text:
how much can changing light enter the eye shap what you see?
Does it change the shape and how objects are seen or does it just stop you from seeing certain things?

Needs clarification: what is "it"?  "changing light"?  What do you mean by "changing light"?

Now that I reread it its really poorly writen. I'm guess I'm talking about light manipulation. How can manipulating light change how you see. Like changing how much light get in the eye changing  the angle. Will these manipulation change how we see and how? Will it just stop us from seeing and nothing more or is that some how linked to hallucinations?

I'm interpreting your question to be: "How much can changing the light entering the eye change the shape of/how objects are seen? Would manipulating that light just stop you from seeing certain things?"
Manipulating the light entering the eye is the exact premise of a virtual retinal display (VRD):

From Wikipedia –  A VRD is a display technology that draws a raster display (like a television) directly onto the retina of the eye. The user sees what appears to be a conventional display floating in space in front of them.

Google Glass and other technologies (virtual reality headsets, heads-up displays) operate through relatively similar projection mechanisms. Light defines everything the eye sees (outside of hallucinations, and even those can be induced by flickering light). Also, the way your brain processes visual information (photons received by your eyes) can be "tricked," which is discussed in this BBC article. Finally, your brain's ability to process visual information can be altered by external forces (e.g. drugs, motion, or even strong magnetic fields).

Thanks also for the link to other information.  This is exactly what I was looking for. Sorry for the bad explanation.


text:
What is the length and number of the parts of a conformational epitope?
I am interested in the question whether exposure to protein A might create antibodies that also bind to protein B.
I am wondering whether, if the antigen of protein A is a conformational epitope, it would still be possible to predict (or at least guess at) the reaction against protein B with only a sequence comparison.
This might be possible if the subunits are long enough and if there are enough of them, which is why I ask about their length and number.

You seem to be using the word "subunit" in a manner that conflicts with that used with respect to protein structure. Do you mean short stretches of primary structure that contribute to the epitope?

Yes, I guess that's what I mean. I took that term from the definition of conformational epitope at wikipedia: "A conformational epitope is a sequence of sub-units (usually amino acids) composing an antigen that come in direct contact with a receptor of the immune system."

I found this paper that analyzes 111 antigen-antibody x-ray crystal structures.
They find that in their dataset that "the large majority of Ag structures (86.5%) have CRS ranging from 20 to 229 aa." CRS stands for contact regions span which they define as "the minimum contiguous amino acid sequence containing all CRs of an Ag or Ab and represents the size of a complete structural epitope or paratope, inclusive of CR and the minimum set of supporting residues required for proper conformation." further on they mention that "The average and median CRS of all 111 Ag structures is 125 and 95 aa, respectively." and "the majority of the structures do indeed have epitope CRs that are clustered together in short, contiguous stretches ranging from 2 to 12 aa, longest contiguous sequence of CR being 5"
I hope this helps.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


text:
Semantics Question: epigenetic mark on a person's DNA?
In an article on biomarkers of child abuse, the author referred to an "epigenetic mark on a person's DNA". It's a popular science article, so the language may reflect a combination of the journalist's scientific competency and his or her desire to communicate complex topics efficiently to a lay audience. Is that an example of such language?
My understanding was that anything in the realm of "epigenetics" is happening to something other than DNA. Is it technically correct to refer to an "epigenetic mark on a person's DNA"? Correct enough? Only potentially misleading? I'm trying to wrap my head around the whole epigenetics concept.

This link is totally unhelpful.  You have to link to the actual paper in question.  https://www.nature.com/articles/s41398-018-0252-1

We may restrict your definition of epigenetics as heritable changes in an organism's phenotype that occur without a change in the sequence of DNA bases. That is, changes to the DNA molecule itself is permitted, as long as the sequence of ATCGs are not affected.
In this sense, it would not be wrong to refer to an "epigenetic mark on a person's DNA". For example, a mechanism of epigenetics that does directly change the DNA molecule would be something like DNA methylation.

Then the article is incorrect, because it does not establish that the chemical modification to the DNA has been inherited or will be inherited, regardless of whether it has any function, which clearly has not been established.

@David I don't see any part of this answer that demonstrates that the article is incorrect, again given the interpretation for "inheritance" in epigenetics, which does not necessarily refer to inherited by the offspring (per our comment conversation on your answer and the final paragraph of your answer).

@BryanKrause — It would seems that an extensive answer — considering and distinguishing the different definitions or interpretations of the term is needed on SEBiology to deal with epigenetics. I'm not sure this is the best question to use, as ultimately the poster's concern seems to be more at the level of base methylation v. histone modification as epigenetic.

It all depends on your definition of epigenetic. The one assumed by @ning, that appears to fit the case, is that cited in the Wikipedia article on the topic is:

“Epigenetics is the study of heritable phenotype changes that do not
  involve alterations in the DNA sequence”

Methylation is a change in DNA that does not involve altertion in the DNA sequence. For observations of such marks to be epigenetic it needs to be proved that they also:

Have a phenotype. In this case the association of the methylation with behavioural changes resulting from child abuse is not asserted or demonstrated.
Be heritable. This is also not asserted or demonstrated in the article.

I am unaware of any circumstance in humans in which these three conditions have been satisfied.
Epigenetics without inheritance
I think the confusion and pseudo-science associated with this topic arises from the fact that DNA methylation can play a role in differentiation of cells during the lifetime of higher organisms, which has also been termed epigentic. This has been confabulated with experiments on inheritance of methylation patterns in bacteria. A resulting epiphenomenon has been a revival of credence in the criminal fraud of Trofim Lysenko.

In literature on epigenetics it is common to take the "heritable phenotype" in your first definition to include inheritance within cell lines in an individual, rather than the more common use of the term to mean across generations, though clearly the article in the OP was referring to generational changes. I'd say this is especially true in 'epigenetic' research into cancer where the term really just means "long-lasting changes in gene expression that are carried to daughter cells."

@BryanKrause — Agreed, as I hope my rider made clear. But the abuse of the real science by gutter journalists and people with a political agenda really annoys me.

Understood, and I know you have been an opponent of (intergenerational) epigenetic studies on previous questions here. I have to say though, although imperfect, I thought this article was actually a very fair assessment for a more pop science article, have you actually read it? It makes the controversy pretty clear and identifies accurately the current state of research: someone is reporting some methylation changes in sperm and are uncertain at this point if those make it through to offspring.

I'm not sure you mean confabulate. Autocorrect?

The word suddenly came to mind, so I checked with Merriam Webster who give one definition as "to fill in gaps in memory by fabrication". Seemed quite a good fit.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Is there a simple incision that would render a man impotent?
I’m writing a novel in which two women (one of whom is a doctor) take revenge on a rapist by performing surgery on him.
What would be the simplest but most effective way of causing permanent and total erectile dysfunction?
I assume cutting one or more nerves but there are several up for contention:
The Dorsal nerve
Pudendal nerve
Inferior rectal nerve
Perineal nerve
Posterior scrotal nerves
Ideally, I’d like the surgery to be so minimally invasive that he wouldn’t even be aware that it had been done to him.

Snake Bite. There is a cobra in Thailand/Asia whose venom interferes with the male pituitary or some deep brain hormone regulation, and the result of enough venom is that he stops growing a beard, his testosterone drops, and he becomes like a 8 year old boy again.

@com.prehensible Thanks! My novel is set in a small English village so getting cobra venom may be a bit difficult, but I may use that for a future novel! Out of interest, why would a question like this get voted down with no explanation as to why? Have I not phrased it correctly? Thanks!

I think the downvotes are from people who might not think this stack is most appropriate for your question. I see the biological relevance, but future questions like these might be better answered in the medicalsciences stack or the writing stack.

Thanks Bruce. On the writing stack we generally migrate questions and explain why rather than just downvote them. But they're a cheery bunch over there. Glad I made the mistake of picking this stack, if I hadn't, I wouldn't have found you!

I'm voting to close this question as off-topic because it's better suited for health.

You want to somehow damage the cavernous nerves of the penis. If you damage the preganglionic root of the cavernous nerves (the pelvic splanchnic nerve), you'll create all kinds of other problems.
You might also  consider using a chemical agent instead of surgery; this will allow for increased discretion and ease of administration. I discuss this after the break in my answer.
Erection is driven by the parasympathetic nervous system; ejaculation is driven by the sympathetic nervous system. Since you're looking for "permanent and total erectile dysfunction," you want to disrupt parasympathetic innervation to the penis. The candidates you've mentioned (dorsal nerve, pudendal nerve, inferior rectal nerve, perineal nerve, posterior scrotal nerves) won't work since none of them provide parasympathetic innervation to the penis. Rather, the dorsal nerve of the penis is a branch of the pudendal nerve and provides sympathetic (ejaculation) and sensory innervation; the inferior rectal nerves are also branches of the pudendal nerve and provide purely somatic innervation to the anus (these lie below the pectinate line, which marks the boundary we use to define internal and external hemorrhoids); the posterior scrotal nerves are a sensory branch of the perineal nerve, which itself is a branch of the pudendal nerve. This plate from Gray's will help you visualize these relationships.

"The Epidemiology and Pathophysiology of Erectile Dysfunction." Melman et al. The Journal of Urology. 1999.
Erectile  dysfunction
is
a
common
condition  associated
with  aging,
chronic
illnesses
and
various
modifiable
risk
factors. Normal penile erection
is a hemodynamic
process
that
is
dependent
on
corporal  smooth
muscle relaxation mediated
by
parasympathetic neurotransmission, nitric
oxide,
and
possibly
other
regulatory factors
and
electrophysiological
events.
As
more
knowledge
is
gained
of
the
physiology
and
regulatory factors
that
mediate
normal
erectile
function,
the
mechanisms
involved
in
the
pathophysiology
of
erectile
dysfunction
should
be
further
elucidated.

So, let's say you want to go after the parasympathetic nerves to the penis – the cavernous nerves. These are postganglionic, meaning they've already synapsed in the cell bodies of their target organ. Here's another plate from Gray's to make clear the parasympathetic (blue) vs. sympathetic (red) innervation in the body:

As you can see, the preganglionic pelvic splanchnic nerve might be an easier target than the postganglionic cavernous nerves, which will be running all over the tissue of the penis, making them difficult to quickly and directly target. However, you risk disrupting other hindgut functions as you move closer to the sacral spine.

"The actions of parasympathetic and sympathetic nerves in human micturition, erection and seminal emission, and their restoration in paraplegic patients by implanted electrical stimulators." Brindley. The Royal Society. 1988.
Appropriate stimulation of the S2 roots causes the erectile tissue of the penis to swell... Implants that stimulate the S2, S3, and S4 anterior roots improve micturition, defaecation, and penile erection in many patients with spinal-cord injuries.

Your desired discretion will go out the window if your antagonist wakes up unable to normally urinate or defecate, so you might target the prostatic plexus, where the branches of the cavernous nerves arise, but this is a relatively deep structure (bound within the prostatic sheath) that you won't be able to discretely injure. When scientists test cavernous nerve injuries, they use a variety of techniques, but none of them are particularly non-invasive:

"Functional Sequelae of Cavernous Nerve Injury in the Rat: Is There Model Dependency." Mullerad et al. The Journal of Sexual Medicine. 2006.
Nerve Manipulation Techniques
(1)  Control  group  (C):  underwent  a  laparotomy
only  to  control  for  the  effect  of  anesthesia.  The
pelvic  organs  were  not  disturbed  and  thus  the
result was no visualization of the CN. (2) Exposure
group (E): laparotomy and dissection of the pros-
tate to enable visualization of the CNs bilaterally
without any direct CN manipulation. (3) Neurot-
omy  (N):  the  CNs  were  transected  bilaterally,
5  mm  distal  from  the  ganglion,  with  as  much  of
the overlying fascia preserved to allow approxima-
tion  of  the  nerve  ends.  (4)  Bulldog  clamp  crush
group  (B):  a  vascular  bulldog  clamp  (60  g/mm
2
,
Fine Science Tools, USA) was applied to each CN,
5  mm  distal  to  the  ganglion.  It  was  applied  for
30  seconds,  removed  for  30  seconds,  and  then
reapplied  for  a  further  30  seconds.  (5)  Hemostat
crush group (H): an ultra fine hemostat (12.5 cm, nonserrated, Fine Science Tools) was applied with
full  tip  closure  in  the  same  manner  as  for  the  B
group.

Understanding the anatomy of the penis will help you decide how to proceed. I think you're on the right track with a neurovascular or nerve injury. "The Physiology of Human Penile Erection" (Weiss, Annals of Internal Medicine, 1972) includes this great figure, where each labelled letter in the pathway relates to a specific site of erectile dysfunction-causing injury:

You're most focused on sites F, G, and H. Here, F is caused by long-term illness and G is caused by, once again, invasive surgery:

SITE  F The  incidence  of  erectile  dysfunction  in  diabetes  mellitus   exceeds   that   in   diabetic   retinopathy   or   nephropathy.  In a random study  of 200  diabetic  men,    59%   were  impotent.   The  incidence  of  impotence  does  not  correlate  with  the  duration  of  the  diabetes,  the  severity  of  the  imbalance  in  carbohydrate  metabolism,  or  the  degree  of  diabetic  control.   Impotence   is   occasionally   the   initial   clinical   manifestation  of  diabetes,  and  diabetes  should  be  considered  as  a  possible  cause  whenever  a  man  complains  of  impotence.  Ellenberg   found  a high correlation between  neurogenic  bladder  abnormalities  and  impotence  and  thereby  postulated  that  an  autonomic   neuropathy   was  the  cause   of   impotence  in  diabetes  mellitus.  Other  causes  of  autonomic  neuropathies  are also frequently  associated with impotence. Simpson   speculated  that  a  diabetic  angiopathy  involving   the   small   vessels   of   the   erectile   tissues   might impede  the blood flow and lead to impotence in some  cases.
SITE  G Radical   surgical   procedures,   such  as  abdominoperineal  extirpation  of  the  rectum,  frequently  destroy  the  nerve  plexuses  from  both  spinal  erection  centers,  resulting   in   complete   impotence.   The   effects    of    sympathectomy  on  potency,  if  any,  have  been  discussed   earlier.   Other   surgical   procedures,   such   as   transurethral   prostate   resection,   that  do  not  interfere  with  the  neural  or  vascular  structures  mediating  erection   usually   do   not   alter   penile   potency.
SITE  H Drugs  that  inhibit  the  action  of  acetylcholine  on structures   innervated   by   postganglionic   autonomic   nerves  (for  example,  methantheline  bromide)  occasionally   cause  impotence.   This   effect   is  consistent  with  the  role  that  cholinergic  fibers  play  in  opening the polsters  and initiating erection.

Alternative method: chemical agent
Site H caught my attention most, since the author mentions inhibitory drugs causing impotence. This might be the non-invasive, discrete route you've wanted.

"Pharmacology of Penile Erection." Andersson. Pharmacological Reviews. 2001.
Phosphodiesterase Inhibitors. The L-arginine/NO/GC/cGMP pathway seems to be the most important for penile erection in some species (see above), and recent results with sildenafil, a selective inhibitor of the cGMP-specific PDE5, further support the view that this may be the case also in humans. Sildenafil is 4000 times more selective for PDE5 than for PDE3, 70 times more selective for PDE5 than PDE4, but only 10 times more selective for PDE5 than for PDE6. Sildenafil is rapidly absorbed after oral administration (bioavailability 41%) and has a plasma half-life of 3 to 5 h.

PDE5 degrades cGMP, which is required for an erection. PDE5 inhibitors (Viagra, Levitra, etc.) prevent cGMP degradation. You might have your protagonist culture PDE5-overexpressing cells and isolate the enzyme (or, she could buy a bunch from Sigma) and sneakily inject the isolate into your villain. This probably wouldn't really work, but I think it might be a better (more plausible) fictional solution than a surgery, which you won't be able to cover up without some other kind of trauma to the area. (Plus, at that point, why not just use the cover-up trauma to create the erectile injury in the first place?)

Bruce, I had no idea erection was so complex! You’re an absolute star for giving up so much of your time, thank you. I should name one of the characters after you but since the only male character available is the rapist, I’m sure you’d prefer I didn’t!

There is a reason I’d like to use surgery: another character will train to be a nurse after assisting with this surgery.
So, if nerves aren’t an option, how about we target blood flow to cause vasculogenic erectile dysfunction?
I found an article on Laparoscopically assisted penile revascularization for vasculogenic impotence, so couldn’t she perform the same operation to cause instead of cure impotence? What if she were to sever either the inferior epigastric artery, the dorsal artery, or the interior pudendal artery?

Long story, but I got to watch a vasectomy and through two tiny incisions, he was able to pull out, cut and cauterise the vas deferens tubes. It would be great if she could do something similar with one of these arteries? Or, failing that, a small incision and cauterise the artery. But I have a feeling you’re going to tell me severing arteries isn’t as simple as severing the vas deferens?

You can definitely sever arteries quickly, but you’ll have two problems: (1) blood is going to want to go somewhere, so you’ll need to cauterize (like you saw with the accompanying vasculature on the vas defrens) or otherwise ligate those vessels; (2) blood is bringing oxygen to those tissues – if you deprive them of blood (to prevent an erection), you risk ischemic necrosis and subsequent amputation. To cause erectile instability, you’ll want to damage the deep artery of the penis, which supplies the corpus cavernosum (the erectile body). As the name suggests, it’s deep!

No need to thank me! If you think my answer was sufficient for your question, you can mark it “correct” and it’ll come off of SE’s unanswered board.

Have marked it!

Bruce, I found some diagrams, you’re right, it’s too deep, impractical. But, I also read that an erection is maintained because, “as the tunica stretches, it blocks off the veins that take blood away from the corpora cavernosa” (sounds like a Harry Potter spell). So, what if she were to stent either the circumflex vein or the deep dorsal vein (which despite its name appears to run along the top surface of the penis)? Would the stent prevent blood from staying in the penis while avoiding necrosis due to blood deprivation?

Obviously, this doesn’t need to be a 100% solution, as a surgeon, she could admit that she’s not sure it will work, nobody’s ever done this before, just as long as there’s a chance it could work. That’s really all you need for fiction!  Thanks!

That's very clever! Ensuring venous drainage is a great, discrete solution – you could place a stent by entering a different vessel (further down the leg, for example) to obscure your work even more (although this stretches realism a little since you'd need to pass through the prostatic venous plexus – easier to go in directly). Venous stripping can treat ED – doing the opposite (stenting/shunting) should work!

BRILLIANT!!  I was hoping you'd say that! But I wouldn't have reached that solution if it wasn't for all your pointers. Going in through the leg would be awesome in terms of discretion, but looking at the diagrams, the deep dorsal vein runs along the top of the penis. I guess, if she does it up high enough where it's buried in his pubic hair, he won't notice the incision. And one of his colleagues will be slipping him pain killers for a few days. Excellent! One impotent rapist! All in a day's work! Thanks!


text:
Are there any particular chemicals that initiate either DNA replication or Transcription ?
When does the nucleus of a cell "know" when to bind DNA nucleotides ( for Replication ) or RNA nucleotides ( for Transcription ). From what i read, they're both structurally different and free nucleotides of both are present in the nucleoplasm. So when one's free nucleotides bind ( mRNA nucleotides for transcription for example ) why doesn't the other ( DNA nucleotides in this case )bind, or what keeps the other from doing so?
Are their any chemical prerequisites of some sort that initiate the processes?
TIA

Your question is too broad for this list, where question sof this sort assume some basic familiarity with the topics asked. You need to read about replication and transcription in some introductory book of biochemistry. Berg et al. on NCBI Bookshelf has well written chapters on these topics.

Enzymes, nature’s catalysts, proteins that speed up chemical reactions.  In this case, creating a linear polymer out of deoxribonucleotide monomers, to yield a polynucleotide (DNA).  This reaction also requires a DNA template strand.  Enzymes contain an active site that brings all of the substrates into alignment, and then key amino acid side chain residues that are located in the active site enhance the intended organic chemical reaction, often by stabilizing a transition state in one or more of the substrates.
You are correct that ribonucleotides and deoxyribonucleotides share many structural similarities, but enzyme active sites can indeed distinguish between the two molecules.  Even if the wrong substrate diffuses into the active site it will usually not be able to participate in the reaction.

Oh ok so basically, its the Polymerase enzymes that sort of "filter" out the right nucleotide additions form the wrong ones and the nucleotides connect to the strand all in their due time?


text:
Genes related to senses and their variation across animals
Animals often have very different numbers of active genes related to any sense. For instance, most fish or even aquatic mammals have very few olfactory receptor genes, whereas this is higher in terrestrial animals. Even among them, there is huge variation; compare dogs and humans, for instance. But this comes at a cost; for instance, dogs are dichromatic, the blind mole is, well, blind. So there is a compensation across the senses which is not merely a plastic change. I was wondering if there is any way to reconcile this with some notion of conservation of the total proportion of active genes involved with sensation.

There are two notions I could think of

There might have a trade-offs about where to spend ressources (energy and nutrients). If an organism spend a lot of ressources in, say, vision (incl. the part of the brain that deal with interpreting the input), then there won't be much left for other things.
When a sensory system is well enough developed that the other sensory systems would bring up only marginal benefits, it is better to just not spend unecceesary ressources on building these other sensory systems.

Please note that

The above two hypotheses are just guess work from me and I did not support any of what I said with an actual evidence.
I assumed that there is a negative correlation between the "quality of the different sensory systems" (whichever way that would be defined) but I don't know whether this is true or not.


text:
Is the structure of human brain white matter fixed at/near birth?
I have been reading that, with exceptions for a few parts of the human brain, no neurogenesis occurs, so no new neurons are created.  I have also heard that no new axons are formed through the white matter of the brain after birth as well.  I also know that the axons are myelinated, minimizing crosstalk and other interesting structural effects that might occur.
Between those, does that imply that the structure of the white-matter of the brain is fixed at a very young age, and never changes through our life?  It seems like a natural conclusion from the data, but it feels counterintuitive when contrasted with the continuous creation and destruction of synapses which happens so close nearby.

No, white matter structure is not fixed at a very early age. Although a person is born with most of the neurons they will ever have, those neurons must form connections between each other, via axons and synapses, and many of the axons become myelinated during this period. Although the number of neurons remains relatively constant, these processes lead to a substantial increase in overall brain volume. After a few years, there is then a period of synaptic pruning (https://en.wikipedia.org/wiki/Synaptic_pruning), in which many of those connections are rationalised. These processes explain many of the characteristics of human development.
For example, mammalian species can be characterised as precocial or altricial. A precocial species is one in which much of the brain's development has been completed in utero. This allows for a relatively sophisticated behavioural repertoire to be immediately available (think precocial = 'precocious'). For example, a foal is born and almost immediately is able to walk, follow its mother, and so on. Meanwhile, an altricial species like a human is born in a relatively helpless state, incapable of independent locomotion and with even very limited perceptual processes. It is the development of axonal and white matter pathways, with associated synapses, that allow learning and development of new skills in the post-natal period.
During this process, the brain is extremely flexible. For example, a baby can initially distinguish between the phonemes of any language. As its white matter connections develop in response to a lot of exposure to the language(s) in its home environment, the brain becomes more specialised. Eventually, past the pre-teen period, it becomes much harder to perceive and articulate subtle phoneme distinctions from other languages, and the acquisition of new grammars shifts from effortless and rapid, to slow and requiring formalised instruction rather than being spontaneous.
This shift to relative inflexibility reflects the second phase of white matter development (i.e. large-scale synaptic pruning). That is, in the first phase, there is widespread growth of connections between neurons via axons and synapses, along with myelination. In the second phase, the flexibility of this system is traded for the efficiency and focus of a brain that has learned what specific abilities it needs to have. This continues up until about age 10, at which stage 50% of the synapses present at age 2 have been lost (https://link.springer.com/referenceworkentry/10.1007%2F978-0-387-79061-9_2856). Learning is then no longer so rapid, but with specialisation and development, an adult is able to focus attention explicitly and maintain discipline towards achieving goals, where a child might get more easily distracted and seek novelty.
Synaptic formation and loss then continues throughout life, as the underpinning of learning processes, but no longer on the mass structural scale seen in earlier development.

Is it only the synapses that are changing, or are the long axions also growing or changing, such that they might terminate somewhere else in the brain?

It is probably the competitive selection and destruction of axons that is the dominant process. eg in the adult macaque there are 50 million axons in the corpus callosum, selected from the 200 million available at birth. Check out chapter 6 of this textbook by Ackerman for a good introduction: https://www.ncbi.nlm.nih.gov/books/NBK234146/?report=reader#ddd00050


text:
Black squirrel in France?
I saw a nearly jet black squirrel in ardeche today,  carolinensis have invaded the UK and Italy, however I didn't find news about their arrival in France. Was that black squirrel really a Canadian species?

Note that "Black morphs may also occur with Eurasian red squirrels" (Wikipedia). I have personally seen some such exemplars. while they are black they are the (smaller) size of European red squirrels. If you've seen both American and European red squirrels (in real life), it's hard to mistake them due to size differences.

Yes you are completely right. I have seen some other black morph squirrels which are Eurasian reds and some which are the same color as tree bark from a fairly dark pine tree.

Yes, Sciurus carolinensis has been invasive in France, Italy and Switzerland for quite a few years already (Bertonlino and Genovesi, 2003).
Note that the "original" distribution of S. carolinensis is over eatern Canada and USA. Not Canada only.


text:
How can two biological sequences be anything but homologous?
If we consider homology between two nucleotide sequences as a yes/no answer to whether they have shared a common ancestral sequence, then given that all life share common ancestry and sequences are carried by living things, then how can two biological sequences be anything but homologous?
One possibility I can think of is perhaps natural transformation in bacterial---but even so, the DNA sequences picked up must have come from a biological source.
(I assume that it must be possible that there are sequences that are non-homologous, because otherwise there wouldn't be a need to point out which things are homologous, i.e. I assume that the concept of sequence homology would not be as widely used as it is right now)

There has been some discussion on my claim that homology should take a Boolean value. As I have stated in the comments, for this I refer to Inkpen, S.A. & Doolittle, W.F. J's "Molecular Phylogenetics and the Perennial Problem of Homology" in Mol Evol (2016), pp. 187.

Nevertheless, there is a general understanding that conflating the extent of similarity and the inference of common descent is always a misuse of the concept—that there can be no such thing as ‘‘percent homology.’

"If we consider homology between two nucleotide sequences as a yes/no answer to whether they have shared a common ancestral sequence..." But we don't. If you think we do, please cite a source that supports this idea. In fact, you are not asking a real biological question, but playing with words to expressing a philosophical opinion that is not the concern of this list.

I'm voting to close this question as off-topic because it is not about Biology in the terms of this list.

@David I refer to Inkpen, S.A. & Doolittle, W.F. J's "Molecular Phylogenetics and the Perennial Problem of Homology" in Mol Evol (2016), pp. 187. Quoting the article: "Nevertheless, there is a general understanding that
conflating the extent of similarity and the inference of
common descent is always a misuse of the concept—that
there can be no such thing as ‘‘percent homology.’"

@David I want to stress that I am not asserting my opinion. Rather, I am stating my premises which have lead to my conclusion. By doing so, I hope to expose these premises to the Q&A in addition to the actual question, to avoid an XY problem. I do not agree that I am 'playing with words'. I truly believe that there can be situations where non-homologous sequences can be created---just that I have not yet thought of them.

@ning You should edit your question and insert new information there. The paper/quote for example might get buried in the comments, or later even deleted...

@ning — There may be no such thing as "percent homology", so the terminology used (as I remember) is "percent identity". You might argue that identity is like pregnancy — all or nothing — but a metric of the percentage of amino acids that are identical (or 'similar') is both possible, useful and used. It is the basis of statistical comparisons (which I don't personally understand) that allow one to place a confidence value on two sequences being 'related'. If you don't like the term homologous sequences, you can use 'related' or 'structurally related' (to avoid any evolutionary implications).

Homology in this context is always a matter of degree exactly because of shared ancestry. Measures of homology are often in terms of "percent homology" (or more often "percent similarity" as evidence of homology) or some other measure that allows representation of that degree.
To emphasize why this makes sense, think about a receptor family. In an extant organism, you might have 3 receptors that all are homologous. However, if receptors 2 and 3 are more similar to each other than to receptor 1, then you can make some better assumptions about the history of the evolution of receptors 1 to 3, that there is likely a "common ancestor receptor" to both 2 and 3. There is more "information" if you consider the degree of homology rather than just its existence.
At some extremes, sequences could be so different that even if they share a lineage they may have now diverged to the point that they are not distinguishable from independent sequences. However, selective pressures prevent such complete reorganization in key sequences and so at least some homology can be maintained across very distantly related organisms.
As far as deciding what is "homologous" versus "not homologous", that is somewhat of an arbitrary threshold that depends on levels of evidence and the purpose for recognizing the homology.

It is interesting that you argue according to degrees of homology. I was taught that homology is strictly answered in binary, or at best likelihoods, and never as a degree. A degree of similarity can estimate a likelihood (but not degree) of homology. Frankly, I do not agree with looking at homology in terms of degrees, but then your answer would not make sense unless I do. Perhaps you could elaborate on why homology should be thought of in degrees?

@ning It all depends on what your goals are. I added a paragraph, does that help at all?

@BryanKrause I feel it is important to stress that degrees of homology as represented by percentage similarity is a very flawed metric, given that degrees of homology is discrete in a certain sense, determined by degrees of common ancestry. See for example Smith & Pease, 2017


text:
Can you help me identify this "thing"?
I found these "things" by chance on my wild strawberries which I grow in my organic garden. Basically, some strawberries are completely covered with them.

They're transparent, they have dots equally aligned and they don't move. I've tried searching for transparent slugs and worms and also faeces but to no avail.

I don't know the answer, but the same thing appears in these two other questions which are unanswered: thing one thing two At this point given the variety of places they have been seen they must be some kind of egg, but surely someone with expertise will eventually tell us.

Alright, I searched for "gelatinous insect eggs", found a similar image, and encountered a 3-part discussion of these things that begins with part 1.   It's a fair amount to read but I think it is your "thing".

Where do you live and how big are these millipedes(just a hunch).Do they have legs because if they don't you can tell they're not millipedes and centipedes

@BryanHanson I don't think theyre the same thing these have a shape and look so much like millipedes but once OP replies it will become clear

@BryanHanson I did the same search as you and after looking at many images I guess I found the species (I am not sure, though). It appears like the egg mass of Chironomus.

@WYSIWYG I think you might actually got it right. I just google'd "chironomus egg mass" and I'm getting back images very similar to mine. Chironomus appears to be a non-biting version of mosquitoes (by how similar they look to an average Joe) and now when we're talking about it, in the area where I live there are mosquitoes but during summer time at night there might be hundreds if not thousands of mosquitoes/chironomuses attracted to lights nearby. I thought they're all mosquitoes but now I'm not so sure.

@WYSIWYG At the very end of the 3 part blog post I referenced above, it come down to caddisfly eggs vs chironomous eggs, with this important distinction, quoting now: "chironomid eggs are nearly always elongated or oval shaped. Caddisfly eggs, on the other hand, are nearly always spherical."  Not all the pictures on SO are clear, but in those that are it seems like the eggs are elongated, so I think you are correct about Chironomous.  I think you should post that as an answer, and also post a reference back to your answer here on the SO questions I linked to above.  Great work!

@BryanHanson I think you should post an answer. I believe you know about this topic better. I am not an expert on this field. My research was just some google searches :P

It appears like the egg mass of Chironomus.

First, I am no expert on this topic, I am simply synthesizing several different sources of information along with the very good work of others.  Since the "thing" featured in this question has appeared elsewhere, it deserves an answer.
These appear to be eggs of Chironomous midges (wikipedia).  This conclusion is based largely on reading the three-part blog by Tom of askanaturalist.com
Part 1, Part 2, Part 3 which is very thorough.  In the last part of that blog, it is stated "chironomid eggs are nearly always elongated or oval shaped. Caddisfly eggs, on the other hand, are nearly always spherical." Looking at the pictures here and on the other SO questions (here and here) it appears that the eggs are indeed elongated rather than spherical.  Hence they are apparently Chironomous midge eggs.

I doubt it can be Chironomidae eggs. These midges live aquatic, or at least in very wet conditions. "On wild strawberries" is way to dry i think.

This link supports that Chironomidae live in aquatic or in very wet conditions. https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.eje.cz/pdfs/eje/2003/04/01.pdf&ved=2ahUKEwilj9-a_vLfAhVHaFAKHWpEC-EQFjACegQIBhAB&usg=AOvVaw0IYCx7tDciVnLlY6JT_ajV


text:
Why do some viruses have only one serotype, but others have many?
Some viruses, like the virus that causes mumps, have only a single serotype, meaning that variants of the disease are immunologically identical. However, other viruses, like the influenza virus family, has many different serotypes. Why is this?


text:
Passing on the DNA of old age
I've often pondered the fact that we only pass on the DNA of our youth. Any mutations to our DNA that occur after having children, that may help us to respond to getting older, are not inherited. Do older parents pass on a different, perhaps more learned "quality" of DNA? Anyone know the answer to this?

Your assumption that the mutations that occur during life are somehow beneficial and help us respond to ageing has no basis in fact. If you think otherwise please provide a source with evidence in support.

I'm voting to close this question as off-topic because it is based on a false assumption.

It is good thinking you're doing here!
Only mutations happening in the germ line can be passed on
Mutations that happen in an individual hand (or any other soma line) will not be passed on the the offspring. Only those happening in the soma line can.
Mutations are random
What I mean here is that it is not because someone is old that all of sudden the mutations that would happen in this person would be beneficial for old people.
Age dependent "quality" of genome being passed on
You are asking

Do older parents pass on a different, perhaps more learned "quality" of DNA?

You seem to misunderstand how natural selection works. An individual alone does not get selected over its lifetime to become better (at least not in the sense of what is meant by "natural selection"). You need a population for selection to happen.
In the females as the pool of ovules is being set early in life. In males the spermatozoids keep replicating during the whole lifetime of the individual. Hence, in males, but not in females, the number of new mutations being passed on to their offspring should increase with age and it does.
In humans the mother transmit on average 15 new mutations and the father transmit on average $25+2(g−20)$ new mutations, where $g$ is the age of the father (Cochrane and Harpending, 2013; this approximation holds only for men older than 20 years of course).
As the vast majority of mutations are neutral or deleterious, the "quality" of the genome being passed on should decrease with age unlike you expected.
Efficiency of selection decreases with age
The fact that after a given age, one does not reproduce anymore (among mammals, this is particularly true for women) does affect the selection pressures on the genetic variants that affect age specific fitness. e.g. A mutation that will reduce health at young age will be quite strongly selected against while a mutation that affect health at old will not.
When talking about this discrepancy between selection pressures at different ages, the concept of antagonist pleiotropy often comes into the discussion. Pleiotropy is the phenomenon where one locus affect several traits.
The idea of age-specific antagonist pleiotropy is that a mutation that will increase health at a young age by a factor $s$ but decrease it at an old age by the same factor $s$ will be selected for. Such process can cause a population to evolve toward lower lifespan. The antagonistic pleiotropy hypothesis is one of the most important hypothesis that we have for the evolution of senescence.
Evolution of senescence
You might want to have a look at the posts:

Why does evolution not make our life longer?
Why do we age? or Do we have a theory of senescence?


text:
What is an "end-to-end fusion" in the context of telomerase?
Telomerase is said to prevent "end-to-end fusion" of chromosomes.
My question is threefold:

What is an "end-to-end fusion"?
How does Telomerase prevent end-to-end fusions?
Why do end-to-end fusions cause problems in cells?

An end-to-end fusion is the result of two chromosome ends fused together. This happens when telomeres (repeated sequences at the ends of chromosomes) lose their protective telomere-binding proteins. In mammalian cells, loss of TRF2 (telomere repeat-binding factor 2) leads to chromosome fusions.
Here is an example of how it looks with metaphasic chromosomes (the DNA is stained in blue and the telomeres are stained in pink; picture from Rai et al, 2016). The left panel shows normal chromosomes, the right panel shows end fusions upon depletion of TRF2.

What causes chromosome fusions in such situations is the DNA double-strand break (DSB) repair machinery, which is normally repressed by telomere proteins (mainly by TRF2; see van Steensel et al, 1998). In mammalian cells, telomere-binding proteins are collectively called the shelterin complex (they literally shelter chromosome ends; see de Lange, 2005).
Telomerase doesn't repress the DSB repair machinery directly. Because of the structure of telomeres (a single-stranded 3' overhang) and of the way replication is primed, linear chromosomes cannot be fully replicated and will gradually shorten at each replication. When telomeres become critically short, they don't recruit enough telomere-binding proteins and therefore fail to repress the DSB repair machinery. Telomerase, when expressed and activated, maintains the length of telomeres in replicating cells at each replication (by adding repeated sequences complementary of the RNA template that is a component of the telomerase holoenzyme), providing binding sites for telomere-binding proteins, and thus indirectly contributes to the repression of the DSB repair machinery.
End-to-end fusions cause problems in cells in part because fused chromosomes will likely not segregate properly during mitosis and meiosis. The resulting daughter cells end up with altered ploidies that can be severe enough to prevent cell viability.

de Lange T (2005) Shelterin: the protein complex that shapes and safeguards human telomeres. Genes Dev. 19: 2100–2110 https://doi.org/10.1101/gad.1346005
Rai R, Chen Y, Lei M & Chang S (2016) TRF2-RAP1 is required to protect telomeres from engaging in homologous recombination-mediated deletions and fusions. Nat Commun 7: 10881 https://doi.org/10.1038/ncomms10881
van Steensel B, Smogorzewska A & de Lange T (1998) TRF2 protects human telomeres from end-to-end fusions. Cell 92: 401–413 https://doi.org/10.1016/S0092-8674(00)80932-0

Hello! This question was deemed worth of an answer, so why not upvote it? Vote early, vote often to encourage new users and keep the community alive!

Thank you for the suggestion. I just upvoted the question.

Merci bien, Guillaume! :)


text:
Which is the correct term haploid daughter cells or haploid parent cells?
Meiosis 2 begins with 2 haploid parent cells and ends with 4 haploid daughter cells (gametes). Gametes from the opposite sex can now merge together and fertilize.
If I were to refer to a specific haploid daughter cell merging with another to produce a zygote; are these daughter cells from Meiosis 2 still called 'daughter' cells or are they now called parent cells?

"Parent" and "daughter" terminology is indeed relative. Any parent cell has been a daughter at some point. However, in the case of the zygote there is no "parent" strictly speaking since it is the result of a fusion between two cells, that you may call "daughter cells" only if you are referring to the previous meiosis event.
In this particular case, there is no cell division, so no "daughter" is formed, so no point in calling the haploid cells from M2 "parents" either.

Hello! This question was deemed worth of an answer, so why not upvote it? Vote early, vote often to encourage new users and keep the community alive!

@LinuxBlanket Don't ask me. I did upvote it. Someone else downvoted back, resulting in 0 votes so far.

Ok! I don't have enough reputation yet to see the vote imbalance, I see only the result. So thank you for voting early and often!


text:
What is this and is it dangerous?

Is this some type of moth, it looks dangerous is it?
I have only seen something like this once before.
Thank you for any information you can give me.

Where did you find this insect?

Black and red, probably dangerous! In case you don't know for sure, don't play with it.

better to say which region / country and what kind of habitat you found that.

That's a wheel bug (Arilus cristatus), a species of assassin bug named for the wheel-shaped projection on their thorax. They tend to prey on pest insects, but they do "bite" humans with their proboscis. The result is an extremely painful, itchy welt, though non-venomous.
These one's don't attack unprovoked, however, so generally just when trying to handle them. You should handle them with gloves.


text:
How exactly do microfillaments change the cell membrane's shape?
I understand that they are concentrated under cell membrane and can contract, but the details aren't very clear. How do they attach to membrane, and in what direction do they pull? Do they draw two points of cell membrane together or what?
Also, actin in muscles doesn't just contract itself but anchors to myosin and "crawls" along it: it's not actin that contracts, but the entire actin-myosin complex. Does something similar happen in microfillaments?


text:
GWAS: marker map based on old genome assembly - can I use the new assembly to look for SNP positions?
I have an old set of pig SNP data and the positions were mapped using v10.2 of the assembly.
I submitted a GWAS paper for review, and the reviewer wants to know if any of the significant SNPs that were located in previously unknown genes are now in known genes, with the release of the latest assembly last year.
I was under the impression that I had to use the assembly the marker map was based on to see where SNPs are located. Is this correct or can I use the new assembly?
Many thanks in advance!

Why haven't you tried using LiftOver to convert the coordinates?
https://genome.ucsc.edu/cgi-bin/hgLiftOver

I didn't even know this was possible! Thank you!

Hello! This question was deemed worth of an answer, so why not upvote it? Vote early, vote often to encourage new users and keep the community alive!


text:
Why are plants unable to take up Phosphorus directly in their organic form like Phytic Acid?
I am researching acquisition strategies of phosphorus by decidious trees. I am reading a lot that plants take up nutrients as their inorganic form. In the case of P according to literature this is mainly $H_2PO_4^{-}$ (Schachtmann et al. (1998), Hinsinger (2001), Buchanan (2015)). So far so good...
In forest soils for instance, Phosphorus is much more concentrated in the form of phytic acids (derivates of inositol hexaphosphate), which are organic acids. Not in any paper which I have read before, it is stated why organic P is not taken up directly, only that it is enzymatically cleaved before it is taken up as inorganic P. The best, which I have found so far is that

Although organic P ($P_o$) is present in soil solution at higher concentrations than inorganic phosphate (Ron Vaz et al., 1993; Seeling and Jungk, 1996), direct uptake of ($P_o$) compounds by plants is considered unlikely. --Hayes et al. 2000

My problem - or rather limited understanding - is that I wonder, whether plants in fact do have the ability to take up nutrients directly as organic forms.  I would prefer not to take the presence of enzymes as a proof that organic P cannot be taken up directly by plants. Also phytate seems to be used in plant tissue for storage of P.
Unfortunately my understanding of biochemistry is limited, that's why I'm pretty sure that I am missing some basic facts, which could clarify the situation. My best guess so far is, that organic sources of P are simply too big to pass through the cell wall.
So my question is: are there certain structural or biochemical barriers or obstancles, which would prevent plant roots from absorbing organic P directly, or is it for some reason better to cleave phytates "outside" the cell?
I would be very happy if you could point me in the right direction. Thanks in advance
Sources:
Buchanan, Bob B.; Gruissem, Wilhelm; Jones, Russell L. (Hg.) (2015): Biochemistry & molecular biology of plants. 2. ed. Chichester, Rockville, Md.: Wiley Blackwell; American Society of Plant Biologists.
Hayes, Julie E.; Simpson, Richard J.; Richardson, Alan E. (2000): The growth and phosphorus utilisation of plants in sterile media when supplied with inositol hexaphosphate, glucose 1-phosphate or inorganic phosphate. In: Plant Soil 220 (1/2), S. 165–174. DOI: 10.1023/A:1004782324030.
Hinsinger, Philippe (2001): Bioavailability of soil inorganic P in the rhizosphere as affected by root-induced chemical changes: a review. In: Plant Soil (237), S. 173–195.
Schachtman, Daniel P.; Reid, Robert J.; Ayling, S. M. (1998): Phosphorous Uptake by Plants: From Soil to Cell. In: Plant Physiology (116), S. 447–453.
https://en.wikipedia.org/wiki/Phytic_acid

Welcome to Stack Exchange Biology, and congratulations on a very well constructed first question.

I am not a plant biochemist but would make a couple of points that may or may not be relevant or helpful.

The living organisms that preceded plants had evolved a wide repertoire of systems for transporting ions across membranes, involving variations on a few general designs. Given the importance of inorganic phosphate in living organisms, phosphate transporters would have evolved early on.
Phosphate may have been more abundant in soil before sophisticated evolution of plants led to secondary metabolites like phytic acid. If this were the case it would explain why roots developed phosphate transporters.

This is not to say that it is impossible for organisms to develop transporters for more sophisticated molecules — there are many such examples — but in this case such a development would only be expected if there was such a lack and intense competition for phosphate that it would convey an evolutionary advantage.
This sort of question is always a matter of conjecture. One imagines there is a tipping point when the difficulty of developing a new system is outweighed by the advantage it would bring. This clearly hasn’t happened, but which of these factors is most important is difficult to say (for me, at any rate).

Might be worth pointing out that this is quite the same in animals; even though we might think of the gut as "inside," developmentally and historically the gut is "outside": all the proteins and other macromolecules a human ingests are broken down into consitutent amino acids, simple sugars, etc before they ever get "inside" and much of that work is done by excreted enzymes. Bacteria do this as well.

Thank you for your answer, it did in fact turn me in the right direction. I looked for inositol transport proteins and actually some exist and are located in the plasma membrane. So far I think at least it has not been clarified whether they play a role in inositol-P uptake from the soil. http://www.jbc.org/content/early/2009/09/21/jbc.M109.030247.abstract


text:
How do I calulcate the amount of concentrated stock solution to add to get the correct dilution?
For example, how much loading buffer (6X) do I need for my PCR reaction with a volume of 25 μl?  What is the general way to calculate it?

For any question regarding volume and concentration, you should consider the equation $C_1V_1=C_2V_2$. We can use it to derive a general equation for the addition of concentrated stock solutions. We want to find the volume of stock solution ($V_1$) to add so that its final concentration is 1X. Here's what we know:

The initial concentration of stock solution, $C_1=X$
The final concentration of the solution, $C_2=1$
The volume of solution we are diluting the stock into, $V_s$

So the equation becomes:
$$XV_1=V_2$$
We don't know $V_2$, but we do that $V_2=V_1+V_s$. Subbing that in:
$$XV_1=V_1+V_s$$
Solving for $V_1$:
$$XV_1-V_1=V_s$$
$$V_1(X-1)=V_s$$
$$V_1=\frac{V_s}{X-1}$$
Then you simply need to sub in your values:
$$V_1=\frac{25μL}{6-1}$$
$$V_1=5μL$$
So you should add 5 μL of your 6X loading buffer to the 25 μL solution to get a 1X final concentration.

@biologist You’re welcome!

Absolutely correct. I leave this comment only as an aside for people who may find it unhelpful to think and visualize mathematically: a 6X buffer simply means it should make up one part in six. You add 1μl of it to 5μl of your solvent. Or add 2μl to 10μl. Or add 5μl to 25μl. Or 1 teaspoon of honey added to 5 teaspoonfuls of tea. Now that's some 6X honey.

Candianer's answer is a generally correct way of solving these problems but, in my opinion, overkill for this situation.
All Nx buffers are mixed to make your life easier, and you will generally encounter 10x, 6x, and 5x buffers. 10x and 5x seem obvious, you just put them in so they make up a tenth or a fifth of your solution, but 6x seems to confuse people. The reason it's x6 is because you are adding it to an existing solution, so as well as you're solution you're going to have one lot of whatever you're adding. This makes it (1+N)x and you can then clearly see that 6x is (1+5)x, so you need to add an amount equal to one fifth of your volume.
One fifth of 25 μL is 5 μL so that is what you need to add.

Certainly one doesn’t need to derive the equation every time; I was just showing how it’s done. It really is as simple as dividing the volume by 1-N.


text:
Is rabies virus infectious outside host?
Can rabies virus remain infectious on environment i.e on soil, grasses, leaves and water?

Cross posted question on medical.sciences.SE

First off all we need to be 100% sure what does be infectious mean. According cambridge dictionary meaning of the word infectious is be able to past from one host organism (multicellular/cellular) from another. So this is actually biggest hole in your question.

But i think you mean something else then word infectious. In my oppinion you wanted to know if rabbies can survived outside of its host. The rabbies virus as many other viruses cannot live outside of its host. Rabbies is exists in "public reservoir". This fact only confirm its variety of hosts such as bat, bears, dogs etc. (technicly all warm blood species) and its long incubation period (for example 1-3 months in humans.

According this site:

Rabies virus is transmitted through saliva and brain/nervous system tissue. Only these specific bodily excretions and tissues transmit rabies virus. If contact with either of these has occurred, the type of exposure should be evaluated to determine if postexposure prophylaxis is necessary.
Contact such as petting or handling an animal, or contact with blood, urine or feces does not constitute an exposure. No postexposure prophylaxis is needed in these situations.
Rabies virus becomes noninfectious when it dries out and when it is exposed to sunlight. Different environmental conditions affect the rate at which the virus becomes inactive, but in general, if the material containing the virus is dry, the virus can be considered noninfectious.

To sum this:
Rabbies viruses need to have contact with host, typicly by biting. It is possible to be infected by other contacts such as kissing, licking not dry saliva, but still the virus cannot live long outside of body. So long incubation and variaty of possible host (most infected is bats) makes the true killing combination.

Yes I was referring to survival outside host. As in if a rabid animal drools on grass or soil, can it survive in those?

Also. Has there been any cases of rabies infection from virus outside of host rabid animal?

https://www.elsevier.com/connect/8-things-you-may-not-know-about-rabies-but-should good article

I didn't find anything relating to virus survival outside host

Because there is not such a case. This is only the possibility. You know, i dont think that any person (not including little children) be so mindless to implated the saliva to his wound.

Btw you can easialy go threw the sites like WHO and you will find deffinitly some information on this topic.

So infection from outside host is a theoretical possibility but there has never be a real case?

I've only read about the virus transmitted from bite and scratches. But wanted to know if it can be transmitted from saliva from a rabid animal thats on the environment.

So i hope this answer is enought for you.

Thank you for your answer. I am just paranoid I may come into contact with rabid animal's saliva without knowing it. So wanted to know if the virus can infect like this.


text:
What is (are) the medium of conduction for an electrical current with an external source in the human body?
I am trying to get some background for some personal research I am doing into the effects of Electro Convulsive Therapy. I don't understand how electric current from an external household source, say, flows through the body. There are no naturally occurring chains of metal atoms in the body, so it can't be electron flow, but my understanding is that the electric field around an electrode is very thin, so I can't see ion flow as accounting for electrical effects in the body at some distance from the electode - particularly with AC, as I would only expect a local oscillation. I am familiar with membrane depolarisation but that is essentially a cellular mechanism - is it (or saltatory conduction) activated by an external current? I know that the body as a whole (and cell membranes in particular) function as a dielectric, but I can't see how this fits into the global picture of current flow between two electrodes. Can anyone help or recommend me a paper?

Electric current flows rather rather easily through water that contains ions, which are electrically charged atoms. Since the human body is more than half water, and that water is filled with ions such as sodium, chlorine, potassium, etc., the body for the most part conducts electricity rather well.  The skin can have a high resistance to the flow of electricity, but it varies substantially, particularly being reduced when the skin is moist.  Medical electrodes, as for heatbeat measurements, are typically applied with conductive paste to overcome most of the skin's resistance.  You may want to look at this "Electricity And Human Body" page, or the article "Conduction of Electrical Current to and Through the Human Body: A Review".

In fact electrons do not flow through water: they are donated or received by ions at the electrodes.

@DonnardWhite, Yes, a particular electron probably doesn't flow further than an atom or three at a time. The reception of an electron by an ion does change the electric field near the ion, causing another electron to be donated to another ion further along. An enormously long chain of this happens through the ionic solution of the body's water and ions.  Eventually some electron pops out into the other electrode.  No particular electron flows from one electrode to the other, but rather each moves a minute distance along the path through the solution.

Ah, that I didn't know, and that is useful. I am trying to get a picture of an end to end passage of charge - problem is mmm - trying to imagine the energetics of this - my thermodynamics could do with some revision - but there is a directional electric field near the electrodes - but I'm guessing pretty random after that if you are saying there is a local electric field change for every electron exchange - would love to have a better idea of the medium - blood? membrane surface? but you have been a help. I'd read the second paper you mention, and: https://www.ncbi.nlm.nih.gov/pubmed/19212042


text:
Dynamic of the number of cells over time as the embryo grows
I would like to investigate the dynamic of the number of cells over time as the embryo grows. I am interested in any multicellular animal species for which we can have some data. How does the number of cells change over time in an embryo?
I welcome any graphs, empirical data and/or mathematical expression for this dynamics.

Its a bit unclear what you are asking are you talking about how it has changed across many species or how it changes in a single species through a single organisms life cycle. in hte case of the former this may be a place to start, https://www.ncbi.nlm.nih.gov/pubmed/10225991

The question seems very unclear but I think this is because OP is using the term "evolution" where she/he should not. I don't think OP meant evolution as in the sense that a population evolve as to change the number of cells in the embryo (whatever that would mean as the stage is not specified) but rather the question is I would like to investigate the dynamic of the number of cells over time as the embryo grows. I am interested in any multicellular animal species for which we can have some data. How does the number of cells change over time in an embryo?. Is that right, @J.A?

@Remi.b it is indeed what I meant. Thx

your biggest limit is going to be how difficult it becomes to count the total number of cells, especially once you get past the blastula stage. In the beginning its fairly predictable often defined by the number of cells (2,4,8,16, ect) but once you reach blastula there just is not much incentive to try and count nor is it terribly consistent.  this may help https://www.researchgate.net/figure/Stages-and-molecular-events-associated-with-early-development-of-the-mouse-embryo-A_fig4_255951891

It also varies quite a lot by animal. nematodes for instance are famous for having exact cell counts (it can even be used to identify a species) which just does not occur in organisms with hox genes.

There are some interesting analyses in mice, zebrafish, and worms. These papers contain a lot of data at the single-cell resolution, so you'll need to read and find the exact numbers about cell counts over time. You might also want to take a look at this classic paper about cell counts in humans.

A starting point could be this very recent amazing movies and the corresponding research article published yesterday.
This is not my field of expertise, but I think you will find relevant information in the references cited by this article.


text:
Cross-species infections
I’ve heard that HIV developed from SIV, etc.
I’ve also heard that most species (including most monkeys) can’t get a common cold like humans.
So then what causes infections to be able to travel across species, or vice-versa?
For the sake of the question, I’ll narrow the scope. Let’s say we have a virus that can infect humans but not infect close human relatives, like Chimpanzees. What about that virus biology or animal biology causes that difference?
I know with some animals it’s about body temperature or skin composition, etc. But humans and chimps are physically pretty similar. Is it all about the immune differences?

Viruses evolve alongside their hosts. If you swapped a human chromosome into a chimp cell for the matching chimp chromosome, there would be a lot of genetic similarities but you would also surface a bunch of incompatibilities because the genes on each chromosome have been evolving independently from the rest of the genome.
Viruses interact with their host genome at many stages. First, they need a way to identify their target hosts (cells) in the environment and gain access to the cells. They do this by recognizing markers on the cell surface. For something like HIV, this identification is far more specific than identifying just humans even: they are identifying particular immune cells.
Once inside, viruses interact with the host to express viral genes, produce and assemble new virions, and get transmitted to subsequent hosts. If an incompatibility occurs at any of these stages, the virus won't be able to replicate.
However, because there is a lot of homology across related species, it is feasible for a virus to infect more than one host. If a virus evolves in a context where it commonly infects multiple hosts, there can be selective pressures for it to maintain those abilities across all the hosts. Alternatively, selective pressures might cause the virus to evolve into separate lineages, one infecting ducks and another infecting sparrows, for example.
For a virus that is specific to a certain host (or range of hosts), it is likely that it will have difficulty in another host outside the context in which it evolved. However, there is also variability in viral genomes, and if many viral copies are exposed to a novel host, there is chance that some of them can survive in that host. This will select for those particular viral genes, and subsequent viral generations will be further selected for traits that help replicate in that host.
Immune reactions could also play a role, but in most cases it is the specialization of the viruses themselves that hold the key to host specificity.

Ahlquist, P., Noueiry, A. O., Lee, W. M., Kushner, D. B., & Dye, B. T. (2003). Host factors in positive-strand RNA virus genome replication. Journal of virology, 77(15), 8181-8186.
Hao, L., Sakurai, A., Watanabe, T., Sorensen, E., Nidom, C. A., Newton, M. A., ... & Kawaoka, Y. (2008). Drosophila RNAi screen identifies host genes important for influenza virus replication. Nature, 454(7206), 890.
Schild, G. C., Oxford, J. S., De Jong, J. C., & Webster, R. G. (1983). Evidence for host-cell selection of influenza virus antigenic variants. Nature, 303(5919), 706.

Great answer and concise, thank you!! One question I have that I may address if I have time (or if you/someone else wants): so your answer says that one possible reason why rhinovirus doesn’t infect mice is that the receptors are different. So (1) what are the receptors that rhinovirus binds to in humans and (2) can we do an alignment between those receptors in mice and humans? Do we know which misaligned residues/change in structure leads to the mismatch?

@CalendarJ That would be an excellent separate question. Not my area of expertise but I am almost certain that rhinovirus cell specificity has been studied, though I'm less certain that specific residues involved in human/mouse differences would be understood. In any case it's a good question that should produce a well-referenced answer.

The biggest key to understanding viruses and their hosts (more specifically, host cells) is external (membrane and ECM) protein structure.
As a general rule of thumb, viruses need to latch on to their host cells. Some viruses abuse transport mechanisms to trick host cells into "eating them" and running their contents. Other types of viruses have nasty-looking clamps (most prominent example that comes to mind are bacteriophages) that grab specific structures on host cells while the central piece of the virus punches a hole in the host cell's membrane to feed it malicious DNA/RNA and enzymes.
Cross-species infections usually abuse structures common to many species. For example, sialic acid receptors are commonly abused as viral entry points (see https://www.ncbi.nlm.nih.gov/pubmed/23873408). If humans had genomic support just like computer operating systems receive updates for vulnerable components, sialic acid receptors would have been labeled a critical risk millennia ago and patched.
Obviously there are other factors that can thwart cross-species infection. A successful cross-species virus needs to use a minimum supported operation subset of cell functions common to its hosts. If a potential (by external structure match) host cell is unable to make a piece required for viral replication, it fails. If a potential host cell (or the host itself, in the case of multi-celled life forms) is built with some oddball anti-infection measures (for example: tamper-detection, integrity check before producing protein from RNA, or unexpectedly robust immunity), then the infection could fail anyway.


text:
Where does weight go when you lose it?
When one loses weight, where does the lost poundage (I assume comprised mainly of fat) go?
Is it urinated out? Defecated out? If a combination of both, does the percentage of each differ depending on how much of what your are losing was pure fat?

You breath it out, for the most part. Fat is "burned" to convert the carbons to CO2, which is breathed out. There's not very much fat-derived carbon in each breath, but you breath a lot, all day long.

At rest, an average 70 kg person consuming a mixed diet (respiratory quotient 0.8) exhales about 200 ml of CO2 in 12 breaths per minute. Each of those breaths therefore excretes 33 mg of CO2, of which 8.9 mg is carbon. In a day spent asleep, at rest, and performing light activities that double the resting metabolic rate, each for 8 hours, this person exhales 0.74 kg of CO2 so that 203 g of carbon are lost from the body. ... Replacing one hour of rest with exercise that raises the metabolic rate to seven times that of resting by, for example, jogging, removes an additional 39 g of carbon from the body, raising the total by about 20% to 240 g. ...
Our calculations show that the lungs are the primary excretory organ for fat.

--When somebody loses weight, where does the fat go? Ruben Meerman and Andrew Brown, BMJ 2014; 349

Hello! This question was deemed worth of an answer, so why not upvote it? Vote early, vote often to encourage new users and keep the community alive!

This answer is very interesting. I think it is a good example of order estimation in biology.


text:
What is a section in botany based upon?
I am a bioinformatician working with plant data. Therefore my formation on plant biology and botany is "ok" but not very strong.
When people talk about sections, I know that they talk about a phylogenetic rank that is lower than the genus but higher than the species. It groups subsets of species belonging to a genus together.
What is the thing that puts them together? Morphology, origin, geography, metabolism, genome identity, ...?

It depends. Sometimes people use it because there is monophyletic group within the genus which share a particular character, but which they don't want to (or can't) segregate into its own genus. Usually you will find sections in large genera which contain quite a lot of morphological diversity.

For more discussion on what makes a "good" name, see comments on this answer: https://biology.stackexchange.com/a/77519/42697

Taxonomic rankings above the species level are arbitrary—that is, they are created just to be a useful handle, much the way one might call the plants in one’s study “my study plants” and the plants in one’s kitchen “my kitchen plants” in order to convey information about them more easily. What makes a handle like “section” or “genus” useful is up to the botanist creating the handle, and, yes, he or she would likely consider many or all the things you mention (metabolism, origin, geography, etc.) while doing such creating. There are some rules, however—-such as respecting taxonomic hierarchy, giving such names only to clades, prioritizing earlier valid names for the same taxon, etc.

Nice answer. I could be improved by references if you can find a suitable one.


text:
Has evolution made a mistake with prehistoric animals?
Let me start this by saying I have very limited knowledge in biology and evolution.
However, when visiting museums and watching documentary movies, I always get impression dinosaurs (and other animals in "dinosaur era") are very huge compared to today's animals, especially land animals.
So I wonder, was the this huge size actually an error in evolution?

You see them as unsuccessful? They roamed the planet for about 170 million years, which I find pretty impressive. If conditions change fast (like they did 66 Mio years ago) such animals cannot adapt fast enough.

Dinosaurs have been roaming the earth for 230 millions years. Birds are dinosaurs. Let's avoid fueling a weird non-monophyletic categorization to please a vague intuition.

You overlook one obvious factor.  It's a lot easier to find big dinosaur bones (or bones of any sort) than little ones.  I'd also guess that the bones of big creatures are more likely to be preserved in recognizable form...

@Chris I don't see them as unsuccessful. In fact, I'm very impressed by them. I am just curious was one trait of them, size, theirs disadvantage (especially when you compare them with todays land animals).

There are two questions here.

Dinosaurs were larger because their basic anatomy is better at being large than mammals. Their spine is better braced (no lumbar region), their breathing mechanism scales better, and their hip structure is stronger. This is called a preadaptation, or when an organism or group of organisms just starts with a head start on a particular adaptation due to unrelated reasons. It is the same reason mammals are the only terrestrial vertebrates to have echolocation: they are the only group with advanced amplification equipment in the ear to give it a head start.
Any era has its giants. Today is the time of the largest whales, largest trees, largest frogs, and largest horse to ever exist. Size is often a decent advantage: it makes you more resistant to resource fluctuation, it's just not a good for surviving global mass extinction inducing bolide impacts.

Evolution has no foresight. Evolution often produces and locks in counterproductive adaptations in the long run; while an adaptation may be an advantage in the short term, it may lock the organism into a disadvantaged position in the long run.
Sexual displays are a classic example: some quirk in peacock brains meant early female peacocks really liked more flamboyant males, that drove peacocks to the point modern males are incredibly vulnerable to predators and can barely fly due to carrying around huge superfluous tails. Both males and females would be better off preferring/having something less detrimental, but a feedback loop has locked in that detrimental feature. Males without it can't find mates, and females who do not prefer large tails male offspring also can't find mates. The term for this is fisherian or runaway selection. As an another example of counterproductive selection, many organisms when no longer controlled by predators or other factors will expand their numbers and consume resources to the point their populations collapse because there are too few resources to sustain them. Parasites often face this: a host with too many parasites dies, which is bad for the parasites but if the host can't fight off the parasites many are perfectly happy to kill their host and then starve.

Another aspect of evolution not having foresight is it cannot prepare you for extremely rare events, like mountains falling from the sky.

Runaway processes (and other evolutionary dead end processes that you quickly describe) is (are) not what killed the dinosaurs though.

no of course not, a mountain fell out of the sky evolution can't do anything to prepare you for that.

tl;dr

There is no mistake if there is no intention
pre-historic is not the term your were looking for
Some animals were big during the "dinosaur era" but not all and the largest animal to ever exist is extant today
Ancient dinosaurs have been around for 170 millions years. That's a very long time, much longer than anything you seem to be comparing to
Most lineages get extinct
NOT ALL DINOSAURS GOT EXTINCT! Some are still around

Semantic - On the concept of mistake
If you look to pretty much any definition of the term "mistake" (e.g. Merriam-Webster) you will find references to the concepts of choice and of intention. Indeed, in order to make a mistake one needs an intention, a goal.
Evolution is not some kind of mystical creature that has an intention for what ought to happen. Evolution has no intention. In this sense, it sounds very wrong to claim anything like "evolution made a mistake".
That makes your whole question (Has evolution made a mistake with prehistoric animals?) a little unclear.
Were pre-historic "huge?"
The concepts of historic vs pre-historic era are not concepts in empirical sciences but in history. The limit between the two is roughly placed at the invention of writing in humans. This boundary separate the past ~6000 years and the 13.8 billions years before it until the beginning of the universe (or the ~4 billions years of life on earth before it).
For the vast majority of these 4 billions years, life forms where definitely not all "huge". For most of this time, lifeforms were exclusively unicellular. First animals appeared ~550 millions years ago. And again, they were definitely not "huge" at the beginning. So a claim like "prehistoric animals are huge" would be very misleading.
Now of course, what you meant by "prehistoric" was actually "dinosaur era" but I still wanted to correct your choice of terms.
Were "dinosaur era" animals "huge"?
By "dinosaur era", someone probably refer to the period of ~170 millions years between the beginning of the triassic and the CP extinction event. Again, please note that in your comparison you are comparing a 66 millions years period to a 6 thousands years (0.006 millions years) period. To give you a little more perspective, there is about 170 millions years that separate a mid-triassic dinosaur (such as the Thrinaxodon) to a late Cretaceous dinosaur (such as the famous T-rex) but there is only ~66 millions years that separate a late Creataceous dinosaur to us, today!
Animal size varied a lot along these 66 millions years but yes, there were very big dinosaurs and also very large insects. This is mainly caused by a higher oxygen content in the atmosphere. Note however, that the largest animal that has ever lived is the blue whale who did not exist at that time but is extant today.
Extinction events
You probably meant to call "dinosaurs" a mistake because they do not exist today. First let me tell you that dinosaurs are not extinct, there are still a lot of dinosaurs alive today (see next section). Second, I would like to talk about extinction events.
Mass extinction events happen! In the phanerozoic only (that is in the past 500 millions years, that is a quarter of the time since life exist on earth), there are 7 commonly accepted mass extinction:

O-S
Late D
Cap
P-T
Tr-J
K-Pg
H

The last one, H refers to the holocene extinction and is the extinction event that is currently happening. Excluding the holocene extinction, the last mass extinction was the K-Pg (Cretaceous–Paleogene extinction event), which is the one who massively reduced the number of dinosaur lineages.
So really, don't think too much of modern life as being more "successful" that ancient dinosaurs because they are still extant. They just did not get extinct yet. If you want to call ancient dinosaurs a mistake, then you would have to call any lineage who got extinct a mistake and that represent the vast majority of all lineages that has ever existed. Also, these ancient dinosaurs have been around for 170 millions years! And also, ... as said above, dinosaurs are not extinct anyway!
Dinosaurs are not extinct
If by dinosaur, you mean Dinosauria, that is the monophyletic group that include all the things that you would typically call a dinosaur and all their descendent, then dinosaurs are still alive. Dinosaurs are still "flying around"! Birds are dinosaurs. They are not just distant cousins of dinosaurs but they are dinosaurs. It would indeed sound very wrong to state that dinosaurs are extinct just because we decided to name "bird" the dinosaur lineages that did not get extinct. For more information please have a look at the posts

If dinosaurs could have feathers, would they still be reptiles?
Were there any flying dinosaurs?

Whether or not you consider dinosaurs extinct depends on how you define "dinosaur". "Dinosaur" in the common sense refers to the extinct species.

That's right. I am using the only well defined definition that exists (the same used on wikipedia). I call a dinosaur any member of the clade Dinosauria

Downvoted because of the "birds are dinosaurs" nonsense.  By the same logic, birds, dinosaurs, and humans are just different kinds of fish :-)

Ha ha. Well, the point (maybe unclear; I tried to clarify that) is that stating dinosaurs are extinct is really silly because there are lineages that did not get extinct we just stopped calling them dinosaurs in the popular language. Nobody would say that all metazoa are extinct just because we got them more specific names.

Yeah, but what you've done is answer the question "what's wrong with this question [insert question]" in Semantics SE rather than try to answer the question that was asked in Biology, you could have probably condensed all the problems you have with it's wording into less than a 10th of this, defined what you thought he meant in less than that & then answered the question, which would have all been fine, you've only done the first bit ("your question is silly & this is why") & took a bleedin long time about it as well :)


text:
How Does the Body Know a Finger is Fully developed?
When a baby is being developed inside the womb,
1) how does the baby's body know a finger, or any other part of the body, has been fully developed?
2) following question, how does it "stop" the development of that part? What kind of signals are being communicated here?
3) I have hairy arms. The length of the hair is almost the same length if i don't cut it. If it breaks, it grows back almost the same length. How does the body know the current length and how to stop when it reaches the "target length"? Is it the same "procedure" as the development of parts inside the womb?

Welcome to Biology.SE. The two first questions are related, the third question is quite different. Please always narrow down your post to a single question. Also, the first two questions are in themselves already quite broad. You might want to read a  bit more about developmental biology

For the third question, you might want to read related posts; Why does hair grow after trimming but remains at a constant length after a while? and Why can hair grow without limit while eyebrow cannot?

I am interested in the "communication part". I chose hair as an example because it regrows. I could have chosen anything that regenerates to the original shape in the body.

Is there a common "algorithm" the body follow for development and regeneration or is there different once for every scenario?

Yes but the case of hair is very different that the case of finger development.

Fair enough. The hair is a bad example,

Yes, there is some kind of "algorithm". Describing this "algorithm" would require writing a whole book. And in fact many people have been writing books on the development of organisms. This is why the question is too broad in my opinion. Your question sounds to me like the question "Can you explain to me how biology works?" might sound to you.

So Developmental Biology is the door for my question, yes?

Yes, it is! If you are interested in following a class, you can for example consider this MIT intro class. More introductory and less complete, there is also this Khan academy series of videos. Note: I have not attended any of these two classes, I just googled them so I can't comment on their quality but MIT classes tend to be pretty good. You could open a new post to ask for good ressources in developmental biology if you want to. Good luck!

Hello and welcome to Bio.SE! Take the tour to learn about the site and earn yourself your first badge. Have a nice stay!


text:
Surface area : Volume Ratio
I just have a quick question. I am currently studying for a test and I am confused as to what my book is saying. On the first page when learning about the gas exchange of insects it states that the insects have a large surface area : Volume ratio and this increases the rate of diffusion allowing the insects to get the oxygen they need at a fast enough rate to allow them to survive. Then on the next page when talking about the prevention of water loss it states that insects have a small surface area : Volume ratio to prevent water loss as it minimises the area at which the water can be lost. I am confused as the book states that an insect has both high and low surface area to volume ratios and because of this I'm not sure which is correct to write for the exam.
Thank you

Hello and welcome to Bio.SE! Can you provide the exact reference?

Hello, thank you for your welcome :) I have added pictures of the textbook where it talks about both things and contradicts itself. Inside the rectangle is where it states that small organisms have a large surface area to volume ratio and underneath the rectangle is where it states that the insect has a small surface area to volume ratio. Which statement is correct or am I interpreting it wrong?


text:
Genetic analysis of one sibling relevant to other
My sister, my only sibling and I have literally no physical traits in common. Whatever trait I inherited from one parent she inherited from the other. We're thinking of using one of those genome analysis services to learn information about our mysterious geographical ancestral origins.
We're wondering if, despite our differences in appearance, if only one of us submitted our genome for analysis, the geographic origin results would still be accurate for the other. Because our parents may both have diverse lineages, the answer might not be so cut and dried.
Understand, please, that we are not so much looking to find out the general "where" of our origins as we are to have each of us know what our individual genetic heritage is.

You should be aware that DNA tests can't give highly localized "geographic origin" information.  Genes spread around, so exact locations can't really be pinned down.  Many gene variants can be confidently assigned to continental areas (Africa, Asia, Europe), but it begins to get hazier as smaller areas are considered.  For example, many British Isles variants can be distinguished from other European variants, but French versus German genes really can't reliably be separated for the most part.  You might care to see what other people think of their results, for example by looking at Reddit posts about 23andMe results.
Most siblings will get pretty similar origins results.  If each of the parents individually has several very distinct origins, then siblings can have somewhat more divergent origin results depending on the randomness of inheritance.  The only way to know what you two each have is for both of you to get tests.  You should consider that if, in actuality, you two are half-siblings, or are not closely related (as e.g., one or both of you were adopted), the results will show that.

If you are siblings, then, outside the Y chromosome (if you are a man, otherwise, you both only have X chromosomes), the results should be very similar. There might be some slight variations of course but it is unlikely to come out as important.
If you are not siblings (e.g. you might be half-sibling if your mother is hiding an affair; sorry for suggesting this possibility but that's no so unusual), then the results might well be quite different.

Hello! This question was deemed worth of an answer, so why not upvote it? Vote early, vote often to encourage new users and keep the community alive!

@LinuxBlanket I was not 100% sure that the question would be considered worth of an answer. It has happen to me a few times in the past to be criticized of answering questions that aren't worth it. But thanks for pointing this link to me and everyone else!

@LinuxBlanket Btw, why haven't you upvote then?

Even if it's not considered worth of an answer by the community, your opinion still counts and can be expressed not only by answering, but also by voting. With that upvote, you gave the OP the chance and maybe the will to participate more. Thanks, and remember to vote early and vote often! :)

I admit that I didn't do it in order to see what was the effect of my comment - I didn't want to have answerers think "the question has an upvote anyway". Now I'll do it!

Ok! I'll make sure to apply this logic. Let's vote early and let's vote often! Thanks


text:
Psychrotrophic Bacteria
I want to know what gene or protein makes bacteria psychrotrophic, as opposed to regular bacteria that prefers warmer conditions. If you don’t know exactly, and you have suggestions as to where I can find the name of the gene, that would be great. I would also need the gene to be accessible so if anyone knows anything, please let me know. Thank you!

what is broader problem you are trying to solve? In other words, what do you want to achieve with this information? If you edit your question, adding these details, it might greatly help

Hello and welcome to Bio.SE! Take the tour to learn about the site and earn yourself your first badge. Also, what did you try in order to find the information you need? Can you give some example of psychrotrophic bacteria?

It is not necessarily about special (psychrophilic) genes, but rather about psychrophilic variants of their mesophilic and thermophilic homologs.
In general, lower temperature means lower rate of enzymatic reactions.
To cope with this problem, psychrophilic bacteria encode enzymes with highly mobile surface loops (higher mobility, higher catalytic rate).
Thermophilic bacteria have a different problem: enzymatic reactions are fast, but the enzymes are unstable; to cope with this problem, thermophilic bacteria encode enzymes with more rigid surface loops (more rigid, more stable).
Sočan et al. (2018) Catalytic Adaptation of Psychrophilic Elastase. Biochemistry 57: 2984-2993.
Åqvist (2017) Cold Adaptation of Triosephosphate Isomerase. Biochemistry 56: 4169-4176.


text:
What change would you expect in phospholipid orientation of the membrane if the enviornment were mostly heptane?
The external and internal environment of the cell is basically water, thus phospholipids organize themselves the way they do (bilayer). If the environment were to magically become mostly heptane, how would the phospholipid orientation change?
Phospholipids maintain their structure in the cell membrane because of the hydrophilic heads and the hydrophobic tails. Much unlike water, Heptane (CH3-CH2-CH2-CH2-CH2-CH2-CH3) is non polar and thus would not cause the heads to present themselves on the outer bilayer and the tails to tuck themselves away.
Because heptane is non polar, I wouldn't expect there to by any hydrogen-bonding going on, so I don't think that we would see an "inverted bilayer". I could be wrong though.
My thought - the cell membrane would cease to exist, I can't think of what would hold it together, but that seems a bit out there.
Thoughts?

Is this a homework question? If so note that the SE Biology policy on homework questions indicates it should be tagged as such.

Yes, this is a homework question. I'll go ahead and tag.  Also not really looking for an outright answer, more just guidance on my current train of thought. Which... do you have any?
Also, I feel like I've met all the rules. https://biology.stackexchange.com/help/homework

I agree that you have followed the rules. Your answer that the membrane would cease to exist seems most reasonable to me, but I suppose you are expected to think about the polar and non-polar parts of the phospholipid and which would orient itself to the hydrophobic heptane. I hate this sort of question, because this only works if you assume that the membrane is still surrounding a cell with an aqueous interior and the membrane still exists. I assume your instructor knows this is so, but you or I would not, which is not fair on you (I don't care).


text:
Why plant tissues end in -enchyma?
Many plant tissue types end in the affix -enchyma.

Etymology: enkhyma "infusion," from en- "in" + khein "to pour"

Examples are parenchyma, collenchyma, and sclerenchyma.

(meaning "to pour beside," "glue infusion," and "hard infusion.")

My question: Where did this usage of -enchyma meaning "infusion" for plant tissues come from?

I'm curious from a biological more so than a historical perspective. I.e., why was this word choice chosen for plant tissues?

The best explanation I've found is from Plant Systematics by Michael Simpson:

Para, beside + en-chein, to pour; in reference to the analogy that parenchyma is poured beside other tissues to fill up space.

So far I haven't been able to corroborate this or expand upon it...

According to Wikipedia, Originally, Erasistratus and other anatomists used [parenchyma] to refer to certain human tissues. Later, it was also applied to plant tissues by Nehemiah Grew. so perhaps further investigation from a human anatomy perspective will be informative

I'm also interested to learn more about the difference between the Greek roots for chyme vs -chyma (khūlos vs khéō) and how their origins inform this question further...


text:
What is my pet tortoise' species?
I got this tortoise from my uncle. He said that it wandered into his yard. Found in Khon Kaen, Thailand during the summer.

Hello and welcome to Bio.SE! Take the tour to learn about the site and earn yourself your first badge. Have a nice stay!

It is a Burmese brown mountain tortoise - Manouria Emys Emys
 I differentiated it from a burmese black mountain turtle by this method.