Reproduction or Cell division Most of the cells in multicellular organism undergoes cell division through Mitosis.

While most of the single celled organism reproduces through binary fission by mitosis.

In both cases,the offspring are very genetically similar to the mother cell.

But one is defined as Cell division and other is defined as Reproduction.

Why?

Both cells from unicellular organisms (for example, E. coli) and multicellular ones (humans, for example) divide by mitosis - you are correct. The daughter cells are not just very genetically similar, they are identical (if everything goes right, which it usually does). Both of these instances are called "cell division". It's also called "reproduction" in unicellular organisms because the entire organism just reproduced, in an asexual manner - it went from one to two copies of itself. On the other hand, many multicellular organisms (and some unicellular) can or must reproduce sexually. This involves (generally) at least one partner and a cellular process known as meiosis, which produces haploid gametes, which then meet somehow, one gets fertilized by the other, and the resulting diploid cell begins mitosis again.


What is this plant in the Butler, Pennsylvania area? This is growing in the woods near my house in the Butler, Pennsylvania (USA) area. I have not seen it around before, and I have no idea what is it. What is it? Is it poisonous to pets (or little kids)?

That looks like a bit like a Smilax to me, possibly Smilax herbacea.

Make sure you have a positive ID on any wild plant before you eat it, but if this is Smilax it looks like you don't have to worry about it being poisonous: from Flora of North America entry on the genus Smilax:

  Smilax has numerous uses. Sarsaparilla, a beverage and medicinal used
  against rheumatism, is obtained from the rhizomes of various species... All species of Smilax are excellent wildlife food and are also browsed, or the rhizomes dug
  and eaten, by domestic stock.

For you, or for other Pennsylvania people, note that the Pennsylvania Flora Project of the  Morris Aboretum is a great resource. You can download species lists by county, and just that and some google image searches can often substitute for a field-guide of your county.

If you want to identify plants the hard way, and are willing to deal with special botanical vocabulary, the Flora of North America that I linked to above is the definitive resource.


Can CRISPR be used in editing primary cells? How is the transfection efficiency? Sometimes people wanna use primary cells to do gene-editing because the cells normally have more interesting characteristics, but can we really do so?

The most efficient CRISPR-based editing of primary cells that I've read about used a technology called prime editing, developed in 2019.

Search-and-replace genome editing without double-strand breaks or donor DNA (PDF download)

Normal CRISPR-Cas9 protocols involve generating double-strand breaks (DSBs), and then either introducing a template for homologous repair or allowing the cell to repair the break without a template, leading to insertions or deletions at the lesion site.  Off-target cutting is common, so normal CRISPR-Cas9 produces undesirable or lethal mutations in a majority of transfected cells.

Prime-editing uses a catalytically impaired Cas9 (generates nicks instead of DSBs) fused to a reverse transcriptase.  The fusion protein is guided to its target by a prime-editor gRNA ("pegRNA") that contains a normal targeting domain at its 5' end and a template for reverse transcription at its 3' end. A nick is generated by the Cas9 on the exposed strand (i.e. the strand not bound by the gRNA), and the 3' portion of the pegRNA partially hybridizes to the the 5' side of the nick, providing a free 5' end and a stretch of ssRNA for DNA polymerization.  Resolution of the resulting "flap" by endogenous nick-repair mechanisms results in editing at the target site without DSBs or exogenous DNA template.

This method was assessed for its efficiency in several cell types, including primary mouse cortical neurons, which are post-mitotic and terminally-differentiated.  The authors observed the desired edit of DNMT1 in 7.1% of cells, with 0.58% indels on average.  Cas9 nuclease editing of the same cell type with the same lentivirus transfection system resulted in 31% indels, on average, an error rate more than 50 times that of prime-editing.


Is Rheumatic fever more Chronic than acute? It follows from the complication of S.pyogenes' pharyngitis.
I am thinking how the inflammatory response behaves: acute or chronic or something between.

I think chronic disease is better description here than acute, however not sure.

What is the type of inflammatory response in the Rheumatic fever?

the inflammatory response it autoimmune reaction, thus it occurs 4 weeks after the Strep infection.

please, look at the picture from the "Nature" -


Why are there no organisms with metal body parts, like weapons, bones, and armour? (Or are there?) Reading this question, Why are there no wheeled animals?, I wondered why no organisms seem to make use of the tensile and other strengths of metal, as we do in metal tools and constructions. I am obviously not talking about the microscopic uses of metal, as in human blood etc.

Why are there no plants with metal thorns? No trees with "reinforced" wood? No metal-plated sloths? No beetles with metal-tipped drills? Or are there?

I can think of some potential factors why there are none (or few), but I do not know whether they are true:

Is metal too scarce near the surface?
Are there certain chemical properties that make metal hard to extract and accumulate in larger quantities?
Is metal too heavy to carry around, even in a thin layer or mesh or tip?
Can metal of high (tensile etc.) strength only be forged under temperatures too high to sustain inside (or touching) organic tissue, and is crystallised metal too weak?
Are functionally comparable organic materials like horn, bone, wood, etc. in fact better at their tasks than metal, and do we humans only use metal because we are not good enough at using e.g. horn to make armour or chitin to make drills?

As a predator, I would like to eat a lot of vertebrates and save up the metal from their blood to reinforce my fangs...

A bonus question: are there any organisms that use the high electric conductivity of metal? Animals depend upon electric signals for their nervous system, but I do not think nerves contain much metal. The same applies to the few animals that use electricity as a weapon.

There are some cases, as hinted at by the comments. But these are relatively small amount of metal.

Its not that there is no metal available, but I can think of several reasons you don't see iron exoskeletons on animals all the time.  Firstly, fully reduced (oxidation state 0) metal has a high energetic cost to create in reduced form.

Iron is the second most common metal after aluminum on the earth's crust but its almost entirely present in oxidized states - that's to say: as rust.  Most biological iron functions in the +2/+3 oxidation state, which is rust or closer to it than metal.  Cytochromes and haemoglobin are examples of how iron is more valuable as a chemically active biological agent than a structural agent, using oxidized iron ions as they do. Aluminium, the most common metal on earth has relatively little biological activity one might assume because its redox costs are even higher than iron.

If there are some reasons why reduced biometal doesn't show up very often, inability of biological systems to deposit reduced (metallic) metals is not one of them.  Bone and shell are examples of biomineralization where the proteins depositing the calcium carbonate or other oxides in the material are structured by the proteins to be stronger than they would be as a simple crystal.  There are cases of admittedly small pieces of reduced metal being produced by biological systems. The Magnetosomes in magnetotactic bacteria are mentioned, but there are also cases of reduced gold being accumulated by microorganisms.

I would say that while iron skeletons might seem to be an advantage, they are electrochemically unstable - oxygen and water will tend to oxidize (rust) them quickly and the organism would have to spend a lot of energy keeping it in working form.  Electrical conductivity sounds useful, but the nervous system favors exquisite levels of control over bulk current flow, even in cases like electric eels, whose current is produced by gradients from acetylcholine.

What's more, it is a fact that biological materials actually perform as well as or better than metal when they need to.  Spider silk has a greater tensile strength than steel (along the direction of the thread). Mollusc shells are models for tank armor - they are remarkably resistant to puncture and breakage.  The time it would take for metalized structures to evolve biologically might be too long - by the time the metalized version of an organ or skeleton got started, the bones, shells and fibers we know probably have a big lead and selective advantage.


Task-dependent "reversed" handedness: why use left hand for some tasks? How is it controlled by the brain? I am right-handed. Which means that when I hammer down a nail, I hold the nail in my left hand, with which I can hold it straight and at a controlled position.

This is true in situations where the task of holding something in place is  simultaneous with a more complex task, such has hammering, done with the right hand. But I note that even when there is no other task, I personally use my left hand to hold in place, e.g., a  bottle that I am filling up in a stream of water.

To generalize a little, it seems to me that while I use my right hand for precise motion or applying a force, I'll use my left hand to maintain a position against forces.

Is this behaviour something documented? Does one develop specific brain control to implement this controlled-position tasks?

The dynamic-dominance hypothesis of handedness states that the essential factor that distinguishes dominant from nondominant arm performance is the facility governing the control of limb dynamics. Sainburg (1) writes that

  It should be noted that dominant arm advantages do not apply to all
  tasks, or all aspects of tasks. Healey et al. (1986) examined an
  extensive range of tasks and found that four factors or groups of
  tasks accounted for 80% of the variance in hand preference among the
  110 subjects tested. Tasks that were almost exclusively associated
  with dominant arm use included activities requiring precision in
  interjoint coordination and trajectory formation. (...) In contrast,
  tasks that involved spatially orienting a body segment posture were
  more often performed with the nondominant arm. These tasks included
  posturing the hand to point toward a distant object, which is similar
  to other functional tasks such as holding a piece of paper that is
  being cut with scissors, or orienting the hand in space for catching a
  baseball. Such postural orientation tasks are less dependent on
  intersegmental dynamics, since the trajectory used to attain the
  posture is not critical for task success. The dynamic dominance
  hypothesis thus appears to account for the extent to which hand
  preferences for specific activities are lateralized.

This appears to be consistent with your experience.


Medium for Pseudomonas? What is a good minimal medium for Pseudomonas bacteria? Do I need different media for different Pseudomonas species?

Pseudomonas bacteria are generally not difficult to grow:

Rugged and opportunistic, Pseudomonas use a wide range of nutritional sources, even very simple nutritional environments without any organic compounds. - Sigma

For specific species, you'll want to use a selection medium. Sigma-Aldrich has a number of  commercial products for selection and I'm sure you can find a recipe that suits your species with a Google search.

Related reading:
Medium for the Selective Isolation of Members of the Genus Pseudomonas from Natural Habitats (Grant and Holt, 1977)
Evaluation of various selective media for the detection of Pseudomonas species in pasteurized milk (Van Tassell et al., 2012)


Are hormones antigenic? I have been asked whether hormones are antigenic.

I would have to think that the answer is no because they are used as various drugs such as FSH in infertility treatments without the need of immunosupressants.

Hormones have antigens.  Usually they are antigens our immune systems recognize as self.

Pretty much any big biological molecule will have antigens.  FSH is no exception.  The binding of FSH to anti-FSH antibodies (in a laboratory system) is one way to measure FSH levels in a human.

 Definition and Measurement of Follicle Stimulating Hormone

  B. High-affinity binding assays
  1. Immunoassays. Immunoassays are widely used for clinical determination of FSH for diagnosis and in physiological studies
  because they are rapid, readily available, relatively cheap, and
  sensitive... Most commercially available assays are now based on
  sandwiches of monoclonal or monoclonal-polyclonal antibodies with a
  variety of detection modes and are generally more sensitive and
  precise than one-site assays. The latter assays are highly specific
  and may exclude some forms of the hormone of interest (e.g., Ref.
  176).

The antibodies used to measure FSH are from other species of mammals - usually mice but sometimes other animals. People (and other animals) normally do not form antibodies to molecules that have been present in their bodies since development.  The immune system is educated early on about what is self and so exempt from attack.  Mouse FSH is antigenically different enough from human FSH that mice can be induced to form antibodies against human FSH and then those mouse antibodies are used to make the lab test.   You can find out how those tests work with a little googling because they are for sale and their owners will brag about them.

It is possible to form antibodies against your own FSH or any other biomolecule in your body.  That is autoimmunity and usually that is not good.  The woman in the linked article was infertile because of antibodies against FSH.  Her FSH level was very high because her pituitary was cranking it out.  Her immune system bound it up as fast as it came out and so the FSH did not work.

Abnormally Elevated Follicle-Stimulating Hormone (FSH) Level in an Infertile Woman

  We describe here a case of anti-FSH autoantibodies leading to
  persisting very high FSH serum levels in an infertile woman.

Bullet points

Any biological macromolecule has antigens.
The immune system may tolerate antigens it has been educated to recognize as self.
Sometimes the immune system becomes intolerant of an antigen it should recognize as self and attacks that antigen.  This is autoimmune disease.


About molecules and their shape When a molecule is being used in some biochemical process it has a certain 3-d structure. Is this maintained throughout it's usage or can one specific molecule change it's 3-d shape while it is being 'used' in the process. Can a specific molecule in all it's interactions in a cell say , take on 4 or 5 distinct 3-d shapes??

All molecules have a 3D shape. This is referred to as it's conformation. Most molecules have certain degrees of flexibility. For example, single bonds usually allow free rotation, while double bonds don't. Cyclic structures have less freedom, but can still twist into several shapes. This can be important because some molecules bend into a certain conformation and then fit into protein binding sites they normally couldn't fit into. And it's not just small molecules, proteins, RNA, and DNA fold into specific shapes, and often must be unfolded, twisted, or bent in order to carry out their function. Protein dynamics is an active field of study. A great example is the ATP synthetase, which has a large rotating portion and acts a lot like a motor.


Understanding F-statistics in population genetics I am reading the classic Weir and Cockerham 1984 paper about $F_{ST}$ estimation. At the beginning (first page, right column), they define 3 statistics.

$F$ is the correlation of genes within individuals ("inbreeding")
$\theta$ is the correlation of genes of different individuals in the same population ("coancestry")
$f$ is the correlation of genes within individuals within populations.

They also state that the 3 statistics are related by

$$f = (F-\theta)(1-\theta)$$

I don't quite understand those 3 statistics and especially I don't understand why this relationship holds true. Can you help me with that?

I am a bit wobbly on the subject, but I think the most important bit of information is that they are re-parametrising Wright's (1951) hierarchical analysis of variation, "F-statistics," "hierarchical partitioning of variation," or "population parameters," depending on whom you ask. The parameters correspond as follows (on the bottom of p.1358): Fit=F, Fis=f, Fst=θ.

The relationship arises given some assumptions. Crucially here, if Fis (or f) is a measure of departure from Hardy-Weinberg Principle, and all populations identically depart from HWP, then Fit = 1 - Hi/Ht. It follows that, 1 - Fit = Hi/Ht. As well, we can rewrite this, so that, Hi/Ht = (Hi/Hs)(Hs/Ht).

Together, you can (maybe) see that, 1-Fit = (1−Fis)(1−Fst). Substituting, 1-F = (1-f)(1-θ).

(I realise that this is not a complete answer, but you can rearrange it with some algebra to get the Weir&Cockerham equation, I think).

[Update Oct 25, 2016]: it eventually yields f = (F-θ)/(1-θ). I think the posted question (above) contains a typo--specifically a missing division operator. Perhaps someone missed the stroke on a typewriter in the original paper?


What is the difference between a polysaccharide and a macromolecule? I'm having trouble understanding the difference between "Polysaccharide"
and "Macromolecule".

I know that polysaccharides are made of chains of monosaccharides.  In addition, I know that macromolecules are made of monomers.

But what is the difference?

A macromolecule is a class of biomolecules that are made of monomers. These include polysaccharides (i.e. sugars) polypeptides (i.e. proteins) nucleic acids (like DNA and RNA) and lipids (fats ans phospholipids).

A polysaccharide is one type of macromolecule made up of monosaccharides like glucose and fructose. An example of a polysaccharide is starch or cellulose.


Does the speed of electrical impulses through neurones decrease with age? From what I read on the NatGeo app, it stated that the speed of the electrical impulses that are sent by a neurone will be approximately 332 kilometers per hour.

Will the speed of this electrical impulse decreases over the years as we age?

As @Armatus notes, it is now generally understood that age-related cognitive decline is related to loss of myelination and axon damage (see, for example, Kohama et al, 2012). Myelin degeneration is also likely the cause of some age-related peripheral neuropathies. Loss of myelination (due to inflammation) is also the mechanism behind multiple sclerosis.

Myelin allows for fast and reliable transmission of action potentials by a mechanism known as saltatory conduction. This is necessary to compensate for axons which have small diameters (unlike the squid giant axon) and travel long distances. Degraded myelin will reduce conduction velocity and can result in propogation failures. The links @nico provided in his comment above are useful references.

Kohama, S.G., Rosene, D.L., Sherman, L.S., 2012. Age-related changes in human and non-human primate white matter: from myelination disturbances to cognitive decline. Age (Dordr) 34, 1093–1110.


What's a mouth ulcer/canker sore "made of", and why do they develop? Mouth ulcers are red/white rings with a crater. They are sore and last for 7-10 days.

What I want to know is what they are 'made of' - i.e., what is the ring filled with, and why is the centre crater so sore? And why do these relatively benign and short-lasting ulcers have to hurt so much when they simply heal in a couple of days

The redden area around the grayish-white indentation of the canker sore isn't filled with anything. This circular area is simply inflamed. The grayish-white area in the center is not filled with puss or anything else as well. This is an area of dead cells but underneath this layer of dead cells the tissue red [1],[2],[3].

Canker sores, Aphthous stomatitis, is an ulcer. An ulcer is a break in the membrane. That is, you have an open sore in your mouth. As with any open wound, pain and discomfort will occur but the mouth is how we consume our food. Since we intake our daily bread in this manner, what we consume can cause the pain to increase; for instance,

acidic foods
spicy foods
abrasive foods

The cause of canker sores is not entirely known, but according to the Mayo clinic [2], possible triggers are

A minor injury to your mouth from dental work, overzealous brushing, sports mishaps or an accidental cheek bite
Toothpastes and mouth rinses containing sodium lauryl sulfate
Food sensitivities, particularly to chocolate, coffee, strawberries, eggs, nuts, cheese, and spicy or acidic foods
A diet lacking in vitamin B-12, zinc, folate (folic acid) or iron
An allergic response to certain bacteria in your mouth
Helicobacter pylori, the same bacteria that cause peptic ulcers
Hormonal shifts during menstruation
Emotional stress

Canker sores may also be caused by the following diseases as well [2]

Celiac disease, a serious intestinal disorder caused by a sensitivity to gluten, a protein found in most grains
Inflammatory bowel diseases, such as Crohn's disease and ulcerative colitis
Behcet's disease, a rare disorder that causes inflammation throughout the body, including the mouth
A faulty immune system that attacks healthy cells in your mouth instead of pathogens, such as viruses and bacteria
HIV/AIDS, which suppresses the immune system


Which kind of tick is this and what is that thing around its back? I was recently bitten by a tick. After having removed it from my body, I put it in a glass. By now, it has stopped moving, so I put it under a microscope and looked at it. I was surprised about being unable to get a sharp image of its body (upper part in the images) – what could that be? And can someone help me identify it?

I found a picture of a tick with a somewhat transparent thing around its back here – maybe that's what made it hard for me to get a clear focus on the back? And maybe it's related to this one?

It was found in Oldenburg, Lower Saxony, Germany. Its length is between 1.2mm and 1.4mm (I don't have anything that's very usable for precise measurement of such small lengths).

If clearer focus on a particular part of that thing is needed for identification, please tell me.

As your link suggests, it looks like a female tick of the genus Ixodus. It is likely female because the scutum or shield only covers part of the dorsal surface. E.g.,

which comes from Bristol University Tick ID. The translucent posterior portion may just be from light passing through.

If you are able to zoom in closer on different parts, you can key out what species it is.


Is it possible to synthesize chiral version of an organism (incompatible with our pathogens)? In theory, it should be possible to synthesize chiral (mirror image) version of some organism: with all molecules replaced with their enantiomers, e.g. L-sugars in place of our D-sugars.

Direct application of such chiral life could be production of enantiomers of proteins in e.g. chiral E. Coli, what might be useful for example as new drugs.

However, the most interesting is that such chiral life would be incompatible with our pathogens, for example allowing to design really sterile ecosystems for harsh environments like Mars. Finally, such chiral human would be immune to most of our diseases.

Nice article: http://wikibin.org/articles/chiral-life-concept.html

The question is if it is technologically possible to synthesize e.g. a chiral version of E. Coli?

Update: Wikipedia https://en.wikipedia.org/wiki/Chiral_life_concept

First off, quick clarification: "chiral" simply means distinct from its mirror image. All current life is chiral, in that it is made up of molecules  which have a "handedness". What you're asking about is life which is made up of molecules of the opposite handedness (which I'll term "mirror chiral").

Such a lifeform is theoretically possible - chemical and biological reactions and reaction rates are entirely the same between the two handednesses - presuming that all participants (substrates, products, catalysts, etc.) are flipped to the opposite chirality. A mirror chiral Jarek would look and function exactly like the normal chirality Jarek, although he would need to eat mirror chiral food instead of normal chirality food.

So what difficulties would you have to synthesize a mirror chiral organism?  The biggest one is the bootstrapping issue. There's a large suite of molecules in the cell which are all needed in order to replicate the cell, or even just maintain it. All of these need to be present in order for the organism to work. The organism can make all these components from scratch, but to do so it already needs to have these components.

Synthetic organisms - that is, organisms with a genome assembled in a computer and synthesized abiologically - have been made. The trick, though, was that the synthetic DNA was then placed into already existing organisms to be replicated and to have its genes expressed. There's no limitation (besides perhaps cost) to synthesizing mirror-chirality DNA - the same machines which synthesize normal chirality DNA can do it if you swap out the reagent bottles. But what do you do with it once you have it? There's no existing mirror-chiral organisms you can place it in to replicate and express the genes.

If one was to make mirror-chiral organisms, you would need to synthesize all of the necessary cellular components in their mirror-image form. So you would need mirror RNA polymerase, mirror ribosomes, mirror t-RNA, mirror ...  If you do things right you can skip most of the cellular components, but you still need a large number of them.

This is not necessarily a pipe dream. Last I knew, the J. Craig Venter Institute, the people who made the first synthetic DNA organism, are actively looking into it. The trick is to trim things down to the bare minimal number of chiral components needed to bootstrap the system. That's (more-or-less) where their current efforts are focused, from what I understand: what's the minimal number of genes needed for a viable cell? Which of these are needed to "bootstrap" a cell from bare DNA?

Personally, I'm pretty confident that a mirror-chiral organism will be created one day. The time frame for this is a little unclear, but there's nothing theoretically limiting it. The biggest issue is our current technical limits in synthesizing sufficient quantities of (non-DNA) biomolecules in a chemical (abiological) fashion. But those are constantly improving, and with additional research into what's needed for bootstrapping a synthetic cell, we'll push down the requirements even further.

Of course, the first mirror-chiral organism will be pretty simple. It's going to be less complex than even E. coli. It will also need to be fed a diet of (expensive) mirror-chiral food (amino acids, sugars), so its use will be limited as well.


What is the relationship between induction of cell differentiation and DNA methylation status? This may sound like a broad question to ask, but I am working on interpreting a review article for my epigenetics course and I'm having trouble reconciling two seemingly contradictory things this review is saying.

Ehrlich, M., & Lacey, M. (2013). DNA methylation and differentiation: Silencing, upregulation and modulation of gene expression. Epigenomics, 5(5), 553-568. doi:10.2217/epi.13.43

On page 554,

  Constantinides
  et al. found that treatment of an embryonic
  fibroblast cell line with 5-azacytidine (5azaCR),
  an inhibitor of DNA methylation, induces the
  formation of [myotubes] [35].

and

  Treatment with DNA demethylating agents
  can not only convert non-myogenic progenitor cells to Mt, but also can induce other cell-
  type interconversions in progenitor cells. For
  example, with 5azaCR treatment, the C2C12
  Mb cell line can be induced to express genes for
  key osteogenic transcription factors as well as
  adipocyte markers [40]. The outcome of DNA
  demethylation treatment is dependent upon the
  cell type as well as the treatment and growth
  conditions [41].

and

  The conversion of a multipotent adult stem
  cell to dissimilar differentiation products by
  treatment with DNA demethylating agents
  can be explained by the hypothesis that some
  genomic methylation restricts the differentiation
  potential of progenitor cells [40].

These three quotes, all on the same page, seem to indicate that at the very least, induction of differentiation is contingent on demethylation. More specifically, DNA methylation restricts the possible differentiation activity that a progenitor cell can undergo. However, just a little further down,

  Terminal
  differentiation predominantly led to increases
  in DNA methylation and both increases and
  decreases in H3K27me3, depending on the
  gene involved.

and

  [...] to
  hypothesize that changing the DNA methylation status of pluripotency genes in vivo is critical to their function [43]. DNA methylation is
  considered a more stable repressive mark than
  repression-associated histone modifications [42].
  The association of differentiation and the loss of
  pluripotency with DNA methylation at previously unmethylated sites (de novo methylation)is consistent with the inability of ESCs to differentiate when Dnmt1, the most abundantly
  expressed DNA methyltransferase gene, is
  homozygously knocked out [44].

I'm working on a presentation on DNA methylation and gene silencing, and I want to make an accurate portrayal of the role of DNA methylation in cell differentiation, and this is only a portion of the whole presentation, so I am not including a lot of data on this topic. However, I want whatever I do present to be self-consistent and accurate. How do I reconcile these two phenomena? From what I can tell, there is no explanation in the intervening text between these passages about how these two phenomena are similar but distinct. Am I accurate in determining that this is a difference between induction of differentiation and terminal methylation status? If so, how is it that ESCs can be differentiated with demethylating agents, but also ESCs have trouble differentiating when Dmnt1, which promotes methylation, is knocked out?

This is a good question. I'm not as steeped in this literature as I'd like, but here is my understanding of the process:

Methylation is one of the key methods by which cell fate is restricted. The review you're reading is giving specific examples of cell lines that are at least partially restricted into cells that are of an entirely different type. Thus de-methylation is a method for de-differentiation, which then allows differentiation along a different line.

Your three examples that it sounds like you're interpreting as induction of differentiation, are actually examples of that effect -- de-differentiation that then allows for differentiation to a different fate. Constantinides work, for example, showed the conversion of a non-myoblast precursor into functional striated muscle cells. Not only can fibroblasts be turned into muscle cells, myoblast cell lines can be made to look like bone cells or fat cells. None of these things would happen without re-programming the cell fate by de-differentiating the cell lines to form dis-similar differentiation products.

This is consistent with other findings about de-methylation in vivo. An important example is the global de-methylation of primordial germ cells, as demonstrated in this figure from the linked review, summarizing the methylation state of the germ line in mice. Pay particular attention to the blue line. The pronucleus of the highly differentiated spermatazoon (along with its highly methylated DNA and histones) undergoes global de-methylation. Its products include the primordial germ cells of the developing mouse, the most de-differentiated state, which, in the case that it is a male, then become methylated as they become primed to differentiate, and then differentiate.


Why aren't the brains of most advanced life forms in the middle of their bodies? This question is designed to be the successor to Why don't most animals have "heads" in the middle of their bodies?

The previous question was flawed as it fails to accurately define what constitutes a "head".

Keeping on topic, the question here is largely focused on placement of brains and brain-like structures.

Intuitively, common sense would dictate keeping the brain roughly equidistant from everything it controls, decreasing the number of potential failure points between the brain and peripherals.

The standard argument in favor of putting the brain in the head rather than in the middle is for dedicated specialized visual processing. This argument is easily debunked seeing that there's no reason why you couldn't have a brain in the middle of the body and a smaller dedicated optical co-processor in the head. (similar to how a certain premium laptop design 7 years ago had only integrated video built-in but comes with a dock that supplies a high-end external video card). The smaller head-brain would run all of the intensive processing and send a compact representation to the central brain, adding a modest amount of extra reaction time lag. Extra credit if the central brain can partially offload high-level or heavily spatial thought processes to the smaller head-brain (think of it as using a CPU and GPU working together to solve a problem more quickly than the CPU could on its own).

Because the head is where most of the sensory organs are, and once the brain started developing there it was basically impossible to move it. There is so much relying on its placement, that if it was moved many nerves would no longer be directed to the right place, as there are myoskeletal constraints around it. Basically most of an animals form around the central nervous system and moving major basal organ complexes just doesn't happen in evolution. Moving the brain would be impossible once you got to things like vertebrates.

Smaller CPU only work in systems with lots of redundancy which is not an animal thing. Centralizing processing has it's own advantage because parts of the brain have to communicate with other parts a lot. You would basically have to have almost an entire other brain, which defeats any advantage.

Lastly, there really is not much of an advantage in moving the brain into the chest cavity, as for most animals the brain is small enough to be just as safe in the head as anywhere else.

That said, there are animals with a brain in their midsection; they are called cephalopods.


Is covid vaccine helpful for a covid patient? I am not a biology student and this question came in my mind out of nowhere.
I read somewhere that the vaccines contain some denatured or almost dead corona viruses and when these are injected in our body , our immune system remembers them and if the actual (killer) corona virus enters our body , our body recognises it and quickly attacks it.
But if we have a  corona patient his body has already identified the corona virus and so if the vaccine is given the body will not have much changes to do and simply refuses it .
So is it okay to give the covid vaccines to a covid patient ? Can it make the infection even worse ?

In short, no. It's not harmful but it won't do anything to prevent or mitigate the current infection.
How vaccines work in general is that they train the immune system to respond to an infection so that they are prepared for it. Generally protein component of the virus or an inactivated form of the pathogen is used as a vaccine. The immune system recognises the proteins as 'foreign' and develops anti-bodies to fight them. Then you are immunised to the virus without having to suffer the symptoms of infection. Vaccines work before you are infected as a preventative measure. Then when you are infected, the immune system is prepared and can fight of the virus with the antibodies already developed since the virus has the same "antigen" proteins as you immune cells have already been exposed to from the vaccine.
So what happens when you are vaccinated when you are already infected? Basically nothing.
The benefit of a vaccine is a head-start to train your immune system how to fight it to prepare for the early stages of infection. If you are vaccinated, your immune system will destroy the virus before the it multiplies or gives you symptoms. If you've already been infected then the active virus has already infected many of your cells and multiplied into many copies. Adding inactivated viral particles or spike protein antigen won't help your immune system, it's already been exposed to them by the ongoing infection. Your immune cells are just playing catch up to the infection that's already taken hold. The virus has already stormed the beaches and the immune cells were not prepared. Vaccination now is arguably pointless. They will eventually produce antibodies against the virus already in your system even if you weren't vaccinated.
Lasting immunity after recovering from infection is not guaranteed and a vaccine could give immunity to other strains. For these reasons, it could still be recommended by medical professionals if you've already been infected. However, you need to be vaccinated before exposure to the virus for it to be effective. A vaccine is not a treatment.
Note: the currently available AstraZeneca, Pfizer, Moderna, and Johnson & Johnson vaccines for SARS-CoV-2 do not contain live or inactivated coronavirus. They trick the host system into producing the spike protein from instructions carried by the vaccine.
Citation for clinical application: Jenner, E (1798) An Inquiry into the Causes and Effects of the Variolae Vaccinae.


What makes a metal safe to use for an artificial joint? What determines if a metal is suitable for transplantation such as in the hip? What I am most interested in however is why might some metals be toxic to animals once in the body?

There are a number of reasons why a given metal may be toxic to an animal:

Radioactive metals are the easy ones.
Some metals can affect the normal biosynthetic pathways within the body.  Lead is a good example of this, as it can take the place of calcium; I believe beryllium does the same for magnesium.
Some metals themselves are very reactive.  Hexavalent chromium ($Cr(VI)$) is highly reactive, and will cause damage through severe oxidative reactions, whereas $Cr(III)$ is largely okay.
A lot of metals are okay, even required, at some level, but become toxic at too high a concentration.  Iron, for example.
People can simply have allergies to metals.  Nickel in silver jewelry is a good example, although in my experience it can be overcome.

The basic gist is that some metals are required for life, some aren't but aren't too terrible, and some are completely toxic to it.  Different organisms can vary a bit in which metals are useful or not.  A good implant will of course not be toxic at all, and will be strong and long-lasting.  Titanium is often used, given its strength and general nonreactiveness, but so is cobalt, despite being toxic to some degree.

Ref: Metal Sensitivity in Patients with Orthopaedic Implants.  Hallab, et al. J Bone Joint Surg Am, 2001 Mar 01;83(3):428-428


Virus cannot survive on surface after certain time period, but why and how? I'm not a biology student at all, but I'm trying to get a clearer picture on what is meant by "virus cannot survive after a certain period".

To my understanding, a virus cannot be killed it can only be inactivated (for example, by means of heat and lowered pH).

So I really don't understand how can virus get inactivated by just being on a certain surface for an extended period.

I've come across numerous articles which told me virus won't survive on a surface. They usually focus on comparing the survival time between different types of surfaces but never touch on how the virus gets inactivated.

Can someone help me understand the "how"?

Many important viruses are coated with a lipid envelope and rely on this to enter the host cell. This envelope is fragile - it's similar to a soap bubble - and it can be disrupted in many ways. Lipids will oxidize in air over time and this will degrade their ability to maintain an envelope. Surfactants such as soap or solvents such as alcohol will disrupt an envelope quickly. Even if the genome inside survives, if the envelope is disrupted the virus won't be able to infect cells.
The exact mechanism of inactivation likely varies a lot from virus to virus, and hasn't been studied extensively.
This paper found that Hepatitis C virus RNA survived alcohol treatment, but lost infectivity, presumably due to envelope disruption. In contrast, heat treatment (80°C) destroyed both the envelope and the RNA.
Another paper found enveloped viruses survived being dried out a shorter time than non-enveloped viruses. (5 days vs. weeks)

Speaking generally, the environment outside a body is hostile! If you were taken out of your home and dropped somewhere in the wilderness, there's many different ways you could die, and it's more remarkable if you survive. A similar situation arises for viruses.


Why is Fast Fourier Transform applied to raw EEG data? I am trying to understand why Fast Fourier Transform (FFT) is used in the analysis of raw EEG channel data.

My understanding (at the 30,000 ft view) is that FFT decomposes linear differential equations with non-sinusoidal source terms (which are fairly difficult to solve) and breaks them down into component equations (with sinusoidal source terms) that are easy to solve. It then combines each of these component/partial solutions to solve the original equation. In laymen's terms, it's like taking a smoothie, and breaking it down into its recipe of ingredients. Doing so would allow us to study and analyze each ingredient as it relates to the final product (the smoothie).

But how does this relate to raw (non-FFT-decomposed) EEG data? My understanding of a single channel of EEG data is that it is essentially a measurement of voltage over time.  What is to be gained by using FFT to break this voltage/time signal down into its constituent frequencies (alpha/beta/gamma/delta/mu waves), etc.? What additional information can each frequency tell us about the raw data?

Update:

Here is my updated understanding of how FFT relates to raw EEG data per @Mark's description below:

Fast-Fourier Transform (FFT) transforms a signal from the time domain into the frequency domain. Basically, any time-dependent signal can be broken down in a collection of sinusoids. In this way, lengthy and noisy EEG recordings can be conveniently plotted in a frequency power-spectrum. By doing so, hidden features can become apparent. By adding all the sinusoids up after FFT, the original signal can be restored, so no information is lost.

A notable application of FFT in EEG is shown in Fig. 1, which shows an EEG in an awake person (top blue trace) and an EEG in a propofol-sedated person (bottom red trace). The traces are different, but exactly how different? Scientists like to quantify stuff.

Now look in Fig. 2, which shows the same data but filtered in the delta band (low-pass filtered EEG with a cut-off frequency of 1.5 Hz, left panel). Here it already becomes more apparent what's going on, but what exactly is the difference between the two traces? That difference becomes readily apparent in the frequency domain by using FFT (Fig. 2, right panel); The frequency spectrum has a peak at 0.2 Hz in both traces, but that peak is about twice as big in the anesthetized state than in the normal state. In other words, the anesthetized brain reveals more low-frequency activity.

Fig. 1. Raw EEG of an awake person (blue) and propofol-anesthetized person (red). source: Wang et al (2014).

Fig. 2.  Filtered EEGs (<1.5 Hz) of an awake person (blue) and propofol-anesthetized person (red) (left panel) and corresponding FFT spectra (right). source: Wang et al (2014).

This is reminiscent of the drowsiness encountered in slow-wave sleep; which is yet another example of why FFT is useful; various stages of sleep are markedly different in their EEG. For example, early stages of sleep are characterized by slow-wave EEG, while REM sleep is characterized by high-frequency EEG activity. By using FFT, these differences in frequency content can be captured in simple, quantifiable data.

Another widely applied FFT-based application is filtering in the frequency domain. Look at the sleep EEG in Fig. 3. By splitting the raw signal up in frequency bands, the noise can be removed (high-frequency components), but even better, the k-complex (a characteristic hallmark of normal sleep) can be beautifully isolated from a messy EEG signal (bottom trace, 12-15 Hz).

Fig. 3. EEG FFT-based filtering. source: Neurology

Reference
- Wang et al., Front Syst Neurosci (2014); 00215


Mutation rate and Evolutionary rate? What is the difference between then?I have read some jobs that describes analysis about mutations rates and another ones with evolutionary rates.I want to know the diferrence between then.

Mutation rate

A mutation rate is a rate at which mutation occur. It is typically expressed as number of mutations per site (per nucleotide) per reproduction event. In humans, the average mutation rate per site per reproduction is of the order of $10^{-8}$.

When a mutation occurs, it will exist in only one copy in the population. This mutations might, over time, reach a higher frequency and even eventually reach a frequency of 1.0 (we talk about "fixation" then) but most mutations will never reach a high frequency and just disappear in the coming few generations whether or not the selection was deleterious.

Evolutionary rate

The term "evolution rate" has no commonly agreed upon definition. Depending upon your definition the mutation rate will be more or less correlated with the evolutionary rate.

Phenotypic evolutionary rate

Evolution rate might refer to phenotypic evolution. The Darwin (named after Charles Darwin, obviously) is a common unit to measure phenotypic evolution. Other unit of evolutionary rate could consist at measuring how much time it take for the mean phenotypic trait to change by one standard deviation of the original phenotypic distribution.

Genetic evolutionary rate

One can also consider genetic measure of evolutionary rate such as the number of neutral substitutions in a lineage per unit of time. With this definition, the difference between the mutation rate and the evolutionary rate become a little more blurry as the expected substitution rate at neutral site is equal to the mutation rate.

Always cite your source!

You say

  I have read some jobs that describes analysis

Please, always include your source. There is no way to give any information about what they mean by these terms without having a look at the original paper.

Related post

The post Are we “more evolved” than present-day bacteria? is somewhat related.


Why do we urinate more often in winter compaired to summer? I have been thinking of this question for a long time, but I do not seem to find an answer yet. Is there a hormonal change in our body during winter due to which we have to run to toilet often?

There is no 100 % sure answer for this as, obviously, nobody is that much interested in studying about urination. But there are some theories, of which the most popular and accepted one is cold diuresis.

  Cold-induced diuresis, or cold diuresis, is a phenomenon that occurs in humans after exposure to a hypothermic environment, usually during mild to moderate hypothermia.

According to this theory, what exactly happens is this (I'll explain in steps for better understanding):

When your body senses cold or low temperature of environment, it constricts the blood vessels near your skin and external organs and restricts your blood to the inner core of your body to maintain its temperature.
Thus, it causes the blood pressure to increase as there is same amount of blood in lesser volume.
This induces negative feedback on ADH (a vasoconstrictor) i.e. its secretion is reduced.
Now when blood vessels in kidney get proper amount of blood (as blood vessels aren't constricted now), they sense high blood pressure and try to reduce it as soon as possible.
So they transfer more amount of water from blood to bladder which fills the bladder more quickly and causes an urge to urinate.
Thus, we urinate more in colder climate.

There are some more theories related to it too, but they aren't as popular. According to another theory, when we are exposed to cold weather, aquaporins are inhibited around the body, making it impossible for water to be taken in by cells, leaving a lot more of it in the blood. Again, the body will try to balance that pressure, pulling water from the blood and storing it in the bladder. You can get a more frank and interactive explanation here.


Why can human viruses that can't infect chickens be grown in embryonic chicken cells? Embryonic chicken cells are commonly used in vaccine production.  The viruses are grown in chicken eggs, or in embryonic cells taken from those eggs, and then inactivated or attenuated to produce the vaccine.   But why can human viruses—some of which are not known to infect adult chickens—infect immature embryonic chicken cells?
For instance, according to this WHO fact sheet (https://www.who.int/news-room/fact-sheets/detail/measles), "Measles is a human disease and is not known to occur in animals." Yet the the measles virus prepared for the MMR vaccine is grown in chicken embryonic fibroblast cells.
N.B.:  According to http://www.ogrod.uw.edu.pl/__data/assets/pdf_file/0010/2161/13a.pdf, while measles may have evolved from domestic animals, it is thought to have its origin in cattle rather than chickens: "Measles, for example, is closely related to two other morbilliviruses-canine distemper and rinderpest (a disease of cattle)" [1]
One guess is that, while a virus would normally require interaction with a species-specific surface protein to initiate membrane fusion (see https://www.frontiersin.org/articles/10.3389/fmicb.2011.00247/full [2]), and thus viral (or viral RNA) entry into the cell, the naive nature of undifferentiated chicken egg cells enables such fusion to occur without such species-specific proteins.
Another guess (in the opposite direction) is that the species-specificity of viral infection depends on species-specific cell recognition factors, and because the cells in chicken eggs are undifferentiated, or minimally differentiated, they possess a broad range of recognition factors (where the non-chicken-specific ones are lost as the cells differentiate).
It was surprisingly difficult to find information online about this.  According to the the following (https://www.jstor.org/stable/30105172?seq=1), chicken embryo cells do become more resistant to viruses as the embryo ages; but this doesn't explain the lack of species-specificity:
"Cells dispersed from young embryos were permissive to viral growth, while those from older embryos were restrictive in an age-related pattern similar to that observed in ovo. The mechanism of natural antiviral cellular resistance did not involve viral attachment or release from cells from older embryos, but apparently depended on intracellular events during viral replication. These observations suggest that increasing natural resistance is based partially on intrinsic cellular changes. Sensitivity of a given virus and responsiveness of cells to the action of interferon may be more important to antiviral resistance than the amount of interferon that the virus induces." [3]
[1] Dobson, Andrew P., and E. Robin Carper. "Infectious diseases and human population history." Bioscience 46.2 (1996): 115-126.
[2] Hashiguchi, Takao, Katsumi Maenaka, and Yusuke Yanagi. "Measles virus hemagglutinin: structural insights into cell entry and measles vaccine." Frontiers in microbiology 2 (2011): 247.
[3] Morahan, Page S., and Sidney E. Grossberg. "Age-related cellular resistance of the chicken embryo to viral infections. I. Interferon and natural resistance to myxoviruses and vesicular stomatitis virus." The Journal of Infectious Diseases (1970): 615-623.

The measles vaccine uses an attenuated virus: one that has been  modified to reduce virulence such that it is (hopefully) no longer harmful to the host but still retains the antigenic determinants to induce acquired immunity. Although in modern times rational attenuation by genetic engineering is becoming established [1], the traditional method involves simply growing the virus under conditions abnormal for it such that it must evolve to survive. This often involves culturing the virus in cell types (or possibly organisms) in which it does not typically cause infection. Due to existing variation within the viral population or novel mutations, the virus may, over time, adapt to infect these cells with some degree of efficiency. Importantly in the context of vaccine development, the genetic changes generated during this adaptation may also reduce the pathogens ability to causes disease in the host organism [2].
This effect was originally observed by Louis Pasteur in 19th century who subsequently used it to develop a vaccine against the bacterium Erysipelothrix rhusiopathiae, which infects pigs [3]. Pasteur noticed that propagating this bacterium in rabbits, in which it did not initially cause disease, increased its pathogenicity in rabbits while at the same time reduced its pathogenicity in pigs. The virus had evolved and this attenuated form was used as a vaccine in pigs.
The attenuated virus for measles vaccine was created by the same principle in the 1950s to 1960s. An isolate of the measles virus from an infected patient was successively passaged through human kidney cells, human amnion cells, fertilized hen's eggs [4] and chick embryonic cells [5]. This attenuated virus, which was now replicative in chick embryonic cells, was no longer infective in humans and was used as the basis of the measles vaccine [6].

References
[1] Bull JJ. 2015. Evolutionary reversion of live viral vaccines: Can genetic engineering subdue it? Virus Evol 1(1):vev005
[2] Badget MR, Auer A, Carmichael LE, Parrish CR, Bull JJ. 2002. Evolutionary Dynamics of Viral Attenuation. J Virol 76(20):10524–10529
[3] Bazin H. 2003. A brief history of the prevention of infectious diseases by immunisations. Comp Immunol Microbiol Infect Dis 26(5-6):293-308
[4] Milovanovic MV, Enders JF, Mitus A. 1957. Cultivation of Measles Virus in Human Amnion Cells and in Developing Chick Embryo. Exp Biol Med  95(1):120-127
[5] Katz SL, Milovanovic MV, Enders JF. 1958. Propagation of Measles Virus in Cultures of Chick Embryo Cells. Exp Biol Med 97(1):23-29
[6] Enders JF, Katz SL, Milovanovic MV, Holloway A. 1960. Studies on an Attenuated Measles-Virus Vaccine — Development and Preparation of the Vaccine: Technics for Assay of Effects of Vaccination. N Engl J Med 263:153-159


What kind of insect is it? I found it hanging on the wall at night. It was approximately an inch long. Near my dormitory there is a lot of birch trees. The photo was taken in Prague, Czech Republic.

This is the heart and dart moth (Agrotis exclamationis). Its name refers to the special black spots, which have shape of dart and heart.

This moth is one of the most common in the Paleoarctic ecozone. It has a wingspan of 35-44 mm. The larva of this moth is brown above and grey below. It is capable of feeding itself on a variety of plants.


Would it be correct to say that viruses are genotoxic? I know it is an unconventional way to describe viruses, but would it still be technically correct?

From wiki

  In genetics, genotoxicity describes the property of chemical agents that damages the genetic information within a cell causing mutations

While some viruses tend to cause mutations, most don't have such a strong mutagenesis effect. As such, they are not really genotoxic. Also, even if a virus is genotoxic, one should definitely not reduce the activity of a virus to its genotoxicity. A virus has a life-cycle and is able to reproduce. It is clearly more than a simple genotoxic chemical agent such as metal chromium.

So, in short

Reducing viruses to their genotoxic effect would be a misrepretentation of what virsues are
Most viruses don't have a strong genotoxic effect and therefore you can not make the claim in the general sense.


What determines if a small protein / large peptide is immunogenic? I'm wondering if there is some threshold in size or a specific structural property that determines if a small protein or large peptide would cause an immune reaction.

Context: there are a number of drugs being developed based on antibody mimetics (small protein scaffolds with stable folding).  These tend to have a size around 50-60 aminoacids (6-7 kD).  These tend to be much easier to design than human / humanized antibodies.  However, it is not uncommon for these to cause anaphylaxis, especially if administered repeatedly.  It may be good to somehow design a version of a small antibody mimetic which itself does not cause an immune reaction.

Are peptides around 10-20 aminoacids typically immunogenic?  What about slightly larger ones up to 30 aminoacids?  Does it matter if they have a stable secondary or tertiary structure?

Edited to delete off-topic section:

Most (all?) proteins are ultimately immunogenic. You can't really design your way around immunogenicity, which is a good thing, because otherwise we'd all be dead from viruses.

Obviously not all proteins are equally immunogenic, but basically all protein therapeutics are immunogenic at some rate. One thing that seems positively associated with immunogenicity in that review is quaternary structure, but it's quantitative not qualitative.

Some of the commonly used synthetic antigens used in biochemistry such as HA C-terminus (24 residue) or FLAG (8 residue) are quite small.

More generally, this study finds that even 3-5 residue peptides can be sufficient to raise immune responses. So likely any polypeptide is potentially immunogenic.

Such small peptides are unlikely to have meaningful secondary/tertiary structure. My guess is that that you would have to have a pretty structurally strange protein to avoid any potential immune response. However if you had an insoluble or somehow sequestered protein you might be able to avoid it, but I'm not an expert so I can't say how.


What is the chance a given gene will end up in a given gamete? Let us say a germ cell had a desired allele. This germ cell was replicated during interphase so that it had two of the desired allele. It then underwent meiosis.
My question then is, what is the chance a given allele will end up in a given gamete that will be involved in conception?
Firstly, there is a 50% chance a chromosome will be assigned to a given daughter cell. This is because of independent assortment. In addition, cross over occurs at chiasmata. Lets assume then that there was a 50% chance that an allele will be crossed over (although this probability may be far from true)
The process during meiosis is that cross-over occurs first. We have two desired alleles, each on one of two pairs of chromatid attached to each other. There is 50% chance for a given allele to cross over. For example, the chance for both desired alleles to cross over is 1/4 (1/2 x 1/2), the chance only one will cross over is 2/4 (since either of the two desired alleles can cross over).
Then there is the first independent assortment during meiosis I which produces the desired daughter cell. In this case there is a 50% chance that a given chromatid pair (containing the desired allele) will be assigned to the desired daughter cell. However, in the case where a desired allele is found in both homologs (2/4 of a chance), then the chance that at least one desired allele will be in the daughter cell is 100%.
Finally, during meiosis II, another independent assortment occurs which produces the desired gamete. The same rule applies with a 50% chance a given allele will be assigned to a given cell (in this case the gamete). However, if the desired daughter cell contains two of the desired alleles, then there is a 100% chance that the cell will have the desired allele.
In conclusion, the chance I estimated that the gamete will have at least one desired allele is 50%. Although, I'm not sure if this is correct. Anyone mind confirming this.

A cell contains two haplotypes (or two set of all chromosomes). One haplotype inherited from the mother, one from the father. A haploid cell, resulting from meiosis, will receive either the maternal (or grandmother if you prefer) or paternal (or grandfather if you prefer) haplotype. It cannot receive anything else. Hence the probably must be 0.5 (or 50%).

Note that you are using the term "gene" incorrectly. You should use the term "allele" instead. And while you are improving your genetic vocabulary you should also check the term "locus". Also, the term "desired gene" is never used. We talk about "beneficial allele" or "detrimental allele".


Can you measure ECG from a single location? I want to make a DIY bracelet to measure my ECG. All I need is the interbeat interval.

Can I design a bracelet on one arm only, with two electrodes slightly spaced from one another, and figure out the beat from the conduction timing differences down the arm?

I am afraid you cannot build the classic ECG using only 1 hand.

Probably, you can measure HR - heart rate accordingly to pressure detection and similar sensors and from that you can simulate ECG by picture. Simulate I mean you cannot build any reliably ECG curve on the monitor, but can show some waves after every heart beat.


How does common cold START? When I searched for the causes of common cold, I found out that it's only cause is the spreading of virus and that it's a myth that you get cold when you get wet. If that is true then how does the virus start to spread if no one else is having cold? Or Simply, Can you get cold by yourself without the virus?

No, only virus or bacteria can cause you cold .Cold weather  causes increase in the spread of virus. Flu virus spread quickly in cold weather. Cold feet can slow down your immune system making you prone for virus attack.Means ,if you are wet you are susceptible to a viral  infection but the cause of cold then would be a virus not the cold weather itself.


Can the theory of natural selection distinguish between two correlated phenotypic traits? Consider the following two situations:

A species X has trait $T_1$ that is gradually selected for by some characteristic $E_1$ in some ecological niche but it turns out that the genes for $T_1$ also "turn on" genes for trait $T_2$ so that eventually species X with trait $T_1$ also have $T_2$. Then it turns out that $T_2$ is evolutionarily advantageous i.e it does help in increasing fitness because of some characteristic $E_2$ in that same ecological niche.
A species X has $T_1$ that is selected for by some characteristic $E_1$ in some ecological niche, this ecological niche also has characteristic $E_2$ that separately selects for $T_2$.

Both of these cases have as the end product $T_1$ and $T_2$ being advantageous for survival but in one case $T_2$ was selected for and in the other it's usefulness was accidental. What in the theory of natural selection distinguishes these two cases? To put things more bluntly, you are an evolutionary biologist and you are telling the standard story that corresponds to situation 2, how do you know (from the theory of natural selection) that we can discount situation 1?

I did a research project for my undergraduate research where I simulated mutations of cells in a petri dish and I know that mathematically these two cases can be disentangled because they lead to two different cluster size distributions with different scaling laws. As a physicist I know what to do but does a evolutionary biologist using theory of natural selection know what to do.

Update: The point is that in case 1 $E_1$ and $E_2$ could act at different times so that only $T_1$ is responsible for survival and $E_2$ while acting $T_2$ was completely useless for it's survival i.e other species disappeared not because they didn't have $T_2$ but because they didn't have $T_1$. Then a naive biologist could tell separate evolutionary stories assuming that $T_1$ and $T_2$ were selected for separately because when the biologist is observing the situation both $E_1$ and $E_2$ are present and $T_1$ and $T_2$ are present.  In other words, he or she would assume case 2 occured. In this case, random mutations and natural selection as told in science classes is completely useless because of $\textit{dynamics}$ in the environment and $\textit{correlations}$ that prevent mutations from being just random.

Why does this bother me? Well, because I hear evolutionary accounts that span hundreds of millions of years and it would seem simply applying the Darwinian story naively could make wrong predictions all over the place. I haven't seen people worry about this as they give evolutionary accounts for everything. From sexual behaviors to marketing.

Are biologists aware of the causation vs correlation problem or are they noobs in statistics?

Evolutionary biologists tend to be pretty good statisticians. For historical consideration, Pearson is the father of the concept of correlation and was a biostatistician and Fisher is (one of) the father of evolutionary genetics and is also a famous statistician (invented the Fisher's exact test, t.test and Anova). Many of the modern developments in modern statistics were brought about by geneticists (incl. developments in HMM, ABC, FDR, etc...).

So, yes we are aware of the causation vs correlation problem.

  In the theory of natural selection, can the two situations be disentangled especially when one is talking about evolutionary accounts that are on the order of hundreds of millions of years[?]

Just like in any other causation vs correlation problem, no it is not easy to disentangle the two. If the specific hypothesis put under testing is subject to experimental manipulation, then yes, it is often feasible to disentangle the two. Otherwise, in a purely observational study, one can logically reason and argue for one rather than another causality relationship but in essence, you cannot know in a purely observational study whether a correlation is representing a direct causation.

The follow-up question might then be

  Is experimental manipulation feasible in evolutionary biology?

The answer is yes. Not for all questions though.

First there are evolution experiments. An evolution experiment is just like what is sounds like. You put a population in a controlled environment and let it evolve. Repeat the process many time to have a decent sample size. There are also many question of interest to evolutionary biology that can be studied through experimental manipulation (and not only observatory studies) that do not require an evolution experiment.

You seem to be particularly interested in the reconstruction of past evolutionary history of a lineage (evolution biology is much more than a 'historic' reconstruction of life on earth), I would like to highlight that in purely observation studies and in experimental studies not involving evolution experiments, there are plenty of methods to reconstruct past events. Consider for example the loss of genetic diversity at linked variants (selective sweep) caused by positive selection. If two traits are correlated through time (which is very hard to figure out in absence of good fossil records) or correlated over several species (consider having a look at phylogenetic contrasts methods and more modern version of inference of selection over phylogenies), then if selection occurred in a single of the two traits, you should expect to see a differential loss of heterozygosity among the genetic markers explaining ariance for one trait and for the other.


What factors, other than its homochirality, make our "brand" of biology unique? If humans were to discover organisms on another planet, it is supposed that (unless both we and they were seeded by the same source) we would have nothing to fear from alien pathogens, as they would likely be totally incompatible with our "brand" of life here on Earth. This is due to a set of fundamental particulars not inherent in all possible biologies (as apposed to physics, where characteristics are more omni-present). I know, for example, that the left-handed chirality of amino acids marks one such trait. There appears to be no reason why life could not arise with the opposite orientation. My question is, what other particulars make up this set?

I think the opposite list---what features of life might be reasonably expected to be the same elsewhere---would be much shorter. Nearly every feature of life on earth as I can think of it is arbitrary in the particular molecules.

DNA. Why only 4 bases? Why the bases that we have (ACTG)? Researchers are able to create organisms with expanded DNA alphabets even here on earth (1). Even if you believe that some form of molecular mechanism of heredity is a requirement for life, there is no reason it need be DNA. And while there has been plenty of controversy about arsenic-based life here on Earth, I don't see why there couldn't be arsenic-based life elsewhere.
Ribosomes. Why a combination of RNA and protein? There is a lot in the overall architecture of ribosomes that is locked in due to historical/evolutionary contingency, not any necessary feature of life.
The Central Dogma. Biology as we know it has certainly made great use of the ability to make temporary copies of messages, but I don't see why life orbiting Alpha Centauri would have to have arrived at a similar solution.
Phospholipid membranes. You could make the argument that some degree of compartmentalization is necessary for life to occur (to reduce complexity and allow evolution via drift and small-number effects to generate change), but I don't think they need to be phospholipids. I can also imagine all life on another planet contained within viral-like particles with purely protein (or some other alien polymer) coats.
Genes. Depending on the level one is arguing I can see this going either way. If a gene is just a modular set of instructions for a limited number of components, then perhaps this will show up everywhere---life on our planet is surprisingly modular, and it is hard to imagine life on another planet being able to get by without some modularity (though of course it is possible in principle). But certainly nothing is inevitable about the details of gene organization into promoters, coding regions (why a 3-base code?), introns and exons (I'm still surprised these exist on our own planet), operons, etc.

I think you get the idea. In fact, it's really hard to envision any feature of life on earth that doesn't smack of contingency in some way or other. Astrobiologists have held on to water as an essential ingredient for life as we know it, but still, that's "as we know it."
I am really tempted to make some sweeping speculative statement about what features I might expect to be "inherent in all possible biologies" (a fascinating idea to think about), but that is way out of my depth. Right now I find it hard to come up with good candidates.
(1): Malyshev D et al. (2014). A semi-synthetic organism with an expanded genetic alphabet. Nature 509: 385-8.


Number of beneficial mutations cataloged? I can see from Wikipedia that there are possibly thousands of harmful mutations that have been cataloged and linked to disease. There are also unnumbered neutral mutations. But, does anyone know how many "beneficial" mutations have been cataloged in scientific literature?

That would be hard to say because really beneficial mutations become well distributed through the genome.  Basically the differences between us and chimpanzees are a catalog of all the beneficial (or completely neutral) mutations since the ~4.7 M years since we diverged from each other.

Separating them from changes which have no special effect would be difficult too, but more to the spirit of your question, its difficult to explain what many mutations do, unless they cause significant changes in something we can observe in the individual (like height, weight, big nasty claws, etc).

For some more specific examples you can look at Online Mendelian Inheritance in Man.  Some mutations which are useful sometimes might be related to skin color for instance (really helps when there is a lot of sun about) or lactose tolerance (a variation which is popular amongst europeans who have been drinking dairy milk for thousands of years).


Centrifuge after sonication I follow a protocol to get protein from E.coli cells after sonication.

I used to grow 6 litres of large cultures and add IPTG to express the protein. I centrifuge for 10 mins at 8,000 rpm and get the pellets.
Then I do sonication and centrifuge again at 20,000 for 1 hr.

My question is: can I do the last step of centrifugation at 4000 rpm for 2 hr? The centrifuge is no longer working at high speed (20,000rpm)

Thanks

No, if you use only centrifugation to separate proteins from other parts of the (bacterial) cell, you need very high centrifugal forces. The actual speed (in rpm) you need to separate soluble proteins from the rest of the cell is mostly dependent on the rotor of the centrifuge, because both together determine the acceleration you get, which should be
in the order of at least 10,000 - 100,000 g.

If you do not have a (working) ultracentrifuge available, you could try to precipitate your proteins from the lysate, which would allow you to use a normal centrifuge to collect it. However, this won't be an option if your protein can't be properly re-folded and you need it functional.


Is there more diversity in marine species? I was reading about how life emerged from oceans, and the following question occured to me. Do land species suffer from the founder effect and is there more (genetic) diversity in marine species? A quick google search pointed to the fact that a majority of species live on land. Is that a paradox?

I know that marine habitats have a higher phylogenetic diversity (see also Faith 2006) than terrestial habitats, even though they host far fewer species, which is a result of their deeper evolutionary history. Unfortunately, I cannot find a good reference to this claim right now (see http://biodiversity.europa.eu/topics/ecosystems-and-habitats/marine for some support though).

I wouldn't really call the difference in species numbers a paradox though, since speciation rates depend on habitat complexity and dispersal rates (which are generally higher in marine habitats). In either case, the knowledge of marine habitats and species living there are much poorer than for terrestial habitats, so differences in species numbers are highly tentative.


Is it possible to make anaerobic media too reducing? I've been struggling to grow an anaerobe (P. gingivalis), I take every precaution to keep the culture conditions free of oxygen, I was wondering if the conditions can be so reducing that they inhibit microbial growth of an obligate anaerobe.

To make the liquid media I do the following:

TSB supplemented with yeast extract
plus 0.5g/L L-cysteine HCl as a reducing agent
plus resazurin as a redox indicator
heat-sparge with nitrogen until the resazurin goes completely colourless
add hemin (5 mg/L) and vitamin K1 (1 mg/L) from stock solutions (1mL/L hemin in water, 200uL/L vit K1 in ethanol)
filter-inject this media into glass tubes which have had the gas in them removed (this takes place in an anaerobic hood)
all materials (syringes, needles, filters, tubes) had been left in the anaerobic hood before use so that no residual oxygen is left in/on them
swap the headspace for a gas mix of 80:10:10 N2:CO2:H2

I don't get any growth after over 72 hours @ 37oC.

Other protocols I have found are much more vague/lax about removing the oxygen, many just say that the cysteine should be added, and the media should be incubated in an anaerobic hood for 24 hours with the lid loose before being used. This got me thinking that maybe I'm removing too much of the oxygen.

What do you think?

I notice that you don't specify pH, which might be important.

I don't know if you can put in too much reducing agent (I suspect not), but a large excess is often required as the equilibrium constants for disulfide exchange reactions are typically close to unity (see Cleland, 1963).

I also don't know if any of following has any relevant to your problem (again, I suspect not), but I want to briefly comment on two aspects of using thiols to as reducing agents in general.

Firstly, the oxidized (disulfide) form of thiols may react with a protein sulfhydryl. Using β-mercaptoethanol as an example (Scopes, 1993, p 320), something like the following may occur, where the reducing agent becomes (reversibly) bound to protein. If the reactive sulfhydryl is at an enzyme active site, this may lead to inactivation.

$$\ce{2 HSCH2-CH2OH  +  O2 -> HOCH2CH2-S-S-CH2CH2OH + H2O2\tag{1}}$$

$$\ce{HOCH2CH2-S-S-CH2CH2OH + HS-{Protein} <=>HSCH2-CH2OH + HOCH2CH2-S-S-{Protein}  \tag{2}}$$

As stated, equilibrium constants for thiol exchange reactions are often close to unity (Cleland, 1963).,
 $$\ce{R1-S-S-R2 + R3-SH <=> R1-S-S-R3 + R2-SH \tag{3}}$$
  For this reason, many protein chemists prefer to use dithiol analogs of threitol (dithiothreitol, DTT, or Cleland's reagent) or erythritol as reducing agent, as the oxidized form of these compounds are cyclic disulfides, where the equilibrium constant is displaced to the right  (see Cleland, 1963).

There is also the question of stability.

The half-life of thiols in solution are markedly pH and temperature dependent, as the  table below shows. The half-life of β-mercaptoethanol at pH 6.5 and 20℃ is greater than 100 hours, but at pH 8.5  and 20℃ it is only 4 hours.

The above table was taken from  Stevens, R, Stevens, L & Price, N.C (1983) The stabilities of various thiol compounds used in protein purifications, published in (the now-defunct) Biochemical Education. The full article is freely available as a pdf from the Wiley website


Should I consider one or two DNA chains to find how many nucleotides are in a gene? I am trying to solve an exercise.

How many nucleotides does a gene contain if information about 287 amino acids is encoded in it? What is the molecular mass and length of this gene?

AFAIK, I have to consider two DNA chains to find molecular mass, and one DNA chain to find the length of the gene (am I right here?).
But I am stuck trying to find how many nucleotides are there in a gene. Should I consider both or only one DNA chain? I suppose that both (as for the molecular mass of the gene) but I am not totally sure.

Counting both strands is admirably correct, but most people will multiply the number of amino acids by three, not six.  For example, nucleotide positions in a reference sequence will increase by 3 for each amino acid in the presumptive coding sequence.  Besides, if you want to be that pedantic, you should say zero, since the DNA contains nucleotide residues, not individual nucleotides, as they have undergone dehydration synthesis.  I think in biology the right answer will almost never be marked correct by a machine. :)
The answer you come up with will also be influenced by whether you would like to include a stop codon (+3) to avoid nonsense-mediated degradation, and a transcriptional start site and polyadenylation sequence (in eukaryotes).  The ''gene'' itself, in the genetic sense, will include enhancer elements over a much longer region of the chromosome and regulatory 3'-untranslated regions.  And then there's alternative splicing to consider...


Hydrophobic interactions in the helix-turn-helix This slide states that the second helix works to stablize the configuration of the two helixes via hydrophobic interactions. What exactly is this hydrophobic interaction? In other words, what molecular interaction does the second helix have with the recognition helix?

To quote Sir Max Perutz, in general, the insides of proteins tend to be "waxy", while the outsides of soluble proteins tend to be "soapy."  Those two alpha helices are interacting in a space that is energetically unfavourable for a polar solvent, like water.  Since the outside of the DNA double helix tends to be highly charged, and the edges of the stacked base pairs also have H-bond acceptors and donors, the portion of the alpha helix that interacts with the DNA sequence, will also contain charged amino acid side chains.

In contrast, the portion of the alpha helix that faces inwards, towards the interior of the protein, will have largely non-polar side chains.


Why is iodine used for metabolic hormones? Iodine and related biological iodine-carrying hormones are phylogenetically very old, at least according to Wikipedia. Humans use iodine as a metabolic indicator, as do axolotls and apparently most multicellular life.

So why? Growth hormones, sex hormones, et cetera don't require strange heavy elements not used for anything else. It's not a requirement of transcription factors that they contain iodine.

All I've got for hints is that selenium forms an essential part of deiodinases, as well as forming an essential part of thioredoxin reductase. Thioredoxin is a component used to reduce things around the cell, like thiols and RNA bits and so on and so forth, which I could see being worth the evolutionary cost of running down some selenium.

What's the point of iodine? People have iodine deficiency 'all the time' (it's common enough to be named). Is that a product of agriculture somehow? Are there any advantages to using iodine for metabolic hormones? If there are, what are they?

Classical thyroid hormones implement a very flexible signaling mechanism. Basically, they comprise two aromatic rings that are connected via an oxygen atom. Optionally, they may contain organic side chains and inorganic iodine atoms.

In the case of iodothyronines, which are represented e.g. by the well-known thyroid hormones T4, T3 and 3,5-T2, the side chain contains an amino group and a carboxylate group. Therefore, iodothyronines are amino acids. Up to four different hydrogen atoms (two at every ring) may be replaced by iodine atoms, and the resulting pattern of iodination determines their biological activity. Generally, iodination of the inner ring and deiodination of the outer ring results in high biological activity (e.g. in T3 and 3,5-T2), whereas iodination of the outer ring and deiodination of the inner ring delivers a receptor-blocking thyroid hormone (e.g. reverse-T3). There are three deiodinases encoded by the DIO1, DIO2 and DIO3 genes that catalyze the "step-up" and "step-down" reactions to active or inactive thyroid hormones, respectively. Multiple molecular processes are able to differentially upregulate and downregulate tissue deiodinases. Therefore, thyroid hormones are subject to both global and local control.

Removal of the amino group results in iodothyroacetates. Their biological effects are similar to those of iodothyronines, but in addition to nuclear receptors they also have a strong effect on membrane-bound receptors, which are only weakly activated by iodothyronines.

Thyronamines lack the carboxylate group. Their biological effect is different to that of iodothyronines and iodothyroacetates. By activating the membrane-bound TAAR1 receptor they have an effect that is in most respects antagonistic to that of classical thyroid hormones. Thyronamines seem to be most active in deiodinated state.

Summarizing, both organic and anorganic modifications are able to modulate the effect of thyroid hormones. This mechanism is a very effective way to encode a high  grade of information entropy in rather small molecules.

References

Gereben B, Zavacki AM, Ribich S, Kim BW, Huang SA, Simonides WS, Zeöld A, Bianco AC. Cellular and molecular basis of deiodinase-regulated thyroid hormone signaling. Endocr Rev. 2008 Dec;29(7):898-938. doi: 10.1210/er.2008-0019. PMID: 18815314

Engler D, Burger AG. The deiodination of the iodothyronines and of their derivatives in man. Endocr Rev. 1984 Spring;5(2):151-84. PMID 6376077.

Piehl S, Hoefig CS, Scanlan TS, Köhrle J. Thyronamines--past, present, and future. Endocr Rev. 2011 Feb;32(1):64-80. doi: 10.1210/er.2009-0040. PMID 20880963.


Will eukaryotic RNA fold in the same way in prokaryotes? As far as I know, there are no specific eukaryotic or prokaryotic factors that aid in RNA folding other than cellular environment (salt and ion concentrations, dissolved molecules, etc). Are there any factors to consider when introducing eukaryotic RNA in prokaryotes? Is it possible to predict the proper shape and folding upon introduction to a prokaryotic cell?

As you have mentioned ions and temperature affect RNA structure. There are also different types of RNA structures and their dependence on ions are different. Mg2+, as Mad Scientist mentioned, stabilizes duplexes; so do monovalent cations like K+ and Na+. However, Mg2+ favors duplex over quadruplex if the same RNA can adopt both these conformations.
Dependence on temperature is a trivial case.

Ions and temperature should be more or less same for prokaryotes and eukaryotes unless we are talking about extremophiles.

Apart from these factors I can think of two other factors that can cause difference in RNA structure between prokaryotes and eukaryotes:

Osmolytes
RNA binding proteins/chaperones (Already mentioned in comments by Mad Scientist)

Osmolytes

It has been shown that TMAO (Trimethylamine N-oxide) stabilizes RNA secondary structures. The metabolism of TMAO is different in prokaryotes and eukaryotes.

From this paper:

  Although eukaryototes can endogenously produce L-carnitine, only
  prokaryotic organisms can catabolize L-carnitine11. A role for
  intestinal microbiota in TMAO production from dietary carnitine was
  first suggested by studies in rats; moreover, while TMAO production
  from alternative dietary trimethylamines has been suggested in humans,
  a role for microbiota in production of TMAO from dietary L-carnitine
  in humans had not yet been demonstrated30-32. The present studies
  reveal an obligatory role of gut microbiota in the production of TMAO
  from ingested L-carnitine in humans (Fig. 6c)

I cannot ascertain that this will affect RNA folding but is possible.

RBP

This is something that you can be certain about. Some RNAs require protein counterparts to adopt a functionally capable structure. In the absence of the protein they may not form the relevant structure. So if an RNA needs Hfq then you have to express it in the eukaryotic system where you want to use the RNA (and converse).


Which sex is homogametic in side-blotched lizards? I'm just trying to find out whether the male side-blotched lizard is the hetero- or homogametic sex in side-blotched lizards (Uta stansburiana) - some reptiles are ZW system (female heterogamete) and some are XY (male heterogamete).

Lizards of the genus Uta are apparently male heterogametic (XY) (Pennock et al. 1969). The XY system seems to be the most common mode of sex determination in iguanid lizards (Kasahara et al. 1983).

Kasahara, Y et al. 1983. Chromosome mechanisms of sex determination, G- and C-band patterns and nucleolus organizer regions in Tropidurus torquatus (Sauria, Iguanidae).  Genetica 60: 151-156.
Pennock, L.A. et al. 1969. Minute Y chromosome in the lizard genus Uta (Family Iguanidae). Cytogenetics and Genome Research 8: 9-19.


Recessive alleles at Hardy-Weinberg equilibrium I've run into a question that I disagree with others on but I would like to receive the input of others. The question is:

If a population is at Hardy-Weinberg equilibrium, which of the following can be predicted for the recessive alleles in the population? 1) They will eventually disappear, 2) They will be selected against, 3) They will be maintained at the same frequency, 4) They will be expressed in the heterozygous condition, and 5) They will become dominant.

Some people said that the answer to this question was that the recessive alleles would be selected against, but I interpreted the question as having the answer that the allele frequency of the recessive alleles would not change and instead would be maintained at the same frequency.

My rationale for this was that Hardy-Weinberg equilibrium means there is random mating and basically no radical shifts in allele frequencies from outside sources, such as gene flow, natural selection, etc. I would think that the allele frequency would not change, but I may be incorrect.

Is my methodology correct?

Let's go through the possible answers. Which of the following could be predicted? Not (1), because we don't know whether selection favors or disfavors the recessive alleles. Not (2) for the same reason. Not (4) by definition. Not (5) because recessive alleles don't magically become dominant.

This leaves us with (3), which also seems correct: not only do we know that frequencies don't change under the Hardy-Weinberg assumptions, but also an equilibrium is by definition a state at which frequencies remain the same.

An aside: this question fairly clearly recalls G. Udny Yule's confusion about the fate of recessive alleles, which lead Punnett to enlist G. H. Hardy's help in deriving Hardy-Weinberg equilibrium. Yule expected recessive alleles to decline in frequency by virtue of their recessiveness; Hardy showed otherwise.


Which was the last significant event in human evolution? What's next? At 10.000 BC (12 ka), we became the last of the Homo species on Earth. In evolutionary terms this is a very little time range to something happen, but I'm wondering anyway, in this meantime which are the most significant changes in our species? Were there any?

Also, I've heard something about how our body hair and nails will be gone 'soon', there's any estimation of when such a thing could happen?!

Background

I'd like to start by saying that phenotypic (loosely speaking phenotypic mean morphological) traits evolve because their variance in the population is correlated with some genetic variance. If most of the phenotypic variance is genetically coded, you'd expect that the trait will change through if different variant of the trait influence fitness (which is a function of both survival and reproductive success). Stated differently and more accurately the change in mean value of a given trait $R$ in the population is given by:

$$R=S\frac{V_{Ga}}{V_{P}} = S\frac{V_{Ga}}{V_{G}+V_{E}} =  S\frac{V_{Ga}}{V_{Ga} + V_{Gd}+V_{E}} $$

, where $S$ is the selection differential, $V_{G} = V_{Ga}+ V_{Gd}$ is the genetic variance where its two components are the additive and dominance genetic variance respectively. $V_P  = V_G + V_E$ is the phenotypic variance which two components are the genetic and environmental variances. The ratio $\frac{V_{Ga}}{V_{P}}$ has a name; it is called the heritability in the narrow sense symbolized by $h_N$ Note: I present here a simplified version of the reality!

So, if the trait you consider has genetic variance in the population and that this trait influence the fitness with a given selection differential you can provide estimates of how the trait will change through time in the human population. Now if the variance does not already exist in the population but you have to wait for mutations to occur, then you cannot really provide an estimate of when will this occur.

Discussion on the future evolution of nail size

Also, when you think about some traits such as our nails. You may consider that they are of no use but do you really think that those people that have no nail would really have a better fitness. At first I would tend to think that I would rather chose a partner that have nails, it is much more sexy! If many people are like me and appreciate nails, nailless people will have difficulties to reproduce or in other words, they will have a lower fitness that nailed people.

I don't think we have data on what loci (positions on the chromosomes) influence the size of the nails and about how much of the variance in nail size is explained by the genetic additive variance. And how do the size of our nails influence fitness. So we don't know about how this trait will evolve through time.

Future evolution of other traits

There are several traits that we can/could more or less predict their evolution. Those are the traits for which we know the ratio of the genetic additive variance over the phenotypic variance and how it influences fitness. I can think of genes that are linked with resistance to new diseases such as HIV for example. If malaria comes to a new area you might expect the allele (=variant of a gene) allowing a better resistance to malaria will increase in frequency (note that this allele is advantageous in heterozyotes (protects from malaria) but it is highly disadvantegous in homozygote because it causes sickle-cel disease). We could estimate the change in frequency of alleles linked with obesity in some countries also. Probably several studies exist on the subject but I don't know them. One might improve this answer by giving some information about how HIV resistant variants is likely to change in frequency through time.

What were the last evolutionary changes in human history?

You can think of the impressive frequency of the Tay-Sachs disease in french canadian due to a bottleneck effect. Or you may think of the evolution of height, about the evolution of the shape of the skull or the evolution of feet. You can think of the reduction of our gut. etc… Your question is not well enough define so that we know if you consider the raise in frequency of Tay-Sachs disease is sufficient for you to be called a significant evolution.

Hope that helps!


Human Demography - Where can I find this statistic? In "An Introduction to Genetics" by David J. Merrell, copyright 1975 by W.W. Norton + Co., p. 742, in the Chapter "Genetic Counseling and Eugenics," the author states: "... 50% of the women produce 85% of all children born in the United States."

The author provides an Additional Reading list, but I'm not a geneticist, nor do I have access to much of the listed material.  With that in mind, 1) where can one find the statistic mentioned above? and  2) has this number changed over time?

OP EDIT: In response to comment (a few examples from Reading List of 30 items):

Davis, 1970, Prospects for Genetic Intervention in Man, Science, 170 279-1283

Dubos,1965,  Man Adapting, Yale Univ. Press

Dunn, 1962, Cross Currents in the History of Human Genetics, Amer. J. Human Genet, 14: 1-13

Ehrlich, 1968, The Population Bomb, Ballantine NY

...

Lynch, 1969, Dynamic Genetic Counseling for Clinicians, C. C. Thomas, Springfield, Mass.

...

Petersen, 1969, Population, 2nd Ed. Macmillan

...

1969, WHO Expert Comm. on Human Genetics, "Genetic Counselling(sic), Tech Rept 416, pp. 1-23

I know I can find stats like average ages, etc from the Statistical Abstract of the United States, but where do geneticists find items like the one cited in the Merrell book?

The CDC has some good stuff. http://www.cdc.gov/nchs/data/nhsr/nhsr051.pdf

But keep in mind that number from your book is likely based on yearly findings in which more than half the women would not be able to have children due to age, voluntary contraception, or other conditions. So it is not reflecting how many children they have over their lifetime. Even in the CDC study more than half the women had no children but few had no plans to have children, couples are moving their first pregnancy to later and later in life, which is going to make it look like few are having children at all on first glance.
 And it's probably not accounting for death rates, the poorest people tend to have the most children but they also have the fewest number live to maturity, which is why they tend to have more (not necessarily consciously mind you) .


Buy bacteria for experiment? Where can I buy paracoccus denitrificans? I need it for an experiment. I cannot find online where I can purchase this.

ATCC- you can get most bacterial strains and cell lines there.

Find P. denitrificans here:

www.atcc.org/products/all/13543.aspx