How does Cas9 interact with CRISPR? I read that Cas9 protein along with guided RNA binds at a specific DNA fragment of foreign organism integrated in a host organism DNA. To make the host immune to virus infection Cas9 along with gRNA which is complementary to viral DNA attaches to it host DNA by unbinding it and then cuts the DNA at this site thereby removing the viral DNA. So the host can only remove the virus that enters second time as it makes a complementary RNA from the first virus that has integrated in it and cannot completely remove virus.

Is the process that I am thinking right?
And can we use Cas9 to cut the DNA at any site of our choice?

We are currently using CRISPR in the lab to modify cells. Like @AMR said, it was modified from the In Vivo immune system to be used in the lab in DNA editing field. The Addgene website features both historical background and an application guide that are very well done. To answer your questions:

The bacteria (S. pyogenes, S. aureus, etc) integrates part of the viral DNA (protospacers) inside its genome, flanked by repeats. When transcribed the RNA derived from this newly combined sequence will direct the Cas9 protein to the viral DNA, which is complementary. Another element required is the PAM (protospacer associated motif) which is on the viral DNA just besides the protospacer. By not being on the bacterial DNA, it ensures that the Cas9 does not cut its own DNA.
The only limitations are the PAM and the off-targets. The PAM is specific for every species (EG S. pyogenes is NGG). Some sequences can be repeated in the genome of an organism, meaning that if you find a sequence that would result in a cut at a desired site, it could still cut elsewhere. That would make the guide sequence a poor choice.


Stochastic parameters in population growth equations I'm more of a mathematician than a biologist, so I had a question about an application of the population growth equation to real-life models, and thus would like to ask biologists for their insights. The equation I'm looking at is the following (in reality, I have n-species but it's just an extension of this two dimensional problem):

$$ \frac{dx_1}{dt} =x_1\Big(b_1-a_{11}x_1-a_{12}x_2 \Big) $$
$$ \frac{dx_2}{dt} =x_2\Big(b_2-a_{21}x_1-a_{22}x_2 \Big) $$

where the $b$ are growth parameters, and the $a$'s are all parameters describing interactions among the species (and carrying capacity). The papers I've looked at for stochastic perturbations with these equations have primarily dealt with stochastically perturbing either the $b$ parameters while holding the others constant, or perturbing the $a$ parameters while holding $b$'s constant. However, these papers are written by mathematicians with no biological experience, so the decision on which sets of parameters to perturb are somewhat arbitrarily decided without any biological basis.

For the biologists, can someone suggest some cases for where it would be more biologically reasonable to perturb the growth parameters and some cases were it would make more biological sense to perturb the interacting parameters? I ask because I'm a part of some interdisciplinary neuroscience project which is using equations of this form to study interacting neuron clusters, but since I'm a math person and not a biologist, I am trying to understand reasonable explanations for what stochastic perturbations mean biologically for these parameters.

Since you are asking for the biological interpretations about these parameters, it is important to realize that the model you are presenting is a non-dimensionalized version of this model:

$$ \frac{dx_1}{dt} =b_1x_1\Big(1- \Big(\frac{x_1 + \beta_{12}x_2}{K_1} \Big)\Big) $$
$$ \frac{dx_2}{dt} =b_2x_2\Big(1- \Big(\frac{x_2 + \beta_{21}x_1}{K_2} \Big)\Big), $$

which can also be written as:

$$ \frac{dx_1}{dt} =b_1x_1\Big(1- \frac{x_1}{K_1} - \beta_{12}\frac{x_2}{K_1}\Big) $$
$$ \frac{dx_2}{dt} =b_2x_2\Big(1- \frac{x_2}{K_2} - \beta_{21}\frac{x_1}{K_2}\Big). $$

This clearly shows how this competition model is merely the logistic Verhulst model, with an extra term attached. This extra term is simply describing to what extent each individual in "species" 2 is using up the resources of "species" 1 ($K_1$), where $\beta_{12}$ describes this relationship (~proportion of species 2 that is counted as species 1). The parameters in the model formulations above are also more easily interpreted in ecological/biological terms than the $a_{ij}$s in your model.

To go from this latter formulation to yours you substitute:
$$a_{11} = b_1/K_1$$
$$a_{12} = \frac{b_1\beta_{12}}{K_1}$$
$$a_{22} = b_2/K_2$$
$$a_{21} = \frac{b_2\beta_{21}}{K_2}$$

As you can see, this means that the $a_{ij}$s are composites of other parameters, and perturbing $a_{ij}$s could correspond to either $b_i$, $K_i$ or $\beta_{ij}$ being perturbed. It also means that perturbing e.g. $b_1$ in your model while holding $a_{11}$ fixed means that you are actually also perturbing $K_1$ to offset the change in $b_1$ (since $a_{11} = b_1/K_1$), which will introduce a positive temporal correlation between $K_1$ and $b_1$. This is a strong assumption to make. This also means that $a_{ij}$s are not strictly "interaction parameters" as you call them, but they include other aspects as well.

Since realistic cases and scenarios for perturbations may often be expressed in terms of the parametrization I give above (e.g. random fluctuations in population growth rate or carrying capacity), these relationships are essential to keep in mind.


Lactobacillales vs LAB (Lactic acid bacteria) As far as I understand bacteria of order Lactobacillales are all LAB (Lactic acid bacteria). So often "Lactobacillales" and "LAB" are used interchangeably.

But I also thought that this is not the whole truth, because there are LAB which are not of order Lactobacillales.

Can anyone elaborate on this topic and is there a paper/review explaining the consensus on this topic?

Lactic acid fermentation is the most common type of fermentation among Eubacteria, and it's found on several genera.

Actually, regarding the fermentation types, we can say as a general rule:

Ethanol fermentation: found in Plants and Fungi.
Lactic acid fermentation: found in Bacteria and Animals.

That being said, according to the Todar's Online Textbook of Bacteriology,

  Although many genera of bacteria produce lactic acid as a primary or secondary end-product of fermentation, the term Lactic Acid Bacteria is conventionally reserved for genera in the Order Lactobacillales.

And according to Lactic Acid Bacteria: Microbiological and Functional Aspects, Fourth Edition:

  They [LAB] belong to the Phylum Firmicutes, Class Bacilli and Order Lactobacillales.

These genera are: Lactobacillus, Leuconostoc, Pediococcus, Lactococcus, Streptococcus, Carnobacterium, Enterococcus, Oenococcus, Tetragenococcus, Vagococcus and Weisella.

The problem here is that not all lactic acid producing bacteria are called a LAB. Therefore, Lactobacillales and LAB can be used interchangeably. However, you cannot say that all bacteria that perform lactic acid fermentation are LAB.

Sources:

Textbookofbacteriology.net. (2017). Online Textbook of Bacteriology. [online] Available at: http://textbookofbacteriology.net/index.html [Accessed 3 May 2017].
Lactic Acid Bacteria: Microbiological and Functional Aspects, Fourth Edition
En.wikipedia.org. (2017). Lactobacillales. [online] Available at: https://en.wikipedia.org/wiki/Lactobacillales [Accessed 3 May 2017].


Identify ~6-7mm long green creature Here is the creature I found on the glass lid of my light bulb. I guess they are attracted to light as they all concentrate on the light source. I live in Hong Kong. The brown things aren't moving (those might be eggs). The green creatures are about 0.6-0.7 cm long in body length (excluding appendages and antennae). They are sluggish in movement.

Can you help me to identify these tiny creatures?

Let's take a look at the magnified body of the insect (it is a nymphe btw) - we can see 2 brown dots one above the other along the body line. This pattern is very suggestive to Chelinidea species (the most common is Chelinidea vittiger aequoris):

I stop my search at Coreidae family, because multiple species (a lot of bugs actually) of this family have similar appearance, for example:

Gonocerus acuteangulatus:

But other enthusiasts can start from here (Coreidae family) and trace it down more precisely - I am sure they will succeed.


The least complex animals with ability to dream People can dream, dogs can dream, cats probably too when they are sleeping.

What about other creatures?

Can a bird dream?

Do rats have dreams?

Are there any studies about that kind of thing? What is the most simple organism that have brain structures that allow them dreaming during the sleep?

Since mammals all share the same neural structures it is quite likely that most non human species dream, but as yet, the simplest animal I could find that has been scientifically demonstrated to dream is the rat, as proven by Massachusetts Institute of Technology (MIT).

MIT not only established that rat were capable of dreaming about the events they had experienced while awake, but that the content of the dreams could be manipulated with audio cues the rats had been trained to respond with in a specific way.

Sources:

http://en.wikipedia.org/wiki/Brain#Mammals

http://web.mit.edu/newsoffice/2012/neuroscientists-achieve-dream-engineering-0902.html


why are malarial parasites specific for anopheles why are malarial parasites specific for anopheles mosquito. why do they need only anopheles, they just need lower temperature to complete their life cycle. all mosquitoes are cold blooded, so they can get a suitable environment in any of them, why only anopheles?

The host/parasite relationship is normally very specific: because there are a lot of molecules that have to bind each other for the parasite to complete its cycle, a parasite is not capable of invading any given organism; the same way, a host is not invaded by any given parasite.

That being said, you have to keep in mind that mosquitoes are also hosts (despite of, in the case of malaria, having less symptoms when compared to the human host). In fact, regarding malaria, some parasitology books classify the mosquitoes as the "definitive hosts", while humans are "intermediate hosts" (because the sexual reproduction of Plasmodium happens in the mosquito, not in the human being). So, there are a lot of molecules that have to be present for the parasite finding its way through the mosquito's organism. A plasmodium cannot survive inside a Lutzomyia mosquito, the same way a Leishmania cannot survive inside a Anopheles mosquito. There is specificity.

Actually, not all Anopheles are the same (just as not all human beings are the same). They have differences regarding the susceptibility to the parasite:

  Some Anopheles species are poor vectors of malaria, as the parasites do not develop well (or at all) within them. There is also variation within species. In the laboratory, it has been possible to select for strains of An. gambiae that are refractory to infection by malaria parasites. These refractory strains have an immune response that encapsulates and kills the parasites after they have invaded the mosquito's stomach wall.

(source: https://www.cdc.gov/malaria/about/biology/mosquitoes/)

Please note that other mosquito species are not resistant to the plasmodium, because we call "resistant" a host that's capable to fight the parasite. The other species are not even hosts!


Pituitary giants - is the fusing of growth plates dependent on amount of growth hormone in blood? I wanted to ask a couple questions related to pituitary giants (people who are giants because of some anomaly, such as a tumor, in their pituitary gland).

Some of these giants seem to keep growing and growing until the tumor (or the gland) is removed. Is this because the fusing of the growth plates is controlled by the amount of growth hormone in blood?

The reason for this question is that many of the giants have been described to grow past when the growth plates should probably have fused. For example (all heights in meter, m):

Bernard Coyne This giant is described as having been 2.36m at the age of 20, but 2.54m at the time of his death at the age of 23.
Edouard Beaupré At the age of 17, this giant was measured as 2.16m tall and at the age of 21, he was measured at 2.50m tall. At the time of his death, at the age of 23, he was listed (in his death certificate) as having been 2.51m tall and "still growing".
Väinö Myllyrinne This giant was 2.22m at the age of 21 but is described as having "experienced a second phase of growth in his late thirties", attaining a height of 2.51m by the time of his death at 54.
Adam Rainer This giant was, unusually enough, a "dwarf" at the age of 18, reaching a height of 1.22m. However he had a growth spurt afterwards, reaching a height of 2.18m at the age of 30 and 2.34m by the time of his death at age 49.

Also, in some cases the giant individuals facial (bone) structure changes as he/she ages. Considering that the human skull does not have any growth plates, or anything that would (as far as I know) put a stop to the skull bones response to growth hormone, can changes in face structure also happen to "regular" people who take growth hormones?

Gigantism is caused by too much growth hormone (GH) and causes increased growth in kids (healthline website). After adulthood, increased GH leads to acromegaly which leads to continuing growth of fingers, feet, forehead, jaw, nose, and lips (UCLA Health website). Note that structures like the nose and ears also keep on growing in healthy folks.

Hence, GH does not prevent closure of the growth plates, which happens normally as far as I am aware.

Taking GH during childhood will likely lead to gigantism, and to acromegaly in healthy individuals.

EDIT: In answer to the QUESTION EDIT: the comment by @Raoul is interesting here, as the first guy Bernard Coyne was an eunich. Perhaps that was why his plates never fused as he will have had no testosterone production. I couldn't find specifics in the other 3 cases, but my guess is they are also exceptional cases (otherwise they wouldn't have made it in the record books). As to the question title I dare say that GH is not involved in plate fusion.


Carbon Monoxide and High-Oxygen-Affinity Varieties of Hemoglobin I recently learned about the concept of "affinity" in regards to hemoglobin. For hemoglobin in humans, carbon dioxide has a lower affinity than oxygen, which allows gas exchange to occur in our lungs.

Carbon monoxide is problematic for us because it has an even higher affinity to hemoglobin than oxygen does. This means that our red blood cells will not exchange carbon monoxide for oxygen in our lungs.

My question is: for high-altitude-adapted organisms such as the bar-headed goose, whose hemoglobin has a higher affinity to oxygen than ours does, is carbon monoxide still poisonous?

My question is: for high-altitude-adapted organisms such as the bar-headed goose, whose hemoglobin has a higher affinity to oxygen than ours does, is carbon monoxide still poisonous?

Yes. To put out a few other facts from the Stritch School of Medicine:

CO has 250 times the affinity for hemoglobin than O2
Hb becomes 100% saturated with CO at PCO = 0.6 mm Hg
Hb becomes 100% saturated with O2 at PO2 = 600 mm Hg

What does that mean? Well, that means that when the partial pressure of CO is 1mmHg, you're well and truly dead. So if the bar headed goose could survive in an environment more than 1% CO its hemoglobin would have to bind to molecular oxygen very, very tightly below 1mmHg. If this was true you would expect their binding curve to reach a high % of O2 saturation below a partial pressure of 1mmHg. Does it exhibit that?

Nope. At 1mmHg (remember, CO has 100% binding at 0.6mmHg) the bar headed goose hemoglobin's saturation is less than 2%. In fact, they're pretty similar to humans:

Is this casual glance conclusive? Well... Not entirely. I couldn't find any carbon monoxide data for the bar headed goose, but to overcome the 250x higher affinity for CO the goose's hemoglobin would have to be very, very different from that of humans while still exhibiting a similar binding curve. I've not received the education to determine if that's possible or how it would occur, but it is a very remote possibility.

Erring on the side of "most likely", however, I think it's safe to say that given a room filled with 1% CO you'd end up eventually killing anything that relied on hemoglobin to move necessary oxygen to tissues.


Mechanism to limit the exponential growth of the number of ancestors that are n-generations away from an organism? The context is organisms with sexual reproduction, with 2 parents per organism.
Construct the family tree of one such organism, back into geologic time.

Take a(n) as being the number of ancestors that are n generations distant.
The function a(n) has an exponential character (at least in the beginning, with n sufficiently small).

For 2^n, simple math gives:

After 20 generations, you have about 10^6 ancestors.
After 30 generations, you have about 10^9 ancestors.
After 50 generations, you have about 10^15 ancestors.
After 1000 generations, you have about 10^300 ancestors.

I've read one estimate that there are about 10^80 atoms in the Universe. What does this mean?

It's important to note the the members of generation n usually aren't all alive at the same time.
As an example, for humans, the birth-dates of generation-20 are roughly between the years 1720-1520, for example.

It doesn't take very many generations for a(n) to exceed p(t), the population as a function of time.
This is accounted for (at least for sufficiently low n) by the fact that a(n) represents organisms that aren't alive simultaneously, while p(t) does.
I understand that.
But, this effect, important as it is, seems to be linear with time.
As such, it doesn't seem capable of limiting the exponential growth of a(n).

In this context, inbreeding is often raised.
But, in my opinion, inbreeding is not germane.
Here, all that matters is that each organism has 2 parents.
Period.
Whether or not inbreeding was involved doesn't change that basic fact.
All inbreeding means is that one ancestor is a member of more than 1 generation.
That's not relevant to my question.

Edit later:
No, inbreeding is germane. It means that 2 members of a(n) can have the same two parents in a(n+1). That reduces the exponential growth of a(n).

It seems that a(n) must be limited by something, for sufficiently large n. What is that something?

Of course a(n) is limited, and much more tightly than by the number of atoms that exist.  The analysis in the question goes off track with "inbreeding is not germane. Here, all that matters is that each organism has 2 parents. Period."

Consider a person whose parents are first cousins. Then:

a(1) = 2
a(2) = 4
a(3) = 6, not 8

While each of the two parents has four grandparents, together the two parents have only six grandparents because they share one pair of grandparents.  This is due to pedigree collapse.

This table shows the actual collapse for some people with ancestry known to nine generations and with significant inbreeding (from de.Wikipedia):


What is the scientific name of this flying insect? It looks like some relative of dragon fly.

To give an idea about its size I picked it by its wings

It had quite a flexible abdomen

I set it free after clicking the pics. I live in central India (If that matters)

This insect is, indeed, related to dragonflies. This is a damselfly.

Damselflies are Odonata insects from the Suborder Zygoptera. Unlike dragonflies (Suborder Anisoptera), damselflies fold their wings when resting. This is the most noticeable difference between damselflies and dragonflies:

Regarding your specimen, I'd say that it is Caconeura ramburi, the indian blue bambootail. Here is an image for comparison:

The site where I found that image, conveniently called Odonata of India, is a good source of information.


What in fast food fries have that regular fries don't? Why is it that a french fry from a fast food restaurant doesn't seem to spoil the same way as one that one would cook at home?

PS: If given enough time will fast food french fries eventually decompose; if so, how long?

I went through a longer winded explanation here:  https://biology.stackexchange.com/a/57877/19432.

In brief, food spoils if water is bio-available to micro-organisms.  In the case of a french fry from say, McDonalds. This fry has a very small volume to surface area ratio, and hence is able to dry out what little water is left after the frying process before micro-organisms can proliferate enough to visibly "spoil" the fry.

If, in your own kitchen, you were take a fresh potato, cut it into fries, and cook them in oil long enough to nearly dehydrate the fry, it would not spoil either in a dry environment.

Take either of those items that had been allowed to cool down and pick up micro-organisms (yeast and bacteria) from the air and place into a sealed ziplock bag with a little water and they would both spoil.

For your last question, in a dry environment, once something has become desiccated, decomposition stops and your fry would only decompose if the environment became more humid.  Think about naturally preserved mummies in an arid environment.

Edit: Light also can break bonds...and lend to further decomposition in the absence of micro-organisms. As can physical abrasion from wind, sand etc... So naturally mummified remains of great age would also have been protected from light and abrasion as well.


How can I obtain a computer readable model of Dr. Gerhard Michal's biological pathways map? I want to run simulations of various metabolic pathways – the project could end up becoming quite large, and having a machine readable chart would make thing a lot easier. Does anyone know if there is a machine readable file of Dr. Gerhard Michal's famous metabolic pathways chart?

Roche's Biochemical Pathways works as a big png image and just put labels on the map. But you could try to extract data using queries like http://biochemical-pathways.com/pol/fts/query?query=Glutarate
It seems to be legal as it's not prohibited.

Escher is a good pathway visualization tool where you can save map in JSON or SVG.

Another choice is VMH (Virtual Metabolic Human) - the virtual metabolic human database provides literature-derived information on human metabolism, gut microbial metabolism, nutrition, and diseases.

Reactome has two layer map - first layer is biological interactions, second layer is pathways.


Has the human 7-day week had any impact on the evolution of species? Most (if not all) industrialized countries follow a 7-day work week now, such that we are bound to follow a certain weekly trend in matters such as pollution generation, where to go (e.g. stay in town during weekdays, more likely to go to parks during weekends), what to do (mow the lawn on weekends).

Is there any evidence of any species evolving to adapt to the pace of the human 7-day week lifestyle?

I have no clear evidence of a specific species, but two pieces of the puzzle:

species can adapt to living in cities: birds living in cities are bolder (i.e. allow humans to come closer before flying away), and apparently even some genetic changes can be detected.
it may be possible for species to evolve a circaseptan rhythm: beach beetles may have a seven-day rhythm to accommodate for different heights of the tides (spring/neap tide). (PubMed / PDF)


Long-term efficacy and absence of side effects of anti-covid vaccines The question is about the methodology/biostatistics of clinical trials (I state this beforehand to avoid accusations of being an anti-vaxxer).
As multiple anti-COVID vaccines are offered on the market, the question naturally arises about their long-term efficacy and possible side effects. As SARS-CoV-2 virus has been known for a bit more than a year, neither of these could be tested directly, so one probably has to rely on indirect knowledge due to the experience in developing other vaccines. Given that multiple vaccines have been approved for a wide use, there should exist well-established procedures to assure their efficacy and safety.
The question is: how does one prove the long-term efficacy and absence of side effects during a short period of time (short in comparison to the expected duration of immunity and absence of side effects).
Update
As @MattDMo have correctly pointed in their answer, the absence of long-term effects is established in the last phase of the clinical trials, while observing cohorts of vaccinated individuals during a long period of time. @MaximilianPress, in their comment, has also correctly brought up the fact that this is done within the framework of survival analysis. In particular, this means that it is sufficient to follow the vaccinated cohort during several years to evaluate the side effects that occur during their lifetime, as the survival analysis keeps track of the sensored data.
Here we are dealing with a situation where such a study could not be done - the best we can guarantee is the absence of the side effects in the next few months. We thus need to rely on a different method, which would account for the similarity between the established and the new vaccines.
I am less concerned about the vaccine efficacy, since the inefficacy of vaccines is usually against different strains of virus, as is in the case of influenza and Dengue.
Update 2
The accepted answer points out two important things:

The long-term side effects of a vaccine/medication can be truly understood only in the Phase IV of the clinical trials, i.e., after the vaccine is in widespread use.
The threshold for approving this specific vaccine is lower due to the emergency of the current health crisis.

This however still leaves open the question of the safeguards undertaken in the Phase III of the clinical trials, before the vaccine approval. I.e., the question is about ranking the candidate vaccines against the above-mentioned threshold.
Remarks:

I understand why this question irritates, but I believe that it is not the asking, but rather refusing to seek the answer that plays in the hands of anti-vaxxers.
I did follow the suggestions in the comments to pose this question in the medical and the statistics communities, but it seems to get there even less traction.

Update 3
Recent suspensions of Astrazeneca vaccine in 9 European countries demonstrate the importance of this issue.

You are correct that we have been creating and approving vaccines for a very long time, so the procedures for looking at efficacy and side effects of vaccines in general long-term are quite well developed. They occur via so-called "Phase IV" trials, also known as post-marketing surveillance.
However, one complicating factor with at least the Pfizer/BioNTech and Moderna vaccines is that they're the first mRNA vaccines ever approved. While I hope the companies have been following some of the volunteers from previous clinical studies of other mRNA vaccines, we're in somewhat uncharted territory right now. The vaccines appear to be safe and effective, at least on the scale of tens of thousands of Phase III test subjects, but we just don't know exactly how they'll behave long-term. They were approved in the US as "Emergency Use" products, meaning the upside of having them available outweighs any known or potential downsides at this point.
So, the technical answer to your question "how does one prove the long-term efficacy and absence of side effects in such a short time?" is that they can't prove it. Based on the available data to date, there's no reason to suspect that some previously-unobserved deleterious effect will become common, but we can't be 100% certain until the products have been in widespread use for years and possibly decades. However, given the seriousness of COVID-19 and its currently unchecked spread across much of the world, the benefits of having "highly, strongly, very most likely safe" vaccines (that are also very effective) are huge.


Can the retina emit light? The retina is light sensor, which converts light to an electrical signal.  LEDs can both emit and receive light. Similarly, is it possible to apply electricity to retina to generate light?

Simply put, in theory, can humans emit electromagnetic waves from their eyes?

Please allow me to start by saying I know nothing about LEDs, so my answer isn't going to address your analogy. I'm also going to keep it more simple.

  Can the retina emit light?

Yes. The retina is able to give off light in the form of fluorescence. Since fluorescence is the emission of light by a substance (granted that substance must first absorbed light or other electromagnetic radiation of a different wavelength.)

  “We can use autofluorescence emission to image the retina and see certain features of it,” said Dr. Sparrow, the Anthony Donn Professor of Ophthalmic Science in the departments of Ophthalmology, and Pathology & Cell Biology. ...Most objects in the environment are visible because they reflect, as opposed to emit, light. However, the retina—which exists within the eye’s back wall, known as the fundus—can generate its own fluorescence.

The cells of the deepest layer of the retina, called the retinal pigment epithelium (RPE), contain fluorescent compounds, which when excited by blue light emit a yellow fluorescence.

This ability changes with age, disease, etc.

  Excessive accumulation of lipofuscin granules in the lysosomal compartment of retinal pigment epithelium cells represents a common downstream pathogenetic pathway in various hereditary and complex retinal diseases, including age-related macular degeneration.

Lipofuscin is one of several fluorophores in the RPE. Different fluorophores may be related to different damage to the eye.

  A major hydrophobic component of RPE lipofuscin is the fluorophore A2E... Given that A2E strongly absorbs in the blue region of the spectrum, together with the known susceptibility of RPE to blue light damage, we undertook to investigate A2E as a fluorophore involved in blue light toxicity.

Science Insight: Using the Retina’s Natural Fluorescent Light to Measure and Treat Disease
FUNDUS AUTOFLUORESCENCE IMAGING: Review and Perspectives
The Lipofuscin Fluorophore A2E Mediates Blue Light–Induced Damage to Retinal Pigmented Epithelial Cells


What type of fish is this- Cabo San Lucas, Gulf of California side Can anybody tell me what this fish is?  Caught in Cabo last week, actually closer to San Jose, with a Joe's Flies 1/4oz spinner.  Cool looking fish for sure, just can't seem to find it online of what it is??

That is a giant hawkfish, Cirrhitus rivulatus. It is identified by its unique markings from other species in the same region. This individual looks slightly young to me from the size, however it is most certainly this species. Giant hawkfish on mexican-fish.com


Can I imbibe seeds before sterilization? For an experiment I want to germinate lettuce seeds. For logistical reasons it would be convenient to imbibe the seeds by placing them in the cold for 2 days, afterwards I would sterilize the seeds using dilluted bleach. I mostly see people apply stratification or imbibition after sterilization, does the order matter? Would there be a difference for cold treatment (stratification) or wet treatment (imbibition)?

Personal anecdote: Once I planned to sterilize seeds of Silene latifolia for tissue culture but after the first step (washing the seeds in water for an hour) I had to do other things and the seeds did spend the night wet in room temperature. The next day some of the seeds were showing first signs of germination - a little crack in seed coat. I decided to sterilize them anyway, since there was nothing to lose. The result: Some seeds did germinate after sterilization and were fine. Some seeds died. Interestingly, in some seeds the bleach destroyed only the exposed root meristem resulting in rootless seedlings.
I have never worked with lettuce seeds but I would consider questions:

How fast the seeds germinate and what conditions they need for germinating? You cannot sterilize seed that have already germinated.
Could the inbibition change the properties of the seed coat and make it easier for the bleach to pass through and kill the embryo? I suspect not, but cannot be sure.
Wet environment is good for bacteria and fungi growth. "Dirtier" seeds are sometimes harder to sterilize - they need longer exposure to bleach or stronger bleach concentration to completely remove contamination. Stronger bleach or longer treatment can sometimes kill some (especially small) seeds. It is hard to say weather two days of wetness can make any difference. The cold should slow down the bacterial and fungal growth.

At the end of the day I reccomend you to try with few seeds and see the result. Maybe include negative control with usual order of steps. If the survival is the same for both groops you are good to go.


How to calculate the quantification of qPCR to the equivalent of the number of nuclei in fungi? I have a question about the quantification through qPCR. The my question is: if I made the qPCR of a fungal functional gene, how is possible to obtain from the quantification number (in nanogram) the equivalent number in number of nuclei?

From your comment:

  "As few as 148 fg of Verticillium dahliae DNA were detected and quantified (through qPCR), which is equivalent to five nuclei". How is possible to make this convertion?

The Verticillium dahliae JR2 genome is 36.2 Mb.  Assuming this organism is haploid and dsDNA has an average mass of 660 g/mol per base pair, that means the molar mass of the genome is 2.40 × 1010 g/mol.  Therefore, 5 nuclei will contain 8.30 × 10-24 mol of your genome.  Multiplying the molar mass by the number of moles gives us a mass of 1.99 × 10-13 g, or 199 fg, which is close to your cited value.


Distribution of hearing loss Low-frequency sounds are more penetrating, damaging. Hearing damage caused by blasts typically occurs at frequencies around 2 - 8 kHz, while age-related hearing loss starts at the high frequencies. The frequency range for noise-induced damage is biased upward, because the low-frequency conductive structures damage first.
https://www.entandaudiologynews.com/features/ent-features/post/effects-of-blast-and-acoustic-trauma-assessment-of-hearing-status-on-war-veterans
Why does hearing loss occur at high frequency first? It should occur at low frequency, because that is the more damaging sound. The distribution of hearing loss is totally incompatible with the noise exposure explanation. It could be due to growth factors, i.e., the high frequency parts die first because more distal.

Short answer
Noise-induced hearing loss affects primarily the mid-frequencies, because the inner ear is most sensitive to these frequencies.
Background
Noise-induced hearing loss occurs typically in the mid-frequencies (Rabinowitz, 2000), typically around 4 kHz (3 - 6 kHz), see Fig. 1. This can be explained by the fact that the human ear is most sensitive in this frequency range (Fig. 2). In turn this relates with the frequency range where speech understanding is most important, namely between roughly 2 and 6 kHz (Killion & Mueller, 2000). Hence, noise exposure neither targets the base, nor the apical parts of the cochlea, as claimed by asker and answerer, respectively. High-frequency hair cells in the rat cochlea have been shown to be very susceptible to damaging noise, but the low-frequency hair cells may go unscathed (source: eMedicine).
The other answerer claims that

parts of our hearing apparatus responsible for perceiving these
[low-frequency] sounds are more fragile...

Hence, the claim that low-frequency regions in the cochlea are more sensitive than the more basal parts is not a claim supported by the bulk of the literature. In fact, as a rule of thumb, cochlear damage (inner ear damage) occurs most frequently first in the base, where the high frequencies are resolved. This holds for age-induced HL where high frequencies are lost first (Ciorba et al., 2011), as well as chemically-induced HL (Campo et al, 2013, barred some specific organic solvents that apparently do not follow this rule (Cappaert et al., 2002.

Fig. 1. Typical audiogram of noise-induced hearing loss showing loss of functional hearing at the mid-frequencies (Rabinowitz, 2000)

Fig. 2. Relation between perceived loudness and intensity (equal-loudness curves) for a normal-hearing person. source: Lumen Phsyics
References
- Campo et al., Dis Mon (2013); 59(4): 119–38
- Cappaert et al., Neurotoxicol Teratol (2002); 24: 503–10
- Ciorba et al., J Laryngol Otol (2011); 125(8):776-80
- Killion & Mueller, The Hearing Journal (2010); 63(1): 10-7
- Rabinowitz, Am Fam Physician (2000); 61*(9):2749-56


Are there fundamental differences between the adaptive immune systems of higher primates and other mammals? I recently attended a Leukemia and Lymphoma Society lecture in which one of the lecturers indicated that there are fundamental differences between the adaptive immune systems of higher primates and other animals.

The Wikipedia article on adaptive immune system seems to indicate that mammals share very similar adaptive immune systems.

I understand that there are (minor) differences between the B cells and T cells (and other cells) of different species, and that two species can differ in their susceptibility to a particular kind of pathogen (virus, bacteria, whatever), depending on small differences in cell surface proteins, etc.  I am not interested in these kinds of small differences.

Rather, I would like to know if there are any fundamental differences between the adaptive immune systems of humans (and other higher primates) as compared to other mammals.  For instance, are there particular kinds of adaptive immune cells in primates that don't appear in other mammals.  Or are there fundamentally different mechanisms (e.g. the mechanism of T-cells activating B-cells) or lymphatic system organs that are markedly different in higher primates as compared to other mammals.

In short, are there big differences in the immune system of higher primates that make them stand apart from the other mammals in the same dramatic way that thumbs and intelligence seem to separate them from other species?

I am not aware of a discriminatory feature between primates and all other mammals. However, there are significant differences for some animals. For example, the anti bodies of camelids and sharks consist of the heavy chain only, or the antibodies of sea lampreys are not of the immunoglobulin protein family.

Those differences have been exploited for biotechnology.

consider this review: http://www.nature.com/nbt/journal/v23/n10/full/nbt1127.html


Caterpillar(?) in Leaf Cocoon identification - Missouri A small chunk of leaves fell off of a potted tomato plant. We noticed our cats taking an interest in it once it started moving. Then a little caterpillar poked its head out. What kind of bug is this and should we worry about our plant?

This is the larvae (caterpillar) of a bagworm moth (family Psychidae).

 Source: Wikimedia Commons; Credit: Bernard DUPONT

From Wikipedia:

  The caterpillar larvae of the Psychidae construct cases out of silk and environmental materials such as sand, soil, lichen, or plant materials.

There are about 240 genera, so I will leave IDing to lower taxonomic levels up to you. However, based on the striations of the caterpillar and your lcoation, the Evergreen Bagworm Moth doesn't seem like a bad guess...


Is one single antibody binding its antigen enough to elicit an immune response? IVIG (intravenous immunoglobulin) is derived from plasma of more than 1000 donors. I wonder if in this preparation is one antibody present that recognize its antigen after infusion - if this is enough to elicit an immune response? Thanks

This is a wonderful question, because it addresses a common misunderstanding.
Short Answer: We have no clear data about the effectiveness of a one single antibody molecule in the immune response of an entire organism, but since many different antibodies can recognize the same pathogen, and . Just as antibodies in a healthy individual are able to find, bind to antigens, and produce an immune response, antibodies from transfusions of IVIG can do the same. They can block, opsonize, activate complement, and regulate B-cells and T-cells.
Long Answer: Surprisingly, brilliantly, our innate immune system is able to generate transmembrane and secreted proteins that bind every possible antigen (or almost every possible antigen, depending on who you ask). See my answer to this earlier question, and the associated general references. We get very excited when we teach this. With our focus on teaching the diversity of antigens and binding regions, it is easy to get the idea that there is a single unique antibody for every possible microbial invader. For students that really take in the problem of antigen diversity and the solution of antibody diversity, this question, or some variation, often follows: how can a single antibody ever do any good? Usually, with some wonder about how to quantitatively match up this diversity with any specific pathogen. This is an example of that question. Here is the answer:
Many different antibodies can recognize a pathogen
A single pathogen has many many antigens, or molecules that, e.g., an antibody could bind to. A single antigen has many epitopes, or specific binding sites for an antibody paratope (the part of the Fab region of an antibody that is specific to the binding site). A single paratope can bind more than one epitope. This is called cross-reactivity. Additionally, a single epitope can be bound by more than one paratope. A good discussion of this principle can be found in Chapter 4 of Frank's Immunology and Evolution of Infectious Disease.
Antibodies are produced in massive quantities
Lauren Somparyic, in How the Immune System Works, estimates that, in the pre-immune state, of the roughly 3 billion B-cells, a single clone is comprised of about 30 cells. Each clone contains many copies of the transmembrane version of its single antibody, and many different clones (as discussed in the paragraph above) will recognize a single pathogen. Once exposed to a pathogen, B-cells that recognize it divide many times over, undergoing a series of changes beyond the scope of this question. At the end of this process, plasma cells, the B-cell progeny that produce secreted antibody, then each secrete hundreds to thousands of antibodies a second. Without ongoing antigen stimulation, many of the plasma cells die, but long lived plasma cells migrate to the bone marrow and continue to secrete enough antibody to allow for the rapid response seen in a subsequent exposure to the same pathogen. The majority of antibodies in the blood of a healthy adult come from these long lived plasma cells in the bone marrow. You can read about this process in chapter 3 and 10 of How the Immune System Works and chapter 7 of Abbas Basic Immunology. Essentially, the circulating antibodies in the $\gamma$-globulin fraction of plasma contain large numbers of each antibody produced in response to exposure to a pathogen. Because of this, we don't have to wonder how one lone antibody in the vast expanse of an organism can be effective in response to many pathogens. We have many, many antibodies that can do this.
IVIG
IVIG is from, as the OP states, pooled samples of antibodies from many thousands of blood and plasma donors. 75% of these are IgG antibodies, meaning they've already undergone class switching and are a result of exposure to antigen. I'm not aware of a good study that clearly catalogues the populations of different clones in IVIG samples, but we can say the set of antibodies in IVIG represent the collective immune memory of the population from which it was pooled, but behave in a similar way to the circulating antibodies in a healthy adult.  You can read more about this here and here. Because of this, the same principles discussed in the above paragraph apply here. We don't have to worry about the lone antibody lost in the massive sea of the human body. Even pooled from thousands of donors, each dose of IVIG contains many, many antibodies that can recognize each important human pathogen.
Transfused antibodies retain their effectiveness
There are a variety of clinical uses for IVIG, but there is clear evidence that the antibodies in these samples retain their effectiveness in their roles as effectors of the immune system. Not only are the antibodies in IVIG effective at blocking and neutralizing pathogen receptors and toxins, but they activate and clear complement, opsonize pathogens and damaged cells for clearance by neutrophils and other phagocytes, control and regulate the B cell population, and interact with the T-cell population, much as they do in the healthy individuals who haven't been given IVIG. The NEJM article I linked above discusses much of this (though it focuses on modulation), this review, which you can access without a paywall, also discusses this.


Orange tipped plant found in Carden limestone plains of Ontario What is species is this plant?

Found in the Carden limestone plains of Cameron Ranch (near Orillia, Ontario, Canada) on September 9th, 2017.

It is located in an old bog that seems to have sphagnum peat moss (to my untrained eye).

It's an odd angle, but I think the plant/flower is an Indian Paintbrush (Castilleja coccinea). It is found in Saskatchewan, Manitoba, Ontario, and Nova Scotia.


Does human digestive system benefit from eating same kind of food consistently? Here's the reason why I'm asking: I've heard that it takes some time for pets(cats/dogs) to adjust to a different dry feed, where the new feed has to be mixed with the old one, slowly replacing the old one. I'm wandering if this advice has any truth in it, and if so, does this apply to humans as well?

For example, a cat eats the same kind of food for months at a time, but humans vary their diet  much more dramatically. Are there any benefits to eating the same kind of food over extended period of time? I'm interested in knowing if the digestive system/symbiotic bacteria in the gut adapts to the food, resulting in better digestion/absorption of nutrients.

Thank you for your input!

I think it would depend on the benefits you are looking for.

If you ate the same thing everyday, it's possible your intestinal flora, and the rest of your GI tract would optimize themselves for maximal nutritional extraction. It is known that the flora in you GI do affect nutrition. I recall reading about obese patients who had gut-bacteria which made more nutrients available.

However, if you were in an environment where your diet could change unexpectedly, this optimization could actually be detrimental, since you wouldn't be ready to switch foods when necessary.


What Makes A Pet Hypoallergenic I know you can purchase dog and cat breeds that are hypoallergenic so those who are prone to pet allergies will have reduced allergies or none at all. These breeds are specifically bred for that trait, and as a result are typically pricey compared to another breed. These breeds are not necessarily hairless or short-haired, so I do not think it has to do with the amount of fur shed.

What makes these animals different from other breeds in their inability to cause allergies?

Pet allergy is an allergic reaction to proteins found not only in the
  animals' fur or hair but also in saliva, urine, mucous, and hair roots
  and in the dander sloughed from the animals' skin. Thus, the
  widespread idea that "hypoallergenic pets" are those that have less
  hair or shed less is a myth.

  Most often, pet allergy is triggered by exposure to the dead flakes of
  skin (dander) a pet sheds. Any animal with fur can be a source of pet
  allergy, but pet allergies are most commonly associated with cats,
  dogs, rodents and horses.

  Some dog breeds have been promoted as hypoallergenic because they do
  not shed their hair, shed very little, or have the same pH as human
  hair. However, no canine is known to be completely non-allergenic.

  Some cat breeds, especially females are likely to have low levels of
  Fel d 1, the main allergenic protein.

  There is only one known hypoallergenic horse breed. The Bashkir Curly
  horse has a uniquely textured coat that lacks the protein (present in
  all other horse fur) believed to be the source of allergic reactions
  to equines.

via


Why are there no wheeled animals? In physics, "almost everything is already discovered, and all that remains is to fill a few unimportant holes." (See Jolly.) Therefore, on Physics SE, people are veering off into different directions: biology, for example.

Thus, it happens that a question about bicycles generates some discussion about evolution in biology and animals with wheels.

Three explanations are offered for the apparent lack of wheely animals (also on Wikipedia, where, by the way, most Physics SE questions are answered perfectly).

Evolutionary constraints: "[A] complex structure or system will not evolve if its incomplete form provides no benefit to an organism."
Developmental and anatomical constraints.
Wheels have significant disadvantages (e.g., when not on roads).

Now, I suggest that all three can be "solved".

With time.
With a symbiotic relationship between a wheel-like animal and a "driver"-like animal, although this gets awfully close to a "driver"-animal to jump onto an actual (man-made) wheel. (So, perhaps, you can suggest a better loophole around this constraint.)
Roads are presumably not the only ecological niche where animals with wheels could thrive. I'm thinking of frozen lakes, although there skates would be better than wheels.

What, therefore, is the explanation for there not being any wheeled animals?
Please consider, in your answer, the counterfactual: What assumption of yours would be falsified once a wheely animal is discovered?

Wheels are possible on the molecular level — bacterial flagella are rotating cores inside a molecular motor, but wheels larger than the flagellum have not really been found.

A single animal with a wheel is an improbable* development that would require a single animal have two separable parts (axle/wheel and body).

[*read as: pretty much impossible]

It's hard to imagine how such a thing could evolve.  A wheel and axle would need to be made of living tissue, otherwise it would be vulnerable to wear and tear.  Wheels also have problems going over uneven terrain, which is really all terrain animals live in.  It's difficult to imagine what sort of selection conditions would be strong enough to push animals away from legs.

If you include driver-vehicle symbionts where the 'car' and 'wheel' are actually two animals, then they have evolved. Parasites can have all sorts of symbiotic control over their victims including as means of transport. The Jewel Wasp is one which is the most suggestive of what you may be thinking. The wasp stings its victim (a cockroach) in the thorax to immobilize the animal and then again just behind its head.  After this, the wasp can ride the beetle, steering it by holding its antennae back to its nest where the roach is immobilized to feed the wasp larvae there.

(see section "Pet cockaroaches" in this reference.)

As to the three schools of thought you added to the question, I would probably rather say there were two strong arguments against.  The first is whether there is an evolutionary path to wheels (argument 1 in your question), which I doubt.  Given even a large amount of evolutionary time you will not see a naked human being able to fly on their own power.  Too many structural characteristics of the body plan have been made to all be reversed so that wings or other means of aerial conveyance will show up. The same can be said for wheels when the body plans have fins/legs/and wings already.

Argument 3, which I also tend to agree with, is perhaps more convincing.  By the time a pair of animals makes a symbiotic relationship to do this, or a single macroscopic animal evolves wheels, they will literally develop legs and walk away. When life came onto the land this happened, and since then it's happened several times.  It's sort of like saying that the random movement of water molecules might line up to run a stream uphill. There's just such a strong path downwards, that the statistical chances of you seeing it happen are nil.

This is a hypothetical case, but arguing this in a convincing way I think you would need to lay out:  a) an environment whose conditions created enough of a selective advantage for wheels to evolve over legs or other similar adaptations we already see. Perhaps based on the energy efficiency of wheels;   b) some sort of physiological model for the wheels that convey a reasonable lifestyle for the wheel.

There are lots of questions that would need to be satisfied in our thought experiment.  Here are some: "the symbiotic wheel would be spinning constantly; if it died the driver creature would be completely defenseless"; "if the ground were bumpy, all these wheeled animals would get eaten"; "the wheel symbiont — how would it eat while its spinning all the time? Only fed by the driver? Even symbionts such as barnacles or lampreys on the flanks of sharks still have their own ability to feed."

For many similar questions the same sort of discussion ensues where there are many disadvantages which outweigh advantages for animals. e.g.
"why are all the flying animals and fish and plants even more similar to airplanes than helicopters?"

Sorry if I seem negative, but way back in grad school I actually did go over some of these angles.

UPDATE: First Gear found in a Living Creature.
A european plant hopper insect with one of the largest accelerations known in biology has been found to have gears!  (There's a movie on the article page.
)

The little bug has gears in its exoskeleton that synchronize its two jumping legs.  Once again selection suprises.

  The gears themselves are an oddity. With gear teeth shaped like
  cresting waves, they look nothing like what you'd find in your car or
  in a fancy watch.  There could be two
  reasons for this. Through a mathematical oddity, there is a limitless
  number of ways to design intermeshing gears. So, either nature evolved
  one solution at random, or, as Gregory Sutton, coauthor of the paper
  and insect researcher at the University of Bristol, suspects, the
  shape of the issus's gear is particularly apt for the job it does.
  It's built for "high precision and speed in one direction," he says.

The gears do not rotate 360 degrees, but appear on the surface of two joints to synchronize them as they wind up like a circular spring.  The gear itself is not living tissue, so the big solves the problem of regenerating the gear by growing a new set when it molts (i.e. gears that continually regenerate and heal are still unknown).  It also does not keep its gears throughout its lifecycle.  So the arguments here still stand; the exception still supports the rule.


Identification - hornet It has around 3cm. Does it look like a European or Asian Hornet?
The place where I found it is Central Europe/Romania but, after the wikipedia picture for Asian Hornet's head .. it looks exactly the same.
Thank you!

European hornet (Vespa crabro). In the Asian hornet, the black body bands are much wider and more uniform. For the European hornet, as in your specimen, the bands are thinner and appear as thin lines connecting triangular black dots. See this image for comparison:
https://www.sciencephoto.com/media/980933/view/asian-and-european-hornets-illustration


How is sugar in fruit metabolized, or digested and used? I thought before, in general, when we have sugar in our food, then the sugar goes in our bloodstream, and if there is too much sugar, then insulin is secreted by our pancreas, and the sugar is pushed into our cells for storage, and to lower the blood sugar (and the insulin may over do it, causing our blood sugar to be too low).

But then recently I heard that sugar in fruit goes through a different route: it goes directly to the liver, and not moderated by the pancreas and insulin?  How does it work?

Do you mean fructolysis?

Here what I found on the textbook  by John L. Tymoczko:

Fructose can take one of two pathways to enter the glycolytic pathway.Much of the ingested fructose is metabolized by the liver, using the fructose 1-phosphate pathway. The first step is the phosphorylation of fructose to fructose-1-phosphate by fructokinase. Fructose-1-phosphate is then split into glyceraldehyde and dihydroxyacetone phosphate, an intermediate in glycolysis. This aldol cleavage is catalyzed by a specific fructose 1-phosphate aldolase. Dihydroxyacetone phosphate continues into stage 2 of glycolysis, whereas glyceraldehyde is then phosphorylated to glyceraldehyde 3-phosphate, a glycolytic intermediate, by triose kinase. In other tissues, fructose can be phosphorylated to the glycolytic intermediate fructose 6-phosphate by hexokinase.


How to find PDB id of an amino acid sequence Suppose I have an amino acid sequence whose PDB id  is unknown. Is there in online server that can find the PDB id of the corresponding amino acid sequence?  is there any site that will find the pdb of a protein closest to the query protein?

One way of doing this is to run a protein BLAST search at NCBI in which you specify the Protein Data Bank as your database, as in the example shown below:

The results will be all for proteins in the PDB.


Does body absorb nutrients less efficiently if we ingest the same amount at the same time, opposed to spreading over a larger period? I would like to understand if ingesting a certain amount of nutrients will result in different absorption from my body, depending on whether I ingest that amount spread over time or everything at once.

For example, considering all the food I eat in one day: does my body absorb the same amount of fat and protein if I eat that same amount of food all at once, compared with eating it spread by different meals?
Similarly, could it be possible that my body absorbs less fat if I eat 4 hamburgers at the same time, compared with eating them spread along the day?

LARGE MEALS AND ABSORPTION

When consumed in usual amounts, the percent of absorbed macronutrients (carbohydrates, proteins, fats, alcohol) should not differ significantly when coming from one large or several small meals.

As an example of the composition of a single large meal, let's imagine something that fits into Acceptable Macronutrient Distribution Ranges (AMDR) in a 2,000 calorie diet: 250 g of carbohydrates, 70 g of proteins and 80 g of fats.

Most carbohydrates are digested into glucose and fructose. Glucose, when absorbed as the only carbohydrate (ingested as glucose or starch), can be absorbed at the rate 60 g/min, but the addition of fructose can increase the absorption of both together to as high as 126 g/min. When fructose is absorbed as the only carbohydrate or in the excess of glucose, it's absorption limit from one meal can be as low as 5 g or as high as 50+ grams. Certain sugar alcohols (see Table 4) (sorbitol, isomalt..) can trigger diarrhea when consumed in amounts greater than ~20 g/meal.

Virtually all ingested protein is absorbed by healthy humans (Surgery Journal). The rate of absorption depends on a type of protein: about 10 g of whey protein and 3 g of egg protein can be absorbed in one hour (JISSN).

At least 60 grams of fat consumed at once can be normally absorbed, concluding from a study in which they investigated the relationship between the amount of fat consumed and atherosclerosis.

In conclusion, the amount of macronutrients (except fructose and sugar alcohols) consumed with a single meal does not seem to significantly affect the percent of macronutrients absorbed, but it prolongs the time in which they are absorbed.

LARGE MEALS AND DIET INDUCED THERMOGENESIS

After eating one large meal, more of the consumed calories will be lost as heat than after eating several small meals:

  Consuming the same meal as a single bolus eating event compared to
  multiple small meals or snacks was associated with a significantly
  higher DIT [diet induced thermogenesis]. (Nutrients, 2016)

  TEF [thermic effect of food] was measured by indirect calorimetry
  for three hours following each meal and was found to increase
  systematically, in a nonlinear fashion, as meal size was increased.
  (Metabolism, 1984)


Why are viruses considered microbes? My question is simple. Why is a virus considered a microbe? Considering a microbe is considered to be a "living" unit of life, which viruses are not.

What is a microbe?

A microbe (or microorganism) is a microscopic organism. Anything that is considered alive and that is small enough is called a microbe.

Note that this definition has two issues.

There is no universally accepted definition of life.
There is no universally accepted size threshold for being called a microbe (to my knowledge). I would go with a threshold of about $10^{-5}$ meters.

Is a virus a microbe?

A virus IS and IS NOT alive depending on the definition. Note btw, that the definition of what is alive is not a matter of Biology but a matter of Philosophy. Most of the time, viruses are considered as not being alive. It is important to understand that the definition of life has absolutely no impact on biology and is nothing but a question of nomenclature.

If you want to call a virus a living thing, then yes, viruses are microbes. As stated on the wiki article:

  Some microbiologists also classify viruses (and viroids) as microorganisms, but others consider these as nonliving.

You can find a discussion of why viruses are generally considered as not being alive here.

Unit of life

The concept of "unit of life" has not much meaning in biology and, to my experience, is most often used as a nice image for teaching young students what a cell is. Most of the time that I heard of "unit of life" (mostly when I was in secondary school and eventually high school) was used to describe a single cell making up a multicellular individual such as a cell of your blood for example and not a unicellular individual.


Enzyme inhibitor leads to higher turnover rate? I'm currently working on a project where I have to deal with enzyme inhibition.
The purified enzyme shows a good substrate turnover. When I try to inhibit it with different inhibitors described in literature, however, I receive quite awkward results.
I have now tested 3 different inhibitor compounds. One showed good results (it reduced the substrate turnover), while the other two compounds instead led to increased substrate turnover?!
I know it sounds ridiculous, but has someone experienced something like this before? The measurements of the "working" and "not working" compounds take place on the same plate.
How can it be that widely described inhibitors lead to such results?

While it's difficult to know just what is going wrong in somebody else's laboratory, apparently paradoxical effects like these are unfortunately common in laboratory work.  Assuming that these are indeed well-established inhibitors that really should be working, let's consider why they might not be in your hands.
The mechanisms of molecular interaction are complex enough that there are many cases where a substance that acts as an activator in one condition can act as an inhibitor in another condition. Another way that you could see such an effect is if your purified system is not actually as good as you think and the problem is being partially relieved by one of the inhibitors, e.g., imperfectly purified and addition of the inhibitor neutralizes some of the imperfections.
Not knowing the details of the compounds you are working with, it is not possible to guess which of the possibilities might be at work. I would suggest, however, that you begin by:

Comparing your quantitative turnover rate with the purified enzyme to the predicted rate from the literature to see if your baseline system is actually working correctly.
Make sure your system is also (not) processing substrate at the appropriate low rate when the enzyme is absent.
Checking for potential differences between your method and the method that you are trying to adapt from the literature, which might give clues to the condition differences that may be impacting your results.


Chills down the spine with certain music? I am sure many of us know the feeling of that tingling chill down our spines when listening to certain music.

I experienced this most when my younger brother played an emotional piano piece for a talent show (brought me to tears).

What causes that?
Is music the only stimulus to elicit that spine-tingling?
And in terms of evolution, why?

It is called a frisson, and actually, there has been a study about it, available here.
The frisson is kind of the same you get from cold weather, fear, or... well, other things not suitable to discuss if not knowing how old people reading this might be.

Actually, they found that this works best if you include familiarity. In their case, asking study participants to bring their favourite emotional music, in you case hearing it played by your brother.

How this evolutionary came by is unclear. But as it resembles the shivers you would call "a tingling sense of danger" it might stem from a reaction to uncertainty or at least unclear danger. In this case, it is meant to enable you to concentrate on whatever is coming, and maybe (but that's one of my own theories) this is how it came to connect to pleasant emotions as well: You want to be able to concentrate, delve into the emotion. This could explain, why it works best with familiar pieces: you already know that you want to listen closely.


Why do morning people have shorter biological clocks? First of all, we all have a circadian clock than is run endogenously by differential gene expression and controls our change in awakeness, temperature, hormone levels, etc.. Circadian clocks are not exactly 24 h and they vary among people: some people have shorter clocks and other have longer ones. Apparently, people who have shorter circadian rhythms are morning people, and those that have longer one, are night owls.
How is this possible? In the following article "https://www.futurity.org/biological-clocks-sleep-disorders-protein-mutations-2289312-2/" it says that a 20-hour biological clock will make a person fall asleep earlier because they will get tired earlier and they will get awake also earlier. But for me, that would only be possible the first period or two if both cycles start at the same point time. Afterward, the cycles will get out of phase and that will not be true any longer.

Circadian rhythms are entrained by light via the suprachiasmatic nucleus, a part of the brain that receives signals from special retinal ganglion cells that are directly sensitive to (mainly blue) light.

However, light is not strictly necessary: the internal circadian clock is the result of shifting gene expression that proceeds without outside stimulus. Light is only used to entrain (or "reset") the clock each day.

When people talk about the duration of an individual's circadian rhythm, they are referring to what happens in the absence of a light cycle (that is, without entrainment).

https://en.wikipedia.org/wiki/Circadian_rhythm
https://en.wikipedia.org/wiki/Suprachiasmatic_nucleus
https://en.wikipedia.org/wiki/Circadian_rhythm_sleep_disorder


What are the advantages and disadvantages of using beta-galactosidase compared to luciferase as a reporter gene? In the University labs, we have used Beta-galactosidase as a reporter gene to quantify the expression initiated by the stress-response promoter in yeast. This was done by exposing one of the two groups to osmotic stress (high salt concentration) whilst the other was unstressed. Then the levels of beta-galactosidase were compared.
A question given to us afterwards asked to give advantages & disadvantages of using Beta-galactosidase compared to Luciferase as a reporter gene in this experiment. And which one would be, overall, more suitable?

Beta-galactosidase (B-gal for short) is an enzyme that will process the substrate lactose. In applications using B-gal as a reporter (lacZ gene), two lactose analogues are commonly used: X-gal or ONPG (as pointed out by @Alan Boyd). Both substrates are colourless, becoming coloured once hydrolyzed by B-gal. The formation of this colour allows B-gal to be assayed by means of either visual inspection, or more accurate means by using a spectrophotometer or camera.

When X-Gal is hydrolyzed, an insoluble blue dye is formed. Evolution of blue colour is intensified as more substrate is hyrolyzed, allowing for quick blue/white screening by visual inspection in common applications of cloning and gene expression. Using the X-gal substrate, B-gal assays are more sensitive to gene expression (the dye precipitates out and retains colour very well), however X-gal is not quantitative (Möckli & Auerbach. BioTechniques 36:872-876 (May 2004)). In contrast, ONPG hydrolysis evolves a soluble yellow dye. This colour developement is quantitative, however is less senstive than X-gal because the linear relationship betwen light absorption (at 420 nm) and substrate concentration is small. Using ONPG as a B-gal substrate allows for quantitative measurement of B-gal activity (and therefore promoter activity). (Note that ONPG itself is not capable of inducing the lac promotor, unlike X-gal.)

Luciferase reporters (there are actually a few different luc genes) operate in a similar fashion. The enzyme cleaves its substrate, however instead of yielding an insoluble blue dye, emits a characteristic photon. Luciferase activity must be measured using specialized camera hardware to detect and count photons emitted from your yeast clones. This assay will still answer yes/no reporter questions, but can also be quantified to look at how much the reporter was activated. Luciferase activity is a quantitative reporter while also yielding spatiotemporal information.

The choice of reporters depends largely on the question you wish to answer. If promoter induction is relevant (eg, the stress-response promoter was activated), then luciferase or B-gal with X-gal are best suited for their higher sensitivity. Given that luciferase requires a special camera and optical filter (such as a gel documentation system), X-gal is ideal because it may be screened by eye. If promoter activity is being assayed, then B-gal+ONPG or luciferase will yield quantitative measurements of reporter gene activity, and require at least a spectrophotometer.

Given these are university labs, I assume that materials costs are to be minimized and ease of experimental protocol to be maximized, B-gal is the ideal reporter. Luciferase requires: more costly substrate; specialized equipment; careful handling of materials, and more time (as screening necessarily takes longer, therefore lower throughput for a lab demo setting).


What is Saccus in Embryology? The word seems to be of German origin.
I have it here

  Saccus lymphaticus inguinalis,
  Saccus lymphaticus jugularis,
  Saccus lymphaticus posterior,
  Saccus lymphaticus retroperitonaealis.

I would like to use the word "sinus" instead.
However, Google search does not give good results for it.

What is the meaning of the word "saccus" here?

Saccus simply means sac or bag and is is closed cavity. The lymph nodes develop from the structures, see this image:

Superior cardinal vein (jugular vein)
Jugular lymphatic sacs
Right subclavian vein
Axillary lymphatic sacs
Left brachiocephalic vein
Thoracic duct (bilateral)
Lumbar lymphatic sacs
Iliac lymphatic sacs

The image is taken from this webpage, which should be interesting for you.


Is there a blood panel lab test that measures all the hormone-producing glands? I understand that there are gland-specific hormone tests, such as:

Secretin: for the pancreas; and
Prolactin/ACTH: for the pituitary; and
PTH: for the payathyroid, etc.

However, are there any "composite" blood panels that test the "entire gamut/spectrum" of organs/glands, similar to what composite metabolic panels do for your cell counts?

There are no composite tests that measure all the clinically important hormone producing glands. There are too many hormones produced by too many hormone producing cells/tissues in the body to test for all of them all at once (i.e. in a panel).

For illustrative purposes only... if you go to wikipedia they have a list of all hormones in the human body which is definitely far from complete! But it gives you an indication of just "how many" hormones there are and why testing for all of them is impossible in a panel.

Even with regard only to pancreatic hormones, there are several hormones produced (e.g. insulin, glucagon, somatostatin) that aren't necessarily a marker of the glands overall function (because they are not necessarily involved in the same function). Each of these hormones has different functions even though they are produced by the same gland.

Regardless, from a medical perspective you would never have a reason to test for all of them anyway. If you tested enough of them you'd find at least one of them that would - by chance - be abnormal.

Additionally, if you asked a handful of scientists to name fifty hormones there would be a lot of different hormones on each of their lists. The definition of hormone is vague, and we are learning more about new hormones every day. In the last decade we have learned that bile acids - chemicals predominately produced by the liver that are involved in dietary fat absorption - also act as hormones. There aren't clinical reasons to study all of these molecules just yet, but this demonstrates that it would be impossible to measure all of them all at the same time in one particular "panel".


Indian Spider Identification Today I saw this curious colorful spider on its web near a sapota tree in my garden.
I have never seen any spider like this,its around 2cm or a little less.
The most curious part is this part of its exoskeleton which looks like when a moth rests.Like a cape.

here's the underside and the yellow patterned legs.

But the spider was bothered by my presence and was trying to crawl away,and I took this angled shot:

I live in South India.
So what is this spider ?
Is there any advantage of the wing like part?
Links to websites with details of the spider are also appreciated.

That’s maybe an oriental spiny orbweaver (Gasteracantha geminata), according to its appearance and location. You can find many more observations of such spiders on iNaturalist: https://www.inaturalist.org/taxa/207992-Gasteracantha-geminata?locale=en-GB
However, I don’t know what advantage there is to the “spines”. They are not the only species. There’s a whole genus of them with at least 70 known species, according to Wikipedia: https://en.m.wikipedia.org/wiki/Spiny_orb-weaver


Brain regeneration - book recommendation Searching for an up-to-date book on regenerative brain medicine with a focus on stem cell therapy.
Also interesting in genetic engineering of neuronal stem cells for this purpose.

Alternatively, a comprehensive review article is welcomed too.

Neural regeneration is addressed broadly in this chapter from a book published in 2013 (though I would say for a topic such as this, you're probably going to want to read primary literature or recent, less comprehensive reviews in addition to any book chapters published in the few years):

Neural Regeneration by Melissa M. Steward, Akshayalakshmi Sridhar, Jason S. Meyer, published in New Perspectives in Regeneration.

The chapter includes two sections on stem cell therapy and one section on reprogramming of somatic cells to neural lineages.


Question about what the liver does NOT do Which of the following functions is NOT performed by the liver?

a) Storage of vitamins and minerals
b) converts glucose to glycogen
c) converts toxins to harmless chemicals
d) produces bile

I chose b and got it wrong, any help?

Liver does all those functions as far as I know. The liver hepatocyctes are stimulated to create the enzyme glycogen synthase which promotes the conversion of glucose to glycogen in the presence of insulin. Glycogen is stored in the liver after its production for further use. The whole process is explained in detail in this page. Regarding the storage of vitamins and minerals, I have a paper which details the absorption and storage of Vitamin A in rat liver.  I am also linking another paper that details the presence of Vitamin B12 in the human liver.


What is the mechanism of labeling a DNA molecule with deuterated water? I have seen a paper in which deuterated water was used to follow dividing cells. The assumption was that deuterated water will be incorporated into newly synthesized DNA molecules. Is there any direct incorporation of water in the replication process? Is there any proton exchange?

The paper describing the method can be found here:
http://www.pnas.org/content/105/16/6115.full.pdf

I would assume that the labeling occurs in the reduction of NTPs to form dNTPS.

This process (catalyzed by ribonucleotide reductase) involves protonating the hydroxyl group on the 2' carbon, allowing it to leave as water, and then adding a hydride to the newly formed carbocation. The two hydrogen atoms (the proton and the hydride) come from two thiols on the enzyme, which in the process are oxidized to form a disulfide bond.

The crux is that, in the presence of heavy water, the two thiols would rapidly exchange their hydrogen for deuterium. That means that the hydride that gets added to the carbocation would be a deuterium, and the resulting dNTP would be deuterium labeled.

This is the only step that I can imagine the labeling working for, as a carbon-hydrogen bond is formed (which doesn't exchange rapidly with the solvent) using the hydrogen from a sulfer-hydrogen bond (which does exchange rapidly with the solvent).


How does a change in the potential across a neuron's membrane get turned into a signal that is sent down the axon? I understand

How a signal is propagated down the axon.
How the membrane potential of a neuron changes during the course of it's "firing".

But I don't understand how physically the change in the membrane potential actual starts the signal down the axon.

A stimulus causes the voltage gated sodium channels to open and sodium ions rush in. This creates a positive charge density inside the cell and negative charge density outside. This difference is by definition a potential difference.  Potassium gates sensitive to this difference then open, the potassium ions to rush out, which again flips the polarity of the inside and outside such that positive charge density outside the cell and negative charge density inside.

But how does that actually lead to the signal that is propagated down the axon? Can someone explain?

As you pointed out sodium as sodium enters the cell depolarizes (becomes more positive). Recall the sodium gates open the more positive the voltage is, which in turn opens more sodium gates. If a patch of neural membrane is depolarized, the charge  diffuses into the nearby patches of neural membrane. This will open the sodium channels of the nearby membrane patch. Now once enough sodium channels open, the neuron will fire a action potential, at this point potassium channels open and potassium rushes out of the cell repolarizing it(making it more negative). Furthermore the sodium gates close at positive voltages which further repolarizes the neuron and prevents back propagation.

So the key is the influx of the sodium ions diffusing down the axon and causing a downstream depolarization of the axon.

I find this website instructive, as well as this picture:

Update:
As the voltage builds up in the soma the charge spills over into the Axon Hillock (an area of high concentration of sodium and potassium gates) If enough sodium ions diffuse into the axon hillock and passes a (somewhat ill defined) voltage threshold then the sodium gates will open and start the action potential. Then the action potential proceeds down the axon as described above

A useful metaphor is the soma, and by extension the Axon Hillock, sums up the synaptic input from the dendrites, and again, if its over the threshold then the sodium gates open, if not, they slowly return to rest.

The synaptic input can be excitatory (cause depolarization) or inhibitory(hyper polarization) depending on the type of receptors and channels in the dendrites, but in general these voltage changes in the dendrite diffuse down into the soma and are eventually reach the axon hillock.


Does an increased reproduction/mortality rate provide an evolutionary advantage? If a species has a high mortality/birth rate, then it is able to adapt to changing environments more quickly than species that live for a long time.

Without a high mortality rate, food and other natural resources are hogged by previous generations and the gene pool is polluted when less evolved, older animals reproduce.

Because of this, wouldn't it make sense to conclude that a high mortality/birth rate is better for a species as a whole?
This advantage could snowball out of control, because faster evolution would lead to superior reproduction methods which would lead to faster evolution etc...

If this is true, then why are mice not more successful and adapted to their environment?

House mice were chosen because of their high birth and mortality rates.
Birth rate:
"Approximately 6 mice can multiply into more than 60 mice in 3 months."
http://www.crittercatchersinc.com/critters/Mice/Mousereproduction.html
Lifespan: 1 year
http://themysteriousworld.com/top-10-shortest-living-animals-in-the-world/
One of the reasons these traits may be more harmful than helpful is that predators benefit from a population increase. I managed to find this article in my research:
http://www.ncbi.nlm.nih.gov/pubmed/12675374
Feel free to include this source in your answer if I have interpreted it correctly. The reason I am posting this question answerless is because I am not sure enough about the conclusions I have drawn to answer it on my own and (mostly this) because I am very interested to see what other disadvantages this evolutionary strategy would have.

The first part of the question is interesting.

  Does an increased reproduction/mortality rate provide an evolutionary advantage?

The concept of evolutionary advantage for a species needs to be used with much cautious as different definition of evolutionary advantage may exist. You should typically have a look at game theory beforehand to understand the issue of definition.

A species that have shorter generation time tend to respond faster to new selection pressure (even more so in species that have short generation time and also have high population size).

  why has humanity not been enslaved by mouse¹ overlords with superior intelligence and adaptations to suit the environment perfectly?

You seem to be viewing intelligence and/or species competitive ability as end goal of natural selection which suggests important misunderstanding of how evolution works.

  One of the reasons these traits may be more harmful than helpful is that predators benefit from a population increase

You might want to have a look at the post What prevents predator overpopulation?


Do any nonhuman species have effective ebola immunity? I've read that ebola is an effective killer in humans because it has the ability to interrupt dendritic cells from manufacturing proteins that cause the immune system to destroy the dendritic cells when they're infected. Do any other animal species have different kinds of dendritic cells that don't get thus interrupted by ebola?

While at least some other primates are suspectible to Ebola, pigs appear to be immune. From the WHO factsheet on Ebola (1):

  Although non-human primates have been a source of infection for
  humans, they are not thought to be the reservoir but rather an
  accidental host like human beings. Since 1994, Ebola outbreaks from
  the EBOV and TAFV species have been observed in chimpanzees and
  gorillas.

  RESTV has caused severe EVD outbreaks in macaque monkeys (Macaca
  fascicularis) farmed in Philippines and detected in monkeys imported
  into the USA in 1989, 1990 and 1996, and in monkeys imported to Italy
  from Philippines in 1992.

  Since 2008, RESTV viruses have been detected during several outbreaks
  of a deadly disease in pigs in People’s Republic of China and
  Philippines. Asymptomatic infection in pigs has been reported and
  experimental inoculations have shown that RESTV cannot cause disease
  in pigs.


ATP Hydrolysis to AMP in the Urea Cycle. What is the Free Energy Change? How is the hydrolysis of ATP into AMP and PPi in making arginosuccinate equivalent to the hydrolysis of 2 ATP?

The answer, I reckon, is that as stated it isn't.
However,the hydrolysis of ATP to AMP and PPi yields considerable more free energy than does the hydrolysis of ATP into ADP and Pi.
That is, the free energy change for the hydrolysis of  ATP into AMP and PPi is considerably more negative that that for the hydrolysis of ATP into ADP and Pi and for the hydrolysis of ADP into AMP and Pi.
If we consider the the free energy change for the reaction ATP  = AMP + 2 Pi  (where, say, the pyrophosphate (PPi) produced by  argininosuccinate synthetase is broken down by a  pyrophosphatase), then  it is the equivalent to  the  hydrolysis of 2 ATP to ADP and Pi and (more or less) to  the hydrolysis of 2 ADP to AMP and Pi.
When dealing with ATP hydrolysis, we must take the 'chemical environment' of the phosphate group into account, not only in determining whether the bond is 'high energy' (in the Lipmann sense) or 'low energy', but also when considering the amount of free energy released by hydrolysis of a  'high energy' linkage: not all pyrophosphate linkages yield the same free energy on hydrolysis.

Cleavage of the 'inner' pyrophosphate linkage in ATP (to give AMP and PPi) 'releases' considerably more free energy than cleavage of this linkage in ADP (to give ADP and Pi).
Cleavage of the 'inner' pyrophosphate linkage in ATP  (to give AMP and PPi) releases considerable more free energy than the cleavage of the 'outer' pyrophosphate linkage (to give ADP and Pi).

If  one 'unit' of free energy is considered to be about 32 kJ mol-1 then:

The hydrolysis of ATP to ADP and ADP roughly releases 1 unit
The hydrolysis of ADP to Pi and AMP roughly releases 1 unit
The hydrolysis of ATP to AMP and PPi roughly releases about 1.4 units
The hydrolysis of PPi to 2 Pi roughly releases about  0.6 units
Hydrolysis of ATP to AMP and 2 Pi roughly releases 2 units.
Hydrolysis of AMP to adenosine and Pi roughly releases 0.4
units.

The question posed by the OP may now be answered as follows.
Hydrolysis the inner pyrophosphate linkage of ATP (to give AMP) rather than the outer linkage (to give ADP) provides a 'thermodynamic pull' of 0.4 'free energy units' to the  argininosuccinate synthase reaction.  If the  PPi is hydrolyzed by a pyrophosphatase an extra 0.6 'free energy units' are obtained and the free energy change for the combined reaction (that of argininosuccinate synthase and the pyrophosphatase) is equivalent to 2 'free energy units' (about -70 kJ mol-1).

As pointed out by Frey, & Arabshahi (1995), hydrolysis of the $\alpha$,$\beta$-phosphoanhydride of ATP, rather than the $\beta$,$\gamma$ linkage, is a common strategy in biosynthetic reactions.  To quote the final line of this paper: Cleavage of the $\beta$,$\gamma$-phosphoanhydride bridge in ATP takes place in metabolic reactions in which a smaller driving force is required.
A Small Piece of History
It was not always accepted that the hydolysis of ATP to AMP and PPi proceeded with a more negative free energy than for the hydrolysis of ATP to ADP and Pi.  To quote from  Standard Free Energy Change for the Hydrolysis of the $\alpha, \beta$-Phosphoanhydride Bridge in ATP , by Frey & Arabshahi (1995).

It  appears to be common knowledge in biochemistry  that the standard free energy change $\Delta G^{'o}$ for the hydrolysis of ATP to AMP and PPi is -7.7   to  -8.4 kcal  mol-1 [-32 to -35 kJ mol-1].  Most textbooks of biochemistry  list  values  in  this  range (Zubay, 1993; Lehninger et al.,  1992; Garrett & Grisham, 1994; Voet & Voet, 1990; Matthews & Van  Holde, 1990). Moreover, many  textbooks  also  list  the standard free energy  for  the hydrolysis of  PPi as  $\Delta G^{'o}$ = - 7.9 to  8.0 kcal  mol-1.  [-33 to -33.5 kJ mol-1]. However,  the  true  value for pyrophosphate  hydrolysis is significantly less negative (Flodgaard & Fleron, 1974). Therefore, the standard free energy change for the hydrolysis of ATP to AMP and PPi must be more negative  than 8 kcal  mol-1 [ 33.5 kJ mol-1]  as is explained in this paper

This reminder should not have been necessary.  The correct value for the free energy change in the hydrolysis of ATP to AMP and PPi is given by Schuegraf et al (1960)  , a paper co-authored by Sarah Ratner
The hydrolysis of UDP-Glucose
$\Delta G^{'o}$ for the hydrolysis of UDP-glucose to UMP and  glucose-1-phosphate is about - 43 kJ mol-1 (- 10.3 mol-1) [Frey, & Arabshahi, 1995], also considerably more negative that that for the hydrolysis of ATP into ADP and Pi
Specifics

The standard free energy of hydrolysis ($\Delta G^{'o}$) of the $\alpha$,$\beta$-phosphoanhydride of ATP to give AMP and PPi is about - 45 to -50 kJ mol-1

The standard free energy of hydrolysis of the $\alpha$,$\beta$-phosphoanhydride of ADP to give ADP and Pi is about -30 to -34 kJ/mol

The standard free energy of hydrolysis of the $\beta$,$\gamma$-phosphoanhydride of ATP to give ADP and Pi is about -32 to -36 kJ/mol.

The standard free energy of hydrolysis ($\Delta G^{'o}$) of PPi to 2 Pi is about 20 kJ mol-1

The standard free energy of hydrolysis ATP to AMP an 2Pi about -70 kJ mol-1.

The standard free energy of hydrolysis ($\Delta G^{'o}$) of PPi to 2 Pi is about 20 kJ mol-1

The standard free energy of hydrolysis ATP to AMP an 2Pi about -70 kJ mol-1.

(For a diagram illustrating the  nomenclature of the $\alpha$, $\beta$ and $\gamma$ phosphates of ATP, see here).
Notes

Following Alberty (2000), all equations are written as 'biochemical equations' where everything is balanced except hydrogen ions.

$\Delta G^{o'}$ for the following reaction is about -50 kJ mol-1 (-12 kcal mol-1)

$$ ATP + H_2O= AMP +PP_i $$

[1 ]  Frey, & Arabshahi (1995) give a value of -45.6 kJ mol-1 (-10.9 kcal mol-1).
[2] Dixon et al  (2000) give a value of  -48.5 kJ mol-1 (-11.6 kcal mol-1).
[3] Schuegraf et al (1960)  give a value of  -43 kJ mol-1 (-10.3 kcal mol-1).
[4 ] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1) of -50.2 kJ mol-1 (-12.0 kcal mol-1)

$\Delta G^{o'}$ for the following reaction is about -36 kJ mol-1 (-12 kcal mol-1)

$$ ATP + H_2O= ADP +P_i    $$

[1] Frey, & Arabshahi (1995) give a value of -32.6 kJ mol-1 (-7.8 kcal mol-1).
[2] Rosing & Slater, 1972 give a value of -31.5 kJ mol-1 (-7.53 kcal mol-1).
[3] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1 ) of -36.6 kJ mol-1 (-8.8 kcal mol-1)

$\Delta G^{o'}$ for the following reaction is about -34 kJ mol-1 (-8.1 kcal mol-1)

$$ ADP + H_2O= AMP +P_i $$

[1] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1) of -34.04 kJ mol-1 (-8.13 kcal mol-1)

$\Delta G^{o'}$ for the following reaction is about -71, kJ mol-1 (-16.9 kcal mol-1)

$$ ATP + 2 H_2O = AMP + P_i  + P_i$$

[1] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1) of -70.68 kJ mol-1 (-16.9 kcal mol-1)

$\Delta G^{o'}$ for the following reaction is about -13.7 kJ mol-1 (-3.3 kcal mol-1)
$$ AMP+ H_2O  =  Adenosine  +P_i $$

[1] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1) of -13.74 kJ mol-1 (-3.28 kcal mol-1)

$\Delta G^{o'}$ for the following reaction is about -20.5 kJ mol-1 (-4.9 kcal mol-1)

$$ PP_i + H_2O= P_i +P_i $$

[1] Frey, & Arabshahi (1995) give a value of -19.24 kJ mol-1 (-4.6 kcal mol-1).
[2] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1) of -20.5kJ mol-1 (-4.9 kcal mol-1)


Real-world examples of Darwinian extinction Darwinian extinction (also known as "evolutionary suicide") refers to processes of selection-driven self-extinction, i.e. the cases where natural selection causes the extinction of an evolving population.

In the literature, there are many models of life-history evolution and (to a lesser extent) experiments with bacteria in which Darwinian extinction has been demonstrated. However, I couldn't find anywhere real-world examples (i.e. not from models or experiments) of Darwinian extinction of complex organisms within more or less constant environment.

Do we know of such examples?
And if we do, could you please refer me to them?

Edit: A mechanism of the Darwinian extinction could be, for example, the emergence of ”selfish” strategies w.r.t frequency-dependent selection, which are beneficial to individuals when rare, but may result in a deteriorating environment and smaller population size once they become common.

Although you don't mention it in your question, I guess you'd like examples of extinction in (more or less) constant environment? Then I guess you'd like cases of extinction due to the introduction of an overseas species out-competing the original one.

Red squirrel is not extinct yet, but its sharp population decrease is mostly linked with competition with newly introduced grey squirrel, although habitat loss and concurrent introduction of a virus are also part of the causes. Read at https://en.wikipedia.org/wiki/Red_squirrel


Reasons why people say that AIDS/HIV doesn't exist It's been recurrent when I hear people saying that AIDS doesn't exist. When I ask why, they give weird reasons like HIV is a virus created to control economy and to develop medicine, etc. Also when I try to watch videos on youtube about people that are infected with this virus, I see a lot of comments saying that AIDS is a lie and some of them base their opinions on a documentary called House of Numbers. So I would like to know scientific reasons if this a myth, or why this is true.

I think no one can really deny the existence of HIV or AIDS, just a search on google scholar will show >1,500,000 hits for each of those terms, and ask (hopefully any) doctor and they will say it does, though AIDS denialists do debate whether HIV causes AIDS. This paper explains the process of HIV causing AIDS. Further, AIDS denialists have not offered up well supported alternatives as to how AIDS arises without HIV being involved.

I think however that there is more debate fuelled by conspiracy theorists as to how the disease came about. This article from TIME magazine on conspiracy theories is a short piece about it, there are two main conspiracy theories:

1) The west invented the disease to "decimate the African population."

2) The US government invented the disease in the 70's and injected gay men to stop the spread of homosexuality.

You should read this section on the critical response to the film House of Numbers, it seems to be thought that the film was driven by funding wishing to promote conspiracy theory and interviews were edited in such a way as to help portray that message.

Caution, the following is my own personal opinion ;)

  To most these seem like pretty outlandish claims and most people do ignore them - apart from anything, placing blame on someone won't stop the continuing spread of this horrendously devastating disease so the conspiracies are quite pointless. I personally think these conspiracies are driven by the uneducated, the scared, and those who want to "bring down the man & corporate/capitalist western society led by a powerful minority" etc..

Back to the science: The people who discovered the disease (Dr. Robert Gallo of the National Cancer Institute and Dr. Luc Montagnier of the Pasteur Institute in Paris) along with the majority of the scientific community say:

  "the virus jumped from monkeys to humans some time during the 1930s"

Molecular analysis of the genetic sequence for the virus supports the theory that the jump from apes to humans was around 1920-1930. Some other studies support the jump being made around this time though some estimate it to be a little earlier, this is due to estimated rates of mutation being used to calibrate molecular clocks.

I recommend taking a look at AIDStruth.org and more specifically start with this page (thanks for the link @MattDMo) if you have watched House of Numbers.


Can a living organism run on electricity? Each time I'm too lazy too cook I think it'd be cool to be able to just plug myselt into an outlet. Yet I know it is not possible - I need amino acids and a lot of other stuff that electricity can't replace.

Can some simple organism live on electricity alone or is it just fundamentally impossible?

No; the problem is, as you pointed out, that no organism will manage to multiply, grow or even sustain itself without absorbing matter to create new cells and fill metabolic losses.

Even photoautotrophic organisms which get energy from light (which is in fact an E-M wave, so pretty close to electricity) collect matter from the environment -- plants for instance seem to grow out of nothing, but in fact gather significant part of their mass from atmospheric CO_2.


What is the average Leg-to-Foot Length/Width Ratio? I'm making a program that estimates a probable size (widest width and longest length) for a human's foot given the length and width of the leg to which it is attached. However, try as I might, I can't seem to find the average foot-to-leg size ratio. Does anyone know this? It would be even better if you have different ratios for males and females.

As a note, I don't want to know that this varies depending on certain circumstances, just a good average number that will let me generate people who aren't grossly out-of-proportion

A brief study I conducted of my peers (10 people of varying genders, ages, and races, all about average body type) revealed a rather consistent foot-to-leg length ratio of 1:3 for males and females (variance is insignificant), and width of 2:3 for males and 1:2 for females.


What is the name of this red plant? I came across this plant yesterday (14th May) and was wondering what it might be? Would anybody know the scientific name and if it's indigenous to the UK (personally I doubt it is)? The plant grows in an Asian style garden near Cumnock, Scotland.

Close up of leaves:

This is the "Acer palmatum" or Japanese maple, which shows a wide variety of different leaf forms (from here):

Specically you found "Acer palmatum dissectum 'Red Dragon'", for more information look here (picture also from this site):