Genes, chromosomes, base pairs and the 23 pairs OK so I'm a bit confused. Does a chromosome consist of genes and do genes consist of DNA? What about the 23 pairs in sexual reproduction? I can't remember what the pairs consist of

I will start from the small and go to the big organisational unit:
All of this is constructed by DNA, the sequence of the four bases: adenosine, thymidine, cytidine and guanosine.  They are abbreviated G, A, T and C and are called the letters of DNA.

Genes are organisational units formed by a specific sequence of the four "letters". Genes encode for all the proteins (in fact this is a simple view, but should be enough for the moment) and are the way the information of how the protein sequence looks is conserved.

All DNA is organised in the form of a long string of bases, which would be very long in higher organisms. To come around this problem, the DNA is organised in chromosomes, in which the DNA is wound around special proteins (the histones) and further wound up to get a compact form.  The image below (from here) shows the relationship:

The 23 chromosome pairs are the 23 organisational units in humans, in which our genetic information is stored and organised.  A picture of them looks like this (image from the same website as above):

Please note that the chromosomes are not X-shaped, although they might look like on the image. They are pairs of long DNA molecules, which are not connected.


Why does our mouth "water"? Whenever we see something delicious, rapid salivation starts in our mouth. Also, it doesn't happen for all other food, which we eat regularly.

So, Is there any particular use of "rapid salivation"? and why doesn't it happen for everyday foods?

Basic biology: saliva in digestion is used to digest starches and fats.  It also lubricates food so that it is easier to move down the esophagus.  It is the first response your body has to food entering your digestive system and occurs in advance of food arrival. Pavlov's dog is a demonstration of this.

Rapid salivation occurs most often in two cases.  The easy example is seeing or smelling something like cake or pie, though this applies to any highly desirable food to the individual.  The case we think less of is that of starvation or even deep hunger.  In this case, even "everyday foods" cause rapid salivation as the body needs any calories it can get.


What is this strange horned, slug-like coral reef dwelling creature? On the first episode of BBC's Blue Planet II they visited a coral reef and showed some odd reef-dwelling creatures as part of their establishing shots, but they did not identify the creatures.

What is this odd horned, slug-like creature?
(Sort of like a slug with legs?)

I tried a Google reverse image search and it very 'helpfully' identified it as "Documentary film". So close, yet so far.

Disclaimer:
This question was split off from another question since the original was effectively two questions.

Here is your animal in Blue Planet II trailer:

This is a sea cucumber (Phylum Echinodermata, Class Holothuroidea).

More specifically, this is a sea cucumber from the Species Pearsonothuria graeffei, the Graeffe's sea cucumber.

Here are other images of Pearsonothuria graeffei for comparison:

Sea cucumbers have an antero-posterior elongated body, as you can see in this image of the whole animal:

Those black structures you see are the tube feet, a distinctive feature of Echinoderms.

Here is a detailed image of the tube feet in Pearsonothuria graeffei:


If plants benefit from carbon dioxide, why is car traffic something bad? This is going to sound really stupid or as a joke, but... Ever since I was a little kid, I have been confused about the following:

Humans need air/oxygen to breathe in order to live.
Plants/trees/bushes/flowers produce this oxygen, and are thus crucial for humans to survive.
Plants/trees/bushes/flowers need "carbon dioxide" to survive, just like humans need oxygen.
Plants/trees/bushes/flowers MAY also need some oxygen/air? (I assume so.)
Cars (traditional ones) output "carbon dioxide"... yet they are... not good for nature?

I don't understand how this fits together. It seems as if nature should absolutely thrive in the middle of highways and nearby, if they get so much nice carbon dioxide from the cars! Yet cars are instinctively seen (also by me) as "evil nature-polluting machines of death". Car exhaust seems to be the opposite of what a plant or tree wants, yet it's full of carbon dioxide, so... why?

Can somebody explain this once and for all?

There are at least two separate answers to your question.  First, with respect to plants needing CO2, they have evolved to deal with the limited amounts of CO2 normally in the atmosphere.  That's really all they need, or "want": adding more doesn't really benefit them.  Think of it this way: you need water to live, right?  And drink a certain amount of it every day.  But drinking large amounts of water can kill you https://en.wikipedia.org/wiki/Water_intoxication and holding you under water for a few minutes certainly will.  (As in the comment above, and even better example would be oxygen: we need it to live, but too much can cause all sorts of problems: https://en.wikipedia.org/wiki/Oxygen_toxicity )   Likewise, plants need nitrates, but applying too much can kill them.  So extra CO2 in the air is of little or no benefit to plants.

The second answer has nothing to do with plants.  It's that atmospheric CO2 traps solar heat, causing the Earth to be warmer than it otherwise would.  Without the extra CO2 from fossil fuels, Earth maintained a comfortable temperature, one that we'd all (and I mean not just humans, but all life) had gotten used to.  Add more CO2, and more solar heat is trapped, making the Earth uncomfortably warm, to the point that many plants & animals can't live where they are, and generally can't migrate.  So you wind up with a lot of dead plants and animals.

Of course there's more going on than this, things that are feedbacks from and side effects of the increased CO2, such as ocean acidification.  If you really want to know more, here's a good starting place: https://history.aip.org/climate/index.htm


How much gas is exchanged in one human breath? When we breathe, our lungs absorb a portion of the oxygen in the air, and replace it with some amount of carbon dioxide and water vapor.  Typically, how much $O_2$ (in grams, milliliters, or moles for instance) is absorbed and how much $CO_2$ and $H_2O$ are released in one breath of a healthy adult?

Of course, the exact amounts will vary from person to person and based on how deeply the person is breathing, lung health, etc.  I'm just looking for a ballpark figure.

According to Wikipedia

  "In a healthy, young adult, tidal volume is approximately 500 ml per inspiration..."

(tidal volume is the volume inspired/expired)

Using this figure, together with values for gas composition also taken from Wikipedia, I estimate that in each breath we take in 18 mg O2 (1.1 mmol) and we release 36 mg of CO2 (1.2 mmol) plus 20 mg H2O (1.1 mmol). These are, as you say, ballpark figures.

Sample calculation:

O2 inspired = 21% by volume; O2 expired = 16% by volume

O2 change = 5% by volume = 5*500/100 = 25 mL

1 mole gas = 22.4 L; 1 mmol gas = 22.4 mL

O2 change = 25/22.4 mmol = 1.1 mmol

MW O2 = 16

O2 change = 17.6 mg

The relative values are reassuringly close to what you might predict from the textbook equation for oxidation of carbohydrate: C6H12O6 + 6O2 -> 6CO2 + 6H2O


$F_{ST}$ when considering a multi-allelic locus Sewall Wright defined the $F_{ST}$ in a metapopulation as being:

$$F_{ST} = \frac{\text{Var}(p)}{\bar p (1-\bar p)}$$

, where $p$ is a vector of frequencies of a given allele and $\bar p$ and $\text{Var}(p)$ are the mean and variance of this vector.

For example, consider a metapopulation made of 4 subpopulations. The allele frequencies in these 4 subpopulations are p=[0.2, 0.5, 0.8, 0.3]. $\bar p$ is the mean of $p$ ($\bar p = 0.45$) and $\text{Var}(p)$ is the variance of $p$ ($\text{Var}(p )=0.07 \space$).

Question

Can we define $F_{ST}$ for a multiple allele locus? Or should $F_{ST}$ be defined for each allele independently?

Short answer: yes, people have formulated ways to estimate $F_{ST}$ for multiallelic loci, e.g. microsatellites. For a review, see here.
Specifically, Nei could define $F_{ST}$ for multiple alleles as
$F_{ST} = \frac{(H_t - H_s)}{H_t}$,
which is to say the proportion of total heterozygosity that is across rather than within populations. This is agnostic to the number of alleles, as it just uses heterozygosity. I believe there are other formulations as well.
There exist alternate statistics such as $G_{ST}$ and $R_{ST}$ (links under each) which are devised specifically for the multiallelic problem, see also the review for further discussion. Basically, microsatellites have high mutation rates such that they deflate the statistic; this will likely be the case for most multiallelic loci.
It's not clear though which statistic works best in practice as far as I can tell.


Hardy Weinberg Equilibrium after 5 Generations 1
There is a population not at HWE where red eye = $a^+$ (dominant) and white eyes = $a^-$.
If:
$a^+/a^+ = 0.6$
$a^-/a^+ = 0.1$
$a^-/a^- = 0.3$
what are the frequencies of the $a^+$ and $a^-$ alleles?
My attempt: So if it's not at HWE then I should divide the heterozygotes equally to get $a^+ = 0.65$ and $a^- = 0.35$.
2
We are now at HWE.  What are the frequencies in the next generation?
My attempt: so if $a^+ (p) = 0.65$ and $a^- (q) = 0.35$ then $p^2 = 0.42$ and $q^2 = 0.12$.  Then using $p^2 + 2pq + q^2 = 1$, I can figure out that the heterozygotes make up $0.46$.  So the frequency of the $a^+$ allele is $0.42 + 0.46 = 0.88$, and then $a^-$ should be $0.12$ (because they should add to 1)
3
What is the frequency 5 generations later in HWE?
My attempt:  Wouldn't it be the same answer as #2. I'm not sure how more generations in HWE would change the allele frequencies.

You are almost correct, but with a few modifications/comments.

The calculations in Q1 are independent of HWE, and are just calculating the current allele frequencies in the population based on genotype frequencies (i.e. would be the same irrespectively of if the population is in HWE or not).
In Q2 it is unclear if the questions is asking for genotype frequencies or allele frequencies. Your answer of genotype frequencies of $p^2=0.42$ ($a^+a^+$), $q^2 =0.12$ ($a^-a^-$) and $2pq =0.46$ ($a^+a^-$) is correct if you assume the allele frequencies from Q1 and HWE. However, your allele frequencies are incorrect and should be $p = 0.42 + 0.46/2 = 0.65$ and $q = 0.12 + 0.46/2 = 0.35$, i.e. the same as in Q1. Remember that the allele frequencies shouldn't change under HWE.
Yes frequencies should not change in Q3. This is the textbook definition of HWE, i.e. that allele and genotype frequencies remain constant between generations in the absence of evolutionary forces (i.e. under the HWE).


Plasmid copy number and Rop protein If i want to transform a bacteria (E. coli) with a particular plasmid (in my case pBR322) will the presence of the Rop gene affect the production of it ?
Is it desirable to use a plasmid without that gene to increase plasmid copy number ?

I found some informations about the protein cited on these links:

https://en.wikipedia.org/wiki/Rop_protein

http://www.proteopedia.org/wiki/index.php/Rop_protein

Since the pBR322 is derived from the pMB1 plasmid (which is closely related to the ColE1 plasmid, it does indeed contain the coding information for the rop gene. It's expression will limit the copy numbers from the plasmid, so if you are looking for high copy numbers, the usage of a plasmid without the rop gene should be preferred.

If it is only for the yield in a plasmid preparation, you could also simply scale up your production and make a midi prep instead of a mini or a maxi instead of a midi. It also depends, what you are planning with the plasmid. For cloning purposes mini preps with pBR322 have always given enough yield for me.


Can some one identify this plant with really sweet smelling flowers? Could someone help identifying this plant?
The flowers on it have a very sweet smell, similar to the night queen.

It's most likely a buddleia of some kind, perhaps Buddliea davidii:

You can see the flower is tubular and has four 'petals' at the end. They also have paired leaves, the underside of which is lighter than the top.

  The flowers are generally rich in nectar and often strongly honey-scented.

I never thought it smelled like honey, but it does have a very pleasant and strong sweet smell.

It is present on four continents.


Is it possible for a prey to become its main predator's predator? This is actually for a worldbuilding project, but I thought I'd just ask it here as it is solely about biology.

Anyway, would it be possible for a herbivore, let's call him X, that is predated by a predator, or Y, to evolve to become a specialized hunter of Y?
For example, wolves hunt deer. Imagine that in millions of years, the deer has evolved into the main predator of wolves.

If that's not possible, is it at least possible for X to evolve adaptations for fighting/killing Y (Not for food)?

If you require any further context or clarification, please let me know.

Also it should be noted as you move from prey to predator, there is less energy to be had. This is why we often do not have a predator of a predator species. There simply isn't enough food at that level of a predator to support another predator above it.

That said, I am assuming you are thinking of an alien ecosystem. In which case you might be able to sustain such a system if there is a massive flux of bio-matter through the ecosystem. Ie plant food is extremely abundant and animals within it reproduce at an extremely fast pace. We can see such an environment at the bottom of a marine ecosystem in the polar regions during summer (near constant sunshine, and an up welling of minerals from the deep sea.

  If that's not possible, is it at least possible for X to evolve
  adaptations for fighting/killing Y (Not for food)?

Happens all the time. While lions do hunt cape buffalo, cape buffalo can and do kill unwary lions.


What is the present tense verb form of apoptosis? For example, if I want to say something along the lines of "this signaling pathway causes a cell to go through the process of apoptosis", but I want to shorten the phrase "go through the process of apoptosis" to one word, what would that word be? I've been saying "apoptose" so far but I'm not sure if that's correct.

According to Google Scholar, there were ~40000 hits for "apoptose" and ~120k hits for "undergo apoptosis" in published literature, both of which had significant numbers of high-impact articles.

Therefore, it is clear that both expressions are sufficiently used in literature for either to be used.

Personally, I would say "undergo apoptosis" being both shorter than your original phrase and not risking coining new word forms.


What are the characteristics of a living organism? It seemed fairly basic at first, and yet I have to ask because even a quick Google search reveals that it doesn't seem to be quite so straight-forward anymore. After more research, I found multiple lists, some with six points, others seven or eight. Some lists shared six points and only differed on one, but others had five different points and divided and named the points differently such as Respiration vs Metabolism, Adapt vs Evolve, Homeostasis vs simply consisting of cells, etc.

Maybe it never really was simple, but when I learned basic middle school life science in the 1990s I seem to remember a clear and concise list of 7-8 distinct terms. I know they were just the summary given by the author of whatever textbook we used, but I remember several sources having similar lists (cannot say for sure if they were exactly the same), including a textbook, an educational video game, and a poster.

I'm also told that this has become a bit of a debate in the biology community, whether such a black and white distinction of "living" or "not living" is prudent. Questions such as this one on viruses are an example of how it is difficult to categorize life. However, I noted in my research that there was still clearly overlap in meaning of definitions, it was just in description and division of points that they differed. This suggests to me there is still a generally agreed upon core definition that is simply described by different people, specifically authors, with a few areas of possible debate.

What are the current generally agreed upon characteristics, the common denominators? (They all reproduce?)
What characteristics are commonly debated and therefore would unwarranted to claim? (Specifying cell structure?)

With the understanding that an answer will require an objective synthesis of a range of content and opinions, debate on what should or should not be characteristics is discouraged. Rather, an impassioned summary of the current  scientific consensus on this question is what I am looking for.

It seems to me that even if this is a topic of opinionated debate, it is certainly at the core of Biology and would be worthwhile to be addressed in an academic manner, be accessible, and available to reference on this site.

(PS - Not in any way a homework question, never was, just a curious 30-year father. Unless you are counting questions I have to answer from a curious little boy.)

First of all, you have to note that there is no such thing as a scientific, objective definition of life, and that many scientists disagree on a given definition, and that every definition has it's limits.

However, the one from wikipedia

  Since there is no unequivocal definition of life, most current definitions in biology are descriptive. Life is considered a characteristic of something that exhibits all or most of the following traits:[10][12][13][14][15][16][17]

  Homeostasis: regulation of the internal environment to maintain a constant state; for example, sweating to reduce temperature

  Organization: being structurally composed of one or more cells — the basic units of life

  Metabolism: transformation of energy by converting chemicals and energy into cellular components (anabolism) and decomposing organic matter (catabolism). Living things require energy to maintain internal organization (homeostasis) and to produce the other phenomena associated with life.

  Growth: maintenance of a higher rate of anabolism than catabolism. A growing organism increases in size in all of its parts, rather than simply accumulating matter.

  Adaptation: the ability to change over time in response to the environment. This ability is fundamental to the process of evolution and is determined by the organism's heredity, diet, and external factors.

  Response to stimuli: a response can take many forms, from the contraction of a unicellular organism to external chemicals, to complex reactions involving all the senses of multicellular organisms. A response is often expressed by motion; for example, the leaves of a plant turning toward the sun (phototropism), and chemotaxis.

  Reproduction: the ability to produce new individual organisms, either asexually from a single parent organism, or sexually from two parent organisms.

Encyclopedia Britannica

  Metabolism
  Respiration
  Sensitivity (responding to stimuli like gravity and sunlight)
  Nutrition
  Excretion (getting rid of CO2)
  Growth
  Reproduction
  Homeostasis


Is "Virus" a part of Acaryote? I am just a beginner of BIOLOGY as a Grade 7 student!
But the information which I got from my textbook and Internet has got me confused as MY TEXTBOOK SAID:-

  Viruses are part of "Akaryote"

And 'Acaryote' (or 'Akaryote' or however 'Akaryocyte') is just a Smaller group of ORGANISM than Prokaryote. Example:- Blood (As said in Wikipedia)

Pic-1:- A VIRUS DECRIPTION BY BBC

(END OF PICTURE 1)

Akaryote is not used for a group of organisms in the way that prokaryotes and eukaryotes are used.  The word akaryote is not a common word, but when used it is a synonym for akaryocyte meaning "a cell that does not have a nucleus" and is used in the context of eukaryotes, in which cells normally do have a nucleus.  (It is not used in the context of a prokaryote, which does not have a nucleus but does have a cell, or in the context of a virus, which does not even have a cell.)

The diagrams in your question have confused two different things.  The first illustration is indeed a virus, as stated.  The remaining illustrations are not of a virus, though.  You may have thought they were visually similar, but they are not similar in the details.  The "fibres" may look like like "flagella", but they are different.  The virus is not a cell and has no cell membrane. Viruses are not prokaryotes.


Are the DNA codon mappings arbitrary? I am a Biology novice so I apologize in advance if I state anything incorrectly....

My question is, are the DNA codon mappings arbitrary? I understand that the DNA code is made up of codons which each consist of 3 base pairs. There can be 64 codons which map to 20 amino acids (some are duplicated and others act as stop codons). So was there a reason why one particular codon mapped to one particular amino acid - or is the mapping completely arbitrary?

Thanks!

There is no reason for why a certain codon came to represent a certain amino acid. But some reason is attributed to similarity of degenerate codons. Usually the degenerate codons only differ in their last (third) nucleotide. The corresponding first anticodon in tRNA usually bears a modified nucleotide such as inosine which can (promiscuously) pair with A, C and U.

You can see the wikipedia page on wobble base-pairing.


What is the benefit of using Gonoline-Euroline in combination? I was heard that this combination first Gonoline and other culture another culture on Euroline is good one.

What is the benefit of using Gonoline-Euroline in combination?

Looking at your other question, I think there's some serious editing that needs to be done to clarify this question.

Still I think there is a quick and easy answer to your question.  Gonoline media makes an excellent transfer media.  If you are out in the field some where and want to take a swab for further analysis, you could easily choose a gonoline media for transport.  Then you would want to follow that up with some selective blood agars that might show a pathogenic species that you were looking for.  Thus to use gonoline media with any other medium, is merely to preserve your sample for plating on your diagnostic media/agar later.

Again, looking at your related question, I could only guess that you meant chocolate agar, because you might be hunting Neisseriaceae (which you should put in the question if you are).


Is this bedbug or book louse? Hello everyone.
I have been seeing tiny critters like this one in bed and I started to worryif they are bed bugs. Although they seem different in appearance as well as the fact that they don't seem to bite, I wanted to be sure.
Sorry if the pic is a bit hazy, they are only about 1mm long.
I also did have a bit of a humidity issue since the roof was leaky.
Does anyone know how to get rid of them. I tried different insecticides around the bed and on wooden part of the bed but nothing works.
Could they have settled in my new mattress? :(

The pictures aren't very clear, but I would put this down as a book louse, not a bed bug nymph, as the body is quite elongated, which is atypical of the bed bugs and more typical of book lice.
Book louse:

Bed bug:

Courtesy of  bedbugger.com.
Check out also this page from the University of Minnesota Extension; the picture nicely matches the photo you posted in body shape.


How to model species interactions on population size dynamic? Here are two classical discrete time models of population size dynamic. The exponential growth model

$$N_{t+1} = r\cdot N_t \qquad\qquad(1)$$

and the logistic growth model

$$N_{t+1} = r\cdot N_t \left(1 - \frac{N_t}{K}\right) \qquad\qquad(2)$$

, where $r$ is the growth rate, $N_t$ is the population size at time $t$ and $K$ is the carrying capacity.

I am wondering how are species interaction generally modelled into this framework. Let's consider three interacting species called "a", "b" and "c" with populations sizes at time $t$, $Na_t$, $Nb_t$, $Nc_t$, respecitively. The effect of these three species on the focal species are $\alpha_a$, $\alpha_b$ and $\alpha_c$.

How do we typically compute, for both a logistic and an exponential discrete time model, the recursive equation of the focal species' population size?

For the exponential model, is it

$$N_{t+1} = r\cdot N_t \cdot (Na_t \alpha_a + Nb_t \alpha_b + Nc_t \alpha_c) \qquad\qquad(3)$$

or

$$N_{t+1} = r\cdot N_t + Na_t \alpha_a + Nb_t \alpha_b + Nc_t \alpha_c \qquad\qquad(4)$$

or something else? And for the logistic model, is it

$$N_{t+1} = r\cdot N_t \left(1 - \frac{N_t}{K}\right) \cdot (Na_t \alpha_a + Nb_t \alpha_b + Nc_t \alpha_c) \qquad\qquad(5)$$

or

$$N_{t+1} = r\cdot N_t \left(1 - \frac{N_t \cdot (Na_t \alpha_a + Nb_t \alpha_b + Nc_t \alpha_c)}{K}\right) \qquad\qquad(6)$$

or something else?

It is possible that we typically define more parameters that just the $\alpha$ values I define above to describe a species interaction even in the simplest models. Ideally, I would love an answer that draws from a source (a textbook in theoretical ecology, a peer-reviewed article or whatever).

You can write these equations in the form of ODEs but it is not really essential.

This is my analysis (just the model formulation and not literature):

The effects of interactor species may or may not be dependent on the population of the species that is being analysed (recipient). Now you have to model based on how you would realistically expect the interactions to have an effect on a species. A simple assumption would be that the interaction improves or reduces fitness (growth rate), additively. So you can model the effects as:

$$N_{t+1} = (r_0 + \beta_a + \beta_b + \beta_c) N_t$$

where $\beta_x$ denotes the effect of species $x$ which in turn you can model as dependent ($N_tN_{x_t}\alpha_x$) or independent ($N_{x_t}\alpha_x$) of the recipient population. Now, you can also impose a condition that the growth rate cannot increase beyond a certain value and so you can model it as a saturating function. A logistic or a Michaelis-Menten like function would work. For e.g:

$$\begin{align} r &= \frac{r'}{K+r'}\\[1em]
 r' &= r_0 +  \beta_a + \beta_b + \beta_c\end{align}$$

You can likewise adapt model using the logistic equation.


Realtime PCR plate cleaning Have anyone used realtime PCR, is that the plate for realtime PCR is one-time using or not ? Otherwise how to clean the plate after reaction to prevent wrong result in next time using ?

A possible solution is to use the DNA ZAP solution, which I know many people used in adjacent labs and were happy with for cleaning their DNA free workbench. The product sheet states

  When 500 ng of template DNA is dried down in a PCR tube, it is rendered unamplifiable upon treatment with DNA ZAP solutions. Additional experiments demonstrate that the DNA is degraded down to free nucleotides.

Please note that I'm not promoting any specific product here and you can purchase any similar product/technology for your particular application. Obviously the best recommendation is to use new plates for each reaction but this/or a similar product can be an option too although the risk of DNA contamination in a PCR based reaction should be carefully balanced against simply using fresh plates considering the product itself is not free either.

The product sheet provides instruction for cleaning/treating PCR tubes hence I assume you use the same protocol for plates if you have the plate centrifuges available in your lab. You can get rid of the solutions by tapping the plates on a tissue to get the liquid out of the wells.


Robotic surgery for treating cancer? We can localise cancer cells in the body. We can manufacture materials thin and hard enough to penetrate the body without harming it. So what stops us from creating an automated surgery where the patient lies down for some time whilst a machine locates cancerous cells and, using micro tubes, kills them one by one?

Actually we aren't that good at localizing cancer cells.
There need to be around 100,000 cancer cells at a single location for the cancer to be visible on fMRI.

If you want to treat a cancer via chemotherapy it's good to be able to see the cancer. It allows you to see whether the drug you are giving works.

When dealing with a metastasized cancer where you don't think you know every location in which cancer is hiding it therefore often makes sense to avoid to take out everything you can see via surgery.


What are hot spots on human body? Recently I have just discovered that a certain amount of the mobile phone frequency can be absorbed by human tissues.

For example, this is the SAR info of iPhone 4s:

Head: 1.180 W/kg 1 g
Body: 0.491 W/kg 1g
Hotspot: 0.491 W/kg 1 g

http://en.wikipedia.org/wiki/IPhone_4S

so hotspot means a hot spot on human body right?

Then question is:

What are hot spots on human body?

Hot spots on the human body caused by cell phones are caused by the EMF/RF (ElectroMagnetic Frequency/Radio Frequency) emitted from the phones (or any mobile wireless device). (There is much conjecture about the safety of  these frequencies and whatnot... That is not what I am here to talk about).

In this case, the term hot spot does not refer to you being a WiFi hot spot! It simply means that since the frequencies are similar to that of a microwave, you will absorb them and they will cause heating internally. These areas will remain warm for a time - whether you can feel it or not, some people can, some can't. Shown here is a thermal image of someone who recently used a cell phone and one who had not.


Can birds raise younglings that are not their own? For example, if a scientist were to move a chickadee or pigeon egg from one nest to another, would the new bird (second mother) in the new nest incubate or raise the youngling? Or would the new mother reject the egg since it lacks its imprints (like scent for example)?

In other words, can birds differentiate between their offspring and foreign offspring?

You may not realize, but you actually have two questions here.

Question number 1 is this:

  Can birds raise younglings that are not their own?

The answer is yes. We call this Brood parasitism, and it occurs in several species of birds.

There is both intraspecific (between members of the same species) and interspecific (between members of different species) brood parasitism. I believe you want to know about interspecific brood parasitism.

By far the most famous examples are the cuckoos (Family Cuculidae). Some species of cuckoos are obligate parasites, meaning that they only reproduce laying eggs in other birds' nests.

It's very funny (for us, probably not for the host) the fact that sometimes the young parasite is way bigger than the host mum:

A Eurasian reed warbler raising a common cuckoo. Source: Wikipedia

Then, we come to your question number 2, which is different:

  If a scientist were to move a chickadee or pigeon egg from one nest to another, would the new bird (second mother) in the new nest incubate or raise the youngling?

The answer here depends on several factors, mainly the species involved.

For species that suffer broad parasitism, there is egg-rejection if the parasite egg is somehow different. If you look at the adaptations to parasitism in the Wikipedia link I shared, you're gonna see that "among specialist avian brood parasites, mimetic eggs are a nearly universal adaptation".

However, species that don't suffer broad parasitism are more prone to accept egg transfer (see @bshane comment here).


Difference between negative allosteric regulation and non-competitive inhibition Both connect to some site other than the active site which controls the shape of the active site and causes the enzyme to be less active. So what is the difference?

There Are Two Similar but Distinct Types of Noncompetitive Binding.
Starting from a pharmacological perspective, there are 2 definitions of "noncompetitive" binding that have similar macroscopic effects but differ slightly in their molecular mechanisms. Depending on which definition you use, noncompetitive ligands can bind either orthosterically or allosterically. Aspirin at cyclooxygenase and alanine at pyruvate kinase have both been referred to as "noncompetitive" (see below), despite aspirin binding orthosterically and alanine binding allosterically. Both types of inhibition involve depression of the maximum response, efficacy or enzyme activity. In other words, they reduce $y_{\mathrm{max}}$, $E_{\mathrm{max}}$ or $V_{\mathrm{max}}$. This is described in (Lippincott. (2015). Illustrated Reviews Pharmacology. 6th ed. p. 34). Similarly, (Goodman and Gilman. (2011). The Pharmacological Basis of Therapeutics. 12th ed. p. 46) gives an operational definition of noncompetitive antagonism as that which depresses the maximal response to the agonist but the molecular mechanism of action "really cannot be inferred unequivocally from the effect". The two types of noncompetitive molecular mechanisms are (1) irreversible antagonism and (2) allosteric antagonism. Lippincott claims that both of these mechanisms are "noncompetitive" antagonism. Textbooks trump Wikipedia on credibility so I'm afraid to say that Wikipedia may have been leading people astray for years by saying that noncompetitive ligands can only bind allosterically. Due to this confusion, I think it's better to avoid the term noncompetitive entirely and opt for "insurmountable" inhibitor if the mechanism is unknown, or "irreversible/allosteric inhibitor" if the mechanism is.
Type 1: Irreversible Antagonism
Goodman and Gilmans' definition in the previous paragraph notes that the effect is for "a slowly dissociating antagonist" (i.e. an irreversible antagonist). This is mirrored in (Rang and Dale. (2015). Pharmacology. 8th ed. p. 11) and (Katzung. Basic and Clinical Pharmacology 11th ed. p. 31), which define noncompetitive antagonism as irreversible antagonism. Rang and Dale also makes the point that the term is ambiguous with other meanings of noncompetitive. Rang and Dale claim that aspirin is a noncompetitive antagonist at cyclooxygenase. It may be an irreversible antagonist but it's certainly not an allosteric one, as it modifies the orthosteric binding site. Another "noncompetitive" drug in this class (according to Rang and Dale) is phenelzine, which irreversibly binds MAO.
Type 2: Allosteric Antagonism
Not to be confused with negative allosteric modulators, (Goodman and Gilman. p. 46), (Rang and Dale. p. 17), (Lippincott. p. 34) and (Katzung, p. 32) all give a second definition of noncompetitive antagonism as antagonism at an allosteric site. This antagonism may be reversible or not but as the agonist can't displace the antagonist, it is insurmountable in all cases. Rang and Dale give the example of ketamine at the NMDA receptor, which depresses the maximal response by binding in the channel (an allosteric site) but doesn't bind irreversibly. For ligands relevant to enzymes, alanine and ATP allosterically (yet reversibly) bind pyruvate kinase. So this would cause insurmountable inhibition of pyruvate kinase activity but not irreversible inhibition. Various authors, such as (Mustafa and Hochachka, 1970) refer to this as "noncompetitive" inhibition.
Interestingly, I can't find any exogenous ligand that is both reversible and allosteric. It seems that allosteric antagonists are more relevant to receptors and transporters than enzymes. To make it even more confusing, Katzung claims that benzodiazepines (BDZ) act noncompetitively, since they bind allosterically. But this doesn't fit with any other definition of noncompetitive binding since BDZ is a positive modulator. Also interesting is that hexamethonium at the nAChR fits the definition of "noncompetitive", regardless of which one you use. It is an irreversible blocker at an allosteric site.
Marangoni, on p. 70 of Enzyme Kinetics: A Modern Approach, also points out the difficulty in distinguishing between irreversible orthosteric and reversible allosteric inhibition. Using an irreversible inhibitor is equivalent to removing some enzyme from the system, so $V_{\mathrm{max}}$ drops. But at the same time, an allosteric inhibitor causes insurmountable inhibition (reduces $V_{\mathrm{max}}$). Neither type of inhibition alters the affinity of the substrate for the active site of the enzyme (apart from the irreversibly inhibited enzymes with no affinity) so $K_m$ is left unchanged. The figure below, from (Jahangirvand et al., 2016), shows the antagonism of catalase by cimetidine on a Lineweaver Burke Plot. A glance at this graph tells us that $V_{\mathrm{max}}$ is depressed, while $K_m$ is unchanged, so we could (arguably) call this noncompetitive inhibition. But this would not tell us the molecular mechanism of the inhibition.


The probability meaning of Covid variants In the CDC webpage about Covid-19's variants the next sentence appears:

This (the United Kingdom) variant spreads more easily and quickly
than other variants.

In the ECDC paper about Covid-19's variants we can see that:

Several modeling studies corroborate the postulated increased
transmissibility of VOC 202012/01 (the scientific name of the United
Kingdom variant)

In a Nature article from last week written:

Several research groups suggested that B.1.1.7, which was first identified in the United Kingdom, was spreading more quickly than previous variants...

The probabilistic meaning of these sentences is not clear to me. Does this mean that the risk to be infected by the British variant is X times greater? E.g. if I was exposed to the British variant for 10 minutes, my chance of contracting is equal to the chance of contagion the original variant for 10 * X minutes?
Is there any nuance I miss?

The studies referenced do not have any such specifics about transmission probability.
What they observe is that a variant is becoming more common. Modeling the spread gives a different R0 value for the variants vs the reference strains:

In line with previous
modelling studies, the R0 for VOC-202012/01 was estimated as 75% more transmissible than other variants [35].
Davies et al. modelled data from three English regions to estimate that VOC 202012/01 is 56% more transmissible
(95% credible interval (CrI): 50-74%) than previously identified SARS-CoV-2 variants [32]. Danish modelling
studies performed in January 2021 estimated that VOC 202012/01 was 36% more transmissible than other
variants [ECDC communication with Danish authorities].

(from your second reference)
They infer that the variant is more transmissible because the modeled number of people subsequently infected per infected person is greater. The reasons for this cannot be easily determined by the methodology they refer to, and there is no simple way to map this onto probability of infection given some exposure; they are just describing what happens in real-world conditions, on average.
What you can infer is that there are some types of contact that occur in the real world that wouldn't result in transmission with the old strain that do result in transmission of the variant. This could be because more infected people produce enough virus to spread to others, it could be because shorter contacts lead to infection, it could be because infected people have different behavior that leads to more contact with people to potentially get infected; you can't tell the difference from these data.


Why do humans have irregular teeth and impacting wisdom teeth? Imagine that horses, dogs, bears, and gorillas had teeth as unreliable as humans do, The interruption in behaviour and stress brought by teeth would cause them to be more prone to sinus infections, jaw abscesses, and general poor performance.

The stress from cavities and wisdom teeth growing sideways would affect their survival rates.

Humans have evolved slow maturation times, including teeth, have shortened jaws with compressed teeth, and errored, unvariable, DNA from inbreeding after near extinction 100k years ago (lake toba caldera) which makes us biologically quirky and unreliable.

Why does our jaw have to be so short that we could live with impacting wisdom teeth? because it places strain on the neck to have a long jaw?

Why didnt face infections and tooth misalignment cause humans to select each other strongly with straight teeth?

Are wonky teeth a feature of cold climates, where people dont have so much fruit, and in hot countries, ethnicities have straigher teeth?

Teeth first:

The vast majority of people have no problems with their wisdom teeth, whether they emerge or not. Impacted wisdom teeth are very common and are usually painless. They do, however, sometimes mess around with other teeth and throw off our bites (which will always readjust, not necessarily in a cosmetically pleasing manner, but the bite will adjust). Today, because we value straight teeth, impacted wisdom teeth are often removed prophyllactically, even if we have no proof that it/they will cause any problems.

Since impacted wisdom teeth are not evident until well after reproductive ability is attained, there is no reason to believe that malocclusion from wisdom teeth should be evolutionarily selected against. If problem teeth are so bad as to cause disability for an individual, that individual is removed from the gene pool.

Given two equivalent males, there's no reason not to entertain the notion that a female did not choose the one with better occlusion. So, it is theoretically possible that what we have now is an improvement over what was the state of our occlusions long ago. But there is rarely only one reason for two individuals to choose each other as partners, so... the teeth are relatively unimportant evolutionarily.

Or, if impacted wisdom teeth hurt enough to interfere with reproduction ("Not tonight, Og, I have a killer toothache.") the individuals who don't reproduce because of it will be dropped from the gene pool.

There may have been selection against wisdom teeth, because there are populations who have a lower incidence of third molars.

80% of all people will have problems with their backs at some point in their lifetime, which is a direct result of bipedalism in humans. You might ask why we became bipedal with that painful trade off. But bipedalism gave us some distinct advantages in survival. So did the expansion of our brains. The greater advantage has precedence in evolution.

Impacted tooth
Ancient Mutation Explains Missing Wisdom Teeth


Confusion related to the use of PCA to determine the background network I was reading this paper related to use of gene expressions for predicting the drug response. I have this confusion, the paper has used PCA on the covariance matrix formed by the genes to get what is called the background network as they say.

I don't know the essence of background in this case. I know PCA gives us components which preserves the greatest variance and used for dimension reduction. What they mean by background network. Is it pathways ?

I am by far not an expert, but I read the paper and maybe I can help clarifing things a bit.

Let's start with the simplest answer to your question:
In the last paragraph of the Introduction paper the authors say

  "Throughout this manuscript [...]'background networks' and principle components are used interchangeably." ([1] Torkamani and Schork, Genetic background and drug response, The Pharmacogenomics Journal (2012) 12, 446-452; doi:10.1038/tpj.2011.35)

So they did not "use" PCA to get the background networks, they just call the PCs background models to indicate how they interpret it: As stated earlier in the introduction

  "...interacting networks cannot be expected to correlate strongly with drug response, as their influence may only be observed when the major determinant of drug response and the interacting network complement one another or are both at a synergistic state. A major problem with identifying these interaction partners [...] is the extremely large number of possible partners [...] and [...] that individual genes are unlikely to accurately represent the overall state of a biological network." [1]

As far as I understand the article, they suggest PCA as a kind of compromise: Ignoring interactions would miss associations of all networks lacking a single gene representing the network's state accurate enough. Including all interactions is infeasable due to the huge number of gene-pairs. By PCA, the number of interactions can be decreased by orders of magnitude while keeping a maximum on information (as in variation): Instead of using the interaction (as in product) of all probes with all probes, they only consider those of all probes with the first six PCs.

I think, in this context 'background' is not used in the meaning of 'background noise' but of 'cultural background' - instead of assesing individual interactions, genes are assigned a 'background'. Since this corresponds to a) the biological network(s) they belong to and b) the principle components(s) they contribute to, those two ideas are used synonymously by calling PCs 'background networks'.


How many atoms has the smallest known bacterium? Background thoughts before this question: is it feasible to simulate a complete bacterium, atom by atom, in a computer simulation? On modern systems, either in an  upcoming exascale computer?

In current research they've simulated an organella with 100M atoms but I don't know on which infrastructure.

On Quora, there is an estimation of E.coli to have about 9x1010 atoms. With 4m base pairs it is though still quite big and possibly would produce too high computational workload in a simulation.

See also:
https://scicomp.stackexchange.com/questions/33941/is-a-complete-bacteria-simulation-with-an-exascale-supercomputer-possible

If they have simulated an organella with 100M atoms atom by atom, possibly you could already completely simulate some viruses, but they are not independent organisms.

So there has been an atom by atom simulation of the polio virus capsid in 2014 on the K computer with 10 petaflops. To include enough water molecules to fill and surround the capsid, Okazaki and colleagues needed to model the dynamics of nearly 6.5 million atoms, which they did for a simulated 200 ns.

Question - which order of magnitude would a small bacterium count on atoms? What about the smallest known bacterium Nasuia deltocephalinicola with its 112K base pairs? How many atoms has it got?

Let's take the example of the model bacterium E. coli, for which one can find the numbers for a wet cell of a dry mass of 0.28pg. If you have a feeling for how much smaller the smallest known bacterium is compared to E. coli, you can ballpark things.

The number of carbon atoms in a single E. coli cell is approx. 7x10^9 carbon atoms.
The ratio of elements in E. coli is C : H(1.77) : O(0.49) : N(0.24) .

More simply, if you multiply the ratios by 4, you get the ratios of approximately 4 carbons, 7 hydrogen, and 2 oxygen atoms for each nitrogen atom.

Taken together, there are approximately the following number of atoms in an E. coli cell:

C: 7 x 10^9

H: 1.23 x 10^10

O: 3.5 x 10^9

N: 1.75 x 10^9

That is around 2.4 x 10^10 individual atoms. As you may have noticed, these numbers do not have any bearing on the complexity of the system whatsoever. They also do not provide any insight into the intrinsic biological plasticity and dynamics of the system.


How does vasoconstriction increase the pressure of blood? Is the increase of pressure due to the decrease in volume? Wouldn't the decrease in volume push the components of blood closer to one another resulting in an increase of repulsive forces, thus increasing pressure? Or is the increase in pressure due to the heart pumping the blood with more force in order to maintain blood flow?

Because pressure is inversely proportional to area. If you consider a pipe, if you squeeze it's tip to decrease it's area you'll observe that the velocity of water flow becomes high due to high pressure. Same is with blood in veins.


What kind of fish is this, caught in Cape Coral, Florida? What kind of fish is this?

It was caught in the canal in Cape Coral, Florida. The canals are clean brackish water — a mix of saltwater from the Gulf of Mexico and freshwater from the Caloosahatchee River — but the canal where the fish was caught has gulf access so it should be saltwater. The fish was about a foot long, a little less maybe.

It looks like the spotfin jawfish, Opistognathus robinsi. The larger ocellated spot on the foredorsal fin is a key identifier for this species. They are not so common in Florida, but do inhabit sandy bottoms, such as canals. Are you sure about the length? It looks about 5 inches from the photo provided, when compared with the the size of the hole on the dock. This species grows to about 5 to 6 inches.

See here for more info.


Is it possible to isolate and analyse intermediates of protein folding? I would like to know if there is an assay which could allow us to analyse a protein before it has assumed its 3D functional form.
While studying structural biology, I only came to know the forces that stabilize the structure, but not the gap between the original random coil and the protein in its native form.

Theoretically by molecular modeling -- see the works by Harold Scheraga:
https://www.ncbi.nlm.nih.gov/pubmed/?term=Harold+Scheraga%5BAuthor%5D

Note: An unfolded protein is not a random coil.

Fitzkee & Rose (2004) PNAS 101:12497-12502; emphasis mine:

  denatured proteins are biased toward specific conformations, in
  ... conflict with the random-coil model

https://www.ncbi.nlm.nih.gov/pubmed/15314216


Help to identify this large, slow-growing mushroom? Here in my backyard in Southern California, there appears to be this relatively smooth, mottled-colored dome-like structure a little larger than a chicken egg in the dirt. Can anyone identify it? Is it some sort of insect nest or a multicellular fungus?

Edit: After a couple weeks, I've observed some changes. It appears as though this is definitely a fungus and it has been growing taller out of the base. I also see a few feet away something that looks a little different, but not that different, which appeared even at first to be more mushroom-like. Right now the closest thing I could find online is something like a Shaggy Mane. Here are the new photos:

Edit #2: It's been about three more weeks, and the fungus has continued growing larger. Also I am pretty confident that the second one is also the same species. Both have been growing longer and have started to crack at the top.

This fungus is known as a puffball, although that is no longer a taxanomic order. Some of these fungi don't have small openings through which the spores disperse, but they burst open when the spores are ripe. This proces can be clearly seen in your last pictures. The brown stuff below the cracks are the spores. I think when you press it, the brown stuff will come out

Looking at the appearance, I think this is a Calvatia, but as I am unfamilair with the American fungi I can't name a species.


Identifying a mushroom. (Pyrenees near Gavarnie, France) Can anyone help me identify this mushroom? (a still frame from video taken in the Pyrenees near Gavarnie in France). Also is it edible or poisonous?

This is almost certainly the parasol mushroom, Macrolepiota procera. The parasol mushroom is edible, but many other often resembling mushrooms are not. Never eat a wild mushroom unless you're an expert or consulted one.
 https://en.m.wikipedia.org/wiki/Macrolepiota_procera


Examples of genes involved in plastic responses Adaptive plasticity involves sensing the environment and responding adaptively to it. Intuitively, I would think that this process may ask for a more or less complex genetic machinery of regulation of gene expression.

Can you give me examples of genes and genetic pathways that are famous for their role in adaptive plastic response?

I assume that you mean gene expression regulation when you say genetic processes. The best example for your question would be that of synaptic plasticity in neurons.

The immediate responses are obviously that of protein modifications (cell signaling). These are fast responses that have immediate effects but are also quite short-lived. During the long term potentiation (LTP) some stable changes happen via gene regulatory mechanisms.

It is to be noted that in a polarized cell such as neuron the distance between the nucleus and the point of action i.e. the synapses (at dendritic spines), is huge. Any event leading to transcription regulation would take a long time to act. Therefore there are post-transcriptional regulatory mechanisms in place. The mRNAs are localized at the spines and are kept in a repressed state; poised for translation when the signal is received. Finally, if the signal is sufficient enough, transcriptional regulation (sometimes stable due to epigenetic changes) takes place.

You can look for the genes involved in this pathway which also include ncRNAs (lncRNA and miRNAs).

Other examples:

Acute stress response (such as Unfolded Protein Response [UPR])
Acute inflammation
Chemotaxis


biologically speaking, what's the difference between sleeping and just resting? I can lay down in a rested position with my mind at ease, but no matter how relaxed I am or for how long i do it, it seems I'll still need sleep eventually.  What's the difference - what is occurring during sleep that can't occur now matter how relaxed or rested you are?

And if you know of any studies that have been done to try and mimic the benefits of sleep in a waking state - ie during some type of meditation or whatnot - I'd consider that relevant and interesting to know.

Difference between rest and sleep

There are many factors which describe the difference between rest and sleep.

Rest

Rest occurs with conscious breathing. This allows the autonomic nervous system (ANS) to rest. The autonomic nervous system belongs to the peripheral nervous system. ANS controls many organs and muscles in the body.

In most situations, people do not know about the workings of the ANS since it functions in an involuntary, reflexive manner. For instance, we hardly notice if blood vessels change size.

This is the same case when our heart beats faster. There are some people who can control some of the functions in the body and can know the heart rate or blood pressure.

Sleep

Sleep it is a natural state of rest for mind and body. It happens in cyclic pattern. This can be one of the reasons to describe the difference between rest and sleep. There are four stages of sleep.

In the first stage of sleep, there is low-frequency, low-amplitude $\theta$ waves. This stage last several minutes before you enters into the next stage of sleep. In stage 2 of sleep, you brain moves into low frequency. In the third stage of sleep, you receive more high-amplitude $\delta$ waves.

During stage 4, the delta waves account for more of your brain activity and then they return back to stage 1.

Resting is more like being couch potatoes.

Rest is important for health and sleep is a necessary factor. You need both for your physical and mental activity to create energy. When the energy level goes down and wastes increase, there is tiredness and body needs rest. When you take rest, energy is restored. All the waste in the body gets extinguished. Rest and sleep are dependent upon each individual’s ability to relax. If an individual is tensed, he cannot be in the state of rest. Rest is taken to counteract fatigue.

Source:

[1] http://www.theatlantic.com/health/archive/2012/09/when-you-cant-sleep-how-good-is-lying-in-bed-with-your-eyes-closed/262484/

[2] http://insomnia.ygoy.com/difference-between-rest-and-sleep/


Improving DNA quality and yield from stool samples I prepared genomic DNA from pig stools but the concentration was very low — about 3~4 ng/µl, when I measured it using nanodrop. The A260/A280 and A260/A230 values also did not come out very well (0.4~0.5 and 1.0, respectively). I also tried filtering the DNA two times but it didn't improve the quality. Does anyone have experience with DNA extraction from stool samples and suggest me how I can improve the quality and yield?

Expected photometric ratios for pure DNA are around 1.8 (A260/A280) and 2.0-2.2 (A260/A230). For reference, if you are extracting pure RNA, its ratio is ideally 2.0 (A260/A280).

Often, lower ratios usually indicate low purity due to contaminants or simply a very low amount of DNA.

EDTA, carbs and phenol among other chemicals all have absorbance at 230nm. If you used TRIzol reagent to extract DNA, you may also get some absorbance from this reagent at 270nm if you incorrectly pipetted some of the phenol phase (pink stuff) or the interface (white cloudy stuff between the aqueous phase and the pink phase). If you measure a low ratio, like you did, it probably means that in your final DNA extract, you seem to have (a) things that are not DNA in your solution, and/or (b) a very low concentration of DNA.

If you suspect you have enough DNA, you can purify to try to remove non-nucleic acids. However, with ratios that low, I suspect you should extract DNA from scratch; it does not appear that you have enough to rescue simply by purifying again.

Which method did you use to extract your DNA? What do you mean by filtering?


Are ion channels/resistancies in Rall's model voltage-independent or not? In the description of the electrical circuit that models a piece of membrane

in Rall's Scholarpedia article on Ralls model, I read:

  "[...] this conductance [$G_e$] is zero under resting conditions, but
  is turned on by an excitatory synaptic input. [...] this conductance
  is [$G_i$] zero under resting conditions, but is turned on by
  inhibitory synaptic input."

Does this mean, Rall is assuming voltage-dependent ion channels? Or why does he stress, that the conductances can (or even must) be turned on and off?

From an electrical point of you, I would guess, that the three resistancy-battery pairs can be replaced by one such pair that would not be voltage-dependent, and maybe even the battery is not needed, as in cable theory:

Or would Rall's model not work anymore, then? This doesn't get clear to me, and would not have been stressed by the author. (Later in his article, Rall doesn't mention $G_r$, $G_e$, $G_i$ anymore, but talks only about membrane resistance $r_m$.)

If you are interested in passive diffusion and not just membrane potential generation in a dendritic compartment, then you need to look at the cable equation:

$$\frac{1}{r_l}\frac{\partial^2 V}{\partial X^2} = c_m\frac{\partial V}{\partial T}+\frac{V}{r_m}$$

Here, every compartment is connected in series with resistances $r_l$.

We define the length constant as
$$ \lambda = \sqrt{\frac{r_m}{r_l}}  $$

and the time constant as
$$ \tau = r_mc_m$$

Then the equation can be re-written as:

$$\lambda^2\frac{\partial^2 V}{\partial X^2} = \tau\frac{\partial V}{\partial T}+V$$

The reason $G_e, G_i$ are not mentioned when talking about diffusion along the dendrite is that they are only involved in the generation of voltage $V$ in the compartment.


What flowering green plant is this? I got this green plant as a gift many years ago, but I have never seen it flower before. It has a strong, pleasant scent and cool flowers so I'd really would like to know what it is.

It looks like a "Spider lily" from the Hymenocallis genus.

Here is a picture of Hymenocallis caribaea from wikipedia for comparison:

There are however ~65 species in the genus (according to wikipedia), and I cannot say exactly what species you have.


Why are butterflies drinking blood? According to this video, butterflies sometimes drink blood. Do they have the organs necessary to digest blood? I thought they eat only salts and nectar, which are easy to digest compared to proteins.

@aandreev

100mg/dL is the human blood sugar content (I assume it is similar in other animals). Afaik. sugar energy density is about 4kcal/g. A butterfly is about 1g of weight, which means 1mL if we count with water. So it can drink around 0.5mL of blood. That means 0.5mL×100mg/dL×4kcal/g = 0.002kcal = 8.4J. The top butterfly speed is about 12 mph, so I think we can count with 6mph by an average butterfly, which is about 2.7m/s. So it needs 1/2×1g×(2.7m/s)2 = 0.0036J kinetic energy to move and 1g×9.81m/s2×1m = 0.0098J potential energy to keep the 1m height of flight. I think we can guess that it loses this kind of energy in 2secs, which means it needs 0.0134J/2s = 0.0067W power to fly. So the 0.5mL blood means 8.4J/0.0067W = 24925s = 21min of flight time, which is not much compared to nectar (30g/dL$, $2500J$, $100h). Ofc. this is just a very rough estimation (the real flight time is probably much lower) based on data coming from non-scientific sources, but I think you can see the difference.

I didn't watch the video so I don't know if this was mentioned. Butterflies will exhibit a behavior called mud puddling which occurs mainly with male butterflies [1]. Puddling is when butterflies seek out moist surfaces in order to consume the fluid. Butterflies will puddle in soil, dung, carrion (rotting flesh/meat), etc. Boggs and Jackson claim that puddling falls into two categories which aren't mutually exclusive [1]:

scarce nutrients for example sodium
competitive exclusion of males or young individuals from flowers

But we can see blood isn't the only option for puddling. Basically anything that provides moisture and nutrients will do.


Why have whales and dolphins not evolved to have gills? It seems at first glance that it would be an evolutionary disadvantage for a sea creature to have to come up to the surface on a regular basis in order to breathe, so why are there animals (e.g. whales and dolphins) which still need to do so?

If there is some advantage to breathing from the air instead of using gills, why haven't animals such as sharks (or indeed fish in general) evolved to do this instead?

I think you're looking at this the wrong way.

Animals evolve to fill niches. Many, many land animals returned to the water as a place to live, including:

  whales, dolphins, porpoises, seals, sea lions, walruses, manatees, dugongs, otters, hippos, pygmy hippos, crocodiles, sea snakes, sea turtles, river turtles, river snakes, etc. etc. etc.

Their success in this environment points to no need whatsoever to "evolve" gills to be better suited. Without the interference of man, there would be yet many more of them.


Is this some kind of parasite crawling about in my yard? I've been living in Jamaica 25 years now and never seen something like this until recently they started popping up around my house at nights by the dozens.  They appear to be blackish purple or maybe just black (I think my light has something to do with it), but I recall seeing a grey one once and longest one I've seen so far is about 3 inches long.

It looks like a terrestrial ribbon worm.

https://upload.wikimedia.org/wikipedia/commons/a/ad/Terrestrial_Ribbon_Worm_%28Nemertini%29_%2822799575773%29.jpg

Nemertean worms are not leeches, but a different group of worms.  Most are marine but there are a few terrestrial ones.  This depicted worm is from Borneo and other terrestrial nemertean worms are from South Asia also.  But I have read that these can stow away in plants and are turning up in other parts of the world.  I found some small ones in San Diego that I thought were terrestrial leeches but were nemertean worms.

I would be very curious where you are in the world that big ribbon worms are partying in your yard.


Does one parent transmit more DNA to the offspring than the other one? Does one parent transmit more DNA to the offspring than the other one? Or do both parents always transmit the same amount of genetic material to their offspring?

In other words, can a baby be provided with a gene from the mother without an "opposite gene" from the father?

SHORT ANSWER

The two parents transmit the same amount of genetic material to their offspring ....or almost

LONG ANSWER

Nuclear versus Cytoplasmic DNA

All Eukaryotes (everything that is neither a Bacteria nor an Archeabacteria) have nuclear and cytoplasmic DNA. Most of the DNA is nuclear DNA. As its name indicates, nuclear DNA is found in the nucleus. The cytoplasmic DNA is found in the cytoplasm, that is, outside of the nucleus. More specifically, in all eukaryotes, cytoplasmic DNA can be found in the mitochondrion. In plants (which are eukaryotes), you can find cytoplasmic DNA in the mitochondrion and in the plastids (including the chloroplasts (plastids active in photosynthesis)). See here for more information about the origin of the organelles (≈ organ of a cell) who carry DNA.

Nuclear and cytoplasmic DNA doesn't have the same mode of inheritance.

Inheritance of Nuclear Genes

In the diploid (see ploidy) phase (phase during which each individual carries two copies of each gene), an individual carries one copy from his/her mother and one from his/her father.

The above sentence assumes that a diploid phase exists (which is not the case of all species) and that genders (male vs female) exist which is by far not the case of each species. It also assumes that we are talking about autosomes (non-sexual chromosomes, see below for sexual chromosomes). These assumptions hold for humans for example. Note that the diploid phase is much longer in human than the haploid phase (spermatozoid, ovule). We say that humans are diplontic. Some species are haplontic (longer haploid phase) and some are haplo-diplontic. See life-cycle for more info.

In short: Inheritance of nuclear genes is bi-parental, each offspring necessarily carry one copy of a given gene from his/her father and the other copy from his/her mother.

Note: there are some exceptions to this perfect bi-parental transmission (see segregation distorter and intra-genomic conflict). Also, have a look at the short section on sexual chromosomes below.

Inheritance of Cytoplasmic Genes

There are many exceptions to what I am about to write...

Globally speaking, offspring inherit cytoplasmic DNA for their mothers only. That means that your mitochondrion is those of your mother only. Therefore, mothers transmit slightly more genes than fathers because of the concern of cytoplasmic genes.

To complete the picture...

Inheritance of Sexual Chromosomes (Nuclear DNA)

Not all sexual species have sex chromosomes but some do. In these species, it is not rare that one of the two sexual chromosomes is shorter than the other (In mammals, the $Y$ chromosome is shorter than the $X$ chromosome). In such a case, the male transmits slightly less DNA to their male offspring than to their female offspring. Also, in such case, fathers transmit less DNA to their male offspring than do mothers but males transmit as much DNA to their female offspring than do mothers.

The evolution of sex chromosomes is a very interesting subject as well and you will find tons of information on this website or on different sites.

Non-genetic inheritance

Nutrient in eggs

Not only genes are transmitted. Parents also transmit proteins and nutrients in the egg. Females transmit more nutrients to their offspring than males.

Epigenetic

Not only genes are transmitted. Parents also transmit modifications on the DNA that are not modifications in the DNA sequence per se. These modifications are called "epigenetic modifications". Not all species can produce epigenetic modifications. In species who can transmit epigenetic modifications, both males and females can produce them. It is possible that in some species mother have a higher variance in the modifications that they transmit than males (or vice-versa) but I am not aware of such things.

Environment and Cultural transmission

Not only genes are transmitted. Parents also offer an environment in which the offspring grow. Some species typically feed or protect their offsprings. Depending on the species males or females may have more influence on the environment experienced by the offsprings. Finally, in some species (human, chimps and orca for example) a set of traditions (culture) are transmitted to the offsprings from the parents. And depending on the species the father or the mother may have more influence in the culture transmitted to the offspring.

Length of chromosomes may differ between two randomly sampled individuals

Not all variants between two chromosomes in a population is caused by substitutions of one nucleotide by another. Some variation is due to deletions of nucleotides or insertions of nucleotides. You can even a very long piece of DNA who get inserted, duplicated or deleted. Therefore between two given individuals, the exact amount of DNA that is transmitted may also differ only because they happen to have different variants. However, this is not a systematic difference in the quantity of DNA that is transmitted by one sex or another unlike the other cases presented above.


What's the proton concentration around a DNA helix? Let's suppose the concentration of a 20-nt DNA strand is $10^{-4}$M and the solution does not contain any salt ions. In a solution with pH 7, $[H^+]=10^{-7}$M, on average each DNA has only 0.001 protons. But the DNA phosphate groups become charged through de-protonation so each DNA should effectively release 20 protons thus we would expect $[H^+]=20\times 10^{-4}$M. How does the system maintain chemical equilibrium while keeping charge neutrality? If $[H^+]=10^{-7}$M because pH=7, where do other protons go?

DNA stands for deoxyribonucleic acid. Acid, by definition and mechanism in aqueous environment, is something that donates proton ($H^+$). HCl dissolved in water will donate proton to solution, thus bringing pH down, since $pH=-log_{10}[H^+]$.

DNA, being an acid, donates protons to water and brings pH down a notch. Just like in case with HCl, it has nothing to do with keeping charge neutrality. Water is not a buffer, that is able to tolerate or smooth change in pH. What happens when you add DNA to buffered solution, say phosphate buffer, is completely different story from biochemistry.


Does muscle growth trigger angiogenesis? So heavier people generally have more blood than lighter people (this is why heavier people generally need to take higher doses of medication for the same effect of medication). They also have more blood to draw from. But this fails to differentiate between muscle mass and fat mass.

So here's my question: Is the net angiogenesis per gram of muscle more or less than the net angiogenesis per gram of fat?

Muscle is heavier than fat so actually it does. Muscle growth directly increases angiogenesis. Particularly the mechanism relies on hypoxia, any tissue with less than adequate blood supply secretes factors which result in angiogenesis. This is seen frequently when muscle is bulking as this increases the oxygen requirement but is also seen in heart muscle where subsequent to a heart attack tissue which isn't dead but mildly suffering caused new blood vessels to grow to supply this tissue (as the other ones are blocked which was the cause of the heart attack in most cases).


Reflexes & Pathologies including the Vagus Nerve I only know the vasovagal reflex. I would really appreciate if someone could inform me about the other ones.

About the pathologies, I already know the effects of direct nerve damage. I am talking about more sparse and indirect ones, for example so far I found Roemheld syndrome, which is a gastrocardiac syndrome.

Actually, any subtle clinical presentation including the vagus nerve could be really helpful!

One pathology affecting the vagus nerve is autonomic neuropathy which can be secondary to several causes-one of the most commonly acquired cause is diabetes mellitus. It can manifest with various symptoms such as resting tachycardia (heart beating fast without exercise), exercise intolerance, orthostatic hypotension, constipation, gastroparesis (delayed gastric emptying), etc.

If you'd like to read more-http://care.diabetesjournals.org/content/26/5/1553.full

Hope its helpful.


Troubleshooting PCR Steps I am troubleshooting a PCR reaction that gives me no product, and there are a lot of different approaches that I can find in books and just in google searching (things like running a gradient, increasing cycle number, etc.). But it would be really nice if somebody could list out in order the steps they take to troubleshoot a PCR reaction. Thanks.

I think 30 cycle PCR is maximum to see bands by electrophoresis in most of cases, because under the ideal efficiency, one copy could be detectable by 34 cycles of PCR. However, if your expected products are longer than 1 kbp, you might extend several cycles.

I usually add DMSO 5% in any PCR reaction. In my experience, DMSO would not interfere PCR reaction--you can amplify your fragments without DMSO; you could get PCR products with DMSO. Betaine sometimes work better than DMSO, so I am shifting my default reaction mix from 5%DMSO to 5%DMSO and 0.5M betaine.

For annealing temp, you can not tell which is better, lower or higher than the first trial which showed nothing. When increasing the annealing temp, primers may be able to access your target sequence more and you could get efficient amplification. So you might want to try both. If you have a PCR machine set various temperatures at once by gradient. You could include lower and higher temp together.

Alternatively, I sometimes use the touch-down method. You do not need to determine the best annealing temp in this case. If you just want amplified products, this could be a quick solution.

Additionally, hot start is also my default condition, because this could not ruin PCR reaction without hot start.

Basically, I change annealing temp. If I do not get good amplification and specificity, I change PCR enzymes. Changing PCR enzymes could mean changing buffer conditions because companies try to give unique features for their products.


Needleman Algorithm for Optimal Alignment of two Amino Acid Sequences I want to compute the optimal alignment of two amino acid sequences as per the following definition from a patent:

  "The percentage of identity between two peptidic or nucleotidic
  sequences is a function of the number of amino acids or nucleotide
  residues that are identical in the two sequences when an alignment of
  these two sequences has been generated. Identical residues are defined
  as residues that are the same in the two sequences in a given position
  of the alignment. The percentage of sequence identity, as used herein,
  is calculated from the optimal alignment by taking the number of
  residues identical between two sequences dividing it by the total
  number of residues in the shortest sequence and multiplying by 100.
  The optimal alignment is the alignment in which the percentage of
  identity is the highest possible. Gaps may be introduced into one or
  both sequences in one or more positions of the alignment to obtain the
  optimal alignment. These gaps are then taken into account as
  non-identical residues for the calculation of the percentage of
  sequence identity."

The Needleman and Wunsch implementation at NCBI (https://blast.ncbi.nlm.nih.gov/Blast.cgi) mostly works but not exactly. Thanks to @David & @WYSIWIG from a related SE Thread that suggested this (Computing Percent Identity between DNA / Amino Acid Sequence)

I want to know if there is a way to fix the mismatch.

e.g. My test case is:

Seq1: ABDE
Seq2: AAAAAAAAAAABCDE

The NCBI implementation yields the following alignment which has only 3 identical residues:

But shouldn't an optimal alignment  with 4 identical residues be possible like so:

Seq1: ----------AB-DE
Seq2: AAAAAAAAAAABCDE

Thoughts? Any way to tweak the implementation to give the result I want? Alternatively any other algorithm that can be coerced into getting this alignment? BLAST or a variant?

Needleman-Wunsch does an end-to-end (global) alignment (BLAST uses Smith-Waterman). Needle from the EMBOSS toolkit performs Needleman-Wunsch alignment. It will report the highest scoring alignment. I am not sure which alignment it reports when there are two of them with equal scores (I don't think it is random).

I just tried your case: replaced B with W as the former does not denote any specific amino acid (it is ambiguous). It does give:

     1 ----------AW-DE      4
                 || ||
     1 AAAAAAAAAAAWCDE     15

Note that you can change this behaviour by altering the gap-open and gap-extend penalties. You can also change the end-gap penalties (gaps in the beginning or end of the alignment; not in the middle) in Needle.

In this case gap-open=10, gap-extend=0.5, end gap penalty=false and matrix=BLOSUM62

For performing a local alignment you can use Smith-Waterman. It just aligns the highest scoring region and does not do an end-to-end alignment. You can change gap-open and gap-extend penalties in Smith-Wateman and BLAST too, but these algorithms do not begin or end an alignment with a gap.

This is the output of Smith-Waterman with gap-open=1 and gap-extend=0.5 and BLOSUM62 as scoring matrix.

     1  AW-D  3
        || |
    11  AWCD 14

For more information see What is the difference between local and global sequence alignments?


What does it mean for a distribution to be "consistent with a two rate-limiting stochastic steps"? I'm reading a study (full text here) that examine the dynamic of nuclear translocation of a transcription factor in budding yeast, in response of calcium stress. They found that it occurs in bursts, which distribution of durations is plotted on this normalized histogram:

In the text they say:

  Normalized histograms, $h(t)$, of total burst duration at two calcium concentrations are both well-fit by $h(t)=te^{-t/\tau}$, with $\tau$ = 70 sec (black line).

And also

  This distribution was consistent with two rate-limiting stochastic steps, each with a timescale of ~70 sec.

Can someone explain me the second sentence cited?

The rate limiting step of a reaction is the slowest component of the reaction. So if there are two steps in a reaction, each of these steps will have a rate, and the slowest of those two rates will determine the overall rate of the whole reaction.

As a simple example, consider the equation

$A + B + C\rightarrow AB+C\rightarrow ABC$

If the rate of $A+B \rightarrow AB$ is fast, but the rate of $AB+C \rightarrow ABC$ is slow, then the overall reaction will still be slow.

The figure in your question is showing the distribution of the burst durations, and highlighting the fact that the calcium level has no effect on the burst duration. The second quote is a bit confusing, this is my interpretation:

The functional form which they fitted to the distribution indicates that the expected burst duration is about 70 seconds. I'm not completely sure which stochastic steps they are referring to, maybe translation and subsequent localisation (I think transcription would happen on a different timescale and so could be ignored in this case).

By the way, this paper is a really excellent example of an organism harnessing stochasticity to its advantage in order to synchronise its response to a stimulus (calcium in this case). I just think that it is so cool that the mean response to the signal level can be different to the response to the mean signal level - so counter-intuitive to me. And so much fun!!


DNA extraction from plants and algae don't use phenol. Why? I don't know if here is the correct place to make this question, but I've been noticing that protocols for the extraction of photosynthetic organisms DNA don't use phenol. Only CTAB / Chloroform.

Why?

Because bacterial or animal extraction are phenol:chloroform based.

Thank you

CTAB is for removing polyphenols and polysaccharides which are found in plant tissues. Animal cells/bacteria don't have these. You can do an additional phenol-chloroform extraction if you want.

See this protocol by Monsanto.

  Weigh out 6g of processed tissue into a 50ml conical tube appropriate for centrifugation. Note: For unprocessed tissue, weighing
  m ay occur prior to processing as long as entire processed sample is
  transferred to the conical tube.
  For each 6g sample add 25ml of a solution consisting of 24.25ml, pre-warmed (55°C) CTAB extraction buffer, 0.5ml 2-mercaptoethanol
  (2-ME), and 0.25 ml of 10mg/ml proteinase K for a final concentration
  of 2% (2-ME) and 100µg/ml (proteinase K).
  Incubate the tube for 60 minutes at 55°C. Cool the tube briefly on bench (10 minutes)
  Add 20ml of phenol:chloroform:isoamyl alcohol (PCI, 25:24:1).  Cap the tube and mix vigorously by vortex or inversion.
  Centrifuge for 10 minutes at 13,000×g and 20-25°C to separate the aqueous and organic phases. Transfer the upper aqueous phase to a
  clean 50ml conical tube.
  Repeat extraction two times for a total of three extractions (steps 4-5).
  Transfer upper aqueous phase to a new tube and add approximately 2/3 volume of -20°C isopropanol and gently invert the tube several
  times to mix.
  To precipitate the DNA place the tubes at -20°C for at least 30 minutes and up to three days.
  To pellet the DNA centrifuge the tubes at approximately 13,000×g for 20 minutes at 4°C.
  Redissolve the pellet in 4 ml of TE pH 8.0. Transfer to a 13ml Sarstedt tube and add approximately 40µl of 10mg/ml RNase, then
  incubate at 37°C for 30 minutes.
  To extract the DNA add 4ml of chloroform:isoamyl alcohol (CIA, 24:1).  Centrifuge for 10 minutes at approximately 13,000×g at room
  temperature.  Transfer the upper aqueous phase to a clean Sarstedt
  tube.
  Repeat step 11 then add half volume of 7.5M ammonium acetate, gently mix by inversion/pipette and add 2 volumes of 100% ethanol. Mix
  by inversion/pipette and place at -20°C for 30 minutes to overnight.
  Centrifuge at 13,000×g for 20 minutes at 4°C to pellet the DNA.


What is this anise smelling plant? On holiday in southern France and we found this small plant growing out of some rocky soil:

It smells quite strongly like anise but seems to be a different plant?

There are several plants in the family Apiaceae with these kind of thin leaves, and some smell strong and/or are used as herbs in the kitchen. This must be Fennel  Foeniculum vulgare, because you describe it's smell as anise. Dill looks similar, but smells different. Fennel is indigenous to the mediterranean, but planted all over Europe.

It can be quite big, but on poor, rocky soil might remain small.

Picture of fennel from Dutch wikipedia:


difference between ischemia and oxygen-glucose deprived medium Ischemia is roughly defined as insufficient blood flow to a specific region of the body and in the literature it is generally considered as causing oxygen and glucose deprivation in the tissue and therefore cells. Can we induce ischemia by depriving cells from oxygen and glucose in the medium or does it require more than that and ischemia is more complicated?

edit: i know the definition of ischemia maybe i should have said 'mimick' instead of 'induce'. Anyway, here is the better version of my question:

Ischemia is defined as blood flow shortage in a tissue and it is one of the main causes of non-apoptotic cell death. In an article i was reading, the authors claim that they induced ischemia in the glucose-serum containing medium. Does this mean they deprived the cells from oxygen and thus mimicked ischemia? Is this the way to create ischemia in a cell culture? What other ways can there be? Should not cells also be deprived from glucose?

Ischemia leads to tissular hypoxia and glycopenia due to an insufficient blood flow (e.g. due to atherosclerosis or thromboembolic diseases). Ischemia always result in hypoxia.

Hypoxia can occur without ischemia (e.g. due to anemia).

Tissular glycopenia can occur without ischemia (e.g. due to hypoglicemia).

Ischemia is a shortage in blood supply. Depriving cells form oxygen and glucose isn't the same as cutting their blood supply.


Hill-Roberston effects and effective population size From this article, first page, middle of the second column:

  Even if harmful alleles do not become fixed, they can still reduce the efficacy of selection on neighbouring loci through a process called Hill–Robertson interference. This effect occurs because individuals bearing deleterious mutations are less likely to survive and reproduce, reducing the number of individuals that contribute genetically to the future population. This reduces the effective population size witnessed by a focal locus

I don't understand the link between the Hill-Robertson effects and the effective population size. Why would the effective population size be greater in absence of Hill-Robertson effects? Can you please make this link clear to me?

Here is another question on the same article.

Hopefully this syllogism will answer your question.

Given the following premises:

In the absence of selection, fitness of individuals are at a theoretical maximum.
If a theoretical maximum fitness is achieved then effective population size is maximum.
If there is an allele that confers both increased and decreased fitness you have a genetic conflict (e.g. an allele that turns you green gives you good woodland camouflage but is un-attractive).
If a deleterious allele is linked to a beneficial allele this is similar to having a genetic conflict.

The conclusion follows:

Strong linkage between beneficial alleles and deleterious alleles (Hill Robertson effects, i.e. 3. and 4.) prevents a theoretically maximum fitness to be attained (1.) and thus a reduced effective population size (2.). Which can only be overcome by high levels of recombination and mating (i.e. by separating deleterious and beneficial alleles).


Alleles notation in SNPPedia criteria I can understand the allele notation when is in the form rs8176719(T;T) or rs8176719(G) but recently i found this ones rs8176719(T;-) or rs8176719(-;T).

So im confused, rs8176719(T;-) is the same as rs8176719(T)? or is the location is important ?

Thanks .

The '-' means that that allele has a single base deletion.


Does food really give our bodies the energies that we have determined by burning them in the lab? You are likely to have come across numbers like sugars 17kJ/g (4kcal/g) as the energy supposedly available to our bodies after eating. Yet these values have been determined using very artificial means, typically lighting up food with a red hot iron in a steel chamber at high oxygen pressure.

Many historic energy values have been proven wrong in the past. For example, salad leaves had zero calories in many historic energy tables before we realized that bacteria in our gut can break them down and we in turn can break down bacterial products, gaining back part of the chemical energy of the plant.

Are you aware of any research that has determined the energy value of different foods in more natural conditions, ideally in humans? I expect some calorie values to change from those determined by the bomb calorimeter, don't you?

The device you refer to is a bomb calorimeter. Inside one of these, a sample of material is completely combusted. Typically, the heat from the combustion warms a measured mass of water and the rise in temperature is used to calculate the Calories/Joules in the material.

Of course our cells don't ignite food and burn it to completion. Even if they did, some of the heat from the process would escape collection. Cells use the process of cellular respiration to harvest the energy. The basic version of cellular respiration describes the utilization of glucose to create ATP, by far the most used substance to power the energy needs of the cell. Here's just one source that takes you through the calculations of how efficient this process is: http://www.tiem.utk.edu/~gross/bioed/webmodules/ATPEfficiency.htm

So, at least for the very common sugar glucose, only about 40% of the total Joules, as measured in the calorimeter, end up as ATP. Most other food substances we use for energy share much of the same chemical pathway as glucose. I haven't seen calculations of their efficiency but suspect it would be roughly similar.

One of the most basic and important lays of physics is that no transfer of energy is 100% efficient. (Read more here: https://en.wikipedia.org/wiki/Energy_conversion_efficiency ). The remaining energy in the glucose that was not converted to energy in ATP is "lost" as heat. By lost, it is meant that it's not avaible to do any useful work other than heat us up. Of course, being homeothermic ("warm blooded") animals, that's useful too.


What is the contribution of viruses to the evolution of mankind? I'm interested in horizontal gene transfer in bacteria, viruses, and organisms such as Bdelloid Rotifers. I've just read in Carl Zimmer's 'A Planet of Viruses' the following passage:

  As a host cell manufactures new viruses, it sometimes accidentally adds some of its own genes to them. The new viruses carry the genes of their hosts as they swim through the ocean, and they insert them, along with their own, into the genomes of their new hosts. By one estimate, viruses transfer a trillion trillion genes between host genomes in the ocean every year.

It's interesting to consider the scale of DNA-swapping that has occurred given the frequency by which it happens and the evolutionary timescale.

Are there any examples of genes in the human genome that we know were deposited by viruses that would have given an evolving human a physical/mental advantage? Where did they come from? What benefit did they provide?

I'm interested in genetic additions from non-human-ancestor species, rather than the transfer of genes that occurred as mutations from other humans.

The processes that control the germline of metazoans (multicellular animals) are highly regulated compared to single cell bacteria and eukaryotes as well as plants.

At this point there are no clear stories of gene transfer into a complex animal, though there are some for plants:

"animals and fungi seem to be largely unaffected, with a few exceptions, while lateral gene transfer frequently occurs in protists with phagotrophic lifestyles, possibly with rates comparable to prokaryotic organisms."

Bacteria fungi and plants are more permissive and more susceptible to gene transfer and it probably is more important to their evolutionary path.

Its been estimated that as much as eight percent of the human genome has been affected by viral integration.  But viral genomes are highly selected against carrying non essential material - other genes rarely come along for the ride it seems.  What is probably more influential is that viral insertions could participate in rewiring the regulatory network of animal cells, not adding genes, but modifying the conditions under which they are active.


Is this plant Yucca filamentosa color? I am trying to find the name of this plant for a while. The closest I got is Yucca filamentosa color. The leaf blades are near 4-5 inches and are almost thin(without pulp). Please help me in identifying it.

Location: Hyderabad, India.

I found out the picture that I posted belongs to  Furcraea foetida 'Mediopicta'. It belongs to "Agave" family like L.Diago suggested in comments.


What causes the preliminary changes in resting membrane potential in neurons? Background: The neuron's membrane resting potential is maintained at a certain voltage. The neuron has a lipid bilayer with certain protein channels which allow the movement of ions in both directions (in and out). Some of these protein channels are gated by:

1) mechanical changes (stretching, pressure, etc)

2) voltage changes- regulated by electrical signals (transport of Na+, K+ through protein channels)

3) Ligands (neurotransmitters, etc)

(Guyton and Hall, Textbook of Medical Physiology, 2016)

Question: If action potentials are brought about by voltage-gated channels which are activated by the change in voltage, what brings about this change in voltage which activates voltage-gated channels?

It sounds a bit convoluted. Here's a quote from Wikipedia's Membrane Potential page:

  Because voltage-gated ion channels are controlled by the membrane potential, while the membrane potential itself is influenced by these same ion channels, feedback loops that allow for complex temporal dynamics arise, including oscillations and regenerative events such as action potentials.

Hopefully this quote will help to communicate my confusion.

You have already listed two possibilities:

  1) mechanical changes (stretching, pressure, etc)

and

  3) Ligands (neurotransmitters, etc)

In the central nervous system, ligands and in particular neurotransmitters are going to be the overwhelming cause of most initial depolarization. Ligand-gated ion channels are the simplest mechanism: some examples include AMPA receptors, GABA-A receptors, and nicotinic acetylcholine receptors, but it is also possible to change the membrane potential via second messenger systems that open or close other channels.

In the periphery and in sensory organs, sensory-evoked potentials can be caused by mechanical gating, as you mention, as well as by specialized channels that respond to particular stimuli, for example the TRP family which includes channels sensitive to temperature (for example TRPV1, which responds to heat and also responds to capsaicin, the chemical that makes chili peppers 'hot') and to certain chemicals in food (resulting in taste).

The other category you missed is that some cells generate a spontaneous depolarization because they contain channels that are activated around the resting potential (and/or potassium channels that close, which also depolarizes the membrane). This is crucial for the cardiac pacemaker but can also be found in the central nervous system in some cell types.


Frequency of dominant phenotype (Hardy-Weinberg) The question is:

The frequency of a recessive allele a is 0.6. If a population is in Hardy-Weinberg equilibrium, what is the frequency of the dominant phenotype?

This question is a bit confusing to me. I'm not sure how to use my knowledge about Hardy-Weinberg in this problem. I know that when q = 0.6, p = 1 - 0.6 = 0.4. But when they are asking for the dominant phenotype, should it be p^2 or the squareroot of p? I have watched several YT-videos about this, but I still can't get the hang of it. There's not much help in my teacher or books. I would be really grateful if someone could clear up my confusions!

p = p(a) = 0.6

q = p(A) = 0.4

Frequency of homozygous recessive, aa = p2 = 0.36

All other genotypes have dominant phenotype therefore the frequency of the dominant phenotype is 1-0.36 = 0.64

(Frequency of homozygous AA = q2 = 0.16

Frequency of heterozygous Aa = 2pq = 0.48)

And if you want a deeper explanation you really should study this answer by Remi.b


How is SARS-CoV-2 'deactivated' for some Covid vaccines (for example Covaxin)? Some Covid vaccines like Covaxin employ a 'Whole-Virion Inactivated Vero Cell'.
How is the virion 'deactivated' for the vaccine?

For Covaxin (BBV152), SARS-CoV-2 was inactivated by treatment with β-propiolactone [1]. β-propiolactone reacts with and modifies, among other things, nucleic acids, thus preventing their replication [2].
[1] Yadav P, Ella R, Kumar S, et al. 2020. Remarkable immunogenicity and protective efficacy of BBV152, an inactivated SARS-CoV-2 vaccine in rhesus macaques. Preprint.
[2] Perrin P, Morgeaux S. 1995. Inactivation of DNA by β-propiolactone. Biologicals 23(3):207-211.


What did the evolution of multicellular animals look like? What did the evolution of multicellular animals look like?

Aspects of this question include:

(1) Are there any living organisms that might be helpful in visualizing "transitional forms" between unicellular organisms and multicellular animals? E.g. I have heard of slime molds as one example. Would love to hear of as many good examples as you can come up with. Not looking for strict hereditary relationships here, and I am fine with plausible but unproven theories. E.g., mudskippers might help a person visualize the evolution of amphibians, even if they aren't in fact closely related to amphibian ancestors.

(2) Do we think that the first animals evolved into sponges, or cnidarians/ctenophoroans, or something else? Did sponges and cnidarians/ctenophoroans evolve multicellularity separately? As this is probably a big topic, feel free to just post a link or two.

(3) For any examples that you can think of for #1, would love to hear of any good citations of articles or books for me to read, but keep in mind that I am not a scientist and not looking for anything extremely technical.

The life cycle of myxobacteria (e.g., Myxococcus coralloides, Myxococcus disciformis, Myxococcus flavescens, Myxococcus fulvus, Myxococcus macrosporus, Myxococcus stipitatus, Myxococcus virescens, Myxococcus xanthus---for references to the original articles describing these species, see Bacteria I. Taxonomy: Genera and Species) includes the formation of fruiting bodies, which is an obligate multicellular process requiring cooperativity between individual bacterial cells (see, e.g., Cao et al., 2015).