What is the mechanism by which lamins regulate gene expression? The heterochromatin is generally localized at the nuclear periphery (also near nuclear lamina), whereas active genes are preferentially found in the nuclear interior.

Children with Hutchinson-Gilford syndrome have a mutation in a LMNA gene, which codes lamin A and C, therefore, mutation in a LMNA gene causes overexpression of genes near nuclear lamina, this shows that nuclear lamina has something to do with gene expression regulation.

What is the mechanism by which lamins regulate gene expression?

So my answer was deleted because it "didn't answer your question."  Except that it did.  The article linked here, Gene expression, chromosome position and lamin A/C mutations, is an entire paper devoted to what we knew as of 2011 about lamins and gene expression, with references.  Your question was not a simple question, and article details how lamins are involved in gene expression.
I shall quote it here in order to "answer your question", and perhaps the moderators will see fit to not delete the post this time.  If said moderators think I should write a review of a review to facilitate your understanding, then I obviously have not understood the meaning for this board.
I don't have enough rep to leave a comment on anything other than my own answer, which seems to have been the appropriate way to link to the paper.  I figured an answer to your question would still be useful.
I would recommend reading the entire article as it is very useful in understanding additional indirect hypotheses for lamins controlling gene expression.

The Lamina as a Regulator of Gene Expression
In most cells, a dense heterochromatin network is visualized as electron dense material adjacent to the inner nuclear membrane and the nuclear lamina. The dense network is typically considered to reflect the association of transcriptionally inactive genes with the nuclear lamina. Specifically, this heterochromatin is thought to reflect a repressed gene state and suggests that the nuclear membrane and lamina may play an active role in gene repression.5 Lamin A/C and its binding partners can interact with DNA, histones, transcription factors and chromatin.6 Lamin-associated domains (LADs) are cis-acting sequences thought to range in size from ∼0.1–10 Mb, and these domains are thought to regulate the interaction of chromatin with the nuclear lamina; generally LADs are considered to be transcriptionally repressive.7 The precise sequences that define LADs have been elusive but nonetheless the LAD concept implies that the lamina and the genome interact in a specific manner. Therefore, it follows that one mechanism by which LMNA mutations may confer pathology is by altering the interaction between the lamina and chromatin. Consistent with this, LMNA mutant cells have altered chromosome territories.4 Meaburn and colleagues first examined chromosome localization in proliferating LMNA mutant fibroblasts and found that it resembled the chromosome organization associated with quiescent or senescent fibroblasts. They suggested that mutations in LMNA produced structural disruption to the lamina inducing a chromatin organization that may resemble an inappropriate cell cycle state. The presence of LADs and the fact that mutations in LMNA associate with altered nuclear architecture suggest that the nuclear lamina plays a vital role in both scaffolding chromatin and regulating chromatin organization. In this model, it is possible that distinct LMNA mutations may alter distinct regions of the genome leading to mutation specific profiles of altered gene expression.


The smell from eating asparagus I am wondering about one thing. I have read different accounts of this (prior to reading it on Wikipedia), so I am wondering.

Here are the two versions I have read:

asparagus leads in a certain percentage of people to a smell that has to do with a reaction of asparagusic acid. That is: not every human body creates the reactions leading to the "smelly" thiol (sulphuric) compounds.
asparagus leads to the processes of the aforementioned asparagusic acid in everybody but only a part of the population is able to smell those compounds.

Which one is true? Or is perhaps some other version I haven't heard about.

btw: The Wikipedia article on asparagus references both versions, too. So I am hoping for a definite answer with references to the respective scientific papers/studies.

Apparently, both are true.

  ...Individual differences exist in both odorant production and
  odor perception. The biological basis for the inability to produce the metabolite in detectable quantities is unknown, but the inability to smell the odor is associated with a single nucleotide polymorphism (rs4481887) within a 50-gene cluster of olfactory receptors. Pelchet et al. 2010

It's an open access paper (yay!), but to cut a long story short:

Pelchet et al. asked subjects to provide 'before-eating-asparagus'
and 'after-eating-asparagus' urine.
The subjects then acted as
urine-smellers for their own and others samples, and were asked to
choose between two unlabeled flasks which contained the 'before'
urine and which contained the 'asparagus' urine.
Most subjects produced 'asparagus' urine in which an odor was perceived
significantly more times than expected by chance, and
Most subjects perceived 'asparagus' urine correctly significantly more times than
expected by chance, however
~8% of subjects were non-producers, and
~6% of subjects were non-smellers.
Finally, looking at the actual amount of successes in perception: for
Caucasian subjects, one third of the variation in the amount of
correct odor perception was related to the A allele of rs4481887
(having AA or AG rather than GG). There was no connection between
this allele and production.

Pelchat, ML, C Bykowski, FF Duke, and DR Reed. 2010. Excretion and perception of a characteristic odor in urine after asparagus ingestion; A psychophysical and genetic study. Chemical Senses doi:10.1093/chemse/bjq081


Regarding the difference between cDNA library and RNA sequencing (Biochem. technique) I was wondering why establishment of cDNA library required the step of reverse transcription (i.e. turning the sequence into DNA) why not directly using the extracted RNA for sequencing and converting the U to T base? Why bother to have one more step? super super confusing

The construction of a cDNA library involves making a DNA 'copy' of the mRNA because the aim is to synthesise a large set of recombinant plasmid molecules, each containing a different cDNA and each propagated in E. coli.

The heyday of cDNA library construction predates the invention of PCR.

The key difference between the two approaches that you are comparing is that one (cDNA library) involves creation of a physical representation of the expressed genome whereas the other is an informational representation.


Explaining a branch with visibly different leaves on Citrus japonica My father was so kind as to send me a tree of Citrus japonica, aka Fortunella japonica aka kumquat (all names mean the same according to Wikipedia). Though I have seen this species many times, it is only now that I noticed two very distinct kinds of leaves.

One kind of leaves that I call  'double leaf' (second image) is only found on one single branch. The branch is still green down to where it merges with the tree, but many of the leaves are among the biggest on the tree. Excepting one sickly not fully formed leaf, all leaves on this branch seem to be of this 'double' type. I checked carefully.

All other leaves are of the kind shown in the first image.

This is the tree as a whole:

How can this different type of leaves on just one branch be understood? Does that branch belong to a different kind of Citrus (meaning grafting occurred), or is this a stage in leaf development? I don't think the latter, because I found small single leaves in the top branches of the tree. But I also don't think the former, because father said no such thing. If it is a mutation, why does it solely affect one branch?

I am a particularly ignorant amateur, but if you instruct me what to observe or photograph, I shall gladly do so.

Edit:

I thought I should supply a picture of where the unique branch emerges from the tree:

The tree bears fruit and at its thickest point is marginally thinner than my thumb.

Edit:

It just occurred to me that the entire upper kumquat might be grafted onto a different kind of citrus, which would explain such behaviour in the lower branch. I will search for evidence of this in the morning.

What you are seeing here is an example of a winged petiole. The petiole is the leaf stalk and these can have wings called stipules.

According to this source kumquat leaves have narrow petioles. I can't explain why you are seeing variation on a single plant, but I recall seeing similar variation on garden citrus in California, so I suspect it isn't unusual.


What animal / insect carcass is this? (Victoria, Australia) During a hike on a mountain in Victoria, Australia, I came across this unusual shedding in one of the small rainwater pools. The pool looks small, but was developed long enough to have several insect species thriving in it such as water fleas and others of which I'm unsure.

This was the only shedding found and no other large insects or animals were found in this pool.

This is a tadpole shrimp. The most common species here down under is Triops australiensis.

Here is an image of it:

Source: https://www.flickr.com/photos/euprepiosaur/23782620153

Here is some info from Western Australia Museum (I found nothing on Victoria Museum): http://museum.wa.gov.au/creature-feature-tadpole-shrimp

PS: This is not a duplicate of this question because the species here is clearly different.


Why do meristematic cells have prominent nuclei and dense cytoplasm? I've been reading about meristematic cells having prominent nuclei and dense cytoplasm. However, I could not understand why it is that way. Could somebody please explain?

Because meristamatic cells are the ones who are undergoing mitosis to increase the height of the plant, and diameter of the plant . They undergo continuous division. So y hey don't mature. They only form the primary cell wall.
I wrote another a answer.  Perhaps this will answer the question


Multicellular organisms as DNA banks Animal -> bacterial gene transfer seems easier than bacteria -> animal (rotifers are an interesting exception); there are bacteria live in close contact to us but our germ-line cells are protected. Given enough time, even free-living bacteria would start to pick up some of our genes (once the introns were lost).

Is this true? If so, do we see animal/plant genes gradually spreading into single cell organisms as time goes on (although "seeing" this would be difficult)? Is this effect "significant" for evolution in microbes?

This paper seems relevant. I just found it and don't have access, so I haven't read it. It does seem to suggest that there is evidence for eukaryotic genes being taken up by a prokaryote.

I would imagine this is rare, though. Eukaryotic cells don't tend to just spew their genetic material everywhere. Most death pathways involve breaking down any genetic material in the cell, I believe.


What kind of red and black insect is in the photo? I was wondering what kind of insect this was that I found on a flower on my deck this morning?

The insect was in my flower pot on my deck. I took the picture from my cell phone and zoomed in for a clearer shot. The body of the insect (not counting the antennae) was about an inch.

This is a nymph of some species of Hemiptera, or true bug.

Specifically, this appears to be the nymph stage of a wheel bug (Arilus cristatus) or some other species in the family Reduviidae.

 Source: David Larson

 Source: Debbie Roos 2005

Here is a picture of an adult (with name-sake dorsal wheel):

 Source: Donald W. Hall

You'll notice that the nymph is quite different looking:

  Nymphs have been described in detail by Readio (1927). Smaller nymphs are bright red with black marks. The last instar nymphs are darker. Nymphs lack the "wheel" or crest. For a diagnostic key to identify nymphs of the family Reduviidae to genus (including Arilus), see Fracker and Usinger (1949). [Source].

If you're truly interested in accurately  IDing to genus/species, you might check out Fracker & Usinger 1949$^1$, Herring & Ashlock 1971$^2$, or papers that cite their work.

You can find more information about A. cristatus here.

Citations:

Fracker S.B. & Usinger, R.L. 1949. The generic identification of Nearctic reduviid nymphs (Hemiptera). Annals of the Entomological Society of America 42: 273-278.
Herring, J.L. & Ashlock, P.D. 1971. A Key to the Nymphs of the Families of Hemiptera (Heteroptera) of America North of Mexico. Florida Entomologist 54: 207-212.


Is it one queen bee per hive or per colony? I've come across lots of information on the lifecycle of bees, but I cannot find the answer to my question.

If a beekeeper had, say 6 hives, would there be six queens (one per hive) or one (for the whole colony)? Maybe they would be considered six separate colonies, I'm not sure, but that would be a different question.

Every beehive contains one colony, and every colony has one queen. (Of course there are exceptions, like if a queen dies or is about to be replaced, but I don't think that's what you're asking.)

A swarm is a specific thing, when the queen and part of a colony has taken off from the original colony to form a new one.

I think Wikipedia works well if you need more information on beekeeping terminology:
https://en.wikipedia.org/wiki/Beehive

https://en.wikipedia.org/wiki/Swarming_(honey_bee)

Edit: To clarify, I only have experience of keeping European honey bees (Apis mellifera).


Has anyone tried Gibson Assembly Optimizations? Has anyone tried the chew back-anneal in vitro DNA assembly method (known as Gibson Assembly) for difficult sequences, like GC-rich sequences? How big constructs could you efficiently assemble? Did you use the original protocol or some optimizations?

I haven't tried Gibson Assembly myself, but I do know the Cambridge iGEM Team in 2010 and 2011 developed a web-based tool - Gibthon - for automatically generating primers for Gibson Assembly.

You could try running your difficult sequences through their tool to see what it suggests for primers.  It apparently gives you a "value for the Gibbs free energy of the worst case secondary structure of the primer."


Is this species a variant of a red flour beetle? Found this little guy crawling around the back garden - South Coast of the UK.

The closest things I could find online (with an admittedly weak knowledge of where to look up these things, aside a google search for red beetle) were the red flour beetles. However, it doesn't look quite like what we had, this being more stockier, with a dark head, and more splayed feelers.

This does not look like a red flour beetle, but more like some species of Melolontha, possibly a cockchafer. For more specific information, we would need to know, where your back garden is and maybe something to scale the bug. I would go for Melolontha melolontha, the common cockchafer.
Of the two other european species of Melolontha, M. hippocastani usually has a black edge of the elytra (see this picture), which this one doesn't seem to have, and M. pectoralis is very rare and mostly (only?) found in Germany.


Do voltage-gated calcium channels affect neuronal conduction speeds? We have a hypothesis that a drug may block the voltage-gated calcium channels (VGCC) in annelid worms. We are wondering whether there are any correlations between VGCCs and neuron conduction velocities.  If there are fluctuations in calcium ion contents, would there be any changes in conduction velocities? Or if the channel is blocked, would it block the entire action potential along the worm's giant axon?

Most of the time, calcium is not the most important ion in terms of active propagation of an action potential along an axon. It is usually sodium and potassium which play the key roles here. In most living things the concentrations of ions for the intracellular and extracellular solutions are similar. For an action potential, you usually have an influx of sodium followed by an efflux of potassium. The sodium influx depolarizes the membrane and the potassium efflux re-polarizes it. The speed of conduction is determined by the membrane resistance and its "leakage". That is to say, how easily can a single travel along an axon? This is determined by the diameter of the axon, the greater the diameter, the faster the conduction. The leakage refers to ease with which ions leak out of the axon as the signal is propagating. Insulation via myelin sheaths help in preventing this, and, less leakage, the greater the signal at the next propagation site.

Calcium is the most important ion for the transmission of a signal from a pre to post synaptic cell. Without calcium, you have no neurotransmitter release. This is because the influx of calcium triggers a series of events involving the snare complex which eventually leads to vesicular release of neurotransmitter in quantal units. If you remove calcium from the extracellular solution, you will have no neurotransmitter release. If you block the calcium channels, you will have no neurotransmitter release.


How are sequential patterns grouped into meaningful objects in the brain? The background how I came up with this question derives from information theory so I am not sure that it will formulate it well.

What I am looking for it is the process how our brain forms patterns.
Lets say I have word “Hello” (It is a complex example, but lets say that our brain is blank and sees it for the first time and somehow it can form only this pattern).

How our brain (neurons, synapse connections) “knows” that certain signals should be grouped and after “H” waits for “e” and “l” and so on.

Why it makes certain connection or just “cuts” and waits for new one.

As our brain is so complex, I am not looking for all scenarios how in could be influenced in terms of chemical neurotransmission, but I am looking for a basic principle of how it is done, i.e., how our brain manages to translate patterns into certain connections inside the brain.

The key here is the Gestalt principle formulated in the early 1900's consists of a set of 'laws' describing how perception elements are grouped into recognized objects. The Gestalt laws "prescribe for us what we are to recognize 'as one thing'". Recent data support this view (Pelli et al., 2009).

On a more fundamental level working memory is essential in this process. It is a form of short term memory. An example where short-term memory comes into play is when information is cut up in pieces, like in your example - 'Chunking' is the organization of material into shorter meaningful groups to make them more manageable.

Short-term memory is supported by transient patterns of neuronal communication in the regions of the frontal, prefrontal and parietal lobes of the brain. Long-term memories are maintained by more stable and permanent changes in neural connections widely spread throughout the brain.

The hippocampus temporarily stores information and gates it to the long-term memory. Typically, information is transferred from the short-term working memory to the long-term memory within just a few seconds,

Reference
- Pelli et al., Cogn Neuropsychol (2009); 26(1): 36-49


What, if any, is the difference between covalently closed circular DNA and plasmids? Are cccDNA (covalently closed circular DNA) and plasmids the same thing? What about DNA topoisomers?

As a descriptive term, we can take covalently closed, circular DNA (cccDNA) at face value: any DNA that is circular, with the ends joined by covalent bonds, can be described as cccDNA. Thus, plasmids are a type of cccDNA, but not all cccDNA are plasmids. Textbooks and lecturers describe plasmids as cccDNA for the purposes of DNA topology. This usage also appears in literature. cccDNA can also refer to circularized viral DNA, which is another type of episome. Note that the linked to papers are merely examples of how the term is used, not authoritative definitions.


What kind of bug is it? I really wonder what this is:

I find it near pound in Czech Republic (Central Europe). It's 2 inches long, AP. half wide. It was quite fast.

It is a Coleopteran insect (Beetle order) in the Ground beetle (Carabidae) family. Based on the elytra (protective wings) and the dark first antennal segment, it looks like Carabus granulatus. C. cancellatus is very similar, but has reddish first antennal segments. I don't think there are any other similar species in the Czech republic, but don't know the fauna there well. Overall, Carabus has many species and several are native to Eurasia and can be a size of 2 inches.

https://en.wikipedia.org/wiki/Beetle#Wings

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

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

https://www.insecte.org/forum/viewtopic.php?t=160369


Is it the case that all changes in phenotype during life are not inheritable? This came up in a talk with a friend. I wanted to clear this doubt. I've read about it before and did again after her remark (my thoughts didn't change: her concept is Lamarck's, not Darwin's), but wanted to clarify.

Regarding Evolution, nothing, absolutely nothing, that a person does to herself in life can be genetically inherited. It does not matter how much this person drinks, the changes they do to their body,  how dark their skin gets over life etc. Such changes can not be transmitted to their offspring in any way, correct?

*Summary:*Is the assertion "You can not change in life what will be genetically inherited in any possible way" true?

The assertion "You cannot change in life what will be genetically inherited in any possible way" is true, as you cannot (healthily) change the DNA in your germ cells.

However, the assertion "You cannot change in life what will be inherited in any possible way" is wrong, because of epigenetics. Parts of your DNA are marked (in different ways), and this can be inherited and have an effect. E.g. the only causal difference between these two mice is the diet of their mothers:

Image source and a further explanation: Nutrition and the epigenome.


Immune response to shock I am studying nursing and have a question regarding the physiological response to shock (decreased perfusion).  In lecture notes supplied by the lecturer, he indicates that there is a neural, hormonal and immune response to shock that is compensatory.

The neural component is the activation of the sympathetic nervous system, and hormonal response is through RAAS, etc.  This makes sense, as these mechanisms attempt to increase blood pressure and blood volume

I don't understand the immune response, though, which is described as the release of pro-inflammatory mediators, which lead to endothelial cell damage, making the vessels leaky, leading to oedema.  So how is the compensatory, it seems disruptive?  And why exactly would pro-inflammatory mediators be released in response to shock in the first place?

First: what is inflammation.  From wikipedia
https://en.wikipedia.org/wiki/Inflammation

  Acute inflammation is the initial response of the body to harmful
  stimuli and is achieved by the increased movement of plasma and
  leukocytes (especially granulocytes) from the blood into the injured
  tissues. A series of biochemical events propagates and matures the
  inflammatory response, involving the local vascular system, the immune
  system, and various cells within the injured tissue.

Second re shock: why does it happen?  If I go into shock from blood loss after a terrible knife juggling accident I will probably not have the inflammatory piece: I am dying from lack of blood and consequent low blood pressure.

What if I am in septic shock?  That means shock caused by organisms, usually bacteria, in the blood stream.  Bacteria are the ancient enemy and we have layers upon layer of defense accumulated over evolutionary time.  The reason we have them is that somehow, our ancestors that had them had some fitness advantage - probably because they survived having bacteria in the blood.

Some of the stuff that comes with that package does not seem very adaptive - like the leaky vessels and lungs filling up with fluid.  Maybe we see the wild extreme of this reaction but to a lesser degree (lesser infections?) those inflammatory responses are good?  Maybe releasing a storm of neutrophils has unavoidable side effects for the surroundings - like the Avengers fighting an alien army in NYC?  It was tough on NYC.  Maybe those extreme shock reactions save the organism 1 time in 10, which is better than the odds otherwise with an overwhelming bacterial infection.

Bottom line though is that bacteria in the blood in great numbers is an existential threat to the organism.  Desperate times call for desperate measures.


Are amino acids of viruses L or D enantiomers? I read a note saying that the amino acids of viruses are D enantiomers but I can't understand how that's possible since their human host can't even recognize that type.

Viral amino acids would almost exclusively be L-enantiomers considering they use host cell resources and machinery to build their proteins and the host cells are built on L-enantiomers.

With that said, you could always have nonstandard exceptions as xusr mentioned, if a virus somehow requires oxidase for example.


Negative Phototropism In Plants Why does the root of a plant go away from the sun? The shoot goes towards the sun, why does the root go away from it?

The roots respond to gravity, not to light.  They display what is called a geotropism (aka gravitropism).  It has nothing to do with the light..  The roots grow TOWARD the force of gravity so the roots exhibit positive geotropism.   The stem grows AWAY from the force of gravity so it exhibits negative geotropism.   Think about a tree planted on a hill.

Phototropism is a plant's response to light.  It has nothing to do with the direction of room growth.  The stem may lean toward the sun (because of it's positive phototropism) but will still grow upward because of its negative geotropism.

**If the light was below the plant, the roots would still grow downward.


Transmembrane Protein Problem Problem
A transmembrane protein has 1000 aa. The 5th aa is found on the external side of the cell membrane. It interacts with the aqueous environment outside the cell. Amino acid 90 is inside the membrane bilayer. Aa 100-600 are intracellular, and 200-400 make a tight ball with minimal exposure to the aqueous cytoplasm. Amino acid 979 is found on the extracellular side of the protein where it forms a weak ionic bond with Cl-.

a. Can you draw the protein and mark positions of all mentioned aa in it?

b. What are the properties of these amino acids?
￼￼￼￼￼

I dont necessarily want/need the exact answers to these questions, rather i would like some guidance in what principles i would need to understand and conceptualize to attack this problem. Thanks all !

I made a quick sketch on the basis of the information you gave (this is not to scale):

Aminoacid 5 (aa5) of the protein is on the outside, aa90 is inside the membrane. What we don't know here where the transmembrane part starts (directly with aa6 or later) and how it is organised (I indicated this as a transmembrane helix, but this can of course be different). Then we know that the border between the transmembrane part and the cytosolic part is somewhere between aa90 and aa100, that aa100 to aa200 seems to be some connecting part. The aa200 to aa400 is a globular domain which shields hydrophobic amino acids from the cytosol, so this part has to contain a high percentage of hydrophobic amino acids.

The part from 400 to 600 is again cytosolic but with no further information about the structure. After aa600 starts a second transmembrane part of the protein, but here we don't know how long it is. The maximum possibility would be until aa977, since we know the aa978 is outside of the membrane.


Why are microtubules absent in and around the nucleus? I was going through fluorescence microscopy and found these four images. The top left corner shows the actin cytoskeleton (rhodamin phalloidin) and the bottom left image shows the microtubule cytoskeleton (Alexa 488). One thing I noticed is that the actin cytoskeleton is continuous throughout the cell as seen in the top right image (rhodamin phalloidin + DAPI composite), but in case of the microtubules, the nuclear position and microtubule localization seem to be mutually exclusive. I can't seem to figure out why this might be the case, and it definitely does not look like a coincidence.

tl;dr Cells are 3D and the cytoskeleton does not exist within the nucleus.
There are several things you have to be aware of when looking at such pictures. Remember, you are looking at a 3D object which is not homogeneous and uniform in depth.
Shape of a plated HeLa cells
You are looking at HeLa cells. When plated like in your case, they adhere to the plate and make a generally thin, 2D-ish shape with lamellipodia (the extruded parts that look like they are grasping the plate on the sides of each cell). The nucleus is the most prominent vertically bulging part of the cell - the nucleus takes up most of the depth of the cell and there is little space around it. You have to appreciate the vertical dimension of the cell around the nucleus especially. The shape is a little like an egg cooked sunny side up; the yolk makes a bulge and the egg white is thinner around the yolk and there is little space for large filaments like microtubules. Remember, cytoskeletal filaments are so in size: small (actin) filaments < intermediate filaments < microtubules. This is exactly why you see more actin, a little less intermediate filaments, and even fewer microtubules exactly on top or below the nucleus in these 2D plated cells. Also, please remember that these cells are not representative of most cells.
The nucleus is a separate compartment
The nucleus is also a separate compartment, within which the actin and microtubule cytoskeleton system do not exist. The nucleus performs its own structure-keeping in the form of the nuclear lamina, which is composed of protein meshes that sit on the inner membrane of the nucleus.
You are not seeing the small actin filaments inside the nucleus, only around it. The microtubules are too large to see above and below the nucleus in most cases, since they are much larger filaments. In some cases though, you would see microtubules in HeLa cells above and below the nucleus.
See picture below: microtubule stain shown in green.

Other images for a more wholesome appreciation of the cytoskeleton.
Here follow a few micrographs of HeLa cells.
In green, actin.
In red, intermediate filaments stained with vimentin:

And now here you can see a microtubule stain in HeLa cells, in pink. Notice that some microtubules do actually make it around and across the nucleus.


Are drug-gene interactions predictable? I have been reading about drug-gene interactions and pharmacogenetic tests. I haven't been able to find many resources that define the process of testing for possible drug-gene interactions without performing trial and error method. For example, drug-drug interactions can be predicted by using several parameters as noted here. Are there any parameters similar to the ones described in given paper for predicting drug-gene interactions if drug characteristics and genetic data is available? Please describe process or provide source.

One can list candidate genes based on their functions.

If a drug acts by inhibiting the expression of gene G in order to reduce process P, then, gene G, all its regulatory elements and all sequences involve in process P are good candidates for such interaction and should be investigated. If there is known genetic variation in the population at these loci and if we know this genetic variation affect phenotypic variance, then definitely, those are good candidates.

However, to my knowledge, this is the extend at which we are able to go. We can list candidates but it does not mean in the absolute that a candidate must present an interaction with the drug of interest and it does not mean that a non candidate gene would necessarily not have an interaction. Only a statistical testing for such interaction would allow one to solve the mystery.


Spironolactone's role with adrenergic agents in heart failure? I am studying the treatment plan of adrenergic agents for heart failure.
Then, in the group discussion, spironolactone was included.
But I cannot understand how it is relevant when considering adrenergic agents for treatment of heart failure.
It is probably that it was only mentioned because adrenergic agents are usually used in combination with ABC therapy (antiplatelet, beta blockers, ...).
This includes also diuretics.

Spironolactone is diuretic and antihypertensive.
But I cannot understand how one can classify it adrenergic.

What is the role of spironolactone with adrenergic agents in heart failure?

Spironolactone works through a mechanism different than the adrenergics.

You said of the ABC approach, "This includes also diuretics." That's why Spironolactone was included.

Spironolactone is a specific pharmacologic antagonist of aldosterone, acting primarily through competitive binding of receptors at the aldosterone-dependent sodium-potassium exchange site in the distal convoluted renal tubule. Spironolactone causes increased amounts of sodium and water to be excreted, while potassium is retained. Spironolactone acts both as a diuretic and as an antihypertensive drug by this mechanism. It may be given alone or with other diuretic agents which act more proximally in the renal tubule. Aldosterone interacts with a cytoplasmic mineralocorticoid receptor to enhance the expression of the Na+, K+-ATPase and the Na+ channel involved in a Na+ K+ transport in the distal tubule . Spironolactone bind to this mineralcorticoid receptor, blocking the actions of aldosterone on gene expression. Aldosterone is a hormone; its primary function is to retain sodium and excrete potassium in the kidneys.

  The lack of a decrease in the neuroendocrine prognostic markers, norepinephrine and endothelin-1, suggests that the beneficial effects of spironolactone are mainly related to mechanisms independent of the adrenergic and endothelin systems. The escape of AII and aldosterone, probably reflecting activated feedback mechanisms, confirms the specific activity of spironolactone on the renin-angiotensin-aldosterone system and supports the hypothesis that the beneficial effects of spironolactone on the progression of heart failure are mediated by the blockade of aldosterone receptors.

PubChem
Beneficial neurohormonal profile of spironolactone in severe congestive heart failure: Results from the RALES neurohormonal substudy


Can the colour of skin change with age Can the colour of skin change with age? Can a dark skinned person become fair or vice versa?  Can Melanocyte production vary?

Vitiligo is a loss of skin pigmentation that causes patches of lighter skin as the immune system attacks melanocytes. It can eventually progress to cover the entire body.

Edit:

Ongenae, K., Van Geel, N. and Naeyaert, J.-M. (2003), Evidence for an Autoimmune Pathogenesis of Vitiligo. Pigment Cell Research, 16: 90–100. doi: 10.1034/j.1600-0749.2003.00023.x


Is there a relationship between efficiency of cellular metabolism and warm-blooded-ness? My BIO 101 book states that when human cells convert glucose to ATP, the process is only approx 35% efficient, and much of the potential energy is lost as heat.  However, that heat is useful to us in maintaining our overall body temperature.

Cold-blooded animals (reptiles, for example) are not as effective at maintaining their own body temperature.  Does that imply that their cellular metabolism (conversion of glucose to ATP) is more efficient than humans, and thus doesn't produce as much heat?

Or is cold-blooded- / warm-blooded-ness completely unrelated to heat released during cellular metabolism?

While heat is lost during glycolysis, a lot more heat can be lost during chemiosmosis.  This is the movement of H+ (protons) across the inner mitochondrial membrane.  The energy potential of having a greater concentration of H+ on one side of the membrane usually powers ATP synthesis through ATP synthase.  In mammals, however, special proteins called uncoupling proteins (UCPs) can make the membrane 'leaky' to H+, so the energy is lost as heat, instead of being used to make ATP.  This is called non-shivering thermogenesis, and usually happens in brown adipose tissue (because fatty acids are used to enable UCP production).

It is not that glycolysis in ectotherms is less efficient (as far as I'm aware), but that ectotherms have different levels of different types of UCPs. Some UCP genes may have their expression altered in response to colder conditions (e.g. UCP2 and 3 may be upregulated) or the genes may not be present at all (e.g. UCP1 is not present in birds and crocodiles).

A better summary of UCPs in reptiles etc. can be found in this abstract:

http://rspb.royalsocietypublishing.org/content/275/1637/979.long


What is the standard method for measuring soil and substrate acidity Soils and other plant substrates differ a lot in their moisture content. In dry matter a pH is not measurable without adding water, but this has the problem of the resulting value not being independent of the amount of water added. In controlled conditions pKa measurements would be used instead as they are independent of the amount of water, but would this would require information about chemical composition that is generally unobtainable.

What is the standard way of reporting acidity of soils? I would think that there is probably some kind of measurement based on mass or volume. Or, perhaps the log scale renders the amount of water negligible for most purposes?

Soil should first be processed by drying the soil to ensure a standard "dry" sample is analyzed. 55$^o$C in drying ovens for 24 hours works for most non-water-zone soils, but more time at 50 - 55 $^o$C (as long as it's consistent between samples) can be used to dry out wetter samples. One can then put the soil through sieves to remove rocks and other debris (2mm sieve is common).
To actually measure soil pH, one combines 1 part soil with 1 part water and then measure with an electrode (McLean 1982)$^1$.
By always using 1 part soil to 1 part water, you maintain a consistent relative amount of water per sample and therefore can account for different sample sizes.
The final value is reported as pH.
You can find the McLean (1982) resource here for $15 or likely for free from a nearby university library. The paper has been cited over 2800 times.
[1] McLean, E.O. 1982. Soil pH and lime requirement. In A.L. Page et al. (ed.) Methods of soil analysis, part 2. Agronomy Monogr. 9, 2nd ed. ASA and SSSA pp 199–223.
EDIT:
As @Roland pointed out in the comments, other standards do exist.
For example, the International Organization for Standardization (ISO) maintains reports describing  standard protocols for different methods (which therefore are sometimes used):

ISO 10390:2005 specifies an instrumental method for the routine determination of pH using a glass electrode in a 1:5 (volume fraction) suspension of soil in water (pH in H2O), in 1 mol/l potassium chloride solution (pH in KCl) or in 0,01 mol/l calcium chloride solution (pH in CaCl2).
ISO 10390:2005 is applicable to all types of air-dried soil samples, for example pretreated in accordance with ISO 11464.

The USDA describes several standard protocols used by their laboratory at the National Soil Survey Center to measure soil pH (Hydrogen-Ion Activity) in their Soil Survey Laboratory Methods Manual (version 5, 2014). See specifically, pages 265-281 for various soil suspension and soil extract methods.

Note: They cite repeatedly the McLean (1982) paper as a  source for determining pH using an electrode.

They also provide further notes in this technical note.

The EPA (US Environmental Protection Agency) similarly has a protocol that they use. Their electrometric approach using a digital pH meter involves the insertion of a glass electrode into a soil suspension made by mixing the soil 1:1 with a reagent solution (see referenced notes below).

EPA protocol for soil pH (Method 9045D): Revision 4 (2004) available here

References "Chapter One" of technical note SW846 (I link to Update V revision 2, July 2014), which relates back to 2-2 of EPA-600/4-79-019

Again, the overall takeaways are:

Reporting soil acidity as pH is standard
There are multiple standard methods to measure the pH; Just be sure to properly cite your approach!


Goodness of fit: How to decide which ratio to deal with? While solving problems of Goodness of fit, I'm faced with an issue, how to decide which ratio to consider to find the test statistic from given set of observations.

E.g. 1

  A supplied sample contains four types of seeds and the total number is 64. The types of seeds are large red 42, large white 8, small red 10 and small white 4. Calculate goodness of fit.

Problem: As df=3, Ratio= 9:3:3:1 / 1:1:1:1?

E.g.2

  You are supplied with two different varieties of plant samples;tall-76 and short-24. Determine the observed number, apply Chi square test to state whether it is in agreement with expected ratio.

Problem:  As df=1, Ratio= 3:1 /1:1?

I was vaguely told by my propessor that which ever ratio seems to apply(by logical guess) we should choose that one to determine the expected values and thus the statistic.

I couldn't find any good read in this regard, except those that are full of mistakes. I've been reading Statistics blogs to understand the concepts but they don't cover these typical biological problems and those that did had the ratios mentioned.

I've another question in mind, from experimental result it is also likely that we won't get one of the four types of seeds (given that mating is random and the progenies appeared by dihybrid crosses) so determining the actual ratio behind becomes more difficult as df = 2  =/= 3!

To solve this question you need to have a basic understanding of Mendelian genetics. Contrary to peoples' comments, this problem does provide enough information.

Genes are inherited from two parents. That is, the offspring will inherit one allele from each parent. Genes also interact with each other in a dominant/recessive nature. A dominant trait will be expressed, no matter what if this is carried by an organism. A recessive trait will only be expressed if the organism is carrying two copies of the same allele - the organism must receive the recessive gene from both parents.

In the first question, there are four genes. One gene encoding large seeds. One gene encoding small seeds. On gene encoding red seeds. One gene encoding white seeds.

The dominant genes are those that code for: large & red
The recessive genes are those that code for: small & white

For this question, you assume that both parents are carrying a single copy of each gene. This means, each parent has one copy of a gene coding for large seeds, one copy of a gene coding for small seeds, one copy of a gene coding for red seeds, and one copy of a gene coding for white seeds.

As a side note, this would mean that each parent came from a large red seed. There is also a chance for any of the four genes to be passed to the offspring.

Each parent could pass the genes for: Large red seeds, Large white seeds, small red seeds or small white seeds.

This means that the following gene-combinations are possible:

-large red, large red

-large red, large white

-large red, small red

-large red, small white

-large white, large red

-large white, large white

...etc...

And, I'm sorry, I've been trying for twenty minutes to upload a picture to show you what I mean. But, you can do this yourself also to see what I mean:

Draw a 4x4 grid, and in each box fill in each possible combination of genes that can be inherited by an offspring. They call this a Punnett square, and it is used to predict the phenotype of an offspring bred by two parents. If you search Punett square you will understand how this works.

But the thing to remember is this: If the offspring carries one copy of a dominate gene (large seed, red seed) then these phenotypes will be expressed. In order for a recessive trait to be expressed, the offspring must carry two copies of the genes (small seed, white seed), ie. it must have received the same recesssive allele from both parents.

Now, to solve the problem statistically, you will use the ratio 9:3:3:1. The null hypothesis is that there is no difference between the observation and this ratio. The alternative hypothesis is that there is a statistically significant difference observed from the sample in comparison to the test-ratio.

This means, a p-value < 0.05 indicates that the 9:3:3:1 ratio is false. And the gene-interaction must be explained by another means - not by Mendelian inheritance. Or, I suppose it could also indicate that the parents did not in fact carry one copy of each allele and some other combination, that maybe you need to find. Eg. One parent could have had two copies of each recessive trait, while the other parent could have had in had one copy of each trait. (Play with the Punnett square, and maybe you can figure out if this is true)


Which organs in the body are responsible for measuring temperature? As an instrumentation engineer, I have designed temperature control systems
capable of measuring and controlling temperature with a precision of 0.001K over a
wide temperature range.  I have always wondered how the human body maintains its
temperature within a fraction of a degree; specifically, where and how is the
temperature measurement done?

Human thermo detection comes from a protein, expressed in high levels in the nervous system.
As per comments, there are a group of transmembrane proteins called transient receptor potential cation channel subfamily V (TRPV) ion channels that can detect temperature changes. Although the exact mechanism of the protein remains unclear, a study published in Nature 2010 showed that a protein called TRPV1 opens and closes to allow increased or decreased sensitivity to temperature change.
There is no specific organ that is responsible for temperature detection, however TRPV1 is expressed in high levels in the nervous system.


Correlations between tool use and evolution We humans would be nearly defenseless against large predators without weapons. Even small mammals can outrun humans. Our canines have degenerated to the point where they're almost useless as weapons. A young chimpanzee is far stronger than a human.

So how could our ancestors have survived before the invention of tools and weapons?

Apparently, our species didn't necessarily invent these things at all. As I understand it, more ancient hominids were using tools and weapons even before our species evolved. I would therefore assume that we essentially inherited tools and weapons from the species we evolved from.

At any rate, we are incredibly weak and defenseless compared to chimpanzees and other apes. One might speculate that big canines and physical strength became more irrelevant as our ancestors began to rely on artificial weapons for protection.

Are you aware of any research that supports this? Do our ancestors exhibit a trend towards smaller canines or a decrease in physical strength?

This is a very confusing question! You have many sentences that end in question marks but then you answer them yourself, ending with a final question mark which is basically "are there references that show I'm right" but which is phrased in a way that makes the answer rather trivial (yes, of course our ancestors show a decrease in canine size, I'm not sure how else you would expect to get from there to here. Strength is harder to measure in fossils I think).

I'll address a few points. First I think this question makes humans to be much more hapless and vulnerable than we are:

  We humans would be nearly defenseless against large predators without weapons.

Humans are large predators. It's a nitpick because your other points about the relative strength of great apes and how we use weapons are correct, but I think it's relevant to the "oh us poor squishy defenseless humans" trope. We tend to think of our size as normal but we're actually among the biggest animals.

  Even small mammals can outrun humans.

Not for long they can't. One hypothesis that seems to have some credence in the field of human evolution today is the Endurance running hypothesis, which points out that almost no other animal shares our capacity to run for a very long time and that hunting stragegies based on this may have been a significant aspect of our evolution, that would explain many aspects of our physiology.

Of course this kind of hunting would likely involve weapons, but as you point out humans and proto-humans have been using tools for a long time.

You seem to have an image of weak proto-humans inventing weapons to turn the tables on the large predators that would eat them, but how would they have survived before? I had a similar one about hairlessness and clothes; probably we tend to think of human bodies as immutable human attributes, and all our tools as optional. When the truth, as you said yourself, is that humans as a species aren't separable from our tools and intelligence; our bodies, minds and behaviors all co-evolved. There never was a weak, naked human with no tools; before tools our ancestors weren't weak or naked and with tools of course we are neither. Also, intelligence and social behavior count for a lot; a single human might be vulnerable to a large predator where a coordinated band of hominids, probably armed with sticks and stones and some understanding of how to use them, would be another story.

But you want actual references and evidence, which is harder. I linked to the Wikipedia page on the evolution of canine size but strength isn't so easily measured in the fossil record. I think this paper might be the closest thing:

Body mass and encephalization in Pleistocene Homo

Relevant quote from the abstract:

  On the basis of an analysis of 163 individuals, body mass in Pleistocene Homo averaged significantly (about 10%) larger than a representative sample of living humans.

That's assuming body mass is a good proxy for strength, which isn't clear to me.

The following paper confirms that humans are indeed weaker than other apes and that the genes related to skeletal musculature have changed a lot since our common ancestor with them but doesn't give a timeline:

Exceptional Evolutionary Divergence of Human Muscle and Brain Metabolomes Parallels Human Cognitive and Physical Uniqueness

That paper goes with the hypothesis that loss of strength was caused by diverting resources to our brains, but other papers suggest there could be a trade-off between strength and fine motor control, like here:

The strength of great apes and the speed of humans

  More than 50 years ago, Maynard Smith and Savage (1956) showed that the musculoskeletal systems of mammals can be adapted for strength at one extreme and speed at the other but not both. Great apes are adapted for strength--chimpanzees have been shown to be about four times as strong as fit young humans when normalized for body size. The corresponding speed that human limb systems gain at the expense of power is critical for effective human activities such as running, throwing, and manipulation, including tool making. The fossil record can shed light on when the change from power to speed occurred. I outline a hypothesis that suggests that the difference in muscular performance between the two species is caused by chimpanzees having many fewer small motor units than humans, which leads them, in turn, to contract more muscle fibers earlier in any particular task.

(note that this paper mostly seems to be proposing a hypothesis and not demonstrating it, and it isn't very cited... but a lot of the papers citing it look interesting. Including this entry in the "could pre-humans hunt with weapons" column:

Clavicle length, throwing performance and the reconstruction of the Homo erectus shoulder

  These data (...) suggest that the capacity for high speed throwing dates back nearly two million years.

)

I think the question of how human strength evolved in their evolutionary history is probably very answerable with modern genetics, I've been looking for papers along the line of this one, which is about jaw muscles not upper-body strength:

Myosin gene mutation correlates with anatomical changes in the human lineage

  Using the coding sequence for the myosin rod domains as a molecular clock, we estimate that this mutation appeared approximately 2.4 million years ago, predating the appearance of modern human body size and emigration of Homo from Africa.

but I haven't found any; it's possible this specific question just hasn't been answered yet.


Which living organisms have antibodies? I'm wondering if only humans, or only mammals have antibodies and immune system. Obviously humans and dogs have (we vaccinate both) and in my head makes sense since we're so genetically similar to all mammals that we all have antibodies. Do all synapsids, or even amniotes have antibodies as part of their immune system? Do plants have antibodies or insects?

Apparently, cartilagenous fishes are the oldest extant clade that have the true immunoglobulins (antibodies) and the T-cell receptor (Schluter et al., 1997). All extant gnathostomes, incuding cartilagenous fishes, produce antibodies.

However other animals (invertebrates) and even plants have proteins that belong to the immunoglobulin superfamily (to which the classical immunoglobulins/antibodies also belong). Members of this superfamily are structurally related; they are not necessarily involved in immune responses. Hemolin is one immunoglobulin superfamily protein in insects, that is involved in immune function, but not exactly like vertebrate antibodies.


How many dinosaur genes are in a chicken genome? I read recently that we can "work back" to a dinosaur by selectively turning off certain genes in chickens, and we were able to create a chicken with a snout instead of a beak.

How many dinosaur genes are still hanging around in a chicken genome? I understand there is a lot of overlap for vertebrates, but shouldn't these genes have shuffled out over time?

Otherwise, couldn't we work back to worm or even earlier life forms? Is the whole history of a creature's evolution contained in its genome?

Edit This was a news story about a month ago. Here's excerpts from the BBC's write-up: "Chicken grows face of dinosaur: A chicken embryo with a dinosaur-like snout instead of a beak has been developed by scientists"

  To understand how one changed into another, a team has been tampering
  with the molecular processes that make up a beak in chickens.

  By doing so, they have managed to create a chicken embryo with a
  dinosaur-like snout and palate, similar to that of small feathered
  dinosaurs like Velociraptor. The results are published in the journal
  Evolution.

Link to Evolution paper included.

Also this piece from about a year ago: "Paleontologist Jack Horner is hard at work trying to turn a chicken into a dinosaur"

  In 2009, the world’s most famous paleontologist made a bold claim. In
  “How to Build a Dinosaur,” Jack Horner proposed re-creating a small
  dinosaur by reactivating ancient DNA found in its descendants,
  chickens.

  The toothy snout is already here. At his lab at Harvard Medical
  School, Matthew Harris has made chicken embryos that express ancient
  genes for the growth of conical, crocodile-like teeth.

Be careful when reading media as they tend to exaggerate. That Abzhanov paper is interesting; it will be better when it's published and the figures released. He does a lot of evo-devo work surrounding beak development. What they did in this paper was to inhibit in chick embryos two signalling pathways (which are actually conserved amongst all animals, not just birds and reptiles) so that their expression domain more closely matched that of extant reptiles (which lack medial activation, as opposed birds). They found that doing so results in premaxillary and palatine bones which resemble ancestral archosaurs. While incredibly interesting, this is a far cry from creating living chickens with dinosaur snouts.

To somewhat answer your question, chickens do not contain all of the genes that dinosaurs once had. They will have both gained and lost information. There will be much conservation in the same way that there is conservation between all organisms. For example, the Wnt pathway studied in this paper is conserved across all animals, from chickens to humans to placazoans to, presumably, dinosaurs. It's impossible to say how much has changed since we do not have any whole dinosaur genomes, but it's also important to note that it's not only which genes an organism has but also when and where they are expressed and how they interact.


Is the problem of cryonics only the pressure? According to the pop-sci sources which I drew on from, the only problem with freezing whole bodies its that you can't conserve it without freeze-damage.

If you were keeping a cold-blooded animal in a cold surrounding (well, before that removed the parasites somehow) and optimized the pressure in there so to make the cells not to collapse, could you stop all its functions and bring it back to life again later?

The major problem in cryonics is that when an organism is frozen, all of the organism starts freezing. The cell start expanding since ice expands too. The sharp edges of the ice crystals can destroy a lot. Also, your blood would freeze. Again, the sharp edges of the ice crystals would destroy major blood vessels. That is why currently, they have to insert antifreeze into the blood, but it still might not be effective.

Now, to answer your question, many cold-blooded organisms can survive freezing cold temperatures. Some frogs (like the wood frog), for example, have anti-freeze in their blood vessels! So some actually have special adaptations to survive freezing cold temperatures.

I hope this answered your question. Please ask in the comments if you want more information on this. I will gladly research up for you.


Can emulsion test be used to detect phospholipids? The emulsion test- causes a white cloudy colour when lipid is dissolved in ethanol and then water added.
Can this be used for phospholipids? I am aware that they are polar so may arrange in a circular formation in water but would the test still work?

Thanks

Yes, the test will still work. And you are correct about the phospholipid's process of forming 'circles' in water. The reason the test still works is because alcohol increases the permeability of the edge of these circles by making them less structurally stable. This then allows the ethanol to enter.

The hydrophilic phosphate head is not soluble in alcohol as it is not a lipid, but after the alcohol can bypass these heads, they can interact with the inner hydrophobic 'tails', which are soluble. The white emulsion/layer will then form.

This can be seen in the experiment of using alcohols to test the permeability of cell membranes. -See this investigation carried out by Westminster College.


Why isn't the DNA in bacteria always split up and replicating? Isn't helicase always free floating in bacterial cells, and the DNA without a nuclear membrane and uncoiled and freefloating and so why doesn't the helicase keep breaking the double helix of DNA? Also, since other DNA synthesizing enzymes like polymerase and RNA primer and other replication enzymes also free floating, so why doesn't the DNA in bacterial cells keep replicating at all times?

Bacterial DNA replication is initiated at the oriC by DnaA in E. coli. Think about ways in which DnaA binding or activity can be regulated in a way that inhibits or permits DNA replication. In recently replicated bacterial DNA, the DNA is hemimethylated (parental strand has a methyl group, daughter strand doesn't): An inhibiting protein binds to hemimethylated DNA, that can block DnaA activity at the oriC. A DAM methylase adds methyl groups after a while to the newly synthesized DNA, in which case DnaA may bind. Due to the lag between replication and methylation, DNA replication can't be continuously initiated! This is one of many examples (for example, DnaA must bind ATP for it's mechanism of action), but the take home point is DNA replication must be initiated and if it can't be, then it doesn't take place!

THE INITIATION OF BACTERIAL DNA REPLICATION

Breaking that down: (note, this is in E. coli)

DnaA is a protein with DNA-binding activity. When many DnaA bind at the oriC, it causes the DNA to bend open and loop. At this point, DnaB would have access to the DNA, and this is the helicase that unwinds everything for replication (you'll also see that DnaB must be loaded onto the DNA by DnaC, a helicase loader). So blunty enough, oriC is an origin of replication, everything starts here. There are repeats of AT rich regions denoted 13mer and 9mer in the oriC (number of bases in the region if you will). We know that this is beneficial because AT rich regions are easiest to pull apart due to the number of hydrogen bonds between A and T.

In the example I provided, the assumption is that the DNA of E. coli is methylated on adenines on both strands. When replication occurs, the new DNA doesn't have this methyl group on it's adenines like the parental strand. A protein that recognizes and binds so-called hemimethylated (half methylated) DNA, SeqA, binds where it can, including in the oriC. It blocks DnaA subsequently for a short time, and falls off the DNA on its own. The DAM methylase adds the methyl groups when it can, and once it does the SeqA can no longer bind, but the replication-initiation complex thus can.

There are other modulators of DNA replication, and the concentration of the DnaA itself is a big factor because you need many units of DnaA to bind to facilitate initiation. So then you have to consider is DnaA being expressed strongly enough? And this has it's own pathway outside the scope of this question.


Antigen molecular mimicry Let us consider a situation in which the body is attacked by a microbe, and  the microbe is captured by the immune system for recognition of surface antigens.
The surface antigen recognized mimics one of our self antigens.
It is stated in textbooks that this situation results in the immune system attacking  the microbe along with the tissue containing the self antigen(auto-immunity).
(Reference: Robbins and Cotran pathologic basis of disease)

If a microbial antigen mimicks self antigen, why is the microbial antigen attacked instead of being ignored in the way that all our self antigens are ignored by our immune system?

There are different type of immune cells which falls under either innate or adaptive system.

The cells under the innate are first to respond microbial attack and are able to detect them in extracellular environment by recognizing proteins/peptides called Pathogen-associated Molecular Patterns (PAMPs) on their surfaces; these are only found on microbes.

But when the innate system fails to clear the microbes in time, the adaptive  system is kicked-in. This involves T-lymphocytes and B-lymphocytes. T-lymphocytes are trained to ignore cells that are able demonstrated that they self but B-lymphocytes which produces antibodies/immunoglobulins to the detected antigens do not have a mechanism of ignoring self cells.

So the problem lies with when the immune response gets to the point where antibodies are produced, at that point produced antibodies simply attack without discrimination.

I hope this simplified version would help you.


What is a cortical circuit? I have read about cortical circuits in the context of connectomics (e.g. any example here) and computational neuroscience (e.g. any example here), but a simple Google/Wikipedia does search not show an exact definition.

What exactly is a cortical circuit?

The term "cortical circuit" refers to the generalization that the neocortex is a uniform structure. For the most part, the outer sheet of the brain (the neocortex) is the same structure of neurons all the way around the brain.  It consists of the canonical six layers and it generally looks something like this.  Different research will emphasize different aspects of the circuit.

Anyway, it's quite an interesting evolutionary step for mammals.  The neocortex.. or "associative cortex" as it's sometimes called... is a very dexterous structure.  Someone born without sight will still make use of their occipital lobe to process nonvisual sensations.

Of course, as a I qualified above, it's not strictly true that the neocortex is uniform all the way around; there are exceptions.


Did bilateral symmetry evolved just once? If I understood correctly, all bilaterians come from a single organism (the Urbilaterian) that showed this type of body plan for the first time at the end of the Ediacaran.

Does that mean that bilateral symmetry evolved just once in the entire history of life? Is it correct to say then that bilateral symmetry is not a feature of convergent evolution? That this is indeed a thing that evolution explored just that time in history and never again?

A lack of strong evidence causes the field to be mostly hypothetical. Detailed pre-cambrian fossils are necessary, from the 1bn-600 million years ago, to find a protostome - deuterostome ancestor.

Genetic data is also inconclusive. A search for bilateral common ancestor gives i.e. dev.biologists.org/content/129/13/3021 It's a summary of research, where the accepted view is that there is a common ancestor to all known bilateral organisms.

All the baliteria are classed in the common clade which have a similar cell attributes and physiology, they all have hearts whereas starfish and jellyfish don't, there are various genes that suggest common ancestry. There is currently no evidence of bilateral from parallel evolution, although it's very possible or probable that there were some previously and perhaps even today, i.e. tardigrades don't have hearts, so perhaps some species one day will be found to be convergeant species, although they are thought to be miniaturized lobopodia.

Sea cucumbers and sea anenomes both have a bilateral juvenile stage, so they have perhaps evolved from bilateral ancestors.
researchgate.net/profile/Taha_Soliman4/publication/262415405/…

A new fossil of a bilateral animal has been found from 550mn years ago: phys.org/news/2020-03-ancestor-animals-australian-fossils.html squids are starfish with mollusks on them, there are hybrid symmetries.


Under what category should myosin come? Are myosin microfilaments or intermediate filaments? Or are they simply motor proteins? Under which category should I put them? I am highly confused.

Myosin are motor proteins. Microfilaments (AKA actin filaments) are the tracks for Myosin. Filaments of different sizes are the structural components of cells, giving them their shape, rigidity, etc., as well as providing an intracellular network for transport. Myosin walk along these filaments.

In myocytes (muscle cells), myosin pulls actin filaments towards one another.

Picture from here: https://www.ncbi.nlm.nih.gov/books/NBK9961/


How do I prepare and clone from E. coli DNA? I'm looking for a protocol to get genomic DNA from an E. coli sample so that I can clone a small portion of it using PCR into a plasmid.  (< 500 bp in this case).

It seems OWW (Open Wet Ware) only discusses preparation of fragmented DNA. Does this mean I have to cut it up before I can clone from it?  Any pointers would be really appreciated.

Yes, you must fragment the genome in order to insert it into a vector for cloning; you can't "insert" the whole 5 Mbp genome of E. coli into a vector.  It's difficult to transform cells with huge plasmids, 2-20 kbp is an optimal range.  In any case, if you want a clone of the whole genome, wait 30 minutes and the cell will happily oblige you.

Most procedures that isolate genomic DNA will fragment it in the first place, as it is much too large and fragile to stay together, and if it did it, the majority would be caught up in other cell debris and discarded.  Vortexing with glass beads is a typical first step to randomly fragment it.  After this, you can digest the DNA and your vector to place matching ends on it, ligate it, and transform host cells.

If you want a targeted approach (to extract a specific gene, a technique with which I am unfamiliar), you may be able to use PCR on your extracted, fragmented DNA, as there would hopefully be one intact segment spanning what you want.


Predators on the Galapagos I understand that in many isolated islands, such as the Galapagos, there are no large predators. I find this observation interesting because it has been suggested that the lack of predators unleashes the evolution of new and bizarre species.

However, as new species evolved there (and increase their size, with respect their ancestors), why no small predator species evolved into a large predator species? Or can new predators evolve from herbivorous animals?

This may be a difficult question, because we may not  know the natural history in such great details. More specifically, I wonder if, in general, there is some pressure against the selection of predators or if there are counter examples which show that small isolated islands evolved their own apex predator.

Larger predators need a large range on which to find potential prey. An island might be bigger than the normal range of a predator, but too small to support a large enough breeding population (because of inbreeding, and because a brief lack of food, disease, or other insult could wipe out the entire population, rather than just a few individuals).


The human organism knows what we have to eat? My mother has told that if your organism needs a vitamin, you want fruits include that vitamin. For example you have lack of C-vitamin you would like to eat lemon. Is there any explanation for it, or just it is a myth? The human organism knows that what we have to eat?

Assuming you mean organism, not organisation, it's not entirely false that cravings can be driven by deficiencies. In the case of the eating disorder pica, where a person eats non-food items like dirt and clay, can be caused by iron deficiency (Source). However, that article also suggests the possibility that pica causes iron deficiency by causing the person to eat items that lower iron absorption. So, my answer to your question is, maybe.


What does the term "recruitment of T-cell" mean? With respect to the article, what does the term "recruitment of T-cell" mean? Who recruits T- cell? Does recruiting T-cell mean the T-cells get a sense of directionality to get activated by the APC's?

If I'm interpreting it properly, it's the adaptive response that's recruiting the T cell, evidenced by the last line in their abstract:

"Therefore, the contribution of a T cell clone to the immune response is mostly determined by the time of its entry into the immune repertoire, i.e., the time of first cell division after antigen encounter."

It's strange because when i think of recruiting a T cell it's always to the tissue or site of infection or what have you.


How do penicillin resistant bacteria grow slower in the presence of penicillin? We put 2 flasks inoculated with Bacillus cereus in 37⁰C: one with 100μg/ml penicillin +  50μg/ml chloramphenicol and the other without penicillin. We found that the OD is higher in the one without the penicillin. These strains are supposedly penicillin resistant as verified by growing them in a test-tube containing penicillin (5mg/ml) at 30⁰C. It contradicts my hypothesis that they should have the same growth rate because of the $\beta$-lactamase secretion that would destroy the penicillin. I can't find any explanation in the web.
help me

Your hypothesis is incorrect.

You must be assuming that lactamase destroys the antibiotic with perfect efficiency. This is incorrect.

You must be assuming that the population will remain genetically stable. This is doubly incorrect. Firstly the penicillin will select highly resistant bacteria which suffer a greater fitness burden from expressing the lactamase. Second, in absence of penicillin, spontaneously arising mutants which suppress the lactamase are free to proliferate.

You must be assuming that carrying capacity is identical for Pen+ and Pen- media. Trivially, you claim your experiment disproves this, but the assumption is also baseless since this need not be the case.

Furthermore, your results are inconclusive. You lack crucial controls, such as putting the bacteria from the Pen+ into Pen- and vice versa to see if the growth difference is intrinsic. You have not only failed to provide the error of your measurements, but have failed to provide the quantitative measurements themselves, so we do not even know if the difference is statistically significant.

Lastly, there are several basic things which you could rightfully expect us to assume, but have nevertheless failed to provide. For instance, you do not say if the populations are clonal.


Edible and non-edible leaves For humans, what's the difference between an edible leaf like lettuce, and a non-edible (in the sense of null nutritional value) leaf like grass?

For grasses leaves tend to be inedible due do with the high quantity of silica deposited in the leaves to form structures known as phytoliths Wikipedia.

While this has been shown to inhibit digestion by insects (Hunt et. al., 2008, Massey et.al., 2006), I'm not aware of any studies on how this affects digestibility for humans.  There are however anecdotes about people starving to death with grass stains around their mouths during the Irish Potato famine.


Methods for microbial identification in soil I'm trying to perform a survey of the life in a soil sample. I want to know what species of bacteria, fungi, and other organisms are in it. I've heard that ITS sequencing and 16S rRNA sequencing are both possible ways of doing this, but I don't know enough about these techniques to understand which (if either) I should use, or how you interpret the resulting sequence file delivered by the lab. Will these techniques do what I want? How do I choose one over the other? And how do I interpret the results?

16S and ITS techniques try to identify organisms in your samples by amplifying short, 'barcode' sequences from each organism's DNA, and using those short sequences to try to identify the organism they came from.

16S can be useful for distinguishing between prokaryotes (bacteria), at least to genus level.  It will not always give enough information to determine exact species though.  ITS can be particularly useful for distinguishing between some eukaryotes (plants, fungi, etc), even down to species level.  If you are interested in both bacteria and fungi you would need to carry out both analyses on your samples.

A different approach is to use shotgun metagenomics, where rather than amplify only the 16S or ITS region, you extract and sequence any DNA you can from the sample, and then try to assign each sequence read to a species/genus by alignment with a reference collection (e.g. MEGAN pipeline) or by kmer analysis (e.g. Kraken).

There are some packaged approaches for dealing with 16S. Qiime2 is popular, and will likely involve some amount of work in python to get it working.  There is an R package microbiome, but I don't have experience with this.  Mothur is a long-standing stand-alone package that is resonably easy to use, and MG-RAST is a web-based version that is also reasonably easy.

ITS analysis is less fully developed as pipelines, but I am sure you can find some in the literature by searching for other people's studies of soil microbiomes.

This review of techniques and approaches might be helpful if you are interested to learn more about the whole genome/metagenomics approaches: http://ccb.jhu.edu/people/salzberg/docs/Breitwieser-etal-2017-Metagenomics-review-reprint.pdf


Do somatic cells alter their own nucleotide sequence? I seem to remember reading that embryonic cells will frequently replicate the section of their genome containing rDNA by splicing in duplicate genes. The cells use this to produce ribosomes at a rate which would be impossible with the DNA present in cells from full-grown organisms. Is this real? Are there other examples of cells altering their their own nucleotide sequence?

One case where human cells alter their DNA occurs in the immune system.  In the early stages of the continuing production of B-cells and T-cells, the developing cell recombines (shuffles) genes in a particular DNA region which codes for what are called Variable, Diverse, and Joining gene segments.  This shuffling is called somatic recombination or V(D)J recombination.  This rearrangement gives the cell a genetic template for a random instance out of a enormous set of possible antigen-recognition proteins used by the immune system to recognize foreign molecules (in order to fight infection).


Is eating salt dangerous for the brain? I read somewhere that eating a lot of salt will raise blood pressure, which will in turn damage brain tissue. This is because water molecules gather around salt ions, thus making it harder for the body to remove the excess water from the blood.

Is this true? How much salt is actually dangerous?

Good question. The answer really depends. There is a normal range of plasma sodium concentration that ranges from about 135 to 145 mM. You body has multiple endocrinologic and neurological mechanisms to closely regulate this concentration. So even if you went out and ate a ton of salty snacks, your body would still keep your plasma sodium concentration within this range. A salt concentration much lower or greater than this can start to cause problems depending on how fast it happens and how far from the normal value. Brain surgery patient are often given lots of extra salt to keep their brains "salty" as this protects from cerebral edema and counteracts salt wasting that often occurs with brain injury. However, the opposite or very high sodium concentrations are also not good. As you said, a diet high in salt can lead to high blood pressure and chronic high blood pressure can cause damage the small blood vessels in the brain and cause small strokes over time or very high blood pressure can cause larger bleeds. Usually we see this in patients with very high uncontrolled blood pressures in the 170-200s systolic range. I'm kind of pulling those numbers out of my memory and you would have to check the literature to verify.


Why do E.coli form parallel clusters? Discalimer: I am not a biologist. I am modelling E.Coli growth and in the Wikipedia gif one can see observe some groups where the bacteria are one next to each other, oriented at approximately the same angle. I did some simulations and obtained similar results. Is there any reason why this happens?

Cell division happens by division at the middle of the rod, so the result is two daughter cells that are at nearly the same angle. Over time in the absence of agitation moving cells around, this will lead to a groups of cells that have non-independent cell orientations.

For more information, including how people have induced it to do otherwise, see this paper.


Best method for measuring very young plant growth? Is there a preferable method for measuring plant growth for a plant before the "sprout" stage? Preferably at the microgreen stage? I assume it would not involve some type of leaf based measurument, since they would have few, and maybe then should be based on mass or volume somehow?

I am assuming you want to monitor these traits in controlled conditions because in wild type conditions it will be real challenge to monitor in details unless you have easily accessible way (like leave surface area and related visual traits). Remember these techniques will change according to your plant/seed and your study interest. Lot of things change during development. You need to look at characters which suits your study. You can try following,

Monitor real time oxygen consumption in controlled chamber ( Generally researcher do this by monitoring loss of oxygen in
current chamber by some non invasive method. However there are
other techniques like this which can be also implemented
depending on type of plant.)
There are some automated image acquisition techniques like this or this
Use of volatile organic compound (VOCs) traces
Change is fresh and dry weight during development
Root moisture sensors ( in microgravity environment ) like this
I don't know whether you can use this kind of sensors in any way but these are very useful in monitoring particular element in vivo

This is very big list. There many other components which you can monitor like protein content, lipids etc. However such techniques are most reliable but destructive and you can use if you have large amount of samples.   You can go through papers cited in above list. Take a look at their methods and materials. You will know how to do such measurements and what are advantages/disadvantages.


Why are bed bugs attracted to Carbon Dioxide? All over the Internet it says bed bugs are attracted to Carbon Dioxide. This is why they congregate around beds. Your bed is the only place you are stationary for long enough periods of the day to exhale enough Carbon Dioxide. So, I grant that there seems to be a consensus that they are in fact attracted to Carbon Dioxide. But, why? Certainly they're not breathing it. (Are they?) I was under the assumption that all animals are aerobic.

It's nothing to do with what they breath, they're attracted to carbon dioxide because it's generally a good indication of the presence of a larger organism (such as a person) so they're simply following the "scent" (for want of a better euphemism) to their food (in this case you, or whoever happens to be in the bed), the traps in your links just take advantage of this to trap and kill them.


Are people genetically predisposed to being interested in specific fields/ideas? How does specialization occur? I'm not sure if I formulated my question well, but I'm curious about a couple statements made by Steven Pinker and and James Heckman.

In this interview: http://www.youtube.com/watch?v=KJ9Ad6s8g7I&t=7m51s Steven Pinker says

  "there'd be a wide variety of families I could have grown up with and
  had the same kinds of interests"

and in this interview with James Heckman, he says:

  But anyway, Smith says people are basically born the same and at age 8 one can't really see much difference among them. But then starting at age 8, 9, 10, they pursue different fields, they specialize and they diverge. In his mind, the butcher and the lawyer and the journalist and the professor and the mechanic, all are basically the same person at age 8.
  This is wrong. IQ is basically formed by age 8, and there are huge differences in IQ among people. Smith was right that people specialize after 8, but they started specializing before 8.

Can anyone explain Heckman's statement that people "start specializing before 8"?

What do we know about genetic influence on interests? (Is this the right stackexchange to ask this on?)

I think the concept you are looking for is the one of heritability.

In short, heritability represents the part of the variance for a trait that is caused by the genetic variance only. For more information, you can refer to this, this, this or this post or to wiki.

This wikipedia article talks about the heritability of IQ in human. It has been measured to be around 0.7.

Of course, heritability in IQ is not the same as heritability of "interests". But I don't know about any measure concerning the heritability of "interests". Such measure will be highly dependent on how you classify interests together. Does a mathematician specialist of probability theory have the same interests than a mathematician specialist of non-linear algebra? Does a Mathematician have the same interests than a chemist? and of a engineer? and of an electrician? Does a butcher have the same interests than a backer? and of a waiter? and of a bricklayer? .. Does anyone who work in business have the same interests? The fewer groups you make, the higher will the correlation between parents and offsprings and the higher is the part of the genetic variance that explain the variance in interests choice.


What kind of event would cause the current Mitochondrial Eve to be replaced by a new one? Apparently all living humans are matrilineal descendants of a single woman who lived 200.000 years ago. She is called Mitochondrial Eve.

But at the time she lived there was a different matrilineal ancestor that all living humans shared. And between then and now I imagine many other women have been Mitochondrial Eves of the human population that lived at a particular time.

What I'm wondering is what kinds of events would cause a different, more recent matrilineal ancestor to become the Mitochondrial Eve of all living humans?

One scenario I can image is that the human population is on the brink of extinction and literally only a few people survive. Because there are so few people alive, I imagine that the chance that they share a more recent matrilineal ancestor is high.

Are there other scenarios possible? Does the chance of a new Mitochondrial Eve emerging decrease if the human population is large (billions) instead of small (hundreds or thousands)? Suppose that the human population will not decrease, is it likely future human populations will ever have a different Mitochondrial Eve than the current population? Does it depend on the amount of people that migrate?

The same questions could be posed for Y-Chromosomal Adam and the most recent common ancestor of all humans, I guess...

One possible scenario would be that a particular woman develops a mutation rendering her much more 'fit' (in the evolutionary sense) than her peers. For the sake of argument, lets take the very simplistic case of an X-linked recessive mutation causing the women who bear it to have say 10 children at each birth. If this mutation is then transferred to the offspring, it will very quickly spread across the entire population.

If this continues for a few generations, the crushing majority of the earth's population will be the descendants of that one woman who carried the original mutation, she would be the new mitochondrial Eve.

I want to stress that this is nothing but a very simplistic thought experiment. Such a mutation is i) very unlikely, probably impossible, ii) likely to render the carrying individual less fit rather than more as each birth would be exhausting, increasing the chances of dying during child birth.

Update:

I have specified that the mutation has to be X-linked and recessive. This means that it will only present a phenotype in women who are homozygous for it, women both of whose parents carried the mutation. This is because, as mgkrebbs very correctly pointed out in the comments below, otherwise her sons would mate with women who are not their sisters and their children would have the mutation but not her mDNA. If the phenotype is only expressed when the mutation is homozygous, only women whose mother carried the mutation (and Eve's mDNA) would show it and only then would a new mEve arise.


On enhancers, strands, and zygosity I came across a passage on enhancers that sounds out-of-whack to me:

  ...an enhancer sits on just one of DNA's two strands (usually the same strand as the protein-coding DNA gene itself).  This is unlike a protein-coding DNA gene, which might need to be on both DNA strands——in a so-called homozygous state, in order to surface as a phenotype——like the classic case of blue eyes.

This is what makes no sense to me, since, AFAICT, whether something is in one or two strands has nothing to do with zygosity.

The authors continue:

  And this is [an] evolutionary advantage: an organism doesn't have to wait for a change on both DNA strands.  The bottom line is that evolutionary tinkering is in principle much easier with enhancers...

Is there a grain of truth in what the authors' write, despite their muddled explanation?  IOW: does the fact that enhancers "sit on just one of DNA's two strands" somehow facilitate "evolutionary tinkering"?

...an enhancer sits on just one of DNA's two strands (usually the same strand as the protein-coding DNA gene itself).

Yes and no. Enhancers are in fact sometimes palindromic, so they're mirrored on both strands of the DNA.

  This is unlike a protein-coding DNA gene, which might need to be on both DNA strands

No. Protein-coding DNA is always on one strand only because transcription doesn't suddenly switch strands.

  in a so-called homozygous state, in order to surface as a phenotype - like the classic case of blue eyes.

No. Homozygous means on both chromsomes and has nothing to do with strands or the need for an allele to be homozygous to produce its phenotype because it's recessive.

  And this is [an] evolutionary advantage: an organism doesn't have to wait for a change on both DNA strands. The bottom line is that evolutionary tinkering is in principle much easier with enhancers...

This is completely all over the place and makes no sense to me. Either "strands" is used in the correct way, in which the previous statement is wrong, or "strand" is used as "chromosome", in which case there is no reason why an enhancer should only be on one chromosome. Just like the gene, it can be hetero- or homozygous. The statement about "having to wait for a change on both DNA strands" is more relevant to whether something is dominant or negative. Regardless, I don't think it's possible to make any statements here about enhancers allowing for evolution to progress faster.


Linkage and LD: quantitative or qualitative? My understanding is that the concept "genetic linkage" can be expressed in quantitative form, like:

A predisposing gene X was found in close genetic linkage to Y.

And that linkage disequilibrium (LD) is a quality, like being pregnant, you are either in LD or your are not:

A predisposing gene X was found in close genetic linkage to Y and in
linkage disequilibrium with Z.

Is this correct?

Linkage disequilibrium (LD) occurs when there is a non-random association or correlation between genotypes. Note I used the word correlation; this is a quantitative trait.

Some genotypes may well correlate perfectly (R=1), i.e. they are always inherited together. Others may not be in 'perfect' linkage (e.g. R=0.9), but are still considered to be in LD because there is a strong correlation between the genotypes (I think 0.8 is generally seen in published papers as the 'cut-off').

The correlation coefficient is derived from the D' value - this (simply) denotes the observed vs. expected frequencies of the genotypes (whether they are in linkage or not). Therefore either value can be used, but I think it is more common (and more interpretable) to express the correlation coefficient (or to be more precise, the coefficient of determination, R^2).

If you'd like an example: I might be interested to know if any SNPs are in LD with rs10757278 (located on 9p21, associated with heart disease). Using SNAP (by the BROAD) I can input my search, choose my options (e.g. use 1000 genomes data, and an R^2 cut-off of 0.8) and search. ~5 SNPs are found to be in 'perfect' LD (R^2=1), but a further ~40 are still considered to be in linkage with the input-SNP because their R^2 values are above 0.8.

So in summary, both statements can be used correctly, but it is always more informative to state the degree of linkage (otherwise it might be assumed they are in perfect correlation).


Does sleep duration vary for animals based on time of the year? I'm interested in the sleep patterns of wild animals, that still use sun for controlling their biological clock.

Animals entrain their biological clock to the day/night cycle using light as the entrainment signal. The biological clock follows the day/night cycle: dim light initiates melatonin secretion, while bright morning light stops melatonin production. Melatonin is involved in sleep regulation

Here, I have plotted the day duration over the course of the year for Northeast US, around Washington DC.

My question is given the day duration plot below, would the total sleep duration for wild animals vary over the course of the year?

In other words, would animals sleep longer in the winter time and shorter in the summer time?

Yes, people, as well as animals regulate their drowsiness by light. There's a well known experiment conducted by Michel Suffre on himself in 1972. When he spent a month with no light and no information about the time, his sleeping cycles prolonged up to 48 hours.


How many residues can a reliable ab initio structural model contain? A recent question on ab initio that I answered involved touching on the limitations of ab initio modelling. A review from 2009 put forward that typically only in the order of 100-110 residues could be reliably modelled.

7 years after that paper: I just attended a pre-publication presentation in which a 400+ residue structure had been modelled using I-TASSER. The speaker claimed it was reliable and it did fit well in the biological context, but it still needed experimental validation. Unfortunately they had no in silico validation scores to hand so I had no handle on how seriously I should take the model.

Ultimately, my question is how many residues can I-TASSER (other modern ab initio brands available!) reliably handle for a typical globular domain with today's technology?

Year on year reliable ab initio predictions are becoming more common for longer proteins. 400 residues is not an unfeasible length. Of course, loops still remain more of a challenge than helical and sheet secondary structures.

At CASP13, the Google DeepMind team used AlphaFold to produce a good quality model (T0594) of a 774 residue protein which is a WD40-repeat of RFWD3 (6CVZ).
All of their CASP13 entries are here.


Why do humans suffer anxiety when they view "Trypophobia trigger images"? When you type Trypophobia Trigger Images in google, you see a variety of images with irregular lumps and bumps among some more gory images.

Many people report that these images induce phobia like symptoms of anxiety.

Why do we get anxious when exposed to these images? What advantage is there to be had from this response?

I find the reasons like this ABC news report on ants and spiders. But still didn't get it any info from it.

Trypophobia is not a recognised specific anxiety disorder (Washington Post). It is worth mentioning that anyone can have a phobia to anything, this is merely a question of whether many people associate these spatial patterns with anxiety. Nevertheless, the response of individuals to these images can be quantified (Le et al., 2015). Ultimately the findings show that a response of trypophobia is not correlative with anxiety. Note that here we are discussing anxiety in a phobia response test. Typically anxiety manifests as sweating, dizziness, headaches, racing heartbeats, nausea, fidgeting, uncontrollable crying or laughing and drumming on a desk. This is not merely feeling uncomfortable.

One hypothesis was that these images had irregular spatial patterns that cause revulsion. A study found that in nature some animals and plants may use this patterning as a warning mechanism and that it is associated with poisonous animals  (spatial pattern quantification of 10 poisonous animals versus 10 control animals p=0.03), and indeed spiders were among those that use irregular patterns (Cole & Wilkins, 2013). Note that this hypothesis was presented in a psychology journal so the evolutionary mechanisms remain, in my opinion, not fully explored and scrutinised.

Hover over the below yellow box to view a lotus seed head, which has typical irregular spatial patterning presented in the 2013 study.

This image is often reported as inducing trypophobia.

Answer: In summary, humans do not reliably feel anxious when viewing these images. It also remains unclear why some people do get anxious or uncomfortable when viewing these images. It is perhaps to do with an aversion to some potentially harmful animals, but evidence remains scarce.


Does retinal detachment happen more frequently at night? My understanding and experience is that during the night photoreceptors are less tightly coupled to the retinal pigment epithelium.  Does this make it more likely for a retinal detachment to happen at night?

In case of normal, healthy person, no, I don't think so. In fact, retinal detachment could happen at anytime of the day. Main causes are diseases and illness, such as AIDS, diabetic retinopathy, cancer, or trauma such as post-cataract surgery and being hit/kicked hard on the eyes.


Pancretic Acinar Cell - ATP, calcium concentration data I need to find a decent source of data for concentration of ATP and calcium in the pancreatic acinar cell.

So far all I can find is ATP or calcium 'levels' based on fluorescence , which are not accompanied by a value of concentration in moles/molar.

Is it possible to find this information in a specific book or website, to avoid trawling though vast amounts of literature?

In this study, even though they have used fluorescence based method, they have reported concentrations.

  When we studied basal intracellular calcium concentrations in acini from control rats they were in the low nanomolar range (140 ± 5 nmol).

For ATP concentrations you can see here.

  Is it possible to find this information in a specific book or website, to avoid trawling though vast amounts of literature?

There is the human metabolome database. However, it doesn't have data for all cell types. Either more studies are required or the database needs updation.

Similarly there is the yeast metabolome database (you may not require it for your query but just another piece of information that I thought is worth adding).