What Defines a Food as Edible? With many foods today containing chemicals, agents and preservatives etc... What biological criteria must a new food and its constituent components satisfy biologically, to be defined as edible?

For example do they look at the chronic/acute affects of chemicals in the body?

This question is just limited to chemicals, if a new fruit was discovered, how would it be decided if it was edible or not?

As far as I know, edibility (wow, I'm surprised that passes the spell checker!) is not a strictly defined term, biologically or otherwise. Humans have been around eating and drinking stuff long before the scientific method was around to study this question rigorously, and before there were regulatory agencies charged with approving new products as "safe." As one might imagine, knowledge of what is and is not edible was likely passed down by oral tradition and personal experience.

Honestly, I'm not even sure designating a food (or a substance) as edible or inedible really makes much sense. Let's consider wild fruit, as mentioned in your question. If ingesting 5 or more berries of hypothetical fruit X causes your body to have a nasty reaction, then we could probably agree that fruit X is toxic and inedible (even if eating only 1 or 2 berries might not elicit the same reaction). On the other hand, ingesting berries of hypothetical fruit Y causes no reaction unless consumed in much larger quantities (maybe 100 or more berries). Although fruit Y does cause a reaction when ingested in excessive amounts, it would be a stretch to call it inedible. This principle applies to many foods that we typically consider edible but can be unhealthy or even dangerous when taken in excess.

So where do we draw the line? How much of a substance do you have to ingest without an adverse reaction to deem it edible? I don't think there is an objective answer to this question. It is complicated further by the vast amounts of variation in the human population: food allergies, differences in tolerance to certain substances, etc.


What is special about the N3 buffer for Qiagen minipreps? For those who use Qiagen miniprep columns, they may be aware that the P3 buffer is the acetic acid step to neutralize cell lysis. They may also be aware that the Qiagen P3 buffer cannot be interchanged with the proprietary N3 buffer. It is also known that the N3 buffer is particularly unique since it primes the miniprep columns for binding. I was wondering about that priming step and what chemically primes the columns. Would it be appropriate to use QBT buffer to prime the miniprep columns?

The Qiagen manual for the Miniprep Kit states that buffer N3 contains guanidine hydrochloride and acetic acid. The MSDS for buffer N3 gives a bit more information:

Guanidinium hydrochloride 25-50%
Acetic acid 10-25%
pH 4.3

Buffer P3 uses 3M potassium acetate, the potassium is usually important in plasmid preparations as potassium SDS is used to precipitate the proteins in solution.

This information might be enough to create a buffer that should work with the silica-gel columns.

I also found a patent about a method for isolating nucleic acids that states that silica particles can bind nucleic acids in the presence of chaotropic salts, so the guianidinium hydrochloride is probably the important difference in the N3 buffer.

The patent for this method from Qiagen goes into even more detail, according to this the buffer composition  is:

N3: 4.2M guanidinium hydrochloride, 0.9M potassium acetate, pH 4.8


What is the fastest marine mammal? When I did a research, most of the sources say that orca is one of the fastest. But I could not find a source that says it is actually the fastest.

Some sources say that Dall's porpoises rival orcas in speed. And there are other kinds of porpoises and dolphins that comes into question.

Is there any scientific research with measurements? Or does anyone have any detailed knowledge about this topic?

(Also it would be nice to know top 10 fastest marine mammals, so the question becomes: what are the fastest marine mammals?)

Note: This scientific research might be difficult to conduct also so you can explain the situation as well.

This article by R. Aiden Martin doesn't have citations, but is a great read with a lot of detail on observations and mechanics of animals moving in water. If you trust the numbers the author gives, the top 10 marine mammals in terms of speed (in mph = 1.6 km/h) are:

  Dall's Porpoise (Phocaenoides dalli), leaping   34.5 mph

  Killer Whale (Orcinus orca)  34.5 mph

  Shortfin Pilot Whale (Globicephala macrorhynchus)   30.4 mph

  Blue Whale (Balaenopterus musculus) 29.76 mph

  Fin Whale (Balaenoptera physalus)   25.42 mph

  California Sea Lion (Zalophus californianus)    25 mph

  Pacific Spotted Dolphin (Stenella attenuata)    24.7 mph

  Common Dolphin (Delphinus delphis)  23.6 mph

  Bottlenose Dolphin (Tursiops truncatus) 17 mph

  Pacific Whitesided Dolphin (Lagenorhynchus obliquidens) 17 mph

As noted in the article, higher estimates of speed for, for instance, the common dolphin may be in fact records of them 'surfing' on the bow wave of boats (not propelling themselves through the water).


How can I determine where meiosis occurs in the life cycle of a plant? To fill out this diagram with the mitosis, meiosis, and ploidy , we start with the definition that spores are haploid (N).

Based on knowing that as the sperm and eggs are N, the gametophyte is also N (as only fusion can make something go from N to 2N).

Then I know that the link between spores and gametophytes is mitosis, as we go from N to N.

Similiarly, as zygotes are 2N, and spores are N, either the link between zygote to sporophytes OR the link between sporophytes to spores must be meiosis.

Can I figure out at which stage meiosis occurs with this information, or do I need to know more about the definitions of the different parts of the life cycle? How do I know that sporophyte to spores, and not zygote to sporophyte, is Meiosis?

 (Source)

All of these terms are just names for things that existed long before someone named them, and although you can figure out some of the ploidy from the diagram, you need to know the terms/definitions to complete it all.

Sporophytes are just the name for the diploid cells of a plant/algae that reproduces through a haploid life stage called a spore. You could consider the zygote almost like it is a "special sporophyte" from the perspective of ploidy: it's only special because it's the first cell assembled from two haploid cells. All of the other sporophytes are produced from mitosis from either another sporophyte or from the original zygote.

Being diploid is nice because you have two copies of every gene, which is more robust to mutations (while also maintaining genetic diversity for later generations), and, crucially, it lets one organism make a variety of haploid spawn for sexual reproduction.

Maybe you are wondering just about the terms haploid/diploid, and why "2N" vs "N"? The important thing is it isn't just the total number of chromosomes, it's the number of COPIES of each chromosome: with N you have just 1 of each, with 2N you have two of each. The important thing is that they are homologous, it doesn't matter if N is 1 or 2 or 40.


recolonize earth desert with plants : which plants first? if willing to recolonize earth desert , let's say sahara or any dehydrated and sterile land, without intensive human intervention, what would be the first plants / algae / fungi /bacteria to grow ?

what could be the strategy to slowly bring back biodiversity and trigger new water cycles ?

This is a big idea that's gaining momentum in many people's minds across the world.  This is a brief and probably inadequate survey and hopefully other answers / comments will fill out a better picture.

Most of the plans to reclaim arid regions are not completely hands off.  It seems that the current thinking is that if we waited for microbes and lichen to reclaim arid soil, it would take too long.  Most of them focus on trees.

Trees are fantastic because they can grow in climates that have minimal water once they are established.  They can claim moisture from the air, remove pollution from the air, reduce the ground temperature, sequester carbon, prevent erosion, and make the environment more accommodating to other plants.

Some estimates are that to curb the expansion of deserts worldwide, 30 billion trees should be planted every year for the next decade.

The tree one plants varies depending on the place and application, but the selection of the plant is more than just a climatic choice.  Trees are grown in nurseries when their needs for water are most intensive, and then need to be cared for until they are established enough to survive on their own.

The Green Belt project was the focus of the 2004 Nobel Peace Prize.  Its success in rolling back desertification was because of its understanding of the causes of desertification in many cases as a social effect.*  People harvest the trees, graze the land dry, burn grassland etc.  Green Belt created networks of local people and incentivized them to grow trees, selecting trees which had agricultural and economic value so that they would help the local economy.

The Great Green Wall project is a successor to this idea.  Attempting to contain the Sahara desert's spread across the continent of Africa.   Their plan is to have a different organization in each country, including automation of sorts to collect water from the air and rain for more continuous support of young trees.

there are arguments that ultimately the animal ecosystem needs to be involved.


Copy number regulation & CNV I have some genes which showed copy number loss between two groups. Now I want to see the copy number regulation of those genes. I really don't know about this concept. Can anyone please tell me clearly about this like why we need to check regulation of copy number loss genes? And any idea how to do this?

Thank you

It might be helpful if you showed us what sort of data you are looking at since copy number variations and gene expression can each be detected in similar but distinct ways.

Generally speaking, both gene expression and CNVs are detected by counting the number of reads that map to a given genomic region. The difference is that CNVs are detected using DNA sequencing while gene expression is detected using RNA sequencing. This is an important distinction because CNVs are a more stable genomic feature than gene expression. Reviewing the Central Dogma might help if this is confusing.

In the context of your problem, the main thing to understand is that CNVs can exert an influence on gene expression but gene expression cannot exert an influence on CNVs. Having fewer copies of a gene means that the process of transcribing RNA to express it cannot proceed as quickly as normal. So in an organism with gene X showing copy number loss, it makes sense to expect diminished expression of gene X than in organisms whose genome includes more copies of that gene X. If you're asking for an undergraduate class, chances are this is all you're expected to understand about "copy number regulation": the maximum transcription rate of a gene is dependent on how many copies of that gene are available for transcription.

Gene regulation becomes important for understanding how an organism with fewer than normal copies of gene X in its DNA might have the same amount of gene X RNA expressed as an organism with a normal number of copies of gene X. Suppose that some molecule, M, is necessary for expression of X but degrades after a short time. The cell will send M to the nucleus whenever it needs X to be expressed and the number of X transcripts produced per molecule of M will be dependent on the number of X copies available for transcription. If M is abundant and can be continually sent to the nucleus, then the cell with fewer copies of X can theoretically produce as much X as the cell with a normal number of X copies although it'll take a bit longer. If instead M is a finite resource within the cell, then the amount of X expressed in cells with fewer copies of the gene should be consistently lower than cells with more copies.

Of course if M happens to be produced by a gene exhibiting copy number gain/loss then that could also play an important role in how much X RNA transcripts you ultimately detect (even in the event that X actually has a neutral copy number). Hope this helps.


Can I get 1% of my one of my great great grandparents genes? I basically took a 23andme test and found out genetically I was 1% African. The weird part though is that family records shows that my father's mother's grandmother was African, making me 1/16 African. Shouldn't it be closer to 6%?

The science behind "being X % from a certain place" based on genetic analyses is... approximative at best. It relies on the assumption that some genetic traits are only found in certain (narrow) regions of the planet - which for most of them, is not really true.

Additionally, did your test provide any confidence metric for this result? If not, it may mean that it may be derived from a statistically unsignificant number of traits (and the number could therefore mean anything) or maybe it's simply something like 1% with a confidence interval of several points, in which case the result could be a compatibe the mathematical truth. Genomes are large and have complex dynamics, it it probably difficult to get a precise estimate.

On a side note, there is more genetic diversity in native African populations than on any other continent (for reasons pertaining to Homo sapiens history) so "African" does not describe a homogeneous population.

Source: https://www.nature.com/articles/nature13997 doi:10.1038/nature13997


What happens when the bacteria in the petri dish lack nutrients for long time? If I put some E.coli in a petri dish filled with limited nutrition in room temperature and forget them for months or years. What will happen in the final after they overgrowth and used all nutrition left? Will they die or just stop dividing?

They will die, eventually.

The requirement for energy is a thermodynamic constraint; maintaining cellular structures, repairing molecules that spontaneously damage etc takes some energy, and E. coli is not able to reach a level of quiescence sufficient to survive for years. However some cells might survive longer than expected if they enter low-metabolic activity states; that would not be enough to survive years in a petri dish, though.

Note that other species may be able to survive, through special stress-induced processes such as sporulation or cryptobiosis.


When someone gets infected with influenza, and gains some immunity, is that immunity just as good as getting it from a vaccine? A friend thinks that being infected with a new influenza virus means that little immunity is gained, unless you get a vaccine. But, he is forgetting that new strains can make current vaccines out-dated.
I'm sure the immune system will "remember" that particular strain just as well as getting a vaccine.
When someone gets infected with the influenza, and gains some immunity, is that immunity just as good as getting it from a vaccine?

Natural infections almost always yield a better immunity than that acquired through vaccination. However, vaccines yield a better immune-response than getting infected with influenza. That is so to say the side effects.
I want to backtrack to part of your questions where you say I'm sure the immune system will "remember" that particular strain just as well as getting a vaccine. and add a little bit of interesting information regarding influenza.
Some Influenza (A) stereotypes that infect humans are: H1N1, H2N2, H5N1, etc...
The H stands for Hemagglutinin and N is Neuraminidase. These are important in vaccine development. The H and N are proteins located on the surface of the virus and allow for entry into a cell for infection.
Strains are classified according to their hemagluttinins and neuraminidases. Every year when the vaccine for the seasonal flu is developed we don't know with 100% certainty which strain might be the most prevalent. Rather, surveillance data is used in deciding which flu might be the most prevalent. More info on the CDC Website.
So back to the question:

Does the immune system remember that particular strain just as well as
getting a vaccine?

Yes it does and there's a paper in PNAS that looked at something similar. This is related to something called “Immunological Honeymoon”. A theory that the first infection during childhood provides stronger immunological memory than a later infection.

The paper found that people who were 28 year old were more susceptible to the Spanish Flu (H1N1) in 1918 because they had been exposed to the wrong virus as children.
The elderly, however, had been exposed to H1N1 as children and were well protected. People who were middle aged or in their teens in 1918 had been exposed to H1N8 as children and were partially protected.
This I recon is just as good as vaccine, but more to show that the immunity acquired through infection is, in fact, remembered. For how long? That's a totally different question that varies from infection to infection. Some are life-long (such as measles), other are short lived requiring re-infection, or booster shoots in case of vaccination.


Etymology of PAX proteins What is the reasoning behind naming proteins first found in Drosophila as paired box? All I could find on internet is that it was first found in Drosophila as a protein with paired domain, but I couldn't find anything about the term box along with it. Could anyone please signify the terms paired and box in the name of that protein?

According to InterPro, a paired domain is a DNA-binding element consisting of paired N-terminal and C-terminal subdomains, separated by a linker. PAX proteins follow this motif, and as such typically represent a class of helix-turn-helix transcription factors.

Box is the more interesting term here. In genetics, a box can be used to describe any regulatory element of a gene, including its promoter, UTRs and any enhancer or silencer elements. More loosely they also use box to describe coding segments of a gene, but in older publications.

Going back to Drosophila, however, studies in embryogenesis initially identified a protein called paired, a.k.a. prd. Homology studies into mammalian transcription factors found the presence of a prd-like domain in human HUP transcription factors, and these were renamed to PAX (ref). Thus, the naming of PAX family proteins classicaly denotes the presence not of a PRD regulatory element, but of a coding region for a prd-like domain in the gene product.


How long would it take for a change to the DNA would take effect? I am not a Biology Student (sorry guys!) but I have thought about this question for a while and hope that maybe one of you can answer it. Lets say that I had my DNA changed so that I wouldn't be vulnerable to certain diseases or perhaps to make my body change so that I'd lose weight easier (Just a hypothetical here not sure if sci-fi have skewed my view on DNA).

From the change occurs to the DNA until the changes take effect, how long would that hypothetically be?

OK, let's set up a specific hypothetical situation so we have some details: A virus (we'll call it Human Nasty Virus 1 (HNV-1)) can infect T cells (a type of white blood cell in the immune system) by binding to a certain receptor on its surface, which we'll call the Nasty Virus Receptor (NVR). Scientists have found that HNV-1 absolutely needs a certain protein sequence in NVR to bind, as people with a certain mutation lacking that sequence are completely immune to HNV-1 infection.

You sign up for a clinical trial using gene editing to specifically remove that DNA sequence from the NVR gene. Once that changed gene is transcribed and translated into protein, it is expressed on the surface of the cell, and HNV-1 can no longer bind.

T cells are derived from stem cells that live in the bone marrow. In order for the gene therapy to work, doctors will need to perform a bone marrow transplant - they will remove a sample of bone marrow, give it to the scientists for the gene editing process, then reinject the edited cells back into you. The editing process involves subjecting purified stem cells to a process called CRISPR, allowing them to grow in culture for a while, then screening the cells to select only those where the editing was successful. The successfully-edited cells are separated, cultured some more to expand their numbers, then given back to the doctors, who put them into your body, either into the bloodstream or directly back into the marrow.

So now you have your edited cells back inside you - how long will it take to become immune to HNV-1? Well, the honest answer is that, in the absence of ablative chemotherapy (see the bone marrow transplant link above for more info) prior to reinjection of the edited stem cells, you may never become completely immune. Here's why: Unless all of the bone marrow stem cells in your body are destroyed before reinjecting the edited ones, you will still have fairly high numbers of what are called "wild-type" or un-edited stem cells and mature T cells in your body, and those stem cells will continue making new wild-type T cells. Additionally, there are already wild-type T cells in circulation and in secondary lymphoid organs such as lymph nodes and the spleen, and some of these cells can be very long-lived (months to years). If for some reason you decide to undergo complete ablative chemotherapy to essentially destroy your immune system, the reinjected stem cells will eventually repopulate everything and you'll be immune to HNV-1, although you will have potentially lost your immunity to everything else you've ever been exposed to, unless the chemo is done in such a way as to preserve your immune memory cells.

This is actually a best-case scenario, as we were working with cells that can (relatively) easily be removed from the body, edited, screened, and reinjected. If you were trying to cure a genetic disease that affected solid tissue like the muscles (see Duchenne muscular dystrophy for an example), you obviously wouldn't be able to remove all the muscles and edit them ex vivo, you'd have to do the editing in the body, most likely using a viral delivery system for the editing machinery. The viruses wouldn't infect every single cell, and the editing wouldn't work in every cell that got infected, so the best you could hope for would be a partial cure. For some diseases, this may be enough, and many companies are working on this from various angles. There are also other options besides CRISPR-mediated gene editing that have higher success rates in vivo.

Finally, getting back to your original question of how long it takes from DNA alteration to expression of the gene product, the answer is that it depends on the gene and the context. In the case of our hypothetical situation earlier, as soon as the NVR gene's DNA is edited, the new sequence begins to be transcribed and translated into protein. There is still some wild-type protein left over initially, so it depends on the transcription rate of the gene and the turnover of the existing protein. Some proteins have an extremely long half-life, on the order of years or decades (or more!), while some degrade within minutes to hours of being synthesized.


Determination of the species of a skull Out here in the mid german woods,  the kids found this skull:

Now we would like to figure out what it is. Started to look at various google image search results for all kinds of animals that came to our mind, but not only due to bad reception this takes long and lead to no result.
So what is a good structured way to start detrmining what this is?

If you're serious about this (and it appears you are), you'll benefit by starting with a Comparative Osteology book or webiste that discusses all the various characteristics of skulls that give you clues to exactly what you're dealing with.

This page on Amazon has a variety of such books. Pages such as this one begin with the basics and references help you to pursue the subject further.

On your specimen, although the missing teeth would be very helpful, important identifying features include the very large percentage of the cranium given over to the masseters, the eye socket placement, the size, the jaw shape, etc.


Diffusion to center of the cell I have been researching about the ratio between cell membrane surface area and volume.

Obviously, when the volume increases faster than the surface area, and up to a certain point, there is comparatively less membrane for substances to diffuse through and comparatively more organelles that need these substances.

http://scienceline.ucsb.edu/getkey.php?key=5203

The resource above says that "These nutrients then need to get to the center of the cell."

My question is: why do the resources get depleted before they reach the center of the cell? Aren't all the important organelles in the center anyway? For example, wouldn't the glucose go to the center of the cell, and not be used up "on the way"?

And just to be clear, the "center of the cell" refers to organelles like the mitochondria, nucleus etc?

The center of the cell in this case is a way to say "the nutrients arrive to every part of the cell", and should not really be taken literally as "the center". If the cell is modeled as a sphere, with the nutrients diffusing in from the outside, the whole sphere would be filled with nutrients when the nutrients "arrive to the center". Figure 1 shows how the nutrients would diffuse from the outside layer further in. It is like saying the whole glass would be filled when the water "arrives to the top". It does not particularly mean that the vital organelles are in the center, but is just used to illustrate the fact that nutrients diffuse into and can reach all parts of the cell.

Figure 1: an illustration to show how nutrients would diffuse from the outside to the center of the cell, filling the cell with nutrients. This image is trying to model a cross-section of a circular cell. The nutrients would for example enter from around the green layer, and gradually get to the middle/center dark blue area.

Resources may get depleted before they reach the "center" of the cell because of the rate of diffusion, and also because metabolic processes may convert the resources into other molecules (e.g. converting glucose into ATP; glycolysis happens in the cytoplasm, and can happen in any part of the cell. If that particular glucose molecule is used up, then it will not be able to travel to the center).

Moreover, the "important organelles" are not in the center in particular. If you have seen an image of a typical plant cell for example, most organelles are around the walls of the cell (Figure 2).

Figure 2: a typical plant cell electron micrograph.

Also, you must remember that the Surface Area to Volume ratio is also a restriction for the effective diffusion of waste substances out of the cell. The small volume / big surface area is not only because nutrients have to diffuse in, but also because waste products (like CO2) must be able to diffuse out of the cell, through the membrane.


Are there constraints on where intron/exon boundaries occur with respect to the triplet codons of the reading frame? I did a quick search (here and elsewhere) and couldn't find anything on this subject.
If all introns in a given primary transcript were spliced out in the same way, then this wouldn't matter.  But lots of eukaryotic transcripts have alternate splicing patterns so that one version of the mRNA will contain coding regions that are absent in other alternate forms.

The problem relates to maintaining an open reading frame, avoiding a frame shift and the attendant (and unpredictable) consequences. If a splice donor site occurs within the 3-base codon, it might require that the two (or more) alternate acceptor sites would be in the same relative position in a related codon.

The simplest solution to this problem in my view is to make sure that all splice donor and acceptor sites would be at a codon/word boundary.

Is there any evidence that this is true?

As pointed out by others this is not true. I just verified this for humans (annotations from gencode21).
Methodology:

Obtained the start points of the CDS for all genes
For each exon of each gene, calculated the distance between the CDS start and exon end
Obtained the remainder after dividing this value  by 3 (modulo)

Commands:

Command-1:
    awk 'BEGIN{FS="\t|;";OFS="\t"} $3=="CDS"{print $4,$9}' gencode.v21.annotation.gtf > cdsstart.txt

Command-2:
    awk 'BEGIN{FS="\t|;";OFS="\t"} NR==FNR{a[$2]=$1;next} ($3=="exon" && $9 in a){if($4>a[$9]) q[($5-a[$9])%3]++} END{for(i in q) print i,q[i]}' cdsstart.txt gencode.v21.annotation.gtf

Result:

position | # cases
_______________________
   -2    | 101191
   -1    | 100954
    0    | 99499

As you can see the exons do not necessarily terminate at the third position of the codon.


Pathogenesis of Chronic Venous Congestion in Lungs? I am thinking how CVC in lungs lead to the left-sided heart failure.

I think CVC lead to Pulmonary congestion and edema.
They produce heavy, wet lungs.

Pulmonary changes include

perivascular and interstitial edema, particularly in the interlobular septa;
progessive edematous widening of alveolar septa; and
accumulation of edema fluid in alveolar spaces which contain Hemosiderin and microhemorrhages

Now, the progression of the disease to heart should be discussed.
I am not sure if hemosiderin can go directly from lungs to heart or if it has to travel through circulation and then to left-side of lung.


Effect of the same caloric intake of different macronutrients on body weight To gain weight, caloric intake > caloric expenditure.
To lose weight, caloric intake < caloric expenditure.
But what is the effect of the type of macronutrient ?
That is to say :

does the same caloric intake of carbohydrate, protein, lipid have the same effect on body weight ?
Does X amount of carbohydrate caloric intake > caloric expenditure or X amount of protein caloric intake > caloric expenditure or X amount of lipid caloric intake > caloric expenditure lead to weight gain ?
Does X amount of carbohydrate caloric intake < caloric expenditure or X amount of protein caloric intake < caloric expenditure or X amount of lipid caloric intake < caloric expenditure lead to weight loss ?

This is a hard question because you will find sources that claim that calories from protein have less effect on body weight gain when compared to the same amount of calories from carbs or fats. Likewise you will find other sources that state that a calorie is a calorie regardless of its origin and hence consuming 2000 calories of protein would have the same effect on body weight when compared to consuming 1200 of carbs, 500 of fat and 300 of protein for example.

A proposed mechanism for protein calories having less effect on body weight gain is "thermogenesis" or in order words that some of the energy from protein calories is lost when processed by metabolic pathways after consumption, but this is not globally accepted by the scientific community. Here is an article from the International Journal of Obesity that discusses the subject. I would suggest being VERY picky with the references you find on the subject since there is a lot of info floating around in the web in sites without any scientific backbone.

Something that can be assured though is that different calorie proportions origin-wise cause different results for other variables different from weight such as body composition. In addition to this, there are several studies adressing the apparent statistical find that protein rich foods increase satiety and hence facilitate body weight control; however, the latter is not related to calorie intake count but rather to other factors that decrease hunger physiologically or psycologically.


Why does the funnel-mantle locking apparatus exist, and how / why does it work? I was looking up argonauts, and found this article. As someone who builds things for a living, I was intrigued, but could find no information on how it actually functions in order to help the cephalopod.

Since locomotion is mentioned, I'm assuming that the creature cannot locomote efficiently (or at all) unless this locking apparatus in engaged?

Reference images of some kind (even if scribbled) would really help to explain geometry  / motion.

Argonauts and other octopuses have a muscular mantle which is the outside of much of the body other than the arms.  A cavity is formed by the mantle in which the gills are located.  Water is pulled into the cavity through valve-like flaps and expelled through the tubular funnel (also called siphon or hyponom).  Here is a video of the flaps and funnel as an octopus breathes.

A typical octopus most often moves slowly by crawling across the sea floor.  They have a faster mode of locomotion, though, which is to quickly contract their mantle to force water out the funnel at high velocity.  This jet of water forces the body of the animal in the opposite direction. Here's a drawing of an argonaut moving with this mechanism:

(Here's a video of an octopus using its jet.)

As this jet propulsion is often used for escape, it is important for efficient movement that jet be directed so that the rounded mantle leads the movement and the arms trail.  Since the funnel is flexible, there is a need for a way to keep the funnel aimed away from the mantle.  The funnel–mantle locking apparatus exists for this reason.  A protrusion on the mantle fits into a slot on the funnel and while the animal is propelling itself holds the funnel in place.


How is a T lymphocyte specific to an antigen but not specific to an epitope? In my immunology notes, it states that B lymphocytes (and other APCs) capture and present antigens to T lymphocytes that is specific for an antigen, but that the T cells do not necessarily recognise the same epitope. How can a cell be specific to an antigen but not to the epitope presenting on the surface of the antigen?

I've been in the process of discussing this with a friend and trying to make sense of Janeway's immunobiology and we've come to the theory that the APC recognises the antigen and takes it up, breaks it down and presents the epitope via the MHC where it is then recognised by the T cell. Am I right in saying that the antigen is broken down into many fragments that act as epitopes but each clonal expansion of T cells can only recognise the various epitopes of one antigen?

For this answer lets restrict ourselves to T dependent MHC II mediated responses.

So, an APC like a macrophage or a dendritic cell, takes in a pathogen by phagocytosis and degrades it inside the cell. Some of its broken proteins, which are antigens are presented on the MHC II of this particular APC.

The B cells also do something similar but they identify either free floating antigens or the ones that are expressed by phagocytic APCs. These antigens are broken down in the lysosome. These fragments now are expressed on the surface along with MHC II. This fragment may or may not contain the epitope that the B cell receptor (surface antibody) originally recognised the antigen with. Also, it is not that just one of the fragment is taken to the surface, most of them make it, each with a separate MHC.

The T cell that is going to now interact with this B cell may have a TCR (T cell Receptor) against the epitope in any one of those fragmented antigens on the MHC.

This T-cell is specific to that particular epitope of the antigen it bound to, similarly there could be another T-cell that could recognise some other fragment of the same antigen brought to the membrane by a different MHC II.

So, the epitope that the B-cell and the T-cell recognised the antigen with, needn't be the same. But logically, there's a possibility that they may be.

Note that:

The processing of antigen in the phagocytic APC is not shown in the picture.
B cell recognises antigens not that are displayed on the MHC II (this the T cell does) but those that are tethered on the APC membrane.

Image: Nature Reviews Immunology.


Which point mutations in proteins are OK, and which cause significant change? I heard that some point mutations in proteins are OK, like from alanine to glycine (I'm not sure, it's just an example), some will change the protein significantly. I want to understand deeper but don't know the right keyword. I have tried some but none of them works. Can you give me a good keyword to start searching? Thank you.

There are twenty standard amino acids, and some of them are structurally/functionally similar to each other, such as aspartate and glutamate, or asparagine and glutamine, or glycine and alanine. In general, mutations that cause these amino acid switches don't change the function of the protein, but that's just a general rule - it also depends on where these amino acids are in the protein structure. These are called conservative mutations.


Is the quiescent centre only found in monocot roots? I read that the quiescent centre is present between the dermatogen and calyptrogen. As calyptrogen is only present in monocot root, does that mean quiescent centre is only found in monocot roots?

Note that quiescent centers are typically defined by cell division activity not anatomical placement and are not confined to monocots.

For example, this paper discusses the quiescent center in Arabidopsis roots1.

Reference:
1: Doerner, P. (1998). Root development: quiescent center not so mute after all. Current Biology, 8(2), R42-R44.


Share of water usage by plants From the total water absorbed by the root system, how much water does the plant use for transpiration and how much water does the plant use for photosynthesis?

Your question does not have a single answer, and depends on several factors: the type of photosynthesis (C3, C4 or CAM), the species of the plant, temperature, amount of ground water, relative humidity, luminosity etc.

However, as a good guess, I used to say to my students that around 1% of the absorbed water is used in photosynthesis, the remainder (99%) being either lost by transpiration or used for cell growth. Once more, have in mind that this is a rough estimate, the real number varies.

Now let's have a look at more precise figures, from Bieleski et al. (1999):

As you can see, we have here three kinds of plants (C3, C4 and CAM) here. The column you want is TR ratio (which stands for Transpiration/Photosynthesis ratio). If we consider a C3 plant, the number goes from 450 to 600.

Let's take 600 as an extreme example. A TR ratio of 600 means that the plant loses 600g of H2O to fix 1g of CO2, using approx. 0.4g of water (You'll have to do some math here, using photosynthesis equation), but that tell us that the amount of water used for photosynthesis is less than 0.1% of the transpired water.

Source: Bieleski, R., Farquhar, G., Eamus, D., Atwell, B., Turnbull, C. and Kriedemann, P. (1999). Plants in action. 1st ed. South Yarra: Macmillan Education Australia.


What is frank dehydration? On Wikipedia article about Urine specific gravity we can read:

  A specific gravity greater than 1.035 is consistent with frank dehydration.

What is frank dehydration? How it is different than regular dehydration?

"Frank dehydration" is not really a regular medical term. You can suspect this by using Google search with "frank dehydration" in quotes and site:gov (only 3 websites showing up) and site:edu (2 websites) operators.

The term "frank dehydration" as an informal term can refer to "obvious," "actual," "test-confirmed" dehydration as opposed to feeling dehydrated or thirsty.

Tests to confirm dehydration include a combination of the body exam (dry mouth, prolonged skin turgor, decreased body weight), urine tests (dark urine, increased urine specific gravity, decreased urination frequency and 24-hour urine volume) and blood tests (increased sodium levels - hypernatremia).


What is a mechanical cue? I was attending a talk related to neurogenesis. So one professor was asking a question related to biochemical cues and mechanical cues (related to signaling pathways I believe). Cue as far as I understand is a signal, right? Biochemical cue is understandable for me.

But what does mechanical cue mean?

Mechanical pressure, stress, strain or distortion are mechanical cues. In general, cues sensed by mechanoreceptors are mechanical cues!


If I put a cup over a spider, and leave it there for a day, will the spider survive? Will it travel more slowly since it hasn't had food for a day?

What if I left the cup there for longer?

To answer the first part of your question: it is extremely unlikely that the spider will die or be weakened after just one day.

Wolf spiders (Lycosids) are all predators. Due to variations in prey populations, and low efficiency of consumption at higher trophic levels, they are subject to inconsistent and unpredictable food supply (Greenstone and Bennett, 1980). They are very well adapted to this lifestyle and consequently, long periods of starvation often yield no behavioural changes (Persons, 1999). It is highly unlikely that the spider will die after just one day: Anderson, (1974) observed no changes in activity after starving Lycosa lenta (a species of wolf spider) for 30 days; and Tanaka and Ito, (1982) observed Pardosa astrigera (another species of wolf spider) living for up to 54 days of starvation. Age and sex of the spider are more likely to affect its behaviour and performance than food or oxygen availability (Persons, 1999).

As for oxygen consumption, Greenstone and Bennett, (1980) measure an oxygen consumption of 100µL/hr for wolf spiders. Assuming that your cup is of the size of the unit of volume of the same name, the cup (~0.237L), a small calculation (see figure) shows that there will be enough oxygen for the spider to survive for over 98 days. The oxygen concentration within the cup may decrease as it is used by the spider, however this is likely to have a minimal effect as a cup placed on a surface is unlikely to be hermetically sealed.

In short, oxygen availability is unlikely to have an effect on the spider before other limitations (such as food) are reached. However neither of these effects are likely to cause behavioural changes during the first month.

References

Anderson, J.F., 1974. Responses to Starvation in the Spiders Lycosa Lenta Hentz and Filistata Hibernalis (Hentz). Ecology, 55(3), pp.576-585.
Greenstone, M.H. & Bennett, A.F., 1980. Foraging Strategy and Metabolic Rate in Spiders. Ecology, 61(5), pp.1255-1259.
Persons, M.H., 1999. Hunger effects on foraging responses to perceptual cues in immature and adult wolf spiders (Lycosidae). Animal Behaviour, 57(1), pp.81-88.
Tanaka, K. & Itô, Y., 1982. Decrease in respiratory rate in a wolf spider,Pardosa astrigera (L. Koch), under starvation. Researches on Population Ecology, 24(2), pp.360-374.


Pyruvate dehydrogenase: Apparently anomalous NAD/FAD redox reaction Below is the mechanism for the reactions of the pyruvate dehydrogen complex, which oxidatively decarboxylates pyruvate and transfers the acetyl group to coenyzme A for further metabolism in the Krebs cycle.

The key point is that after $\ce{FAD}$ has reoxidized the dihydrolipoamide, the resulting  $\ce{FADH2}$  is reoxidized by $\ce{NAD+}$, which is reduced to $\ce{NADH}$.
I find the chemical energetics of this difficult to understand. According to standard tables of redox-potential for half reactions, $\ce{FAD}$ is a stronger oxidising agent, and a weaker reducing agent, than $\ce{NAD+}$, which is why it used in the succinate dehydrogenase reaction, for example. How, then, can it reduce $\ce{NAD+}$?
If $\ce{FADH2}$ is really able to reduce $\ce{NAD+}$ it should generate as much ATP in oxidative phosphorylation after oxidation of succinate to fumarate, despite the relatively low free energy change for that reaction. But that is absurd.

Summary
The redox potential widely quoted in text books for the half-reaction reduction of FAD to FADH2 is indeed inconsistent with the observed direction of several reactions involving this coenzyme, including its reduction of NAD+ in the dihydrolipoamide dehydrogenase reaction. The reason for this is that the value quoted is determined for free FAD in aqueous solution, which does not equate to the situation within the enzyme. In its tightly bound state in flavoproteins, the immediate environment (and, in some cases, covalent linkage) alters the affinity of the flavin ring for electrons, hence causing the redox potential to deviate from that in solution. The extent and direcction of this deviation differs in different flavoproteins.
Restating the problem
The basic idea of chemical theromodynamics is that reactions are energetic favourable if the (Gibbs) free energy change is negative (see e.g. Section 14.1.1 of Berg et al.). Although the actual free energy change, ΔG, is influenced by the relative concentration of the reactants, the usual starting point for assessing this in biochemistry is the ‘standard’ free energy change at pH7 and 25˚C — ΔG0′. In the case of oxidation/reduction reactions the standard oxidation–reduction potentials E0′ of each of the two half reactions are usually known (as they can be measured in solution), and one calculates the ΔG0′ from the oxidation–reduction potentials of the two half reactions, using the formula:

ΔG0′ = –nFΔE0′

What is important for this discussion is not so much calculation of actual values, but determining their sign, as for a negative ΔG (reaction energetically favourable) a positive ΔE is required.
Let us consider an example using the much abbreviated version of Table 18.1 of Berg et al. Biochemistry, below:
Oxidant     Reductant       n     E´o (V)
Succinate   α-Ketoglutarate 2   – 0.67
NAD+        NADH            2   – 0.32
FAD         FADH2           2   – 0.22
Fumarate    Succinate       2   – 0.03

Consider one of the energy-generating oxidation reactions of the Krebs tricarboxylic acid cycle:
α-ketoglutarate + NAD+ → succinate + CO2 + NADH
This is made up of two half reactions:
(+ 0.67 V) α-ketoglutarate  → succinate
(– 0.32 V) NAD+ → NADH
which gives an overall ΔE0′ of  + 0.35 V, i.e. a negative ΔG0′, which is consistent with the actual direction of the reaction and the production of energy. (Actual worked numeric examples can be found in Berg et al.)
Now if we consider the dihydrolipoamide dehydrogenase reaction
NAD+ + FADH2 → NADH + FAD
The two half reactions are:
(+ 0.22 V) FADH2 → FAD
(– 0.32 V) NAD+ → NADH
This gives an overall ΔE0′ of – 0.1V, i.e. a positive ΔG0′, which, as the poster astutely points out, is not consistent with the direction of the reaction.
Resolving the apparent anomaly
Berg et al. do, actually, remark on this in section 17.1.1 on the pyruvate dehydrogenase complex:

This electron transfer to FAD is unusual, because the common role for
FAD is to receive electrons from NADH. The electron transfer potential
of FAD is altered by its association with the enzyme and enables it to
transfer electrons to NAD+.

So, how is “the electron transfer potential of FAD altered by its association with the enzyme”? The quotation from Ghia and Massey1 provides a general summary:

The pyrimidine nucleus of the three-membered ring system is electron-deficient and can be viewed as an ‘electron sink’. In thermodynamic terms, any interaction which tends to lower its electron or negative charge density will increase the redox potential. The reduced flavin consists roughly of an electron-rich phenylenediamine moiety fused with a (4,5-diamino)-uracil. The latter is the moiety in which the negative charge (i.e. two electrons taken up by the oxidized flavin) is localized and, most importantly, stabilized. The degree to which this negative charge is stabilized or destabilized is an important factor governing the redox potential. Thus while a positive charge in the protein around the pyrimidine ring will contribute to increase the redox potential, the presence of negative charge or of a hydrophobic environment will lower it.

In the specific case under consideration — dihydrolipoamide dehydrogenase — it has been established2 that a positively charged lysine-57 sidechain (numbering for the A. Vinelandi enzyme) that increases the redox potential (with, perhaps, a small contribution from the backbone N of alanine-326):

[FAD environment in dihydrolipoamide dehydrogenase from A. Vinelandi. NAD is shown in light blue, except for the O and N atoms at the end of the flavin ring interacting with the protein. A section of the latter is shown as a wireframe in salmon pink without sidechains, except for lys57 and ala326. (Own diagram from 3LAD.pdb)]
A second apparent anomaly and its resolution
In drawing attention to the apparent anomaly in the reduction of NAD+ by FADH2, the poster suggested that this would imply one should by able to obtain enough energy to produce 3ATPs from reducing FADH2. The problem with this is that one actually needs FAD to have a lower redox potential to perform the reduction of fumarate that occurs in the Krebs cycle:

This can be seen by considering the redox potentials in the table above:
succinate + FAD + → fumarate + FADH2
The two half reactions are
(–0.22 V) FAD → FADH2
(+0.03 V) succinate → fumarate
Thus, there is an overall ΔE0′ of – 0.19V, i.e. a positive ΔG0′ — another anomaly!
Berg et al. are rather coy on this one. They do not comment, but in their Table 17.2 of free energy changes in the steps of the TCA cycle — where all the other values are given as exact figures — they quote  “~0” for this step.
This implies a higher (more positive) redox potential for FAD than the –0.22 quoted in the table — certainly not the lower one of dihydrolipoamide dehydrogenase.
I turns out that this is, in fact, the case. In succinate dehydrogenase (aka as fumarate reductase) FAD is covalently attached to a histidine residue (his44 in E. coli) at the other side (position 8) of the flavin ring3.

[FAD environment in succinate dehydrogenase from E. coli. NAD is represented as previously. A section of the latter is shown as a wireframe in salmon pink without sidechains, except for his44 and a backbone N. (Own diagram from 1L0V.pdb)]
An extensive review4 of the redox potentials of covalently and non-covalently bound flavoproteins shows that covalent attachment increases the redox potential.
Final observations

Chemistry is a powerful tool for understanding biology at the
molecular level. Biology is subject to the laws of chemistry, but the
chemistry of the special environments encountered (protein interiors,
spaces compartmented by membranes) need taking into consideration,
something that the classically trained chemist, new to the subject,
may not fully realized.
Elementary textbooks often have to walk a fine line between
comprehensibility and truth. The student of biological chemistry
should realize that the initial simplifications that enabled him to
get an overall grasp may mask greater complexities. One of the
intellectual satisfactions in science can be found by resolving these
complexities in a rationale manner.

References
1Ghisla and Massey (1989) Mechanisms of flavoprotein-catalysed reactions
2Maeda-Yorita et al. Biochemistry (1994) 33, 6213–6220
3Kim and Winge (2013) BBA 1827, 627–636
4Heuts et al. (2009) FEBS Journal 276, 3405–3427


How to use Transect-based sampling to select sample trees I was wondering if you help me how to use Transect-based sampling to select sample trees

More detail on what your studying, the question you want to answer, and how you want to go about doing it would be very helpful. But I can answer this basic question of how to select tree's with a transect.

You will need:

Forms to fill out for data.
A compass.
A transect tape (really a very long tape measure, about 100 yards or meters).
A sampling design that fits your study. (I'm assuming you already have this, but if you want to talk more about it see above.)
A wooden meter stick.

Once you are in your 1st area and ready to select a random subset of trees.

Pick a random spot. (Usually done by throwing a stick or water bottle over the back of your head and going wherever it lands).
Pick a random number between 0-360. This will be the random direction you go in from your random spot. Find north on your compass, then which way your random number points. In your mind mark a way point in that distance you can walk to (a mountain peak, a distinct tree, anything).
Stick the beginning of your transect tape in the ground and start walking. The length that you walk should be predetermined from your study design.

Now you'll select trees to perform whatever measurement that you've decided on. But how? Most forests are not so dense that a straight transect tape will touch many of them. This is where the meter stick comes in. Walk back down the transect and choose any tree that comes within 1 meter of the tape on either side. Is the forest not dense enough to include enough trees that way? Then simply increase the length of your transect, or length that you measure out from the transect (ie. 2 meters, or 3 meters).

This is technically called a "belt transect". And it used in natural resources to measure things that are abundant, but not very dense. Such as trees in a forest or shrubs in the desert. It is essentially a giant quadrat.

Why all the randomness? Humans are naturally bias. Even if you think you are not being bias, you could subconsciously be choosing a starting point in a dense patch of trees, or a direction that will let you measure your favorite species. A rigorous study relies on a random sample of a population of interest, and small non-random decisions like this means it is not a random sample, but a bias sample.


Cancer growth and cell division I am confused about the prerequisites for cell division and cancer.

Which of the following is necessary for the cell cycle to progress?

Hormones
Growth factor
Cyclins
Cyclin dependent kinases

Which of the following is essential for cancer proliferation?

Growth factors
Signalling molecules
DNA replication
A control mechanism

How do the cell cycle and cancer relate to each other?

Cyclin dependent kinase is the answer for the first question. Cyclin concentration increases during m phase and falls in g1 s and g2 phase as it is degraded. Cdk is always present in the cell but gets activated during m phase, when cyclin is present. (cyclin dependent)

Cancer cells do not require growth factors to stimulate cell division. They have mutations which disrupts the normal cell cycle regulation. Now can you think what should be the answer ?


Origin, or source, of rhesus negative in human blood This is my first post here, so please be gentle. I recently learned that I have Rh- blood (I'm A-), and was idly looking into blood types on Wikipedia. I was surprised to find that relatively few (~15% of all) humans have it, and most of those seem to be European. Looking just a little further, I found a bunch of crackpot-looking sites that try to explain how people got Rh- blood, and what weird abilities they possess as a result.

I managed to find one site that seemed at least less laughable, which suggested that interbreeding with Homo neanderthalensis (or possibly Homo sapiens neanderthalensis, since the site seemed to indicate that there was some question about how different H. s. sapiens were from H. neanderthalensis) might have accounted for the introduction of the condition.

It seems that from more reputable (medical) sources, the only difference between Rh+ and Rh- is that complications can arise during pregnancy if the mother is Rh- and the fetus is Rh+. Indeed, most sites (e.g., WebMD) seem to explicitly state that there are no other differences of note.

I am not a biologist, or an anthropologist, or a life-science kind of guy at all. However, as a computer scientist, I like to think that I have both an open mind but one which demands scientific and/or logico-mathematical evidence for claims. Lots of the pseudo-scientific, paranormal, etc. theories on the web I basically dismiss out of hand, as explanations which are almost certainly fantasies, but most definitely baseless and untestable.

My question:

  What, if any, is the current scientific understanding of the origin, or source, of rhesus negative blood in human beings? Do individuals with Rh- blood have any common (in a statistically significant sense) characteristics or health issues, aside from the issue with pregnancy and tending to be more European than not? Is there anything to continuing to look into this?

For context, I got started down this rabbit hole while looking into different dieting strategies, and found the "blood type diet". Just as an aside, I don't think there's a lot of merit to that diet... sounds like a fad thing. Any sources or information or help on this subject are appreciated.

EDIT:

I have been looking a little more, and I stumbled across a paper entitled, "The influence of RhD phenotype on toxoplasmosis and age-associated changes in personality profile of blood donors" which looks at the effect of the Rh- trait on personality changes caused by toxoplasmosis (if you Google the title, you should be able to download). Using Cloninger's and Cattel's personality factors, they seem to show a variety of things, including (a) personality differences between Rh+ and Rh- individuals not affected by toxoplasmosis, and (b) different reactions to prolonged toxoplasmosis affection in Rh+ and Rh- individuals.

I didn't even know that parasites could affect your behavior; that seems frightening on the one hand, but on the other, it's fascinating if it's for real, especially since the incidence of toxoplasmosis is not insignificant in most people. Anybody who knows anything about this or who reads the paper and can help me understand what it's saying would be doing me a great favor to answer/comment/chat. Thanks!

Your question has many questions in it.

As for the evolution of Rh factor, Blancher and Apoil (2000) attribute the high level of sequence similarity (92%) of the two RH locus genes, RHD and RHCE to a gene duplication event in the common ancestor of human, chimps, and gorillas. Their analysis of the cDNA from these genes revealed "complex recombination events" after the lineages split.

Basically the most recent common ancestor of apes had the "human" RH genes, which then differentiated after the lineages diverged. Duplicate and differentiate is a common theme in evolution.

As for why it's called rhesus antigen, that's just as experimental artifact:

  The term "Rhesus antigen" was introduced by Landsteiner and Wiener,
  who found that rabbits (and later, guinea pigs) immunized with red
  blood cells (RBCs) from a rhesus monkey produced antibodies which
  agglutinated 85% of Caucasian blood samples (Landsteiner and Wiener
  1940, 1941).

They probably weren't even correct about the antibodies being rhesus:

  In conclusion, if the term "Rh" was coined by Landsteiner and Wiener
  because of the source of antigens (the rhesus monkey) they used to
  obtain anti-Rh in rabbits, it is highly probable that, in fact, they
  produced anti-LW antibodies.


What are the brain structures directly on top of the brain stem? I have been trying to learn the anatomy of the brain, and some information on their functions, through an iPad app called 3D Brain.  Whilst going through the different parts, I have noticed that one area doesn’t seem to be mentioned.

If you look at the image below, you get the brain stem (colour highlighted and labelled).

Going from the brain stem upwards, I am then trying to identify the structures in medium grey which sit on top of the midbrain.

I have seen that the bulbous areas left and right are the basal ganglia.

What are the rest of the structures?  I would like to know what all the mid grey structures are in the first image, but I am especially curious to know what I have drawn around below.

You're looking at many structures in this area.

The region directly above the midbrain is the diencephalon (meaning "across + brain"). From inferior to superior it's composed of the hypothalamus, thalamus, and structures that developed from a developmental region referred to as the epithalamus that include the pineal gland, habenular trigone, and choroid plexus. Between the hemispheres of the thalamus/hypothalmus lies the third ventricle (which may be "bridged" by a structure called the interthalamic adhesion).

Of each of these structures, only the thalamus and hypothalamus are truly visible from your images -- with the hypothalamus articulating with the midbrain and the thalamus emerging superior and slightly lateral to he hypothalamus. The following structures are also visible in your image:

The most inferior structure you see is the pituitary gland, while the "X" shaped structure superior to it is the optic chiasm with cut optic nerves anteriorly and optic tracts continuing posteriorly out of view.
It's not entirely clear, but I believe the two protruding structures posterior to the pituitary are the paired oculomotor nerves.
Finally, the two long ribbon-like structures that extend anteriorly are the olfactory tracts of cranial nerve I that terminate anteriorly in optic bulbs.


How crowded is the bacterial cell? I was wondering what is the protein concentration in an E. coli cell. When studying enzyme kinetics and activity in vitro, I would argue that the substrate and enzyme concentrations resemble those in vivo. As a result, conclusions made by such assays do not apply 100% to the naturally occurring reactions. Are there any examples in literature that address this issue?

Along those lines, what is the concentration of fatty acids/nucleic acids in the cell?

The macromolecule concentration within E Coli is estimated to be around 0.3-0.4 g/ml [1]

The concentrations of your substrate in respect to your enzyme are generally fairly analogous to in vitro studies compared to in vivo studies. However, this is heavily based on the assumption that the diffusion constants for both molecules stay consistent. In many cases that is true and errors can be corrected for using PEG to imitate the crowding effect. And yes, people have begun to look at the question [2]

However, for larger macromolecules like DNA and chromosomes that do see effects from subdiffusive transport, the molecules don't obey diffusive random-wal behavior [3]. The classic model system is the lac repressor which exhibits non-diffusive kinetics due to its interactions with DNA.

http://www.ncbi.nlm.nih.gov/pubmed/1748995
http://www.ncbi.nlm.nih.gov/pubmed/21237136
http://prl.aps.org/abstract/PRL/v104/i23/e238102
http://www.ncbi.nlm.nih.gov/pubmed/7317363


Are there examples of now-living species where one is descended from the other? I'm not a biology person so please forgive me if this question is formulated badly :)

I'm curious. Are there any species that has an ancestor species that is still alive today?

First, you probably want to have a look at this answer who offers an introduction to phylogeny.

There are few subjects that yield to as many semantic issues than the definition of species and the definition of life. Your question is at the border of the species definition. Therefore the question is not so much about Biology than about Philosophy, so let me advertise: The following answer is nothing else than a semantic discussion (philosophy) and has no relevance of our understanding of evolutionary processes. Note however that semantic discussions might be very helpful to evolutionary biologists as well.

Sexual organisms

Dogs and wolves

Commonly, in sexual organisms, species are defined by the concept of reproductive isolation. To address @WYSIWYG's comment, wolves can breed with dog. The offspring is called a wolfdog and it suffers from little inbreeding depression.

Is the MRCA contained in the species of one descendent

But I'll use the wolf example anyway and make some fake assumptions. There are probably better examples I could pick though. Let's assume that wolves and dogs can't interbreed, that they are therefore separate species. Let's assume as well that somehow we manage to recreate the Most Recent Common Ancestor (MRCA) of wolves and dogs (which has some issue due to parental effect incl. culture and epigenetic) and this MRCA can breed with wolves and but not with dogs, then we could eventually say that the MRCA and the current wolf (there are actually 3 species of wolves that are probably not real species) are the same species. One could then say that dogs descend from the wolf.

Feeling that we talk about improvement over another species

I think that much of the issue in saying that the dog descend from the wolf is that some people would understand things like "dog is more evolved than the wolf", which makes no sense. Both the current wolf and the current dog has evolved for exactly the same amount of time. Any living species on earth has evolved for exactly the same amount of time (almost 4 billion years).

Temporal constraint in the definition of species

Therefore, it is eventually possible to say that one node on a phylogenetic tree is of the same species that the previous and the next node. I think that in reaction to the misleading feeling that early evolutionary biologists and current non-biologists people have in hearing that one species descent from another one, we tend to make a temporal constraint to the species. A species is what it is only at the exact moment we talk about it. This prevents us to consider a MRCA as being of the same species of any descendent.

Note that the definition of species yield to various issues such as the case of ring species.

Asexual organisms

Same issue as above

Now, if we talk about asexual species. There is no clear definition of what is a species there. Of course if we were to use the definition based on reproductive isolation, then any asexual individual would be a new species. We therefore define a species when we see a group of phylogenetically related individuals that all share some feature that we find "interesting enough" (very arbitrary) to describe this group as a different species from the some other group of individuals. In asexuals, you may see one lineage that accumulate 10 mutations, while the other lineage accumulates 1000 mutations (this other lineage may eventually live in a different environment than the MRCA of the two lineages). Therefore, you get to the same issue when thinking about asexuals than about sexual organisms. If one lineage ressemble more their MRCA than the other lineage, then is their MRCA part of the species of one lineage?

Is a species a thing?

Well... the concept of species is useful in the sense that it is often not ambiguous to classify one individual into one species or into another. The concept of species allows us to better communicate.. so yes I guess it is useful.

The concept of species existed way before we had any understanding of natural selection, mutations, genetic drift and other basic concepts in evolutionary biology. Aristotle used the concept of species (he also thought without having any good evidence that life evolves). This concept of species has been very well conserved because of the static view we had on what a species is before Darwin. Now that we have a better understanding of evolutionary biology, ecology and reproductive biology we discover that the concept of species is not a natural category but is a man-made unclear category.

Other discussion on the subject

In this post I made an overview of the issue related to the concept of species. I did not go into the details but tried to list important concepts.

You will find many websites that address the concept of species in philosophy. I particularly like discussion in the concern of how current bad semantic may yield to bias in the way we think nature and may yield to bad decision in applied science. Here is a podcast (in french) on the origin and consequences of the concept of species.


How are Stem Cells Produced for Stem Cell Based Therapies? I was doing an initial search on google but couldn't come up with anything I'm looking for. I know were stem cells come from and a bit about their levels of differentiation. For example, embryonic stem still becoming mesenchymal stem cells and what not. I also understand that epithelial tissue cells can be converted to a pluripotent stem cell state but at very low efficiency. So, all that aside how are stem cells obtained in the volumes necessary for stem cell based therapies without causing them to start differentiating during production?

I didn't get your question exactly. If you wanna ask how to maintain the potential of stem cells, yes, there are several compound that could keep stem cells, such as Leukemia Inhibitory Factor (LIF). As far I know, the using of pluripotent stem cell, such as ES, iPS, still has the problem of formatting teratoma in vivo studying. It means totally differentiating pluripotent stem cell still need to be work out.


Question about SAM CIGAR string My question is about the CIGAR specification.

The documentation states:

M 0 alignment match (can be a sequence match or mismatch)

I 1 insertion to the reference

Q1: If I have a CIGAR string 99M170661N26M, does that mean I have 99 matches. Can that also mean 99 mismatches? What about 98 matches and 1 mismatch? The specification states it could be a sequence match or mismatch.

Q2: Assuming I'm doing an RNA-seq experiment. In my CIGAR string 99M170661N26M, does that mean my read aligns to an intron which has 17066 bases? Can I think like: "I have a spliced read which aligns to two exons and an intron. I have 99 matches to my first exon and 26 matches to my second exon. I have 17066 matches to my intron."?

EDIT:

Can I get the number of matches in my read? Does that even make sense? For example, how do I know if I have 10 exact matches?

Q1: Yes, the CIGAR string operation 'M' means you can have both matches and mismatches. For example if you have a CIGAR string 10M, then you could have 10 bases that matched perfectly or you could have 5 matches and 5 mismatches. In this case, you have what are known as SNPs (or single nucleotide polymorphisms).

Q2: In your case, you have 99 matches, 170661 skipped regions in the reference genome, and 26 matches.

Q3: If you want to find out how many matches or mismatches there were, you'd have to take the reads from your SAM file, align them to their position in the reference genome, and compare them base pair by base pair to see if their nucleotides match. You can take advantage of the positional information found in field 4 of the alignment to accomplish this.

You can write your own code to accomplish this or use  something like Samtools, which I believe comes with a variant caller.


Why seeds won't sprout given excess water? What would cause a seed to not sprout despite showing signs of germination given excess water? Oxygen, temperature, and light were sufficient for germination and sprouting in seeds of a slightly lesser amount of water.

You've stated in your question that oxygen was sufficient for germination, but if there's too much water this probably isn't the case. It's likely given excess water seeds will drown- that is they have not got access to sufficient oxygen to continue germination.


Do you produce more sperm after 1 week of abstinence vs 1 year of abstinence Question: I was wondering if the amount of sperm increase with the amount of abstinence?

Side questions:

Is their a max amount of sperm?
What happens with the excess amount?

There is an increase by abstinence.

  The within-subject variability of the semen sperm count (n), volume
  (v) and the total number of spermatozoa (N) was studied on 220
  ejaculates from 36 normal subjects after an abstinence of 7 days or
  less.

  The three semen characteristics for a given subject were highly
  correlated with the length of abstinence: for an increase in
  abstinence of 1 day there were mean increments of 13 × 106/ml for n,
  0·4 ml for v, and 87 × 106 for N.

1979 - Within-subject variability of human semen in regard to sperm count, volume, total number of spermatozoa and length of abstinence

  Semen analysis was performed on six men after various sexual
  abstinence periods (from 2 to 18 days). The variations in semen
  parameters were analyzed statistically as a function of the duration
  of abstinence.

  Lengthy sexual abstinence was found to affect all semen
  characteristics. Semen volume and concentration and total sperm count
  showed significant increases, whereas motility and normal morphology
  decreased significantly with duration of abstinence. Significant
  changes in the percentage of normal sperm forms were observed after
  more than seven days' abstinence.

  The study indicates that the influence of long sexual abstinence on
  semen quality varies with the variable considered. With regard to
  fertility, a long abstinence period might induce senescence of
  spermatozoa.

1994 - Effect of long abstinence periods on human sperm quality.

Sperms can die of "old age", as the previous quotes mentioned long abstinence period induces senescence. It is hard to find anything about their lifetime, it is at least 7 days I think.

  For humans, entire process of spermatogenesis takes 74 days. Including
  the transport on ductal system, it takes 3 months. Testes produce 200
  to 300 million spermatozoa daily.

according to wikipedia

So there is a constant rate of sperm production.

I think the following differential equation can describe the change of the sperm count:

$$ \dot{x} = μ - Dx $$

where

x is the sperm count
μ is the production rate regulated by testosteron (about 250 million per day)
D is the death rate which depends on the age of the population (depends on the lifetime, production rate, elapsed time)

So there will be a maximum amount by abstinence. By that amount

$$ μ = Dx $$

so

$$ x_{max} = μ /D $$


What animal/insect is this? I saw this animal (probably insect) in my house in the Netherlands:

I have searched on the internet but was not able to find what this is, I first thought it was a kind of dragonfly, however there are only two wings which is not usual for a dragonfly. Any suggestions what this is?

It is an insect of family Chrysopidae under the order Neuroptera (net-winged insects).
The insects of this family are commonly called Green lacewings.
Neuropterans have large lateral compound eyes, four wings and a generalised pattern of veins.

(Source: Wikipedia)
Identifying morphological features:

Soft-bodied insects with copper-colored eyes, long thread-like antennae, and lacy wings.
Most species are green, but some are brown, especially overwintering adults of certain species

( Reference: Bugguide )
A similar family of lacewing, Hemerobiidae also exists which are brown, have rounded smaller wings and found throughout the world.
Here's a link to wikipedia showing the phylogeny of the Neuroptera as explored using mitochondrial DNA sequences: link .


Has a beneficial mutation ever been documented? I am trying to find a case/study where scientists documented a mutation in an animal or human that was to the benefit of the host.

The closest thing I have been able to find is sickle cell anemia (SCA) helping to fight malaria. However, the life expectancy for people with SCA is 40 – 60 years, and in 1973 it was only 14 years (source). I am looking for another case, preferably one that is not life-threatening.

Are there any other cases where a beneficial mutation — one where the good outweighs the bad — was documented?

By beneficial I simply mean that it helps or protects the host in some way, while not causing substantial harm. As in my example of SCA it can benefit the host if the host lives in an area with malaria. However, it is also life threatening and reduces the life expectancy of the host.

If — for example — SCA would only cause pain and not be life-threatening, then it would (in my opinion) be a beneficial mutation. While not purely beneficial, it would still increase the life expectancy of people living in an area with a high occurrence of malaria.

The answer depends on what you mean by "observed".

Bacteria acquire antibiotic resistance genes all the time, for example. This happens 'in the wild', but you can see in the lab that bacteria can become resistant overnight - I'd call that 'observed'.

There are many papers about the emergence of antibiotic resistance (not that I'm suggesting this is the only observable beneficial mutation).

In this paper, for example, several spontaneous mutations are induced in H. pylori in the lab in a short space of time:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC90364/

In this paper, estimation of mutation rates are attempted in the emergence of resistance:
http://aac.asm.org/content/44/7/1771.full

It should be pointed out however that the timeframes can vary wildly. If a bacteria acquires a resistance gene by horizontal transfer, for example, this could be considered virtually instantaneous. Spontaneous mutations may take longer to emerge, and might only do so in the presence of steadily increased selection pressure, by contrast.


What species of wasp is this? And how to get rid of them? Yesterday while moving a chair in my garden I got stung by a group of wasps. During the night I went hunting for their nests and managed to neutralize 3 of them: one was in the chair's legs, about the size of a child's fist and with a dozen on them inside. It was made of grey hexagonal cells, similar to paper in appearance.

(Sorry for the blurry image, I was a bit scared :-P)

Then I've found another one in a water hose tube that was slightly smaller, but quite active.

And finally a third one in a vase, it was very small, only had a couple of cells in it and wasps were working on it, almost as if they were building it from scratch.

Given the number and size of the nests I'm afraid that they could be spreading in the garden. I have already noticed that a couple of them survived the massacre of last night and I'm worried that unless I kill every of them they might keep nesting.

I don't know much about the hierachical society of wasps, but I was not able to identify the queen (although I haven't checked every single one I've killed). Reading online I've found that killing the queen might mean that the worker would eventually die.

So what kind of wasp is this? What can I do to make sure that they do not keep bothering me?

EDIT: by the way, I live in northern Italy

These are European paper wasps.

(They look very similar to yellowjacket wasps but you can notice the antennae; they are brown here whereas they are black in case of yellowjackets. There are other subtle differences too.)

See this post on Gardening & Landscaping stackexchange about getting rid of wasps.

(This part is probably not really on-topic here and I don't want to copy-paste an existing answer in another stackexchange site.)

If you are upvoting this post then please also upvote the original one in G&L SE


Help identify this mite? I saw a decimal-sized dot walking on my hand. I wanted to know what this is, so I got it onto some paper and sandwiched below a piece of clear tape so I could keep it in place and photograph it. However it's so small that even with my camera lens almost touching the specimen, I can't get a great photo. It's small, about 0.8mm long, beige or gray or brown with a pattern on the back. It's a little smooshed from the tape so it's hard to tell if it has 6 or 8 legs and is an insect or an arachnid. But hopefully based on the shape, size, and pattern it can be identified.

Location is southern California.

Update: I now believe this to be a rat mite or bird mite. I'll include some additional photos that were better quality (photos were taken with a close-focus camera, mites were on printer paper underneath Scotch tape, back-lit by an LED light):

This appears to be a bird mite (or possibly rat mite) in the genus Ornithonyssus of the parasitic family Macronyssidae.

 Credit: user Aewills on bugguide.com
Distinguishing between species is difficult.
In fact, according to idtools.org, identification of Mesostigmata to family or lower can usually only be accomplished only if the specimen is an adult female.
Blaine Mathison mentions the following features useful for identifying these mites to lower taxonomic levels under magnification [source: bugguide.com]:

chelicerae shape
dorsal plate breadth and degree of dorsal coverage
spiracle present between legs
genitoventral plate width
sternal plate shape and presence of setae

You can find existing answers to posts about bird mites on Bio.Stackexchange below:

Bug Identification: Tiny Bugs
Tiny white very hard cell bug! Please help to identify!


Does Human Female Meiosis II occur after fertilization with sperm? I am reading the answer and I am getting confused by the sentence:

  At the end of meiosis I females have two daughter cells and meiosis II
  only occurs if and when fertilization occurs by a sperm cell.

The clause suggests me that meiosis II starts after the sperm has ignited the fertilization process in female: I do not know how that exactly works.

Wikipedia says:

  The process of fertilization involves a sperm fusing with an ovum.

So female meiosis II must happen before the sperm fuses with the ovum.
Sperm must ignite some process in female that puts female meiosis II going on before sperm can fuse with egg. Is that right? How is that going to happen?

Primary oocytes are formed prenatally and reain suspended in prophase of meiosis I for years until the onset of puberty. An oocyte completes meiosis I as its follicle matures (during ovulation) resulting in a secondary oocyte and the FIRST polar body. After ovulation, each oocyte continues to metaphase of meiosis II. Meiosis II is completed only if fertilization occurs, resulting in a fertilized mature ovum and the second polar body.

So in short, the egg is stuck in metaphase II until fertilization.


About The Selfish Gene Book - How Replicators Molecules forms duplicates? I was reading The Selfish Gene. In the 2nd chapter - "Replicators" I read:

  Think of the replicator as a mold or template. Imagine it as a large molecule consisting of a complex chain of various sorts of building block molecules.

  The small building blocks were abundantly available in the soup
  surrounding the replicator. Now suppose that each building block has
  an affinity for its own kind. Then whenever a building block from out
  in the soup lands up next to a part of the replicator for which it has
  an affinity, it will tend to stick there. The building blocks that
  attach themselves in this way will be automatically arranged in a
  sequence that mimics that of the replicator itself.  It is easy then to
  think of them joining up to stable chain just as in the
  formation of the original replicator. This process could continue as a
  progressive stacking up, layer upon layer.

  This is how crystals are formed. On the other hand, the two chains
  might split apart, in which case we have two replicators, each of
  which can go on to make further copies.

I don't get the part in bold.

If these molecules joins the replicator then the replicator wouldn't change?
To what refers with "The building blocks that attach themselves in this way will be automatically arranged in a sequence mimics that of the replicator itself"? A new sequence? The same sequence?
In the part "It is easy then to think of them joining up to stable chain just as in the formation of the original replicator", what is it joined? replicator with this building block? these building blocks with other building blocks in the soup to form a copy of replicator?
Why you can infer that is how the crystals are formed?

Take into account that I don't have a solid biology background, so it would be great if you can answer it in detail. I really appreciate your help!.

This is how I think about it.  Here is the original large molecule, with each of its 'parts' represented by a letter.  There are a few different kinds of part:

C-A-A-C-T-A-T-A-C-G-A-C

As it drifts around in a 'soup' of parts, new parts stick to it one by one, like for like.  Here it is after two parts stick to it:

C-A-A-C-T-A-T-A-C-G-A-C
  A         T

Here it is after a few more:

C-A-A-C-T-A-T-A-C-G-A-C
C-A   C   A-T   C   A

Eventually, all the parts have got a similar part stuck to them:

C-A-A-C-T-A-T-A-C-G-A-C
C-A-A-C-T-A-T-A-C-G-A-C

Now, if the two halves split, the molecule has replicated itself.


Insect identification, Chennai, India Could someone tell me what the species of this beautiful insect is? Location: Chennai, India.

Thank you!

To me, it looks like a Lepidoptera from the Sphingidae family (Hawk moths). It is similar to species in Hemaris and might belong to this genus.

One similar species from this genus (found in India) is Hemaris tityus, but the moth in your picture doesn't look exactly like this particular species. Another similar species is Hemaris saundersii, which is found in and around India.

(Hemaris tityus, pic from wikipedia)


Why are $\beta_2$ receptors present on bronchial smooth muscles , considering that they have only parasympathetic innervation? It is well known that the bronchial muscles have only parasympathetic innervation. But they still express $\beta_2$ receptors. How does this system still cause bronchial relaxation? What is the exact mechanism?

Good question, but first I'll address a note in the comments.

In bronchial smooth muscle, do β2 receptors receive sympathetic innervation?

Canning and Fischer (2001) claim that bronchial smooth muscle do receive sympathetic innervation. But it would still be correct to say that β2 expression plays little role in regulating smooth muscle tone in the human airway under normal conditions.

How do β2 receptors cause bronchial smooth muscle relaxation?

You already know that this receptor is associated with bronchial relaxation. An article by Billington and Penn (2003) claims it works through Gs coupling. This binds adenylyl cyclase causing it to form cyclic AMP which activates protein kinase A (PKA) which carries out many more functions.

WHY are β2 receptors present on bronchial smooth muscles considering [minimal sympathetic] innervation?

Circulating chatecholamines released due to emotion, exercise and the like. Billington and Penn (2003) note "prophylactic bronchoprotection" as the central role for Gs-coupled receptors in airway smooth muscle.

Why ELSE are β2 receptors present on bronchial smooth muscle?

β2 receptors are important in regulation of airway smooth muscle cytokine/chemokine synthesis, and inhibition of airway smooth muscle growth (DNA synthesis/cell proliferation) i.a. (Billington and Penn 2003).


How to reduce the number of sequences in a Multiple Sequence Alignment? I have a Multiple Sequence Alignment, where there are around 5000 sequences. There also exists many sequences where, there are so much of non-sequenced regions (for instance, AU----CGGGCA--NNNNNNNNNN).

So, by trial and error, I found a threshold value of 25%, so I removed the sequences which contained more than 25% of non-sequenced region (N's here), retaining around 400 sequences in the alignment, by writing a simple R script.

But, I would like to know, if there is any other standard method to do this, because I do not think, removing sequences based on finding a threshold for the percentage of non-sequenced regions, by trial and error is more efficient.If there is, can you please tell me, how to do?

Thanks in advance.

The bioconductor package "ShortRead"  might be what you are after.
It has a function "clean" to remove sequences with ambiguous bases. It also can remove duplicates if you need to.


Identifying statistically significant gene rich and gene poor regions I am just wondering If there any adapted way of Identifying significant gene rich and gene poor regions in each chromosome for a given genome say mm10?

Interesting question. I don't myself know how to do this but a literature search returns some older papers on how this was achieved for pig and chicken genomes over a decade ago. The best way to do this today is to look through annotated genomes (like the mouse mm10) and use a gene density metric. You can achieve this with R code, writing your own code, trying to use some of the rich features provided in-browser at the UCSC genome browser (for mice, otherwise start here), or perhaps try to search literature for gene density stuff. I defer to others for more specialized answers.

PS. Since you're also interested in determining statistical significance, you probably will need to apply this over a sliding window across chromosome lengths, and this kind of question has been answered often elsewhere on SE (example). Sorry I can't be of more help; good luck!


How do insects such as crickets circulate blood through their antennae? Some insects, like the crickets pictured below, have such slender antennae it seems no blood could fit. How do they get blood through their antennae?

Insects primarily get oxygen through diffusion of air through their skin.  I doubt the antennae need hemolymph circulation.


If fully colorblind people only see shades of white,gray, and black, does that mean that the colors black, white, gray are colors humans can’t see? And since the brain can be tricked to thinking that objects with mostly black and grey gradients are moving, like optical illusions, does that mean motion has a color?

Based on your question: if fully color-blind people see whites, blacks, and greys, that means that humans can see them colors. After all, aren't color-blind people humans?

If you actually think about it, is color just created by evolved cells? If so, should we not see just black, grey, and white?


Can you "spam" bird sounds so that birds no longer interpret them right? Is it possible to make birds confused by repeating recorded chirping or singing? Or do they always perceive them as usual, even if the situation is clearly not as described by those sounds?

For example:

mating song when there's no mate
danger/alarm cries when nothing's going on

Specifically, I'm interested in public placed with a lot of traffic using looping speakers to scare off birds that like to dump upon almost unsuspecting citizens. Like underground entrances and city malls. Does the effectiveness decrease over time because of that?

This is at least doing some confusion, probably also harm. A lot of wildlife conservationists warn about using smartphone apps which replay bird songs, as they are confusing the animals. An example is the Dorset Wildlifetrust.

This phenomenon has even be analyzed scientifically, and the results show that birds are irritated. Territorial birds seem to be affected more and it has been shown that, when a fake call was replayed to them, they sang more often and longer. In the first paper they speculate that this will drain too much energy and prevent the birds from doing other important things.

The second paper looks at zebra finches, which are not territorial. Here they find that birds pay less attention, the more often the song is replayed.
The articles:

Simulated Birdwatchers’ Playback Affects the Behavior of Two Tropical
Birds
Habituation in songbirds.


Can MHC class I be used for presenting peptides of extracellular origin by non-professional APCs? Wikipedia says that: "The antigens presented by MHC class II are derived from extracellular proteins (not cytosolic as in MHC class I)."

So does this mean that MHC class I cannot be used for peptides derived from phagocytosis by non-professional APCs? (i.e. peptides that of extracellular origin?).

For example, when non-professional APCs that can undergo phagocytosis (Eosinophil, neutrophil, dendritic cell) engulf bacteria, will they present their antigens using MHC I although the peptides are of extracellular origin? or will they not present any MHC at all? thanks!

when non-professional APCs that can undergo phagocytosis (Eosinophil, neutrophil, dendritic cell) engulf bacteria

Dendritic cells and probably neutrophils are professional APC, so this part of the question is a little confusing.

You're asking about cross-presentation, which is the process by which extracellular antigen can be presented to CD8 T cells on MHC class I.  Cross-presentation is mainly performed by certain sub-classes of dendritic cell. A number of other cell types have been shown to be capable of it, but it's not clear how important they are in vivo.

A decent review of cross-presentation is Understanding the Biology of Antigen Cross-Presentation for the Design of Vaccines Against Cancer.  A review of a related but somewhat different concept (MHC recycling) is Endocytic Recycling of MHC Class I Molecules in Non-professional Antigen Presenting and Dendritic Cells.


What makes alcohol harmful to mammals? During the alcohol metabolic pathway, harmful by-products are made like acetaldehyde, hydroxyethyl, superoxide anions, and hydroxyl radicals. How do these toxic compounds harm our tissues? Many of these intermediates are the compounds that are responsible for hangovers, but are they also the molecular cause of liver damage?

Superoxide radicals , basically damage the lipid bilayers. affecting the efficient gradient.
for example H+ ion gradient across lipid bilayer in ETC is very important. this gradient is affected if superoxide radicals are present.


What is the mechanism that directs myosin walking? Myosin, dynein and kinase all "walk" towards specific ends of the microtubule or actin filament they are on. I'm most familiar with the walking mechanism for myosin, where ATP fuels conformal changes in the binding region, but I don't understand how it chooses to go one direction over another. Actin fibers' positive and negative ends are fueled by the addition of G-actin via ATP and its subsequent reduction to ADP, so I suspect that this process is somehow involved in determining the direction of myosin's movement.

As just a secondary thought, are there differences in the mechanisms of the movement between the three walking molecules listed above?

Good question that got me waist-deep in PubMed. It appears that the directionality of myosin motors is due to the angle at which the actin-binding catalytic domain is attached to the neck region. This review by Vale and Milligan, 2000, sums up the "unzippering" of the neck region that contributes the force for the movement (a video from the review adapted for Alberts' textbook is also informative).

Most myosins move towards the plus end of actin, but myosin VI moves towards the minus end. The neck region of myosin VI attaches to the head region at a different angle than conventional myosins and this is the apparent reason for the change in direction preference (see Figure 1 in review by Rodriguez and Cheney, 2000; also Volkmann and Hanein, 2000; Masuda, 2008).

And for your entertainment, an awesome movie of myosin V walking by Kodera et al, 2010 on YouTube.


Do the enzymes and compounds in saliva help with stain removal? Does spitting on stains help with removal?
Saliva is high in amylase that should help with the breakdown of protein rich stains like blood and semen. It also contains antimicrobial enzymes and antibacterial compounds. Does semen contain any kind of surfactant agents?

So, my questions are:
Does spitting on a semen stain aid in or add to the cleanup?
On which stains are saliva beneficial and how long does it have to sit?

It would depend on the stain - and more specifically the material and staining agent. Saliva contains blood clotting agents so I doubt it would help with removing blood stains. The enzymes in saliva are unlikely to help with the stain removal.

The water in saliva would be more likely to help, dissolving the stain. So your probably better off with water.


How does a thymidine block halt DNA synthesis? The best I've been able to find is that there's a feedback mechanism, but what is this feedback, and how does the mechanism work? If it's just that the concentration of thymidine is too high, why won't excess quantities of other nucleotides do the same thing? (Or do they, and I don't know about it?)

Excess thymidine in a mitotic cell generates negative feedback on the production of deoxycytidine triphosphate from cytidine-5'-phosphate. Excess quantities of deoxyadenosine and deoxyguanosine also block progression through S-phase. However, as a reagent for the control of replication timing, thymidine has been found to work best as its blocking activity can be applied and reversed more consistently.

Xeros N. (1962) Deoxyriboside Control and Synchronization of Mitosis. Nature 194: 682-683.