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Can primary tumor cells grow in 2D culture?
Is it possible to expand primary tumor cells in 2D culture? Are they adherent cells? Do you have any experience especially with culturing non-small cell lung cancer in 2D?
Thank you.

Short answer: Yes, this is possible, it is the way most (cancer) cell lines have been generated.
Long answer: Culturing cells from tumor tissues is done in labs, especially, if you don't want to rely on the often very old cultures used in the labs. Many of these where started in the 1970s and are strange in many ways, e.g. contain many chromosomes multiple times. I have routinely isolated new cell lines from melanoma tissues (mostly metastases from different organs), but the general procedure is the same for other tumors as well.
To isolate cells from a tumor, you first wash the tumor sample to get rid of the blood. Then you cut down the tumors into small pieces using a scalpell, before adding a mix of enzymes like Collagenase, Dispase and Hyaluronidase to dissolve the tissue further in order to get a single cell solution. After the incubation with the enzymes the suspension is passed through a cell strainer to remove all remaining bigger cell aggregates and tissues residues and centrifuge the cells down. They are resuspended in an appropriate medium for the cell type and seeded to an appropriate plate/flask. For our samples this was typically either a 35mm plate (or a 6 well plate, which has the same area per well) or a T25 flask. Most cells from such isolations grow adherent, but sometimes you can observe cells, which do not adhere to the surfaces.
The procedure itself is not very complicated, but needs optimization. Depending on your tissue, the enzyme cocktail can be varied, as well as the length of incubation and the incubation time in this step. Then different plate/flask surfaces can play an important role, also the medium composition.
When we started doing this work in the lab, about 1 in 10 attempts was successfull, after optimization we went up to 6-7 of 10. What is important to take into account is, that the cells change during incubation and adapt to it. This means you need to question yourself, how good of a model they can be and need to be. If you need our detailed protocol, let me know, I can post it somewhere.


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Does it make sense to make my own DNA copy (kind of backup) while I am young?
As I understand, when I am getting older DNA becomes more and more damaged in my body.
Does it make sense to make my own DNA copy (kind of backup) while I am young (38 years old or for my kids) in case that in future there will be the technology which will make possible to restore damaged DNA from this copy and make me younger?
Or it does not make sense, because original not damaged DNA always can be found in some places of my body?
If it makes sense, what is the best way to do this DNA backup? Cut a piece of hair or nails or freeze a piece of saliva?

While your DNA gets damaged, not every single cell will have the same damage.  Your consensus DNA sequence will not change.

I still did not get from your answer if it make sense to make DNA backup or not.

No, it does not make sense. When you ask: "in future there will be the technology which will make possible to restore damaged DNA from this copy and make me younger?" I can confidently say that there won't be such technology, for the following reasons.
1) DNA is only one component of your body's cells; important of course, but not really the 'master regulator' of everything about you (in fact, practically all cellular functions are performed by proteins and other molecules, not DNA). This belief (that DNA can determine every aspect of life) is called 'genetic determinism', and it is known to not hold even in trivial cases.
2) Your environment (diet, air, sun, family, friends, society, random events) plays a major role in who you are and how you age. Even if you were to repair all DNA damage as soon as it occurred (which, by the way, your cells do quite efficiently anyway), you could still not control for all there is outside of you, and thence you could not really 'rejuvenate' with the magic DNA pill. Most people tend to ignore this when fantasizing about DNA's healing powers: there is a world outside.
3) DNA is not something you drink or take as a 'medicine', not now, not in the future. The technology needed to rejuvenate all of your cells will likely not include 'DNA repair'. It might have to do more with metabolism than anything else (also, mutations occur all the time and not all of them are bad, so in fact 'repairing' DNA with your 'juvenile' DNA might not even be good long term).
4) It might make sense to freeze some of your cells for other applications (like tissue regeneration for you/your children), but it is quite expensive at the moment and usually requires a sample of your umbilical cord. I presume the technology to de-differentiate adult cells to totipotential cells is quite feasible, so in the future this application might be accessible, buy still unrelated to rejuvenation (unless there is something like 'whole body' tissue replacement).
As for the previous answer, "Your consensus DNA sequence will not change" makes no scientific sense. Your DNA sequences (of all of your cells) change all the time, and there is no 'average', or 'consensus' inside of you (the term consensus is simply a convention used in molecular biology for simplification).

Thanks for the answer. Let's think that theoretically there will be technology to recover DNA. In this assumption does it make sense to make DNA backup or original not damaged DNA always can be found somewhere in the body?

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Order of samples for RNA extraction
I want to extract RNA from various tissue samples, liver, gut etc, in different treatment groups. Due to the large amount of samples I will extract in sets. I am wondering, in reducing the potential for contamination whether it will be better to extract by tissue type or by treatment?

What you do not want to do is prep all your control samples on one day, and all your treated samples on another day, because you will not be able to separate differences caused by treatment from differences caused by batch effect.  I'd worry more about that than from cross contamination.  Since you probably aren't comparing the different tissues to each other, batch effect between tissues won't be much of a problem.  So do all your spleen samples, treated and untreated, on one day, all your kidney samples the next, etc.

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How does gene affect organs development in eukaryotic cells?
I'm totally new to biology and apologies if you find this basic. The central dogma insists that genetic information flows in this direction:

DNA -> RNA -> proteins

So far so good, it is very clear to me. The question comes here. How does this flow contributes to creating/developing organisms. I want to zoom out from molecular biology to a bigger picture of an organ.
I want somebody to tell me, how does genetic code in a zygote, results in creating organs just in secreting different proteins by different active genes?

The question is very broad and I think can only be answered in very broad terms.
Proteins have metabolic functions. They do stuff! Their actions include catalyzing metabolic reactions, transporting molecules (incl. transport through the membrane), DNA replication, response to external stimuli and many other functions. Humans synthesize almost 30,000 different proteins Muller et al. (2002). The sum of their action put into a specific environment (such as a womb for mammals) end up building up and maintaining an individual.
Let's consider for example Hox genes. From wikipedia

Hox genes, a subset of homeotic genes, are a group of related genes that control the body plan of an embryo along the head-tail axis. After the embryonic segments have formed, the Hox proteins determine the type of appendages (e.g. legs, antennae, and wings in fruit flies) or the different types of vertebrae (in humans) that will form on a segment. Hox proteins thus confer segmental identity, but do not form the actual segments themselves.

For more information, I would recommend you to have a look at an intro course to developmental biology. You might want to learn about HOX genes

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Biochemistry Question: Antibodies
I'm doing conceptual questions in preparation for a Western Blott and needed clarification on a specific question:
Is it possible/ will your Western blot work if you use a primary antibody (say generated in mice) and use a secondary antibody (generated in goats)? Would this combination still work with the western blot? At first glance, I'd say no but I'm still looking into it. Any clarification would be greatly appreciated!

It's not clear what you're asking, but a typical Western would indeed involve a primary mouse antibody and a secondary goat anti-mouse antibody; the primary would bind to your targets, the secondary would have the detector molecule attached and would bind to the primary.

As others pointed out, the question is not clear.. but yes, in general you use a primary antibody recognizing your peptide of interest, e.g. an antibody made in mouse, and then a secondary antibody recognizing your primary antibody, in this case an anti-mouse. The secondary antibody will obviously be made in a different animal than mouse (e.g. in goat), because mice cannot develop anti-mouse antibodies!
I hope I understood your question.

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Filter proteins by domain with InterProScan
I have a bunch of proteins (over 300000) in fasta format, and I want to find the ones that contain a specific domain (using a specific InterPro accession).
I can run InterPro on the proteins and get every domain they have, but with so many proteins, it will take a large amount of time, which I'm short on. I'd like to limit my search to the specific domain I'm looking for, as I assume it will be considerably faster.
Is there a way to do this with InterPro? Browsing the docs doesn't give me any hope. If InterPro isn't capable of that, would it be doable with a single database like Pfam or CDD?

1. Limit the InterPro scan to a specific database:
As you said you know the domain you are interested in so you know which database this is in then you can limit you InterPro scan to that database, which whill save a lot of time:

Then only select the database in which the domain is stored (e.g. ProSite)

2. If your domain is in the ProSite database (which it probably is) you can use
ScanProsite and limit you search to a specific domain.
You do this by going to the above link and select the last option:

Then, if you scroll a little bit down you can enter a ProSite accesion code of the domain/profile you are interested in:

3. Use PFAM scan
I have never used this before, so I don't know whether this would be faster than limiting the InterPro scan to the PFAMa database. You can of course check this out.

4. Clustering your sequences first
This will only work if your sequences look like each other. Depending on the size of the domain and the location in the sequences you can cluster all your sequences first (using for example CD-HIT). And then choose a representative sequences for each cluster and use these to subject to your analysis. For example when you know your domain is always at the end of the sequence then you trim the first part of each sequence and cluster the proteins over the whole length at 100% identity. If you then determine whether each cluster contains the domain or not (based on the representative sequence, which CD-HIT will provide you with) then you can assign these results to the sequences making up each cluster. But of course this will only reduce the search space whenever your sequences look like each other (or if parts do)

5. MOTIF search using downloaded profile or HMM
MOTIF search allows you to query against serveral database, such as PFAM, CDD, PROSITE etc. More interesting, it also allows you to specifiy your own profile or HMM.

So you can download the HMM of your desired domain from e.g. PFAM  or the domain profile from Prosite.

6. Downloading HMM and use HMMscan (or HMMER)
This was suggested by @seven11, you can search your HMM domain in the PFAM database and then use HMMscan.
Conclusion

If you are really interested in one domain. I think downloading the ProSite scan tool would be your best option. Notably, all webtools I mentioned above are available as command line tool, and that is what you need when having that amount of sequences. Back to ProSite scan, you can download this here and don't forget the README. As mentioned in the readme:
Input/Output:
  -e : specify the ID or AC of an entry in sequence-file
  -o : specify an output format : $formats_string
  -d : specify a prosite.dat file
  -p : specify a pattern or the AC of a prosite motif
  -f : specify a motif AC to scan against together with all its
       releated post-processing motifs (but show only specified
       motif hits)

You can use the -p to specify the acc of the pattern you want.
I'm quite busy so I typed this one really fast, please let me know when something is not clear.

Thanks, your answer gave me some very good pointers. I found the HMM for this domain on the Pfam site. I will run it locally using hmmscan.

Aah nice that is a good option and probably much faster as HMM shouldn't take that long @seven11

When your sequences are quite alike you can also choose to first cluster these (lets say at 100% identity over 80% over te sequence lenght) and then choose a representative for each cluster and use these to do searches with. And if your domain is always located at the end of the sequences you can only cluster at these ends and then do your searches. This will only work if your sequences are alike of course @seven11


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Cancer: computing the proliferation of DNA mutations in cancer cells
I have a question about cancer. How is it, that in a cancerogenous cell, once a specific gene changes, subsequent DNAs in cells end up exponentially acquiring more and more mutations?
Can, these mutations, for instance starting from a given, be computed?
Is there key genes, responsible for subsequent sequences of mutations in subsequent cell divisions, that are the subjects of what is targeted with drugs (to, fix, in this way, at a manageable level, the problem (and it's it possible to develop drugs that discover and target the responsible genes, ...?

This doesn't seem to be related to bioinformatics, it's more of a general biology question. You might want to ask on [biology.se] instead. One key thing you might want to consider is that in many cases, the mutation that causes cancer does so by affecting the DNA error correcting mechanisms of the cell. A classic culprit is P53.

Your assumptions are correct. There are genes that amplify mutation rate, once they get mutated/dysregulated.
Mutations in cancer are classified into different types. Each type has its own signature, which can be tracked back to its origin, since the sequence pattern is characteristic for e.g. specific enzymes or failed DNA repair.
One such mutation type is caused by e.g. APOBEC3. This enzyme usually mutates viral DNA. But cancer found a way to have APOBEC3 mutate its own genome. This increases the genetic variability of cancerous tissues and might allow them to gain new survival benefits. Jakobsdottir et al. 2022
Another enzyme that cancer is using to mutate itself is AID.
I don‘t think that drugs are used against APOBEC or AID. However, their relevance as a potential target for therapy is actively discussed (Olson 2018).


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What is the relationship between snails/slugs and clams/mussels?
Slugs and clams are both phyla in mollusca, but how can I tell which features they inherited from an ancestor? Basically, I'm curious about how excatly these organisms are related but can't find any information and do not know where to look.

The Tree of Life web Mollusc page  shows that gastropods (snails/slugs/etc.) and bivalves (clams/mussels) are two of the major groups within Mollusca:

You can click through to get more detail on the individual groups (but there isn't much more information about the defining characters, date of divergence, etc.). At the very least, these technical names for the taxa (and of the Conchifera, their parent taxon) should help you search for more information, e.g. a Google scholar search on "bivalvia gastropoda divergence", which gets to Investigation of molluscan phylogeny using large-subunit and small-subunit nuclear rRNA sequences ("scaphopods are more closely related to gastropods and cephalopods than to bivalves") or Phylogenetic relationships of annelids, molluscs, and arthropods evidenced from molecules and morphology. (You do have to be careful in reading the phylogenetic literature, as it's rapidly evolving; the latter paper is from 1996 and may well be superseded.)

There isn't that much easy information for snails and clams, They diverged 550 million years ago, and their anatomies are well studied. If it wasn't for genetic evidence perhaps not all scientists would agree that they are monophyletic.
The shell is the most obvious common feature, made of silicon (nacre/pearl) and calcium, and the next nearest animal to have a similar growing shell is which animal? a wormy thing with a shell doesnt exist AFAIK. Even the shell is different:
nacre layers in gastropods and cephalods (Nautilus) are formed by the
progressive nucleation of crystals at the top of conical stacks of
aragonite platelets and the lateral thickening and eventual coalescing
of older crystals at the base (Mutvei 1970. Wise 1970a. Wise
1970b, Erben 1972, Mutvei 1978, Nakahara et al. 1982, Wilbur
and Saleuddin 1983). In contrast, in bivalves. growing sheet nacre
has a steplike structure, and at each step, there is a gradient of
maturing crystals overlying fully formed layers (Wise 1970a. Wise
1970b).

Snails and Clams have nearly no articulations, only one major muscle as a result, the grinding and filter apparatus in both is very different, so that only leaves simple things like the heart and circulations and shell and muscle anatomy in common.
https://en.wikipedia.org/wiki/Evolution_of_molluscs
https://www.researchgate.net/publication/259355769_The_Continuing_Debate_on_Deep_Molluscan_Phylogeny_Evidence_for_Serialia_Mollusca_Monoplacophora_Polyplacophora
perhaps someone can tell you from this image of genetic distance the percentage of the genome they have in common.
https://www.researchgate.net/profile/Julia_Sigwart/publication/259355769/figure/fig2/AS:213874457485316@1428003052255/Preferred-molluscan-tree-Maximum-Likelihood-analysis-RAxML-28-hardway-of-pruned.png


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Identify the bird
Please identify the birds and tell about its details

I found this bird in Hyderabad, India

Why those downvotes?


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If senescent cells are removed by the immune system, how can they contribute to ageing?
It is said that senescent cells, also called zombie cells, can cause biological ageing.  These senescent cells are also killed by immune cells. It does not make sense as to how they cause ageing if they are removed?

Who says that senescent cells are killed by the immune system? Do you have a source for that?

Here is a review article talking about immune killing of senescent cells....Cellular senescence: Immunosurveillance and future immunotherapy  https://www.sciencedirect.com/science/article/pii/S1568163718300114

here is a link from a blog....https://www.fightaging.org/archives/2016/03/how-the-immune-system-recognizes-senescent-cells/

In an healthy individual, senescent cells are likely removed by the immune system.  However, as we age, our immune system becomes impaired and may no longer be able to kill senescent cells.  Senescent cells can then accumulate and promote age-related diseases.


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Does trapper/hunter harvest reflect abundance or community composition?
I'm working on a study where a single professional trapper removes furbearers and corvids (who the trapper is changes annually). I would suspect that the composition of the harvest would be strongly influenced by the individual's trapping style, ie. how and where they choose to set their choice of traps, as none of this is regulated. However, others argue that the harvest is reflective of species abundance and community composition. I'm having difficulty finding sources for either argument that aren't fisheries-centric. Can anyone suggest any?

It would be more reflective of relative abundance, rather than actual abundance unless you have 100% catchability.  Comparatively these concepts for furbearer traps should be similar those in fisheries related to catchability and selectivity.  This is my opinion  as a  hobbyist trapper and professional fisheries biologist.


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Are agave plants perennial?
If I were to harvest an agave plant for its nectar, would it kill the plant? I have watched videos of the process and it seems quite invasive.

When harvesting agave nectar, generally the whole plant is harvested at once to get to the core, where most of the sap is. There isn't exactly an easy way to continually get nectar from the agave plant since it is herbaceous, whereas something like maple trees can be tapped because the wood can support the spigot.

Agave is more closely related to asparagus and hyacinths than to cactus. They are perrenial, you can harvest the lowest half of the leaves to make it look like a little palm tree, it will die after flowering, it takes 10-15 years to flower.

Agave are pretty tough. The way I propagate them is to cut the head off, and lay it on the ground, and come back in a year or so. I live in a semi arid climate. They grow faster if I water them every few weeks or so in the dry season.


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This strange looking thing was on the leaf, can you identify what this is?
I found this today on one of the plant that I grow in the container at home. I cannot identify what kind of insect it is.

Where is the leaf located in the world?

That is a butterfly chrysalis. Since it is clear, and you can see the wings, it is about to emerge. A chrysalis is the naked pupal stage of a butterfly, as opposed to a "cocoon", which is covered in silk.


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Is there a biological explanation for a 0.5 difference in allele size with PCR product?
CONTEXT

I am currently working on a set of diversity, this diversity in interspecific (within the same genus). I am using SSR markers, the primers were designed on one species and are working really well within the species (lot of diversity and difference between allele of 1 at least).
When trying them on the other species, I observe the normal non-amplification which could be due to mutation in the primer DNA sequence. But, for some genotypes I have been observing a new allele just between the two older ones (like the new one is 185.5 and the olders were 185 and 186.
QUESTIONS

Is that kind of observation frequent when using primers designed on other species?
I understand how a 1 pb difference could occur CACACA ==> CACCACA, but what could the biological explanations be for a 0.5 pb difference between alleles?

In my experience, working with a similar approach in Campylobacter jejuni, the base pair measurements from these techniques are imprecise and need to be carefully calibrated. I am unsurprised to see 0.5 base pair differences, this can be seen been runs and even, in the worse case situation, between even and odd wells in the same plate(!).
I would use Sanger sequencing to determine the sequence you are getting in one of your isolates, and then use this as a calibration control included in every run.

Thanks for your feedback! I was planning to do a sanger sequencing to understand the problem. The allele though is quite stable (same length on different plates). Usually I see all my alleles in a 0.5 pb variation around the real value depending on genotypes/runs.

@Untitpoi We found that different length targets from the same strain, and the same targets from different strains frequently gave different length results.

@Untitpoi I think it occurs because of differences in the sequence causing sligtht differences in mobility during capillary electrophoresis. If you look at the raw data from a sequencing read, you can see that the peaks appear less regularly than the smoothed processed peak data you usually look at. I would guess there are consistent differences in the progress of sequences based on the physical properties of the nucleotides.


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How a particular composition of molecules result into life in form of cell?
I had read biology in childhood only, but as far as I can remember every living thing/being is made up of cells in the lowest level. Cells again are made up of some particular composition of molecules. But my question is how a particular composition of molecules become alive? Or What's that which turn compositions of molecules sentient?  I'm trying to understand when or how insentient compositions of molecules become sentient.

Welcome to Biology.SE. I don't think one can answer this question differently than giving an entire intro course to molecular biology. I am voting to close as too broad.

For ressources, have a look at Books for beginners

Okay @Remi.b Can you answer that in 1 or more comments? I don't want thorough answer or suggest me the proper SE where I can ask this question.

Taking a biological course is highly impractical just to know the answer. :)

I suspect you might expect a magical simple answer but there is no such thing to this question. There is no essence of life or any specific process that transform non-living matter into living matter. There is just matter interacting in a complex manner that end up making some entities that we like to call life.

Science does not have an answer to how the first reproducing cell came about.  The actual event has left no traces except life as we see it today. There are theories about parts of how it might have happened, but evidence about it essentially doesn't exist.  If you want to get a flavor of recent ideas of scientists in this area, here is a video of a lecture on "The Origin of Cellular Life on Earth".


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Growth mediums required for human cell cultures
So i would like to try a culture some of my keratinocytes just to see if i can do it. Ive read about a few different types of growth medium such as DMEM and RPMI but i am not sure about when to use which medium. So I am asking how do i detrimine which growth medium i need to use to culture human cells

So this paper probably has what you need.
Isolation and cultivation of human keratinocytes from skin or plucked hair for the generation of induced pluripotent stem cells
The first part of that paper covers just the cultivation of keratinocytes.
It's actually moderately difficult to culture keratinocytes, so if you just want to try out cell culture I wouldn't recommend this as your first step.
A good first step to learning the techniques of cell culture would either be bacterial, fungal, or yeast cultures because they are cheap, hardy, and don't require expensive equipment. Yeast culturing would be closest in technique to mammalian cell culture among the three  Yeast culture info here


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Are microwaves harmful to us?
They closed my question on the Physics Stack Exchange because it wasn't a purely physics question, so I'm trying here.
Recently I've come across the topic of scrapping microwaves, and the various warnings about the potential dangers. I've found out that generally speaking higher frequency radiation is more harmful, also that frequency itself is not the sole factor of harmfulness; as one question on the Physics site remarks the fact that microwaves and Wi-Fi use the same 2.4 GHz range, yet Wi-Fi doesn't cook. Anyway, I saw on a website:

Don’t take apart the magnetron or play with it for several good
  reasons! First, there is the obvious danger of 2.45 GHz microwave
  radiation.

There are two problems I see with this warning. First of all isn't 2.45 GHz well into the radio wave category? And also radiation of 2.45 GHz wouldn't be harmful in and of itself, right?
Also a comment from the Physics site:

wifi would be dangerous because of the microwaves, but it is limited
  to very low powers

This seems to imply that microwaves in and of themselves are harmful.

Higher frequency radiations are more likely to cause chemical damage (like to your DNA) because individual photons have higher energy. Lower frequency radiations are easily absorbed as heat but don't cause chemical damage. They are not dangerous at low power, but the high power can obviously burn.

$2.45~\rm GHz$ is well into the microwave region, which is usually defined as radio waves with a frequency of greater than $1~\rm GHz$.
Microwaves can be harmful. If you stood in front of a $1~\rm MW$ microwave dish, you would be cooked basically instantly. But that doesn't mean they are harmful in small doses: if you stand in front of a $1~\rm MW$ visible light source, you would also be cooked. You can hold your hands in front of a fire, but sticking your hands in would be bad. Like heat and visible light, microwaves aren't intrinsically harmful in moderation, but they can be deadly if you have enough of them.

Thank you, this seems to answer my question. The microwave when powered does indeed operate at a high power, but the sentence the: "obvious danger of 2.45 GHz microwave radiation" doesn't make sense if  the microwave isn't powered.  Also the sentence: "wifi would be dangerous because of the microwaves, but it is limited to very low powers", seems to imply that microwaves themselves are harmful, when in actual fact they should be less harmful than for example visible light at the same intensity... I believe.


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Are there mainstream views on the mandrill's coloration's being so unique?

According to the Wikipedia article:

Mandrills are noted as being exceptionally colourful for mammalian
  standards. Charles Darwin wrote in The Descent of Man that "no other
  member in the whole class of mammals is coloured in so extraordinary a
  manner as the adult male mandrill's".

So I know that in many species sexual dimorphism can act as a feature which is selected by sexual selection, I'm not surprised because there are other examples. But the male mandrill seems exceptional, especially according to what I've read, among mammals. Seems very curious to me, especially its face.
I was wondering if there are mainstream explanations for why the mandrill in particular should have such striking colours maybe more than any other mammals.

Mandrills are also extremely sexually dimorphic in terms of size (and fangs and muscularity, I believe). In fact, one of the most sexually dimorphic of all mammals. The extreme coloration and the sex differences in size both speak to a substantial degree of sexual selection.
Now as for the ultimate question, why mandrills have experienced so much sexual selection... I don't know.


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When using a primer to replicate DNA in a plasmid, does it replicate the whole plasmid?
I've been learning about PCR and plasmids. I understand that the reason for having both a forward and a reverse primer is to extract and amplify the specific piece of DNA between these two primers.
What I'm struggling to understand is that why after the first replication, a fully circular DNA strand isn't formed and hence, why isn't a fully circular DNA strand formed for each replication.
For the following diagram , let the strands be labelled strand 1, strand 2, strand 3, strand 4 from top to bottom. (Diagram from Lehninger Principle of Biochemistry, 5th Ed).

For example, in the diagram here. When cloning a plasmid I assume strand 1 is fully circular, so strand 2 (which was transcribed from strand 1) should also be fully circular and in the diagrams it should show DNA to the left of the site of interest.
Does the transcription stop somewhere along the line, preventing it from copying the whole strand? Or does the strand never join up into a circle, so that the DNA that would appear to the left of strand 2 has been copied, but doesn't join up to the site of interest so wasn't included in the diagram.
Thanks for your help.

The diagram clearly implies that strand 2 and 3 are products from the first round of replication. You're therefore correct that it would be more accurate if the diagram showed the grey parts on the left and right side respectively, but then having a small gap between the end of the grey part and the start of the blue part (to indicate the linearity of the product). However, that would make the diagram less illustrative and necessitate more explanation, so I think this is an acceptable inaccuracy.

PCR produces linear DNA, not circular. You can replicate whole plasmids using PCR, but the DNA will still be linear, as if you cut the plasmid with a blunt-end restriction enzyme.
So why doesn't the whole plasmid get copied when using PCR? Let's assume the primers are designed to bind 1000 bases apart from each other. The first round of PCR will probably produce longer pieces of DNA, because the oligos can only bind to the plasmid and the Polymerase can keep going. But the polymerase will fall off at some point, either randomly or when the temperature is pushed up for the next round of PCR. But in round 2, there should be equal numbers of circular plasmid and linear copy. The proportion of linear copy will increase every round. As the linear copies increase, the oligos are more and more likely to bind to linear copies than to circular plasmid.
Binding to linear copies is why the PCR product size is controlled. Let's assume that a linear copy is 1500 bases, because the polymerase ran an extra 500 bases past the other oligo site on the plasmid. But when the reverse oligo binds that site on the linear copy, the polymerase will run 1000 bases and fall off the end of the linear copy. This new copy will have the forward and reverse oligo sites at the ends, so it's the right size. Any copies produced from this strand will also be the right size. As the reaction proceeds, the proportion of correct-sized strands increases, and create more correct-sized strands.

This makes good sense. Thank you. Is there any way to know how long before the polymerase falls off?

@meldob Most polymerases used in PCR are pretty good at staying on. I used to PCR entire 10,000 base plasmids on a regular basis. When setting up the PCR you choose the extension time based on the length you want to copy and the speed of your polymerase. So if your enzyme runs at 1000 bases per minute and you need to copy 2000 bases, use 2 minutes. Going longer probably won't hurt anything, but it wastes time. Going shorter will cut off the reaction before you get the entire sequence copied.

We have different polymerases optimised for different purposes nowadays. Some focus on high fidelity (i.e. low error rate during copying) but sacrifice speed and range, others can copy 1kbp in less than 10s but make more errors and fail if the desired sequence is too long.


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Why are there so many species of large predator on the African savanna?
On the tropical grasslands of Africa, there are loads of large carnivores. Lions, cheetahs, leopards, hyenas and wild dogs are all found, sometimes, in the same place. I was wondering, why is it that there are so many species of large predator in the same place? Wouldn't competition drive all but one species to extinction?
Obviously, this means that each of the predators fills a special niche. So, could anyone tell me what these ecological niches are? What makes the position in the food web of lions, leopards, cheetahs, hyenas and wild dogs different to eachother?

I am not sure but you might overestimate the density of large predators in the African savanna. 1) The savanna covers a very large territory in Africa 2) how many large predators are there? Lion, cheetah, hyena, African wild dog. Looking at a list of apex predators, it does not obviously occur to me that more of them are present in the African savanna than elsewhere.

Note that it is possible that humans have less impacted the African savanna, than say, the European forests, leading to more extinction of apex predators in European forests, than in the African savanna.

@Remi.b Well, there are places, like the Serengeti or Kruger, where you could go on a safari and see all of them, wild, in a day. If they all occupied the same ecological niches, all but one species would die out. So I'm wondering what makes each of their roles unique.

I am playing the devil's advocate but don't get me wrong, I think the question is interesting. You say they all occupied the same ecological niches They are likely not actually. It is not because they live in the same geographical space and all predate that they share the same ecological niche. They might differ because prefer to predate on one or another prey species, or because one target babies, the other adults, because one needs more water than the other, because one needs more shade than the other, etc ...

North American had bear, puma, wolves, coyote, and at one time cheetah and lion, africa does not look all that special.


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How did craniates evolve?
Looking at most chordate phylogenetic trees, it seems that we usually have something like this:
  ,================= Lancelets
 =| ,=============== Tunicates
  \_|
    \_______________ Craniates

So, my question is, what do we think the common ancestor of tunicates and craniates looked like? Did both clades evolve from a lancelet-like ancestor, with the tunicates becoming sessile after the divergence, or are craniates descended from a tunicate-like ancestor?


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Hominidae is to hominid as Poaceae is to what?
I considered asking this on English.SE, but decided against it, since it strictly applies to biological nomenclature, which not many of them will know about - particularly that of plants.
So, in animals, all families end in the suffix  -idae - e.g. Hominidae, Apidae, Canidae or Laridae. When referring to members of a family, you can use the suffix -ids - e.g. hominids, apids, canids or larids.
However, plant families are usually named with the ending "aceae" - such as Poaceae, the grass family. If I want to refer to members of Poaceae (without just saying the common name), what do I say?

Is this a question for an assignment or are you asking out of more general interest?

@BryanKrause Out of general interest, for the most part. Plus, it may come in handy in the future.

Since Poaceae is the plural of Poacea in Latin - like aquae is the plural of aqua - I would say a Poacea, but I'm not a native English speaker so I don't know if this form would be acceptable in English. My guess is that you will have to use the long form a member of Poaceae. In languages like Italian and French it's easier because the Latin nomenclature and grammar are translated. So in Italian you will say una Liliacea for the singular and due Liliacee for the plural, while in French it would be une Liliacée and deux Liliacées respectively.

Seems like most people just call them grasses (or they use the actual family name). I wouldn't suggest using Poacea.

+1 for "a member of Poaceae." Don't use "a Poacea". Definitely don't try the -id ending since that is used for several larger plant clades (e.g. "Rosid" is a much larger category of plants that includes Rosaceae).


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What is the number density of fungal spores per unit of volume of air?
Fungal spores are present all over in the air around us. I understand that they generally range in size from about one to one-hundred microns.
What is the number density of fungal spores in air on a volume basis? I imagine this will vary based on location, season, and indoor vs. outdoor. An ideal answer would account for all of this in the ranges but I'm broadly interested in indoor air conditions around the world.
If measurements of a single spore density are too difficult, I would find the density of CFUs to be acceptable (assuming that those are multiple spores) but would appreciate being directed to information on how many spores typically make up one CFU. Similarly, a mass density of spores would be acceptable as well if experimental methods make that easier. At the simplest level, I'm just curious how much fungal spore material is in the indoor air around us.


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How are asexual species classified?
Are there multiple distinct genetic lineages of asexual species that are closely enough related to not be considered distinct or does any genetic change result in a new species?
I would assume there's tolerance for variety as much genetic material has either no phenotypical expression, or a very subtle one. It's also consistent with my understanding of differential antibiotic resistance. Normally I'd expect a large degree of acceptable differences as long as there could be reproduction that makes viable offspring, but that's obviously not applicable here.

It is a widely held misunderstanding that species are defined by reproduction. (Mayr's biological species concept.) This species concept works for ecologists and high school biology teachers because it roughly describes how species come to be. However, taxonomists, the people who actually define and describe species, almost all use some form of the evolutionary species concept, which does not define species based on reproduction https://academic.oup.com/sysbio/article-abstract/27/1/17/1626671?redirectedFrom=fulltext. , but on lineage patterns or fixed character states.


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Near-zero water loss in a closed hydroponics system?
I know there are a lot of factors that would impact this...

Plant type.
Plant neediness (i.e., even sibling plants will possess different needs, defects, etc).
Automation efficiency.
Water & nutrients quality.

And that is barely touching the surface, but assume that...

We only have 1 healthy adult (meaning fully grown) plant who transpires 90% of absorbed water. The other 10% fuels photosynthesis, cell growth, etc..
Its nutrient levels/requirements are (somehow) perfectly monitored/satisfied.
The hydroponics system is enclosed s.t. nearly all the transpirated water is reintroduced into the water supply, rather than evaporated.
The recycled water is kept clean & nutritious by an automated system.

So my questions are...

Is it possible to create a system where the aforementioned 10% accounts for the only loss of water?
Am I missing any other significant source(s) of water loss?
Are there implementation factors which would jeopardize the plant's health?

don't forget photosynthesis removes water from the system by converting it into oxygen and sugars. thats is why finding the right symbiotic fungi can be important too, they are creating the oxygen and sugar back into co2 and water.

@John "The other 10% fuels photosynthesis, cell growth, etc.". Introducing fungi is an interesting idea but I am not sure that it would be able to reclaim any of that 10%. Glucose gets converted to sucrose, cellulose, & (in times of excess, stored as) starches/oils/etc. Leaking anything back into the water wouldn't be in the plant's best interests. Also, fungi (like all living things) requires water so, if anything, its presence would hasten the rate of water consumption, no?

it would require more starting water, but fungi like animals coverts oxygen and sugars into water, it will never account for all of it but it will reclaim some of it.  You need to make differentiation between water that is lost from the system by being converted into other compounds vs water that is simply absorbed. I may be getting confused by what you mean by "closed system", Is water being lost to the atmosphere or is it an air tight system?

@John "The hydroponics system is enclosed s.t. nearly all the transpirated water is reintroduced into the water supply, rather than evaporated". I will read more about the fungi concept but would you like to take a shot at answering the 3 questions?


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Most optically transparent muscle phantom?
I am trying to use Schlieren imaging techniques to visualize how a sound wave propagates through muscle tissue.
In the past, when needing to experiment with muscle we would use an agar based muscle phantom but they diffuse light. Might anyone have experience with making tissue phantoms that have similar clarity to something like PDMS for example?


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Is there any small animal that can jump over a meter high/long?
By small, let's say less than 5 cm body length. I always thought that grasshoppers were the highest absolute jumpers in this class but the highest jump according to this article is 0.7 m...

no animal smaller than 5 cm can jump higher than 1 meter. grasshoppers and locusts have wings which supposedly disqualifies them. https://www.guinnessworldrecords.com/world-records/highest-jump-by-an-insect.
The immense mechanical power that would be required for any animal to jump so high with such a small size is unbelievably high which is why they have developed different evolutionary adaptations. not to mention that the terminal velocity of such a small creature is very low so a jump would quickly become a fall due to the air molecules slowing them down. https://www.youtube.com/watch?v=f7KSfjv4Oq0


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If women need more dietary iron than men, then do blood donors also?
My understanding that women's dietary iron requirements are slightly higher because I've heard the only way of losing iron from your body is by losing blood, and this happens in menstruation. This got me thinking if someone donates blood does their dietary requirement increase also?
Also, related to this, when a person gives blood we're told that our body remakes the blood we've lost, does this replenish the iron in the blood also, or is this "newly created blood" absent of the iron normally present in our blood?

This can indeed be an issue.  Frequent blood donors are known to get low on iron, which begins to result in fatigue, even before it starts resulting in low hemoglobin and anemia.
The cause is simple: like you pointed out, the loss of blood results in the loss of iron, and it takes the body a certain amount of time to rebuild the iron store.
As for your second question, the "newly created blood" will be low on iron until the body can absorb enough iron to replace that which has been donated.  Even on iron supplements, it can take up to half a year to rebuild the iron stores of the body to where they ought to be.

Sources:

Frequent blood donors risk iron deficiency, Miriam Shuchman, MD
Iron Deficiency & Anemia Treatment, Webmd.com


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Protein misfolding
Protein misfolding is usually prevented by molecular chaperons. Rarely, the chaperons are not able to prevent the misfolding as a result of which the infectous molecules called prions will form.
My question is, why does the misfolding occur like what are the reasons of misfolding and what kind of mechanism occurs? I somehow find limited information on this issue.

Prions only occur with specific proteins. Again please do some research before posting.

Your question is very broad. You can find entire review articles (or even books) dedicated to this topic. Please check out pubmed or Google scholar.

The astonishing thing is not that proteins misfold, but given the astronomical number of possible ways of folding they manage not to misfold. So you are coming at the problem with the wrong mindset. If you can access to it through a university library, try this review.


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What is the difference between optokinetic and vestibular nystagmus?
Optokinetic nystagmus is for stabilising the pictures we see when we are observing moving objects for example if we are rotating on an office chair. If we wear a mask while rotating however, the optokinetic nystagmus will not occur since we don't see. But I read that vestibular nystagmus will occur even if we are wearing a mask.
What is vestibular nystagmus exatly and how does it differ from optokinetic nystagmus?

The vestibular reflexes are the main cause for stabilizing eye movements. The labyrinth canals in the inner ear detect changes in head direction, movement and acceleration. This is important for balancing body and visual field. These are fast involuntary reflexes thanks to almost direct connections between the sensory hair cells in the ear and the eye muscle innervating neurons.
The optokinetic reflexes are complementing the vestibular reflexes for slow movements or visual field motions independent of head movement (source and further reading). It needs the visual input.
In my studies we actually did this experiment ourselves, measuring the eye muscle activity while rotating with opened or closed eyes. The results were basically the same in both conditions. With opened eyes you try to fixate something in the moving image for longer and have therefore larger jumps in the eye movements, but with closed eyes the saccades are still there.
Edit: The two senses can also be in conflict with each other. For example reading a book in a car (your vestibular system detects motion, while your visual field is steady) or watching a movie in the cinema (your visual system detects motion while your vestibular system doesn't). This causes motion sickness.


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Calculation of extinction coeffcient of GFP
I want to convert the absorption of a protein into concentration. Hence ı need to calculate the extinction coefficient of the protein (GFP). ı found the formula (nTrp)5500+(nTyr)1490 on the internet but not able to use it since ı dont understand what n in front of the amino acids stand for and how ı reach to the n value

Only the number ("n") of the aromatic amino acids Tryptophan (Trp) and Tyrosin (Tyr) in your protein contribute significantly to its absorption at 280 nm (and Cystein (Cys), albeit to a lesser extend), see also here.
You could retrieve the protein's amino acid sequence from uniprot (see GFP here). Looking through the GFP sequence, one can identify n=11 (4.6%) Tyr and n=1 (0.4%) Trp. Now you can insert those in your formula and end up with an extinction coeffient of 21'890 M^-1 * cm^-1. This formula is only valid if all Cys are reduced (GFP has n=2 Cys that could form a disulfide bridge).
If you want to avoid all the formulas I suggest you copy the sequence of GFP and paste it into ExPASy ProtParam. This way you get a nice overview of the amino acid distribution of your protein and also retrieve the extinction coefficient under oxidizing conditions, which BTW is 22'015 M^-1 * cm^-1.


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Immunoprecipitation compared to western blotting
Immunoprecipitation and western blotting are both used to locate a specific protein within a sample and to isolate it.  In immunoprecipitation, a specific antibody and agarose beads ( or other insoluble beads) are used to precipitate the protein. In western blotting, SDS-PAGE is carried out and primary and secondary antibodies are used to locate and isolate the proteins on the nylon membrane.
My question is: which technique should be used when? what is the difference between the two? is one of them "better" / does one of them have advantages over the other?

The two techniques serve different purposes:
IP: purifies a protein
WB: visualizes or quantifies a protein
Most often when I have done IPs (in the hazy past) I have turned around and run the protein out on a WB, so one will frequently combine both techniques. Sometimes a protein is very low abundance so you will not see it in a small volume of crude cell lysate on a WB, and you have to IP it from a large number of cells to get enough protein to visualize on a WB.
Note that IPs will also co-purify associated proteins, so a good way to know whether two proteins stick together is to IP one of them and probe for the other on a WB. This "co-IP" analysis is a very common use case for both techniques.
Hope that helps.


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NMDA receptor depolarization
I learnt that two factors for NMDA receptor channels opening are:
1)Binding of glutamate
2)Depolarization of postsynaptic cell (to remove the Mg+2 block)
Given that depolarization starts in axon hillock and NMDA receptors are on dendrites, how does it all work?

"depolarization starts in axon hillock" - this is not true, why do you think this?

Seemingly I confused the term with action potential. So NMDA receptors need a depolarization which is below +30?

Yes, that's correct. Also read about backpropagating action potentials.

Alright, I will. Thank you!


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Do different transcription factors attract different kind of RNA polymerase?
Initiation step of transcription is simply binding of RNA polymerase on the DNA strand and its activation by addition of a phosphate group onto it.
Different kind of promotors are present close to the transcription starting site and different kind of transcription factors (TFIID ,TFIIB ...) are present binding onto promotors making the RNA polymerase bind onto DNA.
is there different types of RNA polymerase II ? I know that it is
RNA Polymerase II which is responsible for mRNA formation but my question is; is RNA Polymerase II further subdivided according to what kind of protein will be synthesised after translation? otherwise why do different kinds of transcription factors exist?

Why didn't you research RNA polymerases before posting? This would have answered your question and saved you wasting other people's time.

"RNA Polymerase II which is responsible for mRNA formation but my question is; is RNA Polymerase II further subdivided according to what kind of protein will be synthesised after translation" shows clearly that ı researched about the subject and I am asking for a further detail that ı am NOT ABLE TO find an answer for.   It is optional for one to share knowledge or not I think, so I am not wasting anyone's time I think. Your use of language is harsh and irritating.

Please read "how to ask a good question" in the Help. You are required to do research before posting. There are ample articles on Wikipedia and elsewhere that describe the RNA polymerases and transcription factors in eukaryotes, as there are text book chapters in reputable books on biochemistry on NCBI Bookshelf. You cannot find anything about the mistaken idea you have about multiple RNA polymerases for the simple reason it is a misconception. The subject of tissue-specific or stimulus-specific transcription is huge — go read about it.

TFs, the DNA they bind to, and the transcriptional machinery (including the Pol II [RNA polymerase 2] enzyme all form a complicated three-dimensional complex. It depends on the topographic conformation of the DNA, epigenetic factors, a whole bunch of things which are orchestrated. However, once the machinery is activated, the Pol II enzyme is capable of transcribing the DNA regardless of its resulting protein. You can get the enzyme to transcribe nonsense, or functional coding regions which will produce functional proteins.
In epigenomics, it is also commonplace to identify mRNA being transcribed on DNA regions which do not bind a transcription factor. This is because the machinery recruits the polymerase at a transcription initiation site, but there may be nearby DNA (looped, for instance, or on a neighboring nucleosome) which is accidentally transcribed, simply because the polymerase was brought into close proximity and began transcribing the wrong DNA.
Such enzyme reactions are a bit like chopping an onion: the knife is the enzyme, the onion is the target DNA, and your stray finger is the non-target DNA. Usually it is the onion that is chopped.
Biology is never perfect, it follows the laws of chemistry and therefore is a stochastic process.


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How likely is it that we will discover a new species of big cat?
So, I've been reading some articles about these "scandals" where everybody thought that there was a new species of feline discovered, from some weird skull or carcass or whatever. And always, by the end of the article, they would have concluded that it was just a jaguar or an ocelot or not even a feline. But, it got me thinking, and I was wondering - Is it possible (As in, are there more than minuscule chances) that we will discover a new species of big cat, or Panthera species?

Welcome to BiologySE! Please cite the source from where you heard that. Also, do take a moment to check out the [tour] of our site.

Extant (alive) extremely small. There just is no place left to hide so to speak. If we do it will most likely be what we thought as one species being split into two along some currently unknown factor, similar to how chimps and bonobos were thought to be the same until fairly recently.
Extinct extremely high, we have discovered such a small fraction of a percentage of the number of species that have ever existed that any group is a candidate for future discovery.

Actually the last big cat discovered was only 2011 so it's remotely possible that another can be discovered.

Comparisons between the clouded leopards of mainland Asia and the Sunda Islands of Southeast Asia, which include Borneo, Java, Sumatra and Bali, revealed the Sunda clouded leopard was genetically distinct, making it the newest species of big cat known to science.
(Despite their name, clouded leopards are not actually a kind of leopard, but are completely separate from the genus that includes lions, tigers, leopards and jaguars.)

https://m.csmonitor.com/Science/2011/0125/That-new-species-of-big-cat-Turns-out-it-s-actually-two-new-species

Yeah, that was one of the things that got me thinking for this question.


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difference between neurotransmitters and hormones
I have been reading a lot about neurotransmitters and hormones but what's the difference between them both or are they the same? It's been confusing for a while now. Also, why do some neurotransmitters act as hormones?

At heart, the distinction between neurotransmitters and hormones is how they are transmitted - not necessarily a difference in the chemicals themselves.
Neurotransmitters are sent over synapses, between neurons. They may be small molecules (e.g. dopamine) or larger molecules such as proteins (e.g. substance P). Conversely, hormones are sent through the circulatory system but could also be small molecules (e.g. adrenaline) or large molecules (e.g. growth hormone).
Looking at the structures of these chemicals, we can see that both neurotransmitters and hormones have an enormous variability in the chemicals they involve. Furthermore, dopamine looks much closer to adrenaline than it does to substance P. But dopamine is primarily a neurotransmitter and adrenaline is typically thought of as a hormone!
There may also be overlap between roles of chemicals as neurotransmitters or hormones. In fact, adrenaline may act as both a neurotransmitter and a hormone. So, to answer your question of "why do some neurotransmitters act as hormones?" - the distinction is in the context of how the chemical is sent through the body. There's variability in which chemicals are used for either purpose, and no rule saying a chemical can't be sent via multiple mechanisms.
Furthermore, neurotransmission also involves spillover of neurotransmitter, which in theory could find its way into the circulatory system. So there could be overlap between neurotransmission and hormone signaling. And lastly, as @Remi.b points out, the particular mechanisms of neurotransmission and hormone signaling have implications on the dynamics of the signaling.

Wikipedia > Neurotransmeter

Neurotransmitters, also known as chemical messengers, are endogenous chemicals that enable neurotransmission.

Wikipedia > Hormone

A hormone [..] is any member of a class of signaling molecules produced by glands in multicellular organisms that are transported by the circulatory system to target distant organs to regulate physiology and behaviour

There is even a section called Comparison with neurotransmitters in the wikipedia > hormone page

There are various clear distinctions between hormones and neurotransmitters:

A hormone can perform functions over a larger spatial and temporal scale than can a neurotransmitter.
Hormonal signals can travel virtually anywhere in the circulatory system, whereas neural signals are restricted to pre-existing nerve tracts
Assuming the travel distance is equivalent, neural signals can be transmitted much more quickly (in the range of milliseconds) than can hormonal signals (in the range of seconds, minutes, or hours). Neural signals can be sent at speeds up to 100 meters per second.
Neural signalling is an all-or-nothing (digital) action, whereas hormonal signalling is an action that can be continuously variable as dependent upon hormone concentration.


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What percent of e coli genes are necessary for survival?
I would like to know, in a typical e coli genome what percent of genes the organism could not survive without. That is, if all the other genes evolved except that one, the organism would not be viable.

There are a few groups worldwide working on a minimal genome; until they've managed to get a reference minimum, we won't know how much is necessary.

About 10% in rich media.
There are lots of papers that try to answer this question. The basic way you do it is you knock out one gene at a time, either in parallel experiments or (more common nowadays) in a pooled experiment, and figure out which knockouts survive and which don't.
The most recent study counts 358 essential genes (out of about 4000 genes in E. coli). http://mbio.asm.org/content/9/1/e02096-17.full . Figure 2 compares a few other papers.
The exact answer will depend on the exact conditions you grow the cells in (if you have fewer nutrients or other stressful conditions, more genes will be essential).


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If all animals were to die, would all plants die too?
Humans and many other animals are able to breathe because plants produce more oxygen than they need. I was thinking if all animals died all of a sudden, then wouldn't plants die too. Eventually they would produce too much oxygen and wouldn't have enough carbon dioxide to go through photosynthesis.

If all animals suddenly died, the large amount of corpses rotting would mean a spike in co2 levels, not a fall

Animals are not the only organisms to respire without photosynthesizing. Fungi, many other eukaryotes and many bacteria respire too (and do not photosynthesize).
Now, if all animals were to suddenly die, there would sure cause a drastic environmental change for plants. Whether or not that would lead all plants to extinction is untestable and it is therefore impossible to give a definite answer. This type of question would be better suited for worldbuilding.SE. I personally doubt all plants would disappear.

Is this an attempt at an answer, a migration vote or a personal opinion? Your answers are usually of much higher standard Remi.b! ;-)


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filtering variant list according to target regions
I have a variant list in VCF file for a particular disease, I want to filter these variants according to exonic regions in a BED file using a Perl script. How I do this?

Sounds more like a question for Stack Overflow to me.

I'm voting to close this question as off-topic because it is not a question about Biology.

Don't reinvent the wheel.  Use BEDTools.
And no one on any Stack Exchange board wants to write you a perl script.

As a fuller explanation, use bedtools with the intersect command:
bedtools intersect -u -a variantList.vcf -b exonicRegions.bed > filteredVariants.vcf

While this should work, if your vcf version is giving you trouble use vcf2bed to convert the vcf to a bed file, then intersect directly.


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is there an easy way to remember taxonomy?
So I have trouble remembering the order of taxonomy for classification.
i.e domain>kingdom>phylum>class>order>family>genus>species
I can never remember it, is there an good mnemonic to remember them? How do you guys remember it?

Of course, Randall Munroe has a solution to your problem: https://xkcd.com/992/

I'm voting to close this question as off-topic because it is not about biology as such.

Have a look at Wikipedia > List of mnemonics#Biology.

Dear King Philip Came Over For Good Soup
Do Kings Play Chess On Fine Green Silk?
Dumb Kids Prefer Cheese Over Fried Green Spinach
Do Kindly Place Cover On Fresh Green Spring Vegetables
Donald Kills People Cause Other Friends Get Sad

Given the current political situation I would go with the last one but it is up to your personal preferences. You can as well make up your own. Mnemonics are like soups; it is always better when homemade. For example, extending upon the last and inspired by @John's comment, here is a homemade mnemonic

Donald Kidnaps People's Children Causing Outlaw Foreigners Great Suffering

Enjoy the game!

do kill purple clowns or face great suffering.


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difference between blastula and blastocyst
What is the difference between these 2 terms. I believe that blastocyst is for animals, but structurally is there any difference? And how would you be able to identify each?

A blastula is a hollow ball of cells, while the blastocyst occurs slightly later in mammalian development and has a defined inner mass and an outer layer of trophoblast.


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Blood pressure in various blood vessels and heart
What are the typical systolic and diastolic blood pressure in arteries,capillaries, veins and the heart?
I know it must be highest in the arteries. arteries>capillaries>veins
Arteries: 120-80mmHg (systolic - diastolic). I also found mean values for capillaries (30mmHg) and veins (10mmHg) but not able to find systolic and diastolic pressure specifically.

Blood vessels have "compliance": that is, they are stretchy. Mathematically, this is very similar to capacitance in electricity.
The further from the heart you go into the vascular tree, the more the oscillations are dampened and the less it makes sense to think of systolic and diastolic pressures. In the capillaries and veins, blood flow and pressure is more or less constant rather than oscillatory (except in the most proximal veins where the motion of the heart again adds some pulsatile influences).
Therefore, for those vessels, you can just stick to mean values for pressure, the oscillations around those values are small.
See another Q&A: Why do people perceive blood pressure as the force that moves the blood forwards (see details)? that has a diagram showing the dampening of oscillations in pressure.

thanks a lot! and what can be said about the pressure in heart? I thought 0 during diastole and around 120mmHg during systole ( I thought during systole it is similar to that of arteries )


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Coelom - Bilateria
Coelom is formed of mesoderm. all bilaterians are triplopblastic meaning they have mesoderm. does this mean that ALL of the bilaterians have a coelom?

No. The coelom has been lost multiple times (for example, in Nematodes). Many parasitic bilaterians also lack a coelom, likely due to secondary loss.


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is it possible that there is no gene at a locus?
"the location of a certain gene on a chromosome " is the definition I know for locus. ı just read that a gene is not necessarily present on a locus. how would that be possible?

A locus is not necessarily the position of a gene. It is a position in the genome, whether or not, there is a gene at this position. A locus often refers to the position of a SNP (which may well be outside a coding region) or any other type of genetic marker.
A gene is typically defined as a sequence that is coding for a protein. Most of a eukaryotic genome, such as the human genome is not made of sequences coding for proteins. It is rather made a various regulatory sequences, introns and especially repetitive DNA. So, if you randomly pick a sequence in the human genome, chance are it is not going to be a sequence that gets translated.

so would this mean that the definiton ı stated for locus is not exact?

Indeed. I edited the answer to clarify that.

Like you said in your question - "locus" means location.  A locus may be anywhere on a chromosome - an entire "gene" coding locus, a non-coding locus (junk DNA), a regulatory sequence locus (example - the promoter region of a gene), or just a single nucleotide locus (SNP) etc.  A "locus" is the location of interest on the chromosome.
Yes, it is also possible that any genetic "locus" may be absent if it has been lost by a "deletion".  A deletion is a type of mutation.  They might be a single nucleotide deletion or a very large deletion of thousands of nucleotides. Genetic deletions can happen in several natural ways (a DNA repair error for example), and by other mechanisms, but also through "man made" genetic manipulations.

Locus just means location, as (non-)specifically as in any other use of the word.
Remember the word originates from traditional genetic studies, which didn't know how genes work. Back then, scientists gave some name to "that region in the genome" and they determined the approximate position relative to other known loci through recombination studies. For many of these, we have in retrospect figured out that all of the findings by these older studies were related to a specific gene and now we refer to that gene by the name originally used for the locus. If you read older papers about the white gene in Drosophila, you'll see this usage.
In vertebrates, functionally related genes are often located close to each other (in a cluster) and it's useful to have a name for the whole group. For example, some transcription factor's function might depend on how the genes are arranged in the genomic region. One example is the human beta-globin locus.
Even when a locus contains something like a "gene", it might not be a traditional protein-coding gene but rather a miRNA (or others like tRNA, rRNA) locus. These again sometimes cluster.
The sequence at that location in the genome doesn't need to be functional in any way. For DNA fingerprinting, you could determine the number of VNTR repeats at each VNTR locus.
And finally, like Remi.b mentions, "locus" can very specifically refer to a single position within a gene's sequence.


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How to linearize target vector by PCR
In my bio class, we learned that you can use restriction enzyme or PCR to linearize a plasmid. Linearizing by restriction enzyme seemed visual and intuitive but how do one linearize a vector using PCR?
I know how PCR works(at least I believe I do), since I watched couple of videos on YouTube explaining them.
But it is not connecting to me how PCR can be used to linearize a "circular" DNA. I have seen videos where a straight double stranded DNA was separated into single strands and using PCR to produce multiple copies with appropriate primers.
But if a plasmid, the circular DNA is not "straight" or linearized in the first place how do you perform PCR on it? Because if they are in a circular state during PCR the strand would never separate in to linear strands. Wouldn't you just have two sperated strands that are circular? E.g a small ring of single strand DNA and a bigger ring of single strand DNA. They are still in circular state after the strands split from each other. Please correct me if I am spitting out nonsense. I just don't see the visual here.

I like your question. I am not sure if "inverse PCR" means that. But "inverse PCR" also needs restriction enzymes.

If you use PCR, the products from the reaction will be linear pieces of DNA. Yes, you'll have two templates that are circular after the first denaturation, but when you anneal the primers and perform elongation you'll be making linear fragments. The exponential nature of PCR means that these linear fragments will far exceed the template after several cycles.
PCR can also be tuned to be selective for shorter fragments. If you use the proper protocol for PCR of the entire plasmid, your PCR products will be a complete copy of the plasmid that is linear.

Why "when you anneal the primers and perform elongation you'll be making linear fragments"? Can you use some graph to explain?

Not sure how do to graphs in this, so I'll try a more detailed explanation. The plasmid is a circular piece of DNA. When you denature it with heat, you'll have two single stranded, circular, pieces of DNA. If we take one of these circular single stranded DNA pieces, and add a primer, the elongation on that circular piece will continue until it circles around and reaches the primer. The polymerase will not ligate the elongated primer back to itself, which creates a linear copy of the circular plasmid when denatured.


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Isolating gene of interest from a large strand of DNA
I was always confused about this in class and never learned it fully.
So say you have 10,000 bp of DNA and you just want to isolate 100bp of specific region(gene of interest) using restriction enzyme.
How can you ensure that at the both ends of your gene of interests has the right sequences for certain restriction enzymes to cut.

What research have you tried to do on your own to answer this question? Please update the question with evidence of such research to avoid having the question closed. Thanks.

Assuming that you know exactly where in the full DNA strand the gene of interest is located, it is fairly easy to isolate the gene. There are several restriction enzymes you can use, it's just a matter of determining which one(s) are most appropriate for your gene of interest.
Remember that it is usually fine to have extra nucleotides on either end of the gene; the ribosomes will start and stop adding peptides based on start and stop codons, independent of how far the ribosome moves before reaching the start codon. Analyze your DNA strand and try to find a restriction enzyme that will slice the strand somewhere before the gene begins, and usually another that will slice it somewhere after it ends, although sometimes the same enzyme will work for both ends of the gene.
Edit: As @Untitpoi mentioned, if the restriction enzyme's slice sequence is found within the gene of interest, it will cut your gene in two (or more). It is very important to ensure that the enzyme(s)s you choose do not slice the gene of interest, otherwise the strand will be useless. It's possible to re-join the strands (which, thanks to sticky ends, isn't too difficult), but why take the extra effort when you don't have to?

won't it be a problem if the sequence is found again in the gene of intersest?

You have to know something about the sequence you want and the flanking sequence then you pick a restriction enzyme that will cut approximately where you want.  There are so many different enzymes with different cutting target sequences, it's usually possible to find a suitable one.


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functionality of protein based on amino acid covalently linked to something
This question is directly taken off from "challenge question" as part of my bio-engineering class.
The functionality of any individual protein covalently linked to a device is dependent on the specific amino acid through which it is chemically linked to the device.
Is this a true statement? I believe that different amino acid has different chemistry and orientation so it would affect the functionality but is it enough to say dependent on them. Also could you please provide an example if possible? I cannot think of an example. I would really appreciate your insight as well.

The if the protein is linked with a residue in the active site, for example, function would definitely be affected.

Your challenge question was meant to challenge you for a reason; your instructor wants you to reason it out. You should not rob yourself of the experience.


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Why is some scat in the form of little pellets?
The scat I most often encounter when out and about is from coyotes, black bears, deers and rodents. The deer and rodent droppings I find are in little pellets, what is different about their digestive system or their food choices that produces these perfectly uniform little balls?

According to this article:

The material that cannot be broken down any further, such as
indigestible fiber, passes directly into the large intestine.  Here
water is reabsorbed and the material is passed, making up the round
droppings you see in your rabbit’s cage.  This indigestible fiber is
important in the diet of the rabbit as it helps to stimulate
intestinal contractions, which keeps the chyme moving through the
gastrointestinal tract.

While this article is specifically about rabbits, all herbivores require high quantities of fiber in their diets. Ruminants such as deer have different stomachs, but it is the large intestine, which is commonplace, that these pellets are formed. Fiber tends to clump together (either because the strands are attached or intertwined), and contractions in the intestine as the material is dehydrated cause these clumps to roll around similarly to pebbles in a rock tumbler, causing them to form round pellets.
Carnivores and omnivores have (and need) less fiber in their diets, so this phenomenon is not present in their feces.


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SNP coding for association analysis
I'm working on a project about detecting SNP association with a disease. As I understand, SNP is a single variation of the nucleotide that occurs for more than 1% of the population. However, I couldn't connect this idea with the dataset in hand. The rows in my dataset represent each patient and the columns contain SNP information. For example:
ID  exm355 exm615
1     T_T   A_C
2     T_T   C_C
3     A_T   C_C

I have no idea why the SNP columns contain 2 nucleotides(T_T, A_T, A_C, C_C). As the definition of SNP, I thought it should show only the variant nucleotide or am I misunderstanding anything? How could I interpret T_T or C_C and how could I know which nucleotide is the variation from the common ones in the population?
Thanks all

Without knowing where exactly your data comes from / how its formatted this is hard to answer. Generally the SNP notation with two bases is used to denote both the 'canonical' and the 'variant' base at each of the SNP positions (this would mean that exm355 doesn't have any SNP at ID 2, since its 'T_T'). You should look up which base is variant/canonical in an description of your data/file format

Each chromosome location which has been identified as being a SNP is a location at which more than one nucleotide occurs at appreciable frequencies in the general population.  This means that there are two or more bases which can occur there, so a person's test must show which bases actually occur there in that person's genome.  Since a person has both a paternal and a maternal chromosome of a chromosomal type (a pair of homologous chromosomes), the person has two instances of the SNP location and so two nucleotides to be detected and reported.  Hence your dataset has two nucleotides for each SNP location for each patient.
Just from the reported base or the SNP name you can't tell which is more frequent in the population.  If you need to know that, you must consult SNP frequency data from some other database. (The SNP names in your example, e.g. "exm355" are not familiar; usually SNPs have names like "rs1234567".)


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Once neurotransmitters bind to its receptors, how does the post synaptic neuron "know" when to start a new action potential?
My textbook seems to gloss over this subject. Once the post-synaptic receptors are activated, do they cause particular ion channels to open, letting positive charge into the cell and inching the neuron closer to the AP threshold?
Also, does the action potential start in the dendrites or the axon? Does the cell body experience membrane voltage? If so, how does the charge get past all the miscellaneous organelles in the cell body? Does it have like a special charge pipe to go down? Or do the ions just float past the organelles?

Welcome - does this answer your question?

Yeah, mostly. Although I'm having trouble figuring out exactly what an ESPS is, Wikipedia is mostly helpful. Thanks!


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Environment requirement for human life
I was wondering, what are the humans needs to fulfill to achieve a human colonisation on mars ?
Let me explain, this is for role play game in a futuristic world where humans colonized mars.
That creates questions that needs answers for background purposes.
I saw like each another some scifi, read novels etc. But I'd like to know scientifically what could help us achieve that.
If this post doesnt have it's place here, do not hesitate to remove it.
In my mind :
breath
eat
drink
dont take radiations (at least not to much)
stay at the right pressure and temperature
any gravity issue on our body ?
try to avoid wandering naked in space
Any help is appreciated
thanks guys :)

This would be more appropriate someplace like Worldbuilding.SE, it isn't really about biology per se. From a biology standpoint, it is under researched for the standards of Biology.SE.

Here is a good write-up for NASA of human needs in space, which applies to other planets, too.
Here is a table of contents with links to chapters that discuss relevant information for you.
The source is described so:

Space Settlements: A Design Study, provides information on space
  settlement development and education and assists teachers and students
  in the NASA Ames Space Settlement Design Contest. The design study was
  the result of a 10 week program in engineering systems design held at
  Stanford University and Ames Research Center in the summer of 1975.
  Participants included professors, technical directors and students in
  a variety of disciplines from physical science and architecture to
  engineering and social science. The goal (see preface) was to
  construct a vision of how people might sustain life in space in a
  large colony.


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Chromosomal structures in S phase and Prophase
Of S Phase:

Existing DNA molecule acts as a template to synthesize new DNA molecule. The cell doubles it's DNA, yet the number of chromosomes remain the same

Of Prophase:

The chromatin condenses and during condensation, DNA strands untangle to form compact mitotic chromosomes

So in the S Phase, we're talking about chromosomes which contain double the number of initial DNA molecules, while the chromosomal number still being the same.
And in Prophase, there's condensation of chromosomes! But the chromosomes are already formed in the S Phase as per the sentence I have quoted from the textbook.
That doesn't make sense to me. I'm very confused.

@AlwaysConfused first of, your explanations back there and here were quite wonderful. Thank you. Secondly, I have one more question. By chromosomes in the S phase, do we mean actual "rod-shaped" structures that are formed from chromatin condensation or it's just the chromatin threads taking the shape of chromosomes (I'm sorry if that sounds a bit naive). Also, can you elaborate on "two chromatids per chromosomes?" Does it have anything relating with visibility in the microscope: that chromosomes with sister chromatids are formed in the S phase itself and they're visible that way in Prophase?

Welcome to SE Biology. When you post a question with a query about a textbook it's always useful to give details of the textbook so if one has access to it one can check for mistakes in transcription or see the context. Is there a graphic to go with this explanation?

@AlwaysConfused Please use comments for clarification or for checking the OP's thinking; if you have an answer to post, use the answer box.

A comment by user AlwaysConfused has answered one part of the question, but I think that the OP's confusion is related to a point of language or teaching. The number of chromosomes doubles during S phase (C number), but the ploidy of the cell does not change (N number). That's what your textbook is trying to tell you, it's just stating it fairly confusingly.
When we say that there are the same number of chromosomes before and after S phase, that's just a lie that we tell ourselves to keep from getting confused. We have invented the C vs. N terminology that AlwaysConfused mentions to try to handle this: we say that the 2N of a diploid cell remains constant across the cell cycle, while the C number alternates between 2C (before S phase) and 4C (after S phase).
For you, this confusion seems to be worse because how we represent chromosomes is not what chromosomes actually look like, and this has gotten mixed up with the definitions of chromosomes.
When we draw pictures of chromosomes we draw them neatly like they are in mitosis, but that is not at all what they look like in interphase. They are still chromosomes during that time, they just aren't pretty and neat ("condensed").
To sum it up more, here is a diagram of chromosomes in interphase (most of the time) vs. during mitosis:
It is only during a very specific part of the cell cycle (mitosis) that the chromosomes are packaged up ("condensed") in such a way that we can readily see them as discrete entities. The rest of the time they're all glommed together and are organized instead according to transcriptional activity etc. rather than according to which molecule they're part of. Remember: chromosomes are very big molecules and if they are "loose" they have a total length that is many orders of magnitude larger than the diameter of the nucleus; so the nucleus is like a big bowl of noodles in interphase.
In S phase it will just be a bowl with twice as many noodles in it as before, because there are twice as many DNA molecules ("chromosomes"; "chromatid" is a term that only applies to the condensed form in mitosis).

Noodles. Great analogy! Thanks a lot!

@yenashah Glad it helps- I think that using familiar objects to get a physical intuition is one of the best ways to understand biology, which is at best a pretty confusing field.


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Does mother feed information?
Does the mother feed information to the child in the fetus? If so, How is that done? IF not, How can the just born baby breath involuntarily if brain doesn't know it should generate impulses to contract and expand Diaphragm ? If information is given, What type of Information it is, And Would it be possible to feed the information of mother's choice?

You might want to look at this question https://biology.stackexchange.com/questions/31459/how-is-instinct-carried-from-one-generation-to-another

It's not like anyone can not breath for long without other access to oxygen. Pain is pretty good informant.

Why was this downvoted? It's a decent question even if somewhat dumb.
Humans don't breathe in the womb. Instead, blood with oxygen and other essentials goes in through the umbilical cord and back out through the same cord after its resources have been partially used.
"Feeding information" would require a neural connection which there isn't any evidence of. Experiments where scientists "link human brains together" generally use an electricity-based computer-mediated connection (for a good example:
https://www.cnet.com/news/scientists-connected-3-actual-human-brains-then-made-them-play-tetris/ )


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Does thyroxine increase BMR or metabolic rate?
I know that thyroxine increases the metabolic rate, but my teacher said it increases the metabolic rate, not the basal metabolic rate, the basal metabolic rate is always the same. What's the difference between BMR and metabolic rate??

The definition of BMR from wiki is :

Basal metabolic rate (BMR) is the rate of energy expenditure per unit time by endothermic animals at rest.

When BMR is calculated for a volunteer some conditions are taken into account:

complete physical rest
sitting upright
at a comfortable room temperature usually around 25 centigrade
at the post-absorptive phase of digestion

On the other hand metabolic rate may be calculated even when one is exercising, at high or low room temperatures, during digestion etc. So it is more generalised.
When you are talking about thyroxine or thyroid hormones, you must keep in mind what (factors) stimulates its secretion.
One such factor is coldness.
So that definitely indicates temperatures below the 25 centigrade mark at which BMR is usually calculated.
So in my opinion it was quite prudent of your teacher to advise you to use metabolic rate instead of basal metabolic rate for the thyroxine effect description.
REFERENCE BOOK:
Biochemistry by Debajyoti Das 14 th edition
Academic publishers P-677 to 680.


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What is the name of this plant with leaves having two different shades of green?
I am trying to find the name of this plant. I am attaching the relevant images. Thank you for your help.

Location: Hyderabad, India

They just look like juvenile leaves...

I have been looking at this plant for a while now and the colour has been consistent with leaves. It might be possible that they are juvenile leaves and are taking their time. Any ideas with what the name of this plant is?

Do you have any images of the flowers of this plant, or if not, would you know how the flowers might look like? This will help, thanks.

With the Help from Taimur in above answer, I was able to deduce that the picture that I posted belongs to Ficus Benjamina.

So after searching a bit, I think this plant is of the genus Ficus:

I am still unaware of the species but the nearest I could find was Ficus retusa. I hope I have been of help.

Yes, Thank you Taimur for your help. You have narrowed my search area.

Hi, I found that the pictures that I attached might belong to Ficus Benjamina. It is grown as ornamental plant where I live.

@vamsidharmuthireddy great, if you are certain of it, you can answer your own question then. I am glad I was of help.


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what is the name of this small plant with yellow flower?
Can someone please help me find the name of this flower. The close I got to is maybe some kind of diasy?.

Location: Hyderabad, India

This looks like Sphagneticola trilobata also known as Singapore daisy, creeping-oxeye, trailing daisy, and wedelia.  It is now found throughout the Neotropics but is native to Mexico, Central America, and the Carribean.  It is a weed that is classified in the top 100 worst invasive species in the world.

Source: Sphagneticola trilobata (ePlants)

Thank you very much Kurt for your answer. It's funny though, how Mexican native species got the name of Singapore daisy.


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What is the rationale behind reverse cholesterol transport?
Reverse cholesterol transport is transport of cholesterol from the tissues back to liver/VLDL. My question is why do the tissues have this extra cholesterol in the first place?
Why would you synthesise extra cholesterol when excellent feedback mechanisms exist - eg. SREBP SCAP INSIG path??
Does this happen only in the case of an atheromatous plaque? Nowhere else?

This is a great question, I have also wondered this many times but found no clear motivation or data in the literature. My guess is that there is some continuous loss of structural (membrane) lipids in all tissues that proliferate or renew themselves. Possibly the cholesterol in membranes of dead cells cannot be completely recycled (perhaps it gets irreversibly modified somehow). Pretty much all tissues have some rate of cholesterol synthesis, and proliferative tissues have high rates, which suggests continuous turnover. But I don't know for sure, just some food for thought ...

The problem is that we are taught all the cycles, and we learn them blindly. The big picture gets lost in the process. :(

Just remembered that I asked this related question some time ago.  No responses yet ...  http://biology.stackexchange.com/questions/41886/is-there-a-way-to-quantify-in-vivo-cholesterol-transport-rates

this source might be helpful: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2390860/


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If chylomicrons can not get into the capillaries, how do they supply to tissues?
The transport of chylomicrons is into the lacteals mainly because they are too big to get into the capillaries and yet they later supply triglycerides in the extra hepatic tissue by traversing in the capillary bed. This seems utterly illogical and self contradicting. So something seems to have gone wrong in this line of thought.

chylomicrons travel via the lacteals into the lymphatic vasculature that forms the cisterna chylii and thoracic duct...chylomicrons and other large molecules that are unable to pass into the fenestrated capillaries of the intestinal tract use this route into the thoracic duct, which ultimately drains lymph directly into the left subclavian vein - completely bypassing any first pass metabolic effects of the liver

But they use the capillaries later to deliver triglycerides to the tissues. So I mean to say, they are anyway able to get there (in the capillaries) so why not absorb into capillaries initially itself?

I have asked my self that as well - though the triglycerides and the particles that carry them (VLDL, chylomicrons) are huge... see this question for some related comments: http://biology.stackexchange.com/q/30883/16299

also - note that the chylomicrons and VLDL particles do not traverse the capillaries - the lipases that hydrolyze the triglycerides are located within the capillary endothelium - so when free fatty acids are released they are able to traverse the endothelium and be taken up by the adipocyte or other cell on the other side of the capillary.

@vance hey! I get it all now. Chylomicron size ranges around 300nm but the capillary diameter is around 40um. So the diameter is very much bigger. So they can very well traverse the capillaries, though they keep getting smaller due to lipoprotein lipase. On some further thought it occurred to me that while absorption in the gut it has to travel BETWEEN CELLS and here it has to travel WITHIN the lumen. So that happens to make all the difference!correct me if I happen to be wrong :)

Its my question too,does anyone know it?

@Nemexia  check ot the comment above, there is a difference between 'within' and 'between'. I assume that's right but yeah, someone has to answer with a reference

Please explain: "but the capillary diameter is around 40um" - that should read 40 n m (nanometer)? You do not speak of  the pores? Pores of/in the capillary endothelium?

@Vance L Albaugh Would be interesting to have your comment as answer, alternatively to have some reference.


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When there's a wound, the end result is a thrombus or thrombosis?
When there's a wound, the blood vessels are damaged. To stop the loss of blood, the clotting cascade starts off and forms a clot. This clot is a thrombus, right? Seems like perfect physiology. Where does the clot occur? As in, if we consider the vessel to be a pipe, the clot is formed at one end to block the flow or is attached to the wall of the vessel on one side?
This doubt arises because thrombosis (considered pathological) is defined as a clot within a blood vessel. Is the same not happening when there is an injury? If we consider the clot formed at one side of the vessel wall, doesn't it become thrombosis? Even if the clot is like a plug, it has to be attached to the wall, right?
In short, what is the difference between a clot due to a wound and one thrombosis (due to the Virchow's triad)? Where are the clots attached in either cases?

Thrombosis is formation of clots without injury due to reasons like ineffectiveness of heparin. Yes, clots are formed on the side of blood vessel, so they prevent blood leakage, not blood flow.

Here are a couple of distinctions,
1) The thrombus is the actual blood clot
2) Thrombosis is the condition of having a clot form in the blood vessel.
3) If the thrombus breaks away and becomes capable of traveling to some distant site, we refer to that as an embolus.
4) If the embolus lodges somewhere disrupting blood flow, we call that embolism, or in the case of a thrombus, thromboembolism.
So referring here, a protein called tissue factor is expressed on the outside of blood vessels, and when ruptured, is exposed to the blood stream that carries Factor VII. This initiates the coagulation response, and through the action of these factors you get platelets sticking to the endothelium, thrombin cleaving fibrinogen to fibrin that sticks to the platelets, and the fibrin/platelet plug forming over the wound is like a gel and RBCs become mired in it. So really, the thrombus is stuck to the endothelial wall.

so thrombosis is a thrombus occurring without an injury?

With or without, there are blood pathologies that can cause clotting without significant injury, such as A-fib, which is particularly dangerous because those thrombus tend to embolise.


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What is the function of CETP?
I read up that CETP transfers cholesterol from HDL, which collected it from tissues, to VLDL. This VLDL is then sent back to the tissues, ultimately forming LDL internalised by cells.
What is the whole point in taking cholesterol from the tissues only to give it back? I read up that reverse cholesterol transport is for sending the excess cholesterol to the liver for excretion as bile. But LDL receptors are everywhere and not just the liver.
There also happens to be a SRB1 pathway specific to the liver but apparently not significant in humans :(
So pls help me make sense.


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Is diarrhoea advantageous to the microbe?
Diarrhoea is a common side effect of many feco-orally transmitted bacterial infections. How does diarrhoea help the pathogen? Should it not have a selective evolutionary advantage? Do all symptoms of the disease need to have a selective advantage for the pathogen? All I can think of is that a more liquidy stool would lead to further ease in feco-oral transmission. Is this true?

It would increase the overall transmission rate, I guess. Diarrhoea is not just liquidy stools (which may be better for dissemination of the bacteria) but also frequent stools (high transmission) + low digestive potential of the gut (which also protects the bacteria). You can have a look at some of the epidemiological models for cholera.

@WYSIWYG "low digestive potential " Not sure that changes anything for the bacteria since gut pathogens are adapted to live in that environnement. Unless I misinterpreted the way it could help them.

Other than that you are totally correct and it is the actual answer to the question

Vibrio cholera for example is actively causing diarrhoea, by stimulating the CFTR channel to excrete chlorine ions, which will attract water from the gut tissue.
The answer of the function seems obvious: to promote dispersal in the environment and as such infect/find new hosts.
See also: extended phenotype (Richard Dawkins): how genes in one organism (mostly a parasite) influence the behaviour of another organism (mostly the host of the parasite) to increase the (reproductive) success of the gene/parasite.
Also: numerous (some horrifying) examples in Parasite Rex (by Carl Zimmer)

Welcome to Biology.SE! Please provide references to your claims (best would be peer-reviewed articles or, for well-known concepts, something like Wikipedia) so that others can check your answer and also for further reading. Additionally, please write comprehensive and explanatory answers and do not just throw hints for what to look for (take a look at guidelines here). Your answer as is might be down-voted. Thanks!