text:
Why do we have only one elbow per arm and one knee per leg, not multiple elbows or knees?
I was surfing on the internet for a long time, but I couldn't find the answer to my question: Why do we have only one elbow per arm and one knee per leg, not multiple elbows or multiple knees per limb?

Possible duplicate of Why do some bad traits evolve, and good ones don't?

The simple answer is: our ancestors did...as did our ancestors ancestors, and so on. We are not optimally designed, but rather, we take what our ancestors give us, and work with that. The horses for example. They have added another joint by essentially extending their toes, and walking on them, which gives them an advantage in running. It is possible to modify the skeleton, but even in this case, the original is modified, not fundamentally changed.

An example or image of our fishy ancestors limbs would improve this answer, not everyone will know what you mean. this may help, http://www.devoniantimes.org/opportunity/images/fin-limb_2006-1.gif

And to carry the examples a bit further, consider how birds & bats have modified that same basic anatomy into wings - but didn't make the same modifications.

We are the way were are solely because of evolution. The only reason we do have a single elbow per arm or a single knee per leg is only because it was advantages to have these bendable joints. Long before humans existed little organisms with small sticks as legs and arms probably roamed the Earth, but there must have been a single time where a mutation came and gave and organism these joints we know have. These elbows and knees are obviously very helpful and preferred. Also the main reason we don't have more than one elbow per arm would probably because no random mutation has come about and on top of that there is no reason we would need it.


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Trying to identify this insect
Can anyone help me identify what kind of beetle this is?
It's ~1/4" in size and was found on some air-dried hardwood lumber in the Pacific Northwest.

This looks more like a hemipteran than a beetle: You can see that the rear part of the wings is membranous. There also seems to be a rostrum starting from the front of the head. https://australianmuseum.net.au/what-are-the-differences-between-bugs-and-beetles

thanks for helping! I think you're right;  it looks like it might be some sort of chinch bug.

I am reasonably certain we have a member of superfamily Lygaeoidea here, but which of the many families that group now contains (aside from Berytidae; the stiltlike legs of that group are clearly not present here) is represented cannot be ascertained from the evidence we have available.

source: Stack Exchange

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sort: votes


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Can combining C3, C4 and CAM plants in a greenhouse/vertical farm increase the efficiency of plant production?
I am reading a little about different types of photosynthetic systems in plants because I want to learn something about plant production in greenhouses/vertical farms (I have no experience in this field).
Can combining C3, C4 and CAM plants in a certain way have positive effects on its production value? So for example C3 and CAM plants are planted in the same area close to each other and they have in some way a positive effect on each other because they use different methods for assimilating energy and thus one can bring down the energy use in the greenhouse/vertical farm.
This is an interesting article.
https://www.khanacademy.org/science/biology/photosynthesis-in-plants/photorespiration--c3-c4-cam-plants/a/c3-c4-and-cam-plants-agriculture
It explains the different aspects of the different plants very well. Maybe the best answer to my question is a simple: NO, because all 3 types of plants grow naturally in different environments, but I can imagine a system were energy that is gained from their photosynthesis at different times of the day can be shared among the plants and thus an increased energy efficiency can be reached. Maybe someone can

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How does the counter-current multiplier work in the nephrons?
Why is the counter-current multiplier called like that? What is flowing in the opposite direction to the glomerular filtrate for it to be called "counter-current"?
Can you please explain the counter-current multiplier mechanism in the loop of Henle in the nephron, including details about the ascending limb, descending limb and the collecting duct?
I have searched it everywhere and I cannot find a satisfactory explanation that I can fully understand.

Countercurrent multiplication

What is flowing in the opposite direction to the glomerular filtrate for it to be called "counter-current"?

The filtrate is moving in the opposite direction of the filtrate. It's a loop. Filtrate moves in two directions relative to the nephron, down (from the cortex toward the papilla/through the medulla) and up (from the medulla to the cortex). We'll start with up, because that's where the active transport occurs

Up: as filtrate moves up the ascending limb, $Na^+$, $K^+$ and $Cl^-$ are actively pumped out of the filtrate and into the surrounding ECF. This limb, the ascending limb, is impermeable to water, so water doesn't follow the active transport of solutes and the fluid becomes more concentrated in the ECF than in the tubule lumen. So on the way up, the filtrate becomes more dilute.

Down: the descending limb is permeable to water and to ions along with it, so as filtrate moves down the descending limb, the osmolarity of the filtrate equilibrates with the concentrated ECF. This equilibration between descending limb filtrate and the ECF, makes the filtrate more concentrated, so on the way down, the filtrate becomes more concentrated.

By itself, the active transport of solutes out of the filtrate and into the ECF on the way up the ascending limb, (with dilution again by the water on the way down the descending limb) would seem to make only a small difference, but consider what happens as the filtrate continues to flow, while the ECF doesn't.
Consider this diagram from Constanzo Physiology, Chapter 6:

First, the active transport of solutes out of the ascending limb brings the ascending limb filtrate from 300 mOsm to 200, while the ECF becomes concentrated. The descending limb and ECF equilibrate, and you're left with an ECF and descending limb osmolarity that has gone from 300 mOsm to 400. This gives you the state represented in frame (1). The increase in ECF and descending limb filtrate osmolarity that is caused by active transport of solutes from the ascending limb is called the single effect.
When fluid moves, 300 mOsm filtrate flows in from the glomerulus, replacing the 400 mOsm filtrate at the beginning of the descending limb (which equilibrates with the ECF), but 400 mOsm filtrate from the end of the descending limb flows around the hairpin and continues along the ascending limb, giving you the state represented in frame (2). This new state is the result of the flow of fluid.
Now the single effect operates on this new state. At each point along the ascending limb, active transport of solutes dilutes the filtrate in the ascending limb and concentrates the ECF, which equilibrates with the filtrate in the descending limb, giving you the state represented in frame (3). Here you can start to see an up/down gradient establish. Continue these steps, and you can see how a substantial gradient can form.
Countercurrent exchange
After being presented with countercurrent multiplication, students will often ask how it is that solutes and water equilibrate horizontally in this diagram (i.e., between the descending limb and the ECF), but not vertically. This is a different question, and is where you start to need yet another compartment, the blood in the vasa recta. This mechanism is called countercurrent exchange, but is the answer to another question (how come the corticomedullary gradient doesn't dissipate?).
Original paper
In addition to physiology texts (e.g., Costanzo Chapter 6), you can read one of the most important original papers supporting this mechanism. Originally published in 1959, it was reprinted here in 1997 and available for download. See if you can follow the connection between the data and this mechanism.

Water in the glomerular filtrate moves out of the descending loop of henle due to the higher concentration of salt in the medulla. The higher concentration of salt in the medulla also moves down it's concentration gradient into the descending loop. The salt is pumped from the glomerular filtrate into the medulla in the ascending portion of the loop of henle. Salt, water and additional molecules can also be reabsorbed into the body in the distal convoluted tubule and collecting ducts and can be regulated by hormones to control salt and water excretion and retention which can affect blood pressure. The proximal convoluted tubule reabsorbes an increased amount of necessary molecules such as 100% of glucose and amino acids.

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Why does a frog's oxygen intake through the skin and lungs vary throughout the year?

Why does a frogs oxygen intake through the skin and lungs vary throughout the year?  And why does the intake through the skin vary slightly while through the lungs dramatically? (Blue line = oxygen intake through lungs and orange line = through skin.) Thanks.

Cutaneous respiration is based, as every type of respiration, on diffusion of gases from a higher concentration (in water or air) to a lower one (in capillaries).
Citing from Johnson, Peter H. Raven, George B. (2002). "Respiration". Biology (6th ed.). Boston: McGraw-Hill. pp. 1053–1070:
In general, the rate of diffusion between two regions is governed by a relationship known as Fick’s Law of Diffusion:
R = D - A x ∆p/d

In this equation,

R = the rate of diffusion; the amount of oxygen or carbon dioxide diffusing per unit of time;
D = the diffusion constant;
A = the area over which diffusion takes place;
∆p = the difference in concentration (for gases, the difference in their partial pressures) between the interior of the organism and the external environment; and
d = the distance across which diffusion takes place.

As you can see, the rate of diffusion R can be increased:

By increasing A, the diffusion area;
By increasing ∆p, the difference in concentration;
By decreasing d, the diffusion distance.

In cutaneous respiration, nr.2 is not really an option; yes, capillaries can be optimised to bring blood rich in carbon dioxide and poor in oxygen really close to skin surface (which brings us to nr.3), but it's a lot less efficient than, for instance, lungs that can exhale air filled with carbon dioxide and replace it with fresh air. While the intake of oxygen of the skin remains more or less the same even with different metabolic demand, lungs can quickly adjust the breathing rate depending on the metabolic demand of the moment.
So, the answer to the question

why does the intake through the skin vary slightly while through the lungs dramatically?

is that skin cannot regulate its gas exchange rate, while lungs can. This brings us to your first question:

Why does a frogs oxygen intake through the skin and lungs vary throughout the year?

The answer lies in the biological cycle of the frog throughout the year: during cold months, frogs hibernate. In winter, frogs slow dramatically their metabolism and they don't need so much oxygen; thus, in this season they are able to rely only on cutaneous respiration. In other seasons they are active, and they have to breathe actively through their lungs to supply their blood with the necessary quantity of oxygen.

Thank you for the in depth clarification and helpful information, highly appreciated!

Another factor contributing to these results may be that some of the most of the most common species of frogs such as the  leopard frog(Rana pipiens) and the American bullfrog (Rana catesbeiana) both hibernate.


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Are humans known to be "poisonous" to any animal?
Are there examples of non-herbivorous animals that could be poisoned if they feed on humans because of the composition of our bodies/blood?

Human is not in the menu of other animals (in normal circumstances) and there aren't any studies regarding to this (as you can guess) so we don't know if human meat is toxic to any other animal. There are instances where other animals ate human though (for example: great white sharks and lions). On the other hand,  cannibalism can lead to a disease called Kuru which is caused by abnormally folded prion proteins. Thus, we could say human meat is toxic for humans.

Hmm, this "non-science related" book claims that: "Human meat can be poisonous for protected species like crocodiles."


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How did shellfish and coral survive acidic oceans in earlier eras?
Throughout most of Earth's history, the planet has had more CO2 in its atmosphere, correct?  Therefore th pH of the oceans was even lower, right?  So how did CaCO3-using animals create their shells back then?

organisms can evolve to cope with more acidic condition albeit slowly, https://cen.acs.org/articles/95/i20/shellfish-adapt-ocean-acidification.html. There are may factors that affect vulnerability which is why some shell building organisms survived.

They didn't survive when carbon dioxide levels in the atmosphere passed certain thresholds in the history and increased ocean acidity significantly; leaving less carbonate for marine life to use for shells or skeletons. For example, up to 96% of marine life (including organisms with CaCO3 skeletons) went extinct in the Earth's most severe known extinction event, Permian–Triassic extinction. Another event called Paleocene–Eocene Thermal Maximum caused a mass extinction of benthic foraminifera.

Five times in the Phanerozoic [the past 542 million years (My)], more than three-fourths of marine animal species have vanished in mass extinctions. Each of these events is associated with a significant change in Earth’s carbon cycle. However, there are a great many disturbances of the carbon cycle  whose imprint in the geologic record is almost exclusively environmental. These other events are relatively benign, with extinction rates barely, if at all rising, above background levels.
Two well-studied examples illustrate these distinctions. The end-Permian extinction [~252 million years ago (Ma)], the most severe mass extinction in the Phanerozoic, plays out over a period of 104 to 105 years; the extinction interval immediately follows a perturbation of the carbon cycle of similar duration. The Paleocene-Eocene Thermal Maximum (~55.5 Ma) is a carbon cycle event of roughly similar time scale, with unambiguous signs of global warming and ocean acidification. It is associated with a significant extinction of benthic foraminifera, but there is no evidence of other major extinctions. What makes these two events so different? The unambiguous co-occurrence of the end-Permian extinction with massive volcanism provides one indication, as does the greater magnitude of the end-Permian carbon isotopic excursion compared to that of the Paleocene-Eocene Thermal Maximum. However, no general distinction, applicable throughout the Phanerozoic, exists.
Thresholds of catastrophe in the Earth system
  By Daniel H. Rothman
  Science Advances | 20 Sep 2017 : E1700906
http://advances.sciencemag.org/content/3/9/e1700906.full
(emphasis mine, removed citation numbers)

Here is an excerpt from a relevant study of Knoll et al. about the affects of end-Permian mass extinction on biomineralization  which includes the extinction percentages of animals that
form skeletons of calcium carbonate and vulnerable to elevated CO2
levels:

Within the marine realm, animals with active circulation and elaborated gills (or lungs) for gas exchange compensate for elevated PCO2 better than organisms that lack these features. Also, animals that normally experience high internal PCO2 , including infauna and metazoans capable of exercise metabolism at high rates, tolerate experimental increases in carbon dioxide differentially well. And among animals that form skeletons of calcium carbonate, species that can exert physiological control over the pH balance of the fluids from which minerals are precipitated fare better than those with
  limited buffering capacity. Based on these features, Knoll et al. (1996) divided the Late Permian marine fauna into two groups, with high and low expected survival, respectively.
As predicted, 81% of genera in the “vulnerable” group disappeared at the boundary, while only 38% of nominated “tolerant” genera became extinct (Figure 6A). The selectivity is even more pronounced when skeletal physiology is considered alone (Figure 6B; Bambach and Knoll, in preparation). Fully 88% of genera disappeared in groups that formed massive carbonate skeletons but had limited capacity to buffer fluids (sponges, cnidarians, bryozoans, calciate brachiopods). In contrast, groups that built skeletons of materials other than calcium carbonate lost only about 10% of their genera. Intermediate taxa—groups like mollusks that have a substantial commitment to carbonate skeletons but some physiological capacity to regulate the chemistry of internal fluids—lost 53% of
  their genera. Of these, those genera considered vulnerable on the basis of the other criteria noted above went extinct at twice the rate of those otherwise considered tolerant.

Biomineralization and Evolutionary History
  By Andrew H. Knoll
  Department of Organismic and Evolutionary Biology
  Harvard University
  Cambridge, Massachusetts, 02138 U.S.A.
https://web.archive.org/web/20100620222809/http://www.geochem.geos.vt.edu/bgep/pubs/Chapter_11_Knoll.pdf
(emphasis mine)

I should point out that some did survive, but it is true they suffered massive losses and die offs.


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During non-cyclic photophosphorylation, how does NADP+ become NADPH?
I know that NADP+ gets reduced to form NADPH, but what exactly is being donated? Is it two individual electrons (from photolysis or the chlorophyll molecules) and a hydrogen ion (proton)? If this is the case, during the Calvin Cycle, do the NADPH molecules donate the same two individual electrons and hydrogen proton from the light-dependent reactions to become NADP+ again? Thanks.

SE Biology expects you to show what research you have done to answer this question (the title of which should be repeated in its body). Just googling for "non-cyclic photophosphorylation" gives the answer to your title in a  callout box at the top of the page.

Specifically during non-cyclic photophosphorylation, I know that the chlorophyll already has preexisting NADP+ molecules, water is broken to release 2 hydrogen atoms and 1 oxygen atom (two water molecules break down to form gaseous oxygen that we breath), those 2 hydrogen atoms get sent down and along the Electron Transport Chain via solar energy and then I believe one goes to a protein called ATP synthase and the other goes to photostem 1. After photostem 1 that hydrogen binds to free floating NADP+ molecules to from charged NADPH. This should be the gist of it all but I would also recommend listening to someone else's input as well.

Wait, I thought that photolysis splits water into two electrons, 1/2 of O2, and two hydrogen ions which are just protons. I'm pretty sure the hydrogen ions contribute to the H+ concentration, not to the photosystems because that's where only the electrons go in which they ultimately end up reducing NADP+

Okay, I've done some research and yes thank you, that was the part that I was forgetting. The positive hydrogen ions go through the ATP synthase while the electrons follow the ETC, after phyotosystem 1, I believe those electrons will diffuse because they repel while the hydrogen ions are also repelling each other (keep in mind they are both outside of the thylakoid membrane now). This I believe results in the electrons and hydrogen's coming back together to later be randomly paired up with NADP+ molecules.

At SE Biology we're looking for answers that provide some explanation and context. Explain why your answer is right, using citations. How is the poster to be able to check whether your answer is correct?

First, "I believe" is what shows your lack of effort to give a nice answer. Second, the OP themselves stating that you give wrong information in your answer is exactly what is not expected from answers on SE (or at least Biology.SE). Please show some research effort for an answer (this is probably the first time I have said this here)

Thank you @another 'Homo sapien' and David, I'm sorry for the lack of effort.


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How did hydrophilic plants become established on an isolated island with an arid coastal zone?
I find unconvincing the existing explanation of how several hydrophilic endemic plants became established at St Helena. This is one of the most isolated islands in the world, has an arid semi-desert coastline and moist and humid highlands where endemic hydrophilic plants grow. It has been suggested that plants originally arrived either as driftwood from the beaches or arrived inland because occasional birds accidentally blown to the island had seeds on their foliage or claws. However, not only would the brushwood of these hydrophilic plants be unlikely to propagate or survive the arid conditions of the coastal region, these plants normally propagate by root, not by seed.
Has the following third mechanism ever been suggested for the establishment of plants on an isolated island? I wonder whether brushwood fortuitously arrived at the point where streams were discharging into the sea. Despite the arid conditions at all other coastal regions, some plants could take root at these wet beach areas and then spread along the streams growing in the damp alluvial soil into the interior heights of the island. I know the migration of plants along the length of a stream or river (riparian zones) have been studied but I can find no reference to the idea that this can also explain the presence of hydrophilic plants in damp highland regions of an island with a surrounding arid coastal region.

there is an important distinction between normally and only.


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How many strains of influenza can occupy a person at one time?
Could a person's immune system be built eventually to be able to inject all the known strains with in to stay immune?

Your premise is wrong to begin with. It's absolutely not true that everybody eventually catches the flu.

Please edit your title so that it gives a better indication of what aspect of influenza it concerns. This saves people time and, unless this question is removed (as being hypothetical), is more useful for indexing.

@David revised...

@TimonG. - Your comment is incorrect. Eventually, indeed, most people will catch the flu (Influenza A or B). It is the rare individual who will have never, ever contracted any strain of influenza. Up to 30% of the infected are assymptomatic, and the odds of being infected any given year are from about 1:10. (Range: 1:20 to 1:5.) If you live 20 years, your odds of never having gotten the flu are about 2 in 100. What are your numbers?

That what I initially thought I had. I changed it because if an answer. I am talking about intentionally on a safely way of taking all the strains numbers aside.

Hypothetical questions are often sub-par due to the absence of information on the part of th OP. However, the worst part of this question is "Could my blood be used to help others recover or would it be lethal?" Why in heaven's name would it be lethal? Are you dead from it?

@assymptomatic because I would be asymptomatic and contagious and not immune.

@anongoodnurse You are mistaking the notion that everybody catches the flu eventually with the concept that the average person gets the flu eventually. The latter is correct, the former is not. Even your choice of numbers (which I did check and are approximately in the right ball park but you are ignoring re-infections in your calculation) yield millions and millions of people who will never get the flu. I want to note that OP edited his comment to "most" people only now after my comment. OP originally stated flat out that everybody gets it and that is false even acc. to your numbers.

We seem to also disagree on what it means to have the flu. Being exposed to the influenza virus is being exposed to the influenza virus. Flu is the label for the disease which is caused by the influenza virus, not a label for the influenza virus itself. If a person has the influenza virus in their bodies but absolutely no symptoms, I consider it confused and incorrect to state that they have the flu. Diseases are sets of conditions and symptoms, not the mere presence of a pathogen that your immune system is fighting off. This is similar to the distinction between being HIV+ and having AIDS.

@TimonG. - I never said everybody catches the flu. Read more carefully both my statement and the OP's. Also, if you are asymptomatically infected with influenza virus, you have caught the flu. Again, where are your numbers?

OP literally said "Eventually you will catch the flu." in the first version of his question, check his edit history. That was what I originally replied to. OP then edited his question after my comment to instead say "Eventually most will catch the flu.". That is a completely different claim and I already explained this in the previous comments. It doesn't do you any good to be confrontational and accuse me of not reading when you yourself haven't done so.

It's perfectly fine to edit your question to be more clear, @Muze. There is nothing wrong with that. Perhaps in the future a small edit note at the bottom will help people.

where do i find a list of influenza strain weak to worst?

@Muze - if you try ordering some of the bad strains of influenza, you'll very quickly find yourself being visited by large, serious men with bad haircuts and suits. This is not a good idea to follow up.

The question is whether being exposed "to all strains of influenza" would make one immune to all strains of influenza. No, and it's not possible to expose oneself to all strains of influenza in the first place.
It might be technically possible to expose yourself to all subtypes of influenza, if you limited to the hemagglutinin subtypes, of which there are 18. But subtypes are not strains; a strain is an antigenic variant of a subtype, and there are tens of thousands of such variants. Even if you somehow managed to expose yourself to every known strain, presumably by injecting yourself every few hours for years (you probably don't want to literally expose yourself to all the strains of flu, because some of them have mortality rates well over 50%, so you'd be dead before you were immune), new strains arise literally every minute of every day.
And because of vagaries of the immune system that are too complex to get into here, immunity to some strains prevents immunity to some others (one review is Immune history and influenza virus susceptibility), so it's either very difficult, or perhaps intrinsically impossible, to get complete immunity.
There's work being done on overcoming these problems with "universal" influenza vaccines, and your best bet is to wait until some of these are available.

I had no idea that immunity to some strains can prevent immunity to others! Nice to learn something new!


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DNA strand displacement and Branch migration- the same or different or interrelated?
So, recently I have begun studying DNA strand displacement and then I come across the term 'branch migration' (p.s. I am not a biology major student). What I understand is that branch migration is part of the strand displacement process.
Or is it not? If branch migration is not a part of strand displacement, then what is it?
First, does strand displacement refer to the case where a single-strand
(floating freely) is competing with the incumbent strand to pair with the complementary pair, resulting in the displacement of the incumbent strand?
That means we have one DNA complex and one single-strand in the input and output. And second, does branch migration refers to the case where two DNA complexes exchange strands, resulting in two DNA complexes both in the input and output?
To me, both processes are involved in the displacement of strands (but I can't seem to find their differences).
Can someone kindly explain to me their difference, if there are any?

Branch migration is a part of the DNA strand displacement process. http://slideplayer.com/slide/12266786/72/images/46/12.+20+The+Holliday+model+of+homologous+recombination.jpg

@MartinKlvana So this confirms to my second statement on branch migration. Will this apply to the first statement as well?


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Can anyone identify this beetle?

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

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


text:
Can anyone identify this garden orb weaver spider?

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


text:
As electrons are moving through the ETC, how is ATP produced for the active transport to even happen?
A lot of websites aren't being specific and they are just saying that when electrons move from a high to low energy state during the ETC, "energy" is being released and that energy is used to pump (active transport) H+ ions through the membrane. I want to know more. Isn't ATP formed by adding a phosphate to ADP? If so, where do electrons moving through the ETC get that phosphate from? BTW, I'm not talking about ATP synthase, because you need H+ ions for ATP synthase and I'm not understanding how those H+ ions are being actively transported through the membrane in the first place.

On SE we expect you to do more research before posting, as you will find if you read the help on asking good questions. It's not sufficient to say "a lot of websites aren't being specific" — you need to find sources that treat the subject at a more advanced level. And the best sources are books, not websites. If you have the money, buy as many as you can afford. If not, try NCBI Bookshelf. For Biochemistry use Berg et al. — Try Chapter 18.

If you are referring to the active electron transport by complexes I-IV (which I guess you mean, by saying you're not referring to ATP synthase), then the most likely answer is 'we don't really know'. For ATP synthase the mechanism is quite well known, but for the ETC complexes I think I've only ever seen some structural/mechanical theory for one of the complexes.

ATP formation is done using the Complex V called as ATPsynthase (also called as F0/F1 particle) and the theory explaining this process is called as the Chemiosmotic Theory2.
During cellular respirationKreb’s cycle (in the mitochondria) and Light dependent Photophosphorylation photosynthesis (in the chloroplast thylakoids) a set of reactions establish a proton gradient across the inter-membrane space ( hereby referred to as IMS) of the mitochondria/chloroplast( if you remember mitochondria/chloroplast are double membrane bound organelles).
Just as in a battery/cell we have EMF(electron motive force) we have, in the IMS of the mitochondrion/chloroplasts, a proton motive force.
Since substances always flow from higher potential to lower potential, the IMS of mitochondrion/chloroplast having a high amount of protons is a region of high potential and lumen of mitochondrion/chloroplast is a region of low potential since there are less number of protons.
The only way protons can move from the IMS  of the mitochondrion/chloroplast to the lumen of the mitochondrion/chloroplast is via the complex V (also known as ATPsynthase).
The ATPsynthase is a lollipop shaped protein structure that is freely rotatable and it brings ADP & phosphate molecules close together so that a covalent bond can be formed in between them.
How does it exactly do this you ask?
So let’s summarise what all we have here:

ATPsynthase that can rotate about its rotor.
Proton gradient across the IMS ( high potential) and the lumen ( low potential).
The only way out for the protons is via the ATPsynthase.

Now we can see a link here.
So what happens is, there’s the F0 subunit of the ATPsynthase through which the protons are able to move across the membrane and during that movement the rotate the F1 subunit.
During this rotation shown in animation here  the ADP & the phosphate group which are present in the active site of the F1 subunit are brought near each other and due to atomic interactions a bond is formed.
The mechanical energy ( movement of protons across the membrane) is converted into chemical energy ( covalent bond) between the two molecules.
This is the process via which the currency of the cell, ATP, is produced.
Hope that answers the question.

I don't think you should answer questions in which the poster has not done his homework properly, but it you do, please read them first. What he writes is "I'm not talking about ATP synthase, because you need H+ ions for ATP synthase and I'm not understanding how those H+ ions are being actively transported through the membrane in the first place." You have described the ATP synthase — he wants to know how the proton gradient is established in the electron transport chain. I have told him where he can read about it for himself.

Oh, I see. Thank you for pointing it out. I thought he needed the mechanism of it. I think he needs to learn the cycles to completely understanding how H+ ions are being transported. I’ll be more careful next time.


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How accurate is facial reconstruction in forensics?
I’ve seen on tv where they reconstruct heads and faces from the remains of ancient people and I was wondering if anyone had a source that has pictures of maybe side by side of a facial reconstruction Vs. a picture of the actual person being reconstructed. I know it takes a long time to fully decompose but surely there’s been a reconstruction done of a recent person who’s been photographed

So, it isn’t accurate at all then. Eyes, hair, nose and mouth are the things that make a person identifiable, not just the shape of his head with some imagined details.
If you just make all those details up, you may end up with a totally different looking person. You may also get a result that is somewhat similar but that’s by pure chance.
So the rest of it is just art, not science.

I’m voting to close this question because it is about forensics rather than biology.

okkkk. I did a big project on this... and here's some of my research... let's hope it answers your question

Facial reconstruction (also known as craniofacial identification) is a method used in the forensic field.  Many people view facial reconstruction as an art instead of science.  Art is commonly portrayed as the expression or application of human creative skill and imagination, typically in a visual form such as painting or sculpture, producing works to be appreciated primarily for their beauty or emotional power.  Science is thought of as the intellectual and practical activity encompassing the systematic study of the structure and behavior of the physical and natural world through observation and experiment.  But where do science and art blur the lines?
WHAT CAN WE TELL FROM THE SKULL:
The skull provides clues to personal appearance. The brow ridge, the distance between the eye orbits (sockets), the shape of the nasal chamber, the shape and projection of the nasal bones, the chin's form, and the overall profile of the facial bones all influence facial features in life. Using these bones, artists and forensic anthropologists work together to reconstruct facial appearance through the process of forensic facial reconstruction.  There are many ways of telling both the approximate age, and the approximate ethnic background of the victim.  To find age, you can pay attention to the cranial suture (or the place where the cranium fuses to other bones of the skull), the size of the skull can help, as well as the teeth and the formation of the bottom jaw.  When looking for the birth gender of the victim, scientists often pay attention to the brow ridge, eye sockets, mandible, and the slant of the jaw.  Sometimes, it is impossible to tell by looking at the skull what birth gender the victim was.  In cases like this, people look to the pelvis to tell if the human has given birth, and if not, males do not have a ventral arc.  It is often very difficult to find the race of a victim if they are mixed race, or if the skull is very worn out.  However, to find the ethnic background scientists will look at the shape of the skull, the nazel root, and the space between eye orbits.
WHAT ARE THE PROCESSES OF FACIAL RECONSTRUCTION AND ARE THEY ACCURATE:
Facial reconstruction is an exacting process. The finished product approximates the actual appearance, because the skull does not reflect the details of soft tissues-eye, hair, and skin color; facial hair; the shape of the lips; or how much fat tissue covers the bone. Yet, facial reconstruction can put a name on an unidentified body in a modern forensic case, or, in an archaeological investigation, a face on history.
Today, many forensic facial reconstruction techniques are in use, including two-dimensional (drawn), three-dimensional manual and three-dimensional computer-based.  In the manual techniques, including two dimensional a cast of the skull is required, so the facial markers do not become an anomaly when analyzing the skull.  Although all of these methods are used, it is most common that a trained sculptor, who is familiar with facial anatomy, works with a forensic anthropologist and uses clay to build the facial features. The forensic anthropologist interprets skeletal features such as the subject's age, sex, and ancestry, and anatomical characteristics such as facial asymmetry, evidence of injuries (a broken nose, for example), and loss of teeth before death.
Facial reconstruction is used when the victims dental records fail to identify them, and there is no dna to pull from the body.  The process of reconstruction starts with making a mold of the unknown skull with the jaw attached and false eyes in place.  Depth markers are placed on 21 different “landmark” areas of the mold of the skull to approximate the facial tissue thickness that lay on the skull.  These tissue thicknesses are approximated from averages of other people of the same age, sex, and race as the skull is assumed to be.  Facial muscles are placed on the mold next and then the face is built up with clay to within a millimeter of the depth markers as tissue.  The nose and eye setting are very difficult to estimate due to the enormous amount of variation possible, mathematical models are used to make the approximations, the mouth is assumed to be the same width as the distance between the pupils. In facial reconstruction the eyes, nose, and mouth are mostly guess work.  Characteristics such as birthmarks, wrinkles, scars, and such are guesses at best and cannot actually be determined from the skull.  Facial reconstruction is accurate because it has been using mathematics, and calculations as such, in order to determine spaces, amounts, as well as the shapes of the face themselves.
WHY IS FACIAL RECONSTRUCTION IMPORTANT:
Facial recognition, as well as facial reconstruction is very important in the forensic field.  Both have a very important role in catching murderers, and investigating crime.  Without having a facial reconstruction, often times, you cannot identify victims.  Assuming the body is historical and for museum purposes, then without an identity it becomes very difficult to fill in large gaps of information, and time that can be crucial to history.  Also, if you can’t identify a murder victim then scientists could only look into cause of death.  Learning the identity of a deceased victim is as important to crime investigations as learning the identity of the suspect. When human remains are found, then the top priority is often to find the identity of the victim.  Police often also will look for an identity out of respect, for both the victim and the victim’s loved ones if any.  Facial reconstruction has been used ever since 1890.  Before 1890, people mostly used few facial indicators such as the shape of the frontal bone, and the remains of flesh to help identify the victim.  Facial reconstructions, can also show what injuries were sustained previous to death.
WHAT CAN WE LEARN FROM FACIAL RECONSTRUCTIONS:
Our skeleton is an extensive record of our lives. The food we eat, the rate at which we grow as a child, the injuries we sustain, whether we have given birth; all can be determined from our bones. Experts can determine sex, age, and ethnicity, relatively easily from the skeleton, with the skull and pelvis playing pivotal roles in this analysis. Later this week, we’ll be taking a more detailed look at how to determine sex and ethnicity from a skull.Teeth can reveal information about diet and a comparison between dental records of the deceased and the recovered skull is often the primary method of identification.  By looking at the scull (or any bones in fact,) you can tell childhood injuries from injuries that might have been fatal.  You can also look at bone density and other factors to tell if the victim was suffering from any diseases.  People look for the sagittal suture – the squiggly line that runs the length of the skull – If it is fully fused, the remains are likely to be of someone older than 35. After that professionals look for a second line at the front of the skull -- the coronal suture – which fully fuses by age 40. Teeth are also looked at. If they're worn down it could be a sign of a poor diet. If they're well-maintained and/or have good dental work such as fillings, they were able to afford proper dental care—another clue as to the identity of your skeleton. Oftentimes professionals consult a scientist who specializes in teeth, known as an odontologist. They can determine how old a person was at death, what kind of health they were in and what kind of diet they had.
Baby's bones begin to grow in the womb. At birth, the skeleton is partially formed. Many bones are still in "parts." The ends (epiphyses) and bony shafts (diaphyses) of long bones form separately in the womb. At birth, the ends of the long bones are mainly cartilage, with centers of bone beginning to form inside. As a child grows, the shafts get longer, and bone gradually replaces the cartilage epiphyses. Through the growing years, a layer of cartilage (the growth plate) separates each epiphyses from the bone shaft.  By paying attention to this, it is easier to tell age, and follow growth patterns to have a successful reconstruction.
Between 17 and 25 years, normal growth stops. The development and union of separate bone parts is complete. At this point, you and your skeleton are as tall as you are going to get - with many fewer bone parts than you started with.  The bones that enclose the brain grow together during childhood along lines called cranial sutures. During adulthood, bone "remodeling" may gradually erase these lines, at variable rates. Closure of cranial sutures gives general information about a person's age. It is best used with additional indicators to estimate age, or when other age indicators are unavailable.
WHAT ARE THE LIMITATIONS:
It is very hard to estimate a person’s weight and represent that with facial markers.  Since a chart of average thickness of soft tissue is used to estimate the way a person looked, if you were on the skinnier side, your head might appear a lot more overweight than usual and or skinnier.  To help determine weight, scientists look at the rest of the remains for a height.  Facial reconstruction relies on the relationships between the facial features, subcutaneous soft tissues and underlying bony structure of the skull. If there is no clue for potential identity because of impossibility to compare questioned remains with possible familiar material, in such cases one of the last chances is to recreate ante mortem appearance by face reconstruction. Many of the soft tissue thickness values are significantly different from those reported for comparable groups, suggesting that individuals from different geographical areas have unique facial features thus requiring population-specific values. This literature review attempts to throw some light on the important aspects that has to be taken into consideration while setting norms of soft tissue thickness among various populations.
Studying the unknown skeletal remains mostly becomes the only way to find out more information about individual characteristics, which could lead to identification of potential victim. If there is no clue for potential identity the most precise comparative techniques fail, because of impossibility to compare questioned remains with possible familiar material. In such cases one of the last options is to recreate ante mortem appearance by face reconstruction. Following the first introduction of reconstruction in the late 19th century, other techniques have been developed including radiography, 3D statistical model, ultrasound, MRI, CT and Cone Beam Computed Tomography (CBCT).  Facial contours were traditionally considered to be the result of positioning of underlying hard tissue followed by the soft tissue. However, current trend shows a paradigm shift from the conventional hard tissue analysis to also include both hard- and soft-tissue analysis.
IS FACIAL RECONSTRUCTION AN INTERDISCIPLINARY ART:
The skull is made up of 22 bones, 14 of those are facial and eight are cranial bones; it is a complex structure, and small variations during development and growth, together with soft tissue differences, create the enormous facial variation seen in the human population.  Artists have long been interested in the direct anatomical relationship between the skull and facial appearance.
Artist, Gaetano Guilio Zumbo (1656-1701), used facial reconstruction as an art because he believed that math and science are both forms of art.  His work can be found in the Wax Anatomical Collection at La Specola Museum, Florence, became famous for his macabre scenes depicting various stages of decomposition of the human body.  One of his most famous pieces is the head of a dead man, with facial muscles recreated in wax over a real skull.
This is the earliest surviving anatomical wax model created for didactic purposes and exhibits extraordinary anatomical precision alongside an artistic sense of horror and decay. Although we assume that Zumbo was less concerned with facial appearance than anatomical detail, he pioneered the development of scientific art and this work ranks as one of the finest examples of three-dimensional facial reconstruction.
By definition, an interdisciplinary art is relating to more than one branch of knowledge.  Facial reconstruction is often categorized as both a science and a mathematical equation.  Both science, math and art are human attempts to understand and describe the world around us. The subjects and methods have different traditions, and the intended audiences are different, think the motivations and goals, specifically for this purpose is fundamentally the same.

Welcome. Can you add sources?

Interesting essay about forensic facial reconstruction. I've noticed that forensic depictions of people from archaeological remains tend to be flattering, depicting the individual as facially attractive, whether male or female. This tendency most certainly reflects the artistic side of reconstruction.

@CaryCotterman that may have more to do with reconstructed faces always being symmetric and free of small scale flaws, which would not show up on bone. They are not going to add flaws willy nilly because it would adding things they have no evidence of, but completely lacking them makes for a more attractive face. it is the same reason a touched up photo of a model is often more attractive, touching it up is  often just removing small flaws.


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What is the fundamental reason for death from too high or low internal temperature?
I have read something about why we die from too high or too low body temperature but have always found only general reasons. For example, that the liver fails. But why does the liver fail?
I would like to know the most fundamental reason why not possessing the appropriate body temperature can kill us. Ignoring the very extremes where it is I think obvious, such as temperatures below 0°C and above 100°C when water freezes and vaporizes.
I have supplied my reasonings below; if any reasoning here is wrong, please correct my thoughts.
As far as I understand, as the temperature changes, the speed of chemical reactions changes as well. As temperature goes up, the reactions occur faster and if the temperature decreases, the reactions slow down. So, if our body temperature changes, the speed of all reactions in our body change as well. Thus, with higher internal temperature we should just become more active, speedy and so, and with low temperature we should become slower. But that does not fit into the fact that we die from extremely high internal temperatures. So, is it that the speed of different reactions change with different rates, so the organism is not kept "in sync" and dies for that reason?
Or - as temperature changes, the volume of everything changes as well. I think that's called thermal expansion. But different materials have different rates of that process. So as our temperature changes, something inside us just literally breaks or deforms too much and we die?
So why do we (and other organisms) die from not having the right temperature?

Half of your question is answered here: https://biology.stackexchange.com/questions/36258/why-do-low-temperatures-kill?rq=1

Please be more specific about your question. SE is not a place for open discussion.

As mentioned in the comments, half of your question is answered elsewhere. Generally you are right, different processes change at different rates. Blood viscosity changes. Some complex systems, such as the heart, may completely fail to function. The other half of your question has a simpler answer. As heat increases, yes in theory so should enzyme performance. However enzymes have a tendency to denature if they get too hot. When heat is excessive, heat shock proteins are released which are naturally stable in hot conditions and which attempt to stabilize other proteins. This is only possible up to a limited extent, and sufficient heat will cause proteins to become entirely non-functional.

Does the downvoter care to explain what was the issue with this answer?

Myself I don't see any problem. Not sure what the downvoter was thinking.

I am not the downvoter, but I would guess the downvote was for a lack of sources.

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


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Microbiome Context for Amino Acid Essentials and Non-Essentials
Given what we are now learning about the diverse mix and variance of microbiomes (aka bacterias via human gut project), is it possible that synthesis of aminos can be done by specific bacteria and therefore provide the "essentials" if atomic ingredients are available in digestive tract?

Essential amino acids are defined as those required in the diet. Non-essential amino acids as those that are not. In general this is rationalized by known metabolic pathways and rates. I don't see what connection are knowledge of gut bacteria (not baterias) have to do with this. Could you clarify your question, please.

Many bacteria are prototrophic and can synthesize the essential amino acids from other available nutrients. OP is asking whether this could be enough to supply the human host with all the needed essential amino acids. It's a perfectly good question. The answer is obviously yes in theory, but I don't have any data to suggest it happens in practice. Someone else might.

If your body was filled with highly specialized bacteria living in nutrient-rich conditions, what you suggest could happen*.
But in practice, you're not filled with such bacteria, and most of the bacteria in your body are living in rather harsh conditions for rapid metabolism.
That said, gut bacteria do produce a range of other useful nutrients. Look for a review on gut microbiome metabolism, and you will find a number of examples.
*Some basic calculations:
Say we take an optimistic estimate for productivity of 1g AA/g biomass/day. (It's what they got in this paper (one of many) that characterized a strain of Corynebacterium glutamicum engineered to produce lysine for industrial purposes and growing in a bioreactor. There are better strains now, but still, let's call that an unbelievably optimistic estimate of what a bacterium in the body might produce in the right conditions). How much bacterial biomass is in the body? Not a trivial question to answer (How much weight/volume do microbes occupy within the human body?) but let's go with the middle of the road estimate of 1kg. So 1 kg of awesome lysine-producing bacteria might potentially produce 1 kg of lysine a day. Googling around for dietary requirements seems to get you somewhere in the 1-5 g/day range. So assuming vaguely similar productivities for other amino acids, we've got plenty of room to spare if we assume that our bacteria are highly specialized for this function and are exposed to friendly, oxygen-rich and nutrient-rich conditions.


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Is there any danger in putting a magnet in your ear (next to your brain)
I recently bought some wireless earbuds that fit right in my ear, so they're very small.
But the method it uses for charging is magnetic, so it has magnets built into the earbud.
I was wondering if there's any danger in keeping a magnet in your ear for many hours every day? I'm not sure if it would affect things in your skull/brain.

All speakers, all headphones, and all earbuds contain magnets. That's how the speaker diaphragm is driven. Furthermore you are walking around in the earth's magnetic field all day long. There might be an issue with exposure to a superconducting high field magnet, but you wouldn't be able to fit that in your year.

@rasen58 As your question comes from a belief popularized by alternative medicines, your question would be a good fit on skeptics.SE. You might also want to have a look at the posts Do magnets have verifiable effects on humans? and Do magnetic insoles or bracelets increase muscular strength and flexibility? on skeptics.SE

@Remi.b I didn't even know that was a belief popularized by alternative medicine. It was just a question that would seem to make sense from a scientific viewpoint since putting powerful things like magnetic fields close to you seems like it could somehow be dangerous. But thanks for the links!

Every pair of earbuds/headphones have magnets in them, as of now there's no solid evidence that proves that they are harmful or harmless to humans. Keep in mind that, what may be harmful to lab rats may not be harmful to humans as we are more resilient to radiation, etc. (In reference to a study done on truly wireless earbuds.)

You wrote that you a referencing to a certain study, could you please provide a link to that study?


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How to convert a test tube assay to microplate assay?
I am trying to measure Ascorbic acid levels in tissue using Omaye et al protocol (Methods in Enzymology, Volume 62, 1979, Pages 3-11). This method is based on reduction of ferric chloride and subsequent detection by 2, 2'-dipyridyl. However, this assay is a test tube based assay. I want to convert this protocol into a plate based assay, however, I could not find any already published protocol for this. Is it possible to do it?


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What is this whitish jelly incrustation on a plastic tube?
I found this plastic tube hanging in the seawater from a pier in the haven of Taranto, Ionian sea, southern Italy. I'm wondering what is the whitish jelly in the lowest part of the photo next to the yellow Botrylloides violaceus. It didn't seem to come off easily (I didn't insist much though) and it didn't have any macroscopic reaction when touched (no contraction or similar).

The photo was taken on the first days of January. The water was shallow in that point (no more than 2m deep) but close to deeper water, as expected from a haven, and rather polluted.

The orange/yellow jelly organism is very likely a colonial tunicate (sea squirt) similar to the one from this post. I welcome you to do some of your own research to determine more species specifics :)

Possible duplicate of What strange jelly-like thing is shown in the photo?

Can a photo identification post really be a duplicate if it's a different photograph? I guess that's a topic we could pick up on meta.

Thanks @theforestecologist! I hadn't see the question (I sent mine from a cellphone so I didn't see the suggestion) - it's actually Botrylloides violaceus, an alien invasive species. I'll edit my question and make the side quest the main one :)

@TimonG. I don't think it's a duplicate, since it's a different species. However, it's true that I could determine the species basing the research on the similarity to that one. I guess it can or cannot be a duplicate depending on OP's ability to search for similar species. I agree that it's worth raising the issue on meta.

No worries, LinuxBlanket -- just linking up the two questions. You're right that it's a different species and that closing it as a duplicate could easily be voted against. Generally with this type of question, the OP doesn't care about the actual species and knowing the type of organism alone suffices, which is why I voted to close. Interest in the specific species would be fair game for me to rescind my close vote. Regardless, I'll rescind the vote due to your edit. Thanks!

@TimonG. Yes for sure. This happens all the time, especially with common ID questions such as for bed bugs, psocids, carpet beetles, etc. Sure it's not the "same" question, but it serves no benefit to litter the site with IDs of the same species. In these cases, closing isn't a bad thing or form of punishment; it's simply a way to keep the site tidy and allow future visitors ease of finding info they need. But please by all means, start a meta post about it and we'll see how the community feels about that current approach. Thanks


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In PCR what is the chemical makeup of the primer? DNA or RNA?
I'm thinking the answer is RNA. Is that right?

You could improve your question by editing it to add why you think/thought the answer was RNA.

Almost always DNA. While RNA is possible, it’s much harder to synthesize (and keep stable) and DNA results in a purely DNA result that won’t need to be replaced with DNA later.

PCR primers are short pieces of single-stranded DNA, usually around
  20 nucleotides in length.

You can read more about PCR on Khan Academy or Wikipedia.


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Do birds change their diet before migration?
Migration takes up a lot of energy, so I am wondering if birds (in my case mallards) change their diet / food preferences in the weeks before migrating. Do they select for more energetic foods to fuel up, or do they just eat more of the same foods to gain enough energy?

Apparently, yes. This article underlines the changes in diet in semipalmated sandpiper before its 3000 km-long migration:

Near the beginning of their journey, sandpipers stop at the Bay of Fundy on Canada's eastern coast to gorge on mud shrimp, 1-cm-long crustaceans loaded with omega-3 fatty acids. Over 2 weeks, the frantic feeding doubles each sandpiper's body mass [and i]t makes sandpipers' muscles use oxygen more efficiently, enhancing the birds' endurance.

The authors experimented the diet on a similar species to disentangle the effects of the different diet from other effects, for example due to hormonal changes:

To isolate diet's role, Weber and colleagues took exercise and migration out of the equation. They turned to the bobwhite quail, an unrelated sedentary bird that doesn't migrate and seldom flies. For 6 weeks, the scientists fed 40 couch-potato quails a combination of omega-3 fatty acids from fish oil. To the researchers' surprise, the quail's oxidative capacity - their muscles' efficiency at using fuel - shot up 58% to 90%.

This paper reviews the effects of diet changes on the digestive trait of migratory birds; however, it's quite old (2001).
I couldn't find any indication on mallard feeding prior to migration, but these links can be a start for further research.

Geese can build a lot of fat reserves before migration, it's the reason that Fois-Gras is made, because the goose can keep lots of fat in it's liver.
You can buy Spanish foisgras which is made naturally by letting the geese fatten on nuts and rich autumn foods.
Birds generally eat whatever they can get, as rich a diet as possible in protein and carbs, but it's dependent on seasons. So the diet changes anyway at that season, independently from the birds energy requirements. https://sora.unm.edu/sites/default/files/journals/auk/v098n01/p0065-p0079.pdf
"The natural cycle for the wild goose of Europe is to spend the summer in Denmark, Sweden, Norway, northern Germany or parts of Russia and Ukraine. Then they migrate south to Africa each autumn," Labourdette explains. "They stop here in Spain on their way, to eat and gain energy for the long flight. But lots of them never leave because they find such a good habitat here."
Geese are adaptable, he says, and they eat whatever the environment provides. Foie gras from Denmark has a fishy taste, because the geese eat seafood there. Here in Spain, they feed on calorie-rich acorns, olives, figs and seeds.


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At what point in the day do plants start to absorb light for photosynthesis?
My plants sit on a small table in my only window, facing Northwest. They are thriving. They are obviously getting enough indirect light to survive year round. Maybe they have adapted?  They have never really been in direct sunlight.

At what point in the day do they start absorbing this light?
Also, if the sun has risen behind my apartment building on a dull January morning and the sky is light are they reaping any benefits yet?

My plants are:

an asparagus fern with a small grapefruit tree in a tall open terrarium
an African violet
an aloe vera plant
2 sprouting avocado seeds
a small house palm.

I live in Alberta, Canada near the 49th parallel. This is a very sunny part of the province. Your ponderances will be welcome.

You may want to post also at https://gardening.stackexchange.com


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

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


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I found this in my refrigerator water filter. Is it a biofilm? Is it a sign of dangerous bacteria?

When I dispense water form my refrigerator after changing my filter, the following slimy tube like deposits appeared. Does anybody know what this is? Could it be a biofilm growing in the water hose, and if so, is this type of bacteria likely dangerous or benign?

The most dangerous bacteria are those that release toxins, and those that can reproduce very happily at 37 degrees inside the human body. lower temperature bacteria are not typically the most competitive at 37 degrees. you;d need to search reagents that identify biological molecules, lipids, proteins, carbs, amd run some test to identify it..  Biofilms develop with a good supply of micronutrients and nitrogen.


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Which word is used to indicate that a vessel is "blood-filled" during a necropsy?
I'm translating a necropsy report, and one sentence says:

Синусоиды полнокровные. Портальные тракты сохранены, сосуды умеренно полнокровные.
The sinusoids are plethoric. The portal tracts are intact, with moderately plethoric blood vessels.

The meaning of the Russian word is "full of blood". There are three words in English: plethoric, congested, hyperemic. Which one is used more often in necropsy reports when describing the "blood-filledness" of blood vessels and tissues?
Per the comment below left by Bryan Krause: in my text, this feature, "full-bloodedness" of vessels, is clearly not pathological, because each of the several dozen animals has this "plethora of blood" in vessels in many instances across the document, and in the end the researchers come to the conclusion that the animals did not display any negative effects from the treatment.
I googled in Google Books using "congested vessels autopsy", "plethoric vessels autopsy" and "hyperemic vessels autopsy" and found all terms in use:

Those words aren't necessarily synonyms so it isn't as simple as which is more often used, it would depend on what condition the Russian pathologist was referring to.

@BryanKrause - is there a good description of the difference between these three terms in postmortem pathology? It looks like there's only one word in Russian for this, "full-blooded" (polnokrovny). It looks like in English the word "congested" might be used to refer not only to blood (judging by my Google Books search)

I'm not a pathologist so I'm hesitant to say much more because I'm not sure what common practice is for reporting "normal full-bloodedness" - my impression is that all three words are referring to an over filling of blood - in the examples you provided this is certainly the case - but that may be inaccurate. "Blood-filled" might be a safer translation even. And yes, "congested" has many other meanings, such as 'nasal congestion' when the nose is full of mucus or "traffic congestion" when a lot of vehicles are on the road. It is a generic term, not at all specific to blood.

congestion implies increase blood filling on account of a passive process such as congestive heart failure, hyperemic an active process such as inflammation and plethora doesn't assign a cause to the excess blood content of the vessels.  I wouldn't use any of these terms to describe a normal vessel filling at post mortem. But I'm also not a pathologist.


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Identify caterpillars and, if possible, parasitoid (Sabah, north Borneo)
Someone on Twitter posted some photos yesterday of a lump of mud that, when knocked off a chair by accident, revealed a number of caterpillars:
https://twitter.com/solomilne/status/956135158381334528
I've uploaded one of the photos below. The assumption (which seems reasonable, but I suppose isn't certain) is that they were left there by a parasitoid.
Can anyone identify the caterpillars, confirm whether they are likely to have been left by a parasitoid and if so identify a likely culprit? The sample was from a forested area in Sabah, northern Borneo; I've requested a size from the person who posted the photos.

These are wasp larvae, but likely not parasitoids. They are the larvae of predatory Sphecid or Crabronid wasps, both of which build mud nests, generally provisioned with spiders or other arthropods that have been killed (and by some wasp species, dismembered) or paralyzed by the female (mother) wasp. It looks like one or two of them may be pupae (closer to eclosing--"hatching"--as adults) instead of larvae. If kept carefully they can be raised to adulthood for identification (at least by an expert familiar with the aculeate, or stinging, wasp fauna of that part of the world).


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Terminology of the sequences of promoters in relation to DNA strands
I'm studying molecular biology and I'm trying to understand an experiment which shows the importance of promoters in the relative transcription level (RT). The image below comes from Rolf Knippers' book "Molekulare Genetik" (8th edition).

The legend says (among other things):

Die erste Zeile gibt die normale "Wildtyp"-Sequenz der 5'-flankierenden Region wieder.

Which, in english, means something like:

The first line repeats the normal wild-type sequence of the 5' flanking region.

The column on the right gives the relative transcription (RT) level, 1.0 being the highest possible level of transcription. As we can see, the lines where some parts of the "5' region" have been deleted give quite low RT levels, since some regions of the promoter are missing.
My questions are the following:
1) According to this and this, I understand that RNA polymerase reads and uses both coding and non-coding strands in order to synthesize RNA. Therefore, how did they manage to use the sequences strands regions had been deleted to make a polymerase "read them" and perform transcription?
2) If the polymerase reads the template strand in the 3' -> 5' sense, shouldn't we talk of "ATAT box" or "TAAC box" instead of "TATA" or "CAAT" boxes? Does it mean that the "promoter" regions they are using on the graphic above are actually on the coding strand?
Thanks a lot for your help.

Could you clarify your problem. As far as I can see the results are (1) deletion of them globin-specific element reduces transcription to 10% (2) further deletion of the CAAT-box reduces it to 2% (3) further deletion of the TATA box reduces it to 0.5%. Are you asking why the values for (1) and (2) are not zero instead of small but non-zero? (I would say (3) is zero.) Also, the papers you cite say nothing about coding sequences (i.e. those with triplets that contain amino acid info.). Do you mean coding strands?

PS I have used your term "coding strand", but it is one that is best avoided as it causes immense confusion. If you clarify your first question I will deal with your second question, which illustrates the knots you can tie yourself when you use these terms.

@David Yes, I meant coding strand, sorry about that. The main problem that I have (for my 2nd question) is that, since RNA polymerase is supposed to read a template strand (i.e. non-coding strand) in a 3'->5' sense, I don't understand why the promoter's regions (TATA box & co.) are on the 5' side of the transcription's initiation site.
My first question actually concerns the methods of the experiment: how could a polymerase read or use a strand that is in a 5'->3' sense (since she's supposed to read in a 3'->5' sense), and, moreover, how could she use it since the coding strand is not there?

Gene sequences are given as the coding strand by convention. This does not say anything about which strand transcription factors bind to. The protein that binds the TATA box, for example, actually interacts with both strands.

OK. It would seem your problems are those of a beginner unfamiliar with the conventions, which stem from a combination of history, logical consistency and scientific neutrality as regards interpretation. I'll post a comprehensive answer, if nobody else does. But now its Mahlzeit here in Europe and I'm tied up tomorrow morning.

I've edited your question, altering the title to focus on the nomenclature question and making a few other minor changes. You can always revert them if you don't like them.

Related: What direction is a sequence in databases written? and How to infer a given gene sequence is direct seq of a referred gene, or is sequence of its complementary strand?

It appears that this question is one of terminology, so I am answering it as such.
Convention for representing features in DNA sequences
The convention is that in indicating any sequence feature† in a protein-coding gene on double-stranded DNA, a single strand‡ is represented — the one from which the amino sequence could be read using the genetic code (conceptually, with T substituted for U). Like any other nucleic acid sequence§, it is always written in the 5ʹ to 3ʹ direction in the same manner as the mRNA transcribed from it, without this being explicitly stated.
† An exception might be hemi-methylation, in which case both strands would be shown.
‡ I call this the sense strand. I discuss the nomenclature further below.
§ An exception is that tRNA anticodons are sometimes written in the 3ʹ to 5ʹ direction for ease of comparison with the codon, but in this case the directionality is indicated.
Origin and justification for this convention

Historical. The amino acid sequence of the protein (the product of the gene) is central to this convention because knowledge of the genetic code, and hence representation of the region of the mRNA that encodes protein — and by extension the DNA — was the first sequence information to be known.
Logical consistency.  Later other sequences features were identified (some of which initially may have just been genetic features), e.g. ribosome binding sites, polyadenylation addition signals, transcription start sites, promoters, transcription factor recognition sites. It was logically consistent to represent them on the same strand as the coding sequence.
Functional agnosticism. In many cases the function of a sequence followed its description, so there was no reason initially to place it on any particular strand. However, even if it were thought that the function of some sequence were to be recognized on the opposite strand (what I would call the anti-sense strand), it would be unwise scientifically to  change the representation to indicate this. Science progresses and interpretation changes. Better to separate concrete descriptive features from conclusions about their function.

It couldn’t ever be an ATAT box
Even if you represented the TATA box on the anti-sense strand, it could never be called an ‘ATAT box’ (as suggested by the poster) because, according to the basic convention, ATAT is 5ʹ-ATAT-3ʹ, and on the antisense strand the sequence is 3ʹ-ATAT-5ʹ, i.e. TATA!
Terminology for referring to the two strands of dsDNA
Whereas the above is the convention followed universally, the following is just my opinion. In science terminology is important to communicates ideas unambiguously, so I think it worthwhile explaining the ambiguity in some of the terms, the use of which I discourage.
Sense and anti-sense
This is my preferred term because, although not perfect, it avoids the pitfalls of the others. The idea seems to me clear that when you read the string of codons that encode the amino acid sequence from this strand they ‘make sense’. (Anti-sense is used in preference to non-sense, as ‘nonsense’ was the term used historically for mutations that converted amino acid codons into stop codons.) It can also be extended to non-protein coding genes (e.g. for tRNA), where ‘sense’ correlates with the sequence of the gene product.
I shall use ‘sense’ and ‘anti-sense’ as reference terminology in discussing other terms.
Coding and non-coding
This has the disadvantage that it cannot be extended to non-protein coding genes. However my primary objection is that it can cause confusion, as coding only unambiguously refers to mRNA. As the anti-sense strand is the template for RNA polymerase, one might make the mental association between this and ‘coding’, whereas it is the sense strand that is meant in this (admittedly common) usage.
Template and non-template
Template might be a more logical term for the anti-sense strand as this is the template for transcription by the RNA polymerase (although mRNA is also a template — for translation). However it is used only infrequently.
Plus and minus
This terminology is used for single-stranded (especially RNA) viruses to represent the whole genome, where in plus-strand viruses the genome is also the mRNA, i.e. the sense strand. One problem here is that it can be confusing for the beginner, who by extrapolation may assume that in double-stranded DNA genomes one strand is the sense strand for all genes. It is not.  Which brings me to my final point…
…whatever terminology you use, it is better to make sure it is clear that you are referring to the sense or anti-sense strand of a gene, not of the whole genome. You need to employ some other terminology to distinguish between the two strands of e.g. bacterial or plasmid DNA if it is necessary to distinguish them.

Thanks a lot for your complete answer! It was very informative and I will probably come back to it if I get confused about all this again. :)

@David Very helpful answer but could you/anyone please provide a documentation (such as IUBMB) for "The convention is that in indicating any sequence feature† in a protein-coding gene on double-stranded DNA, a single strand‡ is represented — the one from which the amino sequence could be read using the genetic code (conceptually, with T substituted for U)."? Especially because conventions are human-made rules so there must be an universally accessible documentation?

@AlwaysConfused — I did check the IUBMB, but all I could find dated from the 1960s or thereabouts. I think the question of IUBMB approved terminology has diverged from the empirical practices adopted by the databanks. I studied the GenBank format carefully to write a computer program that parsed it, so what I have written is, in effect, my own description of that. The only document I have is "The DDBJ/EMBL/GenBank Feature Table" (2000), which describes the annotation rather than the sequence convention". You might find something at https://www.ncbi.nlm.nih.gov/WebSub/?tool=genbank.

Thank you I'm going to ask it as a separate question as discussed with community. As well which page(s) of BankIt (your link) I'll check? I have clicked the hyperlink there but I could not found anything useful about my question. As well I am not  very much familiar with bioinformatics yet.

I also lack the idea of the programming scripts they are using

@AlwaysConfused — I gave a link to the BankIt because if you are submitting sequences it presumably tells you explicitly what the convention is at some stage. You'd have to take the time to check it thoroughly to find out.

Thank you for teaching me about the database. Currently I'm not submitting a sequence, but I'm trying to learn the basics and in skeptical way.


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Lifespan of helper T cell
CD4+ cells or helper T cells are produced in Thymus. How long these cells live? For example, RBC live for 3-4 months.

I will respond with a "story-like" approach. You may already know some info but I want to be sure I can help you fully understand!
Unlike RBC, you are born with all the CD4+ (or Th, as I refer to them) you will ever need in your lifetime in the primary organs of the immune system -- they are already specialized and ready to be used, and this has taken place in the thymus. On the other hand, RBC get renewed through erythropoiesis every ~120 days.
In utero, the thymus and bone marrow (primary organs) now supply secondary organs (lymph nodes, the spleen, the MALT) with the various cells they’ve made (B&T). However, only 5% leave the thymus, as 95% are recognized as "anti-self" and are killed. So this would be the first "killing" of Th cells. B cells live in the peripheral layer, while T cells live in the deep lymphoid tissue and the lymphoid dullet.
The dendritic cell will "wander" into the lymph node, carrying the fragment of antigen presentation on the MHC class 2 molecule-Dendritic cell resides between the B cell area and the T cell area. Now, the first specific thing occurs in the immune response, when the T cell receptor attaches to the antigen and tells cell says to make antibodies.
Now -- as of here, we have a lot of Th (and B) cells doing nothing while the antibody is being produced. Some of the Th will be killed, while some will serve as "memory Th cells" so that the next time such an antigen is present in your body, the response will be quicker. At this point, it's hard to distinguish which Th cells are dividing, and which are dying. The average lifespan has been reported to be >17 years.
 Source: https://www.ncbi.nlm.nih.gov/pubmed/24492253
I hope I have been able to help.

you are born with all the CD4+ (or Th, as I refer to them) you will ever need in your lifetime in the primary organs of the immune system This is flat wrong. At least read wikipedia before posting misleading answers.

@iayork Hi, this is what I've learned in my immunology class in uni. I checked my lecture notes before posting this and here is a direct quote: "You are born. You have all the machinery for the immune response, but it's sleeping. When you’re born, no antigen has been involved in the making of your cells. They have been specialized by evolution. They will function later in life by antigen exposure." This is what I was taught and I apologize if it was incorrect, but please don't accuse me of posting a misleading answer. I did attempt to verify. Genuinely thought an established prof was correct.

The quote (and prof) is correct, but it doesn't say that all T cells are made by birth, just that the machinery for making them is available.

@iayork that is what I meant to imply... Everything that goes on to occur once an infection/antigen is present results from those Th cells. I go on to say that they do divide. Apologies if unclear.

You still don't get it. New T cells are formed in bone marrow throughout your lifetime. They are not all formed at birth.


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Dopamine involvement in pleasure
There are some psychologists who believe that dopamine is not released during pleasurable activities but before them; my understanding is that a little dopamine is released pre-reward in order to motivate us to complete the action and then a large amount is released when we consume/get the reward. Can you please explain this? Their argument is that dopamine release tells the brain that it is about to feel good and then the brain releases opioids to make us feel good. This doesn't make sense if when addicts take opioids, such as heroin, the brain is flooded with dopamine and the person feels good. In that case we could say that dopamine is responsible for the euphoria. Do you believe this to be correct?

This is an ongoing discussion, and entire textbooks are written in this field, but I will try to clear up some misconceptions and point you toward some further reading that may help.
Is dopamine pleasure?
"Pleasure" is an emotional phenomenon; dopamine is a neurotransmitter. Dopamine can be involved in the perception of pleasure, but there was a now-outdated hypothesis that "dopamine==pleasure".
More recent evidence says that this is not the case, because endogenous dopamine release occurs in some brain regions during the anticipation of a pleasurable event, and really doesn't correlate with pleasure itself at all. Instead, dopamine is currently thought to reflect a "reward prediction error": a signal that tells the brain "hey, we just got something better than we expected!"
Why is a prediction error useful?
This signal can then be used by the brain to upregulate circuits that were recently active, effectively using the heuristic: "I just got something I didn't expect, so whatever I did just before must have been a better thing to do than I previously thought! I should do that more often!"
There are 'degrees' of unexpectedness, however, which is why you get a dopamine signal when a positive event is expected. Let's say a cue, like a bell, signals a coming reward. The reward is now expected, so it won't produce an error signal, but the bell itself produces an error signal: prior to the bell, you didn't know the bell was coming, so you didn't know the reward was coming. Now you update your brain circuits to try to do things to make bells ring!
This is a powerful learning algorithm that is also used, in a form, in artificial neural networks.
Context in drug abuse
If a drug of abuse causes a release of dopamine, that's a signal to the rest of the brain "Hey, something good just happened, let's try to do that again in the future!" Dopamine is the message, not the experience.
Further reading
The two bolded works below are a recent review and a highly relevant original paper, respectively.
Peter Dayan, Wolfram Schultz, and Ray Dolan were recently awarded for their work in this field and you can find lots of popular press that describes their work, as well.

References
Schultz, W. (2013). Updating dopamine reward signals. Current opinion in neurobiology, 23(2), 229-238.
Schultz, W., Dayan, P., & Montague, P. R. (1997). A neural substrate of prediction and reward. Science, 275(5306), 1593-1599.
Fiorillo, C. D., Tobler, P. N., & Schultz, W. (2003). Discrete coding of reward probability and uncertainty by dopamine neurons. Science, 299(5614), 1898-1902.
Glimcher, P. W. (2011). Understanding dopamine and reinforcement learning: the dopamine reward prediction error hypothesis. Proceedings of the National Academy of Sciences, 108(Supplement 3), 15647-15654.
Pessiglione, M., Seymour, B., Flandin, G., Dolan, R. J., & Frith, C. D. (2006). Dopamine-dependent prediction errors underpin reward-seeking behaviour in humans. Nature, 442(7106), 1042-1045.


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How does acacia affect the growth of nearby plants?
I know acacia will make the soil more acidic, but how? I tried to search online, but cannot really find something useful.

What is the source of the claim that acacia makes the soil more acidic?

@LinuxBlanket My teacher told me that it will

The only hint to acacia making soil more acidic I could find at all was this: http://crcleme.org.au/Pubs/Advancesinregolith/Leonard_Field.pdf There it is somewhat stated that because they fix nitrogen, the soil acidity increases around the root. I don't know what to make of this at all, I was just curious and found it unexpectedly hard to find information on.

You say "affect the growth of nearby plants". Is this interaction positive or negative for the other plants?

try reading articles similar to here and here and update your post with what you've learned. We expect question askers to do their own research before posting questions. See the help page for asking good questions. Thanks.

According to Wikipedia:

Allelopathy is a biological phenomenon by which an organism produces one or more biochemicals that influence the germination, growth, survival, and reproduction of other organisms. These biochemicals are known as allelochemicals and can have beneficial (positive allelopathy) or detrimental (negative allelopathy) effects on the target organisms and the community.

Now to the Acacia case.
First of all, Acacia is a genus comprehending almost 400 species, so my answer will cover all allelopathy cases involving one species belinging to this genus.
This article states that Acacia mangium leaf extracts and forest soil negatively affects germination and growth of paddy, and this other one reports phytotoxic effects of Acacia melanoxylon on Lectuca sativa (lettuce) germination and growth.
As to how Acacia species can have an allelopathic effect on nearby plants, this article evaluated the content the phytochemical composition of Acacia cyclops, Acacia mollissima and Acacia cyanophylla pods and seeds and the phytotoxic effect on lettuce seed sprouting. It states that:

All extracts of the three species of Acacia contain saponins and condensed tannins.
The most toxic one was the ethyl acetate extract of seeds from A. cyanophylla, a total inhibition of growth (100%) was registered.
A new triterpenoid saponin called mollisside B has been registered for the first time in the Acacia genus and may be responsible of part of the allelopathic effect on lettuce.


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What amount of light energy is required to produce one O2 molecule? How about one molecule of NADPH?
I know that for each O2 molecule, a total of 8 photons are required (4 per photosystem). Would the amount of light energy required be E=hc/wavelength using 680 and 700? Or would the energy from the initial incident light need to be taken into account (as in when light initially hits the photosystem and gets funneled down)?
Additionally, I know that one NADPH  is produced per 2 electrons. I am puzzled as to how this can be transformed into light energy? Would the amount of light energy required be that of PSI and PSII once again, due to the Z-scheme that ultimately leads to the NADPH production?
I appreciate any help.


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Assays for detecting RNA binding with protein
In a project I'm working on, we are designing a system where specific RNAs bind to proteins - an important part of this is to test whether the RNA binds when we modify the proteins in some way. What assays are there to test whether a specific (or non-specific) RNA is binding to a protein?

I would reccomend an electrophoretic mobility shift assay (EMSA), one procedure for which can be found here.


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Reproduction in horses and donkeys
How are horses and donkeys able to interbreed and produce a mule. Don't their genetypic variation or chromosomal difference prevent them from doing so? If not, then why not?

In closely related species chromosome has only some genetic variations. Therefore there is chance of their chromosomes joins. But if interbreed occurs the species will not be fertile. The ova of female species can take the most compatible from the closest male type .
It's not like that different species can't breed, in many cases they can. For example Donkey and horse , tiger and lion, etc, but the fact is that when different species breed they do not Produce fertile offsprings. Hinney, mules, liger and other animals that are produced by breeding between different species are infertile.


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How outside signals creates different chemical composition in the brain?
Scenario A:
I am walking down the street and my phone rings. I answer and I am told that my ticket that I registered last week was lucky and I won million EUR.
Scenario B:
I am walking down the street and my phone rings. I answer and I am told that my mother died in the car accident.
We have two rather different situations that have totally different “feeling” reactions in my brain. How come outside events can result in a totally different chemical composition of my brain.
Do we create certain dopamine (or any other chemical) release networks in our brain as we develop that are activated (or suppressed) by certain signaling combination?

First, of course, there is no "totally different chemical composition". The changes are very difficult to detect. In experiments with model animals, the usual method is to insert electrodes into the brain in specific regions and to monitor the electrical activity.
As to your two scenarios, it is the anticipation of reward that is most closely associated with dopaminergic transmission, rather than the consummation of reward. Schultz (2016) describes how dopamine signalling codes for a prediction error using a combination of tonic (slow but continuous) and phasic (fast and pulsed) firing patterns. A pause in tonic firing indicates that an expected reward failed to materialise. A burst of phasic firing indicates that an unexpected reward was received. These excursions from tonic firing give rise to changes in behaviour.
Thus one might expect that on receipt of your telephone calls, there may be some dopaminergic signalling, certainly in Scenario A. In Scenario B things are slightly different because you weren't expecting a reward; you simply received bad news. However, there is evidence (Matsumoto and Hikosaka, 2009) that dopaminergic signalling is involved here, also.
The cells responsible for these changes in dopamine signalling project to the frontal cortex. The receiving cells alter their synaptic connectivity in response. Successful connections are strengthened; connections producing poor results are weakened or eliminated.


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Role of processing bodies in mammalian development
I am currently writing a project proposal for university admissions regarding the duration till which maternal mRNA is required for mammalian development. Till now all the literature I have read has data on P-bodies during oogenesis:-
1) https://www.ncbi.nlm.nih.gov/pubmed/22918798/
2) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2785738/
It will be very helpful if anyone can provide a link for research articles showing p-bodies during embryogenesis in mammals.

These papers might be helpful.
http://www.molbiolcell.org/content/19/10/4383.short
https://www.sciencedirect.com/science/article/pii/S1874939913000047

@Divyanshumishra Thanks. I will go through them.


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Are there laws in ecology?
Are there clearly defined ecological laws, as in the science of physics? If not, why is this the case?

first rule of biology: there is an exception to every rule, including this one.  But seriously this article may help you. http://www.ecology.info/laws-population-ecology.htm

I think this is really more of a question of philosophy rather than science. You can read a bit about the meaning of a scientific law on Wikipedia: https://en.wikipedia.org/wiki/Laws_of_science My personal opinion is that the reason people don't talk about laws as much in biology is because laws are too small/specific to be the most interesting answer to a biological question. In physics, a law is something that you are able to reduce a broad phenomena to. In biology, it's rare outside of mathematics to be able to reduce to one statement that describes an entire phenomenon.

What is law and what is ecology?
I always find the definition of "law" a little hard to grasp but maybe only because I am a mediocre philosopher. To me, I don't quite understand the difference between a theory (a theory is not a hypothesis in science) and a law.
It is also hard to know what exactly you would consider being part of ecology and what you would be considered part of evolutionary biology, agriculture or paleoecology / paleogeology and those disciplines are very much related. Here are a few concepts that I don't if they would qualify for an answer

General latitudinal diversity gradient
The concept that symbiosis is more a rule than an exception (it also comes with the discovery that mitochondria are/were endosymbionts).
Theory of natural selection
Positive and negative feedbacks in glacial period
Geographical area law/hypothesis
Parental effects
Adaptive radiation
r/K selection theory
Theory of island biogeography
...

Are there science that create more laws than others?
I am really not qualified to answer this question but I would tend to think that in ecology, there is a lot of important discoveries that lead to a conceptual rephrase or to a reconsideration of the relative importance of different concept or to the realization of a single fact, more than to the phrasing of a law per say.
Laws in ecology
Here are a few concepts in ecology that are often being called law.

Liebig law of the minimum
Ten percent law
Allee effect law
Square-cube law, allometric scaling and the metabolic theory of ecology
Ecological systems theory

as well as all the laws regarding population growth such as

Malthusian, Verhulst and Lotka-Voltera laws.


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Is a microspore diploid?
In  gymnosperms the plant body is predominantly sporophytic. It produces microspores or megaspores my textbook says that these undergo reduction division in order to form male gametophytes pollen grains and female gametophytes that is egg.
The thought of a spore being diploid is revolting, as I have learned in the case of bryophytes and pteridophytes that it's haploid. Can anyone help me asap.

Sadly I don't have a lot of time to study gymnosperms in details again, but my book (Campbell's "Biology", 11th edition) says that "Microsporocytes divide by meiosis, producing haploid microspores. A microspore develops into a pollen grain (a male gametophyte enclosed within the pollen wall)."
It says as well: "While the pollen tube develops, the megasporocyte undergoes meiosis, producing four haploid cells. One survives as a megaspore."
So microspores and megaspores seem to be haploid.

Hi Susan. If either of the answers you received are acceptable and useful, please consider upvoting them (by clicking the up arrow to the left of the answer) and/or "accepting" them (by selecting the check mark below the vote triangles). Thanks.

The spores (microspores or megaspores) in gymnosperms are haploid. The microspores came from the microsporocytes which are diploids cells of the sporophyte, divided via meiosis. So the haploid microspores do mitosis and form the male gametophytes (pollen grains), containing two male gametes (sperm cell) and a generative cell which will form the pollen tube.
The process conducting to female gametes in the ovule is very similar. A megasporocyte (diploid cell of the sporophyte) via two meiosis form four megaspores (haploid). Only one megaspore is functional (the others will degenerate) and do 3 consecutive mitosis to form eight nucleus with different functions, one of them is the egg cell (female gamete).
So the meiosis happens before the formation of the spores (actually it forms the spores) so they are haploid.
Source: R. F. Evert & S. E. Eichhorn "Raven Biology of Plants"

Hi Maso and welcome to Bio.SE. Rather than commenting on your sources, it would be better to include them in the answer by using the edit function.

Short answer:
A microspore is haploid.

Long Answer:
Gymnosperms are heterosporous, and therefore create two types of spores: male and female -- microspores and megaspores, respectively. These spores will develop into gametophytes which then undergo fertilization (i.e., the male/female gametophytes combine their chromosomes). To avoid constantly increasing the chromosome number of these plants, these gametophytes (and therefore the male/female spores), must only contain half of the "proper" number of chromosomes. In other words, these male/female structures must be haploid (1n). Haploid cells develop via meiosis, a process in which cells essentially split twice even though their chromosomes have only been duplicated (replicated) once. In a diploid cell, this means that the resulting cells (4 of them per parent) have only 1/2 the chromosomes as the mature organism.


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What do you mean by non cellular matrix
What do you mean by the non cellular matrix in which connective tissues are embedded?

You're looking for the extracellular matrix:

In biology, the extracellular matrix (ECM) is a collection of extracellular molecules secreted by cells that provides structural and biochemical support to the surrounding cells.

Its main component are fibers, that can be strongly interlaced as in the case of the dense connective tissue or more loosely distributed as in the loose one.