Why are certain cells more likely to be attacked in autoimmune conditions? For example, type 1 diabetes occurs when the immune system attacks and kills beta cells in the pancreas. This is relatively common.
What makes beta cells more likely to be targeted than, say, alpha cells in the pancreas?

Autoimmune reactions each have their target antigens. They'll "attack" wherever those antigens are expressed. In the case of Type 1 diabetes, many specific antigens have been identified, and they all correspond to regions on the surface of pancreatic islet β cells. Ultimately, however, the immune reaction is targeting proinsulin and its processed product insulin, which are produced by solely by β cells. This is an interesting review covering the topic.


Why do people dying of immune deficiency diseases appear sick? Please forgive the obviously silly appearance of this question, and/or of the tenor which may come across as flippant or dismissive of real world suffering. My intention is none of the above.

As a layperson, I have always understood that the expression of our various colds/flus etc, while frequently mis-understood as being caused by the virus, are actually just manifestations of our own immunity fighting same.  In other words, all the snot, and fever and inflammation are not caused *by the virus, they are a reaction *to the virus, as we fight it off.

My question then is why do people with AIDS (or similar immunity destroying affliction) appear sick?  If they have weak or non-existent immune systems, following the above logic, would one expect to see them passing away while looking entirely healthy?

Many of the symptoms of disease are indeed related to inflammation, but inflammation depends heavily (though not solely) on the innate immune response.  Patients with AIDS and some of the other immunodeficiencies lose their adaptive immune response, not their innate response.  Therefore they are capable of mounting an inflammatory response that is not effective in clearing pathogens (because it doesn't have help from the adaptive immune system) but can still cause symptoms.

More importantly, many symptoms of disease are not caused by the inflammatory response, but are related to organ and tissue damage caused by the infection.  A patient with pneumonia may have a reduced inflammatory response but will still have difficulty breathing and signs of reduced oxygen supply simply because the lung tissue has been damaged by the pathogen.


Why is there no way to remove an immune response? We've known for a long time now how to "add a new entry to the database," as it were, of immune responses.  It's called vaccination, and it's been one of the greatest success stories in the history of medicine.

And yet, allergies and autoimmune disorders, both caused by an immune system gone rogue, are still serious problems today.  If it's so easy to add a new immune response, why don't we have any way of deleting one?

It is an interesting question. The reason for why new immune responses can be launched but the memory of old ones are not deleted is based on the concept of irreversibility of certain chemical reactions.

Launching an immune response involves clonal expansion of cells expressing the epitope sensors such as the immunoglobins and T-cell receptors, accompanied by maturation of these receptors. Some of the reactions involved in this process are irreversible, which include VDJ recombinations, class switching and affinity maturation.

In an overall sense, immune response is analogous to natural selection- in the presence of the antigen the best binders are selected and expanded. Now to make a species extinct you would have to find each individual and kill it. Or you may have to develop a technology that will identify and kill a certain species in an automated manner. This is difficult to implement; how to engineer a mechanism that will precisely seek and destroy all the epitope sensors for a particular antigen. In contrast selection happens spontaneously because it does not proceed with a reason. It just selects the best from available stock.


What's the use of DNA sequencing results? Suppose I sequence DNA of some organism (a human perhaphs) and now I have the entire DNA "string" - the sequence of nucleotides.

What's the use of that? It's just a "string" where nucleotides encode something but I have no idea what they encode specifically. So to me it looks like some raw data, just represented as a sequence of elements.

How is having the entire DNA sequenced useful?

It's just a "string" where nucleotides encode something but I have no idea what they encode specifically.

It sounds like you are describing a computer program, represented by a string of bytes on the hard drive.

Unfortunately, the analogy breaks down very quickly because DNA is vastly more complex and a lot of aspects are still poorly understood.

But the basis is the same: a string of symbols encodes information. In the case of DNA, different parts encode different things in a different manner.

The elephant in the room are of course coding sequences: stretches of DNA, contained in so-called “genes” – which code for proteins and other stuff.

Coding sequences use a fairly simple encoding schema that’s known as the genetic code, decoded in 1961. The genetic code has the nice property of being (almost) universal across all species, and easy enough for a child to understand:

Three consecutive DNA base pairs form a codon. Each codon stands for one amino acid (except for a special “stop codon”). Amino acids form so-called polypeptide chains – proteins. There are codon tables, just as you have manuals for assembly mnemonics in computing:

Unfortunately, it’s not trivial to know where genes are on the genome. Just by eyeballing the sequence there is nothing to distinguish one stretch of DNA from its surrounding. But there are certain recognisable stretches of DNA (“motifs”) which we can use to locate genes and other interesting regions.

Grossly simplified, a gene is preceded by a promoter region which is highly conserved between species (but gene-specific). Once you’ve identified one species’ promoter, you know it for other species. Furthermore, all promoters share highly similar elements, for instance the TATA box – literally the occurrence of “TATA” in the genome.

Of course, just looking for occurrences of “TATA” would yield vastly more spurious hits than actual promoters but combined with other information you get a gene model – a statistical machine which can tell you with high confidence where on a genome the genes are located.

Once you have found the genes in a sequence which you can trivially translate to amino acid sequences, you can try to form inferences about the function of the proteins (a protein’s function is an almost-direct consequence of its sequence). Unfortunately, discovering the function of a protein from its sequence alone isn’t possible but we do know the functions of many proteins.

When we now look at a genome and find a mutation in a protein-coding gene we can infer that the function of this protein is probably modified. Most mutations are so-called deleterious mutations (e.g. by deleting a single nucleotide you get a frame shift in the codons, and all the subsequent codons no longer make sense), meaning that they destroy the protein’s function.

Other, much rarer, mutations modify the protein’s function, making it more or less efficient, or giving it another function altogether.

In the simplest case (but these are rare), a single such mutation can explain a complex phenotype. This is known as a Mendelian trait and can be used to explain a phenotypes such as eye colour, but also hereditary diseases.

Usually, though, it is merely one of many adjusting screws which skew your susceptibility to a certain phenotype in one direction. For instance, you might be slightly more susceptible to breast cancer or diabetes.

This is one use of the DNA sequence, there are many more; in the last decade, we have realised that regulation of gene activity plays a much larger role than anticipated, and most research today looks at regulatory patterns on the DNA level. This is also done with sequence data, but there doesn’t appear to be a simple schema analogous to the genetic code to understand regulation. Instead, it’s a complex interplay of many completely unrelated mechanisms.


How did the largest/longest dinosaurs hold their head and necks up? After seeing the images in the articles shown below, I am having a tough time understanding the mechanics of how these incredibly long and heavy necks can be supported outstretched like this. A rigid beam or tube would remain fairly straight through compression on the bottom and tension on the top, and since there is muscle, tendon, ligament and bone, I know the necessary mechanical functions are there somehow.

Is there one "neck muscle" along the top that holds the neck "up", or many short muscles between vertebra? Where is the origin of the tension, the shoulders or the pelvis, or is it all the tension distributed along the whole spine from neck to tail?

How does this work??

above: Titanosauria of Chubut from here.

above: A reconstructed Patagotitan mayorum, a 70-ton dinosaur discovered in Argentina. (Courtesy of José Luis Carballido) from The Washington Post article Which dinosaur is the biggest? There’s a new contender — and it’s alarmingly large.

above: A reconstruction of the newly named titanosaur Patagotitan mayorum. from The National Geographic article New Dinosaur Species Was Largest Animal Ever to Walk the Earth.

There are lots of papers on this. A good summary article is Why sauropods had long necks; and why giraffes have short necks, by Taylor and Wedel.  They list a number of anatomical features that allowed sauropods to support such long necks:

  Several anatomical features enabled this extreme elongation, including: absolutely large body size and quadrupedal stance providing a stable platform for a long neck; a small, light head that did not orally process food; cervical vertebrae that were both numerous and individually elongate; an efficient air-sac-based respiratory system; and distinctive cervical architecture. Relevant features of sauropod cervical vertebrae include: pneumatic chambers that enabled the bone to be positioned in a mechanically efficient way within the envelope; and muscular attachments of varying importance to the neural spines, epipophyses and cervical ribs.

Let's take these one by one.

A stable platform for a long neck. Large, heavy quadrupedal bodies, so the long neck didn't unbalance the animal when it stretched out.
"A small, light head." Sauropods didn't chew their food, so didn't need large muscles or heavy bones in their head, so they didn't have a heavy weight at the far end of the long neck.
Numerous small, elongate cervical verterbrae. Sauropods had 12-19 vertebrae in their necks. By contrast, giraffes have seven, each of which needs to be large and heavy, limiting how long the neck can be.
Efficient respiratory system. Sauropods, like modern dinosaurs (birds) have a more efficient respiratory system than mammals, so they could tolerate the inefficiency of a long trachea.
Pneumaticity of cervical vertebrae Sauropod vertebrae had air sacs (i.e. hollow pockets of air) in them, making them much lighter than mammalian vertebrae of the same size and strength.

Edit to add Figure 4 from Taylor & Wedel, illustrating how relatively light sauropod necks must have been for their size:

  Figure 4: Extent of soft tissue on ostrich and sauropod necks.
  1, Ostrich neck in cross section from Wedel (2003, figure 2). Bone is white, air-spaces are black, and soft tissue is grey. 2, Hypothetical sauropod neck with similarly proportioned soft-tissue. (Diplodocus vertebra silhouette modified from Paul, 1997, figure 4A). The extent of soft tissue depicted greatly exceeds that shown in any published life restoration of a sauropod, and is unrealistic. 3, More realistic sauropod neck. It is not that the soft-tissue is reduced but that the vertebra within is enlarged, and mass is reduced by extensive pneumaticity in both the bone and the soft-tissue.

Muscular attachments.  This is the aspect that most directly answers the original question, but it's first important to understand that other sauropod features as noted above allowed them to get away with less neck strength than you'd otherwise expect.  In fact sauropod necks were much less (relatively) muscled than, say, ostriches. They got away with this by improving mechanical advantage:

  In effect, sauropods inflated their vertebrae within the muscular envelope of the neck, moving the bone, muscle and ligament away from the centre so that they acted with greater mechanical advantage: higher epaxial tension members, lower hypaxial compression members, and more laterally positioned paraxials.

Taylor and Wedel go into this in much more detail, with many helpful diagrams, and the paper is open-access, so I won't repeat all their points here. They talk about neural spines, epipophyses, cervical ribs, and muscle attachments in various combinations.

The cervical ribs are easily visible on the Patagotitan skeleton image in the question:

There's a long description of cervical rib anatomy and possible functions here:

  My favorite hypothesis is that long tendons allow an animal to shift the bulk of the muscle–and therefore the center of gravity–toward the base of the neck, but that long unossified tendons can be distorted through stretching, which wastes muscular energy. Ossifying those long tendons is like putting bony wheelbarrow handles on each vertebra, allowing the muscles to move the vertebra from a distance without so much wasted energy, and probably with finer positional control.

That's just one aspect of the way sauropod necks were structured.

TL;DR: Sauropod necks could afford to be relatively light, because of the small head; their neck bones tended to be relatively hollow and light for their size; their scale and shapes meant that muscles had good mechanical advantage; and different species had other adaptations including ligaments and stiffening bones that also helped.


What is the difference between non-coding and intergenic regions? The initial question was about understanding what is in the downstream of a gene in a eukaryotic organism. I understand that this region is located 3' of a gene, and therefore I would expect to find non-coding regions, but is there a difference between non-coding regions and an intergenic region?
A small background of what I am doing: I am studying the effect of retrotransposons in S. cerevisiae populations, and I already identified the potential impacts of these retrotransposons and these were the consequences:
Upstream gene variant   49
Downstream gene variant 42
Intergenic variant  4
Transcript ablation 3
Coding sequence variant 1
Feature elongation  1
3' UTR variant  1

So is it clever to say that downstream of a gene there are non-coding genes?

"Intergenic" is, well, an embarrassment, though it can be hard to avoid.  Intergenic means, literally, between genes.  Genes are, as you'd expect, genetically defined as regions of the chromosome with some genetic role.  Between genes, we have, well, junk, spam, without meaning or significance, since otherwise, it would be a gene.  In the 1990s everybody knew most of the genome was "junk DNA" and it was pretty straightforward.  And the central dogma was DNA makes mRNA makes protein and if there was no mRNA making protein, or even no long protein, then they assumed there was no gene.
Well, the problem with using these terms nowadays is, first, it is very hard to show any given piece of DNA never has a role.  After all, you can often remove a whole gene without visible effect on an organism, so how can some noncoding sequence 'between genes' be proved conclusively to be meaningless and of no relevance to either of its neighbors?  And second, DNA definitely does have a role even if all it does is produce non-coding RNA, or act as a regulatory sequence that does.  So for example, on OMIM you can look up many records for "intergenic", with results like H19, for which one term is "LONG INTERGENIC NONCODING RNA H19".  Note also H19 is listed as the HGNC approved gene symbol, so it is an intergenic gene.  Tricky, eh?  (I have great respect for OMIM - this isn't their fault)  Also, enhancers can be quite a long way from a gene, even past the end of another gene or affecting multiple genes, so even though a mutation in the enhancer might genetically act as an allele of a specific gene, it might be described in sequence terms as located in an intergenic region.
Bottom line: the intergenic regions you're reading about are going to be between things that are recognized as genes, and may or may not be known to have some effect on one or the other (or both...).  They won't contain CDS, which is always considered to be a gene, nor 5'UTR or 3'UTR because those are transcribed before or after a CDS.  Past that, how they are being distinguished from "upstream sequence" and "downstream sequence", that could be completely arbitrary.  They might have gone to WormBase and pulled out curated gene records, and added some number of base pairs before the start site as promoter - but I don't know that.  You'll just have to try to find the particular reference for whatever tool you are using.


Electrocardiogram: Missed beats in presence of Ectopic beats or Premature Atrial/Ventricular Contraction beats I have been working on analyzing Electrocardiogram data.

So far, i have identified Ectopic beats and Premature Atrial/Ventricular Contraction beats.
I am working on identifying Missed Beat in the Electrocardiogram.

The definition of Missed Beat is:
"The characteristic of a missing beat in ECG is the unexpected absence, together, of P-, QRS-, and T-waves."

My question is, do we have to consider missed beats in presence of Ectopic or Premature beats also ??
For example, if an ECG contains premature/ectopic beats, then should the R-R interval between these beats should be compared to R-R interval between normal beats to search a missed beat ??

After developing and checking the algorithm with simulated ECG data, i found out that premature beats (as the name suggests) itself arrive prematurely i.e. their R-R peak interval is less then the R-R peak interval between normal beats.

In that case, i am considering the averaged interval between normal beats and compare it to the interval between next arriving beats. If that interval is more than twice the averaged normal interval, then i classify it as a missed beat.


Thymus and maternal microchimerism I read in Bruce Alberts Molecular Biology of The Cell :

  ....If,however,cells from one strain of mouse are introduced into a neonatal mouse of another strain , some of these cells survive for most of the recipient animal's life, and the recipient will now accept a graft from the original donor, even though it rejects "third party" grafts.

As far as I understand , in this experiment,they got these results because thymus hadn't yet learned what was "own" and what was "foreign".

Is  the reason for why maternal microchimerism does not invoke immune response related to the above experiment ? Can we apply the same logic here ?

You are on the right track.  This is an example of microchimerism (the maternal part is a bit off), and the key issue at hand is central tolerance.
Background:
A good definition of microchimerism is:

Microchimerism is existence of an allogeneic DNA in a living creature. (1)

Scientist do this on purpose for all kinds of reasons, but mostly to ether is study the immune system directly or to get a near-transgenic model.  It should be noted that this isn't perfect, and that when you try to do this, you often can lead to auto-immune problems and often death of the mouse (30-50% survival in early work).  If you go back to one of (if not the) pioneers of immunology, Peter Medawar, you can see when how this was done:

Mice and chickens never develop, or develop to only a limited degree,
the power to react immunologically against foreign homologous tissue
cells with which they have been inoculated in fetal life. Animals so
treated are tolerant not only of the foreign cells of the original
inoculum, but also of skin grafts freshly transplanted in adult life
from the original donor or from a donor of the same antigenic
constitution. (2)

If you would prefer a visual layout of the experiment, Starlz put together one in his review of transplantation (Pubmed):

After looking over the section you quoted from Alberts, I'm pretty sure he was in fact referring back to these early experiments.  But that was all the way back in the 1950's, what have we learned as the mechanism in 60 years?
Possible Mechanism:
The truth is that we don't have an absolute grasp on how this works when it doesn't cause an autoimmune problem and abort the fetus or even neonate pup.  It's import to note that it probably does cause auto-immune problems and various other side effects (like sex differentiation) in mammals.
But when and how it is tolerated is likely mediated by central tolerance, and the ability to get the foreign MHC molecules tolerated by early lymphocytes.  Essentially, the cells have to get incorporated into the AIRE machinery at an early enough stage that the T-cells are selected against the foreign cells.
There is enough biology here that an in-depth answer could be a dissertation, so I only want to touch on a few more points.  You should note that this was done with relatively genetically similar animals, and most modern researchers use cells modified from genetically pure mouse breeds.   We also know a lot more on how the cells "recognize self" and the HLA types of the population.
You are most likely to succeed when the MHC molecules are very similar (ie from a direct family member).  This happens when the host and foreign cells have an HLA type match.
TLDR:
The lymphocytes, mostly T-cells in this case, of fetal mammals seem to be able to look at very similar MHC molecule on a foreign cell and decide "eh.. close enough," and build negative selection (part of β-selection) against lymphocytes that would kill the foreign cells.  This requires that the cell be in the right place at the right time, and of course, be "close enough."
Do let me know if something is not clear or needs to be expanded upon.  As someone who works in Immunology, I have difficulty determining where the detail line should be.


Why/How do Cyanobacteria Produce Toxins? I've been doing some research on the versatility of nitrogen-fixing cyanobacteria, particularly of the genus Anabaena, and I often run into safety hazards and have to add extra steps to my procedures because of the toxins produced by the genus. After doing some reading, I've found that most cyanobacteria produce toxins (collectively dubbed "cyanotoxins"). The wide variety of different structures and mechanisms of the toxins across multiple genera is astounding, especially because some of them are carcinogens, which would logically affect the host unless a mechanism to prevent this had evolved. This tells me that a lot of evolutionary "effort" must have been put into the evolution of toxin production in cyanobacteria. Originally, I just thought that the toxins were a natural part of their metabolism that evolved normally because these compounds didn't affect them in the same way as they did us. Now that I see the Huge, variable trend throughout the class, I have begun to think otherwise. My questions are as follows:

What is the evolutionary basis for the production of cyanotoxins by cyanobacteria
Are the cyanotoxins a necessary part of the bacteria's metabolism, or can they be eliminated by way of genetic engineering without directly affecting the success of the organism?
How do cyanobacteria cope with the constant exposure to native carcinogens?

These questions are only the major ones that I have, so any extra information is greatly appreciated

This available paper has some ideas,
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3736421/
Search terms cyanotoxin and evolutionary give at least two more promising papers.

https://www.biorxiv.org/content/10.1101/615542v1.full
says:
i) photoprotection due to absorption of harmful ultra-violet radiation; (ii) facilitating the acquisition or more efficient use of available but limiting resources; (iii) impeding growth or resource use of competitors such as green algae or other cyanobacteria; and (iv) limiting predation by inducing toxicity in organisms predating on cyanobacteria. While the role of cyanobacterial metabolites in photoprotection, resource monopolization, and habitat dominance has been demonstrated experimentally, hypotheses regarding the anti-predation role are not entirely consistent


How do butterflies defend themselves from other creatures when they don't have the ability to sting or some other offensive/defensive mechanism? How do butterflies defend themselves from other creatures when they don't have the ability to sting or some other offensive/defensive mechanism?

  Butterflies are part of the class of Insects in the order Lepidoptera. Adult butterflies have large, often brightly coloured wings, and conspicuous, fluttering flight.

Butterflies have a number of defence mechanisms, even if they don't have the ability to sting (as adults - see spines in larvae below). Here is a non-comprehensive list of some defensive mechanisms:

Toxins or repellents, which can be present in both adults and larvae.
Aposematism (warning coloration)
Mimicry, both in the form of resembling other poisonous species and using features such as eyespots.
Spines, bristles or long hairs, often in larvae (see google images), to make ingestion highly unpleasent or dangerous. See the Pine processionary moth (Thaumetopoea pityocampa) for an nice example of defensive larval hairs.
Camouflage/hiding
Sound clicks used to startle or disorient predators. This is most often known from moths to prevent bat attacks (see e.g. Cycnia tenera and Fullard et al, 1994).
Conspicuous features at the edge of wings to make them targets of attack, e.g. eyespots or appendages, which are used to lure predators to attack non-essential body parts (see Olofsson et al, 2013 for an example).


Which are the most important carcinogens in tobacco smoke? I am researching the neoplastic effects of tobacco smoke and would like to measure a set of key molecules in the saliva of several study subjects after they have smoked.

Which are the most relevant carcinogens originating from tobacco smoke that are detectable in saliva? I don't think there will be time or room to measure metabolites, as the saliva samples will only reflect short-term (<60 minutes) exposure to tobacco smoking.

This is not an easy question - as tobacco smoke contains something like 5000 different chemical components, from which 70-100 are carcinogen. The list includes: Oolycyclic aromatic hydrocarbons (PAHs), N-nitrosamines, aromatic amines, aldehydes, volatile organic hydrocarbons and metals. I haven't found articles which specifically concentrate on the carcinogens in saliva, but my guess would be that you find them all because of the "application route" of the cigarettes.

Most of these carcinogens first need to be processed from the livers cytochrome P450 system to reach their carcinogenic potential. The enzyme complex converts these substances into forms which can then covalently bind to DNA.

A list of several different of the carcinogens can also be found in the Wikipedia. For further information see the references.

References:

Hazardous Compounds in Tobacco Smoke
How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis
for Smoking-Attributable Disease: A Report of the Surgeon General.
Tobacco Smoke Carcinogens and Lung Cancer


Is there a program that simulates biology on a molecular level? Is there a computer program that simulates biology on a molecular level? Software that has rules that simulates the rules of molecular-biology?

There is a recent paper that introduced the first molecular-level whole-cell simulation.

Karr, J.R., Sanghvi, J.C., Macklin, D.N., Gutschow, M.V., Jacobs, J.M., Bolival, B., Assad-Garcia, N., Glass, J.I., & Covert, M.W. (2012). A whole-cell computational model predicts phenotype from genotype. Cell 150:389-401 DOI: 10.1016/j.cell.2012.05.044

The authors combined 28 different sub-modules of various biological processes from the literature. Each one operates at the level of macromolecules, although models them in different ways: some by ODEs, some by logic; some by agent-based approaches. If you want to fool around their code is available online and I wrote a basic introduction/summary of the paper.

Here are some related bio.SE questions motivated by that model:

Short-term Lamarckism in asexual single cell organisms
Computational/mathematical models for predicting phenotype from genotype
Macromolecule levels in daughter cells after fission


Limitations of the Self-Incompatibility Mechanism in Plants For a given plant species, how many types of S-loci exists to prevent self-pollination? I would like to know how often a plant stops fertilization process by other plants, thinking the pollens belong to itself due to limitations of SSI/GSI.

Herrera, Sara et al. 2018 suggest that there are at least 33 S-alleles in apricot.

I believe some species of Brassica have at least 60 S-alleles identified.

However, there are dominance relationships among these alleles, so I don't think you can directly extrapolate from the number alleles to to the rate at which non-self pollen will be excluded.  The frequencies of the different alleles within a population will clearly also affect this calculation.

In addition, different individuals with the same S-alleles are more likely to be closely related, so I would hesitate to classify this as a limitation of the system.

Ref: Herrera, Sara et al. “Identification of Self-Incompatibility Alleles by Specific PCR Analysis and S-RNase Sequencing in Apricot.” International journal of molecular sciences vol. 19,11 3612. 15 Nov. 2018, doi:10.3390/ijms19113612


How does low cysteine conditions affect pheomelanin production? So we were studying this amino acid called cysteine. Specifically we were studying it's effect on melanin genesis.
Our teacher told us how excess of cysteine affects the melanin synthesis  by generating more pheomelanin. Low amount of cysteine promotes formation of eumelanin.
 He told us that if the concentration of cysteine is increased in cells then the above reaction starts producing pheomelanin in brown/black skinned people. I searched it on net and it seems to be true.
The question is that if someone who has fair skin (produces more pheomelanin) is forced to live in low cysteine condition, then what happens? Eumelanin production should increase. His complexion must change. But it doesn't occur anywhere. Fair skinned people affected by malnutrition remain fairskinned. How is this possible? The pheomelanin production must stop since they aren't getting enough cysteine. Then how...?

He also told us that onions contain large amount of cysteine yet it can't be used since it is destroyed by stomach acids.

First: Your teacher is right with the statement that a low cysteine concentration affects the synthesis of pheomelanin. To understand this, you need to take a look at the biosynthesis pathway of melanin (from here):

The first steps for both melanin forms are the oxidation of the amino acid Tyrosine to DOPA (L-3,4-Dihydroxyphenylalanine) and the to DOPA quinone by the enzyme Tyrosinase (abbreviated Tyr). In the following step the branches divert, if there is enough cysteine present in the cells, then Cysteinyl-DOPA and subsequently Pheomelanin are synthesized.

If the cysteine concentration in the cell falls below the threshold of 0,13µM (this is taken from this paper), then the switch to eumelanin production occurs.

In the case of you second question, there is a different setting. The overall rate of the melanin production (no matter which flavor) depends on the amount of active Tyrosinase (for the production of the first steps in the synthesis cascade). The production of this enzyme is regulated by receptors in the cellular membrane (and different other factors).

In fair skinned people (classically red-haired and with freckles) these receptors are not fully functional, resulting much less Tyrosinase enzyme in the cells. This results in fewer available precursors for the melanin production and in turn in less need for cysteine. The reason is that the cysteine pool of the cell is not getting exhausted.


How long can a plant generate oxygen from its own carbon dioxide, produced during nighttime? I recently bought one of these miracle fruit plants (Synsepalum dulcificum).  Since they are of tropic origin, they need higher humidity and temperature as we have it here in Austria. So I decided to cover it in a transparent plastic bag, together with a small water basin, in order to maintain better conditions.

Assuming the bag is absolutely gas-tight, allowing no diffusion, my question is:

For how long could the plant generate $\ce{O2}$ from its own $\ce{CO2}$, produced during night? And as a little subquestion: Will the plant eventually run out of oxygen at night?

I know there are no exact answers to this, so an rough approximation is more than enough for me.

Just to give you better notion of my experimental conditions:

enclosed gas volume: ~ 3 L
(onesided) leaf surface area: ~ 0.5 dm$^2$
temperature: ~ 15$-$25 °C

For how long could the plant generate $\ce{O2}$ from its own $\ce{CO2}$, produced during night?

Plants do not generate $\ce{O2}$ from $\ce{CO2}$.

Photosynthesis consists of two general steps, one that requires light and one that does not. The first step occurs in the thylakoid membrane, and splits water into oxygen, hydrogen ions, and energy. The second step is the carbon fixation step, which occurs in the chloroplasts and uses energy to convert the carbon dioxide into carbohydrates.

Step 1: $\ce{2 H2O + light → 2 H+ + O2 + energy}$

Step 2: $\ce{3 CO2 + 6 H+ + energy → C3H6O3-P + 3 H2O}$

The more detailed chemical equations can be found on the Wikipedia Photosynthesis page.

Since the first step which produced oxygen is light-dependent, it occurs mostly during the daytime. To keep growing during the night, the plants break down the carbohydrates they produced and stored during the day. This cellular respiration uses up oxygen and generates carbon dioxide just as animals do.

Will the plant eventually run out of oxygen at night?

As mentioned, plants require oxygen for cellular respiration, which occurs both at day and night. The difference is that during the night, they are not producing oxygen via photosynthesis. Assuming the plant is in sufficient light and temperature conditions during the day, the plant will not run out of oxygen at night. Plants can survive in sealed environments for very long times. A fun example is a reportedly 53 year-old bottle garden. In a bottle garden, which is essentially the system you are creating, the only difference from a plant out in the environment is that the same oxygen, carbon, and hydrogen molecules are constantly being recycled via photosynthesis and cellular respiration.


Urgent: Bird hatchling identification Yesterday evening I found this baby bird in one corner of my house's verandah on the floor. I picked it up and placed it safely in a tray hoping that tomorrow morning its parents will find it (actually I initially suspected it to be a sparrow hatchling). When I saw it today morning I found that it is probably a bird of prey. As you can notice the large long beak and claws.
I'm really confused now what to do with it. Please suggest something.

EDIT

I live in Uttar Pradesh, India.
Its relatively plain where I live. (No mountains or lake nearby)
Temperature: 35-20 degrees Celsius
Added a photo for size estimation

As you've pictured this is a fledgling that you found which has a mixture of adult feathers and immature feathers.  This indicates that it flew to your location, and a nest is nearby.  You should either attempt to find the nest, or just leave the fledgling alone and let it make its own way home as indicated in this online resource.

Fledglings are juvenile birds who have a mix of fuzzy down and adult feathers and are learning to fly. You may come across them hopping along on the ground, perching on low-hanging branches, or hiding under bushes, but as long as they’re healthy, just let them be.
Note: Fledglings are often “rescued” from their natural environment when they don’t need to be.


Using an analytical balance (0.0000 precision) to measure µg (micrograms)? If i needed to prepare 200µg/ml of proteinase K, and the proteinase K  was in a solid powder form, would I  have to weight out 200 µg using an analytical balance, and if so, is it possible with a balance that only goes up to four decimal places? (i.e. 0.0000) I assumed 1 microgram is 1×10-6 gram and therefore 0.000001 gram.

As others have said, that mass is too small to measure with a standard analytical scale. There are two options you could use:

Make a larger volume of your 200 ug/mL solution.
Make a concentrated stock such as 20 mg/mL. This a 100X stock; you can make 1 mL of 200 ug/mL proteinase K with 10 uL of stock and 990 uL of buffer. Small volumes are easier to measure than small masses (with a micropipette).


Please help identify insect found indoor in Malaysia, south east Asia Found this insect in my home. About half an inch long. Would appreciate it if any of you could help me identify it. Thanks.

In the USA we call these insects crickets. Because they make a noise that sounds like the pronunciation of their name. This one looks like a male with two cerci.


What type of Caterpillar is this? What type of Caterpillar is this?

My hand brushed against this last night and it burned and itched immediately. Today it's starting to blister, is red, and itches all around the bumps. I was camping at the John Knox Ranch in Fischer, Texas. It was dark and I reached to grab the chair when I suddenly felt pain. It was about two inches long. This is the reaction I initially got. I didn't even feel when i brushed against it until i started feeling pain.
These were the best pictures I could get.
Any help is appreciated!!

Picture is not very good, but I think this might be an Eastern Buckmoth Hemileuca maia caterpillar.

 Photo credit: Gary L. Spicer ; Source: butterfliesandmoths.org
Description: From the University of Kentucky:

The two-inch long Buck Moth caterpillar is brown to purplish-black with numerous yellow spots. The body is protected with branched reddish spines that may have red or black tips....
Common...from spring to mid-summer.

Reaction: Your wound/reaction would not be an unexpected reaction from touching this caterpillar species. From UFL IAFS:

The spines in the buck moth occur on raised, sclerotized (hardened) portions of the larva's cuticle that are known as tubercles and scoli. The spines found on these structures are associated with venom glands that occur within the caterpillar's body... The sting produces pain immediately, which then spreads to nearby lymphatic nodes. The caterpillar's sting then causes swelling and redness to occur. These symptoms can last for as little as a day to over a week. Wagner (2005) reported that the stings he received from a buck moth caterpillar were still present after ten days and the venom of the caterpillar caused a small hemorrhage where each spine had stung him. According to Diaz (2005), severe reactions to the venom of the buck moth (such as anaphylaxis) are rare.

Treatment: The video here suggests running your hand under cold water, air dry, use tape to get out remaining spines, and then apply some ice. UFL IAFS corroborates this approach as well.

Range: According to the incidence map on butterfliesandmoths.org, H. maia is found in Texas:

Wikipedia corroborates the range of this species to include Texas.


What are these creeping cacti tendrils? During a trek through a small forest-type area on the main island of Hawaii, I came across the following plant:

It did not cover very much area from what I could tell (there was a continuation of the bed just behind me from where I took the picture). I believe it was near Punalu'u Beach but I can't say with certainty.

It's creepy, looks like a tractor load of snakes got loose, and something I find fascinating. Could someone tell me what this cactus-y, bed of vines-like plant is?

It's creepy ... something I find fascinating.

Creepy & fascinating indeed!

  Could someone tell me what this cactus-y, bed of vines-like plant is?

This is a cactus, and I believe it belongs to the genus Hylocereus, possibly the species H. undatus.

As for distribution, Hylocereus are quite prevalent throughout Hawaii, and can also be found scattered throughout the globe.

Hawaii is the leftmost blue dot. image source

More information about this plant can be found here.


Why do wild lizards often tap with their front leg? I have a lot of wild lizards (possibly Podarcis muralis) in my garden, and I have noticed some of their behavior I'd like to understand:

whenever they are in 'still' position on any surface, they are quite often 'beating' with one of their front legs on the surface

in some cases they put the tail of the mate in the mouth

What is this behavior? Some kind of communication?

I found a paper(1) about the 'tail in the mouth' behaviour in the whiptail lizard, Cnemidophorus ocellifer:

Every time that the female moved, the male followed her. During these periods, he often maintained physical contact, covering her hind legs and base of tail region . The male also performed a series of tongue-flicks on the female's back during this activity. During the observation, the female twice executed a sequence of two or three sinuous, figure-eight movements, which were confined to a small area, and after which, the female moved away. After each movement, the male remained motionless for a few moments and then resumed following her while foraging. After 45 minutes and nearly 15 m from their initial positions, the pair entered in dense underbrush, where we could not continue to observe them. While we observed the pair, there was no agonistic encounter between the accompanying male and other males for access or copula with the female.

The paper continues to explain this behaviour as simply a mating strategy:

Two conditional mating strategies have been described for teiid males (Zaldívar-Rae & Drummond 2007).  1) In consensual copulations,
the male courts the female, slowly circling her for several minutes,
then straddling her and copulating; this strategy is often performed
by a male companion, and thus is linked to accompaniment.  2)
Opportunistic copulations are not preceded by courtship, and are
characterized by a male chasing and holding a foraging female, and not
accompanying her after copulation (Zaldívar-Rae & Drummond 2007).

The 'taping the surface they are on' seems like an attempt to induce vibrations, which is a method of communication.(2)

Some chameleon species communicate with one another by vibrating the substrate that they are standing on, such as a tree branch or leaf. Animals that use vibrational communication exhibit unique adaptations in morphology (i.e., body form) that enable them to detect vibration and use it in communication. These include unique adaptations in ear and jaw morphology that give the animal direct contact with the surface they are standing on, and enable them to detect subtle vibrations. Lizards that live on substrates that can be easily moved (such as thin tree branches or leaves) are probably more likely to use vibrational communication than lizards that live on substrates that do not transmit vibrations as easily, such as the ground or thick tree trunks.

1- https://www.scielo.br/scielo.php?script=sci_arttext&pid=S1676-06032011000400031#:~:text=The%20most%20commonly%20reported%20mating,Bull%202000%2C%20Ribeiro%20et%20al.
2- https://en.wikipedia.org/wiki/Lizard_communication


What happens to the hollow nerve cord? The dorsal nerve cord of vertebrates is a hollow structure that develops into the nervous system. This embryonic tissue is hollow and I wonder what happens to this 'hollow' later?

Does it form the ventricles of brain?

The "hollow" i.e. the neural canal develops into the ventricles, the cerebral aqueduct and the spinal canal (Wikipedia; also see this site).

For a more authoritative reference, see this book by Haines and Ard† (page 82 onwards in google books; google book links are apparently transient and they expire; therefore I didn't provide one).

† Haines, Duane E., and M. D. Ard. Fundamental neuroscience for basic and clinical applications. Philadelphia, PA: Elsevier/Saunders, 2013. ISBN: 9781437702941


Why don't birds in flocks fly into each other? I've seen videos of hundreds of birds flying in the same general direction but creating incredible patterns in the sky seemingly instantaneously! How do they all know in what direction to turn at the same time? Is there a "Lead" bird dictating this somehow?

Richard Dawkins discusses this in his book The Greatest Show on Earth: The Evidence for Evolution.

The birds, in the aforementioned example Starlings, 'know' which direction to fly and where to be by obeying simple local rules concerning the distance and spacing of other members of the flock in their immediate vicinity, without any global knowledge of the size or shape of the flock in its entirety.

The key to this behavior is that there is no choreographer and no leader.  Order, organization and structure all emerge as by-products of rules obeyed locally, many times over.

Dawkins equates this to 'bottom-up' design or 'self-assembly'.  This is also how embryology works.  Beautifully 'designed' bodies emerge as a result of single cells obeying local rules.  The idea of a blueprint is a misconception.

Dawkins mentions a man in the book named Craig Reynolds who wrote a program in 1986 called 'Boids' which models the flocking behavior of thousands of birds - http://en.wikipedia.org/wiki/Boids


Can you detect if a mutation is spontaneous or induced? Is it possible to determine if a certain specific mutation had a spontaneous origin (for example from a mistake of the DNA polymerase) as opposed to an induced origin (for example, from some genotoxic agent)?

Here's a quick answer; hopefully someone will give a more complete one.  But meanwhile you've got something.

Some genotoxic agents have predictable results.  For example, they cause Gs to substitute for Cs, or they cause mutations at specific spots on the genome.  So if you had a bunch of mutations in a single cell (or collection of related cells) that matched the modus operandus of a known genotoxic agent, then it would be reasonable to conclude that the mutations were induced.  But not all genotoxic agents are like that.  And if you only have 1 or 2 mutations, that's not enough to prove they were induced.  Also, of course, it depends on your sample size and your controls.


what happens to rna length if we have a termination site in additional to the original one if we have an RNA transcription and we add an additonal temination site in  the middle , will i have two RNA molecules or just a short one ?

Assuming that by termination signal you mean transcription termination signal (and not a stop codon), you would have one shorter RNA molecule. You can have two shorter RNA molecules if there is another transcription start site after the termination signal, but there is no reason to assume this will be the case.

In some cases the RNA polymerase will skip a base and frameshift while transcribing a new RNA strand. This is known as transcriptional slippage, and it is taken advantage of by some viruses in order to make their genomes more compact by having several different mRNAs overlap each other.

In this rare case, having a termination signal does not necessarily mean transcription will terminate, it might be able to skip through parts of the termination signal and continue to the next termination site.


How, on a physical level, does ATP confer energy? When ATP is used as the energy currency to make, say, reaction X + Y → Z happen, is what happens on a physical level down at the molecular scale that during the reaction

ATP + H2O → ADP + Pi       ΔG˚ = −30.5 kJ/mol (−7.3 kcal/mol)

that 30.5 kJ/ mol is conferred by ATP molecules physically bumping around the reactants X and Y, the kinetic energy of the above reaction being what does it?

I mean, is the energy coin of ATP conferred to reactions by molecular collisions, or is it an electric field effect in the spatial geometry the way the ATP molecule tends to break apart?

Usually in biology (and being ATP, it most probably is biology), it's one of two things.

The gamma-phosphate (the third one, the one farthest from the adenosine) is very unstable, meaning the phosphoanhydride bond is easy to break.  The cell "allows" it to break, but only at the cost of moving the phosphate to some other molecule, such as a serine or glycerol or fructose or whatever.  This phosphorylation creates a bond with lower energy than the phosphoanhydride, and so is overall favored.  Imagine the personification: the gamma phosphate hates being attached to anything, but hates being attached to an ADP the most.

Alternatively, if ATP hydrolysis is coupled via an enzyme, it is usually done through transient storage of the energy is protein conformation.  An enzyme binds ATP, which makes the protein structure "bend" or conform around the ATP.  This puts loads of strain (energy = A) on the protein which is offset by the stabilization of binding the ATP (energy = B).  This strain can make an enzymatic surface open up on the protein which itself takes a lot of energy to make (energy = C).  The surface can catalyze some reaction (X+Y->Z in your example) that costs some energy (energy = D).  The completion of that reaction alters the enzyme's catalytic site to something new and higher energy (energy = E), which can be alleviated by cleavage of the ATP (-7.3 kcal/mol).  Alas, ADP and P do not fit well into that site of the enzyme, so they float out, restoring that original ATP-binding surface to it's original state.  Provided A>B>C>D>E>-7.3, the cycle will continue until the ATP is exhausted or you have no more Z to make.

Typing "enzyme catalysis cycle ATP" gives a few examples. Here's a few:
DNA gyrase
Actin-myosin cycle


Process of Transcription During the process of Conversion to Ribonucleoside Monophosphates the various ribonucleoside triphosphates break off their high energy bonds after linkage to the DNA.But the first ribonucleotide triphosphate retains all the phosphates thus chemically distinct from the rest.

Now my question is:
Why does it retain the phosphates?

There is a useful diagram at this site.

During RNA synthesis in vivo the 3'-OH oxygen atom of the growing chain reacts with the α 5'-phosphate of the incoming ribonucleotide (nucleophilic attack), displacing the β + γ phosphates as a pyrophosphate group. This results in a 3'-5' bond between the prexisting oligoribonucleotide and the incoming ribonucleotide. In other words the loss of the pyrophosphate group is an inevitable consequence of the elongation reaction.

At initiation, however, the first ribonucleotide has not been the subject of a nucleophilic attack, because it is first in the chain. Its 3'-OH will carry out the nucleophilic attack descibed above when the next ribonucleotide is added to the chain.


Literature that demonstrates organisms have a competitive advantage in numbers I'm studying two bird populations that are competing against each other for a resource: Population A and Population B.

Population A is present in much higher numbers than Population B, and as a consequence, I think that Population A has a competitive advantage over Population B.

I'm looking for literature that demonstrates that when one population is present in higher numbers than the other population, the population present in higher numbers has a competitive advantage. Can anyone point me in the direction of literature that demonstrates this?

I have found these papers:
http://www.sciencedirect.com/science/article/pii/S0169534713002322

http://www.sciencedirect.com/science/article/pii/S0040580912001360

http://www.ncbi.nlm.nih.gov/pubmed/19416834

http://www.ncbi.nlm.nih.gov/pubmed/21930936

The last two argue that larger groups have better "problem solving" capability, and this is a clear advantage in competition.


Does DNA helicase or topoisomerase actually "unwind" DNA? I am reading through my textbook (Genetics, Brooker 4th edition) and the summary it gives seems imprecise for the functionality of helicase and topoisomerase.

The following is an exerpt:

At each replication fork, DNA helicase unwinds the DNA and topisomerase alleviates positive supercoiling.

Is it proper to say that helicase "unwinds" DNA? In other places in the book, it says the function of helicase is to separate the two strands of DNA, and topoisomerase "relieves the supercoiling" caused by the strand separation activity of helicase.

Pardon my ignorance, but it seems rather like helicase actually induces more winding, and topoisomerase (gyrase) actually unwinds DNA.

Is this just a case of poor wording, or does helicase actually somehow unwind (untwist) DNA? I am finding this particularly frustrating because virtually every resource I can find says that helicase unwinds DNA, but based on the mechanisms they offer, it definitely does not "unwind".

Got a short piece of three stranded rope handy? (I don't think they make two stranded rope.) Hold the rope firmly in each hand about 5 cm apart. Twist in the direction opposite the winding. The strands of the rope will separate in the region between your hands. The unwinding and the separation of the strands are, um, inseparable from one another. You can't separate the strands without unwinding.

The heilcase unwinding is merely straightening out the double helix in a very local area. This separates the strands such that one strand can serve as a template for transcription or replication.

But a consequence of the unwinding in the local region where the strands are being separated, is that other nearby regions get more tightly wound. This occurs because the DNA is far too long for the ends to spin around to accomodate this unwinding. These more tightly wound areas are what is refered to as supercoiling. The topoisomerase alleviates this stressful coiling. https://en.wikipedia.org/wiki/Topoisomerase

So, the answer is both helicase and topoisomerase result in the unwinding of DNA.


How well does the radius of a tree correlate with its age? I'm looking for a cheap non-invasive ways to approximate the age of a tree (a birch). Measuring the radius pops up in the mind as the first alternative. How would one do that? Measure at multiple defined heights?

I'm hoping that I could get some kind of confidence interval for the approximation, so that the data could be used in a scientific publication.

Or is there any reliable DIY radiocarbon dating technique?

The radius of tree is not a good measure of the tree age, the most efficient technique to know the age of a tree is with dendrochronological methods, this is the less invasive technique. However, knowing very well the dynamics of growth of each species you can infer the age, check out this study:

Jan Lukaszkiewicz and Marek Kosmala. 2008. Determining the Age of Streetside Trees with Diameter at Breast Height-based Multifactorial Model (note this is a direct link to a pdf)


If inhibiting S6 kinase decreases protein translation, then could inhibiting S6 kinase could possibly slow down long-term potentiation in neurons? From http://en.wikipedia.org/wiki/P70S6_kinase...

  Phosphorylation of S6 induces protein synthesis at the ribosome.

  P70S6 kinase is in a signaling pathway that includes mTOR (the
  mammalian target of rapamycin). mTOR can be activated in distinct
  ways, thereby activating p70S6K. For example, branched chain amino
  acids such as leucine are sufficient to activate mTOR, resulting in an
  increase in p70S6K phosphorylation (and thereby activating it). mTOR
  is also in a pathway downstream of the kinase Akt. Akt is typically
  activated upon stimulation of a cell with a growth factor (such as
  IGF-1). Akt then activates mTOR (by inhibiting the Tsc complex),
  leading to p70S6K activation.

We also found a paper showing that downregulation of S6 kinase also results in a decrease in protein translation in yeast (but I'm waiting for Matt Kaeberlein to email me the slides from yesterday).

I can't rule it out, but it sounds a lot like trying to tune a piano with sledgehammer.

Neuronal LTP depends on protein translation, but so does absolutely everything else in the cell. Inhibiting protein synthesis at the ribosome will block the formation of all proteins, not just the ones responsible for LTP. Unless there's a link I don't know about between LTP and total levels of protein translation, you're really going to want to look into inhibiting the production of proteins specifically responsible for LTP and not protein synthesis in general.


What is the difference between the mitotic spindle and microtubules? In mitosis, I understand that the centromeres line up on the spindle. I also know that the centrioles form microtubles between the centromeres during mitosis in the metaphase.

But, are microtubles and spindles the same thing? Or do microtubles make up spindles?

Short answer
The spindle is made up of microtubules

Background
From Nature:

  Spindle fibers form a protein structure that divides the genetic
  material in a cell. [...] At the beginning of nuclear division, two
  wheel-shaped protein structures called centrioles position themselves
  at opposite ends of the cell forming cell poles. Long protein fibers
  called microtubules extend from the centrioles in all possible
  directions, forming what is called a spindle. Some of the
  microtubules attach the poles to the chromosomes by connecting to
  protein complexes called kinetochores. Kinetochores are protein
  formations that develop on each chromosome around the centromere,
  which is a region located near the middle of a chromosome. Other
  microtubules bind to the chromosome arms or extend to the opposite end
  of the cell. During the cell division phase called metaphase, the
  microtubules pull the chromosomes back and forth until they align in a
  plane along the equator of the cell, which is called the equatorial
  plane.


De novo mutation selectivity I was recently reading about genetic diseases and came to understand that many of them are caused by de novo mutations in the prezygotic or early embryonic stages of the life cycle of the organism. Most chromosomal aneuplodies resulting in well known genetic diseases such as the downs syndrome caused by trisomy of chromosome 21 are caused due to de novo mutations.
However the thing that I didn't clearly understand was the reason for some de novo defects being more prevalent than others. For example the trisomy of chromosome 21 causing downs syndrome is relatively more common than the trisomy of the other chromosomes. Why are some aneuploidies such as trisomy 21 replicated independently in many different individuals (are more prone to occur) than others?

Edit: I am only addressing aneuploidies as those are the examples given. Other classes of mutation have distinct mechanisms, so I would split those out into another question if you are interested.
Chromosomal abnormalities occur more frequently when it is hard for cells to do meiosis and mitosis properly with a chromosome, or when the chromosome is more prone to "break" for some other reason.
The cell relies on certain architectural features (centromeres) to segregate chromosomes properly during mitosis. When segregation goes wrong, then you find aneuploidy much of the time. Chromosomes have other features such as telomeres and satellite DNA that can lead to chromosome fusion errors by different mechanisms. For example, yeast cells that have aberrant telomeres lead to high rates of aneuploidy.
Different chromosomes of the same genome have some variation in structure, repeat content, and other features that may predispose to aneuploidy formation or otherwise. These can include the quality and functionality of features such as centromeres and telomeres; these can vary even for the same chromosome across the lifespan of an organism.
For example in yeast, people have observed quite dramatic differences in the occurrence of spontaneous aneuploidy between different chromosomes (see figure 1). Yeast cells are much more robust to chromosomal variation than humans as they do not have a complex developmental cycle. However, aneuploidy of chromosomes with certain genes does seem to be selected against in that paper. There also appear to be dependencies in which the aneuploidy tolerance of one chromosome depends on the karyotype state of some other chromosome. "In other words, CIN [chromosomal instability] does not appear to be caused by some general property of being aneuploid per se but rather by determinants associated with specific aneuploid karyotypes."

Figure 1.
Experiments in the muntjac (a mammal) seem to show that the different chromosomes segregate more or less effectively based on centromere size (Figure 2).

Figure 2.
Human chromosomes have quite different rates of aneuploidy formation (see Table 1), so yes there is a bias. This is most markedly a bias in which acrocentric chromosomes and the shorter chromosomes have a somewhat elevated rate of aneuploidy (Table 2, same paper). So having an acrocentric architecture may make a chromosome more difficult to segregate.
When you ask about trisomy 21, note that chromosome 21 is acrocentric in humans. Thus, aneuploidies occur for chr21 at a somewhat higher rate.
However, commenter @MikeyC has a good point that there is a bit of ascertainment bias in how we find aneuploidies. Many aneuploidies are embryonic lethal and spontaneously abort; chr21 trisomy on the other hand yields living babies with noticeable features of their aneuploidy, so we know a lot about it and see it a lot. This seems to agree with the yeast data.
So there are multiple contributing factors. There is some variation in how chromosomes give rise to aneuploidy, but we also need to consider the means by which we observe aneuploidies in evaluating those molecular mechanisms.


Why aren't organelles considered alive? I'm taking a 3-week Bio I summer course, and my textbook says the cell is the smallest/basic unit of life. I asked my professor why organelles aren't a living unit, and her reply was that they aren't self-sufficient. But it seems that cells in multi-cellular organisms need other cells with different specializations in order to survive. You can't just (or can't always) pluck a cell out of a larger organism and leave it to fend for itself outside of it. Same with an organelle. She said only the entire cell fits all the requirements for life, referring me to the textbook, but I couldn't find an actual description of these requirements. So, what is the relevant difference between an organelle and a cell such that only the entire cell is considered alive?

The definition of life is a controversy in itself, and as it is simply a word that can be understood by everyone however they wish, there is no "correct" definition. It is thus not really possible to give a "correct" answer to your question, but here are a list of things you may want to consider:

Replication of DNA is probably the most agreed common feature to all life on earth. Most organelles do not contain their own DNA but are simply lipid and protein constructs.
Independence is a difficult criterion of life, as parasites require a host for reproduction. However, while the organism may require a host, its cells individually can replicate without a host.
Cells are able to replicate when removed from the body - under the right conditions. (We are getting better and better at culturing all sorts of cell types, for example to avoid having to use animals for research.) Most organelles are not able to replicate under any conditions.
In nature, there are single living cells. In fact, the majority of organisms on earth consist of one cell only. There are no organelles living in nature.

Mitochondria and plastids make a complicated exception to these, as they are originally derived from bacteria themselves. It is indeed debatable whether they could be considered alive, as they possess DNA and it is replicated in order for them to divide, like individual cells do. However, the machinery required is not produced by themselves but rather by their "host" cell, making them subject of a similar argument as viruses.


How were (many) dinosaurs' brains so small? Brain size (or its proxy, encephalization quotient) usually varies allometrically with mass -- larger creatures need larger brains to control their larger bodies, apparently.

Dinosaurs are popularly known as small-brained. While this certainly doesn't hold in general -- theropods and especially birds were particularly intelligent -- but sauropods and thyreophorans (ankylosaurs and stegosaurs) seem to have preposterously small brains. How were they able to control their large bodies with such small brains? Are there modern animals with similar proportional brain size, and if so does that give any clues as to how these dinosaurs functioned?

I don't think there is a concrete answer, because we don't really know the minimum size of a vertebrate brain in relation to body size. Many vertebrates, including many fish, get along fine with tiny brains in large bodies.

For many decades, scientists speculated for this very reason of small brain size, that dinosaurs seemed to have an extra brain, or ganglion, at the hip. Especially sauropods and thyreophorans appear to have had a widening of the spinal cord cavity around the sacral area suggesting this possibility. This pelvic ganglion or "hip brain" was then presumed to be responsible for running the hind legs and tails. However, this idea has not gained any further evidence or traction in the scientific community and is generally dismissed.


Use cases of RNA secondary structure prediction I'm an undergraduate currently writing a thesis on RNA secondary structure prediction, specifically building upon analysis done by the RNAStructure and Unafold software packages by modifying certain algorithms here and there. I'm actually not a biologist, however. I've taken all of my classes in physics and computer science, and I sort of stumbled into my current research, and since it seemed to be a good fit for my skill set I stuck with it. However this leaves me curious of a motivation for my current work. Why is RNA secondary structure prediction important and what are some of its applications?

Short answer

I can think of at least a dozen applications for which it would be useful to know the secondary structure of a given sequence of RNA off of the top of my head. In no particular order:

Simulation/visualization of RNA
Riboswitches
MicroRNA
RNA interference (RNAi)
RNA-RNA interactions
RNA-DNA interactions
RNA-protein interactions
Ribosomal protein expression
Ribozymes
Forced evolution of RNA aptamers
Synthetic tRNAs with four and five base-pair codons
Termination of transcription (the process that makes mRNA from DNA)

Basically anything to do with RNA, which is one of the fundamental building blocks of all living creatures.

More in-depth

Simulation/visualization of RNA

Secondary structure (2°) forms the second (yep) level in the standard 4 level hierarchy of macromolecular structure, and consists of short-range interactions between and among residues. In RNA, 2° is usually thought of as being loosely identical with base-pairing interactions. In order to do a proper simulation/visualization you'll probably also need at least the 3° information, but 2° is important too.

Riboswitches

As an mRNA gets translated by a ribosome, in many cases it can form into a complex 3D structure that will affect the translation process. For example, some of the mRNAs that encode proteins related to the metabolism of metal ions have a riboswitch that will themselves bind to metal ions and inhibit/upregulate expression of the related protein. For various reasons it's usually extremely difficult to get the full 3D structure of a riboswitch, so getting to know the 2° remains an important source of information about them.


Example of impossibility in the nested hierarchy? I have conversations with evolution deniers, and I've read that the best single piece of evidence for evolution is the congruence of the genetic and morphological nested hierarchies, and the fact that they are predicted on evolution, but not on intelligent design.

I think I have an example of what would falsify the nested hierarchy; please check me on this, I want to get this right.

Because evolution is a historical process, an organism can only share characteristics, or have varied characteristics, of one of its ancestors.  If an organism had characteristics that came laterally (?) across the nested hierarchy, as opposed to up or down through its ancestry, that would falsify the hierarchy.  An example of this would be a primate with two post-orbital fenestrae (see pic)..

And, we don't find such organisms.

This is not predicted on design because if you design from scratch, without the necessity of varying ancestors' characteristics, you are not limited by not designing a primate with two post-orbital fenestrae.

Do I have this right?

Your view of evolution is wrong

  If an organism had characteristics that came laterally (?) across the nested hierarchy, as opposed to up or down through its ancestry, that would falsify the hierarchy

The expression "falsfying the hierarchy" does not mean much, so I won't comment on it.

Note two things

1) Convergent evolution
 - It is not so uncommon that different lineages evolve similar traits when facing similar selection pressures. This is called convergent evolution.

2) Horizontal transfer
 - It is not so uncommon that pieces of DNA find itself (via a number of different mechanism) in a different lineage. A gene can therefore jump from one lineage to another one. This causes the gene tree of a given gene to not match the species tree. Other processes can cause such mismatch though. This is called horizontal gene transfer.

So, in short, no your view of what you call "impossibility in the nested hierarchy" is wrong.

Intelligent design

Intelligent design is not a scientific hypothesis. It means that it does not make logical sense and it does not make clear predictions that can be tested. By contrast, the theory of evolution is a set of hypothesis all of which that have been formally tested have shown to be confirmed by evidence (that's why the theory of evolution is called a theory;
see here for the semantic).

It is therefore impossible to say whether intelligent design is correct or wrong because it does not say anything. One cannot compare the predictions of the theory of evolution with the ones of intelligent design as intelligent design does not make clear predictions. One can only argue why the theory of evolution
is a set of (confirmed) hypotheses while intelligent design is not a hypothesis (or set of hypotheses).


What is a set of chromosome and what is a pair of chromosome What is the definition of set of chromosomes? Does it differ from pair of chromosomes?

Yes those two expressions refer to different things.

Set of chromosome

The term "set of chromosome" refers to ploidy number. A haploid has one set of chromosome, a diploid has two sets of chromosomes, an hexaploid has six sets of chromosomes.

In humans, each set of chromosome is made of 23 chromosomes (22 autosomes and 1 sex chromosome).

Pair of chromosome

A pair of chromosome refers to the two homologous chromosomes in a diploid individual (one chromosome from each set for a given chromosome number).

Source of information

If the above is unclear, then you should have a look at any intro course to genetic such as these courses by Khan Academy for example.


How does ethanol interact with insulin? I know that ethanol increases insulin secretion--could someone explain why?

All I have found till now is experimental data analyses.  I am interested in mechanism of alcohol consumption.

Alcoholic beverages, ingested casually, deliver two main nutrients the body will metabolize: sugar and ethanol. The body's natural response to a rise in blood glucose will be stimulated secretion of insulin (from B cells of the pancreatic islets). Alcohol is metabolized primarily by the liver, being first converted to acetaldehyde by alohol dehydrogenase and a coezyme NAD+. Acetaldehyde metabolism quickly converts this to acetate. Acetate is then eventually metabolized elsewhere in the body to carbon dioxide and water. The interesting effects are mediated by acetaldehyde, which can accumulate to toxic levels in some people. This ties into insulin because this article suggests that alcohol consumption changes blood flow from exocrine pancreas (responsible for digestive enzymes) to endocrine pancreas (responsible for secreting homrones, such as glucagon, insulin, somatostatin). Alcohol seems to modulate the late-phase of insulin secretion, increasing secretion, which leads to exaggerated glucose disposal and at least for diabetics causes hypoglycemia.

Huang Z, Sjöholm A. Ethanol acutely stimulates islet blood flow, amplifies insulin secretion, and induces hypoglycemia via nitric oxide and vagally mediated mechanisms. Endocrinology. 2008 Jan;149(1):232-6. Epub 2007 Oct 4.


What is the difference between hsa-miR-33a and hsa-miR-33b? Does anyone know what is the difference between two miRNAs like hsa-miR-33a and hsa-miR-33b? The last letter in them shows what?

Also, if we know that hsa-miR-33a targets gene A, can we say that hsa-miR-33b targets gene A, too? or can we say that it is much probable that hsa-miR-33b targets gene A since hsa-miR-33a targets A?

They are paralogs i.e. they have high level of sequence homology. They may have the same seed sequence too (see this). The paralogs can have same targets if they have same seed sequence but it is not essential in all cases. However, the extent of homology required for this kind of classification is poorly defined. miRBase still follows the guidelines mentioned in this (quite old) article:

  When such a candidate is so similar in sequence to the known miRNA
  that the probe designed to detect it would surely cross-hybridize with
  the known miRNA, criterion A need not be satisfied, and the candidate
  can be annotated as a variant form of the known miRNA, provided that
  the candidate itself meets criterion C, and there is also very high
  confidence that one of these paralogs is a confirmed miRNA (i.e., its
  classification is supported by at least three of the listed criteria).
  When there are two or more mismatches between the miRNA paralogs such
  that probes could differentiate between the species on Northern blots,
  criterion A must be satisfied experimentally. Sometimes partially
  overlapping cDNA sequences are identified from the same locus; these
  are assumed to represent differentially processed products from the
  gene.


What is this strange sea creature we found on the beach? We found this on a beach in North Devon, UK. I've never seen anything like it.
There's a yellowy-ball in the middle with 5 pointed shells attached to it, each of which seems to have a single "leg" coming out of the bottom. It almost looks like it's 5 separate creatures feeding on something, but they're pretty firmly attached. Perhaps it's some sort of egg-sac that they're growing from?
Does anyone know what this is?

You have a Dosima: Also known as a Buoy Barnacle. A gallery of observations of these can be found here:
https://inaturalist.ca/taxa/462188-Dosima/browse_photos
They are found in the coastal UK and Spain area, New Zealand, and east and west N.America:

(source: iNaturalist observations)
These barnacles attach themselves to things that float, and if they don't have access to one, they will grow one themselves. Your image looks like five individuals attached to a central float that one of them (or a dead relative) constructed.


Normal cell diffusion in normal organism? We know, that cancer cell can travel across an organism.

Is this ABSOLUTELY impossible for NORMAL cells?

For example, is it EXACTLY ZERO probability to find some bone cells inside liver or some skin cells inside brain?

In non-living things and with molecules this is called "diffusion". Any two contacting things will penetrate inside each other after hundreds and thousands years.

Is something similar happening in living thing?

May be very slow?

Was this phenomenon searched for?

Are there some protection mechanisms against appearing wrong tissue cells inside another tissues?

I understand that cells appear in their places during grow, but in mature state I think it is not impossible for cells to travel.

UPDATE

I know that there are many cells that travel by nature, like blood cells.

The question is namely about "static" cells, those ones we normally regard as non-travelling.

Also, I understand that there are some mechanisms, making cells to prefer their normal places when they divide and grow.

But the question is what about all these mechanisms failed? And how often it happens?

For example, I am 40 y.o. So, how many bone cells from my legs are currently in my brains? Zero? One? Million?

In a healthy body, cells travel.
But this is very dependent of the cell type. Some cell type will travel in all the body (lymphocytes, plasmocytes, etc) while other do not have any migration capability.

The concept of diffusion is wrong to apply here, indeed the scales at which you are looking are not molecular.

Moreover, there are very active mechanism to keep cell type in place, for example, a concept called preferential attachment will maintain the cells grouped by cell type. If you take two balls A and B and A attached more to A and B to B, and you shake, you will see appearance of clusters of A and clusters of B. But that is only one such mechanism and a lot of other take play here.

see this: http://www.ncbi.nlm.nih.gov/books/NBK26937/

Thus, the probability of finding a cell type NOT at its normal position (that is one that does not travel) is maybe not zero, but so close to it that you will not find a cell outside of their normal position.

I hope this answers your question ?

Reference
Cooper GM. The Cell: A Molecular Approach. 2nd ed. Sunderland (MA): Sinauer Associates; 2000


Why is insulin given in type 2 diabetes? For this reason "insulin insensitivity", or a decrease in insulin receptor signaling, leads to diabetes mellitus type 2 – the cells are unable to take up glucose, and the result is hyperglycemia (an increase in circulating glucose), and all the sequelae that result from diabetes $^{(1)}$

Also

  Type 2 diabetes is due to insufficient insulin production from beta cells in the setting of insulin resistance. $^{(2)}$

So why don't we give people a medicine which just increases the number of receptors or increases the sensitivity of receptors? Isn't it illogical to give more of insulin for a deficit amount of receptors? So, what is the logic behind giving insulin?

Isn't it illogical to give more of insulin for a deficit amount of receptors?

Seems like there is some confusion in the definition of type-2 DM itself. According to the American Diabetes Association:

  If you have type 2 diabetes your body does not use insulin properly. This is called insulin resistance. At first, your pancreas makes extra insulin to make up for it. But, over time it isn't able to keep up and can't make enough insulin to keep your blood glucose at normal levels.

So the problem in type-1 DM and type-2 DM is quite same; both because of less insulin present than required, the difference being that in type-2 DM the cells need more insulin than normal. And that apparent deficiency of insulin is overcome by insulin injections. Also, the definition you cite doesn't say receptor deficiency anywhere, it just says decrease in receptor's response to insulin.

So why don't we give people a medicine which just increases the number of receptors or increases the sensitivity of receptors?

This is not quite possible yet. Increasing the number of receptors means increasing the gene expression for that receptor, something that is called 'upregulation'. Now, just to add, the cause of type-2 DM has been regarded to be downregulation of insulin receptors on cell surface by high concentration of insulin. See this article:

  The process of downregulation occurs when there are elevated levels of the hormone insulin in the blood. When insulin binds to its receptors on the surface of a cell, the hormone receptor complex undergoes endocytosis and is subsequently attacked by intracellular lysosomal enzymes. The internalization of the insulin molecules provides a pathway for degradation of the hormone as well as for regulation of the number of sites that are available for binding on the cell surface. At high plasma concentrations, the number of surface receptors for insulin is gradually reduced by the accelerated rate of receptor internalization and degradation brought about by increased hormonal binding. The rate of synthesis of new receptors within the endoplasmic reticulum and their insertion in the plasma membrane do not keep pace with their rate of destruction. Over time, this self-induced loss of target cell receptors for insulin reduces the target cell's sensitivity to the elevated hormone concentration.

Now, coming back to the main point, it is not yet possible to inject transcription factors in every cell of body so that more and more receptors can be produced. It is possible in vitro, but not in vivo yet. However, it is possible to inject something else instead of insulin which might have similar effects on the body, something known as insulin agonist. Researchers are already trying to create insulin agonists, but haven't achieved much success. See this paper for example, in which they talk about a peptide S961. The problem here is that most of the molecules synthesized act as both agonist and antagonist based on different concentrations. That is why this field has not seen much success.

EDIT: As mentioned by @Don_S in comments, some drugs reportedly do increase insulin sensitivity and number of receptors in cells. Though they have indirect mechanisms for this, unlike insulin itself, but this works too (at least in vitro). One of them, thiazolidinediones, activates a nuclear receptor PPAR $\gamma$, which in turn increases transcription of proteins involved in glucose and lipid metabolism and energy balance. Another drug, pioglitazone, works even in vivo and has been suggested to work by activating receptor kinases and thus increase insulin sensitivity.

Thus, in future, it is very likely that type-2 DM patients would get prescriptions of such drugs instead of insulin injections, but not until there are more such drugs available and at an affordable cost.

References:

Type 2 — American Diabetes Association
Downregulation and upregulation — Wikipedia
Knudsen L, Hansen BF, Jensen P, Pedersen TÅ, Vestergaard K, Schäffer L, et al. (2012) Agonism and Antagonism at the Insulin Receptor. PLoS ONE 7(12): e51972. doi:10.1371/journal.pone.0051972
Hauner H. The mode of action of thiazolidinediones. Diabetes Metab. Res. Rev. 2002;18(Suppl. 2):S10–S15. doi: 10.1002/dmrr.249.
Kobayashi, M, Iwanishi, M, Egawa, K et al, Pioglitazone increases insulin sensitivity by activating kinase of insulin receptors. Diabetes. 1992;41:476–483.


Relationship between fatty acid chain and saponification number Why do long chain fatty acids have low saponification number? What is the relation of fatty acid chain( R)  with saponification number?

The saponification number, or saponification value, can be described as...

  the measure of the amount of alkali required to saponify a definite weight of fat. It is expressed in milligrams of potassium hydroxide required to saponify 1g of fat.

(source: Food Analysis: Theory and Practice. Y. Pomeranz and C. E. Meloan)

Notice that, in the definition, we're talking about grams and milligrams, not mols.

Now comes the important information: in the saponification, the base reacts with the ester group, and any triglyceride, regardless its chain length, has exactly three ester groups.

Let's see this is an oversimplified example:

Suppose we have two triglycerides, A and B. A has a chain twice as long as B. So, suppose that a given number of mols of A weights around two times the weight of the same number of mols of B.

However, they have the same number of esters, and they will require the same amount of potassium hydroxide. As A has a greater weight (which is in the denominator on our equation), it will have a lower saponification number compared to B.


Breeder's equation and equivalent expressions for narrow-sense heritability I am trying to model the phenotype of a trait as $X = G + E$, where $G$ and $E$ are the genetic and environmental effects. (I'll ignore the distinction between broad-sense and narrow-sense heritability in this question.) Wikipedia tells me that $$h^2 = \frac{\mathrm{Var}(G)}{\mathrm{Var}(X)}$$ The same page also gives the breeder's equation $R = h^2S$ but also says "Note that heritability in the [breeder's equation] is equal to the ratio [${\mathrm  {Var}}(G)/{\mathrm  {Var}}(X)$] only if the genotype and the environmental noise follow Gaussian distributions." So let $G \sim N(0, \sigma_G^2)$ and $E \sim N(0, \sigma_E^2)$ be distributed according to normal distributions. Then $X \sim N(0, \sigma_G^2 + \sigma_E^2)$ so $$h^2 = \frac{\mathrm{Var}(G)}{\mathrm{Var}(X)} = \frac{\sigma_G^2}{\sigma_G^2 + \sigma_E^2}$$

Now I want to perform a selection, choosing a parent with $X=a$. We can expect the child to have the trait $\mathbb E[G \mid X=a] + E'$ where $E' \sim N(0, \sigma_E^2)$ is some other environmental effect. (I don't want to bother with recombination and multiple parents, so we can just think of it as cloning the parent: given that $X=a$, we expect the parent's genetic part to have been $\mathbb E[G \mid X=a]$.)

To find $\mathbb E[G \mid X=a]$, note that $\mathbb E[X \mid X=a] = a$ and by linearity of expectation, $\mathbb E[X \mid X=a] = \mathbb E[G \mid X=a] + \mathbb E[E \mid X=a]$. To get the terms to cancel, we want to write $E$ as $\alpha E$ where $\alpha E$ has the same distribution as $G$. Since $\alpha E \sim N(0, \alpha^2 \sigma_E^2)$, we want $\alpha^2 \sigma_E^2 = \sigma_G^2$, so $\alpha = \sigma_G/\sigma_E$. Thus we have $$\begin{align}a &= \mathbb E[G \mid X=a] + \frac1\alpha\mathbb E[\alpha E \mid X=a] \\ &= \mathbb E[G \mid X=a] + \frac1\alpha\mathbb E[G \mid X=a] \\ &= \left(1+\frac1\alpha\right)\mathbb E[G \mid X=a]\end{align}$$ Hence $$\mathbb E[G \mid X=a] = \frac{a}{1+\frac1\alpha} = \frac{a}{1+\frac{\sigma_E}{\sigma_G}}$$

Since the parent was selected at $X=a$ and the child has mean $\frac{a}{1+\frac{\sigma_E}{\sigma_G}}$, we have $$h^2=\frac{R}{S} = \frac{1}{1+\frac{\sigma_E}{\sigma_G}} = \frac{\sigma_G}{\sigma_G+\sigma_E}$$

Now my problem is that the two expressions for $h^2$ don't match. They look pretty similar, but one of them has all the terms squared while the other one doesn't. What's going on/where did I go wrong?

ETA: To give a concrete example, suppose 80% of variance in the trait is explained by genes. Then the breeder's equation predicts the child to have $0.8a$. But computing $\mathbb E[G \mid X=a]$ gives $a/(1 + \sqrt{0.8^{-1} - 1}) = (2/3)a$. So the two approaches predict different things (although if it was 50% they would give the same prediction).

I found my mistake, which is where I said "To get the terms to cancel, we want to write $E$ as $\alpha E$ where $\alpha E$ has the same distribution as $G$." What we actually want is to find a constant $\alpha$ such that $\mathbb E[\alpha E\mid X=a] = \mathbb E[G\mid X=a]$. In my question, I assumed that this was the same thing as finding $\alpha$ such that $\mathbb E[\alpha E] = \mathbb E[G]$; hence I was trying to find $\alpha$ to make the distributions of $\alpha E$ and $G$ the same (the means are both 0, so I just needed to get the variances to equal each other). But actually, conditioning on $X=a$ shifts the distributions so the $\alpha$ I found in my question doesn't work.

Since my previous strategy doesn't work, I ended up skipping the step of finding $\alpha$ entirely. I realized that the random vector $(G, X)=(G,G+E)$ is a bivariate normal, because we can write $$\begin{pmatrix}G \\ G+E\end{pmatrix} = \begin{pmatrix}\sigma_G & 0\\ \sigma_G & \sigma_E\end{pmatrix}\begin{pmatrix}Z_1 \\ Z_2\end{pmatrix}$$ where $Z_1,Z_2$ are standard normal random variables.

Now Wikipedia gives the conditional distribution for bivariate normals, which in our case is $G\mid X=a$. We only need the mean, which is $\mu_G + \frac{\sigma_G}{\sigma_X}\rho (a - \mu_X)$. Both $\mu_G$ and $\mu_X$ are zero, and $\rho$ is the correlation which is $$\rho = \rho_{G,X} = \frac{\mathrm{cov}(G,X)}{\sigma_G \sigma_X} = \frac{\mathrm{cov}(G,G) + \mathrm{cov}(G,E)}{\sigma_G \sigma_X} = \frac{\sigma_G^2}{\sigma_G \sigma_X} = \frac{\sigma_G}{\sigma_X}$$ Thus we end up with $$\mu_G + \frac{\sigma_G}{\sigma_X}\rho (a - \mu_X) = \frac{\sigma_G^2}{\sigma_X^2}a$$ which is exactly what we want.


Examples of animals that co-opt toxins? It is known that there are animals that acquire toxins through their diet or through their surroundings. The examples I know of include butterflies stocking up on alkaloids/glycosides while in the caterpillar stage (monarchs snacking on milkweed come to mind), fish acquiring ciguatoxin or tetrodotoxin from marine bacteria, and arrow poison frogs and pitohuis acquiring batrachotoxin and other nasties from the insects they eat. Are there any other nice examples of animals like these?

Glaucus atlanticus consumes and reuses the nematocysts of jellyfish siphonophores. Perhaps not quite what you were looking for, as the animal doesn't simply concentrate the toxin, but actually co-opts entire stinging cells.

Further to your mention of dinoflagellate toxins being concentrated by fish, I seem to recall reading something about some toxins being modified in vivo into more toxic derivatives, but cannot find any mention of it.


Is it possible to lose weight doing brain exercise? According to this article human brain consume a comparable amount of energy with skeletal muscle. So is it possible to do some brain exercise (calculate something in mind etc.) instead of physical exercise to lose weight?
More specific questions:

Is it theoretically possible?
Is there any real-life example?
What kind of brain activity require more energy?
Pros and cons (brain exercise vs. physical exercise)

No The amount of calories the brain consumes is basically the same whether it is doing anything or no. Best case only about 3% increase in calories consumed by the brain or about 50 calories per day, which is miniscule and most studies do not even show that much.
Additionally buring calories is only important for weight loss once consumption is controlled. It is too easy to out eat any amount of exercise.
https://www.scientificamerican.com/article/thinking-hard-calories/


Number of autoregulation and FFL motifs in a network Suppose we have a network with N* nodes (N* is the number of internal nodes). Every directed link in this network exists with probability p. What would be the number of:

motifs that are auto-regulatory?
feed-forward loop motifs
feed-back loop motifs

The average number of auto-regulatory motifs (self-edges), is equal to the number of edges E times the probability that an edge is a self-edge which is $p_{self}=1/N$, with N being the total number of nodes. Therefore, $<N_{self}>_{rand} \approx E/N$
& 3. According to U.Alon's book ("Introduction to Systems Biology"), the mean number of times that a subgraph G occurs in a random network is given by the following formula: $<N_G>\approx a^{-1}N^n p^g$.

Explaining what each term of the formula means:

α: is a number that includes combinatorial factors related to the structure and symmetry of each subgraph, equal to 1 for feed-forward loop (FFL) and equal to 3 for feed-back loop (FBL)
$N^n$: is the number of ways of choosing a set of n nodes out of N. Because there are N ways of choosing the first one, times N-1$\approx$N ways of choosing the second one, and so on..(this approximation is true for large networks)
$p^g$ : is the probability to get the g edges in the appropriate places (each with probability p)


What are the units of enzyme activity? I was looking at this graph of turnip peroxidase activity and I saw that they use units of 1/sec for enzyme activity. What does this unit intuitively represent and how is it calculated?

This refers to the turnover number (a.k.a kcat or k2) of an enzyme and is usually calculated using Michaelis-Menten kinetics. Jump to the summary at the end if you want a simple answer. If you want a more thorough answer, consider the following chemical equation:

  [E] + [S] ⇌ [ES] → [E] + [P]

This says that a certain concentration of enzyme mixed with a certain concentration of substrate will first combine and form a complex depending on the enzyme's affinity for the substrate. Then the enzyme complex will generate a product depending on the enzyme's ability to convert the transition state into product. The k1 constant is the arrow moving from [E] + [S] → [ES] and the k-1 is the arrow moving from [ES] → [E] + [S] (they oppose each other). The k2 constant is the arrow moving from [ES] → [E] + [P].

  Vo = [ES]k2

Vo - this is the rate that product is being formed, which can be measured.
[ES] - this is the concentration of enzyme-substrate complexes.
k2 - this is a constant value comparing the two.

This can also be expressed in terms of maximum rate:

  Vmax = [E]Tk2

Vmax - Vmax is catalytic rate when [E]T = [ES] (when all of the enzyme present is bound to substrate/saturated).
[E]T - [E]T is the total enzyme concentration. [E]T = [E] + [ES].
k2 - the kcat is the catalytic constant. It is a constant indicating how quickly an enzyme can convert substrates into products. It is easily observed by this equation.

Summary

So k2 is basically an indicator of how efficiently or quickly an enzyme operates. Not all enzymes follow standard Michaelis-Menten kinetics. For example, the allosteric properties of some enzymes cause a non-linear saturation curve. Because of this, the turnover number is commonly referred to. The turnover number's units of s-1 indicate one product molecule per second, so a turnover rate of 3000 means you can create 3000 products in 1 second at Vmax.


Fusion of neuron with a S phase cell There was some experiment in which a S phase cell was fused with other cell and the other cell also began to replicate DNA. Would the same happen if fused with nerve cell ? Why or why not?

This specific experiment has not been done. Fusing cells is difficult and it also leads to polyploidy. Cells are immortalized by overexpressing oncogenes (or viral replication genes); for example HEK293 cell line was established by transforming embryonic kidney cells with adenovirus.

Now transforming a neuron would immortalize it but would also make it lose its function; for a cell like neuron, replication would compromise its activity for e.g. loss of established synapses. As mentioned in the comments by har-wradim, it was shown that transforming neurons with oncogenes leads to their de-differentiation. Another experiment of transforming neurons gave a contrasting result. Feddersen et al transformed purkinje cells in mice by expressing SV40 viral t-antigen from a purkinje-cell specific promoter and surprisingly it lead to degeneration of cerebellar tissue. Also have a look at this article.


Are there histones present in the cytoplasm? In this paper the authors depleted core histone heterodimers H3-H4 at 90 % from the cytoplasm of Xenopus oocytes. They state that their concentration is in the order of 6 uM.

My question is, are histones found in cytoplasm besides the nucleus location? (ignoring the newly sythesized ones), and if so, is there any known function?

In early embryogenesis, cell division called cleavage occurs every 30 min and there is no transcriptional activity. Oocytes have accumulated important gene transcripts and synthesize the proteins at right times. However, histone is one of the most abundant proteins and it would be difficult to supply enough histone proteins during early embryogenesis while oocytes translate other gene transcripts regulating differentiation.

This is my speculation, but the article calls cytosolic histones "stockpile". Just in case, I don't mean that I deny some other roles of histones in cytosol if there are any.


Why does B12 deficiency enlarge red blood cells? I'd like to know why B12 deficiency enlarge red blood cells

@SPr has given you a good reference in his answer. I thought I'd add some context to it.

The basic problem here is that red blood cells need B12 in order to synthesize DNA. Red blood cells live for about 4 months, and have to constantly be replaced, so when you have a problem with B12, this is one of the cell populations that will be affected. The problem here is actually the anemia. It's not that the cells are too big, but that there aren't enough of them (see the linked reference, as well as Robbins and Cotran Pathologic Basis of Disease, Ch 13, subsection "Anemias of Diminished Erythropoiesis"). The size itself helps identify why there aren't enough of them, distinguishing this anemia from other anemias that cause cells that are smaller than normal.

The mechanism in lay terms (which hasn't entirely been worked out, again, see both the article and Robbins), is that a problem with DNA synthesis causes the cells get larger before they divide. So you have fewer, larger cells. Because it's a universal problem with DNA synthesis, red blood cells aren't the only cells affected.