To determine no beating cardiomyocytes from ECG or video recording I am trying to find data and some method by which I can see and say that there are some cardiomyocytes not working.
I have reviewed many arrythmia data where I think I can see much cardiomyocetes there and there which are not beating at all.

Is there any method with available data for the recognisition of cardiomyocytes without beating?

I am particularly interested in the paediatric data.
I am using at the moment ECG data after cardiac infarction.

What is the name of this video record?
Picture from House season 3 episode 2:

A number of cardiomyocytes is lost during an infarction. Instead, fibrous tissue forms, but it only preserves structural integrity, having no contractile function [1]. Myocardial infarction is an uncommon condition in pediatrics, happening very rare, when embolization occurs due to blood coagulation affections or heart congenital defects [2].

The fibrous tissue has different properties, thus modifying:

MDE-MRI images [3]
ECG: deep Q wave [4]
echocardiography: hypoechoic and hyperdense echoes inside the fibrotic material (the latter compatible with calcium) [5]

That video record is probably about 3D Echocardiography (look here at Video 2 and figure 2).

References:

Yao Sun, Myocardial repair/remodelling following infarction: roles of local factors
Nicola Carano et al., Acute Myocardial Infarction in a Child: Possible Pathogenic Role of Patent Foramen Ovale Associated With Heritable Thrombophilia
Harikrishna Tandri et al., Noninvasive detection of myocardial fibrosis in arrhythmogenic right ventricular cardiomyopathy using delayed-enhancement magnetic resonance imaging
ECGpedia - Pathologic Q Waves
Berenzstein CS et al., Usefulness of echocardiography and doppler echocardiography in endomyocardial fibrosis


How to know the gestation time of pregnant mice? In lab mice I wish to establish how many weeks my animals are into their pregnancy. Is there some way?

This is generally done by checking for the vaginal plug in the female after you have set up the breeding. If the plug is visible then it means that copulation has happened. However, this is not a foolproof test because the vaginal plug just indicates copulation and not pregnancy. This, nonetheless works in most cases and helps you in timing the pregnancy (Reference: JAX notes).

  For most strains, the rate of pregnancy is highest among
  estrus-suppressed females with vaginal plugs found the third day after
  being placed with a male. As examples, whereas the rate of pregnancy
  is ~100% and 44% respectively for C3H/HeJ and BALB/cJ females with
  plugs found on the third day, it is only 62% and 31% respectively for
  those with plugs found on the fifth day. In contrast, whereas the rate
  of pregnancy for C57BL/6J females is only 39% for those with plugs
  found on the third day, it is 69% for those with plugs found on the
  fourth day.

  If the plugged female is pregnant, the first day of gestation is
  considered to be the day after the plug is found.

You can also monitor for an increase in weight of the mouse. This is not a foolproof technique but serves as a secondary evaluation method.

If you have not timed your breeding and checked for these markers, then you may have to rely on ultrasound.


Why exactly does the immune system weaken with age? Why does the immune system become weaker with age in humans and in some other mammals?  Let's try to be more specific than just "everything degrades with age."

We don't know.

More precisely, we know of many, many different reasons why the immune system deteriorates with age, but we don't really know which are different measures of the same thing, which are independent factors, which factors actually cause problems and which are harmless and incidental, and so on.

There are too many age-related phenomena to try to list. There's a nice recent review Aging and the immune system: An overview which spends time on

Aging and the immune cell repertoire
Cell Intrinsic defects in lymphocytes
"Inflammaging" ("an overall decrease in the ability to cope with different stressors, accompanied by a progressive increase in the organism's pro-inflammatory status")

Each of these broad topics can be broken down into dozens of sub-topics, and the molecular and evolutionary mechanisms underlying each are rarely well understood.

It's a huge area of research, and it's not possible to give a single concise answer.


Where do the 31 spinal nerves start/meet? Which part of the brain is the first place (from top to bottom) where all 31 pairs of spinal nerves (on each side) meet? Or if they all start at one place - where is that?

Nominally, the beginning of the spinal cord is the medulla oblongata, but perhaps the spinal nerves or some sort of "root" of every nerve start at the Thalamus?

They don’t meet.

Some framework:

Spinal nerves contain motor, sensory, and autonomic fibers. Each of these have different pathways.
Spinal nerves don’t go to the brain. Rather, they synapse in the spinal cord with other neurons which in turn go to the brain (sometimes requiring one more synapse).
In the case of motor neurons, we talk about upper and lower motor neurons. In the sensory system, we talk about first order and second order neurons. Explanation below.

Regarding sensory (afferent) neurons:

Touch and limb position sense are mediated by the dorsal column-medial lemniscus system. The first order (primary sensory) neurons from the spinal nerves, synapse on a second order neuron in the dorsal column in the medulla. There it decussates (i.e. courses to the contralateral side) and ascends via the medial lemniscus to the thalamus. There it synapses with a third neuron that courses via the internal capsule to the primary somatic sensory cortex.
Pain, itch, and temperature sense are mediated by the anterolateral system. These first order (primary sensory) neurons synapse at the spinal level they enter. The second order neuron decussates at that level and courses rostrally via the anterolateral column, ending up in the thalamus. There it synapses with a third neuron that courses via the internal capsule to the primary somatic sensory cortex.

Conclusion: It takes three neurons (inclusive) to get from the spinal nerve to the primary sensory cortex in the postcentral gyrus of the parietal lobe.

Regarding motor (efferent) neurons:

Limb muscles are innervated by circuits beginning in the primary motor cortex. These upper motor neurons descend to the medulla, decussate here, and continue caudally via the lateral corticospinal tract. At the level of the spinal nerve, they synapse with neurons in the lateral ventral horn. These are the lower motor neurons that become the spinal nerve.
Axial/girdle muscles are innervated by circuits that also begin in the primary motor cortex. These upper motor neurons synapse in the midbrain, descend, and decussate at the appropriate spinal level. They synapse there with the lower motor neurons that exit the spinal cord and end up in the muscles.

Conclusion: It takes two neurons (inclusive) to get from the primary motor cortex in the pre-central gyrus of the frontal lobe to a spinal nerve.

In the cortex, these circuits also don’t all come together. They are actually quite diffusely organized across the sensory and motor cortices. Here is a representation of the sensory cortex.* It is a schematic of the post-central gyrus with pictures to indicate where the signals from various body parts end up. The motor cortex is similar. (Google homunculus if interested.)

In addition the pathways described for cognitive perception and control, there are others that help with sub-conscious control of movement (e.g. those involving the cerebellum and basal ganglia), sub-cortical perception of pain signals (e.g. amygdala), and even spinal reflex arcs that never reach the brain. Not all circuits that begin or end in the spinal nerves are destined for or originate from the cortex

This is already considerably over-simplified, and the autonomic system is more complex yet and is not confined to spinal nerves, so I won’t detail it. These signals originate in and feed back to an entirely different area of the brain (mostly hypothalamus). Similar to the motor and sensory systems, at least one synapse is required to connect the brain to the peripheral nerve.

Conclusion: they don’t meet.

Reference:

Martin, John. Neuroanatomy: Text and Atlas. McGraw-Hill Medical; 3 edition (March 27, 2003)

*The source of this image is: http://www.mindtrippingshow.com/mind-trip-of-the-week-17-how-do-we-feel-the-world


What type of insect is this? ery bug 1]1

What insect are these? Found them indoors. No wings, just crawling on the walls.

Looks like a termite; male; after loss of wings.


"Next generation" brain scanners, can they detect CTE? I've just read the news that a "new generation" brain scanner is under development. I wonder whether they can detect chronic traumatic encephalopathy. I haven't been able to find the paper about these new brain scanners.

So is it possible to detect CTE (during life of the patient, i.e. non post mortem) with this new device, and if not, is there any chance it will be possible in the future?

I do not know the details of the innovation, but it's based on MEG. MEG is a complementary technique similar to EEG, sesitive to magnetic fields instead of electrical fields (hence the 'M' in place of the 'E'). It is used to read population brain activity in real time, and is less useful as a tool to assess structural changes. MEG is currently mainly used for research purpose, and I don't see this innovation changing that. CTE could manifest in longer conduction delays or disruption of communication, but given that MEG can only access certain areas of the brain, it is probably not going to be very useful in general. I can imagine it being useful for some very specific CTE cases.


What is the use of futile reaction cycling such as Fruc-P to Fruc-BP? One rate-limiting step of glycolysis is the conversion of Fructose-6-Phosphate (Fruc-6-P) to Fructose-1,6-Bisphosphate (Fruc-1,6-BP), catalysed by Phosphofructokinase 1 (PFK 1). The reaction involves hydrolysing one ATP to ADP.

The reverse reaction of gluconeogenesis is catalysed by Fructose-Bisphosphatase (FBP). This reaction uses 1 H2O for hydrolysis and yields 1 phosphate (Pi).

One would expect the cell to be utilising only one of the two reactions at any one time, either to break down glucose or to generate it. However, the case is commonly that both reactions are taking place simultaneously in an equilibrium [ref 'Biochemistry', Voet & Voet, 4th ed., 628-629 (Section 17-4-F-f,g,h,(i))], cycling Fruc-1,6-BP to no apparent benefit, at the expense of valuable ATP.

What is the purpose of such futile cycles?

As far as I am aware there are various regulatory mechanisms (allosteric regulation, hormonal control) in place to minimise futile cycling by ensuring that phosphofructokinase (glycolysis) and fructose 1,6 bisphosphatase (gluconeogenesis) are not both active at the same time.

See this Wikipedia article for a starting point.

  The precise regulation of PFK1 prevents glycolysis and gluconeogenesis from occurring simultaneously. However, there is substrate cycling between F6P and F-1,6-BP. Fructose-1,6-bisphosphatase (FBPase) catalyzes the hydrolysis of F-1,6-BP back to F6P, the reverse reaction catalyzed by PFK1. There is a small amount of FBPase activity during glycolysis and some PFK1 activity during gluconeogenesis. This cycle allows for the amplification of metabolic signals as well as the generation of heat by ATP hydrolysis.

The last two sentences of the quotation are probably what you remember reading about. There is a theory that having some cycling provides an element of regulatory responsiveness. See here for example. I'm not enough of a mathematician to explain this idea well.


What determines the efficiency of electron production in photosynthetic bacteria? Is there a specific gene involved, perhaps? Would one be able to genetically engineer a bacterium to oxidize water and generate electrons quicker? I am speaking about this biological problem in terms of an application to solar cells.

Edit: I am not inquiring to the existence of a gene responsible for photosynthesis, I am inquiring as to why some exoelectrogenic bacteria can produce electrons in electron transport more efficiently than others. Is there a reason for this that can be traced to a certain gene that makes certain exoelectrogens superior to others?

You may or may not consider this an actual answer to your entire question, but it's interesting nonetheless.

A physicist friend of mine did some work recently modelling the quantum dynamics of photosynthetic complexes, and their coupling constants for passing energy throughout the photosystem. His results showed that, (and I believe this is in agreement with the literature), that photosynthetic systems are actually about as efficient as it is possible to be (not only this, but they are the most efficient energetic systems known to man I believe - over something like ~90% efficient).

If you begin altering positions of chromophores and so on, the photosystems exhibit remarkable robustness and you get a more or less logistic decay in efficiency (i.e. removing one or 2 chromophores results in marginal reductions in efficiency, more still in considerably more severe debilitation, until ultimately it's efficiency is markedly lessened, but further manipulation has a plateau in efficacy reduction).

Much of the work that's been done on the quantum biology of photosystems has concerned the FMO Complex (Fenna-Matthews-Olson) which is a simplified model system from photosynthetic algae - you might find more detailed answers to your queries by reading up in this area.

As for discrepancies seen in photosynthetic effectiveness bought about genetically, there are theories that suggest that the organisms are actually protecting themselves. E.g. to avoid over-production of ROS species. I can't offer you much in the way of a well evidenced case for this though, it's just a conversation I had with a post-doc at work recently, who completed his PhD on photosynthetic cyanobacteria.

EDIT Here's one of the papers about optimality in the FMO:

http://aip.scitation.org/doi/pdf/10.1063/1.4930110


What does it mean for a chemical pathway to be conserved? In many papers the MAPK pathway, (along with many others) is referred to as being conserved:

Example: "The mitogen-activated protein kinase (MAPK) cascades are ubiquitous in eukaryotic signal transduction, and these pathways are conserved in cells from yeast to mammals"

example 2 "The Hippo signaling pathway appears to be highly conserved."

What does it mean for a pathway to be conserved?

A conserved pathway is a pathway that exists in a variety of species, by virtue of that pathway being conserved throughout the evolution of those species. A pathway must by neccessity have appeared for the first time in one particular species. If that species gives rise to new species, but the pathway in question is identical or very similar in all the new species, it is sensible to say that pathway has been evolutionary conserved. This may imply that the pathway in its conserved form is important for the fitness of those species.

For some examples, here is a page on evolutionary conserved pathways in Drosophila: http://www.sdbonline.org/sites/fly/aimain/aadevinx.htm


Identification of this Salamander This salamander was found in a small forest pond somewhat near the Oregon coast. In the area are many rough skinned newts and a small number of another type of salamander that I still can't find the species of. I'm guessing it is either the salamander species or a rough skinned newt.

It is a torrent salamander. Most likely this is the southern torrent salamander (Rhyacotriton variegatus)


Why is the human body hair not uniformly colored? Most of my body hair is black however my lip hair is light brown/blonde the rest of my beard region is black. Since hair color is genetic what causes this?

The hairs you mention are also called "androgenic hairs", meaning their growth and pigmentation is influenced by androgens. These include pubic hair, the hairs on the breast and shoulders (almost exclusively for men) and the beard.

It seems, that these hair bulbs have different sensibilities (number and expression of androgen receptors) so they react differently to androgen levels. This includes balding, pigmentation, growth and so on.

These articles should be a good starting point, if you want to dive deeper into the topic:

Androgen actions on the human hair follicle: perspectives.
Mechanism of action of androgen in human hair follicle.


Why do insectivorous birds migrate? Living in northern latitudes, I have always wondered why do migratory birds invest so much time and energy to travel twice a year the vast distances between their breeding grounds and wintering areas. The most commonly found explanation, and the one I am grown accustomed to, is the scarcity of resources, resources meaning food and nesting places.

For years I have considered this a quite convenient explanation but recently I came to rethink it.

As you know, many of the longest migrating birds are insectivorous such as European Pied Flycatcher that breeds in much of Europe and western Asia but spends winters in western Africa. While it is easy to see the scarcity of food (insects) in northern breeding areas during winters, it is more difficult for me to see the scarcity of food in southern wintering areas during summers. - Take, for example, ants, that I expect, are abundant in those places all year around. Considering their total biomass, they would seem to hold a potential for a stable food source for masses of insect eaters with minimal food gathering effort required. So why migrate?

Is it that ants (or any other seemingly overly abundant invertebrates such as termites and mosquitoes) are not nutritious enough? Or are they too stingy and poisonous perhaps?

As for nesting places, I am aware that many birds defend their home range (thereby setting an upper limit for population density), but I imagine that such behaviour could be subject to change (or never had emerged in the first place) if there was no need to compete for other resources (mainly for food).

Or are the primary constraining factors disease and predation that would follow from a larger population density?

So in short, my question is, what is (/are) the primary reasons(s) for insectivorous birds to migrate instead of staying in their wintering areas and feeding on (seemingly abundant) local resources such as ants?

Reason for Migrating Birds:

Migrating for a Meal

Food scarcity: If birds will stay and eat all the bees they find, there will be no bees to feed on for the next generation. So, they fly away to take advantage of these places where there is abundance of food. And when the insects or replenish they come back.

Migrating for Family

Flocks of bird can be easy prey as they are small and are in a huge number. Also for the young ones who can't fly it is very dangerous. (Though they abandon the young one as soon they can fly)

Migrating for better Climate:

Some of the species fly away to sustain the temperature and come back when it is suitable for them. So, Northern birds migrate to tropical places for the winter and come back to north for the summer to lay eggs.

There are too many other theories for bird migration. It had been confirmed that migration is often due to genetics than any other reason.

Further Reading: THEORIES OF BIRD MIGRATION

Sources:

[1] http://birding.about.com/od/birdbehavior/a/Why-Birds-Migrate.htm

[2] http://en.wikipedia.org/wiki/Bird_migration


Why do people look different after a long sleep? What happens during a long sleep that makes people look odd when they have just woken up?  Why doesn't the same phenomenon occur in the case of a person who lies down for an extended period of time, but stays awake?  I've noticed that some nights seem to make a bigger difference than others in the appearance of the sleeper, but haven't noticed a pattern.

Puffy eyes are caused by fluid build up in tear ducts from extended periods of lying down. Gravity from sitting or standing slowly drains them during the day. The crusty 'sleep' that accumulates in the corner of your eyes is the residue from basal tear liquid that has seeped out of the eye and evaporated during the night.


Bioinformatics basics What are the basic differences between genbank, NCBI and entrez gene?
And please tell some books and webpages where I can get more about the databases .(currently I'm using Bioinformatics and functional Genomics by Pavsner)

Genbank is a database of nucleotide sequences that are public.

NCBI stands for "National Center for Biotechnology Information" (in the US).

Entrez is NCBI's retrieval system.

You can find more information in this article

I don't know which kind of databases you are looking for, but there are hundreds of them!
In this wikipedia article there are some of them.


Laurus Nobilis parasite identification In north Italy were I live I have two plants of laurus at the two sides of a garden. One of them has some sort of parasite on its leaves.

Someone know something about it? Leaves are covered with something like an oil.

As @picapica has pointed out, I presume these are scale insects, the first instar of Japanese wax scale, Ceroplastes japonicus.

Laurus sp. is a host of this hemiptera in Italy.

Here is an image showing the second instar from Italy:

These are the adult females :


difference between transcriptional activator and general transcription factors? What is the difference between transcriptional activator and general transcription factors? Are they same or different, and do the transcriptional activators first attract general transcription factors or the RNA-polymerase also, at the same time?

Activators turn genes on - they help or promote RNA transcription of the gene.  Other Transcription factors may turn genes off (prevent or reduce RNA transcription).  Some transcription factors may promote or inhibit RNA transcription depending on their environment/context.

Transcription factors is such a generic term that anything can happen in practice.  They are generically supposed to interact with the polymerase, but if some were found to interact by attracting other transcription factors that would not be a surprise.

I think 20+% of human genes are transcription factors (that is just a guess we haven't been able to characterize more than a few of them.


What´s the origin of junk DNA? Most eukaryotes posses a certain amount of junk DNA in their cell nuclei. What is (are) the origin(s) of this junk DNA, And is it realy junk (superfluous)?

"Junk DNA" is more aptly named noncoding DNA. This is defined as any DNA region that does not encode for a gene or more precisely is not within an open reading frame. In the human genome over 98% consists of noncoding DNA. However the more we learn about molecular biology the more we understand the biological function and importance of noncoding DNA. Examples for important functions are:

Regulatory regions that control the expression of a gene
Regions coding for regulatory RNA
Regions where epigenetic regulation takes place

However, there are also regions which likely do not have beneficial biological function, which may rightfully be called junk:

Transposons are genetic regions that can copy themselves (either by an enzymatically active RNA or by encoding for the protein transposase). They are believed to have evolved as "selfish genes" and several known defense mechanisms against rogue transposons exist (siRNA, RNAi). Transposons and the defense mechanisms have now become powerful tools in molecular biology research.
Endogenous retrovirus sequences which are remainders of retroviruses which have inserted themselves into the germ line and become inactive through mutation.

However, even these "junk" regions are believed to have important evolutionary functions such as protection from mutation through retroviruses: Because there are large DNA regions where the precise order and function is not important, a retrovirus that inserts itself at random positions of the genome is less likely to cause permanent damage.


White residue from ginger juice I’ve been juicing some ginger by grating it and pressing it (by hand). A white residue collects at the bottom of the liquid. What is this?

I believe that this white residue is starch. According to Wikipedia, Ginger is 17.7% carbohydrates by weight, or 14% excluding sugar and dietary fiber.

I let the residue settle and decanted the liquid. The residue behaved remarkably similarly to wet corn starch. From this, I have concluded that it is starch of some form.


Do spring varietes of cereals have a process of vernalization? I was wondering about this question - Do spring varieties of cereals have some process of vernalization?
It would be nice to have some description of the main processes' differences of spring and winter varieties.
Thanks!

The answer depends to some degree on what you mean by "some process of vernalization". As far as I know, the difference between winter and spring varieties is a matter mostly of how strong the response is, not whether the response exists.
One paper writes in the abstract:

Wheat cultivars are classified as two general types: winter wheat with variable low temperature requirement for a proper flowering time (vernalization) and spring wheat without the requirement, based on their qualitative vernalization requirement. Winter wheat cultivars are classified as three types, weak winter, semi-winter and strong winter, according to their quantitative vernalization requirement to reach a vernalization saturation point or achieve the maximum vernalization effect.

The difference is not whether vernalization exists as a process, so much as whether it is required for timely reproductive transition.
See the figure below (from this paper), showing spring (LEG) and winter (MIR) varieties of wheat after various vernalization periods. Basically, even the spring variety has a weak vernalization response; it's just much less notable than the strong response of the winter variety.

With legend:

Frost tolerance (LT50), apical development (DC = decimal code) and days to heading of ‘Mironovskaya’ (MIR) winter wheat and ‘Leguan’ (LEG) spring wheat plants during 12 weeks of acclimation at 2 °C and two photoperiods, 16 h (long day) or 8 h (short day). Vertical bars indicate LSD0·05 and asterisks indicate that the plants had not reached heading by 100 d.


How do we look inside the cell? My sister is in 9th grade biology and her teacher avoided answering the question of how we actually study the inside of a cell. I haven't taken biology in a while but I'd like to give her an answer.

Can someone roughly summarize how we actually learn about what goes on inside a cell? Just mentioning a few of the most common or used techniques would be fine.

Note: I hope this isn't a bad question. It's a bit vague. But I didn't want to leave her without a decent answer.

Techniques to look at whole cells are: Light microscopy (cells, large organelles), electron microscopy (detailed analysis of subcellular structures and even proteins) and confocal fluorescence miscroscopy (look at particular cellular planes, reconstruct 3D images).

And of course you can analyze the insides by Biochemistry by breaking the cell membranes and look at individual proteins and DNA/RNA by extraction and electrophoresis followed by Western / Northern / Southern blotting, or isolate organelles by centrifugation.

It is a broad question, and I just gave the most obvious examples of techniques (not anywhere near exhaustive). By googling the bold-out terms you may provide some details to your sis.


How long does it take for a blocked dopamine receptor to be broken down by the body? Do the blocked dopamine receptors get broken down by the body and if so how often ?

In other words how long does it take for the dopamine receptors blocked by irreversible dopamine antagonists to degrade ?

Partial Answer and Suggestions
As @De_Novo says, this is a complicated, albeit very interesting, question. There are various reasons for this, such as the fact that the receptors aren't just internalised but also recycled and the fact that there may be antagonist and dose-dependent changes in receptor internalisation. There's the added complexity that receptors can have their expression changed in the short term (by internalisation) but also in the long term (by varying synthesis). You should then note that there's not a set lifespan of the receptors - there's a statistical distribution for how long they'll last at the membrane.
But I'd quite like to stimulate discussion about it so I'm proposing some smaller questions:

Do irreversible dopamine antagonists change the rates of receptor internalisation, degradation or recycling? This is likely to be the case as internalisation of receptors is often activity-dependent. Also, the shape of the irreversible antagonist could change how the receptor fits into a clathrin-coated pit.
Do the irreversible antagonists change the rate of receptor synthesis?
What mathematical models can describe the dynamics of internalisation? This might be a bit tricky since there are feedback mechanisms here (e.g. recycling --> internalisation --> degradation --> less recycling).
How does the proportion of blocked receptors affect these factors?

By answering these questions (or even by finding an experiment that measures the half life of the receptors with blocking), you could come up with an answer for the half-life of the blocked receptors.


I'd like to know the name and a few details of a certain time-keeping structure in the human brain I once heard of this structure on the Discovery Science channel and have since forgotten the name. The details I remember about it were that it is the central time-keeping device for the brain located in the geographic center of the human brain. The DSC only mentioned it in passing to describe a person with an abnormality in this structure. Can someone post some reliable research links and a short description of it? I don't trust google much and am not good at using it, so thanks!

You are probably referring to the suprachiasmatic nucleus.

Note that, although this is the central clock, there are also so-called "peripheral clocks", for instance in the liver, pituitary and other organs that can finely tune rhythms in the organism.

You may also want to have a look at the Wikipedia page for circadian clock and references therein.


What implications has the missing 2'-OH on the capability of DNA to form 3D structures? The chemical difference between RNA and DNA is the missing 2'-hydroxyl group in the nucleotides that build DNA. The major effect of that change that I know of is the higher stability of DNA compared to RNA. But I'm wondering whether this difference has significant implications for the ability of DNA to form compex, three-dimensional structures.

RNA is known to be able to from complex tertiary structures and function as ribozymes. It clearly has the ability to form a wide range of structures and can catalyze a variety of chemical reactions.

As far as I know, there are no naturally occuring catalytic DNAs known. But a number of synthetic DNA enzymes have been created in the lab, so it is generally possible for DNA to form catalytic structures (see Breaker and Joyce 1994 for the first created DNA enzyme).

I'm wondering whether the missing 2'-OH means that DNA has less potential to form complex structures compared to RNA? I imagine it changes the ability to create hydrogen bonds, but I don't know if it would significantly decrease the potential structures that DNA could adopt.

Breaker RR, Joyce GF; (December 1994). "A DNA enzyme that cleaves RNA". Chem Biol. 1 (4): 223–9

To make sure I'm not comparing apples and pears, my (attempt to) answer the question will be broken into two parts: comparison of single-stranded nucleic acids and double stranded ones.

Single stranded DNA and RNA

Both DNA and RNA can form single-stranded complex tertiary structures in which the secondary structure elements are associated through van der Waals contacts and hydrogen bonds. The presence of a 2'-hydroxyl group makes ribose ring prefer different conformations than deoxyribose in DNA. Also, since 2′-OH moiety is both a hydrogen donor and acceptor, it provides RNA with greater flexibility to form 3D complex structures and stability to remain in one of these conformations. As Aleadam notices, this paper shows that tRNA and its DNA analog form similar tertiary structures though tDNA is not as stable as tRNA:

  Therefore, we submit that the global conformation of nucleic acids is primarily dictated by the interaction of purine and pyrimidine bases with atoms and functional groups common to both RNA and DNA. In this view the 2-hydroxyl group, in tRNA at least, is an auxiliary structural feature whose role is limited to fostering local interactions, which increase the stability of a given conformation.

These authors also show that at least one loop in the tDNA analog is more susceptible to cleavage by a restriction endonuclease. In this region the tRNA has a water molecule hydrogen bonded to 2'hydroxyl group.

I was not able to find more of such interesting comparisons in the literature.

Double stranded DNA and RNA

Both DNA and RNA can form double-stranded structures. Again, sugar conformation determines the shape of the helix: for DNA helix it's usually B-form, whereas helical RNA forms A-geometry under nearly all conditions. In RNA helix we find the ribose predominantly in the C3’- endo conformation, as 2'-OH stericly disfavors the C2'-endo conformaion, necessary for B-form geometry.

Physiological significance

dsRNA and ssDNA often provide a signal to the cell that something is wrong. dsRNA is of course seen in normal processes like RNA interference but it can also stop protein synthesis and signal viral infections (cf. double stranded RNA viruses). Similarly, ssDNA is much more prone to degradation than dsDNA, it often signals damage of DNA, or infections from single stranded DNA viruses and induces cell death. Therefore, due to their functions, under normal conditions DNA 3D structure is mostly a double-stranded helix, whereas RNA has a single stranded, "protein-like", complex 3D structure.


What are unmapped reads? I am mapping some reads to a reference genome (hg19). I used bamtools to have the percentage of mapped vs unmapped reads.

Total reads:       1150004
Mapped reads:      1052983  (91.5634%)
Forward strand:    624067   (54.2665%)
Reverse strand:    525937   (45.7335%)
Failed QC:         0    (0%)
Duplicates:        0    (0%)
Paired-end reads:  1150004  (100%)
'Proper-pairs':    1046208  (90.9743%)
Both pairs mapped: 1049400  (91.2519%)
Read 1:            575002
Read 2:            575002
Singletons:        3583 (0.311564%)
Average insert size (absolute value): 534.479
Median insert size (absolute value): 215

My question:

What represent exactly these unmapped reads? What information do they tell us? How can we analyze them?

Thanks

In transcriptome (RNA-Seq) libraries, unmapped reads are reads that fail to map to known exons. More often than not, they represent genomic DNA. RSeQC has tools to help identify genomic (also sometimes called intergenic) sequences.

For the most part, the percentage of unmapped reads just provides you with QC information, like how much gDNA you purified along with your mRNA. It's unlikely to be very useful beyond that, but it really comes down to what you're looking for in those sequences.

If you're doing DNA-Seq, then unmapped reads generally represent reads that failed to map unambiguously to known sequences. This will depend on a threshold (usually provided by the user) for alignment stringency.


Land recultivation? Land revegetation? Land reclamation? Land rehabilitation? I'm translating a Russian text about the recultivation (рекультивация) of land formerly used for open-pit mining. The process of 'land recultivation' in Russia involves three general stages:

Preparatory stage: a feasibility study, justification of investment, development of working documentation.
Technological stage: engineering operations that involve large-scale movement of soil, removal of machinery and buildings, etc.
Biological stage: seeding of trees and plants, soil improvement operations, irrigation & drainage work, etc.

It is said that the last two stages can last for "years or even decades".

Which English word should I pick? Recultivation, revegetation, reclamation, or rehabilitation?

Example sentences (I retained the original "recultivation" here):

  All too often a coal mining company implementing a recultivation project in this region limits itself to the use of simplified technological solutions that fail to take into account the need to preserve biodiversity. The range of plants used at the biological stage of recultivation is limited to five tree species, which depletes the genetic resources of the region's ecosystems and exacerbates the existing invasive species problem.

P.S. The authors of the text do no imply that the land should be used for agriculture - to the contrary, their goal is to improve biodiversity.

P.P.S. Here is a newspaper article about this "recultivation" of open-pit mine land in Kuzbass: source (in Russian)

P.P.P.S. I've just discovered that the English-language title of the Russian national standard GOST R 57446-2017 that comes into force on 1 December 2017 translates the term as land reclamation. However, those who translate Russian documents into English are not always correct.

Reclamation can be used in this context, but I think in this situation the most appropriate word would be "remediation", from the Latin word remediare which means "heal" or "cure". It is most often used in the sense of fixing environmental problems such as pollution or contaminants.

https://en.wikipedia.org/wiki/Environmental_remediation

A Google search suggests this is a widely used term in the mining industry for the situation you describe.
https://www.google.co.uk/search?q=remediation+mining

It does depend exactly which stages you're attempting to describe, though. From http://www.miningfacts.org/environment/what-happens-to-mine-sites-after-a-mine-is-closed/:

  The terms reclamation, remediation, rehabilitation, and restoration
  are all used to describe mine closure activities that attempt to alter
  the biological and physical state of a site. [11] The terms are
  sometimes used interchangeably, and are closely linked, but refer to
  distinct steps in the preparation of the site for another use: [11,
  12]

  Remediation: The cleanup of the contaminated area to safe levels by removing or isolating contaminants. At mine sites, remediation
  often consists of isolating contaminated material in pre-existing
  tailings storage facilities, capping tailings and waste rock piles
  with clean topsoil, and collecting and treating any contaminated mine
  water if necessary.

  Reclamation: The physical stabilization of the terrain (dams, waste rock piles), landscaping, restoring topsoil, and the return of
  the land to a useful purpose.

  Restoration: The process of rebuilding the ecosystem that existed at the mine site (where applicable) before it was disturbed. The
  science of mine reclamation has evolved from simple revegetation
  activities to a discipline which involves using native plants to mimic
  natural ecosystem development over an extended period of time. [13]

  Rehabilitation: The establishment of a stable and self-sustaining ecosystem, but not necessarily the one that existed before mining
  began. In many cases, complete restoration may be impossible, but
  successful remediation, reclamation, and rehabilitation can result in
  the timely establishment of a functional ecosystem.

See also this publication by USGS:
Finger, Church, and Guerard. Potential for Successful Ecological Remediation, Restoration, and Monitoring, Integrated Investigations of Environmental Effects of Historical Mining in the Animas River Watershed, San Juan County, Colorado, 2008; U.S. Geological Survey Professional Paper .


Evolutionary term for multiple, related adaptations Is there a term in biology for when adaptations are compounded on (or by) other adaptations?

One example in whales: the tail flukes, reduction of rear limbs and development of the blowhole were all part of a number of shifts that aided the transition from land to water. Is there a term, like chain shift, for that?

Also with humans, encephalization led to pelvic adaptation for larger infants.

Co-adaptation

The term you are looking for might be co-adaptation. Co-adaptation is kind of a generalist term that fits many scneario, its definition (source: wikipedia > co-adaptation)

  In biology, co-adaptation, or coadaptation is the process by which two or more species, traits, organs, or genes undergo adaptation as a pair or group. This occurs when two or more characteristics undergo natural selection together in response to the same selective pressure. While the parts may be functionally independent they are only beneficial when together, sometimes leading to increased interdependence. Coadaptation and its specific examples are often seen as evidence for the broader process of coevolution.

You seem to be thinking about a chain of adaptations, where the first adaptation changes the selection pressure on another trait causing another adaptation. For this purpose co-adaptation is not the perfect term but I am afraid there is no perfect terms. You might want to consider the following ones though that help you express your ideas.

Structural interdependence

Ziegler et al. 2009 talk about structural interdependence and interdependence of internal organ.

Phenotypic space

Of course, you can use the frameworks of the phenotypic space (as in Pigliucci 2007) and of fitness landscape to talk about how a change in a given phenotypic trait affect selection pressures at other traits.

Phenotypic constraint

A phenotypic constraint (as in Pigliucci 2007) is a case of fitness valley in fitness landscape in the correlation between two of more phenotypic trait, hence causing a trade-off. Absence of such constraint are cases of interest to you

Phenotypic plasticity

It is common to talk about the ability of a specific phenotypic trait to vary to fit into the broader context of the whole body as phenotypic flexibility or phenotypic plasticity. There is a difference plasticity and flexibility for many but I don't think all authors use the exact same definition.

Phenotypic plasticity

  Phenotypic plasticity refers to the changes in an organism's behavior, morphology and physiology due to its adaption to a unique environment.2 Fundamental to the way in which organisms cope with environmental variation, phenotypic plasticity encompasses all types of environmentally induced changes (e.g. morphological, physiological, behavioural, phenological) that may or may not be permanent throughout an individual's lifespan. The term was originally used to describe developmental effects on morphological characters, but is now more broadly used to describe all phenotypic responses to environmental change, such as acclimation or acclimatization, as well as learning.5 The special case when differences in environment induce discrete phenotypes is termed polyphenism.

Exaptation

This is a poorly related term but it may eventually be of interest to you. The definition from wiki > Exaptation

  Exaptation [..] and the related term co-option describe a shift in the function of a trait during evolution. For example, a trait can evolve because it served one particular function, but subsequently it may come to serve another. Exaptations are common in both anatomy and behaviour. Bird feathers are a classic example: initially they may have evolved for temperature regulation, but later were adapted for flight. Interest in exaptation relates to both the process and products of evolution: the process that creates complex traits and the products (functions, anatomical structures, biochemicals, etc.) that may be imperfectly developed.

Phylogenetic signal

Phylogenetic signal is used way more often than the term exaptation. It is however also quite unrelated to what you are looking for but I added it because... well we never know what you'll find helpful!

  Phylogenetic signal is a measure of the statistical dependence among species' trait values due to their phylogenetic relationships.

For example, the existence of 4 limbs in vertebrates is a phylogenetic signal (see Why don't mammals have more than 4 limbs?)


What influences the timing of human bowel movements in the morning? I'm trying to understand if the timing of human bowel movements in the morning is associated with the circadian rhythm, and can thus be used to make predictions about the circadian rhythm.

What influences the timing of bowel movements? Is it the timing of meals, caffeine intake or is it a biologically programmed time?

Thank you!

The bowel movements are influenced by a lot of factors. For example, when you eat a meal it induces a movement in your large intestines, to defecate and clear up space for new food.

Also, there is MMC, migrating motor complex, which is responsible for the bowel movements when you are fasting. It causes a flushing effect, which prevents bacteria to overproduce in intestines.

So, the daily bowel movements are mainly influenced by the timing and content of the food that you eat. But as I said there are many other factors. The gastrointestinal system has a very complex nervous system. Even psychological factors can effect the bowel movements greatly, for example extreme physical pain may induce the symphatetic system and cause constipation.

Also caffeine may affect it, like many drugs do.


Chromosome naming convention: Why are there chromosomes named "1" and "1A"? I've been stumbling on multiple genome of birds where there is a "1A" chromosome and a "1" chromosome. For example, the zebra finch has 1A and 4A. What does that mean?

Do you have any resource about naming conventions for chromosomes and if this naming convention is specific to birds?

I would suggest looking at some of the reference genome papers. My guess is that the chromosomes are named as such based on their synteny to the chicken genome; e.g. look at Accessory Figure 3 here for your zebra finch, and note that chromsomes 1 and 4 are split in the zebra finch relative to Gallus.

The direct comparison from that paper is to an Accessory Table 1 that I can't actually find.

I would guess that in most cases it's because of a synteny comparison to some reference, in this case chicken that splits a chromosome in the new genome. For example sequences homologous to the chicken chr1 are on two finch chromosomes 1 and 1A.


Why are amino acids in biology homochiral? Why are nearly all amino acids in organisms left-handed (exception is glycine which has no isomer) when abiotic samples typical have an even mix of left- and right-handed molecules?

I know that you are referring to the commonly ribosome-translated L-proteins, but I can't help but add that there are some peptides, called nonribosomal peptides, which are not dependent on the mRNA and can incorporate D-amino acids. They have very important pharmaceutical properties. I recommend this (1) review article if you are interested in the subject. It is also worth mentioning that D-alanine and D-glutamine are incorporated into the peptidoglycane of bacteria.
I read several papers (2, 3, 4) that discuss the problem of chirality but all of them conclude that there is no apparent reason why we live in the L-world. The L-amino acids should not have chemical advantages over the D-amino acids, as biocs already pointed out.
Reasons for the occurrence of the twenty coded protein amino acids (2) has an informative and interesting outline. This is the paragraph on the topic of chirality:

This is related to the question of the origin of optical
activity in living organisms on which there is a very
large literature (Bonner 1972; Norden 1978; Brack and
Spack 1980). We do not propose to deal with this
question here, except to note that arguments presented
in this paper would apply to organisms constructed from
either D or L amino acids.

It might be possible that both L and D lives were present (L/D-amino acids, L/D-enzymes recognizing L/D-substrates), but, by random chance the L-world outcompeted the D-world.
I also found the same question in a forum where one of the answers seems intriguing. I cannot comment on the reliability of the answer, but hopefully someone will have the expertise to do so:

One, our galaxy has a chiral spin and a magnetic orientation, which causes cosmic dust particles to polarize starlight as circularly polarized in one direction only. This circularly polarized light degrades D enantiomers of amino acids more than L enantiomers, and this effect is clear when analyzing the amino acids found on comets and meteors. This explains why, at least in the milky way, L enantiomers are preferred.
Two, although gravity, electromagnetism, and the strong nuclear force are achiral, the weak nuclear force (radioactive decay) is chiral. During beta decay, the emitted electrons preferentially favor one kind of spin. That's right, the parity of the universe is not conserved in nuclear decay. These chiral electrons once again preferrentially degrade D amino acids vs. L amino acids.
Thus due to the chirality of sunlight and the chirality of nuclear radiation, L amino acids are the more stable enantiomers and therefore are favored for abiogenesis.

BIOSYNTHESIS OF NONRIBOSOMAL PEPTIDES

Reasons for the occurrence of the twenty coded protein amino acids

Molecular Basis for Chiral Selection in RNA Aminoacylation

How nature deals with stereoisomers

The adaptation of diastereomeric S-prolyl dipeptide derivatives to the quantitative estimation of R- and S-leucine enantiomers. Bonner WA, 1972

The asymmetry of life. Nordén B, 1978

Beta-Structures of polypeptides with L- and D-residues. Part III. Experimental evidences for enrichment in enantiomer. Brack A, Spach G, 1980


Is natural selection a tautology, and therefore not truly falsifiable? I've heard the argument from a lot of creationists that all the evidence for natural selection (and by extension, evolution) in general is worthless because natural selection is so flexible that it could cover all the data, no matter what we discovered. In essence, that natural selection is a tautology:

Survival of the fittest. What is 'fit'? What survives.

There are other creationists, however, that admit that natural selection could be falsified. These are split into two groups:

The ones that say, if you rephrase natural selection as a non-tautology, it becomes obvious that it doesn't work:

  Natural selection has been criticized as a tautology. This would be a major problem for evolutionary biology, if true, because tautological statements can't be falsified and, therefore, can't be scientific. There is merit to this critique insofar as the theory of natural selection is indeed generally described in a tautological manner. However, natural selection can be described non-tautologically if we’re careful. Natural selection should be defined as the theory that attempts to predict and retrodict evolutionary change through environmental forces acting upon organisms. However, this re-framing comes at a cost: it reveals, based on our current knowledge of evolutionary forces, the lack of ability to make accurate predictions about expected changes except in the most simple of circumstances.

And those that say that the falsifying options provided by natural science are impossible to actually use. Here are some of those falsifying options:

  Charles Darwin himself proposed a rather strong test of evolution: "If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down." [Darwin1859, pg. 175]. This is the basis of claims by various intelligent design writers that various biological structures, such as the vertebrate immune system or the bacterial flagellum, are "irreducibly complex" -- they consist of multiple components that could not develop in the absence of the others. However, these structures have been exhaustively studied in the scientific literature, and scientists have demonstrated entirely plausible evolutionary pathways. See Complexity.
  Famed biologist J. B. S. Haldane, when asked what evidence could disprove evolution, mentioned "fossil rabbits in the Precambrian era" [Ridley2004, pg. 66]. This is because mammals, according to current scientific analysis, did not emerge until approximately 40 million years ago, whereas the Precambrian era is prior to approximately 570 million years, when only the most primitive organisms existed on earth.
  Biologists had long conjectured that human chromosome number two was the result of a fusion of two corresponding chromosomes in most other primates. If DNA analysis of these chromosomes had shown that this was not the case, then modern evolutionary theory would indeed be drawn into question. This "fusion hypothesis" was indeed confirmed, rather dramatically, in 1993 (and further in 2005), by the identification of the exact point of fusion. For additional details see DNA.
  Modern DNA sequencing technology has provided a rigorous test of evolution, far beyond the wildest dreams of Charles Darwin. In particular, comparison of DNA sequences between organisms can be used as a measure of relatedness, and can further be used to actually construct the most likely "family tree" hierarchical relationship between a set of organisms. Such analyses have been done, and the results so far dramatically confirm the family tree that had been earlier constructed solely based on comparisons of body structure and biochemistry. For additional details see DNA.

Is there any way to save natural selection? To do so, we need to:

Prove it can be explained non-tautologically
Prove that it does make useful predictions
Give falsifying experiments that are reproducable and actually possible.

I think @Remi.b's answer is great and really the only way to answer your questions is with a comprehensive introduction to evolution. However, I wanted to address the tautology issue more directly.

First, the "survival of the fittest" seems like a tautology with "natural selection" because it is not a description of how natural selection works, rather, it is a phrase meant as a synonym for natural selection, to help describe the result to someone unfamiliar with the phrase.

Let me use an analogy: it would be like if you were a very new learner of English, and I told you "Joe's truck has more mass than an elephant!"

If you aren't really familiar with the term "mass" in English, this phrase could be confusing. So I explain instead that "Joe's truck is heavier than an elephant." If you know the word "heavy" this is easier to understand.

However, there is a tautology there! the car is actually heavier because it has more mass, but that does not make either phrase untrue or untestable: it's just another way of saying the same thing within a context (i.e., those statements are the same if they are exposed to the same gravity).

The testable hypothesis that natural selection makes is that, given 2 things: 1) a population where individuals have traits that give them different chances of survival, and 2) some way for offspring to inherit traits from their parent(s), then the population over time will consist of individuals who are more likely to possess the traits that gave a high chance of survival.

Following this, should the environment change in some way such that a different trait is now beneficial, that trait will increase in prevalence.

There are way too many experiments to summarize here that show 1), 2), and a combination of 1) and 2), as well as experiments that show that indeed, when you have 1) and 2) you get natural selection.


How can I accurately predict proper transgenic protein function/structure from different species? I am currently building a synthetic system in E.coli, and am often faced with the need to use genes from other distant prokaryotes. I know that myself and most of my colleagues resort to an educated trial and error approach. Besides the obvious (elimination of introns from eukaryotes, codon optimization, genetic relatedness), is there any predictable or semi-rational way of knowing if a transgene for a different organism will function properly in any given organism?

By looking at the sequence only?  This is an unsolved problem.

Its not clear to me exactly what you are looking for, but here are some thoughts...

On a relatively narrow question as to whether any gene you plug into a bacterium, yeast, mouse, goat or other transgenic organism - the rna may not translate into protein in detectable levels or at high enough levels to get the desired result.  changing the sequence of the DNA of the gene for better transcription/translation is a common necessary experimental.

On the broader systems biology level, other cofactors, substrates that are necessary for the function of the gene may have to be engineered in the host organism. That is also an open question.

All this is assuming the gene in question codes for an enzyme to make a new or different amount of the metabolic product from the host organism, a commmon synthetic biology target.  If you are adding signaling pathway components, tinkering with a more specific mechanism in the cell, getting the function you desire could be a lot of work.  E.g. if you were inserting a new ribosomal component or a gene related to mitosis, that would be hard to imagine a priori how it would function in the new cell or if it would just kill it.

Also, Olga Troyanskaya at Princeton CS is working on the related problem of finding the function of a gene by looking at its sequence and cross referencing to other known data. Electronic functional inference is difficult, esp when we have no complete gene functional description of any living organism to start with.


What kind of kale is this? I'm from Pennsylvania and I used to get this kale all the time at the grocery store, but I moved to the West Coast recently and can't find it anywhere! It looks exactly like this photo:

Image source: http://www.specialtyproduce.com/produce/Kale_Purple_764.php.

I've seen this referred to as purple kale, salad savoy, and flowering kale, but I don't think any of those are 100% accurate. The purple kale I've found here is tougher and more bitter, with spikier leaves and a more reddish color, and it doesn't come as a bunch like this but as individual stems. Does anyone know exactly what this variety is called?

It's just a variant of kale, part of the genus Brassica. I think you'd call this particular variant redbor or purple, bluntly, but you could go further because kale is often classified by the type of leaf. So in your picture, curly 'redbor' or 'purple' kale.

This is your specific name: Brassica oleracea Acephala Group.

(just sort of look at wikipedia)


Is it possible that the recipient of a heart transplant would display some of the donor's personality traits, as if the heart has memories? I've read somewhere that after a person has a heart transplant, it is possible that his/her attitude, action or behavior would change slightly or significantly, as though he/she possesses some aspects of the organ donor's personality because he/she is using the donor's heart.

Anything to support this phenomenon? Does it suggest that there are actually memories 'stored' in the heart and these memories may be retrieved by the person that owns the heart even if he/she is not the original owner?

Although there is clearly no feasible mechanism for such a phenomenon, there is good evidence that transplant patients can believe in some sort of transference of qualities from the donor. See for example (my emphasis):

Inspector, Y. et al. (2004) Another Person's Heart: Magical and Rational Thinking in the Psychological Adaptation to Heart Transplantation. The Israel Journal of Psychiatry and Related Sciences 41: 161-73.
Abstract
The goal of this study was to examine heart transplant recipients' psychological adaptation to another person's heart, with particular emphasis on recipients' attitudes toward graft and donor.
Thirty-five male heart recipients were examined by: the Symptom Distress Checklist (revised) (SCL-90-R); the Depression Adjective Checklist (DACL); a Post-Traumatic Stress Disorder Questionnaire (PTSD-Q); a Heart Image Questionnaire (HIQ); and a Semi-Structured Interview (SSI), aimed at eliciting attitudes and fantasies regarding the transplanted heart.
All instruments indicated high levels of stress even several years after the transplant, but, simultaneously, 73% of recipients felt that acquiring a new heart had had a dramatic influence on their lives with a new appreciation of the preciousness of life and a shift of priorities, toward altruism and spirituality. Sixty percent returned to work after the transplant but some had to adapt to a changed attitude from those around them who regarded them as anything from mystical creatures to vulnerable or still-sick individuals. While all recipients possessed a scientific knowledge of the anatomy and physiological significance of the heart (as revealed in the HIQ), many endorsed fantasies and displayed magical thinking: 46% of the recipients had fantasies about the donor's physical vigor and prowess, 40% expressed some guilt regarding the death of the donor, 34% entertained the possibility of acquiring qualities of the donor via the new heart. When asked to choose a most and least preferred imagined donor, 49% constructed their choices according to prejudices, desires, or fears related to ethnic, racial or sexual traits attributed to the donor.
This study confirms the intuitive idea that heart transplant involves a stressful course of events that produces an amplified sense of the precariousness of existence. Simultaneously, it gives rise to rejoicing at having been granted a new lease on life and a clear sense of new priorities, especially with regard to relationships. Less expectedly, this study shows that, despite sophisticated knowledge of anatomy and physiology, almost half the heart recipients had an overt or covert notion of potentially acquiring some of the donor's personality characteristics along with the heart. The concomitance of the magical and the logical is not uncommon in many areas of human existence, and is probably enhanced by the symbolic nature of the heart, and maybe, also, by the persistent stress that requires an ongoing, emotionally intense, adaptation process.

Another study is reported in:
Bunzel B, et al. (1992) Does changing the heart mean changing personality? A retrospective inquiry on 47 heart transplant patients. Qual Life Res. 1:251-6.
To actually investigate this further I suppose it would be necessary to set up experiments in which patients had transplant operations in which (unknown to the patient) no transplant actually took place, with the expectation that these individuals would display the same magical thinking. Grant application?


How many generations are required for a specific neutral mutation to reach fixation? In population genetics, the term “time to fixation” is defined as the time it takes for a specific mutation to appear in a population, plus the time required for this mutation to spread throughout this population. My question is, how many generations are required for a specific neutral mutation to reach fixation? I need a general formula for number of generations as a function of mutation rate and population size, valid for all kinds of biological entities. Note that a neutral mutation is not fixed by selection, it is fixed by genetic drift.

How many generations are required for a specific neutral mutation to reach fixation?

Kimura and Ohta (1968) showed that the expected time for a neutral allele to reach fixation is

$$\bar t(p_0)=-4N\left(\frac{1-p_0}{p_0}\right)\ln(1-p_0),$$

where $p_0$ is the initial frequency and $N$ is the population size. The model assumes a Wright-Fisher population (panmixia, constant population size, exclusively sexually reproducing hermaphroditic individuals, ...) and negligible mutation rate at the locus of interest.

  how do i calculate po in terms of known quantities, such as mutation rate?

You can compute the expected allele frequency at mutation - drift balance (e.g. see here or any decent intro textbook to population genetics). In short, let $\theta = 4N\mu$, where $\mu$ is the mutation rate, the expected heterozygosity is

$$H = \frac{\theta}{\theta + 1}$$

From that you can compute the allele frequencies $p$ and $q=1-p$ by solving $H = 2pq$.

If needed, you can get the entire distribution of allele frequency given $N$ and $\mu$ (and even $s$ and $h$ if needed) in Wright (1937).


What insect is this with furry wings? Found this on the wall of my house in Kuching, Sarawak, MALAYSIA It is a tiny black triangular shaped insect.

That is a Moth Fly, also known as a Drain Fly. It is in the order, Diptera, family Psychodidae. https://en.wikipedia.org/wiki/Drain_fly


Does mechanotransduction of cells play a role in the biocompatibility of titanium? What exactly is mechanotransduction as the information varies between sources. Some sources indicate that mechanotransduction is the underlying principle where cells pull on the surface they grow on to test their stiffness, so they can stretch and facilitate cell growth and differentiation. Other sources indicate that mechanotransduction is how cells detect mechanical stimuli and turn them into chemical signals.

Is this the main reason titanium is biocompatible to replace bones because it has a low surface resistance and cells on stretch on it?

First off, AOZ has a wonderful page about titanium alloy uses in medical applications you should read and that most of my info is coming from:

Suitability of Titanium for Implant Purposes

I think you're having a couple of easy to correct misconceptions. First, titanium alloys are used for medical implants and replacements because they're lightweight, stronger by tensile strength than steel and judged to be completely inert and immune to corrosion by all body fluids and tissue, and is thus wholly biocompatible. It's also non-magnetic, meaning you can even go through an MRI machine with it! The range of alloys that we're able to produce is also key to the widespread use of titanium in medical applications as different alloys can serve their purpose as anything from hip joints to jaw reconstruction bases to spinal fusion devices based on their composition.

But cells don't exactly "stretch on it" and in fact in many operations additional material is used to ensure that the host body is able to function with the implant. This includes the use of polymethyl methacrylate bone cement to ensure that implant joints stay in place, and the use of roughened bioactive surfaces (hydroxyapatite) to stimulate the integration of the bone and surrounding tissue onto the implant.

As far as mechanotransduction goes, the problem is that it covers an extremely wide range of topics so ascribing it only one definition can quickly cause issues between studies. I usually go off of Nature's definitions for these kinds of things, which in this case says that "Mechanotransduction refers to the processes through which cells sense and respond to mechanical stimuli by converting them to biochemical signals that elicit specific cellular responses" (1). If you peek at the studies highlighted on google scholar for mechanotransduction you can see that the range of work is extreme and that's why ascribing the term one specific meaning at this point is unrealistic.


Which vaccines are damaged by freezing? I have noticed that many of the freeze-sensitive vaccines are antigen only vaccines, for example Hib, pneumococcus, and tetanus vaccines. Why are these vaccines damaged by freezing? Are inactivated or killed vaccines like IPV damaged by freezing? How about live vaccines?

In order for a vaccine to work, antigens in the vaccine must maintain their shape and charge. Freezing a vaccine, particularly vaccines that contain aluminum, can cause antigens or other important constituents of the vaccine to aggregate. This may be what prevents them from working correctly, though we don't know for sure, and it may be something else about the freeze-thaw process. The main thing that we know, though, is that (typically in animal models, as in the last reference) for certain vaccines, if you allow them to freeze, they don't produce a sufficient immune response.

You can look at this very large table of data about which vaccines are freeze stable and which are not.  There are a few patterns to this, as the OP seems to have noticed.

Aluminum adjuvant: Any vaccine that uses an aluminum adjuvant (a chemical used to enhance the immune response) will be damaged by freezing. Polysaccharide vaccines and other purified or recombinant antigens are more likely to require an adjuvant. This is one of the reasons antigen only vaccines are more likely to be freeze sensitive. Some antigen only vaccines can be frozen themselves, and reconstituted with the adjuvant prior to administration (for example, some Meningitis polysaccharide and polysaccharide protein conjugate vaccines).
Live attenuated vaccines: Almost all live attenuated vaccines are freeze stable (e.g., MMR, oral polio). The only ones that aren't, as far as I'm aware, are influenza vaccines: flumist and the live attenuated H1N1 influenza A vaccine. This may or may not just be a precaution, as I'm not aware of immunogenicity experiments that demonstrate freeze sensitivity.
Inactivated vaccines: Most killed or inactivated vaccines are sensitive to freezing. IPV is one of them. Rabies is an important counterexample. This is entirely speculation, but since many of these vaccines are formalin inactivated enveloped viruses or bacteria with cell membranes, freezing a perforated cell membrane may further damage it's antigenicity.

You can read about the basic principles of vaccination (e.g., how a vaccine works, what an adjuvant is, when you need it, etc) in Abbas Basic Immunology Chapter 8, and Murray Medical Microbiology Chapter 13.


Respiration of an animal cell media I want to do respiration process of an animal cell media in laboratory environment.

I don't entirely sure how to supply it with Oxygen to the process because it is a gas, but not a liquid.

Supply of cells growing in adherent culture is unproblematic, as long as you don't fill too much media in the petri dish/cell culture flask.

Oxygen supply here work by diffusion which is getting more problematic if the layer of media covering the cells gets to thick. I usually follow the recommendations of Corning for the amount of media to be used in the flasks/dishes:

The complete information can be found here, other companies have similar data sheets available. With these amounts I do a lot of cell culture work and I have no growth problems.


SPR TRIS or PBS buffer Hey guys I want to ask why I can't get any binding interaction if I use TRIS-NaCl buffer for protein quantification using aptamer as its bioreceptor. But I can see the binding interaction if I use PBS buffer
The procedure step for my experiment :
1.) Self Assembled Monolayer (24-48 hrs) - NHS/EDC Activation (wash with acetate) - Streptavidin (Acetate buffer) - wash with acetate - wash with TRIS - ETH Blocking - wash with TRIS - Aptamer biotinylated (TRIS buffer) - Protein (TRIS buffer)
all washing buffer are using TRIS or PBS
And down below (my other method) I tried to exchange the buffer from PBS to TRIS after aptamer injection
2.) Self Assembled Monolayer (24-48 hrs) - NHS/EDC Activation (wash with acetate) - Streptavidin (Acetate buffer) - wash with acetate - wash with PBS - ETH Blocking - wash with PBS - Aptamer biotinylated (PBS buffer) - Buffer exchange (PBS to TRIS) - Protein (TRIS buffer)
I can see my aptamer signal in 1st and 2nd method, but still no binding occurred between my aptamer and my protein in TRIS buffer.

I presume the aptamer is biotinylated; if not, that’s a likely reason for the outcome.
Have you used a biotinylated positive control to confirm the surface is functional with PBS? I understand you want to buffer exchange to Tris, but this positive control in PBS buffer is important.
Amine coupling involves covalent attachment of the 1-Ethyl-3-(3-dimethylaminopropyl) carbodiimide (EDC) to carboxylate on the chip surface, followed by replacement of this adduct with N-hydroxysuccinimide (NHS), thus creating an active surface to crosslink primary amines at slightly acidic pH. Then the unreacted active surface is quenched with ETH. Residual active surface would react with Tris that contains a primary amine.
Perhaps the ethanolamine blocking agent may not have completely inactivated the active surface following streptavidin amine coupling, enabling crosslinking of Tris buffer to that surface and impacting the ‘Protein’ capture?
Other possible reasons: Binding of the aptamer to streptavidin may sterically hinder binding of the 'Protein.' Also, the loss of the proper secondary structure of the aptamer may impact the 'Protein' binding. Perhaps refolding the aptamer prior to streptavidin capture may help?
Edit: Differences in pH and ionic strength may impact 'Protein' binding to aptamer when tested in Tris versus PBS buffers.


Bicarbonate concentration in saliva From the picture it can be seen that Bicarbonate is secreted into lumen of duct of salivary glands by exchanging Cl- ions.

So if flow rate of saliva is increased then its obvious that less Cl- is taken in the cells and less bicarbonate is secreted out.

  At high flow rates, there is less time for reabsorption and secretion, and therefore the saliva is most like the initial secretion by the acinar cells. Thus, with the increase in flow rate the concentration of ions changes2

But it is also said that when flow rate increases the bicarbonate concentration also increases and when flow rate decreases bicarbonate concentration also decreases.

Doesn't this contradict the former fact?

According to this:

Yet another significant finding was the discovery of HCO3− absorbing mechanisms like NHE3 and NBC3 (NBCn1-A) at the luminal membrane of the ducts, which suggested the ducts absorb and scavenge HCO3− in the resting state.

So, initially saliva is isotonic to plasma, it is both reabsorbed and secreted, if its flow is slow, more of bicarbonate is reabsorbed, if the flow is high less bicarbonate is reabsorbed. Therefore when flow rate increases bicarbonate concentration increases.

Source of image:

At low salivary flow rates, HCO3- is reabsorbed by the striated duct cells and so very little reaches the mouth. At high flow rates, the striated ducts can't keep up and so HCO3- reaches the mouth at high concentration (<25mM)).
This makes perfect sense, from a physiological point of view. HCO3- is valuable to the body and not something to throw into the gut for no reason. The main purpose of unstimulated saliva is to keep the mouth lubricated, help you to talk and so on. Unless you are feeding the plaque bacteria, there is no great amount of acid to neutralise and therefore no need for a high HCO3- saliva. When you feed yourelf, and also your plaque bacteria, you stimulate salivary flow and produce a high HCO3- saliva, with a high buffering capacity, just when you need it.(Source)


Do spinal cord reflexes (such as the knee-jerk reflex) continue to function under general anaesthesia? The knee-jerk reflex (patellar reflex) is an example of a stretch reflex (myotatic reflex). Stretch reflexes are monosynaptic reflexes happening in the spinal cord without involvement of the brain.

Does it mean that this reflex will continue to function in an unconscious person, e.g. under general anaesthesia? Does it depend on the "deepness" of anaesthesia? Does it depend on a specific drug? I would also be interested to know if spinal reflexes keep working in unconscious states such as e.g. alcohol poisoning or a knockout.

The issue is complicated. In general it depends on the specific spinal reflex and on the specific anaesthetic. But it seems that the modern general anaesthetics usually do NOT block monosynaptic spinal reflexes (such as knee-jerk).
Here are two figures from Baars et al. 2009  that show that propofol and sevoflurane strongly inhibit withdrawal reflex (spinal two-synaptic reflex) but have almost no effect on the H-reflex (spinal monosynaptic reflex closely connected to the stretch reflex):

See below for many more details. Disclaimer: I know very little about anaesthesia and am simply writing down what I found after a couple of days searching and reading.

Withdrawal reflex
As @AliceD wrote, withdrawal reflex (a two-synaptic spinal cord reflex) usually disappears under any anaesthesia and this disappearance is used as a clinical sign of anaesthesia being deep enough for the surgery. As an example, this handout on monitoring anaesthetic depth in rodents has the following entry on the list of criteria for surgical anesthesia:

Withdrawal    reflexes    are absent! Try at  least   2   toes    and the ears    so  that    you are  sure   that    this    reflex  is  absent.

Knee-jerk reflex: early history
On the other hand, it is known from the XIX century that stretch reflexes such as knee-jerk (note that they are monosynaptic) are very persistent. They can be abolished under some drugs (such as e.g. chloroform and ether) that act directly on the spine, but keep working under others. I am quoting from three old papers on the topic (here and below emphasis is mine).
Horsley, 1883, Note on the patellar knee-jerk:

In 1881, while experimenting (on myself) with this gas [nitrous oxide] for
a different purpose, it occurred to me to contrast the conditions of the superficial and deep "reflexes," taking the
plantar reflex as an example of the former, and the patellar
phenomenon to illustrate the latter. Being aware of the fact
that deep chloroform-narcosis abolishes all the "reflexes,"
superficial and deep, and yet that with ether-narcosis, however deep, ankle-clonus frequently, appears, I was scarcely
surprised to find that the knee-jerk persisted in the deepest
anaesthesia from nitrous oxide, while the superficial reflexes
all disappeared.

Sherrington, 1892, Notes on the arrangement of some motor fibres in the lumbo-sacral plexus (p 671):

With regard to the effect of anaesthetics on the "jerk," a better proof of
the action of chloroform being rapid and direct on the nervous mechanisms of
the cord itself could hardly be found than in the speedy abolition of the
"jerk" by chloroform inhalation when the cord has been previously divided
in the thoracic region.

Simpson & Herring, 1905, The effect of cold narcosis on reflex action in warm-blooded animals:

The knee-jerk is a very persistent phenomenon. It is known to disappear in deep anesthesia produced by ether or chloroform [Sherrington 1892]. [...] The knee-jerk is as a rule easily elicited, and we find it present when
all the reflexes have disappeared. [...] The lower the
temperature the smaller the jerk. [...] In several animals that died at a low temperature the disappearance of the knee-jerk was simultaneous with death [...] The lowest temperature at which we found the knee-jerk present was 15° C., and this
was also the lowest temperature at which any of our animals were
still alive. [...] Pinching the skin does not provoke any response till the temperature is 25° C. [...] We have compared these results with similar ones obtained from
cats in recovery from deep ether anesthesia and find that the order of
reappearance agrees very closely.

Modern studies in animals
Hara & Harris, 2002, The Anesthetic Mechanism of Urethane: The Effects on
Neurotransmitter-Gated Ion Channels mention in the abstract that

Urethane is widely used as an anesthetic for animal studies because of its minimal effects on cardiovascular and respiratory systems and maintenance of spinal reflexes.

(they don't specify which reflexes specifically).
Ho & Waite, 2002, Effects of Different Anesthetics on the Paired-Pulse Depression of the H Reflex in Adult Rat study the effect of five different anaesthetics (ketamine, halothane, etomidate, saffan, and nembutal) on the Hoffman reflex (H-reflex), a monosynaptic reflex similar to the stretch reflex. They report that it keeps working under all five drugs, but the drugs modulate the decrease of the reflex under repeated stimulation (this decrease depends on the descending controls and is affected differently by different drugs):

The  results  suggest  a  preferential
action  of  some  anesthetics  on  descending  pathways
involved in reflex modulation [...]

Strangely, Ho & Waite do not describe how anaesthesia affects the reflex strength following an unrepeated stimulation, but in any case it is clear the the reflex keeps functioning.
Propofol etc.
What about the anaesthetics widely used in humans, such as e.g. propofol? Matute et al., 2004, Effects of propofol and sevoflurane on the excitability of rat spinal motoneurones and nociceptive reflexes in vitro:

We used an isolated spinal cord in vitro preparation from rat pups and superfused the anaesthetics at known concentrations. [...] Applied at anaesthetic concentrations, [...] sevoflurane produced a large depressant effect on the monosynaptic reflex whereas propofol was ineffective. [...] Sevoflurane produces large inhibitory effects on nociceptive and non-nociceptive reflexes which are likely to contribute to immobility during surgery. Compared with sevoflurane, propofol appears to have much weaker effects on spinal reflexes such as those recorded in an isolated preparation.

Kerz et al., 2001, Effects of Propofol on H-reflex in Humans:

Previous studies of motoneuron excitability using H-reflexes or F-waves during general anesthesia found significant depression after administration of halothane,  enflurane, isoflurane, desflurane, or nitrous oxide. [...]
Recommended propofol doses for induction and maintenance only had a transient effect on the H-reflex and were no longer demonstrable after 10 min of propofol anesthesia. [...] Immobility during propofol anesthesia [...] does not seem to be caused by a depression of spinal motoneuron circuit excitability.

So why is then the withdrawal reflex so easily abolished and the stretch reflex is so persistent (e.g. under propofol)? This does not seem to be well understood. Baars et al., 2009, Effects of Sevoflurane and Propofol on the Nociceptive Withdrawal Reflex and on the H Reflex write

Both H reflex and nociceptive withdrawal reflexes are reduced dose-dependently by propofol and sevoflurane in humans. [...] We have shown a striking difference of the degree to which both reflexes are reduced by the two anesthetics. The relative reduction of the polysynaptic RIII reflex amplitude was more than four times higher than that of the H reflex. This difference can probably be attributed to the higher number of neurons interposed in the RIII reflex pathway in comparison to the H reflex.

Note that the last sentence is very vague; it says that the difference is "probably" due to monosynaptic vs. polysynaptic mechanisms of these two reflexes but does not offer any explanation. Withdrawal reflex is mediated by an excitatory interneuron and propofol acts on GABA (which is inhibitory transmitter), so it remains unclear. This study is from 2009 and I did not find anything relevant in the papers that cite it.


Why don't primates have galactose-alpha-1,3-galactose (alpha-gal), but other mammals do? I read in wikipedia that:

  Galactose-alpha-1,3-galactose, commonly known as alpha gal, is a carbohydrate found in most mammalian cell membranes. It is not found in primates, including humans.

My question is : Why not?

In the sources for the wikipedia article about alpha gal allergy, I spotted the (pay-walled) article Evolution and pathophysiology of the human natural anti-α-galactosyl IgG (anti-Gal) antibody which has this to say in the abstract :

  It is estimated that anti-Gal appeared in ancestral Old World primates less than 28 million years ago, possibly as a result of an evolutionary event which exerted a selective pressure for the suppression of α-galactosyl epitopes expression by inactivation of the gene for the enzyme α1,3 galactosyltransferase.

However this is more than a bit over my head, biology-wise.

The general idea is that infectious agents use certain cell-surface proteins to enter the cell, and presumably recognize them by their particular glycoproteins. There are examples (cited in the extract below) of changes in e.g. blood group antigens in populations that are thought to convey (at least temporarily) an advantage against particular pathogens.

In this context, let me cite the rest of the section of the article that you didn’t have access to:

  However, after the geographic separation of Africa and South America,
  Old World primates appear to have been subjected to a selective
  pressure for the suppression of autologous α-galactosyl epitope
  synthesis and for the subsequent production of anti-Gal. Possibly, an
  infectious agent endemic to the Old World, which was detrimental to
  primates, and which expressed α-galactosyl, or α-galactosyl like
  epitopes, exerted a selective pressure for the evolution of Old World
  primates able to suppress autologous α-galactosyl epitope expression.
  Thus, immune tolerance toward this epitope was lost and anti-Gal
  antibodies could be produced in these primates as a protective
  response to such putative pathogens.

  An alternative scenario for the
  evolutionary suppression of α-galactosyl epitope expression could
  have been one in which ancestral Old World primates suppressed
  expression of these epitopes on their cell surface glycoconjugates as
  a result of exposure to a pathogen which exerted its detrimental
  effect via α-galactosyl epitopes functioning as receptors. A current
  example for such a pathogen is Clostridium difficile. Enterotoxin A
  produced by this pathogen was found to bind to the cells it damages
  through interaction with α-galactosyl epitopes on cell surface
  glycoconjugates [12, 56]. A bacterial toxin with a similar ligand
  specificity and which was detrimental to ancestral Old World primates
  could exert a selective pressure for the evolution of primates which
  suppressed the expression of α-galactosyl epitopes and, thus, lost
  the immune tolerance toward this carbohydrate structure.

  [12] Clark GF, Krivan HC, Wilkins TD, Smith DF (1986) Toxin A from Clostridium difficile binds to rabbit erythrocyte glycolipids with terminal  Galα-3Galβ1-4GlcNAc sequences. Arch Biochem Biophys 257:217
  [56] Krivan HC, Clark GF, Smith DF, Wilkins DT (1986) Cell surface binding site for Clostridium difficile enterotoxin: evidence of a glycoconjugate containing the sequence Galα→3Galβ1→4GlcNAc. Infect Immun 53:573

Whatever the reason, the consequence of this was:

  This also resulted in the loss of immune tolerance to the α-galactosyl epitope and the production of anti-Gal.

I presume this explains the IgE problem referred to in a comment, and I would consider this as an unfortunate side-effect of the change, and not a reason for it.


What is the base cancer rate for an arbitrary carcinogen? Are all carcinogens equally potent? Is the relationship between dose and probability of cancer roughly equal, or are there some carcinogens that provoke cancer significantly more than their cousins?

To answer this question in its entirety we have to split it into two questions:

  What are the underlying mechanisms of carcinogenity?

One of the main mechanism behind carcinogenity is the mutagenity of the cancerogens, i.e. the ability to cause mutations, that are abberations of the cell DNA leading to uncontrolled proliferation. This classical paper investigates the relation between cancerogenity and mutagenity.

One should mention here that there are many types of mutations possible, mutations are not equally dangerous for cells and some mutations can be successfully repaired using the intact strain.

Therefore the following parameters of the source substances need to be measured to estimate the cancerogenity:

Substance concentrations or absolute amounts (both being indirect measures of their chemical activities, the lower concentration is needed for causing cancer the higher is the chemical activity and vise versa).
Substance radioactivity (for the mutagenesis due to radiation).

  How can we measure the carcinogenity of different substances?

The most general approach here is to introduce certain amount of cancerogen into the animal body or to the cultured cell and to see the effect. The effect is calculated as the percentage of cells that undergo the transformation from normal into cancer cells. Two metrics are available here:

  DT = Tumorigenic Dose (the amount of substance causing certain
  percentage of cancer in treated animals, all treated animals are taken
  for 100%)
  CT = Tumorigenic Concentration (same, but adjusted for
  concentration and used in cell cultures).

(They are written CT and DT because in science people tend to used Latin abbreviations where the adjective actually follows the noune).

The common metrics are DT5/CT5 (5% cells/animals get cancer) and DT50/CT50 (50% of the animals). Those are similar to other common metrics, the most common is LC50/LD50 -- lethal dose for 50% of the animals/cells.

Unfortunately I couldn't not find any pre-compiled list with most known cancerogens and their TD/TC values. These seem to be interesting primarily for scientists. But going back to your question: you are absolutely right: some cancerogens are much more potent in causing cancer than the others!


Why did the process of sleep evolve in many animals? What is its evolutionary advantage? The process of sleep seems to be very disadvantageous to an organism as it is extremely vulnerable to predation for several hours at a time. Why is sleep necessary in so many animals? What advantage did it give the individuals that evolved to have it as an adaptation? When and how did it likely occur in the evolutionary path of animals?

This good non-scholarly article covers some of the usual advantages (rest/regeneration).

One of the research papers they mentioned (they linked to press release) was Conservation of Sleep: Insights from Non-Mammalian Model Systems by John E. Zimmerman, Ph.D.; Trends Neurosci. 2008 July; 31(7): 371–376. Published online 2008 June 5. doi:  10.1016/j.tins.2008.05.001; NIHMSID: NIHMS230885. To quote from the press release:

  Because the time of lethargus coincides with a time in the round worms’ life cycle when synaptic changes occur in the nervous system, they propose that sleep is a state required for nervous system plasticity. In other words, in order for the nervous system to grow and change, there must be down time of active behavior. Other researchers at Penn have shown that, in mammals, synaptic changes occur during sleep and that deprivation of sleep results in a disruption of these synaptic changes.


Why are abiogenesis and evolution considered unrelated? When a discussion about evolution comes across abiogenesis - the typical reaction is that they are unrelated (see the headline at http://www.factsnotfantasy.com/abiogenesis.php).

It seems to be that both are stochastic processes in which less ordered structures become ordered.  It seems that, in general, abiogenesis is the process of forming of life (whatever that is) whereas evolution is the process in which life would develop into more complex forms.  In other words, it seems that it's really just two phases of the same type of process and I'm wondering why they are considered as such isolated fields.

I wouldn't go so far as to say that they are entirely unrelated -- our understanding of selective processes can certainly inform our study of the origin of life -- but I would say that they are quite different projects.

One important reason is that evolutionary biologists can use phylogenetic information to reconstruct much of the history of life. For example, genetic sequencing techniques allowed us to definitively work out the evolutionary relationships among humans, chimps, and gorillas. But this approach can only allow us to back as far as the last universal common ancestor (LUCA). LUCA was presumably a DNA-based (uni-)cellular lifeform, given that these characteristcs are shared across the entire tree of life. So we have no phylogenetic information that we can leverage to reconstruct what happened to get us from a soup of organic molecules to LUCA.

Another reason is that evolutionary biology focuses on what happens to a population in which we have variation, heritability, and selection. Early in the origin of life, a structured system of heredity would not yet have arisen and so we would not see natural selection occurring in the form that we usually study it -- though there could be interesting selective dynamics in such a system.


My hand was stabbed with a pencil tip 10 years ago - why is the graphite still visible? I, and multiple people that I know, have permanent marks (up to 30 years) from a graphite pencil puncturing the skin. The palm of my hand still shows a very clear mark where my hand was punctured by a pencil 10 years ago in school.

Why/how does the graphite remain in the skin indefinitely?

I had the same thing happen to my leg. I think it eventually went away, but it was definitely many years.

I am going to go with the Tattoo answer. The way tattoos work is that Macrophages in the skin phagocytose the heavy metals in the inks. Because the heavy metals do not interact with Toll-like receptors, or any of the other pathogen receptors that macrophages have on their cell surface, they do not induce a transcriptional signal into the nucleus of the macrophage to induce it to chemotax out of the dermal tissue and into the lymphatic system, so they just sit there. The YouTube channel Smarter Every Day actually has two interesting videos on tattoos Tattooing Close Up and How Laser Tattoo Removal Works.

Macrophages are long lived, so unless they receive transcriptional signals to get them to move out of the tissue they are in, they will just sit there, and if they happened to have engulfed the heavy metals in tattoo ink, or the graphite from a pencil jab, then they sit there with a vesicle filled with that compound. As graphite is pure carbon, I wouldn't worry that much about it, but it is also not not in a form that the body can use, so it will persist. If eventually the macrophages are induced to move, they will likely take their contents with them, which is why tattoos fade over time.

It also is likely that the graphite was taken up by several macrophages in the region, in particles large enough that they cannot be cleared and remain visible, but not so large that the macrophages could not phagocytose them.