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The space of all human DNAs
This is both a math and biology question but I think it makes more sense for a biologist to answer it. My question is: what can be said, if anything, about the space of all possible human DNAs (for a suitable definition of "human" in the context of this question)? Is it open or closed with respect to a suitable topology?
EDIT: To fix ideas and make it less a matter of opinion, one (admittedly incomplete, this is for the sake of making the question more precise) definition to use might be "those who can reproduce with existing fertile human beings"?
EDIT 2: To be clear, I am not a biologist but a computer scientist and maybe my question is guided by assumptions that simply do not hold. My naive vision of someone's DNA is a string of A,T,G,C which, when "interpreted", becomes that person. I am also under the impression that a single mutation of a letter may render them nonviable. On the other hand, other mutations may produce an individual with altered characteristics, who may or may not be able to reproduce with other human beings. So I was wondering if there is an interesting way to think of the space (in a mathematical sense) of all strings of DNA which produce a viable human being in this sense. If my assumption that a single mutation can render one nonviable, I would expect that this space would be "closed" for some topology.
I'm totally ready to accept that this way of thinking about DNA is flawed and/or unrealistic, and in that case I'd be happy to learn why, if possible in layman's terms.

The question is entirely dependent upon the definition of "human" you are willing to use. There is no obvious "suitable definition", there are only definition each person might want to come up with. I am VTC because an answer will necessarily be opinion-based.

I think the definition of human is less of a problem (one can probably assume we are mostly interested in healthy human cells, preferably in vivo) than the definition of open and closed topology of DNA: DNA chromatin status (which what's usually used as a proxy for the overall DNA topology) is VERY hard to measure directly and is therefore mostly assessd by indirect methods (ChiP, Acetylation state, occupancy by proteins &/ RNA-pol)

I hope I'm interpreting your question correctly; you are asking how large the possible conformation space is for DNA contained within 23 pairs of human chromosomes. The answer is very very large, since there are countless ways to arrange it, loop them, tangle them. Evolution has certainly sampled many ways to do this, but the number of possibilities unsampled is probably much astronomically higher. It's a bit like asking how many ways you can tangle a single, very long string, or 46 of them, for that matter, not including mitochondrial DNA. (cont...)

(...cont) Each cell in your body is unique in this respect, although cells of similar type share similar features that may distinguish it from other cell types. Chromosome conformation is difficult to determine, and the best ways currently we have of looking at it involves looking at the modification of histones (methylation, acetylation, etc.), looking at which transregulatory elements are bound at specific locations (polymerases, cohesins that hold loops in place, which portions of DNA are accessible to DNA-cutting enzymes, etc.), and methods like chromosome conformation capture ("3C").

@user3078439 if you'd like a super simplified explanation of the role of DNA in "creating" a person, see here and then here for 2 quick video explanations (< 5 minutes). It's a very basic (and relatively non-biological) approach to explaining things, but the videos should confirm for you the conceptual role of DNA in a human (cont...)

(...cont) ... Note, though, that I put "create" in quotes, b/c really DNA codes for the production of proteins that either make-up or generate the parts necessary for a body to form and function. In other words, DNA doesn't "become" a person; but rather, DNA provides the instructions for creating the various parts needed to assemble the various cellular and intercellular components in an organism (such as a human).

The best way to answer this question may be to root the answer in data.  We now have human genome sequences for a sizeable sample of humans.These sequences, and the variations between them, already define a sample of what it means to be a human.  We might assume that as the size of the sample grows, it will eventually converge on a definition of the entire genome-space of what it means to be a human.  We can only speculate about whether a genome configuration outside that space could give rise to an individual we would regard as human, but I think this is moot.

To add an opinion of the answer to your question, it seems to me that the space is closed but unimaginably large.


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Is this an imprint of a fossil?
I found this stone in the arizona desert. Sort of far from humans on the side of a Butte

Could you please add the size if that stone/imprint?

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When endothelial cells in blood vessels (arteries or veins) are damaged, does atheroma form first or blood clot?
I have learnt from Khan Academy's video on atheresclerosis that when the endothelial cells of an artery are damaged, atheroma forms at the site, and if the atheroma’s fibrous cap is ruptured, thrombogenic material is released from the atheroma, causing a blood clot. Having read other articles on this issue, this phenomenon is known as the atherothrombosis. And I believe that the fact that atheroma is formed before thrombosis is because thrombogenic material isn’t released when endothelial cells are damaged; thus cholesterol deposits in the area to form atheroma first.
However, in another video, when endothelial cells in blood vessels are damaged, platelet activation occurs due to the exposed collagen, and thrombosis occurs. Why is it that blood clotting occurs first instead of atheroma?
I have also learnt from my other question on Biology StackExchange that hypoxemia in the valve pocket of the large veins can cause endothelial damage that triggers the clotting cascade.
Therefore, I am confused as to which of atheroma or blood clot is formed first when endothelial cells are damaged; and if either one is formed first, why is that so? I’m certain that after a blood clot is formed, atheroma won’t be formed as I’ve not found any article that supports this sequence.
References:

https://www.khanacademy.org/science/health-and-medicine/circulatory-system-diseases/coronary-artery-disease/v/atherosclerosis
https://www.youtube.com/watch?v=R8JMfbYW2p4
https://academic.oup.com/eurheartj/article/25/14/1197/509341
How do veins's valve pocket sinus tend to become hypoxic?

It is unlikely that atheroma would develop as a complication of a thrombus.
Atherosclerosis and thrombosis are two independent disorders and not two stages of the same disorder. Atherosclerosis is a disorder of the arterial wall and atheroma develops in the arterial wall. Thrombosis is a disorder of the blood and thrombus is merely attached to the atheroma or arterial or vein wall.
In veins, only thrombosis, but not atherosclerosis can occur, as mentioned here.
In arteries, thrombosis usually occurs only as a complication of an atheroma or calcification (PubMed, 2017):

The majority of coronary thrombi are caused by plaque rupture
  (55–65%), followed by [plaque] erosions (30–35%), and least frequently
  from calcified nodules (2–7%).

It is very rare that thrombus develops in arteries that have previously not been damaged by atherosclerosis (PubMed, 2015).
Further evidence that thrombus formation is an unlikely initial event in the development of an atherosclerotic plaque:

Thrombosis is not mentioned as an initial stage or risk factor in development of atherosclerosis in various texts: Textbookofcardiology.org, Pathophys.org
Genetic coagulation disorders are not likely risk factors for atherosclerosis (Atherosclerosis, Table 2 (PubMed, 2010):

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How much does calcium reduce iron absorption?
Generally calcium inhibits the absorption of iron, but to what extent? One atom of calcium will not block 100% of iron absorption, that clearly isn't feasible. On the other hand, if someone ate 10 pounds of calcium, they wouldn't absorb any iron. How can we quantitatively determine the inhibition of iron absorption for a given calcium intake?

In short: Calcium can inhibit absorption of iron, but this does not necessary have any significant effect on the long-term iron status in the human body.
Iron (Linus Pauling Institute):

The presence of calcium decreases iron absorption from both nonheme
  (i.e., most supplements and food sources other than meat, poultry, and
  seafood) and heme sources (meat). However, calcium
  supplementation up to 12 weeks has not been found to change iron
  nutritional status, probably due to a compensatory increase in iron
  absorption. Individuals taking iron supplements should take them two
  hours apart from calcium-rich food or supplements to maximize iron
  absorption.

In various studies, calcium from food or supplements in usual amounts decreased iron absorption by about 50%, but the calcium dose/iron absorption relationship cannot be simply quantified, because it is affected by several factors, for example:

Phytates in food inhibit the absorption of both calcium and iron (BiomedCentral).
Calcium may inhibit the absorption of nonheme iron from plant foods less than heme iron from meat (academic.oup.com).
Different calcium supplements may differently affect the absorption of different iron supplements.

The inhibitory effect of calcium on iron absorption is not linear and one may not be able to express it as a simple formula. Below are some examples from studies.

A review of studies, American Journal of Clinical Nutrition, 2010

The reported dose-effect relation between the amount of calcium given
  and the degree of inhibition of iron absorption differs from other
  factors influencing iron absorption.
  This dose-effect pitfall is illustrated by 2 studies...[Read more in the linked article ].

A review of studies, PubMed, 2010

The quantitative effect, although dose dependent, was modified by the
  form in which Ca was administered and by other dietary constituents
  (such as phosphate, phytate and ascorbic acid) known to affect Fe
  bioavailability. The results of most multiple-meal human studies
  suggest that Ca supplementation will have only a small effect on Fe
  absorption unless habitual Ca consumption is very low.

A study, PubMed, 1991

When taken without food, calcium carbonate did not inhibit the
  absorption of ferrous sulphate with doses of either 300 mg Ca and 37
  mg Fe or 600 mg Ca and 18 mg Fe. However, at the latter levels,
  calcium citrate and calcium phosphate reduced iron absorption
  significantly by 49% and 62%, respectively. All calcium supplements
  inhibited absorption of the iron supplement when taken with food. The
  absorption of dietary nonheme iron was also inhibited by all three
  supplements. This inhibition was less pronounced from a meal of high
  iron availability and low calcium content (28%) than from a breakfast
  meal of low iron availability and high calcium content (55%).

A study, American Journal of Clinical Nutrition, 2005

Calcium supplementation reduced heme and total iron without
  significantly affecting nonheme-iron absorption, regardless of meal
  bioavailability.

This doesn't really answer anything because it says nothing about the timing or ratio. Obviously if you don't take calcium supplements at the same time as you ingest iron, there is no problem, but when taken together calcium definitely inhibits the absorption of iron, you will be hard-pressed to find a certified nutritionist who says otherwise. That is why the article still recommends taking them two hours apart. The question still remains: by what percent does a given mass of calcium decrease iron absorption by? This can only happen if you ingest them within two hours of each other.

@VaneVoe, if you are asking how calcium supplements inhibit the absorption of iron supplements, please make this clear in your question. Food can affect iron absorption in so many ways that it makes your question unanswerable. Even with supplements alone, it may not be possible to answer with a certain "percent." They are individual differences in iron absorption, current iron stores in the body and different Ca and Fe supplement forms that affect absorption

You're the one who chose the focus on supplements, I am asking about per-weight inhibition, you chose to ignore that.


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Are microbial antigens selected against?
Antigens provoke a response from the host immune system. Could selective pressures result in microbes losing their antigens? Has this been observed? Or are antigens typically so important that they are constrained from losing them?

Hiya. I find the last sentence a bit confusing and don't really know what you mean by it.. However, I interpret your question as whether there are any selective pressures that would lead microbes to lose/hide their antigenicity. If my interpretation is correct then, yes, that happens / has happened. S. aureus is probably the most famous example.. Antigenic variation as well as antigenic disguises are two "ways" a microbe can escape the host immune system.

Thanks, that answers my question! Sorry I was not clearer in the last point. What I meant was, are there certain antigens that are so functionally important to the microbe that they cannot be lost? And what would an example of such an antigen?


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What species of tree is this (found in Navarre, Spain, many tiny flowers)?
It was planted within the urban area of Pamplona, Navarre, in Spain. It does not seem like it's native to the area, since no trees like it are found in nearby forests. Its size is of 7-9 meters, while its leaves were commonly 4-5 cm long. It was spring when these photos were taken. It had a great number of tiny, dark flowers. It also showed tumor-like growths where the trunk begins to branch.

[

I believe you are looking at Box Elder, Acer negundo.  It's a North American species but according to Wikipedia it is naturalized in Europe.  If you search online for images, you will see the leaves and flower structures in your own pictures.  Specimens I have seen in my area (Indiana, USA) are very similar to your pictures, even identical, and the trunk is gnarly, as you observed.

Nice identification, +1. There's a picture here if you want it.

Thanks. After Googleing it, it seems to be the male plant (landscapeplants.oregonstate.edu/plants/acer-negundo).

Interesting... I did not know or did not remember it is dioecous.


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Why did translation develop a specific codon for initiation?
The translation of mRNA is initiated by a specific methionine-accepting tRNA at a specific initiation codon, usually AUG (complementary to the tRNA anticodon). However translation at suitable (albeit unphysiological) conditions in vitro does not require a specific initiation codon or a specific amino acid, so it is not difficult to envisage an earlier stage in the evolution of the translation apparatus in which this specific initiation system was absent. Instead there might have been random initiation or initiation from the 5′ end of the mRNA.
A specific initiation codon puts constraints on the sequence of the mRNA and adds an unnecessary amino acid to the N-terminus — one that is sometimes unwanted and needs to be removed.

What advantages can one envisage for initiation at a specific internal
  site, rather than at, say, the 5′ end of the mRNA?

I appreciate it is impossible to prove which factor was actually responsible during evolution, but by soliciting concrete explanations I trust that this question is as valid as the original from which it is derived (see Footnote).
FOOTNOTE
This question has been expanded from one part of a three-part question posted some time ago on “Why is AUG the Initiation Codon?”. This recently resurfaced, and as nobody had answered this particular part, and as it is site policy to ask one question at a time, I decided to remove it from the original and repost it here so it could be considered on its own merits, without the distraction of other questions such as the choice of codon or of methionine over other amino acids. I shall contribute an answer with some thoughts of my own, but, of course, anyone can join in.

It could simply be to prevent random fragmentary RNA from being transcribed,  they are fairly common in the cell afterall.

@John — Thanks for your comment. I can include it in my answer if you are not going to answer yourself. One thing — do you have a reference to support your statement that random fragments of RNA are fairly common?

There are many things like ribosomes that are made of RNA, ribonucleases (which are also made of RNA) is one of the many ribozymes which could be transcribed. It is also one of several mechanisms that cut RNA into smaller pieces. https://www.sciencedirect.com/science/article/pii/S0092867409000671

@John — Thanks. I've included your point in my answer.

It is not clear to me where initiation took place in the translation of artificial polynucleotides such as (UC)n which Khorana used in experiments that, following up the work of Nirenberg and Matthaii, helped decipher the genetic code. It may well have occurred at random positions rather than the 5′ end. Such a mode of translation would obviously have been wasteful if it occurred during early evolution as a mixture of products would be formed, many of which would be inactive and might even compete with the active species. If this were the original situation,  it is easy to see how a change to initiation at a specific point would be advantageous.
But why not start at the 5′ end? Contemporary eukaryotic initiation complexes recognize the 5′ end of the mRNA, even though they then scan further to find a specific initiation codon that will respond to the initiator tRNA. As there is no physical separation of  genes on a chromosome, it is obvious why transcription needs to start at a specific point within the DNA, but the need not be true for the translation of individual mRNA transcripts.
I can see two ways of approaching this question.
The first is from the standpoint of the contemporary ‘DNA World’. The arguments one can make  include:

In a general sense 5′-end initiation may be regarded as restrictive
in that it would not allow the 5’ end of mRNA to provide other
functions such as forming a secondary structure to regulate the ease
of translation.
5′-end initiation would preclude the polycistronic mRNAs we see in
contemporary bacteria.
In 5′-end initiation it might have been difficult to distinguish the
ends of mRNAs from other RNAs before the modification of bases that
we see in contemporary eukaryotic mRNAs had developed.
Likewise, as suggested by @John in a comment on the question, 5′-end initiation might have caused translation of fragments of RNA as they degraded.
The selection of a specific codon was secondary to the need for a
single initiator tRNA, which has been discussed in relation to
another SE question, although the arguments there relate to more recent stages in evolution.

However there is another approach which considers the situation in a putative ‘RNA World’.
The difference here is that — like some contemporary RNA viruses and bacteriophages — the genome might also have been the mRNA but without a system to produce many copies of the ‘plus’ strand for translation. Translation may have been on the genomic RNA.

To translate several proteins it would have been advantageous to have
several initiation sites on what would have been a polycistronic
messenger (rather synthesize a polyprotein like poliovirus).
The 5′-end of the RNA may not, in any case, have been available for
encoding protein as it might have another (e.g. replicative)
function, and it is also possible that part of what in contemporary
systems is a separate part of the translation apparatus was
physically incorporated into the genome.


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How does a cell identify itself?
In embryological development, undifferentiated cells developed into specific types.  As far as I understand, a key differentiating factor is the regulation of gene expression via transcription factors.
However, if all cells have identical genomes and, therefore, identical transcription factors, what is the source of difference in their morphogenesis? Does it rely on some element of randomness in external factors?

This is essentially asking 'How does (embryo) development work?' which is even after decades of research and several nobel prizes not a fully solved question. I don't think its possible to write even a general answer here that doesn't omit tons of important factors.

I think you can ask the basic question and get an answer. In fact, there are two good ones below. I particularly like @swbarnes2's answer because, well, that's the answer to the basic question. If you have asymmetry in the initial cell, you can establish different lineages. Re: "this is not a fully solved question", no field in biology is complete (thankfully), but we know an extraordinary amount about this in several important model organisms.

This has been studied this in Drosophila, and a lot of development hinges on where the cell is in the body.  An initial asymmetry of mRNA in the pre-fertilized ovum leads to the establishment of the anterior-posterior axis (which end is the head, which is the tail)  So cells are told what to develop into based on what mRNA signals they receive which depends on where they are along that axis.
https://en.wikipedia.org/wiki/Drosophila_embryogenesis

yes. the most simple answer to this is gradients (established initially by an asymmetrical cell)

If all cells have identical genomes and, therefore, identical transcription factors

Important comment: all cells do indeed have identical genomes, and all cells are therefore equipped with DNA that codes for transcription factors, but that does not mean that all cells have the same state of the genome. It is well understood that different cell types have different chromatin accessibility ('DNA open and closed for enzyme access'), and this is dependent on the modification of histones which DNA is wound around. It is not a complete image to simply visualize DNA as a strand; it is in fact a complicated 3-dimensional structure, and each region or 'neighborhood' of a DNA location is different from other regions. The below image helps in visualizing the levels of ordering. The ordering is very specific based on the current state of the cell and its history (i.e. which progenitors it came from).

Currently, we have a few ways in which we can study DNA conformation and epigenetics (study of things 'on top of DNA') with a few methods, each limited to probing a certain aspect. Among many others, we use:

ChIP-seq and related methods to determine which proteins occupy positions on the DNA (most often we look for polymerases, or histone modifications),
DNase hypersensitivity assays to determine which regions of chromatin are accessible to cutting enzymes, and thus are open for transcription,
3C-based methods to determine which regions of DNA are in close proximity with  other regions (via e.g. looping of the DNA strand to bring distal enhancer or silencer elements to promoter regions)

How do cells differentiate into specific types?

Factors that cause differences in morphogenesis are called morphogens. There is an incredible wealth of information on the topic, and it's difficult to find a good place to start. Indeed, transcription factors are central players. The best known family of morphogenic TFs are homeotic genes that are crucial for patterning the body. They give rise to the body plan, determine which cells are the head and which are the opposite end, they determine where organs arise, how segmentation proceeds, and how organs form. The field of evo-devo is the principal field that studies how body morphogenesis is determined at the cellular and molecular levels.
Here is a simplified image that illustrates how the same conserved elements (a handful of Hox genes) determine body patterning even across species:

For the layman, I think there is an outstanding engaging and mandatory video on the topic. It does a good job at summarizing and depicting exactly what you are asking, without going into the painful details that would do the science justice.


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Why are Barr Bodies usually seen along the edge of the nucleus under the light microscope?
We do a typical class exercise of aceto-orsein staining of buccal epithelial cells from female students to visualize Barr bodies under the light microscope. All the illustrations and pictures in the books depict a Barr body located on the edge of the nucleus, but that is not always the case in the students' samples. Given that the cell is a 3D structure, I couldn't explain why the Barr body would localize itself to the edge of the nucleus with respect to the viewer's 2D perspective.
In this article's introduction, a statement is found saying:

"In interphase, the inactive X chromosome (Xi) is found as a condensed
  heterochromatic Barr body, usually positioned at the nuclear or
  nucleolar periphery (1-4)."

By "usually", does it mean that it is pure luck? Is there any explanation as to why we would have a tendency to see it localized to the edge from our perspective, exactly on the rim of the nucleus, and not just somewhere random?


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Where are Opsonins produced?
I read that opsonins are a type of antibody that play a vital role in chemotaxis and phagocytosis in general. The fact of them being antibodies though, got me confused. Antibodies are, to my knowledge (however inadequate it may be) , released by plasma cells after macrophages present antigens. Yet my book says that pathogens are covered in antibodies (opsonin) which help the macrophage initiate phagocytosis. How can antibodies (opsonin) be present before the APC Present the antigens to activate the production of antibodies?
P.S.: I'm a college student so there's probably a lot of things I'm missing out on. Please do fill me in :)

Did you check wikipedia on opsonins? For a more authoritative reference see this and this.

Yeah i tried, and cheers for the other two links, but i still can't find a clear citation of a source. Found what they do and how they work but not where they are produced. FYI by where i mean what produces them. Probably shouldve clarified that sorry.


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Do bald people not grow hair, or does their hair simply fall out immediately?

This image is not directly related but it made me wonder if there was a relationship between the nature of the hair follicle and baldness, namely that the follicle cannot 'hold' the continuously growing hair, and it constantly falls out in. I wonder if this is the case or if the hair literally just does not grow out from the follicle at all.

There are different causes of baldness. Perhaps you can check out the wikipedia page on hair loss and make your question more precise.

I'm no expert on the whole matter, but I know that at least when it comes to male pattern baldness, it is caused by a hormone called dihydrotestosterone. As those men with the right (or wrong genes, however you choose to look at it) age, this hormone causes the hairs to progressively lighten and thin up until the hair stops growing altogether. The hair follicle dies out basically.

Welcome. Answers need to be backed up by reputable sources, preferably journal paper citations. As of now this is more of a comment and not an answer.


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Gel electrophoresis and foam

I've never seen this kind of thing happen. What might trigger this??

Looks like an agarose gel. What buffer did you use? Did you happen to clean the tank (incompletely) using a detergent?

Gas bubbles are foamed by electrolysis of water, generating bubbles of hydrogen gas on the negative electrode and oxygen gas on the positive electrode.
As for the foam itself... I am guessing there is some form of detergent in the buffer. Some electrophoresis buffers do contain detergent.


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Dragonish caterpillar from North Vietnam
I encountered this caterpillar in North Vietnam (Hanoi) and could not find any reliable web site for this kind of search. I am not an entomologist, so I don't even know how to describe it, except that it has hairy head stalks. I hope my pictures will help.
Thanks to anyone who can help me here.

Please provide approximate size of your specimen.

Subfamily Lymantriinae?

My comment above is actually likely wrong.
Instead, I think this is possibly the larva of the rose-myrtle lappet moth (Trabala vishnou) in the Lasiocampidae. (It may also be the larva of the closely-related roseapple caterpillar, Trabala pallida -- see here and here).
I don't know this group of moths at all, but a series of failed "Lymantriinae" searches and otherwise successful image searches led me to this genus and these species. Lack of reputable resources available in English online make differentiation between species in this genus very difficult for me. Below are some images of Trabala caterpillars:

 Images Source: Koh Chang Nature
You can see a very smilar image to the ones above on flickr.


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Do non-human primates have mental disorders like humans?
I was at the zoo today and watched a gorilla pick at a scab on its finger, compulsively, until it started bleeding. Is this OCD or is it just a nervous thing that non-human primates do at the zoo? Do gorillas share any of the same mental disorders that humans have?

Hi and welcome. What attempts have you made to answer this question? We ask that all question posters show an attempt to search for an answer to their own question, show what they learned, and why iit s still confusing/unknown to them. (Studies exist on this subject.) Our goal is not to just be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail and it will likely be received more positively by out community. Thanks!


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System diagrams showing biofeedback processes or interactions (- and + symbols) in ecosystems
Overview:
I apologise profusely for asking a silly question, but I am feeling confused and I am seeking more clarity on this subject.
Could anyone, please help me understand why the interaction between climate change, habitat loss, and monotonous diets with the energetic suppression of the bee itself (shown in diagram 1) has a positive (+) symbol?
Would these factors not have a negative effect (-) on the bees energetic suppression?
Would you only add + or - symbols to define interactions when:-

Two biotic factors (i.e. foxes predating on rabbits);
One biotic and one abiotic factor (i.e. the effects of elevated temperatures on bee population abundance);

Would you not add + or - symbols for two abiotic factors i.e. elevated temperature produces extreme weather events and negatively affects a species habitat as these interactions don't involve living organisms (as shown in diagram 2)?
If anyone can help me understand better, I would be deeply appreciative!
Diagram 1
Diagram 1 provides an overview of how parasites, pathogens and pesticides as well as other stressors interact to affect honey-bee health, eventually causing CCD in honey-bees.
How do insecticides and pathogens act synergistically to affect honey-bee health?
There are several hypotheses that have been proposed to explain the effects of pesticides (insecticides and fungicides) and pathogens on bee mortality and CCD including:
Exposure to insecticides suppresses the immune response of bees, promoting pathogenic parasitic (Nosema) infection and as a consequence increased viral loads. The mechanism by which immune suppression occurs has recently been elucidated (see Optional material).
Nosema infection induces energetic stress in honey-bees that results in higher food intake by infected individuals. This directly results in an increase in insecticide oral exposure, increased toxicity and higher mortality in infected individuals.
Bees are commonly exposed to plant compounds that can be toxic (called phytochemicals, e.g. nicotine) and use enzymes (P450 enzymes) to detoxify these compounds and also insecticides. When exposed to fungicides, these enzymes are inhibited, increasing the toxicity of insecticides to bees and also making them more susceptible to Nosema infection.
Honey-bees have a form of social immunity (which is found in many social insects) that consists of cooperation between individual group members to prevent disease contamination. This collective immune defence includes hygienic behaviour where diseased individuals in the brood are removed from the hive, as well as the secretion of antiseptics to sterilise brood food. Exposure of bees to a combination of pathogens (Nosema) and neonicotinoids compromises their ability to sterilise larval food by decreasing the activity of an enzyme known as glucose oxidase. This enzyme catalysis the oxidation of beta-D-glucose to D-gluconic acid and hydrogen peroxide, the latter having antiseptic properties. A decrease in hydrogen peroxide allows the pathogens to spread within colonies.

Diagram 2
Currently, the main stressors on bee populations are considered to be agrochemicals, parasites and poor (monotonous) diets. The interactions between these stressors can also increase the stress on bee populations. However, the Goulson paper also briefly discusses how climate change may become an increasing stress on bee populations in the future, and mentions a couple of impacts of climate change that may negatively affect bee populations. In Session 3.3.11, you also learned how ecosystem function can be impacted by climate change through different processes.
Drawing on the information of climate change in bee populations and the knowledge of ecosystem processes, draw a systems diagram that illustrates the potential impact of climate change on bee populations. This diagram should include impacts of climate change that can affect bee populations directly as well as indirectly (i.e. via impacts on other bee stressors). Your diagram should, therefore, show the cascading effects of climate change, acting both directly and through specific stressors, on bee populations.

Can you link the original source of this diagram? +/-  is usually used to denote positive/negative interactions, respectively. Some people also use arrowhead for positive interaction and a "tee" (⊣) end for a negative interaction. So there is no universal standard. In your case it looks weird. For instance, P450 system should reduce toxicity but in the diagram the interaction is depicted with a +.

Hi WYSIWYG. The first diagram was taken from an example supplied from the Open University. I supplied the relevant information that accompanied the diagram. The second diagram, I drew myself to answer the question. I placed as much information as possible so my question might make more sense now. I hope this is what you need to provide insight. Many thanks for your help!

The original diagram is inconsistent with the use of symbols. As I mentioned, P450 should have a negative effect on toxicity but it is indicated by a +. The interaction between deformed wing virus and mortality (which is a positively correlated interaction) is also denoted by a +. Now, again, immune response also has a + interaction on the virus. Overall, this diagram is inconsistent with the usage of the symbols and is hence wrong.

I'm voting to close this question as off-topic because it is based on a non-standard and incorrect premise that is not even a part of a published text.

Hi WYSIWYG. In this systems diagram (diagram 1: which is definitely a published text with the OU and designed by a doctor in his field), the description says "+" and "-" signs are read as "positive" and "negative" in terms of the recipient box in the diagram. There are some boxes with a negative statement/factor, e.g., "Deforming wing virus", it has "+" on the arrow from "Immune response". That means that immune response allows deforming wing virus to develop. So "+" here confirms the strength of the negative statement in the box.

This question may help many people like me who are suffering from confusion over the theory of "+" and "-" symbols in systems diagrams. I really do appreciate your help and advice. Many thanks

I understand. But the most common usage is that + denotes a positive effect (causal) on the on the node where the edge is directed to (conversely for -).  However, I cannot be sure about this diagram because it doesn't really rationalize these interactions. For example, I would expect immune response to suppress the virus and P450 system to reduce toxicity. Both these interactions should have a - but they have a +. The premise is, hence, unclear. By published text, I mean something published in a book or a peer-reviewed article (at least a place that has figure legends).

So, I also asked a fellow colleague and he explained it like this: a systems diagram is not constrained to involving a biotic interaction. For example, the well know positive feedback loop involving sea ice and warming, whereby warming leads to reduction in sea ice, which increases surface albedo (water is darker than ice), further warming the surface and more melting. This could be represented as [warming] -- (-) -- [sea ice] -- (-) -- [albedo] -- (+) -- [warming].

Are you thinking along the same lines?

Let us continue this discussion in chat.


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What happens when too much sodium flows in the cell due to a faulty voltage-gated sensor? What about too little?
The activation gate opens, signaling depolarization. Eventually, the inactivation gate closes, ending depolarization and beginning repolarization.

What is the physiological impact of the inactivation gate remaining open too long, letting in too much sodium into the cell than a normal action potential? This would raise the magnitude of the action potential.
What would be the impact if it remained open for too short a time?

Is this a homework question or related to studying for a course/class?

No, I'm just curious as to what happens and trying to understand the concept. If it helps I'm studying for a 'standardized test.'

To answer the OP directly: You may be interested in looking at diseases that abnormally increase or decrease the activity of sodium channel proteins, changing the degree to which sodium ions cross the cell membrane. Some diseases are genetic in basis, which means they are inherited. This lends them to characterization and study.
This review paper by George summarizes some of the genetic diseases associated with sodium channel mutations, which might give you some direction for further research:

Muscle sodium channelopathies (SCN4A)

Hyperkalemic periodic paralysis
Paramyotonia congenita
Potassium-aggravated myotonia
Painful congenital myotonia
Myasthenic syndrome
Hypokalemic periodic paralysis type 2
Malignant hyperthermia susceptibility

Cardiac sodium channelopathies (SCN5A)

Congenital long QT syndrome (Romano-Ward)
Idiopathic ventricular fibrillation (Brugada syndrome)
Isolated cardiac conduction system disease
Atrial standstill
Congenital sick sinus syndrome
Sudden infant death syndrome
Dilated cardiomyopathy, conduction disorder, arrythmia

Brain sodium channelopathies (SCN1A, SCN2A, SCN1B)

Generalized epilepsy with febrile seizures plus
Severe myoclonic epilepsy of infancy (Dravet syndrome)
Intractable childhood epilepsy with frequent generalized tonic-clonic seizures
Benign familial neonatal-infantile seizures

Peripheral nerve sodium channelopathies (SCN9A)

Familial primary erythermalgia

Generally, you might search on the term "sodium channel mutant" or "mutations" to see what kinds of health problems are caused by under- or over-activity of these proteins.

This answer provides some good information about channelopathies but doesn't address the misconceptions in the OP or answer the 'what happens' question directly.

Thank you for the links... as for the misconceptions... that's why I'm here!


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Maximum recombination frequency
During the process of crossing over, Why is the maximum possible recombination frequency between two genes equal to 50% and not more than that?

Statistically, this is that the maximum mean recombination frequency is 50%.
Recombination defined this way means that Gene A and Gene B from one chromosome are not 'together' on the same chromosome after recombination. That means that the recombination frequency is the probability of an odd number of recombination events between the loci. If there is an even number of recombination events, Gene A and Gene B end up back together again (with some rearrangement between them).
Recombination events can be modeled by a Poisson distribution: that is, recombination events are discrete (you either get an event or you don't) and they don't depend on each other. The rate can be expressed in terms of base pairs, e.g. "mean number of recombinations per base pair" or "mean number of recombinations for 'distance' X."
The probability of getting an "odd" result from a Poisson distribution is always <0.5. See for example this Q&A from Math.SE.
Spoken in plain language, let's start from two loci that are very close where the recombination rate is very low. In most cases, then, we get 0 recombination events so the genes stay together. Now, as we increase the distance, we will get more cases where 1 event occurs. However, as we increase the distance further, we will also start to get cases where 2 events occur. 2 events has the same end result as 0 events: the genes stay together. It turns out mathematically that there is no rate that you can choose where the number of "1"s is more than the combined number of "0"s and "2"s; therefore, the frequency must be <0.5, but will approach 0.5 as the rate approaches infinity. If this doesn't seem intuitive, check the math from Math.SE!


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Detrimental effects of fructose in fruit on the liver?
Fructose is mostly broken down by the liver. During this breakdown, the liver also creates fats (by the process of lipogenesis) which over time can get accumulated in the liver and give rise to nonalcoholic fatty liver disease.
Now, fruits contain fructose. So, here is my question: "Will eating lots of fruit lead to fatty liver disease?" If yes, how much fruit consumption is too much? If no, why not? What about lipogenesis, then?
I got the above information from this article by Harvard Medical School.

Moderation in all things, and all things in moderation.

There is insufficient evidence to claim that high consumption of fructose, when part of isocaloric diet (no weight gain), is a risk factor for non-alcoholic fatty liver disease (NAFLD).
Fructose Consumption, Lipogenesis, and Non-Alcoholic Fatty Liver Disease (PubMed, 2017):

...the available evidence from human epidemiological and
  interventional studies does not support the hypothesis that
  fructose, when consumed in isocaloric amounts, causes more liver fat
  accumulation than other energy-dense nutrients. The observed
  prosteatotic effect of fructose in hypercaloric trials is likely
  confounded by associated weight gain...

Effect of fructose on markers of non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of controlled feeding trials (PubMed, 2014):

Isocaloric exchange of fructose for other carbohydrates does not
  induce NAFLD changes in healthy participants.

Consumption of fruits, if part of isocaloric diet, is also not likely associated with NAFLD.
No association between fruits or vegetables and non-alcoholic fatty liver disease in middle-aged men and women (PubMed, 2019):

No obesity-independent association was found between fruit or
  vegetable intake and NAFLD.

The main source of dietary fructose are probably soft drinks, not fruits, anyway:

Popular soft drinks can contain 60-70 g fructose per liter (ScienceDirect, Fig. 2).
Four apples (150 g each) contain 36 g fructose, which is more than in most other fruits (USDA.gov).

And finally, even if there is abundant evidence that fructose stimulates lipogenesis in the liver, this does not automatically mean that it stimulates the development of NAFLD (according to the first source above).

There is sufficient evidence to apply the precautionary principle, however.


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Is a flower having 12 petals trimerous or tetramerous?
Suppose if a flower has 12 petals. Then 12 is a multiple of both 3 and 4. So which category of flower is it? Is it trimerous or tetramerous?

Suppose if a flower has 12 petals. Then 12 is a multiple of both 3 and 4. So which category of flower is it? Is it trimerous or tetramerous?

Merosity, in the context of your question, is the number of petals in the corolla.
Refer to "Gray's Botanical Textbook: Structural botany", on page 176, section 322:

"322. To designate the particular plan, such familiar terms of Latin derivation as binary, ternary, quaternary, quinary, unary, &c., are sometimes employed, denoting that the parts of the flower are in twos, threes, fours, fives, or sixes. More technical and precise terms, equivalent to these, are composed of the Greek numerals prefixed to the word meaning parts or members, as Alonomerous, for the case of a flower of one member of each ; Dimerous, of two, or on the plan of two members of each ; Trimerous, of three, or on the plan of three members ; Tetramerous, of four, or on the quaternary plan ; Pentamerous, of five, or on the quinary plan ; Ilexamerous,$^{[1]}$ of six, or on the plan of six members to each circle. But, in Monocotyledons, so-called hexamerous blossoms are really trimerous, the sixes being double sets of three.
[1] These may be shortly written 1-merous, 2-merous, 3-merous, and so on up to 10-merous (decamerous), 12-merous (dodecamerous), &c.".

Because counting is done using Greek cardinals a corolla with 12 petals is dodecamerous. One with 4 sets of 3 is trimerous, and one with 3 sets of 4 is tetramerous.


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How can I learn biology by myself?
I am only 15 years old,and my primary school education hasn't been that good,also I forgot a lot of things. I would like to start again,and I am asking for your advice. What are some of the good websites/books/methods that can help me?

I'd look into MOOCs on a site like edX. These courses are recorded by talented and engaging professors and are often available for free (at edX you only need to pay to get a certificate of completion, not to take the course)

There is a game on google where you type 2-3 unlikely words like " silver microbiology horn" and " indigo evolution chemical" and "photosynthesis cell jogging" see what information arises. Wikipedia is good for the main biology course: mitochondria, microbiology, photosynthesis, gametes, recessive, inheritance, all that kind of thing.Read what you are interested in, cell biology, zoology, biomimetics, nature magazine,  paleobiology...

Khan Academy...


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What is a secretion target family protein?
I came across this link: https://www.genome.jp/dbget-bin/www_bget?btw:BF38_3398
What is this protein, is it a secreted effector protein or is it something else?
What is the difference between type VII secretion protein (https://www.genome.jp/dbget-bin/www_bget?sams:NI36_12950) and type VII secretion effector (https://www.genome.jp/dbget-bin/www_bget?bmyo:BG05_3891)?

Have you followed up the links you get from an internet search for type VII secretion? I know nothing about the topic, which sounds quite specialized, but reckon I could hack it in a quarter of an hour. Or is the problem journal access?

@David yes I have tried to find the difference between the two types of proteins but could not find any proper explanation....


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Why "Having chlorophyll without photosynthesis is actually very dangerous" and "like living with a bomb"?
The Phys.org article Scientists discover first organism with chlorophyll genes that doesn't photosynthesize says

"For the first time scientists have found an organism that can produce chlorophyll but does not engage in photosynthesis.

It is referring to the new paper in Nature A widespread coral-infecting apicomplexan with chlorophyll biosynthesis genes (paywalled).

"This is the second most abundant cohabitant of coral on the planet and it hasn't been seen until now," says Patrick Keeling, a University of British Columbia botanist and senior researcher overseeing the study published in Nature. "This organism poses completely new biochemical questions. It looks like a parasite, and it's definitely not photosynthetic. But it still makes chlorophyll."
[...]
Chlorophyll is the green pigment found in plants and algae that allows them to absorb energy from sunlight during photosynthesis.
"Having chlorophyll without photosynthesis is actually very dangerous because chlorophyll is very good at capturing energy, but without photosynthesis to release the energy slowly it is like living with a bomb in your cells," Keeling says.

Question: Why is it that "Having chlorophyll without photosynthesis is actually very dangerous" and "like living with a bomb"?

While I lack detailed knowledge of this organism's internal structure, it's plausible that since it is still carrying out photocapture and acid pump that the acid pump directly powers ATP synthesis like it would normally do in mitochondria. It would take a link between the plastids and the mitochondira to do, but that's not ridiciulously implausible.

It is important to note, at least from my understanding of the article, that the organism doesn't actually produce chlorophyll; it merely has the genes to do so, but they seem to be inactive.

They're referring to the fact that a bomb can release a lot of energy under the right circumstances.

Chlorophyll absorbs photons (light). The energy in the photon extracts an electron from a molecule of water. Electron transfer creates intermediate superoxide and hydroxyl radicals from the oxygen and hydrogen from the donor water molecule.
In normal photosynthesis, these radicals are quickly used to power the reduction of NADP to NADPH and the synthesis of ATP from ADP. NADPH and ATP in turn power the synthesis of sugars from carbon dioxide and water, via the Calvin cycle.
These radicals are highly reactive. If they hang around and don't get used properly in redox reactions, they will just as happily attack DNA, proteins, and structural lipids within the cell, and are therefore dangerous. In normal plant cells that get too much sun, for instance, free radicals can build up and cause cell damage.
My guess is that the author's "bomb" is made up of higher concentrations of these radicals within a cell with no apparent machinery to perform the downstream (photosynthetic) chemical reactions needed to consume them safely.
Edit
I skimmed the (sadly, paywalled) paper, and it sounds like my guess was right, that it is indeed these radicals that are the danger from having chlorophyll, with no light-independent (Calvin cycle) mediated reactions to safely consume the energy in them:

Chlorophyll itself has no natural biological function outside of
  photosynthesis, so if photosystems are indeed absent, corallicolids
  must have evolved a novel use for either chlorophyll or its closely
  related precursors or derivatives. However, these molecules generally
  function in light harvesting, which would be destructive to cellular
  integrity without the coupling of the resulting high-energy compounds
  to photosynthesis. Other possibilities are functions in light sensing,
  photo-quenching or the regulation of haem synthesis, but these too
  leave open the question of what the cell would do with the highenergy end products.

What's not clear to me is that the genes that help generate chlorophyll are expressed, but the cells are unpigmented. I don't see any explanation where the chlorophyll and associated proteins are localized in the cell — seems like a missing part of the paper, or I missed that part when skimming. Or perhaps the organism has evolved interesting and novel ways to manage the damage caused by these oxygen radicals, or has other mechanisms for consuming them, yet to be identified.
Should motivate further research, especially if these organisms share ancestry with malaria and toxoplasmosis — there might be something interesting to learn that would help with eliminating these diseases. I imagine a biochemical "radical bomb" could be very handy for destroying parasites, if there was a way to expose them to light or some other source of photons; perhaps some drug therapies could target the relevant genes and induce the parasite to destroy itself. Interesting paper.

I see what you mean, thanks! So maybe the "bomb" analogy isn't fitting, but this certainly sounds like the situation could be potentially dangerous.

It would be great if you could provide some references.

"It transfers the energy of a photon as an electron to a molecule of water". I believe that's the electron-transport chain you're thinking of. The end-product of photosynthesis is glucose AFAIK.

Chlorophyll (and more commonly porphyrins) are in fact used to kill cells by light exposure in photodynamic therapy (Song et al., 2014)

Is this the main reason why plants get 'burnt' by too much sun?

@elzell I would say that's usual dehydration/UV induced damage. Usually chlorophyll synthesis is regulated and there are anti-oxidants to prevent oxidative damage. Note that excessive sunlight also burns animals.

Well now this just leaves me wondering if these organisms are doing anything with this chlorophyll.  Are they just in some really weird evolutionary niche where they manage to produce chlorophyll they don't need, without it being a large enough burden to stop the species from surviving?

@JMac it seems unlikely to me that its doing literally nothing (especially given how other members of the family have lost the genes for chlorophyll), but biology seems to constantly find weird uses for things. Maybe the free radicals fend off bacteria/viruses or something...

@user1136 most microorganisms are nearly completely transparent to visible light. Deliberately absorbing light via chlorophyll seems unlikely to have a protective effect.

@user1136 Dunaliella is photosynthetic (using chlorophyll), and beta-carotene has a known role in preventing the generation of reaction oxygen from chlorophyll: ref I strongly suspect its that role which is protecting Dunaliella, and not because it is absorbing light. If you lack a photosynthetic system (like the organism in the OP), I struggle to see how absorbing more energy could ever be protective, compared to letting it pass through.

@user1136 see here for general information. Or to quote directly: "In oxygenic photosynthetic organisms, chlorophyll triplets are harmful excited states readily reacting with molecular oxygen to yield the reactive oxygen species (ROS) singlet oxygen. " ref. There is no electron involved, the triplet chlorophyll transfers energy and excites the oxygen, making it reactive and destructive to cells. Beta-carotene quenches excited chlorophyll before this happens and thus protects the cell.

@user1136 I am not sure what article you are referring to but the article I quoted in my last comment directly states "Carotenoids have a photoprotective role in photosynthetic membranes by
preventing photoxidative damage through quenching of chlorophyll singlets and triplets"

@AlexReynolds Your edits are great but I was hoping for a source that says that accumulation of chlorophyll without the other photosynthetic machinery actually increases the cell mortality by induction of ROS. Your theory is quite pertinent but suitable references would be perfect. Your answer is great so I don't want to add another one. Some papers on photodynamic therapy might have a good lead if specific papers on chlorophyll induced toxicity are not there.

Alex Reynolds has explained why “Having chlorophyll without photosynthesis is actually very dangerous”, but I think that the original sensational statement by Phys.org is unhelpful as it distracts from the real question. However that’s what you get with so-called ‘free’ journalism.
Obviously organisms don’t synthesize complex molecules without a reason. If the corals don’t perform photosynthesis, they use the high-energy electrons produced from the light photons for something else. To quote from the paper:

Chlorophyll itself has no natural biological function outside of photosynthesis, so if photosystems are indeed absent, corallicolids must have evolved a novel use for either chlorophyll or its closely related precursors or derivatives. However, these molecules generally function in light harvesting, which would be destructive to cellular integrity without the coupling of the resulting high-energy compounds to photosynthesis. Other possibilities are functions in light sensing, photo-quenching or the regulation of haem synthesis, but these too leave open the question of what the cell would do with the high- energy end products. Moreover, we detected corallicolids in sun coral (Tubastrea sp.) and black coral (order Antipatharia), both of which are considered to be non-photosynthetic corals, which further suggests that corallicolids deviate from classical modes of light harvesting.

The interesting question is what they use it for. Bombs are for writers that don’t do biochemistry.

You probably didn't notice but the article is directly quoting one of the authors. The reference to "bomb" is in quotation marks, with the author's name following immediately. Your bone to pick is with the author himself, not with Phys.org or "free journalism" (which it isn't, Phys.org has advertisements). I also felt it was strange that an author of the paper would use this wording, You may want to fix this glaring error in the beginning of your otherwise helpful answer. Thanks!

(-1) because first and final sentences are inaccurate and should be corrected. You're claiming that the author of the Nature paper doesn't do biochemistry. Yikes!

"Obviously organisms don’t synthesize complex molecules without a reason." I don't see this as obvious; vestigial structures are a counterexample. The reason could simply be random chance that hasn't been selected against.

@user1136 that's an interesting editorial. The paragraph immediately before the one to which you refer also has significance here with respect to this organism producing but not using chlorophyl; "...or indeed the very presence, of a protein may be very significant or totally irrelevant depending on whether it is following a ‘don’t care’ condition."

@Bob Certainly in general you are correct, but in this specific case the evidence is suggestive of selection.

Although you pose an interesting question ("what they use it for"), you don't really answer uhohs' question. And your spike remarks are redundant IMHO.


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Ink blue molds/fungi/dermatophytes
Which of the above has naturally ink blue hyphae? Are there any that make both Ochratoxin A and fumononis toxin and have hyphae that color?

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

I have chased down all research articles thatI can find. I know know there are about 10 Aspergillus Niger subspecies, some used in industry that have this ability. I can’t find references to their specific names and no descriptions or images. Thus, I don’t know what they are named or what they look like. There also may be a remote chance that there are dermatophytes that do the same. I was hoping someone familiar with the specialized nature of these organisms might remember some obscure facts they might have stumbled on or someone who is researching these for possible industry use might know.


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What do we call these containers used in biotechnology?
I'm translating an autoclave instruction from Russian, and it says that these containers (ванночки) (see the black circle on the below photo) are to be sterilized in the autoclave. I'm not sure what they are called in English-language biotech texts.
The Russian text uses the vague term "ванночки", literally "little bathtubs". Maybe just "containers"?

That would be a Reagent Reservoir, or just a Reservoir. These tall and narrow ones are specifically designed for use with a robot, but there are also shorter and wider ones for manual pipettes:

120 mL Reagent Reservoirs


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How are the first mammary glands thought to have functioned?
I happened upon a book (not about biology) containing this text:

A life-changing birth occurred on the planet about 190 million years ago [...] the first tiny shrew like creature brought forth an infant and began suckling her young. [...] this furry little mammal embodied a huge leap in biological evolution

The description is nicely dramatic, but it doesn't ring true for me. While I know that evolution likely wasn't as gradual as high school books represent it, the thought that a non-mammal bore a daughter with fully functional mammary glands who actively suckled her young is a bit too much for me to swallow. For other body systems, I have read stories how they emerged gradually, for example the oldest species having a few nerve cells, then new ones having a whole nervous "network" with a few ganglions, before actual brains emerged. Or similarly, worms having a patch of photosensitive cells on the skin evolved into animals with eyes. I know that platypuses have mammary glands without nipples, but presumably even they are already much more sophisticated than the first mammary glands.
So what are proto-mammary glands thought to have been like? Did they evolve de novo especially for feeding babies, or were they maybe repurposed sweat glands or something like that? What are they supposed to have functioned like?

the production of liquids to nourish offspring has evolved separately in several lineages, mammals have simply taken it further than any other group. it is pretty easy to see how it could evolve, any way of providing even trace nutrients or nourishment to young will have an advantage in organisms that are already engaged in child rearing. it means exposing the young to predators less often.
Mammary glands are modified sweat glands.
Monotremes do not have nipples what they have is a cluster of mammary glands on a patch of skin. the young have to suck the milk of the a cluster of hair.
The exact sequence of how lactation evolved is not well known since lactation leaves no fossil evidence.

Sources:
Lefèvre, C.M., Sharp, J.A. and Nicholas, K.R., 2010. Evolution of lactation: ancient origin and extreme adaptations of the lactation system. Annual review of genomics and human genetics, 11, pp.219-238.
Capuco, A.V. and Akers, R.M., 2009. The origin and evolution of lactation. Journal of Biology, 8(4), p.37.


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The truth behind human urine and marking territory?
So some years ago, I remember watching a survival show in which the host said that human males produce a type of chemical in the urine that animals such as wolves can acknowledge as a territory marker. The host also said that women do not produce it, and therefore cannot mark territory in the same way men can.
Would this be accurate? Would the results of this change at all if the individual was a fully transitioned transgender person?


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Lysosomal Storage Disease
In my biochemistry class today we did a problem detailing two lysosomal storage diseases.
In the first scenario, a cell line for I-cell disease can synthesize lysosomal hydrolases that are perfectly functional which are then secreted outside of the cell instead of being sort to the lysosome. However there is a mutation that inhibits the the kinase domain that normally phosphorylates Mannose-6-Phosphate (M6P), so there is no M6P-labeling in these cells.
In the second scenario, a cell line for Hurler's disease has a mutation that eliminates one lysosomal glycosidase so that it cannot degradte certain classes of oligosaccharides. This results in the cells of this mutant cell line to have engorged / bloated lysosomes.
Now when these two cell lines are co-cultured in the same flask, it is observed the I-cell culture correctys the defect in the Hurler cell culture, while the Hurler cell culture was not able to correct the defect in the I-cell culture.
My question is how can this phenomenon be explain? And why are the Hurler cells still growing?

While you explained the problem quite well, please note that homework questions are considered off-topic on this site unless you show your own effort in solving the question (Please edit your question instead of just commenting).

I-cells produce the normal functional lysosomal hydrolases, however they are secreted outside of the lysosome.
The Hurler cells lack a functional lysosomal hydrolase to degrade the certain oligosaccharides.
When the two cell lines are mixed together in the same media, through non-specific endocytosis, the Hurler cells will simply arbitrarily want to endocytose things such as nutrients from the media into the cell, and some of the times, the Hurler cells may endocytose the functional enzymes secreted outside of the extracellular matrix / membrane from the I-cell.
Thus, the Hurler cell's lysosomal contents can then be degraded to some extend and restore the defect exhibited in normal Hurler Cells.


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What is the origin of plasmids?
As I understand it, plasmids, like mitochondria, have their own genetic material and are capable of self-replication.
According to Wikipedia: Plasmids are considered replicons, units of DNA capable of replicating autonomously within a suitable host. However, like viruses, they are not classified as life. Plasmids are transmitted from one bacterium to another through conjugation. Unlike viruses, plasmids are "naked" DNA. However, some classes of plasmids encode the conjugative "sex" pilus necessary for their own transfer.
My understanding of that is that a bacteria gets their plasmids not because of the replication of their circular chromosome, nor because that chromosome have genes to code for the plasmid (I don't really know if that's possible), but because of the self-replication of their own plasmids.
So, my question is how the first plasmid got into the first bacteria, if they are not in their chromosomes? Were they a virus other prokaryotic cell that had circular DNA, and got phagocytosed by that bacteria ?

Do you mean plastids? Becaue otherwise I get a feeling you don't seem to understand what a plasmid actually is: a piece of (circular) DNA. Also note that the human genome does contain a majority of the genes that are needed for / originate from mitochondria.

@Nicolai, I really meant Plasmids, see if the explanation is better now.


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16S rRNA and 5S rRNA datasets
I need 16S rRNA and 5S rRNA (Gammaproteobacteria - E.coli) Secondary structure files in ct format.
I tried looking for them in different RNA databases, could not find one. Can someone tell me where to find such datasets?
Thanks in advance.

This site has secondary structure maps for rRNA from different organisms but they are just pictures. Not sure if it is helpful.

Thanks. But I was looking for the secondary structure files in ct format. I found it in RNA STRAND v2.0, please check the answer below.

RNA STRAND v2.0 - The RNA secondary STRucture and statistical ANalysis Database
http://www.rnasoft.ca/strand/
16S rRNA: secondary structure file in ct format
http://www.rnasoft.ca/strand/show_file.php?format=CT&molecule_ID=CRW_00111&check_out_the=View+the+RNA+sequence+and+secondary+structure+for+molecule+CRW_00111
5S rRNA: secondary structure file in ct format
http://www.rnasoft.ca/strand/show_file.php?format=CT&molecule_ID=CRW_00573&check_out_the=View+the+RNA+sequence+and+secondary+structure+for+molecule+CRW_00573


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Reference request: Lipid composition in bacterial, yeast and human membranes
I would like to know about the lipid composition of different kinds of cellular membranes. I remember going through such a table once in a paper, but I am unable to find it anymore. What I am looking for is a kind of tabular data which shows the percentage of phosphocholines, cholesterol, sphingolipids and other kinds of lipids organism-wise (and if possible tissue/organ/organelle wise wherever applicable).
So please share the papers/links/books etc where I may find this information. Thank you.


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Is coral photosynthesis dependant on the wavelength or frequency of light?
When buying a light fixture for a marine fish tank, it is often sold with some technical data reguarding the spectral output of the light, with a peak in the blue region of visible light, somewhere around 430 to 460nm in air.
As light enters the water with a refractive index of approximately 1.33, the peak wavelength will reduce, but the frequency of light will remain constant. So, for example, a monochromatic light with wavelength 460nm in air would have a wavelength in water of about 345nm, but the frequency is the same. Physics so far, so here comes the biology question....chlorophyll a and b have peak responses between 400-500nm light, so is it the wavelength of light in water that is important to photosynthesis, or is it actually the frequency(therefore the photon energy) that is what counts?
If we were to discover a purely theoretical new plant that grew equally well in air or water, and discovered that photosynthesis only occurred at 650nm wavelength light in air, and not at all to any other wavelength. Then we place this plant in water indoors in the dark and shine a monochromatic 650nm light source at if from air, into the water,  would photosynthesis still take place because the photon energy is the same in water or air (e = hf). Or would we need to shine a monochromatic light source of approx 865nm in air, which would reduce to 650nm in water (865/1.33)? I suspect the answer is that photsynthesis is dependent on the photon energy not wavelength, but I am far from sure about this!

Its is my hunch that it is the photon energy/frequency that counts not wavelength in much the same way our eyesight works with colours, but i would like to see it confirmed either way. I often wonder if artificial lighting for plant growth should be aimed more towards replicating natural sunlight (there is a Japanese company doing just this), especially regarding corals from shallow waters or propagated frags from tanks where some red light still makes it through the first few metres of water. Still I am interested to know what drives photosynthesis specifically underwater.

Short answer: Coral doesn't need the light, it's the zooxanthellae that is symbiotic with some corals that relies on light to grow; it adapts to the frequency spectrum available at the depth the particular coral grows, full spectrum at shallow depths and at over ~30m the zooxanthellae relies on blue light because other frequencies are absorbed by water.
Some species of coral, such as Lophelia pertusa, grow in water so deep that there is too little light for them to rely on zooxanthellae, instead their polyps gather food directly with their tentacles, feeding heterotrophically.
There are even instances of coral feeding on jellyfish, see: "Opportunistic feeding by the fungiid coral Fungia scruposa on the moon jellyfish Aurelia aurita" (May 21 2009), by A. Alamaru, O. Bronstein, G. Dishon and Y. Loya
Longer answer:
The physics portion of your question is best answered on our Physics.SE site's question: "Why doesn't the frequency of light change during refraction?"
Light's wavelength and frequency are related to each other based on a mathematical formula, it's the intensity that is affected by passing through a medium; different materials will attenuate some frequencies more than others. Water doesn't transpose light's frequency or wavelength as much as it absorbs (filters) the frequencies of light affecting which color can penetrate deeper.

"What is a light wave?
Light is a disturbance of electric and magnetic fields that travels in the form of a wave. Imagine throwing a pebble into a still pond and watching the circular ripples moving outward. Like those ripples, each light wave has a series of high points known as crests, where the electric field is highest, and a series of low points known as troughs, where the electric field is lowest. The wavelength is the distance between two wave crests, which is the same as the distance between two troughs. The number of wave crests that pass through a given point in one second is called the frequency, measured in units of cycles per second called Hertz. The speed of the light wave equals the frequency times the wavelength.".

See this other Physics.SE question: "Does light color change when refracting?":

"The color will not change. What you're not taking into account is the speed of light in the medium. It's not the same $c$ en vacuo. The frequency stays the same. What changes is that speed of light in the refracting medium and as a result wavelength.".

Here is what sunlight (natural light) looks like underwater:

Despite that fact in shallow water enough full spectrum light penetrates sufficiently, and the zooxanthellae adapts to the spectrum available, no longer requiring blue light for growth.
See: "The spectral quality of light is a key driver of photosynthesis and photoadaptation in Stylophora pistillata colonies from different depths in the Red Sea" by T. Mass, D. I. Kline, M. Roopin, C. J. Veal, S. Cohen, D. Iluz, O. Levy in the Journal of Experimental Biology 2010 213: 4084-4091; doi: 10.1242/jeb.039891

"Depth zonation on coral reefs is largely driven by the amount of downwelling, photosynthetically active radiation (PAR) that is absorbed by the symbiotic algae (zooxanthellae) of corals. The minimum light requirements of zooxanthellae are related to both the total intensity of downwelling PAR and the spectral quality of the light. Here we used Stylophora pistillata colonies collected from shallow (3 m) and deep (40 m) water; colonies were placed in a respirometer under both ambient PAR irradiance and a filter that only transmits blue light. We found that the colonies exhibited a clear difference in their photosynthetic rates when illuminated under PAR and filtered blue light, with higher photosynthetic performance when deep colonies were exposed to blue light compared with full-spectrum PAR for the same light intensity and duration. By contrast, colonies from shallow water showed the opposite trend, with higher photosynthetic performances under full-spectrum PAR than under filtered blue light. These findings are supported by the absorption spectra of corals, with deeper colonies absorbing higher energy wavelengths than the shallow colonies, with different spectral signatures.".

"Fig. 4. Percent surface irradiance received of different wavelengths at 3 m (grey) and 40 m (black) depth in the waters adjacent to the Interuniversity Institute for Marine Sciences, Eilat, Israel, on 3 April 2008.".

So if you deep dive for your own coral you should be aware that it will thrive under blue light. If you obtain shallow water coral, or buy from the local aquarium supply store, white light is suitable.
Also from: "The spectral quality of light is a key driver of photosynthesis and photoadaptation in Stylophora pistillata colonies from different depths in the Red Sea", (full info above):

"Studies in the Caribbean have found that other corals that are found along a broad depth gradient switch from hosting clade A or B zooxanthellae in shallow water to clade C in deeper water, possibly owing to the ability of the different clades to adapt to different light levels (Rowan and Knowlton, 1995; Baker et al., 1997).".

Hi Rob. Thanks for the detailed answer. I'm not sure it answers my actual question though. I have a physics degree, I understand electromagnetic radiation, so my question was not about physics. I understand that light will be scattered, reflected, absorbed in different ways in water. I also understand that it is the zooxanthellae that photosynthesize. I am not a biologist though, so,  very specifically my question is this - is photosynthesis dependant on wavelength or frequency, baring in mind the wavelength changes in water, and the frequency doesn't (and therefore photon energy)?

@Justanengineer Is this answer more helpful, that is the frequency or wavelength in a vacuum, depending if you want to measure in THz or nm. Moving from space to air, glass or water affects the wavelength because the medium is changed, it affects the diffraction and filters which frequencies can pass more freely than others but it doesn't alter the frequency, the color, of the light by transposition. Changing the speed of light by passing through water only affects the wavelength.

Hi Rob, all the information you have provided is great, although I feel i already have a good grasp on the physics of this question. Its the biology i need to learn about! I understand refractive index, downwelling irradiance from the sun, the filtering of different wavelengths of light dependent on water depth. Its the biology of photosynthesis i do not understand. It seems to me that it would be more helpful to measure solar irradiance in THz or electron volts, as this does not change in different media. I need to rephrase my question I think somehow....

Maybe a better way to phrase this question is: "Is it accurate to say that photosynthesis occurs under light irrandiance of frequency 430-770THz, regardless of the refractive index of the medium it takes place in, and therefore regardless of the measured wavelength in that medium"?

Am I on the right track here...1.82ev is needed to activate the chlorophyll complex p680, which drives photosystem 2 at the start of the light dependent reactions and is needed to oxidize h20. So when we think of light for photosynthesis, we should think in terms of electron volts required for redox reactions? Can anyone point out my beginner mistakes or point me towards some further reading?

Ok I apologise for upsetting you but it IS still the same question it always was. Is coral photosynthesis dependent on the wavelength or frequency of light? That is all. That is the title question and the only question I am asking and it hasn't actually been answered. The scope has not expanded in any way the question still stands. All the rest is background because I was finding it hard to clearly ask the right question, so I tried to give it context. Its my first post here, so in future I will just ask a very straight question and see what comes back.

If you deep dive for your own coral it will want bluer light, as will some non-aclimatized coral (which a reputable aquarium supply store won't sell a beginner. --- I do appreciate that it is difficult to 'ask the right question' or figure out what it is you want to ask. I have to assume that you've done some initial research and that upon reading your question that either I can answer it or I can not. --- You don't want to worry about electron volts, just don't buy to big a light for your tank. You don't want your coral and plants to grow like crazy unless you are trying to sell them.

Hi Rob. Thanks for all your input it's really useful. The fault is mine, in that I did not know enough biology to ask the right question. I know a little more now and realise the question I needed to ask should have been very specifically about energy needed for photosynthesis to occur. I am going to put it that you have answered this question because you have given so much relevant information to a question that wasn't worded clearly enough to answer.

@Justanengineer I'll clean out my superfluous comments. If you have enough information for a different question ask and see if someone can help you here or elsewhere.

For the non-biologists,
@Rob isn't wrong about the existence of heterotrophic coral—they exist alright. But the absolute vast majority of productivity (creation of biomass), ecosystem function (e.g., facilitation of diversity, nutrient cycling, energy flow, trophic complexity), and density of corals are features of symbiotic corals. The mentioning of heterotrophic corals here doesn't seem to be relevant to the question.

@ChrisMoore There used to be another half dozen back and forths that you are missing. Currently, I'm working on something else. If you can offer a better answer we all welcome that.

@Rob I imagine more context would help. I nevertheless think it's a really good post, I would just cut the "shorter answer" section. (It's more of a digression than a short answer.) Everything after that is apt and relevant. I'll edit it.

Yes, coral photosynthesis and growth (actually, Symbiodinium symbiont photosynthesis) is dependent upon the spectra of light provided.
Each photosynthetic organism has a characteristic 'action spectrum' which is the photosynthetic rate (Y axis) plotted vs. the wavelength of light (X axis).
Or, we could plot an action spectrum for growth, which is a step removed from photosynthesis.
Either way the action spectrum is a product of:
-absorbance of light at a given wavelength
-yield of conversion of absorbed light to achieved photosynthesis (or growth), at a given wavelength.
-second order effects related to the complex propagation and scattering of light through tissue or coral matrix
For any oxygenic photosynthesis the action spectrum is going to include absorbance by chlorophyll a (peaks at ~440 nm and at ~680 nm), but will be modified by other secondary pigments.
http://jeb.biologists.org/content/206/22/4041
Fig. 6, rough action spectra.
Some methodologies.
https://www.advancedaquarist.com/2014/5/aafeature
The situation is complicated because:
-some wavelengths (short blue, ~420 nm) can drive photosynthesis but also drive photoinactivation of photosynthesis more so than longer wavelengths. This can lead to cumulative light stress, depending upon the absolute level of light, the duration of illumination and the wavelength.
-corals 'use' light for many things other than photosynthesis and these regulatory and signalling functions can be disrupted if the spectrum or duration of light is not appropriate.
-different corals will have different requirements.
Long answer, tough question, still a research topic.


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What the name of this fish?
Well saw this on a fish group on facebook. Noone can give a decent answer so I came to you guys hoping you can help us? The one who posted lives in the Philippines and he said he caught it in the river that is somewhat connected to sea.

This fish called neon velvet damsel fish (Neoglyphidodon oxyodon)
Check wikipedia

I don't think this is right. The asker's fish has a brown tail, no golden spot/stripe on its back and very different "fluoro" markings. The asker's fish was caught in a river but yours lives in the sea.

@DavidRicherby maybe if the asker added many pictures from different sides, I can see the blue color under the fish eyes which says everything ..

There's only one photo available and it already shows significant differences from your suggestion. Having more photographs of the unknown fish can't make it look more like a neon velvet damselfish.


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How does (action potential) hyper-polarisation work?
I understand that after depolarisation, repolarisation and then hyperpolarisaiton occurs and that an area in hyperpolarisation is in its "refractory period".
Why does this prevent Na+ ions diffusing "backwards"? Since an area of the neurone membrane in hyperpolarisation will have a very negative charge so surely positive Na+ ions would diffuse towards them rather than away from them - "forward".
Similarly, why does this prevent another action potential firing too soon?
(I know this is kind of 2 questions in one, but as they are so very related I thought it more prudent to combine them).

Possible duplicate of: https://biology.stackexchange.com/questions/56621/why-does-the-refractory-period-of-neurons-only-allow-signals-to-pass-in-one-dire

Yes, that answer kind of answers my first part of my question (about being uni-directional) but doesn't answer the part about another ap firing too soon. Although I see why you might think it's a duplicate :)

I'll borrow a diagram from another answer to a similar question, but not quite a duplicate (I hope @AliceD won't mind my laziness):

Fig. 1. Refractoriness. source: University of British Columbia
One important concept to understand about the refractory period is that it has two components. One is the hyperpolarizing part, which is due to open voltage-gated potassium channels. Because there is more potassium conductance than at rest, the membrane voltage gets closer to the reversal potential for potassium.
If you were to open a sodium conductance during this period, you would indeed get a larger sodium current than you would get at rest (because you are further from the sodium reversal potential), however it will also be accompanied by potassium leaving the cell (because there is more potassium conductance), such that the net current and net change in voltage may not be much larger than at rest. Voltage-gated sodium channels that open to cause an action potential are gated by voltage, not by sodium. However, this type of refractory period is referred to as a relative refractory period because you can overcome it if you open a large enough sodium conductance (or inject a bunch of current with a patch clamp amplifier).
However, there is also a second part to the refractory period, the "absolute" part, which is shown in the diagram above. The voltage gated sodium channels themselves are not only closed but they are also inactivated. While inactivated, those channels will not open even in response to depolarizing voltage. It takes some time for the channels to return to the 'closed' state where they can be opened by voltage.
Summary
To speak to your question more directly, nothing prevents sodium from diffusing 'backwards', but action potentials travel quickly, sodium channel inactivation prevents them from traveling into axon segments where the sodium channels were just recently open, and the open potassium channels that cause hyperpolarization will 'shunt' current out of the cell while they remain open. Lastly, voltage-gated sodium channels are gated by voltage, not sodium.

"or inject a bunch of current with a patch clamp amplifier" --> Current is the flow of electrons, would hence current injection not make the membrane more negative (and make it hence harder for sodium channels to open)?

@Pugl The convention is to refer to positive charge as positive current. In neuroscience, it is not in fact electrons that are moving but ions of positive or negative charge. You can hyperpolarize or depolarize a cell freely when you have access to a cell via patch clamp, it doesn't matter what is flowing in the circuit of the amplifier.

So, one would in fact inject cations (= positive current) for instance to depolarize a cell?

@Pugl Physically with an electrode it's probably more accurate to say you are attracting electrons/anions towards the cathode but it really doesn't matter mathematically.


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Can sperm cells penetrate the cell membrane of non-ovum cells?
Sperm cells have tiny bags of enzymes on their tip (the acrosome) which allow them to penetrate the ovum. My question is whether or not the process that allows sperm cells to penetrate the cell membrane is specific to ova, or if it allows them to penetrate other types of cells.
In either case, a quick description of the process would be greatly appreciated!

I was about to ask this question. I just bought a microscope and of course I was looking at my sperm, what intrigued me (even though I have little knowledge on biology) is that I saw a sperm cell incide a another [what looked like] another cell, from my own semen. (Took pictures and recorded with my cellphone!).

It is very possible that the specific enzymes that penetrate the cells can be used to lyse other cells or at least manipulate the plasma membrane. That being said, I don't think that sperm cells can be used to do that because the acrosomal reactions that you discuss are only activated by the presence of the zona pelliculada of the egg cell. Since that doesn't exist in any other type of cell a sperm cell can't be used for Acrosomal enzyme delivery for somatic cells, for example.
If you want to read more, the Wikipedia page about the Acrosome reaction is pretty good.

Thank you for your response. The specificity of the acrosomal reactions to the zona pelliculada was the information I needed.


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Can anyone help me with these Biology evolutionary properties homework questions?
my teacher assigned these worksheet questions, they are ungraded, but he said something might come up on the test really similar to this so I really want to get all of them right. I am pretty confident with all of them except for two,
In the layer below a mass extinction that devastated the region, the paleontologist observed that shells of species A was present in small numbers over a widespread area whereas species B was abundant and found in a few restricted areas. Which of the following predictions about the fossil record in the layer above the mass extinction is the MOST likely to be supported by further excavations?
A.

Species A survived because of its widespread range including some areas that were not as affected by mass extinction.
B.

Species A survived because the low number of individuals meant that there was less competition for resources.
C.

Species B survived because it was the more abundant and more individuals survived.
D.

Species B survived because the population was concentrated in a few areas and had a higher chance of survival.
and
A scientist analyzes the vision receptor molecule in invertebrates and vertebrates. The results show that the genes for opsin, the protein part of the photoreceptor, share strong homology in the regions that code for domains involved in light response. Which of the following conclusions is the MOST likely?
A.

The receptor molecules will be structurally different but respond to the same light cues.
B.

The receptor molecule will be similar in invertebrates and vertebrates because of convergent evolution.
C.

The receptor molecules will be different because invertebrates and vertebrates perceive visual cues in different environments.
D.

The receptor molecules will be similar in invertebrates and vertebrates because they appeared early in evolution.
For the first one, I reasoned that it was most likely A, however, D caught my attention and now I am seriously doubting myself on it. This is due to the fact that the wide range of an organism might lend itself to higher survival, as some regions might better be protected or missed by harm, however, it could just as likely be D, in my opinion, as more animals might lend to quicker recuperation in any instance. For the second, I am pretty confident it is A, as homology means they come from the same source but may evolve to differ, but again, D is pretty tempting as it may be simply as it was an element that appeared early on and thus is present in both. I am only an undergrad premed, so not too savvy yet, but any help would be great.

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. See also https://biology.meta.stackexchange.com/questions/3377/homework-questions Please edit your question to have an informative title, limit your question to a single specific question, and explain the reasoning behind your answer attempts rather than just your guesses and confidence. It would also be better to phrase your question as a conceptual question rather than multiple choice.

Thank you for the reply, I explained my reasoning further and updated my title. But I didn't see anything about asking one single question in your links, thank you very much for them by the way, I am not being rude! I will totally cut it down if necessary

We really don't answer homework questions, as @BryanKrause stated very politely. Our goal, ado, is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :)  I was about to close vote, but it's better after the edit.

Thanks for taking the time to reply :) I totally understand that, I can add more to my question, I really want to completely grasp the topic, or I can rewrite it completely if you guys think that would be best. I would ask my prof but I wont be able to until a little while.

Your two questions are unrelated (other than the fact that both of them are parts of your homework). Therefore I am voting to close your question as broad. Your edit is good enough to make the question on-topic. I recommend that you ask two separate questions and rephrase your question titles accordingly.

The first question is poorly designed the only things with a high chance of surviving mass extinctions are organisms that occur in large numbers over a wide range of environments, without more detail neither A nor B would have a strong preference for survival compared to the other. Mass extinctions are too unpredictable, neither by itself gives you a large advantage.
It really depends on how they define terms the only organisms that occur over a truly wide range of environments that is both marine and terrestrial ones are tiny and thus have huge population numbers. the more localized the measure of widespread the less being widespread matters. for instance Ammonites occured in every marine environment in large numbers (so a wide range of local environments) but were completely wiped out because the ocean PH changed which hits every portion of the ocean equally.
The best you might be able to say is A might have a slight advantage because it is more of a generalists as it occurs in more environments but that use of the term "within a region" means it does not help much.
The second question is easy, if the genes are sequentially similar it is due to a common ancestor. since the sequence is part of the functional component then the ancestor likely used it for the same function, so D would be your best answer.


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Why does our body absorb toxic substances or toxic concentrations of a substance if it is capable of regulating gastrointestinal absorption?
Our gastrointestinal system is filled with regulatory molecules that place brakes in the absorption process. For instance, the food that we consume daily is filled with harmful substances that our body does not absorb, and these substances are later excreted. However, when ingesting poison or a potentially poisonous substance at high quantities our gastrointestinal system ends up absorbing these poisonous substances in sufficient quantities (if present) to kill us. Why can't these regulatory mechanisms not entirely prevent the absorption of toxic/poisonous substances that can cause us harm or death?

Is there a  specific substance you are thinking about?

regulating is not the same as control entirely, your skin is proof against many materials but DMSO or mercury pass right through it.

Yes Arsak, any pharmaceutical drug, for instance Ibuprophen. If any person ingests enough Ibuprophen,the pharmaceutical will no longer be therapeutic, as it would get absorbed in sufficient quantity to cause toxicity.

Thanks for the insight John. However, the gastrointestinal tract, contrary to the skin is under more scrutiny in terms of absorption regulation. We rarely abosrb substances through the skin, but continuously need to regulate which substances are absorbed or excreted in the gastrointestinal tract. Hence, my question. Why can't the gastrointestinal put a momentary full stop on absorption, say for 2 hours. Is it so important for continual absorption to occur that it cannot be stopped?


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What properties of the pathogens of infectious diseases make recovered individuals susceptible to the disease?
I was wondering what properties of the pathogens of infectious diseases make these diseases more prone to making recovered individuals immediately susceptible to the disease? I was thinking that with Salmonellosis, for example, there are different variants of the Salmonella type of bacteria, but I'm not sure if having more variants of a pathogen necessarily makes it more difficult for the human body to recognize these pathogens.

gonorrhea is a good example. https://mbio.asm.org/content/2/3/e00095-11


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What culturing process / experiment needs a "grid" petri dish (one with a vertical division)
You can buy petri dishes with separations in them like this:

I have studied biology and biochemistry and never come across one of these before.  What cell culturing / experiment would this be used in?
** Edit: **
Perhaps it's not cell culturing but instead used for containing different macroscopic organisms like woodlice or something?  But then I'd have thought they'd climb over the divisions.

I am not sure about 'vertical' division. But in general there is article describing use of Divided Petri Dishes

We grow plant explants on petri dishes. They grow paifully slowly, so having several on one dish is major space-saver. Howewer, I wouldnt use prefabricated divider. Drawing marker lines on the bottom is usually enough to keep track of what is what.


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How is fructose absorbed into the body
I’m finding contradicting methods of   Fructose  transfer to blood
page no 264(10)One of which saYs fructose is absorbed by simple diffusion
And another sources like this say that fructose is absorbed by facilitated diffusion
I Believe that second source is true but still which one is correct ?

Fructose is absorbed by facilitated diffusion in the small intestine by the help of transport molecules GLUT5 or GLUT2.
Sources:

https://en.wikipedia.org/wiki/Fructose
http://diabetes.diabetesjournals.org/content/54/10/3056.long

The source you've mentioned (http://ncert.nic.in/ncerts/l/kebo116.pdf), says that certain monosaccharides, such as glucose, can be absorbed by simple diffusion, but it says nothing specifically about fructose.
In fructose malabsorption, in which the transporter GLUT5 is deficient, fructose absorption can be very decreased, which suggests there is probably no additional absorption of fructose by simple diffusion (PubMed).