text:
Understanding genetic similarity in humans
I was reading "Blueprint" by Robert Plomin (online preview on webpage) and got stuck when I got to these two sentences in the prologue:
"We are the same as every other human being for more than 99 per cent of these 3 billion DNA steps, which is the blueprint for human nature." (page X)
"familiy members differ a lot genetically - you are 50 per cent similar genetically to your parents and siblings, but this means that you are also 50 per cent different." (page XI)
How does it fit together? Is he talking about different measures of similarity here?

If you search the site, I think you will find that this question has been asked before.

How can someone share 50% of their DNA with their parents yet all humans share 99.9%? is an even better duplicate.

Yes, these are different measures, and agreeably confusing. The "more than 99%" figure refers to pairwise distance. This figure (actually 99.9%) means that if you were to line up the 3 billion nucleotides of DNA from of any two people, on average, 1 in 1000 of these nucleotides would be different. Among siblings, this number would be even smaller. The 50% figure refers to the origin of DNA stands in a diploid organism: you get one exact copy of each of your genes from your mother, and an exact copy from your father. So half your DNA comes from each parent. But the DNA from each parent is still nearly identical. Siblings will get all their DNA from their parents, but for any particular section, they will get either their maternal grandmother's or grandfathers gene from their mother, and either their paternal grandfather's or grandmother's gene from their father.
For reference, you often hear that humans and chimps share 98% of our DNA. This is the not exactly a pairwise difference value, because it only counts changes in amino acids (http://humanorigins.si.edu/evidence/genetics). The amino acids between chimps and humans are about 98.8% identical to humans. The DNA across the whole genome is about 94% identical. There are about 50 genes present in humans that are absent in chimps https://www.genome.gov/15515096/2005-release-new-genome-comparison-finds-chimps-humans-very-similar-at-dna-level


text:
Osmosis/ Facilitated diffusion
Water can move across the (Semipermeable non polar lipid) membrane by simple diffusion (osmosis).
But polar molecules cannot pass through the non polar lipid bilayer, they require carrier proteins to facilitate their movement.
But water as well, is a polar molecule. How and why does it simply pass through the non polar lipid bilayer by simple diffusion and not by facilitated diffusion (i.e., through carrier proteins)?

@user1136 If you have an answer it should be posted as an answer rather than as a comment.

source: Stack Exchange

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text:
Do histones constitute the largest proportion of the protein in chromosomes at mitosis?
Do histones contribute more (by mass) than non-histone proteins in the chromosomes formed during mitosis?

I restructured your question in clear direct English, but wonder why this information is important to you.

If you are asking if histone mass represents a larger percentage of total chromosome mass then the answer is yes when considered at the level of the nucleosome. Each histone-octamer wraps ~147 base pairs of dna around 1.7 turns. The histone-octamer consists of  two copies of each of the four structural core proteins (H2A, H2B, H3 and H4). The sequence encoding for H2A histone family member B1 (H2AFB1) is 517 nucleotides long (RefSeq). Based on nucleotide length alone and inferring a consistent contribution to mass from nucleotides at the single base level and in triplet at the amino acid level, each nucleosome should be roughly 95% histone by mass. But this doesnt account for stochasticity in the mass and density due to DNA-methylation and to heterochromatin and euchromatin along the genome, respectively.
Consider DNA methylation, these features represent a non-zero contribution to total chromosomal mass that would decrease histone mass as a portion of the total and would not be considered if whole genome sequencing of a single organism was employed to answer this question at the genome level for a single sample. Now consider histone acetylation, this is another feature that represents a non-zero contribution to mass but swings the pendulum in the other direction. Beyond a local calculation at the nucleosome level this relationship would be nearly impossible to quantify.
During replication specifically, histone translation seems to be as tightly regulated as DNA replication.
Ma Y, Kanakousaki K, Buttitta L. How the cell cycle impacts chromatin architecture and influences cell fate. Front Genet. 2015;6:19. Published 2015 Feb 3. doi:10.3389/fgene.2015.00019
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315090/
nature has a great open source overview related this topic.
https://www.nature.com/scitable/topicpage/chromatin-remodeling-in-eukaryotes-1082

Does the 95% figure account for presence of variable-length linker DNA between the 147 bp canonical nucleosome cores?  If not then this would reduce the 95%, but I think your point would still stand.

It did not, it was a rough estimate using nucleotide sequence length as a metric of weight. Using the lengths of the sequences that encode the four core histone proteins H2A, H2B , H3, H4 in relation to the length of genomic sequence  wrapped around the complex the number is actually closer to 98 %
`>(2*(2223 +437+917+1077))/((2*(2223+437+917+1077)) + 147))

.9844527'
H3
H4
(https://www.ncbi.nlm.nih.gov/nuccore/NM_003517.2)
(https://www.ncbi.nlm.nih.gov/nuccore/NM_003528.2)

Something like 20% of the DNA is in linkers between the segments wrapped around the histones (here's a reference from plants http://www.plantphysiol.org/content/168/4/1406), so this would take the 98% down to 79%.

This furthers my point about the quantification only being possible at the nucleosome level. The linker segment is variable across the genome and represents another feature that prevents global quantification beyond the local nucleosome. Using your estimate of the linker region also incorporates a standard deviation associated with that estimate in nearly equivalent magnitude to the quantified region. Its a broader estimate of global proportion but greater uncertainty is associated with the estimate

"Genomics regions associated with active promoters/enhancers, marked by H3K4me1 and H3K27ac, contained the shortest spacing of 178 to 187 bp. By contrast, heterochromatic regions, marked by H3K9me3 and H3K27me3, contained the largest spacing of 205 bp in the human genome"
((2223 * 2) + (4372) + (9172) + (10772))/((2223 * 2) + (4372) + (9172) + (10772) + 147 +205)
Using the larger spacer value only drops the estimate to 96%

No problem @schokakola. Happy to help. It's a pretty deep rabbit hole with implications for potential experiments. If you find the answer helpful and sufficient, you can accept it and upvote it. Why are you insterested in histone mass? Or are you more interested in potential changes to histone mass during mitosis?

I am reinforcing the statement made by the previous answer. Yes, histones are the most abundant proteins in the chromosome (Ohta et al. 2010); they can contribute up to ~38% of the chromosome mass. Other abundant chromosomal proteins include toposiomerase-IIα and condensin-I (SMC proteins). Apparently many non-chromosomal proteins i.e. proteins that are not a structural part of chromosome but bind non-specifically to the chromosome, can contribute up to 12% of the total protein mass. Of the purely chromosomal proteins (68%), histones form ~48%.

  (D) The 28 classes of proteins found in chromosomes.
  (F) Estimated percentages of total chromosomal protein mass in the major classes of proteins.   From: Ohta et al. (2010)

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Which plant's part is this?

I found this plant in Rajasthan, India.
This sample is 4-5 cm long.
This is an ornamental plant. It was a potted plant.
I put my fingertip in the photo to give an idea of size of the specimen.
I can't figure out which plant this part belongs to.
Please give the species name if you can.
I would be very thankful to anyone out there who will help me.

This is a bit hard to say exactly, since there is a number of possibilities. We can be pretty sure that these sample is from a Cypress, belonging to the family of Cupressaceae, but which subfamily or species this is exactly, can't be identified here. Therefore a wider image would be necessary, but since this is a potted plant, even this might not be enough, as a lot of these plants are used in gardening.

Can u explain how one can figure out that this sample belongs to a cypress?

@Anonymous Members of the Cupressaceae family are the predominant group with scale (or scale-like) leaves. See here & Schulz, Knopf, and Stützel (2005) for more info.

Those scale-like green structures are likely to be the foliages of Platyclaudus species, they are attached densely on the branches of the plant. Hence the whole thing in your picture shall be the branch with the leaf from some kind of gynosperm tree.
It's common in Gynospermum the foliage is highly abbreviated and deformed(comparing to Angiosperm).

Welcome to Biology.SE! It isn't clear that this adds anything to the existing answer. In addition, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. Thanks!

It is called Leyland Cypress. For more details, refer the following link. https://en.wikipedia.org/wiki/Leyland_cypress


text:
Why are prions in animal diets not destroyed by the digestive system?
According to CBC:

Mad cow disease is the common name for a condition known technically as bovine spongiform encephalopathy, or BSE. [...] The only known source of mad cow disease is from animal-based feed contaminated with tissue from a diseased animal. The original source of BSE is believed to have been feed containing tainted meat from sheep with a related disease called scrapie.

As prions are proteins, I would expect any that were contaminating food to be broken down to amino acids by the proteases in the digestive system. Why does this not occur?

I have reworded your question which confused me so much originally that I downvoted it (now revoked). There is no question that prions are proteins, so my rewording focuses on the question of proteolysis during digestion.

Proteases are enzymes in your digestive system that help break down food, acting like molecular-sized scissors that cut up proteins.
Proteases have clefts, or subpockets, into which proteins fit, where the substrate (protein) gets cut.
Infectious or pathogenic prions are resistant to proteases, because of their three-dimensional shape, which hides away parts of the prion that would normally fit in proteases and which would cause the prion to be digested.
Prions that do not cause disease — normal prions — have a different three-dimensional shape that allow them to fit into proteases, and so they are not resistant to digestion:

A wealth of evidence contends that the infectious pathogen causing the prion diseases, also referred to as spongiform encephalopathies, is solely comprised of PrPSc, the pathogenic isoform of the prion protein (21-23). Both PrPSc and its normal cellular counterpart, PrPC, are encoded by a cellular gene (2, 19). Physical and molecular characterization of PrPSc and PrPC has failed to reveal any chemical differences between the two isoforms (32). However, PrPSc acquires distinctive conformational characteristics upon its conversion from PrPC. Whereas PrPC is soluble in most detergents and can be easily digested by proteases, PrPScis insoluble in detergents and maintains a protease-resistant core, designated PrP27-30, which polymerizes into amyloid (25).

Dr. Neena Singh also discovered that prions "piggyback" or attach to another protein called ferritin, as they make their way through the digestive system:

Disease-causing prions are thought to have passed into people when they ate beef from infected cattle, triggering the brain wasting condition called new-variant Creutzfeldt-Jakob disease, or vCJD. But researchers have not been sure exactly how prions enter the body.
To find out, Neena Singh and her team at Case Western Reserve University in Cleveland, Ohio, mimicked the process of eating and digesting infected meat.
They mashed up brain tissue that contained prions from patients who had a form of Creutzfeldt-Jakob disease. They then exposed it to a range of harsh digestive enzymes from the mouth, stomach and intestine, which normally break proteins into pieces.
Prions, which are known to be enormously tough, escape this attack almost unscathed, they showed, as does a second type of protein called ferritin, which stores iron and is abundant in meat. The two proteins seem to stick together, they report in the Journal of Neuroscience.
The researchers next added the digested slurry to a lab model of the human gut: a growing sheet of cells from the intestinal lining. By attaching fluorescent tags to the two proteins, they showed that they are transported through the cells hand-in-hand. "Prions probably ride piggyback" through the gut wall into the body, Singh says.

Attaching to ferritin may provide additional protection from digestion, insofar as this removes prions from the digestive system, where proteases are concentrated.

Proteolytic enzymes present in human body mostly catabolize the Alpha helical protein. Prions are Beta sheet proteins hence they survive during digestion.
(We also can't digest silk because it is made up of beta sheet protein)
A protein is very resistant (Biological molecule) towards the environmental conditions. As chances of survival for a protein coat virus is higher then a virus having lipid envelope in the environment.
When we intake a pathogen by food. The food is contaminated with thousands of pathogen. Digestion may destroy most of the pathogens but many get access to infect the person.

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text:
Chargaff Rules (confusion)
A professor of mine wrote that: $\frac{A+T}{G+C}$ is constant in double stranded DNA of different origin. However
The Chargaff rules state that due to base pairing in the DNA it holds that :
$A=T$ and $G=C$ and from that follows that $A+G=T+C$ in all DNA molecules
and thus: $\frac{A+G}{C+T}$ should be constant, no?
Who is in the wrong?

Was your professor talking about Chargaff rules or about GC content? Why didn't you ask the professor to clarify?

Constant in what sense? For all organisms? Please edit your question and make sure you recall correctly and completely what your professor said. And please, no ‘rules’ in any argument — just invoke what is known about the structure of DNA.

It states verbatim: for double stranded DNA of different origins it holds that : $\frac{A+T}{G+C}$ , the ratio is wrong, and the one I gave in my answer is correct, right?

Context is important.
A/T ==  1 and G/C == 1 (approximately, to within a measurement error) are Chargaff's rules for double-stranded DNA, occurring because A pairs with T and G pairs with C.
(A+T)/(G+C), or (G+C)/(A+T+G+C), are completely different ratios unrelated to Chargaff's rules. These are roughly constant across individuals for a given species and can be used to distinguish different species' genomes in an approximate manner.
I am not your professor, but it is possible in writing what they wrote, the professor was referring to whole-genome GC content within members of a species, in which case the professor is correct. If the professor was discussing Chargaff's rules, then the professor was wrong, but probably just made a mistake in writing: these things happen.

He states (verbatim): with double stranded DNA of different origin , the ratio $\frac{A+T}{G+C}$ is constant. Your answer doesn't really answer or help with anything , and just creates more confusion.

@schokakola I prefer to not just assume your professor is an idiot: in my experience, assuming people are idiots is counterproductive when other explanations exist. Thinking through multiple possible meanings is a good way to test your knowledge, so that was the intent of my answer. I've clarified my answer to make clear that if your professor wrote that ratio referring to Chargaff's rules, it is a mistake.

Read your "answer". It doesn't answer anything that I stated in my question. Do yourself and me a favour and stop replying to me please and let somebody who understands what I am asking answer instead!

@schokakola Can you clarify what exactly is still unclear to you compared to what you already know? "Your professor is right" or "your professor is wrong" is not an appropriate answer for Biology.SE, answers need to explain the concept and underlying biology.

I am asking whether the ratio I stated is correct or not. It's a very simple matter if you understand what I am asking. The answer is either yes or no. What you are doing is posting mindlessly anything that could peripherally have anything to do with the question in order to sound smart without answering the question itself. Stop.

Let me remind you of the Code of Conduct - I am being very patient with you because you are addressing me, but if you were addressing anyone else I would not have such patience. See also https://biology.meta.stackexchange.com/questions/3377/homework-questions

As I've said before. You not only didn't answer (or read and understand) my question, you intentionally added more confusion to make things MORE unclear just to sound smart. I don't want to have to deal with "you". I'm looking for somebody who is knowledgable in this area and can give a clear answer for which I'm very thankful.

@schokakola The answer to your question depends on the context. I don't want you to go to your professor and tell them they are wrong if they are actually correct but you misunderstood. Therefore, my answer gives two explanations: a case where they could be wrong (if they were in fact talking about Chargaff's rules), and a case where they could be right (if they were talking about something else). Now you'd have to go to your notes and find what the context was so that you know which one is the case. The only one here who is knowledgeable about what was said in your class is you.

If you don't understand the question, or it is unclear to you, then don't answer! Judging from your answers, you have no clue what I'm asking (you didn't even consider the ratio I gave because you are only interested in posting whatever you want to sound smart). After 100 comments, I still don't know whether the ratio I wrote is the correct one or not, instead you started a discussion about why I did or didn't ask the professor etc. etc. everything that has nothing to do with the question itself. Just save yourself the time and don't answer/reply if you don't understand the question.


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Why darwins, a measure of evolutionary change, is calculated on the log scale?
In a famous paper, Haldane is describing the idea of rate of changes in "darwins". Here below is the excerpt where he introduces the math about the concept.
Haldane, J. B. S. 1949. Suggestions as to quantitative measurement of rates of evolution. Evolution 3:51–56.

Now suppose that in time $t$ the mean length of a structure has
  increased from $x_1$ cm to $x_2$ cm, the mean value of the
  proportional rate of change
$\frac{1}{x}\frac{dx}{dt}$ or $\frac{d}{dt} (\text{log}_ex)$ is
$\frac{\text{log}_ex_2-\text{log}_ex_1}{t}$

I don't understand why he is arguing that the difference should be logged. Why can't you just use:
$\frac{x_2-x_1}{t}$?
What justifies this line below?

$\frac{1}{x}\frac{dx}{dt}$ or $\frac{d}{dt} (\text{log}_ex)$

Why not just using:
$x\frac{d}{dt}$?

The reason why there is a logarithm in the mean value is because the original equation has the form (1/x)dx/dt. The author wanted to remove the (1/x) factor by taking the antiderivative which is log(e)x and absorbing it into the dx symbol so they could rewrite dy/dt as Δy/Δt. Unless your question is why is there a (1/x) there in the first place?

If you have an answer for "why is there a (1/x)?" I'll take it! Is it because it is how you write a geometric mean with a derivative?

I don't think so. This isn't my field of study, but if r = growth rate = (1/x)dx/dt and if you rearrange that formula as rx=dx/dt then it takes on the form of the population growth formula x=x0e^rt maybe that helps?

There are several purposes for log transformations, but one of the most common that occurs in biology is when changes are relative aka multiplicative. See for example this answer from CrossValidated.
If I told you that one lizard has a tail 5 cm longer than another lizard, that doesn't actually tell you much about how different it is. If the first lizard had a tail 1 cm long, that's a pretty massive difference! If the first lizard had a tail that was 100 cm long, the 5 cm difference is pretty minor.
Taking the log shows this:
Big (relative) change:
$log_e(6) - log_e(1) = 1.8$
$6 - 1 = 5$
Small (relative) change:
$log_e(105) - log_e(100) = 0.049$
$105 - 100 = 5$
The simple differences are both 5, but the log differences show you a big change versus a small one.
Logarithms are also more convenient than ratios for rates of change because they are easy to manipulate to predict change over any time interval assuming a constant relative change over time.
Taking the 6cm vs 1cm example above, lets say we want to guess the change when only half of the time is elapsed. If we take half of 1.8 = 0.9 and solve the following for X:
$log_e(X) - log_e(1) = 0.9$
$X \approx 2.5$
So we'd expect after only half the time, the length would have been about 2.5 cm.
$2.5/1 \approx 6/2.5$ meaning that the relative change for each subdivision of time is equal.
You could try this for any dt, too, and plot out X as a function of time with any dt when you use logarithms. You can't do this directly with a ratio like "6/1" because you can't directly subdivide that "6/1" into smaller time intervals (trying to do so would take you into the world of logarithms again :) ).
test <- function(time,x1,x2) {
  out = exp(log(x1)+(log(x2)-log(x1))*time)
  return(out) }
time = seq(0,2,0.01)
plot(time,test(time,1,6),
     xlab = "Time",
     ylab = "X",
     type = "l",
     main = "Change in morphology through time")
points(x = 1,
       y = 6,
       pch = 21,
       bg = "black",
       col = "black")

Ultimately, what matters most is what thing you are measuring and how you want to interpret a particular type of change. For things like lengths or average counts, often a relative multiplicative change makes the most sense.

I did tested your example. Here is the script below in R.
y = x*2

(y)-(x)
log(y)-log(x)
test <- function(time,x) {
  out = exp(0.6931472/time+log(x))
  return(out)
}
plot(test(1:10,25),xlab = "Time", ylab = "X")``` It shows a reduction in X as time goes by, in an exponential manner. Is that what you were trying to say?

@M.Beausoleil Maybe something more like `test <- function(time,x1,x2) {
out = exp(log(x1)+(log(x2)-log(x1))*time)
}
time = seq(0,2,0.01)
plot(time,test(time,25,50),xlab = "Time", ylab = "X")` Starts at 25 at t=0, increases to 50 by t=1 (that is, the original time difference between x1 and x2), continues to increase up to t=2 at the same growth rate (that is, doubling every 1 dt). Function is the same as yours but I think its easier to interpret this time axis.

Another related point: plotting in log scale shows reductions in a better way. Usually, if the reduction appears to be smaller than increases for the same absolute magnitude of fold change. With log transformed data, your reductions will just be negative but the magnitude will not appear smaller.

I would also want to add that although log transformed data is easier for representation of relative changes (or in cases where the data span several orders of magnitude), it is difficult to say if effects of traits on fitness would be dependent on absolute differences or relative differences. For e.g. if the trait is growth rate: a small linear increase can magnify into a high fold change after several rounds of division.

This might help also: Why is it that natural log changes are percentage changes? What is about logs that makes this so?: https://stats.stackexchange.com/questions/244199/why-is-it-that-natural-log-changes-are-percentage-changes-what-is-about-logs-th

I don't know why this doesn't make sense, but when you look at it on the "linear" scale test2 <- function(time,x1,x2) {    out = x1+(x2-x1)*time   return(out) }  you get  test2(0,1,6);test2(0.5,1,6);test2(1,1,6)
test2(0.5,1,6)/test2(0,1,6);test2(1,1,6)/test2(0.5,1,6) . For the first time interval the rate approximately doubled  3.5 compared to the rate for the second interval of time 1.714286. Why is it the case? Basically, why is the "relative change for each subdivision of time is equal" not the same in the linear scale?

@M.Beausoleil What's the confusion? For the log scale, we've said the proportional change for a unit time is constant: increasing 6 fold for every 1 unit time (so from 1 to 6 and then from 6 to 36). For a linear scale, the absolute change is constant: +5 for every unit time. So 1+2.5 at time 0.5, 1+5 at time 1, 1+10 at time 2. If we want the relative change to be constant, we need to use a log scale (that's the answer to your original question about why Haldane is using a log). As WYSIWYG mentioned in a comment and me in my last paragraph, that's not always what you want, but often it is.


text:
Does anyone know what this purple plant is? (picture taken in Turkey)
Is anyone familiar with this plant species, picture taken in the Dalaman region of Turkey. It has large purple leaves.

This shrub is called Tradescantia pallida. You can read more about this shrub on this website https://florafaunaweb.nparks.gov.sg/Special-Pages/plant-detail.aspx?id=2521
I hope this helps you


text:
How does evolution explain the apparation of different group like: mammals, insects etc
When I am learning about evolution I barely see any source that explains how insects, mammals, reptiles and fish came to be. Can someone show me a source where I can learn about this? Especially insects and mammals - I want to know how those 2 distinct group came to be.
And I have a related question: can a fly evolve into a rabbit given enough time with the necessary condition? (I know the question sound stupid but please can someone explain me that)
I have a layman understanding of evolution. So please can any of your source or explanation be simple? Thank you.

Re a fly evolving into a rabbit, theoretically yes, practically no.  Insects (and invertebrates in general) made some evolutionary "choices" like having an exoskeleton & breathing through trachea that put serious limits on their maximum size.  (And vertebrates, particularly warm-blooded mammals & birds, likewise have limits on their minimum size.)  So to get a rabbit-sized fly (in Earth gravity & atmosphere) you'd have to make a bunch of major changes, with no obvious environmental niches for the intermediates.
But where the size limits and other constrants overlap, convergent evolution can produce remarkably similar results.  I think perhaps the best example is the hummingbird https://en.wikipedia.org/wiki/Hummingbird and the hummingbird moths https://en.wikipedia.org/wiki/Hemaris  They're about the same size, live in the same habitat with similar lifestyle, and from a distance are almost indistinguishable, yet evolutionarily speaking, they're about as different as animals can be.

Insects and mammals diverged from one-another over 500 million years ago. For most of Earths 4.5 billion year history, life was single-celled, or organized into colonies of single-celled organisms. Likely sometime shortly before the Cambrian, multicellular animals evolved. The first multi-celled animals were likely a kind of colony that was not differentiated into tissues. It didn't have a head, or tail, or look much like an animal. From these simple undifferentiated, multi-celled building blocks, came most of our animal phyla, during a burst of innovation called the "Cambrian explosion". At this time, one lineage headed down a path that would lead to insects, and another lineage, toward mammals. Although theoretically, it is possible, given enough time (as in billions of years) for a fly to evolve into a rabbit, this is highly unlikely. Evolution works with what it starts with and modifies it under natural selection to favor fitness. So having six legs and wings works pretty well for flies, and having 4 legs and fur works pretty well for rabbits. The hurdles to go from one form to another, given that these lineages are already well adapted, would be enormous. It was much easier, 500+million years ago, to go from one colonial lump of cells to a rabbit, and another lump to a fly. As an example of how evolution works with what it starts with, virtually all tetrapods (amphibians, reptiles, and mammals) have 5 digits on their limbs. This is because they share a common ancestor that did. Not because 5 is somehow special. Another example, humans choke to death because we share a common ancestor with fish, and fish share a tube that connects both the mouth with their swim bladders and their gut. Swim bladders were modified into lungs, but the common connection from our fish ancestors remains (a really bad design, but we are stuck with it).

The two groups that you mention belong to two separated branches in the animal kingdom. The fly and all insects are protostomes and the rabbit and all mammals are deuterostomes. In the first, the embryonic opening (the blastopore) becomes the mouth, while in the second, it becomes the anus. Wiki
At first glance, it seems like a simple difference. But it became a total change in terms of body structure and allow the appearance of animals whit the nervous system in the back, like us (insect have a ventral nerve cord).
In theory, it is possible for a population of flyes to accumulate the mutations to become something similar to a population of rabbits. All the intermediate forms should be viable and able to reproduce them self.


text:
What is this insect or lake dweller?

Found on my deck. We live next to a lake. Don’t know if a bird dropped it?  Not sure whether to save it?  Has scalloped front legs and a point from the end of what I think are wings. Antennae, mouthparts. Back legs either deformed or partly missing because can’t propel forward, just rolling side to side   I put it in a pen to keep it safe for now.

That is a mole cricket. Order Orthoptera, family, Gryllotalpidae https://en.wikipedia.org/wiki/Mole_cricket
I'm not surprised you live by a lake. They burrow in sandy soil or sand, often right up to the water's edge. They can fly, but spend most of their time underground. You do not need to save it, as it will find its way back to its home if you just let it go. They are not pests. They don't bite, or spread disease.


text:
What is the cause of "imbalanced" linkage disequilibrium?
With perfect linkage disequilibrium ($D' = 1, R^2 = 1$), you might have the following table of counts for the alleles:
    B     b
A  100    0
a    0  100

With "partial" linkage disequilibrium ($D' < 1, R^2 < 1$), you'll see something like this:
    B     b
A  100   25
a   25  100

But I've sometimes seen the following "imbalanced" linkage disequilibrium ($D' = 1, R^2 < 1$):
    B     b
A  100    0
a   50  100

What gives rise to this sort of situation, where aB occurs, but Ab never does? Is there a name for this phenomenon? Which is a better measure of linkage disequilibrium in this case, the normalized LD coefficient $D'$, or the squared-correlation $R^2$?

This can occur if the Ab genotype is lethal, i.e. you won't observe individuals with a Ab genotype.
Allele lethality is a common mechanisms that can explain non-mendelian inheritance of a trait.
For the question of which LD metric to use, this is tricky. Under the assumption that allele lethality is indeed at play, you observed perfect haplotypes, so D'=1 wouldn't be incorrect. Yet the correlation coefficient is also correct in the sense that SNP A is not a perfect proxy for SNP B.


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Can you identify this mold? (Aspergillus?)
I took some macro pictures (see below) of some black mold growing on wet straw. I noticed this creature that I think to be Aspergillus niger, but looks bigger than the one depicted in many pictures (the fruiting body is visible by naked eys) and since I am not an expert mycologist, I would like to ask the following questions:

Do you think it is Aspergillus niger?
If not what it is?
Is it dangerous (toxic/poisonous/infective) to keep it growing for the sake of making pictures?

Update. I am still getting this mold infection running on some of my cultures. Eventually, I managed to add some extra pictures.

Can you post the pic of growth? Normal shot not the macro one?

@AmodBhat Those are all the pictures I got. I trashed everything since a cloud of spores would be released after any vibration and I preferred not taking any risk. The first and the last pictures represent the colonies well though.

@AmodBhat Eventually, I got an ordinary pic of it. The piece of straw is about 4cm long.

I though it might be aspergillius niger also, but since it appears to be growing somewhat like a filament i would think it could be some sort of rhizopus. Aspergillus niger can produce mycotoxins (some strains) but generally it's safe. If it is rhizopus, the only health problem can occur if you're immunocompromized, but i'd be carful not to inhale or get near eyes. Also be careful not to spread spores (shaking, etc...). Mold can be persistent and hard to get rid of. Look into Rhizopus stolonife which is black bread mold.

@m4rio I am not convinced. The pic I find about Rhizopus are all microscopic ones. The fruiting bodies of this mold are visible with naked eye. Can you back up your conclusion with some pics?


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How does blood pressure substantially drop in the capillaries and arterioles?
Is this due to increased frictional resistance which decreases the velocity of the blood? You would think using Bernoulli's principle that the velocity of blood in the capillaries would increase due to the decrease in pressure but the inverse is true.

There are two main reasons why the pressure in the capillaries is lower than in the big arteries:

Arteries are elastic - they increase in diameter with every pulse, so the blood pressure is falling as the blood is moving along.
The total cross-sectional area of the capillaries is greater than the one of the big arteries.

Biology-pages.info

The pressure of arterial blood is largely dissipated when the blood
  enters the capillaries. Capillaries are tiny vessels with a diameter
  just about that of a red blood cell (7.5 µm). Although the diameter of
  a single capillary is quite small, the number of capillaries supplied
  by a single arteriole is so great that the total cross-sectional area
  available for the flow of blood is increased. Therefore, the pressure
  of the blood as it enters the capillaries decreases.


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Size distribution of all known species in the domain bacteria
I have found the smallest bacteria are around 200nm (e.g Mycoplasma genitalium an ultramicrobacterium) and largest are around 700um (Thiomargarita namibiensis). I am looking for a graph that illustrate the size distribution of all bacteria species. I have googled with no luck.

You can find the average size of all characterized bacteria. That information is documented but perhaps nobody thought that a plotting a size distribution is useful (especially if you consider all bacteria and ignore the habitat and demographics).

You say you are looking for a graph. I assume size is the variable you require on one axis. What is the other?

@David in x-axis average size and in y-axis number of species

Sorry if I gave you false hope of an answer. I had forgotten you wanted physical size rather than genome size. You certainly will be out of luck for "all" bacterial species, because in recent years the number has increased vastly from genome sequencing of uncultured species (e.g. in the gut) which have not been characterized physically. You might like to take a look at the abstracts of this recent Nature paper and this one to get an idea of the scale of this.


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I did an agar gel electrophoresis but I could not see DNA, why?
After performing a PCR, I ran the products (700 bp) in an agar gel electrophoresis along with a Genedirex ladder (100 bp), but the transilluminator did not reveal them.

Please give us information as to how your prep was done, because otherwise our guess is as good as yours.

Dinesh, could you take a photo of the gel? It would be helpful.

Assuming you loaded everything correctly, if you CANNOT see the ladder, you forgot to add EtBr. If you can see ladder but no product, then there is no product, or at least not enough. You can try to concentrate or amplify your DNA sample to increase the signal, if you have anything.

One common reason you can't see your DNA is because you didn't put any EtBr / GelRed into your gel. Do you have enough PCR product to run it on another agarose gel?

When i ran the same ladder(100 bp) again on the same gel i got ladder on the gel.

I think you should check if you added following two before loading on a gel

EtBr
Loading dye

Since you can't see the ladder either, amount of PCR products may not be the reason.

The same thing happened with me again this time i could see the loading dye but not the pcr product and ladder.


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Preparing sample for SDS PAGE
I have more than 10 cell lysate samples (70 µL each) whose concentration varies from 1.9 mg/mL to 4.8 mg/mL. I have 5X and 2X SDS sample buffers. I would like to prepare SDS PAGE samples in such a way that the final concentration of all the protein samples would be equal. I am struggling to deal with it.
What I know is while using 5X buffer, for 4 parts of sample we use 1 part of buffer to make it finally 1X. Similarly, for 2X buffer, we use equal amounts of buffer and sample to make 1X. Also, I would like to know will it be a problem if I make it more than 1X? Why we need 1X?

Usually you would want to keep the amount same, not the concentration. However, if you still want the concentration to be the same then you can add suitable amounts of PBS or your lysis buffer.
For e.g. if you have two samples with 1mg/ml and 4mg/ml concentrations and you want to load 20μg of total protein, then you can take 20μl of first sample and add 5μl of 5x loading buffer. For the second sample, you would take 5μl of the sample, 5μl of 5x loading buffer and 15μl PBS.

Why 1x?

Because researchers before us found this composition to be optimal (or just simply stuck to it as a matter of practice).

Would it be a problem if the final concentration of the loading buffer is more than 1x?

Apparently not, in my experience if it is up to 1.5x. Never checked higher concentrations.

Thanks for your answer. I want same concentration in order to load equal volume to the gel. I know it's the amount to be the same not the volume/concentration. But as I have many samples (10+) it's more convenient to pipette out equal volume & less error prone.

@Science123 Then you can use PBS to make up that volume. Usually, I do the concentration calculations on Excel. It is also convenient to calculate how much extra PBS to add, in Excel.

Yes. Exactly I used Excel because it is very convenient when we have multiple samples.

Your buffers come concentrated so that smaller volumes can be packaged, shipped and stored. They're intended for use at a 1X concentration, unless otherwise noted. So for example, if you get a 5X buffer then you should use an appropriate diluent to obtain a 1X concentration in the volume you need. This might be 5 mL (1 part) of 5X buffer into 20 mL (4 parts) of diluent to get 25mL of 1X buffer.
You would have to study the effect of using a more concentrated buffer in your process, but it can may affect your results, and it would certainly cost you more money.
A good question to pose yourself would be: If I use a more concentrated buffer for my SDS-PAGE, and there is variability in the results, how would I be able to tell if the variability came from the buffer concentration or not?
Instead, you can try bringing your protein samples up to the same concentrations first, and then dilute into your buffers as needed.


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Can consuming acidic drinks help kill bacteria in the stomach?
All around us we hear and read articles which suggest that soft drinks or carbonated beverages are acidic and damage our body but we still consume them (or atleast a significant proportion of us do). Why doesn't consuming such drinks during a bacterial infection in stomach help to kill all the bacteria?

The stomach is already full of gastric acid (pH 1.5 - 3.5). So anything that lives in the stomach must already be able to survive low pH conditions

@divibisan Thanks Man totally missed this point

I don’t know if soft drinks can help ward off bacterial infections in the stomach, however if you’re not taking antibiotics, other acidic compounds can be helpful for that. One of these is apple cider vinegar, you will find many videos on youtube about it. Another is betain-HCL, which is actually hydrochloric acid, the same acid we have in our stomach but it’s more expensive than ACV.
There is a big misconception regarding stomach acid problems and their treatment, and people should first check whether they have low or high acid level in their stomach, as both have almost the same symptoms. You can do that with a simple bicarbonate test.
I was diagnosed with mild GERD (gastroesophageal reflux disease), and I was surprised to learn that, contrary to popular belief, this common digestive problem does not arise from excess acid in the stomach but on the contrary from having too low acid, which causes the valve that we have at the bottom of our esophagus, called LES, to relax, so that the acidic content of the stomach goes up and reaches the delicate mucosa of the esophagus triggering the burning sensation, especially after a heavy meal.
Having low acid is something you want to avoid not only because you are more prone to digestive problems due to improperly broken down proteins, but also to infections - our food is not 100% sterile, bacteria are everywhere and even after washing or cooking there will always be some in our food, they don’t create problems to us simply because they get killed in the stomach.
The worst part of the GERD epidemics in the Western world due to excess and bad eating, is that doctors prescribe you acid reducers (so called proton pump inhibitors, they go with various brand names that contain omeprazole, lansoprazole, etc.) which further lower the acid content of the stomach. Doctors should know that, right? Well this drugs put you at higher risk of infections, given that in the long term they can lower the acid content in the stomach down to 5% of the normal level! Which is like inviting bacteria to a party. As if this were not enough, once you take them is very difficult to stop and get rid of their side effects, as there will be a rebound effect after a few days, with symptoms even worse than before you started the treatment, so you are literally bound to them. The only way to get rid of them is decreasing the dosage very slowly over a long period of time, usually months, while taking substitutes.
My doctor didn’t give me acid reducers, instead he told me that if I like soft drinks I can try coke zero, which has zero calories but still retains the acidity necessary to raise the stomach acid and help with digestion, and it works! Later I found that the same effect is given by apple cider vinegar and also vitamin C, aka ascorbic acid, and now I tend to prefer the vitamin over the rest.

The bicarbonate test in the video is not a reliable test for the lack of stomach acid. Acid is secreted during meals, but between meals you can have very little acid in the stomach. There's another video in which someone claims that GERD is caused by lack of gastric acid, but I have found any evidence from any reliable source. The question is if acidic drinks can kill bacteria. I have found no evidence that apple cider vinegar kills them. Can you provide links for your claims from reliable sources?

There is insufficient evidence to claim that soft drinks can kill microbes in the human gut; sugar in them could actually stimulate their growth.
Natural acidity of the gastric juice with pH 1.5-3.5 kills a lot of microbes (Medline Plus, Journal of Medical Microbiology). The pH of common soft drinks is 2.5-3.4 (PubMed, Fig.1). So, drinking soft drinks does not likely make the gastric juice more acidic.
According to one in vitro study, soft drinks can help to kill some bacteria (ResearchGate, 2015). In another in vitro study, they did not observe any antimicrobial activity of Coca Cola (Journal of Food Protection, 2007).

This article shows that carbonated beverages (Coca cola and Beer) have no direct bactericidal effect. However, these drinks may possibly increase stomach acidity.

Yes, OK; it's always some study will say something works and another study it doesn't. I'll search into it a bit more.

I'm a bit skeptical of that traveller's diarrhea quote... if a carbonated beverage is sealed from a safe source (e.g., a 20oz bottle of Coke), it's safe to drink but that safety has nothing to do with the acidity. If a carbonated beverage comes from a soda fountain it's local water mixed with a syrup. It would have to be acidic enough to kill pathogens present in the original water source, and if those pathogens can't survive 5 minutes in an acidic soda they aren't going to last any longer in the stomach. Am I missing something?

I deleted that part to prevent confusion, because the emphasis in the question was only on acidity not on carbonation.

Carbonic acid (H2CO3) itself in the human body is not stable and falls apart to water and carbon dioxide. When you consume anything by eating/drinking it and swallowing it via the gastro-instestinal tract, it does not enter your bloodstream directly but instead is filtered by various organs first and in many cases undergoes a transformation (First pass effect). In this case the main organ dealing with the drink would be the kidney.
So to answer your question more concisely: it is not stable, and it can not pass the apical cell membranes freely (especially in the proximal kidney tubuli). This is done by the body on purpose because if it could pass freely it would disrupt the pH balance (more specifically the bicarbonate buffer system) of the body. There are different mechanisms in the body that regulate this (look up any physiology textbook).


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Can you increase the microbiota in an insect?
I know you can suppress the microbiota of an insect with antibiotics, but I´m am looking for a way to increase it. For example, can I feed an insect with something that helps boost the bacteria like agar or something.

The answer is absolutely yes.
There are 3 main ways:

Faecal transplant: faecal sample from other insect could be
transplanted in order to colonize the gastro-intestinal tract
Injection of bacterial culture into the desired tissue
Use of functional foods to increase the abundance of specific bacterial
genus.

See this review for more detail


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Can two populations of the same species pollinate during different times?
My question comes from the Barron's SAT Subject Test Practice Test #1 question 2
It states:

Two populations of rhododendron, R. ferrugineum, grow in the same region of Connecticut. Although rhododendrons are able to cross-pollinate, these two population never hybridize. Which of the following is the most likely reason for this phenomenon?
A) Genetic drift has caused one populatoin to be betteer adapted than the other.
B) Self pollination is more advantageous because it increases variation in the gene pool.
C) One population produces pollen in early June when the pistils of the other population are not ready to receive pollen.
D)The two populations demonstrate convergence of two separate species over time.
E) The two populations fill different niches

The Barron's book says that the correct answer is C. Why? If the it's the same species, shouldn't they produce pollen at the same time?

Yes, they can.  Consider an original population that produces pollen over a fairly long time, and then something happens to select earlier & later times for different populations.  This is actually quite common for domestic plants such as fruit trees, where different varieties are selected (by humans) to produce fruit at different times.
As far as the question itself goes, it's more a case of the other answers being either obviously wrong, or not supported by the information in the question.

You are obviously right (+1). I do however find the answer peculiar, because I doubt how often this occurs in the wild. A much more logical explanation would be that the two populations are seperated by a mountain range or a desert (and afterwards the pollen time started to grow apart).

@RHA: I don't know how often it would happen naturally, though logically it could be caused by a random mutation, and like anything that produces reproductive isolation, would be the start of the two populations eventually evolving into different species.

given the number of imported or specially bred rhododendrons have two populations end up with different seasonal triggers is not unbelievable. Nowhere does it say they are native species.

@John: Good point!  You got me curious.  I don't recall rhododendrons as being native to the northeast, though apparently there are some.  However, the R. ferrugineum of the question is native to Europe, so ones in Connecticut would almost certainly be garden varieties: https://en.wikipedia.org/wiki/Rhododendron_ferrugineum  So now we can pretty well assume that the populations were selected for different bloom times by humans :-)

There are species native to the US appalachia https://en.wikipedia.org/wiki/Rhododendron_maximum but yes R. ferrugineum is invasive. Because of that the two populations could have two different origin events.


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What is the correct value of Neuronal Resting Potential - is it -65mV or -70mV?
Some books show the resting potential of neurons as -65mV, such as Neuroscience: Exploring the Brain, Fourth Edition (2016, published by Wolters Kluwer).

However, a majority of internet sites, including Wikipedia, show the resting potential as -70mV.
Which one of these is the correct value, and why is there this small difference?

This seems a rather specialized question. Why are you concerned about what you admit is a small difference? Does it have any practical relevence to your work? We would be interested to know.

@David I  was just reading about the resting potential of the neurons in the book mentioned above.The book uses -65mV in all the pages ,when i checked the internet ,it is -70mV everywhere.So i was curious.

@David Why are you concerned about what you admit is a small difference?  I am new to the field so i was confused.  ** Does it have any practical relevence to your work?**  No,I am not building anything,just reading only

Neither is incorrect. Neuronal resting potential is a function of the internal and external concentrations of ions and the conductance of the membrane to those ions via ion channels. Different neurons exhibit a range of resting potentials.
You can calculate the resting potential for a given cell using the Goldman Equation.


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Antibodies combine with antigens in the presence or abscence of macrophages?
There was a mcq in book that antibodies combine with antigens when.... And the correct answer was if macrophages are absent. As far as I know macrophages release interleukin 1 which stimulates T helper cells to release interleukin 2 which further activates b cells. Plasma clone b cells then produce antibodies.  With respect to that macrophages presence is important.   Kindly clear my confusion.

Could you provide more complete context about what your book is saying?

It wasn't from the text.  It was just an mcq.

I suspect there is further context to the question that would help explain your confusion, without it I can't say much. If it's just completely isolated then I don't think it makes much sense as a MCQ by itself.


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Can someone help me identify this larva?
I found this creature in my toilet bowl and very curious as to what it is. The main reason is I want to make sure this wasn't a parasite living in me.  Everything I've researched tells me this is some sort of fly larva, possibly a fungus gnat larva or a drain fly larva.  The fact that it has no long hairy like things makes me think it is not a pet flea larva.  This was in Southern California and it was almost exactly 1cm long.  Any help is greatly appreciated!

Singular larva, plural larvae.


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What allows grass eaters to digest cellulose?
Scientists are saying that it was a small step for the Panda to move from a meat diet to a grass diet. The article only refers to differences in the Panda's skull, presumably for better chewing.
I've also heard that the Japanese are able to digest Nori because they have the right gut biome because Nori has been part of their diet and the appropriate bacteria has developed over time.
Does that suggest that if the cellulose of bamboo and other grasses were pre-chewed by mechanical means and the right bacteria were introduced into the human gut that we would likewise be able to digest grasses?
Related story

fresh foods contain the right bacteria, especially if they are fermented of left to get a bit old in the right way. taboulet and grass salad after a few days would contain colonies of bacteria that digest grass and taboulet.

There are edible varieties of bamboo, which are used in Asian cooking.

You might find the answers to a similar previous question interesting:
Human Digestion of Cellulose?
Summary of those answers: It seems that some humans do host cellulose-digesting symbiotic bacteria, and do digest some of their cellulose.  According to Cellulose and the Human Gut, finely ground cellulose with low lignin content is most readily digested by humans who host the right bacteria.

Note if you read the linked answer humans digest an insignificant amount of the cellulse they ingest. The problem  is the human gut is to short and has nowhere to house the bacteria to allow long term breakdown. bacterial digestion is slow.

Hi John.  You might find the paper I linked interesting.  In some cases - e.g. the digestion of cabbage in some individuals - it appears that up to 75% of the cellulose was digested.

The only paper you link is about tiny amounts of a single type of purified cellulose It does refer to a paper that has little to do with digestion, cellulose need to be broken down and absorbed, that study never controlled for large intestine breakdown which is not absorbed. this is why some animals like rabbits use coprophagia to digest cellulose.  Cabbage is also a domesticated crop with low fiber content.

No there is something else missing besides bacteria
humans often already have the right bacteria but they don't digest most of the cellulose they ingest because digesting cellulose with bacteria is SLOW. Too slow to keep up with normal mammalian digestion. You need a specialized gut that  either has a large complex stomach to keep recycling the cellulose in the system (foregut fermenters) or has large storage chambers to keep the cellulose a long time and allow it to be digested slowly (hindgut fermentation).
humans have neither. To make matters worse Humans have huge caloric needs compared to other animals of the same size. Brains are calorie hogs and our brains are so large they consume 1/4 of all our calories. That is 3 pounds of our mass consumes a quarter of all the calories we eat. honestly without the advent of cooking (which drastically improves the caloric availability of food) human brains could never have reached the size they did.
Further reading
More further reading

What about panda bears? Do they have said requisites?

Just barely, that would by why they have to eat so much compared to other herbivores,  bears already have a longer digestive track than humans, and the giant panda has expanded the stomach and intestines further. but they are still only able to barely survive. https://www.theguardian.com/science/2015/may/19/hard-to-bear-pandas-poorly-adapted-for-digesting-bamboo-scientists-find Note human have a much higher caloric demand than an bear of the same size our brains are calorie hogs.


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Is drinking your urine an effective way to stay hydrated in a hostile environment?
There are quite a few stories about people trapped or otherwise incapacitated resorting to drinking their own urine in an attempt to stave off dehydration, ignoring the long term consequences, my problem with this idea is that the main cause of death when dehydrated is kidney failure, resulting from the buildup of urea and uric acid when the body can't package those chemicals with water to execrate them. Because of this, I'm tempted to assume that drinking your urine (without somehow purifying it) is a futile action as you are consuming both the water and the exact chemicals you need to remove with the water. I'm however not confident with this analysis, so any sources on the subject would be appreciated.

Drinking urine could help you stay hydrated a bit longer, maybe a day, but only when you are well hydrated at the start. You could get about 0.5-1 liter extra water this way. This doesn't work anymore when you start drinking urine the 2nd or 3rd day without water - the amount of urine will be very small and will be too concentrated at that time.
A man, drinking his urine has survived for 6 days under the ruins of the earthquake (Slate.com). However, people have survived for as long as 8 days without water or drinking urine: a 7 and 11 years old kids under the ruins of 2010 Haiti earthquake, and a 35 years old woman trapped in a lift.
According to Guyton and Hall Textbook of Medical Physiology:
...to excrete an average amount of waste products, let's say 600 mOsmols, your kidneys need to excrete at least 500 mL of urine, because they have a limited ability to concentrate urine.
If you drink 1 liter of urine with 600 mOsmols of waste products, you will need to excrete 500 mL of urine to excrete those 600 mOsmols and additional 500 mL to excrete 600 mOsmols from your normal metabolism. So, drinking 1 liter urine forces you to lose 1 liter of water, which means no water gain.
If you are very well hydrated at the time of first urination, your urine will be more diluted, so containing less than 600 mL of urine (minimally about 50 mOsmols/kg according to Wikipedia). Drinking such urine can provide net hydration, but your next batch of urine will be much more concentrated and will provide much less hydration. At the point when the kidneys need to excrete more water to eliminate the waste than you have drunk by urine, you will be in the negative water balance.

You may want to emphasise in your first sentence that this is only true if you are very well hydrated to start off with.

OK, I did......

Thank you, sadly a lot of people will just read for first sentence than downvote which would be unfair

Oh, I don't know. I actually don't want to encourage anyone to drink urine, to be honest; it's just to answer that it makes some logical sense, but then, one could vomit or get diarrhea after drinking urine, which would make dehydration worse. Also, most of those people who said they drank urine and survived, would probably survive without drinking it, anyway.

Under the vast majority of survival situations it is counterproductive, people do it and survive survive despite doing it. but under the super rare circumstance where someone is super hydrated the urine can be used to recover water, but as you said it is a small one time benefit that relies on you basically not needing the water in the first place.

I agree, and no medical or military guideline recommends it.

@Jan I thought I already accepted this answer, I'm sorry it took so long

@ShmuelNewmark...to me it's like "just now."


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Can someone identify this creature?
I discovered a few of these while cleaning an outdoor fish pond north of Sacramemto California. What is this?

Check the species ID tag info for some ways you can improve your species ID question to help get a good answer.

mayfly nymph of ephemoptera species

Wonderful! Now I will go intimidate my friends with this knowledge. Thank you!

This is a Burrowing Mayfly nymph (order Ephemeroptera), more than likely of the family Ephemeridae.  The Bugguide site has very few photos of nymphs, but you'll find a near miss here (the species shown is not Californian, but the related Ephemera simulans Walker, 1853 is; see here for other possibilities [you'll want to look for nymph photos of the species listed from "USA: SW"]).


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How to search for a DNA sequence in a genome on ENA (European Nucleotide Archive)?
I have to do a search for small DNA sequences in the genome of an organism in ENA. I have the accession number and project id. However, I can't download the whole genome because of the download size and would prefer to do it online if possible. I have a rough idea of the part of the genome I wish to scan in, don't know if that's relevant.

Do you want an exact match? Did you try BLAST? You can adjust the parameters according to your needs.

Have you already tried to submit accession number into advanced search? https://www.ebi.ac.uk/ena/data/warehouse/search

@WYSIWYG Yes I  do need exact matches. BLAST would search it against multiple sequences wouldn't it? I don't see how you can find DNA sequences in a particular genome using it

While it is much better/easier to download and do the exact search on your own, it is possible to do something similar, online. You can use NCBI-BLAST and increase the word length and mismatch/gap penalty. It also allows restricting the subject space; you can even align two sequences. The BLAST on ENA does not have much flexibility (subject restriction/word length). Perhaps you can look for a duplicate sequence on NCBI.
If this genome is available on UCSC genome browser then you can use BLAT too. However, it only accepts sequences larger than 19nt.


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What substances can selectively destroy certain cells?
Recently, I've watched a documentary about how, in the 1980s, people were buying and using drugs from the streets and then becoming paralyzed a few days afterwards. The drugs that they were using were contaminated with a substance called MPTP, which was able to selectively destroy dopamine-producing cells in the brain, essentially causing end-stage Parkinson's Disease, but leaving higher cognitive functions intact. Is MPTP unique in its ability to selectively destroy a certain type of cell, or are there other substances that can selectively destroy certain body cells while leaving the others intact? If yes, then by what mechanism do they work?


text:
What species of frog is this?
I was walking around outside my house when I found this little guy clinging to the outer wall of my house. The house in question is located in Indiana, United States. What is interesting to note is that the skin that is normally covered up by the frog's hind legs is yellow, but the rest of its belly is not, and this can only be seen when the frog is spreading its hind legs. You can see some of the yellow skin poking out from behind the left hind leg in the picture. This was at night, and the frog couldn't have been longer than an average person's index finger.


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Why we can't feel our internal organs?
We have lungs,kidneys, stomach etc.But why we can not feel them consciously?

We do feel some sensations in the internal organs; it depends on the distribution of the sensory receptors in them.
TOUCH
Receptors for touch are in the skin, outer ear canal and eardrum, cornea, nasal cavity, mouth, throat and upper third of the esophagus, trachea and bronchi, vagina and anal canal, but not in other internal organs. For example, you can feel the inhaled foreign object in the bronchi (cough reflex), but you do not usually feel the movement of the food through the gut.
On the other hand, you can feel the distension of the urinary bladder or rectum. Distension of other hollow organs may be perceived as pain rather than just distension.
TEMPERATURE
Temperature receptors are in the skin, cornea, tongue and urinary bladder (Wikipedia), liver and skeletal muscles (ScienceDirect).
PAIN
Pain receptors (nociceptors) are in the skin, surfaces of the joints, joint capsules, synovial membranes and ligaments, tendons, blood vessels, periosteum, endosteum; other organs, such as the gut and muscles, have fewer pain receptors (Health24.com, McGill University).
Within the skull, pain receptors are in the pia and dura matter and their feeding vessels, and small cerebral vessels but not in the brain parenchyma (PubMed, McGill University). This explains why brain tumors cause pain only when they invade blood vessels or other pain-sensitive structures or when they result in increased intracranial pressure (Hopkins Medicine).
In the hollow organs (esophagus, stomach, intestine, gallbladder and bile ducts, bladder, ureter, urethra, uterus) pain can be due to their distension (ScienceDirect). This is why a stone in an ureter can cause pain
 (Clinical Methods, NCBI).
In the muscular organs (the skeletal muscles, heart, stomach, uterus, intestine) pain can be due to ischemia (WebMD).
In the parenchimal organs (liver, spleen, lungs, pancreas, kidneys), the pain does not arise from the parenchyma, but from the blood vessels in them or from the distension, inflammation or injury of their capsules or membranes (Scielo.br). This is why cirrhosis with a shrunk liver usually doesn't hurt, but hepatitis with swollen liver (and hence distended capsule) does (MedicineNet).

note much of our digestive system has some of those, temprature and pressure mostly.

@John, in most of gastrointestinal part (except in the mouth, throat, upper esophageus, rectum and anus), you do not feel food or hot water or normal (physiological) distension.  You can feel pain from excessive distension, as I mentioned.

I updated the answer.


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What brazilian snake is this?
(1) Is it possible to identify the snake in the picture below?
If (1) cannot be answered:
(2) In view of the pattern of colors, is it possible the snake in the picture below be non-venomous? If so, what kind of non-venomous snake?
Additional informations:

Size: 62cm.
Region: South of Brazil, noutrh of Paraná.
I do not have a picture of the head.

Pictures:

The triangular pattern and the lightly colored underside resemble typical patterns of Bothrops (lancehead viper). Without the head it is quite difficult to tell which species this is. Given the location, the most common lancehead viper would be Bothrops jajaraca, simply called Jararaca by the locals.
Images can be found here


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Mushroom Identification: White mushroom growing on tree (South America)
Near the place I live in I noticed a little white mushroom growing on a tree trunk (a dead palm tree). I was curious to identify it, but from the little I learned so far white mushrooms are the worst to identify. I’m on Brasil, near the tropics in an Atlantic Forest predominant area, and I haven’t yet found a field guide for my region (if anyone knows any, or a field guide from a region that grows similar mushrooms I’d love to hear suggestions).
Also, I'm very novice when it comes to mushroom identification (still learning the basics), so if I missed some important characteristic, or misinterpreted something that can be spotted in the pictures I'd love to hear it. The whole point of identifying this mushroom is learning.
Below are some characteristics I noticed and some pictures from the mushroom:

Region: Brazil southeast coast, state of São Paulo, predominantly Atlantic forest
Grows in very small colonies, but every fruiting body comes from an individual point (No Cespitose)
Presence of Volva
No presence of partial veil (No Annulus)
Pileus Color: White with some brown spots
Stipe Color: White
Wasn’t able to get a spore print, but when it grew old (at least I think that's what happened) and shrunk it looked like the spores where brown as can be seen in the pictures
Narrows gills? (The fruiting body is small, so maybe relatively speaking it isn't narrow)
Fruiting body leaves white stain in wood
Margins of the Pileus are cracked

There's a new colony growing, so I might be able to collect a sample once it grows big enough and gather more information, as a proper spore print, since my guess of the spores being brown might be a mistake (maybe those brown things in the dead mushroom are not spores).

Pictures:
Older colony

Recent colony

Shrunk fruitbody

Does it have a hollow stem? stem and cap size? The gills are like a Marasmiellus, and it's larger. A image of the gills in daytime and perhaps a lengthwise cross section would be cool. What's the region? There are s many more species of tropical mushrooms.

@com.prehensible Not sure about the hollow stem (would have to wait the new colony to grow so I can get a sample). Cap was about 1.5-2cm in diameter on the bigger ones, stem also about 1.5-2cm long. I'll update the question with a more specific location: it's Brazil southeast coast, state of São Paulo, on an area that is predominantly atlantic forest. Can you indicate a good field guide for this region? By the way, I looked at some pictures of different Marasmiellus species and some do look very similar to the ones growing here!


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Can one assess muscle strength through imaging (e.g., MRI)? If so, though which type of imaging and how accurate is it?
Can one assess muscle strength through imaging (e.g., MRI)? If so, though which type of imaging and how accurate is it?
On How does muscle size relate to strength?, I read this answer from  Moses (mirror):

Strength training will increase the size and quantity of myofibrils, and subsequently increase the size of the respective muscle fibers; this process is called hypertrophy, and it results in larger and stronger muscles.

As a result, I assume that a medical imaging processing the physical strength of a muscle should assess both the size and quantity of myofibrils. That being said, it can be easier to assess the size as an approximation of strength, and if so, I wonder about 1) the quality of such an approximation 2) how to measure the size of a muscle that what cannot directly easily measured with a tape ( e.g., gluteus minimus or piriformis).

Direct measurement of muscle strength something isn't possible or advised, e.g. if the tendon is injured. Also, some muscles are difficult to isolate when testing. In the case of a tendon injury, assessing the muscle strength would be useful to find a good balance between muscle strengthening and tendon recovery.

Can you please add some details on what parameters would you consider for "strength"? Different imaging techniques can measure different parameters.

@WYSIWYG Thanks, I am interested in any parameter that has an effect on the muscle's physical strength.

To the close voters: this isn't a homework, and please let me know if the edit I made satisfy the "attempt at an answer" requirement.

@FranckDernoncourt The answer linked from Fitness.SE as well as the second answer on that question both make clear that there is a correlation but not a particularly strong one between muscle size and strength. It's unclear to me why this question is even relevant when there exist both simpler and by definition more accurate ways to measure muscle strength directly that don't require expensive medical scanner time (which is also valuable for diagnosing disease and injury).

@BryanKrause Direct measurement of muscle strength something isn't possible or advised, e.g. if the tendon is injured. Also, some muscles are difficult to isolate when testing.

@FranckDernoncourt Why would you be interested in muscle strength when a tendon is injured? What is the point of assessing the strength of some particular muscle independent of some real physical output (like the amount of weight lifted, the velocity of a thrown ball, etc)?

@BryanKrause E.g. to find a good balance between muscle strengthening and tendon recovery, in the case of a tendon injury.

One of the criteria for good SE questions is "You should only ask practical, answerable questions based on actual problems that you face." - I think your question would be better received if you situate it in the context of injury recovery in which case the measure of interest is probably not 'strength' per se but some measure of health, if that is what you are interested in. It would also be beneficial for you to do some further research on your own to properly scope the question.

@BryanKrause Thanks, sounds good I edited the question to mention the use case. The measure of interest is strength though, as the muscle itself is healthy, and muscle strength is often regarded as an important factor during tendon recovery.


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What structural features make a molecule a potent opioid receptor agonist?
For instance, take morphine. It is used as a baseline for measuring the potency of opioid agonists. Its structure looks like this:

But then, take heroin, around three times as potent, its structure is this:

6-Monoacetylmorphine is around 30% more potent than heroin itself:

If, however, the acetyl group is bonded to the top instead of the bottom, the resulting substance is less active than heroin.
U-47700, a research chemical, has a totally different structure but has around 7.5 times the potency of morphine in animal models:

Desomorphine is 8-10 times more potent as morphine:

Oxymorphone is 10 times as potent as morphine:

The common explanation that I've heard for these substances being potent opioid agonists is that they mimic the endorphins produced in the human brain. However, Beta-Endorphin is 18-33 times more potent than morphine, and its structure is thus:

That looks absolutely nothing like any of the substances mentioned above. How can molecules with structures so radically different from those of endorphins mimic the action of endorphins? And how come U-47700 has a potency similar to the more powerful morphine analogues but looks nothing like them?
But then, there's Fentanyl:

100 times more potent than morphine, making it a more powerful Opioid receptor agonist than the body's own endorphins, and its structure looks nothing like them or any of the other ones so far. Other analogues are even more potent. So what is it about a molecule's structure that makes it a potent opioid? The only structural similarity that I can spot is the presence of a tertiary amine group in the structure. And how does U-47700 have a potency similar to the more powerful morphine analogues?

Are these comparative numbers you report receptor affinities? Or bioavailability?

I could only find receptor (relative) affinities reporte in much less concrete form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3555047/table/tbl2/

Specific parts — moieties — of an agonist molecule bind to the receptor protein, causing the receptor to change shape, which in turn initiates a signaling pathway inside the cell.
Some agonists are better at causing the receptor to change to its "optimal shape" for relaying signal. These are called "full agonists".
Other agonists cause a partial change in receptor shape and reduced signal. These are called "partial agonists". The strength of the resulting signal is called "efficacy".
In addition to differences in efficacy between agonists, the parts of the agonist that bind to receptors can have a different chemical makeup and so create a different environment of electrostatic attractions and van der Waals forces between atoms in the agonist and in the atoms in the binding site in the receptor. Agonists that bind more strongly will stay bound to the receptor longer. These are said to have higher "affinity". Agonists that bind more weakly have lower affinity.
It is affinity and efficacy together that determine potency, or how well an agonist works.
In a biological environment, as well, these agonists swim in a pool with other agonist and antagonist molecules. For example, your agonist of interest might do a good job of changing a receptor's shape, but if it binds weakly, it will "pop off" the receptor quickly — perhaps too quickly to trigger the necessary signal. Another, different agonist molecule comes in and binds more tightly, but it doesn't create as strong a signal. Or perhaps a passing antagonist molecule floats around and pops onto the receptor, stopping any signal from that receptor and also keeping any agonist molecules from binding again for a while.
The population of agonists, antagonists, and receptors all change the number and kinds of binding events that take place, which determines whether you get the signal you want, as strong as you want it.
While the opioid molecules you are looking at have different numbers and varieties of atoms, it is the molecule's shape and electrochemistry that matter. Most specifically, it will be the part of the agonist molecule that actually binds to the receptor that matters most: how well it causes a conformal change in the receptor, and how strongly it binds.
These molecules could look very different from one another, but ultimately it is the part of the molecule that binds to the receptor, and how well it binds, that matters.
I don't know about the receptor-ligand kinetics of how different opioids bind to pain receptors, specifically, but hopefully there is some terminology in this answer that helps with further research.

Another point that can be very important (not sure about this particular case) for the potency of drug/pharmacological molecules is its Pharmacokinetcis: drugs have to pass from their entry site through various organs until they reach the point where they are active and the efficiency of all these 'steps' is also determined by chemical properties & structure.

@Nicolai I believe I read a paper that attributed almost the entire difference for fentanyl to PK, so perhaps quite relevant indeed.

That's an excellent point and should make a great answer!

@BryanKrause: actually fentanyl has very low oral bioavailability, that's why it's injected/sprayed/patched. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3555047/

@Fizz Is that bioavailability based on plasma? The thing about fentanyl that makes it potent from a PK standpoint is lipophilicity such that it partitions into tissue like brain. I could be wrong though.

Ah it's because of first pass liver metabolism. In any case, check out the table you linked in another comment. That shows the partition coefficient differences (which that paper says little about...) I was referring to, where fentanyl stands out a bit.

@BryanKrause: you're probably correct. The issue I'm seeing is that the OP didn't really say what his relative "potency" numbers were. (See my comments under this question.)

@BryanKrause: It thinks his potency number are based on DEA data. So maybe someone can answer: https://psychology.stackexchange.com/questions/23232/when-the-dea-says-a-drug-is-x-times-more-potent-than-another-what-do-they-mean

@Fizz Those potency numbers are commonly reported by clinical effect. They are referring to the (probably IV) dose required to get a similar pain relief effect to equivalent morphine. Partly why they are ranges and not more specific values. The remaining biology question is what actually causes the differences, and simple mu receptor affinity is not sufficient to explain it. So people argue about partitioning, effects on other opiod receptors, effects on non opiod receptors, etc.

I think you are confusing potency with receptor affinity.
The (unsourced) numbers you indicate appear to be DEA-style "potency", which probably refer to the effective dose (of some kind).
The fentanyl to morphine ratio on the κ-opioid receptor affinity, from human studies is only 1.35 to 1.14 (on average). In contrast the N-methyl fentanyl is estimated from animal studies to have a receptor affinity of around 18,000 (±3,000).
As pointed in the other answer, there numerous other issues besides receptor affinity that affect potency, like bioavailability by the various administration routes.
Receptor affinity alone is somewhat easier to deal with (e.g. in computational chemistry models), e.g. by "molecular docking":

Molecular docking, a type of virtual screening, places compounds or ligands into potential binding poses within the binding site of a biological target and assesses binding affinity with a scoring function. The scoring function evaluates the non-covalent interactions between the ligand and target to provide a binding energy (score) which can be used to rank compounds with increasing binding affinity

It's actually quite difficult to measure receptor affinity in practice; there's a large margin of error, better shown in this graph, from the source that that previous table is based on for human studies.

Also there are three opioid receptors to worry about. (The graph above is for μ.)
I think the reason why fentanyl (and its derivatives) is stronger than morphine in analgesic test is/are largely unknown. According to a 2014 paper

A large number of fentanyl analogs have been synthesized and structure activity relationships revealed, but the knowledge of their action is still incomplete and many questions remain unanswered. In general, the order of activity at receptor parallels that of binding affinity. However, the comparison of ED50 values, for μ- analgesics with their IC50 and Kd numbers at the corresponding binding site does not always correlate with experimental data. How to explain, why fentanyl (6), methylfentanyl (42), sufentanil (88), lofentanil (82) are more potent than it would be suggested from obtained binding values. Another example, the Kd of ohmefentanyl for the μ- site is approximately 5–10-times less than that of morphine, but it is nearly 7000-times more potent than morphine in analgesic tests. There is another contradiction, absence of correlation between lipid solubility and analgesic effect [195,196]. Another observation is that **in general fentanyls are compounds with the highest affinity for the μ-receptor and the most potency at that receptor. However not all fentanyl derivatives are highly μ- selective. They also produce actions through δ- and κ- receptors. Lofentanil (82) is the least and R30490 (90), are the most μ-selective compounds, among fentanyl series. Although their structures are very close, and affinities at the μ-receptor are similar, R30490 displays much lower δ- and κ-affinities than lofentanil.


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What is this tree growing in my town?
Can anyone tell me what kind of tree this is? I took this picture today. It's in Iowa City, Iowa.

Have to see the bark to know, it looks like a fruit tree, perhaps an ornamental apple or cherry tree.

@com.prehensible I added a picture of the bark, as you requested. Also, thank you!

It looks like a white crab apple or an obscure cultivar of apples, of which there are many.
The best identifier will be the fruit. Because there are not millions of flowers, It looks like there may be less fruit and bigger than a crab apple, although it varies by year.
The fruit of crab apples are small apples which can be used to make jelly. Crab apple trees can grow to 10m, a lot bigger than table apples.
White flowering crab apple:

https://en.wikipedia.org/wiki/Malus
comparison images.


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What is tissue gel?
My book consists of following lines."The interstitial fluid is entrapped in minute space among proteoglycan filaments. This combination of proteoglycan filaments and the fluid entrapped within them has a characteristic of gel so called tissue gel.  Instead of flowing interstitial fluid mainly diffuses through gel.  This diffuion allows rapid transport of interstitium of water nutrients,oxygen,cell excreta e.t.c.
I can't get the meaning of these lines.  I tried to search on net but didn't get a satisfactory explanation.  Please explain this to me.

In the question, "tissue gel" clearly refers to "proteoglycan filaments and the fluid entrapped within them" and which appears in the interstitial space.
This is the same as what the Wikipedia article says about Extracellular matrix:

Gels of polysaccharides and fibrous proteins fill the interstitial space and act as a compression buffer against the stress placed on the
  ECM. (Source: Essential cell biology, 2004)

A.C, Guyton et al from University of Mississippi School of Medicine, 1973 also says the same:

Though 1/6 of most tissues is composed of interstitial fluid, this
  fluid is generally held tightly in place in the form of a gel. The
  reticulum of this gel is composed mainly of hyaluronic acid, but this
  is cross-linked slightly with collagen fibers to form a meshwork in
  which the interstitial fluids are trapped. The presence of this gel
  reduces the mobility of fluid in the tissues...

The exact term "tissue gel" is very rarely used in biology or histology, though.
You are probably confused because of this sentence, which is messed up: "This diffusion allows rapid transport of interstitium of water, nutrients, oxygen, cell excreta e.t.c. " It should be: "This diffusion allows rapid transport of water nutrients, oxygen, cell excreta e.t.c. through the interstitium."


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difference between population genetics and genomics
I don't have a biological question therefore, this might be be quite basic. But I want to know does genomics entail population genetics or these are completely different fields?

Did you read the wikipedia entries for these two terms? Can you add them to your post and comment on what is unclear?

They are different. Genomics is the general science of sequencing whole genomes (or sometimes, the majority of the genome, or all the protein-coding genes, as in transcriptomes). Population genetics uses molecular data (usually DNA sequences, but not always) to make deductions about the characteristics of a population, or the relationships among biological populations. Genomic data could be used to draw conclusions about population genetics, but genomics can be used in many other sciences, and population genetics can be performed with other kinds of data besides genomes.


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Can any one ID my tortoise?
I have got a pet tortoise and I was wondering if any one could identify it. I think it's a male around 2 years old.
I'm not quite sure, it is quite small, very shy and goes very fast.
He likes carrots, pears, apples and tomatoes.
At the bottom of his shell there's sum light orange color.
Basically light line of orange on each side but only on the bottom of his shell.
If this helps at his last owner house he was bitten by a dog and his shell was repaired by a local farmer with fibreglass.

For getting more accurate answer I would add some more details like if you found the tortoise in the nature or if you got from another way. Telling which country you're living would also add better match if you found it in the nature. For me it looks like a Hermann's tortoise but as I am not specialist, it could be another one from the Testudo family (or even another if yours is not coming from Europe).

Normally for determining the gender, i think it's the length of the tail which differs. I would add one more picture with the tail fully out. The end of the tail can also detarmine the family / genus of the tortoise.

Another point about size: it is quite small is very subjective and as they grow very slowly, the specimen you shows does not look so small. If you can just put how many Centimeter (or Inch) it is (ideally length, width and high) it would also help other people to have a better estimate.