text:
How to mark an ant with the least disturbance to the ant and the nest
How would one go about marking one or more ants in a nest so as to least disturb the ant and the nest? The goal is to be able to know which ant you marked months, or many years up to a lifespan later, while at the same time have the least influence of the markings on the behavior of the ant and the interaction between the marked and not-marked ants.

lots of previous research has been done marking bees and ants.

For this purpose, people usually paint ants on top of the thorax (not on the head where it can prevent eyes and antenna to function normally, nor on the abdomen where it can block the spiracles and prevent respiration), with a bit of acrylic paint applied with a toothpick. Combination of colors are used to identify individuals.
These techniques are currently being replaced by the use of RFID tags and Flashcodes in science, to automate recordings.


text:
How many end segments does the axon of a typical cortical pyramidal cell have?
I tried to do some research - starting with a Google search for "typical axonal trees" - and found the following pictures:

source

source (axons are red)
but didn't find a concise answer to this and some related questions:

How many end segments (which don't branch anymore) does the axon of a typical cortical pyramidal
  cell typically have. I guess it's a much smaller number than the
  number of end segments of a typical dendrite, but how large is it
  roughly: some tens, sometimes less than ten?

I'd like to exclude from this question the typical axonal "end trees" which branch into the axon terminals.

@vkehayas: I followed your advice.

Some things to consider: What do you think that this is measure is relevant for? Are you making the implicit assumption that these terminal branches make more synapses? Please edit your question to help us understand what is the underlying question you are trying to answer.

In my original question - where I asked it all together - I made a distinction: number of synapses = number of end segments times number of synapses (= axon terminals) per end segment. But I am quite sure that not every kind of "end segment" has the same number of synapses (= axon terminals) (not even roughly). This number most probably depends on other things.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
How many synapses are there in the different target regions of a typical cortical pyramidal cell?
I found the following pictures of axon trees:

source

source (axons are red)
but didn't find a concise answer to the following question:

How many (in relative terms) branches terminate and how many axon
  terminals (synapses) are there in the different target regions of a
  typical cortical pyramidal cell, i.e.

same cortical layer
other cortical layers
same cortical column
other cortical columns
more distant cortical regions (e.g. in the same gyrus)
subcortical regions

I take it that you mean how many synapses are formed with a pyramidal neuron and $X$. Talking about branches doesn't make too much sense. You should know that there are 4-7 different types of cortical pyramidal cells, depending on how you count (e.g. Oberlaender et al. 2012 for the higher estimate). Every single presynaptic source you are asking about is going to have a different estimate for every different type of pyramidal neuron, and some of them are unknown. I'd say this is too broad.

You "just" say there is no typical pyramidal neuron? I know that

... but 4-7 is not such a big number one couldn't give a partial answer: for type X it is so-and-so, ... Should I rephrase my question? To which of the 4-7 types would you recommend to restrict my question?

I'd say we only have numbers for the number of synapses or the volume of axon that comes or goes inside or outside the column, with no estimates about specific neurons, but I really do hope that someone will prove me wrong.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Are there axon branches that go up to cortex layer 1 and spread there?
I found the following pictures of axon trees:

source

source (axons are red)
but didn't find a concise answer to the following question:

Are there axon branches that go up to cortex layer 1 and spread there?
  (This is not indicated in the pictures above, maybe because there are no.)

Short answer: It depends on the layer.
Axons of some neurons in deep layers will project back to L1 (Brecht et al. 2003a, Oberlaender et al. 2011), but neurons of superficial layers extend their axons laterally (Brecht et al. 2003b).
Besides focusing on specific pyramidal cell sub-classes it's worth considering what proportion of inputs to L1 comes from intracolumnar or extracolumnar inputs. From the wikipedia article on the cerebral cortex:

Layer I, the molecular layer, contains few scattered neurons and consists mainly of extensions of apical dendritic tufts of pyramidal neurons and horizontally oriented axons, as well as glial cells. [...] Inputs to the apical tufts are thought to be crucial for the ‘‘feedback interactions in the cerebral cortex involved in associative learning and attention. While it was once thought that the input to layer I came from the cortex itself, it is now realized that layer I across the cerebral cortex mantle receives substantial input from ‘‘matrix or M-type thalamus cells (in contrast to ‘‘core or C-type that go to layer IV).

Most of the inputs to layer 1 (L1) are indeed thought to come from the "non-specific" thalamus and other cortical areas, such as the primary motor cortex in the case of primary sensory areas.[citation needed] I am only aware of circumstantial evidence for the relative prevalence of thalamic inputs in L1. According to staining for different vesicular transporters of glutamate (type I is thought to label mostly cortical neurons in adult animals, type II subcortical), about half of the input to L1 is subcortical (Kubota et al. 2007). It's worth noting that the slender-tufted neurons described by Oberlaender et al. (2011) to project heavily in L1 are considered to be the main targets of the "non-specific" thalamus in the cortex (Brecht et al. 2003a). The extracolumnar origin of cortical inputs to L1 matches with the overall trend observed accross layers for the majority of inputs to come outside the cortical column (Stepanyants et al. 2009).

Depends on the layer the pyramidal cell lives in?

Anyway a great and concise answer!

@HansStricker Correct.

Having learned that there are such axons resp. branches of axons, and assuming that they play a functional role (and are not just outliers): How far do you think do they spread in layer 1 (typically, roughly, on average)?

I didn't mean to imply that they are outliers, but rather a sub-class of cellls. I've updated the text to reflect that. If I understand you correctly, the answer is in Figure 3 from Oberlaender et al.

Figure 3 is hard to grok for me (at first sight). What does it tell me?

And no, I didn't want to suggest that you implied them being outliers. It was just for the case.

The average slender-tufted L5 pyramidal cell projects ~50 mm of axon in the superficial layers (L1-3) outside its principal column, in comparison with ~10 mm inside the column.

Just to add, cortico-cortical inputs to layer 1 originate from many areas (not just motor cortex), usually in a 'feed-back' pattern from 'higher' to lower-order cortex, and many of them travel quite some distance once there.


text:
Are intracortical axon branches myelinated?
I found the following pictures of axon trees:

source

source (axons are red)
but didn't find a concise answer to the following question:

Is it possibly true that the intracortical axon branches (i.e. those that don't leave the gray matter) are not
  myelinated?  (The first picture seems to indicate that they have at
  least a smaller diameter, making them slower?)

A great reference for this question is Tomassy et al. 2014. Axons of cells from all layers lack a myelin sheath at their proximal segment, often called the axon initial segment. This stretch of unmyelinated axon is longer for more superficial pyramidal neurons (~150 $\mu m$) and shorter for those located in deeper layers (~25 $\mu m$), something which does not depend on axonal caliber. These authors observed that some of the superficial neurons didn't have any myelin for the length of axon observed (> 200 $\mu m$). They speculated that these are neurons that send their axons through the corpus callosum.
What is interesting is that superficial pyramidal neurons often displayed intermittent myelination away from that initial segment, with long stretches of axons (up to ~55 $\mu m$) being unmyelinated. Note that these myelin gaps are more than an order of magnitude longer than Ranvier's nodes.
What are these gaps in myelin good for? If these axons target other intracortical neurons, it is unlikely that the predicted transmission delay will have an important impact given the short distances in the cortex (~1 mm). For those neurons targeting other brain areas it may be somewhat more important. It is interesting, however, that these patches of unmyelinated axons both made and received synapses, suggesting that they may have a functional role.
The neurons in the OP's images are corticothalamic cells residing in (lower) layer 2/3 of the visual cortex (upper half) and thalamorecipient cells in layer 4 of the motor cortex (bottom half). Thus it is likely that their axon initial segment is unmyelinated. Although not yet conclusive, the results of the cited paper support the view that the axons of those superficial neurons that project to deeper layers or other brain areas are completely unmyelinated.

modified from wikipedia, CC BY-SA 3.0


text:
Why difference in degree of folding in a cell?
For a cell to maintain constant volume, input should be equal to output of substances.

My question is, if the basolateral membrane, by less folding can attain the same rate of transport as of the apical surface with microvilli, then why do cells produce more foldings (microvilli)?
Why is there a difference in degree of foldings on each side?

This is not my area of expertise, but assuming that the concentration gradient is significantly different on each side of the cell, there should be different transport rates over a given membrane surface area simply from the different diffusion rates. Throw in varius pumps and transporters, which can differ in localization and numbers and there should be no reason to assume identical transport rates in the membrane. Therefore I would suspect that the increased surface area on one side serves to maximise passive absorption while the other side acts as an active transporter expending energy.


text:
Flora of Ice Age Europe
I'm trying to get a very in-depth idea of the ecosystem of Pleistocene Europe, somewhere around 40,000 years ago, and I can't seem to find what types of foliage (other than the obvious grasses and lichens) grew in that place and time. I'm particularly interested in the species of tree that were present; can anyone help?

40,000 is not very long ago! it would be similar to today. tundra and deciduous similar species. check this from 50,000,000 years in america, it's still similar: http://geology.com/articles/green-river-fossils/plant-fossils.shtml

It strongly depends on how far North in Europe you mean. Scandinavia would be very different from France, which would be very different from Spain or Italy. But trees would not be very abundant North of the Alps I think.


text:
Do IgM and IgG differ for different infections?
I am not that much educated in the medicine and immunology fields. So I noticed that there are tests for IgM and IgG immunoglobulins for various infections. I was not able to google quickly if IgM for one type of infection differs from the one for another type of infection.
I guess they differ because otherwise there would be only a few tests in the laboratory instead of dozens. But it would be great to hear some solid explanation.

IgM (Immunoglobulin M) is the first antibody to appear in response to an antigen. It can be produced by the fetus and cannot be crossed by the placenta.
Typically one might test IgM to diagnose hereditary and acquired IgM immunodeficiencies or diagnose Waldenstrom macroglobulinemia. It can serve as the earliest Ig serologic diagnosis of infectious disease.
Lab tests for IgM may be increased in liver disease, chronic infection, hyper IgM syndrome, and secondary to nephritic syndrome; Waldenstrom macroglobulinemia, lymphoma, CLL, multiple myeloma (rare), Schnitzler syndrome, cold IgM antibody agglutin, and MGUS.
Lab tests for IgM may be decreased in protein-losing syndromes, non-IgM myeloma, and infancy/early childhood.
IgG (Immunoglobulin G) activates complement and fights infection. IgG represents 70-80% of the total serum immunoglobulins in normal adults. It exists in four subclasses (IgG1, IgG2, IgG3, and IgG4). IgG1 predominates as 65% of the total IgG. IgG of maternal origin provides passive immunity to the neonate. It is transported across the placenta.
Typically one might test IgG to diagnose IgG myeloma, diagnose hereditary and acquired IgG immunodeficiencies, and provide a serologic diagnosis of infectious diseases and immunity.
Lab tests for IgG may be increased in multiple myeloma, solitary plasmacytoma, MGUS, lymphoma, CLL, sarcoidosis, cirrhosis, autoimmune diseases, parasitic diseases, chronic infection, and intrauterine contraceptive diseases.
Lab tests for IgG may be decreased in protein-losing syndromes, pregnancy, non-IgG myeloma, Waldenstrom macroglobulinemia, primary immunodeficiency states, and agammaglobulinemia (if combined with other immunoglobulin decreases).
Sources:
https://5minuteconsult.com/collectioncontent/2-152356/lab-tests/immunoglobulin-m-igm
https://5minuteconsult.com/collectioncontent/2-152354/lab-tests/immunoglobulin-g-igg

Taylor, thank you for your answer that's all wonderful. But it actually does not address my question. I was asking why there is an IgM test for e.g. Borrelia burgdorferi and also the IgM test let's say for tick-borne encephalitis and they are priced differently.
In other words I was asking how exactly the IgM for one infection differs from the IgM for another infection.

IgM will be specific for certain epitope on the antigen. Basically, it will detect a "signature" of the various pathogens and be specific for it. Most of the IgM molecule will the be the same apart from a section called the hypervariable region. This hypervariable region will have different characteristics and specificity for each antigen that an organism has been challenged by.

Joseph, thanks a lot. Could you put this comment as an answer and I will accept it.

The CDC currently recommends a two-step process when testing blood for evidence of antibodies against the Lyme disease bacteria. CDC
If Lyme Disease is suspected in at-risk patients, a sensitive serum serology screening test is performed to detect IgG and/or IgM antibodies to Borrelia Bugdorgeri. More specifically, an ELISA (Enzyme Linked Immunosorbent Assay) is a type of test that is used to detect IgM and IgG B. Burgdorgeri antibodies which is then followed by a Western blot test.
In tick-borne Encephalitis (TBE), laboratory diagnosis depends on the detection of specific IgM in either blood or CSF (Cerebral Spinal Fluid), which usually appears later, during the second phase of the disease. CDC
Pricing is dependent on the number of tests required to accurately diagnose one or both conditions, associated laboratory fees, your medical insurance coverage, etc.

You are very welcome Alexander. Glad I could provide some clarity.

My mistake, sorry for that.


text:
Using viruses to treat altered or misconfigured DNA
Consider how a Retrovirus can modify existing cell DNA to 'execute instructions' on its behalf.
I wondered: Why can we not utilize lab-generated viruses to infect sick patients with a 'healthy' virus that would rewrite bad segments of DNA with something either correct or non-malus? This of course is assuming that we have a solid understanding of the relationship between genomes and precise viral functions, additionally that we had some sort of gene replacement functionality.

Consider how a Retrovirus can modify existing cell DNA to 'execute instructions' on its behalf.

Not only retroviruses do that. Actually, pretty much all viruses use the machinery of the host cell on its behalf.

Why can we not utilize lab-generated viruses to infect sick patients with a 'healthy' virus that would rewrite bad segments of DNA with something either correct or non-malus?

We actually do that. We use viruses (incl. retrovirus but not only) to insert DNA segments into eukaryote genome. See vectors in gene therapy > viruses

Retrovirus to reverse another retrovirus

Note that I don't really understand your title so, I ignored it a bit focusing on the content of the post.

Updated the title. That makes sense, thank you for giving me a direction to continue research!


text:
What is the largest animal that has no hard parts?
Some examples of "hard" animal parts are bones, cartilage, and exoskeletons. What animal has the most mass while being completely "soft". I don't think it's the colossal squid, since it has a hard beak and cartilage in their mantle. My guess is the heaviest jellyfish.

What do you consider hard and what as soft? My [now deleted] answer received a downvote and below answer also struggles to find a definition of what 'hard parts' are.

@AliceD Why don't you post a new answer as per his definition?

@TalhaIrfan because the question is ambiguous and below answer is not too bad.

Please forgive me for plagiarizing the open source wikipedia, here are some species of large soft bodied animals. I honestly don't think I could re-write this more clearly for any logical reason:
Citation:
The lion's mane jellyfish (Cyanea capillata) is the largest cnidaria species, of the class Scyphozoa. The largest known specimen of this giant, found washed up on the shore of Massachusetts Bay in 1870, had a bell diameter of 2.5 m (8.2 ft), a weight of 150 kg (330 lb). The tentacles of this specimens were as long as 37 m (121 ft) and were projected to have a tentacular spread of about 75 m (246 ft) making it one of the longest extant animals

The largest roundworm, Placentonema gigantissima,[174] is a parasite found in the placentas of sperm whales which can reach up to 9 m (30 ft) in length
The largest nemertean is the bootlace worm, Lineus longissimus. A specimen found washed ashore on a beach in St. Andrews, Scotland in 1864 was recorded at a length of 55 m (180 ft).[183]
There are a couple of animals that are of interest but they are not technically soft bodied:
The colossal squid (Mesonychoteuthis hamiltoni) is projected to be the largest invertebrate. Current estimates put its maximum size at 12 to 14 m (39 to 46 ft) long and 750 kg (1,650 lb),[185] based on analysis of smaller specimens. In 2007, authorities in New Zealand announced the capture of the largest known colossal squid specimen. It was initially thought to be 10 m (33 ft) and 450 kg (990 lb). It was later measured at 4.2 m (14 ft) long and 495 kg (1,091 lb) in weight
The largest known species of sea sponge is the giant barrel sponge, Xestospongia muta. These massively built sponges can reach 2.4 m (8 ft) in height, 80 kg and can be of about the same number of feet across at the thickest part of the "body". Some of these creatures have been estimated to be over 2,400 years of age.
https://en.wikipedia.org/wiki/Largest_organisms#Invertebrates

I received critiques from another user and deleted my answer. Issue is the species should be devoid of any 'hard' parts - a sponge has a rigid calcareous skeleton and the squid was dismissed in the question too.


text:
How many ancestral generations do I have?
Following on from this question: How many humans have been in my lineage? Is it almost the same for every human currently living?
How many generations back do my ancestors go? Not just human ancestors, but all ancestors, right back to the first lifeform.
I recognise that there are some impossible unknowns here, so I’m looking for some kind of Fermi estimate.

sexual reproduction changed the generational thing so you have perhaps 1 - 4  billion sexually reproductive generations since your precambrian times, if you have an average 1 to 4 generations per year, seasonally, on average. since 4 billion years, zircons from australia have isotopes of oxygen that suggest life, and stromatolites date from <3.7, so we are talking about 4-400 billion prokariote and eurkariote zygote meioses.


text:
What do you call mRNAs that translate to the same protein?
For example AUAACC and AUCACG in distinct mRNAs may both be translated to the same dipeptide Ile-Thr.

This is by no means a consensus, but this paper from 2000 proposes a new term: Isotranscript.
According to the authors:

Duplicated genes often encode distinct proteins that differ by only a few amino acids, such as the two mammalian S27 isoforms, S271 and S272, documented here and the yeast and Arabidopsis S27 isoforms identified previously. On the other hand, we have found that different S27 transcripts encode 100% identical proteins. This phenomenon has also been described previously for the histone subtype, H3.3, in which two different transcripts encode the same H3.3 amino acid sequence . We have chosen the terminology “isotranscripts” to describe such mRNAs. (emphasis mine)

Source: Thomas, E., Alvarez, C. and Sutcliffe, J. (2000). Evolutionarily Distinct Classes of S27 Ribosomal Proteins with Differential mRNA Expression in Rat Hypothalamus. Journal of Neurochemistry, 74(6), pp.2259-2267.


text:
Bumble bees and wasps
Location:India
My father was telling me yesterday that wasps were building a nest over an abandoned store room in our backyard...But he noticed that the wasps were attacked by a bunch of bumblebees...And the two were locked up in a duel.Several wasps were also found dead on the land...
Today he told me that the nest had almost diminished and several bumblebees were surrounding it...which seemed like they were destroying it
My question is:
Why would bumblebees destroy the wasp nest?
I guessed that they would build their own nest instead (after a few days perhaps) but there were plenty of other places in the yard too like there is big mango tree... it's only a guess and I am too curious to know any biological cause.


text:
Nervous stimuli and neurotransmitters and impacts
As far my knowledge, in body parts generally **acetacholine ** is the neurotransmitter. Which is responsible for most nervous impulses.
Consider a body part, say, foot. Only one  nerve reaches here. When ant bites there, the impulse of pain and irritation moves from there ;
Secondly, when some soothing agent comes there the impulse of comfortness moves from there
Now, neurotransmitter is the same, nerve is the same, but different impacts are observed.
My teacher said that the impulse moves to different parts of the brain.
But how are the impacts really understood, analysed and sent to different regions ( as entrance of all stimuli enter through the same brain stem,)
In short,
My question is that how does our brain analyses two different stimuli when neurotransmitter is the same, nerve is the same and enter the brain through the same brain stem. They must be going to different regions of the brain but how is that decided

Please see this related Q&A. Although that question's focus is on the motor system, the answer also provides adequate coverage for the sensory system. If you still don't understand something after reading the linked Q&A, please edit your question accordingly in order to let us know what more specific details you need help with.

Would you be kind to tell that What specifications you require?

Did you read the linked question? Does it cover your question? Or is there something more you need to know?

This related question talks about the action of peripheral nervous system. By presenting two models. I am not talking about that. My question is that how does our brain analyses two different stimuli (like i have written in the post), when neurotransmitter is the same, nerve is the same and enter the brain through the same brain stem. They must be going to different regions of the brain but how is that decided?


text:
Peacock species identification
A few weeks ago I encountered a peacock while driving to a friend's house in Central KY, USA. I don't believe I've ever seen a peacock in KY, and when attempting to ID [just through Google searches], I could only find restaurants & musical artists that contain "peacock" in their name.

Can someone help me ID this bird? And, are peacocks wild in KY? Have they always been, and are just rare? Aside from species ID, any insights about this bird and its prevalence within KY would be most appreciated.

The answer below is correct. I just wanted to add, having kept peafowl, that the male looses all of the beautiful feathers of his tail once a year, and as a result, looks pitiful (to my tainted eye; after all, he's "supposed to be proud of his tail") for a number of weeks while the new ones grow back. Your peacock is in the process of growing his back, and looks pretty good, although note the absence of the long trailing green/blue iridescent tail feathers. (I didn't know this and panicked when my first male molted!)

That is the male of the Indian peafowl species (Pavo cristatus), also called the blue peafowl or common peafowl.  The male is called a peacock and the female a peahen, collectively peafowl, although often "peacocks" is used instead of peafowl.  The hen does not have the impressive tail of the peacock (although she does have a similar crest on the head).
They are not native to Kentucky, or anywhere else in the Americas, but have been widely introduced (because of their appearance).  There are only 3 species of peafowl, the green peafowl being similar and native to southeast Asia, and the Congo peafowl being much more subdued and native to Africa.

They're a reasonably common ornamental bird among farmers &c, and also kept in some parks for the same reason, e.g. https://www.mcmurrayhatchery.com/peafowl.html  They've also become naturalized in some places, such as IIRC the Santa Rosa area of California.


text:
Organisms that do not wish to reproduce
Are there any organisms that do not want to reproduce?
As humans, there are people who do not want to reproduce with the opposite sex. Do any other organisms replicate this behavior? Also, why does this behavior exist? If the end goal of an organism is to reproduce, why has evolution allowed organisms that do not want to reproduce to exist?

Are you talking about homosexuality?

See also: Which species has the highest proportion of homosexual individuals? and Can animals, like monkeys, be homosexual?

Hydra dont age and only have sex when food is scarce to leave spawn for next season. they devide. komodo dragons dont need sex to have eggs, whiptail lizards, marbled crabs and many many other animals are asexual: https://www.cuteness.com/article/animals-use-asexual-reproduction some 10 pc of rams, male sheep, stick insects, sawfish, snakes ... search for asexual animals. parthogenesis.

@Remi.b — The poster did not mention homosexuality. Have you never encountered heterosexual couples that don't want to have children and are able to fulfill their wishes through contraception. The question is silly in attributiing human emotions to non-human animals, but it is not about homosexuality.

@David You're right. I'd think however, that the answer remain similar I would guess. It will be hard to talk about 'will of having babies' with heterosexual couples in animals.

@David You're right that I was asking this question with homosexuality in mind, but the explanations there gave me the answer i was looking for. Thank you!

Animals and especially female animals might not "want" to reproduce when circumstances are bad for babies.  Pregnancy and rearing of infants is a big commitment of resources for female mammals.  If a female is under stress, or sick she might avoid having sex even though she could get pregnant because evolutionarily that was a winning strategy for her ancestors - committing the physical and nutritional resources to a pregnancy and fetus unlikely to survive current circumstances puts the mother and subsequent pregnancies at risk.
A more extreme example is the Bruce Effect.  Pregnant females exposed to the pheromones of a strange new male "decide" not to reproduce - their bodies resorb the fetuses.  Presumably this is because the new male is a risk to the fetus and they would do better calling off the doomed project, and possibly having a new litter with the new male if he shows up.
Weirder is the circumstance of parents that kill and sometimes eat their young.  That happens in mammals, birds, fish and others.  It is hard to see how this sort of thing advances genetic fitness - it seems like a crossed wire or misfire of some sort.  Certain animals, however, seem to do it all the time; hamsters come to mind.  Maybe stress causes weird behavior?  In any case this too would seem like a case of deciding not to reproduce.


text:
Acid/basic chemicals that can be used without extraction hood?
I need to use some meat dissolvent for my thesis, I’m working in forensic anthropology, but in my university, we are not allowed to use those which might be extremely harmful (such as HF or HCl due to the fumes).
Friend of mine suggested me to use CaO and KOH, since you only need normal lab equipment. Do you have other suggestions that might come in handy?
Thank you! All the help I can get is really appreciated


text:
Why does the upper respiratory tract not fill with water when diving?
When we swim, I know we close the some of the vestibular folds in the larynx part of the throat to hold our breath (and to avoid water from getting into the lower respiratory tract, I suppose).
I wondered, what avoids water from running into the upper respiratory tract (such as the nasal cavity and pharynx), when we e.g. dive to the bottom of a swimming pool and lie on our back on the bottom of the pool?
I've tried googling for an hour (during which I learned most of the above anatomical words), but I have not been able to find any bodily mechanic that prevents water from entering the nasal cavity... How does the body avoid this, since there is clearly two holes in our nose, which could lead to water filling our whole upper respiratory tract, if they are not closed?
Thanks!


text:
What is the justification of Chargaff's second parity rule?

First parity rule
The first rule holds that a double-stranded DNA molecule globally has percentage base pair equality: %A = %T and %G = %C. The rigorous validation of the rule constitutes the basis of Watson-Crick pairs in the DNA double helix model.
Second parity rule
The second rule holds that both %A ~ %T and %G ~ %C are valid for each of the two DNA strands. This describes only a global feature of the base composition in a single DNA strand.

[source]
It makes sense that in the context of dsDNA, that A = T and C = G, but I don't see an obvious reason why in a single strand of DNA, A ~ T and C ~ G.

Please avoid uploading text in images. They are not searchable, they are often hard to read (it is the case here) and they pose problem to visually impaired people. Also, please add a link when you cite from a source.

This is an excellent question, which was the cause of some confusion in the field over the years:
"The validity of the second Chargaff rule was unexpected. Obviously it should be regarded as a global rule, i.e. applicable to large sections of chromosomes. Nonetheless, not being derived from a compelling principle, such as the one underlying the first rule, it remains a mystery. This is even more so, when one studies extended versions of Chargaff’s second rule." (paper)
There are a few things to note here:

Chargaff's rules were purely observational; they pre-existed the double helix (see your same Wikipedia ref), and thus pre-existed the double helix model (which was in fact famously a rendering of the first rule in a 3-D model, as Watson wrote about in his book "The Double Helix"). There is thus no logical or mechanistic justification for the rules; they were simply what Chargaff et al. observed for dsDNA and ssDNA. Perhaps I have misinterpreted, but I felt the question implied a belief that there must be some logical requirement for this.
Note that the first rule uses "=" and the second rule uses "~" ("approximately"). That is, if we believe that all bases in a genome are paired, then it follows as a mechanistic/logical requirement that Watson strand and Crick strand must match up compositionally. This is obviously not the case with ssDNA, as I think you indicate in the Q. However, it is nonetheless true that genomes have overall compositional biases; they tend to have consistent (G+C)/(A+T) ratios across the molecule (on average). More recently, it has become clear that this is true not only for single nucleotides, but also for $k$-mers, or short DNA sequences of length $k$ (paper). Indeed, these patterns have been used to match up different pieces from the same genomes (paper). These biases exist on both strands, therefore each strand of a genome is subject to these biases. (The reasons why these biases exist are often argued over, but may have something to do with mutational biases). Therefore, both ssDNA strands of a dsDNA genome have the same compositional biases, and they must complement each other's similar biases, so even within a strand the statistical expectation is Chargaff's second rule. Chargaff, again, probably didn't know many of these things when he came up with the rules. This explanation for Chargaff's second rule has been explicitly discussed in the literature, in the first paper cited.

Notably, the second rule only holds reliably for long sequences, because in short sequences sampling error may lead to a failure to match the biases of forward and reverse strands. This is more or less what everyone means when they call it a "global" rule.

In addition to the answer by Maximilian Press, the papers

[1] Intrastrand Parity Rules of DNA Base Composition and Usage Biases of
Synonymous Codons
[2] Properties of a General Model of DNA Evolution Under
No-Strand-Bias Conditions

show that under a no-strand-bias assumption, the base frequencies of a single strand at equilibrium, denoted as $A^*,T^*,G^*,C^*$, are such that $A^*=T^*$ and $G^*=C^*$.
I would try to explain it briefly here, but please refer to the original papers for a complete and better explanation, as some of my explanation is simplified.

First, we denote the base frequencies (in time $t$) of a single strand $A(t),T(t),G(t),C(t)$.
(each frequency is in $[0,1]$, and $A(t)+T(t)+G(t)+C(t)=1$)
Next, we denote the substitution rates in a single strand $r_1, ..., r_{12}$, as follows:

(diagram copied from [1])
E.g.:
$$\frac{dA}{dt} = -\left(r_{1}+r_{4}+r_{6}\right)\cdot A\left(t\right)+r_{2}\cdot T\left(t\right)+r_{3}\cdot G\left(t\right)+r_{5}\cdot C\left(t\right)$$
Similarly, we denote the substitution rates in the other strand (in the double helix) $r'_1, ..., r'_{12}$.
If we assume no-strand-biases$^{(*)}$ (i.e., the substitution rates are independent of the strand: $r_1=r'_1, ..., r_{12}=r'_{12}$), then using Chargaff's first parity rule we can deduce:
$$r_1=r_2,r_3=r_9,r_4=r_{10},r_5=r_7,r_6=r_8,r_{11}=r_{12}$$
(because $r_7=r'_5$, etc.)

$(*)$ If I understand correctly, there is another implicit assumption here - each substitution rate in time $t$ is independent of the base frequencies. E.g., regardless of whether the frequency of $A$ bases in one strand is different from the frequency of $A$ bases in the other strand, we assume that $r_1=r'_1$.

So we can (under a no-strand-bias assumption) denote the substitution rates in a single strand $a, ..., f$, as follows:

(diagram copied from [1])
I.e.:
$$
\left(\begin{matrix}\frac{dA}{dt}\\
\frac{dT}{dt}\\
\frac{dG}{dt}\\
\frac{dC}{dt}
\end{matrix}\right)=\left(\begin{matrix}\left(-a-e-c\right)\cdot A\left(t\right)+a\cdot T\left(t\right)+b\cdot G\left(t\right)+d\cdot C\left(t\right)\\
a\cdot A\left(t\right)+\left(-a-e-c\right)\cdot T\left(t\right)+d\cdot G\left(t\right)+b\cdot C\left(t\right)\\
c\cdot A\left(t\right)+e\cdot T\left(t\right)+\left(-b-d-f\right)\cdot G\left(t\right)+f\cdot C\left(t\right)\\
e\cdot A\left(t\right)+c\cdot T\left(t\right)+f\cdot G\left(t\right)+\left(-b-d-f\right)\cdot C\left(t\right)
\end{matrix}\right)
$$
Or equivalently:
$$
\left(\begin{matrix}-a-e-c & a & b & d\\
a & -a-e-c & d & b\\
c & e & -b-d-f & f\\
e & c & f & -b-d-f
\end{matrix}\right)\left(\begin{matrix}A\left(t\right)\\
T\left(t\right)\\
G\left(t\right)\\
C\left(t\right)
\end{matrix}\right)=\left(\begin{matrix}\frac{dA}{dt}\\
\frac{dT}{dt}\\
\frac{dG}{dt}\\
\frac{dC}{dt}
\end{matrix}\right)
$$
At equilibrium:
$$
\left(\begin{matrix}\frac{dA}{dt}\\
\frac{dT}{dt}\\
\frac{dG}{dt}\\
\frac{dC}{dt}
\end{matrix}\right)=\left(\begin{matrix}0\\
0\\
0\\
0
\end{matrix}\right)
$$
So we have to solve:
$$
\left(\begin{matrix}-a-e-c & a & b & d\\
a & -a-e-c & d & b\\
c & e & -b-d-f & f\\
e & c & f & -b-d-f
\end{matrix}\right)\left(\begin{matrix}A\left(t\right)\\
T\left(t\right)\\
G\left(t\right)\\
C\left(t\right)
\end{matrix}\right)=\left(\begin{matrix}0\\
0\\
0\\
0
\end{matrix}\right)
$$
It turns out that every vector proportional to the following solves the equation:
$$
\left(\begin{matrix}d+b\\
d+b\\
e+c\\
e+c
\end{matrix}\right)
$$
The relevant solution to us is a solution such that each frequency is in $[0,1]$ and $A(t)+T(t)+G(t)+C(t)=1$:
$$
\left(\begin{matrix}\frac{d+b}{2\left(d+b+e+c\right)}\\
\frac{d+b}{2\left(d+b+e+c\right)}\\
\frac{e+c}{2\left(d+b+e+c\right)}\\
\frac{e+c}{2\left(d+b+e+c\right)}
\end{matrix}\right)
$$
I.e., $A^*=T^*$ and $G^*=C^*$.

I’m too old to follow your maths (it was different when I was a school boy), but if I understand you correctly, Chargaff’s second “rule” is a mathematical consequence of his first. Pity he didn’t devote himself instead to understanding the basis of the first — he would have died a less embittered man.

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


text:
Can a phosphodiester bond form between RNA and DNA?
In the initiation of DNA synthesis:

the RNA segments are first synthesized by primase and then elongated
  by DNA polymerase (Wikipedia).

What does 'elongated' mean in this context? Is it possible for RNA and DNA to form a phosphodiester bond to make a single strand which is part RNA and then part DNA?

A biochemistry book, such as Berg et al. online, is far better than Wikipedia. Your question is answered in section 27.4.1 — see Figure 27.26. Try other books on the NCBI Bookshelf searching for Okazaki fragments.

@David thank you very much David , I've read the section 27.4.1 and the figure 27.26 but a bit unsure about it. It mean that a RNA and DNA can forms a sugar backbone bond between them to make a single strand RNA-DNA ?. I used to think that the RNA cannot forming bond with DNA like that and I was wrong. Thank you again!

The problem is not forming a phosphodiester bond between ribose and deoxyribose (chemically the same) but that one would expect a DNA polymerase to discriminate against the 3'OH of the ribose. You are in good company being surprised that it happens — it was an unexpected discovery at the time. I suspect that some component of the DNA polymerization process confers this changed specificity, but it is not my field and I haven't time to check this. If anyone knows the details I suggest they formulate them into a more comprehensive answer.


text:
Is the cranial nerve blood supply encapsulated by the blood brain barrier?
I understand the origin of cranial nerves are within the blood brain barrier. I'm assuming as they extend distally there's a point at which their vasculature is not encapsulated by the blood brain barrier. Is this true? Any idea where the blood brain barrier stops?
Thank you.

Did you google (e.g.) Blood Brain Barrier? The Blood Brain Barrier isn't a membrane or sac, like the dura mater. It exists because of capillary structure within the central nervous system. The origin of all nerves (anything coming off the brain or spinal cord) is "within the BBB". I'm unsure of what you're asking.

Thanks anongoodnurse. I've researched it quite a bit. Although I haven't found anything to confirm or deny, I'm assuming the cranial nerves as they emerge from the Pons, etc. would be encapsulated in the BBB. I'm also assuming that the BBB doesn't extend all the way along the cranial nerves until they end, because that would mean you have a Blood Brain Barrier outside of the CNS. Somewhere along the way from the Pons to the end of the cranial nerve, it stops. Is this right?

I will ask you a question which can answer yours, though I think you still don't quite understand the BBB. How can you administer a drug which can bypass the BBB? Think cancer treatment. I'm sorry to use the Socratic method, but that's largely how doctors are taught. Teach a man to fish and all that.

I can't find a great answer to this either, but there is a known concept of a CNS-PNS transition zone, specifically as it pertains to myelination of cranial nerves. With the exception of CN 1 & 2 (which are effectively wholely CNS) the other cranial nerves are anatomically similar to spinal nerves, i.e. they're myelinated by Schwann cells and have an endoneurial blood supply. But they are also myelinated by oligodendrocytes for a short distance (varies by nerve) after taking of from their CNS nuclei before reaching that transition zone. According to this paper, that transition zone should mark the end of the astrocyte coverage which is necessary for BBB function. It's not a dead-ringer of an answer but this explanation makes as good physiologic sense as anything I've seen.
https://www.ncbi.nlm.nih.gov/pubmed/10697296


text:
Interbreedability between current humans and his ancestors
I want to know the first point of time in the past when genomes have diverged so far from modern human genomes so that they both (human and ancestors) are not interbreeadable anymore and can be seen as separate species.

Does pre-zygotic isolation count?

Related (but definitely not a duplicate): How could humans have interbred with Neanderthals if we're a different species?

"Does pre-zygotic isolation count?" I don't think so ;-).

Short answer
Considering only post-zygotic isolation and based on below discussion, I would tend to think that 20th century human could interbreed with our ancestors living a 1 to 2 millions years ago. I would give a range between 100k years and 8 MYA for safety.
Long answer
Concept of species
The post How could humans have interbred with Neanderthals if we're a different species? makes a good introduction to the difficulties behind the concept of species.
Pre-zygotic isolation
Anatomically speaking, it is probably possible to get a spermatozoid cell from a 20th century man start fusing with a Homo abilis ovule (and vice-versa). The potential pre-zygotic isolation will rather be caused by aesthetic appearance.
To the risk of sounding posh, I would say that Homo abilis hairy face does not exactly fall within my standards! I suspect it will be the same for many of us, humans of the 20th century. It is hard to really know how much time one needs to go back to consider that we don't disgust each other enough to refuse mating together. There are a few reasons why this is hard

Reconstruction (esp. facial reconstruction) is often too inaccurate to really allow to tell how ugly their faces were.
It is going to be super hard to tell what they would just about our faces today! I bet they'd laugh at our ridiculously small jaws!
It is hard to fully separate the environment from the person. In middle-age (in Europe at least) people would bath a few times in a life-time. Again I would consider this not in my standards!

But let's focus on post-zygotic isolation.
Post-zygotic isolation
Humanzee

The humanzee (Homo sapiens sapiens × Pan) (also known as the chuman or manpanzee) is a hypothetical chimpanzee/human hybrid. An unsuccessful attempt to breed such a hybrid was made by Ilya Ivanovich Ivanov in the 1920s. There have been occasional reports of human-chimpanzee hybridization, notably regarding a performing chimp named Oliver during the 1970s, but none of them have been confirmed. Similarly, the possibility of a chimpanzee–gorilla hybrid, known as a koolakamba, also remains unsubstantiated.

There is no evidence of humanzee but it is important to realize that the idea of such hybrid is not fully unthinkable. Human and chimpanzee share a common ancestor about 6 millions years. So, if a humanzee is consider eventually possible, I would quite definitely consider that a H. abilis (~1 MYA) or H.erectus (~2 MYA) and 20th century human could well interbreed if we were to live at the same time.
Sumatrans and bornean orangutans can hybridize (Malinson, 1984) despite that their lineages have split about 1.3 MYA!
So putting all of that together and follwing some vague intuition, I would personally tend to think that 20th century human could interbreed with our ancestors living a 1 to 2 millions years ago. I would give a range between 100k years and 8 MYA (MRCA with gorillas). But really, it is a rather vague intuition.
See also CrashCourse > How to Make A Humanzee

Ok. I posted this question in a german q&a website. They also came up with estimations of about 500000 to 7 Million years.


text:
Does the brain store information and personality traits in different areas?
I'm aware that muscle memory, language etc can remain largely intact after brain injury that impairs other forms of memory, suggesting that different kinds of memory are stored in different places in the brain.
Are your personality traits also stored separate from memory?

If I'm a bigot, I probably came to be that way because of my experiences and what people who are influential in my life have told me. If I forget those experiences and people due to memory loss following brain injury, will I not be a bigot anymore?
I may have certain nuances in my personality because I'm rich - like body language, or that public transport makes me uncomfortable, never having been used to it. If my memory loss is so severe that I don't recall anything about my life so far, will I still have my nuances?

You're talking about several different things, not just information and personality traits.

@anongoodnurse Being a bigot, disliking public transport, body language.. they're all personality traits, surely? Is it the "information" part which is not properly worded or termed? How can I improve the title or description?

The only way I can make sense of your question is if you are asking whether personality traits are innate or not. Is that what you are asking?

@vkehayas No, I'm pretty sure they're acquired. Based on "information". But is that information stored in a different part of the brain than the personality it creates? If so, does its loss change the personality? (Usage of the term "information" depends on further comments from anongoodnurse, who seems to feel it's not really what I'm asking about)

I think your confusion comes from the fact that you take traits and memory to be distinct from each other. The brain processes information and we know that some of the connections between its cells are altered in the process --some call that memory. You are convinced that this is the only way that traits form, through experience at some developmental stage. You are then asking if cells in areas other than those that change during the formation of traits are affected more by the experience of forming a trait. If that were true, they would by definition be included in the areas that are associated with the trait in the first place. Can you see the problem in the logic of the argument?
Many people have followed similarly flawed reasoning, including trained neuroscientists that have been indoctrinated to believe in extreme forms of functional specialization of the brain, a more subtle version of the now debunked theory of phrenology.


text:
Can somebody identify this insect?
It has transparent wings which covers the body like an armor. It has shining red orange colour.

I found it in the western ghats of kerala.

Now, that's an interesting insect. But, we post pictures here on the insect, and it's likely a better photo is needed (but not absolute.)

This is a tortoise beetle, a coleopteran from the Family Cassidinae.
According to the Queensland Museum:

tortoise beetles are quite distinctive because they’re actually quite flattened and their wing covers are expanded around the edges. So the wing covers are the hard forewings that protect the hind wings in beetles and because they’re spread out at the sides, they look somewhat like a turtle or a tortoise. So that’s how they get their common name.

There are many beautiful specimens, like these:

Your photo is not exactly the best one, but based only on it I'd say that your specimen is a golden tortoise beetle (Aspidimorpha sanctaecrucis):

Here is another image of it, even more similar to your specimen:

That's my favorite insect from this day!

Mine is the passion fruit bug: https://biology.stackexchange.com/a/65070/24284


text:
Is it possible to affect a brain with electromagnetic waves?
A human brain can generate electrical signal. So it generates magnetic field as well. Is it possible to affect a brain with electromagnetic waves?

Sorry... your post is incomprehensible in its current state.  What exactly are you trying to theorize can be done, and what do you mean by "mind connect with EM wave controlling device"?  Please clarify.

Yes.  As a trivial example, put the brain in a microwave oven and cook it :-)

One can use transcranial magnetic stimulation to modulate neural activity. This is effectively inducing a current in the tissue under a magnetic coil.


text:
What is the use of male plants in nature?
If pollination is done by insects like bees and through the air, then what is the use of male plants in nature?

They are just the delivery service for Pollen

Pollen, spermatozoid, ovules and bees
The pollen is a coarse substance containing the spermatozoids. Males plant creates these pollens. As bees visit the flowers, the pollen get stuck on their body. When the bee covered with pollen visits female plant, then the pollen may randomly stick onto the female organ. The spermatozoid grow into a tube within this organ and goes to fertilize the ovule.
In short, bees are ...
In other words, you need females for the ovaries, males for the spermatozoids and bees for the delivery services.
Note that bees don't do this delivery services just to be nice with plants. They do so because they get nectar (substance full of sugar) in the flowers.
Reality is more complex and more diverse
Note also, that reality is more complex and more diverse than what I explained. Not all plant species are pollinated by bees. Not all plant species have flowers. Most plant species are hermaphrodite (have male and female flowers or even have male and female organ within the same flower).


text:
What are hyphal compartments?
The hyphae are the branching filaments that make up the mycelium of a fungus. Hyphal compartments are part of the hyphae. What are they exactly?

I did a quick lookup on google for "hyphal compartments" and the number of online texts/books/citations using this term is quite meagre to say the least. One of the images that I found was this-

And I have reached to the conclusion that--
Hyphae cells (only in septate species) are known as hyphal compartments.
Quoting from wikipedia (read if you don't know about septate and coenocytic varieties of hyphae)

A hypha (plural hyphae, from Greek ὑφή, huphḗ, “web”) is a long, branching filamentous structure of a fungus, oomycete, or actinobacterium.In most fungi, hyphae are the main mode of vegetative growth, and are collectively called a mycelium.
A hypha consists of one or more cells surrounded by a tubular cell
wall. In most fungi, hyphae are divided into cells by internal
cross-walls called "septa" (singular septum). Septa are usually
perforated by pores large enough for ribosomes, mitochondria and
sometimes nuclei to flow between cells. The major structural polymer
in fungal cell walls is typically chitin, in contrast to plants and
oomycetes that have cellulosic cell walls. Some fungi have aseptate
hyphae, meaning their hyphae are not partitioned by septa.
Hyphae have an average diameter of 4-6 µm.


text:
How can potassium rich foods reduce blood pressure?
How come sodium increases blood pressure, but potassium, which has to some extent similar properties helps lower it?

potassium is really the main guy in charge of everything that happens involving action potentials which in turn govern homeostasis such as blood pressure.
k+ lowers blood pressure due to making it harder to get an action potential going, which in the macro scale causes the heart to pump less.
too much k+ kills the person as it stops the pumping of blood (lethal injections are just lots and lots of k+ along with some pain killing drugs)

This provides some information but does not fully answer the question. Why is $K^+$ the main "guy" rather than $Na^+$.  The question assumes that they have similar properties. In what ways relevant to the question are these two ions different?

I agree with @vkehayas but I'd go a step further to say that this answer is completely wrong as far as the mechanisms for what the OP is asking about. We aren't talking about lethal injection levels of K+ or anything about K+ concentration effects on action potentials when talking about K+ effects on blood pressure.


text:
Are the asymmetrical positions of owl ears consistent across species with this trait?
While at a raptor speech a while back ago the naturalist mentioned that owls have offset ears. One ear is located higher in the skull than the other. This is supposed to help the owl detect the location of prey due to the tiny time difference in which the sound reaches each ear. After doing some more research online, it seems that the offset ears are primarily found in owls that are nocturnal hunters. Specifically, I have found that Barn Owls left ear is higher than the right.

Barn Owl (Tyto Alba)-www.robinsonlibrary.com
Are the ear openings are always higher on the left for each species of owl that has asymmetrical ear openings? I would guess that they are predominately the same unless this characteristic had evolved in more than one instance.  Any additional information would be appreciated.

Are you asking if the left is always higher?

Yes, that is correct.  Is the left always higher?

Great question. I checked a few of my ornithology texts and they conflict. Cornell Handbook of Bird Biology (2nd ed) states the Boreal owl right external canal is higher than the left. Ornithology by Gill, 2nd ed, states that the barn owl left is higher than the right.

@JYelton - Thanks for looking into this.  I wonder if there is some confusion in the texts with point of view when it comes to right or left.  I asked the naturalist that was giving the talk on raptors the same question and he wasn't sure either.

This is a good question indeed. If owls with asymmetrical ear canal openings have different arrangements, it would suggest that the asymmetry has evolved more than once and arrived at different solutions.
The Cornell Handbook of Bird Biology (2nd ed.) states that the Boreal owl right ear is positioned higher than the left. Ornithology by Frank B. Gill (2nd ed.) states that the barn owl left ear is higher than the right. If both of these reports are accurate, then we have two species that differ.
The Wikipedia entry on Sound Localization in Owls (section 3) also suggests that the asymmetry of different owl species may be a product of convergent evolution:

For example, in barn owls (Tyto alba), the placement of the two ear flaps (operculi) lying directly in front of the ear canal opening is different for each ear. This asymmetry is such that the center of the left ear flap is slightly above a horizontal line passing through the eyes and directed downward, while the center of the right ear flap is slightly below the line and directed upward. In two other species of owls with asymmetrical ears, the saw-whet owl and the long-eared owl, the asymmetry is achieved by different means: in saw whets, the skull is asymmetrical; in the long-eared owl, the skin structures lying near the ear form asymmetrical entrances to the ear canals, which is achieved by a horizontal membrane. Thus, ear asymmetry seems to have evolved on at least three different occasions among owls.

(Emphasis added)
I presume the source of the Wikipedia information to be from Konishi, Masakazu and Susan F. Volman, 1994, though it is not cited in the relevant paragraph.
Perhaps some other ornithological journals will have more specific information, perhaps even allowing us to trace these separate evolved structures. It may even become a great thesis project!

I saw that reference in Wikipedia too.  I'm glad you have a pretty good idea of the source of the information because it's hard not to be a little skeptical  - especially if it's not cited.  It would be interesting to see if other nocturnal raptors have similar asymmetrical ears too.


text:
What are some examples of interbreeding between species that are separated by 5 million years or more?
Interbreeding is constrained with that the offspring shares the gene pool of the parents. What are some examples of interbreeding that has occurred, where the two species were separated by 5 million years or more?

Consider many cases of horizontal gene transfer. Are you interested in a given lineage in particular?

Animal kingdom, vertebrates, mammals

Years are not really the appropriate measure here, I think.  A horse for instance might have 5 years between birth & sexual maturity (thus 1 million generations in those years), while many birds grow to sexual maturity in a single year, so would have 5 million generations of divergence in the same time.

I depends a little bit about what you mean by interbreeding. In any case, my answer won't be fully satisfactory.
Horizontal gene transfer
If you are referring to any exchange of genetic materials than, you can have a look at Salzberg et al. (2001) who report 40 genes that were horizontally transferred from bacteria.
Elysia chlorotica is sea slug which is able of photosynthesis thanks to a horizontal gene transfer (Schwartz et al., 2014)
Typical interbreeding
If you are thinking about some kind of more common type of inbreeding, then you might want to consider
mule who is the hybrid between a male donkey and a female horse. Donkey and horse share a common ancestor that is about 4.5 millions years old (according to Live Science). Mules are often sterile but some of them have been fertile (Rong et al. 1988; see also this article from the Denver post; thanks @iayork)
Platanus × acerifolia is a hybrid between Platanus orientalis and Platanus occidentalis. Platanus are a rather old genera with fossils of 115 millions years old found (from wiki). However, I don't know how old is the common ancestor between P. orientalis and P. occidentalis
There are plenty of other examples in wikipedia > hybrid but I failed to find good estimate of common ancestry for those who may have had a common ancestor older than 5 millions years but it probably exist given that the mule example is already 4.5 millions years old.

Mules (and hinnies) are not always sterile; see here, here, and many other cases.

Here's some research about a fern hybrid converging after 60 million years:
http://www.iflscience.com/plants-and-animals/distant-species-produce-hybrid-60-million-years-after-their-split/
Some yeasts in a brewery apparently after 10-20 million years:
http://www.iflscience.com/plants-and-animals/distant-species-produce-hybrid-60-million-years-after-their-split/
a Goat Sheep Geep after 7 million years: https://whyevolutionistrue.wordpress.com/2014/08/03/a-new-geep-a-sheepgoat-hybrid/
for timing evolution
http://www.timetree.org/


text:
Do prey animals fail to see incoming pythons/snakes?
I understand that pythons are considered ambush predators, and I was under the impression that they tend to employ the sit-and-wait strategy: quietly staying in a coiled position near a trail frequented by prey animals, and striking when a prey passes by. However, this is in contrast to the stalk-and-strike strategy I encountered in every video I could find of snakes hunting prey in the wild.
In this video compilation of pythons hunting prey (warning: it's graphic), in every instance shown, the snake can be seen closely approaching the prey, the prey appearing to not notice the snake, and striking when the snake's head is within a few cm/inches of the prey animal.
This seeming appearing-to-not-notice-a-large-snake-nearby behavior can be seen in different animal species:

Pigs: Here
Mice/rats: Here, here, here, here, here, and here
Rabbit: Here
Bird: Here
Possum: Here

Similarly, the-fail-to-notice can be seen another video and here too.
Question: Is the stalk-and-strike strategy the more common hunting strategy that snakes tend to employ? Do the prey really fail to notice a looming large snake? Or do they "play pretend to not see it" as a some sort of adaptive strategy?
My sample of videos could also be biased, but it seems that the sit-and-strike strategy would be more easier to film and thus should be more easy to find in popular video sharing sites. No?

It looks like being close to the ground and having certain patterns send little information to prey about their motion or they blend into the environment.  They tend to be silent also. https://academic.oup.com/beheco/article/24/5/1237/256081


text:
Does the term "fitness advantage" or "fitness disadvantage" make sense?
Same for the terms "selective advantage" and "selective disadvantage" which I intend to use synonymously.  There are usages of each on Google Scholar, but do evolutionary biologists understand what is meant?

What is unclear to you?
If you could highlight what is unclear to you, or what exactly are the semantic issues in your opinion, that would help to really address your misunderstanding. In absence of that, I will just give you a general explanation of their meaning.
What does 'fitness advantage' mean?
If a group of individuals has a fitness advantage, it means that this group of individuals has a higher fitness over some other group of individuals. The other group, then has a fitness disadvantage.
Natural selection
If we grouped these individuals based on genetics, then the genotypes having a fitness advantage will likely raise in frequency in the population. If we used phenotypic trait to group individuals and if the trait is heritable, then the frequency of these phenotypic traits is also likely to raise in frequency in the population.

Thank you.  That is about what I expected.  I just haven't seen that term frequently.  I just wasn't sure whether if a group has a fitness it, by definition, has an advantage.

What about the terms "less well-adapted individuals" or "less well-adapted natural enemies"?

The saying "les well-adapted" is less common the saying "fitness disadvantage". To me they sound very much the same. I would tend to think that we use the term "fitness disadvantage" when there is fitness variance in the population and we want to refer to it, while we could use "les well-adapted" to refer to the idea that the entire population has a lower mean fitness than some other hypothetical population (a load). In any, it really is the same concept but just eventually applied in slightly different context.


text:
Species Identification: Beetle having trunk!
Today morning I found this beetle in Cynodon dactylon grass. It had this beautiful head bearing a trunk like structure. I'm wondering what beetle it is
Images:

Approximate size: 1.75 cm
Temperature: 29°C
Location: Uttar Pradesh, India

Did a bit of research. Its one of the Snout beetles from the family Curculionidae. Couldn't get any further.

Looks like a weevil (Curculionoidea). What was it's approximate size?

@theforestecologist I guess around 1.75cm

This is a weevil called Cleonis japonica. Here is a link to a specimen which was collected in 1904. (http://weevil.info/sites/weevil.info/files/Cleonis_japonica.jpg)
Here is a link to same site and one other which show where it was found.
(http://weevil.info/content/cleonis) and (https://www.iso.org/obp/ui/#search)
NP means nepal. Here is a link to something which I hope is a little more descriptive.
https://www.zin.ru/Animalia/Coleoptera/pdf/arzanov_grebennikov_2017_cleonini.pdf
I wish you had taken better pictures.


text:
Are there two varities of dandelion leaves?
This is in India. I noticed a dandelion plant which had the familiar leaves.

Right next to it there was another plant which had similar flowers and white tufts, but the leaves were different.

Is the second plant also dandelion? I'm asking because I was considering feeding the leaves to my budgies, but needed to know if it is a dandelion, to avoid having the birds consume a toxic plant species.
Did a Google search, but all of them show the arrow-style leaves only as dandelion.

I'm not familiair with the flora of India, but these both look like sonchus species to me, not taraxacum (dandelion).

Although the leaves are similar, these are both not Dandelions Taraxacum species, because:
1. Dandelions have leaves in a rosette, not distributed along a stem.
2. Dandelions have a stem with a single flower at the end, not multiple flowers.
3. The shape of the closed flower heads after flowering is too pointed.     Dandelions usually have the pappus (white hairs) sticking out a little.
These distinctions can be clearly seen in the picture below:

I am not familiair with the flora of India, but I think these could be Sonchus species. Sonchus is known to have  variable leaves.
For comparative purposes, see how Sonchus looks like

Very good answer! I hope you don't mind I added a Sonchus picture!

Dandelion is the commom name used to make reference mainly to Taraxacum officinale, but actually is also used to virtually any species of the genus Taraxacum. I mean, a lot of species are known as Dandelion, hence this name comprises a lot of morphologies.
Also, there is something called "Phenotypic plasticity", which refers to changes in the organism characteristics due to adaptation to environmental factors. (I.e. one species may have different morphologic and physiologic traits in response to environmental variation).
Regarding to the photos you posted, it's not safe to tell you if these are the same species or not, because one would need way more detailed images, mainly from flowers, to give you a more accurate identification.
There is a Fabebook group named DetWeb, where botanists identify plants if you post good enought photos... It's a brazilian group, but you can post in english, of course.

In my opinion, this doesn't really answer the question, which is if these are dandelions or not.

yes, you are right... but it's a brief explanatin on why it's not simple to tell if these are two dandelions.. Do you think I should have provided this information as comment instead of answer?

It is probably to long for a comment. And one can easily tell these are not Dandelions.


text:
What are the (correct) terms for these flagella-arrangements?
I came across the following diagrams depicting two kinds of arrangement of flagella over cells.

Now according to my (very unreliable) school textbook, the arrangements are termed as:

A - Cephalotrichous (tuft of flagella on one end)
B - Lophotrichous (tufts of flagella on both ends)

Whereas another (equally unreliable) book states the exact opposite:

A - Lophotrichous (tuft of flagella on one end)
B - Cephalotrichous (tufts of flagella on both ends)

A spot of cursory Googling reflects this sort of confusion online (compare the images and their labels here) as well.
According to Wikipedia that arrangement A is lophotrichous, but it makes no reference to arrangement B though.

I tried to figure it out, going by the smattering of Greek I picked up as a Bio. student ( Cephalos = Something to do with the head ; Lophos = something to do with a peak/protuberance ), I arrived at:

Hmm... so cephalotrichous probably means you find the tuft on one "end" (so arrangement A), and ipso facto lophotrichous is arrangement B.

But I guess, I ended up putting a little too much thought into it...

Cephalotrichous is probably used to indicate you have a tuft on the "head" in addition to another tuft on the "tail" (so arrangement B), and ipso facto lophotrichous is arrangement A.

 At this stage I'm not sure what's more serious: my inability to find an authoritative answer to my question... or my tendency to overthink stuff

I'm in a fix.
Could someone clarify, citing (multiple, if possible) authoritative sources, on the distinction between a "cephalotrichous" and a "lophotrichous" arrangement?

Whup! You're right! My bad :3  ( <--- Flag as obsolete)

A good source on this subject is Tortora's Microbiology. Unfortunately, it uses a different terminology.
Have a look at this image (click on it for a bigger size), chapter 4, page 81:

As you can see, the lophotrichous arrangement is the one with the flagella at one end of the bacterium (which agrees with the arrangement at the Wikipedia page).
However, the opposite arrangement (flagella at both ends) is called amphitrichous (which, by the way, makes more sense), not cephalotrichous.
The text below that image says:

Lophotrichous: a tuft of flagella coming from one pole;
Amphitrichous: flagella at both poles of the cell;

If you assume that "amphitrichous" is synonym of "cephalotrichous", then the correct book would be your second one, which says:

A - Lophotrichous (tuft of flagella on one end)
B - Cephalotrichous (tufts of flagella on both ends)

However, there is no evidence that one should consider "amphitrichous" and "cephalotrichous" as synonyms. Besides that, things seem to be way more complicated: if you search those terms at Google Books, you'll see that most books say that amphitrichous bacteria have only two flagella, one at each end. And, indeed, some have completely opposite definitions.

Source: Tortora, G., Funke, B. and Case, C. (2010). Microbiology. San Francisco, California: Pearson Benjamin Cummings.

Meh, I don't see a better answer coming anyways, so I guess I'll have to equate amphitrichous with cephalotrichous (non-existent) then. Thanks!

Amphi- Gr. ἀµϕι- on both sides.
Cephalo- Gr. κεϕαλή head.
Lopho- Gr. λόϕος crest (a tuft of . . . upon a head).
In the context of bacterial flagella, cephalotrichous and lophotrichous are synonyms for they both denote a bacterium with a tuft of flagella on one end only, conventiently called "head" (for things tend to have one head, not two, and, with some imagination, bacteria with a tuft of flagella on one end only do look like hairy heads, don't they?); the latter term, i.e., lophotrichous, is more commonly used.


text:
Questions about apoptosis

Is apoptosis a part of cell division?
Can apoptosis occur if DNA is damaged beyond repair?

Please show your attempt at trying to find the answer to the question!

Welcome. If this is a home-work question please show some of your efforts in answering it. What do you think the answer is and why?

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. I am voting to close.

I think this question could basically be summarized as "What is apoptosis?"  I will attempt to give a brief answer to that question, answering the two aspects of the question along the way.
Apoptosis is at its root programmed cell death (PCD).  It is basically when a cell (healthy or not) dies so that it can be replaced.  It is happening all the time in multicellular organisms such as me, you, and the lion in the zoo.  Basically, it allows all the cells to be replaced as the tissues of the body grow.
For instance, as your skin grows, cells in the dermis are dividing to produce a new epidermal layer.  At the same time, cells on the outside are dying (at the stratum corneum) so that the skin does not grow infinitely and we aren't covered with 20 inches thick of skin by the ends of our lives.
The same thing is happening in, for instance, the liver.  As the liver cells split, old ones are also dying.  This allows us to rebuild the liver to its normal size after a surgery in which we remove a section of it.  We simply have to stimulate cell growth so that it counterbalances PCD (apoptosis) and the liver grows to its normal size.
Cell death is initiated, not by the DNA, but rather by caspase activity.  All cells have inactive procaspases which will destroy the cell as soon as they become active.  When what we call an initiator procaspase bonds with a procaspase within the cell, the procaspase is activated, and the signal is spread across the cell.  This initiator procaspase is usually triggered by a death receptor outside the cell.
More reading here


text:
How are bioremediation microbes removed from the environment once they perform their function?
In the case of bioaugmentation, microbes are introduced into the environment to clean up and absorb a certain pollutant. My question is how is that microbe then removed from the environment once it performs its function?

A bit broad.  Sometimes it will die off when food supply is too small to support the population; sometimes it will need to be removed with poisons or predators; sometimes it doesn't need to be removed as it is relatively benign to the environment.  What case of bioaugmentation are you referring to specifically?

Heavy metal bioaugmentation.

Usually you have to introduce conditions which hinder multiplication of the microbe such as altering the pH and emperature. This is hard to achieve in a large environment, alternatively, you can introduce a recombinant of that microbe which posses a survivability threat to the initial microbe.

Could you add some sources describing these steps actually being performed?


text:
Need to identify this insect and ways to eradicate it
I need some help in identifying this unknown insect that was found in my kitchen.
Thanks in advance.

It might help if you added localization and size information.


text:
What is the field of view of humans (not just fixed angle eyes)?
What is the human field of view also counting the maximum vertical and horizontal eye movement (rotation), with the head still.
It is unclear from this question whether the answer relates to the field of view from both eyes when a person is looking at a fixed angle or also what he/she can see if the head won't rotate but the eyes will.
What is the field of view for the human eyes?
There are many articles and diagrams online as well but they too don't make it clear whether the eye rotations are also taken into account or not and it is just the FOV at any given moment at a given eye angle.

Pretty sure the question you linked assumes fixed head position and includes eye movement. Eye rotation is taken into account.

@Diio - why do you assume that?


text:
Why can fish survive out of water?
Obviously, humans can survive underwater for a short while. I've assumed this is because at some point it benefited us to stop breathing momentarily, and so we evolved a respiratory system that was able to take short breaks.
Similarly, fish can survive outside of water for a short while. However, I can't think of a single instance for most fish where they may have needed to evolve that ability. Even their ancestors originated from aquatic environments, so I don't think it's a residual ability they no longer need.
Why did fish evolve a respiratory system that could take breaks like ours can?

Do not have too a "panselectionist" view of evolution!
You can survive in a bath of mercury for a little while. You can survive naked in the outer space for a while (see here). Yet none of your ancestors where exposed to such conditions. We can be tolerant to certain conditions without having been selected to tolerate it.
Similarly, you managed to survive in your very specific environment. Yet none of your ancestors ever encountered this specific environment.
In other words, evolution is more than just natural selection. Not every phenotype in every environment you can think of is the result of a direct selective pressure acting on it. A classical and easy to read paper on the subject is Gould and Lewontin (1979).
Why fish not die suddenly outside of the water?
The main reason why fish die outside of water is that they cannot intake oxygen from air (see Breathing under water; not considering lungfish). So once fish are exposed to air only, they stop intaking oxygen, consume the oxygen that they have left in their circulatory system and tissues and slowly die of asphyxie but there is no reason for the death to be direct and sudden.

As I understand it, we could survive a mercury bath because we evolved a barrier (skin), and our homeostatic levels for mercury are far lower than instant death. The same goes for space and temperature (I don't die at 98.5 degrees). I'm pretty sure we evolved a resilience to things like that when we left the roughly-constant temperature and alkalinity of the ocean, since we needed to respond to huge environmental fluctuations. Fish do encounter a pretty standard environment though. Is it nutrition perhaps or other factors which led to them needing a response to changes in homeostasis?

Or is your first point that there's not always a reason?

I just mean fish still have oxygen in their tissues and there is no reason for them to die instantly. They were not selected (not that I am aware of) for surviving to this condition, they just happened to be pre-adapted due to various reasons, including the fact that they are big and therefore always keep a certain amount of oxygen in their tissues.

Do you consider lungfishes as fishes? When their pond dries they can survive hybernating in cocoon for up to four years.

A lot of fish (not just lung fish) can breath air quite well they start dehydrating quickly however and no organisms breathing mechanism works onces it dries out. .

The answer is simple. A fishes gills are exposed to air that is oxygen rich. Gills can take oxygen from the air. We do not inhale water, so humans under water must hold their breath. I am assuming the question is not referring to lungfish, who have modified their swim bladders (homologous to our lungs) to take up oxygen.

Gills cannot take up sufficient amounts of oxygen from the air - this is why fish cannot survive out of water for long.

Also, do we know that lungfish modified their swim bladders to take up oxygen? I can't recall offhand if the current consensus says that lungs are ancestral to swim bladders, or that we don't know which is derived from which, but I'm pretty sure it's one of the two.

Correct that they cannot take in "sufficient" amounts, but a bit is all it takes them from asphyxia for an hour or so. The question was not why can't fish live their entire lives out of water, but why they don't die immediately.

Actually there is a huge group of fish that need to breath air, swamp living fish, stagnant water is very low in oxygen that is why many fish gulp air (air contains a lot more available oxygen than stagnant water) even house goldfish will do this is poorly oxygenated bowls (see below). in fact the early ancestors of terrestrial vertebrates show a lot of adaptations for swamp living, legs also work better in swamps than fins (at least above a certain size) that is why so many swamp fish develop leg like fins, such as the snakehead fish. These are not adaptations for land but for shallow stagnant water, air gulping for hypoxic water in particular.
Note most of these fish are not lungfish (or lobe finned fish) they are ray finned fish, they are using their swim bladder to extract oxygen. Aquatic surface respiration is actually a very widespread behavior in fish, and can be triggered in a very large number of ray finned fish. The behavior is quite well studied and has lead to better developed air breathing multiple times.
Fish that cannot do this (like sharks) will die very quickly on land as the suffocate, since gills don't work in the air. The risk for normal fish is dehydration of their breathing tissue, of while they are IN water this has a easy solution.


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How much vitamin C has a noticeable effect on E.coli k12
I am doing a research on effects of different concentrations of vitamin C on serial dilutions of E.coli k12. I am looking for literature that has already shown effects of vitamin C on E.coli, but there is a vast amount out there (26 thousand Scholar hits).
What might be the main effect of Vitamin C on E.coli? Is 1000mg vitamin C enough to have noticeable effects on the bacteria?

Can you please clarify what is 'noticeable effects' and give us some background of your research?

Aren't you doing the research to answer this exact question?

I don't think you should be doing research if you ask questions like "Is 1000mg vitamin C enough to have noticeable effects on the bacteria?". To how many bacteria in what volume under what conditions. I think it best to close this question.

@canadianer are you suggesting that you shouldn't do a literature review before running a series of experiments?

@DanHall Did I say that? My comment was on the initial revision of the question and perhaps makes more sense in that context. Perhaps.

@canadianer I see! And I see this is an old question by an inactive user. I suppose my heartfelt advice will just echo in the cyberspace, then.

I found a 'short communication' paper by Akira Murata et.al where they did In Vitro testing of Vitamin C on L. casei showing no inhibition of growth, and also tested on E.coli and B. subtilis and found that Vitamin C inhibited the growth. Also I believe Suzanne Humpries stated the same thing somewhere in this 1.5 hour long video, indicating she may posses more knowledge as to studies.

Ascorbic acid did not inhibit the growth of L. casei even at high
  concentrations, and rather stimulated the growth at certain
  concentrations (2~3 X 10- 2 M). This observation indicates that
  ascorbic acid can be used as an antiviral agent.
In E. coli and B. subtilis, unlike L. casei, a high concentration
  of ascorbic acid acted so as to lessen their growth rates (Fig. 3).
  Particularly, in B. subtilis W23, cell lysis was observed about 100
  min after the contact with ascorbic acid and, moreover, when a drop of
  the lysate was placed on a plate seeded with B. subtilis 168 and
  incubated overnight at 30oC, there appeared a clear zone around the
  placed lysate. Since B. subtilis W23 is known to possess an inducible
  defective phage PBSZ able to kill B. subtilis 168,3 ' 41 the observed
  result maybe ascribed to the induction of the defective prophage from
  B. subtilis W23 by action of ascorbic acid. Lwoff and Siminovitch51
  reported once that the lysogenic phage in B. megaterium was induced by
  treatment with ascorbic acid.

You have @arberg's answer showing a report of an inhibitory effect of vitamin C on E. coli. Here's a PLoS One paper, in different conditions. It shows vitamin C rescues cultures that had no growth the previous night.

As the comments suggested, expect to see different results in different conditions.
Literature reviews before an experiment are important. When you're new to an area they are VERY HARD. Do them anyway. Give yourself a set amount of time, sit down at your computer, and start chugging away. Then do it again. And again. And again.
If you have a large number of possible articles, try narrowing your search. I often do this by tweaking my search terms or by limiting my search to a particular subset of journals that are more likely to give me what I'm looking for. Set up a hierarchy for how you read. Start by scanning the abstracts. If it looks helpful, pull the article and look at the figures. Note the article, your conclusion, and the authors' conclusions in a file somewhere that you can find later. If there is something interesting or useful in the introduction, follow the references.
Again, this is VERY HARD, but VERY IMPORTANT. Don't skimp on this step by just asking people.

Maybe you have to think about vitamin C from another point of view. You start from the postulate that Vitamin C could destroy E. Coli. Maybe the action of vitamin C, rather then destroying E.coli is destroying the endotoxins generated by the bacteria, leaving the body immunity healthy and boosting the phagocytes that can therefore destroy E. Coli way more easily.
About the dosis of vitamin C to use, I would just use it to bowel tolerance. Body will take what is needed and just flush what's in excess. testing Lyposomal vitamin C would maybe also a good idea.
Many years ago , I had a monstrous and painful "tourista". It usually take a few days to cure. Well, I felt so bad that I took 2-3gr of vitamin C orally and, to my great surprise (and relief), Tourista symptoms were gone within 2 hours and I felt good.

Could you add sources to your answer to allow others to background read on your material?

It’s proven quite hard to find research on the effects of vitamin C on gram-negative bacteria.
http://www.sciencedirect.com/science/article/pii/S1089860301903714
This paper suggests that vitamin C (sometimes also referred to as ascorbic acid) can help inhibit the growth of E. coli when in the presence of mildly acidified urine with added nitrite. Keep in mind that this paper is quite old, and inside the first few paragraphs it states:

despite numerous studies the mechanism of any antibacterial action of
  vitamin C still remains unclear.

It later states

we have recently shown that large amounts of NO gas are released from
  nitrite-containing urine after mild acidification and this release is
  greatly potentiated in the presence of ascorbic acid.

So it seems this first paper doesn’t offer us much in terms of toxic effects of vitamin C on bacteria in isolation.
http://jb.asm.org/content/98/3/949.short
I found another paper that suggests that vitamin C can kill gram-negative bacteria, but again not in isolation, but in combination with other agents as well.
Perhaps your research is among the first to offer any insight on the effects of vitamin C on E. coli. I’ll be interested to know if anyone else finds a publication on this specific topic (I only searched for about 30 mins on the subject).


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What is this bizarre insect?
Well, a friend of mine sent me this picture of an creepy insect. I'm wondering if the picture is photoshoped or if it is real. It is said the insect lives in Indonesia, but I'm not sure.

Can anyone identify this? Thanks.

This is a Creatonotos gangis
This nice arctiine moth was described by Linnaeus in 1763.
The species  lives in South East Asia and parts of Australia.
C. gangis went viral earlier this year because of a post in The independent where they wrote about a facebook video on the species... I don't know if this is the same video that was popular at facebook, but take a look:
https://www.youtube.com/watch?v=hn1ms8qfqzM
Furthermore, I can tell you that those weird tentacles are in fact scent organs which secrete pheromones in order to attract sexual mates. And also, their larvae cause huge problems because they eat pomegranade leaves

Oh thanks, it is so freaky I thought it was a fake picture.

@Thai If I am not mistaken, these scent organs are called coremata (aka. Hair-pencils)


text:
What is this insect? Seems to be in Indonesia
https://www.facebook.com/gadik63/videos/707361412787259/
This video has me completely baffled.

https://en.wikipedia.org/wiki/Creatonotos_gangis
Creatonotos gangis is a species of arctiine moth found in South East Asia and Australia. It was described by Carl Linnaeus in his 1763 Centuria Insectorum.


text:
Finding steady state concentration given half life and production rate
Intracellular molecule B is normally synthesized at a constant rate of 1000 molecules/second. The lifetime B = 200 s.
How do I find the concentration of molecule B when it is at a steady state?
I Tried:
For molecule B. P is concentration of molecule B.
2^-(dt/200) * P + 1000 * dt = P
"2^-(dt/200)" is the half life formula. I multiply it by P to give me current concentration of molecule B. Then I add 1000 * dt to give me the amount of molecule B being produced at an exact moment. Rearranging the variables:
P = (1000 * dt) / (1-2^(-dt/200))
Now I limit dt --> 0 to give me P:
lim t->0 (1000 * dt) / (1-2^(-dt/200)) =
l'hopital's rule: lim t->0 1000/ (0.005 * ln2 * 2^(-dt/200))
Plugging in dt = 0, what I get is a steady state concentration of molecule B = 200000 / ln(2).
However, the correct steady state concentration for molecule B is just 200000.
Suggestions?

It's not clear to me how the problem is formulated. It sounds like you have a system at steady state, with synthesis rate = breakdown rate, and you want to relate half-life to concentration, which is fine. But then what do you mean by "reach steady state" -- the sought concentration is a constant? Also, I don't see where your equations derive from. The first equation seems to violate dimensions since 2^(-dt/200) is dimensionless? Somehow, your answer is actually the correct concentration for the steady-state problem. But I don't see how you got there ...

tl;dr besides making this a bit harder than necessary, your main problem is that you have confused the lifetime (average time to removal of a molecule), not the half-life (time until half of the molecules are removed, which is $\ln(2)$ times the lifetime ...) Wikipedia has some formulas ...
You can translate the problem into a differential equation (not as scary as it sounds):
$$
\frac{dB}{dt} = \underbrace{1000\vphantom{\frac{1}{200}}}_{\textrm{production}} - \underbrace{\frac{1}{200} B}_{\textrm{removal}}
$$
The only tricky part here is recognizing that if the lifetime is 200 s, a fraction 1/200 of the existing molecules will be removed per second.
Now we have to solve this at equilibrium: $dB/dt =0$. We get
$$
\begin{split}
1000 - \frac{B}{200} & = 0 \\
1000 & = \frac{B}{200} \\
B = 200000
\end{split}
$$
Or you could memorize Little's Law: steady state = arrival (1000/s) $\times$ lifetime (200 s).

Concentrations are molecules or moles or grams per liter. From molecule numbers alone you cannot calculate concentrations. You need information of the volume it is related to. E.g Substance A has a concentration of 1 mmol/L solved in water.

I understand your point. My question is actually simply referring to the number of molecule Bs the moment it reaches equilibrium.

Then don't use the naming "concentration". It is just the number of molecules at steady-state, nothing else.


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E.coli fermentation - process flow
I have an engineering background and have been assigned a project to look into to failures during E.coli fermentation process using the data available before/during/after the process
I have learnt some of the procedures involved in the process from SIP/ CIP and few things about inoculation during fermentation. But I am still lacking some basic knowledge of E.coli fermentation process using glucose and other media components. I consider and value these steps with extreme care during this project.
Any suggestions for resources from where I can learn about this process at a more basic/ intermediate level without focusing too much on any individual step.
I have looked at this youtube video and found it helpful to understand the fermentation process but I am looking into E.coli fermentation in particular, so I have posted my question here. I learnt a good deal about what OD measurement is, d02 values, KLA etc. during this project. I am looking for resources or suggestions to understand how these parameters affect E.coli fermentation process
Bioprocessing Part 1: Fermentation
I also browsed through BiFlo reactor product pages to try to understand some basic information about E.coli fermentation.
E. coli Fermentation Using a BioFlo® 110 Bench-Top Fermentor
I can provide more information if it helps anyone to provide some suggestions. I don't have biology background. So I am not aware of any decent textbooks or papers to read about E.coli fermentation process
Thanks


text:
Reference request for Sydney Brenner's "it might come in handy in the cretaceous" quote
In {1}, Richard Dawkins attributes a quote to Sydney Brenner without giving a citation. I'm preparing a publication on the same topic and if possible I would like to track down the original reference for the quote. Does anyone know the work (if it exists) in which Brenner made the argument Dawkins refers to?
Here is the text from Dawkins' paper where it is mentioned:

It is all too easy for this kind of argument to be used loosely and unrespectably. Sydney Brenner justly ridiculed the idea of foresight in evolution, specifically in the notion that a molecule, useless to a lineage of organisms in its own geological era, might nevertheless be retained in the gene pool because of its possible usefulness in some future era: "It might come in handy in the Cretaceous!" I hope I shall not be taken as saying anything like that.

Edit: it looks quite likely that this is referring to something Dawkins heard Brenner say, rather than anything that can be cited. There is a footnote in {2} that reads:

...Brenner... has a sardonic wit to match his scientific brilliance. I once heard him lampoon the 'evolutionary foresight' fallacy by imagining a species in the Cambrian that retained in its gene pool an otherwise useless protein, because 'It might come in handy in the Cretaceous.'

So it seems likely that there is no citable source for the quote besides Dawkins' paper, but in any case it would be useful to know if there is a pre-1988 publication in which Brenner made a similar argument.
{1} Richard Dawkins (1988) The Evolution of Evolvability. In C. Langton (Ed.) Artificial Life, SFI Studies in the Science of Complexity. Addison-Wesley Publishing Company.
{2} Richard Dawkins (2009) The Greatest Show on Earth: The Evidence for Evolution. Random House.


text:
Expressing bacterial proteins in mammalian cells
Does anyone have experience/knowledge of expressing bacterial (or other microbial) proteins in mammalian cells? I am interested in this for a project where we are trying to introduce a new enzymatic activity in human cells. I have been looking for examples in the literature, but haven't found anything so far.
I can imagine that various problems might arise. Presumably transcription and translation should not be a problem; but I can imagine the protein may not get sorted/localized properly, or might not be properly degraded and so could  accumulate to toxic levels ...  or what not.
Any advice or pointers to literature would be much appreciated!


text:
what type of insect is this? is this a moth? (southeast asia - Malaysia)
i found this insect in the garden behind my house a few months ago.This is the first time i saw this insect.On that day the weather is very hot.I found the insect in the afternoon.I am from Kelantan,Malaysia.The climate in Malaysia is equatorial, hot and humid, heavy rain falls in the monsoon season between november and february.

Oleander Hawkmoth (Daphnis nerii)
Same fellow? (From oocities.org)

And a better picture from ukmoths.org.uk:

For more reading, here's a wiki article.


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Can our body adapt to periodic fluctuations in sleep?
Suppose that if I've to attend a morning class then I must wake at 5 AM in morning. Next, if I don't (attend the class) then I wake up at 7-8 AM.
I've experienced that, since I do attend those classes almost regularly, my body has adjusted itself (sleep cycle) to wake at 5 AM almost precisely without a alarm set and has also decided when to sleep (it seems to demand 7-8 hour of sleep). This, I think, is common to most of us.
Now suppose that I attend classes only on alternate days. Put simply, I wake up at 5 on first and at 8 on the next day and so on. This implies that I am constantly switching my sleep cycle every day. Would my body, now, be able to adapt to this continuously varying cycle (which is but periodic).
I suppose no, and that is just a guess based on my experience. But provided I give my body enough time, I think that it may really adjust to this scenario.
On a side note, assume that (in case it matters) I take a sleep of 7 hours during class days and a sleep of 8.5 hours during holidays to make this data realistic. .

There's a time bias after which it is less healthy and good sleep to be very clear mentally. the circadian rhythm works on a 24 hour basis and also a 4 hour basis, which is why we have meals every 4 hours. It also depends on age and how robust the person is. 7 hours sleep on week days and 9 hours at the weekends isn't stressful for some young people. I know a russian who works 24 hour shifts as a receptionist twice a week and she never got used to the sleep deprivation.

Oh that's interesting, this example perhaps proves that alternating sleep cycles is inpossible. Thanks for the real life example.

In the same way that it takes time to fully adjust to jet lag (~ 1 timezone/day), it is unlikely that the body can adjust to alternating patterns of 3hr gaps on wake time on a daily basis [Ref. 1].  We simply have not evolved to jump timezones.  The most healthy thing to do is to have one time to get up each day (5am) so that your body is in sync.
[Ref. 1]: Review about circadian rhythms

Definitely your body will adjust. All you have to do is make it a thinking point that you have to wake up early at 5 and trust me you will, if you don't think hard about it then you will wake up later than 5.

Perhaps you haven't read my full question I suppose. Since the answer doesn't, in any way, relate to it.