Data repositories for data on the Tumor Microenvironment? Does anyone know of any data repositories for data on the Tumor Microenvironment? I know of the The Cancer Gene Atlas and the Gene Expression Omnibus databases but I'm more curious about data on the (molecular) composition of the TME. (I'm also curious about any databases with data less specific.)

Have you seen the St Jude Children's Research Hospital Pediatric Cancer data repository PeCan?
They have a bunch of data on a wide range of different types of pediatric cancers. These are all in the form of genomes and RNA-seq. However, they also have a bunch of visualizations set up so that you can see how these profiles work from a perspective of mutations and RNA in tumours of all sorts.


The effects of dust particles When sun rays shoot through my house from a window, sometimes if the lighting is correct, it will reveal a huge amount of floating particles and dust.

Are these particles dangerous to humans if you live with them constantly?

You asked the single most difficult questions ever, so be proud of yourself! I've spent some time in the lab with a post doctorate trying to answer that particular question. It all is based on something called the hygiene hypothesis: the belief that as we are getting cleaner we are seeing less and less bacteria and so our immune system isn't working as it should so we get allergies. There's lot to this theory with regards to the different white blood cells in our body (specifically Th1, Th2 if you've ever heard of them). Of course there are reverse hypotheses, because we avoid eating stuff like peanuts, but minute amounts is found in dust, dust exposure (which also contains bacteria) makes us think peanuts are harmful so that's why we have allergies.

Realistically a bit of dust to the most of us isn't harmful but if it contains things like dust mite poop which many people are allergic to, cat skin (another seriously common allergy) or is leaking from a place with mould... you should be okay :)


How to define "evolution"? The standard answer found in intro course to evolutionary biology to the question:

  what is evolution?

is:

  It is a change in allele frequency over time!

I believe a complete definition should encompass the following concepts:

mutations
copy number variation (CNV)
codon usage
chromosome numbers
phenotypic change (whether heritable or not)
Complex phenotypic trait such as plasticity and developmental noise
maybe some other things...

My questions are:

Would it be worth it to talk about phenotype in a definition of evolution?
What are the alternative definitions that have been proposed?
What is your definition?

Note: I would rather talk about genetic evolution, but if you think it is worth making one definition for genetic and cultural (and some other stuff maybe) evolution, you're free to suggest it!

What is evolution?

In a non-biological sense, evolution means change:

  "a process of [...] change"

Biological evolution (seeing as this is Biology stack exchange) then needs to be tweaked to give a biologically specific context. Many textbooks etc. give definitions of evolution and here are a few good ones from across the history of evolutionary biology:

Charles Darwin:

  "Descent with modification".

Mark Ridley1:

  "Evolution means change, change in the form and behaviour of organisms between generations. ... When members of a population breed and produce the next generation we can imagine a lineage of populations, made up of a series of populations through time. Each population is ancestral to the descendant population in the next generation: a lineage is an ancestor-descendent series of populations. Evolution is then change between generations within a population lineage."

Brian and Deborah Charlesworth2:

  "Evolution means cumulative change over time in the characteristics of a population of living organisms. ... All evolutionary changes require initially rare genetic variants to spread among the members of a population, rising to high frequency..."

All of these have a common theme. Biological information is moving through time, descending with a degree of directionality (e.g. parent $\rightarrow$ offspring), and the information is modified with time.

Personally I would define evolution as:

  Evolution is a change in gene frequencies, resulting from four mechanisms (mutation, migration, drift, and selection) which can all affect the transmission of heritable genetic information within populations. Evolution has the potential to cause phenotypic change (when genotype affects phenotype) and has the potential to cause both adaptation (microevolution) and divergence (macroevolution).

This definition captures that biological evolution occurs through changes in heritable genetic information, the prerequisites of evolution, the mechanisms of evolution, and what the consequences of those changes can be.

I think it is important to include mutation (and drift, selection, and migration) because these explicitly state how evolution occurs. I don't think it is necessary to include copy number variation, chromosome numbers, or codon usage as they are not central to the process of evolution (though they can be important).

Whilst only the first sentence of my definition is critical, I think it useful to include the latter part (or something of a similar effect) whenever possible as it helps to clarify evolution and it's relevance.

ISBN: 978-1-4051-0345-9
ISBN: 978-0-9815-1942-5


What is the biochemical explanation for tingling and burning sensation in brain due to certain food? Consumption of mustard (spicy English Mustard), wasabi and horseradish based food dressings usually result in a burning, tingling or freezing sensation in the brain/scalp and nostrils as the vapour goes through the nasal cavity.

I read somewhere, the checmical which gives the burning sensation is isothyocyanates. And some of the posts roughly mention about sinuses being agitated due to this chemical vapour.

How to explain this from biochemical and biology aspect? e.g. What sort of a cell reaction, if any receptors involved etc. (Appreciate an answer that is similar to the type of explanation here.)

You are right the compounds provoking this burning/tingling sensation is called allyl isothiocyanate.

We (human) perceive these compounds in two different ways when ingested, namely via the gustatory and olfactory systems. The molecular receptor sensing isothiocyanates is called the transient receptor channel A1 (TRPA1) [ref].

Here a simplistic view of how ingredients are perceived:

Gustatory sensation

First we get a burning sensation in the buccal cavity due to TRPA1 receptors present on the surface of the sensory neurons of the trigeminal nerve. In essence isothiocyanates dissolved in the saliva will activate those neurons via TRPA1 provoking electrical impulses in the trigeminal nerve which leads to a burning sensation.

Retronasal olfactory sensation

For several food ingredients we also perceived an aroma (taste = gustation, aroma = olfaction, taste + aroma = flavor). The aroma of an ingredient is perceived by olfactory sensory neurons in the nasal cavity and because some of the ingested ingredient will be vaporized inside the buccal cavity and travel through the nasal cavity where they are perceived (retronasal perception).

Not so surprisingly, isothiocyanates will again be perceived by sensory cells of the olfaction system via TRPA1 hence a burning sensation in the nostrils.

How receptor activation leads to a neuronal stimuli

This is a very broad subject and I will only give an overview of what is happening. We first start with the activation of a receptor by an agonist (in your question, isothiocyanates binding and activating TRPA1). Upon binding of the agonist the conformation of the receptor will change from an inactive to an active state. The way the signal is transduced varies according to the type of receptor but for the TRPA1 channel what happens is that the channel opens leading to an influx of calcium ions ($Ca^{2+}$) in the cells which changes its electrical state (as calcium ions are positively charged), a phenomena called depolarization. Depolarization of specific sensory cells (here the one expressing TRPA1) start an electrical signal in the nerve which travels to the brain where it is then decoded. The exact way the brain decodes sensory signals is still under debate but a likely explanation is that only some neurons within the nerve are activated which allows the brain to decode the sensory signal based on the nerve activation pattern. As an analogy, it would be the same as having only specific wires (neurons) turned on within a bundle of wires (nerve).

Further reading

If you want to further extend your knowledge on taste perception at the molecular level read this excellent review Chandrashekar, 2006. For a in-depth review on olfaction refer to this book. For a book on signal transduction refer to this while for TRP channels activation this is a good reading.

The field is quite broad and there are many good references. Sensory perception includes two distinct and broad fields namely neurosciences and cell signalling.


How are geneticists able to isolate gene functions? As an example, this Scientific American article describes a known area in the dog genome that metabolizes carbohydrates.

How is it that researchers are able to determine specific functions such as this?

@LanceLafontaine suggested a few ways above, but I would recommend reading this section
in Alberts' Molecular Biology of the Cell, which gives a more descriptive overview of some approaches, but even that is not exhaustive.

An extremely simplistic and also not exhaustive summary:

observe mutants, see what processes are disrupted, and map these back to particular mutations
mutate a gene and see what processes are disrupted
biochemical studies to see, for example, which proteins (which are gene products) interact in vivo and things like where they're localized, which may hint at function.
analyze structure of proteins, see how similar they are to other proteins with known function, and infer that the protein of interest probably has a similar function

EDIT: The link to Alberts is to the 2002 edition (which is free online; the latest edition of the textbook costs around $200), so things have come a long way since then, but the underlying approaches are still in use.


Amphibian blood circulation In an amphibian blood entering the right atrium shows higher levels of oxygenation than that in left atrium when :

A.It is hyperactivated

B.it is hibernating

C.it is submerged

D.it is in the terrestrial habitat

I think it should be C.

I think the answer should be C because when it is submerged, cutaneous respiration takes place and hence right atrium receives more oxygenated blood.


Can UV radiation be safe for the skin? It is well known that UV radiation can damage the DNA and generally harm our skin.
We also know that UV radiation helps on the production of melanin and Vitamin D.

From what I could find, the DNA absorption spectrum goes to almost zero for wavelengths higher than 300 nm. This seems to suggest that we would be safe to use UV radiation between 300 and 340 nm in our skin (as long as the power or exposure is not too high/long to make burns), for therapeutic purposes such as the stimulation of Vitamin D production.

Is this assumption correct? Are there any evidences that we could use this UV wavelength range safely?

You're talking about long-wave UV, or UV-A radiation. In the 80s, experts claimed that this was a safe wavelength. Protection against UV-A was not part of sunscreen in the early days. Consequently, UV-A was (and still is) used in tanning beds due to its perceived safety over UV-B. However, a lot of research has been done since.

UV-A is well understood now to also be unsafe in unreasonable amounts. Currently, UV-A protection is a typical feature of sunscreen and tanning beds are still not a healthy alternative to moderate, healthy doses of sun. Here is a recent review covering some of the aspects comparing different UV range effects on skin. I really suggest you put a search engine to good use here; it makes little sense for us to expound on the literature when it is so clear and easily available.

In summary,

UVA certainly contributes to the development of skin cancer.
UVA penetrates deeper into the skin than UV-B (which is largely responsible for 'burning' of the topmost layer of skin, without directly affecting the deeper layers). For this reason, UV-B is associated primarily with burning and UV-A is primarily associated with aging and aging diseases like cancer.
It is important to note that 95% of UV light in every day life is UV-A, because it does not vary seasonally and can penetrate clouds and windows. Therefore, in spite of the fact that short wavelengths carry more energy per photon, the ratios of UV-A and UV-B exposure are far from equal.

These are only a few of the explanations as to why we observe an incidence of aging and skin damage and disease upon UV-A exposure.


Heterozygosity and the Wright-Fisher model I was reading the textbook Probability Models for DNA Sequence Evolution by Durrett. In chapter 1, he discusses the Wright Fisher model and the coalescent theory which I am interested in.

He defines heterozygosity as the probability that two copies of an allele are the same. In theorem 1.3, he derives the expected value of heterozygousity, but what he seems to derive is the expected value of the probability that two allelles have a common ancestor. This does not seem to be the same as heterozygosity to me. Am I missing something here?

The following borrows from Gillespie, J.H., 1998. Population Genetics: A Concise Guide. The Johns Hopkins University Press. It is a good concise guide, and reduces to some extent the mathematics.

Theorem 1.3 is used to show the decay of heterozygosity in a population due to genetic drift.

Consider alleles in a population.  Two alleles drawn at random can differ by state, meaning they have two different DNA sequences. In other words, they are different alleles. Or the randomly drawn can have the same state, meaning they are the same allele. For alleles that are identical by state, they could differ by origin, meaning they are the same allele from two different chromosomes. The two alleles in a homozygous individual differ by origin (sampled from maternal and paternal homologs) but are identical by state.  Or, two identical alleles could differ by descent, meaning they are the same because they trace ultimately back to a common ancestor.

To calculate heterozygosity, you can first account for homozygosity, the frequencies of alleles that are identical by state. First consider two alleles identical by origin.  If you draw two alleles identical by origin when t=1, the probability that the two alleles are copies of same original allele (from the same chromosome) is

$$\frac{1}{2N}$$

because there was only a single copy of that allele on that one chromosome in the population prior to the round of mating, so it is 1 out of the 2N alleles at time point 0 ($t=0$).  The probability that two alleles identical by state are not identical by origin then is

$$1-\frac{1}{2N}.$$

Therefore, total homozygosity ($G'$) in the population (identical by state) after one round of random mating is

$$G' = \frac{1}{2N} + (1-\frac{1}{2N})G,$$

where $G$ is the homozygosity prior to the round of mating.  Of course, anything not homozygous is heterozygous. So, heterozyosity ($H$) is simply,

$$H=1-G.$$

By substituting the formula for $G$ into the above equation, the equation for $H$ becomes,

$$H' = 1-G' = (1-\frac{1}{2N})H$$

where $H$ is the heterozygosity prior to the round of mating.  This formula represents the change in heterozygosity after one round of random mating.  This can now be expanded for several rounds of random mating. For example, the change from $t=0$ to $t=1$ is

$$H_1 = (1-\frac{1}{2N})H_0.$$

The change from $t=1$ to $t=2$ is,

$$H_2 = (1-\frac{1}{2N})H_1$$

Therefore, the change in heterozygosity from $t=0$ to $t=2$ is

$$H_2 = (1-\frac{1}{2N})^2H_0.$$

This can be expanded to any time $t$ with the equation,

$$H_t = (1-\frac{1}{2N})^tH_0,$$

which you will recognize as Durrett's Theorem 1.3.

In short, in the Wright-Fisher model, two alleles that have a common ancestor are by definition identical by state and so cannot contribute to heterozygosity.

I hope this helps. I was a bit rushed and have not explained this often (mostly to myself in my mind) so if I can clarify something, please let me know.


Does the tannin level in plants go down or up after they die? Or does the tannin level stay the same regardless? Does the tannin level in plants go down or up after they die? Or does the tannin level stay the same regardless?

As they decay, do they release more tannins or does the production stop?

Well maybe I'm confused, but do plants not produce tannins? If they do
  does the production of the tannins stop after death?

That depends on how you define death. Tannin is secondary product, so I don't think the plant cells will produce more tannin when they are starving probably because of cutting off the leaves, roots, etc... when the plant dies. The plant won't bother to degrade tannins (I guess it does not even have the pathway necessary to do that), because it is a defense mechanism against insects, mammalians, etc... and not an energy storage material. Tannins can be degraded by microbes, heat, UV radiation, chemical reactions, etc... So if you can't protect the tannins from all of these then they will degrade. (Note: you can't, all you can do is slowing down the process.)


How to get started in bioinformatics I'm a second year bachelor electrical engineering student and self-taught programmer. I've always had a interest for biology, but never got into it (besides two year biology in secondary school and some basic biochemistry in chemistry class).

I'm especially fascinated by the interplay between computer science and biology, both computer science used for biology and computer science concepts inspired by biology. Think of things like the human genome project, genetic algorithms, deep learning, protein structure prediction etc etc. I think many of this things (the computer science used for biology things) are - as far as I know - part of bioinformatics.

I've done challenges on Rosalind and although they are nice, it feels more like training/reinventing the wheel. Althrough it may be too much to ask, I'm want to do something "real" which could actually be used. Not that I want to start straight away without learning, but I don't have a picture in mind of what I can do after learning some theory.

I'm looking for an overview of the field of bioinformatics and some guide on how to get started. Some examples on what I can work on. Maybe there are some power intensive algorithm I can start designing chips (ASICs) for, in order to speed up the process. This just one example.

I hope you can help me, thanks in advance.

You will find various bioinformatics tutorials on: https://www.biostars.org/t/Tutorials/

As a computational biologist I would however strongly suggest to attend biology lectures, and read many textbooks that cover topics outside of the favorite topics of today's bioinformatics (Bruce Albert's "Molecular Biology of the Cell" would be a good start):

Technical aspects are easy to solve, and learn (and also to outsource). The difficult part is to find smart problems, and to understand how you can solve some things faster than your competitors by combining bioinformatics with other approaches.

BTW: I really like your idea to approach bioinformatics from the hard-ware side (also see evolvable hardware).


What are these white areas of coronary thrombosis? Please, see the picture where the areas (1,2,3) look little yellow:

I think these areas are fat, platelets and/or air.
I think 3 is fat/platelets while 1 is air/platelets.
There also exists white thrombosis, which can explain something here.
However, I do not it is that because those white areas do not contain thrombocytes or leucocytes (not sure, since I have no more closer picture; probably you can see it from this).

I think at the moment that these white areas are endothelium-lined spaces.
However, I am not sure about (3).

What can these three areas be in the coronary thrombosis?

Low density lipoproteins can be taken up by the macrophages under a number of circumstances (typically high circulating levels is the most important). These macrophages are called foam cells. The macrophage can then die and deposit this cholesterol and fatty material onto a vessel wall in the context of atherosclerosis. Additionally tissue damage as a result of release of damaging chemicals from the macrophage can induce an inflammatory response recruiting more macrophages (worsening the problem in a cyclical manner) and result in fibrosis and platelet activation. I think this would cause the white stuff you point to.

In summary I think you're right, it's a combination of fat, cholesterol, fibrotic tissue and platelets. 3 is more likely macrophages and platelets whilst 1 and 2 are more likely a combination of all the above.


To which ungulate species does this tooth remainder belong? Found on the beach in Çanakkale, Turkey.
I have found a lot of these, but this is the first one that has parts like long teeth. My other findings have sometimes 4, sometimes 6 tubes. Very solid, stone-like objects. Is this from a marine animal or is it a non-living formation, I wonder.
Below image is for scale in centimeters.

View from top and bottom

Other similar findings without teeth-like parts

Its definitely not a marine mammal, just based on size and general configuration.
those convoluted ever growing teeth are pretty diagnostic of non-cetacean ungulates.
Just based on the pattern I would say bovidae, but that does not narrow it down much in turkey, the H shaped central portion is fairly diagnostic of bovidae. However you have several antelope species not to mention domesticated animals that each would fit that category.
I suggest changing the title to ask for ungulate tooth identification. You need someone specialized in mammalian teeth to narrow it down to species. if you can add more shots of the tooth crown (the complex ends like those below) that is the part most useful for identification. See the examples below. The more you have the better.

Source


Distribution of nutrients throuought a drink made of plants? In an attempts to eat my veggies for the day in one shot, I blended together a bag of salad with some water. The mixture separated by density, a thick top layer containing the bits of leaves, and a bottom layer of just juice. My question is: how many vitamins and nutrients are actually found in the top layer compared to the bottom, and how efficiently would the body process them?

If we assume the drink was very well blended most of the water-soluble vitamis (B and C) as well sugars could dissolve in the juice. Fiber would mostly remain in the plant debris. Oils and fat-soluble vitamins (A, D, E, K) would form their own oily layer or be found in an emulsion with the fruit juice.


Why isn't there a standard unit of promoter strength? Sometimes in synthetic biology, we need to know rates of transcription of one promoter in relation to others (particularly inducible vs constitutive) in order to perform tasks like balancing transcription products and ensuring an excess of one product over another. As far as I know, there is no standard method of characterizing promoter strengths in relation to one another. However, a logical unit for transcription rate made (by organism or in vitro) could look something like:

Promoter Strength = number of transcript made / (concentration of RNA polymerase) (length of transcript) (unit of time).

Why hasn't this been done yet? What other factors could contribute to rate of expression in a particular organism? Is there another system for comparing promoter strengths?

Note: a similar system could be used for strength of repression.

Transcription rates are very context dependent. This shouldn't surprise you, since the same genes aren't expressed in your lungs and your eyes. They're also very environment dependent, this shouldn't surprise you either, since it's pretty obvious every organism is going to respond to temperature, their current nutritional state and so on.

So, in order to define promoter strength, you'd first need to define the exact conditions under which you're measuring it, including the exact strain you're measuring it in. Because if you get any of those even slightly different you're going to get a different answer. Doing this might get you a consistent number but you're abstracting away the most important parts of differences in transcription anyway: how it varies between cells and contexts.

Moreover, even if got past these hurdles you'd not have a particularly useful answer anyway since the rate of transcription is only a small part of the whole process. Why not consider mRNA durability, or rates of translation, or protein durability? What matters very much depends on what you're considering.


What's the name of this Heteroptera bug from Toronto, Canada? My friend already identified it as belonging to the Heteroptera order, but I was wondering if anyone knows the name of the species.

Found in Toronto, Ontario, Canada, on July 21 2017, in a residential bathroom.

This is, indeed, a Heteroptera bug.

Luckily, this is not a kissing bug (which could be infected with Trypanosoma), but just an assassin bug, from the Species Reduvius personatus. Its common name is masked hunter.

Here is an image of the same bug, also in Ontario, from the Canada Pest Control website:

Source: http://pestcontrolcanada.com/5723-2/

And in this photo you can see the long rostrum, just like in your second photo:

Source: https://www.youtube.com/watch?v=9fIBT7IJHn8

Finally, to see an assassin bug in action (a different species, though), have a look at this video from the Smithsonian Channel: https://youtu.be/hXFRAmWiaa4


Descendants of dinosaurs It is commonly accepted that birds are descendants of dinosaurs. It is nice that not all dinosaurs died out.

Are there other animals, descendants of dinosaurs,
 that survived ? (Maybe not till our time, but survived the time when most dinosaurs died).

By the way, what made flying dinosaurs survive and not die like other dinosaurs?

No. No other group found in the fossil record after the K-T boundary (the extinction "event") descends from dinosaurs.

It is likely that the extinction event was not itself instantaneous so if you wanted to be extremely picky you could argue that small numbers of individuals survived the K-T boundary but, apart from birds, none of these survivors went on to form long lasting lineages.

Non-avian dinosaurs that survived the extinction event are referred to as "palaeocene dinosaurs", there are some links on Wikipedia that might interest you.

You can see a diagram linking vertebrate groups here, similar diagrams can be found in most evolution texts.


Do nerve cells cause action potential in cardiac muscle? I think the answer is no, but I am not 100% sure.

If it was yes, then the dendrite of the nerve cell should each time receive a stimulus causing Na+ channels to open, when the contraction happen.
Also, then it would mean that outside events could alter the function of hearth, which would be dangerous.

The heart has a special excitatory system and a contractile system - Sinoatrial node and Pacemaker cells, which control the action potentials in different portions of the heart.
So heart and primarily myocardium i.e. cardiac muscle can depolarise without any external influence with a slow, positive increase in voltage across the cell's membrane.

Do nerve cells cause action potential in cardiac muscle?

The vagus nerve controls heart rate. This is the best example of a direct nerve action potential impacting cardiac muscle, although one could argue the adrenaline system to be an indirect mechanism.

The vagus nerve is part of the parasympathetic system, it acts to decrease heart rate. Resting heart rate is maintained by permanent vagal stimulation/tone by the release of acetylcholine.


What is the difference between Molecular and Cellular tolerance? Although I've read that there are three types of tolerance, molecular cellular and behavioural, I cannot seem to find any mechanism of cellular other than desensitization of receptors. If someone can clear it up, or inform me that cellular tolerance is not a thing, that would be much appreciated <3

Personally, I find these distinctions a bit silly but I also understand they have some use.

People sometimes divide neuroscience into molecular, cellular, and systems levels of understanding. Molecular covers all the "one cell" phenomenon: expression of particular receptors or related proteins, for example. Cellular is one step above of molecular and considers the collection of all "molecular" entities and also considers a circuit level, recognizing that neurons exist among other neurons. Systems level neuroscience sometimes ignores these low-level interactions and sometimes embraces them, but overall is more connected to the behavior and state of the whole organism, approaching psychology.

The reason I think this separation is a bit silly is because, well, none of these levels of understanding are independent. That said, it's a good framework especially for novices to drive home that stuff happens at different levels of explanation. This is true for drug abuse as it is for many other concepts in neuroscience. It also lets someone that is writing a textbook focus on these different levels of explanation in sequence, in a way that is easier to process. A professional in the field is unlikely to draw the same boundaries, but they also have enough background to consolidate knowledge at all levels of interest.

I included a reference that makes the same distinctions I'm making here, but it's likely to be hard to find a canonical one. Different textbooks are going to draw different boundaries as they explain what we know in their own ways, and that's okay. I hope students recognize that A) There are different levels of explanation for neurobiological phenomenon, and B) These levels are interconnected. It's important to recognize that it's possible to study addiction at these different levels of abstraction; it shouldn't be important to draw boundaries between them, however.

Pietrzykowski, A. Z., & Treistman, S. N. (2008). The molecular basis of tolerance. Alcohol Research & Health, 31(4), 298.


Red neurons - Acute neuronal injury “Red neurons” are evident by about 12 to 24 hours after an irreversible hypoxic/ ischemic insult. The morphologic features consist of shrinkage of the cell body, pyknosis of the nucleus, disappearance of the nucleolus, and loss of Nissl substance, with intense eosinophilia of the cytoplasm.  -Robbins textbook of pathology

Taken from Robbins pathologic basis of disease, 9e, pg.no1265, fig: 28-13B

Why in case of neurons there is shrinkage instead of swelling as in other cells?

There is not some simple dichotomy of "neurons shrink and other cells swell" in response to hypoxia/ischemia.

Neuronal death can be necrotic or apoptotic or both, and at different stages different morphology is observed: generally swelling earlier, shrinkage later, though both are observed together early as well. Eosinophilia/"red neurons" tends to occur later as mentioned in this passage (after 6 hours, consistent with 12-24 hours) so that's probably why the author is referring mostly to shrinkage. Cells can also have swelling of some organelles, like mitochondria, despite shrinking overall.

Without further context of the passage you provided it's hard to say much more.

Garcia, J. H., Yoshida, Y., Chen, H., Li, Y., Zhang, Z. G., Lian, J. I. N. Y. I. N. G., ... & Chopp, M. (1993). Progression from ischemic injury to infarct following middle cerebral artery occlusion in the rat. The American journal of pathology, 142(2), 623.

Jenkins, L. W., Povlishock, J. T., Lewelt, W., Miller, J. D., & Becker, D. P. (1981). The role of postischemic recirculation in the development of ischemic neuronal injury following complete cerebral ischemia. Acta neuropathologica, 55(3), 205-220.

Portera‐Cailliau, C., Price, D. L., & Martin, L. J. (1997). Excitotoxic neuronal death in the immature brain is an apoptosis‐necrosis morphological continuum. Journal of Comparative Neurology, 378(1), 10-87.


HLA typing between siblings to identify a genetic disorder If a patient  suffering from a complex array of signs and symptoms for a disease and is having an 8/8 loci match with his sister who suffers no such symptoms can you conclude that the disease is an X-linked recessive disorder? Can u rule out autosomal dominant disorders and autosomal recessive disorders from the diagnosis?

No, you can't conclude that.

First of all, two siblings being HLA identical tells you very little about the rest of their genome. HLA genes are closely linked, and each haplotype is transmitted in mendelian fashion as a single gene.  For non-linked genes (on other chromosomes, or further away on chromosome 6), they are as or nearly as likely to have the same genes as non-HLA identical siblings.

Further, the disease of interest may (is highly likely to) be multigenic and have incomplete penetrance. The heritability of common disorders generally varies from 20-80% (Cecil Medicine Chapter 41, the Inherited Basis of Common disorders).


Books for learning how plants function Can you recommend a good, detailed book on how plants function? A book that explains plant processes on a molecular level from roots up to the fruit.

I am interested in home crops production, such as tomato and peppers, but I expect the principles to be the same for most of the plants. There are lots of "how to garden" books, but this books don't explain things, they just tell what to do.

Background: I have a degree in chemistry so I am confident in my knowledge of chemistry and chemical analysis. But this knowledge is useless unless you mixed it with other science branches, such as biology.

I wanted to comment because I don't think my answer will be the best, but I can't because of my low reputation... Anyway, here are two suggestions:

Plant Physiology and Development, by Lincoln Taiz, Eduardo Zeiger & al.
Biochemistry and molecular biology of plants, edited by Bob B. Buchanan, Wilhelm Gruissem and Russell L.Jones

These are the two main books we are using in my university (I'm studying biology) and I think that together they cover a lot of topics. You can probably buy the pdf versions online as well. I hope it helps!


Why does BLAST employ local alignments? Why does BLAST use Local alignment, not Global alignment? And when would a global alignment be useful?

BLAST was devised to compare one sequence (the query sequence) with all the sequences in a database (target sequences), in particular the Genbank database(s). In 2012 Genbank contained over 3x1011 nucleotides in approx 109 sequences. So it is not feasible to do a rigorous comparison of the query sequence with each of the target sequences in the database, e.g. by the dynamic programming method, either local or global. It would just take too long. Instead BLAST uses heuristics to get the most likely best matches in a reasonable time.

The key assumptions of one of the heurists used is that any good overall match between sequences will contain some high-quality short matches, called high-scoring pairs (HSPs). (HSPs would be perfect matches of short runs of nucleotides, or high-score matches of amino acids (tripeptides) when one uses an amino acid comparison scoring matrix.) The program can make an index or library of those HSPs present in the query sequence and then just compare these (i.e. make a local alignment) in turn with target database sequences — a great time saving. So that is the basic answer to the first part of your question.

Just to quickly complete the story, an attempt is then made to use these high scoring pairs as 'seeds' to extend the alignment in either direction, and high scoring target sequences are saved and ranked.

An answer to your second question is you would do a global alignment when you were working with just a couple of sequences and had some scientific reason to believe that they were related, even though there were regions that had diverged appreciably. For example, you might be aware of key rare amino acids or nucleotide sequence motifs that should align in these regions and want to display them. Or you might want to align a protein of unknown three-dimensional structure with a related one of known structure to model it. But you wouldn't use BLAST to do the alignment, you'd probably use an implementation of the Needleman and Wunsch dynamic programming algorithm.


Is the 'fluttering feeling' when under stress neurological or physical? I'm sure that everyone is familiar with the sensation commonly known as "butterflies in the stomach".  It is commonly experienced during periods of anxiety or stress (e.g. before high stakes job interviews or roller coaster rides) and apparently (after my web research) often felt in new romances without an obvious cause of tension.

However, whilst my googling did turn up an inordinate amount of rubbish regarding love-sicknesnes, I have been unable to find even a suggestion as to a mechanism as to the physiology behind this feeling.  Is it a sensation of physical change in the stomach (some sites vaguely mentioned the restriction of blood flow to critical organs but it was entirely unsupported) or is it neurological in nature?

If you want to find out about the the relationship of this response to romance in particular, there's a pretty comprehensive research paper called Love is more than just a kiss: a neurobiological perspective on love and affection[1] which reviews a lot of the work done in this area. This is pretty good as it discusses all the different stages including breakup.

Essentially, there seems to be a lot factors at play which elicits various responses through different stages of love.

In terms of anxiety and stress, initially, there's a large increase in levels of cortisol[2] and a marked drop in serotonin. Depletion of serotonin is found in many psychiatric conditions such as depression, anxiety and panic disorder. There's even been evidence that these levels at early stages of love are similar to those suffering with OCD. Obviously, the 'symptoms' of early love are quite similar to these conditions so it's hypothesised that this, at least in part contributes to those feelings.[1]. It was found that these levels are back to normal in 12-24 months.

The elevated levels of cortisol contribute to the feelings of stress but this hormone has also been shown to promote attachment.[2].

There are also changes in activity of the amygdala. Responsible for regulating a lot of emotions such as fear and sexual drive, the amygdala can activate autonomic nervous system responses through the mechanisms which Kevin described.

There are a bunch of other things at play here including dopamine, oxytocin, vasopressin, nerve growth factor (NGF), testosterone, increased activity in the hypothalamic-pituitary-axis (HPA) and variations in activity in other areas of the brain.

Again, that first reference gives a pretty comprehensive overview of the mechanisms involved.

To answer the actual question about the fluttering feeling, as Kevin mentioned, it's hypothesised that this is caused by reduced peristalsis in the intestines as a result of sympathetic stimulation. I don't have an academic reference for this but there are plenty of non-academic sources that talk about it (a quick Google of butterflies in stomach and physiology will probably show them).

A lot of the mechanisms noted above can contribute to, sensitise for or cause sympathetic activation. For example, panic attacks and anxiety, mentioned earlier with the serotonin relationship, can cause the same feeling.

Boer, et al. Love is more than just a kiss: a neurobiological perspective on love and affection. Neuroscience. 2012. 201:114-124.
Marazziti, et al. Hormonal changes when falling in love.
Psychoneuroendocrinology. 2004. 29(7):931-936.
Guyton and Hall. Medical Physiology. 11th ed. Elsevier Saunders.


Why did Darwin say "the misfortune to undertake"? Why did Darwin say "the misfortune to undertake"?

"Every naturalist who has had the misfortune to undertake the description of a group of highly varying organisms, has encountered cases (I speak after experience) precisely like that of man; and if of a cautious disposition, he will end by uniting all the forms which graduate into each other, under a single species; for he will say to himself that he has no right to give names to objects which he cannot define."

One reason, is that he was challenged with a difficult task.

Another is that he is unhappy because he could not name more than one species and had to say they are all one species because they graduate into each other.

If you read the subsequent paragraph it is clear that he is speaking of the difficulty in drawing borders between species.

It is not possible to draw definitive species boundaries, especially if you follow species over time  rather than classifying organisms with a snapshot in time: these issues come up time and time again on this Stack. Some examples:

How could humans have interbred with Neanderthals if we're a different species?

Usage of "lineage" over "species"

Transitivity of Species Definitions

Because all species descend from common ancestors, there is a time at which any two organisms shared an ancestor. For related organisms, you can recognize that shared history, emphasize the similarity and at some point group two subspecies together as one species, or you can focus on differences and separate them. Whichever you choose, someone can argue that the species should instead be separated or grouped.

Ultimately, the distinctions are based on somewhat arbitrary decisions, and counterexamples are abundant whichever rule you try to use (for example, a rule that organisms that have viable offspring should be considered species renders many examples that one would argue should be separate species, and examples of individuals that should be one species that are nonetheless not able to produce viable offspring).

It's not so much the misfortune of the task being difficult but rather of it being not possible to come to a definitive answer.


How is a specific fragment isolated for PCR amplification? For background I am interested in studying engineering applications of a specific protein, which is not commercially available. My end goal is to express the gene for the protein in bacterial cells, most likely E. Coli, if that is a feasible procedure. I am mostly familiar the process of forming recombinant DNA, and though our lab does not specialize in Biology, we will be working with another lab in our Biomedical department which can provide necessary equipment and some advise.

The last time I did a lab where we expressed a new gene in E. Coli cells was a biotechnology class in high school, though much of the set up was done for us. I recall that our first step was amplifying the desired DNA fragment through PCR, but what I don't know is how the fragment was initially isolated. I know the primers help by essentially setting the start and end positions for the DNA cloning, but if you were to use an entire chromosome that contains the desired gene, it would seem likely that there would be many possible sites that the primers could attach besides the desired region. So if the DNA sequence for the protein I want is already known, how would I get a fragment that contains the gene I want?

Additionally, how difficult will this process be? Since the end goal is actually to study the protein, I do not want this step to turn into a full thesis on its own. For some specific proteins, the process seems well documented and can be done using relatively common materials and by following simple instructions, but how much should I expect the procedure to diverge for attempting this with gene that has not been specifically done before?

There are a number of primer testing tools that will compare primer sequences against the genome to ensure specificity, or help you design specific primers to amplify a specific region. One place to start is NCBI Primer BLAST; the linked page explains how to use it to generate primers to amplify a specific gene.

Doing PCR on genomic DNA can be a bit tricky, though, since you have to deal with a lot of confounding factors like DNA accessibility, contamination, and PCR inhibitors that get through your purification procedure. In addition, genes often contain huge introns, so you're going to end up doing PCR on an extremely long template (which is very hard or even impossible, depending on the size of the gene) and you'll end up with the whole gene sequence with introns which is not what you need in order to express it as a transgene.

Instead, I'd recommend purchasing a cDNA clone of your gene of interest and amplifying it from that. cDNA is made from the spliced mRNA sequence, so it will be a much more managable length and will prevent problems with alternate splicing.

If you go to the NCBI page for a gene, on the right sidebar under "Related Information" you'll see a link to Order cDNA clone. This will give you a few options to purchase a purified plasmid containing that gene for around \$60 - \$90. It will be much easier to work with this plasmid than genomic DNA and it will definitely save you time and money, especially if you're still inexperienced at molecular cloning.

Of course, it's not 2003 anymore and there's a good argument to be made that the whole idea of doing molecular cloning yourself is a waste of time and money. If your budget allows it, the easiest and fastest way is to pay a company to synthesize your gene for you. Genewiz, for example, offers snythesis for $0.28/bp, but you can probably get a better deal if you shop around.

The advantage of synthesis is that you can get the exact sequence you want cloned into exactly the right vector done perfectly the first time. If you don't have experience with it, trying to clone a gene yourself will take longer and cost more money than you think. It's better to just get it synthesized so you can move onto your real experiment.


What is the most complex plant form? At school we were told on scale of 0 through 1000 the animal kingdom ranges from amoeba the simplest/primitive being at 0, and Humans the most complex animals at 1000; what are the equivalent complexity species (?) in the plant kingdom? What is the least complex plant, and the most complex?

That whole thing of being more complex is non-sense, you can't say that for animals and you can't say that for plants either. It all depends on how you look at it. Average number of cells? Size of genome? Size of the proteome? Adaptability to different environments? Mental abilities? You can't place human on the top of any of them (maybe we could argue about if you define it as mental abilities but that doesn't sound right) and you can't place amoeba at the bottom either.

Also, if you look at a phylogenetic tree, an organism is also not more complex by the number of nodes it has behind them (I've seen people thinking this means more evolved and associate that with more complex).


Is it possible to insert DNA without cutting the recognition site with CRISPR/Cas9? We are looking for a way to insert DNA into a genome, but we would like to do it in a way that the recognition site stay intact to be able to add again DNA at the same location. Do you know if it is possible or if it is already the way CRISPR/Cas9 does it? Apparently multiple systems were already engineered but the few papers we read weren't about our problem.

Sincerely,

Emilie

Look into site-specific recombination.  You can use a site-specific recombinase, specifically an integrase, that can insert a sequence of DNA at a certain attachment site.  You can add an identical attachment site into the DNA sequence to insert, allowing for the reintegration of a new attachment site.  Note however that you might get SSR onto the insertion plasmid itself, so don't do this if you need a specific amount of integration.

Look at the bottom subfigure of A for an example of integration.  Recombinases can also do other things, such as excision and inversion, based on the orientation of the attachment sites.


Batch convert miRNA names to Accession IDs? Does anyone know of tools to convert lists of miR names to their miRBase Accession IDs? I know they exist, but my search keeps pulling up gene ID converters.

EDIT: both @rg255 and @shigeta have provided solutions to the underlying issue, but I am curious to know if something exists for miRNAs that is similar to a site like this.

EDIT 2: miRNA names are of the form 'hsa-let-7a' and Accession IDs are of the form 'MI0000060'

If you want it all, download the mirRNA.xls.zip file from mirbase here:

ftp://mirbase.org/pub/mirbase/CURRENT/

its a spreadsheet that includes these data as columns and also more information besides - for the entire database.


Why is GTP, not ATP, produced in Gluconeogenesis & TCA Cycle? In both gluconeogenesis and the TCA cycle, there is a point in each that GTP is produced instead of the usual ATP. My question is why GTP and not ATP for these 2 specific steps?

Nice question. Beginning with Krebs cycle, there is actually no specific answer as both GTP and ATP are produced. First, see this article for why GTP is the more frequent product:

  It may be that at the beginning, both GTP and ATP were equally available for energy and that the succinyl CoA synthetase reaction happened to choose GTP and that reaction is still with us today, billions of years later, even though we run the TCA cycle clockwise (forward) instead of backwards.

So, actually both ATP and GTP can be produced. And indeed both are produced, depending upon the organism. See this article:

  A step with significant variability is the conversion of succinyl-CoA to succinate. Most organisms utilize EC 6.2.1.5, succinate–CoA ligase (ADP-forming) (despite its name, the enzyme operates in the pathway in the direction of ATP formation). In mammals a GTP-forming enzyme, succinate–CoA ligase (GDP-forming) (EC 6.2.1.4) also operates. The level of utilization of each isoform is tissue dependent. In some acetate-producing bacteria, such as Acetobacter aceti, an entirely different enzyme catalyzes this conversion – EC 2.8.3.18, succinyl-CoA:acetate CoA-transferase. This specialized enzyme links the TCA cycle with acetate metabolism in these organisms. Some bacteria, such as Helicobacter pylori, employ yet another enzyme for this conversion – succinyl-CoA:acetoacetate CoA-transferase (EC 2.8.3.5).

So, there is no strict rule that only GTP will be produced instead of ATP at that step. And, afterall, it does not matter much as both of them carry equal energy.

Now coming to Gluconeogenesis, GTP is hydrolyzed by the enzyme Phosphoenolpyruvate Carboxykinase or PEPCK. This enzyme can also work with both ATP and GTP, depending on the sepcific type of enzyme. See this article (links added separately):

  It is classified under EC number 4.1.1. There are three main types, distinguished by the source of the energy to drive the reaction:

  4.1.1.32 - GTP (PCK1, PCK2)
  4.1.1.38 - diphosphate
  4.1.1.49 - ATP

Thus, there is no strict protocol for using specific energy carrier in the process, both ATP and GTP can be used in the reaction. Its just because GTP is more frequently used that it is mentioned instead of GTP/ATP in the reaction.


Is there a link between digestion and nightmares? A common belief is that eating too much before going to sleep can cause to have nightmares. In fact, I often experience it: I systematically have nightmares after eating too much in the evening.

Then I was wondering: is there really a link between digestive system's activity and unconscious brain's activity?

If it actually exists,
- is the influence linked to the neurons we have in out gut?
- or is it linked to the augmentation of the concentration of a nutrient in our bloodstream (which can then reach our brain and)?
- or is the neuronal activity which control digestion that interferes with the process of dreaming?

If the influence is linked to the augmentation of the concentration of a nutrient in our bloodstream, does this mean what we eat actually controls our mood or level of anxiety, or any subconscious process? (regardless of compounds known for having a particular effect, like theobromine, etc...)

A nightmare is basically an alarm; typically your subconcious mind trying to wake you. Nightmares often occur when you are experiencing pain or discomfort (like needing to use the bathroom).

Dreams are a way of sorting through questions in a "what if" sort of way. When it comes to a nightmare, you are in a panic-situation, often without a solution, or where a "logical" solution is unsuccessful.


What are the reactions in the body that triggers dizziness after cigar(nicotine) smoking in non-smokers? Suppose there is a person that has never used nicotine in any form in his/her life. Why does the person get dizzy after a few "shots" from a cigar(nicotine)? What's the difference between using other plants(e.g. marijuana)?

It's all about the synapses, the places where separate neurons connect to one another. All psychoactive drugs act in some way so as to modulate the signals that are passed from one neuron to another. Nicotine acts by increasing the effect of signals that pass through a particular type of synaptic receptor called nicotinic acetylcholine receptors (they're named after the fact that they're affected by nicotine). The dizziness and other effects of nicotine are caused by this interference with normal neuronal communications.

The reason why regular users of nicotine don't get dizzy is because they've gained a tolerance to the drug. Tolerance isn't super well understood at the molecular level, but it has been associated with long term changes in the quantities and types of receptors that are present at synapses in certain regions of the brain, it particular the nucleus accumbens.

Marijuana is similar to tobacco, only its main psychoactive component, THC, acts on the cannabinoid receptors.


Why don't most animals have "heads" in the middle of their bodies? For example, humans. It would seem like, to me, if our brains and eyes, ears, etc. were situated in our stomach area they would be more protected from harm and more central than up at the top in and on a fragile skull. The same goes for other organisms. For example, horses have eyes on the sides of their heads; why wouldn't the eyes be near their stomach area? To me, it would seem like it would make it more safe and the horse could still see alot. I looked at this question, but it didn't fully answer my question.

We generally define a "head" as something that comes at the top/front of the body. I think that, we're likely to ignore examples of animals with nervous systems / sensory systems not at the top/front of their body as "animals without heads" rather than "animals whose heads are not at the top/front". For example, sponges and jellyfish.
Some animals who do, arguably, have heads, have their heads in the center of their bodies:

Image by james_michael_hill (CC BY-NC-ND 2.0)

The evolutionary - developmental roots of head position (or having a "head" at all) go very deep (although despite this, some organisms, like the starfish above, shifted evolutionarily and shift developmentally from bilateral to radial symmetry).


A New Antiviral Drug Strategy? I am studying viruses and I have a question about antiviral drug strategies. Why haven't researchers tried finding small molecule drugs that will bind to receptors on the host cell, thereby preventing viral attachment to the host cell? I feel as though with this strategy, virus resistance and mutation wouldn't be an issue. Thoughts?

According to wikipedia, there have been drugs targeting CCR5 coreceptor approved for treating HIV. These drugs work by binding to CCR5, thereby prevent binding of HIV and CCR5.

However, drug resistance can still develop. Some HIV can bypass it by shifting tropism to CXCR4. While others can increase its affinity to CCR5.

And some receptors are vital for the functions of cells. If we design drugs to these targets, we should make sure that the drugs only prevent binding of viruses specifically without disrupting their normal functions.

  Maraviroc was approved for use by the FDA in August 2007.It is the
  only one thus far approved by the FDA for clinical use, thus becoming
  the first CCR5 inhibitor. A problem of this approach is that, while
  CCR5 is the major co-receptor by which HIV infects cells, it is not
  the only such co-receptor. It is possible that under selective
  pressure HIV will evolve to use another co-receptor. However,
  examination of viral resistance to AD101, molecular antagonist of
  CCR5, indicated that resistant viruses did not switch to another
  coreceptor (CXCR4) but persisted in using CCR5, either through binding
  to alternative domains of CCR5, or by binding to the receptor at a
  higher affinity.
  https://en.m.wikipedia.org/wiki/CCR5

http://www.ncbi.nlm.nih.gov/pubmed/11782552
http://www.sciencedirect.com/science/article/pii/S0042682206008245


Does "mind" has any physical reality in biology? Or is it just an assumptive concept? Biologically,  Brain controls our thinking,  ideas,  decisions everything along with controlling each body parts. My question is,  is there anything real as "mind "?  If it's controlled by brain then how does brain controls the mind?

The mind is an abstraction which arises from physical and chemical processes within the brain.  For a crude analogy, think of the brain as an incredibly complex, self-modifying, multithreaded program.  The mind would then be the abstraction arising from the behavior of the program as it runs.  Consciousness would be the abstraction arising from the behavior of one particular thread in the program: a thread which has access to a limited buffer of its own (that thread's) behavior, and control over limited input and output from the body.  All of the other (unconscious) threads may affect the conscious thread, but the conscious thread has very limited access to information about the behavior of the other threads.

Since the conscious part of the mind has access to information about its own behavior, there is actually some recursive looping going on when it comes to thinking and feeling.  The feeling that this goes in circles somehow (which you seem to be expressing) is a common intuition, and it's almost certainly a correct one.  But the manner in which this occurs is not well-understood, and it's definitely not well-understood within biology at the macro level because the brain is unbelievably complex and plastic.  We really don't have a clue how to begin modeling the brain's processes.  This is one reason artificial intelligence is still extremely crude today (despite what Elon Musk and Bill Gates may try to say).

If you want to read a scientifically-inspired theory of from whence consciousness comes, and of how it arises from the brain, I would recommend the book Godel, Escher, Bach by Douglas Hofstadter.  Douglas does a good job of combining computational theory with biology, music, and art to illustrate a theory of consciousness the reader can grasp even if you don't have a strong background in any of those subjects.


Computational engineering of protein binding pocket I have an X-ray structure of an enzyme with reported activity to a small molecule.
This activity is rather low since it is not the native substrate.

I can run molecular modeling simulations (e.g. using DOCK) to estimate the enzyme's binding behavior to different compounds. However, what I would like to be able to do is to mutate the binding pocket so that it better binds my small molecule of interest.

Exploring all possible amino acid substitutions is computationally too expensive, so I am wondering whether smarter ways of looking at this problem have been developed.

Can someone point me in the right direction? I've searched Google but can't really find a straight forward answer

You can try an evolutionary algorithm. If you can quickly evaluate the binding affinity you can initialize a set of copies of your protein but with random mutations. You can assign them a fitness score based on the affinity of the binding. The ones with highest affinity you replicate again with some probability of mutating each amino acid and you continue for as many generations as you need. If you find your parameters (mutation rate, population size, etc) correctly you can easily optimize the binding without knowing anything a priori about the different sites. There is a lot of literature on this, I suggest you do a quick Google scholar search on directed evolution or evolutionary algorithms to optimize binding affinity.

Paper on in silico evolution to optimize protein-protein binding


What equation to compare protein isoforms in a Western Blot? The protein isoforms I am interested in comparing appear as distinct bands on the gel I have already run. I have an Excel sheet with optical density measurements I obtained using ImageJ; it looks something like this:

Lane    Iso1       Iso2       GAPDH
1       149.06     194.646    893.08
2       832.654    494.473    148.335
3       49.998     490.539    147.361
4       29.347     208.53     120.652

For the other proteins I've analyzed so far, I've been computing fold-change relative to my loading control, GAPDH, with the following equation:

Fold-Change = Log2(Protein/GAPDH)

I'm not sure how best to compare my isoforms to each other and considering the following two equations:

1. Fold-Change = Log2[(Iso2/GAPDH)/(Iso1/GAPDH)]

2. Fold-Change = Log2(Iso2/Iso1)/GAPDH

I've already computed both of these values for all my samples, graphed them and found that the resulting graphs look pretty different. Which of the two equations do you think is a better way to compare the relative quantities of these proteins?

Alternative equations are also welcome.

In my opinion you should use this formula:

$$ \frac{\text{log}_2(\text{Iso}_1/\text{Iso}_2)}{\text{log}_2(\text{GAPDH})} $$

This will normalize the relative fold differences between the isoforms with the loading control- GAPDH.

Since both numerator and denominator are log transformed they are in comparable domains unlike the formula-2 that you mention in your question. This is just a modified formula-2.


What kind of spider? I’d much appreciate help figuring out what kind of spider this is. I’m in Western Washington, in the northern suburbs of Seattle. Its outside, on the eaves of the house. Particularly wondering if a yellow sac spider.

Interesting!  The size, shape and posture, as well as the visible patterning on the body, are all reminiscent of Dolomedes tenebrosus, the common terrestrial fishing spider here in the east.  However, there are a couple of odd things here:
1.  Dolomedes is a genus only found (as far as I know) in the eastern half of the US,
2.  The abdominal color pattern is a bit off from what I would expect (dark flank marks at the front of the abdomen, especially), and
3.  That looks like an egg sac the spider is sitting on top of, as if it was guarding, but fishing spiders (as far as I know) do not make egg sacs like that - they make ball-shaped egg sacs which they carry around with them using their fangs to hold them.

The thing is, nothing else rings a bell with me - the only other large wandering hunter that would be anything like that in the Pacific NW, that I know of, is the Giant Crab Spider Olios giganteus, which doesn't look much like that, although it does make a silken retreat/egg sac protection.

I confess that I am stumped, although I can confidently say that it is not a Yellow Sac Spider.

However, I can suggest two good options for identification:
the Burke Museum: https://www.burkemuseum.org/collections-and-research/biology/arachnology-and-entomology/contact-form

and Bug Guide: https://bugguide.net/node/view/6/bgimage

both of which can often do identifications from photos alone (although with spiders, this can sometimes be tricky).
Good luck!


Why does no one get vaccinated against plague in Europe? I've read on Wikipedia that only people who work with Y. pestis and people in 3rd world countries get vaccinated against it:

  Since human plague is rare in most parts of the world, routine vaccination is not needed other than for those at particularly high risk of exposure

But I know that it is easy for plague to conquer Europe. All your need is just some fleas and half of the continent dies, as proved in history.

So why does no one in Europe get vaccinated against plague?

Ask yourself when was the last time that you went to a friend's home and had to worry about getting flea bites? Modern cities still have lots of rats, but modern construction, pesticides, and hygiene have greatly reduced the number of encounters between fleas and people. Contrast that with the early 18th century. When the young George Washington wrote an essay on civil behavior, he felt it worth while to include this item:

  13th Kill no Vermin as Fleas, lice ticks in the Sight of Others, if
  you See any filth or thick Spittle put your foot Dexteriously upon it
  if it be upon the Cloths of your Companions, Put it off privately, and
  if it be upon your own Cloths return Thanks to him who puts it off.

Plague is almost exclusively transmitted to humans by fleas (the pneumonic form of the disease can be transmitted by aerosols but is rare). Few encounters with fleas, few cases of the Plague.

Mumps and measles (for example) are transmitted by human to human contact. No fleas needed. Modern life may have done away with flea bites, but it has only increased the number of persons we come in contact with each day. If you think about it, all the diseases we commonly get vaccinations for are ones spread by direct human to human contact: smallpox, polio, diphtheria, whooping cough, mumps, measles, flu. Tetanus vaccines are an exception, but that's a bacteria that is ubiquitous in the environment, and causes a very nasty disease.


Simple computational biology project for AP Biology class. Ideas? Our teacher assigned us a project to do with an extremely open-ended prompt and it should be completed within a month.
I was planning on doing something related to computation and evolution in terms of biology although I'm not really sure where to start. I say simple because I'm not a professional programmer, rather, extremely interested in the field and I hope to use this as an opportunity to stretch by skills.
Any ideas on a project or where to start would be greatly appreciated.

You can use BLAST or NCBI resources to do an analysis of something like the duplication of a gene in the HIV virus, for example. If you're looking for a place to start, I would recommend just learning the NCBI database resources.


Evolutionary advantage of consciousness What possible theories are out there, regarding the evolutionary benefits of having consciousness? Why is not all information processing done subconsciously?
Can it have something to do with language and communication? But then, a lot of animals can be considered to be communicating without "qualia".

EDIT:
Some background. Philosophy student here. Recently ventured into reading a bit of genetics. Every aspect of life seems to be slowly evolved out of need, either survival or atleast survival till reproduction occurs.
Consciousness, according to me, would be the constant "subjective experience" of our lives, the inner movie as they would say.
My question, then, is why would a part of the brain be dedicated to generating an integrated coherent experience when zombie-like information processing could suffice? Did the ability of movement, along with certain cognitive skills, really make the upper mammalian habitat so unpredictable that genes had to adapt to "every-situation-might-be-a-new-situation" level of brain capacity?
Has any biologist written about the evolution of intelligence (which is a precursor to the consciousness I'm talking about) corresponding to early humans?

DISCLAIMER

I know little on the subject. I want to first express my personal views of the existing difficulties at answering this question and then I will attempt to give a short overview of the potential answers I could find.

ISSUES WITH THE QUESTION

Consciousness vs higher cognitive abilities

I personally find it hard to disentangle evolutionary advantage of consciousness from the ones linked to other cognitive abilities especially the social ones such as for example cooperative hunting, Machiavellian intelligence or advanced communication. I think a big part of the issue in this question is in the exact definition of consciousness.

So, a very important issue with the question is that 'consciousness' is not well defined.

Only few peer-reviewd papers on the subject

While there are a number of ressources in the non-peer reviewed literature (mainly books or popular articles) on the question, I could not find a lot of papers in the peer-reviewed literature. I suppose again that part of the issue that prevents much discussion in the subject is the absent of a commonly agreed upon definition of consciousness. Some of what I'm about to quote is not peer-reviewed and some are not written by biologists but philosophers.

Evolutionary psychology remains very theoretical

One would note as well that most work in evolutionary psychology remains mostly theoretical as it is often hard to perform meaningful empirical testing for the existing hypotheses.

Quoting for safety

As I often failed to make sense of what I just read(!), I will try to quote quite  a bit to avoid misinterpreting other authors.

ANSWER

Definition of consciousness

I recommend having a look at Perlovsky (2007) for a semantic discussion (and opinion) on the concept of consciousness. Quoting their full abstract

  The knowledge instinct is a fundamental mechanism of the mind that drives evolution of higher cognitive functions. Neural modeling fields and dynamic logic describe it mathematically and relate to language, concepts, emotions, and behavior. Perception and cognition, consciousness and unconsciousness, are described, while overcoming past mathematical difficulties of modeling intelligence. The two main aspects of the knowledge instinct determining evolution are differentiation and synthesis. Differentiation proceeds from and unconscious states to more crisp and conscious, from less knowledge to more knowledge; it separates concepts from emotions, Its main mechanism is language. Synthesis strives to achieve unity and meaning of knowledge; it is necessary for resolving contradictions, concentrating will and for purposeful actions. Synthesis connects language and cognition. Its main mechanisms are emotionality of languages and the hierarchy of the mind. Differentiation and synthesis are in complex relationship of symbiosis and opposition. This Leads to complex dynamics of evolution of consciousness and languages. Its mathematical modeling predicts evolution of cultures. We discuss existing evidence and future research directions.

Consciousness as a by-product

To my personal experience, consciousness is in general viewed as a by-product of the selection for specific cognitive abilities. Again, without much of a definition of consciousness it feels to me that selection for specific social skills, such as those requiring the Theory of Mind (ToM) would yield to increase consciousness.

If consciousness and ToM (and other related cognitive skills) are the same thing, then we got our answer, otherwise, the standard view is to consider consciousness as a by-product of the selection for those higher cognitive skills.

On the topic, see for example Judd (1910) (did I really cite such an old paper?) or Dennett (1980) (Dennett is a philosopher, not a biologist).

In the comments the OP said

  To me, it feels either too complicated and inefficient or just a chance byproduct of "useful intelligence"

I would note that, if taken as an argument, then it would be a logical fallacy called argument from incredulity.

Consciousness as a result of higher social abilities

This opinion seems quite related to the previous one. Quoting from Ingold (2005)

  Becoming a person is thus a matter of gathering social relations into the structures of consciousness: the movement in development, as Vygotsky put it, is ’not from the individual to the socialized, but from the social to the individual’

  [..]

  as relationships unfold in the course of purposive social action, they are
  enfolded in the consciousness of persons, that is, in the structures of the self.
  The connection between social relations and consciousness should thus be
  understood in terms of unfolding and enfolding, rather than in terms of cause
  and effect

  [..]

  This view of sociality, and the theory of direct perception on which it is
  founded, suggests that it is possible for persons to engage with one another on
  the basis of shared perceptual experience prior to the objectification of that
  experience in terms of collective representations encoded in language and
  validated by verbal agreement. Thus sociality is possible in the absence of both
  language and the kind of objective self-consciousness that (probably) depends on language

Conscioussness as result of the logistics of decision making

Quoting from Merker (2003)

  Consciousness will be interpreted as a biological
  function evolved by mobile animals as a solution to neural logistics problems inherent in the
  control of orientation to their surroundings. The interpretation is motivated by the conspicuous
  absence from the contents of consciousness of two significant classes of information known to be
  present in brains, one on the afferent and the other on the efferent side of neural function. In fact,
  the thoroughness of their exclusion from consciousness suggests that their absence represents a
  design feature of consciousness providing important clues to its nature and biological function.
  This in turn helps constrain conceptions of its neural implementation as well as the search for its
  origin in the phylogeny of life forms


Which statement about phenotypic plasticity is false? This was a test question, and I'm not too sure about the answer.

Which statement about phenotypic plasticity is false?

a. Because the plasticity of a phenotypic trait may be costly to maintain, it will not be favoured in stable environments.

b. A trait that is an adaptation will not vary with environmental conditions within one generation.

c. Phenotypic plasticity can itself be an adaptation to varying environmental conditions.

d. Variation in phenotype among populations of a given species across different environments is only caused by phenotypic plasticity.

If you could explain the answer to me, that would be great.

I'll try to answer but I'll encounter some difficulties: first because I don't know what you mean by "plasticity". Does it mean non-reversible developmental plasticity or reversible flexibity. Then, because, I don't really like the word adaptation! Anyway'll try...

a: Plasticity  is some kind of mechanism allowing organisms to adapt to various environment. If the environment is stable and under the assumption the plasticity is associated with a intrinsic (physiological for example) cost, then a population would tend to evolve so that they always display the most optimal phenotype. I would argue that this is under the assumption that we gave enough time for the right mutations happen and under the assumptions that such mutation might exist!

b I don't really understand this statement. Does it mean that between two generations (which mean in one generation time) an adaptation cannot vary.…in what terms? in frequency? Through time any trait vary because of selection, environment, genetic drift and mutations. And to what environment is the trait under consideration adapted for? Can we accept that the environment is changing from one generation to the other in this question? What does this question has to do with plasticity? I guess that when one says that a trait is an adaptation it means (among other things) that the population has no more variance for this trait. Therefore, only mutations would bring variations if there were no environmental change making the trait not adaptive anymore.

c: Well, yes. Plasticity is an adaptation to fluctuating environment. It allows to display a rather optimal phenotype in multiple different environments.

Answer d is wrong for sure. There is variation within a population due to genetic variance and non-adaptive environmental variance (and their interactions). Variance due to plasticity is just some kind of subset of the variance du to the genetic-environnment interaction

Hope this helps a bit!


How do you find pre-miRNAs from mature miRNA Blast output? So in short, I did a blastn with standalone blast using all known miRNAs against the EST sequences in a genome (word length 7 and e-value 0.01). Now to confirm one of the next steps would be obtain the pre-miRNA sequence of each hit and do an mFOLD for structural confirmation. Each paper I read always mentions to get a sliding window (of 70 - 100 nt length) but how do you get this sliding window from the BLASTN output.. Do you have to code something yourself or is there an easier way to do it. Thanks.

DISCLAIMER: I have never worked with miRNAs.

However, from what little I know, the mature miRNA is produced by modifying the pre-miRNA. This means that you should be able to infer the pre-miRNA by mapping your miRNA to the genome using a tool like BLAT. Since you already have an EST which represents a transcribed sequence, you can map your EST back to the genome. You can simplify this by using a tool like exonerate that also models splicing.


What is the function of the Moderator band? The moderator band in the right ventricle is a band sorts of muscle which consists of a significant branch of the AV bundle. Does it mean it delivers impulses to the anterior papillary muscle faster? If it does, how does this help? and why only the anterior papillary muscle? What makes it special to have a moderator band?

Does it mean it delivers impulses to the anterior papillary muscle faster?

Yes.

  If it does, how does this help?

To facilitate the conduction time thereby allowing coordinated contraction of the anterior papillary muscle.

  and why only the anterior papillary muscle?

This is because its chordae tendineae insert into anterior and posterior tricuspid valve leaflets, so only their contraction before systole would be optimum.

  What makes it special to have a moderator band?

For effective Cardiac Output because it helps in coordinated contraction of ventricular cells. The ventricles must maximize systolic pressure to force blood through the circulation, so all the ventricular cells must work together.


Is there a correlation between total neurons and intelligence? Thanks for looking.
First off, I am not a biologist, just a curious layman, so I apologize in advance if this isn't a "good" question.  Please don't downvote me into oblivion.
I read today that the human brain has about 100 billion neurons and that got me wondering: is that number pretty standard for everyone or does someone like say,
Einstein, have many more neurons than this daft poster.
Question
Is there a correlation between total neuron count and intelligence, or does intelligence depend more on the way neurons are used--or some other factor like previous experience--rather than their total count?
Can this question be answered?
There are two very valid points-of-view posted as answers below, but it sounds like we simply don't have a solid answer to this question at this point in time, so I hesitate to select a "correct" answer.

There are an estimated 100 billion neurons within the human brain. In general a minor variation in the number of neurons should not effect individuals too much, however when there is a more significant loss, such as brain injury or in some forms of dementia cognitive abilities do decline. So in this sense yes the number of neurons does relate to intelligence. However this variation is not what accounts for general variation of intelligence in the population.


How to name a case of convergent evolution where the same mutation is involved in both lineages? Definition of Convergent evolution - from Wikipedia > Convergent Evolution

  Convergent evolution is the independent evolution of similar features in species of different lineages. Convergent evolution creates analogous structures that have similar form or function, but that were not present in the last common ancestor of those groups.

Examples

-- Lactase --

Humans have evolved the ability to digest lactose at adult age twice; once in Europe and once in Africa. Different mutations are involved in European lineage and in African lineages.

Source: Tishkoff et al. (2007)

-- White fur --

Beach mice and mammoths have both evolved white fur independently. The same mutation is involved in both lineages.

Source: Römpler (2006)

Question

Is there a term to differentiate convergent evolution that involves the same mutation in different lineages from convergent evolution that involves different mutations in different lineages?

I'm not aware of a specific term for this. In the places I can find the concept discussed in the literature (here and here), the authors simply describe the pattern as "the same [...] mutation in two lineages" and "parallel mutation in two lineages".


Animals as organ donors and organ's life expectancy Recent attempts to find reliable organ donors was using genetically-engineered (GE) pigs as heart donors.
The pig's DNA is altered so that its tissues will appear identical to the patient's tissue and will not be attacked by the patient's immune system and rejected. A pig's heart is anatomically close enough to a human heart to fit to the task. All it takes is to make a GE and raise it until it is of the right age.

The issue is as follows: a human's life expectancy is much higher than that of a pig. If the patient is young enough, and the transplant succeeds, then the human will live far longer than the average pig. Will the heart hold-up throughout the lifetime of the human, or will the human need a new heart in say a decade or two?

EDIT: I have realized that actual attempts were so far limited to valves, and not entire hearts or other organs. Looking for an analogy in a human-to-human transplant, or animal-to-animal experiment, what would happen if the organ receiver is much younger than the donor itself? will the transplanted organ live the lifespan of the donor (its "original" lifespan), or will the transplant extend the life of the organ to that of the receiver?

tl;dr
Graft survival, even with allotransplantation (human donor to a human host), is not equal to an average human lifespan. It's much shorter (11-16 years on average). Porcine grafts (which often last over 15 years) do not seem to be limited by the average pig lifespan (which, google tells me is 6-10 years). In both allo and xenotransplantation, graft failure and host survival are issues of the immune response to the graft, not of the expected lifespan of the donor.
Full answer:

Will the heart hold-up throughout the lifetime of the human, or will the human need a new heart in say a decade or two?

Lets answer this, first, for a heart transplanted from a human donor, an allograft. Even from a human donor, the heart is unlikely to hold up for a normal human lifetime. Heart transplant survival has improved greatly over the last five decades, but median survival in an adult is now 11 years. In pediatric patients, it's 16 years. The main problems are cardiac graft vasculopathy, malignancy, infection, and immune rejection. Transplant is a treatment, not a cure, and a major challenge of transplant as therapy is managing the immune response. Rejection and graft vasculopathy are (generally) related to immune injury of the transplanted organ. Malignancy and infection are related to immune suppression of the host.
Xenotransplant (transplantation from a non-human donor) adds an additional complication to the challenge of managing the immune response. Here, the range of non-self antigens is even greater, and the graft will be attacked by complement and other aspects of the innate immune system, as well as the adaptive immune system. This leads to graft destruction, often in the first hour after transplant. There have been advancements using transgenic pigs that solve some of these problems, with improvement in survival in pig to primate trials. Personally, I'm skeptical that CRISPR techniques will easily solve all of the problems of transplant immunology, but transgenic animals have moved things forward substantially over the last 15 or so years (see this review)
As far as porcine valves are concerned, they are treated to reduce their antigenicity (a protocol that hasn't worked for cardiac xenotransplants). Paradoxically, graft survival in older patients is quite good, with most valves lasting beyond 15 years. This may have something to do with age related decrease in immune function, but regardless, porcine tissue (at least from a valve), seems to hold up quite well.
There is good access to data on cardiac allotransplant survival (both adult and pediatric) directly from the international society for heart and lung transplant. There is a good review of pediatric transplants here. You can read more about cardiac graft vasculopathy here
As far as xenotransplantation is concerned, there was an excellent issue of the international journal of surgery, november 2015, that has a number of articles reviewing xenotransplant. Many are available without a paywall, and it's a good place to read up on this. This article from that issue discusses immunological challenges in xenotransplantation from pig to primate. You can read more about this here, but it's beyond a paywall. A good discussion of the overall history of xenotransplantation was reprinted in that issue, here


At what minimum distance the direction at which eyes point becomes parallel? This is very similar, but different than this question about focus, let me explain why it's not a duplicate at all.. That other question is about the distance of EACH individual eye FOCUS, this one is about VERGENCE, focus plays no role in this question, here what matters is the angle formed between the direction each eyes points. When objects are close to our noses, eyes get cross-eyed. As objects get further away, the eyes get more parallel, so called wall-eyed. There must a distance just become totally parallel, I deduce this by analogy to what happens to the focus, for which the distance is 6 m as this answer says. What is the corresponding distance for vergence?
I couldn't find the answer in the relevant wikipedia article on vergence.

Mathematically, the eyes are parallel when they fixate at, and only at, infinity. Now, because of noise, there is a distance after which it's not really going to make a difference (otherwise you would be able to tell the distance between stars at night). There are 2 parts for your question. First, at what distance it doesn't matter because the eyes won't stay still enough to accurately maintain this vergence angle. Second, at what distance it perceptually makes no difference because you can't tell if the object is closer or not. Concretely it means looking at the distance where each of these metrics is smaller than detection threshold (the value below which your performance on a detection task is lower than a specified value). Conveniently, Chopin et al. (2016) measured both values (these numbers can of course be found in older papers too).

For the first question, they measured vergence noise of 225 arcsec (or 225*pi/(60*60*180)=0.0011radians). The distance for which vergence becomes smaller than that is approximately 55 meters (vergence~=IPD/FD, with IPD interpupilary distance of approx 6cm). So farther than that you wouldn't be able top tell whether they fixate at infinity or not.

For the second question they measured relative disparity thresholds. Relative disparity is the difference in vergence angles between 2 points. So for relative disparity angles lower than threshold you cannot tell whether point A is closer or farther than point B. They unfortunately don't report the exact value but from the graph it looks like 300arcsec, corresponding to a distance of about 40 meters. In other words, after this distance you can't tell whether an object is farther than where you look at.

Finally, you could also ask: at what distance can't I tell whether an object is at infinity or not? The distance of a point in isolation is called absolute disparity, and is known to be much worse than relative disparity (i.e. it is much easier to compare the distance of 2 points than to report the distance of a single point in isolation). This distance turn out to be quite shorter. From the same paper the absolute disparity threshold is about 3000arsec (again, they unfortunately don't report the exact value). This gives a fixation distance after which you cannot tell whether you fixate at infinity or not of about 4 meters.

This is all very approximate and making lots of assumptions but I hope this more or less answer your question.

Chopin, A., Levi, D., Knill, D., & Bavelier, D. (2016). The absolute disparity anomaly and the mechanism of relative disparities. Journal of vision, 16(8), 2-2.


Widest angular of binocular vision Which out of eagle, rat, duck or owl has the widest angle of binocular vision?

I am pretty sure it's not rat and duck but I am confused between owl and eagle. Can anybody help me figure out which one would have the widest angle of binocular vision?

Take a look at some pictures of eagle and owl and observe their beaks. It will help you in concluding which might have the widest binocular vision angle.


Foveal ganglion cell density (Tay-Sachs Disease) I’m currently reading on Tay-Sachs disease and have stumbled upon something regarding the typical “cherry red” macula symptom.

On the one hand it is mentioned that the macula is almost devoid of ganglion cells (GCs) and this actually the reason for the high acuity in this region since there is not obstruction of light [Suvarna JC, Hajela SA. Cherry-red spot. J Postgrad Med 2008;54:54-7].

On the other hand google books gives me numerous textbooks that highlight the fovea as the location of highest GC density and conclude that this leads to the high acuity because a GC only receives information from one or two cone cells.

I guess both are correct but how does one fit the other? It seems contradictory to me.

To be precise some sources specifically mention the boundary regions of the central fovea to have the high GC density, this could leave the fovea devoid of them and therefore combine both facts, however if this is correct I still wonder:

1: Where are the GCs that the cones in the central fovea are connected to?

2: Why is the “cherry red” spot in the macula so large on all the pictures. If my explanation is correct only the tiny area of the central fovea should be red and the surroundings the complete opposite due to the high GC density, right?

I’d really appreciate if someone could shed some light into this.

As you've already mentioned, cells near the primate macula tend to make one to one connections.  Due to this lack of convergence they can be somewhat smaller than normal cells (particularly in the size of their dendritic arbors) earning them the moniker "midget" ganglion and bipolar cells (also P cells).  By reducing the magnitude of photoreceptor convergence onto ganglion cells, the retina sacrifices luminal sensitivity for spatial acuity.  Or put another way, a downstream neuron in the LGN/V1 can be more "certain" about which photoreceptor is sending information when light is bright, but less certain that any information is being sent when light is dim.

The other side of the question you bring up is how the retinal ganglion cells themselves alter the image formed onto the photoreceptor layer.  For those that don't already know, photoreceptors are located at the very back of the retina.  Since they're the major light sensitive part of the retina, that means light has to go through the ganglion cells, bipolar cells, amacrine cells, and all of their associated processes before reaching the actual photosensitive part of the eye.  So, why not put photoreceptors at the front of the eye?  One major reason is metabolic, photoreceptors are tightly coupled with the retinal pigment epithelium which helps to re-process used photopigment as part of the retina's vitamin A cycle.

How can those two factors, a one to one correspondence and a decrease in thickness be present at the same time?  For reference, let's locate a cross section of a primate macula

Dark areas are cell nuclei.  The innermost layer of cells (bottom of the image) are ganglion cells, the next layer of cells up is bipolar cells (the inner nuclear layer) and the next layer up is photoreceptor cell bodies.  you can make out the cilial stalks of the photoreceptors pointing upwards toward the RPE.

From this image we can see a few transformations happening in the macula:

The photoreceptor layer is thicker, up to 7 or 8 cell bodies deep.  This means higher photoreceptor density.
The outer plexiform layer (photoreceptors to bipolar cell connections) is considerably thicker.  A single cone should connect to fewer bipolar cells in the retina, so how does this make sense?  We'll find the answer in #3.
The outer nuclear layer is only one cell thick.  This is the first layer that is actually thinner in the foveal region.  The cell bodies for photoreceptors from tis region have been displaced laterally, and the outer plexiform layer from #2 had to be larger to accommodate this lateral shift
The inner plexiform layer, connections between bipolar cells and ganglion cells, is nonexistent.  Also absent is the ganglion cell layer itself.

So how do these observations resolve your question?  Quite simply, the lateral movement of information from the foveal/macular photoreceptors happens predominantly in the outer plexiform layer.  That buys the inner plexiform layer considerably more space to further spread those signals laterally to ganglion cells, and avoids the problematic situation you suggested of having an extra-thick ring of ganglion cells immediately around the fovea.  The end result is that ganglion cells that respond to photoreceptors in the foveal region of space are even further out from the retina than the bipolar cells they connect to, which are themselves displaced.

As far as why a cherry red spot looks so large, that honestly depends on two factors: the disease or disorder in question and the zoom used.  Bear in mind that the red color comes from, as far as I know, the blood vessels in the choroid itself.  It would therefore not necessarily correspond exactly to the size of the macula, but instead to any area which is thinned in that vicinity.  I think you'll become more comfortable with that idea if you look back at the thickness of the total retina in the above figure and notice that even outside of the foveal region it is still growing thicker.

I think your question shows good instincts, because I believe that if the eye evolved to have a larger "true" fovea then you would get exactly what you describe: a large area of super high density vision surrounded by a region with non-linearly worse vision designed to support the central region.  Instead it appears that the primate macula is just large enough that we have a moderate sized central acute region and a (relatively) linear drop in spatial acuity moving out from it.