Relation between a compound's toxicity and it's concentration level I know that ammonia is toxic for the body since it disturbs enzymes of mitochondria.
I want to know that why the ammonotelic animals don't get affected by it?
I mean that even if there is plenty of water to remove ammonia from their body, does ammonia not cause any damage till it's inside body?
Does toxicity depends on concentration level?
Can anyone tell me its evolutionary significance?

Sorry for the previous question. .
Actually it was a easy one and I got the answer.
Sorry for the unclarity.;)

The article at linked at the bottom says that the marine organisms keep the concentration of Ammonia under very strict control.

pH of the ECF (Extra Cellular Fluid) is said to play a very important role.
The concentration of ammonia in the environment (ambient ammonia levels) also plays an important role.
Less importantly temperature also plays a role.
Ionic strength of water also is involved.

The NH3:NH4+ ratio seems to be more important than the abosolute value of ammonia.

Ammonia is more toxic than ammonium ion. The lipophilic (ammonia is amphiphilic - soluble in both water and lipid) nature of ammonia allows it to easily cross the cell membrane and the blood brain barrier (in organisms where BBB exist) and affect the physiologic functions. The ammonium ion on the other hand can't enter the cell as easily, as it is not as soluble in lipid as ammonia.

For ammonia and marine organisms see http://www.sciencedirect.com/science/article/pii/S1546509801200053
For more on ammonium toxicity see: http://www.ucl.ac.uk/~ucbcdab/urea/amtox.htm


What are the metabolic concerns associated with hard water? If humans can maintain a consistent blood pH, then what problems does alkalized water cause us?

Why is it recommended that we filter and boil hard water? Is the issue that hard water can affect the pH of our blood?

Right now, there is no evidence shows hard water can cause any healthy problem.
Previously people were concerned about the high mineral content, such as calcium and magnesium, may cause disease such like cardiovascular disease.
But from the report World Health Organization published in 2003 Hardness in Drinking-water, it says "Although a number of epidemiological studies have shown a statistically significant inverse relationship between the hardness of drinking-water and cardiovascular disease, the available data are inadequate to permit the conclusion that the association is causal. No health-based guideline value for water hardness is proposed."
And the United States National Research Council thinks hard water can supply the calcium and magnesium ions that dietary need. Hard Water Hardness Calcium Magnesium Water Corrosion Mineral Scale
And at the same time, I have to say the filters cannot directly work for hard water because ions cannot be isolate by filter. We can filter the precipitation after boil the water. Boiled water is better because tap water may contain microbes in some country, that will be harm for our health. And also you don't want to feel some "precipitation" while you drinking water. That's it.
For my personal view, I prefer soft water because it tastes a little bit sweet.


Human genome, chromosomes I have a very basic question, but it seems the hardest to me.
So we have 46 chromosomes (23, 2 copies of each). Do all chromosomes have the same DNA? If so, does it mean that in different cells with different functions some genes are expressed and some aren't? Also, if each chromosome has different lets say "fragment" of the genome, how is the genome interconnected?

Do all chromosomes have the same DNA?

No.  Not any more than each chapter of a book has the same words in the same order.

  If so, does it mean that in different cells with different functions
  some genes are expressed and some aren't?

Yes.  In general, all cells in your body have all the same DNA; what makes your retina cells function differently from your pancreatic beta cells is which genes they express.  Like if every chef in a restaurant had the same recipe book which had every recipe the restaurant can make, but the pastry chef only makes pastries.

  Also, if each chromosome has different lets say "fragment" of the
  genome, how is the genome interconnected?

The genome is not physically connected except for all the genes on a chromosome being physically connected.  But a gene product from one  chromosome might control expression of another gene by physically binding to the DNA close to it, which can affect its expression.  But most gene-gene interactions are really protein-protein interactions.  (Or in some cases, RNA interacting with RNA)


Simulating Migration in SimBit Software Program How is migration incorporated into the SimBit program of Remi Matthey-Doret and Michael Whitlock?

Is an island model or stepping stone model assumed?

In SimBit, no specific model is assumed as the user can very much chose for himself/herself what migration scenario to be simulated. The migration scenario can be set with the option --m (or equivalently with --DispMat).

There are four ways (what is called "Mode" in the manual) to indicate migration.
 A, LSS, OnePatch, Island and LinearNormal.

A

This mode stands for "All". This mode allows the user to enter a matrix with the migration rate between any two patches. Any migration scenario including the ones achieved with the below modes can be achieved with A. The interest of the other modes is to simplify the user's life esp. when dealing with many patches. I rather recommend using the other modes when these apply.

LSS

This mode stands for "Linear Stepping Stones". It allows the user to set linear stepping stones with any number of stones and potential asymmetry.

OnePatch

This is the default. It means no migration scenario apply as there is only one patch (or one deme if you prefer)

Island

This is a classical island model. The user must input the probability of not migrating.

LinearNormal

This is just like a linear stepping stone model except that the dispersal kernel follows a normal distribution.

Note also that the migration scenario (as well as the number of patches) is a time specific argument and therefore it can vary through time at will. You can have a look at the manual for more information.

Note that I have been working quite a lot on new versions that I have not put online yet, mainly because I was too lazy to rewrite the manual! The last version online is 3.69 but I am currently working on version 3.139! I will upload a more recent version in the coming week(s). Most notable improvement with the new version include:

Easier user interface; no need for all these quotation marks. Migration scenario will be given by the user as forward migration while it currently is backward migration which is a little less intuitive for the user.
More freedom on demography.
Possibility to simulate several species interaction with ecological relationships. One can simulate a whole ecosystem!


What kind of Brazilian Arthropoda is this? It looks like a Diplopoda, but I've never seen anything like that. A friend took those pictures in the Brazilian Cerrado (Goiás state, Brazil) these days (October, start of rainfall in Spring). It was inside a country house, she already found it dead.

She said it has about 3 cm (~1.2") long. We can see it's not so small as a Symphyla or Pauropoda. Looks like it has 12 pairs of legs.

I was fooled by the red marks in its back, that made me believe they were each pair of marks in a segment. Looks like they're distributed in one pair of red marks for each 2 segments. Maybe that's a mimic of some similar Diplopoda (which usually have such colored marks, see for instance Rudiloria)?

Looks like it's some species of Scutigera or some related group.


Countercurrent multiplier mechanism How exactly does the countercurrent multiplier mechanism work in formation of urine in the body? I am unable to find a satisfactory answer to this.

The countercurrent system permits forming a concentrated urine

In the presence of ADH, which increases water permeability, the hyposmotic fluid that enters the distal tubule (DT) from the thick ascending limb (TAL) looses most of its water by osmotic equilibration with the surrounding cortical interstitium along the CNT and cortical collecting duct (CCD). It also continues loosing NaCl through reabsorptive transport along DT, CNT and CCD, until the tubule fluid becomes isoosmotic with plasma, by the end of the CCD.

The relatively small amount of isoosmotic fluid that flows into the medullary collecting ducts losses progressively more and more water to the hyperosmotic medullary and papillary interstitia and is finally excreted as hyperosmotic, highly concentrated urine.

The countercurrent system permits forming a dilute urine

In the absence of ADH, the hyposmotic fluid that enters the DT from the loop of Henle, continues to be diluted by transport of NaCl via NaCl (thiazide sensitive) cotransporters into DT cells and via Na channels (amiloride sensitive) along the CD. Water reabsorption is limited so that the tubule fluid becomes more and more dilute along DT, CNT and collecting ducts (CCD, OMCD and IMCD), until it is excreted as a large volume of hyposmotic urine.

Sources:

Barac-Nieto, Prof. Mario. "Countercurrent System and the Loop of Henle." Countercurrent System and the Loop of Henle. Kuwait University. Web. 08 Feb. 2016.
Wikipedia. Wikimedia Foundation. Web. 08 Feb. 2016. https://en.wikipedia.org/wiki/Countercurrent_multiplication.
"7. Urinary Concentration (countercurrent Mechanism)." 7. Urinary Concentration (countercurrent Mechanism). Web. 08 Feb. 2016.


Can we change the direction of a neurological signal? My question is can we change the direction of a neurological signal? When a neurological signal is generated it goes to the brain. Along the way it passes synapses. Can we make it change it's pathway to go through another neurone instead of the neurone it was going to ?

"Neurological signal", or as I would put it, action potential, or activity propagation can be modeled as current in an electrical circuit. Trick is that such a circuit contains a bunch of highly regulated and non-linear and non-static elements. Imaging bunch of potentiometers (variable resistances) in your circuit. And all of them behave depending on something else in the system. So certainly currents will go somewhere, but level of control and complexity is phenomenal.

An example that should let you appreciate possibility of rerouting is simple Pavlovian conditioning. Neutral stimulus (bell) that has no evident connection to stomach, after conditioning elicits response there. Even though circuitry is very complicated and signal propagation is hard to investigate, this is an evidence that changing path of signals is very possible in some way. (Of course, conditioning require changes in higher-than-stomach systems, some intermediate levels).

On more practical note, we can readout neuronal activity in region A (of brain, muscle or else) and rely it via electrical stimulation somewhere in brain or muscle or gland. Both parts of this are available technology. As of drugs, some people report "seeing" sounds while intoxicated, this might be an example of such temporary effects.


Causes of monozygotic twins Twins could be monzygotic i.e. identical twins and dizygotic i.e. non-identical twins.Well, monozygotic twins occur when a single egg is fertilized to form a zygote which later divide into separate embryos.

Now, My question is Why does the embryo collapse splitting the progenitor cell into half?
While searching for the answer I found certain theories (possibly without evidence). Following are those theories;

An enzyme in the sperm causes them to split.

I have known only a few hyaluronidase and hydrolysing enzymes present in the sperm acrosome which helps penetrating the ovum by lysis of Zona pellucida.

A mutation in the mother's RNA which may control embryogenesis in the first nine days.
The splitting of embryo is more of a random process then genetically governed one.
Genetic mutation which leads to rejection of one group of cells by the other.

A few possible explanations are named in the Wikipedia article you link:

  Regarding spontaneous or natural monozygotic twinning, a recent theory
  posits that monozygotic twins are formed after a blastocyst
  essentially collapses, splitting the progenitor cells (those that
  contain the body's fundamental genetic material) in half, leaving the
  same genetic material divided in two on opposite sides of the embryo.
  Eventually, two separate fetuses develop. Spontaneous division of
  the zygote into two embryos is not considered to be a hereditary
  trait, but rather a spontaneous or random event.

  Monozygotic twins may also be created artificially by embryo
  splitting. It can be used as an expansion of IVF to increase the
  number of available embryos for embryo transfer.

Interesting references for this are:

"The epidemiology of multiple births"
Twinning.
On the possible cause of monozygotic twinning: lessons from the
9-banded armadillo and from assisted reproduction.
Monozygotic twinning associated with assisted reproductive
technologies: a review.
Developmental biology: Two by two (on overview article conatining a
lot of other references)


What does it mean to have a Y-DNA Haplogroup "R-M512"? I did a DNA test to learn about my origins, but the results are highly technical.

I see I have a Y-DNA Haplogroup R-M512 and a mutation (zero marker in DYS448). I Googled these terms and came across a bunch of technical papers, but I don't have the expertise in Genetics to make much sense of them.

I wonder if one of you can shed light on this?

Normally Humans inherit from each parent one sex determine Chromosome. If you have a XX chromosome pair you are female. If you have a XY pair you are male. Therefore the Y-Chromosome get only passed on from father to son. The Chromosomes itself consist of DNA. The DNA consists of base pairs in which an A only pairs with a T and a C only pairs with a G. The Y-Chromosome has about 57 million of these base pairs. DNA is normally relative stable but from time to time only one of these base pairs randomly changes from a C-G base pair to an A-T base pair. This phenomenon is called a pointmutation. So imagen two brothers. One has the unchanged Y-Chromosome of their father the other has one this pointmutations. So the descendants of the one Brother have the same Y-Chromosome, with exception of the pointmutation, the same Y-Chromosome. This is called a Single Nucleotide Polymorphisms (SNP). In the millennia the Y-Chromosomes acquire more and more of these SNPs. One combination of these SNPs is called a Haplogroup. By the amount of SNPs and the kind of them you can reconstruct which Haplogroup descended from which one. You have the Haplogroup R-M512 which is a rather old one (https://upload.wikimedia.org/wikipedia/commons/d/d4/R1a._Info-19.05.2014.jpg) and could be found in great area. M512 is actually the name of the last SNP that defines your Haplogroup. Here some people had write down which Haplogroup they belong to. By the ethnicity of the name you can assume how far it is spread ( https://www.familytreedna.com/public/R1a?iframe=ysnp ).
Another Name would be R1a1a. Maybe these papers help you more to understand the nomenclature ( http://www.ncbi.nlm.nih.gov/pmc/articles/PMC155271/  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1288547/ ).
Short tandem repeats (STR) are small DNA sequences that repeat multiple times.  On the Y-Chromosome these STR can be referred to as DNA Y-chromosome Segments (DYS).  DYS448 has the sequence AGAGAT  with 20 to 26 repeats. Here ( http://cstl.nist.gov/strbase/ystrpos1.htm ) is visualized where actually  it is located on the Y-Chromosome.  In your case the laboratory was not able  to measure any repeats.


Is there a difference in the energy produced from the hydrolysis of GTP and ATP? Is the energy produced from the hydrolysis of GTP greater than/less than or the same. I know that GTP can be converted to ATP through a pathway and so my thinking was that GTP would be less.

As @WYSIWYG said in comments, there is no effect of change in nitrogenous base on the third phosphate. Why? Simple, they are too far to directly influence each other's stability. See the diagram (of ATP) below from wikipedia:

and of GTP from here:

What one can clearly interpret from these diagrams is that there would be no effect on the energy released by hydrolysis of the third phosphate by the nitogenous base present. It will remain -30.5 kJ/mol(1) in both cases.


How Scientists sequence, assemble and annotate plant genomes? I previously read this question and this paper and learned good things about this topic. my current question is that scientists use which tools, algorithms, soft wares... to sequence, assemble and annotate plant genomes?
For each genome project do they develop new tools and algorithms or there are some tools that are useful for (almost) all genome projects?
Are there any comprehensive site, book or paper that have plant genome sequencing and annotation protocols?

Let's try and answer all three parts of your question.

Sequencing
The general method is the same. Sequencing is just sequencing. But as for every single sequencing, there are factors to consider and protocols to be selected.
One important thing is, that you might want comparably long reads to cope with the repeats and the general large size of plant genomes. To get long reads, you need long input DNA sequences. Therefor you would want to follow a suitable protocol for high molecular weight plant DNA. That might be hard, because plant DNA can be difficult to extract based on the plant and tissue you have, as most easily put you have to "crack open" the cell wall in the very beginning.
After that, it is general sequencing. Although, as I already said you might opt for long reads (PacBio) and/or good coverage. If that is not at all feasible, you might choose to do targeted sequencing and only capture the whole exome (or only the genes you are interested in) to reduce both cost and analysis complexity.

Assembly
Now you have probably accumulated a lot of sequence and also potentially long sequence. There are multiple tools you could use for assembly and generally you can use the same for plants that you might want to use for example for a human genome assembly. One example that works well on large plant genomes is MaSuRCA, another is Allpaths-LG. There are some assemblers designed to cope with long repeats, but quite often you just assemble and then try figuring out the repeat regions later, for example by improving a shotgun read assembly with long reads from another technique.

Annotation
This one definitely has specific tools for plant genomes. Well, large genomes. The main thing in annotation is finding potential genes and comparing them to databases to annotate them with function. Plants do splice and plants can have long introns, even ones including long repeats.
One gene prediction software example that works on plants is Augustus, but for some model organisms there are even organism-specific pipelines and tools for this task. And of course, on the database part you would choose to rely on a plant specific database (if you do not use NCBI-NR anyway). Those can also be species or genus specific like the ones you find on the TAIR (Arapidopsis) project.

TLDR:
It's in fact complicated. On one hand, there is a need of specific tools and databases, on the other you might go well with standard tools, but would have to adapt parameters, do additional pre- or post-processing steps and so on.


Is ATP Synthase a channel or an enzymatic protein? Today in a biology lecture about plasma membranes and functions of proteins, we learned about channel and enzymatic proteins along other kinds of proteins. ATP synthase is considered an enzyme that synthesizes ATP, but it also creates a channel for H+ ions to pass through into a lower concentration area.

My question is could ATP synthase be considered a channel protein as well as enzymatic protein? Or no since the ion channeling is part of the enzymatic reaction? Also are there more examples were some proteins could have more than one kind of protein to them?

ATP synthase is an enzyme, a molecular motor, and an ion channel all wrapped together in one structure (Fig. 1). It is an enzyme, because it generates ATP. It is a molecular motor, because the central rotor part turns about 150 times every second during ATP synthesis (Source: MRC mitochondrial Biology Unit). It is an ion channel, because it funnels protons into the mitochondrion during ATP generation (Source: Davidson College).

ATP synthase. Source: Ace Biochemistry

ATP synthase is composed of two subunits, F0 and F1. The 0 subunit is embedded in the inner membrane, and the other, containing the catalytic parts, protrudes into the matrix.

F0 contains the proton channel and is connected to F1 with a stalk.

F1 consists of five polypeptide chains, alpha (a), beta (b), gamma (g), delta (d), and epsilon (e). The alpha and beta chains make up the bulk of F1 and are arranged in a hexameric ring. Both chains bind nucleotides, but only beta participates in catalysis (Source: ACE Biochemistry).

Another example of complex proteins are G-protein coupled receptors, for example those linked to ion channels (Fig. 2).

G protein coupled receptors. Image source: Wikipedia

Here, a receptor is bound to a G-protein, that becomes activated after receptor binding. The G protein then leaves the receptor and travels to an ion channel and activates it (or inhibits it).


How much energy is used to construct a pound of fat tissue? A widely cited figure is a pound of fat contains 3500 calories of energy in fatty acids.

However, a pound of fat also contains adipose cells, arranged in adipose tissue, connective tissue etc.

When a human breaks down fat to use as energy, from what I understand it doesn't break down the fat cells, just liberates the triglycerides stored inside those cells.

Those fat cells, and connective tissue took energy to assemble as well.

How much energy is used to create a pound of fat tissue?

Let's assume that all the cells and the triglyceride stored inside them are created from scratch.

A rough answer to a rough question

According to a study conducted in the 1960s, human adipose tissue, on average, contained (per 100g wet weight) 87g fat, 2g protein, 2g sodium and potassium and 10g water. (Nothing else was measured.) This suggests that approx. 3% of adipose tissue is solids other than triglyceride.

The figure quoted is presumably the energy yield for the complete oxidation of triglyceride. The energy yield for the complete oxidation of the non-triglyceride solids in adipose tissue  — the appropriate, if hypothetical, comparison would be less than that for triglyceride, which is much more chemically reduced, so the yield for the oxidation of non-triglyceride might be approx. 1–2% that of triglyceride.

The energy needed to bio-synthesize any organic compound (triglyceride, carboyhdrate or protein) is more than is obtained from it by oxidation because a negative free energy change is needed to drive reactions. Hence, as regards the relatively constant (slowly turning-over) portion of the adipose tissue, the cost would be higher — perhaps 2–3% of that quoted produced by oxidizing the triglyceride.

The problem with this question

Some people say that there is no such thing as a stupid question. Nevertheless, there are questions that are formulated as if their answer will establish solve some problem, when in fact it will not because the premise on which it is based is false.

In this case a comparison is made between the triglyceride and non-triglyceride content of adipose tissue with the implication being that the latter should be assessed in the creation of the former:

  “Those fat cells, and connective tissue took energy to assemble as
  well. How much energy is used to create a pound of fat tissue?”

As already mentioned, it is invalid to make a numerical comparison between the energy required to synthesize one compound with that released by the oxidation of another compound, as it costs more to synthesize a compound than is released by its oxidation.

However, quantitatively more fundamentally wrong is the implication that the one-time synthesis of the structural components of the cell should be costed into the repeated oxidation of triglyceride in that cell. How many grams of triglyceride are synthesised per gram of cell structural material during the lifetime of a cell? Very many, I should imagine if the cells turn over much more slowly than the lipid they contain.

It would be more pertinent (assuming that you are interested in such things) to ask what the cost is in terms of the energy used by whatever muscles are used by the lungs to breath in the oxygen needed to oxidize the fat, and the energy used by the heart muscle to pump the blood containing the oxygen to the fat cells so that it can be oxidized.

Finally, it is naïve to think of the energy cost of maintaining a fat cell in terms of the synthesis of its structural components. Other metabolic processes are continually occurring that require energy even in fat cells.

No doubt it would be possible to perform a calculation that took all these things into account (although what would you start with “from scratch” — ingested carbohydrate or carbon dioxide and water?). Personally, I am happy to accept that the system makes a profit and interest myself with the details of how it operates and adjusts to different circumstances.


Can I use grayscale images when working with ImageJ? I am using ImageJ to analyze Western Blots. I have scanned films in as grayscale images because this is how we did it in my old lab. People in my current lab are not satisfied with that explanation and think I should consider using color images. I've been searching for protocols but they all seem to address how to use the program once you have some films scanned.

Can anyone help me figure out what considerations go into choosing how I scan my films?

There is no evidence that one is better than the other, most likely because it differs from case to case. Neither you, nor your critics, are right. There is a tiny bit of science in a paper on digitizing blots, generalizing from blots of a specific protein (PMID: 19517440), and they use grayscale for no given reason. Come to think, that is the best paper in the field of immunoblot quantification., and it still lacks evidence.

Immunoblot is semiquantitative, meaning it may sort and order bands (and protein amounts), but it fails often at estimating differences and ratios, and may even fail to see differences. Just try your best to find a difference, in the knowledge that if there is no difference in protein amounts, any fiddling with contrast won't create a difference in bands quantitation.

There is almost no difference between color and black-and-white digitized images of an immunoblot. The parts of the blot that are black will still appear in the computer as White = 0, even though a tri-color image file will detail it to Red = 0, Green = 0, Blue = 0. The parts that are nearly black will still be very close to zero.

The only thing that changes a lot between RGB and color is the background.  The background may change, for example, from White = 200, to Red = 190, Green = 190, Blue = 220. There is one consequence of such switching between values for background. (These changes may be induced by switching between grayscale and RGB, but also by altering exposure time etc.) When you use a method where the background gets too close to the blots, the "amplitude" of the blots, the height of the peaks in ImageJ, will be reduced. This loss of contrast should wash out some of the differences between blot bands and lessen support for differences between bands (i.e., for the alternative hypothesis), making you miss a genuine protein difference.

Again, if your blot bands are different enough so that your percent increase / decrease is huge, and your p value is small, you are all set, regardless of the method you chose. Ask your critics to explain your observed differences other than by differences in protein. But if your quantification fails the p test, I think it will be a honest effort, to change the color from grayscale to RGB, or the other way around, just in case your first choice had been the one that dampens contrast.


How do muscle cells synthesize glycogen? Hexokinase enzyme is present in all cells (including muscle cells) and can be suppressed by excessive G-6-P product. So that's why in the liver, glucokinase can act on glucose without inhibition of it despite excessive G-6-P product; that's why it can generate glycogen and not let excessive glucose flow back in bloodstream. My question is then: why muscle cells can generate glycogen despite having HK instead of GK? Because as i said above, HK activity is dependent on intracellular glucose level, and cannot phosphorylate glucose to hold it inside the cell. So glucose enters back to bloodstream and prevents the synthesis of glycogen?

Hexokinase catalyze glucose to form G-6-P is only the first step of the glycogen synthesis, and then the G-6-P will continue to processing a series reaction and finally become glycogen. So once the G-6-P forms, it will keep reacting, which will not inhibit the activity of hexokinase.


How does consumption of vinegar affect food chemistry? For example: does consumption of vinegar somehow change digestion of flour (bread, cakes, pasta, puffs) ? May be there are some benefits to eat flour meal with vinegar ?

In the case you're talking about (just using vinegar to taste), there should be no effect whatsoever on a healthy stomach. The stomach already contains a significant amount of acid, and a little bit more from the acetic acid in vinegar won't change much, just like eating some citrus fruit with a meal (oranges, lemons, and whatnot) won't change much. Acid-mediated hydrolysis of chewed food is only the first of many steps in digestion - a significant portion is performed by enzymes and commensal microorganisms in the gut. Changing the type or amount of acid by a small amount won't affect anything significantly in the long run.

The only exception I can think of is for people suffering from peptic ulcers, whether from over-use of NSAIDs (Non-Steroidal Anti-Inflammatory Drugs such as aspirin, ibuprofen, naproxen, etc.), infection with H. pylori, or possible genetic/developmental issues (most often seen in young children). In these cases, consuming an overly-acidic meal may aggravate the symptoms of peptic ulceration.


What is the name of the smallest self-replicating thing? Some time last year, I found an article on Wikipedia about the smallest something to be able to reproduce.

I don't remember exactly what it was, but I am fairly certain that after the initial discovery another of the previous organism (this one slightly smaller) was discovered.

I think that the smallest something might have been the smallest self-replicating protein, or smallest self-replicating molecule, or something like that.

It was not mentioned in this thread: Which organism has the smallest genome length?

It had a strange, stand-out name and I believe it was discovered in the 90s.

You're probably thinking of the Spiegelman Monster. It was actually discovered in 1965, but it was discovered that it became shorter over time in 1997.

It also wasn't included in that thread, and it has a strange name.

http://en.wikipedia.org/wiki/Spiegelman_Monster


What is the impact of selection on orthologous and paralogous genes? How would this impact differ in different regions of protein coding genes? Since paralogs increase the size of the genome and provide more opportunity for the evolution of novel characteristics, would they be more prone to selection?

Exactly .
Paralogs and orthologs , both go under natural selection. But harmful mutations tend to have a less fatal effect if they happen to paralogs as there would  be a backup for the malfunctioning protein. In paralogs, if a bad mutation happens to a protein, the paralogous protein will compensate and help the organism maintain its function but in orthologs one mistake is enough to do harm because there are no other proteins to perform the function of the wild protein.

All the different members of the tubulin family of genes (and
proteins) are sufficiently similar in sequence to suggest a common
ancestral sequence. Thus all these sequences are considered to be
homologous. More specifically, sequences that presumably diverged as a
result of gene duplication (e.g., the α- and β-tubulin sequences) are
described as paralogous. Sequences that arose because of speciation
(e.g., the α-tubulin genes in different species) are described as
orthologous

Reference : Molecular Cell Biology of Lodish et al 8th edition page 325
Also see Campbell Biology 9th edition chapter 26 section 26-4


Can the human eye distinguish colors in the periphery? In the back of my mind I have the idea that human eyes can't notice the color of objects in the far periphery, and that any subjective perception of colors is done by the brain that tries to fill in the color percept.

Is that true?

It depends to some degree on what you define as peripheral vision. Until relatively recently, color vision in the peripheral field has been thought to be substantially less developed than color vision in the central field.

Most estimates of peripheral color perception place the limit of trichromatic (RBG) vision at no more than 30 degrees from fixation; the visual field was thought to be completely color blind at about 50 degrees of eccentricity.

Within the last 30 years, an increased understanding of the changing spatial scale in the peripheral field has led researchers to reevaluate what is believed about peripheral function. Virtually every measure of peripheral color perception can be improved by using a suitably large stimulus in the peripheral field.1

Here is a schematic of distribution of cones in the retina. While cones are decreased in number at 60°, they do exist.2

Here is a schematic of angles on peripheral vision.2

Previous measured sensitivity curves farther into the periphery than thought. In one paper, detection thresholds for colored disks showed that color vision, in particular color vision mediated by the L – M cone-opponent channel (luminance or blue–yellow colors), persists up to at least 50 deg. The larger the color disc, the better the peripheral color vision.[3]

  The range of eccentricities over which red–green color vision is still possible is larger than previously thought. Color stimuli can be reliably detected and identified by chromatically opponent mechanisms even at 50 deg eccentricity. Earlier studies most probably underestimated this range. Differences could be caused by technical limitations and the use of stimuli of non-optimal size. (Emphasis mine) In agreement with previous studies we found that the decline in reddish-greenish L − M color sensitivity was greater than for luminance and bluish-yellowish S − (L + M) signals. We interpret our findings as being consistent with a functional bias in the wiring of cone inputs to ganglion cells (Buzás et al., 2006) that predicts a decrease but not a lack of cone-opponent responses in the retinal periphery.

1 Color vision in the peripheral retina
2 The Retina: Rods and Cones
3 Color perception in the intermediate periphery of the visual field


Is there a free software for manual sequence annotation? I'm looking for a software that would allow me to make a quick graphical annotation of the structural features of a sequence. Something that would look like what you get in jalview, with your sequence on top and tracks at the bottom that highlight which part is an alpha helix or a beta sheet.

My final annotated sequence would look like this:

You might find some success with using WebApollo or JBrowse

WebApollo allows you to perform many manual annotation functions for your genes, such as editing exon boundaries, fixing coding sequences, and merging or splitting gene predictions, which looks like what might have been done in the UCA-At2g42245. It can also be used for adding various attributes, GO terms, pubmed info, or generic attributes. WebApollo actually uses JBrowse, but JBrowse itself has very flexible options for displaying annotations. The part about highlighting the alpha helix/beta sheets is not built in, but JBrowse can be configured to do lots of different renderings, and I could provide more details if you are interested. Disclaimer: I'm a WebApollo developer/JBrowse contributor.


Why is chromatin not condensed during interphase but is in prophase Cell cycle goes through three processes:

Interphase
Mitosis
Cytokinesis

Why are chromatins not condensed during interphase but instead condensed at prophase of mitosis? What makes them condense at prophase?

Here's an image that explains the cell cycle:

And here's one that explains Mitosis as a subcategory of the cell cycle:

Chromosomes condense on the metaphase plate before they are pulled apart by kinetochore microtubules in a Tug-of-war. Chromosome condensation is not yet fully understood, but nucleosome structure is hypothesized to play a role. This is a very good question and is definitely not too broad.


Santa Fe xeric indigenous tree The hills around Santa Fe are covered in a particular xeric tree which is quite small and looks like some kind of juniper which I have been unable to identify:

What is this species?

I eventually figured it out. It is the one-seed juniper, Juniperus monosperma.


How likely is it that a person's progeny has an inheritable disorder based on this pedigree? Case study:

A person (let's just call him "John") had 3 aunts that died back in the 1950's in early childhood due to an unknown form of neuromuscular disorder. One died at birth, one at 2 years and one at 3 years. John's father was the only surviving descendent of John's grandparents. John and his brother do not show any symptoms. John's brother has a daughter who shows no symptoms. John has two sons, one does not show any symptoms and his other son is a 4 month old who is exhibiting signs of some sort of neuromuscular problem.

John has provided me with a pedigree that he believes is correct (note, the ones with the blue square are the ones that exhibit the symptoms):

I took a bit of genetics in university, but basically I am just trying to understand the genetics here. These are my assumptions. Please correct me if any are wrong:

Since the disorder appears to prevent developing past childhood it must be autosomal recessive because everyone who exhibits symptoms is not be able to reproduce due to their early death.
Both of John's grandparents must have been carriers.
The probability of John's dad and any aunts and uncles having the disorder is 25%, and the probability of being a carrier is 50%. The 3 aunts who died must have just lucked out.
John, his dad, and his wife must all be carriers of the disorder.

However I really feel like I'm wrong about these assumptions since the math really doesn't add up. The likelihood that so many carriers for a relatively rare disorder all coming together and the fact that 3 of the 4 offspring of the grandparents died with only a 25% chance all seems improbable.

It could be that John's son doesn't have the disorder and what he has is something completely different. What do the geneticists say?

This is a very rough draft about the case, not verified, and should not be used for any medical conditions. Ask your own doctor. It is just for demonstrating some Mathematics and genetic passing generally.

Condition: Muscular atrophy
Differential conditions: TODO
Support: history of genetic passing in -1 and -3 generations

Disease

Muscular atrophy as a condition jumps over a generation. The environment/living of your greatgreatgrandfathers determine your grandfathers future, as a rough estimate.
The disease's common feature is recessive autosomality.
Assumptions

Autosomal recessive disease because everyone who exhibits symptoms is not be able to reproduce due to their early death.
TODO genetic passing
What is the genetic profile? Is there any other autosomal recessive diseases in the gene map?

Proposed probabilities where the random variables $X = disease$ and $Y = carrier$ such that the subscript 0, -1, -2 and -3 is about new children's, John's, parents' and grandparents' status, respectively.
Both of John's grandparents must have been carriers
\begin{equation}
P(Y_{-3}) = 100\%
\end{equation}

The probability of John's dad and any aunts and uncles having the disorder is (TODO think this again with the correct genetic passing)
\begin{equation}
P(X_{-2}) = 25\%
\end{equation}

The probability of being a carrier is for dad, aunts and uncles (TODO think this gain with the appropriate genetic passing)
\begin{equation}
P(Y_{-1}) = 50\%
\end{equation}

Disease as a process

$X \sim P_{i}(\mu, \sigma)$, $i = -3, -1, 1, ...$  where I propose the mean $\mu$ and the variance $\sigma^2$.

To understand this better, we should know how the generation $-5$ lived.
Can you get it?

Assumptions

Assume the events of individual probabilities independent i.e. (-3) events do not affect (-1) events in the series.
...

Test if the two independent statistics $X_{-3}$ and $X_{-1}$ are from the same population.
If you assume it, put it to assumptions.

Probability Density Functions in Generations -3, -1, 1, ...

Probability density function

At $X_{-3}$, the 3 aunts of 4 died. The mean $m = 0.75$ (=3/4).
You cannot use Binomial because sampling is not with replacement, not Poisson because occurrence probability is not less than 10%, ...
...

Conditional probability and Bayes theorem

Consider the conditional probability $P(X | Y)$ that is what is the probability of getting the disease for the generation when given the carriers ...
...

You propose 25% probability for generations series $-3, -1, 1, ...$.
You can test this. Select the statistical significance $\alpha = 0.05\%$. Select the appropriate probability density function or teach neural network to it.

False assumptions

John, his dad, and his wife must all be carriers of the disorder. Why wife should be a carrier?

Literature

Blythe, Peter.  Mathematics for the international student Mathematics HL (Options). Haesa & Harris Publications. I recommend this for beginners.
TI-84 and TI-86 have good manuals about the statistics.
Some publications about teaching a neural network doing some of the genetic analysis.
...


Percentage of genome devoted to regulating gene expression Recently I've been studying the p53 tumor suppressor gene as a model for regulation of gene expression. It's amazing how many different post-translational modifications are known to regulate p53 activity, and how many different factors are involved in this regulation.

It is postulated that there are between 20,000 and 30,000 genes in the human genome. Is there an estimate for the percentage of these genes whose primary function is related to regulation of gene expression?

Okay, I'll take this out of the comments and put in an answer for all of us to work on.

To directly answer your question:

  "Is there an estimate for the percentage of these genes whose primary
  function is related to regulation of gene expression?"

It depends on how you define "gene expression." And what cellular processes you want to include in that definition.

Larry's answer is the usual standard response, especially for people (such as me, ha) that have spent significant time studying transcription factors. About 1% of human genes have DNA binding domains and are thought to be directly involved in regulating the transcription of genes into mRNA - these are transcription factors (TFs). Closely related are cofactors, which regulate expression by binding to TFs or RNA polymerase machinery, but not directly to DNA.

Regulation of gene expression could also include modifications at the chromatin level - here you would include chromatin remodelers, histone acetylases, deacetylases, methylases and the histones themselves.

mRNA transcripts can also be regulated by miRNAs: post-transcriptional regulators that bind to complementary sequences on target mRNAs, which leads to translational repression or target degradation and gene silencing. So you would also include the proteins involved in this process, most notably the RNA-induced silencing complex, which includes Dicer.

There are also proteins involved in mRNA stabilization and turnover, which effects gene expression.

I'm not sure if anyone has added up all of the genes above to determine an overall percentage of the genome.

If you include in your definition of "gene regulation" post-transcriptional modification, folding chaperones, intra-cellular transport, extra-cellular and intra-cellular signaling, and so on - then Shigeta is right, you begin approaching 100%. In the most basic sense, life itself is gene regulation.


Does anyone know of a study supporting predictions #2 or #9 of the Extended Evolutionary Synthesis? Regarding the 12 predictions made by the Extended Evolutionary Synthesis (http://extendedevolutionarysynthesis.com/about-ees/), does anyone know of a study that supports #2 or #9?

It seems like #1, #3, #5, #8, #10, #11, and #12 do not violate the modern synthesis.  #2 and #9 would though.  Agreed?  But I know of no study that supports them.  Not sure about #4, #6, or #7.

There is no debate

The so-called Extended Evolutionary Synthesis (EES) is just a new term for a whole lot of knowledge that roughly speaking everyone acknowledge to be true. EES is really just an extension but does not say anything that conflict with previous theory. There is no conflict and no contradiction.

The only debate stand upon whether or not our current understanding of evolutionary processes deserve a new name or shall we just stick with what we call the modern synthesis.

Shall we use the term ESS?

I talked about this renaming with about 20 evolutionary biologists and all of them consider such renaming useless. However, by the end of the day, they all mainly did not care much.

My personal opinion about the renaming

IMO, one reason such naming is silly is that there has not been a major work that have completely and suddenly changed our understanding. We just keep discovering more and more as we always did. All the new things we discover we just used to integrate it what we already called modern synthesis. Those advocating for a renaming define the modern synthesis not as most people do (that is everything we know about evolution so far) but as the set of knowledge that existed in 1950.

It is funny that even the discovery of DNA did not bring about a renaming of our theory of evolution as we only considered that it added up to our current understanding. I doubt that the emergence of new fields (such as niche construction and its heritability or developmental noise) would be in any way sufficiently revolutionary to cause a renaming. And I say so even though I also work in the field of mutational and developmental noise.

Unclarity

The points listed in the link are rather unclear and it is therefore impossible to comment on them. Take the #2 you are interested in

  heritable variation will be unbiased

The term variation has no strict definition. The term variance is clearly defined. However, a variance in itself cannot be biased, only the distribution it comes from can. So, this simple sentence mainly makes no sense (to me at least). If it does make sense to those who wrote this list, then, OP, you will need to provide explanations from other source or ask for its meaning before asking for its validity.

Further reading

This paper will offer you opinions from both sides. As implicit from the above, one side (namely, the "counterpoint" side as referred to in the paper) seems to me to represent the vast majority of evolutionary biologists.

Addressing your comments

  Thank you for the clarification. I think by "heritable variation," the authors mean mutation. You feel it's still true that they are unbiased?

"mutation" is not a variable, it does not follow a distribution. It cannot be bias or unbias.

Mutational effect on fitness is a variable and follows some distribution which is most definitely biased (deleterious mutations are much more common than beneficial mutations; usually modelled with a double gamma distribution; see here).

Mutational effect on the phenotype is a variable and follows some distribution. It may well be biased indeed. The distribution of mutational effects on the phenotype were mainly unconsidered by evolutionary biologists who contributed to place the first bricks in the modern synthesis (Fisher, Wright, Haldane, Muller, etc...).

These "early" evolutionary biologist never made predictions about the distribution of mutational effects on the phenotype that would contradict today's predictions. They just had little understanding and did not talk about it much.

Again, in your question you are opposing EES with Modern Synthesis as if they were to be opposed. But by doing so, you need to clearly define Modern Synthesis. By default, one just consider the Modern Synthesis to include all the knowledge we have in evolutionary biology and therefore by definition, elements like niche construction, biased mutational effects of phenotype and other field of knowledge that one might want to specifically associate to EES only.

  Do you still feel it's true that natural selection is the only source of the evolution of adaptation?

This question depends only on the definition of adaptation. If, for example, you consider a lineage being poorly adaptive becoming adaptive as the environment changes to match their phenotype (and not the other way around) to be an adaptation, then typically nobody would have never thought that only natural selection would cause adaptation. I would personally be happy to call that an adaptation.

The question is not a question of evolutionary process but only a question of the definition of adaptation.

Note, as an extra source of confusion, when talking about adaptation one may refer to the changes yielding to higher fitness (whether the change is genetic or not is up to you) and/or to the resulting state of having a high fitness.

  For example, if there is an epigenetic modification that is transgenerationally stable and adaptive, is it an adaptation?

Again, it depends upon what you call adaptation. I would be happy to call that an adaptation.

  the discovery of DNA would not cause a reconceptualization of the modern synthesis because it was consistent with it.

Everything from the EES is consistent with the modern synthesis. Most of it are just add-up subjects that brought little consideration before. Some of it might break some simplified generalization that may have been done before though. Many does affect our view of the grandeur and complexity of evolutionary process but none is contradicting what we previously thought.

  what you mean by "becoming more adaptive as the environment changes." Would you give an example?

Imagine a population is perfectly adapted to live at an environment where the temperature is 18˚C. The current temperature is 15˚C though. Let's imagine a case where the population does not change much through time (eventually due to a lack of genetic variance to select from, eventually due to a low mutational variance or a recent bottleneck) but the environment is getting warmer and after some time the environment is at 18˚C. The population is now perfectly adapted.


Why is the blood thick in Wet Cupping / Hijama I have just witnessed the wet cupping procedure being performed and have questions regarding the blood that is seen in the cups. I understand there are no studies that show cupping is an effective treatment for many diseases as some claim it to be but my question is regarding the blood that is released.
The procedure aims to eliminate the 'bad blood' which leaves clean blood to circulate the body, the practitioner pointed out the difference between the clean and bad blood and there was a substantial difference in how it looked and flowed. The blood was very clumped up and thick and didn't flow well at all whereas some of the blood was a lot more fluid and was able to flow easily. I was told this runny blood is clean blood and is what we want in our bodies.
My questions are what is the thick clumpy blood and why is it like that?
Is it actually bad blood?
Thank you in advance!

We had a demonstration of blood coagulation/clotting in a biology lesson with the school nurse. She just took half a test-tube of blood sample from a class pupil and we waited a moment, and the blood became a solid lump inside the test-tube.
The process is there to protect you from leaking blood if you cut yourself, the process uses fibers and platelets and complex proteins.
https://www.youtube.com/results?search_query=blood+clotting
wiki: Coagulation
Blood letting is a very ancient practice that used all sorts of methods like annelids/leeches, which has not been proven to have any benefits. The blood in your body does not seperate into good blood and bad blood by sitting in a jar.


Isotropy of sarcomere bands in skeletal muscle cells As seen under a polarization microscope, the A-Band in skeletal muscle fibres is so named because it is anisotropic in its refractive index which is a characteristic of orderly crystalline structure. On the other hand, the I-Band is so named because of its isotropic nature, as far as its refractive index is considered, which is characteristic of Amorphous substances or substances which lack long-range order. Both are filamentous (as opposed to globular) in the sarcomere (Actin is present as F-Actin).

  But then why this difference in the characteristics of refractive index,
  which is indicative of order (i.e crystalline or amorphous?) in their
  molecular structure?

Moreover, is the H-Band anisotropic?

If not, then the anisotropy of the remaining part of A-Band must be a consequence of the relative arrangement of Actin and Myosin which are independently isotropic, and hence cannot give a possible isotropic arrangement.

If yes, then that indicates that the myosin filaments are anisotropic in themselves and actin filaments are isotropic. But, in the region of their overlapping (A-Band minus H-Band), the overlap is between an anisotropic (myosin) and an isotropic (actin) component which shouldn't be anisotropic because the randomness of actin filaments (i.e. its isotropicity) should make the entire configuration isotropic?

I am sorry if I am wrong in my understanding of isotropic and anisotropic characteristics, or if my question sounds too "physics-related", but this has been bothering me for quite some while now.

Here is a directly related question I asked on physics.se. It partly solves the problem of possible arrangement of isotropic elements to generate anisotropy.

This is sort of technical answer, but I hope its helpful I hope.

All these bands in the sarcomere are anisotropic.  Isotropy would imply that the structure/properties of something is equally ordered or coherent in all 3 directions.  The sarcomere has definite structure along its longer axis so the H band is anisotropic.

Since the H band is a small structure compared to the actin and myosin components of the sarcomere, much of the signal that one measures via diffraction or polarization experiments is from those two fibers and less information would be discernible from the anchoring portion (H band) of the myosin filament.

In the case of the A and H bands, which are identified by electron microscopy, the structure along the sarcomere axis is not very strong - they are thin sections of the sarcomere and tend to function structurally to connect the actin and myosin axes.

Because of this the information that you might get from A and H band segment studies will be that 'these bands are not very ordered along the axis of the sarcomere'.  That's not a lot of information, and we know this from other experiments.  But it is information nonetheless because they have some spatial organization.


What is proton leak? I have some idea about it. Is it the wasteful back flow of H+ ions through uncoupling proteins during aerobic respiration?

Thank you

Short answer: yes.  It also includes unspecific leakage without the aid of uncoupling proteins, since the mitochondrial inner membrane is not entirely impermeable to protons. For example, protons might fall backward through the proton-pumping complexes, through other solute carriers, or through other openings or irregularities in the membrane.


What are the statistical tools for distinguishing molecular analogy from homology? Scientists have developed statistical tools that distinguish "distant" homologies from coincidental molecular homoplasy in extremely divergent sequences.
What are these tools?How are they used ?

I have very less knowledge about statistics.

There are lots of statistical algorithms that allow you to evaluate the similarity between two given sequences. For instance, blast allows you a rapid comparison between your sequence and other sequences in a database; while Clustal, with a similar functioning, allows you to compare a set of given sequences between them. They are very simple algorithms, but very fast and useful, and basically they score an alignment by counting how many positions between the two entries are the same. Other algorithms function in a similar fashion, but they use hidden Markov models to compare your sequence with a consensual sequence in order to identify motifs and domains. I'm sure there are even more advanced programs, but I don't know them and don't think it's the point.

Homology usually refers to things that share the same origin, while analogy refers to things that do the same function but their origin isn't shared. While the algorithms I've described you only search for similarity or identity, you must notice a few things:

a) Homology of function doesn't necessarily correlate with high similarity. Two proteins can have the same global structure and their sequences be completely different. The three-dimensional structure is the same, and probably there'll be key amino acids that will remain very similar. This is very obvious in many proteases, which share only the three catalytic amino acids (catalytic triad) between them, and vary enormously even between strains of the same species.

b) Protein domains vary in size from a few dozen to a few hundred amino acids. The odds that exactly the same sequence evolves in two separate moments are very low. Especially in highly conserved domains, which usually carry out key functions.

c) Proteins usually have a modular structure with more than one domain. New proteins often evolve by switching and combining domains by translocation. So, even if the same domain has evolved in two separate times, the association between these two "twin" domains with other domains will probably reveal its unusual origin.

That's why usually the term molecular analogy is not used, and if so, it would refer for example to structurally different domains that catalyze the same reaction or that share the same structure. Note that even if the analogy as you describe isn't impossible by itself, the software won't be able to differentiate them unless the sequence appears associated with others. Furthermore, the origin of many of the current protein families is so far in the past that it's quite impossible to reconstruct it, even more so with the high diversity in prokaryotes.


How are minerals formed by biological processes? News to me is that about 4500 of the 4900 minerals on Earth have been created by life. What are some examples of such processes? Are some minerals formed inside the human body?

News to me is that about 4500 of the 4900 minerals on Earth have been created by life.

After reading the article, this isn't what was said.

What was said is that life increases mineral diversity on a planet, most notably through biproducts reacting with existing minerals (like Oxygen - a biproduct of photosynthesis - reacting with iron to create iron-oxide).

So, life doesn't create new minerals, but it does change the abundance of elements at the surface which can undergo reactions with pre-existing minerals to form other minerals.

Not all of the 4500 "new" minerals on the Earth can be attributed to life. We don't know how many new mineral formations have formed because of life, but the article suggests the theory that increased surface diversity of minerals might be a good indicator of life.


Name and Behaviour of Arthropods near a Cactus Background Story

I have a small, old cactus on my sunny, south-facing window sill in southern Germany. Since a few years, small black dots gathered around its pot. At first, I thought the dots were dust or sand and wiped them away. But the dots appeared again and again, so I had a closer look at them and saw that they were tiny insects or arachnids, probably lice or mites. We just call them arthropods from now on.

More information

The following picture shows my cactus with some of the arthropods around the pot. Click here for higher resolution.

Here are some close-ups.

The arthropods seem rather dead. They do not move and most of them lie on their back. However, they are not dead. Once they are picked up and set on a paper towel they start to move. If they get on their legs (with a little help) they walk around, which can also been observed by the naked eye.

I inspected some individuals using a detached camera objective as a magnifying glass. The arthropods are brown, shiny, somewhat translucent, and have 8 legs. I could recognize a small head without a neck (like most bugs have) but couldn't recognize a mouth or eyes – probably because of the size.
I couldn't take a picture, but tried to draw what I saw:

Later I got hold of a cheap microscope and took a few videos. The video quality is miserable. In reality, the arthropods are not that dark, see my drawing and the photographs.
Here's on individual laying on its back, flipping over, and walking away.

Here's another individual walking.

The Strange Part

As said, the arthropods keep on re-appearing around the plant pot. But in all those years, I never saw any of them on the pot, inside the pot, or on the cactus. I also have other cacti right next to the "infected" cactus, but their pots were never surrounded by the arthropods.

Question

What are these arthropods, where do they live, and why do they leave their habitat?

My Theory

I suspect the arthropods to live inside the dead and cracked part of the cactus. They could walk on the spikes of the cactus and jump from the ends of the spikes to the ground. If they land on their backs, they cannot get up and stop moving after some time.

I don't think that the arthropods live inside the soil. Two reasons for that:

The arthropods could have drowned often. From time to time I put too much water in the pot, such that all soil is fully covered by water, often for more than 8 hours (yes I know that can't be good for a cactus *cough*).
In order to get to the window sill, the arthropods would have to walk quite a while. Over time, I should have seen at least some of the arthropods on their way to the outside world.

It's hard to tell from these photos (you'll need a macro lens for good shots), but they seem indeed to look like mites (Acari).

There are mites that feed on rotting cacti, Bonomoia opuntiae for example. There is a film here about this cactus mite.


Which is the most extreme thermophilic bacteria known? Extreme thermophilic bacteria thrive at any temperature above 40/50°C. Thermotoga Maritima seems to be the bacteria that can survive at the highest temperature up to 90°C (reference 1, table 2). I wonder if there is a more exhaustive list of extreme thermophilic bacteria and if there is a known bacteria that can survive at higher temperatures than Thermotoga Maritima.
References:
Ref.1 Front. Microbiol., 05 November 2015 | https://doi.org/10.3389/fmicb.2015.01209
Extremely thermophilic microorganisms as metabolic engineering platforms for production of fuels and industrial chemicals

Geogemma barossii, initially designated Strain 121, can survive and reproduce at 121°C, with an optimal growth temperature of 103°C. It's not a bacterium though, but a member of the Archaea domain.


What happens during metamorphosis? We were studying butterflies in class and I asked my 7th grade teacher, but she deemed the concept "too complicated." I'm really curious now, not only about butterflies but insects in general...

Thank you!

It depends of what order and even what family of insects we are talking about. Insects may have complete or incomplete metamorphosis, being the complete more complicated. Even inside the first group (wich in fact contains most of the insects since coleoptera, diptera, lepidoptera and himenoptera have complete metamorphosis) there are important differences. However, I'll try to explain some basics.

First of all, metamorphosis is a molting-related process. It's regulated by the same hormones and they share many characteristics. In insects with uncomplete metamorphosis, this is very visible, since the "metamorphosis" is the last molt, wich usually involves growth, sexual maturity and the development of functional wings.

The choice between a regular larval molt is determined primarily by the levels of juvenil hormone, wich decays during the last larval instar (pupae and adult are instars, too). The molting is triggered by a peak of ecdysone, an steroid.

Once the insect has entered into the state of pupae, the organs start to suffer diverse changes. The formation of adult organs de novo arise from some special structures called imaginal discs, wich are clusters of stem cells that are more or less isolated in the larvae.

Position of the imaginal discs in Drosophila. Source.

Note that diptera larvae lack legs, mandibles and even head, while coleptera larvae usually have true legs, a set of mandibles and many other adult features.

A typical larva of a coleoptera of the genus Lucanus. Note the mandibles and the legs. Source.

Some other organs remain more or less the same, such as the hearts or many parts of the nervous system. On the other side, some larval organs needs to dissapear and suffer programmed cell death. The gut, many parts of the nervous system, between others, suffer modifications that may be more or less drastic. In many cases this happen by simple growth and differenciation of the tissue or degeneration by apoptosis, but in some others the whole organs suffers apoptosis and regenerates itself with adult characteristics.  For example, the innervation of the abdominal parapods (false legs) in caterpillars suffer a progressive degeneration, while the opposite happens in toracic nerves, wich will have to control legs and wings. This whole process is pretty similar to embrionic development and it shares many traits with it.

Finally, metamorphosis in other animals, such as crustaceans, vertabrates (fishes and amphibians), echinodermae, annelidae, cnidaria and many others will probably vary widely. I know for sure that amphibians metamorphosis is regulated by tiroid hormones, but I'm not even sure that many of the other examples have even been studied at a phisiological level.


Will humans ever evolve to cope with the rising temperature of our planet? I am a complete layman of this field(Biology).I went through an article about global temperature rise and i wanted to ask this question.

  Federal science agencies announced Wednesday that 2016 was the warmest year on record, beating the previous record of global temperature set in 2015, which had beat the previous record set in 2014.

(As seen in the graph temperature is rising rapidly and will increase even more in the near future.)

Can we evolve to cope with high temperature?Will we evolve?Is mutation the only answer?

(Frankly not looking for an answer saying by natural selection,the last thing i want to hear)

A change in temperature of 1 degree, or even 4 degrees, is less than the variation in temperature that is seen between different areas that are inhabited by humans and less than the variation which is seen annually in those areas. Accordingly it seems that humans are already adapted to these differences in temperature and that our response to the temperature changes are more likely to involve habituation and cultural changes in behaviour and technology use than evolutionary change.


Advantage of cup-like shape of blood cells, spores? Mold spores sometimes have the same shape as platelets in blood. If I were designing a spore it would probably be spherical. Is there any advantage to this cup-like shape?

Maybe there is some advantage in flow properties in fluid or air? And maybe the physics of structures on that scale differ from that of everyday objects?

Thanks.

The functional implications of the biconcave shape of human red blood cells are not fully understood. Several hypotheses have been suggested as explanations, including bending energy (1) and effects on oxygen transport (2). More recently, it has been hypothesized that the shape is important for the flow properties of the blood cells in capillaries. Uzoigwe (3) states that

  The deleterious nature of turbulent flow on the cardiovascular system
  suggests that the biconcave disc form has evolved out of a necessity
  to maximise laminar flow, minimise platelet scatter which in turn
  suppress atherogenic activity in the large vessels.(...) The biconcave
  profile of the discocyte means that much of the mass is distributed in
  the periphery. This increases the moment of inertia of the cell and
  subsequently renders the erythrocyte less prone to rotation during
  flow in the large vessels. Here it is suggest that this reduction in
  rotation promotes laminar flow and discourages platelet scattering by
  minimising the "Eddy currents" and it thus anti-atherogenic. A number
  of pathological mutations result in the red blood cell adopting a
  spherical shape as opposed to the biconcave disc profile. The sphere
  has a smaller moment of inertia when compared to the discocyte, as
  much of the mass is distributed round the centre. The spherocyte is
  hence much more prone to rotation during flow in the large vessels.

The advantages of various structures do depend on the scale of the system, as you say. For red blood cells, the size of capillaries and veins are of importance. The shape of red blood cells differ in animals that have blood transport systems with different structures than humans. Thus, the red blood cell shape is likely optimized with respect to movement in the human blood transport system, with oxygen diffusion also being a possible factor. To determine what advantages a specific shape of spores would give, you would need to consider the expected environment the spores would live in and their typical lifecycle.


Would my hands sweat this much if I wasn't wearing gloves? I've wondered about this for a long time, and hopefully someone here has a reasonable answer. I'm a cell and molecular biologist, and much of my time at the bench is spent wearing (usually nitrile) gloves. I've noticed that if I wear them for longer than 10 or 15 minutes they start accumulating sweat. However, my hands aren't clammy or damp when I'm not wearing gloves, so my question is whether my hands are always sweating at approximately the same rate, and the impermeable barrier of the gloves just traps the moisture, or does the enclosed environment inside the gloves promote sweating? My hands don't seem particularly hot when I have the gloves on, and the gloves themselves are pretty thin, although they do have some insulating properties, as I can handle items taken from a -80°C more easily gloved than bare-handed. What causes this diaphoresis?

Hand sweating has been fairly well-studied, both because sweating from the hands is one of the main mechanisms of heat dissipation at higher temperatures and because there is a significant effect on palmar sweating by the autonomic nervous system (the main cause of hyperhydrosis of the palms).

Disregarding autonomic effects (stress response), the single most important determinant of hand and foot blood flow is the thermal status of the body core. Heat dissipation is more marked in the hands than feet, and remains so as temperature increases.

Studies have been done of palmar sweating in extremes of temperatures, palmar sweating changes with aging (decreases), palmar sweating in disease, etc. But what has not been studied is the effect of localized heat on sweating of the palms, which would be of interest to you if sweating was a result of the insulating capacity of the gloves.

What is known about palmar sweating is that it is an ongoing and important process in both genders, at all temperatures, and at all ages. The most reasonable assumption then, given the limits of the literature, is that your hands sweat continuously and steadily at a given temperature, and it is highly likely that you are noticing it when wearing gloves only because the vapor barrier caused by the gloves prohibits evaporation.

The roles of hands and feet in temperature regulation in hot and cold environments
OBSERVATIONS ON THE ACTIVITY OF SWEAT GLANDS WITH SPECIAL REFERENCE TO THE INFLUENCE OF AGEING
Why do I get sweaty palms?


Is there a good analogy that illustrates the difference between early DNA sequencing techniques and shotgun sequencing? My first university biology classes begin in September. In preparation, but increasingly out of curiosity, I've been studying some basic biology. Saying that to say, I know as much about DNA replication as the Khan Academy videos teach.

Presently, I'm reading about the two efforts to sequence the genome. From what I've read, Collins' project used "polymerase catalysis and nucleotide labeling"; whereas, Venter's project used "shotgun sequencing". I didn't know enough to understand the article I read on "shotgun sequencing" and couldn't find one that described the other technique.

I suspect that, in order to comprehend a concise description of the two techniques, I'd need to learn more than I could learn from an answer to this question. That said, it'd still be nice to have a very rough idea of what each process involves and how they differ from each other. A crude analogy to something concrete would be great.

The public effort, led by Collins, relied on a physical map of each chromosome.  Very large pieces of genomic DNA were sub cloned into cloning vectors and used to create genomic libraries in cosmids, BACs and YACs.  The sub clones are ordered using hybridization probes from either known genes, or RFLP genetic markers. In this way a physical map of each chromosome was built up, and then the project would march down the ordered clones, sequencing the sub clones.  If the physical map is good then you have a very good idea of where the sequence comes from.

Shotgun sequencing, in contrast, involves randomly fragmenting the entire genome into small fragments (using sonication, for example), sub cloning those pieces and sequencing everything.

In the first method each base is sequenced a minimal number of times, whereas in the second approach each base ends up being sequenced many times (on average).

For a whole genome, shotgun sequencing requires an excellent computer algorithm to "assemble" the resulting data into overlapping contigs.


Have we ever observed two drosophila lineages that evolved reproductive isolation in labs? Background

The standard definition of species refers to the concept of reproductive isolation. If two lineages are found to be reproductively isolated, then we consider these two lineages to belong to different species. My question concerns evolved reproductive isolation in Drosophila sp. following labs due to experimental evolution.

Question

Have we ever demonstrated that two Drosophila sp. lineages that could initially interbreed (in nature or in labs) evolved through artificial selection (and drift and mutations) in labs to finally not be able to interbreed anymore either due pre- or post- zygotic isolation (see wiki)? Or, in other words, have we ever demonstrated that two drosophila lineages evolved to become different species (reproductive isolation definition) in labs experiments?

If not, have we ever observed some partial reproductive isolation such as inbreeding depression for example?

Note: This question is motivated by @LotusBiology that could not receive the answers she/he was waiting for because he/she failed to ask questions that are possibly answerable! So I wanted to ask this question that somehow addresses this question he/she asked (now on-hold)

For more information about the concept of species, please have a look at How could humans have interbred with Neanderthals if we're a different species?

Rice and Salt$^1$ bred fruit flies for 35 generations and from one line of flies created two groups that were isolated from each other reproductively. They could not interbreed because they no longer bred in the same environment. Depending on one's definition of 'species' this could be a case of artificial speciation.

$^1$Rice WR, Salt GW (1988), Speciation via disruptive selection on habitat preference: experimental evidence". The American Naturalist 131 (6): 911–917.


Identify an insect (beetle?) Body size: 30mm
Location: Poland, in the middle of a large meadow
It was flying and landed directly on my cap :-)

After consulting wikipedia it look similar to some of Tenebrionoidea but can't find an exact match.

Help!

This is a Buprestid beetle, and I think the species is Chalcophora mariana. It doesn't look all that coppery in your photos, but the large size and shape is perfect. Their larvae live mostly on pines, so perhaps there were pines close to your meadow?  (Image from Wikipedia)


Can enzymes catalyze thermodynamically unfavorable reactions? Can biological enzymes catalyze thermodynamically unfavorable reactions? I read that an enzyme lowers the activation energy of a reaction by offering an alternative reaction pathway with a lower activation energy, however the ΔG of the reaction is unchanged. If enzymes can do this, then how exactly does this work?

Enzymes can catalyze a thermodynamically unfavorable reaction by coupling it with a thermodynamically favorable reaction. Most often, enzymes use ATP hydrolysis reaction (energetically favorable) as a source of energy (in simple terms) to drive the unfavorable reaction forward. One important point to keep in mind here is that enzymes don't drive a reaction equilibrium forward or backward; they just help in achieving the reaction equilibrium faster. Also pay attention that enzyme itself does not change the thermodynamics of a reaction (as you say, ∆G of the concerned reaction remains the same, except at equilibrium), coupling of a favorable reaction with an unfavorable one only helps in making the overall reaction favorable. This phenomenon, of one reaction changing the rate of another reaction, is called induced catalysis and has nothing to do with the enzyme itself.

I will talk about how enzymes do this using examples, while the other answer talks about the semantics. An example which will help you understand this concept is ATP synthase. It is an enzyme found in the inner mitochondrial membrane which allows the movement of H+ from the inter-membrane space towards the mitochondrial matrix, using the energy of movement (since this is favorable and exergonic) to generate ATP. The reaction would look like this:

$$\ce{ADP + P_i + 3 H^+_{IMS} \rightarrow ATP + 3 H^+_{matrix}}$$ (remember that exactly 3 H+ are not required, this is a simplified version)

But, ATP synthase does not drive the reaction forward; it just helps in reaching the following equilibrium faster:
$$\ce{H^+_{IMS} \leftrightharpoons H^+_{matrix}}$$ i.e. keeping the amount of H+ in inter-membrane space and matrix the same. This is why a constant gradient is required to keep them in working condition. For this, the electron transport chain continuously throws H+ into the inter-membrane space to maintain an electrochemical gradient. Along with this, enzymes ATP-ADP translocase and phosphate carrier continuously take out ATP from the matrix and throw in ADP and Pi. However, this lowers the electrochemical gradient (exchanging ADP3- for ATP4- in inter-membrane space, while phosphate carrier catalyzes electroneutral reaction), making the final reaction: $$\ce{ADP + P_i + 4 H^+_{IMS} \leftrightharpoons ATP + 4 H^+_{matrix}}$$

However, since the enzyme just helps in maintaining equilibrium, it can also work backwards i.e. it can also transport H+ against electrochemical gradient (unfavorable), coupling it with ATP hydrolysis (favorable) to reach equilibrium. The enzyme is now called ATPase and the reaction becomes: $$\ce{ATP + 4 H^+_{matrix} \rightarrow ADP + P_i + 4 H^+_{IMS}}$$

There are many more such enzymes which couple ATP hydrolysis (or other favorable reactions) to catalyze reactions which are either unfavorable or very slow (i.e. require a source of activation energy) under normal cellular conditions. Another factor, as the other answer explains, which helps in this is changing the concentration of products. As seen above, ATP-ADP translocase and phosphate carrier continuously decrease the concentration of products (ATP) and increase concentration of reactants (ADP and Pi) so that the overall equilibrium shifts forward and the enzyme keeps on driving the reaction forward (this, again, has nothing to do with with the enzyme itself, it is called Le Chatelier's Principle). Again, the other answer focuses on this issue.

References:

Enzyme - Wikipedia
Cellular Respiration


Can ELISA be used to detect a plant enzyme? Creating assay for a new enzyme If the goal is to generate a rapid assay for an enzyme of plant source what are the typical options?

i.e. Could one do something like: Generate an antibody to the enzyme and then use it to create an ELISA? Would animal-injection be the way to generate the specific antibody needed?

If not, what is typically done in such cases. How does one go about creating an assay for a new enzyme of plant source. Are there alternative approaches that avoid the antibody creation?

I want to add something on top of Chris answer.

The production of an antibody it is usually a quite slow (and expensive) process, an alternative that worth to consider is phage display (https://en.wikipedia.org/wiki/Phage_display). Once you find the phage that effectively bind your protein of interest, you can use it instead of an antibody in what is called a Phage-ELISA assay.
However, mind that the ELISA (or Phage-ELISA) will give you information about the presence and the concentration of the enzyme, it will not give you any hint about its activity.


Does tardigrade eat mould? There is a problem of devastating mold in ventilation of old buildings in Europe. I guess tardigrades might be better solution because chemicals is not a good idea for ventilation because people are breathing with this air.

Mould in buildings can be serious.  It is treated by removing and destroying (fire is good) the things the mould is growing on, and lots of cleaning.

The mould grows on wet cellulosic material like fiber board, gypsum board, paper, or wood.  It can be prevented by fixing the leaks so stuff doesn't get wet, and more cleaning.

You could pour bleach on the contaminated material, kill some of the mould, and what survived would grow back.  Neither chemicals, nor tartigrades are any help here.  Just more cleaning.

Details:  http://www.cdc.gov/mold/stachy.htm


Why do you need the intrinsic pathway when you have faster extrinsic pathway? There are two pathways in blood clot fromation; the extrinsic pathway and the intrinsic pathway.

The extrinsic pathway is faster than intrinsic pathway because it has less number of steps. So, why do we need intrinsic pathway then?

In short: The extrinsic cascade reacts to damages of the blood vessel, the intrinsic pathway reacts to damages of the walls. But as with all things, the long version is ways more complicated:

The extrinsic pathway is activated when you damage tissue and factor VII come in contact with tissue factor (also known as factor III). Tissue factor is located in the membrane of the cells and is only released when the cells are damaged.
Then the cascade starts and delivers a very fast large amounts of active thrombin, which then converts fibrinogen to fibrin to build a block of the damaged blood vessel. The step from the thrombin is common between both pathways.

The intric pathway is also called the "contact pathway", which starts when the factor VII comes in contact with collagen or anionic surfaces.
The main advantage of this pathway is the strong amplification of the initial signal from the intrinsic pathway by a factor of about 1000 fold. The intrinsic pathway is also co-activated by active thrombin (which stands at the end of the cascade) meaning it is also a powerfull feedback loop to make the initial reaction much stronger. This also overcomes weak activation which where the active thrombin will be inactivated by Tissue Factor Pathway Inhibitor.
The coagulation cascade has a pretty nice article in the Wikipedia.

Interestingly it is now believed, that the start of the intrinsic pathway plays no or almost no role in vivo. There are people which "suffer" from a deficiency in factor XII which is necessary to start the intrisic cascade. These people have absolutely no problems with their coagulation, so the first steps are not necessary (any more?). This article presents findings, that it stabilizes a thrombus:"The intrinsic pathway of coagulation is essential for thrombus stability in mice."
Here are some further articles about the intrinsic pathway:

In vivo roles of factor XII.
Factor XII: what does it contribute to our understanding of the
physiology and pathophysiology of hemostasis & thrombosis.


Determination of genes to be modified in epigenetics It seems that during reproduction particular genes are targeted for modification (mutation, deletion, insertion, etc.) given environmental inputs of either or both of the parents.

If a creature was fit given its environment, its seems there is little mutation. However, if the creature becomes less fit (i.e, due to increasingly becoming prey to a predator) it will undergo increased rate of mutation to find a successful adaption to the new environment. But it seems that the mutation is also targeted to particular genes that maybe most beneficial to mutate (i.e, to develop camouflage).

This begs the question - given environmental inputs, is there something that controls gene modification during reproduction? More specifically, is there a process that targets a specific gene or trait?

Mutations are not performed targeting a specific new phenotype. There is no way an organism can "know" the impact of a specific future mutation anyway. A mutation is just a mistake in the replication process. As a consequence the majority of mutations are deleterious and only a handful of mutations are beneficial.

It is true though that the mutation rate can be affected by the environment or the stress induced by an individual (Agrawal 2002). It seems more intuitive that these are just a consequences of the cost of the DNA replication machinery and DNA repair machinery but it is not impossible that such changes in mutation rate could eventually evolve as a bet-hedging strategy. In the extreme case where the same types of environmental change happen over and over again, it is not impossible that a lineage could evolve the ability to modify the mutation rate at a particular locus. However, to my knowledge this has never been found.

You might want to follow an introductory course to evolutionary biology. You might also want to read this post too that gives a mixture of related information


Are prosauropods ancestors of all sauropods? My daughter, while reading a book about dinosaurs, asked me if prosauropods are ancestors of all sauropods. Are they? From the name ("pro-sauropods"), I guess that they are, but am I right?

Welcome to Biology.SE! Your daughter asks interesting questions!

The question is debated. It is currently mostly thought that sauropods and pro-sauropods are sister lineages and therefore, one does not contain the other. In other words, the pro-sauropods are no more the ancestors of the sauropods than were the mammals are the dogs are the ancestors to the cats.

One of the most updated source of information for phylogenetic questions of the kind is tolweb.org. You should have a look. Here is the page for the Sauropodomorpha (which contains the sauropods and the pro-sauropods). You have a nice list of reference on this page including some from Sereno, who is the author who first defined the pro-sauropods.

I quickly sought through the literature. It seems indeed that all phylogenetic analysis were based on phenotypic comparisons and not on genetic comparisons. Citing from wikipedia:

  Evidence against sauropod ancestry within Prosauropoda comes from the fact that prosauropods had a smaller outer toe on their hind feet than the sauropods. Many maintain that it is easier for digits to be reduced or lost during evolution than the reverse, however there is no evidence for this. The lengthening, or gaining of extra digits is common in marine reptiles, and within the theropods digit lengthening occurred at least once. Therefore, using this as evidence against ancestral prosauropods is questionable.


What can be used for DNA preservation? I am neither a student nor really advanced in biology, I am just writing a tabletop role-playing game scenario that I want as realistic as possible. In the story, the players find an old laboratory where genetic mutations were studied, but as the electricity is off since 40 years, most of the embryos are "rotten". I still need to have some embryos still "fresh" so someone could get DNA from it and continue the experiment.
Problem is, I thought about formol (the experiment is supposed to have taken place in the 1980's, so the health problem is not one right now), but I've read that formol alters and destroys the DNA. I've seen older ways with alcohol, but the process doesn't seem as efficient.
What liquid (or technic) could have been used in the 80's to preserve embryos and their DNA so we could still exploit it 40 years later, and with not electricity?

There are a few plausible ways:
As someone mentioned in the comments; Alcohol works well for this. We have samples from a hundred years ago (e.g. Thylacine), which have been stored at room temperature in a museum for that period of time and have had DNA easily extracted from them.
Unfortunately for many species, alcohol preservation fell out of favour due to it shrinking (by dehydration) specimens, so that they no longer look "realistic" in terms of morphology (something that is very important for classical identification methods). In addition, ethanol and other alcohols tend to evaporate fairly fast if not sealed properly. For these reasons aldehyde based solutions came into favour about 100 years ago. The downside to this is that formaldehyde and other aldehydes cross-link the genetic material, making it more or less impossible to extract and use.
Another possible method is dehydration - mummification. Small samples like embryos or tissues can be dehydrated quite fast. In the absence of water, these samples should last more or less forever - we can extract DNA from mummies in many places around the world, but these ones might interest you in particular.
There are also specialist chemical solutions such as RNAlater that are routinely used in labs for preservation of precious genetic material.
Given that we knew these sorts of things in the 1980's and that the lab was staffed with competent scientists, and that they knew that the lab was going to shut down but would re-start at some time in the future, then it is entirely plausible that they would have used alcohol or something like RNAlater.
In the absence of this knowledge, but still competent scientists, it is much more likely that they would have used some sort of cold (frozen) storage method;  whether this was cryopreservation (liquid nitrogen), such as is used for storage of cells or a specialist -80 $^\circ$C freezer or a -20 $^\circ$C freezer like you might find at your house. Some samples may have been still stored in chemical preservation in the interests of space-saving in freezers though.


Does this patient have HHV6 or HCMV after transplant surgery? I have been given mock results from a PCR test on blood samples taken from kidney recipient patients and their donors. The PCR reaction can detect single copies of viral DNA. I have been asked to determine whether 5 patients have been infected with either human herpesvirus 6 (HHV6) or human cytomegalovirus (HCMV) following kidney transplants. I have results for patients pre-transplantation and 1/3 weeks post-transplantation.

The results are as follows:

Donors:

Donor for patient A = HCMV+
Donor for patient B = HCMV+ & HHV6+
Donor for patient C = Neg for both viruses
Donor for patient D = HHV6+
Donor for patient E = HCMV+ & HHV6+

Recipients:

Patient A = HCMV+ before and 1 & 3 weeks post-transplant
Patient B = Neg for both viruses before, then HHV6+ at week 1 & HCMV+ at week 3 following transplantation but negative for HHV6.
Patient C = HHV6+ before and 1 & 3 weeks post-transplant.
Patient D = HCMV+ before and HCMV+ & HHV6+ 1 & 3 weeks  post-transplant
Patient E = HHV6+ before and HCMV+ & HHV6+ 1 & 3 weeks  post-transplant

Answers: I am guessing that Patient A was re-infected by donor A. Patient B was neg for both viruses, developed HHV6  week 1 but this test was neg week 3 & instead positive for HCMV – these viruses do not disappear, you either have it or don’t so assuming there is no contamination error then what virus did he develop post-transplant?? Patient C was HHV6+ prior to transplant but donor is neg for both, so what virus did he develop following transplant? I can see that Patient D was infected with HHV6 from donor post-transplant. Patient E was infected with HCMV from donor post-transplant.

I am struggling to determine what virus Patient A, B and C was infected with following transplant. Can anyone help? I know almost 100% of us are infected with both viruses but do not cause disease in healthy people, that both latent and active viruses show positive when in blood and that both viruses can re-activate under certain conditions such as via infected organ transplants and immunosuppression.

I get the feeling that there's something we should probably know from your textbook or notes that you have not included. As-is, here's my best shot:

It is impossible to determine if Patient A was infected by the transplant since the virus they had before the transplant is the same virus carried by the transplant itself. Without running further tests to separate the two lineages you can't tell. It's likely, though.
While HHV6 has been known to precede HCMV in certain cases the conditions don't seem to apply here. My best guess, which is something I'm pretty loathe to say, is that if you're positive the tests are accurate then it's possible that Patient B's immune system alternately suppressed each virus below detectable levels. Since Patient B is receiving donor tissue with both viruses, and transplant patients are put on immunosuppressants following surgery, it could simply be that at first the immune system was capable of dealing with HCMV for the first week, but not HHV6. Then as it adapted to HHV6, HCMV evolved to evade so it showed up on the assays. That is entirely speculative, though. Another explanation might be that the viral titers of HCMV were too low to detect at Week 1, but it had reproduced enough to show up at Week 3 while the immune system dealt with HHV6. There's a lot of information that's missing on how the virii behave, the characteristics of the immunosuppressants given to the patient, and so on.
Patient C was clearly infected with nothing. They already had HHV6, and that's what showed up post-op.
Patient D was infected with HHV6. They had HCMV before, and both after.
Patient E was infected with HCMV, although like Patient A they could have been infected with a different strain of HHV6 as well, but the tests probably aren't specific enough to determine viral lineages for the before and after strains.


What are key factors when evaluating and comparing miniprep columns? I'm looking to comparing different protocols for minipreps for plasmid DNA purification. What factors should I be looking at? A few things come to mind:

Cost
Yield
Time per step
Replacement with other reagents
Spin vs. vacuum
Color and caps or lack thereof

Storage conditions and shelf life are some of the things that you should consider in comparing columns.


Would non-human carnivores be able to survive on farmed foods? Certain creatures that are considered carnivores are non-obligate carnivores and are technically omnivores (such as wolves/dogs).  How different is the potential digestive ability of these species compared to humans?  If they theoretically developed sapience and the intelligence for agriculture, would they be able to survive on the same wide variety of plant foods that we do (i.e. could wolves survive on wheat, rice, etc)

The foods people in the developed world typically feed their carnivorous pets (including dogs and cats) are not made primarily from meat.  Instead, they are made from plants, specifically grains, such as corn, rice and wheat.

In order to get our pets to eat foods that are so different from the meat-rich diets of their ancestors, we add flavors to the food.

Check out this episode on the making of pet foods from the television series "How Its Made", http://www.youtube.com/watch?v=220PSFJWHao.

So, to answer your question directly-- yes, in places like the USA, domestic dogs and cats are already living on a diet that is almost entirely plant-based.