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Is working with (nitrile) gloves around a bunsen burner safe?
Recently I have started in a new microbiology lab, and with a new lab come new habits. When I was working with my bacterial (liquid) culture next to the flame (Bunsen burner) wearing nitrile gloves, my colleague warned me to not wear gloves close to the flame. Personally, I never experienced any problems with them and I think that wearing them provides better sterility.
Is it more dangerous to work with gloves close to the Bunsen burner than without?

new microbiology lab

What're the entry requirements for your lab? If you're working in BSL-2 or greater, the appropriate PPE ensemble is listed and required at all times while you're in there. Likewise, gloves are required whenever you're in contact with potentially infectious materials (OSHA 29CFR1910.1030). There shouldn't be leeway to decide when and when not to wear your PPE ensemble.
As bunsen burners do present a burn hazard, your work with a bunsen burner should be preceded by general lab safety training, and subject to work practice controls. It's safe to wear nitrile gloves working with an open flame, and your gloves are not readily combustible. Burns will typically result from a failure to exercise universal precaution and/or use the burner properly.
If you're working dangerously close to an open flame or with heated materials, consider controlling for injury with thermal gloves, tongs, or engineer out the burner with a biosafety cabinet.

Wearing gloves increases the risk of injury when working next to an open flame since they can melt onto your hand.
Not wearing gloves increases the risk of infection when working with pathogens.
As for sterility, standard examination gloves may be helpful but are not necessary. The gloves aren't packaged sterile, you don't use sterile technique when putting them on, and nothing you touch with them is sterile.
So, whether or not you wear gloves near a flame really depends on what you're doing and the safety requirements of your laboratory.


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Can there be multiple EPSPs with constant current injection to a neuron?
I am performing a current clamp experiment and measuring the change in membrane potential of a neuron with different current injections. A constant current of 50pA is injected to the neuron for 100ms. The current is not enough to cross the threshold for the neuron so there are no action potentials. But will the neuron have multiple EPSPs in this setup?

If you stimulate the soma you shouldn't get any EPSPs except for spontaneous but they'd have to be larger than the membrane depolarization you induced. You expect to see a step increase in membrane voltage.

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Why does decreasing ion channel density result in an action potential not firing?
I'm pretty confused, when i run a simulation of an action potential reducing the sodium and potassium channel densities gradually over time results in an action potential not being fired, and when i only reduce sodium channel density it stops the action potential from firing even faster. My question is why? what role does density have in firing an action potential?

It is very straightforward. More the density of sodium channels, more the influx of sodium ions. More the influx of sodium ions, more the depolarization. If there are sufficient sodium channels, then the large influx of sodium ions will cause membrane depolarization above the threshold value, thus resulting in firing. If the density of channel is reduced, the depolarization value will not cross the threshold. Thus causing a net change in membrane potential, but not firing.
Potassium channel acts in coordination with sodium channel. Only if there is an influx of positive sodium ions into the cell, potassium channel will act and release potassium ions outside the cell in order to maintain the membrane potential. If sodium channel is reduced, no further processes happen, thus no firing.

Actually, the depolarization can still cross the threshold given sufficient synaptic input even with a reduced sodium channel density.
Also, in the case where only sodium channel density is reduced, the rate of sodium influx will be lower than the rate of potassium outflux and hence action potentials will be harder to produce

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Is summation linear in a passive membrane?
I am not too sure what it means for summation to be linear? I am running a simulation and as I decrease time for the second EPSP the amplitude decreases. Does summation being linear mean that there is a direct negative linear relationship between delay of onset and amplitude? I also noticed there is no change when I double or triple my conductance value.
I am just not too sure what the relationship is telling me.

For a membrane to satisfy the conditions for linear summation implies that when two EPSPs of amplitude $A$ and $B$ are summed at the integration zone, the resulting output signal will be of amplitude $A+B$. Since the signal dissipates due to time and length constants, increasing the delay between the two inputs means that the later input will be dissipated so $A+B$ will be smaller than it would have if the delay was shorter. Under this scenario, inputs $A$ and $B$ are still summed linearly. However, if the delay is shorter than the time constants or the inputs are delivered closer in space than the length constant, then you may get non-linear summation since the output signal at the integration zone will be larger than $A+B$.
Have a look here for more information (especially Figure 7):
Silver RA. Neuronal arithmetic. Nature reviews Neuroscience. 2010;11(7):474-489. doi:10.1038/nrn2864.


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How can I verify my true genetic relationship with my close relatives with simple physical traits?
Question
I don't know if it is ethical to ask a question like that, but I would like to know every simple physical trait that I can observe on me, my parents and my siblings which are regulated by a single or really low number of genes.  I don't want any disease-related traits, just simple traits that could illustrate genetic relatedness.
Already done search
During my research I've found about:

Hair on the second phalanx which is controlled by a single gene and absence of hair being recessive. (Recessive means you need two copies of the allele to have the trait absence of hair!) So if both parents have the trait absence of hair (on second phalanx), every child must have it as well.
Merged ear lob is also a recessive trait.

These are some for which I am not sure of the underlying genetics.

Hair in V on the forehead
Presence of dimples
Able to make a U with tongue
Able to detect Phenylthiocarbamide (PTC)

Don't hesitate to answer with references
EDIT: This site is saying that both hair in second phalanx and merged ear lobs are not as simple as they seemed...
Question: What trait can I use to illustrate genetics?

What do you mean by "physical trait"? I assumed you meant something visible, but "Able to detect Phenylthiocarbamide" doesn't come under that. Put another way, what would a "non-physical" trait be?

Well, it would mean something easy to assess for a classroom (and no lab studies), To be honest I wasn't thinking about PTC when first writing the question. for example blood type is not easy to assess without a lab. I agree physical is not the best way to say that

Here are the answers for your four questions:

Widow's peak (hair in V): dominant: Dominant and recessive characteristics, blinn.edu; Dominant Inheritance, Genetics Generation
Dimples: irregular; tendancy toward dominant *: Mendelian Genetics, uni.edu; What Is the Genotype for Dimples?, seattlepi.com; Understanding Genetics, genetics.thetech.org
Curling tongue: complex; tendancy toward dominance: Myths of Human Genetics, udel.edu; Debunking the biggest genetic myth of the human tongue, Cathrine Woods
Phenylthiocarbamide detection: dominant: Phenylthiocarbamide tasting, Encyclopedia Britannica; Genetic study of phenylthiocarbamide (PTC) taste perception, Egyptian Journal of Medical Human Genetics, Volume 13, Issue 2; PTC The Genetics of Bitter Taste, genetics.utah.edu

Hope it helps!
*See comments

So i shouldn't use Curling tongue to illustrate genetic trait :-(.

@Untitpoi probably not.  There's even some discussion about the phenylthiocarbamide gene being more complex than a simple dominance.

I found that Dimples is irregular as it can change along the life (like curling tongue) http://learn.genetics.utah.edu/content/basics/observable/

Hmm, interesting, I wasn't aware of that one.  I'll edit to reflect that.

Well these was more complicated than i have expected, almost no trait are really controlled by one gene... the only one i have found with no doubt on it is dry earwax http://udel.edu/~mcdonald/mythearwax.html

"no trait" is a bit of a harsh judgement when so many single genes control so obvious traits like having a symmetrical body plan, two fore and two hindlimbs, five fingers... :) to find inter-individual differences within one species, you're looking at extremely high-level genetics.

The other side of this is that you're unlikely to find common genetic traits that are shared by close relatives, yet not fairly common in the generatl population.


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Technical reason that specialized embryonic cells form
During the embryonic stage of human development, rapid cell division occurs and specialized cells form to build the various parts of the developing fetus.
I'm curious:

Why technically do specialized cells (such as brain cells) form?  I suspect this is due to a DNA sequence, but why chemically / mechanically should a genetic combination cause a certain specialized cell-type to form?
Have we (the international scientific community) reproduced the fundamental chemistry that causes any specialized cell-types to form?

There is indeed chemical signaling that triggers the differenciation. There are gradients of chemical species during the development. Look at https://en.wikipedia.org/wiki/Morphogen ! There are also other references there.
PS: there is a stack exchange question from today about something related Can gap genes delay their expression?

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Nocioception (pain perception) in subcutaneous tissue
There seem to be no nocioceptors (pain and temperature sensitive nerve endings) in subcutaneous fat. there are nocioceptors and other receptors in veins running through fat, but these can be avoided. Does this mean that subcutaneous fat can be cut, or otherwise traumatised, such as with diathermy (burning) without causing pain?

No nerves no pain I guess...

"no nociceptors in subcutaneous fat"

Well nerves innervate tissue, but only the layers of skin above the hypodermis (Subcuteaneous fat layer).
You are correct.
If one was to burn below this layer they would not feel pain in that area due to having no nociceptors.
There is a great Kharn Academy video on this topic here.

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For how long can animal body cells survive outside the body?
I'm researching on the topic that if bacteria have souls then animal cells and plant cells also do for an article.
1) Is there a way to make any of the body cells survive outside the body for a reasonably long time?
2) What is the longest time that human cells have survived outside the body?
3) Can we consider each human body cell as a living thing, the same or more complex than a bacteria? Why? Why not?
4) If a cell is unable to survive outside the body, is it considered to be not a living thing in biology?
5) What are the properties of a living thing definition that animal body cells do not meet?
6) What is the stance of biologists on animal cells being living things?

Whoa whoa whoa. Too many questions. Choose one or two of them, not more. You can ask the other ones in another question.

Partly duplicate of: https://biology.stackexchange.com/questions/7053/can-you-consider-a-human-as-alive-or-is-it-the-cells-on-the-body-that-are-alive?rq=1. Disregarding all talk about "souls", the question revolves around the definition of life.

depends which ones, and the temperature, and protection, and robust attributes.

HeLa cells would be a classical example of a human cell that can live indefinitely outside of the body.

I am voting to close as too broad because the post contains way too many questions!

The concept of soul is undefined in science. Please use terms that are clearly defined or define them in your post.

The soul part might be better suited to the philosophy site, or to the one for your religion of choice. For survival (in culture) outside a body, AFAIK the record is HeLa cells, which have been cultured since 1951: https://en.wikipedia.org/wiki/HeLa

I think it is very likely that this will be closed as "too broad" in the near future, but if you plan to narrow it down to (2), then you need to clarify whether you mean a cell line or an individual cell. Either way, it should be fairly easy to answer (incidentally if you mean option 2 then it's not far off https://biology.stackexchange.com/questions/45790/which-are-the-last-cells-of-the-human-body-to-die, but that doesn't have an answer yet).

As @LinuxBlanket stated, that's too many questions. But I thought this interesting so wanted to answer anyway.

I'm researching on the topic that if bacteria have souls then animal cells and plant cells also do for an article.

Since there's no evidence of "souls" anywhere, the topic is moot. I encourage you to read this.
Concerning your main question

Can animlal body cells survive outside the body? For how long

That has nothing to do with a soul - if souls did exist, then they'd only really matter when the organism dies. So how long something lives has nothing to do with your topic.
You should also think about what "alive" means, as there isn't a solid definition in Biology. usually the definition is around replication and/or metabolism, but then would you say a virus is alive? If yes, what about prions? If you cut a tree to the stump, when exactly does it "die"? Where do you draw the line?
OK, to answer your questions.

Yes. Think of a cell as an enclosed unit that metabolises and respirates. As long as the cell gets what it needs to continue those two processes, whether within the tissue or in a synthetic setting, it'll "survive". See this.
So as I explained, you can keep a cell ticking along as long as you can keep those basic processes going. At some point, a cell will want to replicate. So now you have to think - is my 1 surviving cell becomes 2, then 4, etc., then cell number 1 dies, am I still classing it as survival? If you want to keep cell number 1 alive indefinitely, you can adjust its environmental conditions to slow the pace of its life - cool the cell down, chemical reactions for metabolism and respiration slow down and the individual cell will "live longer". You can even freeze a cell for years then thaw it, and it will continue to live. See this.
That's for you to figure out. I encourage you to look up the definitions of cells, tissues, organs and organisms.
If a cell dies, it's considered dead. Even in biology.
Again, the definitions of "living" aren't set in stone. Personally, I reduce a living thing into these two requirements:

Something that replicates
Something that metabolises

But, I would say that animal cells meet the requirements of the general consensus more than viruses and prions (they replicate), but less than plant cells. This might be a good start to exploring why. But in short, animal cells tend to work together as tissues. Plant cells are a little more viable on their own. You can take a plant cell and grow an entire plant from it. You can only do the same with an animal if you use stem cells.

You should be able to answer that question yourself now =)

@MartinKlvana "that which can be asserted without evidence, can be dismissed without evidence". If no physical instrument can detect and measure soul, how did lamblichus could conclude that the soul existed in the first place? Just because I disagree with the Greeks, doesn't make me "against them". Pythagoras' theorum's grounded in maths, so it's difficult for it to be contrived. But they didn't have the scientific instruments of today, nor the discoveries of Newton, Einstein, etc., to test their assumptions and correct their errors.

@RonaldGreeff The 4 point is about if the cell doesn't have the ability to survive independently can it be considered alive according to biology. Not if it is dead, is it dead.

1) Is there a way to make any of the body cells survive out side the body for a reasonably long time?

HeLa cells have been living outside of their owner's body since 1951. Admittedly, cancer cells are trying hard not to die in the first place...

Cell lines are cancer cells or virally or chemically transformed cells that can continue to replicate indefinitely, as long as they get fresh media. Primary cells are native cells that are grown in culture, but they eventually die off. Some primary cells are short lived, both in vitro and in vivo, like neutrophils. Other primary cells can grow, differentiate, and replicate for weeks, particularly if growth factors are supplied.

I think it is unlikely that cells have souls, especially not culturable cells.


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Calcium and nitric oxide: does a numerical relationship exist?
Currently, I am trying to understand how nitric oxide and calcium are related during the production of the former (I am not a biologist nor a chemist, so my knowledge about these topics is very poor). I would like to know if there are some papers or experiments that present a model (or, at least, some numerical data) that relate the concentration of nitric oxide with the concentration of calcium.
I've read somewhere that one of the effects of nitric oxide in synaptic transmission is the reduction of calcium influx, but how does it happen quantitatively? I've started my research considering the model reported here where NMDA is assumed to be main calcium source so that the time derivative of calcium concentration is directly related to the NMDA current. Now, I think this model should be slightly modified if I would consider the effects of nitric oxide; I've found a model that describes how nitric oxide synthesis occurs, but what is missing for me is the link between calcium concentration and nitric oxide concentration.

It seems that you want to have a look at neuronal nitric oxide synthases. Not an expert on this but there seem to be some references in this paper:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3514612/pdf/fncir-06-00082.pdf

@vkehayas Thank you for your reply. I will read the paper you cited hoping to understand something more about the topic. However, at first glance the paper explains detailly all the biological aspects of nNOS but I don't see how nitric oxide is related to calcium. I will check later.


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What is the response vector in the fMRI GLM model?
In fMRI, univariate analysis typically makes use of the general linear model (GLM), where the relation between experimental condition and BOLD activity is estimated with a linear regression model for each voxel separately ("mass univariate model"). However, I found it surprisingly hard to find out what the response vector $Y$ contains. I am aware that it is some measure of the blood oxygenation level dependent signal (BOLD signal) - but what is measured exactly, i.e. what are the units? Is it the oxy/deoxy ratio, or is it another property?

Short answer
The units aren't important, and are typically normalized.
Longer answer
The name "BOLD" is actually very instructive: Blood Oxygenation Level Dependent contrast (or signal). BOLD is not directly measuring anything like oxygenated/deoxygenated ratio, or we would probably call it something more similar to that: oxy/deoxy ratio.
Instead, "BOLD" is just the MRI image you get when you set up the scanner properties in a way that happens to be influenced by the oxygenation level of blood. Oxygenation level is far from the only contributor to the BOLD signal, but experimentally you try to factor out any influences that are time-varying but not interesting, and you ignore baseline levels that don't change.
fMRI works because the transverse relaxation time T2 of water in blood depends on oxygenation of the blood. From the original paper showing BOLD contrast in a rat brain Ogawa et al. 1990:

At the 7-T field strength used in this study, T2 varies from 50 msec at 100% oxygenation to 4 msec at 0% oxygenation. The venous blood signal becomes very weak when the T2 value becomes comparable to or shorter than the echo time of the signal acquisition. At 60% oxygenation level, the estimated T2 value is 18 msec, similar to the echo time used in this report.

In other words, if you produce gradient-echo images with an echo time of 18 ms, the images you get show very different signal levels at 100% vs 60% oxygenation. Depending on the strength of your magnet, you can tune this time to go after the differences you want to see.
There is no straightforward way to compare images recorded in different conditions (i.e., different scanners, different parameters) on any useful scale of measurement. Instead, people typically report relative values, either in time or space. For this reason, you often see BOLD signals expressed as a % change or in terms of standard deviation (i.e., z-scores).
Ultimately, for fitting a general linear model it doesn't matter: you can freely scale a dependent variable without changing the structure of the model fit, all you influence is the interpretation of the magnitudes of the intercept and coefficients.
References

Ogawa, S., Lee, T. M., Kay, A. R., & Tank, D. W. (1990). Brain magnetic resonance imaging with contrast dependent on blood oxygenation. Proceedings of the National Academy of Sciences, 87(24), 9868-9872.

Hi Bryan, my question w.r.t to units was to clarify what the response vector is quantifying, and I am aware that scaling does not affect the strength of the relationships between response and regressors quantified in the GLM - so I am not quite sure still about the original question: Are you saying that the response vector quantifies changes in properties of the magnetic field?

@Pegah It's measuring a radio signal from magnetically excited hydrogen atoms. However, it takes a lot of signal processing to go from that radio signal to a 3-dimensional image. See https://en.wikipedia.org/wiki/Physics_of_magnetic_resonance_imaging


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


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How long ago did the mutation arise that gives rise to sickle-cell disease?
Is it known how long ago the mutation arose in Africa that gives rise to sickle-cell disease and protects from Malaria in heterozygote carriers?

Is it safe to assume that the mutation arose after the out-of-Africa migrations, since sickle-cell disease is almost exclusively prevalent in people with more recent African ancestry (i.e., black people)?

In a fairly recent review P W Hedrick surveys a number of gene variants associated with resistance to malaria.
He explains that:

The impact of malaria is thought to have increased between 10,000 and 5,000 years ago when there were the beginnings of agriculture and consequently more human settlements. During this period, the numbers of both the human population and the mosquito vector increased, resulting in higher spread of malaria.
  Recent molecular studies suggest that malaria in humans from Plasmodium falciparum may have originated from gorillas. Using these data, an initial timeline for the origin of P. falciparum as a human pathogen suggests that it may be more recent than previously thought.

As you can see from his Table 1 (reproduced below), the S variant of β-globin is suggested to have arisen 1440 years ago.

The study of the origin of sickle cell anaemia is complicated by the fact that the allele responsible is found associated with five different β-globin haplotypes (four from Africa, one from Saudi Arabia/India). This has sometimes been interpreted as indicating that the allele arose on several independent occasions. However, the picture is complicated by patterns of human migration, and recent papers suggest that the observed distribution of the S variant is not inconsistent with a single origin, e.g. this paper.


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How long ago did protein synthesis from DNA start?
How long ago did DNA start to include sequences that code for protein?

where have you looked for information on this? online, google, wikipedia?

Protein isn't synthesised from DNA it's synthesized from RNA.

I've googled it first yes, I could not find it. And yes, I realize that protein get synthesized from RNA, but the protein is coded in the DNA. My question is, when did DNA code start to contain information on the proteins that are the result of gene expression. Sorry if my formulation caused confusion.

There are two questions being asked here.
1) When DNA was used to encode RNA via DNA dependent RNA polymerase
It is uncertain if the Last Universal Common Ancestor (LUCA) had this enzyme. There is some debate.
Also some  DNA polymerases of family A, B are structurally related to RNA polymerases https://www.ncbi.nlm.nih.gov/books/NBK6360/. So DNA may have come after RNA. The switch to DNA has been proposed to be a result from a reaction to the evolution of RNAse.
2) When RNA was used to encode protein via ribosome
LUCA has ribosome. So LUCA had proteins made from RNA
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2926754/
And LUCA has been estimated to have appear around 3.5-3.8 billion years ago. https://en.wikipedia.org/wiki/Last_universal_common_ancestor

Please define the abbreviation LUCA in your answer.

Last Universal Common Ancestor.

I worked that out, but I shouldn't have to. Define it in your answer so that everyone knows. The use of undefined acronyms is lazy and inconsiderate and decreases the value of an answer.

DNA and RNA... which actually stand for Deoxyribose Nucleic Acid and Ribose Nucleic Acid.

I am afraid that this will not wash. More people know what DNA and RNA are than know what it stands for. As you are not willing to clarify your answer, then I shall your do it for you, although I hardly think it worth it for such a poor question. Also the last common ancestor hasn't been around since 3.5-3.8 billion years ago — that would imply it is still around. It was thought to have lived then.

Thank you very much JayCkat, I found your answer to be clear and satisfactory. Sorry we did not meet your requirements David :/


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Chart of blood pH across different animal species?
How does blood pH vary across species?  I can't find an article or chart listing this kind of information.
So far I've found bits and pieces like:

Human blood pH is nominally 7.4.
7.4 seems to be a good value for dogs and cats (¿and probably all mammals?).
For racehorses it seems to be roughly 7.4.
Silkworm, Bombyx Mori, blood (hemolymph) has a pH of 6.45 (larval) and 6.57 (pupal).
Bullfrog muscle(!) pH runs roughly 7 to 7.3.  (Link to The Journal of Experimental Biology article, PDF) It's not clear if this is also blood pH.

But no real comparison.
Is there an authoritative comparison of blood pH between: mammals, reptiles, fish, invertebrates, etc.?
Is nominal/average pH at least constant across all mammals, or across all reptiles, etc.?

Don't forget most plant life needs soil that has a pH of 6.0 to 7.4 to dissolve nutrients easily, so you might as well add plant life to your list

@TheVoid, Sure, any plants that have blood. (^_^)

Its all life that needs a pH of level of 7.4 to be in the Alkaline. That is wear life can thrive at its fullest potential.

in reptiles variation from 6.5 to 8.1 have been observed. ectotherms in general have a broader range. http://jeb.biologists.org/content/jexbio/203/13/2065.full.pdf

@John, that's the exact same reference I used and I don't see anywhere where it says blood pH was in those ranges.  What paragraph or table are you looking at?

oh sorry that was the reference for the ectoderm statement. here s the reference for the PH values. http://www.seaturtle.org/pdf/dessauerhc_1970_inbiologyofthereptilia_p1-72.pdf

@John, Thanks!  Just skimmed it so far, but it seems to show that baseline is about 7.4-ish but it lowers dramatically during dives or other activities where CO2 builds up.  That would be extreme (in the) ocean acidification. :)

Crocodiles can do some weird things with their blood and even have different ph values for different parts of the body, http://compphys.bio.uci.edu/BENNETT/pubs/65.pdf but crocodile circulation is weird to begin with.

for non-crodilian reptiles there is also a strong relation ship between body temprature and PH, this alone could account for why birds and mammals are so stable.

insects have some wide ranges too. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2140737/

birds average 7.5 -7.6 http://www.sciencedirect.com/science/article/pii/0300962982902006?via%3Dihub


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What does "out-titration" mean?
I am reading an article on developmental biology and cannot understand (even after searching the internet) what is meant by "out-titration".
For example, in this phrase:

We have previously shown that Drf1, together with Cut5, Treslin and Recq4, are out-titrated on chromatin by increasing N/C ratios in vitro.

From this article: Chk1 Inhibition of the Replication Factor Drf1 Guarantees Cell-Cycle Elongation at the Xenopus laevis Mid-blastula Transition
Thank you!!

It does seem oddly phrased, but is still understandable. The paper explains how the combination of low zygotic transcription and increasing amount of DNA due to rapid cell division can function as a switch to trigger the mid-blastula transition. Before this event, most factors in the cell are of maternal origin (ie they are not being expressed in the zygote) and are thus in limited supply. As cell division progresses, the stoichiometric ratio between these factors and DNA decreases until, eventually, there is more DNA than these replication factors. At this point, you could say that the DNA has titrated the replication factors in that there is no unbound form left. This is analogous to the equivalence point of acid-base titrations commonly encountered in first-year chemistry courses.

Thank you for your input! I had correctly understood the general sense of the expression, but was wandering if it was a specific process.

@BeatriceBaldi No, it's just part of the description of the process described in the paper. I often say something is "titrated into/out of solution", which I believe is a more standard phrasing.


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Is water released when a phosphodiester bond is made between two nucleotides during DNA replication?
I know that when two sugar molecules (like glucose) connect to each other, H2O is released because of the -OH and -H groups in both of the molecules. I want to know if the same thing happens when two nucleotides connect to each other during DNA replication.

Welcome to Biology.SE! What research have you done before asking it here?

yes there is no water release during phosphodiester linkages because the 3'OH of the growing daughter strand exerts a nucleophilic attack on the phosphodiester linkage between the alpha phosphate with the beta & gamma phoshate of the deoxyribonucleoside triphosphate.
During such formation there is no hydrolysis rather it would precisely be a transesterification type of organic reaction.
REFERENCES:TEXT BOOK OF BIOCHEMISTRY(T.M. DEVLIN)
https://en.m.wikipedia.org/wiki/Transesterification

No, nucleophillic attack by the activated 3'-hydroxyl on the α-phosphate of the incoming nucleoside triphosphate results in the formation of a new phosphodiester bond and release of pyrophosphate (PPi), which is subsequently hydrolyzed.

[image source]


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Can a human be made with ovum but without sperm?
This article says that scientists were successful in making a mouse using only a sperm and no egg (ovum). The article also states that this procedure could be applicable to humans.
However, I want to know why didn't they try with only an ovum?
Can a human be made only with an ovum, i.e. without sperm?

Nice question! It is actually very difficult to do so because humans, obviously, are far more complex than some animal species which naturally show parthenogenesis. Just to mention, there are female-only animals also present in nature, such as New Mexico whiptail, which reproduce only by parthenogenesis, meaning that it is not as impractical as one might think.
There have been many parthenogenesis tests on mice and monkeys, but they usually result in abnormal development. This is because mammals have imprinted genetic regions, where either the maternal or the paternal chromosome is inactivated in the offspring in order for development to proceed normally. A mammal created by parthenogenesis would have double doses of maternally imprinted genes and lack paternally imprinted genes, leading to developmental abnormalities. It has been suggested that defects in placental folding or interdigitation are one cause of swine parthenote abortive development.
During oocyte development, high metaphase promoting factor (MPF) activity causes it to arrest at the metaphase II stage until a sperm fertilizes it. The fertilization event causes intracellular calcium oscillations, and targeted degradation of cyclin B, a regulatory subunit of MPF, thus permitting the oocyte to proceed through meiosis. The most precise and exact mechanism is not known yet.
But this does not mean that it is not possible. Actually, it has been done quite a few times; once on June 26, 2007 by International Stem Cell Corporation (ISCC), and once (controversially) on August 2, 2007 by Hwang Woo-Suk. Even the procedure for parthenogenesis (in swine though) in lab is available. To initiate parthenogenesis of swine oocytes, various methods exist to induce an artificial activation that mimics sperm entry, such as calcium ionophore treatment, microinjection of calcium ions, or electrical stimulation. Treatment with cycloheximide, a non-specific protein synthesis inhibitor, enhances parthenote development in swine presumably by continual inhibition of MPF/cyclin B As meiosis proceeds, extrusion of the second polar is blocked by exposure to cytochalasin B. This treatment results in a diploid (2 maternal genomes) parthenote Parthenotes can be surgically transferred to a recipient oviduct for further development, but will succumb to developmental failure after ≈30 days of gestation.

The major problem with parthenogenesis in humans is the abnormal development of embryo. This has been accounted by a phenomenon known as genomic imprinting. Genomic imprinting is the epigenetic phenomenon by which certain genes are expressed in a parent-of-origin-specific manner. For example, if the allele inherited from the father is imprinted, it is thereby silenced, and only the allele from the mother is expressed. The death of diploid parthenogenetic or androgenetic mammalian embryos is determined by the absence of expression of the genes of imprinted loci of the maternal or paternal genome, which leads to significant defects in development of tissues and organs. How this exactly works is not known yet, but it is supposed that it evolved to prevent parthenogenesis. Bi-parental reproduction is necessary due to parent-specific epigenetic modification of the genome during gametogenesis, which leads to non-equivalent expression of imprinted genes from the maternal and paternal alleles. Thus, genomic imprinting seems to be ineffective during normal reproduction.
As a side note, in the article you refer to, the researchers did not just mix two sperms and produce diploid zygote or something like that. In the procedure, they injected a normal sperm to the above explained abnormal embryo, which later on proved to be viable. They, thus, showed that these kind of embryos can also become viable if they get fertilized by a sperm within time.
References:

Abnormal development of embryonic and extraembryonic cell lineages in parthenogenetic mouse embryos; Karin S. Sturm, Margaret L. Flannery, Roger A. Pedersen
Parthenogenesis - Wikipedia
Patient-Specific Stem Cell Lines Derived from Human Parthenogenetic Blastocysts; E.S. Revazova, N.A. Turovets, O.D. Kochetkova, L.B. Kindarova, L.N. Kuzmichev, J.D. Janus, and M.V. Pryzhkova
Genomic imprinting is a barrier to parthenogenesis in mammals; Kono T.
Genomic Imprinting and Problem of Parthenogenesis in Mammals; E. S. Platonov
Mice produced by mitotic reprogramming of sperm injected into haploid parthenogenotes;
Toru Suzuki, Maki Asami, Martin Hoffmann, Xin Lu, Miodrag Gužvić, Christoph A. Klein & Anthony C. F. Perry
Stem cell fraudster made 'virgin birth' breakthrough; Silver lining for Korean science scandal; 3 Aug 2007, Christopher Williams

"As a side note, in the article you refer to, the researchers did not just mix two sperms and produce diploid zygote or something like that."I asked that whether it can be fulfilled without sperms.Anyway,a beautiful answer

It was just to clear things out, just in case someone might get it that way. Thanks :)

Also, the cloning process that made Dolly the sheep would work on humans as well. That just involved nuclear transfer from one adult cell to an ovum.

@swbarnes2 maybe it could work, but I couldn't find any scientific paper related to its testing on humans. Also, I'd speculate that it would also lead to some kind of abnormal development of resulting embryo; you never know where complications might arise.


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After the primer is removed from the leading strand, how does DNA polymerase I add dNTPs without a 3'-OH?
I have a question about replication in prokaryotes. I learned in school that:

DNA polymerase needs 3'-OH to add a dNTP.
The chromosomes of prokaryotes are usually circular.
The primer in the leading strand (of course the primers in the lagging strand too) is removed by the 5'→3' exonuclease activity of DNA polymerase I.

It makes sense that on the lagging strand the primers are removed and then replaced by new dNTPs using the 3'-OH of the previous Okazaki fragment. However, for the primer on the leading strand, there is no Okazaki fragment upstream and thus no 3'OH that DNA polymerase can use for polymerisation.
How is the primer replaced by new dNTPs on leading strand?

It seems you're asking about the leading strand, but you may have made a typo that made it unclear what you are actually asking. I tried to clarify your question, but please roll back the edit if it changed the meaning.

@canadianer — I think you must be right. I have had to scrap my answer which assumed the lagging strand, because the question makes no sense for the leading strand where the primer is the growing DNA chain which is not removed.

@David Sorry for making your original answer obsolete. However, the leading strand does have a primer at the origin of replication that needs to be removed. The gap can be filled using the upstream Okazaki fragment as a primer. See this image for example.

@canadianer — No problem about my original answer. And you're right, but I wasn't thinking about the ori. I doubt the poster was either, but I guess I should update my answer to cover that. That way it will be of some value. Tomorrow perhaps.

@canadianer — where was your figure from? I have now  extended my answer and should acknowledge the source.

@David Nice update. The image is from the following website: http://www.mun.ca/biology/scarr/iGen3_03-09.html

Can someone please explain what they mean by stating that the RNA primer on the leading strand does not need to be removed? I mean it is an RNA hybrid. The DNA pol cannot initiate replication by itself and can only elongate the primer. Thus primer removal is required. I have the same question as the poster and haven't found a satisfactory answer as yet. If someone does, pls do share.
Thanks!

@SarveshAnandas — If you are referring to the statement in my answer you should comment on my answer, not the question. But I would read that answer again, where I first talk about the situation at the replication fork (where the leading strand is not being primed by RNA) and then consider the case of the origin of replication (where it is and needs to be removed).

The leading strand post-initiation
First consider the DNA replication fork after initiation has occurred.
The 3′-OH primer on the leading strand is the 3′-end of the strand of DNA being synthesized in the 5′ to 3′ direction (circled in the diagram below, modified from Berg, Biochemistry). It is not removed because there is no need to do so. (The primer on the lagging strand is only removed because it is RNA.) So the problem posed in the question does not arise.
Remember that the reason for Okazaki fragments is that there is no DNA 3'-OH primer for the lagging strand, so a temporary RNA 3′-OH primer is generated instead, RNA polymerase — unlike DNA polymerase — is able to copy DNA without a primer. There is no such problem for the leading strand.

The leading strand at the origin of replication
As @canadianer points out in a comment, the remarks above do not apply to the initiation of DNA replication, the single instance where the leading strand must have an RNA primer. In the case of prokaryotes such as Escherichia coli replication proceeds in both directions so that a short time after initiation one has a replication bubble as shown in the figure below (adapted from Russel, iGenetics) :

It can be seen that, at the origin, the 3′-OH of the DNA from the lagging strand of the other direction of replication (boxed in red) can act as a primer for the DNA synthesis function of DNA polymerase I, after its exonuclease activity has removed a nucleotide from the start of the RNA primer on the leading strand.
References
Berg et al. Ch.27
The Cell, Ch. 5
Sandwalk: Blog page
Footnote
There was a typo in the original question which caused confusion about which strand the poster was concerned with. This answer assumes the leading strand.

I am very sorry for my late response, and I guess someone already modified my question, but indeed my question was how the primer on the leading strand at the site of initiation could be replaced by a DNA fragment when there is no 3OH' (on the lagging strand, the 3OH' of an okazaki fragment just behind the primer can be used), but as you say, we have a 3OH' from the lagging strand which results from the replication in the opposite direction!!! Wow, that was very interesting. Thank you.

However, I still have a small question if you allow me. I thought that the leading strand starting from the Ori would continue until the very end (when two forks meet) without any addition of another primer, so I'm confused about the first diagram. Does it mean that during the replication in procaryotes (my question has been always the case on procaryotes), on the leading strand, far from the initiation site, a few primers are added and in this case they are DNA primers? Or the explication with the first diagram is a general description of the replication in eucaryotes? Thank you so much.


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How do chemists calculate the existence of billions of organisms?
So the packaging of Bio-Cultures Complex says that it contains a minimum of a billion viable organisms per capsule.
How has such an estimate been drawn?
Have they counted a smaller amount and then multiplied it?

Aren't you just describing statistical sampling?

Have you mistaken chemists for chemists?

It says a "a billion viable cells". The viable is important because it tells you that they employ a method that determines whether the cells are alive or dead. Most likely they did a simple colony count.
The approach is simple, you take bacteria in suspension, serially dilute them in order to reduce the concentration to numbers that can be counted, and then spread onto a solid media plate (usually containing agar) and leave for 1-3 days (depending on organism) and count the number of colonies produced. You can then multiply up this number by the amount you diluted by to get the number of viable cells present in the original.
A billion is not a lot of bacteria. You can expect 100-1000 billion cells per ml in an overnight culture of these bacteria.
Looking at the product description, it specifically mentions CFUs (colony forming units) so I think we can be pretty sure that this is the approach they are using.
(Note that this is standard microbiological technique rather than something chemists would be doing)


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How are single-stranded binding proteins removed from the lagging strand during DNA replication?
The lagging strand, downstream of the Okazaki fragment, is covered in single-stranded binding proteins (SSBPs) during DNA replication. What is the mechanism which ensures that SSBPs are removed from the lagging strand to allow for the binding of the next Okazaki fragment?

Actually, there has been some evidence that the SSBPs keep the bases facing outwards so DNA polymerase can still replicate the lagging strand with the SSBPs on them. There has also been other evidence that they can pop off spontaneously.
You can learn more about this by watching the lectures on https://www.edx.org/course/molecular-biology-part-1-dna-replication-and-repair

Your answer may well be correct but there is no way for anyone to know without reference to some external source that supports your answer. At the moment it is likely to be automatically flagged as low quality by the system. Please take a moment to read the Help on writing the sort of answers that are appropriate here, and then edit your answer.


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Can 5 alpha reductase inhibitor drugs work for life or do they lose effectiveness?
Do 5 alpha reductase inhibitor drugs like finasteride and dutasteride lose their effectiveness over time? Why do some drugs, like in an HIV regimen, work for a prolonged time without tolerance whereas other drugs, for example antidepressants, have tolerance issues after a short time?

This is a very broad question. From the [help/dont-ask]: Your questions should be reasonably scoped. If you can imagine an entire book that answers your question, you’re asking too much.

As noted in a comment, a truly thorough answer to this question would require one or more books (1,2) or scientific journals (3), but a simpler, necessarily incomplete answer can be provided.
The short answer is: transmembrane drug transporters of the ABC family (4)
But what are those? Well, you should read the wikipedia article for a detailed description, but essentially they're proteins that burn energy in order to remove a broad range of drugs from the cytoplasm, making them less "bioavailable". The answer to why some drugs (or broad spectrum treatments with multiple drugs) are more or less susceptible to export by ABC family proteins is much more complicated (buy books from (1) and (2) or similar texts(5)), but the broad spectrum HIV regimen prevents resistance by a completely different mechanism (6).
Briefly, ABC transporter-mediated resistance involves no evolution, simply a "transcriptional response" to the presence of harmful drugs, while HIV actually evolves to become resistant or immune to antiretroviral drugs. However, it's difficult or impossible to be virulent (fast replication) and hardy (drug resistant and/or immune system resistant) at the same time, so mutations which increase resistance to one drug also decrease virulence - if you treat HIV with enough drugs then the mutations required to be resistant to all of them will result in a virus that has very poor virulence.
(1) http://www.wiley.com/WileyCDA/WileyTitle/productCd-0470927941.html
(2) https://www.amazon.com/gp/search?index=books&linkCode=qs&keywords=9781782620693
(3) https://scholar.google.com/scholar?q=human+drug+transporters&hl=en&as_sdt=0&as_vis=1&oi=scholart&sa=X&ved=0ahUKEwjVh6-a8aPPAhVK1B4KHfxABSsQgQMIGjAA
(4) https://en.wikipedia.org/wiki/ATP-binding_cassette_transporter
(5) https://www.google.com/webhp?sourceid=chrome-instant&ion=1&espv=2&ie=UTF-8#q=human+drug+transporters&tbm=bks
(6) https://en.wikipedia.org/wiki/HIV_drug_resistance


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Sodium concentration during action potential generation

At the peak of the graph, is the concentration of Na+ outside the cell more than inside? That must be to overcome the electrical force in the opposite direction.
When is the concentration of Na+ greatest inside the cell? At the peak assuming the Na+ channel close immediately at it then it is also greatest at 3. If there is still passage of Na+ then 3 is the maximum. Is this true or false?
One last question: is the inside of membrane actually negative, or only negative relative to the outside? In a galvanic cell for example, a given rod isn't actually negative, but it is negative relative to another.

As you said, it is negative relative to another.

Below is a schoolbook example of the membrane potential combined with the individual conductivities of Na+ and K+ during an action potential (AP) (Fig. 1);

Fig. 1. Membrane potential and conductivities of the two most important ions in AP generation. source: Physiology Web
And in Fig. 2 is an example of the currents of Na+ and K+ during an action potential (AP) (Fig. 1). Note that K+ stays high due to amanipulation of ion concetrations.

Fig. 2. Sodium and potassium currents during AP generation.
However, you ask about the concentrations of Na+ in the cell. As far as I know, this has not been investigated directly. Intracellular Ca2+ concentrations, for example, can be imaged with various imaging techniques, but absolute Na+ and K+ concentrations have to be measured with intracellular electrodes. So while the conductivities and the currents are depicted quite clearly in the above figures, they do not show the absolute concentrations of Na+ or K+ and I doubt it can be found anywhere in the literature. It can of course be mathematically deduced, by calculating the number of ions entering the cell using the Nernst equation and correcting that for the background effect of the sodium-potassium pump and other factors that alter Na+ concentration in the cell (protein transporters and what not). It will at least give an approximation of [Na+]i.

Thank for the information about the current and how absolute concentration weren't measured.
Can you just solve this question for me?
At the peak of the graph, Is the concentration of Na outside the cell is more than inside? because that must be to overcome the electrical force in the opposite direction
Because our book shows that at the peak the concentration of Na outside is lower than inside which is not reasonable to me.

@user3733086 the idea I have is that, even though the peak Na+ concentration inside is still greater than outside, the amount of Na+ that exits the cell is sufficient to revert the the electric potential. Remember that there are other ions intervening, and that the potential differences are measured in mV

See my answer to another question: the emphasis there is on resting potential but it is relevant to this one too. tl;dr: Very few ions actually move across the membrane (relative to the total number of ions present) during an action potential. The intracellular concentration of sodium does not change much during a spike, far less than 1%.


text:
How does the body count time in the short term?
So I've done some research and found out about the different circadian cycles that use chemical clocks to help us keep time in the long term (hours, days, etc.). This doesn't seem to explain how we can so accurately count seconds. Musicians can count time extremely precisely in even shorter intervals than seconds. Is it a chemical clock responsible? If you could explain the whole process to me it would be great. Thanks.

I've nominated this question for reopening because it is clearly about counting time in the short term, whereas the duplicate marked is merely about circadian rhythms. This question explicitly differentiates itself from circadian time and is talking about time on the order of seconds.

"One mississippi, two mississippi..."

@Charles But what biologically enables musicians to do so? By practicing, they must be essentially just fine tuning whatever biological function that helps us keep time. As an analogy when riding a bike, at first we must consciously make an effort to balance. Eventually we fine tune our vestibular system to the point where we can subconsciously do it. I am look for that "vestibular system" for hearing. At least I think this is the way it works. Am I right?

Detection of rhythm is a separate function from general musicality, but both can be affected by the same brain damage, or they can be independently affected:

A range of rhythmic deficits has been described, including the inability to reproduce rhythmic patterns or to discriminate between them, and the inability to perform music rhythmically, or to keep time to music, including dancing in time. These deficits may occur in combination with other musical deficits, such as impaired vocal and instrumental skills ... rhythmic and metric organisation can be differentially impaired in brain damaged patients, supporting the relative independence of functions of the rhythmic system. In terms of cerebral lateralisation, Peretz and Morais [43] suggested that metric organisation may be ascribed to the right hemisphere, whilst smaller rhythmic groupings are encoded by the left hemisphere. ... Neuropsychological studies of groups of patients, however, have generally shown more variable lateralisation effects, particularly in recent research [25,36,46]

--Modelling rhythmic function in a musician post-stroke
So it seems that the detailed neuroanatomy and function of rhythm isn't completely understood, but it is a fairly specific function.  One suggestion is that it's  linked to language ("We conclude, then, that this effect is linked to language dominance and not handedness." -- Rhythm and dominance), but I don't know how widely this is accepted.  Possibly Common neural mechanisms for explicit timing in the sub-second range. offers more insight, but I don't have access to the full article and the abstract isn't very helpful.


text:
moltype controlled vocabulary?
In submitting sequences using tbl2asn to NCBI/GenBank, the documentation states that there is a controlled vocabulary for the key "moltype", but no where on the Internet can I find a full list of that vocabulary.  "mRNA" and "genomic" are given as examples on several pages, and I can see from Sequin documentation what the GUI descriptors of all the vocabulary terms are (e.g., "genomic DNA"), but I can't find the terms themselves.  Any ideas where I can find this list?

Kind of a hassle, but could you download Sequin see what it outputs in the fasta for each molecule type?

I hadn't realized Sequin output fasta files.  I just checked, and it doesn't seem to include any of those descriptors in the FASTA file that will be exported when you use the Export command.

Sorry, I actually don’t know anything about it. Just a thought I had.

It was a good thought.  As you can see, I (perhaps inappropriately) edited my comment because I tested it out, and it didn't seem to work.

There is this "Controlled vocabulary for /mol_type qualifier" page created by the International Nucleotide Sequence Database Collaboration in 2013.  It says the allowed values are:

"genomic DNA", "genomic RNA", "mRNA", "tRNA", "rRNA", "other RNA", "other DNA", "transcribed RNA", "viral cRNA", "unassigned DNA", "unassigned RNA"

I found this as the second result of a Google search on moltype vocabulary.

I found that too.  The issue with this is that in the examples provided by NCBI, "genomic" is one of the valid values "moltype".  "genomic" by itself does not appear on that controlled vocabulary list.

Of course, another possibility is that the other NCBI documentation if invalid, and that this is the controlled vocabulary they use as well.

I just heard back from NCBI.  Even though this controlled vocabulary conflicts with their own documentation (which I suspect is out-of-date), it is the vocabulary they now use.

I've found an archived version of Sequin for Database Submissions and Updates:
A Quick Guide, published by NCBI.

moltype should use one of the following values. Example: [moltype=genomic]

genomic
precursor RNA
mRNA
rRNA
tRNA
snRNA
scRNA
other-genetic
cRNA
snoRNA
transcribed RNA

Great job!   That looks like it is what I need.  Odd that this isn't public.

The other possibility is that the OTHER documentation is out of date, and that the controlled vocabulary the mgkrebbs found is the one NCBI also uses.

@DavidMaddison Yes, it is odd. It may be worth contacting NCBI about it.

Yes, I sent NCBI a note asking about this earlier today.  I will report back!

See my new comment to mgkrebbs answer.


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Why does something taste less sweet after eating something else that is sweet?
Why does something taste less sweet after eating something else that is sweet, especially if you don't drink water in-between.

Welcome to Biology.SE! What research have you done before asking it here?

It happens for food of any taste, not only sweet.

It's a general flaw (IMO bad design) in organic/neural sensor frameworks where inputs tend to be measured relative to previous experience rather than absolute quantitative.
This happens with weights as well. There have been plenty of experiments where people are asked to pick up a heavy weight and then a light weight, then record/estimate the perceived light weight. The next day, they pick up a medium weight and then the same light weight and record the perceived light weight.
The 2nd recording turns out "heavier" because of relative perception.
Suggestion: Computer-mediated nerves designed to measure in absolutes.

Ugh, I can't disagree with you enough about it being a 'flaw.' Sensory adaptation is almost certainly a feature, not a flaw, and is incredibly well preserved across senses and species.

Downvote an otherwise fine answer just because you personally disagree with 1 part of it? pathetic... if relative measurements are a feature, perhaps all the measuring instruments you use should use relative measures, everything from weighing scales to CPU Hz configuration and the speedometer in your vehicle. While you're at it, perhaps your electricity and water meters should use relative measurements so you get a ridiculously large bill if your neighbor uses those utilities sparingly. Precision is a virtue, and mechanical precision is something that everyone should aspire to.

Have you considered that organisms aren't solving the same problems that machines are? I'm not saying relative measurements are good for all things, I am saying they are useful in biology. I'm downvoting because I think your answer is wrong, because it contains no references or explanation the process, and doesn't even contain the word "adaptation" which is the term given to this process in sensory systems.

"Precision is a virtue, and mechanical precision is something that everyone should aspire to." - Citation needed.

If your keyboard ever stops typing the precise keys you press, I'm going to laugh. While relative measurements might be good enough for primitive animal life, modern civilized society requires mechanical precision. Example consequences of lack of precision: missing your highway exit and ending up in the wrong town, accidentally putting lower amounts of food/drink in commercial packages and bottles (infuriating customers), and screwing up a recipe because you couldn't measure the ingredients straight.

When your brain starts receiving non-adapted sensory information, I'm going to laugh. While precise, invariant measures might be good enough for machines and computers, biological organisms need filters that make relevant information salient. Example consequences for not filtering out unnecessary information: not being able to operate a car at all because you are dazzled by the sun and unable to adjust, deafened by the roar of the road that you can't ignore, distracted by being bombarded by dozens of odors from your own body, the air coming in from outside, and the upholstery.

"When your brain starts receiving non-adapted sensory information" It could be part of what's informally called "human 2.0". Some machine learning frameworks and programs filter or transform data in a way that doesn't use relative measurement yet makes it vastly more useful, such as a database view or a numeric array transform. Filtering out sunlight is handled by the eyes rather than in the brain. The road doesn't roar, and even if it did you would be able to hear everything else by mentally "subtracting" the background noise. You obviously have no clue what you're talking about.


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Why does the ova remain viable for only a day after ovulation?
The ova remains viable for approximately 24 hrs after ovulation to be fertilised by a sperm.

...chances of becoming pregnant increase dramatically if you have sex during the 5 days before ovulation and the 24 hours after ovulation.
  [source]

My question: what prevents it from remaining viable for a longer period?
My assumptions:

Could be because it is arrested in metaphase II so cannot undergo transcription
Could also be because its haploid
Due to progesterone effect.

So what is the real phenomenon behind this? Also note that, compared to the ova, the sperms remain viable in the female reproductive tracts for a longer time (approx. 4-5 days).


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Dominance and recessive relationship of alleles
You can find easily in textbooks that definitions for dominant and recessive alleles as follows:
Dominant allele: produces working protein and shows its effects in hybrid state.
Recessive allele: produces defective protein and remains suppressed in hybrid state.
But I have these confusion:

Defectiveness or benefit is relative thing.
There are many genetic diseases which are caused by dominant genes, for example short toe fingers. The protein related to it is also defective.

Another definition includes dominant as wild type most circulated while recessive as mutant allele. But even this seems to be unsatisfactory as every mutation cannot be recessive or defective.
Then, finally, what determines dominance of an allele over others?

These definitions are wrong. Can you please directly quote a definition from a specific textbook(s) (so that we can boo the author if the textbook is indeed wrong). While the recessive allele is probably more often associated with the production of a non-working protein, it is definitely not how the term recessive is defined.

Yeah, these are bad definitions.  A better one would be "Two alleles are in a classic dominant/recessive relationship if the heterozygous phenotype is the same as the homozygous dominant phenotype, and different from the homozyogus recessive phenotype"

Possible duplicate of Is protein production doubled if you have homozygous dominant genes as opposed to heterozygous genes?

Phenotype determines dominance. The "rules" you state are just general possibilities that are most likely; they are not correct definitions. "dominant as wild type most circulated" is just completely totally false.
It's common to have mutations that cause loss of function. These often end up as recessive alleles, because the second copy still makes a functional protein. It's not about the allele being suppressed necessarily, and doesn't have anything to do with benefit or not, it's just that the other copy is able to do the job, so you don't see much effect. Because there are often feedback mechanisms for gene expression, having 1 less copy in the genome often means much less than a 50% reduction in protein.
It's also common to have mutations that cause negative gain-of-function: these are often dominant, because you only need one copy for that negative effect to be observed.
However, as you point out, these aren't always the case. You could have an allele where loss of a single copy causes a deleterious phenotype. Sometimes these might more appropriately be considered "incomplete dominance."
I think it's important to note that these terms are really labels based on phenotypes, they are not biological realities. An allele could be thought to be completely dominant, but under further study actually demonstrates a form of incomplete dominance or co-dominance.
The Wikipedia page on dominance has some better definitions for you.


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How can i confirm that the given pedigree chart is of an autosomal dominant trait?

This image is from the NCERT textbook. In diagram A, which represents an autosomal dominant trait, I found out that autosomal recessive inheritance also satisfies the pedigree. Yet, the NCERT text book states that it is a dominant trait. How can that be? Is it because the dominant trait is more probable here? If so, how is that it is more probable in this case?

Sure, both are possible here!
Your book probably makes an implicit assumption of low frequency for the "red allele".
Assuming, "red" means "disease", it is quite standard to assume that the "red allele" is at low frequency in the population. If this is the case, then it is unlikely that partners of the members of the main family being represented in the tree carry this allele. It is therefore quite standard to assume that partners does not carry the "red allele". If this assumption is made, then recessive autosomal cannot explain the observed tree.

Both are possible here, as Remi.b stated.
It could be autosomal dominant, assuming that the first male in the pedigree is heterozygous for that trait (assuming that "red" means the trait). Since he is heterozygous, and the female is homozygous recessive, there is a 2:2 chance of their children getting that trait or not, which is actually shown!
So if the male is heterozygous recessive for autosomal dominant, and passed it on to 2 of his children, then those children that received that trait are also heterozgous, resulting in the person with that phenotype from the F2 generation.
Also the trait could be seen as autosomal recessive, as you had said, if the females in the parent generation and F1 are carriers.

how about X-linked dominant trait? It is also possible for this pedigree. So, how can is test which is more probable, autosomal dominant or X linked dominant?

If it was sex-linked dominant, the other female offspring would also be seen as having it.


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Rate of Diffusion Through Cellulose Membrane
From what I understand, the larger the molecular size, the slower the rate of diffusion and vice versa. However, after doing a lab (similar to this one) about diffusion through a cellulose membrane, my instructor said that despite substances having different molecular sizes, the rate of diffusion (thru the membrane) will be the same. Could someone further explain or did I hear incorrectly?

Yes, diffusion coefficient varies with molecular size, so it is difficult to imagine a mechanism whereby a membrane would precisely nullify this relationship, but could you describe your experiment in a little more detail?

@AlanBoyd
http://mayhewbiology.com/laboratory/Diffusion%20lab.htm
This is essentially what we did

I think that your instructor was wrong.
For the type of experiment that you describe the dialysis tubing (cellulose acetate with pores) is acting as a semi-permeable membrane which can block the diffusion of a polymer (starch) but will allow the passage of a small molecule (glucose). The molecular weight cut-off of the tubing was probably 10 kilodaltons or greater, so glucose (180 daltons) would diffuse through the pores without hindrance, as would sucrose (342 daltons). But would the monosaccharide and the disaccharide move through the membrane at different rates?
This table gives values for the diffusion coefficient (D) of these two sugars as:

glucose 6.7 cm² s⁻¹ × 10⁻⁶
sucrose 5.2 cm² s⁻¹ × 10⁻⁶

The time τ to travel distance L by diffusive movement is given by
τ = L²/6D
Here all that matters is that τ is inversely proportional to D, so we can estimate that glucose 'diffuses' approximately 30% faster than sucrose.
Bulk diffusion is, of course, driven by a concentration gradient: if you were to start with, say, 0.1 M each of glucose and sucrose in a dialysis tube the glucose should reach equilibrium with the surrounding liquid faster than the sucrose.


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How do people actually find codons in a DNA transcript just by looking at it?
I was looking at this transcript of a DNA sequence, and the article kept referencing what the first codons are, but a codon like AUG isn't in the sequence...there's no "U" in any sequence. What am I missing?

In DNA, the first codon would be "ATG"

as far as i know genomics, you can align your transcripts (mRNA) to your peptide, as well as align mRNA to genome and cDNA, to detect first codon. Also, starting sites are conserved and have canonical sequences (on average)

Codons refer to sequences of nucleotide triplets that translate to amino acids. As you know, polypeptides are translated at the ribosome using a messenger RNA (mRNA) blueprint produced by RNA polymerases from the DNA.
DNA consists of four nucleotides: adenine, guanine, cytosine and thymine. Thus, DNA sequences read, for example, ATAAGC. RNA, however, replaces thymine with uracil. So to transcribe the above DNA nucleotide sequence into mRNA would result in UAUUCG.
The mRNA may also get spliced into various isoforms coming from the same gene. In short, it may be difficult to determine the gene product from the DNA sequence.
Does that make sense?

There are also start codons other than AUG.


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Bird Identification
I found this bird when I came back home. I have never seen a bird like this. Also, she is not moving even if I touch her slightly.

Welcome to Biology Stack Exchange. For species ID questions, it is often helpful to include some information on where and when the animal was found: for birds, information on the location (i.e., country / state / province) and local environment (coastal, forested, urban, etc) would be especially helpful.

Also some indication of size.

It looks like a Bulbul to me.

Thid bird looks a young one to me, based on the type of feathers it has around the neck.

It's a scaly breasted munia or spotted munia (Lonchura punctulata).
A relatevely common bird in captivity, probably escaped from someone cage? (check for rings)
Here a picture from the web:

Here you find more facts about it:
http://www.hbw.com/ibc/species/scaly-breasted-munia-lonchura-punctulata


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Why can't pyruvate be used directly in the Krebs cycle?
Why can't pyruvate be used directly in the Krebs cycle? Why does it have to be converted to acetyl before it enters the cycle?
Excluding the reason that the shape of pyruvate is different than acetyl and therefore it would not fit the enzymes involved in the Krebs cycle, what is the advantage of converting pyruvate to acetyl?

"Excluding the reason that the shape of pyruvate ... would not fit the enzymes involved in the Krebs cycle" -- that's a pretty big exclusion. Obviously pyruvate cannot be used directly because it doesn't fit. It rather sounds like you're asking why the cycle isn't made up of completely different enzymes? But metabolism is evolved, and there is no special reason why it looks the way it does, except that this solution was found by evolution. I'm not sure the question is answerable. (But maybe I don't understand it correctly.)

Oxidative decarboxylation of pyruvate to acetyl-CoA by pyruvate dehydrogenase is coupled with reduction of NAD+, which can feed into the electron transport chain.
CoASH activates the acetate: hydrolysis of the thioester is thermodynamically favourable and drives the reaction catalyzed by citrate synthase.
Conversion of pyruvate to acetyl-CoA commits it to a subset of possible fates (including the tricarboxylic acid cycle) and is therefore a key regulatory step.

You can read more about this in most introductory biochemistry texts, like this one.
Also note that pyruvate actually can enter the TCA cycle via carboxylation by pyruvate carboxylase to oxaloacetate. This reaction requires energy in the form of ATP and is used to regenerate TCA cycle intermediates as they are siphoned off for anabolic pathways.


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Does any molecule other than DNA have a double-helical structure?
DNA is known to have a double-helical structure. Do any other molecules have this structure?

Probably also interesting to ask: was their molecular structure known before that of DNA?

Double Stranded RNA Actin Filament Collagen protein Starch is kind of similar too

A few examples:

Starch
A polymer of glucose that can form a double helix and functions primarily as energy storage in plants.

[image source]

f-Actin
Filamentous actin forms a helical structure with two strands of polymerized g-actin. This is a structural component of the cytoskeleton.

[image source]

Coiled Coil
Protein motif with a helical structure formed by two (or more) α-helices. Coiled coils are found in a diverse range of proteins from structural proteins like keratin to transcription factors like c-Fos.

[image source]

Gramicidin
A peptide-based antibiotic that has been shown to form membrane spanning double helices.

[image source]

Yes, double-stranded RNA as found in some viruses.

Do you know of any other such molecule? RNA is very similar to DNA, but is there a molecule that is very different from DNA and yet still has a double helix structure?

Yes, I thought you'd be only half satisfied with this answer. I do not know of any other molecules (but I am not a good chemist) but the answer may depend upon how different the structure of a molecule can be until you start considering its structure to really be different.

The structural protein collagen consists of a triple helix of polypeptides. Whether this answers the question is arguable—you could say that the triple helix contains double helices. In any case, depending on what prompted your question, I thought it might be an interesting structure to consider.


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How does selection affect allele frequency?
Question
People who are carriers for Blooms Syndrome have developed a selective
advantage. How would this affect the allele frequency of the disease allele?
My thoughts
Natural selection will occur, only the carrier is selected and the affected will be selected against, leading to an imbalance of the Hardy-Weinburg equilibrium.

At Biology.stackexchange we expect that people show some effort to find an answer by themselves, otherwise questions are considered off-topic and will be closed. The same happens to homework/assigment questions with no effort to solve them. So, what have you found out?

i found a few different things. Natural selection will occur, only the carrier is selected and the affected will be selected against. Leading to an imbalance of the hardy-weinburg equilibrium. - sorry, it is my first time asking qns and even coming to this page so i dont really know the 'rules' of this website.

Welcome to Biology.SE! I edited your post (title, tag and I added your comment onto it), to make it on-topic. Feel free to roll back if you don't like the edit.

This is slightly tangential, but I question one of the premises for your question ("People who are carriers for Blooms Syndrome have developed a selective advantage"). On Wikipedia https://en.wikipedia.org/wiki/Bloom_syndrome and briefly on Pubmed, I don't see any such evidence. Or was this meant to be a hypothetical for the purpose of understanding population genetics?

Question

People who are carriers for Blooms Syndrome have developed a selective advantage. How would this affect the allele frequency of the disease allele?

Your answer

Natural selection will occur [..]

This is correct. Anytime you have a fitness differential among different genotypes, selection will affect allele frequencies.

[..] [l]eading to an imbalance of the hardy-weinburg equilibrium.

Hard-Weinberg equilibrium describes the relationships between allele frequencies and genotype frequencies. Selection can sure affect this relationship at some stage of life but it will not affect this relationship just after fecundation.
In any case, the question does not seem to expect you to talk about that. The question is asking about allele frequency only.
If you want to understand Hardy-Weinberg, you should definitely have a look at Solving Hardy Weinberg problems.
What I would answer
Not assuming any extra knowledge, the only simple, logic answer is to say that the frequency of the allele coding for the Blooms Syndrome will likely increase in frequency in the population, eventually reaching fixation. This increase in allele frequency would yield to an increase in the frequency of carriers of Blooms Syndrome.
Of course, if there is heterozygote advantage (aka. overdominance for fitness), then in an infinite population, the allele should never fully reach fixation.
If we were to know more about the genetics of the Blooms Syndrom or the specific selection advantage (and eventually many other things one may want to consider) one could formulate a more quantitative answer.

Won't reach fixation if homozygote Bloom syndrome genotype is deleterious (as seems to be true) and only carriers have a fitness advantage (cf. sickle-cell allele)

Is there heterozygote advantage (a.k.a overdominance for fitness) in the locus causing variation for Blooms syndrom? I edited the answer adding a "if there is overdominance" type of paragraph. Thanks

Original question might need to be closed with "unclear what you're asking". If OP is referring to Bloom syndrome https://en.wikipedia.org/wiki/Bloom_syndrome , it seems pretty clear that being homozygous for the variant allele is deleterious. Thus I was guessing that the question was a hypothetical "suppose there was overdominance at this locus, what would happen"?


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What Kind of Bug is This?
I took a picture of this bug when I was camping with my boyfriend in Ontario, Canada. The little guy (or gal) kept wanting to climb onto my hand which kind of freaked me out. I'd love to know what kind of bug this is!

It looks like an assassin bug. Spined assassin bug perhaps?

Ogre71, I looked at the picture to which you refer,and I think you are correct. It has a smaller abdomen,but it might mean that it is male.


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Is lumosity.com based on science?
I always see these Lumosity ads on TV, and I personally feel they are just trying to "sell me something". I did some layman's research (wikipedia) and read that "Studies of Lumosity's effectiveness have shown mixed results".
Does anyone with knowledge on the topic of learning know if the "brain games" they post are simply games? I guess the proper question would be:
Can games like the ones Lumosity offers increase cognitive ability?

This question on Cognitive Science SE has a couple good answers about this topic: http://cogsci.stackexchange.com/questions/1705/how-valid-is-lumositys-brain-performance-index-and-what-normative-information-i

Most advertisements are trying to "sell you something", namely, the product being advertised.

I'm voting to close this question as off-topic because the purpose of SE Biology is not to make judgement on television programmes or advertisments. This is not therefore a question about biology that allows an objective answer.

Zickefoose et al. did a study, and showed that while you might improve while playing the game, it called into question if you actually improved outside of just getting better at the game.
Redick et al. also reported that when they did a double blind study in brain games like Luminosity that you improved in the games, but they didn't see any transfer from game to every-day life.
Also see my previous answer on the topic: Cognitive Science Forum

I figured as much, although only based on personal opinion more than actual data. Thanks

wow, that's even harsher than I was expecting :O (expected it to at least have some effect, though less than most other/better forms of studying/training/etc.)


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Are prions a recent biological phenomenon?
Is there evidence to suggest whether prions have existed for a large portion of evolutionary history, played a role in evolutionary history, or could they actually be a recent biological technology invented by mother nature? Is there evidence or biochemical data that prions may predate cells?

Knock-out experiments on non-pathological prion proteins ("PrP") show damage to neurons. So there is evolutionary pressure to conserve their sequence and expression. Mutations to PrP and related regulatory regions appear to be deleterious and the organism will not likely get to reproduce.
A paper here explores this question and demonstrates empirically that pathology-causing prions — normal PrP that refolds into a form that causes disease — themselves undergo selection pressure:

In summary, prions show the hallmarks of Darwinian evolution: They are subject to mutation, as evidenced by heritable changes of their phenotypic properties, and to selective amplification, as documented by the emergence of distinct populations in different environments.

To the extent that organs susceptible to aberrant prions have undergone evolution, one could infer from this that prions themselves would be under selection pressure to adapt, as their host environment changes.
Further, there is another paper that discusses sequence-level similarity of PrP between clades:

The presence of the human and mouse PrP genes within conserved syntenic groups (Sparkes et al. 1986) and the presence of aPrP gene in chicken (Gabriel et al. 1992) argue that the PrP gene existed before the speciation of mammals. In mammals, DNA sequences of the ORFs encoding PrP generally exhibit ∼90% similarity. As expected, the degree of similarity at the amino acid level increases to >95% when PrPs of different primates are compared (Schätzl et al. 1995) but is much lower when human PrP is compared with that of a marsupial (∼70%) (Windl et al. 1995). An even lower degree of homology is found when human PrP is compared with that of the chicken (∼30%) (Harris et al. 1989; Gabriel et al. 1992). Attempts to find PrP-related genes in lower eukaryotes have, to date, been unsuccessful (Oesch et al. 1991).

There is an estimation of 600M years of evolutionary distance between humans and chickens, back to their common ancestor:

The last common ancestor of birds and mammals (the clade Amniotes) lived about 310 – 330 million years ago, so 600 million years of evolutionary time in all separates humans from Aves, 300 million years from this common ancestor to humans, plus 300 million years from this ancestor to birds.

This would suggest to me that PrP has been around for a while, at least 330M years and probably longer, and that aberrant and pathological folds of PrP would have been evolving since (along with PrP, itself).

Update: note that prion-like proteins have now been discovered in Archaea.
Note that prion proteins are an important component of yeast natural history.
If they are shared between yeast, amniotes, and Archaea (which branched off at least a billion years ago), one could argue that prions are:

Extremely ancient (>1 billion years since that split).
a phenomenon that arises spontaneously in proteins. There is some support for this, see e.g. here.

If prions arise spontaneously in proteins, then it is reasonable to assume that they have been around as long as proteins have been made in any diversity (e.g. since the origin of cellular life).

A wise biologist told me once that, if some biochemical event is energetically feasible, it will likely happen. Protein folding, TF binding, whatever.


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Tools that take a kinship matrix for phylogenetic decorrelation
I have plant genotypes that have been classified as Invasive, Wild or Domestic. I am trying to investigate what explanatory variables (such as "leaf size", "width of petals" and other continuous variables) affect the probability of being classified a sone of the three groups. I therefore have to perform a multinomial logistic regression. However, I would like to account for phylogenetic non-independence using a kinship matrix.
Are there R tools that can perform such regression?
I considered lmekin for example but I don't think it manages to take a response that can take 3 different categories. Is there some function I would be interested in (in the ape package for example)?

If you willing to do Bayesian model fitting, this is likely possible but will take some tinkering to make sure the models are what you think they are. Stan (via rstan or brms), can fit multinomial logistic regressions (A demo from Thinkinator).
If you can convert these models to pure stan code, then you can incorporate phylogenetic/kinship/arbitrary correlation structure into the model following this example on github (or this one). I have had better luck getting phylogenetic regression to work correctly in pure stan than via convenience functions.

Thanks, that was helpful! Here is also an explanation for similar analysis with MCMCglmm


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Background correction when reading ELISA with TMB substrate
I'm doing some ELISA development, and I'd like some justification/best practices for background correction. I'm using a horseradish-peroxidase (HRP) detection system along with a TMB substrate and an acid-based stop solution, which is quite common. When TMB is cleaved by HRP, it produces a blue (maximum absorbance (Amax) of 650 nm) product. The addition of the acid not only stops the reaction for endpoint detection, but it amplifies the signal two- to three-fold, and turns the solution yellow, so that it should be read at its Amax of 450 nm. The acid itself supposedly has an Amax of 540 nm, which is why you should use that wavelength for background correction, subtracting it from the A450. Other sources claim the A540 reading is supposed to correct for "optical imperfections" in the plate.
Using either of these explanations, one would assume that the A540 would be relatively uniform across the plate, independent of the A450 of the same well. However, in my experience, that is not the case at all. My blanks and negative controls are averaging about 0.041 absorbance units (AU) at 540 nm, with an average A450 of about 0.065. However, an A450 of 0.9 gives an A540 of 0.051, 1.4 gives 0.6, 2.0 gives 0.73, and 3.5 gives about 0.14. The absorbance spectrum (Fig. 2) of the substrate appears to be quite minimal at 540 nm, so why am I seeing this dose-dependent increase as the A450 increases?
More practically, how should I do background correction? Currently, I'm subtracting each individual well's A540 from its A450. Should I continue this practice, or should I determine an average plate background at 540 nm using my blanks and negative controls, and subtract that value from each individual A450?

Using different wavelength for reference give some advantages. You can measure a baseline of each well. All well might not have the same baseline because each well might not be the exactly same as others. In addition, you could make scratches on it, you might touch the bottom, or you get some dirt from your bench. And this can be corrected by A540 in your case. So, variations at a lower range are not much concerned. Sometimes, even if you choose a wavelength where the absorbance seems not to change after reaction, there might be a small change. This is not concerned ether, because both absorbances are concentration dependent unless states in solution do not change (froming complexes or something like that).
But still, you get high background from samples showing 1.4 or more at A450. I do not have experiences for this substrate, but you might want to think several possibility:
1)You might get bubbles on the top of your solution in the wells,
2)You might not get accurate values because OD is too high,
3)The solution might get precipitates
4)This may be a very less possibility, but some secondary reaction occurs.
For 2), 3), and 4). You might want to check linearity by drawing a standard curve, and avoid to use the range deviating from the liner relation.
PS
I should've mention that you would check the specification of your plate reader. OD=3 could be way to high to measure it. Because light intensity decreases to one thousandth though 1 cm light path at OD=3. It is very hard to measure such weak lights exactly. Probably many specifications of plate readers say you could measure ODs up to around 2, but some people think it is ideal to measure ODs up to around 1.


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Why can action potentials not be initiated at dendrites?
Why are action potentials not initiated at dendrites, although dendrites are the first to receive input from the presynaptic cell?
In fact, excitatory postsynaptic potentials (EPSPs) at the dendrites are smaller than in the cell body and axon.
Considering the fact that dendrites have enough voltage gated ion channels, why is it that cation influx through these channels is not able to depolarize the dendrite above threshold and generate an action potential?

What makes you think there are enough voltage gated sodium channels?

@DevonRyan There aren't enough voltage gated sodium channels at  soma and dendrites as there are at the nodes along the axon. But there are VGCCs.So can't action potentials be initiated at dendrites and soma with the help of VGCCs ?What are the channels required for AP?Also how is it that action potentials are initiated at axon hillock,although the input is at dendrites?Why can't enough depolarization happen at dendrites and soma?As a corollary,if enough depolarization cannot occur at dendrites and soma,how then is it propagated to the axon, which is further down anatomically , in the neuron ?

They can't? https://en.wikipedia.org/wiki/Dendritic_spike

The exact site of action potential generation is debated, as is the underlying physiological mechanism (Colbert & Johnsten, 1996). It is generally agreed upon that the initiation site is beyond the soma, at the axon hillock, or even further in the initial segment of the axon.
The reason for the distal axonal initiation site of action potentials is, according to the classical view, that the density of Na+ channels is not high enough in the soma, while the density in the axon initial segment is substantially higher and sufficient. However, it has also been proposed that the threshold of action potential generation is lower at the initial segment (Kole et al., 2008).
Regarding your questions in the comments:

So can't action potentials be initiated at dendrites and soma with the help of VGCCs?
Answer: No. Channel density is too low;
What are the channels required for AP?
Answer: Basically Na+ and K+ channels;
How is it that action potentials are initiated at axon hillock, although the input is at dendrites? Why can't enough depolarization happen at dendrites and soma?
Answer: Either due to a low density of Na+ channels, and/or a higher action potential threshold (e.g., due to the presence of K+ channels in the soma counteraction depolarization);
As a corollary,if enough depolarization cannot occur at dendrites and soma,how then is it propagated to the axon, which is further down anatomically , in the neuron?
Answer: If the EPSP reaches a region with sufficient Na+ channels, depolarization becomes sufficient to activate a critical amount of Na+ channels that causes a sufficient increase in the membrane potential to sustain a full-blown action potential. Along the way, leaky K+ channels decrease the depolarization so a critical amount of channels is necessary, otherwise the EPSP dies out.
What about backpropagating APs from axon hillock to dendrites ? How is that possible?
Answer: the soma and dendritic region are believed to represent too big an electrical load to ensure action potential propagation in both the orthodromic and the antidromic direction. This impedance mismatch can be overcome for an action potential propagating from the axon back into the somato-dendritic region when the initial segment and axon hillock provide additional current. This can be achieved with a high density of sodium channels in that region (Lüscher & Larkum, 1998).

References
- Colbert & Johnsten, J Neurosci (1996), 16(21): 6676–86
- Kole et al., Nature Neurosci (2008); 11: 178-86
- Lüscher & Larkum, J Neurophysiol (1998); 80(2): 715-29


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Serial dilutions
A student wants to make serial dilution of a sample. She starts with a 1mg/ml sample and 10 tubes, (labelled 1-10) each containing 2 ml buffer.
The student puts 1ml of sample solution into tube 1
Repeating the process.
What is the concentration of the sample in tube 4?
Give your answer to 2 decimal places and in µg/ml
I've started this question and I assume I would do 1/2^4 which would give me 0.0625
But i'm stuck if this is right?

I think 1/3^4 is the right factor which gives 12.3 microgm/ml
step #1 consists in adding 1ml of the sample to 2 ml of buffer in tube #1
which then contains 1mg in 1+2=3 ml's i.e  has concentration 1/3 mg/ml.Repeating we get 1/3^2  in tube #2 and  ...1/3^k in the kth tube.
for k=4 we get 1/81 mg/ml=1000/81 microgram/ml
As @xusr remarked this line of reasoning is a good first order approximation based on the additivity of volumes.If one needs a more exact answer in general
e.g for mixtures of organic and aqueous buffers etc one must consider the partial molar volumes of the components involved which will be be dependent both on their chemical nature and the thermodynamic state parameters of the
experiment leading to nonadditivity of the volumes mixed or in worst case to
phase separations(i.e solute is present only in one portion of the resultant
solution)

I think you are correct, could you please show your work for the serial dilutions. I think it would be beneficial for @user135629 to have your work shown

OK @xusr.Of cource if  one wants to be very exact one has to consider the

@xusr.I have discussed the matter completely in principle by adding to my answer what has to be considered in general when the first approximation I