Examining antibody - target interactions in PyMOL I'm a student currently looking at antibody responses against a viral target protein of interest.

I have my own, annotated PyMOL session of my protein and I also have .pdbs of crystallised antibody structures that bind to this protein and rougly know whereabouts it binds. I would like to know if it is possible to combine these two structures into a single session to observe or at least overlay the two structures together. Many thanks!

Multiple structures may be read into a given session using the following for each pdb:
File -> Open

In the narrative below, the reference antibody has the name AAA and the second antibody has the name BBB. The heavy and light chains have pdb chain IDs A and B, respectively. Adjust those as needed.
Whole molecule overlay
Make visible the reference and the moving molecules.
From the menu item next to the BBB molecule name (right panel), select:
A -> align -> to molecule (*/CA) -> Object: AAA

Antibody's variable domain overlay
I think it may be more helpful to align the variable domains than the whole antibodies or Fabs. Typing the following on the command line is a temporarily adequate way to align proteins:
align BBB and chain A+B and res 1:109, AAA and chain A+BL and res 1:109


translation of scientific names I am trying to determine the "translated" meanings (not seeking the common names) of different insects, (presently some bees and wasps).  Does anyone know of a printed or internet resource that defines the various names. I have one for plants, but not for animals.  Knowing the (English) meaning of the Latin / Greek/ etc. is often very informative -- IF I can find it.

I can give more specifics if you want.

Thanks.

Glen B
Olympia WA, USA

Glen, sometimes there are many species that have same colloquial name. For e.g. frog includes hundreds of species. If you require high level of detail, you may need to look for more comprehensive lists.

There are zoology dictionaries such as this. I think it should serve your purpose.


Relationship between action potentials and EEG recordings It is possible that I am overthinking this but I have difficulties relating the neural activation to the amplitude and frequency of EEG recordings.
For example; if at the EEG location P3/P4 we observe alpha waves at 10Herts, what will that tell us about the action potentials and membrane polarisation within the population of neurons generating the wave at this frequency?
Also, high amplitude within alpha frequency may indicate attention deficits, but how is the high amplitude related to or explained in terms of electrochemical activity within a neuron?
Informed replies are very much appreciated!
Many thanks

Most of the EEG waves are not directly generated by action potential, because it is too short and has a high frequency. They are generated by synaptic activity (overall propagation potential of axons).

The amplitude of this propagation potential depends on the impedance of the brain. Higher impedance means higher amplitude. Impedance is higher for low frequency signals.

The amplitude is also affected by the direction of the EEG vector so parallel axons which go in the same direction should produce a higher wave in amplitude.

Reference: Rudell AP, Fox SE. The propagation potential. An axonal response with implications for scalp-recorded EEG. Biophys. J. 1991 Sep;60(3):556-67. doi: 10.1016/S0006-3495(91)82085-9. PubMed PMID: 1932547.


Identification of that red and black bug Found in France countryside, few hours ago, on a bushlike plant in direct sun light.

There is dozens of individuals, by groups of 5-ish, everywhere on the plant, along aphids, maybe sucking the plant's sap.

Looks like a stink bug, with unexpected colors. Some of them were attached two-by-two by their bottom (mating, probably ?).

Sorry for the bad photo quality.

This looks like Graphosoma italicum (aka G. lineatum; it is a stinkbug):

Graphosoma italicum had been regarded as either a subspecies, or a mere synonym to G. lineatum.
G. italicum can reach a length of 8–12 mm (0.31–0.47 in). The body is almost round, with a large shield. The basic color of the upperside of the body is bright red, with wide black longitudinal stripes. The pronotum has six black bands. The antennae are black. Also the sides of the abdominal segments (connexivum) are red with many small black spots. The legs are black.
Wikipedia

I think you are right that they are mating. Here is another picture of the species mating:

ibid

(Despite it saying that the legs are black, they are clearly striped in some specimens, like in your picture.)
It's found in France, according to Honeyguide.


Immunomic Microarray "One can measure two or more signals simultaneously determined by a single feature, i.e.,
  epitope in immunomic microarray DNA microarrays measure one response value for each gene per sample; that is, mRNA concentration produced by the gene but a single epitope
  can generate different response values corresponding to different epitopes in peptide–MHC chips. In case of B cell epitope, it can be recognized by different isotypes of immunoglobulins, so here, one can measure both intensity and quality of antibody response."

These few lines are from the book:
http://www.springer.com/biomed/immunology/book/978-1-4939-1114-1
Chapter 3

What does measure of one response value for each gene per sample mean?
Different response value means??
how is intensity and quality both are being measured??

epitope in immunomic microarray DNA microarrays measure one response
  value for each gene per sample; that is, mRNA concentration produced
  by the gene but a single epitope can generate different response
  values corresponding to different epitopes in peptide–MHC chips.

The excerpt looks grammatically incorrect and is therefore confusing. I guess what it tries to convey is — like there can be several probes for a single mRNA in a normal gene-expression microarray, there can be several antibodies binding to different epitopes in the same protein. Different antibodies will bind to their cognate epitopes with different affinities. This is what is referred to as "response value"

By quality I guess what the authors mean is that for the same epitope it is possible to quantify the binding interactions between that epitope and antibodies of different classes (but same antigen binding site).

Having looked at this excerpt, I would not recommend this book to anyone.

You can also have a look at these two articles:

From Functional Genomics to Functional Immunomics: New Challenges, Old Problems, Big Rewards
Prospects for the Future Using Genomics and Proteomics in Clinical Microbiology


How heavy are all foreign microorganisms in and on the human body? I define "foreign microorganism" as a microorganism which is not produced
by the human body (not antibodies or leukocytes) including bacteria, viruses, fungi, biofilm aggregates or small lifeforms independent if they are benign or hostile.

Let's say I have currently a weight of exactly 100 kg. How much of it consists of organisms not belonging to me?

Edit: Matters Arising

In this Nature News article, Scientists bust myth that our bodies have more bacteria than human cells, and in the bioRxiv pre-print article, Revised estimates for the number of human and bacteria cells in the body, a new estimate of the ratio of microbial cells on the human body to human cells that make up the body has been revised down to close to 1-to-1, with there being slightly more microbial cells to human cells.

It should be noted that near 90% of the human cells taken into account were red blood cells and platelets.

- Revised estimates for the number of human and bacteria cells in the body, Sender et.al. bioRxiv preprint.  doi: http://dx.doi.org/10.1101/036103

Note: Preprint articles have not been refereed. The information in them is subject to change, may not pass review, and in the end my not be accepted for publication.

  Readers should therefore be aware that articles on bioRxiv have not been finalized by authors, might contain errors, and report information that has not yet been accepted or endorsed in any way by the scientific or medical community.
  - bioRxiv.org: What is an unrefereed preprint?

Original Post

  The human body contains trillions of microorganisms — outnumbering human cells by 10 to 1. Because of their small size, however, microorganisms make up only about 1 to 3 percent of the body's mass (in a 200-pound adult, that’s 2 to 6 pounds of bacteria), but play a vital role in human health.

From: NIH Human Microbiome Project defines normal bacterial makeup of the body

Additional Information on Microbiome and Obesity

From Cell

Altering the Intestinal Microbiota during a Critical Developmental Window Has Lasting Metabolic Consequences

From The American Journal of Gastroenterology Supplements (a Nature Press Journal)

Disclaimer

  This article was published as part of a supplement sponsored by the Gi Health Foundation, a nonprofit 501(c)(3) educational organization dedicated to increasing awareness of the effect of gastrointestinal disorders in the United States. The foundation's goal is to provide health professionals with the most current education and information on gastrointestinal health.

Impact of the Gut Microbiota on the Development of Obesity: Current Concepts


Measuring body size in flies/insects "Mesothorax length (the distance from the tip of the scutellum to the
  most anterior part of the mesothorax)"

From Bergland et al 2008.

Would that be this distance (green line)?

If not, how would you describe that distance?

I think you are correct, but I'm not an expert in Diptera/Drosophila morphology. Since the prothorax (pronotum) and metathorax are greatly reduced in flies, you mostly see the mesonotum in dorsal view, and this includes the scutellum. Personally, I think it would have been more accurate of them to label this structure mesonotum, or at least dorsal mesothorax length, since mesothorax could just as well imply a ventral view (mesosternum).

More information can be found at this webpage: Flies - Morphology and anatomy: Thorax, which state that:

  The mesonotum occupies most of dorsal view of the thorax. In order anteroposterior we can identify four parts, called as follow (McAlpine, 1981): prescutum, scutum, scutellum, and postnotum. The scutum is the most large, condition considered apomorphic for the entire order of Diptera.

Also see this picture of the mesonotum from diptera.net


Why APC's present antigen to T cells? the macrophages are pretty known well for antigen presenting process and to present the antigens which are bound to pathogens unlike exotoxins (which are free) the pathogen first should be digested and destructed and derive the antigenic portion and present it to T cells then stimulate the B cells to make antibodies. If the macrophages can destruct and digest the pathogen to derive the exact antigenic portion so then whats the need of humoral immunity to be activated because they have already destruct and kill the pathogen if your answer is that the pathogen gets knocked out quickly by antibodies for the second if they invade,so there are millions of other infecting agents every day         invading our body and are omitted by the first line defenses?

Let's consider some situations real quick:

(1) A bacterial microbe enters through a fissure in the skin. What does an innate, systemic immune response look like? In short: it's lengthy, uncoordinated and has a lot of potential to damage tissue in the area of infection.

(2) A bacterial microbe enters the blood. The bacterium produces an AB toxin that enters cells and kill them.

(3) The host is infected by a helminth.

In situation 1: Innate immune responses are associated with the secretion of many cytokines and chemokines. Cytokines are associated with the inflammatory response, and chemokines are associated with lymphocyte trafficking. Inflammation and recruitment of lymphocytes, macrophages and the like are good for clearing the infection, but there's a lot of potential to damage the surrounding tissue. Effector cells from the adaptive response incl. humoral immunity don't elicit the same level of damage, and we can illustrate this in mucosal immunity. Since commensal (and some pathogenic) organisms are constantly stimulating mucosal immunity, there are (1) epithelial effector T cells, (2) plasma cells and (3) dendritic cells that make the response to these pathogens fast, efficient and little damage occurs to the tissue involved.

In situation 2: So let's say the pathogen has escaped the immune response, maybe it's encapsulated. There are AB toxins being produced that kill cells endocytosing them. What good will it do for a phagocyte to eat something that ends up killing it? Antibodies are particularly efficient for this extent because they can neutralize toxins they've encountered with the same fast, efficient response as we described above. This is achieved through antigen presentation. The host will then need to find other ways to clear the infection, however.

So: In situation 1 we illustrated that an innate, systemic response isn't always desirable due to tissue damage, and through the presentation to T cells by APCs, a later adaptive immune response mitigates this effect through formation of effector cells. In situation 2, we then illustrated that the first-line defenses can't always respond to the imminent threat for various reasons, which are overcome by the presence of effector cells.

Situation 3: This is the more complex concept. You have different subsets of CD4+ T cells that can be formed in response to the type of interleukin or cytokine that is present when the CD4+ T cells are being activated. This differentiation is driven largely by secretions of activated APCs! The APC performs this critical step based on what kind of receptors the specific types of pathogen are detected by. The differentiated CD4+ T cells, or T-helper cells of class: Th1, Th2, Th17, Treg, etc. each perform different roles which are effective in different situations. For example, you wouldn't see any benefit in throwing Th1 cells at a helminth infection, Th2 is the best effector for this. Treg cells are capable of abrogating autoreactivity, and Th17 cells are needed to assist B cell differentiation in response to antigen detection (which in the case of helminths, the B cell must class switch to IgE and this is stimulated by Th2 cells via IL-4).

Now, in situation 3, we've illustrated that CD4+ T cell intermediates are providing your overall immune response: flexibility, specificity, and checks/balances which are all-at-once critical to healthy functioning. I disregarded MHC-I responses and CD8+ CTL's because this is about APC-driven responses.


Doesn't meiosis form two pairs of similar cells and two pairs of opposite cells? I am learning about meiosis in biology. I've learnt that the crossing-over in metaphase I only exchanges small portions of DNA at the tips of the chromosomes. Doesn't this mean that:

After meiosis I, there will be two cells that will be almost opposites (for each chromosome, if one cell has the mother's chromosome, then the other will have the father's chromosome), except for the parts where crossing-over happened
After meiosis II, each cell produced in meiosis I will produce two similar cells (the only differences will be where crossing over happened in one but not both of the chromatids)

This means that there would be a rare chance of two of the sperm cells produced by a single meiosis fertilizing two eggs, in which case we could have:

Almost-identical twins
Very different twins, which would have less than the normal 50% of DNA in common

Am I right about this?

Great question - I think there are two misconceptions in your question that are interfering with your understanding.

First, crossing-over occurring at just the "tips" is just for clarity in textbooks so you can easily follow the different pieces of chromosome.

Although crossover events tend to occur at particular sequences, these don't have to be at the tips. There can also be multiple crossovers on the same chromosome, or none at all. See this link for some estimates of recombination rates for different species.

Second, gamete diversity doesn't depend only on crossing-over during meiosis, it also depends on the incorporation of just a single chromosome from each pair. Humans, for example, have 23 pairs of chromosomes. There are therefore 2^23 = 8388608 different combinations of chromosomes - with NO crossing over! Therefore, even without recombination, the odds of two genetically identical sperm fertilizing two genetically identical eggs are incredibly small.


Are quaternary protein monomers unique to a particular protein complex? I know that quaternary protein structures are formed exclusively via non-covalent bonds. My biochemistry professor discussed a viral capsid that is essentially one quaternary structure with 240 individual monomers of 4 kinds. I suspect that for this protein coat to be stable, the non-covalent bonds holding it together must be rather stable. He also mentioned that different monomers can join to form the functional protein complex from relatively far distances, like across an entire cell, which once again leads me to believe that both monomers must be interacting with each other very strongly.

My question is: Since a strong non-covalent interaction is required between (at least) two protein monomers to form the functional quaternary structure, can one particular protein be a monomer to an array of different quaternary complexes? Are there any examples of this?

If I understand the question correctly, you're thinking something along the lines of modular tertiary domains, but in a quaternary sense?

For a reversible interaction, heterotrimeric G proteins spring to mind. Once activated by a G protein coupled receptor (GPCR), the alpha subunit and the beta-gamma complex dissociate from the receptor and from each other. They can both go on to affect signaling by binding to various effector proteins, depending on the particular pathway in which they are involved, and their activities can be mediated by other proteins (e.g. the alpha subunit GTPase regulated by GAP proteins).

I spoke to my Protein Engineering professor, and she also directed me to a few examples, although I'm not sure they're quite what you're looking for in the strictest sense.

Cyclin-dependent kinases, as @Armatus mentioned, bind to all sorts of different cyclins. (I get the sense that subunits found in multiple protein complexes will probably be more common in signal cascades. I don't have any real data on that, but it makes sense that a signal protein could interact with two or more protein complexes and even have slightly different functions in each.)
Alcohol dehydrogenase (ADH) is an example of a protein with different quaternary structures between species. According to my professor, it occurs as a homodimer in mammals, but as a tetramer with some slightly different residues in budding yeast. I can't say whether the sequence changes are what affect the oligomerization, although my prof also mentioned "oligomerization domains" that could mediate protein-protein interactions.
She also directed me toward a slightly more interesting example (in my opinion), though, again, it's also more along the lines of oligomerization. Small heat shock proteins (sHSPs) undergo something called "dynamic subunit exchange" and can take on a wide variety of oligomeric architectures. Binding is transient, but it's still kind of neat. There's a review here: http://www.sciencedirect.com/science/article/pii/S0968000411001903. Figure 3 shows different oligomeric architectures from the one monomer.

It seems that pretty much any protein that interacts with two or more separate protein complexes could be considered an answer. Neither I nor my professor have managed to come up with an example of an irreversible assembly of common subunits, but she is of the opinion that, in all the different possible protein structures, there is probably at least one example of everything, no matter how outlandish it seems.


What regulates these two methods of splicing? Alternative splicing can shuffle the exon order and select from the exon sequence of a single gene site to provide a combinatorial selection of possible transcription products from the one gene. Can intergenic trans splicing can do this starting from multiple gene sites?

What regulates these two "non linear" gene combination, transcript-splicing processes?

As Alan Boyd said, this process is called trans splicing where exons of different RNAs are joined together. Physical proximity is conducive for trans-splicing. This study shows that trans-splicing frequency is higher if the genes are proximal. Proximity not only means closer in the genome but also the 3D proximity governed by chromosomal interactions.

Now, what factors  promote trans splicing is not properly understood.


Could humans theoretically see infrared better than regular light? I have noticed that in infrared film, people's eyes reflect that light within their eyes much like nocturnal animals (and many other animals for that matter) do with regular light. I know that this is in order to maximize their night vision capabilities by reflecting more light onto the retina.

My question is this: If a human had the nerves in our eyes to process infrared light, would someone with these 'special' eyes be able to see better than someone with 'regular' eyes? What would they see? What about in low-light conditions?

...Infra-red illumination of the eye produces the 'bright pupil' effect

Source: http://www.museumsandtheweb.com/mw2003/papers/milekic/milekic.html

(most of the way down the page)

No, retina doesn't have or has too few infrared receptors.

Practical example: most remote controls use IR LEDs (infra red light emitting diodes) to send commands to a receiver device. So take a remote control, keep pressing a button and look at its front. Do you see any flashing light? Now take a camera (phone camera, photo camera or video camcorder) and look with it at the remote while pressing a button. Now you see it producing white light. The camera sensor detects IR. That is how night vision in cameras work.

What you read in that article is about how light is reflected by the eye (the pupil). There is nothing to do with the retina which is on the 'back wall' of the eye ball.


What do butterflies eat? I found a beautiful scarce-swallowtail butterfly in my storeroom, but it was kind of frozen and couldn't fly away. So, I put it on my terrace in the sun. After a little bit, it flew a few meters away and fell. I was wondering what could these beings eat, so that I can help it...
Any answers would be great appreciated!
Thanks in advance

Adult butterflies don't eat! I mean.... not in the sense of chewing on food. They rather drink. They get their nutrients via ingestion of liquid substances. Their mouth consists of a long tube called a proboscis that acts as a straw.

What do butterflies feed on?

The vast majority of butterflies eat nectar from flowers. Many species are quite specialized and feed on the nectar of a few species only.

There are a few exceptions though. Some species feed on tree sap, dung, mud (see mud-puddling), pollen, or rotting fruit. Butterflies are attracted to sodium and may as well try to feed on human sweat but I doubt there exist any species would get a non-negligible source of nutrients from human sweat. Coming to exceptions, you should definitely consider reading @DmitryGrigoryev's answer as well.

What do caterpillars feed on?

Of course, you are probably aware that butterflies have a complex (-ish) life cycle. The larva is called a caterpillar, while the adult is called a butterfly. So what do caterpillars eat?

Caterpillars have mandibles, so they can chew tissues and not just drink. Most caterpillars eat leaves and other plants parts. Again, many species are specialized to only a few plant species.

There are of course exceptions. For example in the Phengaris genus, (such as the famous large blue (Phengaris arion), caterpillars live in ant colonies and mimic the larvae of these ants. Some of them are able to trick the ants into feeding them as though they were ant larvae (e.g. Phengaris alcon, Phengaris rebeli). Others (e.g. the aforementioned Phengaris arion) will act as predators and eat the real ant larvae!

When the butterflies emerge from their cocoons after metamorphosis, the ants finally figure out the trickery and start attacking the butterfly. The butterfly has therefore very little time to try to fly away from the colony before getting killed. It is a critical life stage for individuals of this species.

How to feed a butterfly?

This section exists thanks to @Rodrigo's recommendation.

As a substitute of nectar one can simply use sugar water. The optimal sugar concentration (in mass-mass) is around 35% (Kim et al. 2011) although it likely varies among species.

Kim et al. 2011 explains that what limits optimal sugar concentration for insects is the viscosity of the solution. Too much sugar renders the solution too viscous and difficult to forage on. Interestingly, the ability to drink viscous solutions depends upon the drinking technic (active suction, capillary suction or viscous dipping) which vary, not among butterflies but among insects. The article is interesting.


What is the relatedness of sisters in a haplodiploid system if you mate virgin queens with 1 of their sons So I'm having trouble wrapping my head around this. In haplodiploid insects, sisters are related by 75% on average due to all sharing 100% of dad's genetics and 1/2 of mom's. (males are produced from haploid eggs)
The question I have is, if you take a son of a queen and mate her with her own son, what is the genetic relatedness of her resulting daughters to one another?
Here is an illustration of the haplodiploid system in insects.

Thanks in advance!
source: https://en.wikipedia.org/wiki/Haplodiploidy

This question may not be duplicate but I would reconmmend reading the answers of this question first How to calculate relatedness in haplodiploid organisms (mainly full sisters and full brothers)?

I think an image is worth a lot of words so here it is:

To calcul relatedness, I used the formula
$ \text{relatedness} = \ce{prop_{mother}} \times \ce{shared_{mother}} + \ce{prop_{father}} \times \ce{shared_{father}}$

The little trick here is that we know the father (son of queen) is unique, so we can focus on either of the two possible son of the queen. This gives us a 0.875 relatedness between sisters with a father being the son of the mother.
I hope it is clearer now.


What kind of snake is this Found this outside on patio in northern Virginia, Ashburn area, September 2018. It's about 12 inches. Is it a water snake or rattlesnake?

It looks like an Eastern Hognose Snake, which is characterized by an upturned nose and high likelihood of playing dead.

These are described as variable in coloration:

  "Two color phases are common in Virginia: (1) a patterned phase (79.6%, n = 98), characterized by a series of 19-27 (average = 23.2 ± 2.4, n = 12) black or dark-brown blotches along middorsal line, with alternating black spots on sides; body color consists of varying combinations of gray, tan, pink, yellow, orange, and red; venter of body and tail immaculate cream to dark gray;"

If you replace the tan in this image (www.virginiaherpetologicalsociety.com) with gray in yours, I think the pattern match and overall body form are very similar:


how many copies of tp53 (p53) gene do we have? I just started studying biology so I almost have no knowledge.

I learned about the tp53 gene and I just wanted to know how many copies of tp53 gene we have?

Humans have one copy of the p53 gene per set of chromosomes along with most other mammals (a notable exception being elephants with 20)[1]. Since it is located on an autosome (chromosome 17), each parent gives one copy of the gene[2]. Meaning two copies per human cell (and 40 per elephant cell).

A little extra information on p53 and the effects of only having 2 copies:

Since humans only have two copies per cell and p53 forms a homo-tetramer, it only takes one mutated copy to lose functionality.[3] This is because p53 needs to tetramerize to function, meaning only 1 out of 16 p53 proteins are effective if one copy is mutated (24 possibilities and only 1 combination has 0 mutated copies, ~6% are functional). This makes p53 a rare human tumor-suppressor gene with dominant negative mutations.

But with elephants, the more copies they have, the less and less one mutation affects the amount of functional p53. ($\bigl( \frac {39}{40}\bigr)$4 probability of having a functional tetramer = 90% functional, which is very high)


Why is my DNA below the ladder? I have run a gradient PCR.. and band 6 after the ladder is clearly the brightest. But all bands appear below the ladder. What does that mean? It is extracted mDNA that was loaded.

Thank you in advance!

Below the ladder means primer dimer.  You have no product.


Why does opening of the Ca-channels trigger the release of neurotransmitters? I understand that the opening of the Calcium channels trigger the release of stored neurotransmitter in granules, but what is it about the flow of positive ions that makes the vesicles fuse with the cell membrane? Does the vesicle itself carry a charge or concentration gradient?

Synaptotagmin is a protein that is part of the synaptic release machinery. It binds calcium specifically, which leads to a conformational change that encourages vesicle fusion with the membrane, therefore the ultimate release mechanism is not via voltage or charge but by calcium itself.


Winogradsky column and hydrogen sulfide For a science experiment for school, I have set up 15 Winogradsky columns, and will be looking at the microbial growth inside the columns over a period of 25 days.
I have read that, due to gas produced by the microbes, it is good to leave the cap loosely closed to prevent an explosion from gas buildup. However, I have also read that sulfate-reducing bacteria that grow in the column can produce toxic hydrogen sulfide gas. Wouldn’t the hydrogen sulfide also escape in small amounts and pose a health risk? What would be the correct protocol to follow here?

Hydrogen sulfide can be toxic at high concentrations, however, the amount that your columns will make is likely very low, and will almost certainly degrade/oxidize into something safer before it hurts anyone (who isn't a small organism in the column!). It will noticeably smell bad at levels well below what is dangerous. So maybe just make sure that the columns are in a ventilated space.
Remember, what is happening in the column is basically just rotting organic matter, like leaving a bunch of food waste in a highly compacted, sealed environment. It is sort of intrinsically gross, but it isn't any more dangerous to your health than forgetting to take out the garbage for a month (actually, it's probably a lot less dangerous than that!).
For example, this guide says the following (after constructing columns with different inputs such as e.g. eggs):

You may have seen worms, snails, shrimp or other small organisms in the water, but probably not many (if any) in the bottle with the egg yolk, because hydrogen sulfide is toxic to most organisms!

So, depending on what you put in there, a very H2S-productive medium is likely to create enough H2S to kill tiny animals that are trapped inside the column. But apparently not enough to hurt large animals like you, as long as you don't huff the column.


At what point, when connected, do DNA strands become a helix? When synthesizing DNA strands and beginning to "connect" them, how quickly does it become a helix?

In this answer, canadianer says

  The helical structure is more stable than the "straight" form (because of base stacking interactions), and so it forms spontaneously.

This then makes me think of the following scenario: say one is constructing two strands of DNA out of deoxyribonucleotides. Then, one begins connecting them with hydrogen bonds. Before the hydrogen bonds are added, my understanding is the two strands would be straight and not helical (if this is wrong, please correct me on this) so at some point as the two strands are connected, it would "spontaneously" become helical.

The question, then, is at which point. After one "connection"? Two? All of the connections necessary to complete the piece of DNA?

In general, a single stranded nucleic acid is helical in the absence of other secondary structure. The base stacking that drives helix formation does occur  between adjacent bases in the same strand. Note, however, that such structures are dynamic and dependent on properties such as temperature and salt concentration. You can see an example of a single-stranded RNA helix in the following crystal structure (1MHK):

Note the blue helix at the bottom of the image is actually a duplex in the crystal.


Is there a taxon that "adaptively" radiates faster? It seems that there are some taxa that have a greater potential to radiate through adaptations. Off my head, I can think of birds:

Darwin's finches
Hawaiian honeycreepers
House finches (Carpodacus mexicanus)
Manakin (or other passerine birds)

Also, there are some fish:

Cichlid fish (Lake Victoria in east Africa)
Threespine Stickelback

Plants:

Hawaiian silverswords
Erythranthe lewisii (Lewis' monkeyflower, great purple monkeyflower)

Lizard(s):

Anolis lizards

Insects:

Heliconius butterflies
Drosophila (Hawaiian Drosophila particularly)
Spider (Maybe peacock spider)
Leaf beetle

Generally:

Angiosperm plants
Dinosaurs
Marsupial mammals
etc.

So, is there a group of organisms (taxa could be any level: family, gender, species...) that is consistently radiating more than other?

By radiation I take the points that Grant defines here:

  These examples have the following in common: (1) they comprise
  several to many species, (2) the species vary morphologically in
  conspicuous ways, and relatedly, (3) they occupy a diversity of
  ecological niches. Most of the species were (4) derived from a single
  ancestor in their current environment, and (5) most diverged
  relatively rapidly.

The species from your list have some common traits:

Fast metabolism of themselves, food and fertilizers
sexual reproduction is more complex than crabs and coral
complex ecosystems and fast changing ecology
lots of ecological competition generally advanced compared to ferns, moss and crabs
More Possibility to travel through gene bottlenecks
recent in fossil history
prevalently small
possibility of population explosions
generalist and robust flexible habits and traits like tree nests, live birthing, flying, fangs, close inter-animal relations i.e. with bees,

If you study animals that have sedate speciation habits like platipus, they are limited in many of the common traits from that list.

The animal is therefore mostly dependent on it's ecosystem's stability, richness and opportunities, as well as the specie's own physical wealth, opportunism and stability. Those species have very complex and flexible ecology cycles working over them at a high rate. The rate of change of the ecology is also dictated by the other's organisms ability to radiate in record times, so today's species are in an arms race of the fastest rates of change in predator-prey-reproduction traits, with all the tools of the trade, i.e. fast movement, strong protection, freaky efficient cell-type mutations, locomotive, feeding, protective and spacial habits that by themselves can define the base of the most prevalent recent families.

Some species RNA is more susceptible to change and has to be be counterbalanced with different checks, it's to keep up with the arms race of competition in the complex ecology spaces of most of the planet.


What worms devour the body? I was reading this site which broached comedones, an esoteric word to me; so I thought to look up its etymology which I find exceptionally singular and peculiar (I would have never guessed that the word originated from to eat up !) :

  Etmyonline: "blackhead," etc., 1866, from Latin comedo "glutton," from comedere "to eat up" (see comestible). A name formerly given to worms that devour the body; transferred in medical use to secretions that resemble them.

Footnote: ODO also offers an etymology.

A maggot typically feeds on carrion. A maggot is the larva of a fly and usually  particular to the larvae of Brachyceran flies, such as houseflies, cheese flies, and blowflies.

Interestingly decomposition from maggots has a lot of use in forensic science as the presence or development of maggots on a corpse can be useful to a forensic entomologists to determine the approximate time of death. Depending on the species and the conditions, maggots may be observed on a body within 24 hours. The eggs are laid on the body and when the eggs hatch, the maggots move towards their preferred conditions and begin to feed. Insects are usually useful  25–80 hours post mortem and is contingent on temp humidity and oxygen availability. After 80 hours, this method becomes less reliable.


Why do bacteria need messenger RNA? Why do bacteria need mRNA? Isn't the DNA free floating without nuclear membrane so why doesn't the tRNA read the code directly off of the split DNA strands? (ofcourse after helicase splits them). Wouldn't this be more efficient?

Ribosomes don't read DNA.
Transcription adds several layers of regulation tactics: you can control transcription itself, you can control mRNA.
mRNA amplifies genetic information that you need at the moment. Having many copies of a matrix really helps.
Some prokaryotes have splicing. It's not a good idea to splice your DNA.

EDIT per your request of some elaboration.

  Why did they evolve to read RNA in the first place as they are primal
  to all other organisms, why did they develop this

The "RNA world" hypothesis (which is the most realistic early life model, considering the ever-growing body of evidence) postulates that RNA had been the main thing long before DNA was introduced into cells. The ribosome (being an RNA enzyme that doesn't require any proteins to bind amino acids together), along with many other RNA enzymes and regulators, is believed to be a relic of that world. Wiki has a good page with all the references you might want to read.

  Also, the regulation tactics, isn't DNA free floating and so are all
  the replication enzymes like Helicase, primase and RNA primer etc. So
  how do they regulate the action of these enzymes as they are just free
  floating?

First of all, it's a common misconception that prokaryotic cells are mere bags stuffed with enzymes and whatever. Prokaryotes posses highly complicated compartmentalisation systems (some even possess nucleus-like compartments). Second of all, DNA is not "free floating": it's located at a specific site with a special molecular environment. If you want details, ask a separate question, or better a series of questions with narrow scope, because bacterial regulation is too diverse, bizarre and sophisticated to cover here (we had a 3 years-long course on this matter when I was a student).

  Could you explain a bit of how the extra copy helps as is it not just
  more data to deal with?

When you have many copies of a matrix, many ribosomes can synthesise a protein at once. This comes in handy when you need to make tons of something as fast as possible. Remember, ribosomes are quite ubiquitous in all active cells for this very reason: to facilitate fast protein synthesis (at least as far as copiotrophic organisms are concerned).

  What exactly do you mean by splicing?

I mean splicing: a group of processes by which introns are excised from primary transcription products.


How long can an octopus survive out of the water? I saw videos of octopuses crawling on the ground and I was wondering how long an octopus can survive when out of the water? Does it depend on either its size (i.e., does a big octopus from deep sea survive longer than a tiny octopus) or the species?

Short answer
Under ideal conditions, an octopus may survive several minutes on land.

Background
Octopuses have gills and hence are dependent on water for the exchange of oxygen and carbon dioxide. Gills collapse on land because of the lack of buoyancy (source: UC Santa Barbara). Octopuses have three hearts. Two of these are dedicated to move blood to the animal’s gills, emphasizing the animal's dependence on its gills for oxygen supply. The third heart keeps circulation flowing to the organs. This organ heart actually stops beating when the octopus swims, explaining the species’ tendency to crawl rather than swim (source: Smithsonian).

According to the Scientific American, crawling out of the water is not uncommon for species of octopus that live in intertidal waters or near the shore (Fig. 1). Because most species of octopus are nocturnal, we humans just don't see it often. Their boneless bodies are seemingly unfit for moving out of water, but it is thought to be food-motivated, e.g. shellfish and snails that can be found in tidal pools.

Octopuses depend on water to breathe, so in addition to being a cumbersome mode of transportation, the land crawl is also a gamble. When their skin stays moist, a limited amount of gas exchange can occur through passive diffusion. This allows the octopus to survive on land for short periods of time, because oxygen is absorbed through the skin, instead of the gills. In moist, coastal areas it is believed they can crawl on land for at least several minutes. Mostly they go from pool to pool, never staying out of the water for extended periods. If faced with a dry surface in the sun, they will not survive for long (source: Scientific American).

Fig. 1. Octopus on land. Source: BBC

Your sub questions; I think small octopuses may survive longer, since passive gas exchange is the mode of survival on land. In general, an increase in diameter causes the volume to increase with a third power, while surface increases with a power of two. Therefore, an increase in body size reduces the surface-to-volume ratio and leads to reduced gas exchange. Because passive gas exchange needs large surface-to-volume ratios, I am inclined to believe small octopuses may cope better with terrestrial environments. However, in hot, arid conditions it is likely a bigger one will have an advantage, because it can store more oxygen in its blood.

In terms of species, I have to say I couldn't find any sources going in so much detail on this. Likely, as said, smaller species may do better in cool, moist conditions, while larger specimens may be better off in dry environments.

Reference
- Harmon Courage, Sci Am; (November 2011)


Why does a lightsource postpone the time it takes for the leaves falling from a birch tree? It is autumn and the leaves have already left their trees on all birch and other trees that has leaves, except one. This birch has a spotlight pointed to the tree and it is on 24/7. I have recognized that this birch have lost almost no leaves. And if we take a closer look at this birch, the back side of the birch, which is faced away from the spotlight have lost a noticeable amount more leaves than the front side which is directly hit by the light from the spotlight.

My conclusion is that having a lightsource pointing to a leafy tree will postpone the time from when it loses its leaves, relative to trees that does not have a lightsource pointerd at them.
 But I have no idea why this is happening. I do not know anything about trees, leaves, chloryphyll or the reason why trees drops their leaves in the autumn.

If any one is a expert in this field and might know why this is happening, or just have a hypothesis of why this is happening please provide it since I find this really interesting and I can't find anything on Google about this phenomenon.

You can make your anwer as complicated as you wish, I will understand it even if I might need to Google some of the things in the answer :).

Thanks!

It's to do with the chemistry taking place in the system, and then in turn the balance of energy resources.

Leaves contain chlorophyll, a molecule that traps light energy. It is large molecule containing a long carbon chain and a magnesium atom surrounded by 4 nitrogen atoms. In terms of a plants energy resources it is an 'expensive' molecule, but it is worth it as it is important to the plant.

The conversion of light energy by plants, using chlorophyll, is called photosynthesis. The chemistry of photosynthesis using chlorophyll is complex, but essentially Carbon Dioxide (CO2) from the air is combined with Water (H2O) from the roots to produce sugar and oxygen. Excess sugar is transported to the roots and stored as starch, and some sugar is used to keep the living cells throughout the plant alive. They need energy and this gained through respiration. Again, the actual chemistry is quite complex, but simply put the cells take in Oxygen from the air and 'burn' the sugar to release energy, this gives off Carbon Dioxide and Water. (There is plenty of resources and explanation on the actual mechanism - search for "ATP and ADP in plants")

Notice that it starts with carbon dioxide and water and ends with carbon dioxide and water, the energy is held within the chemical bonds.

When there is plenty of light (and water) the rate of photosynthesis, and therefore the rate of energy production, is high. The plant is producing excess energy, and the leaves are 'worth' the energy needed to keep them alive and functioning. Note that temperature also has an influence. The warmer the temperature (to a point) the greater the rate of photosynthesis.

So, in temperate climates with markedly different day lengths and temperatures between the summer and winter seasons some plants have evolved to be deciduous and shed their leaves in the autumn. The point at which this will start to happen will be when the day length shortens, and the temperature drops, and so when the amount of energy that the leaves are able to produce starts to balance the amount of energy being used to maintain the leaf.

If a plant has an artificial light source then the leaves will continue to be able to produce more energy than they use and so will be retained for longer.


How do I make conclusions from the autoradiograph of a Southern blot? Here's another question taken from "Concepts of Genetics," Klug et al (10ed), revolving around a paternity test. PCR and a Southern blot were carried out in order to determine whether 3 chimpanzees (lanes 3, 4, 5 in the blot below) were the "legitimate" offspring of 2 potential parents (lanes 1 and 2).

The question makes a point of saying that the primers used to bind to the chimp DNA originates from humans, and that they "flank highly polymorphic sites in human DNA that result from variable numbers of tandem nucleotide repeats." My first question is what exactly does "flanking" mean in this context? It sounds to me like the human DNA "mirrors" the chimp DNA, and so makes it good enough to use as a primer, but I'm not sure.

I've come across a few other examples not in the text about how to infer whether a potential parent is indeed a parent based on whether the offspring's lane contains bands found in both the maternal and paternal lanes, which leads me to believe I can rule out the chimp in lane 5.

I'm given five answers to choose from to decide which of the offspring, if any, are legitimate:

None
A only
A and B only
Not enough data; more polymorphic sites should be examined
No conclusion can be made because "human" primers  were used

Main questions: Does that fact that we're using human DNA as primers cause any problems? Do we know enough from this blot to determine paternity?

As @canadianer pointed out in the comments section flanking sequence is a sequence that is immediately near the target on either side. Since chimps and humans are closely related and the sequence different is minimal (according to this paper its approx 4% for the entire genome)  so using human primers is totally fine.  Now if take a look at the picture of the gel:
 The answer is 2. only A because only this offspring has a variant in large amount (that can be determined from the width of the band) that can be acquired from both parents and in this case chimp A actually did inherit the 136bp variant from both parents.

For chimp 4 either parent can be the same (as for chimp A) from the two because it has the 136bp variant as well ( that can be inherited either chimp one or two), but has a different one that cannot come from chimps 1 and 2.

As you said chimp 5 can be ruled out instantly because it has a large band that cannot be found in either of the two parents.


Can (any) human cells learn? I'm not talking about single celled organisms, but actual cells in your body. Is there any evidence that they can learn to, say, navigate an environment or avoid an aversive stimulus like an animal could? Is their behaviour understood well enough to say that it's entirely mechanistic, or are there things we still don't know?

For this specific question, let's divide the cells into two categories:

Cells that rarely "navigate" are the cells that are connected to give the tissue its mechanical properties. How do these avoid an "adverse stimulus"? Well, they don't avoid it. But if that stimulus "harms" cells they react in some way:

if the cell is destructed by the pathogen, it will release chemical compounds that have chemotactic properties and attract specialized cells.
if the pathogen has intracellular tropism, the cell may release some chemical compounds (see interferon) to "alert" other cells that something is wrong. Most cells can also present antigens on their surface.
there are also some stimuli which change cellular life cycle turning cells into cancerous cells. These cells can gain excretory properties and produce substances that destroy intercellular jonctions. This is how metastases occur.

Cells that "navigate" are the blood cells. White blood cells respond to different kind of stimuli (chemical) in two ways: either they are attracted (by inflammatory cytokines for example) either they are repelled. Macrophages are attracted by cytokines released when a pathogen agent triggers inflammatory response. They "ingest" that pathogen through phagocytosis and expose some parts of it (the antigens) on their surface receptors. This stimulates lymphocytes which process that antigen and decide if it is self or non-self. If it is non-self, they stimulate proliferation of specialized cells against that antigen. Another type of blood cells, the platelets, although they have no nucleus, have interesting properties: they can adhere to the broken endothelium where they change shape and start to produce different chemical mediators.

Read more on:

Wikipedia contributors, "Chemotaxis," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Chemotaxis&oldid=600637322 (accessed June 28, 2014).
Wikipedia contributors, "Interferon," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Interferon&oldid=608718450 (accessed June 28, 2014).
Wikipedia contributors, "Adaptive immune system," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Adaptive_immune_system&oldid=612379171 (accessed June 28, 2014).
Wikipedia contributors, "Platelet," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Platelet&oldid=614627651 (accessed June 28, 2014).


What does the 'V' stand for in ECG electrode names? In electrocardiography, electrodes have the typical names of:

RA (Right Arm)
LA (Left Arm)
RL (Right Leg)
LL (Left Leg)
V1, V2, V3, V4, V5 and V6

What does the V stand for? Is it perhaps from vector, ventricular, or maybe from something else entirely?

Short answer
V stands for voltage.

Background
The various leads in an ECG montage are shown below:

ECG electrodes. Source: American Heart Association

I am not an expert in ECGs, but as far as I can see, RA, LA and LL are return electrodes as they are situated far away from the heart. In other words, they act as reference electrodes. RL is the ground, basically to correct for baseline shifts. This leaves the V electrodes, which are the chest leads, or precordial leads, and are situated right above where the action is, i.e., the heart. The ECG is determined between the V electrodes and a distant reference, with a ground added. The V electrodes are the active electrodes, picking up the signal. The others are references and a ground only.


What are all the possible developmental stages an insect can be in? I'm making an app which allows the user to report insect observations. Many bugs may exist in different forms throughout their life time. For example, a butterfly will exist as an egg, a catterpillar, a pupa and lastly as a butterfly. A greenshield bug can live as a nymph and then as an adult.
I want to make one list that contains all morphological stages that insects can be in. Then the user can select the appropriate one for the species he or she observed. My question is: What are the names of these stages? Are there any other stages next to the egg stage, caterpillar/larval stage etc?
Thank you

This process is refereed to as Metamorphosis, is a biological process by which an animal physically develops. Furthermore, Animals can be divided into species that undergo complete metamorphosis ("holometaboly"), incomplete metamorphosis ("hemimetaboly"), or no metamorphosis ("ametaboly").
Otherwise there is the process known as Holometabolism, which more specifically pertains to insect development. This process defines almost all the types of insect development.
Others include: Ametabolism and Hemimetabolism.


Is it possible to be (briefly) aware you had been decapitated? If a person's head was cleanly and rapidly decapitated by a sharp blade slicing through the neck, such as would happen on the guillotine, could that person remain conscious? If so for how long? Long enough to be aware of (the head) falling down and hitting the ground?

Obviously it would be brief due to lack of blood supply, but it seems plausible that it could be a few seconds.

Or is there some inherent neurological shock due to the severing the top of the spinal cord that would cause near instantaneous loss of conciousness?

Could Marie Antoinette have seen her own severed neck from the basket below the blade?

According to this, in rats it takes about 17 seconds after decapitation for the EEG to become iso-electric. But there is no known correlation between EEG and consciousness. Also at 50-80 seconds after decapitation, EEG being iso-electric, a very slow, late wave appears on the EEG record.

The same article concludes that it takes about 3-4 seconds after decapitation for the animal to lose conscience and perceive no stress and pain.

Also, dr. Harold Hilman states in An unnatural way to die article from october 1983 issue of New Scientist, page 277 that:

  Consciousness is probably lost within 2-3 seconds, due to a rapid fall of intracranial perfusion of blood.


Why does the blood not clump and result in death? In this question's accepted answer, it is said that the blood type will slowly change to that of the donor's.

When the blood in the person is about 50% his own and 50% that of the donor's.
i.e, 50% A group blood (his own) and 50% O group (donors blood),won't the antibodies in the O group react with the A-antigens and clump?

Some people do die from graft vs host disease after bone marrow transplants involving ABO incompatibility, but not usually from blood clots.

Foreign red blood cells don't usually form significant clumps (or clots) as a result of an antibody interacting with a surface cell antigen. They can form tiny clumps, however, that are not life threatening, but simply plucked out of the bloodstream by macrophages.

The typical reaction consists of foreign red blood cell detection and destruction (broadly called hemolytic anemia.) So anemia is a problem, but normally not significant clumping/clotting.

Safety and impact of donor-type red blood cell transfusion before allogeneic peripheral blood progenitor cell transplantation with major ABO mismatch.
Blood transfusions and the immune system
Consequences of ABO incompatibility in allogeneic hematopoietic stem cell transplantation.


What pH ranges are used in industrial scale fermentation? When reading

  Hans-Peter Meyer, Wolfgang Minas, and Diego Schmidhalter (2017) Industrial-Scale Fermentation. Industrial Biotechnology: Products and Processes, First Edition. Edited by Christoph Wittmann and James C. Liao.
  © 2017 Wiley-VCH Verlag GmbH & Co. KGaA. Published 2017 by Wiley-VCH Verlag GmbH & Co. KGaA.

I came across the following passage describing industrial up-scaling of fermentation processes (in general):

  1.3.1

  Process Development – Scale-Up Starts at Laboratory Scale

  Process scale-up should be considered early on while the biological expression
  system is still under development. Factors such as genetic stability for at least
  the number of generations needed for a scaled-up production, and the need and
  impact on the environment of selection markers, should be evaluated before
  process development is started. The use of antibiotics as selective markers in the
  production medium should be avoided. Throughout development of media and
  cultivation conditions, it is important that parameter settings remain realistic and
  scalable, always indicated with upper and lower limits reflecting the safe operating
  range (process design space), for example, pH 7 ± 0.3.

I am quite surprised about the narrow pH range specified (pH $7 \pm 0.3$). I assumed that the pH range would be much wider, similar to lab scale. Is this really common practice?

Fermentation pH will differ a great deal depending on the bacteria or fungi being used and the process. But it is not uncommon to have a relatively narrow range of pH as a target. Remember pH is the -log[H+] so the pH scale is not linear. Also some fermentation reaction involve very expensive pharmaceuticals or intermediates, a single fermentation batch may have a value in the hundreds of thousands of dollars so keeping +/- 0.3 range in pH is trivial.


How does acupuncture work? Can anyone actually tell me how acupuncture works?

There are numerous websites with little actual explanation, but assert that it works. For example the below article:

http://www.health.harvard.edu/blog/acupuncture-is-worth-a-try-for-chronic-pain-201304016042

However I have failed to find any article about how acupuncture works, or the mechanism at play. Can anyone tell me how it works?

It works via the placebo effect which according to recent research, is not the sort of trivial effect as it was thought to be.


Endothermy in different species Birds and mammals are both endothermic, meaning they metabolically generate the heat they need to keep their body within a certain temperature ranger.

But birds are closer relatives to reptiles than they are to mammals, and reptiles are not endothermic. Thus birds and mammals developed endothermy independently; and here is the question:

How does thermal regulation differ in birds and mammals?

This is in between a comment and an answer...

Notes

reptiles can have several definitions. Some of them causing birds to be a reptile.
You probably meant "evolved" instead of "developed".
Thermoregulation is performed by a set of different mechanisms and it is plausible that your question would be considered as too broad. Note however that I am NOT a physiologist and might overestimate the scope of the question.

Similitudes between birds and mammals

From wikipedia (here)

  In cold environments, birds and mammals employ the following adaptations and strategies to minimize heat loss:

  Using small smooth muscles (arrector pili in mammals), which are attached to feather or hair shafts; this distorts the surface of the skin making feather/hair shaft stand erect (called goose bumps or pimples) which slows the movement of air across the skin and minimizes heat loss.
  Increasing body size to more easily maintain core body temperature (warm-blooded animals in cold climates tend to be larger than similar species in warmer climates (see Bergmann's Rule))
  Having the ability to store energy as fat for metabolism
  Have shortened extremities
  Have countercurrent blood flow in extremities - this is where the warm arterial blood travelling to the limb passes the cooler venous blood from the limb and heat is exchanged warming the venous blood and cooling the arterial (e.g., Arctic wolf[3] or penguins[4][5])

  In warm environments, birds and mammals employ the following adaptations and strategies to maximize heat loss:

  Behavioural adaptations like living in burrows during the day and being nocturnal

  Evaporative cooling by perspiration and panting
  Storing fat reserves in one place (e.g., camel's hump) to avoid its insulating effect
  Elongated, often vascularized extremities to conduct body heat to the air


Why ravens play with garbage? Why ravens play with small plastic details and other garbage?

Could you explain how this behavior was formed by evolution for birds-scavengers?

Ravens and other corvids are among the most intelligent birds. Of note, crows and ravens are known for their ability to solve problems that require tool use, memory, and delayed rewards (patience).

Many animals play, and ravens and crows are no exception. (A study entirely on raven nestling play.) The evolutionary purpose of play activity is thought to improve coordination/dexterity, provide exercise, strengthen muscles (such as wing-flapping by young birds that have yet to fledge), and develop social skills.

As to what type of objects ravens find most interesting to play with, I'm unsure of a definitive answer. Some birds, particularly the satin bowerbird, even collect colorful objects. My hypothesis is that the choice of object is likely due to simple availability (discarded) and conspicuous nature (color). In other words, ravens more easily find such objects because they are colorful, which in turn are frequently human-manufactured.


Is there an evolutionary explanation for the black spots around a pandas eyes? I couldn't seem to find one elsewhere, at least not with a scientific source.

It would seem as it's quite a striking feature there would be an advantage it would infer.

As your commenters have suggested, no.

In order for an explanation to be a good evolutionary explanation, it needs to have a testable hypothesis and a mechanism to test it.

The most common mechanism for testing the crypsis (camouflage) hypothesis is to take a large number of closely-related species, and see if their coloration differences are correlated to a particular habitat. Since pandas have few black-and-white relatives, there is no statistical power in this analysis.

Another option is to take a large number of pandas, create a treatment and control group and bleach the treatment group (or their eyespots) white, and compare survival or visual acuity. Unsurprisingly, this has not been done.

Here's a nice article to animal coloration for those that have access:

Caro, T. I. M. (2005). The adaptive significance of coloration in mammals. Bioscience, 55(2), 125-136.


Elution of biotinylated RNA I am using Neutravidin Agarose beads to isolate biotinylated RNA. The thing is, in the manual it says to use 8M Guanidine-HCl, pH 1.5 for elution biotinylated molecules. As far as I know it is a very harsh elution buffer. Do you think it would effect my RNA? I have isolated my RNA with TRIzol which also contains Guanidine salt but the concentration is not that high.

As a second question, do you know other ways to elute my biotinylated RNA from beads?

Thanks!

The biotin-streptavidin interaction is extremely strong, one of the strongest (if not the strongest) non-covalent interaction between biomolecules. So you'll need pretty harsh conditions in any case.

Extreme pH values are generally a very bad idea for RNA. I'm pretty sure that the conditions you mentioned are not meant for elution of nucleic acids. Such low pH values (and high pH values as well) lead to a quick hydrolysis of the phosphoester bond of RNA, you can read more about the mechanism of that in this review.

A quick Google search lead me to the following protocol:

  To dissociate biotinylated nucleic acids from Streptavidin-Coupled
  Dynabeads®, incubate the beads in 95% formamide + 10mM EDTA, pH 8.2
  for 5 minutes at 65°C or for 2 minutes at 90°C.

This sounds reasonable to me, as formamide is also commonly used in sample buffer for denaturing gel electrophoresis of RNA. I haven't done anything like that myself, so I can't guarantee that this would work in your case.


Why would growth hormone (somatotropin) cause both lipid AND glucose release? GH increases lipolysis (lipid breakdown) and the release of fatty
  acids from adipocytes into the blood. Fatty acids then can be used as
  energy sources to drive chemical reactions, including anabolic
  reactions, by other cells. GH also increases glucose synthesis by the
  liver, which releases glucose into the blood. The increased use of
  lipids as an energy source accompanies a decrease in glucose usage.
  Overall, GH activates the use of lipids to promote growth and protein
  synthesis.

(From Seeley’s Anatomy and Physiology, 10th edition.)

That passage has gotten me confused. So more lipids are used by cells instead of glucose, yet the body releases more glucose into the blood in response to GH. What would be the point, or benefit, of this occurring?

Great question... and an important point about glucose and lipid utilization! The body can't turn fat into sugar, but it can turn sugar into fat. The more technical way to say this is that the body can't convert acetyl-CoA into glucose, but it can convert glucose into acetyl-CoA.

The enzyme that converts glucose to acetyl-CoA, pyruvate dehydrogenase, catalyzes an irreversible chemical reaction. Pyruvate dehydrogenase converts pyruvate into acetyl-CoA, which can be used in the Krebs Cycle, fatty acid synthesis, etc. Once acetyl-CoA is produced it cannot be converted back into glucose (carbohydrate) within the body. This is important because certain cells/tissues can use only glucose for energy production, while other cells/tissues like the liver can use both glucose and lipid for energy production.

This is where your question becomes very important, because the liver is the predominate organ that maintains glucose homeostasis (i.e. maintains blood glucose concentration) in-between meals or during periods of fasting. In periods of fasting, the liver uses free fatty acids released by adipose tissue for energy/ATP production in order to produce glucose through gluconeogenesis, an anabolic process that requires energy.

So, growth hormone increases fatty acid release from adipose tissue stores for uptake by the liver. The liver takes up the fatty acids from the plasma and uses them to produce glucose for release into the circulation for glucose-dependent tissues to use. During this time of fasting, tissues that can use fatty acids and glucose tend to switch to fatty acids as their energy source, while tissues that only can use glucose will continue to rely on glucose production from the liver for their energy source.

Here is a nice summary (open source) from National Library of Medicine explaining in more depth the basis for why fatty acids are oxidized to provide ATP for gluconeogenesis - "Energy Metabolism in the Liver".

Also, George Cahill, a famous physician-scientist at Harvard University who studied metabolism and starvation has an excellent review of fuel flux under fasting and starvation conditions that demonstrates the above mentioned principles as well "Fuel Metabolism in Starvation" - namely that free fatty acids released from adipose tissue are oxidized in the liver and used for anabolic processes in the liver, such as gluconeogenesis that maintains blood glucose concentrations.


Aquatic forest insect identification I found it in the forest but I've never seen anything like it so I took it home to see what it is. Does anyone know?

This is a caddisfly larvae (Trichoptera). They live in streams and other water that are rich in oxygen.
They protect themselves by building there own 'house', with whatever is available, e.g. plant or wood fragments, gravel or even snail shells (see picture below)

Picture from Dutch wiki

https://en.wikipedia.org/wiki/Caddisfly

Id to species level probably requires microscopic work.


Stomach sagittal section Can anyone please tell me where is exactly the stomach in this image?

This is a sagittal section from the University of Michigan Visible Human Browsers.

Thank you.

The below structure circled in green clearly is part of the stomach antrum. The location is correct, and the mucosal folds are characteristic. Kerckring valves of the small intestine and semilunar folds of the colon both look different.


Why is an intron (or exon) still called intron (exon) if retained in (excluded from) mRNA? In most explanations, the sections of RNA removed during splicing are called introns, and the remaining segments that are stitched together are called exons.  That is, introns and exons are defined in terms of the splicing process.
But I've come across several counter-examples.  For instance:
From A simple answer for a splicing conundrum:

Exons without these elements [exonic splicing enhancers (ESEs)] are
generally not recognized and tend to be excluded from the mature
mRNA.

And from Wikipedia on alternative splicing:

Intron retention: A sequence may be spliced out as an intron or
simply retained...

In what sense is an exon still an exon (and not an intron) if it tends to be excluded from the mRNA?  In what sense is an intron an intron if it included in an alternatively spliced mRNA?

You must know that:

Introns are non-coding regions of an RNA transcript, or the DNA encoding it, that are eliminated by splicing before translation.
An exon is any part of a gene that will encode a part of the final mature RNA produced by that gene after introns have been removed by RNA splicing.

Now, about the exceptions, alternative splicing: Here,

  particular exons of a gene may be included within or excluded from
  the final, processed messenger RNA (mRNA) produced from that gene. There are numerous modes of alternative splicing observed, of which the most common is exon skipping. In this mode, a particular exon may be included in mRNAs under some conditions or in particular tissues, and omitted from the mRNA in others.

Apparently, this greatly increases the biodiversity of proteins (since there are differences in their amino acid sequence and, often, in their biological functions) which might explain why it is so common.

So in this case, it becomes easier to understand if you use 'coding' and non-coding' as the difference instead of 'spliced' and 'not-spliced'.

EDIT- The coding region of a gene:

  In DNA, the coding region is flanked by the promoter sequence on the 5' end of the template strand and the termination sequence on the 3' end. Although this term is also sometimes used interchangeably with exon, it is not the exact same thing: the exon is composed of the coding region as well as the 3' and 5' untranslated regions of the RNA, and so therefore, an exon would be partially made up of coding regions. The 3' and 5' untranslated regions of the RNA, which do not code for protein, are termed non-coding regions.

I had previously forgotten about the UTR's, so I have included that. Now, if there is a definite sequence where coding regions are found, it points out to the fact that coding regions must be intrinsic. Another point in favour:

  The evidence suggests that there is a general interdependence between
  base composition patterns and coding region availability.The coding
  region is thought to contain a higher GC-content than non-coding
  regions. There is further research that discovered that the longer the
  coding strand, the higher the GC-content. Short coding strands are
  comparatively still GC-poor, similar to the low GC-content of the base
  composition translational stop codons like TAG, TAA, and TGA.


Sporophyte and gametophyte My textbook says that in both groups of seedless plants (vascular plants, non-vascular plants) the gametophyte is a free-living plant, independent of the sporophyte.
I don't understand this statement and am now wondering if the sporophyte and gametophyte  are stages in a plant's lifecycle, or are they individual parts of the plant, or are the sporophyte and the gametophyte different plants altogether? Secondly, does this differ depending on the organism?

Different plants or different structures that make up the same organism?

The sporophtye is the diploid stage in the life cycle. In comparison, with humans, you and I would be sporophytes.

The Gametophyte is the haploid stage in the life cycle. In comparison, with humans, spermatozoids and ovules are gametophytes.

Independence

Note for what follows: "independent" can be understood in terms of "ability to survive". Being independent according to its ability to survive. One might use the word "independent" for other concerns though! For example: "Independent" in the sense "no nutrient exchange between the two"

Therefore, one could say that in humans, the gametophyte is not independent (in it's ability to survive) of the sporophyte. Similarly, in moss (bryophyta), the gametophyte is not independent of the sporophyte because the gametophyte grows on the sporophyte using its nutrients (one could say that the gametophyte parasitize the sporophyte but that would be a bit misleading!). If the sporophyte is independent of the gametophyte (or vice-versa), it means that there is alternation of generations. In other words, sporophyte and gametophyte live separately (like two different individuals).

Life-cycle

You can find tons of examples of weird life cycles, in particular in plants, fungi and parasites but not only. And you may find many examples for which the type of sexual reproduction or the type of life-cycle are hard to defined with these relatively simple concepts.

Identity

The question of identiy (how separate or genetically different should two individuals be so that we consider them to be two different individuals) is rather a question of philosophy. Such discussions about identity occur when we talk about clones (ramet and genet), about life cycle or about level of organisation/level of selection. The book Major Transition in Evolution (Revisited) provides many of the philosophical discussion on the subject of identity in population genetics.


How can I convert plate reader measurements of Pichia pastoris OD to cells per ml? I am performing experiments with the yeast Pichia pastoris where it will be beneficial to calculate product yield per cell. I plan to use a plate reader to measure OD600 of my cultures and then somehow relate this to cell number.
The Pichia pastoris expression manual from ThermoFisher says that 1 OD600 is equivalent to 5x10^7 cells/ml, and Weis et al (2004) have a similar number of 1.5x10^8 cells per 1 OD.
However, there are now calibration protocols (Beal et al 2020) and packages (Fedorec et al 2020) for using absorbent beads to convert OD measurements to cell density in E.coli. These rely on the beads scattering the light in a way that is equivalent to cells, so that one can compare measurements of OD with a standard curve of known amounts of beads to estimate cell number. Pichia is about 5µm in size size, compared to E. coli which is about 1-2µm, therefore I do not believe that using the same protocol will work for me.
Is it necessary for me to develop a new protocol, or can I just convert by multiplying OD by the numbers given above? If it is necessary, how can I develop such a protocol? Can I just use the E. coli protocol that I linked with different size beads?
Refs:

Weis, Roland, Ruud Luiten, Wolfgang Skranc, Helmut Schwab, Marcel Wubbolts, and Anton Glieder. ‘Reliable High-Throughput Screening with Pichia Pastoris by Limiting Yeast Cell Death Phenomena’. FEMS Yeast Research 5, no. 2 (1 November 2004): 179–89. https://doi.org/10.1016/j.femsyr.2004.06.016.
Jacob Beal, Traci Haddock-Angelli, Markus Gershater, Vishal Sanchania, Russell Buckley-Taylor, Geoff Baldwin, Natalie Farny, Richard Tennant, Paul Rutten 2020. Calibration Protocol - Plate Reader Abs600 (OD) Calibration with Microsphere Particles. protocols.io
https://dx.doi.org/10.17504/protocols.io.bgy6jxze
Fedorec, Alex J. H., Clare M. Robinson, Ke Yan Wen, and Chris P. Barnes. ‘FlopR: An Open Source Software Package for Calibration and Normalization of Plate Reader and Flow Cytometry Data’. ACS Synthetic Biology, 27 August 2020. https://doi.org/10.1021/acssynbio.0c00296.

From a technical perspective, for the FlopR package you mention (and I believe also for Jacob Beal's protocol) you can simply change the bead size and perform a new calibration. The only information that you need is the bead count at each point of your calibrant curve.
However, using calibration beads of a given size assumes that your cells will remain approximately the size of the beads for the duration of your experiment. We know that cell size and shape vary based on growth phase, antibiotics etc. [1] This can cause substantial misreporting of cell counts but is currently brushed under the carpet. I would suggest that if your Pichia change significantly in size or shape during their growth, it would be worth using a range of beads sizes and attempting to calibrate different growth phases of your samples against beads that correspond to cell size at during that phase.
[1] K. Stevenson, A. F. McVey, I. B. N. Clark, P. S. Swain, and T. Pilizota, “General calibration of microbial growth in microplate readers,” Sci. Rep., vol. 6, no. 1, p. 38828, Dec. 2016.


What type of jellyfish is this I have been swimming in the seas around Minorca and saw a jellyfish I had not seen before.

I have tried to find it and have (eventually) found 1 single picture of the jellyfish.

The problem I have is, the image is from one of these "buy our picture" website and offers no information about the creature.

What type of Jellyfish is this and can I assume from the picture that it does not actually sting humans?

I have researched, and viewed sites like (As well as Google/Bing images)

http://www.holidays-majorca.co.uk/trips/beaches/types-jellyfish-around-majorca
http://www.seafriends.org.nz/indepth/jellyfish.htm (I know, it's NZ but I'm looking everywhere I can)
http://www.glaucus.org.uk/Moonjell.htm
http://www.whatsthatfish.com/browse/tags/limit/Jellyfish
http://www.imenorca.com/en/entrada-de-blog/jellyfish-minorca
http://www.menorca-tips.com/EN-jellyfish.html
http://www.mcsuk.org/downloads/wildlife/Jellyfishguide.pdf

Eventually, I've stumbled upon an article which calls it a cigar jellyfish.

Further research even shows a very empty entry on Wiki about it, which consists of the single line entry:

  The cigar jellyfish (Olindias phosphorica) is a species of jellyfish from the Central and East Atlantic, and the Mediterranean Sea, including off Malta.[2]

Also an interesting article about it being 'rare' in Malta (despite the above information)


Is touching or inhaling 70% isopropyl alcohol dangerous to humans? I bought 99% isopropyl alcohol and made 70% alcohol + 30% water in small spraying bottles as a disinfectant.

I also read that this solution is safe and recommended by Apple for cleaning iPhones.

My worry comes from reading on the 99% bottle how extremely dangerous it is to humans. Basically touching, inhaling and of course consuming it is very toxic.

On the other hand 70% alcohol solutions are found in most hand and surface sanitizers which are usable against COVID-19.

So my question is: how much should I be afraid when cleaning surfaces with my small 70% spray bottle? Since alcohol evaporates, I'd be naturally inhaling it, I mean where else could it go in the air? I'm also just spraying it on a wipe to clean my mobile, not using a rubber glove for that.

What are the health concerns when using such solution?

If you're interested in the biological or health effects of various chemicals, try to look up the Safety Data Sheet, or "SDS" or "MSDS", for that chemical compound.
Going to your favorite search engine and plugging in your chemical of interest to the search term "SDS" or "MSDS" will almost always get you to some kind of answer — either what you're looking for has a safety data sheet or it doesn't!
In the case of 70% isopropyl alcohol, there are SDSs/MSDSs out there that will tell you what potential health effects are. Here's one example for 70% isopropyl alcohol:

Potential Health Effects
Eye: Produces irritation, characterized by a burning sensation, redness, tearing, inflammation, and possible corneal injury. May cause transient corneal injury. In the eyes of a rabbit, 0.1 ml of 70% isopropyl alcohol caused conjunctivitis, iritis, and corneal opacity.
Skin: May cause irritation with pain and stinging, especially if the skin is abraded. Isopropanol has a low potential to cause allergic skin reactions; however, rare cases of allergic contact dermatitis have been reported. May be absorbed through intact skin. Dermal absorption has been considered toxicologically insignificant. The cases of deep coma associated with skin contact are thought to be a consequence of gross isopropanol vapor inhalation in rooms with inadequate ventilation, rather than being attributable to percutaneous absorption of isopropanol per se.
Ingestion: Causes gastrointestinal irritation with nausea, vomiting and diarrhea. May cause kidney damage. May cause central nervous system depression, characterized by excitement, followed by headache, dizziness, drowsiness, and nausea. Advanced stages may cause collapse, unconsciousness, coma and possible death due to respiratory failure. Aspiration of material into the lungs may cause chemical pneumonitis, which may be fatal. The probable oral lethal dose in humans is 240 ml (2696 mg/kg), but ingestion of only 20 ml (224 mg/kg) has caused poisoning.
Inhalation: Inhalation of high concentrations may cause central nervous system effects characterized by nausea, headache, dizziness, unconsciousness and coma. May cause narcotic effects in high concentration. Causes upper respiratory tract irritation. Inhalation of vapors may cause drowsiness and dizziness.
Chronic: Prolonged or repeated skin contact may cause defatting and dermatitis.

Safety data sheets sound terrible! But in reality, people use rubbing alcohol with common sense, without putting into their eyes, without drinking it, etc.
Mainly the point of this answer is to help you find the answer for yourself, if you want to find out about this or other chemicals you might be worried about.


How are micelles formed from the byproducts of emulsification in fat digestion? It is known that fat droplets are made into emulsion droplets via the addition of bile salts. It is then said that the emulsion droplets are made into micelles through some sort of lipase, which can be absorbed and transported to different cells through the LDL and HDL pathway.

My question is what is the biochemistry for transforming emulsion droplets into micelles? How does water, lipase, and other factors make these micelles?

Fat (triglyceride) enters the small intestine in the form of an emulsion of droplets which are stabilised by surfactants from the diet including proteins and phospholipids.

Bile salts (BS) bind to the surface of these droplets, displacing proteins. The BS-stabilised droplets are the substrate for pancreatic lipase which can adsorb to the BS-stabilised surface and convert the triglycerides to monoglycerides and free fatty acids.

The products of lipolysis then enter micelles that are formed by BS and phosphatidylcholine (PC: also in bile). The prevailing view is that these micelles take the form of discs of bilayer-like structure with BS situated both around the edges protecting the exposed acyl groups, and also embedded within the PC bilayer.

I think that the mechanism by which the products of lipolysis move from BS/PC micelles into enterocytes is not known. However, once they have entered they are re-esterified to form triglycerides which are packaged into chylomicrons (a class of lipoproteins) and exported into the lymphatic system.

Maldonado-Valderrama et al. (2011) The role of bile salts in digestion. Adv Colloid Interface Sci. 165:36-46 doi: 10.1016/j.cis.2010.12.002


Books on machine learning applications in Biology I have recently engaged with a collaboration, which requires me to construct, then train an unsupervised artificial neural network (ANN).

However, I have only a very coarse understanding of what machine-learning classifiers try to do, and how they work. For example, Chen et al.'s random forest (RF) classifier (ensemble of decision trees) for protein-protein interaction prediction. Additionally, I have very little idea about which types of machine-learning are useful to different classes of Biological problems.

So -if they exist- I would very much appreciate information on books that discuss applications of machine-learning classifiers in Biology/Bioinformatics. Preferable criteria are:

Intuitively introduces key concepts.
Illustrates a variety of Biological/Bioinformatics problems and their solutions by appropriate types of machine-learning (e.g. when is it appropriate to use ANNs versus RF classifiers?)
Relatively short (I'm planning to read from cover to cover).

Related

Stack Biology: Machine-learning for light microscopy problems to solve (I would consider this question a sub-class of the present question; personally, I am more interested in the sequence analysis / genetics domain of Bioinformatics problems)
Stack Biology: Historical connection between neuroscience and machine intelligence
Blogs about deep learning implementations in Biology
GitXiv: Collaborative on-going (and also published) computer science projects pertaining to machine-learning (search using relevant Biology-related queries to filter)

At NIPS 2016 most ANN implementations I saw were related to biology were trained on imaging data, thus the kind of comprehensive book you are looking for probably doesn't exist yet.

However, if you utilize the search feature on Amazon.com you'll find:

Neural Networks for Applied Sciences and Engineering: From Fundamentals to Complex Pattern Recognition

Artificial Neural Networks (Methods in Molecular Biology)

and this, which seems to best meet your need:

Neural Networks and Genome Informatics, Volume 1 (Methods in Computational Biology and Biochemistry)


Collective name for the X- and Z-chromosomes Chromosomes are grouped as sex chromosomes or autosomes, with the X, Y, Z and W all falling in to the former category. The Z and X are present both in the homogametic and heterogametic sexes, and the Y and W only in the heterogametic sex.

Is there a collective name for the chromosomes in such groupings (X/Z & Y/W)?

I want to talk about Z- and X- (and analagous) chromosomes in general. Rather than having to write "The X-chromosome, and analagous chromosomes such as the Z-, are present in both sexes...." I'd like to say "The blank chromosomes are present in both sexes...."

I think you can safely use the terms heterogametic (Y/W) and homogametic (X/Z) chromosomes, meaning that a heterogametic chromosome is the chromosome which makes one of the sexes heterogametic (i.e. defines the difference between the two types of gametes of the respective sex).

These terms applied to chomosomes do have some usage in the literature, e.g. in this article.


What is it about the housekeeping genes that makes them almost immune to gene regulation? When it comes to eukaryotes, including ourselves, we have all different kinds of specialized cells and tissues that are so different, yet originally all came from the same single cell. And apparently the reason for that is differential gene expression, where different genes get to be expressed in different cells. But there are, however, a set of genes that gets to be expressed in almost all of the cells.

My question is not why, but what is it about these genes that in a way makes them above the laws of regulation? Is it in their sequence? Or are they located on a single chromosome or perhaps regions that are somehow non-regulatable?

Housekeeping genes aren't clustered on a single chromosome. It is perhaps not that 'housekeeping' genes - broadly expressed genes - are 'above the laws of regulation'; rather that their regulation is merely more straight-forward than that of specialised genes.
I can think of 2 factors that could be relevant:

Abundance of methylation sites (CpG sites)
Promoter sequences and hence the transcription factors regulating expression of housekeeping genes are distinct from those controlling specialisation

I think the second (promoter sequences) is the better explanation, since housekeeping genes are abundant in CpG islands; but I'll explain a bit about both.
tl;dr: Housekeeping genes have simpler promoter and enhancer regions that are not bound by particular complexes which act to inactivate regions of the genome in a hierarchical manner during differentiation (according to the transcriptional program). http://genomebiology.com/2007/8/7/R140
Preamble
In forming tissues during development, cells must differentiate from embryonic stem cells, which have very wide potential to express many genes and give rise to all cell types; to partially specialised stem cells e.g. hematopoietic stem cells (HSCs) which are limited to give rise to all blood cells but not, say, neurons or pancreas or skin. Completely differentiated cells have a much more restricted domain of possible expression, and are more-or-less condemned to their fate.
Waddington's developmental landscape is a nice metaphor for how cells specialise:

DNA Methylation
A major mechanism behind this one-way narrowing of potential is methylation of DNA, which suppresses transcription. As the ball rolls down the landscape it acquires new stretches of methylation on its DNA, rendering it inactive which (for our purposes) is permanent and irreversible.
DNA methylation consolidates its chromatin inactivating function by acting as a signal for proteins which chemically modify histones (around which DNA is wrapped in chromatin) with further signals to condense chromatin, which occludes the transcriptional machinery from doing what it does best. (There are also activating histone modifications, and we imagine chromatin being, roughly, in OPEN and CLOSED states regarding the possibility of RNA polymerase gaining access to the DNA.) Since histones are ubiquitous & regularly spaced over the genome, there aren't "non-regulatable" regions - chromatin is opened or closed by the interactions of various DNA binding proteins, some reading and writing signals on to the chromatin.
So one plausible hypothesis is that housekeeping genes are relatively devoid of CpG sites (where methylation occurs). However I think this is not true. Many human genes have regions abundant in CpG (called 'islands') around their promoters, and in particular virtually all housekeeping genes. When genes are active, these CpG islands are unmethylated - hence in most tissues housekeeping genes have unmethylated CpG islands, something else is keeping them unmethylated.
Specialised cells, through a hierarchical transcriptional program of 'master regulators', successively close unneeded regions of their chromatin during differentiation, and keep open regions containing housekeeping genes, and the 'specialised genes' that relate to its specialism - these regulators are transcription factors which recognise the regions they act upon by binding promotor or enhancer sequences.
Housekeeping promoters and transcription factors
Transcription factors bind to enhancer or promoter sequences and open or close the chromatin for RNA polymerase, usually as part of a co-operative complex of many factors, including proteins that modify the histones or methylate DNA.
A good hypothesis is that the promoter/enhancer regions of housekeeping genes differ from those of specialised genes which are inactivated in many tissues. The transcriptional programs in differentiation must call forth factors that bind and inactivate specialised genes but keep active things like actin, ribosomal genes, etc.
This paper finds that upstream regions of housekeeping genes are less conserved, and a particular set of promoter motifs are over-represented. This suggests that housekeeping genes have relatively simple regulation by a few transcription factors; they lack binding sites for those transcription factors with important specialised roles in development.
To summarise, I think the following is likely: Housekeeping genes' promoter and enhancer regions exempt them from the complex transcriptional programs of hierarchical inactivation responsible for cell differentiation that many other genes are subject to. Housekeeping genes simply lack the relevant binding sites for these specialised transcription factors; they have instead more simple 'core' promoter elements. All the DNA methylation and opening/closing of the chromatin is a consequence of the transcriptional program.

http://en.wikipedia.org/wiki/CpG_site
http://en.wikipedia.org/wiki/Embryonic_stem_cell
http://en.wikipedia.org/wiki/Hematopoietic_stem_cell
http://www.nature.com/scitable/topicpage/the-role-of-methylation-in-gene-expression-1070
http://en.wikipedia.org/wiki/Histone
http://genesdev.cshlp.org/content/25/10/1010.full
http://genomebiology.com/2007/8/7/R140   < most relevant thing to read, and the basis of my own conclusion


If proteins have an overall charge, how do membrane proteins traverse through the hydrophobic region of the plasma membrane? These two concepts seem almost contradictory, proteins have a net negative charge due to the amino acids in them each having a small negative charge, yet membrane proteins are able to exist traversing the plasma membrane, which is impermeable to charged molecules (hence the need for membrane proteins).

How do these two statements remain true simultaneously?

Transmembrane proteins are inserted into the membrane in the ER in a rather complicated system, there is a whole chapter about translocation of proteins in "Molecular Biology of the Cell".

The proteins are moved through an aqueous pore in the Sec61 complex, which explains how charged parts of a protein are moved across the membrane.

The parts of a transmembrane protein that remain in the membrane are usually composed of hydrophobic amino acids that aren't charged.

I strongly recommend you to read up on the whole translocation stuff in a cell biology book like the Alberts I linked. There's a lot more to it than what I wrote here.


What makes a protein structure discernible? In Lehninger's Principles of Biochemistry, Pg. 116 states that "parts of proteins lack discernable structure." What exactly makes this protein not readable? Is it the complexity of the shape that makes it difficult for scientists to understand the structure?

There are two main methods for discerning a protein's structure; x-ray crystallography, and more recently cryo-electron microscopy. Both methods work by firing a high-energy beam through the sample and observing how the path of the beam has been changed by passing through the sample. The data obtained by measuring the beam includes "signal" information on the structure of the sample, but also a lot of random data, or "noise". If the signal from large numbers of copies of identical proteins can be averaged together coherently, it can be separated from the noise and the positions of the atoms that make up the protein can be determined. In crystallography, this is achieved by getting the proteins to arrange into a crystal, and in cryo-EM by a computational process after data has been collected. Either way, if the many copies of the protein are not quite identical, the signal averaging will not work, and the positions of the atoms cannot be determined as accurately, or at all. In some cases, the protein has two or a few distinct structures that it switches between, and these can be separated and determined accurately. In other cases, the protein only takes a specific shape when it is bound to another molecule, and just flops around randomly when nothing is bound. Here is the abstract of a review on this second type of protein:

Many gene sequences in eukaryotic genomes encode entire proteins or large segments of proteins that lack a well-structured three-dimensional fold. Disordered regions can be highly conserved between species in both composition and sequence and, contrary to the traditional view that protein function equates with a stable three-dimensional structure, disordered regions are often functional, in ways that we are only beginning to discover. Many disordered segments fold on binding to their biological targets (coupled folding and binding), whereas others constitute flexible linkers that have a role in the assembly of macromolecular arrays.

Finally, some proteins will not crystallize unless a portion of their sequence is removed. These portions may have a consistent structure, but it can't be determined by crystallography.


Could tumor cells have normal genomic profiles? I have thawed primary tumor cells and performed FACS. They were EpCAM positive cells. Then, I expanded them as organoids in 3D and did another FACS analysis. Again, they were EpCAM positive. I also sent organoids to pathology for IHC. Results showed they expressed EpCAM, EGFR, and panCK. But to my surprise, the Ampli LowPass sequencing results showed they had a balanced profile like normal cells. How could that be explained? Any help (comments, papers, ...) is appreciated.
Thank you.

I think this is the paper about the Ampli LowPass sequencing technique. Although, I didn't read it thoroughly but from the abstract and result section titles, it appears that this technique is designed for detecting CNVs. Since it is low pass (i.e. low coverage), it may not detect substitutions and small indels accurately.

Your cells may have mutations but not big chromosomal rearrangements. It is not necessary for tumour cells to have such chromosomal aberrations. In fact a simple overexpression of an oncogene or a point mutation causing reduced/loss of activity of a tumor supressor (for e.g. p53) is enough for tumorigenesis.


Can someone die from pain? I'm a CNA and I just got home from a very long day at work. I just started this job and I got hurt at work last night which made me wonder can enough pain cause death (without suicide)?

I think the answer is yes, but I'd like to know how/why.

Yes, you can go into shock from bleeding, emotional disturbance, a heart disorder, and/or a blood infection. It causes not enough oxygenated blood to get to important organs in your body and if it isn't treated it's normally fatal.

I would think that enough pain could cause a large emotional disturbance which could result in shock.