?report=fasta
http://www.ncbi.nlm.nih.gov/protein/23491729?report=fasta
**Actually double that to account for mouse evolving from the common ancestor but like I said, wanted to be conservative

There are six different types of evolution and they all happen on different levels.

Cosmic evolution- the origin of time, space and matter. Big Bang
Chemical evolution- the origin of higher elements from hydrogen.
Stellar and planetary evolution- Origin of stars and planets.
Organic evolution- Origin of life from inanimate matter.
Macro-evolution- Origin of major kinds.
Micro-evolution- Variations within kinds. Only this one has been observed. For instance poodles and great danes are descendant from the same thing. A wolf.

Are you asking about macro evolution or micro evolution? Or one of the other 4?
Speciation does not show macro evolution in any way, shape, or form. And the ring species you refer to moths changing colors, that is micro evolution. A moth changing into another moth would even be micro evolution.
Man thought up species and defined them. If it looks like a duck and quacks like a duck, it didn't evolve into a different animal because it changed the color of it's feathers.

You're using some rather strange terminology, your first 4 points are generally not called evolution, the Big Bang and abiogenesis are not part of the theory of evolution. And the division into macro- and microevolution is misleading, it is exactly the same process.

It is not the same process and they are all forms of evolution. Define macro and define micro and let's see if they are the same. Micro are finite changes that can happen independently of macro evolution. Are you saying you can't have micro, without macro? Or are you saying you can't have macro, without micro? If you can have micro without macro then they are different.


text:
Why is history not called science even though palaeontology is?
In the scientific method, we propose models to explain a phenomenon and propose falsifiable tests for it. In palaeontology, we cannot do direct tests to verify our models, but we still make predictions that this particular kind of fossil would be found within a particular time period, or a rabbit wouldn't be found among the Cambrian  fossils. I assume that's why, even in the absence of experiments, we can call palaeontology science.
But in history also, we do a similar thing. We propose models (Jesus existed, let's say), and then make (implicit) predictions that no future discoveries would contradict that hypothesis, or better, mention him by name in a non-theological context.
Then, why is doing history not considered science, when palaeontology is?

Because of this

I'm voting to close this question as off-topic because it is about the philosophy of science and not biology.

Tests need not be direct to be scientific 2. Direct tests are common in Paleontology. For example, the prediction that non-avian dinosaurs went extinct from an impact event can be directly challenged by finding a dinosaur skeleton above the impact layer.

Paleontology is not only guessing and estimating how old a fossil is... And it's also not only imagining how dinosaur XY may have looked like during lifetime.
Paleontology also is:
Paleobiology
Understanding the biology, physiology, anatomy, reproduction, evolution, and whole way of life of prehistoric animals, including trophic networks, life communities etc.
Taphonomy
The way from a biocenosis to a thanatocenosis and a taphocenosis. What happens after the death of an animal? How it is transported (allochthonous/autochthonous), what changes in chemistry lead to decay and preservation of hard and soft tissues? E.g. the principles of local self-eutrophication for phosphate-based soft-tissue preservation. How is the fossil embedded in the rock? Is a fossil spirit level preserved? What diagenetic processes happen after embedding?
Paleoclimatology
Understanding prehistoric climate changes by studing e.g. isotope levels, paleo-monsoon conditions during the formation of huge continents like Pangaea or Gondwana, the influence of plate tectonics on the conveyor belts of the oceans etc.
Paleobiomechanics
The mathematics and physics part... Breaking down animal locomotion to equations and calculations of forces and moment arms. This helps to understand how animals of giant sizes or with a completely different locomotory musculature were able to walk and to take a look at the forces, which were exerted on the joints during locomotion/mating/standing up etc.
So you see... Paleontology uses so many different natural sciences disciplines like physics, chemistry, biology, and mathematics, that practicing it becomes a natural science itself. Can you say the same thing for history?
My list could have been much longer... There are so many sub-disciplines in paleontology that it would habe taken too long to mention them all.


text:
Do mosquito repellent sprays work on all insects?
I would like to know the mode of action of mosquito repellent aerosols. Are these specific to mosquito or are other insects affected too?

Are you specifically interested in the aerosols. The sprays are sometimes insecticidal as well.

Citronella oil is also used as an insect repellent and is seems effective on mosquitoes[1] and head lice[2] as well. Though I was not able to find information on the mode of action, just the effectiveness of citronella.
Wikipedia also says DEET is effective for fleas, ticks, and chiggers (though this lacks a references). Anecdotally, I know the Off brand of repellent is useful when the dogs get fleas to avoid getting all bitten up (Off contains DEET I believe).


text:
Why do pigeons kill their chicks when touched by a human?
I used to have many pigeons around the house. If by chance one of the chicks fell out of the nest, we used to put it back using gloves.
Usually, if we would touch the chicks with our bare hands, however, the other pigeons would usually kill the chick. I want to know why they do that?

This is covered at Skeptics.SE: http://skeptics.stackexchange.com/q/3132/43

This is a story I have been told as well when I was a kid. Usually this is related to the foreign smell that the humans leave on the chick. However, this seems to be an urban legend, as birds have not a great sense of smell.
Snopes says about this:

However, Mother birds will not reject their babies because they smell
  human scent on them, nor will they refuse to set on eggs that have
  been handled by a person. Many birds have a limited sense of smell and
  cannot detect human scent, or if they can detect it, do not react to
  it.

What can happen is that the birds returning to their nest which find the nest disturbed compared to the situation when they left might cause them to temporarily or permanently abondon their nest.
You can find this and more urban legends about birds here and here.


text:
The effect on the efficacy and potency of a non-competetive antagonist binding to the active site of the receptor (dose-response curve)
According to the book "Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy" by Golan et al, non-competetive antagonists can bind to both the allosteric site and the active site.
I know that a non-competetive antagonist that binds to the allosteric site causes a decrease in efficacy, but no decrease in potency (see figure below). Figure A shows the agonist alone and the agonist together with a competetive antagonist. This causes the dose response curve to shift to the right, thus increasing the EC50 and decreasing the potency of the agonist. Figure B shows the dose-response curve for the agonist alone and agonist together with a non-competetive antagonist that binds to an allosteric site. As you see this type of antagonist causes a decrease in efficacy, but no decrease in potency is observed.

But how does a non-competetive antagonist that binds to the active site affect the dose-response curve? Does it lead to both a decrease in efficacy and potency? Unfortunately, there is no figure in the book to answer my question.

I slightly modified your question. Please feel free to roll back. Thanks for this interesting question.

Short anwer
'Non-competitive active site–binding inhibitors' are called mixed-type inhibitors. These inhibitors exhibit features of both competitive and non-competitive inhibitors, as they increase Km (like a competitive inhibitor) and decrease Vmax (like a non-competitive inhibitor).

Background
What an interesting question!
In theory, a reversible inhibitor binding to the active site of an enzyme is per definition competitive. In a review by Blat (2010) the author mentions that active site–binding inhibitors that display non-competitive inhibition are indeed unusual. Such inhibitors are referred to as mixed-type inhibitors. In many cases the unusual behavior is observed with (1) enzymes utilizing an exosite for substrate binding, or (2) isomechanism enzymes, (3) enzymes with multiple substrates/products and⁄or (4) products and two-step binding inhibitors.
(1) Enzymes with an exosite have a substrate recognition site that is different from the active site. For example, some proteases bind their target on the exosite and then catalyze proteolysis in the active site. Mixed-type inhibitors then bind to the exosite, thereby inducing non-competitive behavior, as the active site is not bound.
(2) isomechanism enzymes are enzymes that undergo several structural transitional changes during catalysis. When one of these conformations is rate limiting and binds the mixed-type inhibitor, it may non-competitively inhibit the enzyme when another conformational form binds the substrate.
(3) Enzymes with multiple substrates or products sometimes follow a sequential binding and release of two substrates (or products). Suppose substrate A and cofactor B (e.g. NADPH). The enzyme converts substrate A into A' and cofactor B to B'. Now suppose that the enzyme obligatory has to release A' before B' can be released and that the B' bound state is unable to bind substrate A in the active site, but is able to bind the mixed-type inhibitor. In this case, again, a non-competitive inhibition pattern is observed.
(4) Two-step binding inhibitors refer to inhibitors that cause a conformational change of the enzyme after binding its inhibitor, that very slowly reverts back. In the conformationally changed state, the enzyme cannot bind the substrate and competition with substrate is lost. The most extreme case are inhibitors that covalently bind to the active site (note this is the mechanism addressed by @RoverEye).
You ask what the dose-response graphs are of mixed-type inhibitors. A more common way of displaying inhibitor behavior is using Lineweaver-Burk plots. Many enzymes follow Michaelis-Menten kinetics (Berg et al., 2002) and by plotting the enzyme kinetics as Lineweaver-Burk plots more insight is gained into the affinity (Km, you call this 'potency') and maximum rate of the enzyme (Vmax, you call this 'efficacy') compared to dose-response graphs. In Lineweaver-Burk plots the reciprocal velocity of the enzyme is plotted against the reciprocal of the substrate concentration, resulting in a straight line out of which affinity an maximum velocity can be easily obtained via linear regression.
The following graphs obtained from Illinois Institute of Technology show the three different modes of inhibition discussed, starting with the two common types:

Competitive inhibitors increase Km (i.e., decrease substrate affinity).

Non-competitive inhibitors decrease Vmax (i.e., decrease substrate turnover)

Mixed-type inhibitors increase Km and decrease Vmax

References
- Berg et al. (2002). Biochemistry, 5th edition
- Blat, Chem Biol Drug Des 2010;75(6):535-40

There is one more type of inhibition called uncompetitive inhibition where the inhibitor binds to the ES complex. y-intercept increases with increasing inhibitor but the slope remains constant. [Example].

@WYSIWYG,  I left it out for clarity as it wasn't mentioned in the question.

Also you can perhaps add that the dose response curves shown in the question have Hill kinetics and these graphs are for normal Michaelis-Menten.

@WYSIWYG - which graphs do you mean with these graphs, mine or PO's graphs?

Your graphs are for MM but OP's graphs look like Hill.

@WYSIWYG Thanks I'll look into it. Does it invalidate my answer?

No no.. Not at all.. :)

@WYSIWYG,  pheww :) I spent a lot of time on this one. Will work on it asap.

Wow thank you @AliceD for this answer. It really helped me.

@Sarin - no worries, my pleasure! It was a tough and interesting question :) It took me several days to have a satisfactory answer in place. With the comments from WYSIWYG it ended up as a decent answer. Glad I could be of help.

This is a tough question. I was reading this paper Patrono, C., et al. "Clinical pharmacology of platelet cyclooxygenase inhibition." Circulation 72.6 (1985): 1177-1184. and they seemed t mention this paragraph in the introduction.

Platelet Cycloxygenase or prostaglandin (PG) H synthase (i.e., the
  enzyme that converts arachidonate released from membrane phospholipids
  into PG endoperoxides) is the target of several antiplatelet agents
  that can reversibly or irreversibly block the activity of the enzyme
  by competing with the substrate or permanently altering the active
  site, respectively.Such drugs belong to the class of so-called
  nonsteroidal anti-inflammatory agents (e.g., indomethacin, aspirin),
  but also include a uricosuric agent, i.e., sulfinpyrazone.

So we have to look for  DRC of a NSAID to say COX. Now I was unable to find a good DRC for aspirin (If you find it, let me know in the comments below. I would love to take a look at it). But I did find DRC for other drugs that inhibit COX.
It led me to this paper Walker, M., et al. "A three-step kinetic mechanism for selective inhibition of cyclo-oxygenase-2 by diarylheterocyclic inhibitors." Biochem. J 357 (2001): 709-718. which described the inhibiton of COX2 by a NSAID called celecoxib.

The inhibition of COX isoenzymes by NSAIDs generally conforms to one of three inhibitory mechanisms: simple reversible inhibition, as demonstrated by ibuprofen ; time-dependent reversible inhibition, which includes both weaker binding inhibitors, such as naproxen , and tight binding inhibitors, such as indomethacin and meclofenamic acid ; and irreversible covalent inhibition, as demonstrated by aspirin  and o-(acetoxy-phenyl)hept-2-ynyl sulphide ('APHS') . Most of the traditional NSAIDs display similar inhibitory mechanisms against both COX-1 and COX-2 , and are relatively non-selective. However, COX-2-selective diarylheterocyclic inhibitors demonstrate distinct inhibitory mechanisms for the two isoforms . For example, celecoxib  has been reported to be a reversible competitive inhibitor of COX-1 while demonstrating time-dependent irreversible inhibition of COX-2.

Considering the highlighted statement, I think you can consider the COX1 curve as a standard competitive inhibition and COX2 as non competitive inhibition. The resulting change is essentially the curve shape itself (being shifted to the right).
The DRCs were reported here: Tacconelli, Stefania, et al. "The biochemical selectivity of novel COX-2 inhibitors in whole blood assays of COX-isozyme activity." Current Medical Research and Opinion® 18.8 (2002): 503-511.

Interestingly the second paper (By Walker) also described how (the authors proposed) the binding occurs. A very interesting read.

Thank you for the answer, I appreciate it. But it really doesn't answer my question, which was about an irreversible antagonist that binds to the active site (apparently there are non competitive antagonists that do bind on the active site) and how this affects the dose response curve. The figures in my first post (fig B) and in your post (fig B) show the dose-response curve for a non competitive (irreversible) antagonist that binds to the allosteric site. But thank you, once again, for the time and answer!

@Sarin Apologies. I corrected the answer with what I think happens. I know its not ideal, but I do hope it does this help a bit? It was a very interesting journey to find the answer I must add. I am still trying to find the DRC, but atleast I was able to find an example to start and give a general direction to go in.

Indeed, this one is a really great and interesting answer. It does help. I thank you once again for your effort. Appreciate it man!