Can you replace glucose with glycerol in cell media? In order to feed an animal cell in process called Respiration, can I replace Glucose with Glycerol?

The Equation bellow:
Glycerol + Oxygen -> Water + Carbon Oxide

In most cases, it's not a good idea to replace glucose with glycerol in animal cell media. Animals do possess the ability to metabolize glycerol, via a pathway starting with the enzyme glycerol kinase. However, glycerol kinase is only expressed in certain cell types, such as liver cells and kidney cells.

References:

http://www.brenda-enzymes.org/enzyme.php?ecno=2.7.1.30
http://www.ncbi.nlm.nih.gov/books/NBK22591/


How does blue white screening work in selecting E coli that have taken up a plasmid vector? The plasmid vector I am referring to is pCR 2.1 - TOPO. I added the vector to the E coli and plated them up onto LB+amp+X-gal plate, then incubated. After incubation the plates had two types of bacterial culture on them, one white and one blue.

I think that the blue cultures have accepted the plasmid as they are able to grow on ampicillin, so have the ampicillin resistance gene, and are able to convert the X-gal substrate to blue via the lac Z gene. What i'm confused about is the white colonies. If the colonies are able to grow on ampicillin, surely they have accepted the gene because they have the resistance, and surely they should to be able to convert the X-gal?

So why are these not expressing the lac Z gene? Is it that the lac Z gene and ampicillin resistance aren't on the same plasmid, or is it that the lac z gene didn't make it into the plasmid?

The traditional blue/white screening is set up so that blue colonies are considered negative for the insert, and white colonies are positive for recombinant DNA. The gene responsible is the lacZ gene, or beta-galactosidase. This enzyme converts a synthetic substrate, X-gal, into an insoluble blue compound.

The pCR2.1 TOPO plasmid is a blue/white selection plasmid in which white colonies are considered positive for the insert. The way this works is by inserting the DNA sequence to clone inside the coding region for lacZ. By having any inserted DNA interrupting the sequences of lacZ, so that the enzyme has lost its function (because it is no longer being translated correctly in the bacteria). On the other hand, no insert present means that lacZ is ligated back together, and the entire enzyme is correctly made, and therefore can metabolize the X-gal substrate to form an insoluble blue dye.


Fatty Acid Synthesis I have a problem in my reasoning on the fatty acid synthesis in the human body.
In the synthesis process you have this homodimer.

So the synthesis starts with the transfer of a acetyl group from acetyl-CoA to the sulfhydrylgroup of the condensing enzyme (CE) with help of the acetyltransferase enzyme (AT) and this on 1 of the 2 monomers.

At the same time a malonyl group from malonyl-CoA is transfered to the sulfhydryl terminus of phosphopantotheine from the ACP, and this on the other monomer and with help of the malonyltransferase (MT) enzyme.

AND HERE THE PROBLEM STARTS

The acetyl residue will be condensing with the malonylACP and at the same time there will be a decarboxylation (CO2 goes off) and CE goes off from acetyl. At the end acetoacetyl-ACP is formed. So if I got it right; the acetyl residue is being 'cut off' from the CE from the first monomere and binds to the malonylACP on the other monomere. Right?

And after that the acetoacetyl-ACP will be swept back to the other monomer (to the reduction part), is this also right?

Then the reduction-dehydration-reduction steps are happening and at the end of the road you will get butyryl-ACP which will cut off from the ACP and migrate on the same monomer to the cysteine residue at the condensing enzyme (CE) (= translocation).

And after that you can start a new condensation-reduction-translocation cycle and go on until you end up at palmitoyl-ACP.

So the actual question is; is my reasoning right about how the product is going from one monomer to the other several times?
In my book it's a pretty messy explanation and so I want to be sure I'm right.

I hope somebody can help me out =)

Greetings

The textbook descriptions of fatty acid synthesis can be confusing because although the underlying chemistry of the process is universal, the way that it is organised is different in the systems that have been characterised, which include E. coli, yeast and vertebrates.
In vertebrates:
The fatty acid synthase is a dimer of identical multifunctional single polypeptides. The synthesis process involves two -SH groups: one is the terminal group of the pantothenate of the acyl carrier protein domain (Pan-SH) and the other is an -SH group of the condensing enzyme (CE-SH).
For the first condensation step the initiating acetyl group is attached to the CE-SH of one monomer and the incoming unit (malonyl CoA) is attached to the Pan-SH of the other monomer.
The condensation reaction between these two results in the new elongated unit being attached to the Pan-SH. This unit then goes through the reductase/dehydratase/reductase steps to form the new acyl CoA which is finally transferred to an CE-SH group, opening up the Pan-SH for the next incoming malonyl CoA.
This will happen repeatedly in each cycle of the process. Obviously since each monomer has both -SH groups a single fatty acid synthase dimer can be engaged in two elongations at the same time, but these will always include a transfer. It is thought that the initiating acetyl group comes in via the Pan-SH group.
You say:

And after that the acetoacetylACP will be swept back to the other monomere (to the reduction part), is this also right?
Then the reduction-dehydration-reduction steps are happening and at the end of the road you will get butyrylACP which will cut off from the ACP and migrate on the same monomere to the cysteïnresidu at the condensing enzyme (CE) (= translocation).

The diagram that you included clearly shows that the acetoacetyl group is formed via the reduction-dehydration-reduction steps on the same Pan-SH where its precursor was formed by condensation. Only then is it transferred to the CE-SH group. The diagram also indicates that the acetoacetyl group is transferred to the CE-SH of the same monomer. This implies that a growing chain never transfers from one monomer to the other. I have seen other sources which seem to suggest that this step does involve a transfer between monomers.
In fact it would appear from the discussion on the WP page for fatty acid synthase that this is an unresolved issue - see for example:
Joshi et al. (2003) Engineering of an Active Animal Fatty Acid Synthase Dimer with Only One Competent Subunit Chemistry & Biology 10:169 - 173

Abstract
Animal fatty acid synthases are large polypeptides containing seven functional domains that are active only in the dimeric form. Inactivity of the monomeric form has long been attributed to the obligatory participation of domains from both subunits in catalysis of substrate loading and condensation reactions. However, we have engineered a fatty acid synthase containing one wild-type subunit and one subunit compromised by mutations in all seven functional domains that is active in fatty acid synthesis. This finding indicates that a single subunit, in the context of a dimer, is able to catalyze the entire biosynthetic pathway and suggests that, in the natural complex, each of the two subunits forms a scaffold that optimizes the conformation of the companion subunit.


Specific primer design I'm designing primers for species-specific amplification (inside ITS1-ITS2 region). The problem is that when I blast (GenBank) my primer pair, the Forward primer anneals with some isolates (of the same fungus species that i'm targeting) that have one base polymorfism:

Ex:

Predicted Tm= 58-61ºC
product length = 189
Forward primer  1    TTCATCTCCGACTCGCATGT  20
Template        130  ........G...........  149

Reverse primer  1    GAATACCAAGGAGCACAAGGT  21
Template        318  .....................  298

My goal is to amplify only the 100% specific sequences. Would a higher annealing TºC be able to prevent this unspecific binding?

Question 2: The fungus species i'm targeting have isolates with a diversity of polymorfisms (deletions, insertions, one nucleotide substitution,..) and sometimes the predicted amplicon lenght may vary: 189bp, 190bp, 191bp. Will it be problematic for a RT-PCR quantification assay?

Thanks in advance

If your primers are not specific enough, you should design other primers. Try shifting a few bases upstream or downstream. Also, you can add a few extra bases to your primer, you can safely reach 68C as annealing temperature.

If you want your PCR to be able to distinguish a single base mismatch, then the mismatch should occur at the 3' of your primers, ideally one of the three last bases.

If your goal is just to quantify the initial DNA, then RT-PCR will be ok. But if you want to detect the composition of the different polymorphisms, then you should go for sequencing.


Is the human ovum visible to the naked eye? I'm a student in a field unrelated to biology or medicine, however I very much enjoy reading about it. I just read in Merck Manual that

Human cells vary in size, but all are quite small. Even the largest, a fertilized egg, is too small to be seen with the naked eye.

A very quick google search (caused by basic elementary school biology knowledge) results in Wikipedia article that says The egg cell is typically not capable of active movement, and it is much larger (visible to the naked eye)

Did I misinterpret something here, or I'm reading an unreliable source?
Merck Manual was reccommended for learning about these things since it's maintained by MDs so I was just wondering. Thanks!

The line that you quote from the Wikipedia page is talking about ova in general, whereas your question relates specifically to human ova. The "Human and mammal ova" section of the same article states that

  The ovum is one of the largest cells in the human body, typically
  visible to the naked eye without the aid of a microscope or other
  magnification device.

With the stated average size of 0.12 mm in diameter (same Wikipedia article), an ovum is very, very small, but presumably a person can still see it unaided.


single units vs ensemble recording for signal detection I would like to know, when looking (in vivo electrophysiology) at response properties (latency, magnitude) in response to sensory stimuli, is there any advantage to looking at single units over ensembles of neurons? My ensemble data is really good, while my single units are only ok.

Any advice or resources regarding this would be helpful. I've talked to members of my lab, and looked for answers elsewhere, but havent really found what Im looking for.

Best!

First spike latency or similar measures when looking at ensembles only tells you about the latency of the least affected unit when you are talking about latency increases, or the most affected unit when you are talking about decreases.

For example, if you record from 30 cells on a multiunit cluster and the latencies of 29 of them increase but 1 does not change, you might conclude no effect on latency.

Also, changes in detection probability can be harder to recognize in multiunit recordings. If a pharmacological manipulation increases or reduces activity overall, including at distant sites, this might change your threshold of which cells' spikes you can accurately detect as spikes by increasing or decreasing the noise floor.

For example, if your threshold decreases, you might be recording spikes from ~20 cells in your control condition, but then sample from ~50 in your pharmacological manipulation. Note that in this circumstance the total number of spikes you record might actually go down, but you would underestimate the affect because you don't know how many cells you are actually sampling from.

Of course there are problems with single cell recordings too. Sometimes it's really the ensemble activity that matters more, in that case the single units aren't as informative. You also have the problem of tracking accurately a single unit throughout a pharmacological intervention, which can be problematic depending on the time course of the manipulation (electrodes drift, cells die) or if the manipulation itself affects spiking properties (it may be more difficult to ensure you have the same cell if spike widths or amplitudes change).


How many agarose gel bands are typical for circularised DNA I am aware that circular DNA can be both relaxed and super coiled. However when running an agarose gel of the circular plasmid along with singly digested plasmid with BamHI and HindIII, I see 1 band for the linearized plasmid (lanes 2-5) (as expected) but 5 bands for the circular plasmid (lanes 6 and 7).

What are these various conformations?

I don't have hands on it, but I will not be surprised if supercoiled DNA migrates at different distances according to some inner topological conformation (i.e., more or less coiled AND/OR more or less nicked). Similarly, this picture highlights >8 conformations. What is run in the gel is circularized phage DNA with some degree of knotting due to the circularization (phage DNA is otherwise linear).

Figure from: Arsuaga et al. 2005, PNAS 102 (26) 9165-9169 (free on PubMed Central)

Another theoretical possibility is that two or more plasmids of different sizes were grown in the same maxiprep because of some contamination. But in this case, you will spot the problem also in the digestion, so it does not seem to be your case.


What is the developmental basis of the placental sac? The placental sac is the organ that provides nutrients to the embryo from the mother.

My question is that, since this obviously involves a lot of complexity, where does the sac originate from  (maternal / embryonic) ?

Also, what is the genetic basis of the above? do the genes intercommunicate between the embryo and the mother ?

We used to spend a few days studying the placenta in our embryology course. The short answer is, both.

Organ level embryogenesis:

The placenta connects the fetus to the uterine wall, and is the organ by means of which the nutritive, respiratory, and excretory functions of the fetus are carried on. It is composed of both fetal and maternal portions. The placenta can be traced right from the moment when the blastocyst is implanted into the uterine wall, though it takes a good portion of 12 weeks to develop.

  After this adhesion, the invasion process starts, during which the cytotrophoblast cells from the trophoblast layer migrate deeper into the decidual layer. The formed vacuoles of the embryo become confluent to the uterus with the formation of the lacunar space 13 days after fertilization. The lacunar space will develop into the intervillous space for blood circulation a few weeks later. The placental progenitor stem cell is the cytotrophoblast cell. These cells are responsible for the cellular growth of the placenta, and they have the ability to proliferate and differentiate throughout gestation. The proliferating cytotrophoblast cells provide, after differentiation, the villous syncytiotrophoblasts as the outer cellular layer of the placenta.

I took the above paragraph from here (http://www.medscape.com/viewarticle/780615_2).You can read more about it here (https://embryology.med.unsw.edu.au/embryology/index.php?title=Placenta_Development.)

But for a serious scholarly study, you might be better off using textbooks.

Genetic basis of placental development:

As for the second part of your question, that is the genetic basis of development for a placenta, allow me to lift a paragraph from a book. You must remember that the embryo as it were, is not a distinct entity genetically, in that it contains half of the genes of the mother, and half of the genes from the father. And this is where biology becomes more complex, beautiful and truly mind boggling. It involves intricate interactions between evolution, organogenesis and developmental biology.

  These results [in mice] led to an extraordinary conclusion. Paternal genes, inherited from the father, are responsible for making the placenta – maternal genes, inherited from the mother, are responsible for making the greater part of the embryo, especially its head and brain…

  David Haig had begun to reinterpret the mammalian placenta, not as a maternal organ designed to give sustenance to the foetus, but more as a foetal organ designed to parasitise the maternal blood supply and brook no opposition in the process. He noted that the placenta literally bores its way into the mother’s vessels, forcing them to dilate, and then proceeds to produce hormones which raise the mother’s blood pressure and blood sugar. The mother responds by raising her insulin levels to combat this invasion, yet, if for some reason the foetal hormone is missing, the mother does not need to raise her insulin levels and a normal pregnancy ensues.

  In other words, although mother and foetus have a common purpose, they argue fiercely about the details of how much of the mother’s resources the foetus may have - exactly as they will later during weaning. But the foetus is built partly with maternal genes, so it would not be surprising  if these genes found themselves with, as it were, a conflict of interest. The father’s genes in the foetus have no such worries. They do not have the mother’s interest at heart, except insofar as she provides a home for them.

  The father’s genes do not trust the mother’s genes to make a sufficiently invasive placenta; so they do the job themselves…. Modern evolutionary theorists, led by David Haig, now think of the placenta as more like a parasitic takeover of the mother’s body by paternal genes in the foetus. The placenta tries, against maternal resistance, to control her blood-sugar levels and blood pressure to the benefit of the foetus.

Taken from: Matt Ridley, Genome: The Autobiography of a Species in 23 Chapters, Fourth Estate, 2000

For a more scientific explanation, I'd suggest reading the following papers.

Wang, Xu, et al. "Paternally expressed genes predominate in the placenta." Proceedings of the National Academy of Sciences 110.26 (2013): 10705-10710.

Hemberger, Myriam, and James C. Cross. "Genes governing placental development." Trends in Endocrinology & Metabolism 12.4 (2001): 162-168.


Can DNA be considered as a fractal antenna? I was reading about the consequences of using mobile phones and came across the statement that mobile phones are a potential source of cancers because DNA is a kind of a fractal antenna. The reason put forward for this was that it shares with mobile phone antennae the properties of self-similarity and electric conductivity.

The scientific paper which is the source of this statement appears to be: Blank and Goodman, “DNA is a fractal antenna in electromagnetic fields” Int J. Radiation Biology, 87:4, 409–415, DOI:10.3109/09553002.2011.538130. Is anyone able clarify this assertion and explain whether or not the arguments in the paper support it.

I looked at the original paper, Blank and Goodman "DNA is a fractal antenna in electromagnetic fields" Int J Radiation Biology, 87:4, 409-415, DOI:10.3109/09553002.2011.538130.

To be honest I can't give concrete reasons to doubt it, but here are a few things that raise my suspicions:

it is a review article that relies heavily on self-citation (15/50 citations are authored or co-authored by the two authors of this paper, including most of the primary experimental references)
in my judgement "responding to many different frequencies" and "having structures on several different scales" (Table 1) is not particularly strong evidence to support the conjecture that DNA acts as a fractal antenna; I would be much more convinced by an analysis based on physics rather than analogy (this comment on the paper by Foster reviews the physics of fractal antennas and its application to DNA and concludes that "Loose and implausible conjectures about DNA as a fractal antenna do not substitute for careful discussion of these matters"; I don't find the authors' rebuttal particularly convincing)
the authors cite epidemiological evidence that non-ionizing/low-frequency radiation causes cancer: according to the US NIH's National Cancer Institute, this evidence is weak. (However, one of the authors of this paper is a contrarian on this subject and believes that the mainstream view is wrong, for a variety of reasons.) (See Are low-intensity radio-waves carcinogenic? for more discussion on Biology.SE.)
the paper uses very disparate lines of evidence (not necessarily a bad thing, but in this case it feels haphazard): in particular, the authors discuss both low-frequency and ionizing radiation (this is part of their "DNA is sensitive to many different frequencies" argument, but ionizing radiation operates in a very different way)
it is highly speculative in places (e.g. "EMF is believed to have been an important driving force in evolution", p. 413, no reference; the authors go on to attribute the faster evolution of eukaryotes to the fact that their DNA structures are more fractal)
at least one of the references cited (de Pomerai et al. Nature 2000) was retracted in 2006 (5 years before the current paper was published)

What I can say in favor of the authors is that exploring the mechanisms by which low-frequency electromagnetic fields/radiation (ELF) affect cellular biology is indeed interesting; many of the epidemiological studies, while finding very weak effects, have also downplayed risk because so little is known about mechanisms of operation. If we could come up with a rigorous mechanistic understanding of ELF effects, that would be scientifically worthwhile.


Are there ontologies for the description of the look of plants? Are there existing ontologies for the description of the look of plants?
I am looking for something formally defined giving me at least or better more information like in descriptions:

They are mainly deciduous shrubs and trees, often with brush-like foliage, often spiny to deter grazing, and masses of small, pea-like yellow blooms which are sometimes fragrant.

which I took from https://en.wikipedia.org/wiki/Genista .
The use case is to be able to procedurally generate 3D models of them, which are not too far away from the reality as far as an ordinary person would notice.

To transform an object in an ontology to an image of that object?  Sounds unlikely, I doubt that any botanical ontology is that developed and detailed.  It would be great if it worked.  Could be used to check the ontology.  The website https://www.ebi.ac.uk/ols/ontologies lists 251 biological ontologies.  There are several on specific plants or groups of plants (brassica, beet, oats) and several that might be more relevant to you: Plant Ontology, Plant Phenology Ontology, and Plant Trait Ontology,


Stimulating an axon causes impulses to travel both ways? A diagram is presented as such above.
The question given states What would be the effect of stimulation to cause a nerve impulse with a microelectrode at the middle of the axon?

I thought the nerve impulse only travels in one direction to the muscle fibres, but the book says "A nerve impulse would pass in both directions."

Why is that the case?

Allow me to do a silly analogy: think about the electric wire going from your outlet to your computer, conducting electricity. If you make two cuts in this wire, rotate it 180 degrees and weld it again at the cutting points, what will happen? It will conduct electricity just as it did before.

The same happens to an axon (but please have in mind that this is just an analogy, an action potential is not an electric current). That is, the axon doesn't determine or influence the direction of the action potential. If you cut a piece of that axon, rotate it 180 degrees and join it back in the cutting points, it will conduct the action potential the same way.

That being said, imagine that you stimulate that axon at a given point. There will be two action potentials, going to opposite ways:

unmyelinated (A) and myelinated (B) nerve cells

In your figure (given that is a motor neuron), if you stimulate that axon in the middle, the action potential going to the neuromuscular junction, which is the normal direction, is called orthodromic (from the greek orthos, "proper", and edramon, past of "run"), while the one going to the soma (the perikaryon) is called antidromic (from the greek anti, "against").

According to Oh (2003):

  The sensory nerve conduction study measures the conduction of the nerve impulse along the sensory nerves. The routine method measures the conduction velocity of the large diameter sensory nerve fibers of the nerve being tested. There are two methods of obtaining sensory nerve action potentials (SNAP), orthodromic and antidromic. The orthodromic method includes recording of the sensory nerve action potential proximally and stimulating the nerve distally whereas in the antidromic method the location of the stimulating and recording electrodes is reversed. The latency and conduction velocities are identical with the orthodromic and antidromic methods if the recording and stimulating electrode positions are constant. (emphasis mine)

In a simplified scenario, the orthodromic impulse will reach the neuromuscular junction and stimulate the muscle contraction, while the antidromic impulse will be canceled by another orthodromic impulse or, if it can reach the dendrites, it will simply end, since there will be no neurotransmitter release.

Source: Oh, Shin J., 2002. Clinical Electromyography: Nerve Conduction Studies. Third. LWW.


What happens to the holes in the skull where teeth were developing? In Skeptics.SE, a question regarding the skulls of children arose. Depicting a scary skull where the permenent teeth are "hidden" inside the jaws and the milk teeth are in the their place.

After all milk teeth fall out, and the permanent teeth "rise", do the holes left by them filled up, or do we go around with holes in our jaws?

The question on Skeptics

The picture:

Bone growth continues in the human body for quite awhile after permanent teeth come in. Generally, the complete closure of all growth plates doesn't occur until the mid 20s.

As the top and bottom primary teeth come in, the empty space left behind is gradually filled by growth of the maxilla and mandible, respectively. During the time period when teeth are actively coming in, teeth can displace into the empty space left by other permanent teeth that are no longer there, resulting in crooked teeth.


What problem does kin selection solve? I'm trying to understand what problem led to a development of kin selection.

The explanations I've found consist roughly of the following:

  The existence of some altruistic and cooperative behaviors in social
  insects like honey bees, the phenomenon of sterile castes formed by
  non-reproductive individuals that leave no offspring and the suicidal
  role of these insects in defending the hive, were traits that natural
  selection could not favor. Kin Selection | Nectunt

What I do not understand: Why could natural selection not favor the phenomenon of sterile castes?

From the perspective of the sterile worker: Since it can't reproduce, no strategy will affect the number of offspring it has (will always be 0). So there is no conflict with natural selection.

From the perspective of the queen bee: Her offspring consist of sterile worker bees and a new fertile queen bee. The worker bees improve the viability of the next queen bee. This is consistent with natural selection.

Therefore, I can't see the relevance of the worker bee sharing lots of genes with its sister queen bee. This seems to be nothing but an ancillary effect of the mechanisms of evolutionary change.
Imagine, the queen bee could produce worker bees without a genome (like a robot), or a genome that is not related to its sister queen bee, those worker bees would still show altruistic behavior.

What am I missing?

Why natural selection leads to selfishness
Imagine a population of individuals. At a given locus, some individual carry the A allele and some others can the S allele (A for altruistic and S for Selfish). For simplicity, we will assume organisms are haploid. Individuals carrying the S allele are selfish and will take care of themselves only. The A allele are altruistic meaning that they produce behaviours (and non-behavioural phenotypes) that will reduce their fitness and increase the fitness of other individuals in the population.
As the altruistic behave as to reduce their fitness, they will be at a selective disadvantage and therefore, over time, only selfish individuals will remain.
How can altruism evolve then?
The study of the the evolution (and evolutionary consequences) of behaviour (and non-behavioural phenotypes) that affect the fitness of other individuals in the population is called social evolution. Social evolution is a wide field of knowledge and I will here attempt a very short summary of it so many concepts will be left out!
There are two main (non-exclusive) ways by which altruism can evolve:

Repeated interactions (False altruism)
Kin interactions (True altruism)

Repeated interactions
The concept is grounded within game theory. A good introduction to game theory is definitely out of the scope of this question but I just want to give a little bit of an intuition. I will over-simplified the concepts of game theory but you should definitely have a look at it. Those concepts are very enlightening for questions of evolutionary biology, economy, psychology, sociology and even philosophy.
If for example, the altruistic individuals are actually only altruistic to those
that have shown altruism in the past (via a Tit-for-Tat strategy for example or through the use of reputation), then altruistic individuals may end up have a higher fitness than the selfish individuals. Imagine for example that selfish individuals give nothing and receive nothing. Let's assume that all altruistic individuals, all make one good deed and receive one good deed. Giving a good deed comes at a cost of having, say 0.8 fewer offsprings on average. Receiving a good deed comes at a benefit of 1.2 extra offsprings. Overall and on average, each altruistic individual will produce 0.4 more offsprings than the selfish individuals and therefore, over time the whole population will become altruistic.
We often refer to these concepts as false altruism because altruistic individuals actually has a fitness increase over their life time. Let's now talk about true altruism where altruistic individuals really just give without receiving but yet, the allele coding for altruism thrives.
Kin interactions
Note first that any kin interaction follows within a give game theory scenario. As such kin interaction is just an add-on on what I discussed earlier. For those used to Hamilton's rule, please note that Hamilton's rule apply to Prisoner's dilemna (a type of game theory scenario) only.
So, imagine now that altruistic individuals are being altruistic with their family members (their kins) only (either because they direct their altruism or because there is a strong population structure). Note that such altruistic behaviour can pretty indirect as helping your partner (who we will assume is not part of your close family) will have for consequence that your partner may offer better parental care and therefore by being altruistic to your partner, you are actually being altruistic to you offsprings (which are your kins).
Because the kins of altruistic individuals probably carry the A allele, eve if the altruistic individual is experiencing a lifetime cost in fitness, the A allele may still thrive and the recipients of this altruism are likely also carrying the A allele. In other words, a truly altruistic individual is an individual that sacrifice itself for helping the allele A present in its kins to thrive. In yet other words, true altruism is when an allele is ensuring that copies of itself present in other individual will manage to get passed on.
And this is called Kin Selection. I can now clearly answer your question
Your question

What problem does kin selection solve?

Kin selection explains "true altruism"!
Only "true altruism" can yield to such separation of the reproductive task as that some individuals are perfectly steriles. In your post, you say

From the perspective of the sterile worker: Since it can't reproduce, no strategy will affect the number of offspring it has (will always be 0)

What is missing from this logic is that, 1) at a time workers could still reproduce and 'gave it up' and 2) in many (maybe most?) social species (honeybees, termites, ants and also in non-hymenopteran eusocial species), workers are still able to sometimes reproduce and are also able to overthrow the queen.


Do strictly anaerobic organisms use metabolic reactions requiring oxygen? When looking through genome annotations of strictly anaerobic organisms I see reactions featuring oxygen. I suspect these are likely an artifact of the annotation process. But I am wondering if it is possible for such organisms to have oxygen associated metabolism. Strict anaerobes are known to die in the presence of oxygen due to the lack oxidative stress pathways. So I cannot think of any reason for oxygen to be part of their metabolism.

Strict anaerobes do not use molecular oxygen for oxidation reactions.

The oxidation of ferrous iron to ferric iron (viz. the example given by Septimus G) can be done anaerobically by anaerobic purple bacteria [eq. 2 in Ehrenreich & Widdel (1994) Appl Environ Microbiol 60: 4517-4526]:

4 FeCO3 + 10 H20 --> 4 Fe(OH)3 + (CH20) + 3 HCO3- + 3 H+

https://www.ncbi.nlm.nih.gov/pubmed/7811087


What is the meaning and significance of extreme pathways Can someone please explain me what extreme pathways are? I found this definition in this article:

  Extreme pathways are a unique and minimal set of vectors that
  completely characterize the steady-state capabilities of genome-scale
  metabolic networks.

Now, frankly speaking, I did not understand the head or tail of this definition? What is steady state? What does it mean by steady state capabilities? Can someone please explain me in a simpler way?
PS: I am a computer Science student

For any dynamic system defined by different components, the steady state is the state of the system in which the components remain constant over time. If you consider the example of growth (by cell division) the point at which the total number of cells remain constant would be the steady state. This is a point at which birth rate = death rate. Similarly for a multi-component system such as a gene and its activator, the steady state would be the point where the mRNAs and the proteins of the gene and its activator are constant. If only few components are constant then the system is said to be in a quasi-steady state.

A point to be noted that in chemical (or biochemical) systems steady state, as a term, is different from equilibrium (in physics these terms are used interchangeably). Equilibrium is a condition when, for a single reversible reaction, the forward rate = backward rate.

In mathematical terms steady state is a point where the rate of change of components = 0. In an ordinary differential equations based model:

$$\frac{d\bar{X}}{dt}=0 \\$$
where $\bar{X}$ is a vector in which each element is a component of the system. In case of the transcription example, $X(1),X(2)..$ would be mRNA, protein, activator mRNA and so on. In other words $\dfrac{dX(i)}{dt}=0$ for all $i$.

Steady state capabilities should mean the properties of the system at its steady state.

The kind of study described in the question is called metabolic flux balance analysis in which different metabolic reactions are described in the form of linear equations represented by $Sv=0$ where $v$ is the vector of all fluxes (metabolic reaction rates) $S$ is the stoichiometry matrix (which has the stoichiometry of all components in different metabolic reactions). The RHS is zero because we are evaluating the system at its steady state i.e. we are interested in finding out the condition in which the net metabolic reaction flux is 0. In other words all metabolic reactions, balance each other.

You need to read more about this. There are a lot of books on this topic. You can start with this review.

In flux balance analysis, the linear equations are overdetermined i.e. there are many solutions. People generally use linear programming (simplex algorithm) to find optimal solutions. In the space of the optimal solutions, the vertices represent extreme reactions. The entire optimal solution space can be described as a linear combination of these extreme reactions.

  Schematic representation of a convex cone characterized by five
  extreme pathways. Extreme Pathways 1–5 (EP1, EP2, EP3, EP4, and EP5)
  circumscribe the solution space for the three fluxes indicated (vA,
  vB, vC). EP4 lies in the plane formed by fluxes vA and vB.
  Consequently, flux vC does not participate in that extreme pathway.
  EP3, EP4, and EP5 are all close and represent different uses of a
  network to achieve a similar overall result. All points within the
  convex cone can be described as a non-negative linear combination of
  the extreme pathways [1].


is Xanthosine Xanthine plus ribose? I'm so confused. I used to think Xanthosine is Xanthine with a ribose instead of H but it appears to me as if it isn't. If you look at the picture in top-right of its wikipedia page you will see that the Imidazole is reversed from the picture in here also the picture in the bottom of this page in additional images section is like the second one. I'm sorry if didn't use the right chemical terms! I'm no chemist. Also I while I was searching I saw different images for Adenine and Guanine where the Imidazole loop was reversed in some by reversed I mean like the position of NH and N was reversed with respect to the Benzene loop!

P.S. It would be great if you could also teach me the correct way to ask this question by means of the chemical terms I should use.

P.S.S I hope it is not a wikipedia problem!

The two structures are tautomers of one another:

Tautomers are often considered the same compound even though they are really constitutional isomers. Technically they are called 7H-xanthine and 9H-xanthine, respectively (thanks to gilleain for the links).


What nutrients do I lose in the water when I boil vegetables? What nutrients do I lose in the water when I boil vegetables. Has to be some water-soluble and heat labile ones right? Which ones?

Vitamin C and the B complex vitamins are water soluble.   Thiamine and folate are also heat labile.

Overall there are hundreds or often thousands of kinds of small molecules (not protein or DNA) in the cell and many of them are water soluble or heat labile.  Plants especially have many unusual small molecules.  Its not known how many of them affect human health, but may affect factors like the gut microbiome quite a bit and have an effect on well being if not mortality.

Some people think that live uncooked vegetables have enzymes and other proteins which are good for you since cooked proteins are denatured and may be taken in differently.  At the very least they are probably easier to digest when they are not heat denatured.


What is meant by "neurotransmitters flooding the brain"? I frequently hear expressions like "Dopamine flooding the brain" or "X neurotransmitter flooding the brain" used to communicate with general audiences. For example: "Following [orgasm]? oxytocin floods the brain, causing feeling of deep connectedness between people"

What exactly do they mean by "Oxytocin flooding the brain"? I'm interested in where and how it happens. Do they mean that excess neurotransmitters are released in the synaptic cleft? Is it localized to some brain areas, or is it indeed throughout the brain?

If they are indeed talking about the synaptic cleft, then I'm interested in how such "flood" triggers the change in state - the answer to this question suggests that the half life of dopamine is only about 2 seconds in prefrontal cortex. Assuming that the half life of oxytocin is similar, in the "oxytocin floods the brain and produces feeling of connectedness" example, does it mean that a single burst of oxytocin(x seconds in synaptic cleft) is enough to produce such feeling, or are they talking about sustained release or some kind of release loop mechanism?

It is very likely what they mean by "neurotransmitters flooding the brain" is the phenomenon called Volume Transmission.

I paraphrase from this source:

  When a neurotransmitter is released at a synapse, it reaches its
  highest concentration inside the narrow space of the synaptic cleft,
  but some of it is certain to diffuse away before being reabsorbed or
  broken down. If it diffuses away, it has the potential to activate
  receptors that are located either at other synapses or on the membrane
  away from any synapse. The extrasynaptic activity of a
  neurotransmitter is known as volume transmission. It is well
  established that such effects occur to some degree, but their
  functional importance has long been a matter of controversy.


Can neurons divide if somehow centrioles are introduced in nerve cells? I am a biology student, so i know that centrioles are required for cell division, and i also know that nerve cells lack centrioles.

My question is that if somehow compatible  centrioles were introduced to the nerve cells, would their division be possible?

Induced Pluripotent Cells
https://en.wikipedia.org/wiki/Induced_pluripotent_stem_cell?wprov=sfla1

You should probably look into this. This introduces what is called iPSCs, which are stem cells derived from adult cells.

What it is is that  they use signals that are found in embryonic cells, and the adult cells revert from their differentiated form into cells that can become virtually anything.


About. Autosomal recessive diseases in genetics What happens if homozygous dominant  alleles are present in an individual for an autosomal recessive disease will he be affected ?

You are talking about an extremely simple system of inheritence that is a single bi-allelic locus with simple dominance relationships. You are talking about a autosomal recessive disease. In other words, let a and A be the two alleles, where A is dominant of a. By definition of your model, the individual expressing the disease is the individual carrying both a alleles (a aa individual). Anyone carrying the dominant allele would not express the disease (by definition of the term dominance and because you define a model where a and not A is causing the disease).

In short aa express the disease, while aA, Aa and AA individuals don't express the disease. aA and Aa are carrying the allele causing the disease though and might have kids expressing the disease if they mate with an individual that carries at least one allele a.


Do couples having children later in life act as an evolutionary mechanism? Ok, this may be just wild nonsense and I have to warn that my knowledge on the subject is limited.

I was reading about how in some countries people choose to have children later in life. After that this question came to my mind?

If human couples chose to have children later in life, lets say 40s 50s - disregarding keeping an younger self gamete preserved - wouldn't this result in the people less resistant to the effect of aging being unable to reproduce,  creating a more longevous generation? thus enabling future generations to reproduce even later lenghtening the average lifespan of humans?

ps: After reading this sounded a little too eugenic, by no means I'm trying to make this an legitimate theory or suggest an experiment, it's just a doubt - maybe good for some science fiction story...

Many factors have to be considered.  First, although more women are delaying pregnancy until after the age of 35, the overall percentage of women doing so remains very small, as shown by this figure from this New York Times article. Only about 9% of pregnancies in the United States (for 2008) were in women over the age of 35. Most pregnancies still occur in younger women. I suspect this is especially true when considered globally.

Getting pregnant later in life is more difficult, is more likely to result in miscarriage, and is more likely to result in some types of birth defects. The issues are discussed by the Mayo Clinic, WebMD, and summarized by Parenting Magazine. On average, individuals with birth defects are themselves less likely to reproduce (Skjaerven 1999).
For natural selection to favor a particular trait (such as later pregnancy), the individuals with the trait must have higher relative fitness, meaning they produce more offspring on average compared to other individuals. However, relatively few women have late-age pregnancies, more of the offspring are likely to have birth defects, and those offspring are themselves less likely to reproduce. In other words, on average, late-age pregnancies would have reduced fitness compared to individuals that get pregnant at earlier ages.
Most importantly, though, the decision to wait until later in life is a conscious choice, not a genetic trait. Natural selection can only work on genetic variation associated with particular traits. If the choice for delayed pregnancy has no genetic basis, then it is invisible to natural selection, and so cannot evolve.

Citation
Skjaerven, R. et al. 1999. A population-based study of survival and childbearing among female subjects with birth defects and the risk of recurrence in their children. The New England Journal of Medicine 340: 1057-1062.


Nicotine levels in non fruit/edible parts of plants (that are not tobacco) I am an ex smoker who now vapes (uses e-cigs). Various authorities are equating vaping with smoking by calling it a 'tobacco product' - which is in a sense true given that the majority of nicotine sold is extracted from the leaves of tobacco. I am interested in the practicality (or otherwise) of extracting nicotine from other botanical sources.

Of course, it is not just tobacco that contains nicotine, it is common in other plants of the nightshade family, as suggested by The Nicotine Content of Common Vegetables & Nicotine: Occurrence and biosynthesis. The second source notes:

  Nicotine is a natural product of tobacco, occurring in the leaves in a range of 0.5 to 7.5% depending on variety.[84] Nicotine also naturally occurs in smaller amounts in plants from the family Solanaceae (such as potatoes, tomatoes, and eggplant).[85]

Reference 85 points back to the first link, which shows this table.

But looking at the numbers, it seems unlikely. At even .5%, the 'low nicotine' tobacco leaf comes in at 5 mg/g, which is 5,000,000 ng/g - around 50,000 times more concentrated than eggplant. In fact, here is a graph of the log10 value (2 is ten times larger than 1) of each.

On the other hand, the ability of a plant to produce nicotine is retained and handed down to ancestors because nicotine is a pesticide that ..discourages insects from eating the plant, and larger herbivores will also get sick if they eat too much of it. Logically, levels of nicotine would be higher in the leaves and stems of a plant than in the fruits/food that we & animals are more interested in eating. That again makes sense, since most fruits are 'designed' to be put through the stomach of a larger animal as part of the process of regeneration.

That logic seems to be borne out by the levels of nicotine in tomatoes, that start around 40 ng/g in green tomatoes, but end up at just over 4 ng/g in ripe tomatoes (not sure what's going on with that 'pureed tomato' level of over 50 ng!). The drop suggests to me that's the plant's way of preventing consumption while the fruits are still developing, but making them safe(r) to eat once ripe.

But what about the nicotine content in the leaves of those plants? Logically they might have a higher nicotine content. Does anyone know of studies of the levels of nicotine in the other parts of plants of the nightshade family?

Tomato leaves have something like 184 ng/g of nicotine, in the same ballpark as tomatoes (the fruit) and not close to tobacco.  I think this is not peer-reviewed, but it cites other papers that are: Nicotine Analysis in Several Non-Tobacco Plant Materials
And this is a PDF of a slide deck providing a simple presentation of the results from the same article: Nicotine Analysis in Several Non-Tobacco Plant Materials - PDF


How to determine the direction of regulation of a gene by comparing gene expressions? I am just learning about the gene expressions and regulation. Several researches focus on finding the genes of altered gene expressions on a microarray to claim that they have a correlation to a specific disease.

I am confused about how people can determine whether a gene is down-regulated or up-regulated by its gene expression.

Assume we have a few samples of a gene: some of the samples are normal patients samples and rest of them are disease-infected samples. Do we determine the direction of regulation of a gene by the ratio of gene expression of normal/disease-infected samples?

For example, if the ratio of expressions is a negative value, do we say that the gene is a down-regulated gene, otherwise, it is a up-regulated gene ?

If you have control expression values $c$ and e.g. disease expression values $d$, you take the ratio: $\frac{d}{c}$. If this is greater than one, it's up-regulated. Usually, the log-ratio is computed: $log\frac{d}{c}$. Now, if this is positive, the gene is up-regulated.

Gene expression values are usually measured genome-wide and then normalized before computing the ratios. So you rarely deal with individual raw expression values.


Is this a bacterial colony? On the physics StackExchange site people are trying to figure how and why these branching structures formed. The two questions can be found here and here. The latter had no cooling fans and was situated in an unventilated cupboard. There are many processes that could explain such structures without them being a bacterial colony, for example by Diffusion-limited-aggregation as explained in my answer here. To me it looks like this could be a bacterial colony. Is there any way to rule this out or say with precision that this is a bacterial colony?

I think some organic material and humidity could latch on to the irregular edges upon which bacteria could then grow in a warm environment.

What ways are there to tell from just a picture if this is a bacterial colony or  not?
What ways are there to tell if this is a bacterial colony or not if you have the structure at hand?
What ways are there to rule out or say that this is some kind of fungus or living thing if you have the structure at hand?

The second pic was taken by Wossname:

  "the equipment is in a temperate climate in a non-aircon area of an
  office building near the external door. In high summer it would get to
  probably 40 Celcius and 85% or more relative humidity in my
  estimation. It's an area of the building that people most definitely
  don't loiter in during July/August. :)"

These look like crystallization structures when liquids dry up. But if it were to be a living thing, I'd go with fungal colonies. In my opinion, the best methods to tell is to scrape off a small piece, flood with KOH, and observe under a microscope, if you see filaments then it is definitely a fungus, and alternatively you can inoculate an agar (Sabouraud agar could work, or LB agar) to see if something grows. If its a fungus, it can take from 4 days up to 3 weeks to grow depending on the species and the growth conditions provided.

Good luck.

Here's a ref that might help you.

Microscopic potassium hydroxide preparation:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3994805/


Nucleotide frequencies in Kimura's two-parameter model Here's an excerpt about Kimura's two-parameter model from Felsenstein's Inferring Phylogenies:

  "The model is symmetrical, and one can immediately see that, after
  enough time has elapsed, it will be equally likely for the base to be
  a purine or a pyrimidine."

I think I understand the assumptions of the model but it's not obvious to me why the equilibrium frequencies are equal. Why is that so?

If sufficient time has elapsed, there will be a large number of transversions present between the original base and the final state. The initial state will therefore not matter.

Say, you flip (turn over, not toss) a coin at random intervals. For short time and few flips, the initial state will matter. But if you go on flipping it for millenia, the final state will be essentially random -- you will not be able to tell what was there in the beginning.


Why is cancer not a communicable disease? I read another question where the author is asking about the infectivity of viruses. In the same vein, I am curious why cancer is not a communicable disease.

A cancer is not a pathogen

Cancer is a group of cells that (because of several specific mutations) start to duplicate abnormally. This group of cancerous cells are the own cells of the sick patient. It is not another species infecting the individual carrying the disease. It is the individual itself who developed the disease. Cancer is not a pathogen (but see below) that infect hosts and get transmitted from one host to another. It is more correct to picture cancer as an internal mistake of the body rather than as an external attack on our body. You might want to have a look to the wiki page for cancer for more information.

Transmissible agents that can cause cancer

Some cancers are caused by transmissible agents, such as oncoviruses. the transmissible agent may jump from one host to another and cause cancers giving the sensation that cancer is transmitted. It is just a sensation of course because in reality only the oncovirus gets transmitted and not cancer itself jumping from one host to another.

Cancers that become transmissible

Note however that it is not impossible to imagine a tumour jumping from one individual to another in cases where the immune response cannot detect cancer as 'non-self'. Some cancers are transmissible. Those cancers are called clonally transmissible cancer (As indicated by C Rags in the comments). Here is the list:

The Devil Facial Tumor Disease which occurs in Tasmanian Devils
The canine transmissible venereal tumour (article from Chris Stronks in the comments)
The Contagious reticulum cell sarcoma occurring in the hamster.


What does cell-to-cell variability means? I'm reading an article where they claim that transcriptional bursting could play a role in cell-to-cell variability.

  Cell-to-cell variability plays a critical role in cellular responses and decision-making in a population, and transcriptional bursting has been broadly studied by experimental and theoretical approaches as the potential source of cell-to-cell variability.

I was looking for a definition of Cell-to-cell variability and I found only the one of Single-cell variability

  In cell biology, single-cell variability occurs when individual cells in an otherwise similar population differ in shape, size, position in the cell cycle, or molecular-level characteristics. Such differences can be detected using modern single-cell analysis techniques. Investigation of variability within a population of cells contributes to the understanding of developmental and pathological processes.

I won't ask a question that's related to an article before reading it completely! The answer was in the first paragraph.

  Cell-to-cell variability defined as when genetically identical cells in an identical environment behave differently, leading to significant consequences in many biological processes from bacterial decision-making to mammalian development.


What kind of soil-dwelling flying insect is this? In the UK. They are roughly 1.5mm long, appear to crawl much more than fly, and seem to live in the soil of indoor potted plants. They are fast and tiny, so apologies for very shallow DOF. The first is on an aloe, the second is on a pot. They really like the soil around some capsicum plants.

Those look to me like fungus gnats. If you're looking to get rid of them, I've heard that putting a layer of rice hulls on top of the soil keeps them from reproducing. From what little I've read my identification doesn't go much deeper than superfamily, taxonomically, but it's a least a common name to work from.


Is it impossible to increase skeletal bone mass, as opposed to just bone density? I've heard exercise and resistance/strength training increases the density, but doesn't increase mass. So basically, experimentally or theoretically possible at least, can modern science do this/is it feasible?

Density is just how "packed" the current bone is on the micro-level -- i.e., doesn't affect total mass potential. Filling or adding "density" is just like putting water in a fixed-size bucket until it fills. By "adding mass" I want the bone's bucket to be able to hold more density, i.e., a larger potential of density along with an overall greater weight to the bones themselves. I can't find any evidence that this is possible with long and flat bones alike, AKA the spine, leg and arm bones, clavicles and etc. -- or any bone.

I've heard facial bones are more malleable, but their bone mass cannot change with diet/training either.

So to make this as easy to understand as possible: Can bone mass in an adult be significantly changed somehow? Can I make my whole skeletal set heavier somehow, rather than just dense? Like for example, say I am considered "small framed." Rather than just density, could I make my frame bigger? Could I make my entire frame base more robust through some possible bio/drugs/etc. means?

And since I know someone will come along and claim this is a "medical/personal question," explain to me how this would be possible to ask in a non-medical/personal way then to enlighten me. Go ahead.

If you search for
 - bone growth training
 - bone hypertrophy athletics,
 - bone diameter increase,
 - bone strengh hunter gatherer,
on google, you will find more articles than I could possibly summarise:

stimulation of longitudinal bone growth and widening of the joint space (cartilage hypertrophy) occur. The possibility of bony hypertrophy as a result of athletic training, especially with regard to increases in of bone density and bone diameter, should lead to incorporation of sports medical considerations into the prophylaxis and therapy of osteoporosis.

https://www.ncbi.nlm.nih.gov/pubmed/7856798

https://www.ncbi.nlm.nih.gov/pubmed/7478507

I have slender bones and it was the gain of muscle which helped me to balance my physique.


Why is menstruation in wild animals not a disadvantage to organismal survival? When I watch wilderness specials for more than a few minutes, I notice a familiar pattern: predators are depicted as being alerted by the scent of blood. Wounded animals seem to make the best prey and predators seem to have a heightened awareness for the smell of blood.

It would seem that it would then be a disadvantage to evolutionary survival for female organisms to menstruate. How do females of a species not attract predators to the signal of menstrual blood?

Do female organisms in the wild actually menstruate? If so, is there a difference in the composition of menses that does not alert predators? How would this not at the very least give predators an idea of the general vicinity of the female?

If wild animals excrete their menses, do they have ways in which they are able to mask the evidence of its release or are they somehow internalizing the tissue so that they are not released?

If female organisms in the wild do menstruate, then why is this not a survival disadvantage?

Thanks to the other answer for pointing me in the right direction with some references. It seems that two biologists in the early 1990s had a back-and-forth over this topic in The Quarterly Review of Biology.1,2

A statement of the problem:

  The function of menstruation is a central enigma of mammalian, and especially primate, reproductive physiology. Each cycle the uterus builds a glandular epithelium with a high secretory capacity and an elaborate microvasculature, only to reabsorb or void it with the menses if implantation does not oc-cur. Why does the endometrium not maintain a steady state of readiness for implantation by the blastocyst? What is the selective advantage of cyclical regeneration and regression?1

One hypothesis2

In  1993, Margie Profet hypothesized that menstruation is primarily advantageous as a defense against pathogens transported by sperm. During mammalian insemination, she stated, bacteria from the male and female genitalia cling to sperm tails and are transported to the uterus. Menstruation, triggered by the abrupt constriction (causing necrosis of endometrial lining) followed by dilation (causing shedding of said necrotic tissue), forces loose not only the endometrial lining but sperm-borne pathogens contained therein. In addition to shedding the uterine tissue harboring these bacteria, menstruation delivers immune cells to the uterine cavity, triggered by the mechanical pressure exerted via the shedding of endometrial lining.

In this 50 page (!) article, Profet also points out that other mammals with covert menstruation take advantage of some of these same benefits, as the immunological stimulation includes phagocytosis of pathogens by cells that may be expelled in cervical/vaginal mucous. Further, proestrous  bleeding (i.e. that preceding ovulation, 180 degrees off from the human cycle), which occurs in some mammals (domestic dog, coyote, etc), seems to serve a similar function.

  If not eliminated prior to estrus, these tenacious pathogens might otherwise attach to incoming sperm during estrus and ascend the oviducts.

As to why humans and other primates are subject to overt bleeding in contrast to other mammals, she lays out a theoretical argument that selection pressure to menstruate should increase with decreasing per-cycle “fecundability” (the probability of pregnancy) because copulation not followed by bleeding risks infection. In contrast to, e.g., mice (98% fecundability), humans have some of the lowest fecundability rates, primarily due to “concealed” ovulation which de-couples copulation and ovulation. (Contrast this to most mammals whose females have a defined estrous period during which they are receptive to male sexual advances; the data for the existence of such a period in humans are controversial, and sexual behavior is driven primarily by “higher” social, environmental, and cognitive cues.)

A different view1

In response/objection to this paper, Beverly Strassman in the same journal published an article outlining an alternative hypothesis about the potential adaptive value of menstruation. She proposed a hypothesis based on energy conservation:

  [T]he uterine endometrium is shed/resorbed whenever implantation fails because cyclical regression and renewal is energetically less costly than maintaining the endometrium in the metabolically active state required for implantation.

Her research determined that, in its regressed state (i.e. s/p endometrial shedding), oxygen consumption in the endometrial tissue is markedly declined, nearly sevenfold. Although this would seem to be a trivial component of whole-body metabolism, she argues otherwise:

  Metabolic rate is at least 7% lower, on average, during the follicular phase than during the luteal phase in women, which signifies an estimated energy savings of 53 MJ over four cycles, or nearly six days worth of food.

Her argument shares with Profer’s the implication that mammals with lower fecundability are more likely to menstruate. In those with high probability of pregnancy at every cycle, the energetic benefits of ridding the body of the need to support endometrial lining (relevant only in the absence of pregnancy), are decreased. Her hypothesis also predicts the larger volume of menstrual shedding in humans and chimps in contrast to other mammals related to the increased uterine size relative to the female body (a ratio that is largely determined by the especially large head of the human fetus).

Conclusion

As noted in the comments, only primates have overt menstrual bleeding. The adaptive benefits have been variously explained, and it is probable that there is more than one operative explanatory model. Whatever the small decrement in survivalship incurred by the intermittent and uncontrolled depositing of blood in the wild, it is apparently outweighed in these species by the processes described above.

References and Notes

1. Strassmann, Beverly I.  The Evolution of Endometrial Cycles and Menstruation The Quarterly Review of Biology, June 1996; Vol. 71, No. 2 pp 181-220.

2. Profet, Margie. Menstruation as a Defense Against Pathogens Transported by Sperm. The Quarterly Review of Biology, Sept 1993; Vol. 68, No. 3  pp. 335-386.

Note: Your comparison to urine and feces is an interesting one. Perhaps a vaginal sphincter would be a good idea…..were it not for men and babies….


intravenous (IV) in the tail vein of an anaesthetized mouse I trained myself to do intravenous injection on live mice. However, on anaesthetized mice you don't see the flux of your product showing that your injection was successful. In the same way, on live mouse a slight back pressure can be used to pull blood into the syringe to confirm proper placement in the vessel before injecting. On anaesthetized mice, I really have difficulty to obtain blood. All my following experiments rely on this injection, so I really need to be sure that the injection was successful and I have no choice that to do the injection on an anaesthetized mouse. Of course I warm the animals before injection to dilate the veins but I don't know how much I can warm an anaestethized mouse.
I thought to put a catheter before anesthetization the mouse but I don't know if it will stay in place until the mouse is anaestetized.
Do you have any tips?

Cleaning the tail with ethanol is of some help and also, as you said, warming the tail. We sometimes put one of those flexible lamps (such as this) to heat up only the tail.

When anesthesized (ketamine/xylazine or isoflurane) we keep our mice on a heated pad anyways.

Cannulation in the tail does not sound like a good idea to me, especially if you are going to have the animal wake up afterwards. If you're going to cannulate then go for the jugular, but be aware that doing it on a mouse requires quite a bit of experience and it's definitely way longer than a tail injection.

It really depends on your experiment


How accurate does the alignment of molecules in DNA have to be? We have learned that the same information is saved in the DNA in the same place. So when DNA splits and then connects again (during reproduction); how does it maintain the integrity of the information? In other words, do they split and come back like a zipper, or does something else happen?

In the case of replication the parent strands do not pair up back into the original helix. Instead, as your picture and the one below show, the complementary bases are paired up on one of the parent strands, resulting in two copies, each with one parent strand and one new one.

Source: Kathy's webpage on DNA


Technical term for water entering a semipermeable membrane? Would the word happen to be diffuse? I have tried imbibtion but that word is invalid because it isn't specific to osmosis.

Research: http://www.majordifferences.com/2013/12/difference-between-osmosis-and.html#.V9xc4fkrLIU

This is not imbibition, as water molecules don't get absorbed in the semipermeable membranes commonly found in biological structures like Membrane around cells and cellular organelles (I took this example as you asked it in Biology forum). The water molecules pass through biological membranes via protein channels, that may be an active, secondarily active or passive process. Percolation and permeation are also inappropriate.

If the membrane doesn't hinder a particular solvent it can be said to be permeable to that solvent (e.g. Permeable to water etc.). "Osmosis" is also applicable. As osmosis is only a type of diffusion, you can use the term 'diffusion', but it would be too broad or generalized.


Binding of Multivalent Antibody to mutiple epitopes? A multivalent antibody molecule such as Immunoglobulin M Immunoglobulin A etc bind to more than one antigens or epitopes but I am confused about that wheather these multivalent antibodies bind to identical epitopes or can bind to different epitopes? means if one molecule of Immunoglobulin M being pentameric can bind to 10 epitopes at a time the 10 epitopes that it binds Will be identical or can be different..? Confused about that..       2. And also another Question I want to ask that as Immunoglobulin G,Immunoglobulin D and Immunoglobulin E are monomers but all of them have 2 antigen binding sites so we consider them as Mutivalent antibodies or not and if we cnsider them as multivalent antibodies then what are the Examples of monovalent antibody that Specifically only bind to One antigen molecule or epitope? Because as far as i Have studied Antibody or Immunoglobulin molecule hae specific "Y" structure that contains 2 binding sites. Similarly in this case also want answer that these momomeric ImmunoglobulinsG,D,E each binds to 2 identical antigens or epitopes or can bind to two different epitopes. Means that if Immunoglobulin G is binding to two epitopes these epitopes will be identical or can be different...??? :/

Non-engineered IgM (such as is produced in vivo) has the same binding domain on all "arms" of the pentamer. They don't bind to more than one antigen, instead they can bind to multiple copies of the same epitope. Due to steric hindrance, a single IgM molecule generally will not bind at all 10 binding sites.


Name two reasons why it is impossible to determine a gene's nucleotide sequence from the amino acid sequence of the polypeptide I can only think of one reason, which is because different codons can specify the same amino acids. However I am having trouble thinking of another reason.

I can think of at least 3 reasons in addition to the one you gave:

1: As mentioned in the comments, RNA splicing takes place on most messenger RNA encoding proteins in eukaryotes. Sections of the mRNA may be spliced out, therefore multiple mRNAs with different codon sequence can encode the same gene.

2: Translation is a stateful process, since it depends on the frame of the codon. Therefore, a gene with the sequence GGATGATGATGTAA will encode the same protein as a gene with the sequence ATGATGATGTAA, due to the start codon shifting the frame of translation downwards.

3: Genes contain untranslated regions in regions before the start and after the stop codon. These nucleotides cannot be predicted from protein sequence, but are generally important in regulating protein expression.


What is the rationale behind tapering of immunosuppressant dose a while after transplant? MMF, Cyclosporine, Prednisolone, Tacrolimus the dose of whatever immunosuppressant used is reduced in around 6 months - 1 year after the transplant.

What is the rationale behind this?

Wouldn't any allograft, howsoever old, still remain foreign? Does the body learn to consider the graft self? Or is the response still there but the destruction is reduced?

Why should a new graft elicit more response than an old one?

This is a very interesting question. One of the most important considerations in patients on long-term immunosuppression is the risk of complications, whether infections or (more dangerously) cancer development; because of this if we can taper the dose then we would like to. This paper specifically discusses a lot of those risks. You mention prednisolone which is a glucocorticoid, and the side-effects (see also here) of chronic steroids (due to very wide-ranging immunosuppression) are well-known and always borne in mind when they have to be prescribed. The tapering of corticosteroids in long-term immunosuppression is often early to replace them with other drugs (mentioned here). With regards to the other immunosuppressives you mention, I'll mention mycophenolate mofetil and tacrolimus later with regards to how this is feasible biologically; with regards to cyclosporine, this study (admittedly old) has data illustrating the rates of rejection of renal transplants when patients withdrew from or tapered cyclosporine (here for financial reasons, but this drug also has significant adverse effects) and you can see from Figure 1 in the paper that although the patients who withdrew completely had many allograft rejections, those who tapered did not.

I'll start with answering your question about what clinical evidence we have for being able to do this; there have been quite a few studies which might help to throw some light on this. This study specifically considered kidney transplants, testing patients who were on standard immunosuppression for the 2 years after a transplant, and specifically measuring the quantity of CTLs (cytotoxic T-lymphocytes) reactive against donor cells, and they found that these cells were significantly downregulated in most patients 2 years after the transplant (while activity against third-party cells was mostly preserved). Since they found other T-cell responses to be unimpaired, they concluded that there was specific downregulation of the donor-specific cells occurring.

This paper also has some data which you can have a look at. This study specifically looked at moving patients from cyclosporine to azathioprine and mycophenolate mofetil and then tapering those. I've reproduced one of their graphs below which shows the activity of donor-specific CTLs before transplantation (the no dose group), 1 year after (still on high dose immunosuppression) and 2 years after (on low dose immunosuppression). The units are the ratio of activity of donor T-cells to activity against third-party T-blasts from spleen tissue (i.e. a control). Although you can see that some patients have ended up with increased activity after tapering, most patients appear to have low activities similar to (or even lower than) their pre-immunosuppression values, and these would be the patients considered for this tapering. This means that they now respond less vigorously to allograft cells than to control cells, and the ratio has decreased during treatment (presumably the reason why almost all of them have ratios under 1.0 before treatment is that the donor is not a random individual but matched for a lower immunological response):

And for another comparison with the body's response to non-donor substrates, the same study looked at response to tetanus toxoid. As you can see in the graph below, although the high dose caused the response to drop, it appears to have bounced back up again in most following the taper, similarly to the 3rd-party T-cell response but unlike the allograft response (the y-axis is proliferation of patient spleen cells in response to the toxoid divided by control rate):

As to the immunological reasons that we can taper the immunosuppressant dose, this is not particularly clear but there are known processes which might help to elucidate it. This paper (also on kidney transplants) suggests that there is a specific downregulation of the activity of CTLs directed against antigens presented by the direct pathway, and that this could be caused by anergy, deletion or regulation. The authors suggest that the most likely cause is an effect of the chemotherapeutics (here MMF and azathioprine) on the T-reg cells, and they speculate from the tests they did (the Discussion of the paper has the details) that the cessation of suppression of T-regs that occurs during the taper is what is responsible. They also mention a role for IL-2 signalling (necessary for T-reg function, and some immunosuppressants suppress it leading to rebound on tapering) and dendritic cells (whose costimulatory function may be altered by MMF).

As to the precise mechanism, it is not yet particularly clear, but it is thought that in the interaction between a suppressing T-reg cell and a CD4 effector T-cell, the latter actually induces the T-reg cell through as yet unknown mechanisms, so that continued activity of T-cells (e.g. in chronic inflammation or the presence of an allograft) may upregulate T-regs that suppress them. It is known that T-regs are important in downregulating chronic inflammation (presumably this is responsible for the pattern in the first graph I reproduced above where the activity against donor cells seems to drop more than that against control cells, even on high immunosuppression), through mechanisms which have been hypothesized to include CD4 T-cells undergoing receptor-ligand interactions with T-regs and providing signals to them to upregulate their production of IL-35 (which is important in suppressing all types of T-cells). Given that it is known that upregulated suppressive activity of T-regs in chronic inflammation downregulates the immune responses of all non-T-reg cells, it appears that donor-reactive T-helper cells will induce T-regs which will then downregulate donor-reactive CTLs. This paper I mentioned previously postulates that on release of immunosuppression this population of T-regs would bounce back and greatly downregulate the donor-reactive CTLs and T-helper cells.

This paper also mentions the fact that an introduction of tapered mycophenolate mofetil in liver transplant patients promotes immunological tolerance to allogeneic transplants. They mention the effect of this on T-regs as well as other immune cells.

For interest, this paper presents some interesting alternative speculation on the nature of the T-regs involved in organ transplantation tolerance. In certain cases, self-tolerance may develop to 'new' tissues, and the authors postulate that the main T-regs involved in transplantation tolerance are newly formed in response to the prolonged presence of the allograft, rather than predefined. Because of this, the tolerance might develop to some extent regardless of the chemotherapeutic regimen.

Finally with regards to tacrolimus, this study has data on the immune response during weaning off the drug after an intestinal transplant. They found that patients with a low immune response prior to weaning had a better response to the weaning, and that their immune function remained low after weaning. This is a bit different to the MMF situation I mentioned above where immune function in general seems to return and only donor-reactive immunogenicity remains low (this tacrolimus study doesn't specifically mention the effect on infection rates, but their Figure 7 seems to imply that those patients with low immune function (presumably those weaned) had lower intervention rates). Specifically the authors conclude here also that self-downregulation of the immune system (probably by T-regs) is likely to be the cause.

So in summary it is not yet fully elucidated as to why we can do this, but the upregulation of T-regs that downregulate donor-specific effector cells, and (at least for certain chemotherapeutics) the release of T-reg suppression on tapering may be important.


Why is there extreme itching when we touch a hairy caterpillar? What are ways to stop itching? I mean there are lot of caterpillars or hairy caterpillars to be more precise when we touch those hairs we get extreme itching on that area i want to know why we got that itching? Ok i know that it must be some chemicals but which? And if one has got itching how to remove it?

It would seem that you're referring to caterpillars that have urticating hairs, such as the goldtail moth caterpillar.

Erebidae similis

  .. when we touch those hairs we get extreme itching on that area i want to know why we got that itching?

In this case, the itching sensation is the effect of a hair-specific, soluble protein known as Thaumetopoein. According to this publication, in where they studied the urticating hairs of the Thaumetopoea pityocampa moth caterpillar when applied to guinea-pig skin:

  The hairs are hollow inside with sloping spikes toward the distal end. There are no holes or pores on the hair and the irritating factor can only be obtained by crushing the hair. This suggests that when stinging occurs the hair is broken in the skin and the substance [Thaumetopoein] is released.

More information about this immunological reaction begins on page 5 (numbered 350).

  And if one has got itching how to remove it?

Remove all caterpillar hairs by first using tweezers to extract any embedded hairs, then the sticky side of tape to remove surface resting hairs. Do not use your bare hands, as this will only spread the caterpillar hairs.
Rinse the affected area with warm water & soap.
Apply some kind of hydrocortisone cream.

Poison.org - Caterpillar Stings


Absorption rate of Infrequently eating animals? Clearly, creatures such as us humans, after vastly increasing the entropy of our food, expel most of the mass that we consume.

Some creatures, however, do NOT get the opportunity to eat nearly as often, even though these creatures are if anything more competitive (and perhaps cannibalistic!) than we are - snakes come to mind here, as do spiders.

Such a lifestyle implies that growing large - or at least to adult form - quickly has a huge advantage evolutionary.

So the awkward question that arises is thus: do such animals have a higher "absorption rate", if you will, then humans and other frequent feeders?

In other words, do such animals maximize their diet by incorporating more of the mass of their food and expelling less of it, or is there some physics/chemistry which makes this difficult?

Thanks!

I'll take a stab at this.

What fraction of your food is absorbed and what fraction is expelled is a function of what kind and how much indigestible material there is in the food, and not related to how often the animal eats.

How often an animal eats is a function of its metabolic demands(how many calories it needs) and how many calories it can get in one meal. Reptiles, as ectotherms, have a lower metabolic demand than endotherms. In addition, snakes can swallow huge amounts(relative to body weight) of high-calorie food in one sitting. As a result, snakes eat infrequently. Pet snakes are fed weekly or biweekly, depending on a number of factors. A reticulated python can swallow and digest something up to its own body weight. Ten weeks of digestion gives 1.4% of its own body weight daily, even without fasting.

Elephants are a migratory large mammal and eat about 4% of their body weight each day, more or less. This takes about 12-18 hours to collect, according to these people.

Elephants eat high-fiber, low-calorie foods, and as a result about 20% of their food mass is turned directly into poop. They feed often, and don't absorb much. Hummingbirds eat constantly, consuming their own body weight in food each day, but poop almost not at all. Their feces contains the indigestible parts of their food, just as the elephant feces does. The different is that large parts of elephant diet is indigestible fiber, while a tiny part of the hummingbird diet is indigestible insect exoskeletons.

All creatures absorb as much nutrition from their food as they can, and expel the remainder. How much remainder there is depends on what kind of food they eat.

Growth rates versus digestion rates and mass intake is a totally different and much more complicated question. Generally speaking, the growth-limiting factor is DNA replication or an essential acid or mineral deficiency and not a raw mass problem.


What is the lower temperature limit for ion channels function? What is the cold-block temperature of ion channels? (not of nerves or axons)

The lower temperature limit of ion channels likely is dependent on various factors, including the type of channel and the recording conditions (tissue type, medium etc.). Reports on the suppression of voltage spikes (i.e., the inhibition of action potential firing) range from 1 to -20oC in squid axons, dependent on the species (Leuchtag, 2008). I couldn't find information on specific channels.

Reference
- Leuchtag, Voltage-Sensitive Ion Channels: Biophysics of Molecular Excitability (2008)


What kind of snake is this? First, we are located in Missouri. In between St. Louis and Cape Girardeau. St. Francois county to be precise.

We just walked outside and found this on the porch so we carried it off. Normally this wouldn't be a big deal, but we have a little one now and I didn't want to take any chances.

The snake, pictured below, was approximately 6 inches long. He seemed timid in nature, he didn't let us get very close to him before he started to slither away.

I assumed he was a juvenile black rat snake, from my highly deductive google searching, but I also know that snakes sometimes change color, shape and design as they get bigger. So I wanted to find out if my guess was correctly or completely mistaken. Thanks for you help!

Great find!
I'm pretty certain that is actually a Prairie Kingsnake (Lampropeltis calligaster - likely the subspecies L. c. calligaster).  The biggest indicator to me are the two alternating rows of dark spots on sides, with some blotches fusing.  They are distributed all over Missouri, although pretty rarely seen due to their microhabitat:

They tend to be fossorial, spending much of their time underground and
out of sight. As a result, there is little known about the biology and
status of these secretive snakes. Most [prairie] kingsnakes are observed
hiding under boards or other debris or crossing roads on warm
evenings.

I actually used to study herpetology in St. Louis, and we caught a few of these.  The juveniles tend to have well defined spots that fade in time, although there is some degree of polymorphism here.  Looks like yours is somewhere in between.  See pictures below for reference.
Juvenile:

Adult:

Worth mentioning these snakes are nonvenomous, and typically docile.
Photo cred: Edward Prenzler


What are the best detection medias for cholera? I heard this fact that you can use some [hypertriade] for vibrio cholera diagnosis which has compontents

sucrose (yellow)
mannose (yellow)
arabinose (do not ferment; stay dark pink)

I did not find this hypertriade agar on Google.
It reminds me of Egg Yolk Agar, but I think cannot be it because of the arabinose.
Otherwise, it seems to be similar.

What are the best detection medias for cholera?

You should use Thiosulfate-citrate-bile salts-sucrose agar for the detection of all vibros, including cholera.  When cholera is presant, you should expect round, largish (not huge), yellow colonies.  This is the CDC recommended diagnoses method.

Again this question might be better phrased "what are the best detection medias for cholera," or "what plate screens should be conducted when vibros are suspected?"


What causes the localization of myoglobin in turkey to regions of muscle tissue? I've read that myoglobin localization is responsible for the darker colour of leg muscles in turkeys. Why does this localization occur in terms of any of cell biology, molecular biology, or biochemistry? I'm not looking for bigger picture explanations at the levels of physiology or evolution, although I understand that they'll be connected to this question.

"Localization" is probably the wrong term, but I think I know what you mean... It more has to do with "expression."  While the exact mechanism to my knowledge is not elucidated, it has to do with the type of motor neuron innvervating the fiber.
This has been demonstrated by studies where they cross-inervated; that is, they took the neurons which usually innervate Type I muscle fibers and innervated Type II muscle fibers with them and vice versa.  The Type I fibers took on fast glycolytic properties, whereas the Type II took on the slow oxidative features (such as higher levels of mitochondria and myoglobin that you're talking about).

Source:
Sherwood L, Kell R. Human Physiology, First Canadian Edition. pp. 282-283.


How do I find a protein from this DNA sequence? I have a DNA sequence from a sequencer. How can I determine what protein is it? I tried some translator but it didn't help. What protein is this and how can I determine it?

The sequence: CGTTCTATAGATACGCGATGACGGTATACCATCCGCAAAGT

Thank you very much!

You might want to try searching against NR/NT database using BLAST. This way you will get to know what this sequence might be similar too. The length of the sequence is too short to code for any meaningful protein.


Which life is supported in sterilized 100% pure water? As sterilized 100% pure water does not contain any mineral and ion, so which type life can survive in sterilized 100% pure water?

Of course many life forms can survive for some time in 100% water. A human for example can survive about 4 minutes in 100% water but I doubt this is what you are interested in! Although there is no commonly accepted definition of life, I think we can say that we all agree that any life form needs to reproduce or somehow grow. So I take your question as

  What life forms can reproduce or at least grow "potentially indefinitely" in 100% water?

Any life forms, to grow or reproduce needs matter to make its own constituents. As such, pure water won't provide with such nutrients and no life form can survive in the long run in 100% water.


How to deduce if RNA virus infection or DNA virus infection Is there any general rule to say this must be RNA virus infection and the other one DNA virus infection?

Example of a case: 5 children develop a bright red rash on the face and turns violet after a few days and then disappears. Then maculopapular rash appears on the trunk, buttocks and extremities. It soon fades from the trunk but persists on the thights and forearms. Two children have also had a slight fever and a sore throat, but all were not terribly sick. What is the genetic material of the most likely causative agent?

Right answer is: Single-stranded DNA, since most probably causative agent is erythema infectiosum caused by parvovirus B19.

I do not want to remember all microbes by heart.
How can you deduce that this must be a DNA infection and probably single-stranded?

If you mean simply by looking at symptoms, then there is no way, especially if in the context of a medical visit.  You're better off learning the usual suspects and figuring out the patients risk and likelihood for a given infection.  A good example is Hepatitis.  Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) have similar (enough) outward symptoms, but the former is a DNA virus and the latter an RNA virus.  In fact, looking at enWikipedia's list of acute causes, it's all over the place!

If you can actually assay for it in the lab, then of course.  Although...


Why are some human injections intraperitoneal? In humans, what benefit do intraperitoneal (IP) injections(old/cheap rabies vaccines, or cancer related injections) offer versus traditional intramuscular injections?

For example, where I live, the rabies are not administered right away after a bite because of the associated discomfort(cheap IP injections) or cost(newer intramuscular injections) they represent versus the low probability of a dog having rabies and the long incubation period(instead, the offending dog is observed carefully for 10 days to decide, or the vaccines are administered in the fourth day if not found). So, since speed of action doesn't seem to be an important factor, what are the benefits of IP injections?

IP injections are used for a variety of reasons:

The peritoneum provides a large surface area for absorption of drug (compared with intramuscular (IM) or subcutaneous); can thus inject a larger fluid volume.

Easier to inject that intravenous.

For some chemotherapy, such as ovarian cancer, IP injection is used to attempt to localize the drug near the tumor (it's through a catheter, rather than with a syringe and needle).  Essentially the goal is to provide chemotherapy to the abdominal region where cancer has spread rather than systemically.

 It is commonly done in animals, such as mice, because it is difficult to find a vein in small creatures.

https://en.wikipedia.org/wiki/Intraperitoneal_injection
http://www.cancer.org/cancer/ovariancancer/detailedguide/ovarian-cancer-treating-chemotherapy
http://www.ncbi.nlm.nih.gov/pubmed/20156151 courtesy of @AMR
http://cpharm.vetmed.vt.edu/VM8314/Administration.htm


How does a baby deer stand the day it's born? I know most creatures take time to learn some things.

Birds take some time to fly.
Human beings take some time walk or stand.

But in the case of the deer species, it's different. It can stand the same day it's born. Why is this so?

If you compare placental mammals in how much time they need to start walking, you'll see that deer are no exception. Humans are an exception.

Hypothesis of Obstetrical Dilemma

The hypothesis of Obstetrical Dilemma states that humans are born premature. We very much think this is because if we were to be born more developed (like other mammals), our big brain would not be able to make its way through the pelvis. Also, bipedalism leads to a narrower pelvis making the passage of the big brain even more problematic. For this reason, human babies are very dependent on the care of their parents for a long time. This hypothesis is called the Obstetrical dilemma (see Rosenberg 1992, Weiner et al. 2008 among many other papers as well as several books such as Ancient Bodies, Modern Lives for example).

Counter arguments to the Hypothesis of Obstetrical Dilemma

Note however that this hypothesis comes with a few potential contradictions, such as the fact that human gestation is no shorter than the gestation of humans' sister species. Indeed, in chimpanzees, for example, gestation lasts 243 days on average against 280 days on average for humans. These counter-arguments can be found in Dunsworth et al. 2012.

Thanks to @MattThrower and @AdamDavis for their helpful comments.


Finding and Comparing Homologous Genes I have a gene of of interest that I would like to compare between homologues. How does one go about finding a gene from known coding sequences across phyla? Afterwards I imagine I could do a Clustal sequence alignment to see how the sequences match.

There are various databases of homologs, for example:

eggNOG
Ensembl Compara (accessible via BioMart, I think)
Homologene
OMA
TreeFam

The advantage of using an existing database is that more sophisticated methods for detecting orthologs than simple BLAST searches have been used (see "Computational methods for Gene Orthology inference" for a review), and everything is already precomputed, so it's much faster. The downside is that all precomputed methods need to use a snapshot of the genomes from the past, so not all currently available genomes will be there.


How does use an action potential from innervation selectively modify tropomyosin over time? Within a myofibril, the myofilaments move past one another to product muscle contraction if and only if the actin binding sites are exposed to the myosin by locally removing the tropomyosin by binding it with calcium ions

What isn't quite clear to me however is: what does a pulse from a motor neuron do to the tropomyosin in order to to excite this initial change to move the tropomyosin away and expose the actin?
Then, how does the muscle cell and/or motor neuron sustain this state of contraction, and then finally decide to end this state of contraction and return the muscle cell to its relaxed state?
Also, where exactly is the tropomyosin going after it binds with calcium ions?

At the neuromuscular junction, motor neurons release acetylcholine which binds to nicotinic acetylcholine receptors on the muscle. These receptors are ligand-gated ion channels that are permeable to small cations.

Opening these channels depolarizes the muscle cell membrane, which causes the opening of calcium channels, primarily on the sarcoplasmic reticulum (SR) for skeletal muscle. The key channel is called the ryanodine receptor and is either mechanically coupled to a voltage-gated calcium channel (skeletal muscle) or activated by calcium released from voltage-gated calcium channels (smooth & cardiac muscle), but in both cases the change in voltage is the initial signal.

Calcium concentrations are very low in the muscle cell at rest, but high within the sarcoplasmic reticulum so calcium rushes through and some of it binds with troponin (not tropomyosin itself, but they are associated/attached with one another), which releases the hold of tropomyosin on the actin filament.

The calcium-bound tropomyosin doesn't go anywhere, but as calcium is quickly pumped into the SR or buffered up by calcium-binding proteins, troponin is no longer bound to calcium, allowing tropomyosin to block the myosin binding sites.

The increase in calcium concentration is transient, and travels in a wave down the muscle. If there are no further action potentials, the muscle will relax. Constant contraction requires a constant train of action potentials, and the overall strength of the contraction can be regulated by the firing rate of the motor neuron.

The Wikipedia pages for muscle contraction, tropomyosin, voltage-gated calcium channel, and ryanodine receptor can all be helpful. I'd also recommend a basic textbook on neuroscience, which typically covers neuron effects on muscles and some of the mechanics of muscle contraction. I typically recommend Purves, see https://neuroscience5e.sinauer.com/ or a library or anyplace you get books from (any edition is fine).