text:
What is this bug?
I recorded a video of this bug:

https://youtu.be/0eoWfHLEo7A
I counted 8 legs, the front legs are a little curved. The drawing on the flat back is dark and looks like the image of Jesus with some light from behind, hahahaha. I found it on the curtain of my bedroom. I believe it belongs to some tree where it can use its camouflage. Can anyone identify it?
Location: Valencia, Spain.

Where (geographically speaking) was it found?

Grao de Gandia, Valencia, Spain.

Welcome to Biology S.E.! If you need any assistance, please visit The Help Center.

I think it looks a lot like a European Pigeon Tick (Argas reflexus).

They infest pigeons and they die when infesting humans, which they only do if they are very hungry (yours looks hungry though).
May also transmit diseases.
Edit:
It could also be an Blyborough Tick (Argas vespertilionis). They infest bats and are a little rounder in shape but look otherwise similar.

Thank you very much! I'm glad I killed it in time. Although it went inside a hole and I had to stick something to kill it.

By the way, we live close to a park full of bats and some have tried getting in. So, it is highly likely to be an Argas vespertilionis

My best guess is a soft-bodied tick, perhaps of the Ornithodoros genus, although the determination of the species is a little more difficult. Though, if it's O. erraticus they're known for causing african swine fever in Spain and Portugal (1).
Ornithodoros
In response to the comments, here's a link from Texas A&M which notes the ticks pump waste+water back out into the host, and this is why they transmit so many infections.

That wiki page says "The opening between the midgut and hindgut has been lost, making the ticks unable to pass digestive waste products out of their bodies", so do these ticks just fill up with waste?

If that is true, no doubt why they carry diseases and viruses.

@user137 I've updated the answer to respond to your comment. The ticks pump the waste back into the host.

@Kendall That makes these ticks even worse.


text:
Who are these biologists?

I know the third one in the front row is James Watson.
Does anyone recognize the others?

This has no relevance in biology

Should we put the species-identification tag?

While not being an ideal question (where and when was the photo taken? why do you want to know?), I still think these kinds of questions should be allowed here. We have the history tag, which is relevant for this Q (history of biology), the Q has a definite answer, and BioSE should be as good a place as any to ask about the identification of prominent biologists.

I agree with fileunderwater. I vote to reopen

Without the context of where (geographical location + setting) and when this photo was taken - I vote to leave closed on the basis of being unclear what you are asking -slash - homework (no effort whatsoever / poorly researched)

Sitting next to Jim Watson is another Nobel Laureate, Wally Gilbert (on the right in the photo) but actually on Watson's left.

Plus there is a History of Science and Mathematics SE site, so wouldn't it be best to keep this question there?

Front row, left to right; Victor McKusick, Maurice Wilkins, James Watson, Walter Gilbert and John Kendrew.

Great! +1 Do you know where/when the picture was taken? Seems to have a high density of Nobel laureates.

Unfortunately I was unable to find any context for this photo, I just recognized the scientists. It appears to be a relatively formal meeting and most of them are molecular biologists/geneticists, but I'm not sure why they would be holding papers if it was anything but an experiment (though I can't imagine what experiment they would attend that involved molecular biology) my only other guess would be perhaps some sort of a conference because they all seem to be taking notes and looking in the same direction. Again, I'm not sure. I apologize for not being able to find anything on it.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
Hopeful Monsters in Plants?
Does anyone know of any research/examples on Hopeful Monsters in Plants?
I define Hopeful Monsters as organisms of a species that have macroevolutions to prompt new speciations. These macroevolutions being themselves, prompted by smaller gradual microevolutions in the species. See this paper for more details. I'm interested in a plant based example, or any good recent example, if plants can not suffice. Ideally research that is easily read and recent, and useful for arguing the existence of themselves?

Could you please add more context to your question? I'm not particularly familiar with the term Hopeful Monsters.

I found a review on the topic for those who are also not familiar of the different versions of evolution theories: http://www.evolocus.com/publications/Theissen2006.pdf

@poka.nandor       I define Hopeful Monsters as organisms of a species that have macroevolutions to prompt new speciations. These macroevolutions being themselves, prompted by smaller gradual microevolutions in the species. I want a plant based example, or any good recent example, if plants can not suffice.

I didn't the term "Hypoeful Monsters" before. From Wiki, the term "hopefull monsters" designate a concept (a hypothesis) and not an organism. In the same logic, the term "macroevolution" has a meaning that depends only on the observer and not on the underlying evolutionary processes. It means "evolution observed at a scale of separated gene pool". In any case, the term "macroevolution(s)" as a noun don't have any meaning to my knowledge. What do you mean by "macroevolutions"? Also, what do you mean by "microevolutions"?

I've edited these extra info along with the paper I found into your question, so it has all these details and don't get lost in comment section. You can roll back at any time if you wish.

Is your question "Can you give examples of plant lineages that underwent major mutations (such as chromosomal rearrangement or hybridization or change in ploidy level)?" or maybe it is something like "Can you give examples of plant lineages which fundamental niche has suddenly and drastically changed in response to a single (or few) mutations?" or stated differently is would be "Do you know examples in plants lineages of mutations that had a major impact on the ecology occupied by the species?"

What do you mean with a species having "macroevolutions" that are "prompted by smaller gradual microevolutions"? This doesn't make any sense to me.

@fileunderwater   Sorry, I am not too great with biology( im a stupid undergrad). Can a species have macroevolution happen to it? Am i phrasing it wrong? If a species can have macroevolution happen to it, can then this macroevolution be caused by microevolution(small, gradual, changes in  allele freq in a population).

@RoSiv Macroevolution is mostly a label describing a level of studying evolution (macroevolution ~= evolution above the species level), and not a type of evolutionary change. Most evolutionary biologists would find it rather meaningless to talk about macroevolutionary changes "happening" to  a species. Macroevolution is the accumulated  result of many small evolutionary changes (i.e. microevolutionary changes). So in that sense, macroevolution is caused by microevolution. Sure, some  single mutations can have larger effects than others, but this is not macroevolution.

@fileunderwater   Can I ask you then how you would define and relate the four terms, Hopeful Monsters, Macroevolution, Microevolution, and polyploidy? So that I can get a solidified view on this, because to be honest I have some confusion with the concepts now. Thank you.

@RoSiv A starting point for the relationship macroevolution and microevolution (or simply just evolution) can be found in my previous comment. I hadn't heard about "Hopeful monsters" before, so I cannot really say anything about that. Polyploidization is a full genome duplication (polyploidy is just the state of having more than two homologous chromosomes), a common cause of speciation in plants and a good example of a single event that can have large evolutionary consequences.

I am not sure what your question is but here is an example that may interest you.

The three sunflower species Helianthus anomalus, H. deserticola, and H. paradoxus are all of hybrid origin of the same two "parent species" (H. annuus and H. petiolaris).

Major ecological transitions in wild sunflowers facilitated by hybridization is a paper that will likely interest you. This paper has been written by L. Riesberg and colleagues. You may want to read through some of the work of L. Rieseberg (CactusWoman already linked one of his articles).

One example of what you may consider to be a macroevolutionary change is a whole-genome-duplication, or polyploidy event. These are not uncommon in plants, and can promote speciation due to a reproductive barrier arising between the polyploid progeny and the diploid parents. You can find many papers about this topic, here is one from 2009: http://www.pnas.org/content/106/33/13875.short

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Are there single-celled organisms that have evolved from multi-cellular ones?
I'm reading this paper about transmissible cancer cells in clams (Metzger et al. 2015) and I was wondering if there are any single-cellular organisms that are around today that are suspected as having descended from a multicellular organism
My question is different from this question as I'm not asking about cancer specifically but rather single-celled organisms evolving from multicellular organisms in general.

Related Post: I am not sure if I can call this a duplicate.

@WYSIWYG I think the answer in the related post answers this question, but the question is different. Not a dupe question, therefore, if you ask me. Given the quality of both questions and answers I would definitely not vote for close as dupe

I would consider HeLa cells to be an example of a unicellular eukaryotic organism that evolved from humans. It can survive independently and replicate within cell culture plates, but cannot survive in the wild, however.

HeLa cells are, like in your example, cancer cells, in this specific case human cervical cancer cells. They were propagated as an immortal cell line, and completely match the replication characteristics of eukaryotic cell lines when propagated in the laboratory.
It can be even considered the case that HeLa cells are actually a kind of unicellular eukaryotic model organism not unlike S. cerevisiae, since they are widely used in experiments involving human-like cells.
As WYSIWYG has said in the comments, some biologists have even assigned the binomial name Helacyton gartleri to the cells (albeit with some controversy).

Hela cells have a scientific name: Helacyton gartleri. They are classified as a separate organism because they can grow beyond human control and have chromosomal differences compared to a normal human cell.

@AliceD http://en.wikipedia.org/wiki/Directed_evolution

Great answer and thanks guys for explaining. +1 here!

Excellent, this is very interesting, especially that some biologists consider them to be a separate organism. Very interesting that they can survive in culture. I'm wondering if there are other examples (discovered or undiscovered) of single cells that broke off and can survive in the wild

great perspective, thanks for sharing! also, thanks go to @WYSIWYG

@MarchHo Thanks for adding that the classification is in some controversy.

This is very interesting, but the OP only contextualized this with cancer. The question seems to instead be about natural occurrences of reversion from multicellularity to single celled organisms. (The Tasmanian devil answer is more along the lines of the question posted, despite being in the context of cancer.)

Inspired by the answer by @MarchHo, I came to think of the contagious cancer that attacks Tasmanian Devils - Devil facial tumour disease - which should provide a very similar example to the clams in your question. I don't think it has been given a species name though, but for most purposes it functions as an independent species. This "organism" lives as a parasite on Tasmanian devils, but has originated from a cancer tumour in an individual Tasmanian devil. You could maybe argue that it is not single-celled, since it develops into tumours, but it most likely spreads as single cells and I suspect that the cells functions as independent entities. However, I don't know enought about the disease to really say if e.g. cells in the tumours differentiate into different types. The cancer is spread by bites, and only affects Tasmanian devils (see http://www.tassiedevil.com: The Disease). This disease is apparently one of only three known cases of contagious cancers (also in dogs and hamsters), but this is maybe 4 now if the clams are a similar case).

(picture from Wikipedia)


text:
Why does the membrane of a neuron not stay at its depolarized state?
When an action potential is transmitted along the axon, the membrane reaches its depolarized state by opening Na+ channels. Both K+ (potassium) and Na+ (sodium) are now on both sides with close to equal concentration-ratios. It is the next step that confuses me: the K+ rushing out of the cell, thus repolarizing the membrane.
Wouldn't the two substances balance themselves out according to the Electric-/Substance-Concentration-Gradient once the Na+/K+ channels are open? I don't understand where that energy comes from, the energy that not only mediates polarization, but also the subsequent re-polarization.

I edited the question to improve clarity. If the current question does not reflect your original question anymore feel free to roll back

As a short answer: K+ is high in the cell, so it rushes out along its concentration gradient

Three facts:

The K+ ions are heavily concentrated on the inside while the Na+ ions are heavily concentrated on the outside

The Na+/K+ ion pump is unidirectional. It can only pump K+ ions inside the cell while expelling the Na+ ions.

Finally only the Na+/K+ ion pumps can restore the ionic equilibrium.

The full scene:

Once the threshold is reached the Na+ voltage gated channels open up. So Na+ ions rush in, causing depolarisation.

Then the Na+ channels close while the K+ channels open. This causes rushing of K+ ions outside, thus slowly reducing the potential difference starting the process of repolarisation

Now the Na+/K+ ion pumps are geared up as the extracellular concentration of K+ and intracellular concentration of Na+ ions are high (which is the ideal environment for the pump to work.

PS:
Without the high extracellular concentration of the K+ ions the pump can't function any faster than the basal rate even though the intracellular concentration of Na+ ions exceed the normal value by many times. High concentration of K+ ions in the extracellular environment is essential for restoration of the ionic equilibrium.

Edit:
I meant unidirectional in the sense that when actively pumping sodium is always pushed out while potassium is always pushed in.
Thanks to AliceD for pointing out that when the gradient is reversed, the pump synthesizes ATP due to forced movement of ions in the opposite direction.

Correction - Na,K-ATPase is not unidirectional - it is an enzyme, which per definition means it establishes a certain equilibrium. In effect, Na,K-ATPase is an ATP synthase under the correct conditions, such as reversed Na/K gradient: http://link.springer.com/article/10.1007%2FBF00592639

@AliceD I meant unidirectional in its pumping action. Though synthesizing ATP when gradient is reversed is new to me! Thanks for that!

@OneFace Reverse behavior takes many interesting forms. ATP synthase in mitochondria can become proton pumps, for example.


text:
Why is it harder to sequence plant genomes than animal genomes?
Plants seem to be less complex organisms than animals, but despite that there are less plant genomes sequenced. Is that because plant genomes are more complex, for example in terms of regulatory regions and transposons that make sequencing more difficult, or are there other reasons why the number of sequenced plant genomes is smaller than animals?

I edited the question to improve clarity. If the current question does not reflect your original question anymore feel free to roll back.

I know the genomes tend to be much larger, and often have many more copies of the genome than animal cells.

There are multiple problems. One already mentioned is polyploidy, another is the fact that plant cells have cell walls and it can be tricky to extract DNA without fragmenting it too much. Also, some plants have quite a lot of repetitive sequence which makes it harder to assemble. But as with every other organism it also depends on the plant, the variety, the technical possibilities one has and much more.

The authors of this 2012 review article summarize the problem well in their introduction:

In contrast to the tremendous advances in throughput, assembling sequencing reads remains a substantial endeavor, much greater than the sequencing efforts alone would suggest [22-24]. Large complex plant genomes remain a particularly difficult challenge for de novo assembly for a variety of biological, computational and biomolecular reasons. Plant genomes can be nearly 100 times larger [25] than the currently sequenced bird [26], fish [27] or mammalian genomes [28]. In addition they can have much higher ploidy, which is estimated to occur in up to 80% of all plant species [29], and higher rates of heterozygosity and repeats [30] than their counterparts in other kingdoms. Furthermore, the gene content in plants can be very complex, as shown by the presence of large gene families and abundant pseudogenes with nearly identical sequences derived from recent whole genome duplication events and transposon activity [13]. Plants tend to have high copy chloroplasts and mitochondria organelles, which complicate assembly of their remnants in the nuclear genome and skew coverage levels [12]. Finally, it is often very difficult to extract large quantities of high-quality DNA from plant material, making it difficult to prepare proper libraries for sequencing.

From: Schatz, Witkowski and McCombie. "Current challenges in de novo plant genome sequencing and assembly". Genome Biology (2012). 13:243
As you can see, all of the key reasons have been touched on by the various people who have commented below your question.


text:
Is there any alternative to cryopreserve cell lines without -80 freezer?
My university's -80 freezer just broke down and the repair will take 4 months according to the vendor. Is there any other way to preserve cells? Maintaining lot of flasks until the freezer is repaired is not viable option.
Is there any alternative to cryopreserve cell lines without -80 freezer?.

A tank of liquid nitrogen is not just an alternative, but a much better substitute, IMHO. The problem of gradually cooling inside a isopropanol container can be overcome by using a box full of dry ice (-79°C as I recall).


text:
Forensic genetics- why is mtDNA comparison sometimes better than nDNA comparison?
Why is (in forensic genetics) in some cases more appropriate comparison of nuclear DNA but in some other cases comparison of mitochondrial DNA?
Is it because geneticists are sometimes unable to find nDNA or if nDNA is too damaged? Also could it be because of the structure of mtDNA (it's more protected against degradation, which is good for identifying old biological material)? I can't see any other advantages, since mitochondrial DNA mutations occur frequently, due to the lack of the error checking, but are there any that I am missing?
Thank you in advance.

Degradation of mDNA is more difficult than nDNA as you said and it's present in more copies. But also, in some cases, when you just want to know the identity of the victim, and you already suspect who it might be, it can be compared the mDNA with the mother/brother/sister/grandmother. It can be useful as well to know the geographical ancestry.

mtDNA is present in a much higher copy number per cell than nuclear DNA.
According to this paper, there are approximately 4000 or so mitochondrial DNA copies per human muscle cell.

copy number of mtDNA per diploid nuclear genome in myocardium was 6970 ± 920, significantly higher than that in skeletal muscle, 3650 ± 620 (P = 0.006).

This makes it far more likely that a non-degraded copy of mtDNA exists, considering that there are normally only 2 or 4 copies of nuclear DNA per cell per locus for almost all kinds of cells.

Doesn't  a cell (or at least a human cell) usually have one copy of nDNA, only in phase S they can have two?
When would it have 4 copies?

@cherry8.8vanilla Humans are diploid, therefore "2 copies". Arguably if you consider the 2 alleles from each parent (which might be different) you can call it 1 copy as well.


text:
What is correct MVM vs. MMV?
I'm writing up a report and I see conflicts everywhere on the internet. Should it be Murine Minute Virus (MMV) or Minute Virus of Mice (MVM).
The followup question is does it really matter.

i would say no, but just an opinion

According to the International Committee on Taxonomy of Viruses, it has had several official variations of that name over the years:

Minute mouse virus
Minute of mice virus
MVM Virus
Minute virus of mice
Mice minute virus

The current (2014) accepted name is: Rodent protoparvovirus 1
"Does it really matter?" As long as you write in full the name you're using the first time you use it, people will know what you're talking about. However, for consistency amongst current literature, perhaps we should all strive to keep up with current taxonomy.

Given the wide variety of academic sources using each abbreviation, it's fairly clear that there is no standardised usage; as such, as long as you state the full phrase the first time you use it and use whichever form you pick consistently throughout your report, it doesn't really matter which you use.
To avoid confusion, I would recommend mentioning that both are used to refer to the same thing the first time you introduce the term.


text:
What is the purpose of using two layers of gel in SDS- PAGE?
I just made a SDS-PAGE with a top layer of stacking gel and a bottom layer of separating gel with different pH values of 0.5M Tris-HCl. The stacking was 6.8 and the separating gel was 8.8. What about this pH change makes the gels different? What effect does this have on the proteins that I ran?

The stacking gel concentrates proteins loaded into the sample wells so that they are resolved as a unified "line" once they enter the stacking gel.  The reason for the lower pH is that this "lower ionic strength implies higher electrical resistance and consequently a higher electric field, provoking the faster movement of the proteins and of every other charged particle in the gel. Such a high electric field coupled with the glycine in the running buffer (that will not go into the resolving gel due to the pH), helps to clean the sample from the Cl- ions from the Tris-HCl buffer. That concludes in a stack of clean, denatured, and equally charged proteins in the boundary with the resolving gel; this will account for a good quality PAGE."
Bassically, in the stacking gel the pore size is larger so it gives a chance for the larger proteins and smaller proteins to equalize with each other.
"As the proteins are denatured and linearized by heating, SDS and dithiothreitol (if there is any di-sulfide bond), the proteins are loaded onto the wells on the stacking gel. The denatured proteins have a uniform mass to negative charge ratio. Since the current run from negative (top) to positive (bottom), the proteins move toward the bottom. When the electricity is turned on, the proteins and Tris-glycine enter the stacking gel. In stacking gel with pH 6.8, the N-terminal amino group of the proteins and amino acids are protonated at equilibrium which makes them less negative. The average electrophoretic mobility is very slow. A Gly-chloride ion boundary is formed since glycine moves slower than chloride ion. However, glycine still runs slightly faster than other proteins. As a result, the glycine keeps pushing the protein towards the chloride ion. In other words, the proteins are trapped between glycine and chloride ion. The proteins form a very tight band inside the stacking gel.
Once the protein reaches the resolving gel, the pH changes from 6.8 to 8.8 and the pores are smaller. As pH increases, the N-terminal amino groups are deprotonated. Amino acids and proteins are more negatively charged at equilibrium than in stacking gel. As a result, glycine moves faster than proteins. Glycine and chloride ions move ahead of the proteins. As the pores are smaller in the resolving gel, the size of the protein determines the mobility (speed). So the smaller the protein is, the faster it will reach the bottom."
SDS-PAGE stacking gel

The other major difference between the two is the amount of acrylamide in the upper (stacking) gel - it's generally around 4%, while the lower (resolving) gel can vary from 6 or 8% to 20%, depending on the size of the protein(s) you're looking for.
When you load your samples in the wells at the top of the gel, then start the current, not all of the sample enters the gel at the same time. The purpose of the stacking gel, with its lower pH and low acrylamide percentage, is to "stack" all of the proteins in your sample into as narrow of a band as possible, so that they all enter the resolving gel at essentially the same time. If you didn't have that stacking gel, your band(s) of interest could be very diffuse, and may not match up with your molecular weight marker.


text:
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.

To be fair, genetic analysis of dinosaurs would be very very hard, phenotypic comparisons are probably the best we can ever do.


text:
Genetic Relationship Matrix
The classical definition of the Genetic Matrix
G = ZZ'/2p(1-p)
where Z = M - P
where P = 2(p-0.5)
I don't have a background in biology but understand Maths and Computer Science very well. I am trying to wrap my head around
1) Why do we define P the way we do?
2) Why do we subtract  P from M
3) How to interpret a negative entry in G?
4) Does the j,k element of G give me the genetic distance between j and k individuals?

Welcome to Biology.SE. What is P? what is M? What is this genetic matrix suppose to represent? Is it a matrix of genetic variance and covariance for $n$ traits? Can you link to where you found those things?

Sure, here it is. http://nce.ads.uga.edu/wiki/lib/exe/fetch.php?media=uga_3_relationship.pdf

Any clarifications you could provide would be much appreciated.


text:
Why do plants produce so many hybrids as a kingdom?
Why do plants produce so many hybrids? I have read that they are the largest kingdom of organisms to do so. Does this have something to do with polyploidy events?

Might be a bit related

Yes, it has very much to do with the poliploidy events. Specifically if you look at the grasses, most grasses that are diploid (eg., AA, BB), cannot hybridize, but in some rare events when they form polyploid (AAAA, BBBB), they can readily hybridize to form fertile progenies (AABB).

Do you have a citation for this claim?

I don't have the citation, but I recently attended a talk by Dr. Kellogg, who talked about this. I think her paper talks about it briefly.

I found no evidence to your claims in the paper you linked. thus -1, I'll revoke if you can point me to it.


text:
Do macrophages get nutritional value from the pathogens that they eat?
X-posted on reddit AskScience here.
I know that macrophages engulf foreign bodies and transport them to various waste excretion pathways (sorry if the terminology is wrong), and if the foreign bodies are cellular in nature, they get trapped in phagolysosomes and get digested by enzymes.
Does the macrophage get any "nutrition" by destroying the cells, the same way that a person would if those same cells were to pass through their digestive system? Is there any chemical energy produced by the catalysis that the macrophage then uses, e.g. pyruvate for its mitochondria? Or scavenged cellular components that it can use to build its own cytoskeleton?

Maybe there is a study showing if  labeled phosphate of phagocytosed bacteria ending up in the macrophage DNA or mitochondria? I will search for this.

In this article it is described that starved macrophages 'consume' heat inactivated bacteria through phagocytosis with enhanced ability. Starving can also induce (macro)autophagy and the pathways are connected with phagocytosis,in the macrophages under investigation it was shown that autophagy did not play role in the enhanced ability of phagocytosis. The paper however does not mention anything about macrophages utilizing the resources obtained by the digestion of the bacteria. although it would seem logical. I'll keep looking.
Edit:
I found a text book that says:

in general cells of the macrophage series have two major functions. On f their functions ,as their name ("large eater") implies, is to engulf and, with the aid of all the degradative enzymes in their lysosomal granules, break down trapped materials int ismple amino acids, sugars and other substances, for excretion and reutilization.

Source : IMMUNOLOGY A Short course 3rd edition by Eli Benjamini, Geoffrey Sunshine and Sidney Leskowitz 1996 pages 23-24. ISBN 0-471-59791-0. I only have printed copy, but I'll try to find online version.
The other function is antigen presenting.
Thus I can say that yes macrophages and other cells do utilize resources from digested pathogens.

I've found an old paper using radioactively labeled bacteria to track their fate in macrophages. According to the data, both $^{14}$C and $^{32}$P are reutilized in the host cell.
COHN ZA. (1963). The fate of bacteria within phagocytic cells. I. The degradation of isotopically labeled bacteria by polymorphonuclear leucocytes and macrophages. J Exp Med. Jan 1;117:27-42.

It would make sense that nutrients are consumed from the breakdown of the phagocytosed object. Gotta love some of these old papers probing fundamental (yet relatively minor, by today's standards) questions


text:
Does freezing microorganisms such as probiotics kill them?
Does freezing microorganisms such as probiotics kill them?  If not, what is the process that allows them to "come back to life" after the temperatures are increased?
As an example, lets say you freeze a yogurt (whether it be Greek, Australian, Turkish, Indian, Russian, European, or Western) and eat it while frozen.  Would the probiotics in the yogurt "come back to life" and be beneficial?
Specifically, I am referring to freezing refrigerated yogurts, and not products that are sold as "frozen yogurts".
What's the biological basis for this?

I can't say anything about the bacteria in yogurts (usually Lactobacillus) but labs routinely freeze E. coli to -80 degrees C without killing them.

@MarchHo Are those glycerol stocks? If so, the glycerol probably acts as a cryoprotectant. I don't know if anything in the yogurt would have similar enough properties to protect the cells.

This question inspired me to freeze some vanilla yogurt with added chunks of chocolate. No word on the bacterial content, but 100% of survey respondents agree that the results are delicious

@Luigi Yep!  For an even better culinary experience, stick a popsicle stick through the seal or lid before freezing it!  In a few hours, you'll have a delicious frozen treat on a stick!

I work for a probiotic manufacturer. We use a cryoprotectant in the process. We are able to freeze and thaw bacteria many times with little to no loss in cell count. Odds are most of the bacteria in your yogurt are still alive after you freeze it. If there is loss it is probably not much. Don't have any exact numbers, but know from experience.

Yes, they do. For a look at survival of Lactobacillus and other bacterial species after multiple freeze/thaw cycles, check out Harrison 1955 (below).
The awesome hand-drawn graphs show that many bacteria survive after being frozen for 11 weeks. There's also a figure on the following page showing that many bacteria also survive after multiple freeze-thaw cycles, but I won't include that page here for brevity.
Prof. Don Schaffner of Rutgers also supports this conclusion:

So it's possible, even likely, that frozen and thawed yogurt will contain
  living lactic acid bacteria, although it may only be 10% or 1% of the
  total number of bacteria that were there before the yogurt was frozen.

I couldn't find a great deal of official resources on the topic, hence the paper from 1955 and random quote from a food science professor. However, in a lab setting, scientists regularly freeze bacteria and even eukaryotic human cell lines. Usually scientists use a cryoprotectant like glycerol, but many foods (like yogurt and ice cream) may contain an FDA-approved cryoprotectant (Wikipedia):

One recent, successful business endeavor has been the introduction of [anti-freeze proteins] AFPs into ice cream and yogurt products. This ingredient, labelled ice-structuring protein, has been approved by the Food and Drug Administration.

So, yes, at least some of the bacteria in your frozen yogurt are still alive, and will have whatever beneficial/harmful/lack of effect when you ingest them.

Judging from figures 1-3 above, bacterial survival depends on how long and how many times you freeze the bacteria. My rough estimates of the graph above say 40%-10% after a single freeze, and after multiple freeze-thaws getting into the 1% range. Also, it doesn't matter whether you thaw it first or eat it frozen as far as bacterial content is concerned, the bacteria will be unfrozen either way when they reach your digestive tract.

Thank you for your answer.  After reading your answer, I realized that my question needed clarification.  After you contributed your answer, I updated my question to clarify that I am speaking about freezing standard yogurts, and not products sold as "frozen yogurts".  It's a little unclear if your answer needs to be updated accordingly.  I'm sorry that my original question needed to be clarified.

Thanks!  Now the big question: how much survives?

Judging from figures 1-3 above, it depends on how long and how many times you freeze the bacteria. My rough estimates of the graph above say 40%-10% after a single freeze, and after multiple freeze-thaws getting into the 1% range.

Note that even 1% of bacteria left is still a lot of bacteria

When thawed, wouldn't the remaining (live) Lactobacillus grow and populate in the yogurt?

usually the growth of bacteria is slowed down as they are in freezing temperature and they almost carry out no metabolic reaction at this stage.but another problem occurs that is ice crystals formation which disrupts or pierce the bacterial cell wall causing the death of bacterial cells,this problem can be solved by adding  glycerol or any other cryoprotectant into it which will make the concentration equal,inside and out side the bacteria,thus bacteria will not be harmed.
in case of lactobacillus,they are psychrophile and also facultatively anaerobic so yes,they can survive in freezing condition
http://www.ncbi.nlm.nih.gov/pubmed/10843056


text:
GWAS: why is replication in another cohort so crucial?
Almost all the landmark GWAS (Genome-Wide Association Studies) reviews agree that, for a GWAS finding to be valid, it needs to be replicated in an independent cohort. What exactly is the rationale behind this? Is this criterion still valid even when the objective is looking for genes to do functional studies, instead of a clinical perspective of searching for susceptibility loci? Considering the difficulty in replicating some phenotypical characterizations in a large numbers of subjects, for a biologist this whole thing seems irrelevant.
Consider the following scenario: Suppose I have 5000 phenotyped individuals with a budget to genome-wide genotype them all. The phenotyping requires state-of-the art methodology with immense costs, and the cohort was phenotyped through another grant. What would be the point of dividing my cohort to two as a discovery and replication groups, other than to save money in exchange for stat power. To this, add the subsequent functional studies on the associated loci, what would the point in genotyping a few SNPs in 500 more people be? If one can indeed find that additional cohort, wouldn't it be a better option to combine any available cohorts in a meta-analysis, rather than using them for replication?

Think of it like this, if the study can't be replicated in an independent cohort, what does that mean for your results in terms of applicability?

Great question. The answer is non-random technical biases correction. Will expend on that in an answer as soon as I find some time. You are not supposed to divide a genotyped cohort in two, by doing so you might correct for population structure (and not really as you can correct for it anyways using a simple PCA based on the genotype) but definitely not for technical biases. Population might also be a reason but it is not the principal one (population specific SNPs are informative).

As an elaboration of my comment.
Summary: Replication is required in GWAS studies to account for non-random technical biases.
An example of such bias is, for example, a chip used for genotyping giving consistently incorrect genotypes for a locus. In this situation adding more subjects will not correct for this effect and therefore the only solution is to genotype additional subjects with another method (e.g. another chip or experimental protocol). Another source of non-random technical bias is at the phenotype measurement level. You might want, if possible, to measure the phenotype using other techniques to make sure that bias will be corrected.
A replication cohort does not need to be huge and the actual size needed will largely depend on the effect size of the SNP seen in the discovery cohort. A "power-to-detect" calculation would help in predicting the cohort size needed. For a SNP to be significant, it must pass Bonferroni correction but as you can run a statistical test at the candidate site only the correction will be usually not very astringent (i.e. you might run association tests on "only" a few dozens or hundreds SNPs).
Historically GWAS replication was also required to correct for population structure but as the tools evolved substantially (e.g. the use of principal component analysis) and the cohort sizes are now substantially bigger compared to the first GWA-studies, this is less a concern. What was required is to sample independently other subjects from either the same or a different population.
For your situation what you could do is to split your cohort into a discovery and a replication panel, genotype your subject in the replication panel using an independent technique, eventually do the same with the phenotyping and replicate you candidate SNPs. The replication panel needed is usually must smaller than the discovery cohort for the reasons stated in the previous paragraph.
For your last question about the meta-analysis. Yes this could also be a way to go but be careful that you will still need a replication cohort to validate SNPs found this way therefore resulting in the exact same problematic you described.
I hope this help!

As with all serious scientific result GWAS results need to validated by others. In this case it think is extremely important because these studies link mutations to diseases or in more general given genotypes to phenotypes, thus pointing out possible causes. So validating these results with the use of independent "samples" is indeed crucial. But as I said all serious (noteworthy) scientific finding should be reproducible.
Edit: the point in it is randomness and sub sampling. Such large cohort should not come from a small sub-population but many regions of the world, and by randomly dividing your individuals to two or even more groups you ensure that other background effects such as local gene allele variation frequencies, life-style differences etc average out. Imagine a scenario where you have 90 individuals in 60 of them you can link the genotype to the phenotype. that is 2/3 of the individuals. But if you take 3 sub samples of 30 individuals and get 7/23 , 17/13 and  6/24 (not linked / linked), that is 76.6% (23/30) , 43.3% (13/30) and 80% (24/30). From these you can get tbe same average of 66.6% but with standard deviation (15,5), and confidence interval not just a number.

Let me elaborate the question: Suppose I have 5000 phenotyped individuals with a budget to genome-wide genotype them all. What would be the point of dividing my cohort to two as a discovery and replication groups, other than to save money in exchange for stat power. To this, add the subsequent functional studies on the associated loci, what would the point in genotyping a few SNPs in 500 more people be?

Also, in the above scenario, where SNP chips costs much less compared to phenotyping individuals, wouldn't it be a better option to combine any available cohorts in a meta-analysis, rather than using them for replication?

It's not really due to population and sampling but rather technical biases. As you pointed out at such large population size (>5000) you are not expecting to get so much variation due to local population variation or sampling biases. Also reviewer don't ask you to replicate your results in another population but rather another cohort (could be the same population "type"). Last point, no you don't have to run a GWAS on people coming from all over the world, you can run a GWAS in a very specific pop if you want and replicate the discovered associations in a replication panel from the same pop.

I agree, yet I wanted to give a 'general-view' answer on doing paralells, rather than focusing the actual GWAS (as it is like any other experiment from this point of view) I totally agree with your last point, but again my aim was to emphasize the positve effects of diving your sample into sub groups.


text:
Current Trend in Evolution of Human Intelligence
Up front, I am specifically not interested in philosophical or ethical considerations re Eugenics and related concepts. In an effort to receive a concise answer I'll post a narrowly defined question following this preamble to set the stage.
Preamble:
In the movie Idiocracy there is a montage at the beginning "explaining" how the human population degrades, vis-à-vis intelligence, to an alarming (and absurd?) extent due to unplanned differential breeding resulting from several generations of the intellectually "more capable" people limiting their number of progeny, through active and passive family planning, while the bulk of humanity leaves caution to the wind. This exponential social differentiation eventually makes for a global imbalance that degrades our species' overall intellectual fitness to a debilitation level.
Question:
Is the premise of this movie merely a gag or is our species already doing something very much like this?
If yes or no, how might one measure the impact of differential procreation of this sort? Since testing results are always relative to the population as a whole and computers along with the Internet of Things would tend to obfuscate the initial degradation of mental capacity.
EDIT:
Based on the brief discussion in the comments - a summary of fecundity and IQ would potentially answer my question but only if it accounted for the current selection process we see going on in modern technophile societies. That is, it must account for the effect of our most educated couples generally choosing not to procreate and here I'm assuming there is in fact an effect (cf. Idiocracy for the (absurd?) degree to which the present-day trend may work itself out).

Welcome to Biology.SE! You might want to read about the Flynn effect

@Remi.b - Thanks. I was aware of this phenomenon. Thus my last sentence in the question that says, in part, "Since testing results are always relative to the population as a whole". This covers both the Flynn Effect and testing bias resulting from test design in a given culture. - --- - There are many ways of measuring welfare spending against population data but, all politics aside, it seems to me that the 50-year trend (which no one disputes) may be a proxy for an answer to the question I ask above.

Here is a Ted talk by Jim Flynn

@Chris (or Matt) --- I understand the Flynn Effect. I am not asking a question about it. --- What I want to know is if there are any published studies that are looking for the Idiocracy Effect. --- It's a well known phenomenon that kennel breeding in dogs (e.g.), if poorly managed, can engender many genetic diseases and otherwise increase susceptibility to health problems in general. --- Won't the same thing happen with humans? How is this controversial? --- I understand that such a question can engender poor quality answers but that's why I posted on a moderated forum.

Sorry, I was unclear. I really didn't mean that the links I posted would answer your question. I just hope it could eventually help. I know nothing on the subject. From wikipedia I read that it doesn't seem to have any correlation between fertility and IQ.

@Remi.b - Actually the comments attached to the Ted Talk helped the most but still leaves me hanging. I was hoping for something about "regression to the mean" ameliorating bad breeding choices over the long run and how that might apply to human culture generally under our current experimental regime. Something like that. --- I read the SE rules on how to ask questions and, reviewing them again just now, am still at a loss as to how this is a bad question... other than it has gotten zero answers but that could be because it's on hold. ?? O_o

It is not clear to me either why it has been closed. Would be good to give comments when voting for closing. Would a summary about the research on the correlation between fecundity and IQ answer your question? Eventually a discussion about statistical issues in these studies (I am assuming this is what you mean when talking about the effect of regression to the mean)?

@Remi.b - voted to re-open too. Without some constructive comments to improve it it deserves to be active

There appears to be some - note that this, of course, is highly controversial - evidence pointing at the direction that intelligence declined in the US and UK during the last century. There is a relatively new review by Michael Lynch (2016) in which he suggests that modern humans are accumulating slightly deleterious mutations with increasing rate due to relaxed purifying selection (a consequence of technology, medicine, ...), resulting in a 'future genetic load'. Let me just sum up some of the major points he makes that are relevant to assess current evolution of human intelligence:

Heritable mutations that lead to a reduction in fitness of 1% take about 100 generations to be eliminated by selection. Many of these mutations have a direct or indirect effect on the mutation rate (mostly increasing) and relaxed purifying selection on them might cause a positive feedback loop that causes even more mutations. Additionally, parental age increases the number of mutations passed on to the offspring. Most mutations will be slightly deleterious (keep in mind that the majority of new mutations is neutral, the majority of the remainder is deleterious and only very few mutations are beneficial. Therefore the really deleterious ones will still be selected against, but the slightly deleterious ones will not be removed by purifying selection). Accordingly, relaxed purifying selection increases the amount of slightly deleterious selection and decreases the efficiency of getting rid of them.
Lynch argues that the brain might be particularly sensitive to mutations as brain function depends on the finely tuned expression of thousands of genes which for him leads to the proposition that the effect of germline mutation rate on psychological disorders could be higher than expected by chance. In support, he cites Iossifov et al. (2015) who have suggested that autism spectrum disorders might be caused by de novo mutations in at least 30% of the cases and also looked at mutations interfering with IQ measurements.
Finally, he cites two papers that are of interest here as they deal with the change of intellectual abilities of humans over time (Crabtree (2013) and Woodley (2015)). The latter is a meta-analytic study based in the US and UK and Lynch already points out that there there are the usual issues with entangling genetic and environmental factors. However, in that study a slow decline of general intelligence of about 0.39 points per decade due to selection and about 0.84 points per decade due to mutational load is suggested. Interestingly, Woodley points out that there are two major hypothesis for this decline: (i) Since the industrial revolution people with lower general intelligence have higher average number of offspring (that might be the 'differential procreation' you have been hinting at). (ii) Mutation accumulation due to relaxed purifying selection against deleterious variants. Woodley concludes that the decline is a combination of both.

Of course, these points are strongly debatable. One of the major conceptual criticisms on Lynch's view is that slightly deleterious mutations (that Lynch claim to be accumulated as a consequence of relaxed purifying selection) are not slightly deleterious but totally neutral if they do not have a fitness effect. In terms of evolution it does not make a difference if an allele is neutral or negative selection is not acting on it because of technological interference. Another objection - more relevant to your question - is that measuring intelligence in general, or the IQ in particular, is a controversial thing to do and not at all easy to standardize which causes great difficulty in obtaining comparable data. Moreover, tracking down underlying genetics, estimating heritability of intelligence (a trait we even have difficulties to properly define and that is known to be strongly influenced by the environment), and consequently putting together a comprehensive assessment of the evolution of intelligence in humans is really tricky, set aside the ethical problems that may arise which we have not even touched yet.

A last note: In your edit you write:

[...] a summary of fecundity and IQ would potentially answer my question but only if it accounted for the current selection process we see going on in modern technophile societies.

This is problematic as to date it is really difficult, if not impossible, to detect recent selection. This is mainly due to the fact that most methods depend on detecting changes in allele frequencies over time and this needs a considerable number of generations to integrate over.
There have been some efforts to develop more accurate methods, but looking at selection in the last 100 years (which you would need to be able to when looking at the technologically modern populations) is not possible so far. The best attempt I am aware of so far is Field et al. (2016, preprint) who looked, based on genome-wide association study data, at recent selection in the last 2000 years. However, they do not mention intelligence.
Update: This paper was a pre-print. It is now published in Science: Field et al. (2016).

"One of the major conceptual criticisms on Lynch's view is that slightly deleterious mutations are not slightly deleterious but totally neutral if they do not have a fitness effect." -- This criticism of Lynch is not valid. In the absence of human culture the criticism would be true (a truism) but the non-natural selection imposed by human culture is precisely what I think would be interesting to measure.  -- And yes, the whole concept is "loaded", a politically correct bombshell. I hesitated asking the question for just that reason. You'll note the paucity of answers my Q has garnered!

@user23715: I see your point, but selection does not differ depending on the source of selective pressures. It is totally unimportant if we as humans classify it as 'artificial' or 'natural' selection. It is the same thing. This would only not be true if human culture would disappear instantly as this would take away the neutral status of some of the mutations Lynch considers as slightly deleterious. This is actually what Lynch is hinting at: Intelligence levels might drop so strongly that modern medicine cannot be maintained, exposing all these mutations. For me this is a bit far-fetched ...

Human selection, especially modern human selection, is more Lamarckian than Darwinian. -- It's possible genetic medical science will exceed our ability to harm ourselves through non-selective breeding. Maybe the next generation (or three) AI after IBM's Watson will get us what we need to keep from running off the cliff. -- I would think the rate of bad mutations would increase geometrically at some point so the cliff could seem far away and then... too late! -- Thanks for the answer. I'll let it sit for a week or ten but it will likely become the accepted answer.

@user23715: As you might have seen in my answer, I also still have to let it sit as it is a very difficult topic both scientifically (intelligence is the on of the 'worst' trait one can work with) and ethically. Interesting to think about though.

You're right that the Field et al paper is the best broad attempt at an answer. -- I found How fragile is our intellect? Estimating losses in general intelligence due to both selection and mutation accumulation to be useful too as a primer on the topic with an excellent short list of citations going back to the heyday of eugenics. -- As Woodley points out, this topic is critical to human flourishing; too bad the "well was poisoned" with politics in the 1920's/30's. -- Germline repair will be a worthwhile investment.

@user23715 My guess is that the advances in genetic research regarding intelligence will make it possible in a couple of decades to screen/select for intelligence. At that point someone will start providing services for future parents, perhaps in China and in Russia. The undeniable success will very quickly change the mind in the West because competitiveness is at stake. The hope is then that everyone has access to this technology so as to select/engineer their embryo/child, not just the rich.

@user23715 There is already evidence that average IQ is going down, despite the Flynn effect (the effect has come to an end, as the Flynn effect was most likely due to poor nutrition that afflicted the lower strata of the population). Rindermann has collected some data about this. As sad as it is, the modern welfare state we all treasure seems to have adverse effects. If you really want some bad news from the verboten corners of the internet, check out Nathan Cofnas, for some good news about progress in the science check out Steven Hsu.

@user23715 You might also want to visit Gregory Cochrane's blog. I think he discusses the paper you linked to and criticises it. Somewhere in his twitter feed there is a discussion of this paper with people disagreeing as to whether Woodley is too pessimistic or optimistic. One thing is for sure, the Flynn effect has not much to do with genetics. If it would, the constant rise in IQ that was observable for most of the last century would have lead to a significant increase in geniuses, and we failed to see that.

@AlexDeLarge You wrote "measuring intelligence in general, or the IQ in particular, is a controversial thing to do and not at all easy to standardize". Could you elaborate? It might be controversial in some circles but IQ research is some of the most robust research there is in psychology. And intelligence is actually quite easy to measure. For a good defense of psychometric testing see Russell T. Warne's "In the Know".


text:
Correct/complete representation of RTPCR statistics
In papers reporting a relative quantification of gene expression by RTPCR, I often see a bar chart with mean ± standard error or deviation, with the deviation belonging to biological replicates. This ignores all the previous layers of technical replicates. In the regular $2^{\Delta(\Delta Ct)}$ estimation with 3 reactions per primer/template, we have the standard deviation (SD) from each technical replicate, then the SD from normalization, end finally the SD from quantification. If the end results are fold changes, add one more layer to this. I'm not even including normalization with the geometric mean of 3 housekeeping genes (the better method)  How can I  correctly calculate / depict the statistical variations in this case?

Maybe these articles show relative expression changes between time points? In my institute we do these as well and the SD comes from the biological replicates in these cases. Also it might only be a data representation issue.

I think you can follow this method:

Test the statistical significance of a single experiment by comparing technical replicates (lets say Tests: T1, T2, T3 and Controls: C1, C2, C3). This will tell you if the instrument can reliably detect difference or not. Note that you should compare the relative expression (i.e. wrt your reference gene) and not the CT values. The ΔΔCt method is fine but you should note that it is not necessarily a power of 2; 2 denotes perfect PCR efficiency. See these posts:

Real time PCR normalization algorithm
Real time PCR standard curve

If the difference is found significant in all technical replicates then test the difference between biological replicates by using the means of the technical replicates in each experiment; for example mean of T1, T2 and T3 in biological replicate-a ($\bar{T_a}$) used as the sample value for that replicate. You can proceed with t-test for computing statistical significance which will tell you if the difference in expression is because of a random cellular behaviour or not. You can also do an ANOVA to compare the variance between technical replicates (within an experiment) and biological replicates (mean of the technical replicates between experiments). ANOVA lets you know some aspects of reproducibility of a measurement technique.
Fold changes (FC) are a problematic issue because many biologists seem to mess up with the interpretation of the data. First of all a t-test cannot be applied to FC directly (especially if FC is calculated pairwise for each replicate). Now all you have is a single random variable i.e fold change that you cannot statistically compare with anything. Fold changes are not really bad but I would recommend that a t-test be done between the control and the test samples and if the difference is found statistically relevant then report the FC. I personally know many people who do the other way round and set variance of the control sample as zero (because pairwise FC would be = 1 in all cases): This is a blunder.


text:
Do bacteria precipitate in static liquid culture media?
We performed 36h biofilm cultures and would like to know if this time is enough to planktonic bacteria to precipitate.
Since we observed biofilm formation one the surface of the microtiter plate. Were  biofilm bacteria derived from precipitation of suspended bacteria or rather replicated from some initial attached bacteria cells?
Specie: Haemophilus parasuis. A facultative anaerobe.

Maybe the question is irrelavant for the final outcome. The number of inoculated bacteria cells was so small that would not influence the numbers of biofilm bacterial cells observed, almost sure all were derived form initial attached cells.

You didn't specify the species, but I have left E. coli transformations (in 500µl of SOC) overnight due to rushing/forgetting to dispose of them after the transformation, and they were precipitated in the morning.

yup, e.coli for mini preps can precipitate pretty quickly (overnight growth in 3 mL culture). I notice clearing of media (sort of supernatant) after maybe 12-24hr. But other species might behave differently


text:
Organisms that contain rare chemical elements
By accident, I found a slide from a Polish chemical presentation, that talks about a small group of biological organisms which contain chemical elements not found in the human body, like:

B (boron),
F (fluorine),
Si (silicon),
V (vanadium),
Cr (chromium),
Se (selenium) and
Sn (tin).

Can someone provide a list of examples of organisms containing these chemical elements?

Our body contains quite some fluorine in bones and teeth...

There is separate wiki page on selenium in biology, and vanadium has this paper dedicated to it. Your assumption that these "chemical elements not found in the human body" is wrong.

Selenium is an essential trace nutrient, what makes you think humans don't have it? For example, we have ~22 (or 25, depending on how you count them) selenoproteins, each of which contains at least one selenocysteine amino acid which is a cysteine analog with Selenium in the place of sulfur. In fact, I would be surprised if any of these elements is not present (at least in trace amounts) in the human body. Do you have any references that support the absence of one of these?

OK. Thank you for your enlightening comments. However, this question is asking about non-human organisms, that contains these elements (for example, tin, which isn't mentioned yet in any comment or answer). You proven, that my assumption was wrong and probably all of these elements are found in human body, but question remains unanswered actually (with little exception for Thaina's answer and silicon).

In that case, please [edit] your question to reflect what you're currently asking. Most of the elements you mention will be present in, basically, most organisms. Which ones are you asking about? Oh, and this article suggests that tin is an essential nutrient in humans as well. Please [edit] and narrow the question down to something specific that we can answer.

This slide only says that these elements aren't used by all organisms there's nothing about small group...

All the elements you mention (B, Fl, Si, V, Cr, Se and Ti) are listed as (probable) essential trace elements in humans by the World Health Organization. The WHO document "Trace elements in human nutrition and health" mentions a host of studies addressing the functions of these elements in species ranging from bacteria and plants to primates. The following list provides some of the functions these trace elements have in humans:

Boron - essential for cell membrane characteristics and transmembrane signaling (Nielsen, 1991);
Fluoride - necessary for the prevention of caries and it is associated with bone health (WHO);
Silicium - probably essential for healthy connective tissue and bone (WHO);
Vanadium - possible role as an enzyme cofactor and in hormone, glucose, lipid, bone and tooth metabolism (WHO).
Chromium - essential trace element that potentiates insulin action and thus
influences carbohydrate, lipid and protein metabolism (WHO);
Selenium - essential component of one of the antioxidant defense systems of the body (WHO);
Tin - expected to have a function in the tertiary structure of proteins (WHO).

References
Nielsen, FASEB 1991; 5: 2661-7
WHO, Trace elements in human nutrition and health 1991

Silicon is not rare at all. Silicon Dioxide is Sand and Sand is content of every soil. Even just rice hull and grass blade contain silicon
If you just read in wiki page of silicon there you would see this

Silicon is an essential element in biology, although only tiny traces
  of it appear to be required by animals.[10] However, various sea
  sponges as well as microorganisms like diatoms and radiolaria secrete
  skeletal structures made of silica. Silica is often deposited in plant
  tissues, such as in the bark and wood of Chrysobalanaceae and the
  silica cells and silicified trichomes of Cannabis sativa, horsetails
  and many grasses

Also in each wiki page you place about each element. Some of them have content about biology/organism chemical component. Such as Boron and Fluoride. You can search their page with {organ} or {bio}


text:
How does a metronome help in controlling breathing rate?
I'm new to the Bio/Medical field so kindly bear with me. I am doing studies on volunteers to formulate algorithms for evaluating Respiration rate from ECG and accelerometer data. I learned about this device when I read this paper. I'd like to know how exactly the metronome device helps in controlling the breathing rate, how is it to be used and precautions to be taken?

The paper in question used metronome to aid test subjects control their breathing rate. This seems like a good approach, much better, than asking "please, breath with 0.1Hz frequency".

The subjects were asked to remain at rest in a supine position for 10 min, and then to control their respiratory rate with the help of a metronome at different breathing rates: 6 (near 0.10 Hz), 10 (near 0.16 Hz) and 16 (near 0.27 Hz) breaths/min.

Metronome is a device that produces any perceivable ticks (sound clicks or, maybe, light flashes can be used) with given and constant frequency. So patients were asked to synchronize their breathing with metronome clicks.
Only precaution in mentioned experiment is that high frequency of breathing can cause voluntary hyperventilation. Or if preset frequency is low and patient is trying to follow it, hypoventilation might occur. Fainting seems among the worst of consequences in both conditions (if person is relatively healthy).


text:
Fats as energy source
As we know that the preferred source of energy for our body (source) are carbohydrates but heart muscle is an exception and need some explanation for this exception, that why the preferred source of energy for  or cardiac muscle are FATS?

What is the source of this claim?

http://www.ncbi.nlm.nih.gov/books/NBK22436/ (point no. 2, last paragraph)                                                                                2. William's Basic Nutrition and Diet Therapy by Staci Nix , 13th edition. Chapter no. 2 Carbohydrates, page no 22.

Nice question! I've found a great article about fatty acid metabolism in heart muscle in healthy and disease conditions. As it is stated in this paper long chain fatty acids are utilized through beta-oxidation to meet the high energy need of continuous contraction. Beta-oxidation of long chain fatty acids produce far more ATPs than glucose. According to wikipedia:

For an even-numbered saturated fat (C2n), n - 1 oxidations are necessary, and the final process yields an additional acetyl CoA. In addition, two equivalents of ATP are lost during the activation of the fatty acid. Therefore, the total ATP yield can be stated as:
(n - 1) * 14 + 10 - 2 = total ATP or 14n-6 (alternatively)
For instance, the ATP yield of palmitate (C16, n = 8) is:
(8 - 1) * 14 + 10 - 2 = 106 ATP

While a single molecule of glucose produces 36 ATPs (under aerobic conditions)
Thus use of fatty acids (fats) in cardiac muscle is beneficial because of their higher energy concentration. Also it is noteworthy that this does not occur in isolation, so this is a response to contractile work and other competing energy sources (such as glucose, lactose etc). Also excessive uptake and beta-oxidation in disease conditions can even endanger cardiac functions. See details in the linked paper.


text:
Biofilm microtiter experimental design
We sequenced RNA using RNA-seq from biofilm (attached to bottom) and planktonic growing bacteria (supernatant) in 3 mL microtiter plates.
I'm not sure how is possible to obtain planktonic cells since they may have precipitated. For bacteria growing on the bottom I'm convinced these were derived from initial attached cells and then formed biofilms growing anaerobically (this is a facultative bacteria). However, since this bacteria is not motile, how is possible I obtained planktonic bacterial cells RNA? Maybe was a suttle layer on the surface growing aerobically. Wouldn't them have precipitated after the 36h of the assay?
Specie: Haemophilus parasuis. A facultative anaerobe.


text:
A non human adaptive behaviour with a spandrel
Is there any adaptive behaviour in non humans which, when it is functioning as it was selected to do, creates a spandrel behaviour?

In evolutionary biology, a spandrel is a phenotypic characteristic
  that is a byproduct of the evolution of some other characteristic,
  rather than a direct product of adaptive selection

One of the first example of spandrel that has been suggested by Gould was the genitalia of hyenas. At the time the term was created, behavioural consequences of having a big brain was a common example and of course, this does not concern only humans but many other animals.
The riddles on the knuckles is another example (that is not specific to humans only either). Those riddles are a by-product of the need the make movement with your fingers.
I am personally not a big fan of the term spandrel as used in evolutionary biology. This term easily leads to limit cases and it depends on how you define the phenotypic traits and the functions they serve.

then everything i a byproduct of some need. eyes -- byproduct of the need to catch prey. something wrong with that attitude...

I think indeed that this kind of terminology easily lead to some issue. But the example of the eyes doesn't jump to my intuition as being a by-product of catching prey.

i am over-stretching argument here. maybe, vision example is bad, but i do see general problem with such definition like for spandrel.

While some academics contrive spandrels or non-adaptive byproducts to account for human art and religion, actual empirical support in the scientific literature for non-adaptive byproducts, behavioral or otherwise, is virtually non-existent. The few papers that tackle this question tend to criticize the concept. In Adaptations, Exaptations, and Spandrels, lead author David Buss (1998) says, "Hypotheses about functionless by-products must meet rigorous scientific standards." (p. 542) He concludes, "We could not find a single example of an empirical discovery made about humans as a result of using the concepts of exaptations or spandrels." (p. 545)
Several proposed examples of possible phenotypic non-adaptive byproducts are male nipples, the navel, and the female hyena's gentalia, which is very male-like. However, there is no analysis in the peer-reviewed literature that meets the scientific criteria for these to be accepted as legitimate non-adaptive byproducts, and there are good reasons why they are not non-adaptive byproducts. The non-adaptive byproduct or spandrel is much like the way in which religion solves the mysteries of life: it is inappropriately utilized to construct answers in the absence of better explanations.


text:
What determines the spiral direction of plants?
Some plants and vines spiral clockwise as they go along (right direction) and some spiral anticlockwise (left direction). What determines which direction they spiral along? At first, I believed it to be determined by which hemisphere you are in (influenced by the Coriolis Effect), and this result could be tested by finding spirals in both northern and southern hemispheres and comparing their directions. However, the very first spiral I found seemed to cripple that idea.

The spiral I found spirals first in the right direction, then suddenly decides to spiral in the left direction, and then further along in the right direction again. Since the Earth does not arbitrarily change its rotational direction, this phenomenon must be explained by some other explanation. The change in rotational direction seems to be abrupt, almost like a catastrophic event. A few that I thought of:
1: Arbitrary. The spiral seeks merely to latch onto something, and will try both directions to see if either work out.
2: The spiral is somehow influenced by the night day cycles. Since the spiral switches from right to left back to right having been subjected to two sudden changes, the only large changes I can think of is the day night cycle.
I live in Australia, by the way.

Relevant article: http://www.nasa.gov/vision/earth/livingthings/16jul_firemoss.html (moss grow in a spiral in microgravity conditions).

Sometimes called a 'genetic spiral'. Diection of helicity in various helical-patterns in living plants and animals usually solely depends upon genetic make-up.

Related: https://en.wikipedia.org/wiki/Tendril_perversion

Related: https://en.wikipedia.org/wiki/Helix

Wikipedia article on tendrill perversion, deals it in a way that it is yet not explained.

Also read related articles on sinistrorse and dextrorse vines. on http://www.biologydiscussion.com/shoot-system/stems/forms-of-stems-erect-and-weak-form-with-diagram/13189 and https://www.wordnik.com/words/sinistrorse.

Note that the terminology "dextrorse vine" indicates a left-handed spiral!! and a "sinistrorse vine" indicates a right-handed spiral!! . This is because, when we use the term "dextrorse" or "sinistrorse" for vine, we consider the L/R dir. of bending while growing upwards, i.e. we are taking our eye down to upwards; whereas while telling "right-handed spiral or left-handed spiral"; we tell about "screw" direction, i.e. in what-direction turning the screw it will rise upwars, i.e. our eye downwards. I.e.  the frame of reference is opposite in the 2 systems. A bit trickey. Isn't?

Related : https://en.wikipedia.org/wiki/Chirality#Biology

This question is not 'wrong' from any viewpoint. Only, the hypotheses in te question, could be right-or-wrong ... that is why they are hypotheses, and included in the question.

Is the rare change in direction of spiral possibly due to the weather conditions of a particular day? Such as a cloudy morning in spring with a sunny late afternoon? Or any weather conditions counter to the seasonal daily normal weather?
Just an un- researched, unstudied thought while trimming my Wisteria!

First of all, you assumption seems to be incorrect. Plants in same part of the world can twine in opposite directions.
Little seems to be known exactly. Gravity has nothing to do with plant's chirality (or "handedness") or spiraling:

How plants do this is still unknown. Darwin proposed that it was "autonomously induced." This came to be known as the internal oscillator theory. In the 1960's the gravitropic overshoot theory explained mathematically how circumnutation could spontaneously occur as a result of forces related to gravity and growth. Recent experiments on the Space Shuttle have demonstrated that gravity is not necessary for circumnutation.

Here is another link to a blog, but it does contain reference to original paper on observation of chirality. Main conclusion, taken from the abstract, is:

The predominance of right-handed helical growth in climbing plants cannot be explained by hypotheses attempting to link plant growth behaviour and global location. One alternative hypothesis for our findings is that the widespread phenomenon of anticlockwise twining arises as a function of microtubule orientation operating at a subcellular level.

To elaborate a little on that, remember that actin filaments as well as microtubules are all chiral polymers. That is, they form spiral structures with defined orientation. Even more, microtubules all start roughly from the nucleus away to membrane, so this might suggest cellular mechanism for preference toward twining chirality. However, this does not address your observation that given plant changes direction of growth twice.

This answer is outdated; The mechanism has been identified recently, and published in Science. See below for an answer from user42885 that provides the explanation.

Having had a self-sown pumpkin grow in my back yard I can tell you what happened with the tendril in your picture.
The tendril started growing straight, with a couple of branches. When one of the tendril branches touched something (looks like the middle one in your picture), the tip began to curl as it grew, in order to latch onto it. Shortly after, the previously straight section of tendril began to contract, and in the process, to curl.
Curling helps the contraction process hugely. For each rotation in one direction, another part of the tendril has to curl the other way, since both ends are now firmly attached to something (the ground and whatever the end touched). Note that going from the bottom, the tendril curls three times one way (labelled right), five times the other way (labelled left) then twice the first way again (labelled right). There are a total of five rotations in both directions.
It would be interesting to see if every tendril starts curling the same direction as every other one, so maybe you can check a few different ones to see if this is the case.
The entire process is touch sensitive. The tips of the tendril will grow in the direction of what they are touching, so I would guess that the chirality would be random, depending on the particulars of how the tendril was touching the other object. I have, however, seen the tips grow back on themselves, causing one layer in one direction and another layer on top in the other direction, so it seems environmental, not predetermined.
Here is a link to a time lapse film showing the process in motion.

The math seems to add up. Interesting explanation!

Very interesting observation. Would be interesting, whether it is consistent with the recent Science publication, referred to in the answer of user42885, that provided a mechanistic explanation for the century old problem.

tendril coiling occurs via asymmetric contraction of an internal fiber ribbon of specialized cells. Under tension, both extracted fiber ribbons and old tendrils exhibit twistless overwinding rather than unwinding, with an initially soft response followed by strong strain-stiffening at large extensions.

Source: Gerbode et al. 2012, Science, How the Cucumber Tendril Coils and Overwinds (link to scientific article) (link to press article)
PS: I was searching for an explanation to the twisting, and came across the above article before this one. What a wonderful world that we all observed this phenomenon, and that our curiosity was excited by the observation. Thank you for the article.

So, this discussion began several years ago now. I recently decided to grow up, more than out, to conserve space. So, I've tried climbers more. When I had several different plants growing, I noticed they all climbed clockwise.
If the original author still lives in Australia,  I propose an experiment.
I live in the Northern Hemisphere,  just outside Vancouver, Canada. Australia and Canada have differing growing seasons. If we were to exchange seeds and observe the same seeds, from the same packages, and document their growth, it would rule out hemispheric affects.

We call this a common garden experiment

The best reading for the topic is "a comparison of chirality patterns of climbing plants in Peru and Brazil" from "assymetry in plants" which sais that:
The mechanical or physiological basis for dextral versus sinistral orientation of circumnutation among apically twining plants has not been determined, despite several papers on the topic in recent years ((Thitamadee et al. 2002, Kitazawa et al. 2005, Goriely and Neukirch 2006, Edwards et al. 2007, Mugnai et al. 2007, Edwards and Moles 2009, Isnard and Silk 2009, Stolarz 2009 Bastien and Meroz 2016, Smyth 2016). The majority of the data supporting a general hypothesis that twining is caused by microfibril orientation and their overlying microtubules is based on research on the roots and seedlings of mutant forms of Arabidopsis thaliana ...
Chapter 12 states that 80% of plants in brazil from 20 species have the same winding chirality.

I have been told that the direction of twist should be clockwise as long as the growth is vertical. This would mean the tendrils going out horizontal could go either way but the twisting vines should be prodominately clockwise as they grow upward. Googling pictures of American Bittersweet vines provides a good example of this.
Tendrils that have twists in both directions are better suited to holding up under tension as they tend to be able to just untwist without kinking when pulled on. You might see this occur during high winds for example. What I am suggesting is that tendrils may be a special case as they have a unique fuction and often a non-vertical orientation.

Welcome to Biology.SE! Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. In particular, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— This is a good example of how to format references. Thank you!

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


text:
How is instinct carried from one generation to another?
How can non-structural information, specifically instinct (a fixed pattern of behavior that an organism reverts to as a response to certain stimuli), be passed on from generation to generation (such as an unborn baby's instinct to begin inhaling and exhaling amniotic fluid while still in the mother's womb to "practice" breathing, a sea turtle's inclination to enter the sea after hatching, etc.)?
Does DNA have anything to do with it? I can't imagine what else it could be, considering that the genome is the only thing an organism passes on to it's progeny.

This stuff is hard-wired into either the organism's nervous system, or endocrine signalling pathways (e.g., hormones), or possibly a combination of those two mechanisms.  In that sense, yes it is encoded in the genome, but not in a language that we can understand or interpret yet. Also, don't overlook all of the macromolecules that the female provides to the developing egg during oogenesis, your mother gave you lots of things besides a copy of her genome--you just don't have any of those macromolecules left now--but you wouldn't be here without them.

and also epigenetic factors, just look on recent Nature paper, memory can be transferred without change in genetic code per se: http://www.nature.com/news/fearful-memories-haunt-mouse-descendants-1.14272

Please try adding some explanation along with citations for how instincts are hard-wired. What you are essentially talking about is the physiological mechanism whereas the actual question appears to be about the genetic basis.


text:
variance in zygotic gene expression across species
I found this review on the Maternal-to-Zygotic transition (MZT), describing how developmental control switches from maternally deposited RNAs to zygotic expression. I was struck by figure 1, and the apparent difference between viviparous and oviparous life histories.
My maybe naive question is, Could the sharp increase of zygotic expression reflect conflict between the maternal and zygotic genomes?

MZT review

In this figure only the Mouse is viviparous.  I don't have a clear sense of what you mean by "competition." In sexually reproducing species, like these five, fully one half of the zygotic genome is identical to the maternal genome.  I suggest that you try thinking about like this: the main purpose of oogenesis is to create a cell that will provide everything that the zygote needs following fertilization.  The eggs are getting loaded up with proteins and mRNA the zygote will use until its own genes get transcribed. In mice and worms it only takes 1-3 cell divisions for the embryo to take over.

What seems so striking to me is that the length of a single cell cycle is so drastically long in the viviparous species. That tells us that if your mom lays eggs then those first cell cycles are incredibly fast, which really means that oogenesis is stuffing those eggs full of DNA polymerase and dNTP's.


text:
Help me identify this spider from my garden
Found this in my garden today in Sydney, Australia (specifically Lane Cove). Can you tell me what it is?

Can you get a close up shot of the top?

I believe it is a Garden Orb Weaver spider. The Australian garden orb weaver, Eriophora transmarina, has a strikingly similar body

Haha, yours is WAY closer than mine! You have to cut me a break though, this is my first attempted species-identification. Perhaps I should delete my answer to spare myself the humiliation... all the same, great job. +1

@CDB thanks. Species identification can be difficult but it is fun to play detective.

It looks like Neoscona Crucifera to me, but I could be wrong.
Here is a picture of her:

Another one, only this is more of the web:

wrong continent for Neoscona crucifera, which is found in the US and Mexico.


text:
Difference between facilitated diffusion and secondary active transport in cells
Specifically, what is the difference between facilitated diffusion carrier processes (passive transport) and secondary active transport co-transport processes (active transport)?
They seem to be the same thing - doesn't the passive process with the carrier transports substance $x$ against its gradient together with substance $y$ that is moving down its electrochemical gradient?
Similarly, in the active process, substance $x$ is transported against the gradient, and substance $y$ down its electrochemical gradient?
I don't see how energy differentiates the active transport in this case from the passive transport.

it is not very clear what you are asking. Also, have you read through corresponding wiki articles? e.g. http://en.wikipedia.org/wiki/Active_transport

Yes I have, and hopefully after these edits what I am asking is clear. There are many types of transport processes in the membrane but I do not see the difference between two that are listed under completely different processes the active symport, and the passive cotransport. Yes I have read the articles, the problem is I have found listing stating Glut1 is a carrier protein, and also Glut1 is an active symport. I tried to find a difference between the two processes and this furthered my confusion because I cannot find the difference.

Short answer
Facilitated diffusion is a passive process in which membrane channels mediate the transport of polar, or big molecules that are not solvable in the cell membrane. Co-transport, on the other hand, is active transport, as it depends on the electrochemical gradient of ions across the cell's membrane, particularly Na+. Because ATP or other energetic compounds are not directly involved in co-transport, it is referred to as secondary active transport. The electrochemical ion gradient is mainly established by the Na+,K+-ATPase.
Background
As commented upon by others, your question is not entirely clear and the best way to approach this question is by defining the various terminologies and physiological mechanisms used in your question:

Active transport needs an energy source such as ATP. For example, the Na+,K+-ATPase is an enzyme that pumps Na+ and K+ ions against their concentration gradients into the cytosol (K+) or out of the cell (Na+). Note that both Na+ and K+ are transported against their chemical gradients (and Na+ also against its electrical gradient as the cell is negative). Therefore your statement that [...] in the active process, substance x is transported against the gradient, and substance y down its electrochemical gradient is untrue, and likely the cause of your confusion.
Passive transport is mediated by diffusion, which typically occurs through a concentration gradient. Only small, relatively hydrophobic molecules are able to diffuse across a phospholipid bilayer at significant rates. Examples are gases (such as O2 and CO2) in the lungs, and small polar but uncharged molecules (such as H2O and ethanol) (Cooper, 2000).
Facilitated diffusion is an example of passive diffusion, but aided by membrane-spanning channel proteins that span the lipid bilayer. Therefore the particles (molecules or ions) do not have to dissolve in the cell membrane's hydrophobic lipid bilayer, allowing hydrophylic and larger molecules (carbohydrates, ions) to be transported into the cell. No external source of energy is needed and  travel across the membrane in the direction determined by their concentration gradients and, in the case of charged molecules, by the electric potential across the membrane (Cooper, 2000).
Co-transport is active transport, where the energetically unfavorable transport of a particle against its electrochemical gradient is facilitated by the co-transport of a favorable one down its gradient. In other words, multiple particles are transported so as to neutralize the sum of the transport. For example, sodium-dependent glucose tranporters transport glucose into the cell against the concentration gradient (unfavorable) and Na+ is transported along with it into the cell which is a favorable transport (Haraki & Inagaki, 2012). This is an example of a symporter. An example of an antiporter is the Na+/Ca2+ antiporter found in the heart to transport Ca2+ out of the cell against a steep concentration gradient and electrical gradient, while 3 Na+ is imported into the cell to balance the unfavorable Ca2+ transport. Note that all these mentioned co-transporters and many others are dependent on the Na,K-ATPase that ultimately generates the Na+ and K+ gradients by pumping Na+ out of the cell and K+ into the cell using ATP (Freeman, 2000). This generated membrane potential works like a battery being charged, and co-transporters discharge it by using the energy stored by importing Na+. Hence, it is referred to as secondary active transport, as no direct energy input from ATP is needed, but instead it utilizes the electrochemical gradient created by the Na+,K+-ATPase.

These considerations should clarify your issues and answer your question on what co-transport exactly is. Specifically, the glucose transporter mentioned, GLUT1 as you refer to, is a symporter that mediates secondary active transport.
References
- Cooper, The Cell, 2000
- Haraki & Inagaki, J Diabetes Invest 2012; 3: 352-3
- Molecular Cell Biology, 2000

"Specifically, what is the difference between facilitated diffusion carrier processes (passive) and secondary active transport co-transport processes (active)?"
Facilitated diffusion creates alternative paths for polar/charged substances to move down their electrochemical gradients across the hydrophobic interior of the membrane, thus greatly speeding up their movement into the cell.
Secondary active transport is a form of active transport where the transport of a substance AGAINST its electrochemical gradient (endergonic) is coupled to the movement of another substance DOWN its electrochemical gradient (exergonic), thus providing energy to transport the first substance against its electrochemical gradient.
The key difference is really that passive transport does not require energy whereas active transport does.
According to wikipedia the GLUT1 you mention is a uniporter that facilitates the diffusion of glucose into the cell, so it is a passive transporter. It does not require energy as it simply helps glucose move down its concentration gradient.

It's an old article I know, but after a bit of thinking my answer would be that while facilitated diffusion is a single step process (not counting the confugurational changes within the CARRIER* protein of course), secondary active transport couples a step of facilitated diffusion with the movement of another molecule/ion in the direction against its (electro)chemical gradient. There's both a passive and an active displacement. (*It's a carrier, not a channel.)

Please add some references to your answer.

The difference between the two definitions is not scientifically justified. Here is an example to clarify this point. A facilitated transport through a carrier A will dissipate the gradient of a substance a. This dissipation will consume energy indirectly if the gradient for that substance is maintained by an active (ATP-dependent) pump. Hence a voltage-gated sodium channel dissipates the sodium gradient maintained by the Na/K ATPase. We think of these sodium ion channel as facilitating the movement of Na down its gradient but in fact they also need the energy indirectly provided to maintain the Na gradient. Now let us consider a coupled transport, Na+/glu for instance. The favorable transport of Na down its gradient largely overcomes the energy cost of the transport of glu against its gradient. Our textbooks commonly justify that this type of transport is secondarily active because it needs the energy necessary to maintain the Na gradient. But isn't the same thing for the voltage-gated sodium channel? If there is no Na gradient, then the transport of glucose by the Na/glu cotransporter will not exist, same thing for the Nav sodium channel: there would be limited flux of sodium ions without the Na gradient (there will be a little due to the membrane potential).

I see what you are saying, but isn't the other key difference that a protein involved in facilitated diffusion is only transporting a single substance whereas proteins involved in secondary active transport transporting two substances so that the link between the energy from one gradient being used to move something else is more direct?


text:
Comparative Genomics
Are orthologs and paralogs examples of conserved genes? Orthologs are the genes or DNA that is present in 2 different species, having once been present in a common ancestor. It comes about by a speciation event. Paralogs come about by gene duplication events.
So, would we characterize these genes as conserved genes?

Relevant discussion on orthologs vs paralogs: What is the difference between orthologs, paralogs and homologs?

Could not fit in a comment...
To my understanding, paralogs and orthologs refers, as you said, to the relative isolation of gene copy to the isolation of populations (and eventually species).
Gene conservation on the other hand refers to the variability of a given gene along many species. If a gene does not show any variance along many species, than we say that it is a conserved gene.
Eventually, gene duplication may allow for neo-functionalisation, sub-functionalisation or loss yielding to variance among this gene copy. Aside the philosophical problem of what is the identity of the gene, there is no relationships between the concepts of orthologs versus paralogs and gene duplication.

Yes, of course they are conserved. Conservation is basically a measure of sequence identity. It can be used to describe the relationship between both paralogs (genes created by a duplication event) and orthologs (genes created by a speciaton event). Any type of homology relationship can be described in terms of the conservation (sequence similarity) between the genes investigated.
Even entire genomes can be described as more or less conserved.