How do kidney cells excrete their own wastes? The kidney is composed of tissues, and those tissues are made up of numerous cells - so how do these cells excrete their wastes?

Lastly, are there any wastes in the venous blood (renal vein), what makes the renal artery and vein different? - what substances do they each carry?

I checked my anatomy notes and online figures about the kidney. There is no mention about dedicated arteries for feeding kidney cells. So it does not work the same way as the heart does, where there is a dedicated coronary artery. The kidneys use the same blood vessels for filtering and for nutrition/waste transport purposes too.

Figure 1 - kidney anatomy - source

Figure 2 - nephron anatomy - source

The urea is created from NH4+ and HCO3- in the liver (mostly) and the kidney because of blood pH regulation purposes. It neutralizes the HCO3- created by the lungs from CO2 and OH-.

  The urea cycle (also known as the Ornithine cycle) is a cycle of
  biochemical reactions occurring in many animals that produces urea
  ((NH2)2CO) from ammonia (NH3). This cycle was the first metabolic
  cycle discovered (Hans Krebs and Kurt Henseleit, 1932), five years
  before the discovery of the TCA cycle. In mammals, the urea cycle
  takes place primarily in the liver, and to a lesser extent in the
  kidney.

  In chemical terms, urea synthesis is an irreversible, energy driven
  neutralization of the strong base HCO3- by the weak acid NH4+, and the
  average daily excretion of 30 g of urea is equivalent to the disposal
  of about 1 mol of HCO3- per day. Thus, a major function of hepatic
  urea synthesis is to effect this neutralization, without which the
  body would otherwise be confronted by a major load of alkali.

  Urea is excreted by the kidney, and is normally present in plasma and
  body fluids at a concentration of 3.0–6.5 mmol/L.

wikipedia - Ornithine cycle
Textbook of Hepatology - Ammonia, urea production and pH regulation - Dieter Häussinger
1984 - The role of ureagenesis in pH homeostasis

The kidney reabsorbs urea in order to concentrate the urine:

Figure 3 - nephron with material transports - urea resorption at the end of the urine creation process - source

  About 40% of the urea filtered is normally found in the final
  urine, since there is more reabsorption than secretion along the
  nephron.

wikipedia - Renal urea handling:
2007 - Critical Role of Urea in the Urine-Concentrating Mechanism

The kidney secretes the urea to the urine, but it absorbs more by the reabsorption than it secreted.

  The kidney freely filters urea at the glomerulus, and then it both
  reabsorbs and secretes it. Because the tubules reabsorb more urea than
  they secrete, the amount of urea excreted in the urine is less than
  the quantity filtered. In the example shown in Figure 36-1A (i.e.,
  average urine flow), the kidneys excrete ∼40% of the filtered urea.
  The primary sites for urea reabsorption are the proximal tubule and
  the medullary collecting duct, whereas the primary sites for secretion
  are the thin limbs of the loop of Henle.

Medical Physiology by Walter F. Boron and Emile L.

So if we are talking about urea, then it is secreted to the urine. If we are talking about other waste products, then e.g. CO2 is certainly handled by the veins.

The kidneys keep the composition, or makeup, of the blood stable, which lets the body function.

Each kidney is made up of about a million filtering units called nephrons. The nephron includes a filter, called the glomerulus, and a tubule.

The nephrons work through a two-step process. The glomerulus lets fluid and waste products pass through it; however, it prevents blood cells and large molecules, mostly proteins, from passing. The filtered fluid then passes through the tubule, which sends needed minerals back to the bloodstream and removes wastes.


Why can't I smell things that aren't there? I can close my eyes and imagine a red cube with a yellow star on it. Although I don't literally see it -- if there was a red cube with a yellow star on the inside of my eyelids, I'd know the difference -- I can experience it in much the same way as if I was seeing it.

I can do much the same thing with sound, imagining (say) the sound of a bird, or of a bell ringing.

But I can't imagine any tastes, or smells. I know what cinnamon smells like: if several spices were placed in front of me, I could readily identify the cinnamon. But I can't call a familiar smell or a taste to mind in the same way I can call a familiar sight or sound to mind.

I don't think it's merely a memory thing. Even if I've never seen the box, I can still imagine it. I can imagine the sound of a bird tweeting in a large echoing hall, even though I've never heard it. But I can't synthesize unknown smells or tastes in my imagination in the same way I could unknown sights or sounds. I don't think I'm unusual in this respect (correct me if I'm wrong).

Are there any theories as to why this is?

Couple of contributing theories:

The olfactory system does not project to the thalamus, which serves as a relay to other higher processing areas.
Lack of a specialized working memory subsystem; we have fairly robust subsystems for movement,visual and auditory buffers of information, what is normally called working memory, things we can hold on for a little while, but it seems they are not as developed or engage the same areas for smell. see for instance:Working Memory in Another Dimension
It is not as useful,used or adaptive ( beyond recognizing odors) as the other senses, there is a relationship in between how much we use something ( could also be the above working memory systems )and the cortical real state devoted to it's processing, this is a competitive part of the brain and in comparison to other senses like vision the portion of the cortex devoted to olfaction is small.
Another way of looking at it, is that we do have the capability to imagine smells and gustation, but they are not as developed as the others since we don't use them as much.
Anectodally, I would argue that people whose jobs revolve around combining nice smells or tasty things do develop certain abilities like those in vision as well as for those who have been exposed to the same odor repeteadly and can imagine it at will.


Why should plants transform glucose into sucrose before transporting it to other parts? I've learned that plants transform glucose into sucrose before sending it into phloem. But the process seems to be complex and energy comsuming. Why should plants do it? Is it really necessary?

Glucose, fructose and galactose are the three dietary monosaccharides. Glucose and Fructose are  simple monosaccharides found in plants. A monosaccharide is the basic unit of carbohydrate and the simplest form of sugar, glucose are aldose and Fructose are ketose.

  If the carbonyl is at position 1 (that is, n or m is zero), the molecule begins with a formyl group H(C=O)-, and is technically an aldehyde. In that case, the compound is termed an aldose. Otherwise, the molecule has a keto group, a carbonyl -(C=O)- between two carbons; then it is formally a ketone, and is termed a ketose. Ketoses of biological interest usually have the carbonyl at position 2.
  http://en.wikipedia.org/wiki/Monosaccharide

Whereas Sucrose is a disaccharide composed of glucose and fructose. A disaccharide is more complex than monosaccharide, more complex compounds like oligosaccharides and polysaccharides exists. Sucrose synthesised within the cytosol of photosynthesizing cells is then available for general distribution and is commonly trans located to other carbon-demanding centers via the phloem.

Sucrose and starch are more efficient in energy storage when compared to glucose and fructose, but starch is insoluble in water. So it can't be transported via phloem and the next choice is sucrose, being water soluble and energy efficient sucrose is chosen to be the carrier of energy from leaves to different part of the tree. Another problem exists,   glucose is highly reactive and this may result in some intermediate reactions while transporting glucose. Being a complex structure, sucrose is not as much reactive as glucose. So plants uses the sucrose as a medium to transfer energy. Inside the cells, sucrose is converted back to glucose and fructose. Energy is yielded when it is needed. So plants transfer glucose and fructose in the form of sucrose in order to:

Increase energy storage
Efficient energy transfer
Removing in between reactions

References

Carbohydrates
Sucrose & Starch Biosynthesis
Sucrose Metabolism
Sucrose and starch synthesis
Disaccharide

there is no free glucose in the photosynthesis. Stop to spread that myth. The net product is G3P. The end products of photosynthesis are sucrose and starch, but never glucose. Do you test glucose in the leaves? No... it is always for starch. ;) The G3P is converted to sucrose and other molecules, for example, thiamine. Glyceraldehyde 3-phosphate occurs as a reactant in the biosynthesis pathway of thiamine (Vitamin B1), another substance that cannot be produced by the human body. Part of sucrose is then translocated to the phloem. Starch is stored in the stroma of chloroplasts. It is also stored in the amyloplasts in the roots, stems cells after sucrose suffers a conversion to starch.


Why do humans bury their dead? As far as we know Ape Men or the Neanderthal Man was the first to bury its dead. My question is why.

I don't think they practiced religion or believed in spirits or faith or stuff like that. Therefore what was their main reason to bury their dead in the first place?

(Also correct me if I'm wrong but i think that religion only emerged after Homo sapiens came to be.)

Some theories:

Dead bodies died of something. In the earliest ages these were generally infection. Burying them protected us from something that could kill us too. This is also why we would be evolutionarily programmed against cannibalism
They make great fertiliser. Burying waste, dead animals etc resulted in the growth of plants etc which not only food we could eat but animals that would then eat the plants we could kill and eat.
Dead bodies are unpleasant. They stink and so we would want to get rid of them. Also they would attract carnivores which are likely to target humans too

All these would be evolutionarily advantageous so any cultures practising burial would be likely to survive and pass on those customs. Whether this is genetic, that's open to debate because I'm not sure.

In my opinion smell could have an impact on why we buried the dead but I also theorize we did this so our family members or friends would not get eaten by a scavanging animal.  I would assume being eaten was a constant worry while alive and probably a fear among early man to be eaten after death. That's just my theory though.


Please give information about this insects I took this photo of a small insect which I found near to my house (Maharashtra state, India). What insect is this?

It looks like an insect belonging to the family Cicadidae. Further information is needed to identify this cicada species.


Is recognizing one's own mirror reflection a valid test of animal intelligence/self awareness? I've been looking at this Ted talk on interspecies internet, and it appears that they have selected a small number of species of animals (dolphin, elephant, and some ape(?)) and are intent on developing interfaces for these animals to be able to connect with other animals over the internet.

From the talk, it appeared as if one of the criteria for animal selection was whether or not an animal recognizes itself in the mirror. This got me thinking - there are many more cats that have access to technology like the internet or TV or cats that have been interacting with touch screen displays. Yet apparently cats cant recognize their own reflection as themselves.

What is so special about being able to recognize one's own reflection? Is it a true measure of self awareness? Does it only appear in animals with larger brains?

I think it is a necessary test of self-awareness. In order to make the connection that "I am the being in the mirror" and that every action I do will be reflected in the mirror (or, vice versa, every action I see the being in the mirror take is a reflection of my own action), one must first have a concept of self. One requires a constant present-tense (at least) story of oneself: "I am doing this. Now I am doing that. Oh look, I am doing this and that guy is doing the exact same thing." And then there's the ultimate realization, "Ah ha! That's me!". That realization would make no sense if the individual has no sense of "me"!

[speculation] On the other hand, perhaps it is too strict. It seems that it would unfairly favor social species, since it requires not only recognizing another member of the species (and being able to associate the anatomy of another member of the species with one's own anatomy), but it may also require the recognition of intent. That latter requirement is complicated by differentiating between intent and compulsion: at some point, one must realize that the being in the mirror isn't trying to copy but rather it always, inevitibly reflects one's motions. So, perhaps a cat is self-aware, in a sense that it has a constant story in its head of what it is doing and what it intends to do, but it cannot easily ascribe intent to other members of the species and thus cannot figure out that the cat in the mirror is automatically mirroring all of its movements. [/speculation]

Herein lies the rub: there is no perfect test for self-awareness; we can cast doubt on any outcome. The best would be if these animals could communicate with us by language. In lieu of that, we have to think of such tests that demonstrate with reasonable confidence that the species carries all of the characteristics that we attribute to self-awareness. I think another good test would be determining whether the species can plan individual actions in the future; in order to say, "first I will do this, then that; finally, that will allow me to do that", it seems like it would reasonably require an understanding of self and the consequences of one's actions. An example would be birds solving sequential puzzles.

To the answer above:  "I am the being in the mirror", one has to ask themselves:  Is it so strange that a cat seeing it's own paw in front of it and recognizing it as it's his OWN, and not chasing it's own tail because it knows it's his and he's not a kitten anymore?

So how much different is that when they come to understand, especially after you hold the cat several times in front of the mirror with you, making the association and he's no longer weirded out?  Many cats making this transition look in curiosity and awe and move on, never really caring that much about it -- much like kids.

Bring a cat into a bathroom with a mirrored wall behind the sinks, when he's dealing with something where the mirror is in his line of sight.  Walk in behind.  When the cat turns around to look at you to play instantly, instead of trying to play with the mirror -- it recognizes that it shows whats behind him.  I have observed this.

If a cat recognizing it's own tail out of it's "perif" is nothing special, neither is recognizing that it's him in the mirror.  He may not be cognitively advanced to think deeper than "Yep, that's me, I have THIS look.  Oh, am I getting fat?" -- they care less about that.

A good test would be to have a cat with whom you can put something on his head and he doesn't care -- unless it's something he HATES by its LOOK.  Once you've established that over and over 100%, and have been able to put it on him without him caring without him SEEING it -- put him in front of the mirror and see if he tries to take it off.

A red dot isn't going to do squat.  They don't give a shoot about things like that.  If you want to know whether they know IT'S THEM, put them in position where there's something they DON'T WANT on them -- and they try to get it off... where it's something they don't mind on them, they don't try to get it off after seeing themselves in the mirror.

Not fool-proof, though.  They may not mind it on them because it's purely how it looks.  They can just walk away from the mirror and they don't have to worry about it.

But back to the original point:  I don't think it's a big deal that they can recognize that it's themselves.  To UTILIZE that for deeper thinking in making connections is another matter.


Is it possible to distinguish between coding and template strands from the sequence? Let’s say you have the following DNA sequence fragment:

5’-ACCAGTACTTCGT-3’
3’-TGGTCATGAAGCA-5’

Is there any way to determine which strand is the template strand and which is the coding strand for RNA synthesis solely from the above information?

I don't know about your specific example (perhaps look for triplets that code start codons?), but machine learning has been used to predict promoters from sequence information (from promoter regions, you get downstream initiation of transcription of DNA to RNA). You would probably need more sequence to predict a promoter with more certainty. Cites: https://en.m.wikipedia.org/wiki/Promoter_(genetics) and https://academic.oup.com/bioinformatics/article-abstract/35/16/2730/5270663


Was the mitochondrion or chloroplast first? I still don't  know if the mitochondrion or chloroplast was first? I've looked for it on the internet and in various books but haven't found anything. Does anyone have the answer and a theory which backs up this answer?

Mitochondria evolved before chloroplasts.

We know this because Mitochondria form a monophyletic group: e.g. all life with mitochondria traces back to a single common ancestor (source). Since the group with chloroplasts groups within this clade, it must be the case that either (a) chloroplasts were obtained by an organism that already had mitochondria or (b) chloroplasts were independently lost by multiple lineages within the Eukaryotic clade and then many of these lineages re-acquired chloroplasts by secondary endosymbiosis. Since (a) is a (much) more parsimonious explanation it is the one it makes sense to accept.

Why would a mitochonrion be of any advantage in a world without oxygen?
Chloroplasts evolved to fill the atmosphere with oxygen then mito's exploited that situation.


How do plant cell divide without centrioles? Most plants do not have centrioles, so what organelle enables them to multiply?

There are many different ways to make a spindle in plant cells:

  Mitotic spindles may be organized at centriolar centrosomes (only in final divisions of spermatogenesis), polar organizers (POs), plastid MTOCs, or nuclear envelope MTOCs (NE-MTOCs).

Of these, only the latter has been observed in angiosperms (flowering plants). For more info (and the source of the quote), see Brown & Lemmon, "The Pleiomorphic Plant MTOC: An Evolutionary Perspective"

Spindle formation in plants is very different from most other eukaryotes owing to the fact that plant cells lack centrosomes or spindle pole bodies, which act as the microtubule organizing centers in animal cells. The evolutionary advantage that animal cells gain due to the presence of centrosomes is the ability to direct drastic changes in their shapes during mitosis. On the other hand, plant cells have a rigid cell wall that does not undergo any major changes in shape during mitosis; and the cell wall itself can organize many of the microtubules that form the spindle during mitosis.


Why and how is DNA synthesis so much faster then RNA synthesis in bacteria? DNA synthesis in E. coli is 20x faster than RNA synthesis at 1000nt/s vs 50nt/s. (Mirkin'05)

I find that perplexing since DNA polymerization has better proofreading than the RNA variety, which requires extra time as you need to backtrack, excise, and replace. Also, in bacteria there's almost no splicing, so that doesn't slow you down. And the 1000nt/s is a single replication fork. We are not talking about several replisomes together clocking 1knt per second.

Is there an explanation of this or, in the absence of evidence, hypotheses?

I wouldn't call them hypotheses, but the question is intriguing, and, as it seems to be ignored in the literature, I'll make a couple of suggestions.

Perhaps it has something to do with recognition of termination signals in relation to selective pressure for speed in the two processes.

Perhaps if elongation of the RNA chain were any faster it wouldn't be able to respond to the rho-independent termination signals which are thought to be specific stem–loops in the DNA that cause the RNA polymerase to pause and fall off the DNA. The speeding RNA polymerase might disrupt the loops instead. The termination system for DNA replication may have evolved to be much more robust so as to be able to bring faster elongation to a stop. (Note: my suggestion of different ‘robustness’ in termination is not based on any data, it's pure speculation.)

If this were true, it would beg the question of why transcription hasn't evolved a more efficient termination system in concert with the a evolution of a smarter RNA polymerase. Perhaps the answer here is that there is no selective pressure for faster transcription — the rate is clearly sufficient to supply the needs of the cell — whereas the rate of DNA replication determines the time between cell divisions and thus the rate of growth, which is subject to selective pressure.

Perhaps it has something to do with error frequency in relation to selective pressure for speed in the two processes.

First I'll make it clear that I think the proofreading argument in the question is a bit of a red herring. If the rate replication is 20x as fast as transcription, the occasional backtracking will not have much effect on the overall difference. However errors and proofreading could be involved in a different explanation.

RNA transcription does not have proof-reading. The length of RNA transcripts is such that the cell can tolerate the errors that occur. However if the speed transcription were increased it is reasonable to expect an increase in error frequency, which might be detrimental. The current rate of transcription may be a trade-off between efficiency and accuracy. Of course one can imagine a proof-reading system for transcription evolving if it were necessary, but, as discussed above, if the rate of transcription is adequate there would seem to be no selective pressure to produce.

This is because of the fact that DNA polymerase does the fast process that is 1000 nu/sec as compared to the RNA polymerase that 1000-2000nu/min because this process is done without discrimination and also DNA pol has exonuclease activity


Why don't housekeeping genes have TATA Box regions in their promoter sequences? Housekeeping genes are genes that are continuously transcribed. Like all other genes they have promoter sequences, but they don't have TATA box sequences that are used to specify from where transcription is going to begin.

Why don't housekeeping genes have a TATA Box in their promoter sequences?

Two possible answers:

First, TATA boxes has been found to cause increased "noise" in gene expression, such that the expression of genes that have a TATA box is highly variable. See this review for example.

A different set of results suggests (here) that TATA acts only as an amplifier of expression.

Regardless of whether TATA amplifies expression or also increases expression variance, this is not suited for housekeeping genes, which generally have low and constant expression.

Quick googling located online version of Lodish et al Molecular Cell Biology. 4th edition.

From TATA Box, Initiators, and CpG Islands Function as Promoters in Eukaryotic DNA section:

  These genes, which generally are transcribed at low rates (e.g., genes encoding the enzymes of intermediary metabolism, often called “housekeeping genes”), do not contain a TATA box or an initiator

Also, from Transcriptional Regulatory Sequences of the Housekeeping Gene for Human Triosephosphate Isomerase (Boyer et al, J Bio Chem 1989):

  In contrast to facultative gene promoters, these promoters are
  characterized by [...] and, notably,
  the lack of an appropriately positioned TATA box
  [...]
  Based upon these structural differences,
  the possibility exists that initiation of housekeeping and
  facultative gene transcription proceeds through distinct mechanisms.

I can imagine you can google more information, but it seems to me that reason for lack of TATA is necessity for constant low-level expression (hence no strong promoter) and separate mechanism of regulation (hence some common structure). Last point might arise from redundancy argument: when regulation of TATA-containing genes become faulty, housekeeping genes regulation stays same because it is somewhat independent.

However, you should be aware that your original assumption is at least controversial (from same J Bio Chem paper):

  Unlike most housekeeping gene promoters that have been
  described to date, the human TPI promoter harbors a canonical
  TATA element (5’ TATATAA 3’) that spans positions
  -27 to -21. LS mutagenesis demonstrated that this TATA
  box clearly represents a control element, the integrity of which
  is essential for the maintenance of both the fidelity and the
  frequency of TPI gene transcription initiation.


Are "sympathetic nerves" the same as "cardiopulmonary splanchnic" nerves? I've gathered from a number of sources (e.g., Patel (2015), Wikipedia, and here) that the sympathetic nerves leaving the sympathetic trunk to innervate the heart and lungs are called "cardiopulmonary splanchnic nerves".
However, I've noticed that both the 14th and 15th edition of Tortora & Derrickson's A&P textbook seem to suggest that these nerves are simply called "sympathetic nerves," even though they make reference to abdominopelvic and adrenal splanchnic nerves more specifically.  See below from Tortora & Derrickson (2013):

...Then, the axons of the postganglionic neurons leave the trunk by forming sympathetic nerves that extend to visceral effectors in the thoracic cavity (Figure 15.4). Sympathetic nerves provide sympathetic innervation to the heart and lungs.

Here are subsets of images from Patel (2015) [LEFT] vs Tortora & Derrickson (2013) [RIGHT] (my emphasis):

My question: Are "Sympathetic nerves" the same as "cardiopulmonary splanchnic" nerves?

Are these names interchangeable? I can't find further evidence supporting Tortora and Derrickson's usage of this phrase in such a specific manner to refer to postganglionic neurons leaving the trunk to innervate the heart and lungs. Are they acting rogue? Are they simplifying? Any insight would be appreciated.

Cited works:
Patel, T. R. 2015. "Chapter 36 - Anatomy of the Sympathetic Nervous System." Pages 495-506 in Tubbs, R.S., Rizk, E., Shoja, M.M., Loukas, M., Barbaro, N. and Spinner, R.J. eds. Nerves and Nerve Injuries: Vol 1: History, Embryology, Anatomy, Imaging, and Diagnostics. Academic Press.
 Tortora, G. J. and B. Derrickson. 2013. Principles of anatomy and physiology, 14th edition. John Wiley & sons, Inc.

You might consider cross-posting to SE Medical sciences who know more about this stuff.

I think that they are simply using a more general term than other authors. In the same way, most people call crabs crabs, but some people might occasionally refer to them as crustaceans.

Based on wikipedia, it seems that cardiopulmonary splanchnic nerves are a subset of sympathetic nerves. The sympathetic nervous system innervates a large number of organ systems of the body (see image), such that the cardiopulmonary splanchnic nerves are simply the sympathetic nerves that innervate the heart and lungs.

Looking further at the wikipedia for splanchnic nerves, it seems that this is a technical term relating to the fashion in which organs are innervated by the sympathetic nervous system; e.g. in my crude understanding they are organ hookups to the sympathetic nervous system.

In other words, all cardiopulmonary splanchnic nerves are sympathetic nerves, but most sympathetic nerves are not cardiopulmonary splanchnic nerves.

Cardiopulmonary splanchic nerves consist of:

sympathetic nerves
the vagus nerve (a part of parasymathetic system)


Why are there so few multicellular anaerobes? There are a few documented cases of multicellular anaerobic organisms, but I can't see a reason for it to not be more common. On the contrary, it seems pretty useful to be able to create energy even when deep inside tissues, yet the Loricifera are the only ones I've found documented. Given how often multicellularity has arisen, is there something that's fundamentally difficult about being anaerobic while multicellular?

One thought that might inspire others- multicellular organisms certainly tend to be bigger than unicellular ones, and in an oxygenated world larger organisms are more likely to run into oxygen than unicellular ones. However, there still exist an abundance of anaerobic niches for large organisms- the deep sea, for example.

I'm also drawing a distinction between facultative anaerobes and obligate anaerobes- there are plenty of facultative multicellular anaerobes, and I'm not as curious about that.

Useful sites that I came across while searching:

Journal article announcing the first anaerobic metazoa

Anaerobic fungi, presumed to be unicellular?

I did a bit of reading myself, and it seems as if Loricifera are the only multicellular obligate anaerobes.

I see your point with niches for anaerobic organisms in deep water. Many organisms near the hydro-thermal vents use anaerobic cellular respiration.
From my understanding of Loricifera, it seems as if they would utilize chemosynthesis as their method of obtaining energy.

  Loriciferans are found exclusively in marine habitats, and live in the spaces between sand grains or in the mud at the bottom of the deep sea. The nanaloricids prefer sand with low levels of detritus (material derived from the decomposition of once-living organisms) or clean shell gravel, whereas the pliciloricids are often found in such deep-sea sediments as the white abyssal Globigerina ooze and the red deep-sea clay from the hadal zone (below 20,000 ft; 6,100 m).

--From Encyclopedia website: Loricifera (Girdle Wearers).

Lociferans live in a rather oxygen-less environment.

So you're right about niches in the deep sea.

But typically the deep sea has extremely high levels of pressure that few multicellular organisms are built to handle.

Additionally, I was able to find a few other obligate anaerobic Eukaryotes, but those were Protozoa, so thereby not unicellular.

About it fundamentally being difficult to be exclusively anaerobic while multicellular, with multiple cells, there is more upkeep and more energy is required to run the "system". Aerobic processes tend to be a lot more efficient, producing more ATP for usage.

Only 1 ATP (from my understanding) is produced from this, whereas with aerobic respiration:

Aerobic ATP sum

Much more ATP is produced from aerobic processes.

In the end, the majority of obligatorily aerobic organisms are unicellular, or are extremely small.

  Their sizes range from 100 µm to ca. 1 mm.

So... that's why multicellular organisms are typically carry out aerobic cellular respiration.

Also, about the fungi you mentioned, it goes through Horizontal gene transfer, which unicellular organisms typically use:

  Horizontal gene transfer (HGT) or lateral gene transfer (LGT) is the movement of genetic material between unicellular and/or multicellular organisms other than by the ("vertical") transmission of DNA from parent to offspring. HGT is an important factor in the evolution of many organisms....
  Most thinking in genetics has focused upon vertical transfer, but horizontal gene transfer is important, and among single-celled organisms is perhaps the dominant form of genetic transfer.

--From Horizontal Gene Transfer Wikipedia page

So yes, it seems as if the fungi that you mentioned and other similar types of fungi would be strictly unicellular, such as yeast (thought yeast is a facultative anaerobe).

One must wonder if there was an abundance of multi-cellular anaerobes that existed before the Great Oxygenation Event (2.45Ga), but were never recorded (or discovered yet) in the fossil record.

The wikipedia article also suggests that ancient anerobes, before the Great Oxygenation Event, may have had more nickel to work with: "Modern methanogens require nickel as an enzyme cofactor. As the Earth's crust cooled and the supply of volcanic nickel dwindled, oxygen-producing algae began to out-perform methane producers, and the oxygen percentage of the atmosphere steadily increased.[23] From 2.7 to 2.4 billion years ago, the rate of deposition of nickel declined steadily from a level 400 times today's."


Lack of skin in a certain area of the body --- hypo[what]? Lack of skin in a certain area of the body. How shell I name this?

Hypocutaneousis?
Hypo[somethingElse]?

What is the correct term?

First, this is not an area where I have any education or experience. However, out of curiosity I consulted google and found two genetic castle diseases that should be relevant to your question:

Epitheliogenesis imperfecta (vetbook.org)
Ectodermal dysplasia

Both diseases are very serious, and Epitheliogenesis imperfecta is fatal (due to infections).

I chose not to include any pictures of the diseases in this answer since they often look quite horrible, and some people might find them unsettling. If you click the links there are pictures of the conditions though.

A "similar" condition in humans might be  Epidermolysis bullosa, which is caused by decreased anchoring between dermis and epidermis, which cause a very fragile skin:

  Epidermolysis bullosa (EB) is a group of mainly inherited connective tissue diseases that cause blisters in the skin and mucosal membranes, with an incidence of 20 per million newborns in the United States.[1] It is a result of a defect in anchoring between the epidermis and dermis, resulting in friction and skin fragility. Its severity ranges from mild to lethal.

(Wikipedia)

You can say skin atrophy or just thinning where dermal thickness is reduced.

https://m.iliveok.com/health/skin-atrophy_77524i15941.html


How does Darwinian Evolution work? Let me explain... A friend and I read some articles, part of a Biology book, and watched a video on evolution. We then tried to explain what Evolution is to each other.

My friend said that Natural Selection is a mechanism inside the organism that mutates the DNA to make its offspring survive in an environment; that natural selection mutates the DNA beneficially and that random mutations are not useful (like blue eyes). But I disagree and think that it is closer to Lamarkian theory.

I told him that DNA from male and female recombines and randomly mutates making a new "recipe" for the offspring (adding a new characteristic(s)). If the offspring is well suited for the environment, then it survives and passes on its characteristics to its offspring. If it does not have fitness for its environment, it dies. So, Natural Selection is were nature "selects" who survives and reproduces a lot.

So is the DNA mutation process random or is mutation directed to make an organism that is suited to survive its environment?

None of my friends are Biology students, so I can't ask then which explanation is correct (or at least more valid).

I'd prefer you don't answer: "None of these explanations are correct," but to say which one is more valid and correct misconceptions or add more that is missing (of course these are only summaries of our discussion). But of course, you can answer that neither of our explanations is correct...

I accidentally wrote a lot!

I first discuss the term Darwinian evolution. I then describe the main evolutionary processes insisting on the two elements of interest in your question, that is mutations and natural selection. In the end, I directly address your two statements and bring a few more complications into the subjects.

Did you say Darwinian evolution?

Evolution is more than Darwinian evolution

The expression "Darwinian evolution" easily yield to misunderstandings. Darwin was probably the most important scientist and one of the first (if not the first) to develop the theory of evolution but evolutionary biology today is so much more than Darwin's theory of evolution.

Examples of very basic things Darwin did not know

We discovered the structure of DNA in the 1950s-1960s only with Miesher, Chargaff and most renowned Watson and Crick (history of the discovery). Darwin had no idea of the existence of DNA and had not even hypothesized about the existence of such a molecule (which came first by Erwin Schrödinger).
Darwin was not aware either that inheritance was through the transmission of "particles/atomic" and not through the inheritance of some kind of "fluid/continuum". In other words, Darwin did not know the Law of Segregation by Gregor Mendel (even if they lived in the same epoch).
Darwin had no idea about Evo-Devo, that is he had no idea about the similitudes in developmental processes among related (even distantly related) organisms.
Globally speaking, while Darwin managed to touch a little bit about many of the subjects of modern evolutionary biology (which is very impressive), he only manages to mention them and failed to provide any prediction. This is a large part because no one had no concept in genetics at that time.

Evolution is more than natural selection and mutations

Evolution is not only about natural selection. Even C. Darwin knew that evolution is way more than natural selection. It is for example very important to consider random events. One of them is mutation, another is genetic drift (I am not trying to list every process that influence evolution but only to give you a sense of why natural selection is different than evolution with a goal of explaining why a trait that is needed do not necessarily appear). Both mutations and genetic drift explain why a species will not necessarily be perfectly adapted to its environment. Evolutionary biology is a big field of knowledge and there is a lot to know about evolutionary processes.

Natural Selection and Mutations explained by the Lewontin Recipe

The Lewontin's recipe is a good way in order to understand what is natural selection and when it occurs. The Lewontin's recipe says that natural selection occurs whenever:

Individuals in a population vary in terms of a given trait
This trait has some (additive) heritability. Here is one of the several posts that explain the concept of heritability. It might be slightly a post that is a bit advanced for you though but shortly speaking it means that offspring are more similar to their parents more than they are to other non-kin individuals in the population.
The fitness varies (not necessarily linearly) as the trait varies.

Simple example:

In a population, there are blue pens and red pens
Reproduction is asexual and blue pens create other blue pens while red pens create other red pens.
blue pens make more offspring than red pens.

In such a situation, natural selection occurs yielding the frequency of the blue pens to increase in the population while the frequency of red pens will decrease.

Natural Selection

Natural Selection is the process by which variants of genes called alleles are selected and therefore increase in frequency. This selection result from a differential reproductive success.

Mutations

In the broad sense mutation is any change in the DNA sequence. Some changes are more likely to happen than other but in any case, the likeliness of these changes to happen is not dependent on the consequence they will have on the phenotype (shortly speaking, a phenotype is how an individual looks like) and on the reproductive success. So mutations occur randomly and the specific mutation that would be needed in the population may not occur. Therefore saying, if a trait is needed (in the sense of "if a trait would be beneficial"), then a mutation will occur to make this trait existing is wrong. Note that most mutations are deleterious (decrease the reproductive success) while few of them are beneficial (increase the reproductive success) and those that are beneficial are more likely to rise in frequency in the population.

Genetic drift

If the change in frequency of mutations would depend exclusively on natural selection, then I would not have said before that a beneficial mutation is more likely to raise in frequency but I would have said that a beneficial mutation will raise in frequency deterministically. An intuitive explanation of what is genetic drift can be found on this post. It will also allow you to understand why small population undergo a more random change in frequency of their genes than are big population.

Considering your opposing statements

Hopefully, the following is clear from the above discussion but I would like to directly address your statements.

  My friend said that Natural Selection is a mechanism inside the organism that mutates the DNA to make its offspring survive in an environment; that natural selection mutates the DNA beneficially and that random mutations are not useful (like blue eyes). But I disagree and think that it is closer to Lamarkian theory.

You are right that your friend is wrong!

It indeed sounds more or less Lamarkian. In any case, it is very wrong, as you said. Mutations are not caused deterministically under the pressure of natural selection to do specific things.

Are mutations completely random?

See Are mutations random?.

I do not want to go into too many complications. The sentence "mutations are random" is unclear. Does it mean that the mutation rate is random? Does it mean that the effect of a new mutation is random? And also the concept of randomness only make sense if we consider a set of a priori knowledge. So it is a little hard to fully answer this question and the easy, close-enough approximation for a starter in evolutionary biology is just to say that mutations are random (whatever that means). A slightly better approximation of reality is that mutation rate is an adaptive trait and can vary depending on the environment where the individual is found (adaptively or not). However, the effect of new mutations is really not deterministic.

The mutation rate varies with the type of sequence considered. For example, a microsatellite sequence is a sequence or repeated DNA. For example AATAATAATAATAATAATAAT etc.. (note that the genetic code is written with 4 letters, A, T, C and G). Such sequences are highly mutable. So a mutation is more likely to occur in this region than in the middle of a coding region. And it is more likely for a mutation occurring in a coding region to affect fitness than for a mutation occurring in a microsatellite (it is possible that a mutation occurring in a microsatellite will affect fitness).

Depending on the level of stress some organisms (plants mostly to my knowledge) can change their mutation rate. Consider for example an individual that is maladapted to its environment. If it mutates little, then the offspring will likely be as maladapted and in the long run, the lineage will disappear. If the individual is mutating a lot then, most offspring will have a very low fitness but eventually one will receive a beneficial mutation that will make it very strong and by itself, this offspring may save the lineage. This is what is called a bet-hedging strategy. The concept of bet-hedging can be summarized with the expression "Don't put all your eggs in the same basket".

You will note that the mutation rate is an evolving feature of an organism. This yield observation such as what is now called Drake's rule (original paper). Drake's rule indicates that the genome-wide mutation rate is always at the order of 1 (there is quite a bit of variation but it is a good approximation).

  I told him that DNA from male and female recombines and randomly mutates making a new "recipe" for the offspring (adding a new characteristic(s)). If the offspring is well suited for the environment, then it survives and passes on its characteristics to its offspring. If it does not have fitness for its environment, it dies. So, Natural Selection is were nature "selects" who survives and reproduces a lot.

Sounds quite right!

You pretty much nailed it. Mutation adds genetic variation and natural selection selects from the available genetic variation. Your wording is a little uncommon though :). For example, an individual, it is incorrect to say that an individual has fitness or not. Each individual has a fitness, that is some value that encompasses both its fertility and survival probability. In a simple model, fitness is simply the expected number of offspring.

Note also, that the majority of mutations that affect the fitness of the individuals are not so much dependent on the details of the environment. Many mutations are just bad wherever you are. Think about a mutation that would reduce the efficiency of energy production (ATP in mitochondria). Such a mutation will be deleterious regardless of whether the weather is hot or cold for example.

Introductory course to evolutionary biology

You probably want to have a look at an introductory course to evolutionary biology such as Understanding Evolution.

Short Answer: As far as we know, it doesn't.

Mutations at Conception

The mutations you describe as occurring during conception which generate new information have never been observed to take place. Instead, we have observed mutations which reduce existing information. In humans, approximately 100 such mutations take place every generation.

Necessarily if information-additive mutations existed, they'd need to produce a lot more information to make up for the loss. Necessarily, descendants would have a larger and more complex genome than their ancestors. The opposite has been observed, where descendants have smaller genomes than their ancestors.

Abiogenesis

Before Darwin had written On the Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life, Pasteur was disproving the idea of abiogenesis, as the theory had gone around that germs could spontaneously appear. Despite this, Darwin took abiogenesis as part of the theory of evolution, which has consistently proved impossible in tests with no observable data to the contrary.

Genetic information is fragile and is quickly destroyed over time if it doesn't have enzymes to continually maintain it. There is no gradual process of accumulated information that can result in life able to reproduce, as far as we have found from study and observation. The very difficult process of creating amino acids to bond and form the nucleotides (necessary to form DNA chains) is complicated by the chirality problem, where artificial tests have resulted in both left-handed (L) and right-handed (D) optical isomers were created in a racemic mixture. In biological systems, almost all of the compounds are non-racemic, or homochiral, and biological creatures only use left-handed amino acids in the construction of DNA and RNA. All subsequent have tests run into the same problem.

Theory

As for the theory itself, you and Remi.b have described it accurately. As genetics was an unknown field at that time, it was the mistaken idea that natural selection changed a creature through the creation of information, rather than the reformation, sharing, and loss of existing information.

Sources: Genetic Entropy and the Mystery of the Genome by John Sanford. The Miller–Urey experiment.


What is the difference between local and global sequence alignments? There are a bunch of different alignment tools out there, and I don't want to get bogged down in the maths behind them as this not only between software but varies from software version to version.

There are two main divides in the programs; some use local alignments and others use global alignments. My question is threefold:

What are the fundamental differences between the two?
What are the advantages and disadvantages of each?
When should one use either a global or local sequence alignment?

The very basic difference between a local and a global alignments is that in a local alignment, you try to match your query with a substring (a portion) of your subject (reference). Whereas in a global alignment you perform an end to end alignment with the subject (and therefore as von mises said, you may end up with a lot of gaps in global alignment if the sizes of query and subject are dissimilar). You may have gaps in local alignment also.

Local Alignment

5' ACTACTAGATTACTTACGGATCAGGTACTTTAGAGGCTTGCAACCA 3'
             |||| |||||| |||||||||||||||
          5' TACTCACGGATGAGGTACTTTAGAGGC 3'

Global Alignment

5' ACTACTAGATTACTTACGGATCAGGTACTTTAGAGGCTTGCAACCA 3'
   |||||||||||    |||||||  |||||||||||||| |||||||
5' ACTACTAGATT----ACGGATC--GTACTTTAGAGGCTAGCAACCA 3'

I shall give the example of the well known dynamic programming algorithms.
In the Needleman-Wunsch (Global) algorithm, the score tracking is done from the (m,n) co-ordinate corresponding to the bottom right corner of the scoring matrix (i.e. the end of the aligned sequences) whereas in the Smith-Waterman (local), it is done from the element with highest score in the matrix (i.e. the end of the highest scoring pair). You can check these algorithms for details.

You can adopt any scoring schemes and there is no fixed rule for it.

Global alignments are usually done for comparing homologous genes whereas local alignment can be used to find homologous domains in otherwise non-homologous genes.

Take look to the attached image file. It will clear your doubts about difference between local and global sequence alignments.


What is the distinction between chemokines, cytokines, interferons and interleukins? They all seem to describe molecules of similar function and many people seem to use them interchangeably.

Also please include any other similar molecules if I've forgotten any in the list above.

Cytokines is the general class of molecules to which chemokines, interferons, interleukins and others belong. Biologists dispute whether something is a hormone or a cytokine, but generally the consensus goes with if it's to do with immunology it's a cytokine or if the resting concentration is in the picomolar range, but that's a very rough distinction.

Chemokines are molecules that drive cellular chemotaxis. That means they make cells move towards a desired place. Generally chemokines refer to immune cells and there's loads and loads of them.

Interleukins are anything which are messenger molecules between immune cells (inter- means between and -leukins means leukocytes/white blood cells). They're typically denoted by IL + number. However the interferon and tumour necrosis families come under interleukins too in most people's opinion. The interferons are a special group that typically inhibit viruses by making cells non-permissible to viral replication. They also do a few other things like activate macrophages or promote Th1 response, which both also interfere with viruses but there is bacterial overlap. The TNF family is a bit weirder as some are interleukin-like but others aren't as much. TNF-alpha (the classic one) is involved in macrophage maturation. However not all interleukins are strictly between white blood cells, as IL1 acts on the hypothalamus among other leukocytes.

See the problem is everything is a bit grey because most cytokines (if not all) have more than one role and there's never consensus in the world of immunology when it comes to cytokines because more and more keeps getting discovered.

Pharmacology cross reference: Recombinant type I interferons are injected as therapeutics. Viral infections would seem like logical indications, but interferons are both expensive and have considerable adverse effects, e. g., flu-like symptoms on injection, anemia and depression. Their application is therefore limited to life-threatening viral diseases, e. g. hepatitis C.


Can you eat enough to make your stomach explode? Background

After eating a large meal last night, I noticed that my tummy had significantly enlarged. After that, I started wondering if eating too much could cause a stomach to explode. Could this actually happen?

Question

  Are you able to explode your stomach by eating too much? Can it pop or break?

I assume your body would just regurgitate the extra food.

  What if you held in the regurgitation? Then would you explode?

Here's a simple cross-section of the stomach (from here):

The stomach accomplishes much of its function by mechanically breaking down the swallowed food particles and mixing them with acid and enzymes into a sort of slurry. To do this, there are three major layers of muscle surround the stomach - from the outside, the longitudinal layer, the circular layer, and the oblique layer. The stomach also has two holes in it - the gastroesophageal opening, coming from the esophagus with the swallowed food/saliva mix, and the pylorus, where the food/acid/enzyme slurry exits into the duodenum, which is the beginning of the small intestine.

Due to the three layers of (rather strong) muscle, the stomach doesn't have a lot of expansion capability once it is filled completely to capacity. Fortunately, this almost never occurs (despite how we may feel after a large meal) because material is always leaving the stomach on its way to enzymatic digestion in the intestines. Additionally, once the stomach is filled to a certain extent, hormones such as leptin are secreted that give you the feeling of being sated, or full, triggering the brain to make you stop eating.

Of course, as we can see with the current epidemic of obesity around the world, the stomach can change its size over time. However, this is a rather slow process (weeks to months to years) of adapting to continuously consuming large meals.

But what would happen if you completely ignored these internal warnings, or were being force-fed, or whatever? Instead of rupturing (the biological equivalent of "exploding"), food would most likely be expelled either into the small intestine or back into the esophagus and back up the way it came down, i.e. causing vomiting.

For this answer to be complete, however, I should point out that stomach or gastric rupture is technically possible, although it is an extremely rare occurrence. Cases have been described in the literature (1, 2, 3, etc.), but they are rarely correlated with overeating or eating disorders like bulemia. In cases that are, other pre-existing conditions such as gastric ulcer have been found on autopsy that likely weakened the stomach wall in the first place. The bottom line - if you're an otherwise healthy person, a single instance of massive binge eating is very unlikely to end in stomach rupture, as vomiting will most likely begin well before you are in significant physical danger.

First of all, you must understand the way that our(human like) digestive system, simply digests the food. Here is some information about what happens when you eat:

Digestion is the process of changing food into a form that the body can absorb and use as energy or as the raw materials to repair and build new tissue. Digesting food is a two-part process that’s half mechanical, half chemical.

Mechanical digestion begins in your mouth as your teeth tear and grind food into small bits and pieces you can swallow without choking. The muscular walls of your esophagus, stomach, and intestines continue mechanical digestion, pushing the food along, churning and breaking it into smaller particles.

Chemical digestion occurs at every point in the digestive system, beginning when you see or smell food. These sensory events set off nerve impulses from your eyes and nose that trigger the release of enzymes and other substances that will eventually break down food to release the nutrients inside. The body then burns these nutrients for energy or uses them to build new tissues and body parts.

ALSO HERE ARE THE COORDINATES OF YOUR "TUMMY":
Your stomach, a wide, pouchy part of the digestive tube, is located on the left side of your body above your waist and behind your ribs.

Now, lets get to your main body of your question:

Like the walls of your esophagus, the walls of your stomach are strong and muscular. They contract with enough force to break food into ever smaller pieces as glands in the stomach walls release stomach juices — a highly technical term for a highly acidic blend of enzymes, hydrochloric acid (HCl), and mucus. The stomach juices begin the digestion of proteins and fats into their respective bodily building blocks — amino acids and fatty acids.Churned by the stomach walls and degraded by the stomach juices, what started as food — apples, pears, potato chips, steak, cake, you name it — is now a thick, soupy mass called chyme (from chymos, the Greek word for juice). The stomach’s wavelike contractions push this messy but still intact substance along to the small intestine where your body begins to pull out the nutrients it needs.

Moreover you should consider that the stomach is made from muscles; that makes it strong and immune to HCL. So, if even a very strong acid like HCL can do any damage to the stomach, will a very big meal make it to explode? Simply it will force yourself to vomit just because the very big ammounts of food can't be digested.


Can you tell me what species of insect this is? I live in Verona, Italy.
Today I found this black insect and I don't know what species it is. My mom claims it's a kind of mint but I don't think so.

This looks like a horsefly (family Tabanidae, in Italian "tafani"), maybe Tabanus bromius but I'm not sure. If it's so, be careful: they bite and their bite is painful. Here you can find some quick suggestions about horseflies and their bite.

However, as you live in a city, don't worry too much: as the female horseflies feed on horse and cattle blood, they are normally present in the countryside, so those that you saw are exceptions more than the norm!


Neurons competing for survival I was reading in a book that in the process of neurogenesis - when new neurons are born -  neurons compete for survival. Or in other words they have to make themselves useful to the brain otherwise they die and become processed as brain food.

To what extent is this real and how often does this happen?

i think that in the book I was reading it the author mentions it happening in early life, but I'm not entirely sure.

Would be great to know.

Thank you!

It's definitely real ;)

Depending on your previous knowledge, this review from 1987 might be a good starting point.
http://science.sciencemag.org/content/237/4819/1154.long

To give you an idea of recent developments this article is an easy read. Be sure to browse the references.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612357/


Can rats pass on memories of a maze to their offspring? A friend of mine told me once about a documentary movie he saw some years ago. On this movie he saw scientists talking about particular experiment. This experiment involved rats and probably electrical traps. The rat had to get to the cheese, there were traps on the shortest route to it, and obviously it got shocked few times. What is interesting is that my friend says that when they took its offspring (probably born later) they avoided those traps.

I'm aware that its not how "genetic memory" works. Its not memory of individual, but of species (so it requires evolution). This is what I'm trying to explain to him, but he says "he knows what he saw".

Anyway maybe someone here is aware of such an experiment. I believe that he is wrong about something (or conclusions drawn where changed later), so I would like to find out more about it.

To sum up:

Its not Tryon's Rat Experiment
It involved: rats, traps (probably electrical), more then one path to cheese, rat's offspring and some sort of memory/learning amongst rats.

The phenomenon you're talking about was a fad in the 60's, called 'interanimal memory transfer'. It started out when James McConnell performed a later-discredited experiment in which he found that if you chopped up flatworms which had been exposed to some stresses, and fed them to other unexposed flatworms, the unexposed worms became wary of the source of stress quicker after eating their dead companions. He jumped to the conclusion that a 'memory molecule' was being transferred, and that the cannibal worms gained the food worms' memories of the stress.

People then started looking to see if they could:

repeat the experiments
find the same phenomenon in other animals

In the first case, nobody could replicate the experiments in worms, but because McConnell was such a PR genius he managed to convince the public that his results were valid (see Rilling, 1996 for more on this).

In the second case, Frank et al. (1970) and others tried working with rats - I think this is the experiment you're talking about in the question. They found various interesting results including that if you trained rats to run through a maze by using particularly stressful negative reinforcement (like electrocution), then those rats' children would be able to learn the new maze much faster. However, Frank et al. didn't make the same mistake as McConnell - first of all they wondered if the parent rats might be leaving a scent trail. So they used duplicate mazes with the exact same design, putting the children into clean mazes. The children of adults who had already learned the maze continued to outperform the control rats - the explanation was not scent trails.

Next they wondered whether it might be that the second generation rats had been born with a higher wariness as a result of the stress their parents suffered; i.e. it could be a hormonal transfer from mother to child (e.g. cortisol, the stress hormone).

Frank et al. tested their hypothesis by torturing some rats for a while (rules about animal welfare were not strict in the 70's). They would lock some rats in a small jar and bash them about for a long time, then kill them, chop them up, and take out their livers. They fed the livers to other rats, and found that after eating the livers the other rats learned the maze much faster. They interpreted the results in what now seems a sensible light: the stressed rats were producing high concentrations of a stress-signalling molecule. When those rats either had children or were fed to other rats, they passed on high doses of the stress molecule. This raised the alterness and wariness of the receipient rats so that they were much quicker to learn which parts of the maze were dangerous.

There is no evidence that the child rats actually 'remembered' the maze - they still had to find their way around, but they were extremely wary of the electrocution plates and so avoided them, finding the safest way to the end. This is not a case of genetic memory.

 Frank B, Stein DG, Rosen J. 1970. Interanimal “Memory” Transfer: Results from Brain and Liver Homogenates. Science 169: 399–402.
 Rilling M. 1996. The mystery of the vanished citations: James McConnell’s forgotten 1960s quest for planarian learning, a biochemical engram, and celebrity. American Psychologist 51: 589–598.

https://www.facebook.com/ScienceNaturePage/videos/1319435594855362/

I’m not sure if this is the right link, but there was a video on Facebook called “memories can pass between generations DNA” posted by hashem al-ghaili, it is 4 minutes and refers to an experiment where mice passed on maze knowledge to their offspring...


Why do people say that trans fatty acids are bad for your health? I've heard from several sources that trans FAs are bad for you and their consumption will lead to cardiac problems, and that they are indigestible.
But I also learned from biochemistry that they are digestible. What is the reason for this, or is it true at all?

Trans fatty acids are digestible, but they cause an increase in LDL and a decrease in HDL, which is the leading mechanism for atherosclerosis. So, they increase the risk of a cardiac infarct.

LDL means Low Density Lipoprotein, it's one of the 5 major lipoprotein groups. Lipoproteins carries the fatty acids and cholesterol which were absorbed from intestines (because lipids are hydrophobic and cannot be carried within the blood directly like glucose or proteins.)

So, LDL mainly carries cholesterol and fatty acids from intestines to tissues. (fatty acids and cholesterol are essential for cells.) But in excess levels, they tend to accumulate in vessel walls, which also starts and inflammatory response and makes the situation worse. (mainly includes macrophages and T cells) This is the main mechanism for atherosclerosis.

In the other hand, HDLs serve as a reverse cholesterol transport system, which carries the cholesterol back, mostly to the liver (for bile secretion) or steroidogenic organs such as adrenals, ovary, and testes by direct and indirect pathways. So a high HDL reduces the atherosclerotic process.

You are right the biology text books claim that trans-“unsaturated” fatty acids can be metabolized. Note : - The text books make it clear that “Trans” means the fatty acid is unsaturated and can be monounsaturated or polyunsaturated.

Trans fatty acids are generally being blamed so as to keep to the unfortunate false “theory” that certain poly unsaturated fatty acids are essential for humans. This false “theory” is the basis for the epidemic of obesity and most of the strange and lifestyle diseases. The actual culprits of the epidemic of lifestyle diseases is the high levels of polyunsaturated fatty acids (both trans and cis) we consume through the processed unsaturated vegetable fats.

Check from your text books, atherosclerotic plaque is made up of oxidised polyunsaturated fatty acids and cholesterol (which has been labelled LDL cholesterol).

Prostaglandins, which are produced in the body by polyunsaturated fatty acids, have been identified by many different research studies as the molecules underlying diseases and ailments such as diabetes, asthma, cancers, dysmenorrhea (menstrual pains), baldness, cramps and muscle pull, migraine, glaucoma, delivery and labour problems, etc.

Aspirin according to the research results, reduces the chances of cancer occurrence or dying early from cancer. Aspirin stops the production of prostaglandins in the body.


Validation of houskeeping genes in a mixture of cDNAs of two species I have a parasite sample (mixed with host blood) and I need to check gene expressions of parasite using relative quantification (RT_qPCR). For this, I need a good housekeeping gene. I chose 10 genes (suggested as housekeeping) that I need to validate and after choose the most stable one(s). My problem is that my parasite cDNA is mixed with host cDNA and it is impossible to separate them or count the parasite. I do not know how I could choose the best housekeeping gene in this case? I do not have the real amount of parasite cDNA used for qPCR, and I do not have any good internal control. Basically, it is circular problem: In order to validate my target gene I need a good housekeeping gene for internal control, but I do not have an internal control to make relative quantification of my housekeeping genes and to chose the best one. Could you please suggest any study or method that deals with such a case?

Two possibilities:

Design primers based on differences in the sequences of the gene for the same protein between the two organisms. (Suggested by @Artem)
Identify an aspect of the metabolism of your parasite that is not present in the host, then use enzymes from that pathway. If the parasite is a worm and the host a mammal, for example, you should surely be able to find something.


Relationship between lifespan and reproductive age? I remember reading a while ago that there is a "general rule" in biology between an animals lifespan and when they reach reproductive age.

In other words, an organism that reaches sexual maturity after a short amount of time (for example, less than a year) will have a short lifespan (for example, 2-3 years) and an animal that reaches sexual maturity after a long time (elephant, 10-12 years) will have a much longer lifespan (40-60 years in case of elephant).

Is there a special name for this "law" or "rule"? Are there any major papers/theories supporting it that also attempt to propose why (perhaps from an evolutionary perspective) this trend exists?

Some quick supplemental questions:

1.) Is there also a trend between lifespan and animal size?

2.) Is there also a trend between lifespan and base metabolic rate?

3.) Do the two aforementioned "trends" or "rules" have technical names that I could look up as well?

The sort of thing you're talking about would be called a Life History Invariant: a dimensionless ratio between two life history traits $A$ and $B$, such that although the traits themselves vary widely between species, the ratio $\frac{A}{B}$ is relatively constant.

Eric Charnov has written a lot about this, including a book.

One of the invariants which has been suggested is the ratio of age of maturity $\alpha$ to adult lifespan $E$. Charnov claims that it is relatively invariant within taxa, but has a different value for eg. fish vs. mammals vs. birds vs. reptiles.

From Charnov and Berrigan, "Dimensionless Numbers and Life History Evolution: Age of Maturity Versus the Adult Lifespan", Evolutionary Ecology (1990).

(If the ratio $\frac{A}{B}$ is invariant, then plotting $A$ vs. $B$ for different species on a regular graph will give you a straight line passing through the origin. The slope of the line gives you the value of the invariant.

Sometimes, in looking for an invariant researchers will instead graph the quantities on a log-log plot: they then look for whether the curve is a straight line with slope 1 (whose height gives the value of the invariant), with a good fit. This method has been criticized: the fact that some quantities are just about necessarily a fraction of other quantities (eg. you can't really lay an egg bigger than yourself), together with the fact that log-log plots "squish down" variance about the regression, opens the possibility of observing artifactual yesses. I tried to give an intuitive explanation of this criticism in a quora answer. Charnov and company have dismissed it as not applying to the invariants they found, however.)

This invariant is slightly different than the one you describe, in that they deliberately ignore pre-maturity deaths. (If infant mortality were high enough then it would be possible for average lifespan to be less than the age of maturity.) Also, they measure the ratio of pre-maturity lifespan to post-maturity lifespan $(\frac{\alpha}{E})$ instead of the the ratio of pre-maturity lifespan to total lifespan $(\frac{\alpha}{\alpha+E})$. These are just two different ways of talking about the same thing, but the former has an upper bound of 1, while the latter has no upper bound.

Finally, it's important to note that even if a quantity is relatively invariant, it can't be expected to be perfect; you have to decide how much noise you want to allow while still finding an approximate invariant interesting.

I can't find a very fine writings/documents to support this or satisfy your question.

I think, it's related somehow. Let's take a sample: (It's not super accurate but you can make a search)

 ------------------------------------------------------------
|  Creature        Lifespan              Reproductive Age    |
 ------------------------------------------------------------
  Butterfly        7 week           Until become a butterfly
     Dog        around 14 yrs            around 9 months
    Human       around 80 yrs            around 10 yrs
   Whale        around 80 yrs             around 8 yrs
  Jellyfish    can be immortal        depends on a situation

The data above is some-kind the "usual" but still it's not the 100% of proof. There are other factors that affects the lifespan and reproductive age relationships like:

Usual/Common ability to produce no. of offspring/s --- Like whales or elephants, they can't produce a ton of offspring in one shot so their lifespan can be longer. Or those cockroaches, they have short lifespan but they can produce a ton of baby roaches in one egg.
Environment Capability --- If one can survive longer in one place, then there's a possibility of late reproduction maturity but when a creature has less of percent of survival in one place then there's a possibility of early production of offsprings. It all depends on the environment.
Lifestyle --- Bad habits and unhealthy foods can shorten ourlives but good habits and healthy foods can help use for longer lives.


Do birds have quadriceps and thighs fused into their hips? I'm looking at 3D modeling a large bird like an emu or ostrich, but I don't know how the muscles surrounding the femur connect to the hips/back. It seems weird that the entire thigh and quadriceps would be fused into the hip because that would greatly reduce the range of motion of the femur which affects how I animate it, but I can't find any reference that shows it either way.

This is probably WAAAAY to late to be of any use to you but hey...
So the simple answer is:
Kinda.
You were actually correct to intuit that the femora of birds have a limited range of motion, with most of the limb motion being provided from the "knee"-down.
So you shouldn't animate bird legs the same way that you would the legs of other non-bird animals.
That's not to say that the femur doesn't move - it does but not my much (it typically doesn't extend posteriorly beyond the vertical). Much of the thicc thigh musculature is there for support.


Can pulmonary infarction be asymptomatic? I think it can because there are many parts in lungs.
Like for some COPD patients.
However, I am not sure if COPD patients can have infarction.

Lungs have parallel circulation.
Red infarct is possible there.
Blood can flow there.
One symptom should be at least pain.
So now, I think no asymptomatic possible.
But still, I am not sure.

Can pulmonary infarction be asymptomatic?

No. Based on experience. Lungs are very active organs.


What is "beto carotene" and how can it turn lakes pink? The BBC News article Pink lake in Australia attracts and delights tourists describes an artificial salt lake in Westgate Park, Melbourne, Australia that tuns pink around February and then in "late Autumn, until cooler temperatures restore it back to blue."

I am not sure about the autumn part as it's in the southern hemisphere, but my question is about the color change.

Could they mean beta carotene rather than beto carotene?
And if so, does the pigment stay inside the algae or is it released into the water to produce this color change?
And why pink, rather than the orange color we associate with carrots?

  In those conditions, the lake's algae produces a red pigment called beto carotene

  The lake's pink colour typically lasts through to late Autumn, until cooler temperatures restore it back to blue.

The "beto" is a typing mistake. Beta is an organic chemistry label referring to a beta-ring of 6 carbons that exists at either end of a carotenoid polymer C40-Hx.

It is localized in the chloroplast. The plants don't really have a mechanism to release pigments, they can re-metabolize chlorophyll. The volvocalean algea Dunaliella salina is used to harvest beta-carotene in Karratha, Western Australia, from salt lakes. The can have 12% beta-carotene as dry-matter content, the highest of any known source.  The squares are probably salt.

the algea afterwards:

There are over 1,100 known carotenoids of which at least 700 have been identified in plants. They include carotene and xanthophylls, and carotene include beta-carotene. The plants and algea use it to protect themselves from intense sunlight and UV's. It is an anti-oxidant.

Pink doesn't actually exist as a color. It is imagined when green and blue light is sensed by the eye, while red is at a maximum. In the lakes, we know there is 80% red and 20% green pigment in the algea. All that is required would be 20% blue to percieve pink. I don't know where the blue color comes from, the sky/water.
Orange is complex for the eye, and so is pink, because we can only see red green and blue.

Not sure which kind of microorganism they talk about, but beta-carotene is a red-orange~ish pigment (as you pointed out, also produced by carrots). The pink coloration I would assume is the product of the color mixture of the pigment with green-blue from the water (not the water itself but the blue reflection from the sky + any other algae in the water). If they release it (the beta-carotene) to the water, again not sure which organism they talk about but it's probably not like it, since beta-carotene is a photosynthetic compound. Therefore is pretty likely they may want to keep it inside.


Why aren't we ambidextrous? It seems so simple that if my brain can tell my right hand to do something, then it should be able to tell equally well to the left ? This seems like a pretty major evolutionary advantage. Why haven't we evolved so during millions of years ?

Having a dominant side is advantageous. Instead of seeing it as the brain influences our fine motor skill, think of it the other way round. The way we use our hands or any other part of our body sends feedback to the brain to increase the portion of the brain devoted to that region of the body and of course with disuse the reverse occurs. The more you do a certain task the more that portion of the brain gets better and coordinating the movement. The portion I talk about is the primary and supplementary motor cortices. So basically we are specialising. In the same way a heart doctor is better with treating conditions of the heart than a foot doctor. So we can either devote our experience to the one hand, or both or the other hand. If we use both hands equally our brain adapts so that we are ambidextrous, if instead we use just the one hand our brain develops just that side. But if you do focus on both you are using your dominant hand less so overall same amount of development just over both sides of the brain rather than just one side. You can probably see the benefit of having this plasticity of improving only what is used because why improve what we don't use and waste resources? And you may also see the benefits of higher specialising of one hand rather than having two slightly specialised hands. There are few tasks that require both hands to be very specialised, but if that were the case then the body would go ahead and do that but in spending time training your hands you are probably training your legs or something else less.

///

Why not have a switch between the two hemispheres to give the hand currently being used the fine motor skill located in the other hemisphere? (from comment)

I see. In my answer I only talked about one aspect. The brain doesn't have to learn skills for each hand completely independently. For example imagine if you learn to play a musical piece with your right hand only. If you try it with your left you won't be amazing but you'll definitely be better than a complete novice. Our brain can learn how to do by seeing which is vital for development. But there's a limit to that, your hands aren't completely identical so there's still a portion that needs fine tuning. Your muscles have different stregth, fatigue, resistance, recruitment patterns, places they innervate. Your hands are mirror images. The weight of your hand is different. And not only that but these variables aren't fixed, there's lots of them and they are different for different tasks. So to use your analogy, the more expensive remote can be used but it wasn't bought for use with the black plane. It'll give more control to the black plane but it still won't be the best ever until it learns what the muscle strength is etc. then it will be just as great.

A simple answer to this is that at some point our brain's architecture was wired to have a dominant side, at which point it became too expensive evolutionarily to have drastic brain re-organisation or size changes.

Another answer to this is that the two sides have many different specialisations and functions. While having similar bodily control from both sides might seem to be an advantage, that would mean that one of the hemispheres would have to dedicate more neural circuitry to finer motor control. This means less neural material will be available for other tasks. Alternatively, if you want to be able to do other tasks equally well like now (and keep the specialisation of the hemispheres) , but have ambidextrous ability, you'd possibly need a bigger brain.

So, while it might seem like a good idea to be ambidextrous, it would probably come at a high cost on other brain functions or brain size.


Can a blood type O be born from AB and A parents? I have a basic understanding of genetics, and I'm really puzzled by this. My grandma's blood type is A (I don't know if it's heterozygous or homozygous) and my grandpa is AB. Yet my mother is type O.
Grandma says that my mom is 100% my grandpa's child, so how did it happen?
I have a few hypotheses regarding this. Either my grandma is lying, which I find to be really implausible, or there's some genetical anomalies either in my mom or my grandparents.
I suspect that grandma is heterozygous, having the IAi genes for blood type, and grandpa has a weird case of IAIBi alleles, coming either from a failed disjunction which caused both alleles for A and B to be present in one sperm cell, and the i allele to be present in the egg, resulting in the IAIBi genotype. Then, when grandpa had my mom, both i alleles got combined and out came my mom with O type.
My other hypothesis is that mom is heterozygous, either IAi or IBi, but the dominant allele underwent a deletion (or something else) and was inactivated, and as such only the recessive allele remained, giving her type O blood.
Could I get some insight on how this happened? I can't seem to find anything related to it on the internet.

The ABO blood type is controlled by a single gene (the ABO gene) with three types of alleles inferred from classical genetics: i, IA, and IB. The IA allele gives type A, IB gives type B, and i gives type O. As both IA and IB are dominant over i, only ii people have type O blood. [1]
So from this standpoint, normal Mendelian genetics cannot explain the blood-group 0 offspring, given the AB parent.
However, besides errors in testing, the (pseudo?) 0-bloodgroup could be explained by the Bombay phenotype. I don't know the incidence rate in your region, so I can't comment on the likelihood.
To give theoretical background, this would be considered a pseudo 0-phenotype, as the individual genetically does not need to be ii. Instead, the individual lacks another effective enzyme that is required for the A or B alleles to be effective; the blood-type specific sugars (N-Acetylgalactosamin|Galactose) cannot be attached to the red blood-cell membrane, as the anchor of these sugars (called H-substance) is not present.
Finally, to address your hypothesis of a gene-duplication followed by a gene knock-out: There is no need for a preceding duplication. The more probable cause is a single point mutation (or multiple) near the active center of the inherited A/B enzyme, or a nucleotide insertion/deletion in its coding region, causing a frame-shift. A completely (not partially!) inactivated A/B enzyme would effectively represent a novel 0-genotype.

Given that your grandmother is type A and your grandfather is AB, there is very small, minute chances that your mother is in fact the biological child of one or both of them.  For your grandmother to say that she is 100% your grandfather's child, maybe he had her with someone other than your grandmother, and due to unfortunate events, that woman died giving birth or shortly thereafter.  It may hurt your grandmother to admit that. Or, she could have the same views as many others, like myself, and recognizes that there is a BIG difference between being a father and raising a child, and just being a sperm donor and disappearing. There are many different situations that could be possible, that your grandparents may not be ready to admit for whatever reason, or it could very well be a simple mistake at the lab who did the testing. But does it honestly matter if she is the biological child of both grandparents, or whatever the truth may be? Will knowing the answer change anything?


What are evolutionary implications of contraception and reduced childhood mortality rates worldwide? I've heard the following idea this morning: Before the introduction of contraception, humans conceived quite a lot of babies (there was little to do to avoid that), but the population was kept in check by very high childhood mortality rates. This mortality rate ensured that only the fittest survived.

The idea seems common sense, but I decided to investigate if this is really true. I know that for evolution, even 2000 years should be an instant.

I did some research, for example the worst childhood mortality rate currently in the world is around 17.5%, which is still about half of what it was in "developed" countries during the 1700s, according to the table below. But looking at the wikipedia map of childhood mortality, it seems that a baby nowadays has only around 1-3% chance of dying before adulthood, because even the weakest baby can be kept on life support long enough for the danger to pass.

What are the implications of reducing childhood mortality rates worldwide on human evolution? Maybe evolution is a wrong term to use here. Would it be fitness as species? I'm particularly interested in how this relates to developmental defects and genetic disorders. Is there any evidence that people who lived in a world without contraception and with high childhood mortality rate were more physically or mentally fit?

Here's an paper that deals with the subject and the table is from the paper below:

IS CHILD DEATH THE CRUCIBLE OF HUMAN
EVOLUTION?

Before the introduction of contraception, humans conceived quite a lot of babies (there was little to do to avoid that), but the population was kept in check by very high childhood mortality rates. This mortality rate ensured that only the fittest survived.

Woh! Let me stop you there. No, high rates of childhood mortality do not ensure that whom Natural Selection is acting upon are the "most fit." That title is given to individuals who are able to survive long enough to breed.

Many, many conditions that affect humans do not interfere with a person's growth or ability to perform physical or intellectual feats - but can definitely reduce or completely eradicate a person's ability to reproduce. These individuals are evolutionary dead-ends, and thus - while they survive in the environment - are not "fit" in the context of this topic.

  What are the implications of reducing childhood mortality rates worldwide on human evolution? Maybe evolution is a wrong term to use here. Would it be fitness as species?

What it means is that populations will rise. As populations rise and intermingle, alleles get spread around. Perhaps rarer alleles become more common, or more common alleles become rarer. We're talking about Hardy-Weinberg equilibriums in the allele frequencies. However, with populations large enough true equilibriums are impractical to reach.

The more pragmatic explanation is that more mutations will arise, they'll be passed around, rare mutations will see more exposure, and humanity - in a very general sense - becomes more diverse genetically until a Selective Pressure is applied. Until there's a detriment to having a particular gene, there isn't a need to eliminate it from the population.

Your example is children who are too weak at birth to live outside of an NICU for their first few months - well, because we're capable of providing such care, until that care goes away it's not negatively affecting us. If it comes with an additional cost - say that, for whatever reason, premies can't digest mother's milk until the 8-month mark, then Natural Selection would pressure humans to evolve so that only 8+ month or older babies are born.

There's no evidence of significant pressures in human populations at this time, though. At least not in politically stable and technologically apt countries, although in areas undergoing long-time drought or other dangers it is seen. Sickle-Cell Anemia is though to be an adaptation to rising Malaria rates - which was quite fatal until medication was devised to treat it in the last 50 years or so (not even a blip in evolutionary terms).

  Is there any evidence that people who lived in a world without contraception and with high childhood mortality rate were more physically or mentally fit?

Not that I can think of or find easily. While there are detriments associated with being born prematurely, and some evidence that women waiting until they're late 30's and men until they're 60 or older can negatively affect their gametes and consequently the development of any children born from them - it's been such a short time since the introduction of hormonal contraception and modern medicine that we may not see results tangible results for hundreds of years. Although condoms have been around for several hundred years, and there's been no associations with condom use that I can think of.

In the short term, what it has done is affect the ethnic diversity of countries. For the first time ever, Hispanic births have outnumbered Caucasian births in 2012 in the United States. Other countries, mostly European countries, are seeing declines in birth rates - which means their populations will decline with age or be compensated for by immigration. Higher birth rates, however, are associated with lower income brackets or very religious communities - both of which are associated with ethnic Minorities, at least in the United States. So while minority populations have more kids, they do so on fewer resources which may negatively affect their children in the long-term, whereas higher-earning segments of the population might have fewer children later in their lives, but can provide a much more stable environment and opportunities to continue that success.

One thing that hormone-centered birth control has done, however, is eliminate rape as a viable form of passing on one's genes. As gruesome as it might be to consider, pregnancies as a result of rape can produce "fit" offspring. It is a legitimate reproductive strategy in nature, and is in humans... unless the woman is using contraception. In the long-term this will probably show some interesting results (nominally an enhanced "Female Choice" effect - which is already evident in human evolution), but nothing right now.

It's also worth considering the ability for humans' increasing abilities to manipulate our own genome. At this point, we're nearly able to remove detrimental genes at-will and replace them with more effective versions. Because of this bio-engineering ability, the generations after ours might never be susceptible to inherited diseases - or they might all hop on the trendy "genes" and end up completely identical to each other. That's part of the fun of being human, though; we're very messy when it comes to Evolution. We tend to muck things but up good. :)

Well , Ime sorry but sometimes a question have to be rephrased in order to reach the ''elefant in the room''  : The important question is if the existence of contraceptives in itself wil change the direction  of human evolution . After the invention of contraceptives the meaning of ''survival of the fittest'' is something very different , from now on the RESISTANCE to the effect of contraceptives becomes the dominant factor in determining fitness for suvival .
 This resistance can be compared to the resistance develped by a population of insects being subjected to a targeted poison :  before or later the population will develop some kind of resistance , even in cases where this can only be achieved by a complicated and indirect mecanism .
  Humans can achieve such resistance in several ways easy to imagine , and probably also in others very hard to imagine .
 The most obvious is by cultural adabtion , by developing a culture that prevents the efects of contraceptives . This can already be seen in the demografic growth of several population groups dominated by strict compliance with a beliefsystem damning contraceptives... . Many would argue that this has nothing to do with genetics , but actually a very strong case can be made for the opposite position .
 A less obvious way to devellop resistance is selection for a maternal or parental instinct , operating seperately from the sexual drive which has been ''poisoned'' .  In any population , even with an extemely low birthrate , there will always be a few individuals who will have lots of children , no matter what .  Given time enough ,and especially in a low-bithrate population , this behavour will be selected again and again until the underlying genetic mecanism  will cause it to be come  truely hereditary .  Such is the lessons of  selective breeding towards a derirable quality in  everything from horses to tomatoes , and there are  no reason to believe  humans to be different .  The million dollar question is how many generations this proces wil take ....


Why can't a human regenerate limbs like some other species? When a person's arm is amputated, the arm will no longer be able to grow back. However, in salamanders, the arm actually grows back.

In comparison to a human, what is really happening to the cells in the wounded area in salamander ?

After salamanders (or certain other amphibians) lose a limb, the epidermis migrates to cover the wound, forming a structure known as the apical epidermal cap. The underlying "stump" then generates a de-differentiated mass of cells from normal tissue. In most cases, these cells will express genes that are vital to the proper formation of limbs, such as HOX genes. This "lump" of cells at the stump of the wound are typically referred to as a blastema. Basically, the blastema continues to grow and regenerate the limb in a way similar to fetal growth. Though mammals (including humans) also have some regenerative capabilities, they are much more limited. In addition, many regenerated limbs will also be mildly deformed (square fingernails). In axolotl salamanders, it was found that certain retrotransposons, such as the LINE-1 element, were prevented from "jumping" around in the developing blastema during limb regeneration. The two active proteins PL1 and PL2 were responsible for inhibiting the activity of LINE-1 and other such retrotransposons. Active retrotransposons can potentially rearrange the genes in germ cells can be detrimental to the mechanisms that allow the blastema to replicate and differentiate, so the PL2 and PL1 proteins play a vital role in their regenerative capabilities. When the PL2 and PL1 proteins were "switched off" in certain axolotl salamanders, their regeneration was much less efficient. Since mammals lack the PL1 and PL2 proteins and have a different LINE-1 retrotransposon, they have reduced regenerative capabilities.

Sources:

Wei Zhu, Dwight Kuo, Jason Nathanson, Akira Satoh, Gerald M. Pao, Gene W. Yeo, Susan V. Bryant, S. Randal Voss, David M. Gardiner, Tony Hunter. Retrotransposon long interspersed nucleotide element-1 (LINE-1) is activated during salamander limb regeneration. Development, Growth & Differentiation, 2012; 54 (7)

Wei Zhu, Gerald M. Pao, Akira Satoh, Gillian Cummings, James R. Monaghan, Timothy T. Harkins, Susan V. Bryant, S. Randal Voss, David M. Gardiner, Tony Hunter. Activation of germline-specific genes is required for limb regeneration in the Mexican axolotl. Developmental Biology, 2012; 370 (1)

Odelberg SJ (August 2004). "Unraveling the Molecular Basis for Regenerative Cellular Plasticity". PLoS Biology 2 (8)

For salamanders, when they lose a limb, they have cells called fibroblasts that migrate to the wounded area. These cells are not differentiated and are able to be differentiated to whatever is necessary for regeneration. That sort of cellular differentiation for repair doesn't happen for us humans, yet. Give synthetic biology about 20 more years. :D