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Why to use transgenic mice in ALS models?
In ALS mice model with mutant SOD1 - there are use of transgenic mice, with insert of human mutant SOD1.
Why is that? Why not to mutate directly mice SOD1 ?
In transgenic mice, after few generations these human gene thrown out and not present any more.. Why thrown out? Is the second question.
Looking for an answer for a while. Thanks a lot.

Have you done any research what-so-ever on humanized mice and transgenics? You are manipulating the gene one way or the other. Starting with a null background then adding the human gene of interest through homologous recombination is how you produce an animal that can actually give you data for the question you are investigating. Your third paragraph is completely wrong. Doing speed transgenics it will take you about 4 generations to breed the humanized allele into a homozygous state in the animal. Once it is homozygous, you can then start to analyze the data you are producing.

The use of a mouse with the replacement of one of its genes with a human version is to better mimic the human disease phenotype, or to prove something about the biology of the human phenotype with research that can't be conducted in humans.
Genes and their corresponding proteins or RNA usually differ somewhat between mouse and humans. If you wanted to study whether a certain SNP in a gene (found in humans) was the reason for part of your phenotype, you may want to use transgenic mice to test hypotheses with different exacerbations (treatments).  One way to do this is to create a mouse with the human gene replacing the mouse gene, and another mouse with the human gene containing the trait-linked SNP.
If you tried to do this with the mouse gene, you couldn't be sure that the same SNP would have the same functional consequences.  If you didn't remove the endogenous gene from the mouse before replacing it with the human version, you would never be sure if observed experimental phenotypes weren't confounded by both copies of the gene and their corresponding gene products being active in the same animal.
In your example, with SOD1 and ALS, creating a humanized mouse with human SOD1 allows researchers to more fully study the same protein product made in humans, while giving the mouse treatments that would be unethical in humans.
Your understanding in your last part is incorrect. Mice don't lose genes after a few generations.

Thank you. You wrote about replacement. Is there some reference for this, in ALS SOD mice? Thanks again.

http://www.informatics.jax.org/reference/J:76718 contains the reference for the original humanized mice with WT human SOD1 and mutant human SOD1 containing a SNP.  Pubmed reference to that paper is here : http://www.ncbi.nlm.nih.gov/pubmed/8610185?dopt=Abstract .  Manuscript is here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC39778/pdf/pnas01514-0539.pdf  From a cursory reading, it doesn't appear that the endogenous mouse gene was removed first.  Making the results even more interesting, and very convincing that a G93A mutation in human SOD1 contributes to ALS phenotypes. Hope that helps.


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What kind of animal can do this?

When I was moving to another house, I found this plastic bag on the top of the cabinet of my old house. It looks like someone cut it all with a scissor, but no one have access to my bedroom, and it was not me.
I don't thing it could be rats. That bedroom was very tiny and closed, there's no way for a rat to enter.
The house is very near a university with a little "forest", there are many types of mosquito and little flying animals, but I can't imagine which could do this.
I'm just curious. (and not sure if "zoology" is the correct tag here, but I had to choose one)

How old is this bag? How is been exposed to light for a long time?

@Chris about 2 years old. Exposed to lamplight from 19h to 22hs (when I was home), and not directly exposed to sunlight. The cabinet was on the same wall as the window, and it's top (where this bag was) was higher than the window. But a little sunlight was entering the room during the day, through the glass window. Not directly, as the windows was close to another wall outside.

Then I would suspect this is due to decay of the material of the bag. I have seen similar bags which sat on shelves for years and literally fell into pieces when touched.

Although your plastic bag tears are most likely due to light damage as @Chris mentioned above, there is a type of ant that chews its way through plastic, rubber and other manufactured polymers: Monomorium pharaonis, the Pharaoh ant.

It is capable of destroying many manufactured materials and is a great example of budding, a method by which new ant colonies form. They are very invasive and difficult to control.

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Recombination frequency as a function of genomic location in E coli?
Are there any databases or papers that give recombination frequency as a function of position in the E coli genome?

What kind of recombination do you mean?

Homologous recombination.

No, I mean: which process? There are several processes involving recombination in bacteria, which require enzymes and different substrates. For example, recombination-mediated DNA repair occurs at sites of DNA damage (which can happen at any location, albeit with unequal frequencies), while conjugational recombination is much more location-bound.

A recombination map of the E. coli genome was recently published (several years after question was asked).

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Why aren't genetic triplets roughly evenly found in DNA?
Sorry, the page I linked to is huge and you'll need to do a text search for "CG" to find the part I'm talking about.
I found a graph on this page (http://www.oftenpaper.net/sierpinski.htm) showing that the eight DNA sequences including CG, i.e. four *CG and four CG* sequences are much rarer than the others in a human X chromosome. I realise that this is only for one sample of a human X chromosome (not even all human chromosomes) but I was wondering why this is? Obviously, if *CG is rare CG* will be too.
From my limited understanding the equivalent RNA sequences would be *GC (redundant codes for four amino acids) and GC* (the only codes that produce Alanine). According to the Wikipedia page on Alanine it accounts for 7.8% of genetic amino acids, well over the average.
Is this representative across all DNA? Across all human DNA? What does DNA have against coding CG sequences, even if only in the X chromosome? Do other chromosomes have an abundance of CG sequences but are rare in others?

http://en.m.wikipedia.org/wiki/CpG_site

Or https://en.wikipedia.org/wiki/CpG_site for desktop computers.

No, it's not specific to the X chromosome. It's a general trend. CG sequences are underrepresented in mammalian genomes. In fact, the very nucleotides C and G are underrepresented. Instead of the ~25% you'd expect by chance, the real numbers for the human genome are (calculated on the hg19 version of the UCSC human genome):
N: 234350281 = 7.5702%   <-- N means unknown
A: 844868045 = 27.2917%
C: 585017944 = 18.8978%
T: 846097277 = 27.3314%
G: 585360436 = 18.9089%

If we break this down by chromosome (chrM is the mitochondrial genome which should probably be ignored here), we get:
chrM    A:5113 (30.9%)  C:5192 (31.3%)  T:4086 (24.7%)  G:2180 (13.2%)  N:0 (0%)
chr1    A:65570891 (29.1%)  C:47024412 (20.9%)  T:65668756 (29.1%)  G:47016562 (20.9%)  N:0 (0%)
chr2    A:71102632 (29.2%)  C:47915465 (19.7%)  T:71239379 (29.3%)  G:47947042 (19.7%)  N:4994855 (2.1%)
chr3    A:58713343 (29.6%)  C:38653197 (19.5%)  T:58760485 (29.7%)  G:38670110 (19.5%)  N:3225295 (1.6%)
chr4    A:57932980 (30.9%)  C:35885806 (19.1%)  T:57952068 (30.9%)  G:35890822 (19.1%)  N:0 (0%)
chr5    A:53672554 (30.2%)  C:35089383 (19.7%)  T:53804137 (30.3%)  G:35129186 (19.8%)  N:0 (0%)
chr6    A:50554433 (29.5%)  C:33143287 (19.4%)  T:50533923 (29.5%)  G:33163423 (19.4%)  N:3720001 (2.2%)
chr7    A:45997757 (29.6%)  C:31671670 (20.4%)  T:46047257 (29.6%)  G:31636979 (20.4%)  N:0 (0%)
chr8    A:42767293 (29.9%)  C:28703983 (20.1%)  T:42715025 (29.9%)  G:28702621 (20.1%)  N:0 (0%)
chr9    A:35260078 (29.3%)  C:24826212 (20.7%)  T:35243882 (29.3%)  G:24813259 (20.7%)  N:0 (0%)
chr10   A:38330752 (28.3%)  C:27308648 (20.1%)  T:38376915 (28.3%)  G:27298423 (20.1%)  N:4220009 (3.1%)
chr11   A:38307244 (29.2%)  C:27236798 (20.8%)  T:38317436 (29.2%)  G:27268038 (20.8%)  N:0 (0%)
chr12   A:38604831 (28.8%)  C:26634995 (19.9%)  T:38624517 (28.9%)  G:26617050 (19.9%)  N:3370502 (2.5%)
chr13   A:29336945 (30.7%)  C:18412698 (19.3%)  T:29425459 (30.8%)  G:18414776 (19.3%)  N:0 (0%)
chr14   A:25992966 (29.4%)  C:18027132 (20.4%)  T:26197495 (29.7%)  G:18071947 (20.5%)  N:0 (0%)
chr15   A:23620876 (23%)    C:17247582 (16.8%)  T:23597921 (23%)    G:17228387 (16.8%)  N:20836626 (20.3%)
chr16   A:21724083 (27.5%)  C:17630040 (22.3%)  T:21828642 (27.7%)  G:17701988 (22.4%)  N:0 (0%)
chr17   A:21159933 (27.2%)  C:17727956 (22.8%)  T:21206981 (27.3%)  G:17700340 (22.8%)  N:0 (0%)
chr18   A:22465380 (28.8%)  C:14838685 (19%)    T:22489493 (28.8%)  G:14863671 (19%)    N:3420019 (4.4%)
chr19   A:14390632 (25.8%)  C:13478255 (24.2%)  T:14428951 (25.9%)  G:13511145 (24.2%)  N:0 (0%)
chr20   A:16523053 (27.8%)  C:13107828 (22%)    T:16725227 (28.1%)  G:13149412 (22.1%)  N:0 (0%)
chr21   A:10422924 (21.7%)  C:7160212 (14.9%)   T:10348785 (21.5%)  G:7174721 (14.9%)   N:13023253 (27.1%)
chr22   A:9094775 (17.7%)   C:8375984 (16.3%)   T:9054551 (17.6%)   G:8369235 (16.3%)   N:16410021 (32%)
chrX    A:45648952 (30.2%)  C:29813353 (19.7%)  T:45772424 (30.3%)  G:29865831 (19.8%)  N:0 (0%)
chrY    A:7667625 (29.9%)   C:5099171 (19.9%)   T:7733482 (30.1%)   G:5153288 (20.1%)   N:0 (0%)

As you can see, C and G are consistently less frequent than A and T across all chromosomes. The exception is the mitochondrial genome but that is not the genome of a vertebrate. So, overall, A and T occur almost 10% more often than C and G. But why does this happen?
As far as I know, the reasons are not entirely clear. Some factors that affect this, however, are:

The C of the CG dinucleotides can be methytlated. Methylation is a chemical modification of the nucleotide and plays an important role in the regulation of gene expression. The regulatory sequences that control the way that genes are expressed (promoters), are often rich in CG sequences (these localized overrepresentations of CG are called CpG islands) which enable the control of the associated gene's expression by the mechanism of methylation (which can "turn off" a gene). Not the kind of thing you want to have occurring randomly in your genes.
Methylated Cytosine (C) is often converted to Thymine (T):

This would result in a gradual loss of C in favor of T. This theory had long been considered to be the main reason why CpG is so rare in mammalian genomes, but see the next point.
I found a study from 2004 [1] that shows that, among other things, there is no correlation between CpG and TpA shortages, suggesting that the deamination of Cytosine to Thymine is not enough to explain the phenomenon.

I should also point out that the fact that Alanine represents  7.8% of all aminoacids in proteins does not say anything at all about the frequency with which its codons appear in the genome at large. Only ~2% of the human genome (genes are ~5% and exons, those parts of genes that are translated into proteins, only ~2%) actually codes for proteins so it is only in that 2% where you will see this overrepresentation (if one exists) of Alanine.
In conclusion, yes, the CpG shortage is a general feature of the human genome and not of chromosome X, but the precise reasons for this are not yet entirely clear (as far as I know, anyway).
References

Jabbari K., and Bernardi G., Gene 333:143-149, 2004


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Hydrogen bonding and the blocking thereof in nucleic acids during nuclear processes
In transcription, RNA polymerase unwinds the DNA double helix and begins attaching RNA nucleotides to the template strand. In its wake, the DNA double helix closes back—this is only natural, seeing as the DNA bases have the tendency to hydrogen bond. In DNA replication, this closing is prevented by single-strand binding proteins.
I have three questions regarding this:

In transcription, the pre-mRNA strand peels off the template strand in the wake of RNA polymerase. Why? There are just as well hydrogen bonds between the pre-mRNA strand and the DNA template strand as there are between the two DNA strands.
Why doesn’t the pre-mRNA stick onto the DNA indefinitely and block the non-template DNA strand from reattaching to the template DNA strand?
In DNA replication, why is it imperative that the separated DNA be stabilized by single-strand binding proteins? Won’t the replicated strand block the template strands from closing together?


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Does the body prioritise the use of available sugar before fat?
Let's say you eat a very unhealthy snack that contains 90% sugar and 10% fat. Would somatic cells not start using the fat for energy until all the sugar is used up?
Does the body not use fat at all if there is more bio-available sugar to be used? Or is there always a proportion of fat being used for energy?

I think this is an interesting question; adding your own research would make it a better question. :)

In a very simplified explanation  - the body usually picks the process which is easiest/ fastest which would be to absorb the glucose  then the fat would be used for energy as this takes longer to digest and absorb because it is a relatively complex molecule which also requires bile to emulsify it.
Starchy/ high glucose products will already be broken down in the mouth by amylase and absorbed in the intestine + pancreatic amylase etc. which takes around 20 mins-1hr whereas soluble fats are digested primarily in the small intestine (by enzyme lipase) for (very approx.) 1-4 hours depending on the amount ingested. Insoluble fats are broken down into soluble fatty acids and glycerol which can be absorbed into the blood.
The amount of either you use for energy just depends on how much energy you expend.


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What is the relationship between independent assortment and cross over?
During meiosis, the independent assortment will be made first and then cross over will be made. I am so confused, what is the difference between this two process? I looked at the diagram on internet.It is said that law of independent assortment is alleles of genes on non homologous chromosomes assort independently during gametes formation, but I don't quite understand that.
So, another way for understanding this topic, independent assortment is tetrads can line up four different ways between homologous separate. Is that right.
Appreciate your help.

During meiosis, the independent assortment will be made first and then cross over will be made.

No, independent assortment occurs after crossing over. Crossing over occurs in prophase I while independent assortment occurs in metaphase I and anaphase I.

I am so confused, what is the difference between this two process?

During prophase I, a process called synapsis occurs. That is, homologous chromosomes (one from your mother and one from your father) come together and bind together, forming a tetrad. This binding is due to crossing over, which is when the genetic material on the maternal chromosome and the paternal chromosome exchange places. The maternal chromosome gives some of its genes to the paternal chromosome, and the paternal chromosome gives some of its genes to the maternal chromosome. Crossing over increases genetic variety by creating a new chromosome with a new combination of genes.
During metaphase I, the tetrads line up at the equator of the cell. During anaphase one, the tetrads are broken apart and each homologous chromosome that made each tetrad up is pulled toward one end of the cell. Look at the image below, where the blue represents paternal chromosomes and the red represents maternal chromosomes.

Independent assortment describes the phenomenon where the paternal and maternal chromosomes can be lined up randomly at the equator. There are many combinations. For example,

Both red chromosomes could face the top pole and both blue
chromosomes could face the bottom pole.
Both blue chromosomes could face the top pole and both red could face the bottom.
One red on the left and one blue on the right could face the top, as shown in the picture.
One blue on the left and one red on the right could face the top.

This random alignment at the equator makes it so that during anaphase, random proportions of maternal and paternal chromosomes get assorted into each of the resulting daughter cells. Some cells could get more maternal chromosomes and the other would get more paternal chromosomes, and vice versa. On the other hand, they could get similar amounts. Independent assortment increases genetic variation by allowing daughter cells to each randomly receive a different proportion of paternal and maternal chromosomes.
In conclusion, crossing over and independent assortment (sometimes called random assortment) are different independent processes that both lead to an increase in genetic diversity.

References

Reece, Jane A., Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, and Robert B. Jackson. “Meiosis and Sexual Life Cycles." Campbell Biology. 10th ed. Glenview: Pearson, 2014. 252-266. Print.
https://www.quia.com/files/quia/users/dschnepp/Meiosis/Metaphase-I

I'm interested in the randomness of the "Independent assortment" of the genetic material. How specifically is randomness achieved, to create the specific unique variation out of the 2^23=8388608 possibilities. Are certain combinations naturally more likely than others, and how does the cell make the components line up randomly at the equator?


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Most painless method for killing insects
I'm planning on having a small farm of crickets or grasshoppers.
I would like to cause them as little suffering as possible, so I'm wondering what is the most painless way to kill them?
So far, the plan is to put them into the fridge (+4C) to slowly chill them (that way they will not notice it as much), and then to freeze them in the freezer (once they are chilled and are either unconscious or barely so).
EDIT: It is important to note that I am planning on eating them.

They have a wikipedia page for euthanising insects, to my surprise. I'm far from experienced here, though.

I think the freezing method makes sense, since that is how they do it with lobsters. And lobsters are just underwater large bugs really. You could try decapitating them?

4⁰C won't kill them.. see here.. You can freeze them in a deep freezer, if you have one..

As far as I'm aware, there really isn't conclusive evidence that insects can actually feel pain in the same sense that we do, as their nervous systems just aren't that complex. So, I really wouldn't get too hung up on this.

I commend you for a) growing your own and eating insects (so 21st century; not a joke), b) caring that they not suffer. An uplifting question!

I doubt if it is possible for such small nervous system to produce any sentience. Human finger probably contains more neurons than grasshopper.

The faster you kill them, the lesser they can "feel". So the best way should be shock freezing and or throwing them into boiling water.

@AstronAUT at what temperature do they die? Boiling, I would say is a pretty bad way to go, unless it's a second or less.

Thats true. You only need to exceed the temperature, which leads to denaturation of their body proteins. That could be already at >41 °C.

The terrestrial invertebrate taxon advisory group of the Association of Zoos and Aquariums recommends anesthetizing the insects with carbon dioxide and then placing them in a freezer to euthanize them.

Can you post a link to this information? It sounds correct, as CO2 is used by Drosophila labs, but it is always a good idea to source your answers with a link.

Hi and welcome to Biology StackExchange!  Do you have any links to reference your answer?  I see that group mentioned on Wikipedia but usually in reference to freezing.

Using CO2 doesn't feel very practical to do at home though, if the purpose is to grow them for on a large scale for food.

@fileunderwater well, you could always breathe at them. :P


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Help me identify this insect
Over the last week or so as warmer weather has arrived, I've noticed small insects crawling around in the bathroom. I'm located in western Europe. They are perhaps 1mm in length, quite difficult to see without a magnifying glass. I used a macro lens to capture these pictures. What might they be? Ticks? Aren't ticks larger? Why are there so many?
Note: these pictures are heavily magnified (they are on an old wooden door with cracking paint), and I've applied lighting auto correction. Actual size of each insect is 1mm or less.

I can't tell if those have 6 legs and large antenna, or 8 legs and no antenna. If 8 legs, then I suspect some sort of mite.

At the moment, my guess is louse or first instar nymph cycle of a bed bug. Can you obtain better pictures?

It looks like 6 legs and large antenna to me.

@rozmarin Yeah, the last 2 images show it better.

Definitely a spp of mite. And definitely not a bed bug. Sick of people always suggesting that small unknown insects are bed bugs -_-. Need bus do have their own distinct appearance...

After a long hunt it seems they are Dermanyssus gallinae. It appears I have a pigeon's nest somewhere near my building.
http://en.wikipedia.org/wiki/Dermanyssus_gallinae

You should add the picture.


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How long do the periods of systole and diastole last?
The background to this is i'm doing some work using ECGs for an animation of the heart and i'm having trouble defining the end points of these periods, particularly diastole. Currently, the only information the animation uses is the time (in seconds) when a R peak was detected in an ECG.
So i was wondering what the normal lengths of these periods are and what could affect the lengths of these periods.
I assume that the lengths of the periods is mainly affected by pressure/blood volume and not electrical activity so an ECG won't tell you how long these periods are (unless a heart beat is interrupted by another?). Is that assumption correct?
On a side note: what would happens to the heart physically if there is a large gap between beats. Does it sit relatively still during that period?
EDIT:
My original post could have worded better, so: I want to know specifically about long it takes for the ventricles to physical contract and relax. How would i determine the length of these two periods in seconds and where could i find the "normal" lengths of these periods? in the cause of relaxation, i'm wondering about what to do when there is a substantial gap between heart beats.

I've edited my answer, I hope it helps! If not please let me know, so I can refine to mach your needs.

I assume you are talking about humans?

The following image from wikipedia answer what you need. You can check corresponding page for details.

The top part shows the details of the different processes during a heart beat. Corresponding to these events the ECG reads are marked. As you can see the distance between the T wave ( the small bump after the QRS complex) and the next P wave corresponds to the diastole. As you can see the pressure changes correlate well with the electric reads from the heart. This wiki page has great descriptions of the features of the ECG and the corresponding events.
For example P to QRS corresponds to the conduction of stimulus from the sine node to AV node, or QRS depicts the rapid depolarization and repoliarization of the ventricles. This latter leads to strong muscle contraction and this causes intaventicular pressure rise, that is followed by aortic pressure change.
Edit: Sorry, for missing the key point, I totally misunderstood what you needed. I'll try to correct my mistake (I'll leave the previous info as it may be useful for others) The authors of this paper did a really nice work on modeling and measuring left ventricle contraction time and other things.
The reference: (Beyar and Sidman 1984)
Long story short: the contraction of the ventricle depends on the initial amount of blood (preload), aortic blood pressure at the end (afterload), and intial contractility. The results are summarized in three tables:

As you can see in the last columns, the ejection time varies with the parameters. The ejection time that is required for the ventricle to push the blood out to the aorta. Under normal circumstances a complete heart cycle is about 0.8s (or 800ms) this pie char shows the time ratio of main events. (Image taken from: tutorvista.com)

Note that complete cardiac diastole is when all the heart muscles are relaxed (this can be shortened if higher heart rate is required).
According to wikipedia

Isovolumic relaxation time (IVRT) is an interval in the cardiac cycle, from the aortic component of the second heart sound, that is, closure of the aortic valve, to onset of filling by opening of the mitral valve. A normal IVRT is about 70 ± 12 ms, and approximately 10 ms longer in people over forty years. In abnormal relaxation, IVRT is usually in excess of 110 ms.

Isovolumic relaxation is when the muscle relaxes, yet the volume of the ventricle remains the same, thus only the internal pressure changes (it is analogue to isovolumic contraction - when the volume is unchanged, but pressure is built up, this happens at early ventricle contraction).

Systole lasts about 3/8 and diastole 5/8 of a cardiac cycle.
Keep in mind though that such values vary with heart rate. The higher the heart rate, the shorter the fraction of diastolic time compared to the entire cardiac cycle.
That said, an ECG is not the best thing to look at if you wish to determine systolic and diastolic time intervals. What you would need is a heart ultrasound, so you can actually see the valves opening and closing. These events can be considered to happen in an instant. The potential you see on an ECG instead can vary with continuity and it would be a little harder to tell the exact timing.
So your assumption is correct.
Yes, a large gap between beats would show a heart expanding very slowly (this typically happens just before the atrial systole).
With substantial gaps between heart beats, consider those time intervals to belong to diastole.


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Before I move my arm the brain sends signals - what causes the brain to send signals?

Please tell me what causes the brain to send signals, how does the brain send signals?
can you tell me what happens between the point when you make an intention to pick up a glass of water, and before the brains sends signals to the body which excites the muscles.

So what happens at the moment when you make the intention to pick up a glass of water but before the brains sends signals after you reach to pick up a glass of water.

subquestion one seems too broad, but the remainder is interesting.

Action potential - I haven't read through the entire Wikipedia article so I can't vouch for its accuracy (not that my neurophysiology is good enough to critique it), but it's probably a good start.
Broadly speaking: the brain contains different regions that are each responsible for fairly specific tasks. In the case of picking up a glass of water we can, at a high level, describe the mechanism behind thirst. Your blood contains electrolytes in water; you can consider the electrolytes as being like cordial (reduce the water and you have a higher concentration of cordial / electrolytes). A sensing mechanism (beyond the scope of this answer) will trigger action potentials between the relevant areas of the brain (motor, memory, etc.) to result in the final movement.

satisfying answer. nice answer to the question. good attempt because this question I think is not asked before I think.

i think question is bizzare, so there is no need to judge any answers posted

question isn't bizarre, question is good, god wants mankind to learn more about his creation, you just don't know, you are not knowledgeable enough to know what questions are good or not. just be quiet

1) There is always a persistent sodium current which is slowly inactivating in comparison with the fast transient sodium current that occurs when a neuron is depolarized. The effects of this persistent sodium current brings the resting membrane potential near the threshold. Furthermore, neurons do indeed fire and reach depolarization state due to these fluctuations in membrane potential, but those action potentials will not always cause a depolarization of the post-synaptic neurons, since those neurons have inputs of convergence from inhibitory neurons that produce inhibitory post-synaptic potentials. There is no moment or situations where all of your neurons are quiet.
Further information about persistent sodium current can be read in French et al.,1990., "A Voltage-dependent Persistent Sodium Current in Mammalian Hippocampal Neurons"., J. Gen. Physiol., Vol 95;1139-1157 http://jgp.rupress.org/content/95/6/1139.full.pdf
2) The brain center which is thought to play an important role, not only in decision making, but also in behavioral control of the decision making dependent on the reward and outcome, is the prefrontal cortex. Except for its associative learning capabilities prefrontal cortex is thought to have neuronal connections with many part of other brain structures and it must first gather information and integrate the information before deciding what to do. In your question the reward is the glass of water, the emotional response you would get to drink that cold water would aid to the decision making, and the motoric movement is initiated by the subsequent firing of neurons when you see the glass of water and when you recall/remember the feeling to drink it. Prefrontal cortex is therefore activated and can thereafter send action potentials to motor cortex and then to your peripheral nervous system and muscles, so you can pick up the glass of water.
More about this here: http://ac.els-cdn.com/S0959438800001926/1-s2.0-S0959438800001926-main.pdf?_tid=83268f2a-eed1-11e4-ae1f-00000aab0f6c&acdnat=1430354614_ddc06d6aeae4543af28ebe02e29486cc


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How do DNA viruses keep themselves in the nucleus without inserting themselves into genome?
If I'm not mistaken only RNA viruses insert themselves into the host genome. As an example of DNA viruses, herpes viruses for example do not insert themselves in the host genome.
Then how do DNA viruses keep themselves inside the nucleus? Do they just float around without their capsid? And if the cell duplicates, would the DNA of a DNA virus also be duplicated even though it isn't inserted in the host's genome?

If my question makes some weird assumption, I'm sorry. I'm here to learn and the fact that I'm asking a question is precisely because I don't know all the facts.. Thanks for your answer already!

Hi Yuri. We require that all question posts ask a single question on this site. You need to choose whether you want your 1st (How do DNA viruses keep themselves in the nucleus without inserting themselves into genome?) or second (Can CRISPR remove them too?) question answered. Choose to keep one and delete reference to the other. You may ask your second question in a second post. Failure to do so will result in question closure, but I think you'll not find it too troublesome to split up your post. In both, please indicate explicitly that you've researched each question and how. Thanks

@theforestecologist done!

Great, thanks! Now, if you explicitly add where you've already researched your question on your own and what you've figured out, you'll receive much more positive reaction from our community. (for example, try YouTube, wikipedia, pubMed, Google search results, Google Scholar, a school textbook, etc etc.). Our goal, Yuri, is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :).

Herpesviruses maintain themselves during the latent state as "episomes", circular DNA elements, with no capsid, that are in the nucleus but that are not integrated into the host genome. Host enzymes replicate these episomes, and different viruses have evolved different strategies for ensuring that the episomes are passed on to newly-divided cells.

After they first infect cells, many herpesviruses establish a latent lifecycle with the viral genome existing as circular genetic elements called episomes inside the host cell’s nucleus that are closely associated with, but not integrated into, the host DNA. During latent infection, episomes are replicated during S phase, but new viral particles are not produced and the infected cell survives. The maintenance of herpesvirus genomes as episomes contrasts significantly with retroviruses, which insert their genome within the host cell genome to ensure their replication and inheritance by daughter cells and establish long-term infection. ... EBV uses a mechanism to tether the EBV genome to host DNA, facilitating the equal distribution of episomes in daughter cells with a larger number of cells having at least one EBV genome. In contrast, KSHV uses a clustering strategy that promotes a higher number of episomes per cell, but at the expense of not passing on the episome to some daughter cells

--How herpesviruses pass on their genomes
Another mechanism many herpesviruses use is to establish their latent infection in non-dividing cells, especially neurons, so that there's no concern about daughter cells.

"The maintenance of herpesvirus genomes as episomes contrasts significantly with retroviruses,..." - and contrasts with some non-retroviruses the DNA of which gets integrated into host DNA by host enzymes (by chance).  Does herpesvirus care about maintaining its integrity, in other words: does herpesvirus, by any means,  make sure it's not being absorbed by host DNA? (another question: "without 'being' inserted"?)

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


text:
Can DNA test of my grandparent's brother reveal my heritage from that branch of the family?
I'm thinking about doing that DNA test on all my grandparents to know where their genes come from. They are getting very old and I don't want to let the opportunity pass to gather more knowledge about my heritage, something I find very interesting.
One of my grandparents died long ago, but he still has a brother and I was wondering if DNA testing him would reveal relevant information about my heritage from that branch of my family tree. Obviously all of his genes come from family of mine(his parents) but not all of his genes are the same as my grandparent's. Just how should I look at his tests to find information about my heritage?
By the way can I really trust these sort of tests?

if he is the brother of your grandparent then his DNA has some degree of probability that it is identical by descent to that of your grandparent - siblings on average share half of their DNA, though theoretically could share 0-100% of their DNA. Given how broad this is and that it borders on product/service recommendation, while seeing very little in the way of a proper question about biology, I am downvoting

I can take the recommendation part off even the name of the company, but my question is pure biology

I disagree that this question is too broad. It is asking for a very specific case of the genetic tests which need to be carried out to determine the relationship of less closely related relatives.

@rg255 you should develop a little and post your comment as an answer.

As Rayoub's answer points, you are likely to share a random part of your genes with your grandparent's brother, and therefore analysing his DNA won't tell you where all your genes come from, since he has some genes you don't have and you have some genes he doesn't have.
However, I understand that you aren't that interested on your particular genes, but on what genetics can tell you on the history of your family - that is, to shed light on who were your ancestors and where they came from. Then, if your grandparent's brother was your grandparent's full brother, his ancestors are your grandparent's ancestors and therefore analysing his DNA can be as useful as analysing your grandparent's DNA.
In addition, since your grandparent and his brother doesn't share all the same DNA (likely just about 50% for full brothers) and each of them just have a 50% of each of their grandparent's DNA, if you could analyse DNA from both a grandparent and one or more siblings, you would be able to gather more information. In fact, you would be getting closer to get the same information you could have got from analysing your grandgrandparents'DNA.

You should be able to learn some things about your family's heritage from your great uncle's DNA, but, if you're looking to find out about where they lived previously, a stable isotope test might be useful. However that would only he able to tell you where that individual (and siblings who were with them) lived, but nothing farther back. I know your question is 4 years old at this point, but maybe this is something helpful.

Wouldn't you need bone or tooth samples? That sounds rather invasive for the living.

Welcome to Biology.SE. We're looking for long answers that provide explanation, context, and include references to reliable sources. Don't just give a short answer; explain why your answer is right with appropriate citations. Answers that don't include explanations may be removed. Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly.
@JiminyCricket. — Ridiculous! I'm sure he wont mind "donating" an otolith ...


text:
Does the effect of light on melatonin release adapts to light level over long periods of time?
Or do you go to bed with low levels of melatonin when you stay behind a computer screen all day?

Melatonin influences sleepiness but isn't necessary for sleep: you can sleep even if you are in the light all day.

but how about the levels of melatonin under constant light? does the brain realize at some point it's not going to get dark somehow and starts producing melatonin, or will the brain simply not be able to produce it like it normally would do? @B

I think that would be a better question than the one you posted. I would try to avoid words like "realize" since even though we are talking about the brain we aren't really talking about cognitive control. What you seem to be wondering is whether the effect of light on melatonin release (it is release that is affected by light, I believe, not production) adapts to light level over long periods of time.

This paper, for example, shows that indeed, melatonin is suppressed more in the light after a week of dim light exposure compared to after a week of bright light exposure.
However, the authors note that although the result was statistically significant, the effects were fairly small compared to the overall variability in the data.


text:
How the pattern of fertilization path is determined before the cell division to form the blastocyst? Is it individually specific?
After sperm meets ovum,the inactive nucleus starts following a particular path inside the zygote rather chase a path.This path is biologically known as fertilization path (as mentioned in an article of a local magazine named "science reporter"). But my question is how the pattern of the path is determined?  I came to know from the article that for every individual this particular path is very specific. Is it true?  If so then what does that specific path determine and why is it specific for every individual?

Can anybody please make me understand it?

This is a tad unclear.. are you asking about molecular pathways that underlie embryogenesis starting at fertilization? Even so, this is very broad and there are many players involved. You may need to clarify exactly which aspects need explaining.

Is the article one of these: http://nopr.niscair.res.in/handle/123456789/30751 ?  It seems like "Science Reporter" is behind a pay wall, but I was looking at least for the article.

No..I don't think they post online articles. But I checked. The article isn't from here.

First of all, the more commonly used term is "copulation path," and I don't ether is used as a formal biological term, but rather in models for the public.  The term that is used in literature is "pronuclear fusion" for the process as a whole, and I don't know of a more technical term for the path itself.  Your inability to find information may have been linked to terms used.
Anyway, the copulation path doesn't have as much variability as the penetration path, which is what determines the copulation path.  The copulation path tends to be a relatively straight line between the two pronucleoli, dictated by and pushed along the cytoskeleton (Lian et al, 2014).  It is worth noting that it is often not the shortest straight line (think of the number of lines between a smaller sphere and a larger one), but still a relatively straight line.  People tend to care about this, because what ever the copulation path, it sets the axis of division, which can effect in vitro fertilization techniques, particularly in plants.
Getting at what I think you are trying to ask, the penetration path is variable because it is an oscillatory phenomenon.  You actually have to move back in the fertilization process to the sperm impact angle (Hedrih et al, 2015 is the coolest model I've seen of this) to see how this can change.
To understand oscillatory phenomenon in general, you need to understand that a lot of the processes in biology are driven by the chaotic (used in the formal since) vibrating or shaking of molecules and fluid microcurrents.  This means that we can not know (regardless of how sensitive we measure) the conditions specific enough to create the specific path.  These things are not tied to genes or to the person in general (perhaps exuding of mutations/disorders that effect the morphology of sperm or egg).  Rather it is specific to any single fertilization reaction simple because of chance/chaos.

Thanks a lot. You really understood my problem well and I am sattisfied with your answer.

@Demietra95 It's still not a wonderfully worded question.  The "because I read..." section is both poor grammar and doesn't say where you read it.  You should always include references/links to the source materials you've been looking at that lead into a question.

I am really sorry for my mistakes :( Actually I read it in a local science magazine and there it was referred as fertilization path.

@Demietra95  That's fine, you can go back and edit the question to include a reference to the magazine article.  It doesn't matter if it's not in English.

Thank you so much. Just edited it. Though the magazine is an English science of magazine, it's local,  it's mostly popular in our country but probably not outside.


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Does "mind" has any physical reality in biology? Or is it just an assumptive concept?
Biologically,  Brain controls our thinking,  ideas,  decisions everything along with controlling each body parts. My question is,  is there anything real as "mind "?  If it's controlled by brain then how does brain controls the mind?

This might be a better question for the Psychology SE.  Neuropsychology studies the relationship between the brain and the mind, to an extent.  Neurology can touch on this, however, because self-report of experiences (as unreliable as it may be) is often the easiest way to get information about the mind.  A patient describing depersonalization isn't describing anything that you can measure easily without talking to the person, for one.  I'll try to answer below.

@TrixieWolf - Psychology SE does not exist as separate entity anymore. Please refer users to Cognitive Sciences instead.

@AliceD  Thanks.  I apologise for not checking first (I belong there more than here anyway).

@TrixieWolf - Please don't apologize :) I have been pointed out to it myself by others :) Still going through your answer - it looks good, but have to dig it through before upvoting :)

The mind is an abstraction which arises from physical and chemical processes within the brain.  For a crude analogy, think of the brain as an incredibly complex, self-modifying, multithreaded program.  The mind would then be the abstraction arising from the behavior of the program as it runs.  Consciousness would be the abstraction arising from the behavior of one particular thread in the program: a thread which has access to a limited buffer of its own (that thread's) behavior, and control over limited input and output from the body.  All of the other (unconscious) threads may affect the conscious thread, but the conscious thread has very limited access to information about the behavior of the other threads.
Since the conscious part of the mind has access to information about its own behavior, there is actually some recursive looping going on when it comes to thinking and feeling.  The feeling that this goes in circles somehow (which you seem to be expressing) is a common intuition, and it's almost certainly a correct one.  But the manner in which this occurs is not well-understood, and it's definitely not well-understood within biology at the macro level because the brain is unbelievably complex and plastic.  We really don't have a clue how to begin modeling the brain's processes.  This is one reason artificial intelligence is still extremely crude today (despite what Elon Musk and Bill Gates may try to say).
If you want to read a scientifically-inspired theory of from whence consciousness comes, and of how it arises from the brain, I would recommend the book Godel, Escher, Bach by Douglas Hofstadter.  Douglas does a good job of combining computational theory with biology, music, and art to illustrate a theory of consciousness the reader can grasp even if you don't have a strong background in any of those subjects.

+1 - You should definitely check out Cognitive Sciences too! But there's definitely overlap, so don't just run away - expaND :)

The Emperor's New Mind by Roger Penrose is another book on the subject that's worthwhile.


text:
Bubbly foamed cone with insect inside
Location: In a lawn 20 km south of Vienna, Austria
Date & Time: 13th of May 2024 at around 2pm
Estimated size of the  ellipsoid, foamy cone:  y-axis 10mm, x-& z-axis 6-7mm
Estimated length of the insect within the foamy cone: 4-5mm
Please excuse the poor quality of the second picture - focus was off a bit and I was using an old smart phone..

I discovered some bubbly, foamy cone attached to a blade of grass which I never noticed/seen before. It  looks like the insect inside that foamy cone is maybe in its nymph or molt stage.
I have to admit that due to my curious nature I took another blade of grass to gently scrape away some of the foam to see what's inside - I attached another photo showing how it looks when it is still intact.
I tried searching the web with all sorts of combinations of 'insect', 'nymph', 'foam' and the like but unfortunately couldn't find anything that comes close. It also seems that its shell/molt is also present within the foamy cone.
Anyone can share some insights on what that could be/evolve to?
I also find that foam amazing - is this quite common?

This is a very cool question! Thank you for providing a image and location
The insect which made the spittle is in the Subfamily Aphrophorinae, which contains most if not all spittlebugs.
Spittlebugs damage plants by biting into them and sucking all of their nutrients out. The Spittlebug then uses the plant nutrients to create the spit which it will feed on when it emerges from its egg.

Spittlebugs damage plants by piercing plant tissue and sucking out juices. The damage stunts plant growth, distorts leaves and interferes with fruit production. Effective spittlebug control focuses on reaching these pests before they're covered in protective foam.  Source: https://www.gardentech.com/insects/spittlebugs

The species is best identified by range, as the only spittlebug in the Vienna area is the Meadow Spittlebug (Philaenus spumarius)

Philaenus spumarius, the meadow froghopper or meadow spittlebug, is a species of insect belonging to the spittlebug family Aphrophoridae. In Italy and America, it is economically important as one of the vectors of Pierce's disease (Xylella fastidiosa)  Source: https://wikipedia.org

The brownish thing inside the spit is the molt of the spittlebug.

Spittlebugs overwinter as tiny white eggs in plant stems. The eggs hatch in early to mid-spring. Over the next month or two, the nymph feeds within it spittle, molting two to four times. The nymph finally molts to an adult in late spring or early summer, emerging from its froth.  https://hort.extension.wisc.edu/articles/spittlebugs/

You should refrain from touching the spittle as it carries disease and touching it will spread bacteria:

...With a wide geographic range and the ability to thrive in climates spanning from Hawaii to just south of the Arctic Circle, the spittlebug is also a serious agricultural threat because it can carry bacteria from plant to plant while it feeds.
“Thirteen hundred host plants means 1,300 opportunities to spread pathogenic bacteria in natural and agricultural environments, a sobering wake-up call,” said the study’s lead author Vinton Thompson, a research associate in the Museum’s Division of Invertebrate Zoology.

The bug is also impactful as being a significant carrier of the devastating Pierce's Disease:

Philaenus spumarius is economically important as one of the vectors of Pierce's disease (Xylella fastidiosa)

Here are some examples of the meadow spittlebug:

Image one reference: https://www.inaturalist.org/photos/83085896, Photo 83085896, (c) Thomas Barbin, some rights reserved (CC BY-NC), uploaded by Thomas Barbin  Image two reference: https://www.inaturalist.org/photos/140353568, Photo 140353568, (c) Paul van de Velde, some rights reserved (CC BY) Image three reference: https://www.inaturalist.org/photos/77769829, Photo 77769829, (c) Mason Maron, all rights reserved, uploaded by Mason Maron

Can you provide a reference for the claim that "touching the spittle as it carries disease and touching it will spread bacteria"? That seems quite surprising, are you saying that they act as a substrate for specific bacteria that can be harmful to humans?

@terdon Absolutely! I just did. It doesn't carry diseases harmful to humans but diseases harmful to plants. Sorry for the mixup, and thanks for pointing that out :)

The larvae of "froghoppers" are called "spittlebugs" because they make these little balls that look like foamy spit to protect themselves:
https://hort.extension.wisc.edu/articles/spittlebugs/
https://en.wikipedia.org/wiki/Froghopper
I won't attempt to identify the particular species in your picture, maybe someone else will, but the "meadow spittlebug/froghopper" seems to be a quite common one in Europe as well.

Thank you for your answer  - could you also include your thoughts on  which stage this froghopper might be and if the greyish object is indeed its shed/molt/shed in your answer? In the linked article it mentions 'immatures, or nymphs'..

What I found amazing: _"The immature bugs feed face down on the stem, and as excess sap is excreted out the anus, A spittlebug nymph peeks out from a mass of bubbles on a strawberry leaf. A spittlebug nymph peeks out from a mass of bubbles on a strawberry leaf.
it is mixed with a substance secreted by epidermal glands that enhances surface viscosity and stabilizes the foam to make it last longer. This mixture is forced out of the abdomen under pressure and as it is mixed with air, it forms bubbles. Some species can produce as many as 80 bubbles per minute. "_ Very impressive..

@iLuvLogix It would definitely be a nymph, but sorry, I'd be completely guessing at which nymph stage it might be.


text:
Does size correlate with sensory abilities?
On average, do smaller animals have senses inferior to those of bigger animals?  I ask because it seems like a somewhat logical assumption: smaller eyes would in theory collect less light, and smaller ears would in theory collect less sound.
Or is size just irrelevant?

this is a broad question that probably depends greatly on the types of senses that you're referring to. what research have you done trying to fine an answer to this question?

Size is not likely to have anything to do with sensory acuity. A simple example can be seen in the fact that rodents have much more sensitive sense of smell than humans, and some birds have much sharper visual senses than humans. It has much more to do with the number of olfactory/light sensors, sensory pathways to the brain and how that information is processed by the brain (i.e how much priority is assigned). Sensory organ size per se is less relevant (think of elephant ears).

can you add some references or links to back up your answer? posts without any evidence of reference material don't get very far on BiologySE - even if this maybe common knowledge to you, you still need to try and provide some references that others might be able to read more to better understand the answer

Guess thats true. Unfortunately my answer comes from years of working in scientific research animal facility, with small animals. References for something more on the 'common knowledge' spectrum would be very labor intensive and difficult to find. I will remove my answer shortly as i cannot provide a citation. Just want to give the poster a chance to view this answer and maybe help them get where they need to get.


text:
Why draw blood from veins rather than arteries?
Why draw blood from veins rather than arteries? Is it more convenient or safer?

Veins have several advantages over arteries. From a purely practical standpoint, veins are easier to access due to their superficial location compared to the arteries which are located deeper under the skin. They have thinner walls (much less smooth muscle surrounding them) than arteries, and have less innervation, so piercing them with a needle requires less force and doesn't hurt as much. Venous pressure is also lower than arterial pressure, so there is less of a chance of blood seeping back out through the puncture point before it heals. Because of their thinner walls, veins tend to be larger than the corresponding artery in the area, so they hold more blood, making collection easier and faster.
Finally, it is somewhat safer if a small embolism (bubble in the blood) is introduced into a vein rather than an artery. Blood flow in veins always goes to larger and larger vessels, so there is very little chance of a vessel being blocked by the embolism before the bubble reaches the heart/lungs and is hopefully destroyed. Blood flow in an artery, on the other hand, always moves into smaller and smaller vessels, eventually ending in capilllaries, and there is a chance that a bubble introduced by a blood draw (generally rare) or more commonly an intravenous line (IV) could block a small blood vessel, potentially leading to hypoxia in the affected tissues.

+1 - all good points. The main risk, though, is bleeding. Puncturing an artery can cause it to bleed until it tamponades, causing a hematoma which can  cause ischemia downstream and might compress/damage the nerve in that neurovascular bundle. Because of that, pressure must be applied for a while (longer for larger arteries). Before doing a radial artery stick (common for blood gasses), one should do an Allen's test for collateral circulation. The risks are acceptable for blood gases or monitoring but not for blood collection.

(Oh, btw, the paper deals with cannulation, not just puncture, but the principles are the same.)

Yes, arteries are punctured when arterial blood gas readings are required. Patients then wear compression bandages for days.

Right of the bat, veins are superficial so it is much easier to hit a vein than an artery. Arterial sticks are very difficult if you are not practiced at them while veins are much much easier. Also arterial sticks have a very specific purpose usually for example arterial blood gas. Also veins are low pressure compared to the higher pressure of arteries so less chance of bleeding.

Blood is not always drawn from the veins depending on the medical need and situation. For example critically ill ICU patients will often have an arterial catheter placed to provide an accurate measure of blood pressure. Blood is sometimes sampled from this line to provide a more accurate measure of blood gases and cardiac performance.
But the risks of dealing with arterial blood are greater as others have mentioned.


text:
Which sex of trees bears fruit?
Which sex of trees bears fruit? The males or females? And what specifically cause that one to bear fruit. Is it the same as it is with blossoms in trees?

The distinction between male and female is not that clear in plants, at least at the level of individuals. Actually the details may be rather complicated (see [1]), but in general we can distinguish between plants that have:

male and female individuals (dioecy)
male and female flowers on the same individual (monoecy)
flowers that have both male and female structures (bisexuality)

In the first case, only female individuals produce flowers that -- when fertilized by the pollen from the flowers of a male individual -- develop into a fruit. Examples are Hazelnut, common nettle and a few other species [2]. However, dioecy is rather rare among extant flowering plants [3].
Monoecious plant species are somewhat different. A good example is maize. The male flowers of a maize plant are located in the tassels at the apex of the stem, wheres the female flowers are are in the leaf axils. Note that each corn developed from a single flower and that the cob is actually the infructescense.
Then there are bisexual plants. In these, every flower has the potential to be fertilized and develop into a fruit, which is why they are also called perfect flowers. Plants have developed several strategies to prevent self-fertilization, e.g. the temporally delayed expression of female/male structures within the same flower.
Resources:
[3]: Bawa, K. S. (1980). Evolution of dioecy in flowering plants. Annual review of ecology and systematics, 15-39.


text:
Are the irises an exact match in a human's set of eyes?
Are the irises an exact match in a human's set of eyes? Assuming the eyes are healthy with 20/20 vision.

Short answer
No. Not two irises are alike, including the irises of identical twins and even the two irises of one and the same person. This uniqueness of the human iris is used in iris scans. The variety of the iris is caused by its complex structure and coloring pattern.

Source: Jean-François Mainguet
Background
The iris is explained on Biometric Technology's website, and I quote:

The iris [...] is a thin, circular structure in the eye, responsible for controlling the diameter [...] of the pupil [...]. “Eye color” is the color of the iris, which can be green, blue, or brown. In some cases it can be hazel (a combination of light brown, green and gold), grey, violet, or even pink. In response to the amount of light entering the eye, muscles attached to the iris expand or contract the aperture at the center of the iris, known as the pupil.

A striking example of the dissimilarity of the iris in one person are people with heterochromia. Heterochromia can result in both eyes having a different color. Examples are given in the figure below: On the left is Demi Moore (if you look closely her right eye is hazel, while her left eye is green). On the right-hand side a more striking example is shown (taken from the Kliproject):

Heterochromia iridium (differing iris colors) and heterochromia iridis (a variety of color within a single iris) are relatively rare in humans and result from increased or decreased pigmentation of the iris. Most cases are the result of an alteration in the expression of the EYCL3 gene (which codes for brown/blue eye color) and EYCL1 (which codes for green/blue eye color), among other genes within the cells of the entire iris or even a particular section. Other potential causes include trauma around the time of birth or later in life, congenital pigmented nevi or even medications such as those used in the treatment of glaucoma.
Fun fact
David Bowie's eyes are in fact of the same color - his pupils are of a different size:

Reference
Scientific American (November issue, 2001).


text:
why do some cells in the body prefer necrosis to apoptosis as a means of cell death?
There are many programmed cell death pathways, but some cells show a greater preference for some over the other. I'm wondering as to why if necrosis is an inflammatory response that causes damage to neighboring cells, why some cells would prefer this as opposed to a more controlled mechanism such as apoptosis or even autophagy.

Necrosis often happens in case of mechanical injuries or diseases. Apoptosis is programmed and controlled cell death. If tissue damage is too severe, however, the necessary steps can't take a place. A severed cell membrane pretty much prevents apoptosis

What makes you think some cells prefer necrosis? I think the condition leading to cell death is deterministic

There is actually no preference for apoptosis or necrosis in cells of the human body - both types can occur in all cells and they have different triggers. The main differences can be seen in this figure (from here):

Apoptosis (also called programmed cell death) has three different triggers (intrinsic, extrinsic and Perforin/Granzyme pathways), see the image below for details (from reference 1):

All three activate different components and caspases in the beginning but finally all activate Caspase 3, which finally activates endonucleases (which degrade the chromosomal DNA), Proteases (which degrade the proteins in the nucleus and the cytoskeleton) which leads to the degradation of the cell. In the end apoptotic bodies are formed from the cell. Additionally the mitochondria break down and release cytochrome c and ATP. Their release from the cell attracts macrophages which take up and eliminate the apoptotic bodies and in turn release cytokines which suppress an inflammatory response.
Apoptosis goes on in a ordered way and does not trigger any further reactions in neighbouring cells (except these receive the same signal). See also reference 1 and 2 for more details.
Necrosis is triggered by external stimuli of the cell as injury of tissues or toxins from infections. Necrotic cells swell, while there internal structures are in a state of unregulated degradation. Finally the membrane will burst and set free cytochrome c and phosphatidylserines from the membranes which cause inflammation in the affected tissue. The necrotic cells are not removed by macrophages which allows the released interior of the cell to spread further and cause problems.  See reference 2 and 3 for more details.
Necrosis is usually not as a beneficial process, but there are also publications which see
the process as a specific form of cell death (see reference 4).
References:

Apoptosis: A Review of Programmed Cell Death
Apoptosis vs. Necrosis
Cell death by necrosis: towards a molecular definition
Review Necrosis: a specific form of programmed cell death?

Necrosis basically occurs when a cell is injured beyond recovery and it does not have sufficient energy and time to undergo apoptosis

@CRags That would the TL,DR version :-)

The answer given above by Chris is correct, but does leave out one relatively recently discovered method of cell death, somewhere between the two responses of apoptosis and necrosis.
It's called pyroptosis. It's a form of programmed cell death (in immune cells, e.g. macrophages), so it is similar to apoptosis. However, instead of a neat and tidy non-phlogistic (inflammatory) death as is the case in apoptosis, the cell purposefully upregulates inflammatory cytokines, swells, and bursts, releasing the cytokines and other inflammatory mediators out into the extracellular space.

The wikipedia page on this is quite good, and for this image and more information you can check out this study.
It's a response to certain Pathogen Associated Molecular Patterns (PAMPs). These are patterns that are present on pathogens - in this case particular bacterial species - and trigger an immune response. Read more about them here. This pro-inflammatory response attracts other immune cells to the area, and helps to drive an immune response, containing and aiding in the elimination of the invading pathogens.
Edit: OP may also be interested to know that if an apoptotic cell is not cleared by a macrophage, eventually it will become "secondarily necrotic", meaning the membrane eventually falls apart and the cell releases it's contents (Source). This turns it from non-inflammatory to an inflammatory response. Neutrophils are particularly adept at keeping their membranes intact, due to the harmful nature of the cell contents. There is a pubmed entry here regarding it, but the actual book I've taken this information from isn't available without subscription.

Necrosis can be described as accidental cell death or damage, triggered possibly from external environmental factors such as exposure to radiation, toxins, excessive heat and etc...whereas, Apoptosis is a programmed form of a cell death mechanism. This process may be used to recycle unwanted cells in the body. Therefore, the particular stimulus that the cell receives may be a key determinant of the cell death mechanism observed.


text:
Why are belly buttons on the stomach (why does the umbilical cord end up attached to the stomach)?
Belly buttons are at the site where the umbilical cord was attached to us as we developed inside our mothers. The same is true for all placental mammals.
Why are belly buttons on the stomach? Why didn't the placement end up somewhere else like the chest, the back, the head, etc.? Is it optimal for the umbilical cord to be near the intestines?

While it doesn't answer your specific question, a really good book for this kind of question is Your Inner Fish, by Neil Shubin.


text:
What's the highest temperature that algae can survive at?
I know there are a lot of different species of algae and that each one has different environmental tolerances. I've seen data on different species:

brown alga Sargassum echinocarpum J. Agardh - grows well at 35°
Dictyopteris australis - grows poorly above 28°
halophilic blue-green algae A. fertilissima - temperatures of 47° stimulates germination

What's the highest temperature that growing algae or its spores can survive at? In other words, what temperature would guarantee that no algae could grow afterwards unless reintroduced?

Based on the habitat of Algaes, a classification called "Thermophytes" can bear high temperature. The Thermophyte algaes use to grow around hot springs and can live around 70°C.
Please find below the reference for all classifications and more details.
http://www.yourarticlelibrary.com/biology/8-types-of-algae-classified-according-to-their-habitats/7098/
http://www.biologydiscussion.com/essay/essay-on-algae/20891


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How does chromosome doubling occur?
Sterile hybrid with genome AB undergoes doubling of chromosome set to form fertile tetraploid with genome AABB.
But since A and B is not homologous, synapsis cannot occur at prophase I, so there is no meiosis.
So how does the chromosomes double? If through non-disjunction in mitosis, where did it occur? Did it occur in one cell only or all of the cells in the organism?
Did non-disjunction occurs at gonad to produce AABB cell, then it undergo meiosis to form AB gametes, and then self fertilise with AB gamete to form AABB offspring?

@AlwaysConfused  DNA replication occurs only at meiosis or mitosis right? So in this case, it occurs in mitosis?


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What are the uses of Helical Wheel Projections in Structural Biology?
I have seen helical wheel projections used to illustrate amphipathic helices in proteins.  Are there any other uses for these models?

Welcome to Biology.SE! The first part of your question is opinion based (what does often mean) and thus is not appropriate for this site — in addition it is not clear how knowing the frequency of this type of diagram is helpful. The second part of your question seems more appropriate for bioinformatics.stackexchange.com since it is a technical rather than biological question. ——— Please take the time to check out the tour: biology.stackexchange.com/tour and then the help pages on how to ask questions on this site: biology.stackexchange.com/help/how-to-ask. Thanks!

I agree with @tyersome — it’s a better fit for SE Bionformatics, especially if you ask more precise questions eg for a program that will generate them.

Apologies. I have edited the question.

Helical wheel projections can be useful anytime you have a protein or peptide with one or more α-helical regions. They allow you to see whether any "property" is present along one side of a peptide. This can be useful in recognizing potential protein-protein interacting motifs such as leucine zippers.
The wikipedia article on "Helical wheels" also looks like a good place to start learning more about this.

Sounds like the questions is asking for uses besides this one.


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What is that? Dry brown fungus? See photo please

It has appeared two days in a row on my balcony, at exactly the same place. There's nothing near that can give me a hint of what it is. The birds can access the place easily. It's an inch in size, it's dry. In the photography you can see a eyelash and some hair, because has been taken after sweeping.
The place is Jerez de la Frontera (Cadiz, Spain).
What it could be? I'm curious and I would like to know why it appears.

Welcome to Biology.SE! For identification questions please: 1) include the location (e.g. country and region — the more specific the better), and 2) include habitat information (e.g.s: what types of plants grow nearby and whether you are near water). ——— The location and habitat can be essential clues for identification. Thanks!

Looks like bits of insulation. Are birds making a nest above where this appears?

No, birds aren't making a nest above.


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Can you identify this insect (orange back, 6 legs)?

Found a couple of them in central europe on a zucchini plant (in august).
They are about a centimeter in size.
Tried looking for insect with orange back and 6 legs but no result.
[EDIT from comment]: The insect in this post looks pretty similar. There is a difference though - the one in my picture has orange legs not black ones. (maybe different stage of larvae or different species of ladybug or just random?)

There is a related question and answer here which identifies a similar creature as the larval form of a 'spotted lady bug' or beetle; and this is probably what you noticed.  Another possibility is the larval form of a burying beetle (Nicrophorus), but that's less likely.

Yeah I think you're right, that's it ... one difference though, the one on my picture has orange legs not black ones

If you find more, and they are larvae, you just have to watch what they turn into.  Right.  I'm not an expert but the related question was too obvious not to let you know about it.

It is a harlequin ladybird larvae.

This is one of the most variable species in the world, with an unusually broad range of color forms. It is native to eastern Asia, but has been artificially introduced to North America and Europe to control aphids.
I figure that Wiki is saying "it has some of the highest color variability of any wild plant or animal".

wiki: harlequin ladybird


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Induce plasmid acquisition in bacteria to make them susceptible to antibiotics
Is it possible to use plasmids as a way of creating antibiotic susceptibility in bacteria.
For example; in Microbiology, an introduction 13th edition by Pearson , Page 230 "the researchers traced the drug-resistance plasmid to a plasmid found in E.coli that resided in the volunteers before the study".
I was wondering if it is possible to induce plasmids that make those bacteria susceptible.
They have to be in a first instance good for the bacteria, for example an enzyme that allows the bacteria to use a compound. But  through an antibiotic it would make that enzyme catalyze useful compounds of the bacteria, working the antibiotic as a cofactor of such enzyme.
Is it possible?
I was thinking on it as a "trojan plasmid".
Thanks.
Edit: Linking to this question: Could plasmids and conjugation mechanisms be used against antibiotic-resistant bacteria? , it talks about those "trojan horse" plasmids referring them in a way that seems to be linked to a bactericidal function, if instead the  plasmids are linked to a good survival rate in one situation (example, 36°C) but to a bacteriostatic situation ( temperature goes up to 39°) or such a way like hemoglobin works with CO, it's fundamental for us but selection hasn't worked to get through this problem and still binds to the molecule.
This type of coevolution in Wolbachia https://en.m.wikipedia.org/wiki/Wolbachia makes the host insect susceptible to needing the bacteria for reproduction despite being good in some environmental conditions it induces infertility in others.
Or inducing variants of genes that are still with functionality but trunked under certain conditions, if those conditions aren't present in the environment, the gene variant could spread without causing problems competing with the original variant until those environmental conditions are met reaching an equilibrium in which a % of the population could be used as a target of that antibiotic.

Check out this question and its answers.

@canadianer Thanks! It has solved some of my questions, but I still feel I am in a slightly different situation, focusing more in the plasmid genetic equilibrium than in the complete widespread throughout the population.


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Embryonic cells, when can you detect them in vivo? (In order to do whole genome sequencing)
I was wondering, when is it possible to extract cells (humans or mice) in order to sequence them and detect diseases.
Extra: Urine of the embryo in humans is excreted in the 16th week, so I guess that then it's possible to extract some embryo cells.
EDIT
In other words, when is it possible to grab enough DNA to know the full genome of the embryo without damaging it?
In order to sequence it and avoid most genetic diseases and regulate the weekly abortion limits.
Thanks

In vivo or in vitro?

Sorry, in vivo, now I'll edit.

So you are discounting human non-invasive pre-natal testing, on the grounds that it uses cell-free DNA?

@swbarnes2  it depends,  I am especially thinking in the abortions and genetic diseases.

So, when are there enough cells to grab enough DNA and fully genotype the embryo?, Then you could know most genetic diseases. My question would be answered.

By "fully genotype" what exactly do you mean?  Are you talking about a large panel like 23andMe, or a whole genome sequence?

My fault, I didn't  mean genotype, I wanted to say sequencing. Sorry!

Are you asking about detecting cells or having enough material to do whole genome sequencing?

@swbarnes2 about having enough material of the embryo to do whole genome sequencing

As usual, the answer is "it depends what you mean". There is a large existing field (prenatal genetic diagnostic testing) which trying to diagnose genetic diseases in fetuses using different technologies. These technologies are described more in points 2 and 3 below, whereas point 1 is a somewhat academic statement about the technical capabilities of genomic technology in pure research settings which are currently not really relevant for medical applications.
I can think of 3 different answers to the question as originally posed:

With currently available sequencing technology you can never know
the full genome sequence of a human well enough to see all the potentially damaging variants. The "finished" human reference genome in
fact has gaps and errors that are constantly being corrected. For
more information about what "finished" means, see here. Only one assembly of a telomere-to-telomere human chromosome exists as far as I know, and that's only the X chromosome. Even accepting that this best available technology is good enough, it also relies on things like the ability to isolate lots of high-molecular-weight DNA, which makes it very tough to do on the amount of cells you could get from a newborn without highly invasive procedures such as e.g. sampling fetal tissue in vivo. My guess is that even amniocentesis would be very hard to get good HMW DNA from.
With currently available sequencing technology you can however test
very early provided you used IVF, at least as early as the 100-cell stage
(probably earlier). This is a chancier method that will miss a lot
of information but gives you good enough info to diagnose
aneuploidies or other very obvious variants.
Alternately, you can screen cell-free fetal DNA as early as 7
weeks (or possibly earlier). However this does not involve
isolating cells so it is potentially not what you are thinking
about. It is somewhat better information than preimplantation
screening, but rather worse information than you can get from whole
cells.

Likely none of those are exactly the answer you want, but it's also a less simple question than it appears at first: a) getting cells is hard and probably not necessary for the current tech, and b) the tech isn't actually as good as generally advertised.

Thanks!, It is a good and really complete answer. Hopefully in the future we will be able of doing a more complete sequence of the embryos or fetus and avoid those diseases developed during the development. Do you know any source (blog, researcher wordpress...) that talk about this area? Or the scientific name of this field? Thanks!! Héctor

@Héctor - see edit. I think you are interested in prenatal genetic diagnostics. I have added a link to the answer, which you can also see here: https://www.acog.org/Patients/FAQs/Prenatal-Genetic-Diagnostic-Tests?IsMobileSet=false

Oops, meant to also link to this article: https://obgyn.onlinelibrary.wiley.com/doi/full/10.1002/pd.5520 and there is a journal "Prenatal Diagnostics" that you may find useful: https://obgyn.onlinelibrary.wiley.com/journal/10970223


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High concentration of primer in PCR
Why is it that higher concentration of primers than the DNA template in PCR will favor the annealing of a template to a primer?

Using high concentration of primers ensures that after denaturation template DNA binds to primers instead of binding to each other. Also higher primer concentration enhanced product yield, as primers act as limiting factor for annealing.
(Reference: https://academic.oup.com/nar/article/24/5/985/1047654)

To simply put it, higher concentration of primers means more primers in the mix, therefore more chances of it annealing to your DNA template, however more is not always good. The optimum concentration of primers in a PCR reaction is between  0.1 and 0.5 µM. For most applications 0.2 µM suffices. Using very high concentration of primers can be troublesome as it can cause your primers to bind to partially complementary sites resulting in non-specific PCR products.
https://www.embl.de/pepcore/pepcore_services/cloning/pcr_strategy/optimising_pcr/


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What causes change of sex in certain monoecious plants such as Papaya?
certain male flowering plants can be converted to female flowering and fruiting such as Papaya plants by just insertion of an iron nail in their/it's stem near it's roots? How can iron nail alter it genetically from male to female? Biochemically  what causes change in sex of plants from male to female?

Might be useful to provide more background or links to what you're talking about.

Please see edited 1... I've sited link to one similar observation, It's common gardening technique. When we plant papaya plant from seeds over ninty percent of plants are male. But when they grow to a desired height gardner either mercilessly prunes large number of leaves or inserts a iron nail in the stem near the roots. Most of the time this might result in conversion from male flowering plant to female flowering plant and fruits can be obtained. This technique may or may not work for other monoecious plants.

@user240988 please [edit] your question to include all necessary details instead of replying in comments. Comments are not searchable and can easily go unnoticed. Therefore the question body should be complete in itself.

@user240988 The scope of the question "What causes change in the sex of plants?" is too generalized. An answer can be provided for "What causes papaya trees to change sex from male to female?" But the phenomenon can not be generalized to "plants" as a whole, as most plants don't and/or can't change sex, nor is it bi-directional even in the case provided as an example. Can you be more specific in your question?


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Artifial insemination in milch varieties?
Artificial insemination is used to produce offspring cows  and other milch varieties like buffaloes.. etc often use same sturdy males. Isn't it a step towards eugenics? What can be possible future harms?

Possible duplicates or related: https://biology.stackexchange.com/questions/14414/do-humans-have-enough-biological-differences-to-be-grouped-into-races-or-subspec https://biology.stackexchange.com/questions/66144/human-genetic-diversity-in-africa-in-comparison-with-the-rest-of-the-world

And what do you mean by "number dominance of Caucasians"?

"number dominance of Caucasians over other human divisions".... The phrasing is unclear but please note that there are ~1.3 billions Han Chinese and only ~0.85 billions caucasians.

Does it make sense to classify all humans in a single species? might also be a possible duplicate.

Possible duplicate of Do humans have enough biological differences to be grouped into races or subspecies?

There is no genetic basis for these classifications. Most human genetic diversity is in Africa. Diversity only decreases with geographic distance from this continent.  There are geographic clines, not the clusters that one might call race.  Here are some results from Rosenberg's 2002 Genetic Structure of Human Populations:

93-95% of variation occurs within populations
3-5% of variation occurs between populations

Local adaptation occurs, such as height and pigmentation but these phenotypes are polygenic and should not lead to binary classifications.  There are some very interesting case studies on local adaptation that you should look into. ex)EPAS1 gene and no hypoxia among Tibetans or lactose persistence on three continents
There is no genetic basis for dominance of one population over another.


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How do different genes on human genome express themselves?
It is said that human genome  contains over twenty five thousand genes, How many of these (can) express themselves as an external or internal trait in human beings (for e.g. like eye-colors, hair colors, earlobe-assosiation etc.). Other genes are responsible for (mostly) what functionalities?

Where is this said? References would help. There are a little over 20,000 genes in the human genome, so itś not clear what you mean by genomes in genomes.

The human genome doesn't contain 30000 genome, rather it contains 30000 genes, as the HGP has said us. Human gene is split gene,i.e., long sections of non-coding DNA is present in between short sections of actually coding DNA. Thus there is a lot of junk present. Different genes express themselves by a two step process, the first being transcription, where DNA is converted first into a mRNA, which undergoes splicing and then finally that mRNA is converted into protein and this is the second step which is known as translation. Thus it is by the conversion of DNA segment into proteins that helps the various genes in expressing themselves.
As for what the other genes do, not all genes are busy in determining phenotypic traits. There is a lot other things also going on.. the various biochemical reactions in our body need to be regulated by enzymes and the production of these enzymes are controlled by these genes. For more knowledge about this field... Google lac-operon concept or the tryptophan operon concept.

What is meta genome ? it is said that it governs activation and inactivation of certain genes in the genome.


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Identify this insect (looks like part of a tree)?
I found this insect and thought it was part of a tree at first, then it moved and so I knew it was an insect. I've never seen it before though so I am posting here hoping someone knows what it is.

The location is North East US, during the day, in a tennis court surrounded by trees. The insect was clinging to the cover seen above (which covers the tennis court fence).
Any idea what this insect is called?

Good pics, clearly some kind of stick insect, someone will know it.  Can you add info about your location etc, as much info as you can as suggested here?

Not posting as an answer since I am not an expert, but apparently Diapheromera femorata is the most common species across much of the US.

Bryan, I think you're right! I just googled "Common walkingstick" based on your link, and under image it shows the same exact one. I will accept an answer once you post it, thanks a million!

Let's try to draw the attention of @KarlKjer he will know for certain, the details to check...

It's really hard to identify species with a photo, and I suspect the user just wanted to know it is a walking stick. Thanks for the vote of confidence, but I' not an expert on walking sticks.

Alight, best guess, based on it being the most common species, a decent match in pictures, and a decent match to the description on Wikipedia is Diapheromera femorata, the common walking stick.


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How do I prepare a Basal medium for autotrophic mutant creation
Minimal medium (MM) was prepared by adding 2.0 g sodium nitrate (NaNO3) to 1 L of basal medium (BM) fol- lowing Correll et al. (1987). Chlorate resistant sectors (CRSs) were generated on two media i.e. MM and PDA containing 2.5% chlorate (KClO3), represented as MMC and PDC, respectively. The chlorate served as a toxic ana- logue of nitrite (Corell et al. 1987). Four phenotyping me- dia (Correll et al. 1987) were used i.e., i) sodium nitrate (NaNO3); ii) sodium nitrite (NaNO2), 0.5 g of NaNO2 was added to 1l BM; iii) hypoxanthine (HX-), 0.2 g of HX- was added to 1l BM; iv) ammonium tartrate (NH4+), 1.0 g NH4+ was added to 1l BM. MM was also used in pairing of the complementary nit mutants
I’ve tried using the procedure on above but the minimal media is not solidifying

Welcome to SE Biology. Please do not present text as images. It discriminates against people with visual problems and is not indexable by the site. Type out as much as is necessary and provide a link to the source.

How do you expect the medium to solidify without adding any gelling substance like agar?

I added agar to it but it still did not gel


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Which predator / prey pair of species have the most drastically different body size?
I'm trying to identify which 2 species, one predator species and one prey species that have the biggest size difference.  Specifically, which predator hunts the largest prey relative to itself?
I'm looking for the pair with the smallest predator taking the largest prey but relative to each other, not the other way around.
Some limiting factors to the question:

Parasites don't count.  Parasites will, ideally, repeatedly feed on the same host for as long as possible. Killing the host will, eventually, remove the resource, which is undesirable for the parasite (it can't keep feeding on the host if the host ceases to exist).  I'm looking for a predator prey relationship that does not do this in any way, shape, or form.  Even if the predator does not consume the majority of the prey, the portion consumed must be vital to the prey, or the prey must be killed in order to access it or overcome resistance to it.

Animals eating plants don't count.  Animals eating other animals only please.

Pack hunters don't count.  Lions, wolves, orcas, army ants, etc., don't count because packs can come in so many shapes and sizes that it makes it impossible to pin down a size ratio between the pack and the prey.  Single predator individuals only, please.

Scavenging doesn't count.  Predators might also scavenge, but prey species used in the size comparison should only include species that the predator actively hunts as part of its regular active hunting routine (even if intermittently or seasonally).

Intentional prey sharing doesn't count.  Sure, a predator might have it's prey stolen after a kill, that's fine.  In many predator species, parents will share kills with offspring until they are capable of hunting for themselves, that's fine too.  But nothing like the Tarantula Hawk that doesn't actually eat the "prey" itself, but rather leaves it to be eaten by offspring later.  But typical behavior, even in the presence of non-self-reliant offspring, and assuming another predator doesn't take the kill by force, should be for the individual predator that makes the kill to also be the individual that consumes the largest share of the nutritive portions of the prey.

Body mass is the primary measurement for "size".  Since length, width, height, etc., can vary widely based on body plan, let's use mass as the measurement for "size" for the purposes of this question.

Size of the predator should be the mass of a 'typical' or 'average' adult member of the species that performs the actual hunt / kill.  For species with significant sexual dimorphism in relation to size between male and female, use the size of whichever sex is generally larger.

Size of the prey should be the mass of the 'average' specimen taken in a predation event.  For example, Lions (yes, I know I excluded them in the 'pack' section earlier, but for the sake of example), lions will eat elephants.  This is most commonly scavenging, rather than hunting.  And when it is due to hunting, it's more often calves, not adult elephants, that are taken in the hunt.  So (if lions were allowed, and were compared to elephants) the scavenged elephants wouldn't count toward the 'average', only the hunted ones, and the average would be closer to the size of a calf, rather than an adult, due to the higher frequency of predation events involving calves.

The ratio matters, not the absolute mass difference.  I'm looking for the pair with the biggest ratio, or percentage difference, not the greatest sheer difference in mass.  For example, Pair A is a 20 pound predator taking a 30 pound prey, this is only a 3:2 ratio and a 10 pound difference.  Pair B is a 1 pound predator that takes a 5 pound prey, which would have a much larger ratio of 5:1 despite only a 4 pound difference.  Pair B is the winner here, by ratio.

Given all of this, which two species, that have a predator and prey relationship, have the greatest mass difference between the predator and the prey?

Have you googled this? Or "tiny animal predators"? Please give evidence of research have you done to answer this question yourself, which is a requirement on this site. Thanks.

@Darlingtonia  I'm actually looking for the pair with the smallest predator taking the largest prey, not the other way around.  I'll update the question to clarify.

@anongoodnurse  Yes, I attempted many such searches, but the question is too complex for that type of search, as far as I've been able to determine.  For example, your suggested search criteria, of "tiny animal predators" would be useless, as the absolute size of the predator isn't actually relevant.  The ratio of the sizes is the relevant factor here, which is all but impossible to put in to an internet search, and yields useless or no results at all, when attempted

I recently found a beetle larvae specialized to kill an earth worm that was 50+ times more massive than it. your question doesn't make sense to me totally... A parasite is just a predator that eats the prey slowly, and some parasites do kill the prey. If a tiny spider kills a human and eats a piece, where does that fit into the relativity of the query? it doesn't make sense to kill a prey which can supply so much food that it goes mouldy when only 0.1% has been comsumed.

@bandybabboon Parasite, parasitoid, predation...Yes, the lines are blurred. There are no spiders that hunt humans intentionally as a food source, so that would be a defensive kill, followed by opportunistic scavenging, not predation. Parasitoids do kill the host, eventually, but keep it alive as long as possible, for other reasons realated to their life cycles, such as feeding young, defense, or environmental concerns, etc. For simplicity, I'm looking for only those that are clearly not parasites or parasitoids, but rather clear and unambiguous predation.

I think the Black Swallower (Chiasmodon niger) is a good contender. This fish can (at least according to Wikipedia and reference therein) can swallow other fish that are up to twice its length and 10x its mass.
For land based predators, the Least Weasel (Mustela nivalis) is capable of killing prey 5-10x its weight, though these instances are believed to be rare (at least rarely observed), though they will take birds like Chickens occasionally too. Diet is normally much smaller - rats, mice etc.

Why would someone downvote this?

If we go with mammals then I would bet on Musteloid group too who are true killing machines. Metabolism of least weasel and stoat is very high so their food intake per body mass per day could be as high as 60%. Mustela nivalis is not known killing adult chicken, they go for chicks, ducklins and young rabbits occasionally when their main prey mice are scarce.  Also there is sexual dimorphism in Mustelids where male is twice as big eg. Least weasel female 68g and males 125 in Britain which may be different elsewhere (Harris & Yalden 2008 Mammals of Britis isles).

Stoat Mustela erminea is more known killing adult chicken and rabbits again in wild they switch to rabbit when their mice are scarce.  Female size 242 g male 367. European rabbit weighs 1.2-2 kg (Harris & Yalden 2008). These animals can eat whole rabbit but true in farms you can see blood lust where whole flock is killed and none eaten.

It's quite human thing to draw borders everywhere. It's not even fully settled what species definition is hence so many subcategories can be seen in taxonomy. It's even more volatile when comparing body masses where it is varying greatly by regions.
To play the game by borders you set then probably biggest predator-prey ratio is some venomous spider vs some much bigger animal.
You didn't determine that predator have to eat whole thing but it's possible to read out that large prey has to be important role in predators' menu not accidental kill.
In mammal world Wolverine Gulo gulo might be the answer. Tundras' most ferocious predator can weight female 8-12kg male 12-18kg and is known capable of killing adult reindeers female 80-120kg male 160-180kg and even elk (200-700kg) that's weakened in winter. In America wolverine is more scavenging but in Fennoscandia they do more active hunting probably because of less big predators who they can follow and scavenge their kill.

Recommend documentary "Wolverine - One tough mother" 2021 Austria, where  wolverine kills 20x bigger reindeer.


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Confirmation of organoid's character with the respective organ
How can we verify that the Organoid formed from culturing stem cells shows the exact characteristics of the organ it is developed for?

Verification of organoids is done by detecting the cellular proteins for particular tissue type using Immunofluorescence.
For verifying intestinal organoid, apical membrane markers  (villin or alkaline phosphatase) and basolateral markers (E-cadhehrin) are detected by immunofluorescence. Transporters present in intestinal membranes are also displayed on organoids.  The peptide transporter PEPT1 and the glucose transporter SGLT1 are located on apical membrane, and the glucose transporter GLUT2 is present on basolateral membrane. So, these proteins can also be used as markers for verifying intestinal cells.
Via:

https://www.nature.com/articles/srep16831
https://www.ncbi.nlm.nih.gov/pubmed/19329995


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Are there any ways to force DNA-origami to create a geometric shape from non-nucleotides (not from DNA)?
I mean, can we create with the help of DNA-origami figures that would not consist of DNA, but, for example, carbon? Is it even possible?

Can you explain your question in more detail, and link to the relevant study you mention? Carbon can be made into a geometric arrangement called fullerene, for instance, but that may be different than what you're asking. https://en.m.wikipedia.org/wiki/Fullerene

Using DNA-origami, we can get various nano-objects of the desired shape. Such objects consist of DNA. I ask, can we in theory with the help of DNA-origami get nano-objects that will not consist of DNA, but some other specific atoms, gold, carbon, etc?

Welcome to Biology.SE! Are you asking whether the folding of DNA in "DNA origami" can be used to manipulate other nanomaterials?  Or did you mean whether DNA structures can be used as a scaffold to pattern other nanomaterials? Something else? Please edit your question to clarify and add links to relevant papers.  ——— You may also benefit from taking the [tour] and then consulting the help pages for additional advice on [Ask] questions effectively on this site and then edit your answer accordingly. Thanks!
(Also note that DNA contains carbon — did you mean graphene or something similar?)

I interpret your question to ask this:
Can DNA origami be used as scaffolds for the guided assembly of other non-DNA structures?
Yes.  From what I've read, two- and three-dimensional DNA structures can be used for nanoparticle assembly and as a nucleation factor in the crystallization of proteins and minerals.  You can find these examples and more in a lengthy review from 2017.1  Specifically, read section 6.6, Programming the Structure and Conformation of Non-DNA Materials.

Fan Hong, Fei Zhang, Yan Liu, and Hao Yan. DNA Origami: Scaffolds for Creating Higher Order Structures. Chem. Rev. 2017, 117, 20, 12584–12640.