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Why have ground beetles never evolved the ability to get back up?
This may seem like a funny question, but I've seen so many ground beetles upside down on the floor and wondered why they've never evolved the ability to get back up. Wouldn't something like this drastically increase their survivability?

Welcome to Biology SE! This is a variation of a more general question that is often asked in this site: Why do some bad traits evolve, and good ones don't?.

By "floor", I'm assuming you mean a smooth floor like that inside a house or building.  I imagine that these beetles are actually quite good at flipping themselves over when they have something to grab onto -- e.g. a blade of grass, a fallen leaf, etc.  The detritus-free environment that is the modern indoor floor (or smooth path, or paved road) is not part of the natural niche of these organisms, and encountering such surfaces was uncommon in their evolutionary history.  Rare encounters are weak selective forces.

Normally, if a healthy bug is knocked onto its back, it can use its legs to rock on its sides until it rights itself. If, however, the bug can't roll back onto its abdomen because it has become too weak or because its nervous system isn't functioning properly, it remains stuck on its back.
An injury, a compromised nervous system due to pesticides or a lack of food or water can also reduce a bug's ability to right itself. Or the bug could simply be at the end of its lifespan and its strength and coordination abilities are declining.
references:
https://www.livescience.com/33334-dead-bugs-lying-on-back.html
https://www.thoughtco.com/why-do-bugs-die-on-their-backs-1968414


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What causes change of sex in certain monoecious plants such as Papaya?
certain male flowering plants can be converted to female flowering and fruiting such as Papaya plants by just insertion of an iron nail in their/it's stem near it's roots? How can iron nail alter it genetically from male to female? Biochemically  what causes change in sex of plants from male to female?

Might be useful to provide more background or links to what you're talking about.

Please see edited 1... I've sited link to one similar observation, It's common gardening technique. When we plant papaya plant from seeds over ninty percent of plants are male. But when they grow to a desired height gardner either mercilessly prunes large number of leaves or inserts a iron nail in the stem near the roots. Most of the time this might result in conversion from male flowering plant to female flowering plant and fruits can be obtained. This technique may or may not work for other monoecious plants.

@user240988 please [edit] your question to include all necessary details instead of replying in comments. Comments are not searchable and can easily go unnoticed. Therefore the question body should be complete in itself.

@user240988 The scope of the question "What causes change in the sex of plants?" is too generalized. An answer can be provided for "What causes papaya trees to change sex from male to female?" But the phenomenon can not be generalized to "plants" as a whole, as most plants don't and/or can't change sex, nor is it bi-directional even in the case provided as an example. Can you be more specific in your question?

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What causes the elongation of Genome down the evolutionary time line
Theory of natural evolution says that complex life forms arose from simpler ones e.g. starting from Eubacteria to modern day multicellular eukaryotes. {If we try to reduce these changes happening at molecular level, it should be like, from Eubacteria like E.Coli. (20 kilobasepair genome/DNA strand size ) evolving, over time, to Multicellular Eukaryotes ( 3 Gigabasepair genome size) e.g. (humans and other hominids.)}
Now if we see molecular changes happening inside cells, the molecular changes are within nucleus as extra nuclear changes are largely function of nuclear information (and a smaller extent external stimuli). For biochemical changes to take place inside cell Nuclear information is the major guiding force. But according to Central Dogma elongation of DNA shouldn't have happened as there is no scope for it in either doubling, translation or transcription. But actually it is not so according to evolution. So what allows changes to be imbibed in the DNA that also increases it's length ?

Your question is unclear. One interpretation is that you think there is some principal of nature that would prevent DNA elongating, and you perhaps also think this is Crick's mistakenly-named Central Dogma. There is no such principle, and Crick's Central Dogma was that molecular genetic information transfer could proceed from DNA to RNA to Protein, but not from Protein to RNA or DNA. Regardless of what Crick said, gene expansion is known to occur and the mechanisms involved are understood and can be found from an internet search. Or did you mean something else?

@iayork — You can say that the word Dogma was ill-chosen (Crick admitted he misunderstood the meaning of the word) and that it is dangerous to give students the idea that there are dogmas in science. Or you can say that the concept is so obvious now that we know the mechanisms of gene expression that it is difficult to justify teaching it as such. However the expression "outdated concept" suggests that it is incorrect. It is not. Suggestions about the nationality of the OP and the teaching of science in India are not relevant, and I suggest you think about withdrawing them.

Yes exactly if information flows from DNA to RNA to protein and in no way from protein towards DNA than how come the changes that happened in external environment (that should mostly affect cellular cytoplasm and not nucleoplasm) went to the DNA and made such changes that started getting reflected in offsprings of the organism (as adaptation to the environmental change that happened). More intriguing is the fact that Nuclear DNA in modern primates have genome size of up to three gigabase pairs but there is no mechanism described that elongates the DNA.

DNA misreplication events can lead to accidental duplication of DNA (even the entire genome), misalignements in recomibination events, integration of DNA from extracellular sources e.g. viruses. All these events can lead to large scale changes in the genome size of an organisms, smaller scale changes can be insertions and deletions in the DNA from repair pathways such as non homologous end joining.

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Which species of rotifer is this?
If found this in a moss sample.

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Also, for [tag:species-identification] questions, please be sure to include all relevant information mentioned here (which you saw when typing the question). specifically, please at least add an approximation of size of your specimen and indicate where you took your sample. Thanks.


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Why is the Tm defined as the temperature at which 50% of dsDNA has changed into ssDNA?
In molecular biology, Tm is defined as the temperature at which 50% of dsDNA is converted to its single stranded form. Intuitively it would seem that the melting temperature should have been defined as the temperature at which the entirety(100%) of the dsDNA converts into ssDNA. What is the basis of using this ratio, i.e, 50% in the definition of Tm?

If you search for DNA melting temperature plots you will see they have a sigmoid shape. It's common for those kinds of plots to be described by the 50% value for example the therapeutic index and the 50% lethal dose of a substance (LD50). This is because at really low and really high temperatures all DNA molecules become dsDNA or ssDNA respectively so that information is not really useful. You could maybe talk about the first temperature at which DNA becomes 100% denatured but the curves are highly nonlinear at that region so it's difficult to quantify. The 50% is an easy way to compare different molecules since that region is usually linear and easy to compare in a meaningful way (basically all molecules have the same ends of the sigmoid shape, but it's the middle part that changes the most).

The point to emphasize is that in both sigmoid or rectangular hyperbolic curves (for MM enzymes and many ligand-binding cases) you never actually get to 100% until infinity — the curve approaches it asymptotically. So you can't measure it acurately. You need a mathematical function that can be measured and will differentiate different cases. A figure would help.


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If bond break absorbs energy, why ATP hydrolysis releases it?
We know that bond formation releases energy and bond break absorbs energy. I still don't figure out why ATP hydrolysis (that breaks a bond between oxygen and phosphorous) releases energy, and it releases a LOT.

Please note that this off-topic for biology (it is a chemistry question) and has already been answered on Chemistry.SE.

This is well within the realm of biochemistry in my opinion.

ATP synthesis is actually an endergonic process, hence the need for oxiditative phosphorylation to drive the formation of ATP. Although the P-O bond releases a large amount of energy, the reverse of this process is not occurring in ATP hydrolysis. During hydrolysis, the ATP is broken down into two products, with the addition of water, these products are more thermodynamically stable, so energy is released. Breaking of the P-O bond does require energy, but because more energy released by adding the water in, the overall reaction releases energy. ATP is a thermodynamically unstable molecule (bond breakage releases free energy), but is kinetically stable (bond breakage has a high activation energy). I am not too sure what the exact reasons for ATPs hydrolysis being exergonic are, textbooks state it is because the major sources of the free energy associated with the P−O bond dissociation are the relaxation of the electronic repulsion, increased resonance of the products and the stabilisation of the solvation free energies of the relevant species after the hydrolyses. However, this paper (DOI: 10.1021/acs.jpcb.7b00637) claims that the solvation effects upon hydrolysis actually destabilise the products, but I am not sure of the validity of this paper.


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Comparion between machine vision & human vision
I hope this is the correct Stackexchange to ask this question.
I am trying to know : What is the current status of knowledge regarding human vision and pattern recognition.
More specifically,

How does the human eye read signals from  the cone cells? Is it row
by row, column by column like a computer? or or there other things
happening ?
When detecting, say, an edge, or a connected component - does the human eye continue searching row by row? or does it jumpimmediately to the next neighbor? Are human cone cells arranged in arectangular gird with 8 neighbors per cone besides for the edges?(my guess is no). Then how are the neighbors addressed? Does somerace condition occur?

As you can see, I am not a biologist, I am a physicist working with computer vision. I have moderate knowledge of anatomy, but I am willing to learn.
Thank you

This is a potentially very very broad question, but I'll try to provide a simple answer that addresses the biggest misconceptions.
First of all, animal vision (and brains more generally) is massively parallel. There may be some serial processing steps, but these are also massively parallel. Computers need to digest information into stereotyped operations that can be executed on a CPU. The brain has separate dedicated machinery to each point in space for early vision, so there is no need to process individual "lines" or points in sequence: it all happens at once.
Photoreceptor inputs are converted into center-surround receptive fields in retinal ganglion cells, where light in the center excites and light in the surround suppresses (ON-center cells), or vice versa (OFF-center cells). These receptive fields are then transmitted to thalamus (the lateral geniculate nucleus), and from there to V1, primary visual cortex.
You can then combine many of these circular receptive fields to detect straight edges, like this:

From https://grey.colorado.edu/CompCogNeuro/index.php/CCNBook/Perception
The cells in V1 that respond to these "edges" are called "simple cells"; there are also "complex cells" that have more complicated receptive fields, and other sensitivity like to motion and color. Some computer vision strategies end up producing receptive fields that look a lot like the ones found in early visual areas, the earliest ones built out of Gaussian-filtered sin waves.
From V1, there are higher order visual areas that respond to things like shapes, motion, optic flow, etc.
Basic neuroscience textbooks tend to contain a lot of information on the early visual system, Purves Neuroscience is a good example, any edition is fine:
Purves, D., Augustine, G. J., Fitzpatrick, D., Hall, W. C., LaMantia, A. S., McNamara, J. O., & White, L. E. (2014). Neuroscience, 2008. De Boeck, Sinauer, Sunderland, Mass.

In this image, the edge has a particular axis. and thus will detect only one particular edge. Are there then many V1 cells responsible for many axes and sizes in different subfields of the frame of vision?
and are the input to the V1 now completely parallel?

i am reading you link - and i will hopefully understand more soon

@Sean Yes. Many orientations, spatial scales, etc. There are lots more in the area responsible for the fovea, peripheral vision is more vague.

Thank you. Do we know anything about the resolution of the orientations and scales?

@Sean The orientations and scales are population coded, it doesn't make much sense to think of their resolution (we aren't coding in binary here). You can look at psychophysics data to get an idea of discrimination thresholds, which will depend on other factors like contrast. Like others interested in machine equivalents of biological perception, I really suggest you start from the ground up and learn about neuroscience if you want to go further.

Okey, thanks. I am specifically interested in vision and perception. Will it be too much to ask you for a few titles and papers?

@Sean I'd recommend starting with a basic neuroscience textbook; vision is often used as a model system in neurobiology and these texts have extensive sections on vision. Purves' "Neuroscience" or Kandel's "Principles of Neural Science" are good choices. Even Wikipedia is okay for background. For the visual processing hierarchy, Felleman & Van Essen 1991 is probably the canonical reference.

The lecture notes I linked above from the University of Colorado are also a good intro.


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Is there an example of a species wherein the female lays eggs in the male?
There are of course many species which lay eggs in the bodies of another species and also many species where either the male is eaten after mating or the male dies soon thereafter. So it seems possible that a species might exist where the female lays fertilized eggs in the body of the male with whom she mated or even a different male. I could see however the problem being that there is a significant time gap between mating and the eggs being ready to be laid, so perhaps there are no cases of the former but perhaps there are cases of the latter?
Note: Looking for a form of egg-laying that is destructive to the "host" -- where the developing larvae eat the host, like in the cross-species case.

Is there an example of a species wherein the female lays eggs in the male?

Yes.
Pipefish & Seahorses to name two.
Both widely mentioned in many wildlife programs as being an example of what you've asked.

Watch a video of flatworms penis fencing.
Nature never disappoints, it created a real kicker. Some species of flat worms are hermaphrodites, they have penises but also produce and carry eggs. No flatworm wants to be the mom as it uses a lot of energy and food, so the flat worms fight to inseminate each other.
They fight with their penises. the loser gets their eggs fertilized and is the designated mother of the relationship.
all information I used was drawn from Matt Simon's "the wasp that brain washed the caterpillar". If you are interested in weird abilities of strange creatures, I would really recommend checking it out.

They're hermaphrodites, so both, not really what the question was asking for then.

I did see that, my answer was more of a comment to share this cool flat worm story. they clearly have an interest in freaky animals. But I was unsure if it would fit. Hope this helps either way


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Do all humans have an identical nucleotide sequence for certain proteins, e.g haemoglobin?
All humans have the same sort of proteins in our bodies. Take haemoglobin for example.
Is the gene coding for haemoglobin in my body identical to everyone else's gene or is there slight variations in the nucleotide sequence?
Are there examples of proteins that are always completely conserved at the population level?

Humans have many variants
There is variation. The project I use to help understand this natural variation is gnomAD.
Using VarMap and a slightly out of date gnomAD file, I counted
16007805 protein-coding variants across the human genome. This number will only go up over time.
Indeed, the 1000 Genome project found that on average each person has between 250-300 loss of function protein variants that are not found in their parents (The 1000 Genomes Project Consortium, 2010).
This is an important concept for human health.
ClinVar is one of many projects that aims to catalogue and study when these variations lead to disease in a clinical context.
Another is the 100,000 genome project by Genomics England which studies NHS patient data in cases of rare disease and cancer.
Haemoglobin has variants, including disease variants
At the time of writing, HBA1 (haemoglobin alpha subunit gene) has 183 gnomAD variants and 17 pathogenic variants in ClinVar (sourced from gnomAD).
Again, both of these numbers are likely to increase because the data will cover more people.
Constraints on highly important proteins
But the underlying question is, I think, "are there some proteins that are so important, that life keeps them highly constrained" i.e any variation will lead to an invalid cell or a disease phenotype.
gnomAD attempts to add "constrained" metrics to each protein record, and some are more constrained than others.
For example:

Haemoglobin scores a pLI of 0.01 (higher scores are more intolerant to variation, specifically loss of function variation).

p53 is a gatekeeper of the cell cycle, mutants of which are common in cancer cells. It has a pLI score of 0.53 which means it is very intolerant to variation compared to haemoglobin.

Ribosomal protein L5 has a pLI of 0.998 implying it can tolerate little if any variation.
The ribosome is critical in protein production, hence altering it may cause a complete breakdown of cellular life.

Variation and Evolution
There is an almost philosophical difference between human variation and human evolution. Variation is a static snapshot of our protein sequence from individual to individual. Evolution in the sense of a Dayhoff Matrix requires looking back millions or billions of years by comparing similar protein sequences across many species.

It is highly unlikely that there exist any protein that is made from completely identical nucleotide sequences across the entire human population. There will certainly be regions within a gene that are highly conserved, but there is little evolutionary pressure to conserve an entire gene's nucleotide sequence across the population.
This is in part due to the fact that different codons can translate into the same amino acid. So, even if a protein is (phenotypically) identical across the human population, the genes making that protein can use different sequences to code for the same amino acids. This alone can allow for an incredibly large number of possible gene variations that can code for an identical protein.

Related resources: Neutral mutation (wikipedia) and the neutral theory of molecular evolution (wikipedia)

Haemoglobin has two distinct chains. It would be better to give separate numbers for each.

Apologies, I'll change the note to be more generic, as "variants" is not a precise descriptor and depends on context, such as in the point @David mentioned.

The fact that different codons can code for the same amino acid doesn't give anywhere near "infinite possibility"! Most AAs are only coded for by 2 different codons, and only one is coded for by 6. Given a fixed length of gene, that is a far cry from infinite variability!

@terdon Hmmm... Even only considering two different codons for each amino acids for a small 100 amino-acids proteins, that gives 2^100 possibilities, a little in excess of 10^30... Not infinite, sure, but rather high !

Rather high indeed, absolutely :) Still a drop in the ocean when considering the full ~3billion bases in a human genome though. But yes, you're not wrong, even only the wobble positions give significant variability.

Anticodon are a funny example for conservation, because tRNA genes actually have a multitude of copies, and while itʼs true that thereʼs considerable negative selection on their anticodon loop, variability certainly exists — even here.

@GenTest This is a great answer, thanks. Just a heads up I edited the question to get rid of the term "mirroring". You might want to tweak your answer accordingly.

Variants are not limited to SNPs. There are rare instances (but a lot because of the size of the data!) of 2 nucleotide changes, and sometimes 3.

Edited answer to better suit edited question. Removed examples and language that may cause confusion. 1st time answering here, appreciate feedback. Please feel free to edit to improve answer, as original answer was provided in context as a reply to the OP's curiosity as a recent High School graduate and was structured as such.

@GenTest I'm glad you weren't put off by the comments and that you made the changes. I think the resulting answer is a great succinct answer to the question. Welcome to Bio.SE!

At the whole-gene level, there is likely no absolute conservation of any human protein-coding gene at the population level, though there might be complete conservation between individuals. Keep in mind that most human genes are on the order of tens of thousands of base pairs long, and only a portion of that length encodes functional motifs. There are, however, ultra-conserved elements on the order of hundreds of base pairs that are identical between humans, rats, and mice.  Most of these elements are non-coding, and some are transcribed as functional ncRNAs.

"At the whole-gene level, there is no absolute conservation of any human protein-coding gene at the population level," Are you sure about this? I wouldn't be surprised if there were a specific, very short gene with at least its coding sequence 100% conserved. Or even one with everything including UTRs conserved (perhaps a single-exon gene with no introns). I also wouldn't be surprised if no such thing existed, but you are explicitly ruling it out without a reference.

@terdon you're right -- I don't give a reference.  I should have qualified that first sentence with "As far as I know, ..." or, as Gen Test said, "It is highly unlikely ... "

@terdon I haven't come across a whole protein that is completely "constrained", but there are indeed heavily constrained regions in both coding and non-coding regions.

@James neither have I. If I had to bet I'd say that there is no case of a protein coding gene whose coding sequence is 100% identical across all (healthy) individuals, but this is the human genome, so nothing can be ruled out! :)

@terdon My delay in response was me awk|sort|uniq-ing my gnomAD file. I have 18922 uniq UniProt codes, so there are a lot less than the complete proteome! That is more likely down to bugs than biology though! I'll report back when I am more confident.

@James ooh, that's actually a bit of a fun project. I have to run now, but give me a ping either in The Biosphere or the Bioinformatics.SE chat room. I'd love to see the results and would be happy to help out if needed.

No gene and no base pair is immune to mutation. It is the natural selection pressure that keeps some gene relatively constant. Neutral mutations are not subject to pressure, so everything changes. And then, there are "almost neutral" mutations that also get passed by.


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What makes synapses stay "fixed"?
What makes synapses not move or pre- and postsynaptic cells neither touch nor move away from each other? I mean the synaptic cleft is a gap between the pre- and postsynaptic cells that is about 20 nm wide (according to Wikipedia), so what makes it of that width? Are there some protein fibers anchored in both pre- and postsynaptic cells? Or do the glial cells keep them at that (often temporarily) fixed position? What prevents them from being displaced by the slightest movement of the body? I'm talking obviously about the chemical synapses.
Thanks in advance for the answer.

Synapses are held together by adhesion molecules, like cadherins and neuroligins/neurexins, so they aren't just loose adjacent membrane, they are securely anchored in place.
The adhesion molecules serve both a structural and regulatory role, being important for synapse formation and plasticity.
Missler, M., Südhof, T. C., & Biederer, T. (2012). Synaptic cell adhesion. Cold Spring Harbor perspectives in biology, 4(4), a005694.


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What species of snake in India "drinks breaths" according to local customs?
In Rajasthan in India, locals know a snake called peevna in the local language. Many of my relatives live there in villages in open deserts. They see many kinds of snakes every day.
The word peevna is basically derived from the Hindi word peena, which is a verb meaning to drink. But in the case of this snake, the drinking being referred to is the process of inhaling the warm air from the nose or mouth of a sleeping man. Hence they call it peevna.
Locals describe this snake as follows:
It is afraid of light. It just sits on the waist of any sleeping human, and then it "drinks" the warm breaths. After the breath gives the snake some comfort, it releases the venom into the mouth of the human. Finally, it hits the man with it's tail and leaves. The man dies once the sun light falls on him if he is not treated.
A similar description of this snake is mentioned on many Hindi blogs. However, I can't trust these stories.
Given all that, what snake is it and is it and is it even possible that this snake behaves like this?
EDIT:
A recent case has been mentioned here. And it is real. The villagers have reported the case. But it's in Hindi. Kindly translate that page, as it would be helpful to answer.
Now a doctor also said that it is a Karait kind of snake.
When I searched it on Google, I found this.
In common names, Peewana is also mentioned. So I guess this is the snake. But doubt is, the photo on the blog I shared is different than this. No only this, my relatives also define the look and feel of the snake like the one on blogs. So doubt remains.

Usually a snake attacks only when it is not provoked/threatened or if it wants to paralyze a prey for a meal (humans are unlikely to be thought of as meals by most snakes). In this site we ask and answer questions about biology and not bust folklores and myths. Hence your question is off-topic.

The folklore or myth could be real. Don't call it myth without proof.

*Usually a snake attacks only when it is provoked/threatened. You yourself said you cannot believe these stories. Stories without proper scientific basis are usually called myths or folklores (depending on how much they are believable). Your description of the snake does not fit any known behaviour of snakes. Moreover, most snake venoms are not lethal when taken orally. The hitting by tail and sunlight have no roles per se. You told a story with no scientific basis. You did not try to check even the most obvious facts and here you are telling me to prove that it is not a myth.

Your comment was written in such a way that you made it myth, which I don't have any problem with. The thing is I wanted it in an answer. The point of question is to know whether what I stated is TRUE or not. What I believe or think is a different thing. If you had written the comment as an answer, all things would have been cleared. Your comment was too intelligent for me to understand whether you called it myth or it is myth. Please don't comment if you can't explain for better understanding.

This Times of India article mentions the name "peevna" in relation to the "saw-scaled viper".
According to Wikipedia, the genus Echis contains 12 species that are commonly referred to as a group as "saw-scaled vipers."
Of these, one clearly is found in India: Echis_carinatus (commonly called the "saw-scaled viper", "Indian saw-scaled viper", or "little Indian viper" in English.).

This same Wikipedia article provides common names in other languages, but the given common Hindi name on Wikipedia is not "peevna" but rather "aphai (अफई)." I'm not sure what to make of this discrepancy...

I have no idea if this is in fact the snake you're referencing. BUT, if E. carinatus IS your snake in question, Wikipedia provides the following info:

 Source: Wikiedi
Habitat:

E. carinatus is found on a range of different substrates, including sand, rock, soft soil and in scrublands. Often found hiding under loose rocks. Specimens have also been found in Balochistan at altitudes of up to 1982 m.

Behavior

E. carinatus is mostly crepuscular and nocturnal, although there have been reports of activity during daylight hours.

This is likely where the "afraid of sunlight" part of your myth arose form. However, the Wikipedia article goes on to say that they have sometimes been found active during the day

Wikipedia goes on to say that they are a very aggressive species known for many snake bites, which again relates to the sinister behavior described in your story:

E. carinatus is one of the species responsible for causing the most snakebite cases due to their inconspicuous and extremely aggressive nature. Its characteristic pose, a double coil with a figure of eight, with the head poised in the center, permits it to lash out like a released spring.

Wikipedia also points out that bites are fatal ~20% of the time, which I assume would be even higher in smaller villages with limited medical response capabilities.

Finally, Wikipedia points out that they move primarily via sidewinding, which in a way could be construed as flicking its tail aggressively when it moves away. This might be where the tail-hitting comes from in your description.
As for the "drinking" of breaths?...
I haven't figured out what that would be due to. My best guess is that (unsurprisingly) this snake can't handle cold weather and is known to hibernate. Perhaps the warm breath comments are relating back to its need to warm up (after hibernation??). Who knows.
This is the best I've got for you.

https://hindi.oneindia.com/news/rajasthan/desert-snake-pivna-attack-on-a-family-in-sedwa-barmer-rajasthan/articlecontent-pf223209-524634.html
Here's a recent case observed and a doctor also said something about it. Please see this and enable english translation.

I wonder why this answer is getting upvotes. 2nd answer seems more promising and more close to description given by me.

This is a misbelief and the possible answer is the "Krait" and its subspecies.

Here is a blog post by a scientist in the Tata institute of fundamental research. The blog contains data compiled from various sources for the "Special Interest Group-Snakes newsletter, I.I.T. Bombay".
As per the blog post
"In northwestern India, kraits are supposed to suck a man's breath away as he sleeps. This is perhaps the farmer laborer's explanation for the respiratory paralysis that a severe krait-bite brings on."
The blog post--Snakes and common misbeliefs.

This research paper further explains this misbelief of people--> "Krait is responsible for most deaths in North India. It bites people sleeping on the floors, mostly at night." Mass awareness regarding snake bite induced early morning neuroparalysis can prevent many deaths in North India.

Hope it answers your question.


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Are most pathogenic bacteria facultative anaerobes?
I know that S. aureus and most gram-negative rods are facultative anaerobes. In terms of number of species, are most human pathogen-associated bacteria facultative anaerobes?

Most bacteria are facultative anaerobes. There are very few, if any, obligately aerobic bacteria. Wikipedia lists Mycobacterium tuberculosis as obligate aerobe but it can survive in anaerobic conditions.

Thanks. Yes, there are only a few as you mentioned. Moraxella catarrhalis, Legionella pneumophila, and Pseudomonas aeurginosa are some examples.

P.aeruginosa can survive in anaerobic conditions.

In the presence of arginine or nitrate, yes. However, in general terms it is considered aerobic.


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How does a ribosome gather tRNAs at a fast enough rate for Translation?
There are many animations of the ribosome in action, and all I have seen show the correct tRNA neatly entering the ribosome and its amino acid being added to the growing protein chain. My question is this: is it really possible that mere brownian motion and diffusion are responsible for getting the right tRNA out of 20 possible types to that point? Presumably that would require tRNAs of every type arriving and most being rejected until the right one meets its codon and is used. Not only that, you would expect orders of magnitude more tRNAs to be arriving at almost the right place but being the wrong way round or hitting the wrong place on the ribosome.
Has anyone in the field ever done any calculations using dynamics equations, along with the known volume of cytoplasm and tRNAs to see if this is even feasible?

I think it has something to do with the cytoskeleton. https://www.nature.com/articles/nrm2818

Forget any animations you have seen — they are irrelevant. But the fact is translation happens at a particular rate. That's chemistry. What else do you suggest? Magic?

@user237650 — Certainly the cellular environment may increase the concentration of components, but the fact remains you can do it in the test tube with purified components.

Please look up the definition of Brownian (names after Brown) Motion. You will find it refers to macroscopic particles, not the molecules that cause it.

And why do you think it matters if there are 20 times as many collisions that cannot be productive as those that can? It would only matter if it competed with the potentionally productive collisions, which it is unlikely to do at the concentrations in the cell. The need for collision of molecules in the right orientation for reaction is a standard feature of chemistry. Catalytic or binding protein in biochemistry often work by facilitating the correct interaction by binding to others. Transfer RNA is brought to the proteins ribosome A-site by elongation factors.

The answer is simply due to the random walk of the amino acids. Over small volumes, this process is incredibly quick and is also responsible for nucleotide delivery to polymerases as well proteins searching for their substrates, in fact, only a few enzymes/proteins are limited by the rates of random walk motion. I'm sure there are lots of papers which discuss the rates of trna movement in the cell, but this is the first one that I found: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2727733/
(You are completely right about competing tRNAs and the orientation of the tRNA entering the ribosome, all of these factors are taken into account in calculations. Ribosome animations are also a massive oversimplification, they illustrate certain points well but they are by no means accurate, they are useful for reaching purposes!)

I have upvoted your answer as you provide a useful reference, but please edit it to remove the reference to diffusion. Diffusion is the movement of molecules down a concentration gradient. The motion of molecules in general (and in this context) is random (stochastic) motion resulting from their kinetic energy. Hence its temperature dependence. You might also mention the existence of elongation factors which have an affinity for the A-site on the ribosome.

Hi David, I think I would disagree with you on that, diffusion is a stochastic process and the paper both mentions this and states several times that the method of transport is diffusion.

I think you misunderstand my point. The basic movement of molecules that allows their collision and reaction is not due to diffusion but to their kinetic energy. The poster is asking a chemical question and seems not to understand that. Molecular diffusion can, of course, occur in addition to this when there is difference in concentration between the point at which there is an accumulation of molecules and that at which they react. The random component of this is in addition to the effect of concentration difference.

Thanks for the answers. I should say I am not a biologist or a chemist but a mechanical engineer by training but now I run an animation company. As per my original question I am somewhat frustrated by the way molecular biology animations always show proteins and other molecules involved in transcription/translation floating around as though they have agency and the ability to 'swim' where they are required. As the replies have asserted, this is not the way it works - I just wonder if there's a way of conveying something more accurate in an animation.. I will have to experiment


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A single leaf in a very strange air current / wind?
Here is my eight years old movie where I have pictured a single leaf moving in a very weird way:
https://www.youtube.com/watch?v=sCjvgdfNCjU
Can someone explain me what is depicted in this movie (what process, event or situation) or otherwise what is causing this single leaf to move there and back in such way / pattern?
By listening to the sound or observing other leaves (barely moving) you can assume that this isn't a wind what is causing leaf to move. There was also nothing in the kind of spider web or no animal around that could influence leaf's movement.
The movie was captured in late September 2011 in southwest Poland, near Jedlina Zdrój in a forest on the hillsides of the "Mały Wołowiec" mountain (approx. 50°44'22.5"N 16°18'28.7"E).
Note: I understand that this question maybe considered a trivia, downvoted or even closed, yet it depicts one of my personal really weird biology-related mysteries, I ever run into. So, I'd really would like to know, what is going on here?


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Can anyone please identify this?

We saw this leech like worm in Kerala, India. Can anyone identify it for us? I saw it today, 10th September. It's about 6 to 7 centimeters long. It was very still, didn't move while we went close and took a picture. Thank you.

Please [edit] your question and give us some more details. Most importantly, how big is that? Is it a centimeter? A meter? What time of year did you see it? What time of day?

It does not look like a leech to me. Looks more like a millipede. Did it have legs?

None that we could see.


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The First Polymerase
Knowing that polymerase protein is needed for the transcription of genes, which polymerase is used in the transcription of polymerase protein itself?

Please clarify whether you are enquiring about the evolution of RNA polymerase, or about the different RNA polymerases (I, II and III) in contemporary higher organisms.

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Possible duplicate of What came first? The DNA or the DNA polymerases?

In eukaryotes its RNA polymerase II. In bacteria it is the normal RNA polymerase. Although it is true that polymerases are now needed transcription of more polymerases, this mechanism may not have always been present. In the RNA world hypothesis, RNA coded for proteins and not DNA, so with the emergence of DNA, RNA polymerases may have formed as well. To produce proteins from RNA, organisms use complexes called ribosomes, which are ribozymes (RNA enzymes), which have undergone many rounds of evolution from original ribosomes, so there wasn't an issue with the production of proteins from RNA and throughout the course of evolution, polymerases were then developed, but they were only necessary with the rise of DNA.

I think you misunderstand the question. I suspect it's the old chestnut of the chicken and the egg. And even in an RNA world, polymerase (RNA-dependent RNA polymerase) must have developed very early — certainly before ribosomes, as these were only needed to make protein. The answer would seem to be that there was non-enzymic methods of RNA replication, followed by a ribozyme-like enzyme. Whether protein RNA replicases developed before DNA came on the scene is a moot point.

I dont know if we have a solution as to how functional RNAs were first formed. I have found a polymerase that was rationally developed for RNA polymerisation, although the paper is unsure as to whether this was feasible DOI: 10.1126/science.1060786. if you know of any research that has gotten any further please let me know!

I prefer a link I can tap on, especially on the phone. I’ll check it out tomorrow.

Thank you. I checked out the RNA World Hypothesis, it is very interesting, though it is a shame that some scientists were criticizing it.

Oh the cell has premade RNA polymerase from the mother's egg cells

@user3742855 Criticism is good and experiments are even better. Both proving and falsifying a hypothesis increase scientific knowledge.


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Protecting an internal clevage site from restriction enzyme while cloning
2 restriction enzymes used to generate cohesive ends in a vector and foreign DNA(gene of interest you want to clone) also cuts the foreign DNA at an internal site. What are ways to overcome this?

What have you tried? Or is this a homework question?

I have tried protecting using DAM nethylases, but thaf gave a ladder of bands on gel electrophoresis analysis. So I am wondering how to solve this

Does your protocol use PCR and does your vector have a MCS?


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Artifial insemination in milch varieties?
Artificial insemination is used to produce offspring cows  and other milch varieties like buffaloes.. etc often use same sturdy males. Isn't it a step towards eugenics? What can be possible future harms?

Possible duplicates or related: https://biology.stackexchange.com/questions/14414/do-humans-have-enough-biological-differences-to-be-grouped-into-races-or-subspec https://biology.stackexchange.com/questions/66144/human-genetic-diversity-in-africa-in-comparison-with-the-rest-of-the-world

And what do you mean by "number dominance of Caucasians"?

"number dominance of Caucasians over other human divisions".... The phrasing is unclear but please note that there are ~1.3 billions Han Chinese and only ~0.85 billions caucasians.

Does it make sense to classify all humans in a single species? might also be a possible duplicate.

Possible duplicate of Do humans have enough biological differences to be grouped into races or subspecies?

There is no genetic basis for these classifications. Most human genetic diversity is in Africa. Diversity only decreases with geographic distance from this continent.  There are geographic clines, not the clusters that one might call race.  Here are some results from Rosenberg's 2002 Genetic Structure of Human Populations:

93-95% of variation occurs within populations
3-5% of variation occurs between populations

Local adaptation occurs, such as height and pigmentation but these phenotypes are polygenic and should not lead to binary classifications.  There are some very interesting case studies on local adaptation that you should look into. ex)EPAS1 gene and no hypoxia among Tibetans or lactose persistence on three continents
There is no genetic basis for dominance of one population over another.


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Can stress and arousal be independent?
I'm trying to figure out if it's possible to have a stress response without being initially, or simultaneously aroused. I'm defining stress to be physiological stress (ie. release of cortisol) and arousal to be activation of the sympathetic nervous system.
Every example I can think of, these two are not independent. In the case of "fight-or-flight," one initially activates the sympathetic nervous system, which is then followed by the release of cortisol. Or in individuals with major depressive disorder, their sympathetic nervous systems are constantly activated while cortisol is being secreted.
So, is it possible to experience cortisol release without activation of the sympathetic nervous system?

Stress response has 2 main components:

Quick response, within minutes, is by the Sympathomedullary Pathway (SAM): hypothalamus > sympathetic nervous system > release of adrenaline and noradrenaline from the adrenal medulla > stimulation of the heart, dilation of the muscle arteries, constriction of the gut and skin arteries, glcogenolysis (the breakdown of glycogen into glucose) > more glucose available as a fuel
Delayed response, within hours, is by the The Hypothalamic Pituitary-Adrenal (HPA) System: hypothalamus > pituitary gland > ACTH > release of cortisol from the adrenal cortex > gluconeogenesis (formation of glucose in the body from other substances) > more glucose available as a fuel

Cortisol secretion from the adrenal cortex can be stimulated by things other than stress, for example, hypoglycemia, but hypoglycemia will simultaneously activate the sympathetic nervous system, which will trigger the release of adrenaline (Neuroendocrine Response to Hypoglycemia).
Some cortisol is also secreted along with aldosterone in response to hyperkalemia or hyponatremia (Vivo.colostate.edu), for example in SIADH (A Case of Transient Hypercortisolism Simultaneously Occurring With the Syndrome of Inappropriate Antidiuretic Hormone Secretion Induced by Olanzapine).
Cortisol can be also increased without stimulation of the sympathetic system in Cushing syndrome due to a pituitary adenoma or, rarely, other tumors that secrete ACTH or in adrenal adenoma, which secretes cortisol.


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Is it possible to buy a DNA sample with a specific mutation?
I would like to test a genotyping method (ARMS) on a specific human snp (heterozygous or homozygous ).
Unfortunally, we do not have any dna samples with the mutation.
Is it possible to buy somewhere a dna sample with the mutation ?
Otherwise, can you redirect me to other solution like directed mutagenesis?
Thanks

There are many companies selling synthesized DNA, most often in the form of short oligo's. But longer pieces are also possible. What exactly do you mean when you say 'DNA sample' though?

I mean no patient with the mutation. I need a DNA with the mutation to test if my genotyping method works


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Regarding hydrolysis of ATP in ABC transporter
So, I was going through this lecture about ABC transporter and one point about it confused me. ABC transporter is not the same as an ATPase but let's take an example of Cystic Fibrosis Transmembrane Regulator. In it 2 molecules of ATP bind with the channel and then they undergo hydrolysis in order for Chloride ion movement to occur. So,if hydrolysis is occurring when ATP was bound to the channel then shouldn't it also function as an ATPase or is it so that it is binding and the channel isn't doing the function of hydrolysis, some other molecule is and it is just using that energy.

"ABC transporter is not an ATPase" - according to whom?

They told me that an ABC transporter is not the same thing as an ATPase

Can you provide a quote? "ABC transporter is not the same thing as an ATPase" is true just like "an automobile is not the same thing as a vehicle" is true. "ABC transporter is not an ATPase" is false in general, though may be true for a specific ABC family member.

See on the topmost of lecture where they write what topic they are teaching, they wrote that ABC transporters are not ATPases but the teacher that was doing lecture said that an ABC transporter is not the same thing as an ATPase. Well by the way can you tell me the difference between the two statements as they seem kinda same to me.

Also, should I edit the question's statement to make it better

@Bryan Krause, I have edited the question so that it'll be more meaningful. But can you please explain that why despite of the fact that hydrolysis is occurring in the channel, it is not the same as an ATPase. Also, why one shouldn't say directly that it is not an ATPase and use not the same thing as ATPase.

I'm guessing your instructor is referring to a family of ATPases rather than functional ATPase activity. But without some sort of quote or actual evidence I'm always hesitant to provide guidance that can mislead a student when there is confusion between what an instructor says and what a student hears.

@Bryan Krause, yes you are right. The teacher was talking about pumps, Na-K ATPase pump to be specific. But as far as evidence goes, I gave you exactly what teacher had said and I'm confident coz I even used subtitles for that video. The teacher had said what you are quoting but I'm confused that despite of the fact that ATP hydrolysis is occurring, why we cannot refer it to as an ATPase.


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What is this ? Found under my bed

Found under my bed. Looked and there was nothing else like it or eggs of any kind.

It was dead. Looked to be dead for a while but I’m not sure

Hi welcoem to Bio. SE. Please provide your location and the approximate size of the specimen. Additional clearer pictures would also be helpful for anyone trying to help you identify this organism. In general, we have a list of expectations for [tag:species-identification] questions here that should be met to avoid having your question closed (and, more importantly, to help you get a correct answer!!). Please [edit] your post to add more of this information. Thanks!

At a glance it looks like a flattened perfectly ordinary dead woodlouse to me.


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Help on selecting 2 tests - unsure if they are paired or non-paired statistical test
I have data that measures the temperature of flowers and leaves on different plant species. These are the comparisons I am trying to make:

Comparing the flower and leaf of the same plant at the same time of day
Comparing the flower or leaf of a plant to the same flower or leaf at different times of day - on the same plant

My current interpretation is that 1 is an independent statistical test because while they are both on the same individual plant, they are separate "individuals" themselves. For 2 I believe it is a paired test as it is measuring the same flower or leaf at different times of day.
What is confusing me is that I have been taught that if it is the same "individual" then it should be paired, therefore 1 should be a paired test. However my interpretation is that "individual" means something different in the mathematical reality of the tests, where they are seen as different pools in this instance.
Am I correct in my thought? Or completely wrong?
Thank you
Edit:
Maybe some clarification to my thought: The difference between my 2 tests is that one uses the same repeated leaf or flower (referring to case 2) at different times of day (therefore it is paired as it is a  measurement of the same thing twice at different times). This contrasts with case 1 as this is comparing 2 different objects at the same time of day. The confusion for me comes in when case 2 is still on the same individual - they are related in a way, but I'm unsure if this is relevant to the test.

I'm voting to close this question as off-topic because it is a question of statistics, not biology. Have a look at stats.SE

I would argue that statistics is the core of Biology! The whole of the empirical method underlying biology is founded in statistics. Even high school level biology uses statistics. Thank you for your opinion either way.

@s33ds Welcome to Bio.SE. You are right that biology relies on statistics! Remi.b isn't trying to say this is a bad question, but you would get a much better answer on stats.SE. For me the question is missing a few details that are important for the statistical analysis. For example in scenario 1: Are you only counting one leaf and one flower per plant? This might cause different sample sizes in the data.

There may or there may not be any correlation between the flower and the leaf of a plant. If you think there might, you ought to account for that. Switching to mixed-effects (or multi-level) models will induce the change in mentality that will make the task of modelling such experimental designs easier.

I imagine that for case 1 you have data of the type:
Plant1, $t_f$, $t_l$;
Plant2, $t_f$, $t_l$;
etc.
If you are interested in comparing the mean temperatures between flowers and leaves, your data would consist of n measurements coming from flowers and n measurements from leaves. You may surely try a t-test for independent samples, especially if you have some missing data in one column or the other. However, I find it reasonable to think that the values of flower and leaves are correlated within plant (possibly because of different background exposures of different plants). If this correlation is strong, you are at risk of not registering a true effect (a significant temperature difference between leaves and flowers).
Therefore, I would opt for a paired test even for case1.

Welcome to Biology.SE!   ——— Please take the time to go through the [tour] and the help pages starting with [Answer] questions effectively on this site. Thanks!


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Is there a minimum amount a muscle can move? And thus, gaps in our movement?
Lately I've been thinking about something, based on my knowledge my chain of reasoning works like this...
When you want to move a muscle your brain sends an electrical nervous impulse along the chain of nerve cells to the muscle you want to move.
A nervous impulse is nothing other then a jolt of electricity, the voltage is uniform and the only difference is the rate the jolts are sent, resulting in faster movement.
When a muscle is hit by electricity it's reaction is to contract, this is what creates movement.
Given all this, is our movement continuous or quantized? Let's say one jolt moves my finger 1 degree, another jolt would move it another degree. Would that not make it impossible to move my finger 1.5 degrees? To me it stands to reason that while you could shut off the power to your finger at any time, making it theoretically continuous, there must be a minimum amount of frequency by the impulses needed to cause any movement.
If this is true then the movement of our bodies is the microscopic snapping through possible positions. And therefore there must be a finite number of possible positions our bodies can take. Like a knob that can only click it's way through the pre-determined positions on the dial.
Is all this true? Do nervous impulses work like I think they do? Are there things about nervous impulses or muscles we don't know? Are we capable of only positioning ourselves in this quantized way? Has anyone proven any of the things I have said? Please consider you answer carefully.
Personally I hope our ability to position ourselves is continuous.

That's not even close to how muscle signals work, you may want to look up something called muscle recruitment or muscle fiber recruitment.

What about the rest of my question?


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Recognise this thing found in beach?

Kindly help me identify this thing found in beach
Chennai, India . Size would be just 1.5 cm in diameter..across maximum size. It's shelled and has something inside it. It make a small noise when it is shaked completely closed on all sides. It's hard surface ( but " fine" texture ) to touch.

Thanks for the edits. Could you explain what you mean by "fine"? It's not quite clear to me what you mean in this case. Thanks.

Did you ever find out was this was? We just found one in Florida.

give us a cross section. describe the material, is it mineral or organic? is it an egg? google lens app will recognize a HD photo if there are other images of the same thing on google images. I just put that specific image through google lens and it returned "chennai, india"...

I believe it’s the seed of a Guilandina bonduc shrub. The seeds are known as nickernuts or sea pearls, and can be found washed up on beaches throughout the tropics. The seeds are often used as counters in the traditional board game manuals.

Welcome to the site. Please take a [tour] and visit the [help] for more information on the Biology Stack Exchange and what we do here. Please note there is a section in the help on what makes a good answer. We particularly value answers here that contain references that support the answer. To improve your answer you could provide links to the shrub and images of the plant and seeds (try wikimedia/wikipedia and iNaturalist) for these in your answer.


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Which one is better to use for water stress experiment GWAS or RNASeq?
This is my first time in this area of research. I am working on 95 varieties of bambara groundnut. I have done the agromorphological characterization of these varieties as well as the genetic diversity using DArT markers. Based on the charaterization result, i have selected 10 varieties to be subjected to water stress with the objective of identifying genes that are responsible for tolerance in this plant. My challenge now is:
1. bambara groundnut does not have a reference genome, so will i be able to use GWAS in getting these genes from the result of the DArTSeq.
2. Bearing in mind that the whole 95 varieties characterized were not subjected to water stress, do i need to set up another experiment entirely for the water stress and go ahead to make use of RNASeq to get the genes?
3. It is obvious that some genes will be upregulated and some will be downregulated, how do i identify these genes and how do i know if they are expressed at the onset of stress, during, or after stress?
4. when is the appropriate time to take my samples, i was considering taking at 50% flowering stage. Is this good?
Any help and insightful articles will be greatly appreciated.

The choice of the experiment to do depends on the question you are trying to ask. RNAseq will give you a direct readout of gene expression which you can relate to a particular condition. GWAS is more difficult to interpret.

bambara groundnut does not have a reference genome

This is your biggest problem if you want to do any sequencing based analysis. Neither GWAS nor RNAseq data analysis are possible without a reference genome (or at least transcriptome).
Depending on the availability, quality & similarity of reference genomes from related species it may however be possible to construct a reference transcriptome for your species from RNA sequencing data you get from RNAseq experiments. I'm whether it's feasible (or indeed possible) to try the same with genome sequencing data, since with only 10 individuals/strains you may only be able to get huge linkage groups for GWAS analysis.
Either way I'd highly recommend you to talk with someone (i.e. from your institute) who has experience in doing RNAseq or GWAS on plants, when planning this. (The experience with platns important, mammalian/model system genomes are much better studied and generally have less genome duplications, so analysis of plant data comes with its own set of baggage)

Bearing in mind that the whole 95 varieties characterized were not subjected to water stress, do i need to set up another experiment entirely for the water stress and go ahead to make use of RNASeq to get the genes?

If you want to use RNAseq to find genes that are differentially expressed between states of water stress and no water stressin the same plant/species you will need to compare samples taken from corresponding conditions. This is only possible with RNAseq data.
Another approach could be to do some other experiments to determine which plants show a phenotype when exposed to water stress, and then look for correlations of this phenotype with (sequence) isoforms variants [GWAS like approach, possible with RNAseq or genomic sequencng data] or with expression levels of certain genes [again only possible with RNAseq data]. In thsi approach you need to be aware that your sequencing data either represents the ground state of all plants (no stress) or a potentially stressed state and missing one of these may mean that you can't find genes that change expression levels based on stress.

It is obvious that some genes will be upregulated and some will be downregulated, how do i identify these genes and how do i know if they are expressed at the onset of stress, during, or after stress?

First, while most analysis tools will always give you some values for up- or downregulation, that does definitely not mean that these values are always meaningful. Only proper statistical testing can tell you which up/downregulation is somewhat reliable (it still wont tell you if its biologically meaningful) and depending on the quality of your data and the actual biological differences you may not be able to find anything.
Secondly, if you care about the timepoint of expression for specfic genes, you will need to some time series experiments. (Doing that for the whole RNAseq/GWAS would be very expensive, so ideally you first identify some candidate genes and then study their specific expression profiles with easier methods).

when is the appropriate time to take my samples, i was considering taking at 50% flowering stage.

If you are not an  expert on the species you#re working with, I'd again highly recomment you to speak with someone who is.

Many thanks, these points are highly insightful for me a start, i will discuss with someone that have experience to see what can be done. Thank you so much.


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Understanding the strategy of Sanger DNA sequencing
The Sanger sequencing method creates large numbers of sequences of all possible lengths, ending with a specific nucleotide, by terminating with a tagged (fluorescent) nucleotide at the end.
But if you already have fluorescent nucleotides of a specific base, why not just do regular PCR  with them, create a huge number of full length copies of the original sequence, and then simply see the locations where the nucleotide fluoresces to determine all the locations of that base. Why do we need a large number of copies ending at each possible location, as with the Sanger method?

It is unclear whether you are asking a) how the Sanger method works, or b) why it is used (or why it was invented) when Next Gen methods are better. However my guess is that you are student who has encountered DNA sequencing methods without any historical or practical context, and has got bogged down in the preparation of the samples rather than the methods for actually determining the sequences. Read Wikipedia on Sanger and more modern Sequencing  methods. (The Sanger method predates PCR.)

why not just do regular PCR with them, create a huge number of full
length copies of the original sequence, and then simply see the
locations where the nucleotide fluoresces to determine all the
locations of that base. How? What instrument do you propose to use to see the sequence of fluorescent tags?

If you mark the full length strand of the DNA with the fluorescent labels, you will get a lot of signals from the same nucleotide without the possibility to discriminate where the actual nucleotide is located on the strand.
Sanger sequencing doesn't end with the preparation of the terminated and labelled DNA strands, the following step is crucial in discriminating where the labelled base actually is. After labelling, the sample is run through high resolution capillary gel electrophoresis to sort them by size. The smallest fragment comes out first, then the one with one base more and so on. The detector which then identifies which fragment is coming through is located at the end of the capillary.
This works like shown in the schematic image (from here):

If you would mark a complete strand, no dicrimination by size is possible (ideally, all DNA would run on the same height of a gel) and all flourescent signals for all positions would come on the same spot. Not very helpful.

Additionally, the original method of Sanger didn’t use labelled ddNTPs at all. The sequence was determined solely on the basis of fragment size and knowledge of which ddNTP terminated it.

And the Sanger method didn't use capilliary gel electrophoresis for many years after its inception. The principle is merely separation, which in a single small laboratory is proably still done by slab gel electrophoresis.

Foreword
I originally suggested closing this question as I think it confuses methodological details with strategy. There is an accepted answer that clarifies things with a clear diagram of the Sanger method. In the circumstances I decided to add a different sort of answer — one that emphasises the principles involved in the different approaches, rather than practical details which are not intimately associated with logic of the different approaches.
General Strategy of DNA sequencing
Irrespective of the method, the determination of DNA (or any linear) sequence requires two pieces of conceptual information:

Knowledge of a particular position in the sequence.
The identity of the base at that position.
This is illustrated in the graphic. In addition, there is a practical requirement:
Means to uniquely detect this.

Let us compare these in three different sequencing approaches.
A. Chemical fragmentation (Maxam & Gilbert)
Here the DNA to be sequenced labelled at one end is treated with different chemicals that cleave at different bases in separate reactions.

The position is indicated by the length of the fragment.
The base is known from the chemical used.
Detection is performed by separating the different fragments by length and using their radioactivity to visualize them (by autoradiography).

B. Chain termination during synthesis (Sanger)
This method uses enzyme-catalysed copying of  the DNA to be sequenced, with termination of the copying produced by the four di-deoxy analogues of the deoxynucleotide triphosphates (dNTPs) in separate reactions.

The position is indicated by the length of the fragment (as in A).
The base is known from the particular di-deoxy analogue used to terminate the reaction.
Detection is performed by separating the products of synthesis by length and using the radioactivity or fluorescence of the dNTPs used in synthesis to visualize them.

(Note to the poster: obviously you need fragments of all different lengths if you are going to identify the base at each the position in the chain.)
C. Phased synthesis (‘Next Generation Sequencing’)
This type of method also uses enzyme-catalysed copying of  the DNA to be sequenced. However, there is no termination of the chains, as in B, but the cycles of addition are followed by various techniques.

The position of a base in a sequence is indicated by the cycle of addition at which the insertion of the base is detected.
The base is known from which of the different dNTPs allow the extension reaction to occur.
Detection methods vary but include detecting the release of pyrophosphate by coupling to a light-emitting reaction (pyrosequencing) and detecting hydrogen ions released during the polymerization using a semiconductor chip (ion torrent).

Coda: Principle and Practice
In stressing the general principles of DNA sequencing the methodology mentioned has been limited to that required for detection — there was no need to even mention PCR. Of course, different methodologies for preparing multiple samples for sequencing have hugely influenced the speed and cost of DNA sequencing. However the student should understand the principles before getting bogged down in the details, which can be found e.g. in this Wikipedia article on sequencing and on the website of ATDBIO (albeit a not disinterested company).


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Can cell mediated immune response be transferred via blood transfusion
I read that human body can develop cell mediated immunity to viral infections and subsequently clear the virus. For example, people clear warts through cell mediated immune response against the wart virus. Is it then possible to transfer the blood from one person to another to transfer the type of immune cells that kill the virus?

May you consider to add some refferences to your conclusion?


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Snake with strange head
This snake was killed in graveyard Peshawar (Pakistan). I just wonder what is this? Is it a snake? Baby crying sounds were reportedly heard from graveyard in Peshawar after months of search the sounds of baby crying were identified and this snake was killed. I have a video. I just want to know what is this?

It makes me sad that it was killed. Looks like Cerastes genus: https://en.wikipedia.org/wiki/Cerastes_(genus)

It seems like your dead snake is already mentioned in Wikipedia: "A member of this species [Cerastes cerastes] was reportedly found and killed by locals in urmar graveyard situated on border of Peshawar and Nowshera districts of Khyber Pakhtunkhwa province of Pakistan. The incident was reported along with a photo of the dead reptile in 'Aaj' Urdu language newspaper published from the provincial capital Peshawar on September 10, 2019."

Aren't Cerastes spp. pretty much found in the Arabian peninsula and west?  Might this be in the genus Pseudocerastes, which is known to be found in Iran and Pakistan?

@mgkrebbs Perhaps. But the horns look more like Cerastes to me.

The picture looks like it's from the Cerastes genus. It looks similar to a head shot of Cerastes Cerastes (Saharan horned viper) shown on Wikipedia:

In fact, the incident you describe is also reported in Wikipedia's Cerastes Cerastes article since it could be the first sighting in Pakistan. However, I sincerely (and respectfully) doubt that this snake was producing the "baby crying sounds". According to Wikipedia they produce a "rasping sound" when threatened.
I'm not sure that the specimen in your photograph is actually Cerastes Cerastes but the genus should be correct.


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Looking for books on How the limbic system works and it role in non-verbal behavior
This is my first post. I just read and I'm currently studying a book called "How everybody works" as a guide to understanding nonverbal behaviors.
After I'm done studying it and while I experiment with its claims; I'm looking to understand more of how the limbic system works and its role in human emotions.
The book's premise is that the limbic system makes us react to certain situations in such ways that nonverbal behavior is expressed; therefore by understanding the limbic system and nonverbal behavior we can ascertain a person's reaction to outside stimuli and gain insight.
If anyone could provide recommendations on books about the Limbic system
that are up to date with current finds or any other books that relate to the topics above I would greatly appreciate it.

not sure if you are still looking, but I have two recommendations for you.

"Limbic systems for emotion and for memory, but no single limbic system" is a really long, but really great article on the topic.  You can find that online here:  https://www.sciencedirect.com/science/article/pii/S0010945213003110?via%3Dihub
It's been a while since I've read this one, but the book Synaptic Self:  How Our Brains Become Who We Are is a good read on this subject.  It's about the brain as a whole, but focuses a lot on the limbic system and amygdala (it's author, Joseph LeDoux, did much of the pioneering work on the amygdala).  It is from 1996, so the science isn't super up to date, but I still think it's a good read if you're just curious about the brain and limbic system.


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Is plasma membrane permeable to sucrose
I searched a lot in the net but don't found a clear answer.
I just want to know if plasma membrane is permeable to sucrose.

No, but yes.
Sucrose is a large polar solute.
Because it is polar, it cannot easily pass the hydrophobic core of the membrane.
So, if the lipids of the plasma membrane are mostly impermeable to sucrose, how do cells take in sucrose?
Plants
In biology, membrane-bound proteins are used for efficient transport across the membrane (Brian, 2011 from a review of Suc transport in plant cells).
The specific group of membrane proteins used for sucrose transport are unimaginatively called Suc transporters (SUT).
So in a plant cell, sucrose can be moved across the membrane.
Humans
In mammals, there are no SUTs. Instead, sucrose is broken down into fructose and glucose by the enzyme sucrase.

From there, glucose transporters GLUT proteins carry glucose and fructose across the plasma membrane.

What I don't understand is that in the osmosis experiment, potatoes shrink for a long time in the solution of sucrose. if plant cells were permeable to sucrose the potatoes will gain their initial size

@medmorad it depends on sucrose concentration and whether sucrose transporters are expressed in that particular tissue.


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Can germs spread by tissues out of box?
Firstly, I don't know if this is the best site to ask this question. Please guide if its not.
Now my question:
If we take out a tissue out of its box, a new tissue comes out partially so we can easily take it next time. Now that tissue can easily collect germs from sneezes and coughing of other people around us.
Can that cause problems/infections? Why doesn't tissue box have a better design?

I think the current design of tissue boxes is more about ease of use than cleanliness.  Though you do bring up a good point, considering that many human pathogens can persist on surfaces

This definitely possible. Due to the microscopic scale of bacteria and viruses, even very light forces(like those from pulling a tissue out of the box) will lead to those bacteria and/or viruses being tossed to the rest of the box.
However, a large portion of the infectious viruses in humans will struggle to survive on the dry, low nutrient substrate of the tissues and box for extended periods of time(especially given high absorbance), albeit the above comment show many that can(depending on the surface).
To answer why there is no better design, I think the simplest explanation is monetary incentive. There is little incentive to create something better both due to R&D cost and inevitable increase in product price, as well as a steep consumer education cost to let customers know, why this is better. However, if you have a good solution in mind that does not raise product cost beyond a few cents per unit, you should a decent shot(if you patent) to license it to the big players.

Maybe it's not better in the long run? Let's say you have a hermetically sealed tissue dispenser under a UV lamp. How will that help when you grab the door knob or touch your clothes that came into contact with who knows what or walk down wind of a group of people breathing? It will probably be very difficult to prove it reduces infection in everyday life.

^ Yes this is correct. The research costs associated with an alteration of this nature will be extremely prohibitive.


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Are PVC&PET bacteria found inside homes?
I am interested in weather PVC and PET eating bacteria can be found inside people's homes. The PET consuming ones were found in or near plastic waste dumps or in the ocean, but would they also have adequate conditions in people's domiciles or they require specific things like the plastic being constantly in contact with water or earth?
I am mainly interested in the probability/possibility of PET eating bacteria being found in domestic spaces.

Sorry, i was away for a while and didn't see it ^^: I am more interested in PVC, and yeah, i have plastics that are 15+ years old and don't have any visible holes or abrasions, i was a bit perplexed about weather a lifeform so proliferous (and with ample ''food'' available) would only be found in dirt/water, if that, and could consume PVC only while there.

Only thing i found that addressed the issue tangentially was a wikipedia article about a strain that eats PET and was found in Japan, and an article about PET degrading bacteria in cold seas, no mention of PVC or household conditions. I guess that i'd do best to find some microbiologist or bacteriologist and ask them directly, but chances of that are low.

I see (X-ray specs you get after a certain time here) that you tried to thank me in an answer (deleted) You haven't enough "reputation" (points) to comment yet, where this would normally go. You are welcome. Although I don't share your particular concerns, it was interesting to me from a biochemical point of view to read about the bacterial metabolism.

If you read the Wikipedia article carefully, and the recent article in PNAS on improving the enzymes responsible for TET degradation, it is evident that Ideonella sakaiensis is the only example so far known of a bacterium that can use PET as an energy source. As it is a Japanese marine bacterium it will not be found in “domestic spaces”.
The requirement for an aqueous environment is presumably related to the need for the enzymes the bacterium secretes to gain access to the plastic and the products of the digestion to be reabsorbed, and perhaps also for access to essential nitrogen, not present in the plastics. The rarity of bacteria that have evolved this facility presumably relates to the ‘difficulty’ of the chemistry — or its difference from that involved in degrading other carbon sources — although there is some similarity to cutinase, the enzyme in certain fungi that can digest the cuticle of plants.

I also found something other of interest, apparently a certain Daniel Burd isolated some microorganisms from a landfill, full info here:
https://oxsci.org/2018/11/27/daniel-burd-17-year-old-eco-expert/
The organisms that he found degrading PET were genus Sphingomonas and Pseudomonas. I couldn't find weather they had PVC degrading capabilities though. As for these being found in ''domestic'' conditions, well, they were found in a landfill, so a level of moisture and soil contact seem to be of some necessity to them.


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Are all endocrine glands associated with common human feelings?
I was looking at endocrine glands and found it interesting that a few of them have some very understandable feelings/mentalities associated with them.  In particular:

Gonads: arousal/romance
Pancreas: hunger (glucose)
Adrenal glands: fight or flight
Pineal gland: sleepiness (melatonin)

Of course, there is a lot more complexity to how these glands work and what they do, but I find the notion of being able to empathize with a part of the body interesting.
As a counter-example, if something is wrong with my spleen, there may be feelings associated with that (ie pain), but they aren't so profound as things like hunger, fear, and arousal.
Anyways, my curiosity here is: do all endocrine glands have a feeling associated with them?
Here's the list of all glands:

Pituitary gland
Thyroid gland
Parathyroid glands
Adrenal glands
Pancreas
Gonads
Pineal gland

Also, I know this is a silly question, but please bear with me here.  It's piqued my interest, and I just want to fulfil some curiosity.

You may not be able to feel or be aware of the actions of all endocrine glands at the time they occur.
The parathyroid gland secretes parathormone, which affects calcium absorption in the intestine, kidneys and bones, phosphate excretion in the kidneys and vitamin D production in the kidneys. I'm not sure if one can feel these actions or its consequences.
The adrenal cortex secretes aldosterone, which maintains sodium and potassium blood levels, which is related to blood pressure and urine excretion. It also secretes cortisol, which affects glucose utilization, fat breakdown and inflammation and affects the actions of some other hormones, but within normal physiological range, you don't feel these effects. Cortisol is also known as a stress hormone, but its actions are much more subtle (on the level of metabolism) than those of adrenaline (heart rate, excitement). Saying that, cortisol secretion can be related to sleep and appetite. There is a lot of speculation how it might affect mood or "energy levels" (adrenal fatigue).
There are many gastrointestinal hormones (gastrin, secretin, cholecystokinin, ghrelin), some of which affect digestion, some peristalsis and some appetite and you may not be consciously aware of all of that.
Some pituitary gland hormones (ACTH, TSH, FSH, LH) stimulate the secretion of hormones from other glands (adrenal, thyroid, gonades) and some (growth hormone, ADH, oxytocin) act directly on organs - I don't think you can say that you can feel these effects.
Some hormones have effects on other hormones (cortisol > adrenaline ; thyroxine > growth hormone, etc.), so it may not always be possible to pinpoint which feeling is directly related to which hormone.
Common human feelings related to hormone secretion:

Excitement or stress response, including fast heart rate and breathing and anxiety: short term response: adrenaline; long-term response: cortisol
Appetite: ghrelin, leptin, adiponectin, cholecystokinin, insulin, glucagon-like peptide, gastrointestinal peptide...
Sexual drive: sex hormones, mainly testosterone and estradiol
Sleepiness: melatonin, cortisol
Depression: cortisol, sex hormones (mainly in women)

The point of this answer is to show that some of your feelings can be simply affected by hormones, which are note some ultimate forces, and that being aware of that can help you to control them to some extent.


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What is a false crocodile?
On the wikipedia page about crocodiles crocodiles are called true crocodiles. Does this mean there are (or where) false crocodiles as well?

Crocodiles (subfamily Crocodylinae) or true crocodiles are large semiaquatic reptiles that live throughout the tropics in Africa, Asia, the Americas and Australia. Crocodylinae, all of whose members are considered true crocodiles, is classified as a biological subfamily.https://en.wikipedia.org/wiki/Crocodile

The only "false crocodile" I found was the False gharial.
What is a false crocodile? if it exists at all. If not what is the reasoning behind the naming of a true crocodile?

If you keep reading the next sentence it makes clear what is meant (emphasis mine):

Crocodiles (subfamily Crocodylinae) or true crocodiles are large semiaquatic reptiles that live throughout the tropics in Africa, Asia, the Americas and Australia. Crocodylinae, all of whose members are considered true crocodiles, is classified as a biological subfamily. A broader sense of the term crocodile, Crocodylidae that includes Tomistoma, is not used in this article

So, the Crocodylidae family refers to crocodiles, the Crocodylinae subfamily are the true crocodiles which includes almost everything known as a crocodile, and indeed, you found the one that gets left out:

The crocodylian family Crocodylidae includes the true crocodiles, which are the members of the subfamily Crocodylinae, as well as potentially the false gharial, the only extant member of the subfamily Tomistominae. The latter is a subject of controversy as to whether it is a crocodile or actually belongs in the family Gavialidae.

(via Wikipedia)
Wikipedia further states:

Gavialidae have conventionally consisted of only one surviving species, the gharial (Gavialis gangeticus), which is native to India and Nepal. Many extinct species are also known

and also

Tomistominae is a subfamily of crocodylians that includes one living species, the false gharial. Many more extinct species are known, extending the range of the subfamily back to the Eocene epoch. In contrast to the false gharial, which is a freshwater species that lives only in southeast Asia, extinct tomistomines had a global distribution and lived in estuaries and along coastlines.

So there are many other extinct relatives of crocodiles in these groups; the question is to which the extant false gharial belongs. In either case, the other Tomistominae would be non-true crocodiles, according to a definition that subfamily Crocodylinae are the true crocodiles.
The words "true" and "false" are not necessarily used in their boolean meaning here, but rather, "true" in taxonomy fits better with other definitions, for example from Merriam-Webster: "typical" (Merriam-Webster explicitly references the "true cats" as a use for this meaning). A synonym would be more like "archetypal" or refer to a clade or other more robust grouping, rather than a linguistic/non-scientific grouping.


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Why use a logarithmic scale when plotting pharmacodynamics/kinetics?
I've seen the plots and they don't look drastically different. Why do this?
Why use a logarithmic scale when plotting pharmacodynamics/kinetics?

Is there a specific type of plot you're referring to?

concentration time profile

Well, for example, plotting log concentration against time for a first order process gives a straight line with a slope equal to the negative rate constant.

@canadianer That should probably be an answer.

There could be several reasons for this. You mention in the comments that your plot of interest is the concentration-time profile. As you can see, plotting the logarithm of concentration vs time yields a very different plot for a drug administered intravenously.
The reason this is done is because the two plots yield different information. The slope of the log(C) vs t plot actually yields the elimination constant, Ke. The logarithmic plot can also be used to assess if the drug is distributed into one or more compartments. If the drug is distributed into two or more compartments, the initial slope would be different than the remainder (but this is not pictured here).
In terms of pharmacodynamics, its often useful to assess how a 10- or 100- fold increase in concentration affects the effect.


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Estimating diffusion constant of a protein based on number of amino acids
Is there a way to estimate the diffusion constant of a protein based on the number of amino acids it is comprised of. I know that the shape of the protein has an influence on the diffusion constant, but I didn't know if there was some estimate that could still be used to good approximation.
If this does not exist, is there still a way to approximate the diffusion constant of certain proteins. I am trying to make a rough model based on reaction-diffusion equations, and I wanted to estimate diffusion constants of certain species in the model.

Also, you can check PDB if the structure of the protein is available. If so you can get a reasonably close estimate of its shape in vivo. If not, then you can check out some software that predict protein structure based on homologous proteins. However, I cannot say that there is a good estimate of protein diffusivity just based on number of amino acids. Are you interested in a particular protein or you want to make a general model?

@WYSIWYG After further reading it looks like I am looking at a cytokine that only has about 25 amino acids (49.5 kDa). I am assuming this might be easier to estimate a diffusion constant for since it is so small?

@AaronStevens someone could have measured diffusivity of cytokines in blood and ECF (for e.g.). If not, you can find the structure of a cytokine on PDB, obtain it's radius and estimate diffusivity using the Stokes-Einstein equation.


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Chromosome naming convention: Why are there chromosomes named "1" and "1A"?
I've been stumbling on multiple genome of birds where there is a "1A" chromosome and a "1" chromosome. For example, the zebra finch has 1A and 4A. What does that mean?
Do you have any resource about naming conventions for chromosomes and if this naming convention is specific to birds?

I would suggest looking at some of the reference genome papers. My guess is that the chromosomes are named as such based on their synteny to the chicken genome; e.g. look at Accessory Figure 3 here for your zebra finch, and note that chromsomes 1 and 4 are split in the zebra finch relative to Gallus.
The direct comparison from that paper is to an Accessory Table 1 that I can't actually find.
I would guess that in most cases it's because of a synteny comparison to some reference, in this case chicken that splits a chromosome in the new genome. For example sequences homologous to the chicken chr1 are on two finch chromosomes 1 and 1A.

This is my suspicion as well, similar to the ape chromosomes 2A and 2B.


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Where can I find extensive information on animal blood types and transfusions?
I'm interested in doing research on different animal blood types, including blood transfusion across different species. What are some resources you could recommend for me?

Welcome to SE Biology. Please finish reading the Tour. It's dubious whether book recommendation are on topic here as they are subjective, but you should use the site search facility to find out if there have been similar questions on this topic. You will find one here that may provide some starting points, although I am not an expert in this area.

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!


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Autoclaving media Question
1.When I autoclave media should I close the cap tightly or slightly?

I put all tools in plastic bag when I autoclave, should I close slightly the plastic and when it finish I close tightly the plastic? The air steam need to go inside the bag?
I read some document told me autoclave 21 minute, but in my lab everyone operate 35 to 40 minute, What you think?
Thank for your help.

For the media bottle, it is better to keep the cap a bit loose to avoid to pressure inside the bottle. A good way is to had autoclaving tape on the side so that it is clear that the bottle has been autoclaved. As Chris mentionned below once autoclaved, use gloves, and close the bottle firm after you open the autoclave and do not wait until it has cooled down completely.
It is not really important if it is slightly to tightly close. In fact you could have them on a tray or a bucket that would be fine to. One caveat is that it might depend on the equipment, the rules regarding the usage of the equipment etc. You would need to check these questions with a Senior person on the site.
The longer the better. If everyone operate at 35-40 min either there is a good reason to do so (often the case) or not. To be safe, I would suggest to be conservative there. Often what might happen is you want to make sure that you have the sample autoclaved at the highest temparature for at least 20 min. Because of leakages or other factors it might be best to leave it longer to make sure it is autoclaved at least 20 min.

Hope that helps!

In addition to 1.: Close the bottle firm after you open the autoclave and do not wait until it has cooled down completely.

Good point I will edit the answer!

So many things are done because everyone else does it, but nobody knows why.


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Bioenergetics book
I already asked this question on the physics SE but redirected here:
In the field of biophysics, it seems there is a subfield called "bioenergetics" about the processes of generating energy by biology. I am looking for a book to be introduced to the physics aspects of bioenergetics. I checked up on Springer and there seem to be quite some books on the topic, but the problem is that I fear that they would require heavy biology basics.

Whether you are talking about generating heat energy, kinetic energy, or releasing chemical energy, you'll certainly need an understanding of the underlying molecular biology and/or biochemistry. It depends on what you mean by "heavy biology basics". For instance, understanding oxidative phosphorylation would require you to understand that mitochondria have a double membrane and are equipped with an electron transporting machinery within one of the membranes. That certainly is biology.

@SPr Understood, but is there a book that is "self-contained" in some way that the biology basics like "mitochondria" are explained?

Ok so the vital force seems to be oriented towards biochemistry, right? And what is the purpose on Harold on the Peter Michell Nobel prize? I didn't understand the purpose of it in the question. Do you, by any chance, have the list of chapters of The Vital Force?

Sounds a bit too advanced, but a good reference nonetheless :)


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Ligand-binding assays: IC50, EC50 and Kd
I am reviewing several MHC-peptide binding affinity predictors trained on  IEDB data. Quantitative records for MHC class I allotypes come from a lot of different assays and, by extension, have different measurement types. Here are the most common measurement type descriptions (I haven't altered them in any way):

dissociation constant KD (~IC50)
dissociation constant KD (~EC50)
half maximal inhibitory concentration (IC50)
dissociation constant KD
half maximal effective concentration (EC50)

All of the predictors I've reviewed so far consider these measurement types interchangeable, which I find extremely odd. While IC50 and EC50 can indeed be similar under certain experimental circumstances, I find it hard to believe that any one of these can be approximately equal to Kd (this site already has a post on this matter). I've contacted several authors and database curators, and all of them have assured me that these values can indeed be considered more-or-less interchangeable, but I can't find any references to support these claims.

Not an answer (I can’t comment yet), but what is the difference between 1, 2, and 4?

@MarkusHeller as far as I understand, 4 means either 1 or 2.


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Are these termites
Found a large number of these trapped between my window and the window frame. Are they termites?
Location: Eastern Massachusetts, USA

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This is an ant in the genus Camponotus. It can only be identified from the habitus on your picture, but clues are that there is only one element between the thorax and the gaster (Formicinae) and the head is large, this with the color and texture pattern leads to Camponotus sp.
Refer to

Bolton, B., Alpert, G., Ward, P. S., & Naskrecki, P. (2006). Bolton’s
  Catalogue of Ants of the World. Cambridge: Harvard.

for more detail on the identification.

Based on the morphology of the abdomen and antennae as well as the darker coloration, I'm going to say they are not. Looks a bit more ant-like (see picture).

Thank you, jmc1094. Mine do not have wings. Is it a seasonal thing?

Not necessarily, I just chose that figure as it illustrates differences in the body types pretty clearly.

Definitely an ant. Ants have elbowed antennae.

Termites are often nearly white and look as if the have 2 body sections instead of 3 as a typical insect.


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What is the water and fat composition of the human brain?
Everywhere I look online says the brain is about 60% fat. But when it comes to water, I see numbers like 70-75%. One webpage even makes both those claims back to back! That doesn't make any sense. So what is it, really?

Can you provide citations (e.g., links) to the competing claims?

Whenever you see a percentage, you should think "Percentage of what?".  Not doing this is usually at the root of the trouble people get into with percentages.
The water and fat percentages mentioned in the question are certainly not percentages of the same thing.  The sources of the figures should make clear what the percentage is of, but non-scientific writing quite often fails to do this.
In the paper "Lipid composition of the normal human brain", there is a table giving percentages of water and lipids (fats), and at the bottom of the table it says:

All values, except water, are expressed as a percentage of dry weight.

This is a common approach, as, for example in this table from a textbook the lipid percentages are also given as percent of dry weight. This is convenient because water is such a large part of most organisms, and also dry weight is what is usually measured in the laboratory.
Thus the water percentages you are seeing are presumably percentages of total weight, and the fat percentages are percentage of dry weight.  You can convert the latter to percent of total weight by multiplying by the dry percentage of the brain, which is what is left when you subtract the water percentage from 100%.
Thus, assuming say 73% of total brain weight is water, the 60% fat figure would translate to about 16% of total brain weight is fat.

mgkrebbs is totally right. It's standard in biology to evaporate the water to get the wet/dry weight, and then to see for the rest. This study is old so it may lack accuracy:

Please give a citation for the source of this table.

The reference is: JS O'Brien and EL Sampson. Lipid composition of the normal human brain: gray matter, white matter, and myelin. J Lipid Res. 1965 Oct;6(4):537-44.

The reference to what? Answers on StackExchange must be self-contained; it's very good to provide references, but also important to include the information that is referenced.