text:
What kind of filter can be used to filter sterilize ADC?
I am using this recipe to mix my own ADC (Albumine+Dextrose+Catalase), without the catalase for a microbiology application.
It says use a filtering apparatus to sterilize the ADC because it can not be autoclaved. We tried using a vacuum filtering apparatus with both 0.22 um and 0.45 um PEF filters, but they clogged immediately.
We have successfully used the same filters to filter other reagents in our lab.
What kind of filtering apparatus/material would be able to filter sterilize this recipe for ADC?


text:
Is it safe to autoclave waste at the same time as lab equipment?
We have recently moved into a lab space where we share an autoclave with other people.
We generally autoclave empty beakers, flasks, etc., before running experiments, and we autoclave waste (Petri dishes, pipette tips) in autoclave bags after our investigations.
Reading up on the proper use of an autoclave, I came across this quote:

Do not mix autoclave bags and other items to be autoclaved in the same
autoclave cycle. Liquid media requires a shorter cycle, often 15- 20
minutes, while autoclavable medical waste requires a minimum of 30
minutes in order to be effectively sterilized

But my understanding was that whatever comes out of the autoclave would be sterile as long as you pick the proper cycle.
To be clear, is it ok to autoclave waste and equipment in the same cycle? For example, liquid waste and liquid 7H9 on a liquid cycle or solid waste and empty beakers on a gravity cycle.

You generally don't want to cook your media any long than necessary to sterilize it,  depending on how sensitive your application is. Excessive autoclave times can degrade media's ability to support certain organisms. It might be less of a problem with lab-adapted strains than wild-type isolates, but still not in line with what I would consider best practices.

Short answer: no.
The reason is that waste volumes are typically variable (e.g. one beaker with 50 ml, but another with 2 litres) and often have high biological loads compared to media or similar materials. If you were to put both into the same autoclave, and sterilized the waster properly, your media would be over-autoclaved (results in sugars being caramelized, damage to other nutrients too).
As your quote suggests, wastes take longer to decontaminate because you need to be certain that the waste is decontaminated before it can be discarded into normal waste streams (landfill or incineration etc.). If the waste is not decontaminated properly, you run the risk of accidental release of unwanted or restricted organisms into the environment. You may not care if your M. smegmatis contains a genetic modification and gets out of containment, but I bet your local biological safety officer/committee do, as do the local laws surrounding this topic.
Long story short - use the appropriate cycle for differing loads.

Thank you bob. How about solid waste  such as Petri dishes in autoclave bags, plus empty beakers/flasks etc? Our autoclave is large enough that we could put the flasks and beakers on a separate shelf from the waste bags.

@JohanWikström this may be OK, but generally you want your glassware to remain clean - sterile isn't the same as clean! In addition "dry" goods cycles usually have a drying process built in to remove most of the water from the items being autoclaved. If you run dry goods through a waste cycle you are likely to end up with a lot of water in your glassware.

source: Stack Exchange

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

sort: votes


text:
Does centrifuging and filtering supernatant confer an advantage compared to just filtering?
We are trying to isolate bacteriophages from environmental soil samples. One of the first steps is elution, centrifugation and filtering of the soil samples.
One protocol suggests to:

Elute the soil 1:1 with buffer solution. (e.g. Phosphate buffered saline)
Manually shake the tube a few times.
Let it settle overnight at 4°C
Centrifuge 3x 10 min, 5000g at 4°C
Prefilter supernatant with 16 um cellulose
Filter with 0.22 um PES filter

The suspended soil will settle somewhat overnight. In the paper they state:

In this optimization protocol, any filtration attempt with pore size < 16 μm was impaired if the single (Fig. (Fig.1,1, route 1–4) or united (Fig. 1, route 5–6) supernatants were not centrifuged thrice at 5000×g for 10 min beforehand.

When we do this same protocol, we find that in most samples the supernatant can be pushed through a 0.22 um syringe filter  without clogging even before centrifuging. Since centrifuging does take a while when processing many samples, we are considering skipping this step.
Now, is the purpose of centrifuging the eluted sample solely to make filtration easier or are there any other advantages to centrifuging when attempting to isolate bacteriophages?

This is the sort of thing you need to use your own common sense for. You have soil you want to get rid of. Centrifugation will do that efficiently and in bulk. But perhaps it is a problem in the field, and in any case you need to filter smaller particles. If you can kill two birds with one stone, fine. If clogged membranes are a pain, not fine. That’s my take, knowing nothing about isolating phage. But I’d try what was most convenient and see if it worked. The main thing is to think about what is going on.

After having read up on this subject and successfully isolated phages from soil I can say fairly confidently that centrifugation can be skipped unless the sample is very dirty and clogs the filter.
For example, here is a direct isolation protocol from soil that does not use centrifugation but lets the sediment settle for 10 minutes before filtering the supernatant.

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


text:
Anyone able to identify this mite?
Located in a chicken coop crawling on windows. I’m guessing this is a bird mite as I’m only seeing them at night on the coop itself, but want to confirm so that I’m able to treat them effectively. I was able to get this picture by using my microscope with the 10x lens. The size of a grain of salt. Located in Wisconsin.

Welcome to Biology.SE. Please [edit] your post to include as much information as possible to improve your chances of getting a good answer: 1) closeup photos of the organism from multiple angles if possible; 2) how you acquired this image (it looks like you may have used a dissecting scope?) and what magnification you are using; and 3) an estimate of the size of the organism. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site.

to get rid of bird mites you can use https://en.wikipedia.org/wiki/Diatomaceous_earth i have used it myself in our chicken coop and it is effective against mites.if you take a look at the ceiling where your chickens rest at night you will find a lot more mites.

Thanks! Just dusted with DE tonight. I bought elector PSP so I wouldn’t have to mess around, but here I am messing around. Sprayed yesterday for the second time. They are relentless.

Your Answer : (CM/Red Mite) https://entomology.ca.uky.edu/ef516

Sorry, without actual access to the mite, identification is practically impossible - there's just too many different species it could be to actually choose one. As for control, clean the coop regularly and dust with diatomaceous earth to kill any remaining mites.


text:
Do lipids have a monomer or not?
My biology class and I have been on the topic of macromolecules for quite some time now. Chapter 2.3 of the Foundations to Biology Textbook says that lipids are not polymers, so they do not have monomers. It is also stated in our Macromolecules powerpoint.
Now here is what confused me. We did a macromolecules review assignment to prepare for our upcoming biology test. We had to match each macromolecule with its monomer, but that is when I noticed that "No monomer" wasn't an answer; glycerol and fatty acids were the only choices for the monomer of lipids.
This really had me baffled, I thought it must've been a typo on the assignment. So I decided to search it up. I searched for "What is the monomer of Lipids", and google said exactly: Lipids - polymers called diglycerides, and triglycerides; monomers are glycerol and fatty acids.
I still didn't believe what I was reading so instead I searched "What macromolecule doesn't have a monomer?", and google said exactly: Lipids are not true macromolecules because the monomers are not covalently bonded together. Simple lipids are composed of subunits made of fatty acids covalently bonded to a triose sugar – glycerol.
This really confused me because it was saying that Lipids aren't a true macromolecule. I did more research and found that Lipids are polymers, but that is not what we've been learning.
We've learned that Lipids aren't a polymer and that they have no monomer, but google is saying otherwise.
So what is it? Do they have monomers or not? Are Lipids actually considered a polymer?

I fear for your education for several reasons, but the most pertinent is that the term lipid has no precise structural chemical meaning, and refers to a group with similar physical properties that includes steroids such as cholesterol. Presumably the ignoramus who set this educational abomination — MCQ — was thinking of triglycerides, but wanted to hide the “tri” portion because of his absurd answer. No modern biochemist has the slightest interest in the application of chemical terminology such as polymer, but  it seems to me fatty acids themselves justify that description.

No, classic lipids are not considered polymers. Organic chemists have specific names for aliphatic chains of specific sizes, so there‘s no need for polymer terminology.
For example, fatty acids are kept at specific lengths and cells generally don’t elongate them to large sizes. (They can be connected by glycerol. And glycerol can carry only three fatty acids. But that‘s it)
Fatty acids themselves might be called a polymer (repetition of CH2) if one really wishes, but that‘s like calling propane  (C3H8) „polymethylene“ or „trimethylene“, treating it like a polymer of three monomers. But no one does that. Also, fatty acids of different sizes have their own specific names (e.g. oleic acid), while polymer naming systems are usually blind to size.
Polymers are generally composed of roughly >100 monomers (Be aware that everyone sets their own threshold at which size something‘s a polymer). With fewer than that they‘re also called oligomers (oligo means few, poly means many)
lipids aggregate together forming membranes and droplets. But that‘s just lipid molecules sticking together like water molecules do. And water also is no polymer.

You are confusing lipids with triglycerides and pulling numbers out of a hat. If you think about the structure and synthesis of fatty acids they are clearly polymers — they result from the repeated addition of malonyl moieties resulting in multiple CH2 groups. Much more similar to chemical polymers than proteins, nucleic acids or polysaccharides.

Yup, that 100 is definitely a hat-derived number. But most chemists will agree with me that they „feel“ that number when talking polymer (you may dig up some definition from your favorite literature, if you wish). And yeah, you can call the aliphatic chains of fatty acids polymers of CH2. Just like you can call water dihydrogen-monoxide. But you‘re gonna be the only one who does that.

@markur  lipids absolutely do polymerize, lipids as David said lipids formed of many CH2 groups just like polyethylene. If lipids are not polymers, most plastics are not polymers. Also don't confuse "lipids" with triglycerides, lipids come in a huge variety, many drastically exceed 100 subunits. And you need a source for a claim like polymers need to be longer than 100 subunits, because that excludes a lot of biological polymers not just lipids.

Please explain why a biology beginner should know about lipids with the size of 100 carbons.

Edited my answer to prevent misinterpretation. Also explaining why calling e.g. „oleic acid“  a „polymer“ is overkill.


text:
What type of brown mushroom is this?
What mushroom is this? Maybe some type of Armillaria?

Welcome to the site, where in the world is this photo located?

Hello, it's in Austria, close to Kufstein.

The ID is incomplete because we can't see the profile of the gills and the stalk.

I added another image


text:
What's the procedure of the antigen recognition by the B cells in a clear way?
Before presenting my confusion, I really sincerely thank everyone for any advices or clarifying , every  single comment  is helpful.  And my english writing skill is still very bad, Just ask anything if you are confused.
I have first referenced JaneWay's immunobiology textbook and this question about roughly the same question.
However, the exact process is still not very clear in my mind.
So for clearance, Let's imagine the entire  process at the beginning, that is, the time a pathogen having already successfully invade to our body and start circulating throughout blood vessel.
So the first question: The antigen could be distinguished into two types, one of which we have already identified and one of which is totally new to our body,is this understanding correct?
Then, the second question:for the identified pathogen, our antibody which is circulating throughout our body will somehow bind the pathogen and triggers a series of immune response, is this understanding correct?
And then The third and seems like the most untrivial question: for the antigen which is totally new (didn't remembered by our immune cells) to our body, How does our cell knows it is at the first place indeed a pathogen?
Just give me some references  will be enormously helpful for me, thank you!

I can't pull resources for you at this time, and my response is too long for a comment, but just to give you some direction to research:
Firstly, if you are not clear, I would try to understand how antigen and pathogen are different terms. Understanding "epitope" and "hapten" may also help with your understanding.

Yes, BUT it's less "type of antigen" and more "state of immune system" - either there is immunologic memory [to the particular antigen] or there is not.
Yes, there is an antibody binding domain on the variable region of the antibody. Keywords: "Fc/Fab, Constant region/Variable region, Heavy chain/Light chain, V(D)J recombination, CDR1/2/3."
It does not "know." Ideally, it recognizes all foreign particles (of sufficient immunogenicity) as "antigens," but this process is not perfect. Common examples of "improper" recognition are autoimmune disorders and allergies. Try looking into T/B Cell Maturation/Activation, Thymus cells, and B Cell Dual Recognition (the classic/dominant method of activation in response to pathogenic infection). I think this will give you a better understanding of how the body tries to limit its immune response to what we consider "pathogenic."

If the question doesn't get locked, hopefully someone can provide a more complete response to you.

Sorry to bother you again, but if let's say if our innate immune system will automatically attack those pathogens which has "Pathogen-associated molecular pattern" PAMPs, then why does those benign bacteria living in our guts doesn't get attacked by our immune system?

I don't think it is well known and upon cursory search, appears to be an area of active research. The question warrants a separate post.


text:
evolution of a preference for cooked meat
When I got a meat thermometer a few years ago, I was startled at how low optimal cooking temperatures are for beef, less that 140 degrees Fahrenheit. Also, as a kid, I remember reading that the desert floor in Arizona gets up to 180 degrees Fahrenheit, which is much higher. I haven't been able to confirm that, and frankly find it a bit doubtful, but if it's even close, it does imply that an an animal carcass lying on the African plains for a couple of days may be legitimately cooked.
Now, I'm not a biologist, and this is pure speculation, but I'm imagining that if proto-humans picked up a diet consisting largely of medium-rare carrion (probably killed by other predators), this might explain why humans prefer cooked meat and why they lost jaw size (because cooked meat is a lot easier to chew).
Has there been any research along these lines?
Addendum: published temperatures in Arizona seldom get above 120 degrees Fahrenheit, but those measurements are taken in the shade at about 5 feet above the ground. What I'm talking about is measurement of the temperature of sun-warmed rocks on the desert floor. I still think 180 is a little high, but 140 wouldn't surprise me at all.

Almost all predatory animals prefer cooked meat when offered it, cooked meat is way easier to digest and your senses can pick up on that. Animals carcasses lying out for a couple of day are eaten by scavengers and insects very quickly. also 140 internal temperature, which means sustained heating, if you a steak on a rock it cools the rock as the steak warms you need a really hot rock or a way to keep heating the rock, which humans did with fire. we were using fire long before our jaws and teeth shrank


text:
How to figure out when my hot (but cooling) drinking water will go bad
I have a 200 liter electric water heater in a secondary building.
The time periods between me visiting the building and using the water vary and do not follow any schedule.
I can be visiting as rarely as once every 6 months or as often as once every two weeks.
The heater is turned off during periods when I am not at the building to save on electricity, but the heater is well insulated and the water stays warm in the heater for up to two weeks, while slowly cooling down.
The issue is that around 3-4 weeks the water goes bad due to being in the sweet spot for bacteria creation temperature wise (30-40 degrees celsius it seems) for a while.
Then the water starts smelling bad and obviously needs to be discarded, which is wasteful and cumbersome.
The question: I want to install a smart plug (and possibly some temperature sensors) to turn on the water heater every once in a while to keep the water from going bad. I want to hit the sweet spot where the water heater is on as little as possible to conserve the most electricity and still keep the water from going bad.
Obviously there is no one perfect answer for this (e.g. "dont allow the water to go below 40 degrees for more than 8 hours and the water will be safe for consumption forever"), as the water contents will be different based on location, filtering setup, etc, but are there any general guidelines on how to approach this? or a way to figure out what the perfect balance would be for my specific setup without resolving to trial-by-error?
I've googled around using "how long does it take for warm water to go bad" query, but this returns results only on how long you need to wait until the water heater reheats cold water, not how long it takes for warm water to go bad.
Reason for me not wanting to go with "just replace with a flow-through kind of water heater instead of tank kind" is this water heater is hooked up to the fireplace of the building (i.e. fireplace warms up pipes with heating water in them that are circulated by a pump through the tank without mixing with the drinking water), and if I am already in the building, I will be running the fireplace and the water in the heaters tank will be heated for me, without needing to use the electrical function of the water heater.

I’m voting to close this question because it's not really an answerable Biology question (even though it's about bacteria). As you stated, it somewhat depends on factors we cannot guess at. There are answers, but they don't work for you, so it's more about water temperature regulation, efficiency and personal economical considerations.

I'd say it's a practical application of theoretical concepts and knowledge of bioligy, but fair enough, I understand why you would think this way. Could you suggest a better stack exchange site to ask this question on rather than bioligy?

DIY maybe? Home improvement? I don't know. Potential biological solutions include keeping the water heater on at 140° all the time/heat the water to 160° for several hours when you return after an absence (hard on the heater, shortens lifespan)/shock chlorinate the tank, hot water pipes (you have to drain off all the sediments first, as it can harbor and protect bacteria insuring you always have a ready supply of contaminants)/get a hot water on demand system/etc. etc. But you will reject them, so it's not really biological at all. Your requirements make it otherwise.


text:
How does AIDS affect the immune system vs. SCID?
AIDS

acquired immune deficiency syndrome

According to wikipedia,
Caused by infection with the human immunodeficiency virus (HIV).Following initial infection, a person may not notice any symptoms or may experience a brief period of influenza-like illness.  As the infection progresses, it interferes more with the immune system, increasing the risk of common infections like tuberculosis, as well as other opportunistic infections, and tumors that rarely affect people who have working immune systems.
SCID

Severe combined immunodeficiency

According to wikipedia,
.....is a genetic disorder characterized by the disturbed development of functional T cells and B cells caused by numerous genetic mutations that result in heterogeneous clinical presentations. SCID involves defective antibody response due to either direct involvement with B lymphocytes or through improper B lymphocyte activation due to non-functional T-helper cells. Consequently, both "arms" (B cells and T cells) of the adaptive immune system are impaired due to a defect in one of several possible genes. SCID is the most severe form of primary immunodeficiencies, and there are now at least nine different known genes in which mutations lead to a form of SCID.
Both the diseases affect the immune system of the human body. So, why they are classified as different disease? What is the property that differentiates the diseases?

The flu and common cold both affect the respiratory system, yet we have separate words for them. Osteoarthritis and rheumatoid arthritis both affect the joints. Why do you think diseases are solely distinguished by what part or the body they affect?

Homework questions and trivial questions about basic biological concepts are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. "Homework" is interpreted to mean any academic or other assignment, test preparation, or task given in relation to a class, educational setting, or self-learning.

AIDS -

It is caused by Human Immunodeficiency Virus (HIV).
HIV attacks helper T cells and, therefore, helper T cells reduce in number, i.e. individual can produce T cells, but they are destroyed by the virus.

3.HIV can be transmitted at any stage.
SCID -

It is a genetic disorder.
The individuals are born without T-cells and B-cells and are incompetent to produce them.
This disorder is found in new born children.

A disease is characterised not by its target organ/tissue, but how it infects that organ.

HIV (Human immunodeficiency virus)
Cause:

HIV is a retrovirus that infects helper T-lymphocytes
Reverse transcriptase allows viral DNA to be produced from its RNA code
After years of inactivity (Th cells continued reproducing), the virus becomes active and starts to destroy T-lymphocytes
This results in lower immunity, as antibody production is compromised
HIV is the lowering of the immunity of a certain individual, over a number of years
AIDS is the final stage where observable symptoms develop

Transmission:

Exchange of body fluids (sexual intercourse, breastfeeding, childbirth, needles, etc.)
There is a very small fraction of people who are immune to HIV (no CD4+T receptor)

SCID (Severe combined immune deficiency)
A severe combined immune deficiency, a rare genetic disorder in which affected children have no resistance to disease and must be kept isolated from infection from birth.

Genetic disorder characterized by the disturbed development of functional T cells and B cells caused by numerous genetic mutations that result in heterogeneous clinical presentations
SCID involves defective antibody response due to either direct involvement with B lymphocytes or through improper B lymphocyte activation due to non-functional T-helper cells
Consequently, both "arms" (B cells and T cells) of the adaptive immune system are impaired due to a defect in one of several possible genes

Sources:

https://en.wikipedia.org/wiki/Severe_combined_immunodeficiency#Classification
https://de.wikipedia.org/wiki/AIDS
http://www.avert.org/about-hiv-aids/what-hiv-aids
http://www.ncbi.nlm.nih.gov/books/NBK22254/
https://en.wikipedia.org/wiki/Severe_combined_immunodeficiency
https://www.genome.gov/13014325
https://www.scid.net/

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


text:
Question about the Derivation of the cable equation for neurites
I read in Wikipedia how the cable equation was derived (here) and had a specific problem regarding one of its equation:
At the start of the derivation it states that we first need to pretend that the membrane is perfectly sealed (Rm=∞) and that the capacitance of the membrane equal zero. Then we can say that the change in voltage over distance depends only on the resistance of the axoplasm, by the equation:
 and from that, the current equal:
But later when they derive the last equation, , they set  as in the equation above, which seems to me incorrect, since the resistance of the membrane also affect  . What did I get wrong?
Thanks!

The part you are quoting is about helping you conceptualize the cable equation by starting from some approximations that let you remove most of the terms. See the sentence beginning (emphasis mine):

To better understand how the cable equation is derived, first simplify the theoretical neuron even further and pretend...

They then walk you through how, because these approximations are just pretend, one needs to include terms to account for the actual permeability and capacitance of the membrane. This means that you do not have a constant internal current with distance as you travel along; instead, the current decays with distance because of leak through the membrane and membrane capacitance.
This is what the last equation you quote from says: the change in internal current over distance x (written as dil/dx) is equal to the current lost to the membrane, which includes two parts: leak through the membrane (V/rm) and charging the membrane capacitor (cm*dV/dt).

Another correction that might be tripping you up: you write

change in voltage over time

in your question, but that is not what the equations are representing, they are representing change in voltage over distance x.

Thanks for the answer. I also corrected another mistake I wrote (I mean I(i) instead of I(m) at the end).
But I didn't understand yet how they can set I(i) (as was derive at the beginning) to the I(i) at the last equation, because when they set I(i) in that equation (the second-order partial differential equation) its the equation which don't take into account the R(m).

@Idop11 Did you miss equations (7) and (8) from the Wiki page? Note that the definitions are changing throughout, this is not a derivation per se, where you can connect different steps algebraically.  Don't confuse symbols that are based on certain assumptions with the same symbols once those assumptions are changed.


text:
Probability of number of boys and girls being born on a single day
I am new to genetics, I have the following question at hand :

If four babies are born on a single day, what are the chances that
$A>$ Number of boys and girls will be equal.
$B>$ All $4$ will be girls.
$C>$ At least one baby will be  a girl.
$D>$ Which combination of boys and girls is most likely?

My solution:
Let $X$ be the number of boys .
$X$ follows $Binomial (4,{1\over 2})$ , since the probability of a child being a boy is half.
So the answers are
$A>{3\over 8}$
$B>{1\over 16}$
$C>{15\over 16}$
$D> $ Equal number of boys and girls.
Is everything right ?

I'm voting to close this question as off-topic because  it's about probability, not biology.http://meta.biology.stackexchange.com/questions/3111/not-all-questions-featuring-something-biological-are-biology-questions

@rg255 I agree. You can do so. But that doesn't mean you will downvote the question !

Voting allows content that is useful and useless to the community to be identified - your question is not biology so not useful to our community, therefore I downvoted.

@Qwerty mouse over the downvote button and read the message: "This question does not show any research effort; it is unclear or not useful." Additionally, please read "Why is voting important?".

I know this is kind of tedious and only practical when you are considering no more than 10 children  (which I think is a lot to parent), but anyway, I like to solve these problems with a binomial expansion.
So we have binomial probability so 2 options - either a boy (n) or a girl (g) at equal probability or 50% or 1/2.
(b + g)^n = a binomial expansion according to the coefficients of Pascal's triangle.
Where n = 4 children, then the row of Pascal's triangle is 4 in which the first row of pascal's triangle is technically row 0.
Equation: (b + g)^4 = 1(b)^4 + 4(b^3)(g) + 6(b^2)(g^2) + 4(b)(g^3) + 1(g^4)
Problem A)
So the probability that the number of boys and girls will be equal is
Probability((6(b^2)(g^2)), where (b^2)(g^2) means two boys and two girls, an equal number.
When b = 1/2, and g = 1/2, or well ... b + g = 1
6(b^2)(g^2) = 6[(1/2)^2 * (1 / 2)^2] = 6 * (1/2)^4 = 6 / 16 = 3/8
B) All four will be girls: Prob((1(g^4))
= 1(1/2)^4 = 1/16
C) At least one baby will be a girl:
That corresponds to 4(b^3)(g), 6(b^2)(g^2), 4(b)(g^3), and 1(g^4)
The probability that at least one will be a girl is
= (4 + 6 + 4 + 1) * (1/2)^4 = 15 / 16
D) Which combination of boys and girls is most likely?
That would be 6(b^2)(g^2), so when b = g = 1/2
Prob(most likely combination) = 6/16 = 3/8 or two boys and two girls.
Note that if you add up all the combinations, the result is 100% of all probabilities:
(b + g)^4 = 1(b)^4 + 4(b^3)(g) + 6(b^2)(g^2) + 4(b)(g^3) + 1(g^4)
When b = g = 1/2, then basically:
(1 / 16) + (4 / 16)+ (6 / 16) + (4 / 16) + (1 / 16) = 16 / 16 = 1 = 100%
You did it right. But I suppose this is another way to evaluate a binomial like this.

A BIG typo- $2$ boys and $2$ girls, not $3$.

Good work, but basiacllly what you did is like - instead of directly evaluatng $3\times 4=12 $ you wrote $3+3+3+3=6+6=12$....

Yeah, I was typing this so quickly!

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


text:
What exactly happens to hydrogen atoms in step 4 of citric acid cycle?

It seems that there are four hydrogen atoms in alpha-ketoglutarate and one in HS-CoA (not counting the ones in CoA), five in total. Two of them go to NADH and H+, so there should be three atoms in succynyl-CoA instead of four. What am I missing here?
picture taken from Molecular Biology of the Cell, 6th ed., by Alberts et al.

Where are you getting "Two of them go to NADH and H+" from? Count the carbons on each side of the reaction, including CO2.

There are 5 of them on each side (not including the ones in CoA). But there is one more proton (H+) on the right side of reaction, and that's what seems problematic to me, that is, reaction would make more sense to me if the product contained NADH, not NADH + H+.

Oops, for some reason I read "hydrogen" as "carbon"- my bad.

Short answer:
There should have been an additional $\text{H}^+$ on the left-hand side.
Long answer:
You have rightly observed that the left side of the equation is deficient in one hydrogen atom. Let me draw your attention to another issue: the charges on both sides are different too. The left side has one negative charge too many. This gives us a clue: possibly there is a missing $\text{H}^+$ on the left.
This reaction is actually the sum of three reactions catalysed by a multi-enzyme complex. If you add the balanced equations for the reactions of $\alpha$-ketoglutarate dehydrogenase, dihydrolipoyl transsuccinylase and dihydrolipoyl dehydrogenase, you will see that there is indeed an additional $\text{H}^+$ on the left-hand side, which is omitted in your textbook.
But that is the case with most biochemistry/molecular biology texts. Biologists are very bad at balancing their equations, especially when it comes to $\text{H}^+$ and $\text{H}_2 \text{O}$. They balance out only the major reactants and products. The rest is often, er, left as an exercise to the reader.

Lodish is a Molecular Biology book. Berg et al., which is a biochemistry book, has it right (i.e. no hydrogen ions at all). However, heaven preserve us from chemistry students who can’t see what’s important in biochemical pathways because all they understand about chemistry is balancing equations.

Sorry Alberts — molecular or cellular biology. But not biochemistry.

NAD+ accepts only one hydrogen ion (H+) and two electrons (2e−), to form NADH + H+.  So only one Hydrogen is used by NAD+, and remaining four are present in Succinyl CoA.
The reaction mentioned in your question is a three step reaction involving decarboxylation of α-ketoglutarate, reduction of NAD+ to NADH, and at last formation of Succinyl CoA. Last step also uses FADH2.

Reference:
http://www.phschool.com/science/biology_place/biocoach/cellresp/closer2.html
https://www.elysiumhealth.com/en-us/science-101/whats-the-difference-between-nad-and-nadh

I am confused. In your second reference the illustration "NAD+ to NADH redox reaction" clearly shows that NAD+ together with 2e- and H+ forms NADH, not NADH and H+, as you claim in your answer.

As this is an redox reaction the two electrons balances out the reaction, which is normally shown, but here they have not shown the electrons.

And this is a multistep reaction using FADH2 also.

Yes, FADH2 is produced in step 6 and there doesn't seem any problem. But I still have problem with the fact that there isn't equal number of protons before reaction and after reaction in the picture I posted, and I don't feel your answer addressed this concern.

I am not talking about citric acid cycle's 6th step. But this alpha ketoglutarate dehydrogenase enzyme complex's 3rd enzyme. Now I added the picture in my answer

So, as far as I understood, this extra H+ appeared from other reactions taking place in alpha-ketoglutarate dehydrogenase complex and which are not explicitly mentioned in the picture I posted?


text:
How long does it take for a person to lose all offsprings due to inheritance?
From this I know we will only inherit some genetic informations from parents, which is about 50 percent. But the problem is, gene has finite size, after some generations a person leaves only $0.5 \times 0.5 \times 0.5$ parts of genes to the offsprings, and it will be casted into zero. My question is, how long does it required for a person to lose all genetic information in the world?

Why would someone (a lineage) lose all genetic information in the world? Definitely the person will mate with someone else from the same world and not from another galaxy.

I think your question conveys some misunderstanding.
A child is related to each parent by a factor of ½. Humans have a diploid genome, meaning they have two copies of each chromosome (see: autosome). When two humans reproduce, they each contribute one copy of each chromosome to the offspring, in other words, they contribute a haploid genome to make a diploid child. Genetic information is not "lost" - the genome is not shrinking by a factor of ½ every generation.
However, relatedness does decrease from generation to generation. You are related to each of your parents by a factor of ½, each of your grandparents by a factor of ½ $\times$ ½, your great-grandparents by a factor of ½ $\times$ ½ $\times$ ½... You are also related to your children by a factor of ½, you are related to your grandchildren by a factor of ½ $\times$ ½... You get the picture, right?
For example, imagine the genome carries just one gene. Your father carries alleles $AA$ at that locus, and your mother $aa$. You would then be $Aa$ and, because half of your alleles came from your father and the other half from your mother, be related to each by a factor of ½, but all three of you have the same number of genes (1) and that gene is the same length (in nucleotides, barring mutations) in all three.

But at some point, your offspring will have increased in number to the point that they're a significant fraction of the population, and will start mating with each other.  So if two of your great-great-grandchildren marry (each 1/16 of your genes, if I counted right), their offspring have 1/16 + 1/16 = 1/8 of your genes, not 1/32, no?

@jamesqf Right idea, but the fractions add up a little differently. Two of your great-great-grandkids marrying would each provide 1/2 of the 1/16 of your DNA they have, giving their progeny 1/16 of your DNA still. If two of your children, each with 1/2 of your DNA, were to have kids (gross, I know), the child would have 1/2 of your DNA, and not be your genetic clone (100% of your DNA).

I feel rg255 answered your question very well, however my mind snapped to an exponential relationship, which is part of what I feel your asking and what rg255 has said (but I have a pretty picture to add).
An exponential graph illustrates the relationship you are speaking of where a substance is infinitely divided by itself.

In this way it will never reach zero. It will inevitably and exponentially shrink but not disappear.


text:
Does a woman contain all the genes needed to make a man?
I know the answer of inverse is at here, but how about this question?
I also read this question, can I imply to human that a woman can also contain all the genes needed to make a man?

Edit:
I think everyone has  the ability of being a man or a woman in terms of their DNA, and that their gender is just determined by the presence of SRY.
Is my concept correct?

Male mammals require a Y chromosome because the genes needed to express masculine features are on that chromosome. Females don't carry a copy of the Y chromosome, so they don't carry those genes, and can't pass them on. A male could hypothetically provide all the genes needed to produce a female because you could copy his single X chromosome to produce two identical X chromosomes.

Your pseudocode is not necessary here. It actually oversimplifies the issue and is likely to generate unnecessary debate. You should verbally explain what you mean.

Human female cells contain most of the genetic information required to make a male, but they do not contain a critical component: The Y chromosome. This is a relatively small chromosome. Wikipedia claims we have identified around 200 genes on it to date, compared to estimates of 20,000 - 25,000 genes overall in the human genome.
Importantly for your question, only other males contain and make full copies of all the genes on the Y chromosome. The Y chromosome does not cross-over* with the X chromosome during meiosis when producing sperm cells, which keeps the Y genes isolated, except for rare exceptions (e.g. gene translocation). So those genes are passed down the male line only. The SRY gene is just one of the genes encoded uniquely on that chromosome, so something else is definitely missing - the question could be re-phrased "how important to being a functional male are the unique genes other than SRY unique to the Y chromosome?"
The linked question (an experiment on mice that produced XX "males" by finding an alternative trigger to the SRY gene to induce male development) demonstrates that in terms what we might consider a physical male specimen, the Y chromosome probably contains a minority of critical unique features. The mice developed into apparently complete physical males. That means genes outside of the Y chromosome cover most of the body development plan for both males and females.
However, such XX males will in most mammal species not be fully functioning males - the missing genes do make a difference. One outcome is infertility - biologically speaking, XX males do not possess a key male function, the ability to mate with a female to produce offspring. There are missing genes related to sperm production.
Human XX males - as in developmentally male - do occur naturally. This can be caused by gene translocation - specifically the SRY gene moves to the X chromosome in a sperm from the father (potentially other Y genes will move in the same event). The symptoms that present with the syndrome vary, but give some indication of which critical components are missing.

Not all animals have the same mechanism. Birds have W and Z chromosomes (with males being ZZ and females ZW). Yet other animals do not use genetic switches, but environmental ones. In those cases, the female does contain all the necessary genetic information to create a male. In cases where there is parthenogenesis (production of offspring without fertilization), then this can be fully demonstrated.
* Technically there are some small regions, about 5% of the Y chromosome, which do cross-over with X, called the pseudoautosomal regions. At the time of writing the linked article mentions 29 genes found in these regions.

You don't explicitly put it this way, but the reason the Y chromosome is critical, is that it couldn't be simulated just by removing part of an X chromosome. Recombination doesn't occur in all regions of the X/Y chromosome pair, and that's why there's stuff on the Y that really is unique to the Y as you describe. If there was recombination along the whole Y then everything there could appear also in an X somewhere, but there isn't so it can't.

Also worth noting the existence of pseudoautosomal regions - "the genes other than SRY on the Y chromosome" are not all unique to men.

Nope. A woman does not contain all the genes required to make a man. Humans are mammals and mammalian male gender is governed by the ~200 genes on the Y chromosome. However a man (XY) does have all the genes required to make a woman (XX).
In birds they have WZ sex determination system. So a hen, is the heterogametic sex,(WZ) does have all the to make a cockerel (ZZ)


text:
difference in genetic instuctions between male and female
I'm a computer science graduate so please bear with me the following computer program :
mov  ecx, -1
INC  ecx
consist of 2 instructions (mov,inc) each working on specific data , can genetics instuctions be expressed in the same way ? if so what is the difference between male and female(humans) when it comes to the number of instructions and the difference if any (eg , n-instuctions being exclusive to female ... etc) ?
Edit#1
:what I mean by instructions is something like a computer program and a programming language commands.

I don't know what do you mean by Instructions ? Can you be more clear ?

As many biologists, I don't know assembly. If possible, can you rewrite your 2 instructions into C, python, R or some other commonly used languages?

As argued here, the analogy between genetics and the digital world can be quite misleading and one should make sure to not push it too far. I think there are 2 questions in your post: "Is there an equivalent to ?" and "Do human male and female differ in their number of 'instructions'?". You should always try to restrict your posts to one question only.

The typical Male has a Y-chromosome, which consists of about 100 genes.
Genes are the instruction sets to make proteins, and proteins do the work of the cell.
Those 100 genes out of about 21,000 in the human genome are what differentiate Males from Females.
That being said, because of how signaling works, Males and Females can exhibit different expression patterns, like function calls, even though they have the same instruction sets, for the most part.
Expression patterns are how genes are activated and deactivated, it is basically a regulatory process that controls the functions of the cell, tissues, organs, and organism.

There are many other things besides the 100 genes on the Y chromosome that differentiate males from females. If that was the case, XXY persons would be clearly male, when they are not. X genes play a significant role, as do somatic genes.

@MattDMo that is why I chose my words carefully. I said the "typical" male and mentioned that expression patterns can differ. Based on the basic nature of the question I didn't think that it was necessary to go into the intricacies of cell signaling and signal concentration as it relates to gene expression, however if you feel it is necessary to expand the answer to include that level then please feel free to expand on it.

@MattDMo A person with Klinefelter's syndrome (XXY), assuming that they do not also have an SRY reversal are considered to be males genetically. The phenotype comes from the additional dose of expression from the Barr bodies, as they are not completely silenced. XXY in drosophila is genetically female, but for humans, they are sterile males. This Bio SE answer http://biology.stackexchange.com/a/3317/16651 provides a chart that corresponds to the 5th Edition of Genetics by Hartwell et.al.


text:
What insect is featured in this picture?
At the end of the summer, we've been finding these insects in our apartment complex in Baltimore, MD. What are they and do they bite? The length is about the size of a US nickel (We've had mysterious bites along our legs the last few days and haven't found any fleas or bedbugs after turning over the bedroom!

Please update with approximate size, location, and species-identification tag. Thank you

This is a cockroach

Note the flattened body, long antennae, "hidden" short head, and spiny strong legs

Without more details, location or better photos, ID to species is not certain. The most likely species to be found as pests in buildings in the US include: Oriental, German, and brown banded roaches. Common outdoor species that also often come into the home or invade commercial buildings include two larger species: the American and less commonly smoky brown cockroaches. Both of these species are found in the highest abundance in the Southeastern US.
Your image does not immediately convince me you have one of these species. Oriental roaches are black and smoky browns are also darkly colored -- unlike your brown specimen. German (vertical) and brown-banded (horizontal) have stripes on their pronotum, which your specimen also does not clearly have. American cockroaches are unmistakably large with brighter pronotums having darker spots -- again, unlike your specimen.
there is a chance that this is a female brown banded cockroach with its colors washed out from the poor quality photo.  (I kind of see some banding along its abdomen).

 Female brown-banded roach. Credit: James L. Castner ; source UFL
Cockroaches really never bite. You'd have to have a really bad infestation for this to happen. Orkin supports this claim

Texas roaches are at least 3X larger as adults. Borax dust will control them if you can expose them to it . Borax is otherwise fairly innocuous. I blew borax into the cabinet containing the dishwasher and that has significantly reduced the number.

Borax can be dangerous for pets and kids. Use caution using this product. Follow safety guidelines recommended by product


text:
Which type of test tube should not be used for blood collection?
The following question is presented in my biology textbook:

You are required to draw blood from patient and keep it in a test tube for analysis of blood corpuscles and plasma. You are provided with the following four types of test tubes. Which one of them will you not use for the purpose?

Test tube containing calcium bicarbonate
Chilled test tube
Test tube containing heparin
Test tube containing sodium oxalate

In thinking through the question, I reasoned that since we are collecting blood from a patient for biochemical assay or hematocrit, we would want it to be in an anticoagulated stage. Sodium oxalate and heparin are both anticoagulants and therefore should serve my purpose well. I don't think a chilled test tube would have any effect directly, except the fact that low temperatures delay clotting. So, I had chosen the test tube containing calcium bicarbonate to be unsuitable, as $\ce{Ca++}$ is one of the factors required for clotting and hence would accelerate the clotting procedure.
The textbook disagrees with me, and gives (3) as the answer.
Is this an error in the textbook key, or a flaw in my reasoning? Which should be the correct answer, and why?

Your reasoning is sound and correct. The answer key is wrong.
An unclotted blood sample needs something to prevent clotting. Extracellular calcium is required for both the coagulation cascade and platelet activation. It even has its own name in this context, Factor IV. This why EDTA, a calcium chelator, is used in some blood collection tubes to delay clotting.
So, as you say, the most correct answer would be (1): Test tube containing calcium bicarbonate. That is the opposite of the kind of tube you should use for this type of sample.
The answer given by the key, (3): Test tube containing heparin, is incorrect. Heparin tubes are a good choice for plasma and whole blood analysis, as you indicated. Heparin is a good anticoagulant, both in vitro and in vivo.
See this nicely laid out list from UCI medical school for an example of specimen requirements for specific tubes.


text:
Can a zombie apocalypse really occur?
Now, before you flag this question as blatantly off-topic, I claim to have a scientific basis for this(!): not some drug or remote control, but parasitic infection.
While reading about behavior altering parasites and parasitoids, I found this:

Parasites that induce behavioral changes in their hosts often exploit the regulation of social behavior in the brain...For example, Toxoplasma gondii attaches to the hypothalamus rather than target a specific cellular pathway; this broad targeting leads to a widespread increase in host dopamine levels, which may in turn account for the loss of aversion to cat odor...This rise in dopamine levels induces a loss of aversion to cat odor in the rats, increasing the risk of predation by cats, T. gondii’s definitive host.

Now, if a parasite can prevent mice from being afraid of cats, how hard would it be for another parasite to prevent humans from caring about each other's life(!)? Can a parasite develop some method by which it can alter behavior of humans in such a way that they just start killing each other for no reason? How easy/hard would it be for a parasite to do so?
Note: although it is just a curiosity question about whether it is possible or not, giving some description of neural pathways which stimulate social behavior in humans and how they are regulated would be much more appreciated.

interesting question, however you might still want to consider posting this question on skeptics.se

@jordizambrino well I didn't  wish to involve skepticism in the question, it is as general as was yours "can magnetoreception occur in humans?" Also, (if you've given close vote) can you please explain how the question is opinion based so that I can improve it?

First of your questions is partly based on skepticism, secondly in my question on magnetoreception I cited a paper by nature (nature.com/nature/journal/v301/n5895/abs/301078a0.html) which suffices as an appropriate source and lastly I did not vote to close this question as I am interested in which direction this question will go.

Okay let me clear this out ( as it seems to me that your opinion would be shared by many others) firstly, as I say in the question that its mere curiosity about whether its possible or not, second I've also cited a wikipedia paper that it occurs in mice, so can it occur in humans (just like you cite that cryptochromes are there in humans so can they attain magnetoreception). Anyways thanks that you didn't flag it, but an upvote won't hurt ;)

Zombies are reanimated corpses, not just people who murder other people for no reason. There are many diseases and conditions that can possibly lead to people losing certain inhibitions and potentially unpremeditatedly killing other people. I suggest you reword the title to reflect the actual question.

@harryvervet I don't actually know what to call it then. I saw a movie in which some people took an infected drug which made them zombie, and the ones who killed them also called them zombies. So I thought it would fit here.

To me the question is likely going to require a primarily opinion based answer

Sorry guys but I just can't understand how the answer would involve opinion. Just some description of what neural mechanisms would need to be affected to bring this condition would be more than sufficient.

The OP specifically asks for a scientific based answer.

There are many examples of parasite manipulation in nature, if you want more examples you can look up the paper of Lefevre and Thomas (2008). I think the key is, in order for a parasite to develop such behaviour, that it should be giving them a fitness advantage. So I don't think it would ever happen for no reason. The paper discusses a few examples where the manipulation results in a higher transmission rate by the parasite.
I guess that because parasite manipulation is happening in many other organisms, it's probable that it happens to some extent in humans too. There are for example indications that when we are infected with  malaria, the malaria parasites can change our odour profile to make us more attractive to mosquitoes, thus increasing it's transmission (Batista et al. 2014, De Moraes et al. 2014). There are also indications that our gut microbiota have an influence on our brain and behaviour, regulating anxiety, mood, cognition and pain, by communicating with our CNS (Cryan and Dinan 2012).

You've given a really nice answer, but I'm gonna wait for some time to see if I get some other response :)

If there are drugs that can cause this kind of disorder you described, then it is possible to engineer a microbe, that can produce these drugs and maintain a chronic infection, which does not necessarily kills the host.
Walking dead is not possible, human bodies cannot move with rotting muscles or without muscles, so you won't see real zombies, just insane ppl.


text:
Can a Turner syndrome patient develop male characteristics artificially?
From an answer to the question Can stem cells from male convert to cells of female-only organs, and vice versa?

Y chromosome is the sex determining chromosome with SRY gene that determines testes development. Absence of the Y chromosome leads to female development by default. That is why XX forms women and there are people with only one X chromosome which are women. (Turner's syndrome)

and Why are mice with a single X chromosome and no Y chromosome males?

The Y has only a few genes (less than all other chromosomes), but it has genes that occur only on the Y. One of these in particular, the one called SRY, is the main gene that causes the individual to develop male characteristics. It mostly does its job indirectly, by making a protein that affects many other genes on other chromosomes that in turn do the work of building and maintaining the male form... they managed to cause mice without a Y chromosome to develop many male characteristics. They did this by faking one or two of the actions of SRY. One of the many actions of SRY is to turn on a gene called Sox9 (which is on a non-Y chromosome), and it turns out Sox9 causes most of the things that make the male mouse form.

My question: Is it possible to make a Turner syndrome patient develop male characteristics by artificial stimulation? Has it ever been tried?

After a lot of research, I've finally found an answer.
In the case of humans, it is practically impossible. See this article from wikipedia:

During gestation, the cells of the primordial gonad that lie along the urogenital ridge are in a bipotential state, meaning they possess the ability to become either male cells (Sertoli and Leydig cells) or female cells (follicle cells and Theca cells)...Once proper SOX9 levels are reached, the bipotential cells of the gonad begin to differentiate into Sertoli cells.

This part is just to clarify why it is not possible. In embryonic stage in turner syndrome patients (and females), since SOX9 is not expressed (due to absence of SRY), the bipotential gonad cells in the urogenital ridge (Müllerian/paramesonephric ducts) of embryo develop into female reproductive system i.e. become mature into that state. After this has happened, any amount of SRY cannot develop male reproductive system as all bipotential cells have differentiated into female reproductive system.
It is practically impossible, but virtually it can happen if you can insert Y chromosome or TDF in the bipotential cells of embryo. Practically, doing such experiments on embryo might not be possible (at least for now).

Source

Source
However, it only means that they can't develop primary sexual characters. Secondary sexual characters can, obviously, be developed by efforts as small as hormone injections. In fact, hirsutism is a condition in which females devlop hairs on chest, face, etc. and even beards! Its causes are as common as obesity. See this article:

Some medications can cause hirsutism. These include danazol, which is used to treat women with endometriosis; systemic corticosteroids and fluoxetine (Prozac) for depression...Being obese causes increased androgen production, which can worsen hirsutism.

So, if a Turner syndrome patient wants a moustache or beard (just in case), it can be achieved by androgen injections too.


text:
How does one predict the methylation pattern?
Suppose, we have a double stranded DNA like

5' AGCTAGGAGAGACCAGGTTCC 3'
3' TCGATCCTCTCTGGTCCAAGG 5'

Where would the methylated cytosine be? Is there any randomness?

It is usually at CpG however there are non-CpG methylations too. It is not easy to predict. You can however use machine learning by training from existing experimental data.


text:
Cloning Ice Age Lion Cubs
It was just on the news that scientists discovered "Two cubs in Russia's Sakha Republic last August in a near-perfect state".  And the South Koreans and Russians are attempting to clone these extinct Ice Age lion cubs. (Link to one such news coverage)
According to this answer, we seem to be able to sequence its genome but cloning may be difficult.  However, is this find likely to be the rare large chunk of well-preserved material that makes cloning possible?

The answer that you link to provides a pretty good overview of what it might take to clone an extinct organism from preserved tissue and what some of the challenges are. I won't repeat that answer, but in a nutshell, two big obstacles are incomplete sequences and a host womb.
To get at your question of whether this preserved "chunk" of flesh will lead to the cloning & revival of extinct species...you're a little late to the game. :-)
In 2003, researchers used preserved DNA to revive the Pyrinean Ibex, a goat native to the Iberian Peninsula, that had recently gone extinct. The results were mixed. The experiment worked, in the sense that the scientists were able to successfully bring a recently extinct animal to term, but unfortunately, the revived goat only lived for a few brief minutes, due to developmental abnormalities. It's important to note that this was achieved using DNA that was even better preserved than that of the cave lions in the Mirror article.
So, will the DNA found in the cave lion cells lead to successful cave lion revival? If such a revival occurs, I'm betting that it will be due to advances in how the ancient DNA is integrated with reference DNA and in how fertilization and implantation are carried out, more than on the quality of the found DNA.


text:
The evolution of poor eyesight: is there weaker selection in modern humans?
Short question:
Poor eyesight might have been a major impediment to survival and reproduction in early man (say, 100,000 years ago), but, with the advent of agriculture, major cultural changes, and modern medicine, one might imagine that genes for poor eyesight would persist more easily.
Is that true? Has selection on eyesight been relaxed, or changed significantly, in modern humans? If so, when? Do we know what might explain relaxed selection? If there are any genes associated with, for example, myopia, has their population frequency increased through human history, or has it remained constant?
This New York Times article discusses genetic changes 8 to 4 thousand years ago related to skin color, amino acid absorption, and eventually milk digestion, but it does not mention eyesight.
Background on why I find the question interesting:
A friend of mine speculated that human eyesight is worse today than it was only a few centuries ago, due to the invention and widespread adoption of glasses: a person with poor eyesight genes will now survive and have children, whereas in 1600 they might have died without reproducing.
I'm skeptical: first, glasses became widespread only a few generations ago; second, blurry vision plausibly has little effect on evolutionary fitness. I see no reason why someone with slight myopia would on average have significantly fewer offspring than someone with 20/20 vision, even in a tribe of hunter-gatherers. A short-sighted person could specialize in making hand-axes, for example, and trade them for food -- so I find it plausible that eyesight-related allele frequencies have not changed much over time.
However, I recently heard someone on the radio speculate that eyesight might have worsened significantly a few thousand years ago with the invention of agriculture; the story is that above-average eyesight is a major fitness advantage for a hunter, but not for a farmer.  What does the evidence say?
Side note: I realize that eyesight is affected by more than just genes -- for example, age as well as time spent reading books probably both affect eyesight. That's not what this question is about -- I'm interested in genetic selection.
Edit:  this question is indeed similar to Bad Eyesight and Evolution, but it isn't identical.  That question asks why poor eyesight can persist at all, while mine asks whether evolutionary pressures have changed over time.  In particular, do we know of any genes associated with, say, myopia?  Do we know whether their allele frequencies have changed over human history?

Hi Adrian, I've substantially edited your question to make it more concise, normally that leads to better answers. Let me know if I've changed it too much for you.

@rg255 Hmm, that's a big edit -- I'll try and come up with something intermediate.

I like the edit better. Note that the question is still relatively long.

I think the use of the phrase "poor eyesight" is a little problematic because we don't have a solid reference point. In reference to "perfect" eyesight (how to define that, there are always costs and benefits)? In reference to historic humans (probably largely speculative without definitive evidence)? In reference to other primates or mammals?

@Remi.b I'm asking a different question.  That questions asks "Shouldn't there be evolutionary pressure towards better eyesight?"  Mine is "has eyesight-related evolutionary pressure changed through time?"

@HarryVervet maybe it would help to think about specific genes.  For example, is there any known eyesight-related gene with a "bad" allele associated with higher rates of myopia?  If so, do we know anything about how allele frequencies in 2016 have changed relative to, say, 10,000 years ago?

@rg255 thank you for your edit, I agree that it was an improvement

There is no evolution towards bad eyesight. Generally, myopic patients are not hereditary, but are prone to it because of modern lifestyle.


text:
Neanderthal and modern human population sizes
Are there any estimates of both the modern human and Neanderthal population sizes over the last, say, 100 k years? Since "purebread" Neanderthals are extinct, their population has to hit zero; that happened sometime around 30 k years ago. We have good estimates of both the Neanderthal (zero) and modern human (millions, billions) population sizes in the recent past -- what I'm wondering is what the numbers were (roughly) when modern humans and Neanderthals came into contact. How many people were there in each group? How many interbred? Is there any reliable way to estimate those numbers given what we know today? If not, would it be possible, if we sequenced the genomes of a large number of Neanderthal fossils, to get a sense of how much variation there was in their gene pool, and use that to estimate the size of their population? Could we also look at how much of that variation survives today in the homo sapiens gene pool?
In Why Did 6 Great Ape Species Survive But Only 1 Hominid Species? the poster states that "following the eruption of the Toba volcano 70,000 years ago, there were between 1,000 and 10,000 mating pairs of Homo sapiens left." Was the Neanderthal population of a similar order at that time? Was it ever larger than the modern human population? We'll never know the exact numbers -- and the exact numbers don't really matter. I'm interested in orders of magnitude. When homo sapiens and Neanderthals interbred, did sapiens already outnumber them, or were the populations roughly equal? Were the number of Neanderthal - sapiens crosses tiny relative to both populations, or were they perhaps large relative to the smaller of the two populations?
A related question:  Of the Neanderthals living, say, 100 k years ago, what fraction have descendants who are alive today?  Is that a question we can answer either now or in the near future, after sequencing more Neanderthal genomes? According to http://www.nature.com/scitable/knowledge/library/what-happened-to-the-neanderthals-68245020

recent research on Neanderthal nuclear DNA has found evidence for
  limited admixture: a small portion (up to ~4%) of the genomes of
  non-Africans so far examined may derive from Neanderthals, suggesting
  that interbreeding probably occurred in the Near East during the
  earliest dispersal of modern humans out of Africa, but prior to their
  arrival in Europe (Green et al. 2010). Demographic modeling of
  admixture combined with territorial expansion, however, indicates that
  this level of introgression would be produced under very low (<2%)
  interbreeding rates and strong barriers to reproduction between
  Neanderthals and modern humans, arguing against assimilation (Currat &
  Excoffier 2011). Pending the completion of the Neanderthal genome and
  ancient DNA analyses of early modern Europeans dating to the Upper
  Paleolithic, and following the recent discovery of a third possibly
  coexisting species from Denisova cave (Krause et al. 2010), it is
  premature to conclude that the currently observed level of admixture
  constitutes assimilation.

That would suggest that the fraction of Neanderthals with living descendants is very small -- most Neanderthal lineages died out. What evidence would it take to conclude the reverse -- to conclude that the Neanderthal population was very small, and was largely assimilated?

Just to clarify: in the second part of your question, I think you're asking about neanderthals with living descendants, rather than ancestors. I would make the edit myself, but you've used the term 'ancestors' twice, so I want to make sure I understand correctly.

You're absolutely right, I meant descendants in both cases.

Briggs et al. 2009, using mtDNA report an estimate of 3500 females. They failed to offer any estimate of the male population size. Their estimates is much  lower than previously thought. They report two hypotheses of why their estimate is so low:
Hypothesis 1 - Low population size
H. neanderthalis population size was indeed really low. After all, they mostly had to live in harsh ice age conditions.
Hypothesis 2 - Slow decline in population size
H. neanderthalis population size were quite high at some point and their population size slowly decreased in size up to the point of being completely wiped out. Such low decline in population size may explain the low level of genetic diversity observed (yielding to an estimate of small population size) in their sample. If the decline of H. neanderthalis was sudden, then even the last survivors of the lineage would have shown quite a high level of genetic diversity. Their decline may have started about 40,000 years with the arrival of Homo sapiens in Europe but this is just a speculation. This second hypothesis is congruent with the evidence of a rather rapid rate of evolution observed in H. neanderthalis
In short, we don't really know what the population size of H. neanderthalis was but it might have been as low as 3500 females only


text:
Differences between synaptic connections
Consider the following synaptic connections (from here):

axodendritic - A term pertaining to an excitatory or inhibitory synaptic connection between the presynaptic axon of a transmitting neuron and the postsynaptic dendrite(s) of a receiving neuron in a nerve impulse pathway; such connections can influence whether or not a graded potential will be generated on a postsynaptic dendrite.
axosomatic - A term pertaining to an excitatory or inhibitory synaptic connection between the presynaptic axon of a transmitting neuron and the postsynaptic cell body/soma of a receiving neuron in a nerve impulse pathway; such connections can influence whether or not an action potential will be generated in the postsynaptic axon trigger zone at the axon hillock.
axoaxonic - A term pertaining to an excitatory or inhibitory synaptic connection between the presynaptic axon of a transmitting neuron and the postsynaptic axon hillock or axon of a receiving neuron in a nerve impulse pathway; such connections can influence whether or not an action potential will be generated in the postsynaptic axon trigger zone at the axon hillock.

What exactly are the differences between the connections in terms of their influence on the neuron?
To my understanding:

axodendritic: influences a dendrite $\rightarrow$ hence influences the graded potential of the neuron
axosomatic: influences the graded potential of the neuron directly
axoaxonic: influences the axon only (independently of the neuron?)

Hence, to my understanding the axodendritic and axosomatic connections yield the same result: they influence the graded potential of the neuron (e.g. whether the neuron "fires"), where the axoaxonic connection only influences whether the axon fires. Is this correct?
If so, then what is the purpose of dendrites? If axons can connect to the cell body directly, then why would they need dendrites (apart from yielding a larger connection surface to the neuron)?
Note: I have read this answer, which partially explains the use of dendrites. However, it also states that the signal decay due to the synaptic location is compensated for by the local potential change. Therefore, IMO, the answer states that the main advantage of having dendrites is that inhibitory axosomatic synapses can capitalize on the location-dependence of the axodendritic synapses. Is that the true and only purpose of axosomatic synapses? (Please, correct me if my inference is wrong!)

I wrote that linked answer. I did not mean to imply that synaptic location is always compensated by local potential change.

@yamad Thank you for clarifying. Do you happen to know the differences (in functionality) between axosomatic and axodendritic synaptic connections?

Neurons are all about specialized structures having specialized roles. You've given a good justification for dendrites---an efficient way to fit lots of connections in a small space. A pyramidal neuron in cortex, for instance, will have tens of thousands of synapses. If you only had axosomatic connections, the soma would have to be enormous to fit all of them (and this would cause lots of other issues).
Dendritic structure also allows the cell more efficient electrical properties (see cable theory) and to process inputs independently. In fact, different parts of the dendrite are now thought of as independent computational compartments. For instance, the cell might want to selectively strengthen a single synapse or all the synapses on one dendritic branch. By physically isolating those synapses in small dendritic structures, it is easier to make those targeted changes without unwanted "crosstalk" on other synapses or cell activities. What's more, incoming connections from different areas often segregate into regions of the dendrite (e.g. in CA1 hippocampal pyramidal neurons, cortical connections to the most distant part of the dendrite, internal hippocampal connections to the part of the dendrite closer to the soma).
When a cell has a large dendrite (some neurons have no dendrites), its useful to think of axodendritic synapses as the normal inputs that contribute to fine-grained computation, and axosomatic and axoaxonic synapses as more global gates. These latter types take advantage of their location to short circuit the "normal" computation in the dendrites. An inhibitory axosomatic synapse, for example, will reduce the effect of all dendritic inputs when activated.

Extremely informative. Thank you. If I may, I would like to know your opinion about the theory that the "firing" of neurons is somehow connected to the specific combination of excitatory dendrites. E.g. if we neglect differences in potential change and assume 3 dendrites to excitate with the same potential effect on the membrane potential, do you think that different combinations of these 3 dendrites have a different effect on whether the neuron fires? Or are the potential changes from the three dendrites always simply summed up? So, given equal potential change, does location matter?

@Jean-Paul Yes, location matters. In general, the spatial and temporal pattern of synaptic activation matters a lot. Two synapses activated at the same time on different dendritic branches will have a different effect from two synapses on the same branch. Two synapses on the same branch will have a different effect depending on the order of activation. Good rule of thumb for thinking about neural computation: if something can vary, it probably matters (and if it doesn't matter, there is probably a very interesting story about how the neuron ignores the variation).

Thank you very much for your time and effort! This is very helpful. I'm just curious now: does location matter in terms of signal strength or does it matter for the pattern in which the neuron fires?


text:
What are the chemicals in the gap at a synapse?
I am learning about (introductory level) biological psychology and the synapse structure came into mind. I do understand that neurotransmitters are transmitted between two neurons via the synapse structure.
What I found about neurotransmitters was that there are several types of them, including amino acid, and other stuff (I don't really know chemistry..). The problem is that, according to the following picture, neurotransmitters are transmitted across the gap. What are the chemicals in the gap at a synapse? There must be some medium that transmits neurotransmitters right?

My guess is that there is a special solution in which neurotransmitters are soluble. Any help will be appreciated. Thanks in advance!

Hello Zang.Welcome to Bio SE.Your question already been answered. Check it here: https://biology.stackexchange.com/questions/85719/what-material-fills-the-synaptic-cleft-is-it-water/85913#85913

@Science123 Thank you.


text:
Do afterload and stroke volume form part of a negative feedback loop in blood pressure regulation?
Blood pressure is the product of cardiac output and total peripheral resistance:
$\text{BP} = \text{CO} \times \text{TPR}$
Since cardiac output is the product of heart rate and stroke volume, we have:
$\text{BP} = \text{HR} \times \text{SV} \times \text{TPR}$
Stroke volume is determined by preload, contractility, and afterload. An increase in afterload leads to a reduction in stroke volume and thus a decrease in blood pressure. [1]
However, it then seems that hypertension, which increases afterload, would lead to a decrease in blood pressure and form a negative feedback loop. Is this in fact what happens in the human body?
Also, when total peripheral resistance increases, it seems to me that afterload should increase, leading again to a reduction in blood pressure. Nonetheless, peripheral resistance also directly determines blood pressure ($\text{BP} = \text{CO} \times \text{TPR}$). Which of these has a stronger effect?
1: http://pie.med.utoronto.ca/CA/CA_content/CA_cardiacPhys_strokeVolume.html

However, it then seems that hypertension, which increases afterload, would lead to a decrease in blood pressure and form a negative feedback loop. Is this in fact what happens in the human body?

Yes and no. If the only parameters affecting cardiac output were peripheral vascular resistance, then yes, a resultant decrease in blood pressure would occur initially with hypertension. And yes, that is what happens. However, it is quite temporary because there are numerous modulators of "blood pressure", as blood flow, especially to the head, is critical to survival.
There are baroreceptors located at points in the arterial vasculature  which, upon sensing a fall in blood pressure, cause the sympathetic nervous system to release positive inotropes, causing the heart to contract more forcefully to push out that increased afterload. There are cordioreceptors assessing the effect of every heartbeat; decreased BP causes an increase in heart rate.  Sensors in kidney arterial vasculature sense decreased blood pressure and preserve water and electrolytes to increase intravascular fluid volume. Etc, etc.
Which in the end boils down to

BP = CO x TPR

Thank you, can't upvote yet but I would. Is there a way to predict with any accuracy what the effect of changing one of these parameters (as in a pathological condition or upon administering a drug) would be? Right now, I feel like the answer is just "it depends on many variables", but I assume that wouldn't be of much help in a clinical setting.

Of course! These things are studied extensively in disease and drug trials. If we couldn't predict their effects, drug dosage recommendations and therapies for diseases would not be possible. I don't need mine to be the accepted answer, but if it was/is helpful, you certainly should upvote it.

Not really following your logic at all, but maybe it helps to think that the parameter that needs to be held constant to deliver sufficient/constant blood to tissues is cardiac output.
All you need is your first equation:
$\text{BP} = \text{CO} \times \text{TPR}$
to see that an increase in peripheral resistance will mean an increase in (mean) BP if CO is constant.
Anything else you argue from subsequent steps has to conform to this, or you've made an error someplace.

I agree that this would be the case if there were no feedback loops and the cardiovascular system could be modeled in a linear manner. However, why do you consider that first equation to be the 'primal' equation? For example, if you agree that increasing TPR increases afterload, which decreases SV and subsequently decreases CO, then surely increasing TPR both increases and decreases BP. I don't think we can simply assume that CO is constant.

@Quin No, you can't assume anything at all; for many possible parameters, the outcome is death and then you can simply assume everything drops to zero. I'm saying that what the body cares about is how much blood it gets, so generally that's the reference point it makes sense to consider from a perspective of homeostasis. From a perspective of illness, all bets are off, but it doesn't make any sense to assume homeostasis is absent, either.


text:
Breathing becomes harder in certain wind conditions
I'm not sure if this is the right site to ask this, but it seemed like the best option.
I've observed on myself that, if I stand on a train platform and a cargo train drives by, creating strong, short gusts of wind, it becomes harder to breathe for me during the gusts, almost like fighting my body into breathing.
A commenton parenting.se leads me to believe this is due to the mammalian diving reflex.
1) is this assumption correct? 2) what causes the change in breathing?

So I'm going to go ahead and tell you outright that it is not the diving reflex.
What you are experiencing is the effect of air pressure.

Our lungs work off of pressure. Specifically our lungs inflate by using "negative pressure" (a word I've always hated). The pressure is not actually negative it is simply lower than the surroundings. Since there is less air in your lungs the air from the atmosphere rushes in because the pressure is higher outside your lungs. This is Boyle's Law (not the pressure outside being higher, but what happens when your lungs expand). Where an increase in Volume means a decrease in Pressure (if all else remains unchanged). In fact plants pull water up using negative pressure.
However to push out the air from our lungs we supply pressure using our muscles that overcomes the outside pressure and forces the air out.
The reason you feel your breathing change is because when that train passes by you correctly observed the strong gust of wind. This gust of wind has some force behind it that normally is not in the air you are breathing from the atmosphere. It has more force which increases the air's velocity. This actually decreases the pressure, but there's no need to get into that here (Bernoulli's).
The reason it feels like your body is "fighting to breath" is because the air is traveling in a direction with some force that you need to overcome by opening up your lungs just enough to "suck" the air in with negative pressure. This is more than the pressure you usually need to produce in order to breath in air that is "still".
What is funny to think about is we don't really have a muscle that "pulls" air in, even though it feels like you are actively doing that. The air actually rushes in on its own. All you do is expand your rib cage, which your lungs are attached to (look up on how, it's actually pretty cool), thereby making inhalation occur.
Now an interesting question for you to ask yourself is why is cold air harder to breathe?

Excuse my comment, but I don't see how your theory holds up, considering your lungs are in equilibrium with the outside pressure. Even in complete vacuum you would be able to perform a thorax motion, that could be perceived as breathing in. The perceived struggle to attempt the motion per se seems hard to be justified this way. Also regarding your comment about trees (especially if above 10m) please consider reading these answers: https://biology.stackexchange.com/questions/11044/how-do-trees-lift-water-higher-than-10-meters.

Also, the diving reflex is known to be triggered by ambient temperature, or better to say, the increased heat-capacity or heat transfer of water compared to air. The sheering forces created by passing air significantly increases the effective heat-transfer, which might be perceived as being submerged in water.


text:
Where can I find a file listing the genetic differences in humans?
I don't know much about genetics. For an arts project I'm looking for a human genome.
I read that:

Only about 0.1% of the genome is different among individuals, which equates to about 3 million variants (aka mutations) in the average human genome. This means we can make a “diff file” of just the places where any given individual differs from the normal “reference” genome. In practice, this is usually done in a .VCF file format, which in its simplest format looks something like so:
chr20 14370 rs6054257 G A 29 PASS 0|0
Where each line uses ~45 bytes, and you times this by the ~3 million variants in a given genome, and you get a .VCF file size of about 135,000,000 bytes or ~125 megabytes.

Is that correct?
Do you know a database to download a VCF file or something similar? It would be amazing if you could provide a link to the file mentioned above!

You may need to rethink your number, that 0.1% number might be a little low... If you are interested in the genetics, you may be interested in this answer, http://biology.stackexchange.com/a/41975/16651. Also, NCBI's databases are open to the public and you should be able to download whatever you want from them.

Technically speaking (and in SI and IEC terms) 135,000,000 is 135 Megabytes (MB) or approximately 129 Mebibytes (MiB).

Have you tried poking around the 1000 genomes project?
Try this link
ftp://ftp.1000genomes.ebi.ac.uk/vol1/ftp/pilot_data/release/2010_07/exon/snps/


text:
What is the maximum/minimum temperature humans can survive at for an extended period of time, and what rate does the body temperature change at?
3 questions:

At what rate does the body temperature of a human change at? That is, assuming the outside temperature is x, is there some sort of formula that can determine how long it takes for the human body to reach any temperature above or equal to x? I understand this is quite variable, but any data will be useful.

a) What are the harshest conditions currently on Earth that we can survive at (That is, the maximum temperatures people actively live at every day for a period of years, and the minimum temperatures they do so).
b) In what ways have their bodies adapted to allow them to do so?

Thanks!

Hopefully you're not asking this because of the covid-heat-yourself-to-56C-cure nonsense.

Why would that be the reason .... starts sweating because he's in a 60C home and doesn't know if he's going to die so he hoped the bio stack exchange would

This depends a lot on what kind of clothing and tools the human has.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, each question should be posted separately — this improves the chances that you will get answers for each question and makes the answers more accessible for future users. ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!


text:
Why do the hormones FSH and LH decrease when the follicle is maturing and does size of follicle change during menstruation phase
There are three phases in menstrual cycle. In follicular phase of menstrual cycle, the level of FSH and LH would rise because they would stimulate ovarian follicle to mature. However, when I check with diagram of menstrual cycle, I find FSH and LH hormones do actually decrease during day 4-14. Is that because of increase of oestrogen? However, by the time when FSH decreases, the follicle hasn't fully matured. Also, will follicle grow during menstruation, because in diagram, the size of follicle actually changes during Day 0-4, and FSH and LH hormones increases.

I find FSH and LH hormones do actually
  decrease during day 4-14. Is that because of increase of
  oestrogen？

You first need to note that during one ovarian cycle, multiple follicles are stimulated to grow at the same time by FSH. However, one follicle ends up being the dominant follicle, and it is the oocyte housed within this follicle that is released on day 14. The dominant follicle is the one whose cells express gonadotropin receptors the earliest and so have the greatest sensitivity to FSH. Its growth would outcompete the other developing follicles. During days 4–14, FSH begins to decline because the granulosa cells of the follicles secrete inhibin, which—just like in males—causes the release of FSH and LH from the pituitary to drop. Only the dominant follicle is capable of withstanding this FSH drop; the other developing follicles are thus eliminated.

Also, another question is will follicle
  grow during menstruation, because on diagram,the size of follicle
  actually changes during Day 0-4, and FSH and LH hormones increases.

As user19099 explains, yes, follicles grow during menstruation. With the degeneration of the corpus luteum, the negative feedback effect of estrogen and progesterone (in combination) on the hypothalamus is relieved. Thus, GnRH levels increase, causing FSH and LH levels to increase (as reflected on the graph you included), and FSH will stimulate follicular development.

References

Marieb, Elaine Nicpon, and Katja Hoehn. Anatomy & Physiology. San Francisco, CA: Pearson/Benjamin Cummings, 2008. Print.

Another question is how can the level of FSH and LH decrease once they start in follicular phase. It's said the level of FSH and LH would increase to mature follicle. Is there a clash between knowledge and fact? As you mention, the drop is because of inhibin. So, body would release inhibin once going into follicular phase?

@Q.MEO FSH and LH increase during the early follicular phase. As ovulation approaches (i.e. late follicular phase), inhibin is released by the granulosa cells, so then FSH and LH decrease. There is a rise in FSH/LH levels, and then a fall, as you can perceive from the graph. I think your graph is unclear, as it makes it seem as though follicular phase lasts from day 4–14. That is untrue. Follicular phase starts from day 0 to day 14. Note that just because FSH falls does not mean there is no FSH to stimulate the dominant follicle; there’s still FSH—just a lower level than before.

Does it mean follicular phase include menstruation???

@Q.MEO Menstrual cycle has 3 phases: menstrual, follicular and luteal phase. Menses occur in menstrual phase i.e. day 0-4.

@Q.MEO Yes, it does. You should differentiate between the ovarian and the uterine cycles. The ovarian cycle includes the follicular phase and the luteal phase, while the uterine cycle includes the menstrual flow phase (menstruation), proliferative phase, and secretory phase. The two occur simultaneously and relate to each other hormonally but occur in different locations—one concerns the ovary and one concerns the uterine lining. The follicular phase overlaps with the menstrual flow phase and the proliferative phase.

My (honest) opinion, don't pay too much attention on the graph. While looking at other graphs on the internet, I found that many graphs show different levels of hormones on the same day. See these two images (upper one from here and lower one from here) for example:

See the level of FSH and LH on same day in both graphs, you'll find difference. In short, the graphs are just to show approximate value, don't try to derive answers from them.
For your next question will follicle grow during menstruation, yes the follicle grows continuously through the menstrual and follicular phase. A primordial follicle (dormant one, which was arrested in diplotene stage) has a diameter of about 25 μm1, which grows upto 16-20 mm2 before ovulation, as a Graafian follicle.

Source
References:
1.http://www.glowm.com/section_view/heading/Follicle%20Growth%20and%20Development/item/288
 2.http://www.fertilitytoday.org/frequent_questions.html

But I am still confused about why there is no increase in follicular phase. According to knowledge, it's said there is a increase of level of FSH and LH. Is there a clash between knowledge and fact. Or it is just about accidents?


text:
What are the secondary structure requirements for cell-penetrating peptides AKA protein transduction domains
Cell penetrating peptides.
Cell penetrating peptides (CPPs) are a class of short amino acid sequences which are sufficient for crossing cell membranes and delivering themselves along with any attached cargo into the cytoplasm of cells. They were branded CPPs recently, while the term "protein transduction domain" (PTD) was used in the early days of their study, when the necessary sequences were being isolated from native proteins with cell-penetrating activity (notably, HIV-1 Tat).
Most of the scientific literature I have found on CPPs focuses on their potential relevance for targeted drug delivery, and mostly discusses the delivery of proteins and nanoparticles via fusion of CPPs to the N-terminus of the target protein. The only Stack Exchange question & answer on CPPs also points to a discussion of N-terminal fusion of CPPs to a cargo peptide. However, research on cell penetrating peptides has come a long way since the 2005 article referenced in that post.
The 2012 Milletti review highlights that there has been a dramatic increase in the number of different classes of cell penetrating peptides, including hydrophobic CPPs, primary amphipathic CPPs, alpha-helical amphipathic CPPs, beta sheet amphipathic CPPs, and proline-rich CPPs, among others. And that is just between 2005 and 2012! The Milletti 2012 article also covers some CPPs isolated from other viruses.
I have not been able to find a review of similar detail written since, although I'm sure much progress has been made in the field.
Although it is not my main question, I would appreciate any citations for more recent reviews which go into detail on the molecular mechanism of cell penetration for one or more classes of CPPs - especially a review of the function of PTDs in their native proteins.
I have only begun to research CPPs and PTDs in their native proteins and in the drug-delivery setting because it became apparent that a protein I am studying for an undergraduate thesis may have an internal PTD which is essential for its function. I am no expert on the topic and I would appreciate information on CPPs/PTDs including further synonyms for CPPs/PTDs to aid in my literature search - especially synonyms specific to native proteins with CPP-like functions.
What are the secondary structure requirements for cell-penetrating peptides?
My question is whether the previously described positively charged CPPs and/or the new classes of CPPs described in Milletti 2012 are only functional as N-terminal fusions, or whether they typically function efficiently when they are incorporated within an internal loop (in terms of primary sequence, but still exposed to the solvent). The 2005 article cited in the previous Stack Exchange question on this topic stated that the CPP derived from HIV-1 Tat is based on residues 47-57, which are internal residues of the 86 amino acid protein - a protein which has cell-penetrating activity in its native role in HIV-1 infection.
Therefore, my question is not whether or not this ever occurs - it clearly does - but to what extent do CPPs isolated from internal sequences of native proteins have CPP-like functions in their native proteins?
The system I am studying for my thesis is a virus, so any information specifically on CPPs and PTDs function in the native proteins of viruses would be particularly useful.

References
Jones, S. W., Christison, R., Bundell, K., Voyce, C. J., Brockbank, S. M. V., Newham, P., & Lindsay, M. A. (2005). Characterisation of cell-penetrating peptide-mediated peptide delivery. British Journal of Pharmacology, 145(8), 1093–1102. http://doi.org/10.1038/sj.bjp.0706279
Milletti, F. (2012). Review: Cell-penetrating peptides: classes, origin, and current landscape. Drug Discovery Today, 17850-860. doi:10.1016/j.drudis.2012.03.002
Vivès, E., Brodin, P., & Lebleu, B. (1997). A truncated HIV-1 Tat protein basic domain rapidly translocates through the plasma membrane and accumulates in the cell nucleus. The Journal Of Biological Chemistry, 272(25), 16010-16017.
If anyone interested in answering this question is not an expert, the best resource I can currently provide for a list of CPPs derived from natural proteins (besides the Milletti 2012 article above) is:
Hallbrink, M., Kilk, K., Elmquist, A., Lundberg, P., Lindgren, M., Jiang, Y., & ... Langel, U. (n.d). Prediction of cell-penetrating peptides. International Journal Of Peptide Research And Therapeutics, 11(4), 249-259.

I will be continuing to research this topic for my thesis, so if you're interested in answering this question but require more information, feel free to comment asking for specific information that would help.
Thank you!

This is a very interesting and thorough question. Although I don't have an immediate answer I'd be interested to know more about CCPs. I'd like to know more about cargo and membrane insertion. Please feel free to respond in the biosphere (and ping me using @James) since comments are not really intended for extended discussion. (Also, I've made some stylistic edits to your question, feel free to roll back!)

@Demosthenes' pars triangularis Are you still in the field of CPPs research?