text:
Normal ECG/EKG Measurement?
I'm getting started using ECG using a 3 lead system by iWorx. I have place the leads on my two wrists and the ground on my ankle and have recorded some data into the provided LabScribe 3 software using the ECG template. Can anyone help me interpret what I'm seeing?

It doesn't look like the standard QRS I see in my textbook, but it's so regular (this is just a snippet) that I don't believe I'm seeing artifacts.
Any insight would be greatly appreciated.
Thanks!

What do you want to know? It looks fairly straightforward. Wandering baseline causing some artifact, maybe a short P-Q Interval, everything exaggerated throughout. Is this what you're asking?

it does look OK, that is P, QRS and T waves are present (means you alive). Weirdness might come from insufficient or incorrect filtering, namely, it seems that T wave is too intense.

If no one answers here, you might request admission onto the Google Plus ECG community. And post this same question there; there will definitely be someone who can help you there.

downvoter! leave a feedback.

How can an ECG be recorded from the wrist? ECGs pick up the electrical activity from the heart muscle? Where is the wrist signal coming from?

These sites provide useful info for understanding EKG signals:
https://ekg.academy
https://www.practicalclinicalskills.com

If you're looking for an explanation of the parts of the waveform you recorded, here's an annotated version:

I hope that helps you map it back to the "standard" QRS you saw. The AV delay is the time between the depolarization of the atria and the ventricles.
I agree, the T-wave is too intense. I'm not familiar with a 3-lead ECG that connects to the wrists--I'm more familiar with chest ECGs. I'm guessing the large T-wave is an artifact of measuring through the wrists (hopefully it's not indicative of a health condition such as Hyperkalemia). It looks like your resting heart rate is around 52 BPM--that's healthy.
The signal itself comes from the heart muscles. It takes a number of milliseconds for the electrical impulse to travel from the sinoatrial (SA) node to the atrioventricular (AV) node, down the His bundle, and finally to the Purkinje fibers in the ventricles. It takes this long because the movement of charge is caused by ions in the cells physically moving. That change in charge is conducted (via normal electrical conduction, such as you see in a wire) through the tissue and muscle to the electrodes on the wrists--this conduction is effectively instantaneous (in this case, it's electrons "pushing" each other, not ions moving within cells as in the case of the heart's electrical system). ECGpedia has some good background on this.

The ECG system takes the voltage from your right wrist (call this VRA), and subtracts it from the voltage at your left wrist (call this VLA), so that Vlead I = VLA - VRA.

So, in summary, the signal you're seeing is produced by the heart's conduction system, not the muscles in your wrists. Muscle noise would manifest itself as noise or random spikes in the ECG.

+1, but where on earth does this signal come from you think?


text:
How is it possible for the absolute fitness to be more than 1?
The wikipedia definition of Absolute fitness is "the ratio between the number of individuals with that genotype after selection to those before selection. It is calculated for a single generation and must be calculated from absolute numbers."
But in one generation there are no reproductive events so it should be theoretically impossible for the population to be larger after the selection event than before it (since no reproduction is taking place).

That definition in the wikipedia is misleading at best. Contrary to what it seems to suggest there, absolute fitness is computed across a single generation, not within a single generation. For simplicity, let's look at an example using asexual haploids with discrete non-overlapping generations. If individuals with the A genotype produce an average of 3 offspring, each of which survive with probability 0.5, the A genotype has an absolute fitness of 1.5. The key is that we've multiplied fecundity (3) by viability (0.5) and this allows us to obtain a value greater than 1.
Things get more complicated if we look at diploid sexuals. The absolute fitness of the Aa genotype is not the ratio of the number of individuals with the Aa genotype at time t+1 to the number of Aa at time t. An easy way to see this: in a population of AA and aa parents only, e.g. as produced by a cross, the ratio of Aa at t+1 to Aa at t is infinite, which would imply infinite fitness if we went this with definition. Rather, the absolute fitness of the Aa genotype is one-half the number of surviving offspring at time t+1 produced by Aa parents at time t. The one-half comes from the fact that a parent individual contributes only one-half of the genetic material of each surviving offspring. For some traits, e.g. those involved in sex ratio determination or parental care, it will not be sufficient to count surviving offspring; in these cases we apply comparable logic to counting grand-offspring.
The wikipedia seems to suggest we are to look only at viability because we are comparing before-selection numbers to after-selection numbers, within a single generation and thus without an opportunity for fecundity to come into play. That is not consistent with the common usage of the term. To be fair, I have on rare occasion seen "absolute fitness" used as a synonym for "viability"--though I cannot think of any good justification for this usage.

That definition is problematic and incomplete. Absolute fitness can be used in different ways, and can be calculated at different levels of organisation (individuals, genes etc). However, absolute fitness always relate to actual growth rate, actual numbers of offspring or other measures of fitness (so an absolute measure), while relative fitness is calculated as a fitness ratio in relation to a specific genotype (so a relative measure).
Absolute fitness is often defined in terms of the per capita growth rate of a genotype (or the intrinsic rate of increase (r) for e.g. bacterial clones), which can clearly be above or below one. However, how to measure this is another thing, and this is where many different metrics are used. In quantitative genetics and life history evolution it is common to use the net reproductive rate (R0) derived from the characteristic equation as a measure of fitness. However, sometimes the number of offspring or other measures are used as proxies for absolute fitness (as fitness components).
The definition of fitness is a tricky subject, and what to use depends on exactly what type of organism you are studying. The Wikipedia definition is clearly inadequate, and I feel that the formulation "...is calculated for a single generation..." is a direct mistake. The section "Measures of fitness" in Roff (1992) and Day & Otto (2001) (chapter on fitness from the Encylopedia of Life Sciences) are both very useful to read to better understand different measures of fitness.

Welcome to Biology.SE!
Definition of Absolute Fitness
Let's forget about the wikipedia definition for a little while. There exists different definitions of fitness. They vary only slightly and usually it does not really matter. Let's talk only about absolute fitness at first. Absolute fitness can be calculated

for a genotype
for a haplotype
for an individual

fitness can be calculated for

for a given period of the lifetime of an individual
for the whole life of an individual.

Also, absolute fitness can be calculated in function of

the number of offsprings
the number of offsprings that survive at a given age (typically age of sexual maturity), that is the number of offsrping after selection on survival.

Very often, when talking about theoretical concepts, we consider exclusively for semelparous species (species that have only one reproductive event and then die like some salmon species for example). In such case, when talking about one generation, we think of a population of adults that gets entirely replaced by a new population of offspring. Thinking about semelparous species has the advantage (among other advantages) to avoid confusion about lifetime reproductive success versus rate at which offsprings are produced. So, yes in one generation there is reproductive events. Even if selection on survival hasn't yet occurred on the offsrpings of the parents in a given generation, the fitness of these parents during this generation is calculated in function of the number of offspring that will survive later. Hope that makes sense.
Relating the above definition to your question
Now, let's relate the above to the wikipedia definition. Absolute fitness is NOT "the ratio between the number of individuals with that genotype after selection to those before selection". It is only the number of offsrpings produced by an individual for a given period (often the whole life of the individual. It can eventually be the number of offsprings that survive to a given age (selection on survival). Wikipedia seems to be wrong unless it has been misquoted. You should indicate where you read that so that one can correct wiki if there is indeed an error.
Relative Fitness
Now, relative fitness of a genotype/haplotype/individual for a given period of time (eventually the whole life of the individuals of interest) is just the absolute fitness of the individuals of interest divided by a standard absolute fitness. This standard absolute fitness is either the maximal absolute fitness observed in the population (or metapopulation) of interest or the maximum theoretical fitness based on some assumptions. For example we may calculate the relative fitness of an individual by dividing the absolute fitness of this individual by the fitness of a theoretical individual that would carry only the best possible mutations even though this individual doesn't exist in the population.

I think that if we want to settle on some definitions we should look into the book: Endler, J.A. (1986) Natural Selection in the Wild
Definition of Relative fitness

Relative fitness can also be measured with reference to a particular
  phenotype (or genotype), in which case $\overline {w}$ is not
  necessarily 1; this is the most common method used for polymorphic
  traits. If the population is sampled twice (or more) within a
  generation so that individuals in the second sample represent a subset
  of those sampled in the first sample (as in a capture-recapture or
  cohort study), then absolute fitnesses can be calculated. Examples are
  the probability of surviving between samples, or the probability of
  mating. On the other hand, if samples are made without replacement, or
  if samples are made of juveniles and adults at a single time, then
  only relative fitness can be calculaqted; information on total numbers
  and mean fitness is lost (see discussions in O'Donald 1971, Horns and
  Harrison 1970, and Manley 1974).)

Definition of Absolute fitness

Adaptedness and Adaptation. Adaptedness is the degree to which an
  organism is able to live and reproduce in a given set of environments:
  the state of being adapted (Dobzhansky 1968a,b). Adaptation is the
  process of becoming adapted or more adapted (ibid.). Unfortunately,
  adaptation.is also used in the sense of an adaptive trait (Lewontin
  1978), confounding the end product with the process (see also Dunbar
  1982). An adaptive trait is "an aspect of the developmental pattern of
  the organism surviving and reproducing" (Dobzhansky 1956, 1968a).
  There are problems in defining precisely what adaptednedd is so that
  it can be measured (Dobzhansky 1956, 1968a,b; Stern 1970; Lewontin
  1978; Dunbar 1982). One solution is to define it in the sense of
  absolute (rather than relative) fitness (Table 2.1). In this case it
  can be measured by the average absolute lifetime contribution to the
  breeding population by a phenotype or a class of phenotypes. It thus
  becomes intimately related to the actual (R) or intrinsic $(r_{m})$
  rate of increase, or "Malthusian parameter," and these have actually
  been used as measures of fitness for populations and species, though
  there are some problems (Fisher 1930; Dobzhansky 1968a,b; Dunbar
  1982). Adaptedness has also been defined as the mean absolute fitness
  (Sober 1984). [...]

Defining Generation
A generation is the interval of time between birth of an organism and the birth of its offsprings (reference from "Biology ninth edition, Rave, Johnson, Mason, Losos and Singer).
So in my interpretation, yes there is a reproductive event in one generation. If some phenotypes or genotypes are producing more offsprings compared to other individuals, and that there is a correlation between their fitness and the trait that hey have, than yes, it is probable that the population could increase. Especially if they survive, and have offsprings, enough resources, etc.

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text:
How come all my family have brown eyes and I have blue eyes?
My whole family tree up to my grandparents have brown eyes,
I have blue eyes, how come?
I don't know if it matters but I have not received enough oxygen at birth, doctors said it's probably the reason I'm left handed while my most of my family is right handed

let's say my grand-grand-grand parent had a blue eye genes, what is the statistic for me to have blue eyes?

How many (genetically related) aunts and uncles do you have, and are any of them blue-eyed? How many siblings do you have?

about 14 aunts and uncles, many more cousins, all have brown eyes. what is the statistic for me to have blue eyes?

While I don't know much about the inheritance of eye color, I suppose that a perfect answer would compare 1) the probability of such thing to occur assuming the alleles that make you eyes blue are inherited by some family member, 2) the probability that you carry a new mutation that make you eyes blue and that your recent ancestors did not carry and 3) the probability that your father is not your real father (my apologies for saying that this might be a possibility).

After wiki missatributed paternity is around 5% (with large standard error). It is important however, when talking about the misattributed paternity hypothesis, to not forget that there is a multiple comparison issue here. Eye color is not just a randomly chosen phenotypic trait but is one that you notice make make you different from the rest of the family.

Since blue eyes are mainly related to recessive alleles (so brown eyed parents can carry the alleles that cause blue eyes) at two different loci this is perfectly normal, even if all your grandparents have brown eyes. This link provides a nice overview of the basics of eye color inheritance: http://genetics.thetech.org/how-blue-eyed-parents-can-have-brown-eyed-children
However, even more genes are related to eye color besides the two main ones, so besides these main modes of inheritance, there are also other possible combinations and cases.

An age-old problem with a fairly obvious solution: "My mother certainly says I am Odysseus' son; but for myself I cannot tell. It's a wise child that knows its own father." - Homer, "The Odyssey. ca 1100 BCE.  (I write this as the only green-eyed blonde in a family with dark hair & brown eyes.)

The eye color follow quite well mendelian inheritance rules...
Probably your parents are heterozygote recessive for the blue color, hence the children have 25% of probability of having blue eyes.
Let's say color of the eyes has 2 alleles "BLACK" for the dark eyes and "blue" for the light eyes. Your parents are probably both BLACK-blue, BLACK-blue. They show the dark eyes because that allele is dominant over the blue one.
During recombination all the possible combination can come out:

BLACK x BLACK=25% resulting color=dark
BLACK x blue=25% resulting color=dark
blue x BLACK=25% resulting color=dark
blue x blue=25% resulting color=light

Check out the wiki page about mendelian rules of inheritance if you wanna know more!!
Of course in realty the situation is much more complicated, however you can still approximate the results to mendelian rules...
have fun!!

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text:
What are the major causes of mutations in DNA?
I know that point mutations can change the base sequence of a gene by altering a specific codon that codes for a particular amino acid. Are these mutations purely random events that occur when DNA is being copied into a cell? Furthermore, can environmental factors play a role in the amount of mutations that occur?

There are physiological mutations too. You may want to read about the hypervariable regions of the Immunoglobulin and the T-Cell Receptor (TCR). In this case, the part of codon that is responsible for forming the antitope undergo mutation randomly causing the formation of a extremely large gamut of paratopes that can recognize almost any foreign substance!

Welcome to Biology.SE!

can environmental factors play a role in the amount of mutations that occur?

Yes! The environmental factors that increase the mutation rate are called mutagens. You will definitely want to have a look in the wikipedia article. You may also want to read the wikipedia page on mutagenesis
Some chemicals increase the mutation rate, physical agents such as radiation also increase the mutation rate. There are viruses that are mutagens as well. Also, the number of mutations that an organism produce can also be phenotypically plastic. For example, plants have been shown to increase thee number of mutations they produced in response to stressing environment. The reason (or at least the commonly stated reason) is that they produce many mutations, "hoping" that at least one of the offsprings will carry a beneficial mutation and will be very fit even in this environment that is stressing for the parents. Many viruses and some bacteria also act as mutagens.

Are these mutations purely random events that occur when DNA is being copied into a cell?

Mutations are random in the sense that it is impossible to predict with certitude that a given mutation will occur at a given locus (locus=position in the genome). As a consequence, it is also true that mutations are random in the sense that it is impossible to predict the effect on the phenotype (and on the fitness) of a future mutation. Mutation rate varies throughout the genome. Typically, repeated DNA sequence tend to have higher mutation rate. Also, transposons causes many mutations and regions in the vicinity of transposons have higher mutation rate. But again, you should have a close look to the wikipedia pages I linked above.
Note that a full answer would require going into the terminology of the term "random" which itself is a question of philosophy. When using the term random, it is always important to specify what is meant exactly (which is not done in the question) as one may argue that since the Big Bang happened everything has been deterministic.

There are many different types ('scales', you might say, and mechanisms) of mutation in the genome.
Maybe your question was really about base mutations, but I want to add one interesting tangential thing (which also points out the importance of clarifying the term 'mutation'):
Segmental Duplications - non-random genomic mutation
There are mutations that you would not call random; that occur again and again in patients of some disorders. By studying patients with Charcot-Marie-Tooth 1A (and other diseases), geneticists identified structures in the genome which act as 'platforms' for large-scale mutations i.e. chromosomal rearrangements.
Certain places in the genome are rich in segmental duplications, paralogous segments of the genome which can be reasonably large (1-400kb), may contain genes, and have very high identity (>90%) making them prone to recombine.
The presence of segmental duplications (SDs) creates local genomic instability; a propensity for recombination, causing rearrangements - the term "genomic disorder" was coined for diseases arising from these rearrangements.
These genomic disorders are typically gene dosage imbalances. In the case of Charcot-Marie-Tooth 1A, duplication of a region between 2 SDs contains a gene involved in myelination. Deletion of that region causes another neuropathy. Haemophilia A can be caused by the inversion of a region between 2 SDs which lies partially within a long gene encoding a clotting factor. Inversion totally disrupts the exons.
Read more here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1226196/


text:
Why HIS tag is not detected in WB or dot blot?
I would like to know why the recombinant protein with his tag at c terminus is not being detected neither in western blot or dot blot.
I'm trying to validate protein expression of four proteins. Three of the four proteins have no assigned protein family or domain (PFAM). The size of the proteins is small:
Locus   Nucleotide length   Protein size    Membrane features   Cloned  WB  Dot blot    Dot blot urea   COG
HPNK_06205  360 120 signal peptide  yes no  no  -   -
HPNK_09829  129 43  signal peptide  yes low low -   -
HPNK_10446  756 252 transmembrane   yes no  no  -   COG1175 ABC-type sugar transport systems, permease components
HPNK_11461  264 88  signal peptide  yes yes yes -   -

Next steps:
-Discard possible his tag hidding by adding urea to dot blot.
-Revise annotation for the proteins. Since all are annotated as hypothetical proteins, maybe there is an alternative annotation that could lead to longer proteins and maybe more stable products.

Some troubleshootings can be found here, pointing to hidden his tag. https://www.researchgate.net/post/Why_am_I_not_able_to_detect_6_HIS_tag


text:
Why have whales and dolphins not evolved to have gills?
It seems at first glance that it would be an evolutionary disadvantage for a sea creature to have to come up to the surface on a regular basis in order to breathe, so why are there animals (e.g. whales and dolphins) which still need to do so?
If there is some advantage to breathing from the air instead of using gills, why haven't animals such as sharks (or indeed fish in general) evolved to do this instead?

Ever heard the expression "there's more than one way to skin a cat"? Living in the ocean does not require gills to breathe, it's just one of the suitable adaptations. Questions like this are near impossible to reasonably answer because the answer is simply "because they didn't evolve gills."

Just to be sure; are you aware of the evolutionary history of whales (i.e. their phylogenetic relationships)?

I don't know many of the details, but I seem to recall that they actually evolved from land animals, is this the primary explanation for why they still lack gills?

@Cliff Whales and dolphins are not just land animals; they are mammals (in fact they are phylogenetically related to hippopotamus). Gills are not present in higher animals.

@WYSIWYG I'm aware of this, but my question is why is this the case?

@Cliff and the answer is: just because that's the way things happened.

@Cliff It is because whales would require too many mutations to restructure their respiratory and cardiovascular system to develop back gills whereas they could survive in an aquatic environment with lungs and few mutations. The likelihood of selection of that many mutations without an obvious advantage is too less.

Another part of the answer is that it's probably a lot more difficult to re-evolve gills than to evolve the simple streamlining &c that is necessary to become air-breathing aquatic mammals.  There'd also seem to be no real pressure/advantage, since air-breathing whales, dolphins and so on are pretty successful top-of-their-food-chain creatures.

Looking at deepsea fish with gills, they tend to be sluggish and at a bare minimum of activity/expenditure due to the utter lack of oxygen at depths whales are known to frequent. So you have these enormous marine mammals, with enormous concentrations of myoglobin packing literal tons of oxygen, it elicits a much greater capacity for hunting etc. at greater depths. There are advantages to lungs in whales.

So first off, during development mammals produce pharyngeal arches, same as fish. Fish development turns them into gills, mammalian development into ears and parts of the jaw. It isn't too much of a stretch to assume that aquatic mammals with slight alterations in their expression patterns during development could revert to developing gills. I think the best answer is what @Kendall suggests. Gills are a pretty inefficient means of obtaining oxygen, and considering the amount of oxygen that a warm-blooded mammal needs to consume, oxygen efficiency would out select expression to form gills.

While the subject is different, the origin of your misunderstanding makes your question very similar to Why don't mammals have more than 4 limbs?

I marked the question as duplicate but did not expect my vote only would be sufficient to close it. I don't think I can undo it now.

I think you're looking at this the wrong way.
Animals evolve to fill niches. Many, many land animals returned to the water as a place to live, including:

whales, dolphins, porpoises, seals, sea lions, walruses, manatees, dugongs, otters, hippos, pygmy hippos, crocodiles, sea snakes, sea turtles, river turtles, river snakes, etc. etc. etc.

Their success in this environment points to no need whatsoever to "evolve" gills to be better suited. Without the interference of man, there would be yet many more of them.

Not to mention penguins (and should we count diving birds like ducks?), and in prehistory the ichthyosaurs, plesiosaurs, pliosaurs, mosasaurs, and probably more that I can't remember.  Becoming an ocean-going air breather seems to be a pretty successful ecological niche.

Gills are a really inefficient means of obtaining oxygen, while you have some cold-blooded creatures on your list, warm-blooded animals have an oxygen requirement that probably could not be supported by gills. Also, we have pharyngeal arches during development. Our developmental pattern produces ears and parts of the jaw, and fish get gills. I think it is less about no need than it would be unsustainable for a warm-blooded organism to try and supply its oxygen requirement with gills.

@AMR - you may have a point there! My point is that evolution is influenced by selective pressure, not "(un)common sense." Land animals returning to the sea started with lungs, and kept them. Fish started with gills, and kept them.  You state, "it would be unsustainable for a warm-blooded organism to try and supply its oxygen requirement with gills." (The great white predator seems to do fine. It is still about niches in my mind. However...) If you could add an answer that covers your point, the OP might get all the information they need.

Natural selection can only choose from the diversity available. Sometimes there are physiological or other constraints that prevent a solution we think should be optimal to arise. For instance, insects are the most diversified group of animals, but there are no marine insects. Why? It seems their respiratory tract (a tracheal system) can't deal with salt water. Or we can think of flying as something very advantageous, but flight has only evolved four times (insects, pteurosaurs, birds and bats; or five, if we include our flying machines). So "you can't always have what you want".
The precursor of gills can yet be seen in the early stages of mammal embryological development (they lead to the channel that allows you to unclog your ears by swallowing). But to turn them back into fully functioning gills would take so many mutations and the re-adaptation of so many working systems, that it's not a much viable option for large animals such as cetaceans. Remember that the gills first formed in the very first, very small vertebrates, and slowly acquired it's present shape we see in bigger fishes.

Welcome to evolution.
Just because the idea is great, the path obvious (in our minds), does not mean it will happen.
Evolution works by random mutations followed by selection to weed out nearly all phenotypes that are less successful than the original.
So you need both the mutations and right selection environment.
So while gills on a sea going mammals is a great idea. The path towards that is not an easy outcome without some form of intelligent design. You see those gills arches fishes have to support their gills... well the tetrapod lineage has since re-purpose those bones to make several structures such as the thyroid gland, part of the jaw, the larynx, and the bones in mammalian ear. https://en.wikipedia.org/wiki/Branchial_arch
So a whale that simply reconverts to gills, would be without a larynx (mute), or inner ear (bad hearing) and parts of the jaw (Can't eat). So you can see alot of other work will need to be done to make such an animal work. And if this process is left to nature, each intermediate must also work successfully in some environment.
Such are the constrains of evolution.
However if intelligent design were available. No problem. It can be done. We can ignore temporary lowered fitness, and work with a desired outcome in mind.


text:
EMBOSS matcher and supermatcher - incongruent results?
I am trying to align a sequence to the mouse genome. I know a priori that part of my sequence should align to chromosome 9, but not all of it.
I gathered that EMBOSS' matcher and supermatcher would be adequate tools to do this locally on my machine - with supermatcher being (a lot!) faster and matcher being (allegedly) more accurate. Strangely enough, the two functions give me very similar fits (quality-wise) which are however at non-identical but very close positions.

How can I explain this?
What are the odds that an ~800-bp sequence has multiple equally good fits right next to each other (how can I test if I hit a repeat-heavy area?)?
Why do match and supermatch not give me both fits then?

My current alignments:
#=======================================
#
# Aligned_sequences: 2
# 1:
# 2: CM001002.2
# Matrix: EDNAFULL
# Gap_penalty: 16.0
# Extend_penalty: 4.0
#
# Length: 357
# Identity:     322/357 (90.2%)
# Similarity:   322/357 (90.2%)
# Gaps:           2/357 ( 0.6%)
# Score: 1458.0
#
#
#=======================================

                   1 AAAAACGTGAAAAATGAGAAATGCACACTGTAGGACCTGAAATATGGCAA     50
                     ||||.|..|.||||||||||||.||||||.||||||.|||||.|||||.|
CM001002.2    35305253 AAAATCACGGAAAATGAGAAATACACACTTTAGGACGTGAAAAATGGCGA 35305302

                  51 GGAAAACTGAAAAAGGTGGAAAATTTAGAAATGTCCACTATAGGACGTGG    100
                     ||||||||||||||||||||||||||||||||||||.||.||||||.|||
CM001002.2    35305303 GGAAAACTGAAAAAGGTGGAAAATTTAGAAATGTCCTCTGTAGGACATGG 35305352

                 101 AATATGGCAAGAAAAATGAAAATCATTGAAAATGAGAAACATACAGTTGA    150
                     |||||||||||||||.||||||||||.|||||||||||||||.||.||||
CM001002.2    35305353 AATATGGCAAGAAAACTGAAAATCATGGAAAATGAGAAACATCCACTTGA 35305402

                 151 CGACTTGAAAAATGATGAAATCACTGAAAAACGTGAAAAATGAGAAATGC    200
                     .||||||||||||||.|||||||.|.||||||||||||||||||||||||
CM001002.2    35305403 TGACTTGAAAAATGACGAAATCATTAAAAAACGTGAAAAATGAGAAATGC 35305452

                 201 ACCCTGTAAGACCTGGAATATGTCGAGAAAACTGAAAATCACGGAAAATG    250
                     .|.|||.|.|||||||||||||..||||||||||||||||||||||||||
CM001002.2    35305453 CCACTGAAGGACCTGGAATATGGGGAGAAAACTGAAAATCACGGAAAATG 35305502

                 251 AGAAATACACACTTTAGGACGTGAAATATGGCGAGGAAAACTGAAAAAGG    300
                     ||||||||||||||||||||||||||||||||||||||||||||||||||
CM001002.2    35305503 AGAAATACACACTTTAGGACGTGAAATATGGCGAGGAAAACTGAAAAAGG 35305552

                 301 TGGAAAATTTAGAAATGTCCACTGTAGGACATGGAATAT--GGCAAGAAA    348
                     |||||.||||||||||||||||||||||||.||||||||  |.|.|||||
CM001002.2    35305553 TGGAATATTTAGAAATGTCCACTGTAGGACGTGGAATATAAGTCCAGAAA 35305602

                 349 ACTGAAA    355
                     .||.|.|
CM001002.2    35305603 CCTAAGA 35305609

and:
#=======================================
#
# Aligned_sequences: 2
# 1:
# 2: CM001002.2
# Matrix: EDNAFULL
# Gap_penalty: 16
# Extend_penalty: 4
#
# Length: 417
# Identity:     377/417 (90.4%)
# Similarity:   377/417 (90.4%)
# Gaps:           2/417 ( 0.5%)
# Score: 1713
#
#
#=======================================

          180       190       200       210       220
       TGAAAAACGTGAAAAATGAGAAATGCACCCTGTAAGACCTGGAATATGTC
       ::  : ::   : :: :  ::  ::::: ::: : ::::::::::    :
CM0010 TGTCACACACTATAATTTTGAGGTGCACACTGAAGGACCTGGAATTATGC
       35305200  35305210  35305220  35305230  35305240

          230       240       250       260       270
       GAGAAAACTGAAAATCACGGAAAATGAGAAATACACACTTTAGGACGTGA
       ::::::::::::::::::::::::::::::::::::::::::::::::::
CM0010 GAGAAAACTGAAAATCACGGAAAATGAGAAATACACACTTTAGGACGTGA
       35305250  35305260  35305270  35305280  35305290

          280       290       300       310       320
       AATATGGCGAGGAAAACTGAAAAAGGTGGAAAATTTAGAAATGTCCACTG
       :: ::::::::::::::::::::::::::::::::::::::::::: :::
CM0010 AAAATGGCGAGGAAAACTGAAAAAGGTGGAAAATTTAGAAATGTCCTCTG
       35305300  35305310  35305320  35305330  35305340

          330       340       350       360       370
       TAGGACATGGAATATGGCAAGAAAACTGAAAATCATGGAAAATGAGAAAC
       ::::::::::::::::::::::::::::::::::::::::::::::::::
CM0010 TAGGACATGGAATATGGCAAGAAAACTGAAAATCATGGAAAATGAGAAAC
       35305350  35305360  35305370  35305380  35305390

          380       390       400       410       420
       ATCCACTTGACGACGTGAAAAATGACGAAATCACTGAAAAACGTGAAAAA
       :::::::::: ::: :::::::::::::::::: : ::::::::::::::
CM0010 ATCCACTTGATGACTTGAAAAATGACGAAATCATTAAAAAACGTGAAAAA
       35305400  35305410  35305420  35305430  35305440

          430       440       450       460       470
       TGAGAAATGCACACTGTAGGACCTGGAATATGTCGAGAAAACTGAAAATC
       :::::::::: ::::: :::::::::::::::  ::::::::::::::::
CM0010 TGAGAAATGCCCACTGAAGGACCTGGAATATGGGGAGAAAACTGAAAATC
       35305450  35305460  35305470  35305480  35305490

          480       490       500       510       520
       ACGGAAAATGAGAAATACACACTTTAGGACGTGAAATATGGCGAGGAAAA
       ::::::::::::::::::::::::::::::::::::::::::::::::::
CM0010 ACGGAAAATGAGAAATACACACTTTAGGACGTGAAATATGGCGAGGAAAA
       35305500  35305510  35305520  35305530  35305540

          530       540       550       560       570
       CTGAAAAAGTTGGAAAATTTAGAAATGTCCATTGTAGGACATGGAATAT-
       ::::::::: ::::: ::::::::::::::: :::::::: ::::::::
CM0010 CTGAAAAAGGTGGAATATTTAGAAATGTCCACTGTAGGACGTGGAATATA
       35305550  35305560  35305570  35305580  35305590

            580
       -GGCAAGAAAACTGAAA
        : : ::::: :: : :
CM0010 AGTCCAGAAACCTAAGA
       35305600


text:
Can ingesting substances that are produced by the body cause a permanent withering of the organs that produce the substance?
This question is about substances such as insulin and some vitamins that the human body is able to produce on its own.
Some substances that are produced by the body are also present in various body building supplements.
What I wanted to ask is, is there evidence that ingesting these types of substances for prolonged period leads to (permanent?) withering of the organs that produce the substance?

Is this question secretly about testosterone?

@Resonating, no it is not, I was just curious about the effects of substances in general.

Yes it is possible but in most cases it will not occur as the body simply halts production. The most infamous manifestation of this is in adrenal insufficiency. That's where when we take glucocorticoids (e.g. prednisolone used in management of lots of inflammatory diseases like asthma and autoimmune diseases) for a prolonged period at high dose. This causes the adrenal glands to atrophy (physically shrink) and following this sudden withdrawal can be dangerous for a patient. That's why we always slowly withdraw steroids when a patient has been on them for a long period of time.

Mostly no. For example, if a non-diabetic person were to be injected with a small amount of insulin, the pancreas would halt its own production of insulin and, if the dose was too large, begin producing glucagon, which stimulates the liver to produce more glucose to match the dose of insulin. If these periodic doses continue, the size of the islets in the pancreas may decrease, but it is always reversible and the beta cell count may return to normal if the doses cease, although it should be noted that a short period of "withdrawal" may occur. The intensity of this withdrawal will depend on how long the supplement was used and what the supplement is.


text:
What percentage of human body's cells are contained in blood?
What percentage of human body's cells are contained in blood vs. the rest of the body?

The background of the question was a (somewhat silly) theoretical question of "how much of your body's cells can you replace with blood transfusion". I realize that the exact biological answers to the two questions will be different, but I think it's a good first approximation.

You should probably edit the question to contain that background then.

When you mean "percentage", do you mean my type or by mass?

@anon by cell count

According to this answer, there are 2.63 × 10^13 red blood cells, which is 70.69% of the 3.72 × 10^13 total human cells in the estimate.

The human body has about $3.72 × 10^{13}$ cells according to Bianconi et al. 2013, although this is disputed.
It also has about 5 liters of blood, which is made approximately 40-45% of erythrocytes. Let's assume 2.5 liters = 2500 $cm^3$ of red blood cells (RBC). Assuming a mean value of 5 millions RBC per $mm^3$ there should be in total $5 \cdot 10^6 \cdot 10^3 \cdot 2500 = 7.5 \cdot 10^{12}$ RBC.
By completely taking out white blood cells and thrombocytes out of the equation, a number of ${7.5 \over {3.72 \cdot 10}} \cdot 100 = 20 \%$ of number of cells are contained in the blood (approximately).

Given the hypothetical 70 kg man, let him be separated into components:
Blood: 7% (70 kg x .07 = 4.9 kg)
Of that, 60% is plasma, so (4.9 kg x .4 = 1.96 kg blood cell weight.)
Therefore of a 70 kg male, ~ 2 kg is blood cells
Tissue and bone: 93% of body weight (70 kg x .93 = 65kg)
Of that, 27% is extracellular fluid, so (65 kg x .73 = ~ 47.5 kg cell weight)
But we need to subtract the weight of bones:
Dry bone weight = ~6.5% total body weight, (70 kg x .065 = 4.55 kg bone weight)
So, cell weight minus extracellular fluid:
Blood cells: 2 kg
Body cells (minus bone weight): 43 kg
2kg/(43kg + 2 kg) = 4.4% of the weight of cells in the body are the blood cells.

Isn't a human being about 75% other organisms though? As in, of that 70kg, about 50kg doesn't actually have the human's DNA?


text:
Are there any DNA sequences shared by all/most Viruses?
Is there any one DNA sequence shared by all or most viruses?
I highly doubt there is mainly because of how different all of them are, but it's still worth a try.
Thanks

What length of sequence did you have in mind?

Around 4 to 8 nucleotides would be perfect.

Statistically it seems very likely that every organism would share a 4 nucleotide sequence.

Very true. I'm looking specifically for any sort of shared sequence that is necessary for the survival of all viruses. At first I thought (for RNA viruses at least) it would be some sequence in a gene that codes for reverse transcriptase, however I have yet to find such a sequence. Any suggestions for a sequence like this or any other would be very greatly appreciated, so feel free to mention any ideas you might think of.

There are commonalities within certain related viral families. But no, there are no universal viral genes, there are many reasons for this:

Viral genomes in general are much smaller than the average cell genome and the pressure for selection against extraneous genes is high due to the need to be able to replicate as fast as possible within the host cell. This also allows for rapid evolutionary rates due to the sheer mass of  viruses creates and spread through a given host.
There are viruses that infect wildly different hosts and thus require highly divergent entrance mechanisms and strategies. Due to this difference, there would be no need for the bacteriophage for instance to share the same proteins or genes with those of HIV or another human virus.
It is possible that viruses have evolved multiple times throughout the history of life, this is however not confirmed as of this time. If it is true however, then it would preclude the possibility of universal viral genes as they would not share a common homology.(Though viruses may be able to mix their genetic material by sheer chance, if they share a common host.)
Viruses, by definition lack the common replication, translation and generally, transcription machinery that is shared by their cellular hosts. Thus, they do not have this source of common genes, as living organisms do.

No, virus are polyphyletic and there are no genes that are common to all viruses. There may be similarities in capsid structure due to convergent evolution, but these are not universal. See Moreira and López-García (2009) for further detail.


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How does the ideal free distribution work?
I have recently completed a study on Brent Goose. I found that Brent Geese occupy high quality habitat first then once this is full of geese, they fill up low quality habitat. However, there were always fewer geese in the low quality habitat.
This pattern therefore seems like a good match for the ideal free distribution…but is it?
Under the ideal free distribution, do birds fill up high quality first, then low quality habitat second?
Or do birds fill up both high and low quality habitats simultaneously, but fill up high quality at a faster rate?
Or does the ideal free distribution not make explicit the order/rate at which birds fill up high and low quality habitats?

The order of settling depends on the resource availability in different patches (in your case the difference between high and low quality habitat), but generally speaking, the pattern you observe conforms to the ideal free distribution.
The key factor in the ideal free distribution is that habitat patches are filled according to the current resource availablity (~per capita resource access), given the current density of individuals in the patch (so the marginal resource availability). If the high quality patch has much higher resource levels than the low quality patch, this means that many individuals can settle in the high quality patch before the marginal resource availability becomes equal to the resource availability in the low quality patch, at which point individuals will start settling in both patches. Therefore, the two observations you make; 1) lower overall density in low quality habitat and 2) the high quality patch being settled first, both agree with the ideal free distribution.
This graph (from wikipedia.org) illustrates this pattern nicely, for the standard version of the ideal free distribution:

Here, the marginal, apparent value of a patch is shown on the y-axis and the number of individuals in the patch on the x-axis, and the numbers refer to the order that individuals will settle in the two patches (so the first 6 settle in the high-quality Patch B, ind. 7-9 in Patch A, ind. 10 in Patch B etc).
However, I encourage you to read about other theories on habitat choice, and the pattern you describe can probably be explained by other processes as well. The ideal free distribution also has some rather restrictive assumptions (e.g. equal quality of individuals and no dominance/territorial/interference behaviours among individuals), which you have have to consider.


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Origin of term ‘confluency’ in cell culture
Since as long as I have been doing cell culture, the word confluency has been used to describe the percentage growth of cells or area covered by them. However, no dictionary that I have found uses this word. I was wondering if anyone could reliably state where the meaning comes from or how the association began, and truly what it means. I don't believe I can post this on another Stack Exchange  because the word doesn't have even a resembling meaning in the dictionary. Cell culture is such an integral part of cell biology, medical research and biological manufacturing. And this term is an integral part of cell culture. I was surprised to be unable to reliably verify its meaning.

I think that's a fair and sensible guess.

Besides the etymologic explanation that @aandreev gave, in cell culture this term is commonly used to describe the density of adherent cells and it is used as a measure of their proliferation. It is usually combined with an estimated (or counted) percentage, so 10% confluency means that 10% of the surface the dish or flask used is covered with cells, 100% means that it is entirely covered. The cells grow twodimensional on the surface of the flask in this case. The picture below (from here) illustrates different levels of confluency:

The level of confluency is important as the cells change their growth with changing densities. Low density cells (10-20%) usually grow slower than 50% confluent cells. If the plate is complete grown by cells, they tend to grow much slower again. This influences their genetic program, behaviour in experiments and transfections.
As @Roland pointed out it is important to say that confluency is not a hard measure, but rather an estimate of the cell density. Different people will get different estimations, but the trend should be the same.

Chris thank you thorough answer, any thoughts on the etymology of the word as used here other than @aandreev above?

@rhill45 Confluence means coming together. It actually does not mean how dense the culture is but this word has been used for several ages now for what Chris has said in his answer. Perhaps this term came from Dictyostelium (this is a wild wild guess)

@rhill45 I think aandreev's answer about the etymology is right. I don't know any other.

This is good answer. I would add though that the % confluence (area covered) is actually pretty hard to estimate by eye, since cultured cells often change size and conformation as they grow more dense. Different people typically give different estimates from the same image (I'm not sure that last one is 90%, for example :)  So confluency numbers are rather unreliable.

@Roland Thanks, this is a good point. I will add it.

@rhill45 — for the record, I think that is not an etymology, as I explain in my comment to the answer in which it occurs.

con- (com-) is prefix that usually means "togetherness", joining. Root fluency/fluent comes from latin fluere, to flow.
Source: Google's definitions for con- and fluency (information scraped from OUP).

Although this is a reasonably analysis of the meaning of the two components of the word confluency it is not a definition from any dictionary as the word does not occur in any dictionary. In my opinion it is invalid as etymology (the origin of a word and the historical development of its meaning) as the word is either a corruption of confluence or (more likely perhaps) a recent formation from the adjective confluent. Neither of these words are derived from fluency in English as explained in note [2] of my own answer.

The word confluency is a variant of the word confluence, although this variant only appears with any frequency in the context of cell culture [1]. The word confluence itself appeared in the fifteenth century and is derived from the Late Latin confluentia meaning “a flowing together” [2]. In English it was initially used for the flowing together of two or more streams, but acquired a large variety of more figurative meanings [3].
The word confluence (but rarely confluency) occurs in various biological contexts in the first half of the twentieth century [4], but the first example I can find in relation to monolayer cell culture is in 1961 [5], although the term confluent appears in the 1950s [6]. The form confluency seems to have appeared at about the same time as confluence [7]. Since the 1960s both forms have been used by different authors, currently with comparable frequency [8]. Some authors employ either one or the other exclusively, others use confluency when indicating a percentage designation and confluence to indicate the absolute concept — or vice versa [9].
The reason that confluency is not defined in general dictionaries (or even in the Oxford Dictionary of Biology [10]) can only be surmized. None of the online dictionaries I have consulted [11] give the cell culture usage as an example of confluence, suggesting that its use is less frequent than in other technical contexts, where the meaning is similar. With this usage of confluence not being thought to merit separate mention (irrespective of the importance or otherwise of cell culture) then the need to define an alternative form would not have arisen.
It should be added that there is there is a Wikipedia entry for confluency [12] but, despite its title, this uses the term confluence in its definition:

“In cell culture biology, confluence refers to the percentage of
  the surface of a culture dish that is covered by adherent cells. For
  example, 50 percent confluence means roughly half of the surface
  is covered, while 100 percent confluence means the surface is
  completely covered by the cells, and no more room is left for the
  cells to grow as a monolayer.”

Notes
[1] The hits reported by a Google Book ngram for the word confluency between 1800 and 1954 were analysed individually, as journal results from ngrams often have erroneous dates. There was one example (1829) of its occurrence before 1900, and 13 before 1950, about half in relation to vaccines or biological phenomena.
[2] The etymology of confluence given in the online etymological dictionary is:
early 15c., “a flowing together, especially of two or more streams,” from Late Latin confluentia, from Latin confluentem (nominative confluens), present participle of confluere “to flow together," from assimilated form of com “with, together” (see con-) + fluere “to flow” (see fluent).
I would emphasize that the word confluence is not a compound formed in English by adding a prefix to the word fluency, but derives from the compound word, confluentia, already evolved in Late Latin (i.e. by the sixth century).
[3] The Oxford English Dictionary quotes an early instance of the extension of the meaning of the word confluence (1606) as “In this confluence of so many prosperous successes”. A variety of examples, appearing to come from the fields of politics, philosophy and mathematics, can be found in the Cambridge Dictionary online for its second definition of confluence, “a situation in which two things join or come together”.
[4] This can be seen by going to the websites of some of the older biological journals (e.g. Journal of the National Cancer Institute or the Journal of Experimental Medicine) and searching for the word confluence.
[5] 1961 Yearbook of the Carnegie Institute of Washington (p.66).
[6] For example W.R.Earle (of Earle’s saline) uses it in a paper on the growth of fibroblasts in 1951, and T.T.Puck  (of Puck’s saline) uses it in a 1958 article in Experientia. The earlier use of confluent (also of 15th century origin) in relation to monolayer culture suggests that the word confluency, rather being a corruption of confluence, may have been formed from the adjective — perhaps in ignorance that a noun form already existed.
[7] Königsberg et al. (1960) J. Biochem. Biophys. Cytol. 8 333–343.
[8] There seems to have been division at the outset. In the US, Harry Eagle and Renato Dulbecco used the term confluency, whereas Howard Green and George Todaro used confluence. What one might refer to as the Glasgow school always used confluence: John Paul) at the Beatson Institute and his student Ian Freshney, both authors of influential books on cell culture. The more recent frequency of use may be judged from a Google ngram for “cell confluence v. cell confluency”.
[9] Searching for confluence in the Journal of Cell Science and examining recent issues brings up results for both confluence and confluency. This recent paper uses confluence exclusively both as an absolute concept and as a percentage, whereas this recent paper, for example, uses confluency exclusively in both absolute and numerical senses. Another paper refers to confluency, but to 70% confluence, but exactly the opposite is found in this paper which refers to confluence, but 70–80% confluency. Some papers — e.g. this alternate at random. The editors of the journal obviously do not care.
[10] The Oxford Dictionary of Biology has nothing between the entries for cone and confocal.
[11] Collins, Chambers, Cambridge, Lexico or Merriam-Webster.
[12] Wikipedia entry for confluency.

If this seems a little over the top, it was my time that was spent. I don't think it was wasted as demonstrates how one can use search indexes of various sorts to try to trace the history of biology. This overturned my previous view of the term which I had expressed in a previous answer that I decided to delete.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Is it possible to process electrical signals from the brain and interpret the results as exact thoughts?
If the brain uses extremely low voltage signals to communicate (from what I understand around 100 mV), what sort of breakthroughs would be necessary to intercept these signals and interpret them as exact thoughts? I know we interface with the brain's electrical field through already at a much higher level, but what is stopping us from being able to interpret it more precisely?

No, it is not possible at all. There is no technology whatsoever at present that can "read" a thought. Only a brain can interpret electrical impulses as thought. I can imagine nothing that can even foreshadow this.

I think it is not possible for one brain to interpret the thought pattern of another brain.

Define "thought", please, and "exact". You can pick up EEG signals for creating brain-machine interface and move your PC cursor around, is that good enough?

The brain activity is electric and chemical. The male adult human brain contains about 86 billion neurons (Azevedo et al). There is about 100 trillion connections between them. Solving a puzzle like that is not easy..

what sort of breakthroughs would be necessary to intercept these signals and interpret them as exact thoughts?

What you are referring to would be called solving the neural code in neuroscience. With today's methods, it is probably not possible.
Consider electroencephalography (EEG). It records the electrical activity of the brain. Ag/AgCl sensors are placed along the scalp (typically 64-256 in research settings). When about 50,000 parallel neurons fire simultaneously, a change in a recorded signal can be seen. While the time resolution is about 1 ms for EEG, the spatial resolution is several centimeters (it is not easy to find which areas produced the recorded signals; it is an inverse problem). A newer technique, called magnetoencephalography (MEG), is becoming more and more used but is expensive. It records the magnetic fields related to the electrical activity and allows better localization.
Is there other complications? Well... lot's of them. Blink your eyes during the recording and there will be a major artefact masking the brain signals in most channels (10-100x greater in amplitude than the brain signals).
Anyway, you would probably be interested in the new research involving the use of machine learning techniques: it has been possible to decode the contents of dreams, reconstruct what a subject is seeing, etc. The best papers have been published by Science, Nature, and PNAS, so using their search engines with the keywords decoding and brain should allow you to explore the topic easily.
PS. I did not have time discuss fMRI; someone else can may be do that..

I disagree to some extent. If you read "thought" as "intention to perform a motor action", then BrainGate (http://braingate2.org/) has been reasonably successful.

Very thorough! That is precisely what I was referring to when I mentioned, "interpret as specific thoughts". In essence, understand the function the brain is performing as specifically as possible. This is part of what fascinates me about machine learning. I will take a look at those sources! I am curious as to how fMRI works and how accurate it is compared to other methods. I have read articles that employed this method.

Possibly but not for a very long time.
Professor Gallant is in the embryonic stages of researching this and is having some success. Right now the computer needs a pool of possible images to draw from to make the possibilities small enough to search and the image resolution is rough at best. But the fact that even something as simple as color of a remembered image can be read means it is possible. But that is space shuttle level technology while we are still at the stage of strapping cardboard wings to our arms.
In all likelihood even when this technology is mature the machine will have to learn your brain similar to how a speak to text program has to learn your speaking patterns, before it works. To me this is hugely interesting for the possibility of seeing what parts of our brain architecture is universal and thus likely genetic.
I am including two other sources for the research but I warn you they are behind pay wall. http://www.nature.com/scientificamericanmind/journal/v25/n6/full/scientificamericanmind1114-40.html
http://www.sciencedirect.com/science/article/pii/S1053811910009109


text:
Immediate stroke/seizure Therapy
Can an oncoming stroke/seizure, be stopped by a setup consisting of a brain-computer-interface (BCI) that immediately detects the variation in wave-form, and then another machine that neutralizes the anomaly by sending a measured voltage to select areas of the brain OR by Transcranial Magnetic Stimulation?

Can you please use names (not initialisms)? What is a BCI? Also, stroke and seizure are two completely different entities. You can't stop a stroke with electricity or transcranial magnetic stimulation.

Welcome to Biology SE. Nice qunction - I think the seizure part is an interesting thought. However, how a stroke could be detected by its electrical signature, or how it could be prevented by electrical stimuli seems a bit out of context here, and hardly possible for that matter. Perhaps consider focusing on seizures to give the question focus.

@anongoodnurse (I hope you get a ping - I am mobile) - when giving it a second thought - if it would be possible to transfer a large current and coagulate the impeding rupturing vessel, one could, theoretically, use currents to prevent a stroke? But again, predicting it by electrical recordings seems impossible.

To give a jolt strong enough to coagulate blood in a vessel might do more harm than good... and then there are ischemic strokes (>80%).

@anongoodnurse - I see, practically it clearly doesn't make sense - thanks for this.

Yes, these devices and treatment programs are being actively developed. General idea is that epileptic episode follows certain path within the brain. It can start in thalamus, after which sporadic activity spreads into cortical areas, for example motor cortex. There is a number of papers on prediction of epileptic seizure, e.g. Seizure Prediction and its Applications.
The device then will detect initiation of seizure before evident symptoms and provide inhibition via cortical electrodes, microelectrode array (MEA). It seems that currently MEAs are used more for research (recording from tens of neurons), but single electrodes are useful for actual control of epilepsy. Also one can control vagus nerve, which causes parasympathetic response (general inhibition, aka "rest-and-digest"). More you can read here.
Transcranial magnetic stimulation, as I understand, is not portable enough to be useful.

This is more of a long comment than an answer:
There have been active research in this area for several decades now. The problem is that once you detect seizure (which is relatively easy), it's usually too late. Therefore, a lot of effort has been to predict epileptic seizures some time before it happens. This has proven quite difficult.
See this review article for the state-of-the-art in 2007:

Mormann, F., Andrzejak, R. G., Elger, C. E., and Lehnertz, K. (2007). Seizure prediction: the long and winding road. Brain, 130(2):314-333.
http://ntsa.upf.edu/system/files/biblio/Mormann-Brain2007.pdf


text:
What do we use as baseline to determine what genetic segments are "mutations" (and what are not)
In order to determine whether a particular segment of the genome is a mutation, there must first be a baseline code on which that code looks somehow different.
How has the baseline genome been determined? Did someone dig up a _very_old_ human skeleton which was subsequently DNA-analyzed to be used as the baseline?
Or do mutations contain some kind of fingerprint that tells researchers that "it is not the original genome"? If so, how does that fingerprint look like?

It may help to think about the genealogy of the sequences in question. In general, we suppose that all DNA sequences from organisms are related by a set of processes. A particularly important process relating DNA sequences is replication. This establishes a parent-child relationship between DNA sequences in one round of replication or an ancestor-descendent relationship when we view more than one round of replication.
For simplicity, consider a single bacterial cell, which replicates its genome and divides, yielding a descendent cell. This process continues for each cell and produces a population of cells over time. This population of cells (and their genomes) are related to each other by this process of replication and division. The structure of this relationship is a tree (in the mathematical sense). The vertices of the tree are the DNA sequences (or cells) and a directed edge from vertex i to vertex j exists if and only if the sequence represented by vertex j is the result of a replication of the sequence represented by vertex i.
In addition to the replication process which makes this tree structure relating sequences, there are mutational processes that lead to sequence differences.
There are many ways for mutations to arise before or during DNA replication. The important thing to note is that these mutations are passed on to descendants. So, a cell is either genetically identical to its parent cell, or it contains some number of mutations (insertions, deletions, or polymorphisms in the DNA) with respect to its parent.
These mutations (sequence differences) are inherited during replication, and you can think of them as "occurring" along a given edge in the tree from a parent cell to a child cell.
Now, if you consider any two DNA sequences, as well as the model just given, these two sequences are related through the replication-mutation process (the tree). If the DNA sequences are not identical, you have many ways to interpret this question of what is a mutation. It is useful to consider the most recent common ancestor of the two DNA sequences in making sense of the differences observed in the DNA. If you think of the genealogy as a tree, and you're considering two vertices in the tree, then tracing backwards towards the root of the tree from each vertex, these traces will eventually meet at another vertex. The first vertex at which they meet is the most recent common ancestor.
It is possible that mutations have occurred along both paths from the (most recent) common ancestor to the descendent sequences you're investigating. If you're investigating N sequences, there are N paths from the common ancestor on which mutations may have occurred.
All of this is to say that mutations occur with respect to this genealogical process. If you just consider 2, or N, sequences without regard to the process that generated them, then it can be meaningless or confusing to consider a particular sequence difference as a mutation with respect to another sequence under consideration. For example, if you observe a single nucleotide polymorphism between two sequences, how would you know which sequence was the result of the mutation? It is possible that one or both sequences carries a mutation event in its genealogical history since the common ancestor of both sequences.


text:
How do similar looking carps, but belonging to different species, differ from each other?
There are some carps which differ in colour, or has some easily noticeable morphological differences. But apart from that, most of the carps look "almost" the same. How does one differentiate one species from another?
Citing behavioral differences, differences in morphological characteristics (maybe subtle) and the likes which addresses this problem would be helpful. The characteristics with broader scope would be better.

This might actually be a more complicated question. The phylogeny for carps and other members of the Cyprinidae family have not been well resolved. Also, "Carp" belong to numerous genera including Carassius, Cirrhinus,  Ctenopharyngodon, Cyprinus, Hypophthalmichthy, Mylopharyngodon, etc. so they're not all actually related (below the family level). I would assume you could find a fairly easy way to differentiate these genera from each other. But...Given all this, are you seeking to differentiate all carp or just Cyprinus species?

I framed this question mainly keeping Cyprinus species in mind.

There isn't actually. Every species of Cyprinidae has its own distinct characters and sometimes for the ones that are too similar, like Labeo rohita, Labeo bata and Mrigel one can only distinguish them after regular examination. There's no set rules/guidelines but ones you develop an eye you know what ways they are different. Yet knowing the fin formula can help. But learning them all for so many species and remembering them is absolutely beyond human abilities.

If you are interested in some specific species. I think this can be answered.

Let's consider a school of fresh water carps which is readily available. I would like to know of some specific characteristics which are more effective than others when it comes to distinguishing between them i.e. if most of them can be told apart using a trait then it is significant. Developing an eye is just an observation, deducing inferences and standardizing them in a way, so that they can be used to understand subtleties, is what science should be all about.

Do you have a region of interest? As above commenters have mentioned, Cyprinid ID's are really hard. My general algorithm for fish ID typically involves a gestalt feel for family, and, depending on my familiarity with local members of the group, either referencing my internal catalog of species present (incorporating local abundance) or finding a field guide or key. But identifying species from afar? That's not going to be easy, esp. Not without some baseline familiarity with morphology and behavior.

I've edited the question.


text:
Does the use of a Thiazide diuretic affect the ability of a hair follicle to absorb substances?
Thiazide diuretics are on the World Anti Doping Agency's, as well as the International Olympic Committee, list of banned substances due to it ability to mask illegal substances in urine. The rapid expulsion of water from the body helps to achieve this. Additionally, with Thiazide diuretics blood levels decrease. The hair follicle is fed by blood, sweat, and sebum. Will the body's inability to retain or reabsorb water and decreased blood level prevent substances from being deposited into the hair cortex?

Central to your question is this concept: "blood levels decrease". Can you explain (and substantiate) this? Also, is this a medication you have been advised to consider for another reason? Hair falls out most often for genetic reasons.

I agree with @anongoodnurse that the question seems to center around hair follicles and the question may need some focusing as it is just the title and last line that address the question proper.

You both could have just answered... "This question is way beyond my abilities."


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Why people fear GMOs? Can't we map a plant composition?
My main question is can we map what a fruit is made of? For instance apples are made of 0.0002% of protein X, 0.00001 of protein Y, 0.001% of amino acid Z... etc...
If we can, then my next question would be why do people fear eating GMOs?
I understand the argument that if you introduce a new compound to your body you don't know its effect on you, but if for instance you insert a new gene into the plant where it is resistant to drought- can we not simply analyze its product and if its composition haven't changed than everything is alright?
Thank you very much!

I think this is mostly a matter of not understanding how the technology works. And also thanks to the fear mongering of some activist groups.

I guess only time can prove if those fears are true. There is too much which we don't still understand to say with certainity that inserting a segment of gene will not have any deteorating effect

Note that 'fear' of GMOs often have two different angles - human health effects and environmental/biodiversity concerns - which are conflated in this question.

thank you guys, my question was however about the health aspects of eating plants where the edible part haven't been changed and is 100% identical to the original source.

Why do some people fear vaccines, nuclear power, radiation from cell phones, or any of a thousand other scare-mongered things?  Usually it's the result of some very cynical people preying on mass ignorance for their own political and/or financial advantage.

People are not always rational when it comes to what they eat, especially when the compounds that make up the food have long, arcane-sounding names.
It is indeed possible to analyse the amino acid composition of a food substance. However, this has no bearing whatsoever on the safety of the food product.
For example, the following are two truncated protein sequences. One of them is a fragment constituent of cobra venom, the other is a fragment of harmless DNA polymerase. Without looking up or otherwise referring to the PDB IDs, it is not obvious which is which, even to an experienced molecular biologist.

3HRZ:A|PDBID|CHAIN|SEQUENCE
  ALYTLITPAVLRTDTEEQILVEAHGDSTPKQLDIFVHDFPRKQKTLFQTRVDMNPAGGMLVTPTIEIPAKEVSTDSRQNQ
1KLN:A|PDBID|CHAIN|SEQUENCE
  VISYDNYVTILDEETLKAWIAKLEKAPVFAFATETDSLDNISANLVGLSFAIEPGVAAYIPVAHDYLDAPDQISRERALE

Furthermore, even if scientists can prove beyond reasonable doubt that the two products are chemically identical, people will still irrationally purchase them. A clear example is the different prices commanded by "natural" versus "artificial" flavourings, as seen in this Scientific American article.

Consumers pay a lot for natural flavorings. But these are in fact no better in quality, nor are they safer, than their cost-effective artificial counterparts.

Thank you very much for the reply.
First of all I must note that I'm a complete layman (who skimmed over Wikipedia about SCOP and protein structures) so I'm probably missing something obvious and my question is stupid...
Those two PDB IDs that you presented seems different, so it is more of a case that is hard to diagnose their function rather than say that they are a 1 to 1 copy. Have I understood you correctly?
As for the article, well, some might say that it is not that health concious consumers are wrong about how bad artificial flavours are, it is that

it is that they are wrong about the meaning of 'natural flavours' (which raise the association of fruit juices/extracts).
Also, I obviously know very little, but are those flavours the same? Even according to this article ----"So is there truly a difference between natural and artificial flavorings? Yes. Artificial flavorings are simpler in composition and potentially safer because only safety-tested components are utilized." "There is little substantive difference in the chemical compositions of natural and artificial flavorings."---- maybe it's my

maybe it's my english but it seems like he's saying that a minute difference is still there (even if the author see this as an indictment toward the natural substances).
The thing is, you are right about peoples irrationality, but in this case the argument that such GMO food (lets say the transgeneic variety) introduces a new set of variables to the human organism which we can't trust unless rigorously tested for many many years (a generation or two if we want to see long term effects)- seems quite rational.
If someone were to

If someone were to sequence every single molecule in that new apple/tomato and show that the new product is a 100% clone of its counterpart then maybe it won't affect everyone, but at least the pro GMO will be on an unshakable ground... (Actually I just googled natural 'colorants' and it seems that some green sites are against them due to the same scientific reason like in your article- so, the trickling of knowledge is present).
If it's possible is there a reason why it is not being done? (or is it simply a calculation of cost/expected results in public opinion?)

Dang it, what happened to my paragraph division?  sorry if my response is too long.

I agree with March Ho in general: people are not rational about food.
That said there are two fairly different kinds of GMO, with different implications on the fears to have about them.
1) GMO embedding genes from the same species
These are not supposed to be any different from plants obtained using classical breeding techniques. The process in brief is for example: you see a wheat individual with short stems, an other with big grains. You want both. In classical selection you have to breed the two, select the descendants, breed again, select etc... until all descendants have both characters. Using GMO you can simply pick the gene you want and put it in the strain of your liking. It is much, much faster and the changes in the genome are much less than what you get by breeding two strains.
2) GMO embedding genes from other species
This can be more problematic as the gene you brought in could be from an organism nobody did ever eat, such as the Bt toxin in MON 810, hence the questions about toxicity. It doesn't mean it's toxic and the controls are very stringent about that but I can understand better why such GMO should be carefully checked.
3) The false problem of GMOs and environment
A Last problem is the indirect effect of the GMO, for example, if it's designed to be herbicide tolerant it might allow more herbicide to be poured on the plants and hence cause more herbicide residuals to be in the food, or in the environment, people then not liking GMO for environmental related reasons. But that should be addressed by checks on herbicides in food or in the environment, not by banning GMOs!
That said, GMOs have been around now for 20 years and people against GMO have a very hard time showing any kind of negative effects (see links posted previously), and some studies "proving" the toxicity have been shown to be statistically weak, not to say fraudulent.
Conclusion
There is no good reason to reject type 1) GMOs based on food safety and very little reasons to reject type 2) GMOs. I would personally push hard for a general adoption of GMOs bearing genes from the same species or other edible plants. It would already make a lot of things easier!

Thank you for the expounding,
I must ask though about type 1, do we know about the concert and interplay of all the genes? Can we predict all the cascading effects in all the plants that we change?
Do we know that all those genetic alterations that occur when you use classical breeding are not actually necessary in order for the edible end product to convey some yet unknwn characteristics (certain protein and etc)?
thx.

Answers to questions in your comment in order: No; No, but this is the case for normally bred organisms too; the organism modified already conveys those characteristics and there's no a priori reason to expect any change in that.

Yes, but if we don't actually know everything about the chain reactions that happen when we artificially introduce a new gene, then how can we tell that no characteristic indeed will be affected?
Like the famous Rumsfeld quote about unknown unknowns, the only way we can be sure that our product is "as nature intended" is if the artificial result will be 100% identical to the classically bred (which we can't compare unless we actually make both).
no?

Do you consider a plant that has a genome recomposed from two different species+ duplicated to be "as nature intended". That's the wheat you eat everyday. Obtained by very artificial selection several thousand years ago. Was there a risk to taste that incredible mix. Probably but I'm fairly happy they tried. All new varieties are extensively tested but I see no reason why type 1 GMO should be prohibited and not just extensively tested.

Perhaps I should have not used the term "as nature intended" since it might bring some association with other ideas...
However, when you say "two species" you are not exactly being accurate and you give a wrong impression as well. If they can cross polinate then they belong to the same family which in genomic terms is (or might be) quite important.
Furthermore, like you said, they started doing it thousand of years ago. The first aspect to this is that there are plenty examples where human behaviour changed our physical evolution (in relatively short time), if we'll all start

start eating somewhat poisonous transgenic GMO right now then our future descendants would indeed have no adverse effects from it.
The second aspect is that even if those experiments were somewhat detrimental to their health, the process was slow (so effects could be noticed among generations), regionally dispersed (so the bad results would be contained and only harm one village) and the changes were gradual (easier to see what went wrong)- they experimented on themselves but those conditions were a far cry from todays globalized, fast paced, risk aware, scien

, scientific western world.
We have volved alongside  this system.
And finally, if you also agree that some risk is involved then why do  you seperate between type 1 and type 2 when introducing to the market?
Don't get me wrong, by no means I object to the idea of GMO, even cross-species (hence my original question about GMOs where the fruit itself is 100% identical to non GMO), like you, all I want is a (very,very,very,2 human generations long) rigorous testings.

"However, when you say "two species" you are not exactly being accurate". On the contrary, I'm very accurate, but plants have porous boundaries between what are considered species, specially if you help them a bit. Triticum aestivum (common wheat) is an hexaploid of Aegilops tauschii and Triticum turgidum himself an hybrid of Triticum urartu and Aegilops speltoides


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How to select genes before log2 ratio on a RNASeq gene expression matrix, based on signal median
I want to transform a TCGA mRNA expression matrix (in linear data format) to log2-ratios and then run a feature (gene) selection, selecting the 1000 most variant genes (genes with higher standard deviation across samples). The workflow is the following:

Select "good" genes before log2 ratio (genes each with median signal at least t in p% of samples);
On selected genes, run log2 ratio, dividing each gene by its median signal and then log2-transforming the result matrix;
Select the 1000 most variant genes along all samples.

How do I select t and p?

Cross posted on biostars: https://www.biostars.org/p/132301/

@DevonRyan biostars is not part of the SE network. It is only cross-posting when posted on different Stack Exchange sites. We can hardly expect people not to poest anywhere else on the internet if they want to post here! We just want to avoid duplicating information across the SE network.

There is no rule for fixing t and p. It depends on the level of stringency you expect. Value of t depends on what is considered to be an active concentration; this need not be same for all genes.
This is an RNAseq data; I don't understand what is the "median" signal you are talking about. For each sample a gene would have a normalized expression value which is typically RPKM (Reads Per Kilobase per Million mapped reads). If you have replicates for each sample then take the mean not the median.
Regarding calculation of log-ratios: Always be careful with this especially in case of zeros. Instead of log ratios you may use some sort of a gain metric:
if
ratio = x/y
then
gain = (x-y)/y
You can also do a principal component analysis on the data and select first n principal components.

Ok for the "median", it was a mistake. I did not understand: "Always be careful with this especially in case of zeros" - what did you mean? Thanks

In case of expression is zero in one sample then log transformation will give you NaN (undefined)


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Can cell exist without Ribosomes?
Last night I came across a question that goes as follows:-
Cells cannot exist without
a) cell wall
b) cell membrane
c) mitochondria
d) ribosomes
I am getting confused with option B and option D

If RBC is lacking ribosomes then where the antigen proteins on RBC are coming from ?

The most essential thing for a cell to survive is a membrane. Without a membrane there is no boundary between cell and its surroundings. A selectively permeable membrane is needed for cells (from single celled organisms to elephants and giraffes and whales) to survive. Cells will die quickly on removal of cell membrane.
The RBCs are good example of cells without mitochondria or ribosomes which survive for 120 days.

Please read the article on Erythropoiesis for detailed information on how RBCs form and how they have proteins in their surface.
In short, the RBCs acquire the surface proteins during their formation period in the bone marrow. Inside the bone marrow the premature RBCs have nucleus, ribosomes, mitochondria, etc... and produce all the required structural and functional proteins. On maturing they loose the nucleus and cell organelles and contain only hemoglobin in their cytoplasm.

If RBC is lacking ribosomes then where the antigen proteins on RBC are coming from ?

I have edited my answer @DhrubaBanerjee Please see if it answers your doubt. Please read the article on Erythropoiesis

There is no cell without a membrane :P (A cell by definition has to have a membrane). Self sustaining cells do need ribosomes but they can survive without mitochondria (prokaryotes anyways don't have one and there are eukaryotes without mitochondria such as Entamoeba)

Good one @WYSIWYG. Really good, lol

There exist some accounts of temporary stages that lack a cell membrane. If these represents a form of cell question of definitions. SSee e.g. http://www.biomedcentral.com/1471-2180/11/255

@fileunderwater very interesting. Thanks for the link.

@fileunderwater The statement in that article seems doubtful. First they say "protoplasts" and then they say "without a membrane". Protoplasts are plant cells without walls but they still have membranes. Without a membrane (long enough to be called a stage) the cell would have no boundaries and therefore the definition of a cell no longer holds (more like a cell lysate)

@WYSIWYG I cannot really evaluate this research, and was just curious about what papers are out there. There are a couple of other articles as well, e.g. http://www.ncbi.nlm.nih.gov/pubmed/12111719 and http://jcs.biologists.org/content/114/11/2009.short. As I said, whether these are cells is a question about how you define a cell. It seems like they survive for ~10h before a new membrane is formed (a "gelatinous envelope" is formed before that though). Quote: "Nucleocytoplasmic aggregates,  ... released after injury ... are membraneless structures that can survive in seawater for 10–20 min."

@fileunderwater Interesting. This means that the enzymes can function in seawater and also there should be some way of preventing diffusion of cellular material(the gelatinous envelope perhaps)

@WYSIWYG Yes, also interesting with regard to the origins of life, since it shows another way that replicating structures can be compartmentalised (at least temporarily).

Cells can survive without ribosomes, but they would accumulate damage and be unable to restore worn out or exhausted supplies of any proteins they may require. The ribosome is necessary to be able to perform protein translation from RNA. Thus, if the cell can survive without protein, then it would be able to survive without ribosomes. No known organism that exists today meets that definition, if I am not mistaken. However, at some point, it is theorized that the earliest cells were able to perform replication and metabolism without the use of protein. So, it is likely, but not something that is seen in life today.
Nicholas H. Barton Derek E.G. Briggs Jonathan A. Eisen , David B. Goldstein and Nipam H. Patel.(2010). Evolution. Cold Stone Harbor Laboratory Press.

Nicholas H. Barton Derek E.G. Briggs Jonathan A. Eisen , David B. Goldstein and Nipam H. Patel.(2010). Evolution. Cold Stone Harbor Laboratory Press.


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Why is carbonylation added as a fixed modification in mass spectrometry peptide analysis?
When using mass spectrometry analysis software we use carbonylation as a fixed modification. What is the significance of this modification and why doesn't it change?

which MS method are you using ?

We are using  dda on a high  res lc- ms


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How can bats achieve good resolution with wide beams?
I have been reading about the echolocation system in bats. papers state that bats tend to produce a sonar beam that has a beam angle (-3db) of about 30-40 degrees. This would be considered a wide beam given the fact the sonar sensors used by robots have beams 15-20 degrees or down to 10 degrees with multi-sonar.
As the beam width increases, the azimuth resolution decreases. Yet, bats have good navigational capabilities and good object discrimination in azimuth. How is that achieved? what is the technique used?
I searched hard but what I found is that they rely on the timing between two ears. however, given the complexity of the environment and the multiple echos that return, how is it possible to correlate which echo in the left ear belongs to which in the right ear?

I have been contemplating about this question for months and although I cannot provide you with a concise short answer, I do wish to share what I have so far.
First off, the acoustic beam that is sent is not really part of the echolocation resolution (the bat's echo-locating acuity). Consider the human field of view, which is nearly 180o wide in the horizontal plane. Covering your eyes and obscuring, say, half of the field will not substantially improve visual acuity, because it simply blocks half of the retinal surface from receiving light - it does not double the retinal surface devoted to the field of view.
Hence, I think it is not so much the bat's projected beam that matters, it is the incoming echo that matters. Note that objects such as a tree may scatter the sound that is reflected back, so the projected beam of 40o may be a dramatic underestimation of the chaotic signals bouncing back to the bat. What can they do to improve spatial detail in the received acoustic field of view?
Bats may increase the pulse repetition rate when they are approaching a target. Hence, they basically build a map by sampling the environment multiple times. Sampling frequencies may exceed 50 Hz (Grinnell and Griffin, 1985). For example, imagine you are blindfolded and allowed to scan an object with your fingers. Scanning it multiple times will definitely help you to mentally reconstruct the image. Indeed, bats can assemble information about echo delay changes over time, enabling them to temporally integrate information of the auditory scene. Moreover, they can change the spectral content of their calls that may help in echolocation (Moss & Surlykke, 2001).
Furthermore, to conclude with a personal thought - I think that bats must learn to decode complex echo profiles. For example, a chaotic huge blob of echo with low-echo efficiency (lots of sound is absorbed) that only changes when the bat moves is probably a tree. A big blob with a large echo-efficiency (a lot of sound comes back) with well-defined edges that only changes when the bat moves is likely a human structure or a rock. A pinpoint-echo that moves with respect to the bat is likely something tasty.
References
- Grinnell & Griffin, Biol Bull (1958): 10-22
- Moss & Surlykke, JASA; 110(4): 2207-26

I think you are forgetting bats can see as well. Bat's that use echo location are referred to as Microchiroptera. Since we are speaking about echolocation, we can disregard the megachiropteral class since there most prominent sense is their eyes. This doesn't mean though that Micro's don't use their eyes in conjunction with echolocation. In Handbuch Der Zoologie: Eine Naturgeschichte Der Stämme Des Tierreiches, Volume 2; Volume 5, the authors state

In experimental situations, when visual information and echolocation were competing, the bats relied on vision and ignored the acoustical cues [1].

From this we can surmise that even with echolocating bats, they still fall back on vision in ambiguous situations. Moreover, researchers have determined that bats have ultraviolet cone receptors [2].
To answer your question, Micro bats have good object discrimination because they use both their eyes and echolocation to discern objects in their environment instead of solely relying on echolocation.

yes sure  they use vision for mapping in environment but many papers mention they can locate targets using sound only for example:
link.springer.com/article/10.1007/BF00292562    bat located prey  passively using its noise
And here it says they are able to get the target location in 3D using difference in sound intensity but how do they correlate sounds at the two ears if many objects existed in the environment?
sciencedirect.com/science/article/pii/S096098220500686X


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What are the white spots?

What are these white spots? It's like Braille writing or something.
How is the appearance encoded in the plant? (which I think is a Pine, though I am not sure).

If I manually made the "spot sequences" into binary strings, would it be possible to search them against some database? GenBank?

Questions should be asked in the question, not as a comment.

What do you want to know about the white spots? The name? Function? If possible please list the questions in a concise manner


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How did multicellular life evolve?
I can imagine several specialized unicellular beings collaborating. But how does life get from that point to a unique pluricelular being that reproduces into another pluricelular being?

The key is specialization: e.g. some cells specializing in getting food, others in producing something sticky to keep them together. Which cell does what is usually determined by chemical signals: depending on their specialization they produce particular chemical compounds. So if a non-specialized cell notes that one compound is rather low because the specialized type of cell producing it is in low supply then it specializes that way.
While initially all cells are capable of reproduction, at some point there also will be cells specialized for reproduction, whereas the others lose the ability to reproduce to better concentrate on their specialized duty. Hence the other cells do not have an independent existence anymore but exist only as part of the larger organism. When such an organism is then to be considered a separate pluricellular entity is a matter of definition: if it is an entity independent of the original (e.g. capable of moving away)? if sexual reproduction happens?
Wikipedia also has some things to say.

Welcome to Biology SE and thanks for your interesting answer. At Biology SE some references are appreciated to substantiate answers to allow people to validate the answer or for further reading. Thanks.

Ps: although wikipedia is a much referenced source, it is unfortunately one of the most unreliable sources as its contents change continuously. +1 for your answer.


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Why are plasmid genes not already incorporated into bacterial chromosomes if necessary for stressful situations?
If plasmids are important for bacteria to express specific genes under stressful conditions, why are these genes not already incorporated into their chromosome to begin with? What is the evolutionary significance for this?

Plasmids do have the advantage that they replicate independently of the cells chromosome and that they can be transferred between different bacteria. This spreads the gene encoded by the plasmid to other bacteria, which then can also survive.
Think about antibiotic resistance. Bacteria which have a plasmid which allows protection against the antibiotic will survive. They can transfer this protection to other bacteria which then also become resistant. This can either happen through pili which develop between bacteria or also via the uptake of plasmid DNA from the environment in a process called horizontal gene transfer.
Additionally mutations on the plasmids are not as dangerous on the plasmids than on the chromosomal DNA, where essential genes might be damaged. Plasmids can also get lost, if they are not needed by the bacteria due to a missing selection pressure, which is also much harder for genes encoded on the chromosome.

Thank you. Would you mind clarifying on how exactly they get "lost"? Do the plasmids still remain inside the bacteria or do they get transferred when unneeded?

I am not sure, if the exact mechanism is known, but I can look into it.

How many copies of a plasmid get made can vary, and then how those plasmids segregate into each daughter after mitosis can vary. It is possible for one of the daughters to wind up with no copies of a plasmid. If that is the cell you or evolution picks to replicate, the plasmid is lost in all descendants.


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What makes substances allergenic?
Is it possible to tell or rule out (potentially a priori) whether any given substance or compound is likely and how likely to cause allergies with high confidence, without the need to conduct experiments, e.g. by looking at its properties, e.g. solubility, molecular structure or reactivity?
From what I've heard is that generally speaking, things that we come in contact with in early years tend to be less likely to cause problems later on, but still, there seem to be differences even with food and substances that do not quite appear to be exotic, e.g. peanuts.
This question is related to these, though I'd consider it more generic.

Meat and mushroom allergies, why are they so rare?
What is the smallest molecule that can present as an antigen to the immune system in the context of allergies?

So, the first time you're exposed to an allergen, atopic individuals generally produce a large amount of IgE antibodies, and in the case of an allergen, to that allergen. These IgE antibodies attach to mast cells. If the allergen is contacted again, they interact with the IgE on the mast cells, and trigger the allergic reaction when the mast cells begin releasing a whole host of compounds into the region: histamines, leukotrienes, cytokines, etc. There's a host of ongoing studies into genetics, heredity, and TGFß as to susceptibility. I'm unsure there's currently a way to predict it though.

You might be right, @Kendall. This could well be a trillion-dollar question. A definitive answer may establish a unified theory of allergies and produce perfect treatments and predict genetic disposition. If I had an answer, it might thus not be worth posting here but rather to file patents for anything related.


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How does ANF increase GFR?
ANF as we know reduce the Na+ uptake and K+ removal in the distal tubules and it also functions as a Vasodialator (?) But again it says that ANF increases the Glomerular filtrate ? But if it is acting has a Vasoldialator (ie, antagonistic to Vasopressin) how is it increasing the GFR ? Shouldnt it lower the GFR ?

ANF - Atrial Natriuretic Factor also called Atrial Natriuretic Peptide
GFR - Glomerular Filtration Rate

ANF (Atrial Natriuretic Factor more commonly known as ANP - atrial natriuretic peptide) squeezes (vasoconstricts) the efferent arteriole. This means the pressure in the glomerulus is higher (like if you squeeze the end of a hose) and so more fluid is squeezed out i.e. the glomerular filtration rate (GFR) is higher. It also dilates the afferent which means more fluid is going in, further increasing GFR (Marin-Grez et al.)

Why is this answer down voted?

Someone has been downvoting all my answers for whatever reason. Assume they're trying to get me under 4000.

I found two downvotes and I upvoted once to get the -1 status. Good answer though. I think it will be reversed soon! Good luck

It seems the community is very reluctant to upvote good answers. Most of my rep comes from answers to silly questions vs well researched answer to good questions

I downvoted because of the lack of references, the unclear picture, the use of acronyms and the ample use of technical terms. Should have let you know earlier. I also downvoted the question for similar reasons, but after@CRags made the edits I removed the downvote and close-vote as well. I am not downvoting person-based btw - everyone is free to like or dislike particular questions and answers isn't it?

And don't assume the worst when folks downvote. Downvoting helps to  improve questions and answers. My downvotes have nothing to do with personal missions to bring someones rep <4k, nor has it anything to do with a reluctance to upvote! Personal vendettas can be reported to moderators btw.

@ChrisStronks: Thank you for your feedback. Comments and feedback help improve answers whereas simply down voting leave the author of an answer confused. In the future make sure to leave comments when you down vote to avoid not being helpful. I have improved the answer by explaining acronyms and adding a reference. There isn't a better picture than this which has ANP on it.

@AndroidPenguin - you are totally right. Normally I leave a comment. My bad. +1 :-)

So the summary is that ANP vasodilates the afferent arterioles and constricts the efferect arteriole ?