text:
Construct Phylogeny form Edgelist
I am working on large scale biodiversity simulations and have collected a lot of data on simulated phylogenies. I have a list of child-parent edgelist species in the form:
list = [1, 1, 2, 2]

      /-- 3
1 -- 2
      \-- 4

children = [1, 2, 3, 4]
parents = [1, 1, 2, 2]

Where the index is the child and the value is the parent. 1 is it's own parent (the root).
I have such a tree for a large dataset upwards of 1000 individuals. I can build the tree programmatically in igraph or networkx easily and visualise it. However, I cannot find a way to convert the tree into a format for phylogenetic analysis. There are function to convert dendropy and ete trees from igraph/networkx into their own formats but no way to re-import the igraph/networkx trees. There also appear to be no way to write the igraph/networkx trees into phylo formats (newick).
There also seems to be no support in dendropy or ete to programmatically build trees and it would be infeasible to manually build all the trees I have.
Is there a way to build the trees so I can analyse and visualise them as phylogenies?
Tried approach
library(ape)
p <- c(NA, 1, 1, 3, 3, 4, 4)
x<-data.frame(name=as.character(c(1:7)) , id=1:7,  parent = c(NA, 1,   1, 3, 3, 4, 4))
x1<-na.omit(x)[,3:2]
n <- c(c(1, 3, 4), c(2, 5, 6, 7))
edges <- matrix(c( x1$parent, x1$id), ncol=2)

tree<-list(edge=edges, Nnode = 3, tip.label = as.character(x$name[c(2, 5, 6, 7)]), node.label = as.character(x$name[c(1, 3, 4)]))

class(tree)<-"phylo"

#plot.phylo(tree, show.node.label=TRUE)

The plot command just causes R to crash and the tree object has an invalid structure.

Perhaps https://stat.ethz.ch/pipermail/r-sig-phylo/2009-July/000405.html, let me know if this works. I'm not very skilled in R myself, unfortunately! (just for converting edge list matrix to phylo)

Thanks. I tried to get this code to work but I keep on getting errors with my edgelist. I also found this question on stack overflow convert df to dendrogram.  However I don't think their code would work for an edge-list as it seems to require all possible paths to mapped into a dataframe. I will add an example of what I tried to the question.

It seems like standard edge list format is two columns (e.g., for igraph: http://www.shizukalab.com/toolkits/sna/sna_data). Can you output your list in that format?

sure ill edit the first example. In the second example the child list is [1:7]. I believe the graph should be possible using graph.adjlist(mylist, mode = 'out')

It looks like the phylo constructor changed since the link posted above: https://stat.ethz.ch/pipermail/r-sig-phylo/2014-May/003467.html

I can't find anything that changed in how they construct the example tree in the documentation.

This will be a complete answer, but it's got code, so it won't work as a comment. Working backwards from rtree(3), here's a way to build a phylo object from component parts, which might be helpful:
children <- c(5, 1, 2, 3)
parents <- c(4, 5, 5, 4)
x <- matrix(c(parents, children), ncol = 2)
tr <- list(edge = x, tip.label = 1:3, Nnode = 2)
class(tr) <- "phylo"
plot(tr)

Doing the same with your children and parents, doesn't work, however.
children <- c(1, 2, 3, 4)
parents <- c(1, 1, 2, 2)
x <- matrix(c(parents, children), ncol = 2)
tr <- list(edge = x, tip.label = 1:3, Nnode = 2)
class(tr) <- "phylo"
tr

Gives
Error in if (tabulate(phy$edge[, 1])[length(phy$tip.label) + 1] > 2) FALSE else TRUE : missing value where TRUE/FALSE needed
I don't know hot to make the edge list conform to the expected order for a phylo.

yeah I get the same problem. Maybe R isn't the answer. I really only want to extract the newick tree so I can analyse the tree probably in python.

@kmm's code works with a few tweaks. One problem your edgelist has is that it contains a singleton node, which ape does not like to deal with. Turning it into a proper phylo object means removing the singleton 'root' node and instead making the child of this singleton node the root. Here is an example using a slightly larger tree, which demonstrates how to make a tree with both leaf nodes and internal, non-root nodes.
The trickiest part is translating the parents and children list into ape's unusual internal numbering system.
phylo_from_el <- function(el){
  i <- 0
  for(n in el[2:length(el)]){
    i <- i+1
    parents[i] <- n
    children[i] <- i+1
  }
  nnode <- sum(children %in% parents) + 1
  nleaf <- length(el)-nnode
  # Translate preorder sequence into ape sequence
  ttable <- matrix(c(1:length(el), rep(0, length(el))), ncol=2)
  ttable[unique(parents),2] <- 1:nnode + nleaf
  ttable[-unique(parents),2] <- 1:nleaf

  parents_t <- sapply(parents, FUN = function(x)ttable[x,2])
  children_t <- sapply(children, FUN = function(x)ttable[x,2])

  edge <- matrix(c(parents_t, children_t), ncol = 2)
  tr <- list(edge = edge, tip.label = 1:nleaf, Nnode = nnode)
  class(tr) <- "phylo"
  return(tr)
}
el <- c(1,1,1,3,3)

tr <- phylo_from_el(el)

plot(tr)

This code did not work for me so I wrote an R Script to generate a Newick code.
I have a edge list tree_data
 head(tree_data)
  parent node branch.length label
1    117  112      5.093319   124
2    117  116      9.090761   128
3    117  136      9.219770   153
4    117  109      9.292008   121
5    117  108      9.370598   120
6    117  118      9.552086   130

Here is the R code:
tree_data$newick = paste(tree_data$label,':',signif(tree_data$branch.length,3),sep="")
nparents = 2
while(nparents > 1){
leaf = setdiff(tree_data$node,tree_data$parent)
parent_leaf = unique(tree_data$parent[!is.na(match(tree_data$node,leaf))])
index_remove = integer(0)
for(i in 1:length(parent_leaf)){
  parent_children = tree_data$node[which(tree_data$parent == parent_leaf[i])]
  all_children_in_leaf = all(parent_children %in% leaf)
  if(all_children_in_leaf==T){
    index_remove = c(index_remove,match(parent_children,tree_data$node))
    tree_data$newick[which(tree_data$node==parent_leaf[i])] = paste("(",paste(tree_data$newick[match(parent_children,tree_data$node)],collapse=" , "),")",tree_data$newick[which(tree_data$node==parent_leaf[i])] ,sep = " ")
  }
}
tree_data = tree_data[-index_remove,]
parent_next = unique(tree_data$parent[!is.na(match(tree_data$node,leaf))])
nparents = length(parent_next)
if (nparents==1) newick_code = paste("(",paste(tree_data$newick,collapse=","),")",colnames(Adj)[parent_next],";",sep = " ")
}

tree <- ape::read.tree(text=newick_code)
p = ggtree(tree, layout="circular")

There is an issue in this code, see here for more info: https://bioinformatics.stackexchange.com/questions/20677/plot-phylogenetic-tree-from-list-of-edges


text:
why didn't natives of south america evolve darker skin?
I understand that darker skin tone is caused by melanin which helps to protect against the extra UV radiation that comes from more direct sunlight. It evolved in Africa before we migrated away from Africa and as I understand it was later evolved away from in areas further from the equator, where less sun meant less need for UV protection, because less sun also made it harder to get sufficient Vitamin D. Thus those near the equator tend to have darker skin and the further from the equator one goes the lighter the skin.
There are parts of South America which reside right on the equator, where melanin would provide important UV protection and where vitamin D deficiency was not a concern. I would expect them to have black skin, as dark as someone from Northern Africa or the Indonesians has, due to the extra UV exposure associated with the equator.
However, natives of Brazil and other equatorial parts of South America don't seem to have the same skin pigmentation as I see in the other equatorial areas.  They have skin darker then Europeans and other northern natives sure, but not to nearly the degree of other equatorial natives.  They clearly have the mutation for melanin, since that existed before we left Africa and they do have partial dark skin, which suggests that for some reason there was an evolutionary advantage to having skin as dark as theirs, but not darker.
Can anyone explain to me why South Americans wouldn't have evolved (or not evolved away from, depending on what part of the world they originated from) the almost-black level of dark skin the other equatorial natives possess?

This question really needs to be pruned down a lot. Focus on the core question (Why are indigenous people in South America not as dark as sub-Saharan Africans living at the same latitude, with the same intensity of sun exposure?) and get rid of all the fluff, background, and other unnecessary material.

The current prevailing wisdom on human migration holds that the Americas were populated last and from groups that migrated from Northeastern Asia. Evolutionary time was likely not long enough and difference in environment, Rainforest or high mountains versus savanna could have contributed. Also it has been shown genetically that H.sapiens that migrated out of Africa came in contact with and integrated with other Homo species that left Africa several hundred thousand years before who had the traits of lighter skin, straighter hair etc associated with Europeans and Asians....

That these genes survived in H.sapien today likely has to do with environmental selection that you mention.

@AMR Your answer is the correct one. Why don't you post it as an answer instead of a comment?

@LeonardoCastro because my comment is inferred from information that does not directly relate to the question. As I cannot cite actual research that tests the idea, this is more my opinion, which is more correctly placed in the comments than a researched answer that has factual evidence to support the answer. Even if I was to write an answer that cited the sources that that led to my "hypothesis," none of the research that I was aware of at the time directly tested the question.

There hasn't been that much time for it to happen, and it may not be that much of a strong selective force. The main Amerindian peoples apparently arrived 14-15 thousand years ago, at the height of the ice age. They were from cold climates, Siberians, travelling a bit like Eskimos in the snows of Alaska. Indeed, they may have not evolved light skin after coming out of Africa 50mn years ago, but they may have acquired light skin from Neanderthals and Denisovans who had lived in cold climates for over 1/2 a million years.

Could not fit in a comment....
Northern Africans and Indonesians have pretty much the same skin color (to my first impression). Sub-Saharan African (that you don't talk about) are darker. And Northern Africa in not an equatorial region (not more than Los Angeles) as it is right under the tropic of cancer.
Also I am a little confused about who you call "we" and who call "they". I think that by "we", you mean any non-sub-Saharan African human but I am not sure. If this is the case just naming sounds more appropriate that to make a big category that you call "we" to exclude some ethnic groups :)
I think that when you are talking about Brazilians (and other people in South America living close to the equator such as Ecuadorians), you are mostly talking about people from Spanish and Portuguese descent. So let's talk about the great migrations
The Indonesians arrived in their lands about 70,000 years ago. The indigenous South-Americans arrived in South America about 10,000 years ago. The Spanish and Portuguese arrived in South America about 500 years ago.
I think you might want to read a bit more about the geography of those big migrations.

Your paragraph about time of arrival should be expanded into a "real" answer (and the numbers verified), as this is most likely the exact reason that indigenous South Americans (and North Americans as well, really) are not darker than they are - they didn't arrive that long ago. Here is a good place to start.

They have been pushing back the dates of the migrations into the Americas with new archeological findings... They are looking at closer to 15k years now. Also with the work of Svante Paabo and others, it may very well be that the mutations that we associate with Europeans and Asians arose in non Sapien humans and that modern humans inherited those traits from breeding between the groups.

source: Stack Exchange

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sort: votes


text:
Is it possible to biologically convert potential energy to chemical energy?
To lift an object x meters it is necessary to expend, at a minimum, an amount of energy corresponding to the increase in that objects potential energy associated with the increase in height. When putting the object down, returning it to the position it was moved from, its potential energy with respect to gravity returns to the original amount. However, this potential energy is not returned to the person who did the lifting. On the contrary, putting an object down gently requires additional energy to be expended to slow what would otherwise be a free fall.
Can any organism convert gravitational potential energy to chemical energy? Is it at all biologically feasible?

Yes of course: The ATP synthase :) But it is chemical potential, not gravitational potential.

I originally wrote "potential energy with respect to gravity" in my question, but simplified it to "potential gravity" as I thought it would be clear from the question. I edited it back in.

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text:
Listing Cluster of Differentiation (CD) markers (immunology)
I hope this question is appropriate for this SE. When listing multiple cluster of differentiation (CD) markers to define a cell population, e.g. CD3+CD8+CD45+CD4-, is there a default order to put them in? I was recently told to list them numerically with the negative populations after the positive ones (i.e. CD3+CD8+CD45+CD4-). However, I have seen different orders in the literature and would personally prefer to order them by whatever I would consider most logical (e.g. CD45+CD3+CD8+CD4-).

There is no convention like that AFAIK.

WYSIWYG is correct, and I would tend to agree with your personal preference - order the markers in the manner that makes the most sense, not necessarily in any numerical or positive/negative order.


text:
What kind of insect is this and what is it doing?
I live in Denmark and found these two insects on a tree. I'm interested in the big fly and have the following questions:

What kind of fly is it?
What is it doing with the little fly?

it is some what looking like a stonefly.. but if you want a clear identification of this insect you can visit this site.. http://www.insectidentification.org/

I think it's a Robber Fly. Those are predatory.

I'd make that certainly a robber fly.


text:
What kind of tree is this?
I live in Denmark, Europe and was going for a walk on a beautiful cemetary in the city. I saw this tree and would like to know what species it is.
Unfortunately i have no photos of the tree from a closer distance.

This is very likely some species of willow tree (genus Salix).
Without a better photo it will be difficult to ID this to species. To complicate matters, willows are very cross-compatible, and numerous hybrids occur, both naturally and in cultivation.
Since it appears your picture is from a garden or park, a fair guess would be the common ornamental tree:
Weeping willow (commonly Salix × sepulcralis)

hybrid of Peking willow (Salix babylonica) from China and white willow (Salix alba) from Europe

It is not a willow, because the bark is whitish (willows are dark) and the leaves of (weeping) willows are longer and smaller. See my answer below.

This is a Birch tree, Betula sp., probably B. pendula, a common species in Denmark that also has hanging branches. It can be identified by the white bark and the leaves, that are not as long as a willow.


text:
Geographic/ethnic distribution of Neanderthal DNA in modern humans
There is a really good chance that various human populations have different levels of Neanderthal DNA in their genes.
And yet, the only thing I was able to find is the percentage of Neanderthal DNA in Europe, Asia and Africa.
Are there any studies with a finer resolution, such as regions, countries etc.?

Welcome to Biology.SE! Are you looking for a more fine grained (country-level say) frequency of Neanderthal DNA? Can you please to link to what you found so far? If you can't find country-level frequency of Neanderthal, it is probably because there is too little population structure at this small scale to be able to see any difference. Note, however, that I expect northern Africa to be much more Neanderthal than in Central Africa.

http://www.genetics.org/content/early/2013/02/04/genetics.112.148213
Region-level (Northern/Southern Europe, Middle East, India) data will be sufficient. Country-level data might produce some interesting insights.

Here is a link to the full text of the final published article.


text:
Why we do not get hurt from HCl secreted in the stomach?
I read in my book that during digestion our stomach secretes hydrochloric acid ($HCl$). Why we do not get hurt from it? It was also said that mucous provides protection, but from where is it coming?

Great answers, but it also is important to note that our HCl in the stomach acid has a low concentration as well, but high enough to kill many pathogens, in particular, bacteria. Also, some of our epithelial cells are destroyed, but the epithelial cells have the highest cell turnover rate in our body, only about one day...

Goblet cells.
These are specialized epithelial cells whose job it is to produce mucins. Mucous role is not only important in protecting the epithelium of the digestive tract from HCl, it is also a very important substance in the innate immune system, acting as a barrier defense to trap pathogens and/or prevent them from breaching the epithelium and gaining access to sterile parts of the body.

Our stomachs are lined with a special mucal layer which protects the organ from its own secretions. People with stomach ulcers have a hole in this layer, allowing the acid to get to the skin underneath.
HCl is present in our stomach to aid digestion - especially with dismantaling the bolus (food) coming from the oesophagus. The HCl separates the larger bolus to more smaller pieces. The stomach has a mucus which protects the tissues from being damaged. People with gastric problems may not have a sufficient layer of mucus to protect their tissue and the pain is from the acid eating through the tissue. Thus, a common solution for people who have Gastric problems is to use tablets which neutralizes the acid so that it is weaker.

The idea of acid causing ulcers was disproven by Dr. Barry Marshall, for which he won a Nobel Price in Medicine and Physiology, and is now known to be cause by inflammation due to an H.pylori infection.

@AMR, afaik Marshall disproved the idea that ulcers are caused by stress, spicy food, smoking, etc. Actually, H.pilory disrupts the mucus at some regions of stomach, thereby enabling the acid to get through and damage the inner layer of stomach.

@Ivan if you read my comment, I say "causing ulcers." The causative agent for an ulcer in 90% of the cases is an H.pylori infection and the damage done to the endothelial cells by the enzymes produced by these pathogens. Acids will aggravate the ulcer, but does not cause it. When you read the list of substances that Marshall disproved, acid is one of those substances. In fact much of the gastritis that occurred when he infected himself with H.pylori was in the absence of acid.

actually the ulcers are caused.. when say.. we didn't have food for long time, then the acid present in the stomach needs to dissolve some materials as, food is not there it starts to effect the layering of the stomach and thus, some kind of blisters and boils.. appears on the layering of stomach causes ulcer.

@Ashwin.N no, that is incorrect. If you read the previous comments, you'd have seen that this has been disproved. Acid on its own does not cause ulcers - H. pylori does.

We have skin under our stomach?

Simply, it's because of the mucous layer around the stomach, that prevents the strong acid, HCl to hurt our stomach.  Not only this, if there were no mucous, the HCl would digest the protein present in the epithelial cells, so the stomach itself would get digested. So the main protagonist here is the mucous layer.

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text:
Energy released during the production of ATP?
When glucose is used during aerobic and anaerobic exercise, how much energy is expended or required?
During aerobic exercise:
$C_6H_{12}O_6 + 6 O_2 \to ATP + H_2O + 6 CO_2$ + energy
During anaerobic exercise:
$C_6H_{12}O_6 + 6 O_2 \to 2 C_3H_6O_3 + 2 ATP$ + energy
For each of the reactions above what is the value of the '+ energy' part?

where did you get this from? i am pretty sure the ATP is the energy, isn't it?

@TanMath I guess "energy" here refers to heat loss, besides the "useful" energy capture in the form of ATP?

Your formulas are not correct: there is no O2 involved in the anaerobic case, and for the aerobic case there is a coefficient N before ATP, typically around 25--35. Please edit.

This is difficult to answer exactly since the thermodynamics of cellular metabolism are not well understood.
These are spontaneous reactions, so there is certainly a loss of Gibbs' energy $\Delta G < 0$; this energy corresponds to your "energy" term on the product side of the reactions. For the anaerobic case (glycolysis) a balanced reaction formula is
Glucose + 2 ADP + 2 Pi $\rightarrow$ 2 Lactate + 2 ATP + 2 H2O
Details like phosphate (Pi) and water is important here. Now, if we know the free energies $G$ of each substrate and product, we can calculate the $\Delta G$ as the sum of the products' energies minus the sum of the reactants. Unfortunately, this energy $G$ is hard to get at. It depends on a number of things, like the molecule structure, concentration, temperature and the pH and ion strength of the solution. These things are not exactly known, so the answer will be uncertain. This is actually an active area of research, and sophisticated methods have been developed for calculating $G$. One of the best are from a groyp at the Weizmann institute in Israel, and is available at http://equilibrator.weizmann.ac.il
If we assume all concentrations to be 1mM, this method gives $\Delta G = -118.7$ for the glycolytic reaction above. This is the energy lost (mainly as heat) in the reaction. For comparison with energy captures by ATP, we can break up the reaction into two parts and calculate
Glucose $\rightarrow$ 2 Lactate $\quad\quad\quad\quad\quad \Delta G = -206.7$
2 ADP + 2 Pi $\rightarrow$ 2 ATP + 2 H2O $\quad\quad\Delta G = 87.0$
which sums to -118.7, as expected. This tells us the fraction of the Gibb's energy captured as ATP is 87/206.7 = 42%, while 58% is lost as "heat". So glycolysis has an efficiency of 42%. (For comparison, a combustion engine is somewhere at 15--20%.)
The aerobic case is more difficult, because the stoichiometry is not even fixed: the number of ATP molecules actually obtained from 1 molecule of glucose depends on the efficiency of the respiratory chain, on cytosolic NADH oxidation, and otherthings. But let's say we get 30 ATP. Then
Glucose + 30 ADP + 30 Pi + 6 O2 $\rightarrow$ 6 CO2 + 30 ATP + 36 H2O
has $\Delta G = -1608$, which can be broken up into
Glucose + 6 O2 $\rightarrow$ 6 CO2 + 6 H2O $\quad\quad\Delta G = -2913$
30 ADP + 30 Pi$\rightarrow$  30 ATP + 30 H2O $\quad\quad\Delta G = 1305$
So here 1305/2913 = 45% of the energy is captured. So in this sense, glycolysis and respiration are similar in efficiency. Varying the number of ATP changes this value; try it! Of course, glycolysis can only partially oxidize glucose (into lactate), while respiration achieves complete oxidation to CO2, extracting much more energy.
Again, these values depends heavily on concentrations of metabolites inside cells, which are not well known. Try changing them at the equilibrator web site and note the effects! Unfortunately, many biochemistry textbooks present values of $\Delta G$ assuming reactants at 1M (!) which is completely irrelevant to actual conditions in living cells.

In biology, anaerobic respiration is a way for an organism to produce usable energy, in the form of adenosine triphosphate, or ATP, without the involvement of oxygen; it is respiration without oxygen. This process is mainly used by prokayotic organisms (bacteria) that live in environments devoid of oxygen. Although oxygen is not used, the process is still called respiration because the basic three steps of respiration are all used, namely glycolysis, the citric acid cycle, and the respiratory chain, or electron transport chain. It is the use of the third and final step that defines the process as respiration. In order for the electron transport chain to function, a final electron acceptor must be present to take the electron away from the system after it is used. In aerobic orgainisms, this final electron acceptor is oxygen. Oxygen is a highly electronegative atom and therefore is an excellent candidate for the job. In anaerobes, the chain still functions, but oxygen is not used as the final electron acceptor. Other less electronegative substances such as sulfate (SO4), nitrate (NO3), and sulfur (S) are used. Oftentimes, anaerobic organisms are obligate anaerobes, meaning they can only respire using anaerobic compounds and can actually die in the presence of oxygen.
Anaerobic respiration is not the same as fermentation, which does not use either the citric acid cycle or the respiratory chain (electron transport chain) and therefore, cannot be classified as respiration.
Aerobic Respiration
Aerobic respiration requires oxygen in order to generate energy (ATP). Although carbohydrates, fats, and proteins can all be processed and consumed as reactant, it is the preferred method of pyruvate breakdown from glycolysis and requires that pyruvate enter the mitochondrion in order to be fully oxidized by the Krebs cycle. The product of this process is energy in the form of ATP (Adenosine Triphosphate), by substrate-level phosphorylation, NADH and FADH2.
Simplified reaction: C6H12O6 (aq) + 6 O2 (g) → 6 CO2 (g) + 6 H2O (l)
ΔG = -2880 kJ per mole of C6H12O6
The negative ΔG indicates that the products of the chemical process store less energy than the reactants and the reaction can happen spontaneously; In other words, without an input of energy
The reducing potential of NADH and FADH2 is converted to more ATP through an electron transport chain with oxygen as the "terminal electron acceptor". Most of the ATP produced by aerobic cellular respiration is made by oxidative phosphorylation. This works by the energy released in the consumption of pyruvate being used to create a chemiosmotic potential by pumping protons across a membrane. This potential is then used to drive ATP synthase and produce ATP from ADP. Biology textbooks often state that 38 ATP molecules can be made per oxidised glucose molecule during cellular respiration (2 from glycolysis, 2 from the Krebs cycle, and about 34 from the electron transport system). However, this maximum yield is never quite reached due to losses (leaky membranes) as well as the cost of moving pyruvate and ADP into the mitochondrial matrix and current estimates range around 29 to 30 ATP per glucose.
Aerobic metabolism is 19 times more efficient than anaerobic metabolism (which yields 2 mol ATP per 1 mol glucose). They share the initial pathway of glycolysis but aerobic metabolism continues with the Krebs cycle and oxidative phosphorylation. The post glycolytic reactions take place in the mitochondria in eukaryotic cells, and in the cytoplasm in prokaryotic cells.
Thus,more energy is released during Aerobic Respiration than Anaerobic Respiration.


text:
Unilateral damage to vagus nerve
Context:
The vagus nerves supply the neck viscera, heart, lungs and gastrointestinal tract. They join around the oesophagus to form the oesophageal plexus.

Question: Would damage to one vagus nerve in the neck have significant impact on heart rate and gastrointestinal tract function?

Thoughts: If the heart and GIT lie below the oesophageal plexus, which then continue in the inferior direction towards the cardiac and gastric plexuses, then surely a major functional failure in either the heart or GIT would require damage to both vagus nerves (?). I'm trying to make sense of the effect of their fusion, and whether or not this provides a compensating mechanism in the event that one of the two nerves is damaged.

It depends how they're damaged. Pressed on so that they fire continuously and simply severed so that no firing happens have different results.

@Hernandez - it also depends "where" they are damaged. There are branches that we routinely encounter during stomach operations that, if we  damaged, would have very different effects compared to damaging the vague as it descends through the neck in the carotid sheath. More distal injury (i.e. further away from the brain) would likely be less debilitating than more proximal injury.

@Hernandez - how high of a injury in the neck or how low of an injury in the neck?

I was thinking more of damage at the level of the neck. I guess if it occurs before the nerves join to supply fibres to the cardiac and coeliac plexi, parasympathetic functions relating to heart activity and the GIT would remain relatively untouched. Perhaps only the more superior pharyngeal innervations would be affected by such damage.

To qualify that further, I was thinking of damage above the level of the C6 vertebral body.

Would damage to one vagus nerve in the neck have significant impact on heart rate and gastrointestinal tract function?

Not that much, because fibers from both sides are fused, so each nerve carries about a 50% of fibers originated from the one side and about 50% from the contro-lateral. Consider that fibers are rewired after each plexus.
References:
 wikipedia page about vagus nerve
 wikipedia category about vagus nerve


text:
What is this brown insect with a large wingspan?
I found this dead creature on my window last night and spent hours looking for something that could explain what this is. I was unable to inspect it in person though, because opening the window would make the creature fall down.
It is roughly three inches in length and has a wingspan of five inches. I found it in the UK in August.
Here are some pictures:

It is a moth from the Sphingidae family (hawk moths). They are generally large, robust and often have lobed wings (like the one in your pictures). I'm not closely familiar with this group of insects, and not with species found in the UK, but the individual you observed is very similar to e.g. Laothoe populi (Poplar hawk moth), which is also found in the UK.

(Laothoe populi, picture from Wikipedia)

what a beauty! +1 :)


text:
How could 45 milligrams of a substance equal 4,500 micrograms?
In this book, the author repeatedly states that 45 milligrams of vitamin K2 equals 4,500 micrograms.  I thought 1 mg = 1000 mcg.  How could this be?

It's a typo. 1 mg = 1,000 mcg.

Conversion tool.

I'm voting to close this question as off-topic because it is a trivial question.

@AliceD, It's only trivial if you have a certain amount of experience.  With vitamins and "nutraceuticals", I've seen errors caused by conflating and mislabeling between "mg", "mcg", and "Mg" (where "Mg" was perversely meant to be convey micrograms!) .  This is so serious that the FDA has repeatedly warned about it

@BrockAdams - you may be right, but then again I doubt this is the right forum for these matters.

This is a typo.  In the text he states:

... only 0.120 milligrams (120 micrograms) of MK-4 ...

So, he knows the correct conversion.
Then:

... the "same" product is almost 40 times more potent in one country
  ...

40 times 120 micrograms is 4800 micrograms -- which is close to 4500.
So, that suggests that the (4,500 micrograms) in the table is correct and that the 45 milligrams is a typo.
It should read 4.5 milligrams.


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Can the human body enter "Power Save" mode?
Once a year, I am fasting for 24 hours. No food or drink at all for whole 24 hours.
Recently I thought about what is happening to me during those 24 hours, and realized there might be something strange going on. I will try to describe the things I find strange:

I do not feel thirst or hunger at all. Not even after 20 hours.
I still urinate after 10, 15, and 20 hours, and unlike what I would expect from not drinking, the color is not very dark. (actually, same as when I drink normally)
I can still perform energy consuming tasks after 20 hours without eating or drinking anything. I'm not talking about running in the park or lifting weights, but I can walk, do house chores etc, and only after 20 hours or so the body starts to "protest" in the form of headache.

All of the above led me to think that maybe when knowing it's going to be deprived of energy, the body enters "Power Save" mode, allowing it to function as usual under those conditions? (to a limit of course, but still - I would expect hunger, thirst, and headaches to appear few hours into fasting)

I just voted to close, because I find it an anecdotal question. Maybe the headache is caused by a lack of coffee etc etc. It sounds all like a personal monologue on your experience.

@AliceD fair enough, wasn't sure if it fits here or not. Still giving it a chance to see if others find it off topic as well and in this case will delete. (for the record, the headache is really not the issue here)

Please leave the question as is, it is just a single vote - no harm done :) And I understand the headache is just a side note. I just took it as an example. If you could try to extend the horizon of your question to broaden its scope I'm happy to retract the vote. Btw: fasting = good, no liquids = nono afaik

Thanks @Alice, not going to delete yet. Any tips how to broaden the scope?

If you are performing the fast for ritualistic or spiritual purposes, then that mental state likely overcomes the feeling of thirst or hunger, especially if you are an otherwise healthy person.
As for the physiological aspects. The Human Body is made up of 2/3 water, and as your kidneys are still functional, they are constantly filtering, and creating urine. The body can last a few days without water.
As for food, the body has about a one day supply of sugar, assuming limited exertion, that it can consume before it begins to break down other substances. Then there are the fat reserves. The average person will likely have on the order of 7 to 15 kilograms of fat in reserve. There are 9 calories per gram of fat, so roughly 63 to 135 thousand calories worth of energy. Since the average adult will use about 2000 calories a day, then you can see that burning body fat alone would allow about a months worth of energy.
I am not saying that these are optimal conditions, but the body of a healthy human adult can easily withstand a 24 hour fast with no adverse effects. You would likely encounter more problems if you tried to go without sleep for the same period of time than if you refrained from food or water.

So in essence, in reply to the actual question of "Can the body enter power save mode" you say "No, it's just a mental state"?

I am saying that while feelings of thirst and hunger are sensations derived from physiological effects, they are experiences which are interpreted by the brain, and as such humans have developed the cognitive capacity to act against their instincts, and things such as meditation, prayer, repetitive ritualized behaviors can overcome the perceived sensations of the body. I said that if the reason for your fast was related to such a behavior it is likely that not experiencing the sensations of hunger and thirst has far more to do with the focus of your state of mind than the signals of your body

Some mammals hibernate, and in those cases, actual metabolic activity is drastically reduced. Humans didn't evolve to do this. The closest we come to this are situations of hypothermia. As far as power save... It is likely that if you have enough of a calorie deficit for a long enough period of time, you could end up needing more rest and not being able to exert yourself, also in the absence of food our body's metabolic processes are altered, but a single day isn't going to shut you down or alter your metabolism in any significant way, assuming again you are a health, non-pregnant, adult.

The human body can last several days without food and (to a lesser degree) water, and often had to. I myself and certainly many others have not had to experience that tho, as modern Western society has pretty good countermeasures against this.
After 24 hours, your body has still sufficient amounts of water, unless it was dehydrated earlier already. Contrary to what an American stereotype would suggest, a few hours without food won't do any harm.
When looking at longer times, however (which is closer to the core of your question!), this is not as easy anymore. Sadly I'm not familiar enough with this topic to give sensible intervals, but there are certainly many papers about this that could explain this in detail, if you're interested.


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What is the effect of antibiotic chloramphenicol on bacterial size?
When low amounts of antibiotics like Chloramphenicol is added in a bacterial culture, the steady-state growth rate decreases but what happens to the steady-state size? Can anybody please refer me to any paper that comments about the effect of these antibiotics on the size of bacteria (or yeast)?

There's this, but it's about a protist.

Thanks @canadianer for the prompt reply. It will be very helpful if I could get some references for bacteria/yeast as well.

Please can somebody help urgently? Thanks


text:
Does the cell internal temperature changes in response to a change in external temperature?
Background
Some species are homeotherm (internal temperature is not affected by a change in external temperature) and some are poikilotherm (internal temperature changes in response to external temperature). These concepts apply to individual levels.
How about cells (unicellular cells as well as cell in a multicellular organism)? I know that cells react to temperature change. For example, the amount of cholesterol in the cell membrane can vary in response to temperature in order to keep a membrane fluidity roughly constant (ref). But that doesn't prevent the internal temperature to change.
Question
When the external temperature of cell changes, does it affect the internal temperature? I am hoping that the process is general enough so that I don't have to specify a particular organism. If it is needed to talk about a particular organism, then consider a yeast for example. How does the internal temperature of a yeast vary with a change in the external temperature?
EDIT
My knowledge in Physics being very limited, I didn't even think of Fourier's law before reading @Eli Korvigo's answer and comment and @AMR's comment. So let's make some calculations:
If we consider a spherical cell of area $4\pi r^2$, where $r$ is the radius, then the loss of heat is $4\pi r^2 \cdot \Delta T \cdot K$ (Fourier's law), where $\Delta T$ is the temperature differential and $K$ is the thermal conductivity. Then the ratio of heat production $H$ over the thermal conductivity $K$ (in order to deal with this change of $\Delta T$ °C) is $\frac{H}{K} = 4 \pi r^2 \Delta T$. If $r = 10^{-6}$ meters and $\Delta T = 2$ °C, then $\frac{H}{K} ≈ 10^{-11}$. Am I right?
Is this ratio really not realistic for a cell? The thermal conductivity for water is $k=0.56 \frac{W}{m\cdot K}$(ref.) and the heat production per cell is $34 \cdot 10^{-12}$ W (ref.). So the ratio is of the order of $10^{-11}$ as well! Am I right?
So is it really impossible for a cell to regulate its temperature?

When you do cell/tissue culture, you learn to work fast so that you do not keep your cultures out of the incubator for very long. You make sure it is set for 37* and that your CO2 take is not on empty. In short cells are adapted to the environment they evolved in. Mammal cells do not respond well to dry, too cold or too hot environment and oxygen and about 5% CO2 to culture. Bacteria are pretty sturdy and have a broader range where they can survive, but they generally won't grow outside oh their ideal range. For E.coli, against that is 37* as they evolved in mammalian digestive tract.

Think about it this way. You reach a few hundred meters from the summit  of The Matterhorn as night falls in January. You can sleep exposed, in a tent, or in a tent in a cocoon sleeping bag, or in a tent with sleeping bag and a few climbing partners. Option 1, you will probably be severely hypothermic in the morning or possibly dead. Option 2 you probably won't be much better off. Option 3 you should be okay, though you may be apprehensive about unzipping the bag in the morning. Option 4 the temperature of the tent will likely also be warmer than the ambient temperature outside.

I understand that cells (unicellular or not) have their ecological niche. But it is not because you have such niche that you won't evolve so to regulate your inside temperature in order to expand over this niche (as mammals do for example). So I think the question remains (Are cells (yeast for example) able to regulate their inside temperature).

I would say that there is a range of response to the environmental change that the cell experiences, but no individual cell has the capacity to regulate temperature. They can respond to the change, but you need systems to actually control temperature. Multicellular organisms are greater than the sum of their parts, so even though systemically we (warm-blooded animals) can make modifications to metabolic activity that regulates out core temperature, it is the result of the collective response more than that of any individual cell.

And that is just considering Mammals. There are some very large reptiles who are not capable of maintaining their body temperature, even though they have the critical mass to do so. Their response to cold is hibernation, or in the case of the really large ones, dinosaurs, extinction.

And I know that you are aware of these things but I think that you are so focused on the technical specifics of your question that you are forgetting what you know about why multicellularism arose in the first place. An argument can be made that prokaryotic cell walls are adaptations to the extremes of the environments that they experience, but does that mean that they are actively managing the situation or are just adapted to a broader range of environments as they have to go it alone, for the most part to survive and pass on their genes?

Homeothermic multicellular organisms have special tissues that burn resources to warm up (usually this involves breaking the electron-transporting chain at the final stages of respiration to transform all chemical energy into thermal energy). And they have special tissues (fat) and enough body mass (this is more about the volume/area ratio) to keep this energy from dissipating. If you recall physics, any unicellular organism has insufficient body mass to accumulate thermal energy for any perceptible amount of time, hence it's useless to burn resources that it can spend to adapt to lower temperatures, i.e. synthesise cold-shock proteins, modify membranes, restructure metabolism. This is basically the same reason why small mammals and birds have to eat all the time to stay alive.

As you can see, the smaller you get the more energy you need to burn (hence increase ${O}_{2}$ consumption) to maintain body temperature. That's why we don't see truly homeothermic insects (some of them can warm up for short periods of time) or other small animals.

Thnks for your answer +1 You said any unicellular organism has insufficient body mass to accumulate thermal energy for any perceptible amount of time, hence it's useless to burn resources that it can spend to adapt to lower temperatures That means that there is absolutely no control over internal temperature at the cellular level in comparison to the extra-cellular temperature. Is that right? That'd be great if you'd have a reference.

@Remi.b I don't mean this is impossible, but thermodynamically irrational. This statement directly follows from the Fourier's law. A cell is simply too small, hence any energy spent to warm up will dissipate immediately. Don't forget about the energetic capacity of water.

Eli's answer makes sense, but here is an example. If you put a substantial mass of yeast in a cask with crushed grapes or wort, they will initiate fermentation to produce alcohol for beer or wine. If you look at a temperature, the temperature within the vat will be higher than the ambient temperature. With enough mass, the yeast produce enough heat to warm the container that they are in. However a culture on a petrie dish would likely generate insufficient heat to overcome the effects of the ambient temperature of the surroundings.

Thanks a lot for the comments as well. I plugged a few numbers into Fourrier's law to see if it is plausible for a cell to regulate its temperature (See edit). Please let me know if that sounds correct to you and whether you still think it is impossible for a cell to regulate its own temperature.

@AMR exactly With ENOUGH MASS, the yeast produce enough heat to warm the container that they are in. Indeed, a culture might get significantly warm, that's why many bioreactors have cooling systems, but a culture is not a unicellular organism :)

@Remi.b there are two possible flaws in your estimations (I can be wrong, since I don't have time for a thorough analysis right now): 1. You applied a 1D approximation to a 3D case; 2. you reference heat production per cell in a culture during growth (=> a lot of spare resources to burn) - the value is not relevant to an isolated cell (and that is the model we are talking about as far as I believe). As you might've noticed Over an 8.5 h period, cell numbers increased by 9% and heat production per cell by 18% - the heat production per cell correlates with the number of cells.

The second is indeed a potential problems in my calculations (+1).

@Remi.b My pleasure. As for the mathematical part, you can't apply that linear approximation to a 3D case. If you really want to estimate the heat loss, you have to solve the integral form.


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How late in a human pregnancy can a zygote split?
This page indicates that the first two days is "very early" for a zygote to split, and that conjoined twins are the result of an "extremely late" split:

If the zygote splits very early (in the first 2 days after fertilization) they may develop separate placentas (chorion) and separate sacs (amnion). ... Most of the time in identical twins the zygote will split after 2 days, resulting in a shared placenta, but two separate sacs. ... Finally, the zygote may split extremely late, resulting in conjoined twins.

What I'm looking for is more specificity. At what time in the pregnancy does a split zygote result in twins who share a placenta and not a sac? What about conjoined twins (I'm most interested in the most common types of conjoined twins)?

This information can be found in the wikipedia Twin article, specifically in the degree of separation section.

Identical twins
Twinning occurring at the two cell stage or afterwards, up to and including the 16 cell stage, which translates to days 1 to 3 after fertilization, results in diamniotic, dichorionic twins.
Twinning at the 32 cell stage (day 4), up to  and including day 6 results in diamniotic, monochorionic twins. The majority of identical twins split at this stage.
Twinning from day 7 up to day 10 results in monoamniotic, monochorionic twins. This is rare and only accounts for about one percent of identical twins.

diamniotic: twins have separate amniotic sacs
monoamniotic : twins share one amniotic sac
dichorionic: twins have separate placentas
monochorionic: twins share the same placenta

Conjoined twins
This is where things get a bit fuzzy. While some sources say that conjoined twins occur when the twinning event takes place after day 10, others say conjoined twins are created when

the twinning event occurs at about the primitive streak stage of development, at about 13–14 days after fertilisation in the human

It is very likely that because of the rarity of conjoined twins (one in 200,000 live births) there isn't enough data available on the very early embryogenesis.
Sources and further reading:
The embryology of conjoined twins
Twinning
Conjoined twins


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How to read this diagram?
I have diagram of oxidative decarboxylation of pyruvate pathway. The pathway is between glycolisis and Krebs cycle.
How to read this diagram?
This excerpt from Harper's Illustrated Biochemistry, 30E, page 173.

The circles are like gears, where the points of contact are chemical reactions.

To me, it is unclear exactly what you are asking about, and the question also reads as unresearched homework.

Take a look on reaction catalyzed by dihydrolipoyl dehydrogenase. It acts upon $NAD^+$ according to following equation:
$NAD^+ + FADH_2\rightarrow NADH+H^++FAD$
Same way you can write other reactions, e.g. by pyruvate dehydrogenase:
$Pyruvate+TDP\rightarrow CO_2+TDP-Hydroxyethyl$

Texts usually have a verbal explanation of these kind of diagrams, so look in the text where it references Figure 17.5 and read the section before and section after.
That being said, if you start at the top with pyruvate, it enters the cycle where the curved circles touch on pyruvate dehydrogenase, which catalyzes its decarboxylation. That product then enters into the next cycle where the disulphide bond is broken and it is added to one of the sulfurs. Co-enzyme A then reacts with that and you get Acetyl CoA as a byproduct and dihydrolipoamide. The cycle continues and you get one hydride (I think) and one proton transfer to FAD and the reformation of the disulfide bond. You then have a hydride transfer to NAD+ and a deprotonation to regenerate FAD.
So each place a curved arrow touches another is what goes into the reaction and then following the split of the arrows is the product that comes out of the reaction. Where there are transfers to different circles means that there are different enzymes catalyzing the reactions.


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Why do insects (flies) put their legs together when they die (as if they're praying)?
Other animals don't seem to have an organized pose to die in. Or do they?

A good working theory is that this is caused by Rigor Mortis and the anatomy of insect legs.
In most cases, the muscles that pull the leg down (or closer together) are larger than the ones that pull the leg up.  This is because those muscles (flexors) must support the insect's weight:
(Click for larger view)

When the muscles contract after death, the larger muscles win out, causing the legs to move together.
From Why Do Insects Cross Their Legs When They Die?:

I suspect this is rigor mortis -- that post-death stiffening that occurs due to a chemical transformation of muscle tissue -- contracting legs as much as possible in the directions of least resistance, says Brian Farrell, an entomologist at Harvard University.


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Is thinking with language efficient?
First off, Im not sure, whether to put this into Cognitive Science or Biology. So sorry, if this is the wrong place.
I wondered, whether it is efficent to think with language (of course its efficient for communication). When Im thinking with long words, it takes longer than thinking with short words. Maybe thinking without words would be even faster?
So, do babies, who didnt learn think faster because they dont immediately try to find words for their thoughts to tell someone about them?
In our everyday life, we almost always need to talk to others about our thoughts. This leads to us thinking with these words instead of just thinking and then finding words for it. Its like writing a manuscript just from front to end instead of first brainstorming and collecting ideas.
Main question: Is it possible to think in a two-step process(and would it be more efficient)? First, thinking with emotions(or whatever you want to call it) and then finding words for that to spread your idea?

I'm voting to close this question as off-topic because it belongs to CognitiveScience.SE.

Yes.  And your "Milk tongue" greatly influences your cognitive style.  See Dennett, et al.


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Questions about a fossil
I have a plant fossil that my dad once found for me at a beach in Denmark, Europe about 15 years ago.

Is it possible to identify what kind of plant it is? There is a fossil water bubble suggesting that this plant lived under water.
What kind of process did the plant undergo in order to become a fossil?
Is it possible to find out how old it is?

Carbon dating could tell you how old it is...

Knowing what layer it came from you can infer when it was formed.

Unfortunately, this is not a fossil, but a pseudofossil: a pretty deposit of iron or manganese called a dendrite.

That is interesting.. +1


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Source of journals collecting titles of scientific publications regarding clinical trials with dogs fed medicinal herbs
After some time researching on the web, you can find a lot of websites telling you that some herbs may have or have specific properties(unfortunately most seem to be "advertised" as if they were wonder drugs), but none or few give references to specific titles of papers.
Another alternative is the pub med website but papers don't seem to pop up regardless of any search words.
Where is all that research information posted?

NCBI tends to be a good one. While this isn't about dogs, they have the effects of mint on exercise. However I did find an article about ginseng and dogs here, here, and here. To find the dog article I typed "NCBI ginseng dogs" into Google.

For a lot of "alternative" medicine there are only claims but not serious scientific studies have ever been conducted. Look at Pubmed, if you don't find them there, they are most likely not existant.

Check the databases mentioned in this post with right keywords.

Thanks to all, don't know if it matters but, I was looking for research on something that is anti-inflammatory such as turmeric.


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Doubts regarding definition of upstream/downstream genes and cognate protein
With respect to the research paper, there are a few things I didn't understand:
1. What is upstream and downstream gene
2. This paper identifies proteins that help in secretion, but does not identify the originally secreted protein. Am I correct?
3. Does cognate protein here mean homologous protein(from common parents)?

Upstream means towards 5' direction from the reference point (conversely for downstream). Reference point can be a single position such as transcription start site (TSS) or a bigger segment such as a gene. When we say upstream of a gene, it means some region of DNA that is towards 5' direction from the TSS of the reference gene. Downstream of a gene refers to the region 3' to the transcription termination site of the reference gene.
Similar terminology is applicable to RNA but obviously, in this case your reference cannot be a gene (it can be an exon, for instance). I have not seen this terminology used in case of proteins.

This paper is about identification of the proteins that aid in secretion (TEC) of certain proteins (effectors). They identified both the proteins that help in secretion and the proteins that are secreted

Here, we report a class of T6SS effector chaperone (TEC) proteins that
  are required for effector delivery through binding to VgrG and
  effector proteins. The TEC proteins share a highly conserved domain
  (DUF4123) and are genetically encoded upstream of their cognate
  effector genes.  [....]
  We validated this approach by verifying a predicted effector TseC in
  Aeromonas hydrophila. We show that TseC is a T6SS-secreted antibacterial effector and that the downstream gene tsiC encodes the
  cognate immunity protein. Further, we demonstrate that TseC secretion
  requires its cognate TEC protein and an associated VgrG protein.

Cognate refers to the correct binding partner which will result in a functional complex. It basically refers to biomolecular partners with a known and validated relationship. This relationship need not be synergistic. For example:

RNA interference (RNAi) is an evolutionarily conserved process through
  which double-stranded RNA (dsRNA) induces the silencing of cognate
  genes. (Source)

my question is, are they identifying protein that gets secreted or are they identifying protein that help in the secretion?

@Rishika both.. they identify a relationship between them. It is clearly mentioned in the abstract. I edited the answer to highlight this.


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Why can't gametes of one species fuse with that of the other species?
I have read that gametes of one species cannot fuse with that of another? For example the sperm of a dog can't fuse with the ova of a cat or a horse?

Note that it does happen and hybrid offsprings are born in case of some pairs such as lion-tiger, donkey-horse and camel-llama.

But its only some why not all ?

Do you have any initial ideas on how to explain this?

You should also narrow down your question such that it is about some few species. Or at least you can restrict your question to different mammals or even better, organisms of different genera but same family; like Rats and mice or gorillas and chimpanzees, etc.

The implied subject of your question is the prezygotic barrier and is one of the possible determining mechanisms of speciation, the others being temporo-spatial (meaning different time or place), behavioral, and mechanical (the organisms don't fit together, physically).
Fundamentally, this means that gamete cells of each organism are chemically incompatible. While the details specific to each species vary, we can take a look at a few examples to illustrate the point.
In order for eggs of Arbacia Punctulata to attract sperm of the same species they secrete a specific chemoattractant peptide we call Resact (a selection of different species' chemoattractants can be found beyond the former link), which is adapted to diffuse well in seawater. Sperm then follow the chemical gradient in the direction of the egg, which is called positive chemotaxis. Resact doubles as an activating peptide for that species' sperm. Pycnopodia helianthoides starfish, which also reproduce through broadcast spawning, use an attractant we call startrak. Internally fertilized animals use roughly the same mechanism to guide sperm through the reproductive tract, though with different chemical adaptations specific to their evolutionary history.
Once the sperm reaches the egg, an acrosome reaction leads to the fusion of the two gametes into a potential zygote (for the reason why I say potential, see  Speciation by polyploidy). The chemistry of this reaction also varies between species.
In summary, the reason is this:

A change in gamete chemistry (chemotaxis, activation, reaction, adhesion) alters the chances of successful fertilization between one or more members of the same species.
Thus, the altered group reproduces more often within itself than it does with the parent group, allowing it to grow in population.
Changes in the altered group further reduce the chance of success with the parent group.
Eventually, the chances of the altered group successfully mating with the parent group are practically zero.

This process is, of course, typically assisted by one or more of the other aforementioned mechanisms. Where two species are capable of producing offspring and successfully do so, you get hybrid speciation.
Further reading

Study.com - Speciation II: Prezygotic Barriers
Recognition of Egg and Sperm
Egg and sperm recognition systems during fertilization

This example applies to only one organism (or few). OP is interested to know why this does not happen generally.


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What happens to the excess immune cells or WBC in our body?
When we have an infection our immune system produces a large amount of white blood cells (WBCs) in our body to fight against the pathogen or parasite. My question is after the immune response has finished fighting the pathogens, what happens to the excess cells and antibodies that presumably are no longer needed? Will they disintegrate themselves, is there a final step in the immune response to dispose of these cells, or are excess of these cells and proteins present as if they are not in excess (they are filtered no more so than when at normal levels)?

The process you are asking about is called the termination of the immune response, and for a long time it was not studied very much for some reason, with scientists preferring to analyze initiation instead. However, this has changed in recent years, and while we still don't know a good deal, the picture is much clearer than it had been a decade or three ago.
Here is a special edition of Immunological Reviews focusing on termination of the immune response. While the site says you need to pay to access each article, they're actually available for free in PubMedCentral, so just look it up there for access. For a very brief overview, this section of the Wikipedia article on inflammation lists some of the mechanisms involved.
In regards to your question about immune cells and antibodies, a couple of things happen. First, the vast majority of responding cells are either "turned off" or directed to commit suicide (apoptosis) by a variety of signaling mechanisms, such as anti-inflammatory cytokines like IL-4, IL-10, IL-13, and IL-35, along with other molecules like TGFβ and IL1RA, soluble receptors to pro-inflammatory cytokines like TNFα and IL-6, or through "death receptors" like Fas/CD95 and others. However, some cells are prompted to turn into long-lived memory cells, which are able to be quickly activated upon re-exposure to antigen, in many cases completely clearing it without the need for a full-fledged immune response (such as one generating fever and sickness).
As for antibodies, like most circulating serum proteins, they are metabolized mainly in the liver and can be excreted via the kidneys. Their half-lives vary by isotype, but can be as long as three or more weeks. This is assisted by FcRn, the neonatal Fc receptor, which recycles antibodies back into circulation, protecting them from breakdown:

FcRn: the neonatal Fc receptor comes of age
Derry C. Roopenian & Shreeram Akilesh
Nature Reviews Immunology 7, 715-725 (September 2007)
doi:10.1038/nri2155

Good answer. The only thing I would point out, for others reading that may be less familiar with immunology is that you are basically referring to the adaptive response and aren't touching on innate WBCs.

@AMR which cells are you referring to as "innate WBCs"? Macs? DCs? Both are involved in antigen presentation and regulation of the "adaptive" response, especially in producing some of the cytokines I mentioned. As time goes on, the line between "innate" and "adaptive" immunity gets fuzzier and fuzzier, and some investigators I know don't even refer to them as such any more, there's so much overlap.

Neutrophils, eosinophils, basophils, and to a lesser degree natural killer cells.

There is however an article on granulocytes that you linked to. When I read your response the first time, the third paragraph sounded like it was focused on the end stages of the adaptive response, but apoptosis is kind of a catch all for the termination of most all the cells raised in an immune response.


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Why does low sequence diversity cause sequencing problems
When sequencers are processing sequence fragments, if there is little diversity at a particular bp locus this can cause problems for the sequencer. I have the superficial understanding that when a flow cell contains a significant percentage of a single base on any given cycle, it has difficulty deciding what base is present in each sequence. Why is this?

I think the problem is more that the software has a hard time identifying individual clusters if way more than a quarter of them are lighting up for a given base.  If you have more diversity in the first few cycles, when the cluster coordinates are being identified, I think this is less of a problem.


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Why do we spend so much time on creating taxonomies?
I spent 3 years building a taxonomic database of plant specimens for the Missouri Botanical Gardens (http://www.tropicos.org/). Myself and two other programmers used a modern database and web pages to share the specimens with the research community. Last I looked there are over 3 million specimens included. Anyway I never got a straight answer as to why there is so much time, money and botanist's lives spent categorizing the earth's flora. What is the end goal here? I'm hoping there are professional scientists here that do taxonomic work that can chime in. Thanks.

Your question is too discussion oriented for the stackexchange format. The answer invariably will be "it depends whom you ask." I suggest looking at the broader impacts section of the grant that supported your work, which should answer the question "why does this matter?".

I think this is a legitimate question. I am not a taxonomist but certainly one reason is to understand life species relatedness and their evolution. Why is that necessary? Well I guess the main goal here is to fully characterize our ecosystem but more precisely, and as an example, when a biologist starts to work on an organism knowing to whom he is related is a precious starting information as one might expect similarities between very close species (i.e. use previous research perform in that close relative to drive studies in the new organism).

Interesting, that makes sense. One of the other suggestions I had heard is that if they find a plant specimen closely related to a rare specimen that can cure an illness, the closely related specimen may deliver the same medicinal qualities.

I agree with kmm. Why do we spend so much time compiling and tabulating Baseball Statistics? Why did we spend so much time figuring out the nature of light, gases, metals, radioactivity, toxicity, bugs? Why in fact do anything other that chase after herds of elks and dig for roots and berries. Oh but wait, you need knowledge to know which ones are poisonous and which ones will provide you with additional calories when the hunters have had a bad time of it.

You have asked a question with the bias of "This is useless, prove me wrong." It would be a more reasonable question if you said "I am a programmer who worked on a taxonomic problem for 3 years but I did not get an understanding of the relevance of the work. I would like to gain a better understanding of the benefits, uses, and values to producing such taxonomical archives and are there shortfalls to this mode of study of natural systems."

Biology is about observation and learning from nature. If you categorize the species, it helps you in quickly understand what the species is about, what are some of its common characteristics, phylogenetics, etc. It has applications not just in understanding evolution, but in population studies, ecology. Why do we give humans names? So we can find them quickly and easily and associate them with certain characteristics. It is the basic human nature of using patterns to quickly identify objects.


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Do ginko trees grow well in Eastern North America (specifically Ontario,Canada)
I have recently noticed many Ginko (Ginko biloba) saplings planted in my Eastern Ontario city (in Canada), and they are looking a bit sickly, with yellow leaves.
They seem to be a popular choice in new developments, but I didn't think they grew well in the region (which is in Hardiness Zone 5).  Could the yellowing leaves just be poor management, or are the poorly suited to the region?
Wikipedia tells me that although these trees are native to China, they have been cultivated in North America for 200 years.

It took a little bit of digging (no pun intended), but this seemed to be a resource provided by Tree Ontario/Forest Ontario. http://www.seedlingnursery.com/resources/item/21-choosing-the-right-tree . Your best bet is always to ask a nursery or parks service in your local area. They usually have professionals with a great deal of knowledge on local conditions and the best choices based on weather, growing season, soil conditions, drainage, and indigenous parasites.

I have now spotted several ginko trees that appear to be mature and healthy; and established in residential/park area rather than in an arboretum or educational/research facility.  I conclude that they must be able to survive here.

As a side note, ginkos are excellent at removing air pollutants and living in toxic environments. It has a wide range of temperature tolerance and is very hardy. It sounds like yours have a possible magnesium deficiency which is common in gingkos, or the plant might be over or under watered. A very helpful link all about the gingko, its habitats, and usefulness

@AMR I actually disagree (to...some degree). Though there are usually no other options than to speak to a nursery or parks service, these sources are often not accurate. Even experienced nursery employees are not always going to get it right. I have experienced this multiple times at nurseries in various US states. Further, while I worked as an environmental educator within the park system, I saw misinformation be presented on numerous occasions. I don't mean to discredit your comment at all, but rather just point out that those sources come with their own risk of inaccuracy.


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Why do we turn darker in the sun?
I tried the all powerful google to answer this question - but I am not getting the answer I seek. I know we turn darker because the skin produces melanin. The question remains - why darker?
I am a physicist and it would make sense to me that the bodies response would want us to turn whiter- since a higher albedo would reflect more UV radiation. It seems that evolution took the way of absorbing more and more UV radiation by this melanin and then converting it to heat. Which begs the question as well - do black people get hotter than white people given the temperature is constant? Although this a side point to my original question.
What sparked this question was the use of thousand of black balls being dumped into LA's water reservoir in the hopes to reduce evaporation. Again... BLACK balls. This makes no sense to me - why the heck not use white balls to reflect more sunlight?

http://biology.stackexchange.com/questions/35713/what-is-happening-when-we-get-a-tan

Well if you used white it would reflect most all of the solar energy back at the water and what happens to molecules when the get a bump from a photon?

Interesting question. I don't know the answer, but I am guessing that either no suitable white pigment has evolved, or maybe it's too costly to produce compared to the benefits over black. The extra heat absorbed radiates away quickly in most situations anyway, and even when it doesn't, sunburns are hardly life threatening.

For the concern of the black balls, I googled black balls California and the first link gave me an explanation. Note, btw that the question for the black balls is off-topic here (but this is not your main question in your post)and would be on-topic on Physics.SE.


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Definition of Phenotype
I'm not a biologist but, I'm trying to enter molecular biology from a perspective. I have noticed that concept of genotype is quite well defined while phenotype is not. If I understand well, gene expression builds up enzymes that ultimately control all chemistry inside the cell, and which are sensible to the environment. Then, how correct/incorrect would it be to state that "phenotype is the enzyme composition within the cell"? Is it at least a good approximate idea?

Phenotype is considered the physical/observable representation of the genotype.

Where is your quote from? The entire enzyme (protein) composition of the cell is correctly referred to as the proteome. As not all proteins play a role in individual traits, then no, that is a bad approximation of the idea.

Have you read this? If not, please do. If so, what specific questions do you have about it?

Genotype:
Simply genotype is the inherited genetic information an individual has, and is conceptually quite easy to grasp. For example, if height is determined by gene $A$ and there are two alleles (variants of the gene, $A_1$ and $A_2$), then the three possible genotypes at that locus are $A_1A_1$, $A_1A_2$, and $A_2A_2$.
Phenotype:
The definition of a phenotype is a little more difficult to grasp, in part because it's so broad. As a quantitative geneticist I would say its any characteristic of an individual that can be measured. There's an enormous variance in the phenotypes that are used, they can be characteristics that are physiological, morphological, behavioural, life-history, even fitness itself. Personally I've used phenotypes from gene expression, which is one of the "lowest" (most close to genotype on the bridge between genotype and phenotype) phenotypic levels, through to lifespan, rates of ageing, and lifetime offspring production. Phenotypes are determined by genotype and/or environment (all non-genetic effects). For example, height may be affected by several genes, but it is also affected by nutrition during development and growth (among other things). As an evolutionary biologist, I feel the need to point out that selection operates on the phenotype, it is because genotype often has some effect on the phenotype that we see evolution by inheritance of genetic information.
Correctness of your statement:

"Phenotype is the enzyme composition within the cell"

Would be sort of incorrect. It certainly wouldn't be appropriately defining phenotype as a general thing. It would be saying that phenotype means enzyme composition within cells, and the appropriate sentence depends on what you are trying to say. The following would say that, in the discussed case, the enzyme composition of the cell is what you consider to be the phenotype:

"In this study the enzyme composition within the cell is the phenotype."

Whereas, the following defined the concept of phenotype:

"Phenotypes are characteristics which could be, in principle, measured, such as the enzyme composition within a cell."

The problem of your statement is it makes it sound like phenotype, as a general thing, is enzyme composition within cells. It's kind of a problem of while enzyme composition of a cell can be a phenotype, not all phenotypes are enzyme compositions of cells. Similarly to all humans are mammals but not all mammals are humans.

Phenotype is the physical result that one sees that is the outcome of genetic makeup. Genotype is the code that is written in the DNA (or RNA if you are a retrovirus). Enzyme composition in the cell, hair color, proclivity towards certain diseases; pretty much everything is a product of genoptype. There are some other factors in the environment that affect gene expression, but you are very much the product of your genotype.

Your answer lacks references and completely ignores environmental effects and gene-environment interactions, which are large components of phenotype.

I also believe this answer can be improved if it includes external factors.


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what is this ant-sized black insect?
I have found these tiny ant-sized black bugs on the floor that are a little hard to kill; I have to hit them with so much force otherwise they stick to the back of my sandals alive! or i have o squeeze them hard between the Kleenex.
Can anyone identify these please so i know how to get rid of them.
I live in Asia, Iran by the way, thanks.

In the edit box there is an icon for inserting pictures to your posts. Please Click that and then drag and drop the photo there so that it will be displayed on the site and not require people to click through to the image.

I don't think you can get a proper species-id based on that picture. It looks like a beetle though.

Can you try taking a higher quality image?

Generic poisons usually work. And they're cheap enough to try.


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Is RNase AWAY in the lab dangerous?
I use RNase AWAY in the lab. I would like to know how dangerous this chemical is for health. For example, when I remove my gloves my hands smell because of the RNAse AWAY

"Also, when i removed my gloves my hands smell because of the RNase AWAY." - so?

@TanMath. Everyone in a lab is entitled to be provided with the equipment and take the necessary precautions to protect their health or address concerns related to their health. If the OP has concerns about the nature of RNase Away in regards to their health, then the smart thing for them to do is ask the questions and get the information that they need to evaluate the risk that they are putting themselves under. That being said, it would likely be better to raise the concern with her lab head or a university safety officer than on a forum.

Have you read the MSDS (Material Safety Data Sheet) for the product? In general RNAse-Away (or whatever brand specific variant) is just considered an irritant.

RNase AWAY is marked for Category II skin corrosion/irritation and Category II eye irritation/serious eye damage. Recommendations by the MSDS followed by definitions as follows:

Skin contact Wash off immediately with plenty of water for at least 15 minutes. Remove and wash contaminated clothing before re-use. Immediate medical attention is required.
Eye contact Rinse immediately with plenty of water, also under the eyelids, for at least 15
minutes. Immediate medical attention is required.

SOURCE
DEFINITIONS FOR GHS LABELING
More information is included in the MSDS provided.
As for any smell, RNase away is reported to be a proprietary alkali hydroxide solution, so without any additional information it's difficult to tell.

You mean I wasn't supposed to be spraying my hands before I gloved? Oops....

If you are doing RNA preps, there isn't much of a way around it. RNase are everywhere and the only way not the degrade your sample is to use proper technique, barrier protection such as nitrile gloves, certified RNase free containers (macrophage tubes, pipet tips, etc.), and saturate your work surface and instruments with RNAse away.
If you really have a concern and it is available to you, a BSL-2 tissue culture hood with laminar air flow, that you get permission to use for the purpose of an RNA prep, is an option for an added level of safety. You still have to prepare your work surface with it, but the laminar air flow will keep any fumes away from you. A regular fume hood would probably be enough of a precaution, again if you are concerned, and it is less likely that anyone would take issue to you working in it if the BSL-2 hood is set aside for the exclusive use of tissue culture work.

Using something like RNAse Away is not always necessary, we don't use it at all. Working entirely with disposable containers or containers that were treated with DEPC or heated up high enough, as well as starting with RNAse free water and chemicals is generally sufficient.

@MadScientist - Who, we? You talk like Louis the Eleventh. user17471 does use RNAse AWAY.

That is fine if you are working in an area that is set aside specifically for RNA work and is isolated so that contamination is limited, and that area was likely treated in some way to begin with to destroy all biological contaminants. But if you are working on your day-to-day bench, you need to treat the work surfaces with something that will get rid of the enzymes and Ethanol will not cut it. I guess you could bleach everything, but bleach is far more corrosive and toxic that RNase Away.

And it is up to your labs protocol anyway. If your lab has decided that RNase Away is not a part of your protocol and you have engineering controls in place that can mitigate contamination, then that is great. Most labs don't and user17471's lab protocol is to prep with RNAse away, so using a fume hood or BSL-2 cabinet is about the only alternative available to them to protect their health if they are concerned.

You should, in general read the Material Safety Data Sheet for whatever chemical you are using. This is always provided by the vendor.
For RNAse-AWAY (Sigma-Aldrich):

Gloves should be worn when handling this product. RNase
  Decontamination Reagent is alkaline in nature and will cause
  irritation if prolonged contact with the skin is allowed. In case of
  contact with eyes, immediately flush with water for fifteen minutes
  and contact a physician. If swallowed, do not induce vomiting. Give
  plenty of water and contact a physician immediately.

According to the MSDS:

Not a hazardous substance or mixture according to Regulation (EC) No.
  1272/2008. This substance is not classified as dangerous according to
  Directive 67/548/EEC.

First Aid measures as per the MSDS.

If inhaled If breathed in, move person into fresh air. If not breathing, give artificial respiration.
In case of skin contact Wash off with soap and plenty of water.
In case of eye contact Flush eyes with water as a precaution.
If swallowed Never give anything by mouth to an unconscious person. Rinse mouth with water.

I would however say that even if the MSDS says the chemical is not hazardous, a person should make the risk assessment themselves and decide how comfortable they feel working with the substance under certain conditions. Take Ethidium Bromide. While it is a known mutagen that intercalates DNA, if you read the MSDS, it is only dangerous if inhaled of if it comes in contact on an area of the skin that is broken, (cuts, cracks, etc.). Yet most people treat it like the plaque, and while it is irrational and not supported by the known science, they should have the prerogative to protect their...

... health how they see fit. And I am not saying your answer isn't implying that, I am only adding that even if the MSDS says its probably safe, it is still up to the person to decide what is best for them.

@AMR In reality EtBr is not as hazardous as people panic about it. It was used as an antiparasitic drug in cattle.

I am one of those who is not panicked by EtBr, but in fairness to those who are, we mark out the area where it is used and only use dedicated equipment. I am far more concerned and careful with bleach, having evolved Cl gas after washing a container, that had been washed before with bleach, that was not supposed to contain an acid, but had residue from someone who performed a plasmid prep.


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Why are VAL, MET and ALA substitutions commonly used for protein behaviour and function studies?
I have seen that amino acids are commonly replaced with VAL, MET or ALA to study the effects of these specific substitutions.  Why are these specific amino acids used in particular, what are the results of these substitutions expected to show, could substitutions of other amino acids achieve the same results, and what is the source of this technique?

It highly depends on what you're trying to look for with your mutation as to which substitute you use.

Substituting a single amino acid and checking the effect this has on a protein is a method to determine what this specific amino acid does in the protein. For example, substituting an amino acid that is part of the catalytic core would almost always make the protein non-functional.
Alanine scanning is a technique that methodically replaces amino acids in a protein with alanine. Alanine is probably the most neutral substitution, you essentially remove the amino acid sidechain. Glycine for example would be problematic because it is more flexible and can adopt secondary structurs other amino acids can't.
If you want to find out what a specific amino acid does, you don't want to introduce any other new effects when mutating it. Depending on what exactly you're looking at, substituting other amino acids is certainly possible. Some changes to alanine might be too drastic and you might want to substitute an amino acid that is more similar to the original one. This all depends on what exactly you are looking at.


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Why might food go bad in an oxygen-free environment?
I was recently watching a video from the International Space Station (Making a peanut butter sandwich in space), and I noticed he mentioned that a tortilla kept in an oxygen-free environment could last up to 18 months. Impressive, but it got me thinking: Why would some foods ever spoil if kept in a state where molds would not be able to grow? Would it be that other micro-organisms in things like the moisture present in the food eventually take their natural toll? Just a curious thought I had while watching through these awesome ISS videos.
Thanks for any answers!

First of all, you assumed that this tortilla went bad after 18 month, not that austranaughts just decided to eat it?
More importantly, there is thing called anaerobs. Just like your muscle don't use oxygen in times of acute stress (force requirement), so there are organisms that don't care much about oxygen. As it happens in muscle, it happens in yeast during fermentation when sugars are turned into alcohols and released energy is used to propel molecular machinery. So, if there are sugar molecules on tortilla, there are still microbes that willing to prosper on it.


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If a given DNA oligo is an aptamer, will the corresponding RNA oligo with the same sequence be an aptamer aswell?
Functionality of aptamers depends upon the oligo's sequence and secondary structure. So, if I take a DNA aptamer and make an RNA oligo of the same sequence (T replaced with U obviously), will this RNA oligo also act as an aptamer?

There is at least one known case where both the DNA and RNA versions of the same aptamer sequence bind the same target (Lauhon and Szostak, 1995).
But you can't generalize this, there are two differences in structure between RNA and DNA, the Uracil/Thymine change and the missing 2'-OH in DNA. Those differences can affect the binding and overall structure of the aptamer.
It is possible that the RNA version of a DNA aptamer binds the same ligand, but this won't be always the case.

But does the backbone really play role in ligand binding for the aptamer? I mean had the backbone been playing any role, aptamer sequences wouldn't have been as specific as they are, because every oligo has the same backbone and hence would have had atleast some amount of affinty for any given aptamer ligand.

@Kunal24 Not just the backbone, the tertiary structure varies between ssRNA and ssDNA with same sequence. The tertiary structure is crucial for aptamer function.

@WYSIWYG: Oh I wasn't aware of the fact that tertiary structure of ssDNA and ssDNA are different. Could you please cite some informative sources for the same? Thanks a lot!

@Kunal24 that may be a question in itself; can't cite all the references in comments. The backbone flexibility (search persistence length) is different. RNA forms GU wobbles too. For wobbles you can see my answer here.


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How do ascending neural pathways filter unimportant information?
In school they told us one of the functions of the ascending neural pathways is to filter unimportant information. But the neural signal I know, is only a chemical-electrical chain of neurons. Is this filtering of unimportant information reminiscent of the gradual attenuation of the signal during the travel from the periphery all the way up to the brain? If so, how does that work?

What exactly do you mean by **the** ascending neural pathway, do you mean ascending neural pathway**s**?

@Troyseph Definitely, if it's only grammar based note.

Was more of a distinction between a singularly important single pathway or them in general. Thanks for the clarification.

A neuron cannot know the importance of a signal in any applied sense, that is, it can't know the difference between one triggered by a feather or one by a hammer... on an individual basis.
A single neuron can however accumulate information in a number of ways, either by requiring multiple incoming triggers (filtering out localised signals, i.e. from a single connected neuron) or they can require repeated triggers (filtering out weak/freak/accidental signals from a connected neurons). This is called summation:
These filtering events occur at the synapses, so how would a neuron filter a signal as it was passing through it? As far as I know, it doesn't!
NOTE:
As noted by @WSYWYG, LTP and LTD are also important, they stand for Long Term Potentiation and Depression. These are names given to the long term increase or decrease in sensitivity of a synapse, that is a neuron can become more or less likely to pass on a signal over long periods of time due to the pattern or frequency of signals it receives. Googling the terms will lead you to a wealth of vastly more detailed information on these topics.
EDIT:
As an addendum, your body can inhibit neurons selectively, so as a wild stab in the dark, it may be interesting to see if ignoring a sensation from part of your body is the direct result of of external inhibiting (filtering) of signals incoming from ascending neural pathways... but don't trust me on that!

I can't imagine how would they lern it - the action potential is just chemical-a physical reaction, isn't it?

Learn? I don't believe I've used that word. I'm simply saying that a bunch of neurons can make simple calculations about whether or not they will pass on a signal that they receive.  A neuron might require 10units of neurotransmitter to fire, if it has 10 incoming connections that only release 1 unit each, it will ignore any incoming signals unless all 10 incoming signals fire at the same time OR one signal fires 10 times in quick succession.

you can also add a note on LTP and LTD

@Troyseph I think I still didn't get it. Do you think there is some natural mechanism that infiltrates known unimportant signals (then we had it from birth - wouldn't be affectable. Is it?)? I wouldn't really see much relations with LTP then, could you please explain to me? And am I understanding you right, that stray paths just won't get as much neurotransmitters? How is that?

I think you're getting mixed up on the meaning of the word "Important". The neuron triggers based ONLY on the neurotransmitter concentrations in its synapse (that it can detect). This concentration has to be above a threshold, if it isn't, then the signal is ignored. It could be said to have been unimportant. The note in my answer suggests that the threshold can be modified externally however that isn't totally relevant to the question.

@Troyseph is the answer on my question: "Is by filtering unimportant information meant more than gradual attenuation caused by long way up? "No?

@Probably I'm not sure anything in your last comment made sense...

@Probably after much re-reading of your comment, I've not mentioned anything about attenuation of signals, I've in no way suggested that an attenuated signal inside a neuron might get dropped as unimportant.

@Troyseph Oh, never mind, I think it makes sense now. Thanks

Short answer
The thalamus is the most important neural station for the filtering of peripheral information to the cerebral cortex.
Background
Sleep is a prime example of where much, if not all, of the peripheral input ascending to the brain is filtered out. The thalamus situated in the brain stem is the major gateway for the flow of information toward the cerebral cortex and is the first station at which incoming signals can be blocked by synaptic inhibition. This mechanism contributes to the shift that the brain undergoes as it changes from an aroused state, open to signals from the outside world, to the closed state of sleep (Steriade et al., 1993).
One way in which the thalamus does this is by generating slow-wave oscillations, so characteristic of the delta waves observed in slow-wave sleep. These slow waves are apparent in the cortical electroencephalogram (EEG) as well as in the thalamus. The slow oscillations are generated by intrinsic oscillations, probably by thalamic cells, and effectively block incoming information to be shunted to the cortex through thalamo-cortical connections. A similar mechanism underlies sleep spindles, also associated with thalamic unresponsiveness to gate information to the cortex (Fig. 1). (Steriade et al., 1993).

Sleep spindles generated in the thalamocortical network. (A) Shows sleep spindles in the EEG during sleep. (B) The trhalamocortical network, including the reticular thalamic nucleus (RTN) central to slow-wave sleep and sleep spindles. (C) single-cell recordings in the network. Source: Steriade et al., 1993
Filtering of sensory information in the wake state is also performed by the RTN in the thalamus. Selective filtering can occur through a top-down process. For example, when watching a movie, the cortex tells the reticular nucleus in the brain stem to filter other irrelevant input (other folks in the cinema, sounds of popcorn etc.).
Reference
- Steriade et al., Science (1993); 262: 679-84

How does the sound of popcorn get filtered as unimportant when sounds in the movie don't?

@Troyseph - By active feedback from the cortex.


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Organ donation compatibility based on DNA
As far as I know, multiple tests are made before organ transplant to determine matching. Would it be possible to do the matching based on the DNA of the patients, rather than the actual serum antigen/antibody? If yes, is it any better/cheaper/easier?

Since the DNA is not recognized by the immune system (in contrast to surface molecules), this wouldn't make much sense.

@Chris but the these molecules are coded by the DNA, aren't they? I know there are post translation modifications (including immune cell maturation), but I was wondering how important/predictable are they

@Zeller If you are trying do test if a chair exists, why would you look for a carpenter rather than a chair? Sure there might be DNA markers, but whilst it's cheaper and (presumably) quicker to do the more appropriate method, why would you need/want to do a DNA test? (That is not necessarily a rhetorical question)

I'm trying to find a better solution for organ transplant matching based on genetic data instead of immunology. Assuming that if all the genes are know for both the donor and the acceptor, it is possible to determine the match. I haven't researched too much as the idea came up today, but I'd like to know if it is theoretically possible. Maybe going to the gene level, you can avoid multiple tests, predict/prevent chronic rejection and so.

@zeller
The better answers are being sought in a field called Regenerative Medicine.
A number of techniques have been tried, among them 3D printing of organs and dissolving the cells from a donor organ leaving the collagen scaffolding, then reseeding the organ with a patients stem cells in a bioreactor.
Most of these technologies, unfortunately, are in the proverbial 20 years from now category, which means that there are an incredible number of technical and biological challenges to overcome, but the ideal result would be organs with the patient's own cells and therefore no rejection or need for immunosuppressant therapies post transplant.
A nobel prize was awarded a few years back to Shinya Yamanaka for creating Human Induced Pluripotent Stem Cells. A technology like this would be the likely source of the stem cells necessary to seed these organs, however there have been problems with these cell lines including their tendencies to become neoplastic and form cancers.
So for at least the near and medium term the best alternative is to find organs that are as close a match as possible for Major Histocompatibility Complexes, and as Moderator Chris said, the best way to do this matching is to test for the cell surface proteins, as these are what will be the targets of immune cells. Also an organ has a very short life span after the donor dies to be usable. Sequencing is much slower than the protein screening that is in place today. You run into ethical questions regarding keeping someone on life support for the sole purpose of harvesting their organs.
And we still wouldn't be 100 percent sure that even people with the same alleles for these molecules express them in the exact same way as there may be slight differences in the post translational modifications that are made. The human immune system has evolved to detect small variations and as such we would still need to test the proteins, even if we found allelic matches. People get autoimmune diseases all the time, so there is no guarantee that even allelic matches would not be rejected.

It's not really (directly) related to this question as such, but you have listed a lot of different approaches & you do appear to still be active in here, so I just wanted to ask if you know of any suggestions of this approach in any available literature? https://biology.stackexchange.com/questions/79881/could-bone-marrow-transplants-be-used-to-prevent-tissue-rejection-of-trans-speci

The human genome is 3 billion letters long.  Most of that sequence has nothing to do with tissue rejection.  Only a handful of genes relate to tissue rejection, so those are what one might want to sequence, but even having the sequence doesn't necessarily tell you how the proteins are shaped, and it's protein shape that determines how they interact with each other.

But the different alleles of each protein, or gene, is what determines compatibility. That could be easily tested. The thing is it is cheaper to analyse serum than Next Generation Sequencing.

The SHAPE of the proteins is what determines compatibility, and that can't be predicted now from sequence alone. Anyway, next generation sequencing takes a week, PCR and sanger sequencing of 10 genes would take 48 hours.

It is the shape, sure, but the alleles are already known. If we look for compatibility we just have to identify them, not predict their structure. And I don't know where you got that NES takes a week. NES takes about half a day depending on jow much you have to mount and sequence (providing you have the equipment in your lab).