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Database of cancer cells
I am looking for a database(or any kind of information source) of cancer cells, which has information about the speed of reproduction of these cells, how fast they grow, etc.
So I could make my simulation as accurate as possible, as close to reality as possible (I am working on developing a software that simulates how cancerous cells spread).
Edit

Are you interested in growth rates in culture or in vivo (e.g. tumours)

Okay, I am a noob in biology, so let me explain it like that.
I am using Voronoi graphs for simulation, so I think that I am interested in tumor level, how each cell interacts with each other, and thus how fast can cancerous cells overpopulate healthy(or other cancerous) cells.

I suggest making your title more specific. You should at least mention proliferation, growth rate or a similar term.

Are you interested in growth rates in culture or in vivo (e.g. tumours)

The National Cancer Institute (NCI) has a list of doubling times for a variety of commonly used cell lines, see
https://dtp.cancer.gov/discovery_development/nci-60/cell_list.htm
I my experience, these doubling times are quite stable/reproducible, provided that cells are kept in standard culture conditions. While doubling times differ a lot between cell lines, they are also very different in size, and larger cells tend to have longer doubling times so that the biomass growth rate is actually rather similar between lines.
Note: these doubling times refer to cell culture conditions. Actual tumors in vivo grow much more slowly, due to lack of nutrients, suppression by immune cells, and what not. Estimating cell growth rates in tumors is a much more complicated business, and I don't know of any database for that.


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What is Biradial Symmetry?
I am trying to visualize biradial symmetry. I have read the section in the Wiki entry on Symmetry in Biology but it is quite brief and there is no example to illustrate it. I haven’t been able to find one anywhere else on the internet.

Wellcome to StackExchange Biology. I've tidied up your question a little. We always like links to sources people mentioned, so I've included what I imagine your source is to make it clear there was only a small section on your topic (which is best included in the body of the question as well as the title).

This blog post provides examples of biradial and trimeric symmetry: http://planetfuraha.blogspot.com/2010/04/illustrating-symmetry.html

In biradial symmetry, in addition to antero-posterior axis there are also two other axes or planes of symmetry at right angles to it and each other such as the sagittal or median verticular-longitudinal and transverse or cross axes. Such animals have two pairs of symmetrical slides i.e there are two planes of symmetry.
You can visualize it as a combination of radial and bilateral symmetry. The body has similarity on either side of a central axis but slight differences in sections next to each other if divided across any plane.
E.g.ctenophores.

for more info
In this image you can see that there are two planes of symmetry, one passing along the oral-aboral axis and the long axis of the mouth. The other passing along the oral-aboral axis and short axis of the mouth. The antimeres on either side of one plane are slightly different from the antimeres on either side of the plane (Imagine in 3D). The comb plates give it radial symmetry and mesogleal layer (jelly-like) give it bilateral symmetry.
If you are interested in the evolutionary aspect, then read this.

Biradial symmetry is a type of symmetry in which there are two planes of symmetry passing through the principal axis. It is different from bilateral symmetry where there is only one plane of symmetry.
The following image shows difference between biradial and radial symmetry:
Another subtype of radial symmetry is pentamerous radial symmetry which has only 5 planes of symmetry, seen in star fish.

lets use a simple quadrant diagram to explain

so in this diagram 2 and 4 would be identical, but 2 and 1 or 3 would not.
or you could say side 2, 3 is the same as side 1,4 but not as a mirror image more as a rotation.
Another way you can picture it is radial symmetry but with only two sides, hence BIradial. Many believe it may be an intermediate stage between radial and bilateral symmetry.

Your explanation illustrates nicely and simply the definition in OP's reference, but how does that apply to a typical shape of a Ctenophore, such as this example? It doesn't seem that II and IV would be identical, because II would contain a tentacle stem while IV would not.

ts because that picture is from the side, from above it makes more sense, http://lanwebs.lander.edu/faculty/rsfox/invertebrates/images/cten13L_x550_x_420x.gif

Imagine in terms of letters.
A has a bilateral symmetry. Left and right part are symmetrical.
X has a radial symmetry (Tetramerous),  anterior part (v) is symmetrical to posterior part (^) but also identical to left part (>) and right (<) as well which are made by a different plane.
Now consider I. It has two bilateral symmetry but they are dissimilar. That is anterior part (T) is symmetrical to posterior part ( ⊥) but different from left part (]) which is symmetrical to right ([). This is biradial symmetry.

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Question about aneuploidy
I am learning about aneuploidy and non-disjunction and just wanted some clarification with regards to terminology. In particular, do the terms monosimony and trisimony refer only to INDIVIDUALS (i.e. a non-disjuction event during meisosi would produce some gametes with an extra chromosome and some lacking a chromosome, however we do not refer to the gametes as having/being monosimotic (?)/monosimony; we only talk about the zygotes and individuals formed from fertilisation involving these faulty gametes as having monosimony/trisimony etc)
Or do we refer to gametes as having monosimony or trisomny also?

Are you asking what the terminology is for a gamete that is missing a chromosome (leading to monosomy) and one that has two of a chromosome (leading to trisomy when it fuses)?

@KoenvdH yes. I am confused as to whether the terms trisimony and monosimony can refer to gametes as well.

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what is the difference between pituitary dwarfism and thyroid dwarfism?
My book (Comprehensive Biology class XI, by J P Sharma ) mentions of two kinds of dwarfism- "Pituitary Dwarfism" and "Thyroid Dwarfism" but does not provide any details about the matter. so please help me.

Did you do and searches of your own (what did you find when you Googled the terms?) Please share what you found, then someone might fill in the details which are missing.

How can this be a homework question? The matter is quite confusing so I asked that. :O :(

Pituitary Dwarfism is a condition where less amount of growth hormone results in abnormally slow growth and short stature. Growth hormone is released under the influence of hypothalamic growth hormone-releasing hormone(GHRH), and is inhibited by hypothalamic somatostatin. Growth hormone deficiency has different negative effects if happens according to age it manifests;  in newborn, the primary manifestations may be hypoglycemia, while in later infancy and childhood, growth failure is more likely. Growth hormone deficiency can be congenital or acquired. It is usually permanent, sometimes transient.
Thyroid dwarfism is a condition arising from the deficiency of a thyroid hormone. It happens when there is lesser thyroid hormone secretion (defect of manufacturing or lesser supply of Iodine) before attaining the full development congenitally. It causes retarded growth and development of bones with disproportionate body proportions (that's dwarfism ).


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Diploid cells and number of chromosomes
I'm struggling to get a hang on this. I'm getting confused by this sentence from one of my tests:
Each human diploid cell has two sex chromosomes and _____ autosomes.
I'm guessing they're meaning 46, but can someone tell me this in another way? Like in a really easy way, so that I can understand it?

if you think Alissa has answered your question, you can check her answer.

By definition, an autosome is a chromosome that is not a sex chromosome. Therefore, as a human diploid cell has a total of 46 chromosomes, including two sex chromosomes, I guess the answer to your question should be 44. I hope it's clear enough for you. :)

YES, that definitely cleared things up. I knew something wasn't right. Another one if you are up to it:
If the normal diploid number of chromosomes in an organism is 8, how many chromosomes are present in each of the daughter cells at the end of meiosis I?
Is the right answer half - 4?

Yes, the right answer is 4. ;)


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What is this animal? Reminds me of a crab because of the way it crawls but it looks like a plant.
Crablike animal however it looks like a plant. Doesn't seem that fast when it comes to speed.

Welcome to Biology.SE. Can you please indicate where (broad scale and finer scale) and when you took this picture. Was the picture taken underwater? Also what do you mean exactly by "not so fast"? Feel free to add any other information that may help.

It looks like a clump of seaweed to me. But I can pick out pairs of legs.
It is a species of "seaweed crab" or "decorator crab": a crab that camouflages itself with bits of seaweed it picks up, so its appearance can vary depending on its surroundings. Here's a video, and as you say, in the speed department, it's a bit lacking.
It is identified as Naxia tumida as opposed to the larger decorator crabs. The cephalothorax is that round brown bump in the middle, and in front of it (in the middle below the long axis) are the pincer legs. The second and third pairs of legs have quite a lot of seaweed attached (making up what I've described as the 'long axis'.)
Here is a screenshot from the video of a Naxia tumida.


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Evolution of sexual reproduction from asexual
How exactly did asexually reproducing organisms evolve into sexually reproducing ones? Why was it considered more favourable?

The evolution of sexual reproduction is very much a field in progress. There in any case not a single simple answer to this question. A number of reviews exist on the subject. One of the reason being that the dichotomy sexual vs asexual reproduction is misleading as reproductive methods are immensely diverse. I think the question is therefore too broad.

You could give it a start with the wikipedia article about the evolution of sexual reproduction or maybe you could have a look at the SE posts Why asexual reproduction? and Why are not all species hermaphrodites?.

You will find in any intro textbook on evolution a whole chapter about the evolution of sex. You should have a look at it.

I agree with "JJ": Answer not good enough.

Why not add a definition with references on what sexual reproduction is?

Sexual reproduction is a process where two cells fuse to form a diploid cell. Unicellular organisms (or even multicellular lower organisms like alga, fungi and protists) prefers to reproduce by asexual means under favourable conditions. But when the conditions become unfavourable, they opt to follow sexual reproduction. This suggests, sexual reproduction evolved to increase the chances of survival under unfavourable condition.
So how does sexual reproduction helps in increasing survival rate? By fusion of cells i.e., sexual reproduction a cell now becomes diploid and hence have two copies of its genome. This increased copy of genome is beneficial in repairing any breaks or alteration in genome, as the other copy will act as a template for repair (via homologous recombination).
To get a better hold of this, let us take an example. Let there be a population of haploid cells. This population was exposed to conditions which would cause damage to genome, specifically would cause breaks in DNA. There were two cells "Fella A" and "Fella B". They both knew that their genome has suffered damages, but neither was successful in repairing the DNA as they required an intact DNA template for repair. Suddenly "Fella B" came up with this great idea to fuse with "Fella A". This would work, reasoned "Fella B", as the position of damage in the DNA in his genome is different from the position in "Fella A". Fusion of cells was the first step towards evolution of sexual reproduction.
Later on the biological system realised importance of variation generated by sexual reproduction and hence this mode of reproduction caught on with various lineages.

But I want to know HOW the change occurred from asexual to sexual

@Tushar You are presenting one of the many arguments people put forward. Barton and Otto 2005 is just one example of another explanation.

@Remi.b: Agreed! There are many hypothesis (arguments) and to the extent I was able to understand work of Barton and Otto, it discusses "if cells gained the capability of fusion (probably for DNA repair, my view) then what factors will promote its spread to entire population". While my answer explains why cells would start fusing leading to sexual reproduction.

@user29774: I made an edit. Does this answer your question?

@user29774 While I consider the the current answer gives a poor representation of the diversity of explanations and diversity of mating systems, I think that if you feel like the post has answered your question, then you should accept it (and check the checkmark).

This isn't really an answer to the first part of the question.  I wouldn't expect the anthropomorphic explanation of two single celled organisms 'knowing' they have genetic 'damages' and one coming up with an 'idea' to fuse together being up to snuff.

This is your own private theory? What are your references? I like the simple logic very much. As other answers show "where two cells fuse to form a diploid cell" is no trivial approach. I guess at school you may learn about maiosis and mitosis without even "diploid/haploid" being called up as words. I would like to hear about Soma cells in mitosis not changing anything whereas haploid cells departed from the same zygote have mingled but will stop that. What's more chromosomal exchange is decisive - very different, still the same.

Do you think of a diploid soma as a prerequisit of sexual reproduction? If yes, prokaroytes would be out?

Sexual vs asexual is not a binary condition it is a spectrum. Many organisms do both and/or a wide range of things in between. One of the most basic is plasmid swapping Bacterial conjunction in unicellular organisms.Even asexual selction has multiple forms of reproduction such as budding vs fission.  Exchanging genes can be highly beneficial for multiple reasons including but not limited to; making infection far more difficult for parasites or giving a  favorable gene a better change to spread since they are not stuck in the same genetic line forever.
Many organisms are opportunistically sexual, using sexual reproduction when they can (when they can find a mate or when resources are abundant) and using asexual selection when they cannot. this implies that there is an advantage to sexual selection even if what it is is debated, but it also shows it is an an either/or question the two forms of reproduction coexist quite well.
As for why sexual selection evolved, this is a hotly debated topic with no clear answer, it might be as simple as a way to get the benefits of gene exchange without the virus vulnerability plasmids create.  It also a vague question by its very nature, because many organism engage in many different forms and combinations of forms of reproduction AND becasue many of these appear to have evolved independently the question is horribly muddled.
In short we know sexual reproduction has benefits but we can not say which ones were the deciding factors in its early evolution partially becasue there are  several different instances of it evolving..

No, you've got the wrong end of the stick... asexual reproduction came from sexual reproduction, not the other way around! Asexual reproduction is a degenerate state that has benefits but is an evolutionary dead end because sexual combination is necessary to promote beneficial alleles and build new genes.  See:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4231362/
The answer that says "Sexual vs asexual is not a binary condition" is misleading; yes, that is true.  Sexual species will start to experiment with asexual forms if they can because that confers advantages.  The ability to be parthenogenic is very useful, but since it is a dead end, the ability to reproduce sexually should not be lost.
Although sex was quite tricky to evolve in the first place, it was necessary from the very beginning.  It evolved from simpler systems of gene swapping and building that were needed from the beginning.

This answer is just plain wrong. The article you cite only claims that asexual animals are an evolutionary dead end. Animals are just one branch of the tree of life, not its root.


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Has kin selection enabled the evolution of interspecial communication?
I know animals often imitate specific behaviour (like when they show their teeth to evoke "danger!" in the reciever) as a form of communication. Although, for a fully-fledged language where we can express anything we can think of to develop, we need more complicated signals.
And for that, we need both the reciever and the signaler to understand the same signalling system. And since for a language as complex, the animals need to share a lot of similar "associations" with similar signals - it's good when the communicating animals orientate a similar environment - such as siblings.
Is this a possible explanation of the evolution of language?
I know the signalling theory is a biological branch on its own, however I seem not to be able to come up with an alternative explanation. Also, I know that this kind of group selection is sometimes used to explain the evolution of altruism. So is this how the evolution of communication happens?

Perhaps better asked on Linguistics.SE?

@anongoodnurse If my hypothesis is true, it applies on all kinds of complex communication systems.

@anongoodnurse Also I was mindblown when I realized that this had to be minimally the way altruism has evolved.

I don't know about this.  I manage to communicate fairly well with my dogs and horses, and they with me.

@jamesqf They've learned that if they'll respond in certain wain on certain stimuli, they'll got some reward. The problem occurs when we notice that the relationships among animals don't often work that way. Similar ideas are discussed in the book The evolution of language

@Probably: But they've also learned that if they direct certain stimuli to me, I will (generally) respond in certain ways, which will get them what they want. That's certainly communication, isn't it?

@jamesqf I think it's the same case - they learn certain behavior to get rewards. But when you signal to your collegue an information about a bear standing behind him, it's an "altruistic" behavior because when the bear isn't after you specifically, you got some time to run while the bear is chewing your collegue. And, of course, it turns out not to be altruistic considering everyone would have done that in your situation. But this situation occurs only if someone goes first with to "try" if altruism pays of - and of course, since he's the only one, his DNA won't be passed on.

So for altruistic behaviour you need the population to evolve this mutation at the same time. And evolution of such trait within a family seemed like a nice explanaiton for me, even though there are certainly ways to avoid that - if the animals interact in the means of the theory of games, they could have evolved altruistic genes as well.

@Probably: Well, all of language is just behavior learned to get rewards (or to avoid punishment).  As for altruism, your example (like most supposed altruism) is really just an example of forward thinking.  That is, by warning the colleague, you trade a small risk that the bear will catch you instead of him for the large potential benefit that he may provide you in the future.

@jamesqf Sure, my point was that being the "first altruist" doesn't pay of. Of course, everything we do is driven by endorphines but it's a different kind of reward system when there's not just stimulus-reflex behaviour

You're probably right to say that, neurologically speaking, there's no difference between the "rationally learned" and "stimulus-reflex" behaviour   (even though some consider the border to be The theory of mind). The difference important for our case is that it doesn't pay to be the "first altruist" but it pays for your horses to listen to you (and that's not even a "rationally learned" behavior btw since they're domesticated)

You're probably right to say that, neurologically speaking, there's no difference between the "rationally learned" and "stimulus-reflex" behaviour   (even though some consider the border to be The theory of mind). The difference important for our case is that it doesn't pay to be the "first altruist" but it pays for your horses to listen to you (and that's not even a "rationally learned" behavior btw since they're domesticated)

@Probably: But it often does pay to be the first altruist, as long as you don't invest too much in the altruistic act.  Further, I'm not sure that I buy into the idea that there's a difference in kind between "stimulus-response" and "rationally learned".  And endorphins are a result, not a cause, though of course they can establish a feedback cycle.

@jamesqf Well, apart from establishing a feedback cycle, I had on mind the neurotransmiters neurons use in a similar way to navigate new paths as well. But about the difference between "stimulus-response" and "rationally learned": you're right, phisiologucally, it's just about the level of complexity of communication but your horses are domesticated so there might be an evolutionary predisposition to listen to you - basically all behavior in smaller mamalls is driven by evolution.

The selective pressure towards cooperation can occur only once they've got an advantage when they start cooperating. Otherwise, you would have to assume group selection for altruistic behavior, which is not accepted among biologists.

@Probably We are starting a Bioacoustics Stack Exchange for people interested in the studies of non-human animal sounds and the impacts of sounds on animals. Please join us! https://area51.stackexchange.com/proposals/126698/bioacoustics?referrer=YjZmYjUxYzJkNDI1YmY5NDk3NzdhMzViMmZlNzI4ZDdiYTAyMWQxNTM5ZWFiNzRhODNkMmFiMzIxZjI3MmY1N_gFvrICTvBsmYNJ2ptRM6lIZEAV-VGkXtIwNyVDja680


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Can HBV pseudotyped oncolytic viruses be used to treat hepatocellular carcinoma?
Chronic hepatitis B is the leading cause of hepatocellular carcinoma (HCC). Oncolytic virotherapy (OV) is an emerging tool to treat cancer. However, one challenge of OV is that our immune system may produce neutralizing antibodies, which impaired its efficacy.
While on the other hand, antibody production against surface glycoprotein of HBV is inhibited in chronic hepatitis B. So can we use the HBV glycoprotein to pseudotype OV (e.g. VSV, measles, MLV), thereby circumvent the host humoral immunity? Can such viruses be used to treat HCC caused by chronic hepatitis B?


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Problems with SDS-PAGE, no separation - what could be the problem?
I work in a lab were we have a common stock of 30% Acrylamide, TEMED, TRIS-HCl (pH6.8 and pH 8.8.) and a 10% (w/v) SDS solution pH 7.2.
We use the recipe for loading buffer (which we of course mix with BME before use):

3.15 mL MilliQ water
1.25 mL 0.5M Tris-HCl
2.9 mL 85% Glycerol
2 mL 10% SDS
0.4 mL 0.5% (w/v) bromophenol blue

Our problem is that there is no separation.
I have tried making 2 gels because I though I might have mixed the separating and the stacking gel, but I made sure i did not do this the second time. Then I asked someone else to make the gel, and it did not work for them either (nothing on the gel, no samples no ladder).
Then I remade the 10% SDS solution and both the TRIS buffers, but again something strange is going on as we get nothing on the gel.
The gels are obviously polymerized as its a solid gel when you take out to stain and destain, and I dont understand how the loading buffer can do this even if you mess it up (because you should see something on the gel as long as your sample in the well, even without denaturing). We obviously remade the loading dye and tried again, but this does not work.
I know there is protein in the samples, as I am putting cell pellet and purified protein (which I have tested the catalytic activity of) on the same gel.
Does anyone have a rational explanation for this, or suggestions of what can typically be wrong.
Bellow is a picture of the gel as it looks when its almost done running at 200V (80mAmp) for approx 40min. When we stain and destain there is nothing on the gel. Also I think the color (bromophenol blue) looks as if its running a bit strange on the gel, not as it normally should, see picture below, but perhaps I'm getting a bit paranoid.

Did you try running a different protein? Or coloring the protein out of the gel to see it really stains?

Also try using a pre-stained protein ladder in one of the wells. (Preferably one that comes ready-mixed and doesn't need loading dye/heating/BME.) That should separate issues with you gel/running conditions from any issues with your protein/loading dye/staining process.

Are other people in your lab able to see protein in their gels? Not your specific protein, but any other protein that they're working with. In case you don't have pre-stained markers, this should also tell you whether it is a gel/staining issue or a problem with your specific protein. Also, how much protein are you loading?

Thanks fot the input, after readjusting the pH of everything and making new running buffer with new SDS solution the separation seems to be back. Its still a bit of a mystery, but perhaps the SDS (suddenly) got old and since its in both the loading dye, running buffer and gel - it just did not work. I have been reading a bit and it seems that some say that the 10% SDS should not be older than 6moths, ours was 5 years old but had been working just fine up till one week ago.

After readjusting the pH of everything and making new running buffer with new SDS solution the separation seems to be back.


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I found a bug on my bedroom floor. Is this a bedbug?

I found this insect on my bedroom floor. I'm worried. I hope this is not a bed bug.
Size: 3-4 mm

It doesn't really look like a bedbug, but the picture is extremely poor and you need a better one for a species determination.

Honestly i just want to know if this is a bed bug or not

It vaguely looks like a flea, but the photo quality is very poor.

Please update the question with your location

I've voted to reopen because I've incorporated some more info into the question AND I have a good answer for the user.

I think the question should remain closed - the pic is too poor for an ID with any certainty. Given the info, it might be a bed bug, but it could also be something else (so it is unclear).

I trust @theforestecologist has a good answer, so I voted to re-open.

@fileunderwater. The body shape (and, importantly, the presence of a notch at the pygidium) is a giveaway to the type of insect. Bed bugs do not have that body structure. It's a terrible picture, but I'm pretty sure I know it.

@theforestecologist This is up to the community, not up to me (and several have voted to keep closed). I don't think it should be open, since it is of extremely limited value to the site. I don't really see how we can have any pretence of maintaining the quality of BioSE if we keep this kind of question open. And whether you think that you can provide an answer doesn't really have anything to do with it; somebody can always imagine that they can provide some sort of answer to all questions that we close as "too broad" or "unclear". That doesn't mean that the Q should be open.

@theforestecologist Anyway, now it is open, so you got your wish. This is more of a discussion for meta though. For the record, I've been talking to an expert on domestic pest insects, and he thought that it is impossible to say for certain whether this is a bed bug (from this picture). This was also my original point, and why I think that the question should be closed (it is too unclear to answer with any certainty).

@Virginia Again, please update with your location. Also please let us know 1. if you have seen any more of these (if so, where? and do you have photos), 2. if you have pets and 3. if you have received any bug bites.

To answer your question this is very likely NOT a bedbug.

See this answer for a positive ID of (and more info for) a bedbug.

However, based on the size and body shape of your specimen, it appears you've found another blood sucking paristic pest: a flea.

 Sources: Here, here and here.
 General Info:

Fleas are small flightless parasitic insects (order Siphonaptera) that consume the blood of mammals (including humans) and birds.
Over 2,500 species of fleas have been described worldwide.
Adults are 1.5-3.3mm long, narrower than wide and brown (or reddish brown). [1,2]
Flea larvae are worm-like (vermiform) in shape with a sparse covering of bristles.  They rarely live on the body of their host.  Instead, they are usually found in its nest or bedding where they feed as scavengers on organic debris (including adult feces).

 Likely Species:

I'm assuming you have a pet (cat or dog perhaps). If that is the case, you're likely looking at a cat flea or dog flea (depending on your locaiton). From UF IFAS:

The most common [American] flea is the cat flea, Ctenocephalides felis  (Bouché). The adult cat flea, unlike many other fleas, remains on the host. Adults require a fresh blood meal in order to reproduce.
The dog flea, Ctenocephalides canis (Curtis), appears similar to the cat flea, but is rarely found in the United States. Cat fleas are commonly found on both cats and dogs in North America, while dog fleas are found in Europe.
The two species are distinguished by a slight morphological difference which is detectable only under high magnification.

 Cat flea (Ctenocephalides felis) from University of florida IFAS
Note: both species will parasitize multiple species (including both cats and dogs as well as humans), and their distinction (as mentioned above) is more dictated by geographic location. However, both can be found worldwide.

Linardi & Santos (2012)1 have an excellent publication for correctly identifying between the dog and cat flea.

For More General Information See:

Wikipedia
 - Terminix
 - Orkin
 - Univ. of Evansville
 - Purdue University
 - UFL IFAS (cat fleas or dog fleas)

 Fleas vs. Bed Bugs
See this Terminix page for "What is the difference between bed bugs and fleas?"

Your specimen is almost certainly a flea because:

The body of the insect in your picture is thin but vertically "tall" (or "laterally flattened"). In other words, it appears to be narrow like a flea.

A bed bug, on the other hand, is wide and vertically very flat.

Though, an engorged adult can appear to be more narrowly long when engorged on blood. See here.

Fleas are narrow so that they can easily maneuver through a host's fur/hair/feathers; while a bedbug is flat to be able to effectively hide in crevices.

The size (3-4 mm) is more appropriate for a flea.

Although some larval stages of bed bugs can range between 2.5 - 4 mm, these larval stages still retain the relatively flat appearance of the adult (except when engorged).

Notice the reflection toward the posterior end of the specimen in your photo. This is not present on bed bugs. This light is reflecting off the flea's pygidium (or sensilium).

Some fleas have bristles on the posterior end of their body. Bed bugs do not. The insect in your picture has these posterior "hairs."
Fleas have powerful hind legs for jumping that stay relatively close to the body, while bed bugs have very skinny legs that spread laterally from the body.

When bedbugs become engorged and appear more like the insect in the question picture (i.e., not flat), their abdomen grows posteriorly but their legs do not extend very far back.
Notice when I brighten the OP's picture from the question you can see the light reflecting on the wide posterior femur that is both close to the body and extends relatively posteriorly as compared to the overall abdomen:

Location & Behavior: Although both fleas and bedbugs are generally nocturnal, both can be found during the day. However, they would generally be found in different places:

Bed bugs are likely to be digesting meals on the piping of your mattress, in and around the bed frame or box spring, along the baseboards and creeping around in other well-hidden cracks and crevices
Fleas, however, (like your specimen) are more likely to be found making themselves at home in animal sleeping areas or lurking around in your upholstery or carpeting, waiting to hop on for a bite. [Source]

Should You Still be Concerned?

Some fleas are well known to transmit diseases (e.g., plague, murine typhus, etc., and a host of issues for your pets) unlike bedbugs. So really, fleas could potentially be more harmful.

Unlike bedbugs, however, vacuuming goes a long way for managing fleas on bedding, carpets, and furniture.
However, one flea can lay between 150 and 300 eggs every week, so do not wait!

 Works Cited:
1  Linardi, P.M. and Santos, J.L.C., 2012. Ctenocephalides felis felis vs. Ctenocephalides canis (Siphonaptera: Pulicidae): some issues in correctly identify these species. Revista brasileira de parasitologia veterinária, 21(4), pp.345-354.

Wow, you did have a good answer!

I had a bed bug infestation a few months ago. That picture looks like it could be a bed bug that hasn't fed in a while. But, the overall body shape looks more like a flea....
Bed bugs look different depending on what stage of life they are and whether or not they have fed recently. The picture below is a bed bug who has recently fed. You'll notice his body is fat and has a reddish color.

You may want to get an ultraviolet flashlight and look in the seams of your mattress and in the cracks of your headboard. Baby bed bugs are tiny and almost impossible to see..... Also, in case you have fleas, use that UV Flashlight to scan your carpets and pet's fur also.
You can find more information on how to find out if you have bed bugs and what you can do to eliminate them at http://ridbedbugsnow.com/how-to-get-rid-of-bed-bugs


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Pyrimidine bases + genetic variation
I don't understand this question, hoping someone can help!
One of the following bases does not belong among pyrimidine bases:
 - Uracil
 -  Adenine
 - Cytosine
 - Thymine
I thought that everyone was bases, expect that uracil is in RNA, and that in DNA it is replaced by guanine.
Also one more question:
Which of the processes would never contribute to genetic variation within a bacterial population?
 - Transformation
 - Meiosis
 - Mutation
- Transduction
I have a hunch that the right answer is mutation, but I don't know why. If you know the answer, it would be very helpfull if you could explain why :-)

Welcome to Biology.SE. A post should never contain more than one question. As such, the post should be closed as too broad. Also, homework question requires that the OP shows its effort at answering the question. Typically, for the first question, it really is just a matter of googling pyrimidine. You can have a look at our policy about homework questions here.

I'm really sorry for breaking your policy! I thought that by asking more than one question I was being efficient for both myself and the ones answering. You're absolutely right about the first question - but stress can be paralyzing. I will follow the rules from here on.

No worries. It takes a few posts to get used to the SE policies, formatting and things. After that, it is in my opinion a fantastic tool to be using during your studies.

You are correct - they are all bases. However there are two types of bases. Purines and pyrimidine bases. Purines have two ring systems, while pyrimidines have only one. With this hint, I think you will be able to find the answer to your first question.
As for your second question. Can you give me a definition for what a mutation is? I think if you are able to define this word you will know why that answer is incorrect.
Also, bacteria are incapable of performing one of the four processes that you have listed - and that particular process, is therefore the correct answer to your second question.

Thank you for your detailed and very pedagogic answer. Forgive me for being a total newbie, but as far as I can see both guanine and adenine are pyrines?
Mutation are permanent changes in the DNA. So it could contribute to genetic variation.... but bacterias are incapable of meiosis, of course!

Yes, guanine and adenine are purines. And bacteria are incapable of meiosis. Well done.
But, one last thing, it is actually thiamine that is replaced by uracil in RNA; and not guanine as you stated in your question.

So the correct answer to the first question is adenine (I mixed up guanine as one of the alternatives, as you may have guessed ;-). Thank you for clearing up my RNA mix-up as well.


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How can facultative anaerobes exist without catalase?

Catalase-negative bacteria may be anaerobes, or they may be facultative anaerobes that only ferment and do not respire using oxygen as a terminal electron acceptor

A facultative anaerobe is an organism that makes ATP by aerobic respiration if oxygen is present, but is capable of switching to fermentation or anaerobic respiration if oxygen is absent

But if facultative anaerobes can be present in oxygen rich environments, don't they have to have catalase in order not to die?

There is another class of peroxide decomposing enzymes called peroxidases. These enzymes can catalyze the reduction of $\ce{H2O2}$ to water using an electron donor. However, unlike in the catalase reaction, the electron donor is not another $\ce{H2O2}$ molecule and no molecular oxygen is produced. Thus their presence would not be detected by the typical spot catalase test (which looks for gaseous oxygen generation). For example, NADH peroxidase catalyzes the following reaction to protect cells from oxidative damage:
$$\ce{NADH + H+ + H2O2 -> NAD+ + 2H2O}$$
Thus catalase negative organisms can still have a means of protection against $\ce{H2O2}$. You can read more in this textbook, specifically the section titled "Oxygen Toxicity".


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Are humans not sexual dimorphic? Can genetic XY but SRY not expressed become pregnant?
My understanding was that XX/XY was how sex is determined in mammals, and so humans as well.
A science teacher posted this regarding transphobia:

"I just commented this on a transphobic post that was all like, "In a sexual species, females have two X chromosomes and males have an X and a Y, I'm not a bigot it's just science." I'm a science teacher so I responded with this.
  First of all, in a sexual species, you can have females be XX and males be X (insects), you can have females be ZW and males be ZZ (birds), you can have females be females because they developed in a warm environment and males be males because they developed in a cool environment (reptiles), you can have females be females because they lost a penis sword fighting contest (some flatworms), you can have males be males because they were born female, but changed sexes because the only male in their group died (parrotfish and clownfish), you can have males look and act like females because they are trying to get close enough to actual females to mate with them (cuttlefish, bluegills, others), or you can be one of thousands of sexes (slime mold, some mushrooms.) Oh, did you mean humans? Oh ok then. You can be male because you were born female, but you have 5-alphareductase deficiency and so you grew a penis at age 12. You can be female because you have an X and a Y chromosome but you are insensitive to androgens, and so you have a female body. You can be female because you have an X and a Y chromosome but your Y is missing the SRY gene, and so you have a female body. You can be male because you have two X chromosomes, but one of your X's HAS an SRY gene, and so you have a male body. You can be male because you have two X chromosomes- but also a Y. You can be female because you have only one X chromosome at all. And you can be male because you have two X chromosomes, but your heart and brain are male. And vice - effing - versa. Don't use science to justify your bigotry. The world is way too weird for that shit."

This question is combining different arguments: human gender based on genetics vs. based on appearances vs based on culture. This is too broad, and can likely only lead to open-ended discussion. In fact the question is unclear and this post seems to simply be seeking discussion. I'm voting to close as too broad and as being unclear what you're actually asking.

If you're asking if humans are a sexually dimorphic species, the answer is "yes".
If you're asking based on the viral response of the science teacher, then the answer is still, "yes".  What is described above are chromosomal abnormalities, or other disorders of development, but they are still describing sexual dimorphism in the phenotype. However, the answer itself is incomplete, as it's written out of political motivation.
Whilst true that a person can present, phenotypically, the opposite of their genetic sex, this isn't akin to them "being male/female" counter to their allosomes.  Of course, this in itself can prove to be a contentious issue - how is sex defined?  Under normal circumstances, phenotype is the obvious way of knowing. If someone has the external genitalia of a male, they can be assumed to be male, and vice-versa for females.  When it comes to chromosomal abnormalities, there is an "error" in devlopment, where the genotype is not properly expressed in the phenotype, and so while presenting as one sex, the "true" sex as determined by the genotype is the opposite.  It should also be noted that sexual characteristics can be ambiguous certain cases, creating abnormal sexual presentation, such as in hermaphroditism/pseudohermaphroditism, or "intersex" (the quote mentions 5-alpha-reductase deficiency, which is associated with male pseudohermaphroditism).
The problem with the quote above (at least in the way it is written) is it appears to suggest that chromosomes have little to do with phenotype, as in sex determination, and that this carries over to gender dysmorphic patients.  These are both mostly false.  Gender dysmorphic patients generally do not have any allosome abnormalities, and the reason that the given examples are deemed "errors" (eg XX male syndrome; 47,XXY) is because that is what they are, as well as being rare.  The typical effect of these problems is that the patient is infertile, (i.e. they are not sexually functioning, and have reduced biological fitness).
In short, the teacher is correct in the examples used, but overstating them with regard to the general population, and with regard to transphobia and gender dysphoria.  Humans are indeed sexually dimorphic but as with any complex biological system, errors expressing genotype can occur.


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Do acetic acid bacteria use the electron transport chain when converting ethanol to acetic acid?
Do acetic bacteria use the electron transport chain when converting ethanol to acetic acid?
And is wikipedia inconsistent here in its definition of fermentation. It says fermentation

Fermentation takes place when the electron transport chain is unusable

(and this is consistent with (academic) microbiology books searchable on google books).
Wikipedia defines acetic acid bacteria as

produce acetic acid during fermentation.

also

Some genera, such as Acetobacter, can oxidize ethanol to carbon dioxide and water using Krebs cycle enzymes. Other genera, such as Gluconobacter, do not oxidize ethanol, as they do not have a full set of Krebs cycle enzymes.

I read in microbiology books on google books, that acetic acid bacteria use oxygen as the terminal electron acceptor, and have a respiratory mechanism.
Brewing Microbiology edited by Fergus Priest p165

Acetobactor spp. possess a respiratory mechanism...Acetobactor spp. are obligately aerobic with a respiratory metabolism (O2 as the terminal electron acceptor)

So is wikipedia wrong to describe acetic acid bacteria as using fermentation?
I see mention of krebs cycle though, which I understand to be associated with respiration rather than fermentation. Also in this reaction/process :
$C_2H_6O\hspace{1mm}(ethanol) + O_2 \rightarrow C_2H_4O_2\hspace{1mm}(acetic\hspace{1mm}acid) + H_2O$
I see water mentioned but not carbon dioxide(if it had both I'd say that really looks like respiration, though it's being called oxidative fermentation).  So I still can't really see whether it's respiration or fermentation, though it's being called fermentation (oxidative fermentation), yet there is the mention of krebs cycle enzymes (krebs cycle being associated with respiration), so it makes me unsure whether the electron transport chain is used or not.

also aside from ethanol->acetic acid,  apparently they might also do glucose straight to acetic acid, skipping ethanol.. not sure whether that uses the ETC or not.  the additional part to this question is related http://web.archive.org/web/20170312205200/http://chemistry.stackexchange.com/questions/69388/in-the-production-of-vinegar-where-does-water-come-from/

Yes
I find it somewhat ironic that in a response a recent post from the poster concerning itself with the precise definition of ‘fermentation’ I argued that this was a semantic question because of the use of the term in the English language before any biochemistry was known. I now discover that the term is used in an even looser sense than I was aware of — in an aerobic context. The conversion of ethanol to acetic acid by acetic acid bacteria is apparently referred to as oxidative fermentation as explained in this extract from a paper in The Journal of Bacteriology:

Acetic acid bacteria are obligate aerobes that belong to the α-Proteobacteria and have a strong ability to oxidize ethanol, sugar alcohols, and sugars into their corresponding organic acids. Such oxidation reactions are traditionally called oxidative fermentation, since they involve incomplete oxidation of these compounds. These bacteria accumulate the corresponding incomplete oxidation products in large quantities in their surrounding environment.

The biochemistry is summarized by Gómez-Manzo et al.:

Ethanol fermentation by acetic acid bacteria is carried out by two sequential reactions catalyzed by pyrroloquinolinequinone (PQQ)-dependent alcohol dehydrogenase enzymes (ADH) and aldehyde dehydrogenase (ALDH), which are located in the cytoplasmic membrane [6] and transfer electrons to ubiquinone Q10 [7]. PQQ-ADH is a periplasmic quinohemoprotein-cytochrome c complex and catalyzes the first step of ethanol oxidation by transferring electrons to Q10 and producing acetaldehyde which usually is the substrate for another enzyme (ALDH), and converted to acetic acid during the second step of ethanol fermentation.

The fact that the reduced pyrroloquinolinequinone is re-oxidised by ubiquinone, indicates that the conversion of ethanol to acetic acid requires the electron transport chain in the bacterial membrane to continue, and that the ultimate electron acceptor is oxygen.

I do not know about the prokaryotic mechanism for ethanol metabolism. However, in eukaryotes, the metabolism of ethanol does indeed eventually show an effect in the ETC.
When ethanol is metabolised in eukaryotes, alcohol dehydrogenase will remove a proton with the help of NAD+ to create acetate and NADH. Of course, NADH is used within the ETC. So basically, the metabolism of ethanol serves as one of many ways a cell can balance its redox potential.
Some organisms fermentative pathways are inhibited by the presence of oxygen, and some are not. I can not tell you with certainty whether or not this is the case for you in particular. But, I would define a fermentative process as, a process which does not result in the complete oxidation of a carbon-substrate.

Apparently bacteria are related to mitochondria. And some bacteria have an ETC in their cell membrane, rather like all mitochondria have an ETC in their membrane.

This is true! But, my point still stands. The ETC would work to provide a means to convert the NADH produced from ethanol oxidation, back to NAD+, provided that there is an electron acceptor present.

Ah thank you for clarifying my answer @tomd. The acetaldehyde step slipped my mind. But also, in regards to yeast, they are capable of both ethanol production, and ethanol metabolism - so ADH will work in both directions.

It appears that the 'main' acetic acid bacteria — Acetobactor sp — do not use NAD to oxidize the ethanol to acetic acid, but pyrroloquinolinequinone. The situation is not the same is in mammalian liver. (See my answer.)

@xusr Yes this had already been noted, nearly 7 months ago.. thanks


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In what range do humans generally interpret sound best?
I am currently working on a speech recognition frameworks. A generally used feature used in speech recognition are MFCC features, which uses the mel scale to extract features with.

The mel scale visualises how humans interpret different frequencies of sound compared to each. The graph shows that by linearly increasing the frequency from 0 -1000 will the sound/pitch be interpreted as linearly increasing. When the frequency is linearly increased beyond 1000 hz, is the sound not interpreted as linearly increasing but logarithmic increasing.
How MFCC make use of this:
When training the system, are audio files processed using band pass filters with center frequencies that are mel distant, meaning that they will be (somewhat) linearly increasing at the beginning and end up being logarithmic increasing.
How do I interpret this:
It seems to me that the human auditory system is very susceptible to sounds the range 0-1000 and not much above, but 1000 hz isn't much and I guess conversation must in somewhat higher range. So why are humans more susceptible to sounds in these ranges?

Well, I know in what range human interpret vocal sound best.... but not a range for all sounds, will that suffice your need?

Since you are working with a speech recognition framework.

I work on voice recognition too. Yes, very brilliant query about sound perception that I can clarify and not answer completely. Most of the text belongs to DSP SE forum, i.e. Voice rec, MFCC, filter, BP, audio processing. You may have confused the readers except for the image and the final paragraph.
I had to rephrase it to clarify it to myself:
Why are humans unable to hear pitches on a straight maths scale, they hear logarithmically? We hear according to a mystery ratio called MEL distribution, a well studied summary of many subjects perception of pitch, averaged to:

0.01% Humans have Perfect pitch, 95% are relative pitch, and 5% are tone deaf. MEL varies by the type of listener. Tone deafness is hereditary, ( info about biology and brain structurehere) and the rest of humans probably follow a gradual distribution of poor to good pitch differentiation, and they also hear amplitudes differently.
As you can see from the wiki page, there is no explanation for MEL theory, it's either neurological, a soundwave energy balance, or because of the ear anatomy.
To answer the title question, your graph shows humans have a continuous response to frequency spacings through all their perceived sound. However volume tests show amplitude sensitivity peaks at about 3kHz, which you can see on inaccurate amplitude perception and equal loudness contour graph.
MEL studies of Steinberg are stagnant since Volksmann, same as Donald D Greenwood suggested in 2009, they overgeneralize and the field needs to be developed a lot further under a different study name than MEL scale, which isn't english.
Why can they hear voice well under 1000Hz?
At least 1/2 of the sound energy of voice occurs below 1000Hz, same reason bass requires a lot of energy.

So humans can hear sub 1000Hz sounds from further away, but the more sound data you have the clearer the voice is, and computer should use nearly all of possible human voice frequencies to measure formants and N/M consonants to best accuracy. Sub 1000Hz may contain enough vowel subharmonic frequency bands at different spacings to represnt the vowels of sound basically, but it is less clear and realistic if the voice is filtered at 1000Hz, the subharmonics of AEIOU go multiple octaves above middle C male/female voicebox peak, near 440Hz.
The sub 1000Hz components are generated by the voice box, which changes tone at a slow rate, whereas the 2000-3000Hz sounds, i.e. Frictives, S,F, and N aspirated P, k, don't require very as complex sound processing to interpret (for digital sound filter processing)
The 625-1000Hz pivot component of the equation doesnt appear less straight under 1000Hz if the graph is from a parametric frequency view.
To resolve your query, Biologists would want to know:

1/Structure of the ear as a reason for sound perception imbalance
2/Child learning and adult learning of complex pitch tasks
3/Brain structures used in pitch recognition
4/Evolution of ears and psychoacoustics, reason for a hearing peak at 3k which is the same as rustling leaves
5/Physics energy and mathematical reason for MEL distribution (ask on DSP SE)

As a Voice rec researcher, you should think outside of the box. Computers don't hear like humans. Frictives like F and S have peaks around 3000-4000HZ, they are the highest and easiest to recognize and similar in all accents. Formants from vowels can peak from 400 to 500HZ roughly in men and women, at 700hz for children.
Vowels are vague and vary by accent are are the least precise element in voice-rec. That's why voice recognition hinges a lot on formants and accents which have energy peaks below 1000HZ, and timbral graphs which change wildly wether it's AEIOU sounds.
As a side not for voice-rec,
English is tougher to recognize than French because of the stress time, swingy nature and the 2-3-4 vowels per syllable, and perhaps that's why French have lost the wild traditional accents faster (I know I speak both since I was 0). Voice rec of French and other syllable time languages is easier.
I don't know why MEL is used at all in voice-rec filters. Perhaps because people use the same intonations as they hear from MEL, so the PC must know too, else because the programmers don't know enough about real sound physics, and have implemented it as a rough power-balancing graph for filter results? else some other physics reason. Other power-related filter shapes should work fine, as DSP SE if this has a known physical basis of if it uses human psychoacoustics for digital audio inaccurately:
mel-frequency cepstrum (MFC) is a representation of the short-term power spectrum of a sound, based on a linear cosine transform of a log power spectrum on a nonlinear mel.
Humans don't need perfect pitch for anything except music. Relative pitch, we nearly all have ok, and it makes sense because biologically relevant sounds, animal calls, physical signals of water, trees, voices, add together to make a continuous freqency spectrum that we have to measure all the frequencies by a similar rating of importance to interpret best. Voice contains lots of micro-expression subtones that represent clear psychological states that humans benefit to hear, and rustling leaves and other sounds all should biologically benefit from a high relative pitch clarity.

I need to know this too so i wrote a DSP version here https://dsp.stackexchange.com/questions/46092/mathematical-reason-for-mcpp-in-audio-recognition

So why are humans more susceptible to sounds in these ranges?
I can't find the references etc. As I'm on my phone, but the accepted wisdom when I was doing a PhD on inner hair cells was that there were more type I spiral ganglion neurons per hair cell in the mid frequency ranges for a given species than at the extreme ends of the frequency ranges. This was about 400-1200 Hz in humans and gerbils and 1000-4000 in mice.
Basically more sensory information is heading to the brain from the frequencies we listen to most.
I don't think it was known if it was genetic, or an acquired feature, but papers by Liebermann from the early 90s should point you in the right direction. I'll try and pull one up.
Edit: this review looks like it has the info: 'For instance, in mice and gerbils, the most heavily innervated hair cells correspond to sound frequencies with more acute thresholds of detection (Ehret, 1979; Meyer et al., 2009), in agreement with reports of dense innervation in the middle of the cochlea in other species (Dannhof and Bruns, 1993; Liberman et al., 1990; Meyer and Moser, 2010).'
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3078955/


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For fish, does a bony skeleton have any advantages over a cartilage skeleton?
I have learned that two important lineages of fish are the bony fishes (Osteichthyes) and the cartilaginous fishes (Chondrichthyes). Many websites mention an advantage of the cartilaginous skeletons of sharks and other chondrichthyans: they're lighter than bony skeletons.
But it has been harder for me to find out if we know of any things bony skeletons do for fish that cartilage skeletons can't do, or don't do as well.
My research and hypotheses
I found an old Manual of Geology by Samuel Haughton (1865) that says

[a bony] skeleton only affords an advantage over a cartilaginous skeleton by allowing a greater variety of points of attachment for the muscles of the Fish, and so admits of more powerful motions.

But maybe other people have discovered more things since this was written. Also, I'm curious if this is just a theoretical argument, or if we have actual evidence that bony fish are capable of using their muscles more effectively than cartilaginous fish.
I have three main hypotheses at present:

Haughton was right, and a bony skeleton is just more effective at serving as an attachment point for muscles.
Bony skeletons are more effective at protecting the fish.
There are no advantages to bony skeletons; bony fish just happened to evolve this way. (As far as I can tell, the early evolutionary history of fish has been a bit unclear and I haven't been able to determine if there is current consensus about whether bone or cartilage skeletons came first, and whether chondrichthyan cartilage skeletons are an inherited primitive feature or an innovation.)

As a fish morphologist, here's my best attempt. I really like the first reference I listed at the bottom, too.
1) Ancestral Condition:: The cartilaginous skeleton of chondrichthyes (sharks, skates, rays, chimaeras) is almost certainly a derived feature--a synapomorphy-- defining the clade. There are a few lines of evidence for this. First, the cartilage in a shark skeleton is a very specialized form of calcified cartilage,  unique to the group. Second, in other gnathostome and pre-gnathostome ancestors (Osteostracans,  other armored jawless fishes) had big bony head shields. The groups most closely associated with sharks (Placoderms, paraphyletic acanthodians) has both bone and cartilage in their skeletons. Basically I guess my point is that, while cartilaginous skeletons were ancestral for gnathostomes, that cartilage was very different from chondrichthyan cartilage, and bone turned up in many stem fishes before chondrichthyan cartilage. So the ancestor for sharks and bony fishes probably had both cartilage and bone but not the specialized calcified cartilage of sharks
2) Bone as a Plesiomorphic (ancestral feature), but not the entire skeleton: If we take what I've said above, it certainly suggests that your point 3 is in the right direction w.r.t. split between chondrichthyes and osteichthyes. The chondrichthyan skeleton is light...But the osteichthyes definitely took endochondral bone and ran with it--which brings us back to your original question: why did they replace their entire skeleton with bone? Why is always a tricky question in evolution, but we can speculate:
3) Potential adaptive value of a bony skeleton:

bone is better at transmitting muscle force than cartilage, so in that sense, you are correct
when fish were coming into prominence and diversifying, there were a lot of big, terrifying, predatory arthropods. Many early fishes have big bony armor plates-- which may have served to project them from their chitonous predators
More evidence for that -- when big scary predators went extinct, fishes began to pare down their bony armor (most teleosts have highly reduced skeletons).

Without a time machine we can't be certain of these things, but I'm pretty sure what I've laid out is fairly close to the common consensus.
Relevant lit:

https://academic.oup.com/nsr/article/1/4/490/1512529
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3237026/

Thanks for the edits, @kmm . I am not good at markdown. Or spelling, apparently!


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Mechanism for earthworms to get into a roof gutter
While cleaning accumulated muck from a roof gutter on my house, I found a few earthworms living in the muck. I am intrigued about what mechanism may have allowed the earthworms to reach that location. Some hypotheses:

Live worm crawls up a downpipe
Live worm dropped by an overflying bird
Cocoon is stuck to the outside of a bird (feet), falls off while the bird is overflying the roof
Cocoon passing through bird digestive system and deposited on the roof

What is the likely mechanism for earthworms to reach that location?

I wanted to use the tag dispersal for this question, but it doesn't exist and I don't have the rep points. But perhaps there is another better term?

Birds dropping their meal :p

I would say that the reason why a given organism reaches a given space relies on four main factors:

Morphology and physiology: can that organism reach that place physically?
Food distribution: is there enough food to reproduce and spread in that specific spot?
Habitat: does that habitat fulfill its environmental/physiological needs? Is it environmentally safe for that species?
Abiotic factors: wind, water, etc...

I know it's a very general answer, but consider that the main goal of every organism seems to be to survive, spread and reproduce as much as we possibly can.
For example, if the gutter accumulates moss, earthworms will most likely crawl up the wall and into the gutter to feed on the precious organic matter. Also, gutters, due to its function, tend to be wet at times, and earthworms need a moist environment, so it seems like an ideal spot for them (earthworm climbing up).

Live worm dropped by an overflying bird

Seems likely too: the term ornithochory defines seed dispersal by birds. I guess it could also be applied to dispersal of other animals (at least anthropochory can be applied to both seeds and reproductively capable animals dispersal by humans, in this case, earthworms being transported by the bird's beak). I think the most likely scenario in this case is food availability and a good environment to proliferate and make more earthworms (mostly because it would take a couple of clumsy birds to drop their prey on top of your gutter to establish an earthworm colony up there although it depends on the specific earthworm species and whether it is parthenogenetic or not, of course, but still within the realms of possibility).
When it comes to species distribution, it normally tends to be a mixing of different mechanisms rather than one single specific mechanism.


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Can HIV be automatically cured by waiting until CD4 T cells count drop to 0?
As I know, HIV needs host cell, CD4 T cell to repicate itself, and at late stage of AIDS, count of this cell in patient will drop to 0, my question is, if we can provide a sterilised environment for AIDS patients at late stage, will HIV be cured because CD4 T cells drop to 0 and hence no host cell for HIV to replicate itself?

Short answer: no. You might be able to put the patient into a sterile environment, but they will always carry into that environment every normal and - worse - opportunistic - organism they have into the room with them. So, no. They will die from bacteria or reactivated viruses or fungi or parasites (e.g. toxoplasmosis) that live in the body.

HIV can hide in many kinds of immune cells, like macrophages.


text:
What does the term "recruitment of T-cell" mean?
With respect to the article, what does the term "recruitment of T-cell" mean? Who recruits T- cell? Does recruiting T-cell mean the T-cells get a sense of directionality to get activated by the APC's?

Read into MHC-class molecules, and how they're processed. You have Wiki for that, but if you're interested in the evolutionary mechanisms that are very importantly in play in our modern times, check out this Biostars tutorial: https://www.biostars.org/p/5817/#95075 for some nice explanations and software examples, @CMosychuk (also relevant)

If I'm interpreting it properly, it's the adaptive response that's recruiting the T cell, evidenced by the last line in their abstract:
"Therefore, the contribution of a T cell clone to the immune response is mostly determined by the time of its entry into the immune repertoire, i.e., the time of first cell division after antigen encounter."
It's strange because when i think of recruiting a T cell it's always to the tissue or site of infection or what have you.


text:
Identify this indoor plant with strange stem-like leaves
It appears that this plant branches multiple times from the base of its stem; however, I'm not sure if the base stems are from one organism. It becomes yellowish in color at the tip each stem-like leaves; one node can branch 3-4 leaves at a time.
Additional information:
As for the specimen location- I am currently living in Japan and this plant was bought as a gift for me. It probably is imported from other countries since it doesn't seem to be native here. For maintenance; I was told to just cut the tip of the leaves if it began to fade in color and die; and water the plant at least once a week.

What's your location?   2.  What happens  when  you  break off a stem?

Thanks for accepting my answer --  I'm glad it answered your question. However, please update your question with the information I requested in my previous comment so that the question can serve better use to others in the future. In general, species ID questions should always contain some information about the specimen's location. Thanks

Looks like a Pencil Tree (Euphorbia tirucalli), sometimes called "pencil plant", "pencil cactus" or "milkbush." This "leafless-looking" plant is not actually a cactus, but actually a "Euphorbia" (i.e., member of the Euphorbiaceae family), and should present a white "milky" liquid latex when broken.

CAUTION: THIS IS A POISONOUS PLANT [See symptoms here].

Description: A succulent, spineless shrub with round, green branches; leaves clustered at the tip of the branches and soon dropping

Although it eventually can grow into a small-sized tree in its natural habitat, this plant is found more commonly as a medium-sized house plant or landscaping "shrub."

Range: Tropical Africa and India

Euphorbia tirucalli is very well adapted to semi-arid conditions, but also occurs in both dry and moist forest, savanna and shrub land, and withstands salt stress associated with coastal conditions, but no frost. It occurs from sea-level up to 2500 m altitude. It grows well on a wide variety of light-textured, neutral to acidic soils. It is commonly associated with human settlements and becomes naturalized rapidly. It is locally common and often occurs in groups. [Source].

I would say it looks like some kind of Rhipsalis. Which exact species i can't tell. Just search for images of Rhipsalis and compare to yours.
EDIT:
Some time ago i had a specimen of rhipsalis baccifera which looked a lot like your plant but wasn't as self supporting as yours. It was hanging down below its pot. But maybe yours is some kind of subspecies.


text:
Why do some vegetables taste bitter?
Bitter gourd, cucumber, etc. are bitter to taste. Which chemical causes bitterness in them?
I found these when I searched online: this says that it is because of calcium, while this and this talk about physical effects.

As far as I know the maximum bounty is 500. It's easy to give away 500 when you have > 5000, not when you have < 1000...

@another'Homosapien' that's not the point in my commentary. The point is that giving 50 when you have < 1000 is good enough to my taste.

@another'Homosapien' Good, so he/she is, indeed, generous.

Actually, Bitter vegetables are composed of Sourmoi, which came from the word sour

Bitter taste is sensed by bitter sensitive gustducin receptors (T2R family). There are different types of bitter receptors and they can be triggered by different kinds of ligands. Different classses of phytochemicals that can trigger bitter taste, are reviewed by Drewnowski and Gomez-Carneros (2000).
The bitter tasting phytochemicals include phenols, terpenoids, alkaloids, flavonoids, glucosinolates and isothiocyanates.
Drewnowski and Gomez-Carneros' review (2000) and @anotherHomosapien's answer provide examples for these different classes of compounds. I guess they have missed alkaloids; so I give some examples: theophylline, theobromine (from chocolate) and caffeine (from coffee); these all are isomers of N,N'-dimethyl xanthine and taste bitter. Many alkaloids are toxic. Different bitter tasting alkaloids are reviewed in this chapter (Fattorusso and Taglialatela-Scafati, 2008. Chapter 3. Modern alkaloids. Weinheim: Wiley-VCH. ISBN:9783527621071).
High amount of salt may also taste bitter. The sensation of high salt concentration is transduced by amiloride-insensitive channels which are different from the amiloride-sensitive ENaC which sense low sodium concentration. Amiloride insensitive channels can also sense cations other than sodium. This taste is aversive in contrast to that due to low sodium concentration. Some of the bitter sensing taste cells have amiloride-insensitive channels (Lewandowski et al., 2016). However, I cannot comment if these channels elicit a bitter taste response.

Nice answer, +1! I totally forgot about amiloride channels ;)

Nice question! Many vegetables taste bitter because they contain compounds known as phytonutrients (Greek phyto = "plant"). There are more than 2500 phytonutrients known, and the most important (and common) ones are categorized as1:

Carotenoids: they are the ones that give red/orange/yellow color to some vegetables. They are mainly antioxidants, but some of them, like $\beta$-carotene and $\beta$-cryptoxanthin, are good for eyes as they can be converted into vitamin-A, whose derivative forms a part of phototransduction cascade.
Ellagic acid: it is found in a number of berries, such as strawberries, raspberries, pomegranates, etc. and has been shown in vitro to be helpful in slowing the growth of cancer cells and aid liver in neutralizing cancer-causing chemicals.
Flavonoids: they are found in a large variety of plants and constitute a large number of phytonutrients. Some flavonoids, like catechins, hesperidin and quercetin are very good for health. For example, see this answer for effects of catechins on the body.
Resveratrol: it is found in grapes, red wine, etc. and shows antioxidant and anti-inflammatory effects. Some researches have also concluded that it may reduce risk of heart disease and certain cancers.
Glucosinolates: these are found in cruciferous vegetables, like sprouts, cabbage, etc. and help checking formation and growth of cancer. This is the one we're talking about, so I'll continue about this below.
Phytoestrogens: they can exert estrogen-like effects on the body because of their structure, and even block body's natural supply of estrogen. Isoflavones can also reduce risk of endometrial cancer and bone loss in women. They are also found in a large number of plants, including soybeans, oats, barley, rice, apples, carrots, etc. (see full list here).

Another category, alkaloids, has been discussed by @WYSIWYG in their answer. These are all made naturally by plants as a part of their defense mechanism against insects and pests. This, in part, explains why they are bitter.
Coming to main point, glucosinolates are organic compounds that are responsible for bitter taste and pungent smell of many cruciferous vegetables. They are derived from glucose and amino acid, and contain sulfur and nitrogen as constituents. When they are cooked, chewed, or otherwise damaged, an enzyme myrosinase cleaves the glucose molecule, while the remaining molecule converts into isothiocyanate, thiocyanate and nitrile2, which cause the bitter taste and pungent smell (think of the isocyanide test you performed in grade XI and the smell it produced ;) The reaction looks like this:
source
A special glucosinolate, sinigrin, has been shown as responsible for the bitterness of Brussels sprouts and cauliflower3. Also, high concentration of glucosinolates are toxic to humans as well as other animals, though tolerance levels vary even within the same genera (Acomys cahirinus and Acomys russatus)4. So, that partly explains why these compounds are bitter.
Talking about the anti-cancer properties of glucosinolates (going a bit off-topic just so that you know why these are good for you), two of the main compounds that are responsible for such effects are sulforaphane and indole-3-carbinol. Sulforaphane (in which R- becomes C5H11OS- in R-NCS), for example, is derived by the action of myrosinase on glucoraphanin (again, a glucosinolate). It has been shown to have anti-cancer properties. For example, Li et al, 2010 have shown that sulforaphane prevents breast cancer by inhibiting breast cancer stem cells and downregulating the Wnt/$\beta$-catenin pathway (yeah, there is something like cancer stem cell!). In another research, Hsu et al, 2011 showed that sulforaphane prevents prostate cancer by inhibiting HDACs (histone deacetylases, which interfere with normal functioning of tumor suppressor genes) and DNA methylation. This example was just to mention about the anti-cancer properties of glucosinolates in general.
Another class of compounds, called cucurbitacins, are produced in plants of Cucurbitaceae family. Unlike phytonutrients, cucurbitacins are considered a type of steroid since they are derived from cucurbitane and stored as glycosides5. Their derivatives are also found in other families like Rubiaceae, Rosaceae and even some marine mollusks, and, much like glucosinolates, they are also produced for defense against herbivores.
However, it is not sure whether only glucosinolates are the only compounds responsible for bitterness of vegetables. A study suggests that increased levels of calcium can also be responsible for bitterness of vegetables6, although its evolutionary cause and mechanism of action are unknown yet. Also, it may even depend on the person(!). If you are a supertaster (which has high chances to be true if you're woman or from Asia, South America or Africa), you will tend to be highly sensitive to bitterness of Brassica oleracca cultivars, such as kale, Brussels sprouts or cabbage7,8. Sensitivity to coffee, green tea, mushrooms, etc. is also known to increase. You can view a full list on Wikipedia.
References:
 1. Phytonutrients - WebMD
 2. Burow, M; Bergner, A; Gershenzon, J; Wittstock, U (2007). "Glucosinolate hydrolysis in Lepidium sativum--identification of the thiocyanate-forming protein.". Plant molecular biology. 63 (1): 49–61.
 3. Van Doorn, Hans E; Van Der Kruk, Gert C; Van Holst, Gerrit-Jan; Raaijmakers-Ruijs, Natasja C M E; Postma, Erik; Groeneweg, Bas; Jongen, Wim H F (1998). "The glucosinolates sinigrin and progoitrin are important determinants for taste preference and bitterness of Brussels sprouts". Journal of the Science of Food and Agriculture. 78: 30–38.
 4. Samuni Blank, M; Arad, Z; Dearing, MD; Gerchman, Y; Karasov, WH; Izhaki, I (2013). "Friend or foe? Disparate plant–animal interactions of two congeneric rodents". Evolutionary Ecology. 27 (6): 1069–1080.
 5. Jian Chao Chen, Ming Hua Chiu, Rui Lin Nie, Geoffrey A. Cordell and Samuel X. Qiu (2005), "Cucurbitacins and cucurbitane glycosides: structures and biological activities" Natural Product Reports, volume 22, pages 386-399
 6. Tordoff MG, Sandell MA. Vegetable Bitterness is Related to Calcium Content. Appetite. 2009;52(2):498-504. doi:10.1016/j.appet.2009.01.002.
 7. Dinehart, M.E.; Hayes, J.E.; Bartoshuk, L.M.; Lanier, S.L.; Duffy, V.B. (2006). "Bitter taste markers explain variability in vegetable sweetness, bitterness, and intake". Physiology & Behavior. 87 (2): 304–13.
 8. Drewnowski, Adam; Henderson, Susan Ahlstrom; Levine, Alisa; Hann, Clayton (2007). "Taste and food preferences as predictors of dietary practices in young women". Public Health Nutrition. 2 (4).
 9. Li Y, Zhang T, Korkaya H, et al. Sulforaphane, a Dietary Component of Broccoli/Broccoli Sprouts, Inhibits Breast Cancer Stem Cells. Clinical cancer research : an official journal of the American Association for Cancer Research. 2010;16(9):2580-2590. doi:10.1158/1078-0432.CCR-09-2937.

If these things are bitter because they don't want to get eaten, why are fruits so sweet?

@MasonWheeler you might be interested in this. I didn't really mean 'they don't want to get eaten', they want to protect themselves from infection, and it might be mere coincidence that they are toxic to us too.

And all the specimens mentioned by OP; are members of cucurbitaceae.

@AlwaysConfused oh didn't notice that! I was more focused on a general answer ;)

@another'Homosapien' It was the first thing i noticed in softest way. Normally; if an ancient sculpture has been found; an archaeologist and a geologist would get a different 'first glance'.


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How to detect Single Nucleotide Variants (SNVs)?
This image is obtained from this paper.

The description of this image is as follows:-
DNA-sequence reads from a tumor sample are aligned to a reference genome
(shown in gray). Single-nucleotide differences between reads and the reference genome indicate germline single-nucleotide variants (SNVs; green
circles), somatic SNVs (red circles), or sequencing errors (black diamonds).
(a)
In a pure tumor sample, a location containing mismatches or single
nucleotide substitutions in approximately half of the reads covering the location indicates a heterozygous germline SNV or a heterozygous somatic
SNV - assuming that there is no copy number aberration at the locus. Algorithms for detecting SNVs distinguish true SNVs from sequencing errors by
requiring multiple reads with the same single-letter substitution to be aligned at the position (gray boxes).
(b)
As tumor purity decreases, the fraction
of reads containing somatic mutations decreases: cancerous and normal cells, and the reads originating from each, are shown in blue and orange,
respectively. The number of reads reporting a somatic mutation decrease
s with tumor purity, diminishing the s
ignal to distinguish true somatic
mutations from sequencing errors. In this example, only one heterozy
gous somatic SNV and one hetererozygous germline SNV are detected
(gray boxes) as the mutation in the middle set of aligned r
eads is not distinguishable from sequencing errors.
This is my understanding below. Am I correct?
There are multiple reads that are aligned such that for a given location in the reference genome,(here fourth), if approximately half or more of the reads covering that location has a single nucleotide mismatch with the reference genome,then it is a heterozygous SNV.
Eg:-

Please add the paper you mention as a valid link.

Also, cross posting to other platforms is very poor form.  It's not nice to make someone on biostars take the time to answer you when you already have answers here.

Your link doesn't link to the paper, and you seem to be ignoring half of what the image is trying to get across.
The point is that since tumors are heterogenous, you very well might have only 40% of the cells heterozygous for a particular SNV, which means it would only be observable in 20% of the reads.  But if multiple reads with different start sites show the same SNV, it's likely to be real.  If coverage is so low that you only get one read showing a real SNV, you won't be able to distinguish it from noise.

The existing answer is correct, but I want to expand on this a bit.
In the ideal world, a tissue sample will be completely homogenous (every cell has exactly the same genomic DNA with 0 differences), DNA sequencing machines will make 0 mistakes, and sequencing experiments will sample each portion of the genome (evenly) to a deep level of coverage. In this ideal world, distinguishing heterozygous SNVs from homozygous SNVs is trivial: for homozygous SNVs, 100% of the reads aligning to the position of interest will have the same nucleotide that differs from the reference; for heterozygous SNVs, there will be a perfect 50%/50% split between reads that match the reference and reads that match the alternate nucleotide.
The big problem is that none of these 3 ideals are true in the real world. Sequencing experiments DO NOT sample the genome evenly, so some regions have many reads mapping (we say these regions have "high coverage") while other regions have few reads mapping ("low coverage"). Also, DNA sequencing machines DO make mistakes, on the order of 1% for Illumina machine and 10-30% for long read sequencers like PacBio and Oxford Nanopore. Since sequencing errors are random, they're usually fairly easy to distinguish from real genetic variation, but only in regions of medium
 to high coverage. Finally, we cannot always assume that all of the cells in a sample will have identical DNA--this is ESPECIALLY true with tumor tissue.
For all of these reasons, we cannot distinguish heterozygous SNVs by simply requiring that exactly 50% of the reads mapping match an alternate nucleotide. As swbarnes2 states, it might be much lower than 50%, but with sufficient coverage you can make a confident decision.


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Flowers in Arachis hypogea, are they clestogamous or chasmogamous?
I have seen the flowers of groundnut, they open and remains open for one day, so they should be chasmogamous, but in my school book, they mentioned it as clestogamous, and I searched for it in wikipedia but it wasn't clear. So how to classify it?


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Why do F- bacteria still exist?
When an F+ bacteria conjugates with an F-, it makes the other bactaria F+ too. So on the long run, all bactaria should be F+.
Is there any mechanism that converts F- to F+? Could it be degeneration of F plasmid?

So an easy way to convert a cell from F+ to F- is to divide it without correctly replicating the plasmid and transferring it to a daughter cell, leaving you with one F+ and one F-. The cells that are F- now have a selective pressure advantage over the F+ cells, as they now don't require the energy to produce a plasmid when they divide. If that advantage is enough to overcome the frequency of conjugation, you'll end up having a population of F- cells.


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Annotation for non-model organism
I want to annotate data while analyzing transcritpome data using DESeq2 , usually Biomart R-package (https://www.bioconductor.org/packages/release/bioc/html/biomaRt.html) does the needful , but for non-model organism for which link to Biomart R package is not available seems troublesome, any way to use the custom annotation file( I have one annotation file obtained from Uniprot) or any other alternative to do so?

Can you elaborate? DESeq2 takes count data where the row names are labeled sequence features and allows you to test for differential expression. If you want to associate an annotation with a given sequence you don't need DESeq2, either the sequence features can be matched to the annotation or you need to go back to how the transcripts were assembled.

What kind of annotation file are you looking for? Can you clarify a bit on what exactly do you intend to do?

I'm voting to close this question as off-topic because this is a question about computation (how should I accomplish X in R), not about biological concepts.


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Microarray with n channels
Recently we've been learning about Microarrays, and the typical method seems to be to run a two channel microarray where your RNA from each cell is labelled with a different fluorescent marker, and then the relative intensity of the fluorescent label can be used to identify a ratio of relative gene expression.
I was wondering if it would be possible to use a larger quantity of DNA sequences on the array and then run a number of sets of RNA fragments - for example, say you extract RNA from cells from a cell culture at constant time intervals, then you label them with fluorescent markers which are orders, and then scan the fluorescent labels to find out how the expression varies over time?
Why wouldn't this work?
Thanks!


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What insect is in the PHP bugs logo?
Well, maybe this is a question more suited to Stack Overflow, but anyway, I am curious, which insect is the one in the logo of the PHP bugs site? Is it an actual insect or just a generic "bug"?

It seems like some kind of Hemiptera for me, probably some kind of "true bug". A quick google search about these insects and I found the Hemiptera suborder Heteroptera, and this critter is probably from this group.
I tried to search by the image in google images, but only found the logo itself, in the same low resolution is the image above (I was not able to find a better version of it). I tried to remove the background from the image then, but still I didn't get any photo of the possible species of this logo.
EDIT: this was the PHP bugs logo up until 24th July 2017; the next day it was changed to another different "bug". This question is about the former logo, not the current one.

It is an actual insect, Lethocerus americanus, also known as Giant Water Bug. See:

Matches the colors, body shape and small eyes and head. And yes, they are very annoying. As expected from real bugs. You know, like the first one.

Most probably it is Boxelder bug, since their other logo clearly depicts it as seen here
As per wikipedia

The boxelder bug (Boisea trivittata) is a North American species of true bug.
  Trivittata is from the Latin tri (three) + vittata (banded).
  Their congregation habits and excreta can annoy people; for this reason, they are considered nuisance pests.

Really, this bug is pretty similar to the one in my logo; the only difference I am seeing is the red coloration, but this can be a graphic design adjust for the logo; unhappily I was not able to find a better resolution version of that logo to compare the details...

Very light orange like coloration can be seen at back of insect in that logo too. Se their other logo which  clearly shows that insect

yes, you are right, in the other logo the coloration is pretty clear; I'll wait a bit if another answer comes, but I think this is the correct one. Thanks!


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Ugly people and genome
Why haven't ugly and dumb people been eliminated be evolution ? Why do they still exist despite Charles Darwin theory of natural selection.

This is essentially a duplicate of Why do some bad traits evolve, and good ones don't?

Perhaps alcohol?

"Ugliness" and "beauty" are not determined by two distinct genes. Environment also shapes body development. Fingerprints are heritable to a degree, but are largely shaped in utero by environment and the pressure exerted on them. Drinking alcohol during pregnancy can produce fetal alcohol syndrome, leaving "abnormal" features on the infant. Traits with low heritability can't be selected so easily, only genes that predispose to developing those traits.

Selection isn't the only evolutionary force. Genetic drift, where traits get fixed or eliminated by chance also occurs. Not everything in biology has to do with adaptation.

As long as there is variation on the traits you mention, there will be one person to call those at the low extreme of the spectrum dumb or ugly. This would be true even if the average IQ was around 200. So the question really does not make much sense!
One will note that directional selection reduces genetic variance but this is quite clearly not what the OP had in mind so let's not go down this path.
On top of that you are assuming that these traits are under selection. Typically, you are assuming that higher intelligence is necessarily beneficial which might very much turn out to be wrong. As a start you can have a look at the wikipedia article on the Flynn effect or this Skeptics.SE post.
You talk about "Charles Darwin theory of natural selection" please note that our understanding of evolutionary processes is much more advanced today than Darwin's understanding. We call our theory of evolution the modern evolutionary synthesis. If you are curious to know a thing or two about what this theory says, you can have a look at Understanding Evolution for example, a free and short online introductory course to evolutionary biology from UC Berkeley.


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Can one use dialysis tubing several times?
I would like to know, if one can use dialysis tubes multiple times. Or is there a risk of plugging the pores? I use the tubes for dialysis of a solution that contains a precipitated enzyme (183 kDa) and ammonium sulfate (132 Da). Thanks!

This is more of a long comment than an answer, since I don't know. It could be okay, but if you are unsure whether it will work, is it really worth the risk? Here are some thoughts:

With high AS concentration, there is an initial large influx of water which can stretch the tubing. If this is repeated several times you may stretch the pores to where they no longer retain your protein. You can determine yield after each dialysis to see if loss increases with use.
Clogging up the pores seems like it could plausibly happen. You could add some low molecular weight dye to monitor whether the membrane remains permeable with use.
Dialysis tubing costs like 5 ¢/cm. Unless you're using 10 meters at a time, it's really very cheap.


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Identification of Anoles
Can anyone help me identify these anole species? All photos taken on St. Thomas, USVI, in close proximity to one another.
(click to zoom in)

Each photo is a different individual, but the overall similarity makes me think they are likely the same species, although I could easily be wrong about that (the third one especially looks different from the others). They are dull brown overall with fairly subtle patterning, a light line that runs down their spine, bordered by a darker stripe on either side, and a broad band between the eyes. My best guess is that they are either Brown Anoles (A. sagrei) or Crested Anoles (A. cristatellus). Searching images online, there are some images identified for each species that are quite similar to these, but based just on comparison with those images, I really could go either way. Is there a definitive criteria to help narrow down the species?

Note: Usually I'd say that a single question asking for multiple identifications is too broad, but because I think these may be the same species, I felt it was appropriate to group them into one.

If they're not the same species. Whoever answers first, please make it a community wiki.

@canadianer. Looks organised. But they can't be zoomed in, looks like it would require some other markdown.


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When is it unacceptable to measure dry mass in an experiment to measure growth of plants?
I'm an A level student (British high school final year) and I was doing an exam question which asked for the design of an experiment to test the effect of light intensity on the growth of a certain type of plant. Here is the paper; it is question 2(c). The marking scheme can be found here.
As my measured dependent variable, I picked dry mass. However, the marking scheme specifically says to 'ignore dry mass' and asks for use of 'mass'. We were always taught that dry mass is the most accurate measure for experiments where we are trying to measure the effect of a certain parameter on the growth of plant. So now I am wondering - when is it unacceptable to use dry mass as a measured dependent variable in such experiments?
As far as my attempts extend, I tried determining what conditions we should use dry mass under, but I could not find any source that talks about detailed use of dry mass (when to use it and when to not use it).
Perhaps a different way to phrase this question is to ask: when do we use mass rather than dry mass? And when do we use dry mass rather than mass? As far as my knowledge extends, dry mass is the most accurate determinant of growth that there is, given that the plants are genetically identical. This is because it ignores the possible fluctuations that may be present due to fluid mass within the plants.

My guess is that because width and height of a plant are more greatly affected by light intensity, the dry mass has less relevance. If the plants were all the same size, and you wanted to know which plant is assimilating the greatest amount of substrate, then biomass would be okay. But,  you just want to know which plant is growing the fastest

Plus, do you really want to be the guy to dry an entire fir tree sapling? I think drying a flower might be easier

But the dry mass can also be used to determine which plants have had the largest amount of growth. If we start off with cloned plants of the same age (I learnt that this is always the correct way to start these experiments) and I know that I will end the experiment after around two weeks, why not use the dry mass? I am merely starting off with seedlings, so they will have grown to a fairly small size, hence we should be able to obtain their dry mass. Moreover, see my edit to the question.

It might depend on what we mean by "growth" though; actual production, or increase in vertical height ? In the latter case you could have some saplings growing faster than others due to different carbon allocation strategies and "dry mass" as a measure might not pick up on the differences.

@Rozenn Keribin, why do you say that dry mass may not pick up the difference in the rate at which the saplings are incorporating carbon? Isn't that NPP (the production of energy through biomolecules within the plants)? So it should indeed be picked up by dry mass.

@Mathematician I says that dry mass might not pick up the difference "in the latter case", i.e. if the variable of interest is increase in vertical height instead of production.