text:
Is WIFI safe for humans?
I have wifi on at my home almost all the time. I learned that the frequency of visible light is around several hundreds of THz, while the frequency of wifi is only several GHz, which is only 1:100,000. But I'm not sure how the amplitude of wifi wave compares to the amplitude of the visible light? Are the frequency and the amplitude the only concerns when we talk about the radiation? Can someone educate me to quantify the effect wifi radiation could have in our life?

Welcome to BiologyBeta.SE. Your question is off-topic here. It would be on-topic on Skeptics.SE. But before asking, notice that this post probably already answers your question.

what is being said here is that there is not enough evidence to sustain a conclusion here, and so its not a great question for this site.  on the other hand you can also take that as the answer to your question.

so digging a little more into your question , this might also be a physics question.  there are two aspects of electro magnetic radiation which are good places to start.  first is the power of the signal, which is related to amplitude and frequency of the wave, but is on the order of Watts usually. The second is how often the frequency of the radio wave is absorbed by the body and what.  that is much more controversial.  1 GHz waves are have a wavelength of about 30 cm - or about a foot.  this is why radio waves tend to pass through walls and through bodies.  Can this still be harmful?

its not a strong number. but small amounts of power concentrated in tiny spaces can be harmful.  so that's the controversy.  Its hard for many of us to believe that a fraction of a watt deposited extremely rarely in the body can be harmful in an extraordinary way.  (say more than commercial radio transmissions)  but its very hard to say it isn't with enough confidence to shut off speculation. so that might give you an idea of what sort of answer you might get.

Thanks @shigeta, actually I asked the same question at http://physics.stackexchange.com/questions/119806/is-wifi-safe-for-humans before I asked here, but unfortunately I met a group of politicians.

@shigeta thanks for your idea. So how do you think if we are exposed to our home lamp vs to the home wifi? Can I say the radiation from the visible light from home lamp is much stronger than it from the wifi?

yes but also visible light does not penetrate the skin (much).  there's really no way to definitively end the argument. that's why you might have gotten some static here.  although that is also true for most scientific questions too - very few scientific papers definitively come to a proof of one thing or another.  a lot of people ignore this when calling questions 'subjective'.


text:
What is the difference between Leloir and Non-Leloir glucosyl transferases?
The following questions were on the slides for my biotech course and I haven't been able to find any information on what the answer is.
What is the difference between Leloir and Non-Leloir glucosyl transferases?

LeLoir glucosyltransferases use uridine-diphosphate (UDP) 'activated' sugars as substrate, for example UDP-glucose, where 'LeLoir' refers to the LeLoir pathway, the metabolic pathway that inter-converts glucose and galactose (or, more strictly, the inter-conversion of UDP-glucose and UDP-galactose)
Non-LeLoir glucosyltranserases use sucrose as substrate and do not require the sugar to be be conjugated to UDP (or to be 'activated' in any way), and as such are very useful in the biotechnology industry.
See
A new pathway for the synthesis of oligosaccharides by the use of non-Leloir glycosyltransferases)

LeLoir was an eminent Argentinian biochemist.
For the enzymes of the LeLoir pathway,
The Leloir pathway: a mechanistic imperative for three enzymes to change the stereochemical configuration of a single carbon in galactose
by Perry A Frey is IMO definitive (and the pdf is freely available).
(Glucose and galactose are epimers: they differ only by the configuratation at C4. A key enzyme of the LeLoir pathway is UDP-glucose 4-epimerase, which contains a tightly bound NAD(+) and epimerization proceeds by oxidation/reduction (strictly, hydride abstraction/addition) at C-4, where the tightly bound NAD(+) is transiently reduced during catalysis: ie, NAD acts a (transient) hydride 'repository'! To the best of my knowledge, no enzyme has ever been found that directly catalyses the epimerization of glucose to galactose (although there appears to be no thermodynamic reason why this is not possible): the sugar must be conjugated to UDP in order to be a substrate for UDP-glucose 4-epimerase)

source: Stack Exchange

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

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

sort: votes


text:
How to write a stoichiometric matrix for a part of the Pentose phosphate pathway
maybe this is more bioengineering than biology but I didn't find any such group.
So I got the following photo:

And I was asked to do the following for the network inside the red area.
1) Write the stoichiometric matrix for the network
2) Draw a pathway map for the network
3) Draw primary metabolite connectivity maps
4) Write the mass balance equations for primary metabolites
I know that for the first one the columns are the reactions taking place and the lines are the "chemicals". Should the markings on the columns be the same as the numbers that are written on each reaction? (like "3.1.1.31")
Almost every reaction can go in both direction, is there anything that says which chemical should get minus and which one gets plus?
My attempt at the matrix was:

As for the pathway map, isn't that basically the photo is given?
And finally what would be a "primary metabolite" in this case?
All help and hints very well appreciated!

This is not a particularly well written homework question. I'll try to give some hints based on how I interpret it.
1) The stoichiometric matrix. You have exactly the right idea. I would write the reactions as enzyme names or gene names instead of the EC numbers (e.g. G6PD or G6P dehydrogenase instead of 1.1.1.49). For the reversible reactions, there's no a priori reason to write them in one direction or another, but convention would be to make glucose consumption the positive direction. I would not include "glycolysis" as a separate reaction. I would also consider including cofactors and byproducts in the molecules affected by the reaction (e.g. CO2, NADP+, NADPH, (maybe ADP, ATP, NAD+, NADH also if those come up)).
2) Yes, it's basically what you already have. It's not a particularly great diagram, so you could draw it in a clearer way.
3) I have no idea what this means, but perhaps the next point will help.
4) Primary metabolite is not a super well-defined term, but I think in this context, I would say that the way they're intending the question, they're looking for a "total pathway reaction" that describes the net inputs and outputs of the pathway.
Something like this:
$$
X_1 G6P + X_2 NADP+ \implies X_3 GAP + X_4 FBP + X_5 CO_2 + X_6 NADPH
$$
(G6P=Glucose-6-phosphate, GAP=Glyceraldehyde-3-phosphate, FBP=Fructose-bis-phosphate)
I'll leave it to you to figure out what the X's are or whether I left anything out (since it's a homework assignment after all.)

Thank you so much!
But okay since H6PD has the same EC numbers as the two reactions below (1.1.1.49 and 3.1.1.31) should that be considered as a separate reaction or is it enough to only have the other two?
Also if glycolysis shouldn't be included as a separate reaction how do I mark down the carbon going in and out of the network?

Yeah some enzymes will catalyze more than one reaction. You'll have the same problem with transketolase. Nothing wrong with suffixing them _A and _B or whatever. I didn't mean to say that using the EC numbers was wrong either -- I would just say that if you want human-readable names, biologists/biochemists are more likely to recognize gene names. Few people have the entire EC number hierarchy in their head.

Sorry, misunderstood your first question. Each reaction should only appear once, however you name it. The EC number (1.1.1.49) refers to the type of biochemical reaction going on. The gene name refers to the enzyme that catalyzes that reaction. They refer to the same reaction, just in different ways.

As for carbon going in out, you sort of already have this (e.g. a -1 for G6P in the G6PD (1.1.1.49) reaction. At the end of the day, the point of this matrix is that if you multiply your matrix by a vector of how much flux is going through each reaction, you'll get a vector with an entry for each metabolite that tells you how much is being produced or consumed. For this to be sensible, every reaction should be mass-balanced (so nothing that produces something out of thin air).

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


text:
Why is it good to use Glycerol as carbon source to produce intermediates in pharmaceuticals?
Why is it good to use Glycerol as carbon source to produce intermediates in pharmaceuticals?
My best guess would be because it produces a lot of ATP per carbon. But I haven't found anything to verify my hunch.

You might get better answers on Chemistry.SE if you are asking about the process of chemically synthesizing pharmaceuticals. However, I'm confused, why are you referring to ATP?

@BryanKrause okay thank you I will. Well okay maybe I'm thinking about this all wrong I just thought about how when using Glycerol as a carbon source for E.coli it produces more ATP/fuels more growth per carbon than for example Glucose.

Are you thinking about pharmaceutical production by E.coli? That's getting a lot more specific than your question suggested originally. If you have a citation to a particular protocol or something that might also help you get better quality answers.

Do you have a reference for the fact that more ATP per carbon is produced from glycerol than from glucose?

First, glycerol is economically and environmentally interesting as a substrate. It is a side product of first generation biodiesel production, which has been increasing in the past years. So large amounts of glycerol are being accumulated, while we make little use of it. Therefore it has become a necessity to develop glycerol utilizing industries. Another consequence is that glycerol is now a cheap and abundant substrate.
The metabolism of glycerol is quite complex and has many end products that are of industrial relevance. For example, 1,3-propanediol and succinic acid have commercial applications and can be produced directly from glycerol by some microorganisms. So depending on the strain you use, you may not need heavy metabolic engineering.
Here is an article that might help you.


text:
What are these black masses floating on my pool?
I've been cleaning them for some time. At first I thought it was some kind of synthetic material, but when I took one with my fingers it disintegrated into filaments. I placed another under my usb microscope and they appear to be an aggregate of green tubular bodies.

They grow (appear) from one day to another, only 1-2mm diameter. My best guess is that they are some kind of algae, but I'm lost to find exactly what. I live in the south of Spain, the pool is treated with chlorine, in a well illuminated zone. There are no other algae growing, and the area is urbanized.

I was looking in the wrong kingdom. After much searching I asked myself: are those eggs? Silly me, of course they are. I should have thought it from the start. Mosquitoes plant their eggs on water over night. I was confused because in the past I've never seen the eggs, only the larvae and the pupae in the water. So, that's what I have every morning floating in my pool, groups of mosquito eggs.
http://animalia-life.club/other/mosquito-eggs.html

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


text:
Antibiotic resistance
I have a biological puzzle that's been perplexing me for years.  Can you review my logic and tell me where I'm wrong or if I'm on to something.
As I understand it, most, if not all genetic engineering uses a marker gene to identify transformed bacteria.  This marker gene was/is usually an antibiotic resistance gene so the transformed bacteria will be the only ones that can grow on an antibiotic laced culture medium.
So, every (most) GMO will contain a copy of a bacterial antibiotic resistance gene.
Also, I believe that bacteria are able to spontaneously aquire DNA from their environment and / or other bacteria.
So, is it a fair question to ask if the unnatural proliferation of antibiotic resistance genes in the wild due to the commercial propagation of GMOs might be at least partially responsible for the increase in multiply resistant organisms that we are seeing?
Has anyone, for example, mashed up GMO matter, added non antibiotic resistant bacteria, grown the mix up overnight, added the antibiotic used as a marker in the GMO, incubated for a few days and then seen if any bacteria survived?

As I understand it, most, if not all genetic engineering uses a marker
  gene to identify transformed bacteria. This marker gene was/is usually
  an antibiotic resistance gene so the transformed bacteria will be the
  only ones that can grow on an antibiotic laced culture medium

Most but color markers (which gives the host cell a color that can be used for selection) are also used. More complicated selectable-counter selectable markers are also used (ie  HyTK gene). A counter selectable marker is a marker that kills a cells when it is present. A selectable-counter selectable marker is a hybrid marker that allows you to both select for cells with the marker using one selection agent and kill the same cell with a second selection agent.

So, every (most) GMO will contain a copy of a bacterial antibiotic
  resistance gene.

Well not quite. GMO ie Genetic modified organism, includes both prokaryotes (bacteria) and eukaryotes (plants, animals, and yeast). The promoters which drives gene activity in prokaryotes and eukaryotes are different. So a eukaryote markers do not work in prokaryotes and vise versa.
Furthermore, genetic modification of eukaryotes is difficult. Hence modified viruses are often used. These viruses are made in such a way that their genome has been replace by desired DNA playload. And as the payload size is limited, often time any unnecessary DNA is also removed, like prokaryotic markers which have no function in a eukaryotic host.
Lastly due to public pressure, there has been a push towards cleaning up after genetic engineering work in GMOs that are to be marketed to the public (GMO crops). So things such a selection markers are removed (either by use of counter selectable markers followed homologous recombination or site specific recombinases).

So, is it a fair question to ask if the unnatural proliferation of
  antibiotic resistance genes in the wild due to the commercial
  propagation of GMOs might be at least partially responsible for the
  increase in multiply resistant organisms that we are seeing?

Given the wide spread use of antibiotic in animal husbandry and by the public general, and move toward removing selection markers in commercial GMOs, I do not think GMOs are the cause of the increase in MR bacteria.
A more likely cause would simply be because we are using so much antibiotics and thus there is a selection pressure to aquire multiple resistance. Remember all our antibiotics resistance genes and most of our antibiotics were acquired from nature.

Has anyone, for example, mashed up GMO matter, added non antibiotic
  resistant bacteria, grown the mix up overnight, added the antibiotic
  used as a marker in the GMO, incubated for a few days and then seen if
  any bacteria survived?

Yes, lots of times around the world to varying degrees of sucess. I have personally spent time doing this and so have my labmates. It will work if you prepare good quality DNA that has not been degraded by endonucleases, the bacteria are very transformable (ie the bacteria has been treated to take up DNA easily), electroporation is use (to force the DNA into the cell) and you have prokaryotic marker. A eukaryotic marker, is a marker that works in an animal cells will not work in bacteria. So you have to engineer your GMO animal to carry both a eukaryotic and prokaryotic marker.


text:
How to choose the most appropriate measure of genetic distance
I am conducting a phylogeography study of a fish species and am trying to construct a phylogenetic tree to describe population structure and ancestry. I have constructed trees using various measures of genetic distance, such as Nei's DA, DS, and Edwards Chord distance. The answers I get between these measures are conflicting, but each explained by a sound hypothesis, and so I must carefully and objectively choose which measure of genetic distance is to be most trusted given my data.
So my question to the community is not, "which should I choose?" but "how should I choose?" I am interested in an answer or (ideally) resource that describes what factors I should take into account and that may bias my result.

I think we are at cross purposes: cenimorgans describe the statistical distance (linkage) of markers from one another on one genome. What I am interested in is the distance in terms of divergence between multiple genomes (population samples) for the same marker or set of markers.

Have you looked at Rogers, Deriving Phylogenetic Trees from Allele Frequencies: A Comparison of Nine Genetic Distances?


text:
How fast can the human body temperature change?
I'm really curious about how fast can a human body temperature change?
E.g. how fast can the human body temperature change when the human has fever?
I'm not interested in how fast fever changes the temperature, more likely how fast the human body is possible to change it?
I found allot information about how much the temperature changes over the day and so on, but now how fast the human body is "capable" to change it in a certain time span.

This depends on a lot of things. It's pretty slow if you are limiting the change to be entirely internal. If we get help from environmental extremes though, the change can be quite rapid.


text:
Are Zebras white with black stripes, or black with white stripes?
I'm not sure it makes sense, but are zebras black or white below the surface?

It is not like someone painted a zebra one color (say white) and then painted lines of the other color (say black) on top. But it does not mean we can't give some thoughts on the question.
What causes these patterns?
The colors are caused by pigments. Melanocytes either produce black pigments or do not and this cause the alternation of white and black stripes. The exact developmental pathway for producing these stripes is still very much unknown. All we know is that several environmental variables seem to affect this pattern. The most important correlate found so far is temperature, where higher temperature lead to darker and better defined stripes (Larison et al. 2015). This pattern can also be observed geographically (although there might have other important covariate driving this pattern, such as genetic typically)

So, are zebras black or white?
According to the Brevard Zoo, under their white or black fur, the skin is always black. This, I suppose, might lead others to rather claim zebras are black with white stripes.
From @iayork's answer, it appears that embryos are first black and then white tripes appear. This an extra reason to claim that zebras are black with white stripes. Note however, that I am not sure whether the skin of zebras are not first white, then turn black and then black fur and then white fur. Under such circumstance, one might want to argue that zebras are white with black stripes.
So if we take your question as phrased

[A]re zebras black or white below the surface?

If by "below the surface" you are referring to their skin, then they are black (according to the Brevard Zoo)!

Zebra embryos start off black and develop white stripes late in development. This is widely used to conclude that zebras are actually black with white stripes, and it's as good an argument as any for this essentially semantic question.


text:
If animals die why dont plants?
I am not a Phd in biology so don't go hard on me.when I was walking to home after swimming class I saw a mouse dead and was intimidated by gods wonder but when I reached home I saw the Devil's ivy and my thoughts flung to the 450 year old tree in my city why didnt it die when the mouse did.

There are whole large groups of plants that die in a relatively short time.  Annuals, for instance, grow from seed to mature plant, produce seed, and die within the space of a year.  Desert ephemerals are even shorter-lived, compressing the whole sprouting to seed process into the few weeks after a rain.

rephrase that question to not talk about intimidation by gods, not Phd, walking, swimming, it's a mouse/tree longevity question only.

plants have a slow metabolic rate. to can go into stasis, they can freeze below -20, they can go without water. complex machinery breaks faster than simple stuff, i.e. a scythe versus a lawnmower.

Many plants don't have the lifespan of a mouse. Many animals don't have the lifespan of a tortoise. This isn't about Biology. It's about learning. Your question is based on misperceptions.

What do you mean by plants don't die? You don't have to have a PhD to comment on this! Haven't you seen dead grass or any dead plant in your life? Some trees have a long lifespan, like the banyan, but they do die. Even turtles have a long life, but that doesn't mean that they don't die.

Plants die of old age too. Trees tend to have a long lifespan but still.... they die of old age.
There are few species that seem to have negligible sensescence such as

giant tortoise
greenland shark
aspen tree root system
mussel

and some that even seem to never age (biologically immortalilty) such as

lobster
hydra
some bacteria
some yeast

but you most definitely cannot make such generality as "animals age, plants don't".


text:
What is the diameter of the measles virus?
I have searched countless studies. None have given this number. In fact there seems to be no details of any kind about the measles virus.

I'm voting to close this question as off-topic because questions like this are far too simplistic for Biology.SE; answering the question is as simple as Googling "measles virus diameter."

I believe this paper answers your question or at least comes very close to it: https://www.ncbi.nlm.nih.gov/pubmed/6540797
I'll reproduce the abstract here, with emphasis mine to indicate the relevant portion:

The molecular length of measles virus RNA and the structural organization of measles nucleocapsids.
Full-length measles virus RNA molecules isolated from purified virions or nucleocapsids and examined by electron microscopy were 5.12(+/- 0.12) micron in length, corresponding to a molecular weight of 5.2 (+/- 0.1) X 10(6). Purified virions examined by negative staining in the electron microscope exhibited a pleomorphic range of particle sizes varying in diameter between 300 nm and 1000 nm. Purified nucleocapsids had dimensions of 21 nm (diameter) X 1254(+/- 7) nm (length) and a central core of diameter about 5 nm. Full-length nucleocapsids were composed of 204 (+/- 3) protein discs. The pitch of the nucleocapsid helix was calculated to be 6.1 nm and the helix angle, alpha, to be 8 degrees 16'. Approximate volume calculations indicate that each enveloped virus particle contains multiple nucleocapsids.

In case of unfamiliarity with the term "virion", see: https://www.britannica.com/science/virion
In case of unfamiliarity with the adjective "pleomorphic", see: https://en.wikipedia.org/wiki/Pleomorphism_(microbiology)


text:
Can anyone identify this garden orb weaver spider?

Found in low foliage in Harare Zimbabwe. Argiope flavipalpis or A.levi


text:
Can anyone identify this beetle?

Fruit Chafer found in Zambezi valley at Victoria Falls on the Zambia/Zimbabwe border

That is a flower beetle in the family Scarabaeidae, subfamily Cetoniinae.
Derby's flower beetle (Dicronorrhina derbyana)
https://en.wikipedia.org/wiki/Dicronorrhina_derbyana


text:
Where do i find microbes like tardigrades in winter
Just bought a microscope and i want to see microbes like tardigrades.  Where should i look? I have found many bacteria and what seems to be motionless single celled organism.  I want to see movement and feeding.  Ps snow on the ground and frozen ground

Tardigrades are best found by soaking moss in water. Even in the winter, under the snow, that is the best place to look. Let tap water sit overnight, uncovered before you add it to the moss to let the chlorine come out. And then strain the water with fine-mesh cloth to see what was in the moss. I would not call tardigrades "microbes" though. Even though "microbes" is not a scientific term, I think of microbes as bacteria, while tardigrades are microscopic animals.


text:
what is the difference between gene and allele?
I want to know about gene and allele As we know allele is pair of genes they are ;present on only one chromosome or on homologous chromosomes? Or its like that;one chromosome has only one gene out of an allele and other homologous chromosome has another gene from the same allele?please clear this

An allele is a variant form of a gene.
You can obtain a more detailed explanation of alleles using Encyclopaedia Brittanica.


text:
why prokaryotic ribosomes have 30s and40s subunits and eukaryotic ribosomes have 40sand 60s subunits?
Ribosomes are protein factories of cell and are composed of two subunits; one smaller and other larger unit I want to know that why ,ribosomes of eukaryotes have a 40s and 60s subunit and prokaryotic ribosomes have 30s and50s subunits ?If we combine 30s and 50s subunits shouldn't it be 80s ribosome instead of 70s ribosome .

What exactly is your question? Are you asking why there is difference between prokaryotic and eukaryotic ribosomal subunit masses? Or do you simply wanna know why these numbers dont add up?

I want to know why these numbers donot add up?I know that difference in their masses is due to difference of masses of their proteins.(of subunits).

The S units are an artifact of the historical way these RNAs were characterized, based on the rate at which they sediment in an ultracentrifuge. S stands for Svedberg, which is a non-metric unit that measures sedimentation rate, based on size and shape. Larger molecules sediment slower. A better way to refer to ribosomal subunits is by calling them large subunit (LSU), and small subunit (SSU), because ALL ribosomes consist of one SSU and one LSU. Even the 5.8S is simply a part of eukaryotic LSU. Put subunits together and the shape changes, so it they would not sediment at a rate equal to the sum of each subunit.

You mean sedimentation depends on shape of subunits as they combine they slightly change their shape and will now sediment at 70s instead of 80s?


text:
Calculating sample concentration factor (opposite of dilution)
I am starting up an algae project, and I am getting a bit confused about some details in calculating density. For example, I take a sample of 250 mL, and concentrate it down to 25 mL with a sand filtration apparatus (factor of 10). I am using a gridded sedgwick-rafter chamber to enumerate the density of algal cells on a cells/mL basis using this formula from Standard Methods 10200F: cells/mL = [(# organisms counted)* (1000 cu. mm.)/ (field area)(field depth)(# fields counted)].
Once I calculate cells/mL, should I DIVIDE that result by my concentration factor (10)? My instinct is to multiply, but wouldn't that be appropriate only if I diluted the sample?

Your original sample is more dilute than the sample you counted. The concentration is less and therefore you should divide your counted concentration by 10 to get the concentration in the original sample.


text:
Why do recessive lethal genetic diseases continue to exist?
I'm trying to understand, in a simplistic representation of a recessive genetic disease (e.g. Tay Sachs), why wouldn't it "disappear" over time (many generations). Please excuse the use of non-professional terminology below, I hope the point I'm trying to make will be clear.
Let's assume that, for simplicity, people marry at random and each couple has 4 children. Denote the probability of carrying the "bad" gene by p, then a couple of 2 non-carrying people will have 4 healthy children, a mixed couple will have, on average, 2 healthy and 2 carrying children, and a couple of 2 carrying people will have 1 healthy, 2 carrying, and one sick child (which we assume will not have children so we ignore it in further calculations).
Assuming large enough population and random couples and everyone gets married (for simplicity):
The probability of a couple of non-carrying: (1-p)^2
The probability of a mixed couple: 2 * p * (1-p)
The probability of a 2-carrying couple: p^2
The expected number of healthy children per couple: 4*(1-p)^2 + 2*2*p*(1-p) + p^2 = 4 - 8*p + 4*p^2 + 4*p - 4*p^2 + p^2= 4 - 4*p - p^2 = (2-p)^2
The expected number of carrying: 2*p*(1-p) + 2*p^2 = 2*p - 2*p^2 + 2*p^2 = 2p
Dividing to get the new probability for carrying the gene:
2p / (2-p)^2
Which for small enough p is clearly smaller than p (e.g. for p = 0.05 we get ~0.0263).
If I'm not mistaken this means that the number of those carrying the genes should become exponentially small (in the number of generations).
I realize this is a very simplistic model, marriages are not random, mutations occur etc. but I would expect the basic intuition to hold. What am I missing?

I haven't read the entirety of the question, but the salient point is that lethal genetic diseases are mostly very rare. Exponential decrease over time and 0 are not the same thing.

Technically you are correct but if my calculations hold, and we start with p=0.05, we'll be at p=10^-16 within 10 generations which is pretty much the same as 0

And yet we're not. There may be an error in the assumptions or the calculations. It would be a hard model to get to a good standard.

Firstly, sorry if this is not so much an answer as a comment, but it is too long to put in the comments section, although I'll try keep it concise...
I can see exactly what you're doing however my math differs at points, and would appreciate you looking over it.
"The expected number of healthy children per couple: 4*(1-p)^2 + 2*2*p*(1-p) + p^2 = 4 - 8*p + 4*p^2 + 4*p - 4*p^2 + p^2= 4 - 4*p - p^2 = (2-p)^2"
Is it not: ... =  4 - 8p + 4p^2 + 4p - 4p^2 + p^2 = 4 - 4p + p^2 = (p-2)^2
Furthermore: "The expected number of carrying: 2*p*(1-p) + 2*p^2 = 2*p - 2*p^2 + 2*p^2 = 2p" - why for the probability of carriers in mixed couples - "2*p*(1-p)" - why have you not multiplied through by two (as with expected healthy children), given that as you said "a mixed couple will have, on average, 2 healthy and 2 carrying children"?
Is it not: 2 *2p(1-p) + 2p^2 = 4p - 4p^2  + 2p^2 = 4p - 2p^2 = 2p(-p + 2)
In this respect I got different expectations. Lastly "Dividing to get the new probability for carrying the gene..." You have done (no. healthy) / (no. carriers). Is the probability for carrying the gene not (no. carriers)/(no. carriers + no. health) - that is the no. carriers as a fraction of the entire population to give a probability?
Using my expectations this would be: [2p(-p+2)] / [2p(-p+2) + (p-2)^2] = [2p(-p+2)] / [-2p^2 + 4p + p^2 - 4p +4] = [2p(-p+2)] / [-p^2 + 4] = [2p(-p+2)] / [(-p + 2)(p + 2)] = 2p / (p+2)
Therefore, with a new probability for carrying of 2p / (p+2), for our "hypothesis" of the diminishing probability of carrying to stand, we need the condition 2p / (p+2) < p to stand, solving for p:
2p < p(p+2) -> 2p < p^2 + 2p -> 0 < p^2 -> p > 0
Since, as a probability, p must be <= 1, and assuming (as we are) that carriers exist and so it must be > 0, p always satisfies this condition - ergo I would conclude that for any value of p - not just small, the probability of carrying will diminish in the next generation. Just as we "hypothesised". However a quick google of "plot y = 2x/(x+2)" would indicate to me that as p approaches 0 it's rate of "diminishing" actually decreases, and it does not get exponentially smaller as you indicated. But solving for y = 0 gives x = 0 so this model would suggest the gene is never actually fully eradicated?! Which of course confuses me, although on a macro scale it might make sense, as you can't have, for example, 0.1 children "carrying", and 99.9 "healthy", only 1 and 99 or 0 and 100.
Thanks for reading this far, any response would be really appreciated, especially given I might be miles off.
Philip.

Philip - Thanks a lot! you caught 2 errors (the first of 3 is just a typo replacing + and - and we arrive at the same result). So interestingly for every generation the new probability is 2/(p+2) the previous probability, and the factor indeed gets closer to 1 as p goes to 0. In practice trying to start with p=0.05 (one of every 20 people carrying) I get after 1,000,000 generations that still 2 of every 1,000,000 people are carrying, so even after a very very long time there genes will still be around. Awesome!

New probability is 2p/(p+2) rather than 2/(p+2), and running a quick simulation in Python I get probability falling from 0.2 to 0.000002 after 1,999,960 generations, but yes I agree with your conclusion that they will therefore be around for a long time- which begs the question how did they ever become widespread in the first place?...


text:
What is the volume of menstrual flow in non human hominidae?
I'm looking for reliable data related to menstruation in animals, with especial focus on apes. I have found that some articles and cientific studies point that only chimpanzees have copious menstruations, but there is not refrence to the volume of menstrual flow at all, and what is more intriguing this alleged copious menses are not consistent with two important observations, first that in a studied carried on some captive female chimpanzees only a keeper reported an observation of menstrual flow in a female on one single day (and the researchers didn't agree it was actual menstruation), and the second one that field researchers reported of a period of adolescent infertility in young female chimpanzees, about two years in which they have intercourses but not pregnancies, and yet they didn't notice a sign of menstruation.

I'm trying to get to a more deep understanding of the evolutive process of menstruation. I'm familiar with the study of Emera and Romero about the evolution of menstruation and think it has left this important matter outside the box. Also I want that the wikipedia article about menstruation in mammals, which is rather ambigous, get to this point in a clear manner.


text:
Difference between Genus, Genus sp. and Genus spp
What is the difference between the three following sentences?

There is significant increase in Bifidobacterium
There is significant increase in Bifidobacterium sp.
There is significant increase in Bifidobacterium spp.

Of course, this could be applied to any genus.

https://en.m.wikipedia.org/wiki/Species#Abbreviations

Is this homework?

Wikipedia:
Books and articles sometimes intentionally do not identify species fully and use the abbreviation "sp." in the singular or "spp." (standing for species pluralis, the Latin for multiple species) in the plural in place of the specific name or epithet (e.g. Canis sp.) This commonly occurs when authors are confident that some individuals belong to a particular genus but are not sure to which exact species they belong, as is common in paleontology. Authors may also use "spp." as a short way of saying that something applies to many species within a genus, but not to all. If scientists mean that something applies to all species within a genus, they use the genus name without the specific name or epithet. The names of genera and species are usually printed in italics. Abbreviations such as "sp." should not be italicised. When a species identity is not clear a specialist may use "cf." before the epithet to indicate that confirmation is required. The abbreviations "nr." (near) or "aff." (affine) may be used when the identity is unclear but when the species appears to be similar to the species mentioned after.


text:
How can a waterborne disease be transmitted
If a disease is waterborne [as in it is based in the digestive tract], what ways can it be contracted other than the obvious drinking of infected water?


text:
Ejaculation without orgasm: is this possible to do it at will without external stimulation?
I know that ejaculation without orgasm is possible for human males with external stimulations, e.g. prostate massage.
My question is, can a human male perform full ejaculation without reaching orgasm without such external stimulation, i.e. with "ordinary" masturbation? Is this technically possible for the body?

Yes, it is possible. It is all in the brain. One can be sufficiently aroused to ejaculate without any contact.
The most obvious example of this is the case of nocturnal emission

A nocturnal emission, informally known as a wet dream, is a spontaneous orgasm during sleep that includes ejaculation for a male, or vaginal wetness or an orgasm (or both) for a female. Nocturnal emissions are most common during adolescence and early young adult years, but they may happen any time after puberty. It is possible for men to wake up during a wet dream or simply to sleep through it, but for women, some researchers have added the requirement that she should also awaken during the orgasm and perceive that the orgasm happened before it counts as a wet dream. Vaginal lubrication alone does not mean that the female had an orgasm.

Depending by what you mean by "without such external stimulation", you might want to read about premature ejaculation

Premature ejaculation (PE) occurs when a man experiences orgasm and expels semen soon after sexual activity and with minimal penile stimulation. It has also been called early ejaculation, rapid ejaculation, rapid climax, premature climax, and (historically) ejaculatio praecox. There is no uniform cut-off defining "premature", but a consensus of experts at the International Society for Sexual Medicine endorsed a definition including "ejaculation which always or nearly always occurs prior to or within about one minute".

Nocturnal emission is not what I meant actually, as it involves an orgasm. Same for premature ejaculation, which involves orgasm, that just arrives too early. I ask about full ejaculation process without orgasm at all. In slang it's called "milking" but everything I've seen (and tried) involve action done by someone else, to which I refer as "external stimulation". Hope my question is now more clear? Thanks! :)


text:
Can we have the action potential an AC current?
As well known brain are connected to our body by neuronal cells. it transmits and receives its data by action potential during neuronal cells. i wonder if any one can explain to me the properties of this current. can we consider this current as an AC current?

No. This question is too broad - there are many resources for you to read up on the basics of action potentials.

Indeed, an action potential really isn't a current at all, at least as an electrical engineer would understand current.  Rather, it's a wave of cell membrane depolarization.

@jamesqf an action potential is indeed no current, it is a voltage difference that changes over time. The action current is definitely a current, namely a net flow of charged ions through the cell membrane.

@AliceD: Yes, but that ion flow current is perpendicular to the axon, whereas the action potential propagates along its length.  It's also pretty fundamental to the nerve's (normal) operation that an AP propagates one way.  Changing it to an A/C current would mean redesigning everything from scratch :-)

You know those analogies of the brain being a computer and nerves being wires leading to and from it?
Those analogies are LIES.
There are no wires in the nervous system. Each neuron is a capacitor, the sodium potassium pumps create an electric charge in each neuron, and the neuron keeps that charge until the neighboring neuron (let's pretend it's not a sensory neuron) gives it a signal, in the form of an electric jolt or neurotransmitters.
That causes the neuron to equal out the charges on the inside and outside, called depolarization.
Watch this video: action potential crash course
A nerve could contain a bunch of neurons in a line next to each other, with one depolarizing the other.
This functions like a wire, in the way that it can transmit signals, but should be though of more like a domino effect, where the dominoes can stand themselves back up after the depolarization.
Electrons do not move from one end of the nerve to the other, only the "wave" of neural depolarization.
And since each neuron operates like a capacitor, it would be DC not AC current.
When I first learned about neurons, I was flabbergasted that it worked this way. I thought it was like wires, with a positive and negative end...
It couldn't be more different...

There are a few inaccuracies here. "Those analogies are LIES." - No, they are analogies. "Each neuron is a capacitor" - neurons have capacitive elements, but that doesn't make them 'capacitors.' "the sodium potassium pumps create an electric charge in each neuron" - only sort of. The Na/K pump establishes ion concentration gradients. The resting potential comes from differential permeabilities in the presence of those gradients. "Electrons do not move from one end of the nerve to the other, only the "wave" of neural depolarization." - Electrons don't move to the end of a wire either.

"A nerve could contain a bunch of neurons in a line next to each other, with one depolarizing the other." - Nerves are bundles of axons. You don't have sequences of cells in a line in nerves, just a parallel bundle of fibers. "And since each neuron operates like a capacitor, it would be DC not AC current." - Besides the problem that neurons aren't really capacitors, capacitors can be present in both AC and DC circuits, they just behave differently.

@BryanKrause electrons DO move to the end of the wire

Not really. On net they do, but you won't find an electron from one end ending up on the other end. The same is true of ions in a neuron.

dc, not ac current.

No, the same is true for DC current. The electrons do not flow down the length. On average they do, but individual electrons do not travel down the length.


text:
What is this? Found in southern Illinois

Found in southern Illinois in the driveway.  What is this?

It looks like a recently emerged periodic cicada that ran into some problems.

Was their grass / bushes around or just rocks?

Nice find! It looks to me like a Bush Cicada or scientificly Neotibicen dorsatus. It also looks like its injured, because we can see the white liquid around its wings and abdomen. Bush Cicadas tend to have a yellow or brown color but as shown here there is a wide variaty to the colourations that it might have:
Size (Adult, Length): 35mm to 57mm (1.38in to 2.24in)
Identifying Colors: yellow, brown, white, gold, black
North American Reach (Though Not Limited To*): Arizona; Arkansas; Colorado; Illinois; Indiana; Iowa; Kansas; Kentucky; Louisiana; Minnesota; Mississippi; Missouri; Nebraska; New Mexico; North Dakota; Oklahoma; South Dakota; Texas; Wyoming; Mexico.
Here are and some photos:
Adults:

The cicada is black eyed and green and brown colored. Yours have red eyes, except for one. There are lots of different cicadas, though.

@anongoodnurse And it is extremelly difficult to find a WHITE identical... XD

Many cicadas emerge white. That's not the issue. Your ID is off.

@anongoodnurse Thanks for the edit I will take care for it right away...

Do you have a source for what the fluids of a cicada look like? I wasn't able to find it.

@anongoodnurse I am checking it on the net... Look it sure something like its blood or gastric liquids? Probably..

It looks like a cicada of the Genus Tibicen, perhaps a "dog day" cicada (because of when they come out.)

Here are others of that genus; they're very similar.

Something is not right, though. I can't account for the white opaque liquid; even pictures of injured cicadas don't show it (at least that I can find.)
It looks like yours was dipped in Elmer's glue or something similar; the fluid is pooling under the wings and around the body. They usually hatch from a dry case, so I'm mystified.

About these white liquids you asked me, I checked and found that some cicadas "urinate" after the molt process, but the cicada above is a adult version...

Cicada urine is clear, and usually colorless or lightly colored.

Then I don't know... ran out of ideas.


text:
Why have mammalian predators been so small compared to their prey compared to theropod dinosaur predators?
So this is different than the question of "why are megafaunal mammals smaller than dinosaurs", which I understand to be a combination of:

live birth limiting size (even sauropods had miniscule egg sizes, on the order of ostrich egg sizes).

Breathing efficiency due to not having to rebreathe the same air breathed out.

Lighter bones

Mesothermy in large bodied animals.

Different life stages filled different niches.

Dinosaur mass estimates have historically been overblown

Dinosaurs weren't that much bigger excluding sauropods (Many members of the paleoloxidon genus were significantly heavier than modern T-rex estimates, and the estimates of most non sauropod dinosaurs, even African Elephants can get 2x the mass of an edmontosaurus and larger than a T-rex, lots of animals and the ranges of megafauna today are also smaller specifically because of human intervention, perverting our perception of animal sizes).

The only thing I can think of is the tendency for mammalian predators to hunt in packs (Even within the same biome, Hyenas, Painted Dogs, Lions, heck even Humans!), replicated in virtually every landscape on every continent except Antarctica and some what to a lesser extent in Australia (cave hyenas, wolves, cave lions plus sabertooth cats, and again, members of the homo genus), and afaik, the evidence for dinosaurs seems to show even those that hunted in groups weren't necessarily doing it to the same extent as mammals are/have been. This still doesn't explain why mammalian predators seem to cap out at around 1000kg -> 1500kg in mass through out virtually all of prehistory, even the "solo" hunters, such as short faced bear, when T rex itself seemed to be similar in mass to much of it's prey, as well as T rex relatives. The largest mammalian land predator (Andrewsarchus) has had it's mass estimate swinging downwards (back towards 1000kg, possibly no longer making it the largest) but even if it had been 2000kg, it still wouldn't be the mass I would be expecting.
So what are the hypothesis on why mammalian predators haven't gotten to the same relative sizes as prey as theropod dinosaurs did, or vice versa why didn't theropod dinosaurs stay smaller relative to their prey?


text:
Calculating ultrametric distance matrix
I am fairly new to phylogenetic analysis, so I'm guessing this is a basic question. If I have a bunch of aligned sequences, and I ultimately only care about pairwise distance (e.g. for calculating phylogenetic diversity) then is there any way to make sure these distances reflect an ultrametric tree without having to first calculate the tree itself? From what I can tell, to create an ultrametric distance matrix I have to first calculate an ultrametric tree and then use this tree to get distances. But this seems a bit backwards to me, since I can create a pairwise distance matrix without needing to create a tree, but I can't tell if there is a way to ensure that this matrix assumes some sort of underlying molecular clock so as to make sure the distances reflect an ultrametric tree.
I assume I'm just fundamentally failing to grasp something. Any help would be much appreciated.

You might also ask your question here: http://cs.stackexchange.com/

In my understanding you cannot skip the tree construction, since there is no guarantee that the pairwise distances are compatible with a tree, even for non-ultrametric trees. That is, to create a pairwise distance matrix that reflects patristic distances between tree leaves you need to create a tree first. Even without the ultrametricity condition.
The complicating factor here is that distance matrices compatible with trees must also respect distances to unobserved internal nodes...
This blog post about how to make a tree ultrametric might be relevant.


text:
What is the difference between ferritin and hemoglobin?
I have been reading that ferritin is the store of iron but hemoglobin is actually the amount of this in blood.
Does hemoglobin get sourced from ferritin? Is it possible for a person to be low on ferritin but normal on hemoglobin? Will he feel any symptoms of anaemia, if so?

Does hemoglobin get sourced from ferritin?

Yes, of course it is. Ferritin is the superior Group.

Is it possible for a person to be low on ferritin but normal on
  hemoglobin?

Yes, since these things don't have something in common.

Will he feel any symptoms of anaemia, if so?
  Why should he?? No, he won't get any crazy feelings from this.

Please do add some references


text:
Interpreting qPCR curves: how to find Ct value in my case?
I am reading my qPCR results and having no idea why Ct value is returned like this:

This is the qPCR curve of my samples, and the software returned Ct values of most of the curves as seen: 33.99-38.4 for the curves that have lower baseline.
The problem is the 2 curves (navy and black) with higher baseline at the first place. I read Ct values of these curves as 32-33, but the software says that the Ct values are 35.4 for these curves.
What could be the problem and what would be the right answer, my values or the software's?
Thanks in advance!

The software is correct. $C_t$ values are chosen to be sufficiently above background. As you can see, the background level is very different for two of the curves, so you can't use the same signal threshold for determining their $C_t$.

Thanks! I understood that the threshold for the black and navy curves should move up as the baseline is higher.


text:
Sub-saharan africans (Andamanese, Semang) have the ancestral hair-type, do they also have pediculus humanus capitis lice?
Do humans with the ancestral hair-type also have pediculus humanus capitis lice? Pubic hair lice, Pthirus pubis, are adapted morphologically to cling onto
coarse body hair, and originates from Pthirus gorillae via a host switch 3.3 Ma1. Pthirus pubis is also, at times, found at the eyelashes of infants.
The ancestral hair type is coarser than the derived, longer and thinner hair type. Is it parasitised by pediculus humanus capitis, or, by a lice that is adapted to cling onto the coarser hair, possibly related to Pthirus pubis?

The ancestral hair form is frizzier and much shorter. It survives in sub-Saharan Africans and in other groups whose ancestors never left the tropics, notably the Andamanese, the Semang, the Aeta, and the natives of Australia and Papua New Guinea. The latter groups are descended from humans who spread out of Africa along the southern route into South and Southeast Asia.2

References

Reed, D. L., Light, J. E., Allen, J. M., & Kirchman, J. J. (2007). Pair of lice lost or parasites regained: the evolutionary history of anthropoid primate lice. BMC Biology, 5(1), 7. doi:10.1186/1741-7007-5-7
Frost, P. (2015) Evolution of Long Head Hair in Humans. Advances in Anthropology, 5, 274-281. doi: 10.4236/aa.2015.54021


text:
How outdoor/wild plants survive without any proper human support?
I will take care of indoor plants because it was growing in my lawn
if I don't care then parasitic vines will destroy my plants.
But how plants take care of itself which are still surviving in forest without any human support?

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


text:
Do Cooper Hawks eat fish?
I have seen a Cooper hawk sitting on a low branch above my small Koi pond 3 times in 4 months. The books and net say they eat birds and some mammals but I wonder if he is looking at my fish ? Or snakes or frogs ?  As I write this I had a thought, song birds come down to a shallow part of the pond, that may be what the hawk is after. But I still wonder about the original question.

Birds learn new tricks very often, using roads to crack nuts, opening foil milk bottles (tits), and Hawks are known to catch Koi.
These pages say that Cooper Hawks specifically do catch fish: http://forums.gardenweb.com/discussions/1997093/hawks-taking-koi
http://www.outdooralabama.com/coopers-hawk
Here is a cooper hawk catching a duck and swimming around with it: https://www.youtube.com/watch?v=A08jxYinAG8
if you put cooper hawk pond into youtube, you will find 10+ videos of them bathing in ponds, and 2 videos of them scouting at a pond.
My aunt saw a buzzard, Buteo Buteo 50cm tall, catching a yellow Koi right out of the water while I was out for the day. The Koi was 30cm long, 12", it dived on the water and flew away with a fish on the wing. The Koi had indeed vanished as my aunt had said.


text:
Does starch need to be cooked?
Does starch need to be cooked for human digestion ? Is the answer different for different starches; potato , wheat, corn, etc ?

See the post Can we digest raw starch? on cooking.SE.

I wonder why someone would call this question as "personal health advice"...

I'm voting to close this question as off-topic because duplicate of https://cooking.stackexchange.com/questions/16891/can-we-digest-raw-starch


text:
Why is there disagreement on the number of surfaces of the human heart?
I am finding that some state that there are 5 and some that say that there are 3.
For example, "Cardiology: An Integrated Approach" that was published in 2018 states that

There are 3 surfaces of the heart: anterior, inferior, and posterior

Radiopedia, Teach Me Anatomy, and others state that there are 5.
Why is there this difference? What exactly is a surface?

Hmm. Curious what answers you get. Anecdotally, I've studied cardiac (and especially coronary) anatomy extensively and have never seen these "surfaces" described. Seems silly to me and not related to the actually relevant anatomy.

Heart surfaces are not clearly anatomically defined but arbitrary determined in the context of the heart orientation, that is the relation of the heart to other organs. Different sources mention 3 or 5 heart surfaces and there seems to be no "official" agreement about this.
Most sources (Dartmouth College, Gray's Anatomy for Students 2004...) agree about at least 3 surfaces:

Anterior (or sternocostal)
Inferior (or diaphragmatic)
Left pulmonary

Many sources (TeachMeAnatomy, KenHub...) mention additional 2 surfaces:

Posterior (or base)
Right pulmonary

The reasons for disagreement:

The heart base may not be considered a distinct surface (as in the picture).
The right pulmonary and anterior (sternocostal) surface are often considered one surface.

Picture: Heart surfaces (source: Echo Class 101)


text:
Calcium carbonate minerals in marine organisms shells
Calcium carbonate minerals exist in seawater in two main phases: calcite and aragonite. While calcite is the most stable phase, it is aragonite that precipitates first in seawater because of the high magnesium content of the oceans today. But for a similar environment, e.g., tropical shallow water, some organisms have a calcitic shell while some other have an aragonitic one. How can organisms choose which phase composes their shell?

The two minerals differ only in crystal structure. changing the assembly proteins is enough. https://www.researchgate.net/publication/232236795_Aragonite-associated_biomineralization_proteins_are_disordered_and_contain_interactive_motifs


text:
Spider identification: male black widow?
Unfortunately I didn't snag a picture but I found a small spider with reddish legs and enlarged fangs in Victoria, BC, Canada. The spider was very quick and looked similar to pictures of male western black widows I found online. The difference was that the spider I found had a light brown body but pictures I found online typically had white stripes.
Is it likely the spider I saw was a Western black widow or are there other species that look similar in this region?

I think it's unlikely.  Without a photo, it's hard to be sure of anything, but Black Widows don't have reddish legs or enlarged fangs, and it's hard to think of any circumstances in which they could be called "very quick".
Your description might fit a spider called Dysdera crocata (here's a link: https://bugguide.net/node/view/3388 ), but that's purely a guess on my part.
The problem with trying to ID something from photos when you're not very familiar with it, is that you may not be sure what to look at to distinguish it.  If you can't get a photo, make sure you include the most detailed possible description, including anything about it, no matter how seemingly insignificant.  What it was doing, where it was, etc., etc.


text:
Why does cell waste energy in meiosis, between meiosis 1&2
As far as I have learnt about meiosis I have read that anaphase 1 is followed by telophase 2 where chromosomes change back to reticulum.but in the very next stage i.e prophase 2 they again start condensing to form chromosomes again.i have also heard that is most species, cytokinesis is simultaneous and not successive( which means that the 4 cells undergo cytokinesis together)..
If this is the case, then what is the need for a cell to waste its energy on making chromosomes back to reticulum at the end of meiosis 1, and again condense it in the very next step
Can't it directly continue on to prophase 2!
It sounds ridiculous,...but I beleive there must be a reason behind it, because the last thing a cell would want to do is to waste its energy in such things.
Thanks in advance

Can someone please give an answer

There is a phase between meiosis 1 and meiosis 2 called Interkinesis.
During this phase centrosomes or centriole pairs undergo replication in animal cells, which is important for bringing true haploidy.
Refer - meiosis-ii


text:
Mitosis in free nuclear divisions
When free nuclear divisions occur(for instance in endosperm formation in coconut etc)....there are many nuclei undergoing kartokinesis at a given point of time...so that means each karyokinesis will naturally have to involve spindle fibre formation for the chromosomes to be pulled apart in anaphase....so when there are no cell walls or barriers and so many sets of spindle fibres...how is it that the spindle fibre of say dividing nucleus 1 doesn't go and attack to the chromosome of another dividing nucleus....shouldn't there be utter chaos out there as every spindle fibre can attach to any chromosome of any diving nucleus.....I hope you have u der stood my question

No one knows about this?


text:
Is it NAD+ or NAD- or neutral NAD ?
In glycolysis why NAD is positivly charged , why it's not neutral or negative ?

Why is this downvoted?

Question can include why is it NAD + and not NAD- or just NAD.

@AliceD I can't see any way to express my opinion about this other than to comment here. This is clearly a question about biochemistry as tagged. I disagree with your decision to put it on hold because you think that it is a better fit at Chemistry. It's really not about chemistry at all, it's about a convention in representing a biological coenzyme which appears to conflict with the underlying chemistry. A chemist would have nothing to say about this unless they were a biochemist. QED

@AlanBoyd perhaps you're right. But then, it shows no research effort whatsoever (homework) and the way it is framed makes it unclear exactly what the why in the question refers to (structural chemistry versus functional relevance of charge for enzymatic reactions), hence the question is unclear as well. I chose the Chemistry close-vote, but as is often the case when I mod-close stuff, it's lacking quality on various fronts. If you can clarify the question it might be re-opened. For what it's worth, I upvoted your answer, but w/o edits this question should be on hold imo.

You are correct in thinking that because of the presence of the diphosphate linkage between the two nucleotides in NAD⁺, both of which will carry a negative charge at physiological pH, together with the positive charge on the nicotinamide N, it would be more chemically correct to write NAD⁻. However I think the idea of using NAD⁺ is to emphasise the N atom in the nicotinamide moiety, which is the 'active site' of the coenzyme.
As it says at the NAD⁺ Wikipedia page:

Although NAD⁺ is written with a superscript plus sign because of the formal charge on a particular nitrogen atom, at physiological pH for the most part it is actually a singly charged anion (charge of minus 1), while NADH is a doubly charged anion.


text:
Can you see the coloration of Sinosauropteryx with the naked eye?
In 2010 this beautiful fossil of Sinosauropteryx was put under microscopic examination in order to determine the colors of the preserved melanosomes. It was determined that the feathers were reddish brown with white stripes going down the tail and a white underbelly.
Is it just a coincidence that that's exactly what I would have guessed by looking at the color of feathers in the fossil? Am I falling prey to
hindsight bias? Or is it the case that the feathers are so well preserved that their color is visible to the naked eye?

By Sam / Olai Ose / Skjaervoy from Zhangjiagang, China - Dinosaurs!, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=4209411


text:
How do bull semen companies get the semen out of the bulls?
Prompted by this article, which discusses the low number of bulls who sire US dairy cows.
How do semen companies extract semen from bulls?
The procedure to extract semen from humans is simple enough, but I'm struggling to picture a lab operator masturbating a fully grown bull until it ejaculates to collect semen. Is there some kind of specialized equipment involved? What does the operating procedure look like?

iirc they have a big fake cow with a hole in the rear end so when the bull mounts it, the semen can be collected.

@Tom: Any odds you might know the technical term? Search results for "Bull sex doll" mostly seem to be adult websites and stories about Devin Nunes' cow.

http://www.vivo.colostate.edu/hbooks/pathphys/reprod/semeneval/bull.html this should give you some idea. This site even has the speed of the ejaculate and other information

Colorado State University has two helpful pages that explain the main procedures (h/t Tom). Semen Collection goes through the 3 ways that are used to collect semen from animals.
Semen Collection from Bulls helpfully expands on bulls specifically:

Semen is most commonly collected from bulls in bull studs using an artificial vagina, as described below. Electroejaculation is an alternative method used with bulls that cannot mount or are too fractious for easy handling (e.g. range bulls). Finally, semen can be collected by message of the seminal vesicles and ampullae per rectum.

In a nutshell an Artificial Vagina (AV) uses thermal and mechanical stimulation to stimulate ejaculation. In the image below, the top item is an AV for use with rabbits and the bottom one is an AV for use with bulls. (The middle item is a director cone, which is used to collect semen from dogs.)

The procedure revolves around using a steer as a teaser to arouse and mount the bull, and then having an operator divert the penis the AV:

As one of the pages helpfully explains:

Prerequisites to use of an AV are that the male be conscious, not significantly frightened of people, and more interested in ejaculating than in killing humans.

The main alternative for less docile bulls appears to be electroejaculation, which involves applying a series of short, low-voltage pulses of current to the pelvic nerves which are involved in the ejaculatory response. You then collect semen using a director cone much like the one in the image further up.

Good self-answer I could not have done it better. Judging by the pictures it is not a job for me though.

@Tom: Same here. Though to be honest, I'm not sure which of diverting a bull's penis into an AV or masturbating a dog with your bare hands and capturing the resulting ejaculate -- which is what the director cone depicted in the answer is for -- is most agreeable.


text:
Poly-symbiosis? What's the name for this?
A mutually beneficial relationship between two species is called symbiosis.
If multiple symbiotic relationships exist with a single common (dominant) species, is this called 'farming'?

A mutually beneficial relationship between two species is not called symbiosis, but is rather called "mutualism." The benefit is measured in terms of fitness; a combination of survival and reproduction. Symbiosis is the degree to which species are "together," which is used in terms of physical proximity or degree of dependency. Pathogens, for instance, have a symbiotic relationship with their hosts and physiologically depend on their hosts by feeding on them. Mutualism and symbiosis are often conflated, and should not be.
Let's dissect: "If multiple symbiotic relationships exist with a single common (dominant) species, is this called 'farming'?" It seems like you mean, if members of the same species increase each other's fitness. Reciprocal fitness benefits between species is called mutualism, and within species is cooperation. There are important differences between mutualism and cooperation from evolutionary points of view and they have vastly different intellectual histories. None of this is really called "farming," except for some ant-insect mutualisms, where ants raise and protect aphids for a reward (honeydew; i.e., plant sugars secreted by some insects).

I think that you are refering specifically to mutualism, check this diagram from Wikipedia . https://en.m.wikipedia.org/wiki/Symbiosis?wprov=sfla1
I suggest you to  edit your question adding mutualism or mutualistic symbiosis, furthermore, I would add the tags "Ecology" "ecological-communities" and "mutualism".
I haven't heard of that term or comparison, personally I would use "multiple mutualistic symbiosis between A and B,C,D,etc...
I can't help anymore, I hope that those changes in your question will help you to find a proper answer.
Héctor.

The term "holobiont" refers to a community of mutualistic organisms that function together as a unit. A human and the many species of gut bacteria that digests their food are the typical example of a holobiont. The term is mostly used to describe microbial life in and around a larger host organism, but coral reefs and the communities of fish, crabs, etc. they support are also cited, so domesticated plants and animals and human farmers could potentially be thought of collectively as a farm holobiont.


text:
Boletus or Xerocomellus?
I have been trying to identify a mushroom I collected in the nearby forest, and while I think I have it identified, it seems to have a couple of names and I am confused about which grouping is correct.
According to one site, the mushroom is Boletus Chrysenteron :http://www.mycokey.org/result.shtml?genSpec=Species&ID=213&showList=DropDown&random=11837
According to Wikipedia it is Xerocomellus Chrysenteron (picture on right) https://en.wikipedia.org/wiki/Xerocomellus
But the info suggests that this Xerocomellus group is relatively new and belongs to the family Bolataceae.
Are these two different mushrooms (Xerocomellus Chrysenteron and Boletus Chrysenteron)? Or is it that the mushroom is now in a new group?

As you will see in the Species section of the Wikipedia Xerocomellus genus page you linked, Xerocomellus chrysenteron has a basionym (original name) of Boletus chrysenteron.  The Xerocomellus genus was first described in 2008.  The Wikipedia page for the X. chrysenteron species similarly gives three synonyms for X. chrysenteron in the box at the top; among them is Boletus chrysenteron Bull. (1789).  Thus the two names are referring to the same mushroom species.
One should note that Wikipedia says about this species:

Macroscopic observation of Xerocomellus chrysenteron is not sufficient
  to determine this species with certainty, as many intermediate forms
  occur between it and other taxa

It appears from this that correct identification of a mushroom as being X. chrysenteron is not a trivial task.


text:
What are some good examples of open-source articles in which the synergy of two medicines is demonstrated?
I am doing research on Stochastic Cooperative Game Theory (a subfield in mathematics), which I will henceforth call SCGT for convenience. In this theory, entities can work together to receive a bigger combined payoff than they would otherwise receive if they had not worked together.
In the stochastic version of cooperative game theory, the payoffs are not deterministic, but follow a probability distribution.
It seemed to me I could apply this theory to drug synergy. If there is drug synergy, there is a (high) chance that two medicines combined are better at healing a patient than just multiplying the dosage of either medicine by $2$. With SCGT, I could determine how much each medicine contributes to the healing of the patient, if some information is known about the drug-response curves. This in turn could tell us something about how much the manufacturers of each drug receive to be paid (in theory).
However, I am not quite well-acquainted with the literature on drug synergy. Furthermore, I can't access many articles on the topic without paying a lot (as I'm with the mathematics department at the university, I can't view articles on biology for free).
So my questions are:

Do you know any open-source articles in which it is shown that two drugs work in synergy according to the Bliss Independence model?

and:

Do you know any open-source articles in which it is shown that three or more drugs work in synergy according to the Bliss Independence model?

The same questions apply to the Loewe additivity framework.

This list is about biology, not about literature. It is valid to ask for examples of studies on the topic that interests you, but not, in my opinion, about articles in a particular type of journal. An good answer describing and referencing such studies would be of general interest here. An answer with a mere reference would not be suitable. The type of the journal (open access, written in English etc.) is no concern of biology.


text:
How do spiders know where food is stored in their web?
I recently caught a new black widow after a previous one died during molting. I added it to the same enclosure I kept the previous one, without removing the old web. The new spider almost immediately after encountering the web, climbed into it and found a bug the old spider had captured and hung in its web for a later meal, and started eating.
Given how quickly the newly captured spider was able to locate food within the old web, I was wondering how spiders (black widows more specifically) keep track of where things are in their web. I assume at least part of it is memory based as the previous spider was much more confident in climbing around its own web, while the new one had to pause occasionally and search for web to climb on. However, given that black widows can produce pheromones for mating purposes which can be detected by sensory hairs, can distinguish between prey vibrations and vibratory courtship displays, and the fact that some males bring a food item to distract females when mating suggests that more than just memory could play a role in how widows are able to locate food they, or potentially another widow, have cached.


text:
Can someone identify this species?
When I was about 5 or 6 years old, a tiny yellow puffball with 2 black spots which I think are eyes landed on my finger. I didn't dare breath, and after a few moments it flew away. Is there any such species that is similar to my description?

Welcome to Biology.SE. Given your description, it is very difficult to answer your question. Try to think of any feature you remember, any characteristic that might help the id. Maybe try to draw or post a picture that resembles what you have seen. As is, your question might be down-voted or closed as too broad.

Sounds like a bee/bumblebee covered in pollen.

It might be helpful to add location, season and daytime of the event.

It's really tiny, about 2 times the size of a pen point


text:
Mealworm beetles in my attic
I'm having a problem which has been troubling me for the second straight summer. Since 2014 I'm living in my parents attic. I had a very small bedroom and since I had my first girlfriend at that time I wanted a bigger bed. The first two years nothing seemed to be wrong. But last year around June when I came home and wanted to sleep I saw all these little insects on my bed. Pretty weird ofcourse, but since my room was a mess(food,clothes,etc.) I thought it was just because of my bad habits. Since then every day when the temperature was 25 degrees celcius or higher these insects appeared. They came from under my bed, they were in closets, they literally came from everywhere. Not during daytime, but around 10/11 am. Since our attic has this crawling space all around it in which we store stuff we almost never use I thought they had a nest there. But when I crawled through it I couldn't find anything. After some research I found out that this creature could be a mealworm beetle. I bought some insect spray and it all around the baseboard off my attic. I also sprayed some other places where they could be hiding. This worked for a day or two before they came again. The problem is that I never have established where they came from. So they just kept on coming until around September.
All of this kept me from sleeping a couple of hours every week, not to mention the graveyard off all these little creatures(I think I killed around 100 of them by directally spraying insect spray on them or other methods). Ofcourse I also found alot of them the morning after killed by the spray.
A couple of minutes ago I found the first one of this year. It was pretty high on a wall(Around two meters) and I killed it by spraying the insect spray on it. It fell down and after a couple of minutes it gave up. I will also include a picture of the dead insect. Some other interesting things about these creatures were that they actually made sound when walking around and falling down. Also when I tried to flat one it made a bit of a crunching sound and it was pretty hard too.
I live in the Netherlands in a remote village.
Can someone confirm me these are in fact mealworm beetles and what is the best way to make sure my attic is not filled with them this summer again. I have a cleaned up room now with no food leftovers but alot of cables everywhere


text:
What is this snake in South Florida, USA
I observed this snake for about 10 minutes. It was slithering back and forth in about 50x20 yard (50x20 meter) area. Just kept going back and forth (then I left). There was a similar snake at the same time in roughly the same 50x20 area, but they didn't seem to be paying attention to each other.
This is in South Florida, near Naples, Florida, USA.
I took several pictures, but I think this one is the clearest.

Google helped me find this site. Using this tool, it might be a North American Racer, but I'm not positive.  It'd help if you had pics of its underbelly color or scale texture

@Punintended - I think I see a white throat. I agree it's a racer. Your guess is probably correct.

Thank you. Any idea what it was doing, running around back and forth?

Laps?  IDK, it is a Racer


text:
Are these termites
Found a large number of these trapped between my window and the window frame. Are they termites?
Location: Eastern Massachusetts, USA

What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

This is an ant in the genus Camponotus. It can only be identified from the habitus on your picture, but clues are that there is only one element between the thorax and the gaster (Formicinae) and the head is large, this with the color and texture pattern leads to Camponotus sp.
Refer to

Bolton, B., Alpert, G., Ward, P. S., & Naskrecki, P. (2006). Bolton’s
  Catalogue of Ants of the World. Cambridge: Harvard.

for more detail on the identification.

Based on the morphology of the abdomen and antennae as well as the darker coloration, I'm going to say they are not. Looks a bit more ant-like (see picture).

Thank you, jmc1094. Mine do not have wings. Is it a seasonal thing?

Not necessarily, I just chose that figure as it illustrates differences in the body types pretty clearly.

Definitely an ant. Ants have elbowed antennae.

Termites are often nearly white and look as if the have 2 body sections instead of 3 as a typical insect.


text:
Is it possible to reconnect a severed tree trunk and save a tree?
I ask this question because I saw in a the news recently (September 28, 2023) that some vandal cut down the famous Sycamore Gap Tree

I know people normally don't put trees back together, but from what little I know about plant biology and tree trunks, I thought it might be possible, with some extra effort. The inner part of the tree is dead wood anyway, so perhaps that could be fused with internal steel rods, sort of like how surgeons use metal to align broken leg bones. Then, perhaps, the sap-carrying outer layer, under the bark, could be realigned and protected in some way so that it could grow back together?
Has it ever been done? Do you think it could be possible?

Potentially, but the forces involved with a tree in wind are enormous, so I don't think it would work. Not certain though - grafting is certainly possible on trees.

I would try reattaching it with an specialized bioreactor pumping some nutrient medium, do periodic analysis, readjust nutrient input, etcetera, but it would cost a lot only doing the very much needed previous research on the topic. Maybe some A-Team of biotechnologists and physicists could pull it off.

I asked a similar question which was closed as a duplicate.  But my question really is, why does this not appear to even have been considered?  I get that there are challenges and it would be expensive, but for something that touches the public to this extent why not at least try?   Is it known impossible for some reason? https://biology.stackexchange.com/questions/113166/why-couldnt-grafting-save-the-sycamore-gap-tree

Maybe because Northumberland council is cash-strapped, but that'd be a question to ask them. @CrashGordon


text:
Why isn't there 1' to 2' direction or something else except 5' to 3' in dna replication?
I hope i would get logical answers. I  request to post it as soon as possible.

Welcome to Biology Stack Exchange. I would highly recommend to read the tour before asking any questions. You will also earn your first badge. Take the tour here: https://biology.stackexchange.com/tour . Your question is a replication of the following question: https://biology.stackexchange.com/questions/15082/what-does-5-and-3-mean-in-dna-and-rna-strands .. Please check the link provided for answers.

[Source]
DNA is a polynucleotide. The above structure is of a nucleotide which has three components, a nitrogenous base(yellow), a pentose sugar(purple) and a phosphate group. These nucleotides form phosphodiester linkages to form a polynucleotide.

[Source]
These phosphodiester linkages are formed between 3' and 5' carbons of the pentose sugar which is shown in the above image.

[Source]
The end of DNA having a free phosphate group at 5' of pentose sugar is known as the 5'-end of DNA, and the end of DNA having a free hydroxyl group at 3' of pentose sugar is called the 3'-end of DNA.
Here, you can play with the DNA.


text:
Why boys who inherit more genes of their mother are not born as girls and girls who inherit more genes of their father not born as boys?
If boys as well as girls inherit the genes of the father as well as mother, does it imply that boys inherit more genes from the father to be boys and the girls inherit more genes from the mother to be girls? Or there is some thing else to it that settles the sex of the children? Since girls may inherit more genes of father and less genes of the mother question arises what decides that they are not born as boys or the other way around why the boys who inherit more genes of their mother are not born as girls?

Related (but a little more advanced): Do males of all sexual species have Y chromosomes? and Does one parent transmit more DNA to the offspring than the other one?

Most genes are not male or female, so receiving more genes from a father or mother would not make a child more male or female. Whether a mammalian embryo grows to be male or female is pretty much determined by a single gene that's found on the Y chromosome. Called the "Testis-determining factor" (TDF), it triggers the development of male characteristics. TDF is a regulatory gene, and its effect is to switch on other genes, which result in the development of testis. All embryos would become female without the intervention of this gene.
The gene TDF is found on the Y chromosome. Male mammals have one Y chromosome and one X chromosome, females have two X. So there's a 50% chance a fertilised egg will inherent an X, and a 50% chance it will inherit a Y chromosome from it's father, which determines its sex.
References:
Testis determining factor, https://en.wikipedia.org/wiki/Testis-determining_factor
General info about sex determination in different animals (it varies a lot),
 https://www.nature.com/scitable/topicpage/genetic-mechanisms-of-sex-determination-314

The second article states that 45,X (Turner syndrome, IIRC) is female, though I didn't see a justification for this. Anyone know if that's correct, and if so, why? To my understanding, Turner syndrome is neuter.

I am assuming that you are asking about human reproduction (which can be generalized for mammalian reproduction).
Humans have $23$ pairs of chromosomes. Of these $1$ pair is known as sex chromosomes. Human sex chromosomes are named $X$ and $Y$. An individual with genotype $44A + XY$ (A denotes the other 44 chromosomes) is a male and an individual with $44A + XX$ is a female.
Ref - https://en.wikipedia.org/wiki/Chromosome#Human_chromosomes
During reproduction the child receives $X$ from the mother and either $X$ or $Y$ from the father. It is the Sry gene on the $Y$ chromosome which gives male rise to male characteristics.
Also there is no such thing as more genes from the mother/father. The gametes (sperm and egg carry equal number of genes from the father and mother.)

Welcome to Biology.SE! Please add some references to your answer.


text:
Probabilities in calculating the kinship coefficient
I've been reading up to try to understand how the kinship coefficient (or coefficient of coancestry) is calculated. https://brainder.org/2015/06/13/genetic-resemblance-between-relatives/ this is the best explanation I've been able to find so far. However, I've not been able to find an explanation that makes a clear distinction between genes and alleles.
In my initial reading of the above I factored in this fact and assumed that often when the author wrote gene he/she meant allele (an assumption which I now think is incorrect), and thus that identity by descent of a single allele between individuals would be enough to satisfy kinship in the context of the definition of the kinship coefficient. This lead me to confusion upon reading the kinship coefficient as mathematically defined from the condensed coefficients of identity:
D1 + 1/2(D3+D5+D7) + 1/4(D8)
Surely, I thought, the kinship coefficient should merely be the sum of the probabilities of all the possible ways in which the two individuals may share the same allele. And thus there is no reason to multiply the sum of D3, D5, and D7 by 1/2 and D8 by 1/4.
Finally to my question; Kinship coefficient is defined as the probability that two individuals are identical by descent at a single randomly selected gene. Remembering this, is the reason it is calculated in this way because in order for the gene between individuals to be fully identical in the case of D3, D5, and D7, an additional identical allele is required from one parent (an event with a probability of 1/2), and in the case of D8 additional identical alleles are required from both parents (an event with a probability of 1/4)?
I'd be very grateful if someone could clarify for me why it's calculated in this way.

You might want to read "Relatedness in the post-genomic era: is it still useful?" by Speed and Balding.

If anyone is interested in a rigorous formulation of the kinship coefficient, please check out the answer https://biology.stackexchange.com/a/95775/8344.


text:
On parents' similarity
I don't know if this is a real claim, I live in Mexico City and most of the people I know are more similar to their father than to their mother? Why is that? Are the x and y cromosomes somehow related to the strength of a particular gen?

It doesn't look like a proper claim. Unless you can support it with verifiable data it's just your opinion.

Good observation:  http://www.dailymail.co.uk/health/article-2977710/People-genetically-like-fathers-mothers-Scientists-discover-use-paternal-DNA.html

Well then, now we have a source, so which characteristics make the father's genes stronger?


text:
Why are antibodies Y-shaped?
I generally know how antibodies work by binding to antigens, but what is the specific purpose to being Y-shaped, as opposed to any other shape? Does this aid their function? Thank you.

In a comment on this question, asking the poster what research had been performed before posting, I drew his attention to illustrations of antibody–antigen interaction in general articles about antibodies. In order to be inclusive to users of this site with visual impairments (who are perfectly able to use the web but may rely on screen readers) I added a rider. The fact that this comment was removed suggests the rider was interpreted as an insult to the poster of the sort "anyone who is not blind…". This was categorically not the case.

Having two antigen-binding sites allows agglomeration or clumping of antigens, which stimulates further immune response (phagocytosis).

Antibodies also known as immunoglobulins consists of two heavy chains and two light chains linked via disulfide bonds to form Y-shaped structure (as shown in figure below).
This Y-shaped structure bestows antibodies with two properties. Firstly, antigen-binding through the antigen binding fragment(Fab); and secondly, interaction with immune cells and proteins through fragment crystallizable region (Fc) to stimulate and regulate host immune defense mechanisms.
Fc and Fab portions of the antibody molecule are joined by flexible hinge region which enables antibodies to interact with the antibody-binding proteins and thus help in mediating immune effector mechanisms. So, this Y-shaped structure provide proper flexibility for binding to antigens and proteins/immune cells of immune system.

Reference
https://www.ncbi.nlm.nih.gov/books/NBK27144/
https://immense-immunology-insight.blogspot.com/2013/10/antibody-structure-simplified.html

Your answer is dominated by a graphic that is predominantly text. While graphics are often important to describing concepts in biology, in this case the parts of the graphic text that are necessary could (and should) have easily been written as text, making them accessible to users with visual difficulties. This might also have helped you focus on what was important in your answer.

Thanks for your advice, will keep it in mind from now onward.

IMHO, this does not explain the Y structure. Single chain Fragments (ScFv) also have an Fab and an Fc, and, due to their smaller size, can even better diffuse into tissue.


text:
Why are dietary recommendations for methionine consumption combined with cysteine?
I want to understand the amino acids missing in certain vegetables. I looked up the US recommendations for amino acids
(source: wikipedia).
I don’t understand why they pair

Methionine + Cysteine: 25 mg/g protein
Phenylalanine + Tyrosine: 47 mg/g protein

I searched for a justification but I cannot find one. While I acknowledge the chemical and structural similarities between them, they are separate amino acids. If these pairs could simply be transformed from one to another, then why bother considering methionine and phenylalanine to be essential? If you could easily convert cysteine to methionine, then methionine could be manufactured by the body. Similarly, so could phenylalanine. But it is commonly assumed this does not occur. Thus, an answer based on the idea that they can be "easily transformed into one another", if true, needs to address these issues.
Here are references for methionine:

The intimate relation between amino acids and protein and nitrogen requirements is well recognized. Nutrition research has focused on the capacity of food to meet the need for nitrogen and indispensable amino acids (IAA) and led to the conclusion that the quality, not just the quantity, of protein is critical. This is especially relevant in regard to the sulfur amino acids (SAA) methionine and cysteine because of the increased understanding of their relation to chronic diseases (e.g., cardiovascular disease, dementia, cirrhosis), immunomodulation, DNA transcription, and RNA translation. Considerable effort has been expended to determine whether and to what extent cysteine can spare the requirement for the IAA methionine. In vivo studies in humans generally concur that the dietary requirement of the SAA ranges between 13 and 16 mg/kg/d, but how much can be met by cysteine relative to methionine remains controversial.
Using the indicator amino acid oxidation (IAAO) approach to further examine this issue, Di Buono et al. (9–11) confirmed the mean requirement for methionine as 12.6 mg/kg/d in the absence of exogenous cysteine but noted that a safe level of intake of total SAA for the population was substantially higher at 21 mg/kg/d.

Naomi K. Fukagawa; Sparing of Methionine Requirements: Evaluation of Human Data Takes Sulfur Amino Acids Beyond Protein, The Journal of Nutrition, Volume 136, Issue 6, 1 June 2006, Pages 1676S–1681S
...and phenylalanine:

Conclusion: On the basis of the 24-h IAAO and 24-h IAAB methods, a mean phenylalanine requirement of 38 mg/kg/d is proposed for healthy well-nourished Indian adults in the absence of tyrosine intake. This finding is similar to that in Western adults.

Anura V Kurpad, Meredith M Regan, Tony DS Raj, Vidya N Rao, Justin Gnanou, Vernon R Young; The daily phenylalanine requirement of healthy Indian adults, The American Journal of Clinical Nutrition, Volume 83, Issue 6, 1 June 2006, Pages 1331–1336
Questions:

Why would amino acid requirements be grouped together?
If methionine is considered an essential amino acid, wouldn't grouping it with cysteine allow a food high in cysteine to appear as though it is satisfying your methionine requirement?
Suppose I consume 12.6 mg/kg/d of methionine, would this affect my ability to consume cysteine?
If the recommended level of methionine and cysteine is 19 mg/kg/d and this article proposes 12.6 mg/kg/d, then is it logical to consume approximately 6.4mg/kg/d of cysteine?
If true, would the same logic apply to phenylalanine and tyrosine?

In humans, cysteine can be synthesized from methionine and tyrosine from phenylalanine (note that the reverse pathways do not occur). Because their synthesis requires essential amino acids and the biosynthetic capacity of the organism does not always meet its need, they have been labelled conditionally essential. Under normal circumstances, an adult human can live with no dietary source of cysteine so long as dietary methionine is adequately supplied since the dietary deficiency can be compensated for by biosynthesis. Because of this, though, less dietary methionine is required when the diet is also supplemented with cysteine since less methionine is required to synthesize cysteine. This effect is known as cysteine sparing and a similar effect is observed with tyrosine/phenylalanine.
The data you cite are the reference values for PDCAAS, which is an indicative tool to evaluate the essential amino acid composition of protein sources. This system was introduced in 1991 by the WHO, and in this report they give the following rationale for their combined scoring of methionine and cysteine as sulfur amino acids:

The total of methionine and cystine [is] used for scoring purposes... Cystine is not an essential amino acid but can be synthesized from methionine. Cystine in a diet can thus "spare" methionine, and the total of the two has been found more satisfactory for scoring purposes than methionine alone.

They also recognize and somewhat address the weakness in this methodology that inspired your question:

While it is known that cystine can spare part of the requirement for methionine, FAO/WHO/UNU 1985 does not give any indication of the proportion of total sulphur amino acids which can be met by cystine. For the rat, chick and pig, the proportion is about 50%. Most animal proteins are low in cystine; in contrast, many vegetable proteins, especially the legumes, contain substantially more cystine than methionine. Thus, for animal protein diets or mixed diets containing animal protein, cystine is unlikely to contribute more than 50% of the total sulphur amino acids and scores calculated using cystine plus methionine will be appropriate. However, in certain all vegetable combinations, e.g. wheat and legumes, part of the cystine value may not be realized. Because of insufficient data on human requirements, however, the total of the two sulphur amino acids should, for the present, remain the recommended approach for computing amino acid scores.
...
A further complication arises from our lack of knowledge of the proportion of the total sulphur amino acid requirement which can be met by cystine. Without that knowledge, expression of protein values in terms of the sum total of methionine and cystine has both theoretical and practical limitations.

It's because of their structural similarity.  Here are some quick pics of the molecules:
Phenylalanine:

Compare with tyrosine:

You can see that the only difference is the methyl group in para position on the benzyl group in the tyrosine.
Similarly, take a look at cysteine and methionine:
Cysteine:

Compare with methionine:

These two look somewhat less similar; you have an extra methyl group on the methionine, a butyl chain instead of a propyl chain, and the alpha carbon bearing the amino group is in R position instead of S.  Nonetheless, they are the only amino acids bearing sulfur  Also, if you go back to the original paper, they say,

While RDAs are provided for each age group for the nine indispensable amino acids, histidine, isoleucine, leucine, lysine, sulfur amino acids (methionine + cysteine), aromatic amino acids (phenylalanine + tyrosine), threonine, tryptophan, and valine, the requirements for these amino acids are used to develop the FNB/IOM Protein Scoring Pattern.

Because of their similarities, some of them can be fairly easily transformed one from the one to the other in the body.  For instance, cysteine can be produced from L-methionine. This results in it being easier to classify them together, since if they can be produced one from another, they become virtually indistinguishable between the intake and usage pathways.

Sources:

Trumbo, Paula, Sandra Schlicker, Allison A. Yates, and Mary Poos. "Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein and amino acids. (Commentary)." Journal of the American Dietetic Association 102, no. 11 (2002): 1621+.

Institute of Medicine of the National Academies. 2003. Dietary Reference Intakes. p. 138.

U.S. National Library of Medicine. Toxicology Data Network: HSDB: (L)-Tryptophan.

Bin P, Huang R, Zhou X. 2017. Oxidation resistance of the sulfur amino acids: Methionine and cysteine. BioMed Research International 2017 : 9584932-6.

I’m afraid a bland statement “some of them can fairly easily transformed…” is not an adequate answer. You need to present and reference the precise pathways for this interconversion in humans. This is the crux of the answer. How do I know if it’s true?

Are you sure that the grouping is based on the metabolic transformation in humen? Maybe the chemical analysis is done that way: the total amount of Met+Cys or Phe+Tyr was measured without distinguishing both compounds. This might be easier (cheaper) due to certain chemical similarities of each pair.

I agree with @David. I take issue with "can be transformed easily enough" as I think that erodes the idea of essential vs non-essential.  I made an edit with pointing out issues I have with your argument.

@Arsak there's definitely something to what you're saying; check out Standardised methods for amino acid analysis of food by Otter DE in the Journal of Nutrition.  The feeling I was getting from my research was that there was the understanding that it's not extremely critical to distinguish them since cysteine can be synthesized from methionine (see The Sulfur-Containing Amino Acids: An Overview by Bronson JT & EB) and similarly for the aromatic amino acids (see The conversion of phenylalanine to tyrosine in man [shortened title] by Clark JTR & Bier DM.)